ENDOSULFAN
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- ENDOSULFAN
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Pesticides May Hann Brain, Study Says
Pesticides May Harm Brain, Study Says: Health: Fetuses and young children in farm
areas are at highest risk, research suggests, with intelligence, motor skills and personalities
affected. By MARLA CONE, Times Environmental Writer.
Children exposed to pesticides in the womb or at an early age may suffer permanent brain
defects that could change their
bj altering
behavior and their ability to do
everything from drawing a picture to catching a ball, according to new scientific research.
Widely used pest-killing chemicals, in amounts routinely found in the environment in farm
areas, seem to be capable of skewing thyroid hormones, which control how the brain of a
fetus or young child develops, according to a study published today.
Scientists say the study and other recent research support an emerging theory that
pesticides may exact a toll on the intelligence, motor skills and personalities of infants,
toddlers and preschoolers.
"Data suggest that we may be raising a generation of children with learning disabilities
and hyper-aggression," said Wayne Porter, a University of Wisconsin professor of zoology
and environmental toxicology.
\
Porter’s study, published today in the journal Toxicology and Industrial Health, shows
that a common mix of insecticide, herbicide and fertilizer found in drinking water altered the *
thyroid hormones of young mice. It also changed their aggressiveness-measured by attacks
on other mice-and suppressed their immune systems.
Although a study of mice alone is not overly compelling, the theory is bolstered by recent
research on human beings.
In tests in the state of Sonora, Mexico, scientists found striking differences in hand-eye
coordination and other mental and physical skills when comparing Yaqui Indian preschoolers
in an agrarian region with those in adjacent foothills where no pesticides are used.
Four- and 5-year-olds living in the farm valley had trouble performing a variety of simple
motor skills-drawing stick figures, catching a 12-inch ball from almost four yards away and
a tennis ball from more than a yard away, and dropping raisins into a bottle cap from a
distance of six inches.
They also had poorer memory skills and stamina, were more prone to physical
aggression and angry outbursts, and were less sociable and creative while playing.
Farm and household pest-killers are widely used there, and high levels of multiple pesticides
have been found in the cord blood of newborns and the breast milk of mothers in the area.
Another study, in rural western Minnesota, found increased birth defects in children
conceived during the spring growing season.
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Most of the new research detects problems in agricultural communities—places found not
just in rural regions but also in more urbanized areas, including Southern California. No one
knows yet what it might mean for people who consume small traces of the chemicals in their
food. Earlier this month. Consumers Union reported that many fruits and vegetables contain
concentrations of pesticides that may be unhealthful fbr chi’dren
The new hormone studies add to a growing body of research from around the world
suggesting that dozens of commonly used pesticides and other chemicals mimic the
hormones that control sexual and neurological development.
Called endocrine disruption, this is arguably the most controversial environmental issue of
the past decade.
From alligators in Florida to polar bears in the Arctic, wild animals in pollution hot spots
have been feminized by hormone-disrupting chemicals that imitate estrogen or block
testosterone, scientists say.
But the impact on human beings—who generally are exposed to much lower levels of
pollution—is more controversial and uncertain.
In addition to the possible neurological effects, some researchers theorize that the
hormone disrupters could be reducing men's sperm counts or increasing diseases of the
reproductive system.
Pesticide company representatives—and some toxicologists and other scientists—remain
skeptical that commonly found levels of pesticides can alter human thyroid and sex
hormones.
’’I’m kind of dubious that low-level exposures to chemicals are raising all kinds of havoc
with the endocrine system," said John McCarthy, vice president of a group representing
pesticide manufacturers, the American Crop Protection Assn. "The human system has so
many protective mechanisms, and our bodies are bombarded with all kinds of things."
*
Still, he said, the industry is highly concerned about the findings suggesting neurological
damage, and would like to see a comprehensive review to evaluate all existing studies and
figure out what they collectively, show.
"Wc ought to be taking a very hard look at it," McCarthy said. "There's almost a study a
week of one type or another, and it's hard to see how it all fits together. We have to take
some time to say, 'OK, what does this all mean? Is this something that should require some
abrupt change [in pesticides] or fine-tuning or more research?'"
No one knows how many pesticides out of 77,000 used in the United States might alter
sex or thyroid hormones.
The U.S. Environmental Protection Agency requires tests that screen pesticides for
cancer and birth defects—but not for hormone effects. A committee last year devised new
testing requirements — supported by the pesticide industry—that are expected to take effect
in 2001.
It has long been suspected that various environmental pollutants can damage brain
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Pesticides May 1 larm Brain, Study Says
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development. Industrial compounds called PCBs have been linked to learning disabilities in
children of women who ate contaminated Great Lakes fish.
The link to pesticides is far from definitive, however, and big gaps in knowledge remain.
Questions abound: How do the contaminants disrupt thyroid levels? What does that
physically do to the brain? What dose of exposure does it take? Does the human body have
some defense mechanism to fend off low levels of hormones? What do mixes of various
man-made and natural hormones do to people?
Some scientists suspect that the damage is passed from a mother to her unborn child early
in the first trimester, before most women even know they arc pregnant.
Thyroid hormones guide the nerve cells that dictate how the brain of a fetus develops and
the number of brain cells created. One theory is that if a mother receives a dose of pesticides
during this critical phase, it can interfere with her thyroid levels—sometimes raising them,
sometimes lowering them—irreversibly altering the child's nervous system.
How the child's brain circuitry develops determines his or her hand-eye coordination,
motor skills and learning ability.
Thyroid hormones also can change behavior—an excess can make people quick to anger,
while a low count could have the opposite effect. The hortnones also can alter steroids that
control aggression and immune systems.
"Thyroid hormones are important to brain development, and that's been known for a long
time," said Dr. Harley Kornblum, a pediatric neurologist at the UCLA Medical Center. But,
he and other neurologists say, it's debatable how important the mother's thyroid level is to
the fetus, and it's even more uncertain what role environmental contaminants may play.
Porter said children up to age 8 who have developing brains and immune systems are
"especially vulnerable" to changes in thyroid hormones.
*
Some symptoms of children exposed to pesticides are similar to attention deficit
hyperactivity disorders, which have been increasingly diagnosed in American children. Some
medical research supports a link between thyroid hormones and those disorders, but the
connection, especially with pesticides, remains unclear.
The implication for adults, and whether pesticides might cause thyroid disorders, also is
unknown.
In the study of 50 Mexican children, the scientists, led by anthropologist Elizabeth
Guillette of the University of Arizona, said genetic and social factors—including income,
education and health services-are so similar between the farm valley and the foothills that
they cannot explain the differences in the youngsters' cognitive ability.
"These children share similar genetic background, diets, water mineral contents, cultural
patterns and social behaviors. The major difference was their exposure to pesticides,"
Guillette and Mexican researchers said in a report published in June in the journal
Environmental Health Perspectives.
Most of the stick-figure drawings by the 4- and 5-year-olds in the farm valley were
unrecognizable as human beings—they look like the scribbles of a 2-year-old. In contrast,
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Pesticides May I larm Brain. Study Says
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drawings by the foothill children had heads, eyes, torsos, arms and legs.
Experts say that the inability to draw a person indicates a breakdown between the brain's
ability to process visual information and its ability to control fine muscles.
"Some valley mothers stressed their own frustration in trying Io teach their child how to
draw. In addition, two valley children drew pictures composed of boxes, arches and lines,
claiming these pictures were people," the researchers reported.
Other tests pointed to recollection and stamina problems. One foothill child could jump
for 336 seconds--over three times longer than the best-performing valley child.
Some scientists remain dubious of the results because the tests on the children were
unusual, and are intrinsically subjective and difficult to interpret.
Dr. Richard Jackson, director of the National Center for Environmental Health at the
federal Centers for Disease Control and Prevention, said his staff was "unimpressed by the
scientific rigor" of the work in the report.
McCarthy said that although the differences between the two populations of children
seem striking, other hidden factors, rather than pesticide exposure, cannot be ruled out.
Other studies, meanwhile, show that pesticide exposure during the first trimester of
pregnancy increases birth defects.
The University of Minnesota and the federal EPA in a 1996 study found a high rate of
birth defects in the children of Minnesotans who work as pesticide appliers as well as the
general population of western Minnesota, a major farm region with heavy pesticide use.
The defect rate was the highest among babies bom nine months after the spring season,
indicating that the risk rises for children conceived during the time when pesticide use
increases.
In Porter's 5-year study of mice, the animals drank water containing a mixture of two
pesticides-aldicarb and atrazine-and nitrates from fertilizer.
The concentrations ingested by the mice were similar to those found in ground w’ater in
many agricultural areas. Porter said. Aldicarb, atrazine and nitrates are the three most
abundant agricultural contaminants in the United States, although they do not rank high in
use in California.
While the mix of the three chemicals altered the mice hormones, each one alone did not.
That points out a gaping hole in the federal effort to protect consumers—the EPA only tests
for effects of pesticides individually, not cumulatively.
The EPA tests. Porter said, "generate a great deal of false confidence in the safety" of
pesticides.
* * #
Drawing an Unsettling Picture
Scientists say children may suffer permanent brain defects from pesticide exposure. In
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Pesticides May I farm Brain, Study Says
Sonora, Mexico, a study found that Yaqui Indian prescnoolers in a farming region exhibited
poor motor skills compared with their counterparts in adjacent foothills where no pesticides
are used. When asked to draw a person, the farm valley's 4-and 5-year-olds mostly drew
meaningless circles and lines. See Results
Source: Environmental Health Perspectives, June 1998.
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F Journal of Environmental Management (2001) 62, 155-169
doi:10.10()6/jema.2001.0428, available online at htlp://www.idealibrary .com on int^r
md
Pin . 695003
I3 •
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t Degradation of endosulfan in a clay soil
I from cotton farms of western
|j Queensland
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H. Ghadiri* and C. W. Rose
The persistence and degradation of endosulfan isomers and their primary degradation product, endosulfansulfate, were studied in a clay soil from cotton farms of western Queensland. Endosulfan degradation in •
k relation to soil moisture, temperature, day and night temperature fluctuation, waterlogging and re-application
f were, studied. The results show that the degradation rates of both endosulfan isomers were greatly affected
K
by changes in soil water content and temperature. Under a high water content-high temperature regime
the concentration of a-endosulfan in the soil fell rapidly during the first 4 weeks of application, followed
p
by a prolonged period of slower rate of degradation. Alpha endosulfan showed a bi-exponenti'al form of
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degradation for al
all! wa
water
content-temperature
!er, content
~temPerature experiments except for extremes in both these two factors.
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In the submerged soils (and also in low-water content, low temperature, hon-submerged experiments) no
such
degradation
of a-endosulfan was observed, and a single first-order rate equation describes
s^c^rapid
aPld^initial
nitialy
eSradact'Pn ofa-endosulfan
the data. Degradation of p-endosulfan was significantly slower than for the a-isomer under all conditions
studied. A half-life of more than a year was recorded for the fi-isomer when both water content and
temperature were low. The degradation of ^-endosulfan showed no sign of the bi-exponential function
observed for a-isomer, and a single first order rate equation described "the
the data obtained fo^each
for each factor
studied. Endosulfan-sulfate was the major degradation product in all non-submerged experiments. Its build
up in the soil very closely followed the disappearance of a-endosulfan. Its highest build-up was in the high
■R of content-low
temperature
experiments^
but■ its
persistence was primarilylnfluencedQbysoil
temperature.
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Both a and fi-isomers, and endosulfan sulfate, persisted longer in the submerged soil. Re-application of
endosulfan, and day and night fluctuation of temperature had contrasting effects on the degradation of the
two isomers. Both factors slowed down the degradation of a-endosulfan and enhanced that of p-endosulfan
but their net effect was to prolong the overall persistence of this chemical in the soil. Submerged conditions
reduced the net formation of endosulfan-sulfate and enhanced its degradation rate.
© 2001 Academic Press
Keywords: endosulfan pesticide, a-endosulfan, ^-endosulfan, persistence, degradation, halflife, attenuation, Thiodan.
Introduction
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Most pesticides used in agriculture have the
potential to affect non-target organisms and
to contaminate water resources. Endosulfan,
also known as Thiodan, is one such pesticide which is widely in use in many parts
of the world in large quantities. Amongst 40
different insecticides, herbicides, conditioners and defoliants applied to cotton farms in
Australia, endosulfan is the most commonly
used (Barrett et al., 1991). It has been in use
Email address of corresponding author: H.Ghadiri@mail
box.gu.edu.au.
0301-4797/01/060155+15 $35.00/0
for more than 3 decades, being first intro
duced as a replacement for the highly per
sistent DDT. Compared to aldrin, dieldrin
and DDT, which are now banned in agri
culture, endosulfan is commonly assumed to
be safer for the environment since it is less
persistent and does not bioaccumulate to the
same extent as its predecessors dieldrin and
DDT. However despite its rapid degradation
in water, it can persist for a relatively long
period of time when bound to soil particles,
which can be a source of delayed contamina
tion, especially in bottom sediments of rivers
and other surface water bodies. In its water
soluble form it is extremely toxic to fish and
id
.....
‘Corresponding author
Faculty of Environmental
Sciences, Griffith
University, Brisbane, 4111,
Queensland, Australia
Received 19 May 1999;
accepted 22 January 2001
© 2001 Academic Press
156
JI
1:
H. Ghadiri and 0. W. Rose
other biota (Gobble et al., 1982; Karin, 1997).
Recent appearance of endosulfan in meat of
Australian beef cattle fed on cotton residues
adds some urgency to a better understanding
of the fate of this chemical in the soil-waterplant system.
Endosulfan has been shown to degrade
rapidly in water bodies with a half-life of
less than a week (Cotham and Biddleman,
1989; Barrett et al., 1991; Peterson and Batley, 1991a,b; Kaur et al., 1998). Although
it has been appreciated that the half-life of
sediment-bound endosulfan could be much
higher than that of aqueous forms (Cotham
and Biddleman, 1989; Ghadiri and Rose,
1994; Kennedy et al., 1994), not much work
has been done on the degradation and per
sistence of soil sorbed forms of this pesti
cide. With its water solubility of less than
0-3 mg I-1, a large proportion of applied
endosulfan is expected to become sorbed to
soil particles, thus providing a source of
contamination long after its time of appli
cation.
Like other sorbed chemicals in the soil,
endosulfan degradation under field condi
tion is often dominated by aerobic degra
dation. However once a pesticide has been
carried off the field and into water bodies,
anaerobic degradation becomes the domi
nant process, the condition which exists in
the bottom sediment of lakes and streams.
Studies of anaerobic degradation of endosul
fan are very limited (Cotham and Biddle
man, 1989; Guerin, 1999). The mechanism of
anaerobic loss of endosulfan, and the relative
significance of anaerobic to aerobic degra
dation of this pesticide and its metabolite
under different soil and environmental con
ditions is not yet fully understood (Guerin,
1999).
Many researchers have demonstrated that
the parameters such as soil moisture and
temperature, which are highly variable under
field conditions, as well as soil pH, organic
matter content and the rate and time of
pesticide application have major impacts
on the degradation rate of most pesticides
in soil including endosulfan (Walker, 1978;
Kennedy et al., 1998). Kaur et al. (1998) stud
ied the effect of temperature and pH on the
degradation of endosulfan in water and soil
and found these factors to significantly affect
the half-lives of both a and P-endosulfan.
More work is, however, required to deter
mine the effect of each of these factors on
the persistence and degradation of endosul
fan isomers in order to be able to predict,
with some degree of certainty, the fate and
behavior of this chemical in the environment.
The aim of this research work was to inves
tigate the degradation of endosulfan and
its metabolites in the cotton farm soils of
Emerald, Queensland, Australia, under dif
ferent environmental conditions. The effects
of such factors as soil moisture content, soil
temperature, waterlogging, day and night
temperature fluctuation, and pesticide reapplication on the degradation of endosulfan
isomers and their primary degradation prod
uct, endosulfan-sulfate, were investigated in
growth chambers under controlled condi
tions. This paper reports on the results of
this investigation.
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Materials and methods
The soil
The soil used in these experiments was from
Emerald’s irrigated cotton farms in west
ern Queensland. The soil was classified as
a brown cracking clay soil, with a pH value
of 8 and a clay content of approximately 70%
(Simpson et al., 1998). The soil was collected
from the field prior to the firsts application
of pre-planting pesticide, and contained no
detectable amount of endosulfan residue from
previous years.
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The pesticide
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Endosulfan
[l,4,5,6,7,7-hexachloro-8,9,10trinorborn-5-en-2,3-ylene)(dimethyl sulphite)
6,7,8,9,10,10-hexachloro-l,5,5a,6,9,9a-hexachloro-6,9-methano-2,4,3-benzodioxathiepin
3-oxide(I)] of 96% purity was supplied by
PolyScience Corp. Endosulfan consists of
two stereoisomers, a and 0-endosulfan, in
an approximate ratio of 70:30. Alpha endo
sulfan is somewhat more volatile and less
wnter soluble than 0-endosulfan. The solubil
ities in water at 22°C of a and 0-endosulfan
have been reported by Worthing (1983) to
be 0-32 mg I-1 and 0-33 mg I-1, respectively.
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Degradation of endosulfan in soils
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Beta endosulfan is hydrolysed faster than
a-endosulfan, and the rate for both isomers
increases with pH. Hydrolysis seems to be
the main initial process in degradation of
both isomers. Half-life in water of various
forms of endosulfan is reported to be 3-7 days
(Worthing, 1983).
The experiments
I
Endosulfan was applied to the soil at a level
comparable to the application rate in the
field (5 ppm). The treated soil was thoroughly
!<
mixed and put into a series of one liter sealed
jars. The jars were kept in growth cham
bers set at the required temperature levels.
Six sets of experiments were carried out on
this
soil, each replicated at least three times,
i:
using four growth cabinets set at 20, 30
and 40°C, and one at a variable day and
night temperature of 35°C (day) and 20°C
(night). In the first two experiments the effect
of soil water content on the degradation of
a and p-endosulfan and their major toxic
degradation product, endosulfan sulfate, was
investigated at three incubation tempera
tures of 20, 30 and 40°C. The gravimetric
water content levels used in these experi
ments were 15, 25, 37 and 45%. Degradation
under submerged condition was also studied
in a similar manner to non-submerged soils,
and at the same three incubation tempera
tures mentioned earlier.
All experiments were run for up to
4 months. About 15 g of the wet soil was
removed from each jar every fortnight from
which two wet sub-samples with equiva
*
lent dry weight of about 3 g were taken.
J The first sub-sample was used for pesticide
a extraction and the second for water con
tent monitoring and the determination of
■d
exact sample dry weight. Pesticides were
extracted from the wet samples immedi
ately after they were taken from the jars
'•
using the method described in what follows.
A
similar procedure of fortnightly sampling
'•1
and pesticide extraction on freshly taken
samples was used in other experiments set
up to study the possible effect of day and
night temperature fluctuation, and also the
W effect of pesticide re-application at time inter® vals comparable to those used by farmers in the field during the cotton growing
season.
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157
Pesticide extraction
The extraction method employed has been
described by Ghadiri and Rose (1993) and
Ghadiri et al. (1995). In brief, an equivalent
of 3 g dry weight of the freshly taken wet
soil was put in a 125 ml beaker with 100 ml of
acetone-hexane mixture and mixed for 30 min
in a sonic bath at room temperature. Super
natant was then transferred to a 250 ml sepa
rating funnel and washed with distilled water
until phase separation occurred. The aqueous
phase was discarded and the hexane mixture
passed through a funnel containing a GFC
filter-paper and anhydrous sodium sulphate
to dry. After reducing the volume of the mix
ture by evaporation in a steam bath, it was
transferred to the top of a chromatographic
column containing 5 g of deactivated florisil
under a 2-cm layer of anhydrous sodium sul
phate. The mixture was eluted with 130 ml
of JV-hexane/diethyl ether mixture (85/15).
The extract was then evaporated to about
3 ml in a steam bath and transferred to a
sample vial for gas chromatographic analy
sis. Extraction efficiency was determined by
applying known quantities of endosulfan to
soil samples and extracting them using the
procedure explained above. Average recovery
of a and 0-endosulfan from the soil were 86%
and 90% of the added amounts, respectively.
Analysis of extracts
Analysis of sample extracts was performed
with a Varian 3400 capillary column gas
chromatograph with ECD (Electron Capture
Detector). Column dimension was 0-25 mm
i.d.x 15 m in length and 0-25 mm film thick
ness. Injector and detector temperatures
were 220 and 300°C, respectively. The initial
column temperature was 50°C and the pro
gram rate was 50°C min-1. The final column
temperature of 170°C was held for 30 min.
Retention times for a and P isomers were
13 and 18 min, respectively. Helium and 10%
argon in methane were used as carrier and
make-up gases, respectively. Flow rate for the
carrier gas was 24 ml min-1, and for make-up
gas, 33 ml min-1. Standard mixtures of endo
sulfan pesticide at different concentrations
were prepared and used to calibrate retention
time and to prepare response curves.
!•
158
H. Ghadiri and C. W. Rose
If':
Results
when soils were submerged. A single first
order rate curve was then fitted to all
data points from each submerged experiment
Effect of soil water content and
(Figure 1)
waterlogging on the degradation of
In contrast to a-isomer behaviour, the
endosulfan
degradation curve of P-endosulfan does not
show any change of slope with time, and fol
Soil water content affects degradation of the lows a single first-order rate equation for
two endosulfan isomers differently. As shown the entire incubation duration (Figure 2).
in Figure 1, except for the submerged soil, The degradation rate is slower for the low
a-endosulfan degrades very rapidly at first est water content of 15%, and increases with
when water content is 25% or greater. Only increase in the soil water content. However,
in the submerged experiments, and in the low once the soil is submerged the rate slows
water content (15%)—low incubation temper down once again (Figure 2). On the whole
ature (20°C) non-submerged experiments the P-endosulfan appears to be much more per
degradation of a-endosulfan followed a single sistent in soil than the a-isomer under all soil
first order rate equation throughout the dura water content experiments. Half-lives as long
tion of the experiments. The rapid decline in as 376 days were recorded for 0-endosulfan in
the concentration of a-endosulfan during the soils with low water content of 15% (Table 1).
first 15 to 20 days of incubation in all high
Endosulfan sulfate was the major degrada
water content soils was followed by a much tion product formed in every non-submerged
reduced rate for the rest of the duration of experiment. Its rapid build-up corresponds
the experiments. No significant difference in closqly with the rapid disappearance of
degradation behaviour of a-endosulfan was a-endosulfan during the first 20 days of incu
observed between the three higher water con bation, reaching its highest concentration at
tent soils. Such degradation behaviour may . about the same time as the rapid degra
be described by two exponential dissipation dation phase of a-endosulfan ended and a
phases termed ‘bi-exponential’ (Nose, 1987).
sharp slope change in its degradation curve
Alpha endosulfan degrades at a signifi took place (compare Figures 3 and 1). The
cantly slower rate under submerged soil con highest level of endosulfan sulfate produced
dition than if non-submerged (Table 1). The was in the higher water contents of 37% and
bi-exponential mode of degradation which 45%, the lowest level being with 15% water
characterized the behavior of this isomer in
non-submerged soil was no longer observed
Table 1. Half-lives of a and ^-endosulfan as
influenced by soil temperature and water content
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Temp,
(°C)
a-endosulfan
0-endosulfan
15
20
30
40
27
13
10
376
75
38
25
20
30
40
8
6
5
100
43
33
37
20
30
40
20
30
40
20
30
40
7
4
5
7
7
7
43
75
30
100
43
38
100
60
43
Water
content (%)
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Half-lives
in days
Experimental
condition
20
40
60
80
100 120
Incubation duration (days)
140
Figure 1. Effect of soil water content on the
degradation of a-endosulfan at 30°C temperature.
15% wc, H; 25% wc, A; 37% wc, O; 45% wc, o;
submerged, □.
45
Submerged
300
150
33
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Degradation of endosulfan in soils
159
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I
20
0
■ I
I
I
I
I
120
|
,
|
40
60
80
100
Incubation duration (days)
140
Figure 2. Effect of soil water content on the degradation of p-endosulfan at 20’C temperature. 15% wc,
■; 25% wc, A; 37% wc, 0; 45% wc, o; submerged, □.
1
content and in submerged soils (Table 2).
As shown in Figure 3 the concentration of
endosulfan-sulfate remained high through
out the incubation period under all soil mois
ture conditions, and this was especially so at
low temperatures.
3.0
ZO
7m
g 2.0
o
-3
-
<1 / /
a
I
I
Table 2. The formation and degradation of endo
sulfan sulfate in the water content-temperature
experiments
g
u
11 /
■g
10
1/
//
*o
Experimental condition
£
Temp.
(°C)
Peak con
centration
(week 4)
g~1
Final con
centration
(week 20)
g-1
20
30
40
1-4
1-7
0-8
1-40
1-00
0-50
25
20
30
40
2- 5
20
1- 6
1-80
1- 00
0-19
37
20
30
40
2- 9
2-8
1- 5
2- 50
1- 50
0-14
20
30
40
2- 8
2-3
1-6
2- 70
100
0-03
20
30
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1-6
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0-21
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Water
content %
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Submerged
o
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□ '
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0
CM J___ ■
20
I I I I I , I , |
40
60
80
100 120
Incubation duration (days)
140
Figure 3. Effect of soil water content on the
formation and degradation of endosulfan-sulfate at
20°C temperature. 17% wc, •; 25% wc, ■; 37%
wc, O; 45% wc, o; submerged, □.
Effect of incubation temperature on
the degradation of endosulfan
A rapid initial degradation of a-endosulfan
followed by a slower phase was also shown
in experiments at all incubation tempera
tures except for the submerged experiments.
The rate was, however, significantly slower
I
I
I
n
60
H. Ghadiri and 0. W. Rose
for the low incubation temperature of 20°C
as compared to the two higher tempera
ture of 30°C and 40°C (Figure 4). There
was no difference in the degradation rates
of a-endosulfan in the two higher tempera
tures of 30 and 40°C. The temperature effect
* - at low
was noticeable only in soil samples
water content of 15% shown in Figure 4. For
25% water content and higher, the degra
dation rate of a-endosulfan was very rapid
with little difference between the three tem
peratures studied (Table 1). Therefore, soil
water content appears to have more influ
ence on the degradation rate and the half
life of a-endosulfan than incubation tem
perature. Temperature effected the degra
dation of a-endosulfan under submerged
condition (Figure 5), but not in a regular
manner.
o
Beta endosulfan _
degraded
at a slower rate
at
than the a isomer i all temperatures studied. Unlike a-endosulfan, the degradation
rate of the p-isomer closely follows a sin
gle first order rate equation (Figure 6). The
degradation of p-endosulfan is consistently
slower for 20° C as compared with the other
two higher temperatures at all water content
levels. The half-lives shown in Table 1 for
p-endosulfan arc significantly higher than
those for a-isomer in similar conditions.
P-endosulfan appears to be more affected
by the changes in the incubation tempera
ture than the a isomer. Low temperature
restricts the degradation of P-endosulfan and
increases its half-life substantially (Table 1).
The formation and the subsequent dissipation of endosulfan-sulfate appears to have
been profoundly affected by the changes in
incubation temperature (Figure 7). The high
est concentration of endosulfan-sulfate coin
cides once again with the sudden change
in the degradation curve of a-endosulfan,
namely approximately 20 days after pes
ticide application. The peak concentration
is higher for lower incubation tempera
tures.. When the incubation temperature is
low (20°C), the concentration of endosulfansulfate remains high throughout the incubation duration of 130 days, with very small
net decay. However such decay occurred at
a more rapid rate for the higher incubation
temperatures after the peak concentrations
were attained (Figure 7), the decay rate
increasing with temperature. At the high
temperature of 40° C lower production rate
of endosulfan sulfate is coupled with its
faster disappearance from the soil environ
ment (Table 2).
,
I
I!
Figure
40°C,
I
3.0 y = 2.129 * 10(-0 0054x) r2 = 0.94
y = 1.395 * lO^ 0097^ r2 = 0.89
y = 1.262 * IO*-0 0115** r2 = 0.85
\\
%
2.0
g
•3
\\
o
g
'k
o
•!
I
0)
1.0 <D
Pi
o
0
Figure 4.
I
20
B
I
O
1,1?
I
P
P
40
60
80
100
Incubation duration (days)
120
140
Effect of temperature on the degradation of of-endosulfan in soil with 15% water content. 20 C,
□; 30°, ■; 40°C, o.
I
Figur
r-). 3C
nr
□;
Th
sulfa
prou
ditio
temj
I
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Degradation of endosulfan in soils
3.0
L
y = 2.495 * IO*"0007*) r2 = 0.97
y = 2.785 * 10(-0 010x) r2 = 0.99
y = 2.683 * lo<-°-004-^ r2 = 0.98
I
2.0
i
ao
!
o
o
s
XJ
•5 1.0
*■8
a>
L
Ph
I
c
0
20
40
60
80
100
Incubation duration (days)
120
140
i
f
Figure 5.
l
40°C, o.
Effect of temperature on the degradation of a-endosulfan in submerged soil. 20°C, □; 30°, ■;
i
}
y = 1.308 * lO^ 003^ r2 = 0.95
y = 1.327 * 10(-0-007x) r2 = 1.00
y = 1.103 * lO^"0-009*) r2 = 0.98
1.5
%
bfl
•S’
g
Is
h
So i-o
g
<D
15
"o
to
0)
CU
0.5
i:
0
I
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B
20
40
60
80
100
Incubation duration (days)
120
140
Figure 6. Effect of temperature on the degradation of ^-endosulfan in soil with 37% water content. 20°C,
□; 30°, H; 40°C, o.
The effect of temperature on endosulfan
sulfate production-degradation is also very
pronounced under the submerged soil con
dition (Figure 8). At the lower incubation
temperature of 20°C the trend is similar to
that for the non-submerged condition (i.e.
rapid formation, high peak, followed by a
very slow decay). However under the higher
temperatures of 30 and 40°C either very little
endosulfan sulfate was formed or its rate of
161
;
162
I
H. Ghadiri and C. W. Rose
degradation was so fast that it did not build
up in the soil. The measured concentrations
of this compound at these temperatures were
low during the entire duration of incubation
(Figure 8). This is in sharp contrast to the
non-submerged condition (Figure 7). Table 2
shows that at the end of the experiments
(about 130 days of incubation) the concentra
tion of endosulfan sulfate is still very high
for most temperature and water content con
ditions tested except for the submerged soils,
while at this time a-endosulfan has almost
disappeared, and the concentration of the
P-isomer is very low.
3.0
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b/
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'-a
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Ph
i
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l ,
l
■
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l XP I
i
140
20 40
60
80 100 120
Incubation duration (days)
0
Figure 7. Effect of temperature on the formation
and degradation of endosulfan-sulfate in soil with
37% water content. 20°C, □; 30°, ■; 40°C, o.
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Effect of day and night temperature
fluctuation on the degradation of
endosulfan isomers
The effect of alternating incubation tempe
rature, chosen to simulate day and night
conditions of soil in the field, was studied
at 15 and 25% water contents. The incu
bation temperature was altered every 12 h
between 35°C (day) and 20°C (night). The
effect was, once again, different for differ
ent isomers. The overall degradation of aendosulfan shows the same bi-exponential
fbrm shown in the continuous temperature
experiments, with an initial rapid rate fol
lowed by a slower period of decline. The
degradation rates for both water contents
were, however, lower for a-endosulfan under g
the alternating day and night temperatures*
as compared to the continuous temperature
of 20°C or even 30°C (Table 3). Alternat
ing temperature had the opposite effect on
the degradation of p-endosulfan. As shown in
Table 3, the degradation rate of P-endosulfan
have been substantially enhanced under the
day and night temperature regime as com
pared with the continuous temperature of
20°C. For the lower of the two water con
tents the degradation rate was faster for day
and night temperatures even as compared
with the rate for a continuous temperature of
30°C. The degradation rate of P-endosulfan
seems to have been influenced more by the
day rather than night temperature.
The net formation of endosulfan sulfate in
the day and night experiments was reduced,
and its degradation rate enhanced, whecompared to continuous temperature exper
iments (Figure 9). At the low water content
of 15% no measurable amount of endosulfan
sulfate was formed. Almost all endosulfan
sulfate formed in the moist soil under the day
and night temperatures disappeared from
the soil after about 80 days of incubation,
while the concentration of this chemical was
still very high in the continuous temperature
experiments after 130 days.
r
II’
MI
I
■
i
i
Q
__1L_
------- B
■
•P7
0
20
40
60
80 100 120
Incubation duration (days)
140
Figure 8. Effect of temperature on the formation
degradation of endosulfan-sulfate in the sub
merged soil. 20°C, □; 30°, S; 40°C, o.
II
Effect of endosulfan re-application
on its degradation in the soil
Table 4 shows the results of the re-application
experiments. Re-application has resulted in a
longer half-life for a-endosulfan as compared
I
' ^1
1
.I
Degradation of endosulfan in soils
Table 3.
t
J
Effect of day and night temperature variation on the half-lives of endosulfan isomers
Water
content
f (°/o)
^-endosulfan
a-endosulfan
Continuous 20°C Continuous 30°C Day/Night Continuous 20°C Continuous 30°C Day/Night
27
13
8
6
50
25
376
100
3.0
%
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100
Incubation duration (days)
120
0
20
e"---- «
40
60
80
100
Incubation duration (days)
120
f
'
h
f
Figure 9. The formation-degradation of endosulfan-sulfate in the soil with 25% water content
under fluctuating (day and night) or continuous
temperatures. Day and night, o; continuous, ■.
Figure 10. The formation and degradation of
endosulfan-sulfate in re-application experiments
with 30°C temperature. 15% wc, •; 25% wc, ■;
submerged, o.
I
to the first application, p-endosulfan on the
other hand with a faster rate upon re
application to soils with low water content,
but degraded at the same rate as in the first
application for the wetter soil. Re-application
gnificantly enhanced the degradation of
both a and 0-endosulfan in the soil under
submerged condition.
As was the case with the first application,
the formation and degradation of endosul
fan sulfate in re-application experiments are
affected by soil water content. In the drier
Table 4. Effect of re-application on the half-life of
endosulfan
soil condition re-apjplication decreased the
net formation of endosulfan sulfate, while
in the wetter soil there was not much dif
ference between the first and the second
application (Figure 10, cf Figure 7). The for
mation and degradation of endosulfan sulfate
appears, once again, to be linked closely with
the degradation rate of a-endosulfan. Under
the submerged condition very little endo
sulfan sulfate was formed in either first or
re-application experiments, with little differ
ence between the two. No measurable quan
tities of endosulfan diol or other endosulfan
degradation products were formed under the
submerged condition.
Water
content (%)
Open-top experiments
j
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r
3
I
i
g
'os
1.0
!
!
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2
g 2.0
X
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0
43
43
?■
3.0 —
g
O’
u
75
43
1
15
25
Submerged
i I
H i; J!
4.0
'bo
bo
u
H
Half-life in days
r‘ 25
15
I•
163
■i
I)
Half-life in days
a-endosulfan
^-endosulfan
First
application
Re-application
First
application
Re-application
13
6
75
50
20
30
75
43
150
50
43
60
Although volatilization of soil-sorbed endo
sulfan is unlikely to occur at a significant
rate, it was nevertheless decided to check
such a possibility experimentally. This was
do by comparing results from a set of water
con nt-temperature experiments with the
1
' 1.
t
I
164
I
I
:[
s
t
V
H. Ghadiri and C. W. Rose
soils. Table 5 brings together results from this
lids of the jars removed with results obtained
study and seeks to compare them with results
in the sealed-jar experiments described pre
reported in the literature. However, the com
viously. Several attempts were made to carry
parison sought in Table 5 is not quite valid,
out such experiments, however due to the
since most studies haven’t fully described or
rapid drying of the samples, especially at the
controlled the conditions under which the
higher incubation temperatures, maintain
experiments have been conducted. Very large
ing a constant soil moisture over a period
of several weeks proved impossible. Applying variations observed in the reported half-lives
of the two endosulfan isomers, over a narrow
constant suction to soils in a Hains Apparatus
also did not prove successful due to cracking . range of temperatures and soil pH values,
may have been caused by the differences
of the clay soil and discontinuity in the hang
in other factors not clearly specified or con
ing water column. Because of insufficient
trolled in the work reported in the respective
data points the results of these experiments
papers. One thing which this table, and the
were not conclusive. However rate of degrada
tion for both a and P-endosulfan in open-top
literature behind it, clearly show, however, is
experiments appeared to be somewhat slower
the need for more work of the type reported
than in the sealed jars for the correspond in this paper where the effect of major soil
ing incubation period. If volatilization had a
and environmental factors on the half-life
major role in the degradation of endosulfan
endosulfan is investigated in a context wh<
in our controlled environment experiments,
there is strict control over all other factors
the degradation rates for the open-top exper
which may influence the results when a given
iments should have been higher than for the
factor is varied.
sealed jar experiments, not lower.
The experimental results reported in this
Volatilization of endosulfan is more likely
paper indicate that, amongst the factors stud
to occur from a water surface. The open-top
ied, soil moisture content and soil temper
experiments carried out on the submerged
ature are the two most influential factors
soil samples were more successful than those
on the degradation rates and patterns of
for the non-submerged soil and produced
both a and p-endosulfan isomers, as well
more reliable results. However, the results
as on the formation and dissipation of their
showed very little difference for both isomers
primary degradation product, endosulfanbetween the two conditions, suggesting no
sulfate. These two factors and their inter
involvement of the volatilization process in t action determine the persistence of endo
our experiments.
sulfan in soil, and thus its disappearance
from the soil environment. The degrada
tion of a-endosulfan is very fast when both
Discussion
soil moisture content and temperature are
high (but not submerged), with an avei
i
half-life
of
around
7
days
(Table
1).
At
iuw
As the last remaining allowable organochlomoisture content and low temperature this
rine pesticide which is very effective against
figure increases to around 27 days, and in
many agricultural pests, including Helioa waterlogged soil to around 50 days. The
this in cotton crops, there is strong inter
degradation curve for a-endosulfan has a
est and concern about endosulfan’s fate in
bi-exponential characteristic, and the sharp
the environment. Its fate, persistence and
slow-down in its degradation rate happens at
degradation have been the subject of a num
about 20 days after application, at which time
ber of studies in recent years in Australia
a significant proportion of this isomer has
and elsewhere (Guerin and Kennedy, 1992;
degraded into endosulfan-sulfate (Figures 1
Kimber et al., 1994; Southan and Kennedy,
and 4). Kennedy et al. (1994) and Kath
1994; Kennedy et al., 1994, 1998; Kathpal
pal et al. (1997) have reported a similar
et al., 1997; Guerin, 1999). However, the
behaviour
in their field studies of the degra
diverse nature of the factors involved in these
dation
of
endosulfan,
calling it two-phased
reported experiments (i.e. soil, environmen
first-order
kinetics.
One
of the implications
tal, atmospheric, management, etc.), makes it
of
a
bi-exponential
mode
of degradation is
difficult to draw any logical conclusion about
that
the
use
of
the
first-order
rate constant,
the effect of any individual or group of fac
k,
in
the
equation
(C
t
=Coe
-/et
)
to predict the
tors on endosulfan degradation in different
I
►
(U
UJ
CD
ifj
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CD
(U
UJ
UJ
A
Table 5.
Comparison of this study with half-lives of endosulfan in soils reported in the literature
Soil type
Experiment type
Temperature (°C)
pH
Other experimental conditions
Half-life (days)
a-endosulfan
Brazilian sandy clay soil (Laabs et al., 2000)
Field study
Neutral soil (Howard, 1991)
Ac.d soils (Howard, 1991)
Unspecified (Howard, 1991)
Gezira, Sudan (El Beit et al., 1981)
Gezira, Sudan (El Beit et al., 1981)
Australian clay soil (Kennedy et al., 1994)
Australian clay soil (Kennedy et al., 1998)
Silt loam (Gildemeister and Jordon, 1983)
Sandy loan (Gildemeister and Jordon, 1983)
Sandy loan (NRA, 1998)
West Bengal soils (India) (Kaur et al., 1998)
Black cotton (India) (Kaur et al., 1998)
Current study
Controlled condition
Controlled condition
Field study
Controlled condition
Controlled condition
Field study
Field study
Controlled condition
Controlled condition
Controlled condition
Controlled condition
Controlled condition
Controlled condition
Controlled condition
Controlled condition
Controlled condition
Controlled condition
Controlled condition
23
(mean annual)
4-3
20
20
7
5-5
37
37
22
22
28
22
22
20
30
40
20
30
40
aFigures in brackets are for the rapid phase of a bi-exponential degradation of endosulfan.
b Figures in brackets are the half-lives of endosulfan isomers under anaerobic condition.
7
7
6-4
4
7
6-3
5-5
8-5
85
8-5
8-5
8-5
8-5
Free-draining lysimeter
Application rate of 6.7 kg/ha
Non-sterile, moist
Sterile, moist
NSW cotton fields
NSW cotton fields
Application rate of 3.5 pg/kg
Application rate of 3.5 pg/kg
Stimulated microbial activity
Test tube experiment, 2 g soil
Test tube experiment, 2 g soil
5% to 45% water content
15% to 45% water content
15% to 45% water content
Submerged
Submerged
Submerged
^-endosulfan
2-5
35
151
60
43
58
30
30 (4)a
27 (154)b
18(144)b
23
27
14
12
75
6-5
43
75
30
38
187
800
30
60
50
87 (5)a
27 (154)d
18 (144)b
58
27
14
169
55
38
300
150
33
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166
I
H. Ghadiri and C. W. Rose
concentration of a-endosulfan at time t after
its application to soil is not valid. Rather two
different rate constants need to be used with
a change over from the use of the first to
the second value of k. The second segment of
the curves in Figures 1 and 4 suggest that
while the bulk of the applied a-endosulfan
dissipates rather quickly, low concentrations
of this chemical can persist in the soil for
a much longer time than suggested by half
life figures based on the initial high rate of
degradation.
The degradation of 0-endosulfan follows
a single first-order rate decay and a sin
gle curve can pass through all the data
points for every temperature or water con
tent studied (Figures 2 and 6). Kennedy
et al. (1994) reported a bi-exponential or twophased degradation for 0-endosulfan as well
as for the a-isomer (Table 5), but this was
not supported by our results. The degrada
tion rate of this isomer is significantly slower
than the a-isomer. The half-life figures for
high water content-high temperature condi
tions are around 40 to 50 days for 0-isomer
as against 6 or 7 days for the a-isomer,
increasing sharply with any decrease in tem
perature and/or moisture content (Table 1).
When both factors are at their minimum (i.e.
15% water content and 20°C) the half-life
for 0-endosulfan is as high as 376 days, or
more than a year. Soil temperature appears
to influence the degradation of 0-isomer more
than moisture content, while the opposite
appears to be the case for a-endosulfan. Such
influences are clearly shown even under the
submerged condition (Table 1). According to
Walker et al. (1988), any pesticide with a
half-life more than 28 days causes environ
mental concerns. The results presented in
this paper show that endosulfan falls in this
category under a wide-range of temperature
water content conditions observed in the field.
Endosulfan sulfate was produced in all
water content-temperature experiments at
varying but substantial rates and quanti
ties. The peak concentration was quite high
for all non-submerged experiments, with
the highest peak being obtained under the
high water content-low temperature condi
tion (Table 2). It appears as though under
these conditions both a and 0-endosulfan
degrade entirely into the sulfate metabolite.
The subsequent degradation of endosulfansulfate into non-toxic products is very much
*
;
a temperature-related process. When temperature is low its degradation from its peak
concentration is very slow, regardless of
what the soil moisture content is, and, as
shown in Figure 3, high concentrations of
this chemical remained in the soil some 120
days after endosulfan application, and some 3
80 days after endosulfan-sulfate attained its (
peak value. This behaviour poses a persistent
source of contamination long after the applied j
endosulfan, in particular the a-isomer, has all
but disappeared from the soil.
Submerging the soil substantially increa
sed the half-lives of both endosulfan iso- ;
mers (Table 1). The half-life of 0-endosulfan !
remained higher than that of a-isomer in
all of the submerged experiments carried
out under different temperature regimes.
Guerin and Kennedy (1992) summarized a "
number of studies carried out on the degra
dation of endosulfan in aqueous system. In
such environment 0-endosulfan appears to
degrade faster than the a-isomer which is
opposite to how these two isomers behave
if sorbed by soils. The degradation of soil
bound a-endosulfan is always faster than
the 0-isomer under both aerobic and anaero
bic conditions. Very little endosulfan-sulfate
was formed under the submerged condition
at high incubation temperatures (Figure 8)
and this agrees with reports in the litera
ture and the proposed pathway of degrada
tion for endosulfan (Guerin, 1999). However,
there is no such agreement once incubation
temperature is lowered to 20°C. At this tem
perature endosulfan-sulfate was once again
the main degradation product and its formation, build-up and subsequent degradation
followed the same pattern observed under
aerobic condition (Figure 8). Guerin (1999)
also observed the presence of endosulfansulfate in sediments incubated anaerobically,
but he attributed its presence in the sam
ples to its transport and deposition from its
site of formation in the field under aerobic
condition. This was not the case with our
experiments as the collected soil had zero
concentration of all endosulfan metabolites,
and endosulfan-sulfate was produced under
anaerobic incubation. The formation and per
sistence of endosulfan-sulfate in submerged
soil (and therefore in bottom sediments) at
water temperatures not uncommon in the
real world, coupled with its extreme toxic
ity to fish and other aquatic biota, makes
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Degradation of endosulfan in soils
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3S,
er
ir-
ed
at
he
ic.es
it a major source of contamination of the
aquatic environments. Increase in soil and
water temperature from 20°C to 30°C or
40°C substantially reduced its formation, but
its concentration, although low, remained
almost unchanged throughout the duration
of the experiments (Figure 8). The formation
of endosulfan-diol as the major metabolite
in flooded soils, as reported in the literature
(Martens, 1977), was not supported in this
study.
Alternating day and night temperatures
had contrasting effects on the degradation
rates of the two endosulfan isomers. While
it significantly slowed down the degradation
of a-endosulfan and increased its half-live by
a factor of 2 to 3, it enhanced the degrada
tion of P-endosulfan and reduced its half-life
(Table 3). The effect on the degradation of
p-endosulfan was more pronounced when
the day-night degradation values where com
pared with the continuous low (night) than
with the continuous high (day) tempera
ture. However the shapes of the degrada
tion curves for both isomers remained the
same, with a-endosulfan retaining its bi
exponential form, and that of P-isomer a
single exponential form. It is possible to say
that the degradation rate of a-endosulfan is
being influenced more by the lower (night)
temperature and that of the P-endosulfan
by the higher or day temperature. With aendosulfan being the more important of the
two, it can thus be concluded that the net
effect of day and night temperature fluctua
tion is to slow down the degradation process
for this pesticide. Endosulfan sulfate produc
tion under the day-night temperature regime
was diminished and its subsequent dissipa
tion enhanced compared with the continuous
high (day) or low (night) temperatures.
In the re-application experiments the
’’J
initial rapid degradation of a-endosulfan,
although still present, was not as pronounced
« as for the first application, thus allowing a
single exponential curve to provide a reason
able fit to all the data points. The half-life
of this isomer was substantially higher in re| application under non-submerged condition
g of the soil, but lower under the submerged
g condition (Table 4). This implies that the
| first application has adversely affected the
a biological population of the soil presumed
L responsible for endosulfan degradation. 11
Sigi; is also possible that the presence of the
I
ill
i
I
I
I
II
1
f
I
more persistent fraction of this pesticide
from the first application has contributed to
this slower rate of degradation in the re
application experiment. The degradation of
P-endosulfan was faster under re-application
compared with the first application which
could be an indication of a slow build-up of
the microbial population responsible for the
degradation of this isomer. Under the sub
merged soil condition both isomers degrade
faster on re-application compared with the
first application (Tabic 4). These results
could be interpreted as endosulfan having
beneficial effect on microbial population in
charge of its degradation under anaerobic
condition.
Conclusions
Soil moisture content and temperature are
the two most influential factors on the degra
dation of both a and P-endosulfan and their
toxic degradation product, endosulfan sul
fate. Alfa-endosulfan appears to be more
affected by the changes in soil water con
tent, while the fl-isomer is more influenced
by temperature. Alpha endosulfan showed a
rapid phase of degradation early in the exper
iments, followed by a prolonged slower phase.
The degradation pattern of a-endosulfan can
be characterized as being of a bi-exponential
function type except at the two extremes
of moisture contents, the submerged and
low water content of 15%. Degradation of
P-endosulfan was significantly slower than
for the a-isomer under all conditions stud
ied, and always followed a simple exponential
decay function. Half-lives as high as one year
were measured for P-endosulfan under low
temperature-low water content conditions,
while those of a-endosulfan were less by a
factor of 10 or more for similar conditions.
Endosulfan-sulfate was the major degra
dation product in all non-submerged exper
iments, as well as in the low temperature
submerged experiments. Its concentration
peaked some 20 to 40 days after incubation
and remained high until the end of incu
bation period of 130 days, particularly in
low temperature-high water content exper
iments. Its build up in the soil followed the
disappearance of o-endosulfan very closely,
but its degradation docs not appear to fol
low a clearly defined simple exponential
>' ’b
167
■ f I
J
. ; ill
i i I ,
i Hl 1
168
H. Ghadiri and C. W. Rose
form. Endosulfan-sulfate was also formed
in all of the submerged experiments, albeit
at significantly reduced rates. The overall
effect of submerging the soil, however, was
to reduce the net formation of endosulfansulfate and to enhanced its degradation rate.
Both a and 0-isomers, and endosulfan sul
fate, persisted longer in the submerged soil
than under the non-submerged condition.
The overall effects of day-night temperature
fluctuation and pesticide re-application were
to prolong the persistence of a-isomer and
to enhance that of P-isomer and endosulfan
sulfate.
Acknowledgments
The authors acknowledge with thanks the research
funds provided by the Land and Water Resources
Research and Development Corporation (LWRRDC) for this project.
References
Barrett, J. W. H., Peterson, S. M. and Batley, G. E.
(1991). The Impact of Pesticides on the Riverine
Environment with Specific Reference to Cotton
Growing. A report for CRDC and LWRRDC.
Barrett Purcell & Associates Pty. Ltd. NSW.
Australia.
Cotham, W.E. and Bidleman, T.F. (1989). Degra
dation of malathion, endosulfan and fenvalerate
in seawater and seawater/sediment microcosms.
Journal of Agriculture and Food Chemistry 37,
824-828.
El Beit, I. 0. D., Wheelock, J. V. and Cotton, D. E.
(1981). Pesticide-microbial interaction in the
soil. International Journal of Environmental
Studies 16, 171-180.
Ghadiri, H. and Rose, C. W. (1993). Water
erosion processes and the enrichment of sorbed
pesticides in the eroded sediment. Part 1:
Enrichment mechanism and the degradation
of applied pesticides. Journal of Environmental
Management 37, 23-35.
Ghadiri, H. and Rose, C. W. (1994). Endosulfan
degradation in cotton farm soils. In Minimizing
the Impact of Pesticides on the Riverine Envi
ronment Using the Cotton Industry as a Model.
Second Annual Workshop, LWRRDC. Brisbane.
s t/i? cil i
Ghadiri, H., Rose, C. W. and Connell, D. W. (1995).
Degradation of organochlorine pesticides in soils
under controlled environment and outdoor con
ditions. Journal of Environmental Management
43, 141-151.
Gildemeister, H. and Jordan, H. J. (1983). Aer
obic Soil Metabolism Study of the Insecticide
I
I
‘ Hoe 002671 (Endosulfan). Hoechest Aktiengesellschaft, Germany. Document No. A29680
dated November 1984. Unpublished report
(Quoted by NRA 1998).
Gobble, H., Gorbach, S., Knauf, W., Rimpau, R. H.
and Huttenbach, H. (1982). Properties, effects,
residues and analytics of the insecticide endo
sulfan. Residue Review 83, 1—122.
Guerin, T.F. (1999). The anaerobic degradation of
endosulfan by indigenous microorganisms from
low—oxygen soils and sediments. Environmental
Pollution 106, 13-21.
Guerin, T. F. and Kennedy, I. R. (1992). Distribu
tion and dissipation of endosulfan and related
cyclodienes in sterile aqueous systems: implica
tions for studies on biodegradation. Journal of
Agriculture and Food Chemistry 40, 2315-2323.
Howard, H. (1991). Handbook of Environmental
Fate and Exposure Data for Organic Chemi
cals, Vol. HI Pesticides. Ann Arbor: MI: Lewis
Publishing.
Karin, M. A. (1997). Pesticide Profiles: Toxicity,
Environmental Impact, and Fate. Boca Raton,
NY: Lewis Publishers, CRC.
Kennedy, I. R., Ahmad, N., Tuite, J., Kimber, S.,
Sebastian, S., Lee, A., et al. (1994). Transport
* and fate of pesticides in cotton production
systems. In Minimizing the Impact of Pesticides
on the Riverine Environment Using the Cotton
Industry as a Model. Second Annual Workshop,
LWRRDC. Brisbane. Australia.
Kennedy, I. R., Sanchez-Bayo, F., Kimber, S. W. L.,
Beasley, H. and Ahmad, N. (1998). Movement
and fate of endosulfan on-farm (New South
Wales). In Minimizing the Impact of Pesticides
on the Riverine Environment: Key Findings from
Research with the Cotton Industry, pp. 33-37.
LWRRDC Occasional Paper 23/98, Canberra,
Australia.
Kathpal, T. S., Singh, A, Dhankhar, J. S. and
Singh, G. (1997). Fate of endosulfan in cotton
soil under subtropical conditions of northern
India. Pesticide Science 50, 21-27.
J
Kaur, I., Mathur, R. P., Tandon, S. N. anJ
Dureja, P. (1998). Persistence of endosulfan
(technical) in water and soil. Environmental
Technology 19, 115—119.
Kimber, S. W., Coleman, S., Coldwell, R. L.
and Kennedy, I. R. (1994). The Environmental
Fate of Endosulfan Sprayed on Cotton. Eighth
International Congress on Pesticide Chemistry
(IUPAC) Washington, DC, USA, 4-9 July 1994.
vol. 1. Abstract No. 234, p. 263.
Laabs, V., Amelunga, A. W., Pintob, A., Altstaedta, A. and Zecha, W. (2000). Leaching and
degradation of corn and soybean pesticides in an
Oxisol of the Brazilian Cerrados. Chemosphere
41,1441-1449.
Martens, R. (1977). Degradation of endosulfan-8914C in soil under different conditions. Bulletin
of Environmental Contamination and Toxicol
ogy 17, 438-446.
Nose, K. (1987). A multi-site decay model of
pesticide in soil. Journal of Pesticide Science j
12,505-508.
j
i
1
■
.
I.
ftj
MJ__
JR.... J!!",
i •1 I
Degradation of endosulfan in soils
NRA (1998). The NRA Review of Endosulfan.
National Registration Authority for Agricul
tural and Veterinary Chemicals: Existing chem
icals program. Volume 2, Section 7. ACT.
Australia.
Peterson, S. M. and Batley, G. E. (1991a).
Fate and Transport of Endosulfan and Diuron
in Aquatic Ecosystems. Investigation Report
CET/LH/IR013. Lucas Height, NSW, Australia:
CSIRO Division of Coal and Energy Technology.
Peterson, S. M. and Batley, G. E. (1991b). The role
of non-settling particles in pollutant transport:
Endosulfan. In Modelling the Fate of Chem
icals in the Environment (I. D. Moore, ed.),
pp. 103-108. ANU, Australia: Cres Publication.
Simpson, B. W., Hargraves, P. A., Noble, R. M.,
Thomas, E., Kushopf, B. and Carroll, C. (1998).
Pesticide behavior on-farm: persistence and off
site transport (Queensland). In Minimizing the
Impact of Pesticides on the Riverine Environ
ment: Key Findings from Research with the
169
Cotton Industry, pp. 38-43. LWRRDC Occa
sional Paper 23/98, Canberra, Australia.
Southan, S. K. and Kennedy, I. R. (1994). Stud
ies on the Degradation of Endosulfan in Soils
and Sediments of Cotton Growing Regions of
North-West New South Wales. Eighth Interna
tional Congress on Pesticide Chemistry (IUPAC)
Washington, DC, USA, 4-9 July 1994. Vol. 1.
Abstract No. 244, p. 277.
Walker, A. (1978). Simulation of the persistence of
eight soil-applied herbicides. Weed Research 18,
305-313.
Walker, W. W., Cripe, C. R., Pritchard, P. H. and
Bourquin, A. W. (1988). Biological and abiotic
degradation of xenobiotic compounds in vitro
estuarine water and sediment/water systems.
Chemosphere 17, 2255-2270.
Worthing, C. R. (1983). The Pesticide Manual:
A World Compendium, 7th edn. London: The
British Crop Production Council.
.•
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HINDUSTAN INSECTICIUE-S^LTD.
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3.3
(A GovL of Indio Enlei pi Isa)
Subject :
ENDOSULFAN
I
CHEiVbS J p%Y: Attention shoulJbe drav/n nature of Endusullcn '.'■■•.‘ch, Dlliiough It Is
cyclodlcnce OC Insecticides d6es not exhibit the typical charwcie.lr'lc of this group lo
the some extent as olherpnembeis ol this group, I hus it Joes ;</. builu-up In' thc iiid
. ol mammals lo Ihe some extent and neither does it persistent In 7-*e envlrornucni lor
decades alter It has been deposited. Il is sensitive to moisture, acids and alkalis. Il
contains sulphur & oxygen which releases SO2 immediately, degradation starts quickly.
1 Recommended on many crops. Some uses need lo be withdrawn particularly
for the conlrol of termites and on paddy crops where llsh cuilure Is common. Suited to
use in IBM and,resistance .management strategy, because ll-hus osen proved to be
SOI- f on beneficial Insects and it is one of the lew remaining sHscbve oc lris?.ollck»es
which can be used In a RM slralegies-Essenlial lor ViabHily of colion Industry.
'I
I2JS120L2GY1:
.1
'
■
GLOMEiTULONEPHROSIS • Degeneration of Kidney • Dose of Endosulfan and leriglh
of time cf exposure are the. peramclcrs.
•
I here. Is evidence that Endosulfan disrupts the Endocrine hormonal system. ADI-'J.OOZ .
mg per kg/day, now it has been revised lo 0 006 mg per kg/day NOEL-0.7 lo 0.75 mg.
per kg/day lo NOEL-0,6 io 0.65 mg/kg/day.
'
.
PUBLIC HEALTH ISSUE : In rals kidney appears lo be Ihe ms'n iargel for Endosulfan
Toxlclly In number of studies.
•
•
RENEL effects seen Include increase in kidney weight and pigments formation In
shorter terms admlnislralion and progressive chronic GLOMERULONEPI-IROSIS or
, toxic Nephropathy alter long terms exposure lo Endosullan.
These. findings
however, need lo be seen in light of Ihe lact that such RENEL ellecls(are common
• In, ageing laboratory rats and also occur at a higher Incidence In non exposed
control’ animal.
; ' 1 '•
■
'
•
«
No evidence lo prove lhal Endosullan induces any functional aberrations which
might resull from disruptive endo.crinc hormone syslcm.
Il does not have any adverse functional eliccl on the Immi.inc status of lab. animal.
AQUATIC TOXICITY :
Very highly loxlc lo equolic fauna. Giidosullan is hydiophublc substance, Ils luxlcily Is
• thought lo be modeiaied In luibid v/aler through soiplive inler-octlons.
TERRESTiViAL NOH-TARGET INVEItTEbllAI E3 :
.
Endosullan Is toxic to honey bees in Ihe laboialoiy but appeals geneially lo.be
without signilicanl impact in the Held, even applied al Ihe lime when bees aie
actively foraging.
2. It Is moderately toxic lo earth-worms.
i
1.
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POST tCXi’O.
815
th
, . 69 ->003
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G :\U S !• I < S\ WIN W OI ID\ N S.N I
3.
■HNDU.IJOC
SSZ2
Irom under-spiaycdLeos
b 7
10 rd=to” "»“.-pd'ellon
‘s
io occur
d 0"e da/ al!ow'dS
Le to controlLdLLged eaith nLe^ e"eC'5
5.
u'l!,:op"''s..corislslcnt with, Its
Endosulfan'residues do not appear to Impair microbial processes In (Ire soil.
>■ r
I-S'll£2[ogy_:
Acute oral LD50 -- rats - 9.6 to 160 rug per kg.
mice - 13.5 to 353,mg per kg.
I 4
Endosulfan lech. Is n°l eye irrila.H in rabbits whin, forri.ulaliun ba severa eye initant.
In vivo.
.■:
.
Negative (or genotoxicity in a wide range 0[ BS5nyCi both In vitro and
hSSSlr^b^’^LZais"3
l'f’Ve a" adVG'Se ,u'lc,i0':’al a,'c='s.on the
r’ludle3 lrl '!il5' B "3liyQ o( lieutrnenl
rei^ed7^ii^I~0^7ved 1 In
pigment formulation In Wdiiey proxlrial miLL l'!':'ensG!!
weight and granular
mgAkg/day. with a NOEL for this eilect ot LLLL2 r^L/Ly1 U°3,GE
SPP'°' 3;^
• .-h
JLZLau'L '‘T. ’
d°r'e ( 20 ,r’«,ka/day ) Reticular
and
necrosis
J neialiori1 3n
^ noc,
°sis of the gc...::rid cells lining the
somniferous tubules.
'
endocrine effects :
experimental aLLT' dLLLLdLaLLl
and reproductive at
do not Indicate
,oxicolo9>' sludies lfl
ASPECTS :
1. Hligh aquallc loxiclly.
2. Well lelahi'jJ In soil.
/
4 Endolul'lan?11D,lfl’ vul3liliRali0|’ a"d pailicle lianspoii
■
-
r
I t
",B "" 3M,Si“
'
l-pacls 0„ ear,„
degradation ofLrdoLLLalthourih |l1,l'i)l(|ly!'''S i 0|’l’eQ' '0 bt? "li'’Or l’alllways [°r
some photodegradation is likely to ucrJr°hriliP
9lkallnS condiUons and
degradation in the enviromiipni k lnniu/ r
vaP(Jur phase
the main mode of
toxicity of Endosulfan
ctdbolism to Endasullan sulphate which retains the
I!
)
PERSISTENCE :
soil
SIW« niodeialely perslsleril In
Dhs^pX'n
Endosullan lalroi-loiv nn r'' 'S .V""0'y
............. .
0.01
lc’1"'1 '"'I'NIy doe to volatility and alpha
»” ».e
mg per litre is tillowcd in wrjtcr
/
L
i
'USb’'<$\W,NWOI(D\NSM.|.;N|)(.,|)( )(-
1
S,o-^CCU/]1UL/\r}c,N :
.Fro,n a animal data it |s
oondudcd llK.it Endosulfan does no! hlo humans.
nut blo-accuiiiulale In
^X':it"^lxz'nclud',d
Endosulfan bio conceiiliaies |fl
fish, particularly as
waler'S^’X'”l«o'ig|'°'!,“ “"•'»« . ..................... ....
melabilis,,, Ir. fish arid lends lo enler ; • : ,,
WS.DUES IN F,C H
’
'
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predominate.
"W entaull.n „d
'
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'
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; ,
Endosullan sulphite, are.
precautions
'■
Don°i apply under J,'
'.could bG execuled Io
D
..,.:?'a“sospi"'iod"iinCC:i*!ai';i'^
-I
....
.'Cl
Do not c 1 •
W"«,..,to9s,Ms„,,0.... u,e,
,v<z
T •
'.•I •.’••
I
Do not ?
forecastI eve., !»o
r
'I
« are
■ °”'’M"''=''«-“-P'»^o.all„sl,„fl3VBa|te,ap-tea||on,
i
found „0 evidence '»
(or low level loxlciiv
”have
a'’
■
dis.upuonVS
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f~^o{/\s-^> c_<<X.£
i
G
Date sent:
From:
Organization:
To:
Subject:
8
■ <4-
Fri, 03 Dec 1999 16:09:18 -0500
Karen Perry <kperry@psr.org>
Physicians for Social Responsibility
Jayakumar <thanal@md4.vsnl.net.in>
Endosulfan fact sheet from U.S. ATSDR
Agency for Toxic Substances and Disease Registry
Endosulfan
September 1995
This fact sheet answers the most frequently asked health questions about
endosulfan. For more information, you may call the ATSDR Information
Center at 1-800-447-1544. This fact sheet is one in a series of
summaries about hazardous substances and their health effects. This
information is important because this substance may harm you. The
effects of exposure to any hazardous substance depend on the dose, the
duration, how you are exposed, personal traits and habits, and whether
other chemicals are present.
SUMMARY: Exposure to endosulfan occurs mainly from eating
contaminated food.
At very high levels, endosulfan affects the cential nervous
system. We don't know if
endosulfan is hazardous when exposure is for a long time at low
levels. This chemical
has been found in at least 143 of the 1,416 National Priorities
List sites identified by
the Environmental Protection Agency.
What is endosulfan?
(Pronounced en’do-sul'fan)
Endosulfan is a cream-to-brown-colored solid that may be in crystals or
flakes and smells like
turpentine. It is an insecticide used to control insects on grains tea
fruits, vegetables, tobacco, and
cotton. In the United States, endosulfan is mainly applied to tobacco
and fruit crops. It is also used
as a wood preservative.
Endosulfan is sold as a mixture of two different forms of the same
chemical (alpha- and
beta-endosulfan). It has not been produced in the United States since
1982; however, it is still used
here to produce other chemicals.
What happens to endosulfan when it enters the environment?
Endosulfan enters the environment primarily through spraying on
I
It does not dissolve easily in water.
In soil, some endosulfan evaporates into air and some breaks down.
It may stay in soil for several years before it all breaks down. ,
It may accumulate in the bodies of fish and other organisms that
endosulfan-contaminated water.
How might I be exposed to endosulfan?
Breathing air near where it has been sprayed as an insecticide on
crops
Drinking water contaminated with it
Eating food contaminated with it
Touching contaminated soil
Smoking cigarettes made from tobacco with endosulfan residues
I
Working in an industry where endosulfan is used.
How can endosulfan affect my health?
Endosulfan mainly affects the central nervous system. Accidental
ingestion and breathing of high
levels of endosulfan results in convulsions and death. Hyperactivity,
tremors, decreased respiration,
and salivation have also been noted in people who ingested high levels
of jt.
These levels are many thousands of times higher than the average
cxpostiK*. We don't know the
etlects from long-term exposure to low levels of endosulfan.
Animal studies have shown effects on the kidneys, testes, developing
fetus, and liver from
longer-term exposure to low levels of endosulfan. The ability of animals
to fight infection was also
lowered.
How likely is endosulfan to cause cancer?
The Department of Health and Human Services has not classified
endosulfan as to its human
carcinogenicity.
The International Agency for Research on Cancer and the Environmental
Protection Agency (ERA)
also have not classified endosulfan as to its human carcinogenioity.
Animal studies have not shown that endosulfan causes cancer, and no
studies in people are
available.
Is there a medical test to show whether I've been exposed to endosulfan?
Tests are available to measure endosulfan levels in the body. These
tests measure endosulfan in
blood, urine, and body tissues.
Because endosulfan leaves the body fairly quickly, these methods are
useful only for finding
*
exposures I hot have occurred within the last lew days.
These tests are not usually available in your doctor's office. However,
a sample taken in the doctor's
office can be shipped to a special laboratory if necessary.
Has the federal government made recommendations to protect human health?
The ERA recommends that the amount of endosulfan in lakes, rivers, and
streams should not be
more than 74 parts endosulfan per billion parts of water (74 ppb).
The ERA allows no more than 0.1 to 2.0 parts of endosulfan to 1 million
parts of food (0.1-2.0
ppm), depending on the type of food product.
The ERA requires that discharges or spills into the environment of 1
pound or more of endosulfan
be reported.
The Food and Drug Administration (FDA) allows no more than 24 parts of
endosulfan to 1 million
parts of dried tea (24 ppm).
The Occupational Safety and Health Administration (OSHA) has set an
occupational exposure limit
of 0.1 milligrams endosulfan per cubic meter (0.1 mg/m3) of air for an
8-hour workday, 40-hour
workweek.
The National Institute for Occupational Safety and Health (NIOSH) and
the American Conference
of Governmental Industrial Hygienists (ACGIH) have established the same
guidelines as OSHA for
• the workplace. These agencies have advised that eye and skin contact
should be avoided because
this may be a route of significant exposure.
Glossary
Carcinogenicity.
Ability to cause cancer.
Ingesting:
Taking food or drink into your body.
Insecticide:
Chemical used to kill insects.
Long-term:
Lasting one year or longer.
Milligram (mg).
One thousandth of a gram
PPB:
Parts per billion.
PPM:
Parts per million.
Short-term:
Lasting 14 days or less.
Wood preservative:
Substance applied to wood to prevent it from rotting.
Relerences
Agency for Toxic Substances and Disease Registry (ATSDR). 1993.
Toxicological profile for
endosulfan. Atlanta, GA: U.S. Department of Health and Human Services
Public Health Service.
Where can I get more information?
ATSDR can tell you where to find occupational and environmental health
clinics. Their specialists
can recognize, evaluate, and treat illnesses resulting from exposure to
hazardous substances. You
can also contact your community or state health or environmental quality
department if you have any
more questions or concerns.
For more information, contact:
Agency for Toxic Substances and Disease Registry
Division of Toxicology
1600 Clifton Road NE, Mailstop E-29
Atlanta, GA 30333
Phone. 1 800-447-1544
FAX: 404-639-6315
U.S. Department of Health and Human Services
Public Health Service
Agency for Toxic Substances and Disease Registry
Karen Perry
Associate Director, Environment & Health Program
Physicians foi Social Responsibility
1101 14th Street, NW Suite 700 Washington, DC 20005
(202) 898-0150 x249 (202) 898-0172 (fax)
Visit PSR’s Web site at http.//www.psr.org!
Atsdr
ENDOSULFAN
AGENCY FOR TOXIC SUBSTANCES
AND DISEASE REGISTRY
CAS # 33213-65-9
Z™ r
*■“
(FAQ.) sboul endosulfan. For m.„
■on, call IhoATSDR Inform.lton Center al 1-S8S-I22-S737. This faei
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HIGHLIGHTS: F
Exposure to endosulfan happens mostly from eating
contaminated food, but may also occur from
-‘amlnmeu air,, or
or drinking
drinking contaminated
IM of 1 577 Not""'"',
"p"”“ • system.
SyS'en'- Endosulfan
E"dos"lfa" has been
b<*" found si" at least
central nervous
of 1,577 National Pnonties List sites identified by the Environmental
Protection Agency (EPA).
What is endosulfan?
(Pronounced en'do-sul-fan)
□ Endosulfan docs not dissolve easily in water. Endosulfan
in surface water is attached to soil particles floating in water
or attached to soil at the bottom.
Endosulfan is a pcsttcide. It is a cream- to brown-colored
solid that may appear in the form of crystals or flakes It
has a smell hke turpentine, but does not burn. It docs not
occur naturally in the environment.
Endosulfan is used to control insects on food and non-food
crops and also as a wood preservative.
Vhat happens to endosulfan when it enters the
-ivironment?
□ Endosulfan enters the air, water, and soil during its
manufacture and use. IIt’ is
’ often
" sprayed onto crops and the
spray may travel long distances before ------it landss on crops,
soil, or water.
□ Endosulfan on ccrops
- f usually breaks down in a few weeks,
but endosulfan sticks to soil particles and may take years to
completely break down.
■I_________
□ Endosulfan can build
I
up in the bodies of animals that live
in endosulfan-contaminated
— —J water;
How might I be exposed to endosulfan?
□ Eating food contaminated with endosulfan, but levels in
foods are very low.
□ People working in industries involved in making
endosulfan or as pesticide applicators.
□ Skin contact with soil containing endosulfan.
How can endosulfan affect my health?
Endosulfan affects the central nervous system and prevents
it from working properly. Hyperactivity, nausea, dizziness,
headache, or convulsions have been observed in adults
exposed to high doses. Severe poisoning may result in
death.
r.s.
lc> h" ’"'’f Siibstuiiet's and Disease Hegistrv
ENDOSULFAN
Page 2
CAS # 33213-65-9
ToxFAQs1'1 Internet address is http://www.atsdr.cdc.< f>ov/to\fa(j.hinil
Studies of the effects of endosulfan on animals suggest that
long-term exposure to endosulfan can also damage the
kidneys, testes, and liver and may possibly affect the body’s
ability to fight infection. However, it is not known if these
effects also occur in humans.
How likely is endosulfan to cause cancer?
We do not know if endosulfan can cause cancer in humans.
Studies in animals have provided inconclusive results.
How can endosulfan affect children?
We do not know if children arc more sensitive to endosulfan
than adults. We do not know if endosulfan can alTcct the
ability of people to have children or if it causes birth defects.
Large amounts of endosulfan damaged the testes of animals,
but it is not known if this damaged their ability to reproduce.
Some birth defects have been seen in the offspring of
animals ingesting endosulfan during pregnancy.
How can families reduce the risk of exposure to
endosulfan?
□ Fresh fruits and vegetables should be washed before
being eaten.
□ Children should not play on grasses that were recently
treated with endosulfan. Carefully follow the directions on
the pesticide label about how long to wait before re-entering
the treated area.
□ People working in a factory making endosulfan and people
using endosulfan should wash clothing, skin, and hair before
going home.
□ Pesticides should be used according to the directions on
the label and stored in the original container in a place that
children cannot reach.
Is there a medical test to show whether I’ve been
exposed to endosulfan?
Endosulfan and its breakdown products can be detected in
your blood, urine, and body tissues if you have been
exposed to a large amount. These tests are not usually
available at your doctors office, but your doctor can send
the samples to a laboratory that can perform the tests.
Because endosulfan leaves the body fairly quickly, these
methods arc useful only for finding exposures that have
occurred within the last few days.
Has the federal government made
recommendations to protect human health?
The EPA recommends that the amount of endosulfan in
rivers, lakes, and streams should not be more than 74 parts
per billion (74 ppb).
The Food and Drug Administration (FDA) allows no more
than 24 parts per million (24 ppm) endosulfan on dried tea.
EPA allows no more than 0.1 to 2 ppm endosulfan on other
raw agricultural products.
Source of Information
Agency for Toxic Substances and Disease Registry
(ATSDR). 2000. Toxicological Profile for Endosulfan.
Atlanta, GA: U.S. Department of Health and Human Services,
Public Health Service.
Where can I get more information? For more information, contact the Agency for Toxic Substances and Disease
Registry, Division of Toxicology, 1600 Clifton Road NE, Mailstop E-29, Atlanta, GA 30333. Phone: 1-888-422-8737,
FAX: 404-639-6359. ToxFAQs™ Internet address is http://www.atsdr.cdc.gov/toxfaq.html. ATSDR can tell you where to
find occupational and environmental health clinics. Their specialists can recognize, evaluate, and treat illnesses resulting
from exposure to hazardous substances. You can also contact your community or state health or environmental quality
department if you have any more questions or concerns.
*•
f H A Z\ L
ro>r (cy i o • r
EXTOXNET
Extension Toxicology Network
Pesticide Information Profiles
A Pesticide Information Project of Cooperative Extension Offices of Cornell University, Oregon
State University, the University of Idaho, and the University of California at Davis and the
Institute for Environmental Toxicology, Michigan State University. Major support and funding
was provided by the USDA/Extension Service/National Agricultural Pesticide Impact
Assessment Program.
EXTOXNET primary files maintained and archived at Oregon State University
Revised June 1996
Endosulfan
Trade and Other Names: Trade or other names for the product include Afidan, Beosit,
Cyclodan, Devisulfan, Endocel, Endocide, Endosol, FMC 5462, Hexasulfan, Hildan, Hoe 2671,
Insectophene, Malix, Phaser, Thiodan, Thimul, Thifor, and Thionex.
Regulatory Status: Endosulfan is a highly toxic pesticide in EPA toxicity class I. It is a
Restricted Use Pesticide (RUP). Labels for products containing endosulfan must bear the Signal
Words DANGER - POISON, depending on formulation.
Chemical Class: chlorinated hydrocarbon
Introduction: Endosulfan is a chlorinated hydrocarbon insecticide and acaricide of the
cyclodiene subgroup which acts as a poison to a wide variety of insects and mites on contact.
Although it may also be used as a wood preservative, it is used primarily on a wide variety of
food crops including tea, coffee, fruits, and vegetables, as well as on rice, cereals, maize,
sorghum, or other grains. Formulations of endosulfan include emsulsifiable concentrate, wettable
powder, ultra-low volume (ULV) liquid, and smoke tablets. It is compatible with many other
pesticides and may be found in formulations with dimethoate, malathion, methomyl,
monocrotophos, pirimicarb, triazophos, fenoprop, parathion, petroleum oils, and oxine-copper. It
is not compatible with alkaline materials. Technical endosulfan is made up of a mixture of two
molecular forms (isomers) of endosulfan, the alpha- and beta-isomers. Information presented in
this profile refers to this technical product unless otherwise stated.
Formulation: Formulations of endosulfan include emulsifiable concentrate, wettable powder,
ultra-low volume (ULV) liquid, and smoke tablets.
Toxicological Effects:
•
Acute toxicity: Endosulfan is highly toxic via the oral route, with reported oral LD50
values ranging from 18 to 160 mg/kg in rats, 7.36 mg/kg in mice, and 77 mg/kg in dogs
[2,9]. It is also highly toxic via the dermal route, with reported dermal LD50 values in
rats ranging from 78 to 359 mg/kg [2,9], Endosulfan may be only slightly toxic via
inhalation, with a reported inhalation LC50 of 21 mg/L for 1 hour, and 8.0 mg/L for 4
hours [2], It is reported not to cause skin or eye irritation in animals [2], The alpha-isomer
is considered to be more toxic than the beta-isomer [2], Animal data indicate that toxicity
may also be influenced by species and by level of protein in the diet; rats which have
been been deprived of protein are nearly twice as susceptible to the toxic effects of
endosulfan [2] Solvents and/or emulsifiers used with endosulfan in formulated products
may influence its absorption into the system via all routes; technical endosulfan is slowly
and incompletely absorbed into the body whereas absorption is more rapid in the
presence of alcohols, oils, and emulsifiers [2], Stimulation of the central nervous system
is the major characteristic of endosulfan poisoning [51], Symptoms noted in acutely
exposed humans include those common to the other cyclodienes, e g., incoordination,
imbalance, difficulty breathing, gagging, vomiting, diarrhea, agitation, convulsions, and
loss of consciousness [2], Reversible blindness has been documented for cows that
grazed in a field sprayed with the compound. The animals completely recovered after a
month following the exposure [2], In an accidental exposure, sheep and pigs grazing on a
sprayed field suffered a lack of muscle coordination and blindness [2],
•
Chronic toxicity: In rats, oral doses of 10 mg/kg/day caused high rates of mortality
within 15 days, but doses of 5 mg/kg/day caused liver enlargement and some other
effects over the same period [2], This dose level also caused seizures commencing 25 to
30 minutes following dose adiministration that persisted for approximately 60 minutes
[2], There is evidence that administration of this dose over 2 years in rats also caused
reduced growth and survival, changes in kidney structure, and changes in blood
chemistry [2,51],
•
Reproductive effects: Rats fed doses of endosulfan of 2.5 mg/kg/day for three
generations showed no observable reproductive effects, but 5.0 mg/kg/day caused
increased dam mortality and resorption [2,51], Female mice fed the compound for 78
weeks at 0.1 mg/kg/day had damage to their reproductive organs [52], Oral dosage for 15
days at 10 mg/kg/day in male rats caused damage to the semeniferous tubules and
lowered testes weights [2,5], It is unlikely that endosulfan will cause reproductive effects
in humans at expected exposure levels.
•
Teiatogenic effects: An oral dose of 2.5 mg/kg/day resulted in normal reproduction in
rats in a three-generational study, but 5 and 10 mg/kg/day resulted in abnormalities in
bone development in the offspring [2,51] Teratogenic effects in humans are unlikely at
expected exposure levels.
•
Mutagenic effects: Endosulfan is mutagenic to bacterial and yeast cells [51]. The
metabolites of endosulfan have also shown the ability to cause cellular changes [2,51].
This compound has also caused mutagenic effects in two different mammalian species
[51] . Thus, evidence suggests that exposure to endosulfan may cause mutagenic effects in
humans if exposure is great enough.
•
Carcinogenic effects: In a long-term study done with both mice and rats, the males of
both groups experienced such a high mortality rate that no conclusions could be drawn
[52] . However, the females of both species failed to develop any carcinogenic conditions
78 weeks after being fed diets containing up to about 23 mg/kg/day. The highest tolerated
dose of endosulfan did not cause increased incidence of tumors in mice over 18 months,
and a later study also showed no evidence of carcinogenic activity in mice or rats [2,52].
It appears that endosulfan is not carcinogenic.
•
Organ toxicity: Data from animal studies reveal the organs most likely to be affected
include kidneys, liver, blood, and the parathyroid gland [51].
•
Fate in humans and animals: Endosulfan is rapidly degraded into mainly water-soluble
compounds and eliminated in mammals with very little absorption in the gastrointestinal
tract [2], In rabbits, the beta-isomer is cleared from blood plasma more quickly thart the
alpha-isomer, with reported blood half-lives of approximately 6 hours and 10 days,
respectively [2], which may account in part for the observed differences in toxicity. The
metabolites are dependent on the mixture of isomers and the route of exposure [2]. Most
of the endosulfan seems to leave the body within a few days to a few weeks.
Ecological Effects:
•
Effects on birds: Endosulfan is highly to moderately toxic to bird species, with reported
oral LD50 values in mallards ranging from 31 to 243 mg/kg [9,53], and in pheasants
ranging from 80 to greater than 320 mg/kg [53]. The reported 5-day dietary LC50 is 2906
ppm in Japanese quail [54]. Male mallards from 3 to 4 months old exhibited wings
crossed high over their back, tremors, falling, and other symptoms as soon as 10 minutes
after an acute, oral dose. The symptoms persisted for up to a month in a few animals [53].
•
Effects on aquatic organisms: Endosulfan is very highly toxic to four fish species and
both of the aquatic invertebrates studied; in fish species, the reported 96-hour LC50
values were (in ug/L): rainbow trout, 1.5; fathead minnow, 1.4; channel catfish, 1.5; and
bluegill sunfish, 1.2. In two aquatic invertebrates, scuds (G. lacustris) and stoneflies
(Pteronarcys), the reported 96-hour LC50 values were, respectively, 5.8 ug/L and 3.3
ug/L [55], The bioaccumulation for the compound may be significant; in the .mussel
(Mytelus edulis) the compound accumulated to 600 times the ambient water
concentration [17].
•
Effects on other organisms: It is moderately toxic to bees and is relatively nontoxic to
beneficial insects such as parasitic wasps, lady bird beetles, and some mites [9,17].
Environmental Fate:
•
Breakdown in soil and groundwater: Endosulfan is moderately persistent in the soil
environment with a reported average field half-life of 50 days [14]. The two isomers have
f
different degradation times in soil. The half-life for the alpha -somer is 35 days, and is
150 days for the beta-isomer under neutral conditions. These two isomers will persist
longer under more acidic conditions. The compound is broken down in soil by fungi and
bacteria [9], Endosulfan does not easily dissolve in water, and has a very low solubility
[9,14], It has a moderate capacity to adhere or adsorb to soils [14]. Transport of this
pesticide is most likely to occur if endosulfan is adsorbed to soil particles in surface
runoff. It is not likely to be very mobile or to pose a threat to groundwater. It has,
however, been detected in California well water [12].
•
Breakdown in water: In raw river water at room temperature and exposed to light, both
isomers disappeared in 4 weeks [12]. A breakdown product first appeared within the first
week. The breakdown in water is faster (5 weeks) under neutral conditions than at more
acidic conditions or basic conditions (5 months) [12]. Under strongly alkaline conditions
the half-life of the compound is 1 day. Large amounts of endosulfan can be found in
surface water near areas of application [51]. It has also been found in surface water
throughout the country at very low concentrations [12].
•
Breakdown in vegetation: In plants, endosulfan is rapidly broken down to' the
corresponding sulfate [9]. On most fruits and vegetables, 50% of the parent residue is lost
within 3 to 7 days [9]. Endosulfan and its breakdown products have been detected in
vegetables (O.OOO5-O.O13 ppm), in tobacco, in various seafoods (0.2 ppt-1.7 ppb), and in
milk [12].
Physical Properties:
•
Appearance: Pure endosulfan is a colorless crystal. Technical grade is a yellow-brown
color [9].
•
Chemical Name: 6,7,8,'9,10,10-hexachloro-1,5,5a,6,9,9a-hexahydro-6,9-methano-2,4,3benzadioxathiepin 3-oxide [9]
•
CAS Number: 115-29-7 (alpha-isomer, 959-98-8; beta-isomer, 33213-65-9)
•
Molecular Weight: 406.96
•
Water Solubility: 0.32 mg/L @ 22 C [9]
•
Solubility in Other Solvents: s. in toluene and hexane [9]
•
Melting Point: Technical material, 70-100 C [9]
•
Vapor Pressure: 1200 mPa @ 80 C [9]
Partition Coefficient: Not Available
•
Adsorption Coefficient: 12,400 [14]
Exposure Guidelines:
•
ADI: 0.006 mg/kg/day [27]
•
MCL: Not Available
RfD: 0.00005 mg/kg/day [8]
PEL: Not Available
HA: Not Available
•
TLV: 0.1 mg/m3 (8-hour) [56]
Basic Manufacturer:
FMC Corporation
Agricultural Chemicals Group
1735 Market Street
Philadelphia, PA 19103
Phone: 215-299-6661
•
Emergency: 800-331-3148
References:
References for the information in this PIP can be found in Reference List Number 6
DISCLAIMER: The information in this profile does not in any way replace or supersede the
information on the pesticide product labeling or other regulatory requirements. Please refer to the
pesticide product labeling.
ENOOSULPH/VN
IS.SIIC
The principal area ofconccrn relates to the bio-accimnilation ol the pesticide endosulphan, used for
spraying cotton crops.
I hive any eases been filed anywhere against the use of eiidosulphan?
Auslralia
•
!Irian McMullin and Leone Margaret McMullin v K'l Australia Operations Ply Ltd and Ors
11997| 541 PC A (24 lune 1997). See: www.austlii.cdu.au and enter “eiidosulphan" as a key word
search.
I his case concerned the potential liability of a manufacturer (K'l) of endosulphan which had been
sprayed on cotton crops. The Federal Court held that ICI, as manufacturers of the chemical, were
negligent in not proving adequate warning to farmers regarding the potential public health risks
associated with feeding cotton residues (such as cotton ginning trash which containing elevated
endosulphan levels) to drought affected cattle.
•
I'livitonincnt Protection Authority r h'rederick Martin Harlow 119931 NSWLEC 42 (23 April
199 3 ). See: wmv-austHi.edn.au and enter “endosulphan" as a key word search.
This case concerned a cotton farmer who was charged with polluting waters contrary to the Clean
Waters Act 1970. Run off of the pesticide endosulphan used on the property had caused a
substantial Fish kill in the local waterways. The court held that it was possible emanating from the
defendant s property may have originated from other sources, it followed (hat it could not be
proven beyond reasonable doubt that the defendant only was liable for (he fish kill. Accordingly,
the offence was not established beyond reasonable doubt.
•
Envitimmcnl Prolection Auihorily v Micheal I'ynn 11992| NSWLEC 62 (5 August 1992). Sec:
wav, an st lii.edu, an and cuter “endosulphan" as a key word search
In this case, (he defendant was charged with on offence undcr#(hc I'nvironmcntal Offences and
Penalties Ad (1989) in that he had polluted waters contrary to (he provisions of (he ('lean Walers
Ad 1970. I he defendant farmer had allowed the pesticide endosulphan to be introduced into the
watcis ol (he local watciway, causing death to a number ol lish. A reduced line was imposed as a
I )ci laity
W hat regulatory controls (legislation, protocols) aie in place or exist?
Protci lion uj the Pra (Powers of Inlervcntian) , ld 10g I Schedule ?. I his Act was enacted
pursuant Io (he Protocol relating to Intervention an the High Peas in ('arcs a/ Pallulion by
Hubstanccxafher than
This was executed in Erusscls in November 1969 and came
genciall) into (on e in 1983. It wax mtified t>y Aiisli.ilia in 1984 I mdosulplLin is spu dually listed
at paiagranh 2 <4 (he Schedule as a “substance which is liable to create hazaids to human health, to
harm living resources and marine life, to damage amenities or to interfere with other legitimate
uses of (he sea. Whenever an intervening party takes action with regards to a substance referred to
in paragraph 2...that Party shall have (he burden of establishing that (he substance, under the
circumstances picscut al (he lime of (he intervention, could reasonably pose a grave and iminent
danger analogous to that posed by any of the substances enumerated in (he list referred lo in
paragraph 2 above".
•
Endosulphan is classed as a restricted substance in relation to Class C and R waters, pursuant to
Regulation 10, Schedule 2 of (he 1992 Water Pollution Regulations (Amendment). Its maximum
concentration is .003 micrograms per litre.
•
Residues containing cndosulphan arc regulated in Australia under the ( hcniical Usage
(. lgn< iilhiral and i'etcrinary) ( 'antral. hl.
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Shell Agriculture
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4 - Product Advice Sheets
lindane
endosulfan
gamma-BHC
gamma-HCH
Common name
Shell trade mark
lindane
(7-BHC, 7-HCH)
endosulfan
WHO Hazard
Class*
Formulation
types
II
EC, WP, LS
II
EC, WP, GR
*The classification refers to the active ingredient.
Hazard summary
i
These are organochlorine (OC) insecticides. They are
hazardous to humans, animals and the environment if
incorrectly or carelessly handled*
It is important that the following precautions are followed during
handling and use.
Storage
All products should be stored under cool and dry conditions in
locked buildings preferably dedicated to insecticides and in a
bunded area. Store out of the reach of children and away from
foodstuffs and animal feed.
Transport
Comply with any local requirements regarding movement of
hazardous goods. Do not transport with foodstuffs. Check that
containers are correctly labelled before despatch.
Transport accident
procedures
P
Before dealing with any accidents ensure that the advice given
under Personal Protection (below) will be followed.
►
►
4
Contact the emergency services (fire, police) and call an
ambulance if there are injuries.
Consult the Tremcard’ (see Section 1.4) carried by drivers of
road vehicles, if available.
Contact the local Shell company and inform them of the
accident and of the actions taken.
Liquid products
►
Keep spectators away from leaking product and do not allow
smoking or use of naked flames at the scene of the accident.
Prevent liquid-from spreading or contaminating other cargo,
vegetation or waterways, with a barrier of the most suitable,'
readily available material eg, earth or sand.
i
Absorb spilled liquid with spill control material, sawdust, sand or
earth, and place it in a cioseable container for subsequent safe
disposal (see ‘Waste disposal’).
I
Shell Agriculture Safety Guide
i
i .
Page 223
•4 '
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'I
<4^^ ■
<
4 - Product Advice Sheets
I
I
i
Solid products
Decontamination
Keep spectators well away from spillage. Avoid raising a dust
cloud.
t
Use an industrial vacuum cleaner or add damp sawdust, sand or
earth to the spilled product, then sweep up the residue into a
suitable container (eg, closed-top drum) for subsequent safe
disposal (see Waste disposal).
As soon as possible after the accident, cover all contaminated
areas with spill control material, damp sawdust, sand or earth.
Sweep up the residue and place it in a closeable container for
subsequent safe disposal (see 'Waste disposal’ below).
L
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4
Scrub contaminated areas with detergent solution and rinse with
water. As far as possible, retain rinsings as contaminated waste.
Avoid run-off into drains and water courses.
Check that other goods or cargo are not contaminated.
Personal protection
When unloading or handling containers, wear protective nitrile
rubber or neoprene gloves.
Avoid contact with the skin and eyes. Wash off any skin
contamination with soap and water. If eyes are contaminated
flush well with clean water. If irritation persists, obtain medical
attention.
If clothes or overalls become contaminated, remove them and
wash the skin beneath. Launder clothes before reuse.
4
i
.i
When handling leaking containers, or when cleaning up leakage
or spillage, wear overalls, nitrile rubber or neoprene gloves and
rubber boots.
Wash hands and exposed skin before smoking, eating or
drinking and after work.
Environmental
protection
These insecticides are moderately persistent. Do not allow to
contaminate soil or water. Keep away from all forms of wild life.
Safety in use
Follow the advice under Personal Protection. Items in the
‘Gardman’ protective clothing pack (see Section 1.5) will give
protection during handling formulations and application in the
field.
Handling formulations
Avoid exposure to the skin, eyes,‘nose and mouth. Wear
overalls or long sleeve shirt and long trousers, neoprene or
nitrile rubber gioves, face shield or goggles and boots or shoes.
Avoid raising a dust cloud from wettable powder formulations.
Application in the field
Avoid exposure to the spray. Wear overalls or long sleeve shirt
and long trousers, hat or cap and.boots or shoes.
I
i
I
I
I
4
Do not spray against the wind.
Triple rinse empty containers with water and add the rinsings to
the spray tank.
>
4
I
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Shell Agriculture Safety Guide
Page 224
4
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f
4 - Product Advice Sheets
After work
Ensure that equipment is thoroughly cleaned and stored away
ready for use the next time. Carry out any essential
maintenance.
Partly used containers should be reclosed and returned to store.
Empty containers should be disposed of as advised below.
Change out of working clothes and take a bath or shower.
Waste disposal
Emergency situations
Leaks and spills
Lindane and endosulfan are not readily decomposed chemically
or biologically and are moderately persistent in the environment.
Waste material, or surplus or redundant stock must be burned in
a proper incinerator (see Section 1.9) designed for
organochlorine pesticide waste disposal. Comply with any local
legislation regarding disposal of toxic wastes. Seek further
advice from your local Shell Chemical Company or distributor.
Ensure that the advice given under Personal Protection will be
followed.
Stofi leaks, if this can be done without risk.
Absorb spillage with spill control material, sawdust, sand or
earth and place in a clean, labelled container for later safe
disposal.
Empty any product remaining in damaged or leaking containers
into clean, empty drums which should be closed and labelled.
■ Empty containers should be rinsed three times with water at the
rate of 1 litre per 20 litres drum capacity. Swirl round to rinse the
container walls, empty and add the rinsings to the absorbents. ■
Scrub contaminated areas with detergent solution and rinse with
water. As far as possible, retain all rinsings as contaminated
waste. Avoid run-off into drains and water courses.
Fire
Powder products will not burn. Liquid products will burn and
emulsifiable concentrates are miscible with water.
Advise the fire service that smoke and fumes could be
hazardous through inhalation, or absorption through the skin.
Wear full protective clothing and self-contained breathing
apparatus.
4
Use alcohol-resistant foam, CO2 or powder.
Confine the use of water spray to cooling of unaffected stock,
thus avoiding the accumulation of polluted run-off from the site.
I
In case of poisoning
These products are toxic by mouth, by skin contact (especially
liquid formulations) and by inhalation of dust from powder
formulations.
Symptoms of poisoning
Headache, dizziness, nausea. Severe poisoning progresses to
vomiting, muscular weakness and convulsions. Death may
result form cardiac arrest. Chronic intoxication may produce
convulsions alone, without earlier symptoms.
1
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Shell Agriculture Safety Guide
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3
4 - Product Advice Sheets
First Aid
If poisoning symptoms occur, particularly if there has been
known contamination or gross exposure, OBTAIN MEDICAL
ATTENTION IMMEDIATELY.
Skin contact:
Remove contaminated clothing. Wash exposed skin with soap
and water.
Eye contact:
Flush eyes well with water. If irritation persists, obtain medical
attention.
Ingestion:
Do not induce vomiting. If the patient is conscious, give a large
amount of activated charcoal powder with water. Do not give
oils or milk as these will assist absorption.
Antidote:
There is no specific antidote.
i
Medical advice
The following is a short text suitable for product labels,
information sheets, etc. For full details of medical treatment of
intoxication by OCs, refer to Section 2.3.
t
Lindane and endosulfan are central nervous system stimulants.
Convulsions are a sign of serious intoxication, but may be
delayed for 48 hours following exposure.
i
Treatment is symptomatic, aimed at eliminating the material from
the body, controlling convulsions and restoring respiration.
If ingested, gastric lavage is indicated, followed by activated
charcoal powder.
To control convulsions, use benzodiazepines {clonazepam or
diazepam). If not available, use phenobarbital sodium.
Diazepam is recommended, injected intravenously. Large
quantities may be required. When convulsions are under
control, continue with phenobarbitone (oral) for up to 2-4 weeks.
Morphine or its derivatives, epinephrine and nor-adrenalin are
contraindicated.
Shell Agriculture Safety Guide
................................................................
Page 226
a
THANAl
POST FOX No. 315
Articles
KaWDI 4P.TMRUVAN
KERALAM.
Pi
iTM
: •? .'03
Environmental Health Perspectives Volume 109, Number 7, July 2001
Endosulfan Exposure Disrupts Pheromonal Systems in the
Red-Spotted Newt: A Mechanism for Subtle Effects of
Environmental Chemicals
Daesik Park, Steven C. Hempleman, and Catherine R. Propper
Department of Biological Sciences, Northern Arizona Uiiiversity, Flagstaff, Arizona, USA
Abstract
Because chemicals introduced into the environment by humans can affect both long-term
survivorship and reproduction of amphibians, discovering the specific mechanisms through which
these chemicals act may facilitate the development of plans for amphibian conservation. We
investigated the amphibian pheromonal system as a potential target of common environmental
chemicals. By treating female red-spotted newts, Notophthalmus viridescens, to a commonly used
insecticide, endosulfan, we found that the pheromonal system is highly susceptible to
low-concentration exposure. The impairment of the pheromonal system directly led to disrupted
mate choice and lowered mating success. There were no other notable physiologic or behavioral
changes demonstrated by the animals at the insecticide concentrations administered. Our findings
suggest that the amphibian pheromonal system is one of the systems subject to subtle negative
effects of environmental chemicals. Key words: amphibian declines, electro-olfactogram,
endosulfan, environmental chemicals, insecticides, pheromones, olfaction. Environ Health
Perspect 109:669-673 (2001). [Online 22 June 2001]
http://ehpnetl .niehs.nih.gov/docs/2001/109p669-673park/abstract.html
Address correspondence to D. Park, Department of Biological Sciences, Northern Arizona University, Flagstaff,
AZ 86011-5640, USA. Telephone: (520) 523-1344. Fax: (520) 523-7500. E-mail: dacsikpark@hotmail.com
We thank K.C. Nishikawa, L.C. Drickamer, L. Rania, L. Mayer, S. Overstreet, and M. Minor for their help
during experiments and for their useful comments on early versions of the manuscript. C. A. Dyer kindly provided
antiserum for the radioimmunoassay.
This study was supported by the Council for Tobacco Research, USA (grant 4661R1 to C.R.P.) and by the
International Rotary Foundation (D.P.).
Received 13 November 2000; accepted 2 February 2001.
I Articles Online First) f Full Article) [Full Article in PDF)
Last Updated: June 22, 2001
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TITLE:
An anthropological approach to the evaluation of preschool children
exposed to pesticides in Mexico.
AUTHORS:
GUILLETTE EA; MEZA MM; AQUILAR MG; SOTO AD; GARCIA
IE
32 SW 43rd Terrace, Gainesville, FL 32607, USA.
AUTHOR
AFFILIATION:
ENVIRONMENTAL HEALTH PERSPECTIVES; 106 (6). 1998.
SOURCE:
347-353.
SECONDARY
SOURCE ID:
BIOSIS/98/26812
ABSTRACT:
BIOSIS COPYRIGHT: BIOL ABS. In this comparative study, we
compensated for many of the known variables that influence children ’s
growth and development by selecting two groups of 4-5-year-old
Yaqui children who reside in the Yaqui Valley of northwestern
Mexico. These children share similar genetic backgrounds, diets,
water mineral contents, cultural patterns, and social behaviors. The
major difference was their exposure to pesticides. Pesticides have been
applied to the agricultural area of the valley since the late 1940s. In
1990, high levels of multiple pesticides were found in the cord blood of
newborns and in breast milk. Building on anthropological methods for
rapid rural appraisal of problems within the environment, a Rapid
Assessment Tool for Preschool Children (RATPC) was developed to
measure growth and development. The children of the agrarian region
were compared to children living in the foothills, where pesticide use is
avoided. The RATPC measured varied aspects of physical growth and
abilities to perform, or function in, normal childhood activities. No
differences were found in growth patterns. Functionally, the exposed
children demonstrated decreases in stamina, gross and fine eye-hand
coordination, 30-minute memory, and the ability to draw a person. The
RATPC also pointed out areas in which more in-depth research on the
toxicology of pesticides would be valuable.
MAIN MESH
HEADINGS:
*MORBIDITY
^NEOPLASMS
ADDITIONAL
MESH
HEADINGS:
ENVIRONMENTAL POLLUTANTS/POISONING
OCCUPATIONAL DISEASES
CHILD DEVELOPMENT
PEDIATRICS
AIR POLLUTION
SOIL POLLUTANTS
WATER POLLUTION
HERBICIDES
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TITLE:
The pesticides endosulfan, toxaphene, and dieldrin have estrogenic
effects on human estrogen-sensitive ceils.
AUTHORS:
Soto AM; Chung KL; Sonnenschein C
AUTHOR
Department of Anatomy and Cellular Biology, Tufts University School
AFFILIATION: of Medicine, Boston, MA 02111.
SOURCE:
Environ Health Perspect; VOL 102, ISS 4, 1994, P380-3
SECONDARY
TOXBIB/95/009826
SOURCE ID:
ABSTRACT:
Estrogenic pesticides such as DDT and chlordecone generate
deleterious reproductive effects. An "in culture” bioassay was used to
assess the estrogenicity of several pesticides. The E-screen test uses
human breast estrogen-sensitive MCF7 cells and compares the cell
yield achieved after 6 days of culture in medium supplemented with
5% charcoal-dextran stripped human serum in the presence (positive
control) or absence (negative control) of estradiol and with diverse
concentrations of xenobiotics suspected of being estrogenic. Among the
organochlorine pesticides tested, toxaphene, dieldrin, and endosulfan
had estrogenic properties comparable to those of DDT and
chlordecone; the latter are known to be estrogenic in rodent models.
The E-screen test also revealed that estrogenic chemicals may act
cumulatively; when mixed together they induce estrogenic responses
at concentrations lower than those required when each compound is
administered alone.
MAIN MESH
HEADINGS:
Dieldrin/*ADVERSE EFFECTS
Endosulfan/*ADVERSE EFFECTS
Receptors, Estrogen/*DRUG EFFECTS
Toxaphene/*ADVERSE EFFECTS
ADDITIONAL
MESH
HEADINGS:
Biological Assay
Breast Neoplasms/PATHOLOGY
Cell Division/DRUG EFFECTS
Drug Synergism
Female
Human
Support, Non-U.S. Gov’t
Support, U.S. Gov’t, Non-P.H.S.
Support, U.S. Gov’t, P.H.S.
Tumor Cells, Cultured
PUBLICATION JOURNAL ARTICLE
TYPES:
#
CONCLUSIONS
Endosulfan should be banned as a compound in India for cashew plantation or
any other crop, just like all other organochlorine compounds. Organochlorines
are not adapted to local growing conditions or to local patterns of use.
Endosulfan’s high short-term toxicity in particular has alerted the plantation
corporations in Kerala against the using of endosulfan as a compound for
cashew plantation.
Decision-making cashew plantation pesticide use in parts of Kerala
should be more consultative, rather than remaining in the hands of PCK. It
needs to be more open and public so that other cashew planter and development
experts, other stakeholders and groups such as consumers’ unions and
environmental NGOs are actively involved. Integrated management of pests,
pesticides, pesticide resistance and crops requires an interdisciplinary and
participative approach that goes well beyond the technical level to include socioeconomic, cultural and ecological considerations, as well as the preferences of
farmers, livestock herders and fishing communities. Personnel and consumers of
food crops from cashew growing areas in this areas..
The CSE project has made a small start by copying the already mixed
Australian experiences and West African with endosulfan use of cashew growing
conditions without adequate consideration of local conditions and patterns of
pesticide use. The result should open up as soon as possible, and actively invite
other stakeholders to participate in the design, elaboration, execution, monitoring
and evaluation or strategies put in place to manage pests, pesticides, pesticide
resistance and crops.
18
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TITLE:
Responses of the L5178Y tk+/tk- mouse lymphoma cell forward
mutation assay: HI. 72 coded chemicals [published erratum appears in
Environ Mol Mutagen 1988;12(3):345|
AUTHORS:
McGregor DB; Brown A; Cattanach P;,Edwards I; McBride D; Riach
C; Caspary WJ
Inveresk Research International, Limited, Musselburgh, United
AUTHOR
AFFILIATION: Kingdom.
SOURCE:
Environ Mol Mutagen; VOL 12, ISS 1,1988, P85-154
SECONDARY
SOURCE ID:
TOXBIB/88/254784
ABSTRACT:
Seventy-two chemicals were tested for their mutagenic potential in the
L5178Y tk+/- mouse lymphoma cell forward mutation assay, using
procedures based upon those described by Clive and Spector (Mutat
Res 44:269-278,1975) and Clive et al. (Miitat Res 59:61-108,1979).
Cultures were exposed to the chemicals for 4 hr, then cultured for 2
days before plating in soft agar with or without trifluorothymidine
(TFT), 3 micrograms/ml. The chemicals were tested at least twice.
Significant responses were obtained with allyl isothiocyanate,
p-benzoquinone dioxime, benzyl acetate, 2-biphenylamine HO,
bis(2-chloro-l-methylethyl)ether, cadmium chloride, chlordane,
chlorobenzene, chlorobenzilate, 2-chIoroethanol, chlorothalonil,
cytarabine.HCl, p,p'-DDE, diazinon, 2,6-dichloro-p-phenylenediamine,
N,N-diethylthiourea, diglycidylresorcinol ether, 2,4-dimethoxy
aniline.HO, disperse yellow 3, endosulfan, 1,2-epoxyhexadecane, ethyl
acrylate, ethyl benzene, ethylene thiourea, F D and C yellow Number 6,
furan, heptachlor, isophorone, mercuric chloride,
4,4'-methylenedianiline.2 HC1, methyl viologen, nickel sulfate.6H2O,
4,4*-oxydianiline, pentachloroethane, piperonyl butoxide, propyl
gallate, quinoline, rotenone, 2,4,5,6-tetrachloro-4-nitro-anisoIe,
1.1.1.2-tetrachloroethane, trichlorfon, 2,4,6-trichlorophenol,
2,4,5-trimethoxybenzaldehyde, l,l,3-trimethyl-2-thiourea,
1- vinyl-3-cyclopetene dioxide, vinyl toluene, and ziram. Apart from
2- biphenylamine.HCI, 2-chloroethanol, disperse yellow 3, ethylene
thiourea, FD and C yellow number 6, phenol, and
1.1.2- tetrachloroethane, rat liver S9 mix was not a requirement for
these compounds. Chemicals not identified as mutagens were acid red,
11-aminoudecanoic acid, boric acid, 5-chloro-o-toluidine, coumaphos,
cyclohexanone, decabromodiphenyl oxide, di(2-ethylhexyl)adipate,
ferric chloride, fluometuron, melamine, monuron, phenesterin,
phthalimide, reserpine, sodium dodecyl sulfate, 4,4-sulfonyldianiline,
tetrachloroethylene, and zearalenone. The assay was incapable of
ENDOSULFAN SPRAY PROTEST ACTION COMMITTEE ( ESPAC)
Perla - Padre - 671552
Kasaragod , Kerala
Correspondence: C/0 Kajampady Nursing Home , Post Perla 671552
19th October 2001
To,
Smt K R Gowri Amnia,
Hon’ble Minister for Agriculture
Government of Kerala.
Respected Madam,
Subject:
White Paper
on the
Report on the visit of the Expert Team of the Kerala Agricultural University
for Investigating the environmental effects on aerial sprayed endosulfan on
cashew plantations in Perla Area of Kasaragod District
We hope you will remember that we had come to meet you to appraise you of the
plight of our villagers who have been exposed to more than 20 years of aerial
spraying of endosulfan - a highly toxic pesticide.
We wish to convey our heartfelt gratitude to you for having taken serious view of
the matter. We are glad and proud to note that you have upheld the
Precautionary Principle and issued a ban order on the use of endosulfan in the
State. This has given us a feeling of relief.
Meanwhile, in February an expert committee set up by the Kerala Agriculture
University had made a visit of the area to study the problems and had submitted
a report on the visit. We found that the report was highly biased, full of wrong
information and an insult to the already affected people. So, we have brought
out a white-paper on this report. Through this white paper we wish to place the
actual facts of the visit, the facts about the chemical-endosulfan and the
regulations, before the people of the State and your kind self.
We feel that such scientists as the ones who came to visit and study the area are
doing irreparable damage to the credibility of scientific institutions and must be
held primarily responsible and suitably admonished.
We have enclosed a copy of this report for your kind perusal. We once again
thank you for the humane decision and for upholding people’s problems above
private profits.
Yours truly,
i
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TITLE:
Environmental chemicals with hormorie-like properties: A human
health problem?
AUTHORS:
AUTHOR
HOLME JA; DYBING E
SOURCE:
TIDSSKRIFT FOR DEN NORSKE LAEGEFORENING; 117 (1)
1997.70-73.
SECONDARY
SOURCE ID:
BIOSIS/97/06661
ABSTRACT:
BIOSIS COPYRIGHT: BIOL ABS. Lately, a hypothesis linking higher
frequency of testicular cancer, reduced semen quality and
malformation of the male sexual organs with increased
embryonic/foetal exposure to oestrogenic chemicals has received wide
attention in the media. There are several examples where point-source
chemical pollution has been convincingly associated with
endocrine-related changes in wildlife. Such changes have also been
reproduced in experimental studies. There is very little evidence,
however, of such an association in humans. Nevertheless, the findings
provide a clear challenge to toxicologists and epidemiologists in order
to elucidate possible public health risks from environmental exposure
to chemicals with hormone-like effects. Better test strategies and
reproductive toxicity test guidelines are needed in order to assess any
such risks, and to provide a basis for possible regulatory action.
MAIN MESH
HEADINGS:
NEOPLASMS/*PATHOLOGY
Avdeling Miljomedisin, Statens Inst. Folkehelse, Postboks 4404
AFFILIATION: Torshov, 0403 Oslo, Norway.
ADDITIONAL
MESH
HEADINGS:
BIOCHEMISTRY
GENITALIA/PATIIOLOGY
GEN ITALIA/PH YSIO PATHO LOGY
REPRODUCTION
AIR POLLUTION
SOIL POLLUTANTS
WATER POLLUTION
HOMINIDAE
CAS REGISTRY 12789-03-6; 8001-35-2; 1746-01-6; 789-02-6; 241-55-4; 115-29-7;
NUMBERS:
88-99-3; 80-05-7; 72-43-5; 60-57-1; 56-53-1; 50-28-2
LANGUAGES: NOR
KEYWORDS:
Biochemical Studies-General
Reproductive System-Pathology
Neoplasms and Neoplastic Agents-Pathology; Clinical Aspects;
Systemic-Effects— ---------------- ------------- .
_
----------- --------------- —CompHa tion . on Zero- IVaete
TTiaiiaI
CONCLUSIONS
Endosulfan should be banned as a compound in India for cashew plantation or
any other crop, just like all other organochlorine compounds. Organochlorines
are not adapted to local growing conditions or to local patterns of use.
Endosulfan’s high short-term toxicity in particular has alerted the plantation
corporations in Kerala against the using of endosulfan as a compound for
cashew plantation.
Decision-making cashew plantation pesticide use in parts of Kerala
should be more consultative, rather than remaining in the hands of PCK. It
needs to be more open and public so that other cashew planter and development
experts, other stakeholders and groups such as consumers’ unions and
environmental NGOs are actively involved. Integrated management of pests,
pesticides, pesticide resistance and crops requires an interdisciplinary and
participative approach that goes well beyond the technical level to include socio
economic, cultural and ecological considerations, as well as the preferences of
farmers, livestock herders and fishing communities. Personnel and consumers of
food crops from cashew growing areas in this areas.
The CSE project has made a small start by copying the already mixed
Australian experiences and West African with endosulfan use of cashew growing
conditions without adequate consideration of local conditions and patterns of
pesticide use. The result should open up as soon as possible, and actively invite
other stakeholders to participate in the design, elaboration, execution, monitoring
and evaluation or strategies put in place to manage pests, pesticides, pesticide
resistance and crops.
t
i
18
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TITLE:
Human red blood cel! membrane damage by endosulfan.
AUTHORS:
Daniel CS; Agarwal S; Agarwal SS
SOURCE:
Toxicol Lett; VOL 32, ISS 1-2,1986, Pl 13-8
SECONDARY
SOURCE ID:
TOXBIB/86/290405
ABSTRACT:
Endosulfan is a chlorinated hydrocarbon insecticide. Its in vitro
toxicity on human red blood cell membrane was studied by staining
with a fluorochrome dye, merocyanine-540 (MC-540) and Scanning
Electron Microscopy (SEM). At a concentration of 0.001
microgram/ml (1 ppb) endosulfan was found to damage human red cell
membranes as demonstrated by fluorescence of 30-50% of red cells on
staining with MC-540. This was supported by the finding of crenation
and threading of red blood cells under SEM. At concentration of 1
microgram/ml (1 ppm) the cells were markedly damaged.
MAIN MESH
HEADINGS:
Endosulfan/*TOXICITY
Erythrocyte Membrane/*DRUG EFFECTS
ADDITIONAL
MESH
HEADINGS:
Erythrocyte Membrane/METABOLISM
Erythrocyte Membrane/ULTRASTRUCTURE
Hemoglobins/SECRETION
Human
In Vitro
Microscopy, Electron, Scanning
Microscopy, Fluorescence
Pyrimidinones/DIAGNOSTIC USE
PUBLICATION JOURNAL ARTICLE
TYPES:
tr
1);.
VI
>
CAS REGISTRY 0 (Pyrimidinones)
NUMBERS:
115-29-7 (Endosulfan)
58823-12-4 (merocyanine dye)
LANGUAGES:
Help)
L
Eng
|Order Documents} | Other Years; [Log off IGM)
[Next Record! | Details of Search} [Return to Results) [Return to Search Screen [Previous Record}
CONCLUSIONS
Endosulfan should be banned as a compound in India for cashew plantation or
any other crop, just like all other organochlorine compounds. Organochlorines
are not adapted to local growing conditions or to local patterns of use.
Endosulfan’s high short-term toxicity in particular has alerted the plantation
corporations in Kerala against the using of endosulfan as a compound for
cashew plantation.
Decision-making cashew plantation pesticide use in parts of Kerala
should be more consultative, rather than remaining in the hands of PCK. It
needs to be more open and public so that other cashew planter and development
experts, other stakeholders and groups such as consumers’ unions and
environmental NGOs are actively involved. Integrated management of pests,
pesticides, pesticide resistance and crops requires an interdisciplinary and
participative approach that goes well beyond the technical level to include socio
economic, cultural and ecological considerations, as well as the preferences of
farmers, livestock herders and fishing communities. Personnel and consumers of
food crops from cashew growing areas in this areas.
The CSE project has made a small start by copying the already mixed
Australian experiences and West African with endosulfan use of cashew growing
conditions without adequate consideration of local conditions and patterns of '
pesticide use. The result should open up as soon as possible, and actively invite
other stakeholders to participate in the design, elaboration, execution, monitoring
and evaluation or strategies put in place to manage pests, pesticides, pesticide
resistance and crops.
18
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TITLE:
Studies on the genotoxicity of endosulfan, an organochlorine
insecticide, in mammalian germ cells.
AUTHORS:
Pandey N; Gundevia F; Prem AS; Ray PK
AUTHOR
AFFILIATION:
Environmental Microbiology Section, Industrial Toxicology Research
Center, Mahatma Gandhi Marg, Lucknow, India.
SOURCE:
Mutat Res; VOL 242, ISS 1,1990, Pl-7
SECONDARY
SOURCE ID:
TOXBIB/90/363236
ABSTRACT:
The genotoxic potential of endosulfan was assessed in mouse germ cells
by 2 in vivo tests: the dominant lethal and the sperm shape
abnormality test. At higher doses, endosulfan induced dominant lethal
mutations in one mating interval (36-42 days) post treatment. A
statistically significant dose-dependent increase in sperm
abnormalities was observed with endosulfan treatment. At high doses
the sperm count decreased up to 39%. No change in sperm motility
was observed at any dose level. On the basis of the present in vivo
results, it appears that endosulfan has a damaging effect on
spermatogonia! cells as well as on sperm morphology.
MAIN MESH
HEADINGS:
Endosulfan/*TOXICITY
*Mutagens
Spermatozoa/*DRUG EFFECTS
ADDITIONAL
MESH
HEADINGS:
Animal
Female
Genes, Dominant/DRUG EFFECTS
Male
Mice
Mice, Inbred Strains
Mutagenicity Tests
Spermatozoa/ABNORMALITIES
Support, Non-U.S. Gov’t
PUBLICATION JOURNAL ARTICLE
TYPES:
CAS REGISTRY 0 (Mutagens)
NUMBERS:
115-29-7 (Endosulfan)
LANGUAGES: Eng
f:
Help'
jOrdcr Documents ; Other Years; jLog off IGM!
! Next Record; | Details of Search!; Return to Results] [ Return to Search Screen] |PreviousJ<ecord!
CONCLUSIONS
Endosulfan should be banned as a compound in India for cashew plantation or
any other crop, just like all other organochlorine compounds. Organochlorines
are not adapted to local growing conditions or to local patterns of use.
Endosulfan’s high short-term toxicity in particular has alerted the plantation
corporations in Kerala against the using of endosulfan as a compound for
cashew plantation.
Decision-making cashew plantation pesticide use in parts of Kerala
should be more consultative, rather than remaining in the hands of PCK. It
needs to be more open and public so that other cashew planter and development
experts, other stakeholders and groups such as consumers’ unions and
environmental NGOs are actively involved. Integrated management of pests,
pesticides, pesticide resistance and crops requires an interdisciplinary and
participative approach that goes well beyond the technical level to include socio
economic, cultural and ecological considerations, as well as the preferences of
farmers, livestock herders and fishing communities. Personnel and consumers of
food crops from cashew growing areas in this areas.
The CSE project has made a small start by copying the already mixed
Australian experiences and West African with endosulfan use of cashew growing
conditions without adequate consideration of local conditions and patterns of >
pesticide use. The result should open up as soon as possible, and actively invite
other stakeholders to participate in the design, elaboration, execution, monitoring
and evaluation or strategies put in place to manage pests, pesticides, pesticide
resistance and crops.
18
Articles ___
Environmental Health Perspectives, Volume 102, Number 4, April 1994
[Citation in PubMed] [Related Articles]
The Pesticides Endosulfan, Toxaphene, and Dieldrin Have
Estrogenic Effects on Human Estrogen-Sensitive Cells
Ana M. Soto, Kerrie L. Chung, and Carlos Sonnenschein
Department of Anatomy and Cellular Biology, Tufts University School of Medicine Boston MA
02111 USA
Abstract
Estrogenic pesticides such as DDT and chlordecone generate deleterious reproductive effects. An
in culture" bioassay was used to assess the estrogenicity of several pesticides. The E-screen test
uses human breast estrogen-sensitive MCF7 cells and compares the cell yield achieved after 6 days
of culture in medium supplemented with 5% charcoal-dextran stripped human serum in the presence
(positive control) or absence (negative control) of estradiol and with diverse concentrations of
xenobiotics suspected of being estrogenic. Among the organochlorine pesticides tested, toxaphene,
dieldrin, and endosulfan had estrogenic properties comparable to those of DDT and chlordecone; ?
the latter are known to be estrogenic in rodent models. The E-screen test also revealed that
estrogenic chemicals may act cumulatively; when mixed together they induce estrogenic responses
at concentrations lower than those required when each compound is administered alone. Key
words: bioassay, estrogens, pesticides, xenobiotic. Environ Health Perspect 102: 380-383(1994)
blipy/ehpnetl.niehs.nih.^ov/docs/l994/102-4/soto.html
Address correspondence to A.M. Soto, Department of Anatomy and Cellular Biology, Tufts University School of
Medicine, 136 Harrison Avenue, Boston, MA 02111 USA.
We thank Howard Bern, M. Fatima Olea-Serrano, and Nicolas Olea for their helpful advice. This work was
partially supported by grants from the W. Alton Jones Foundation, EPA-CR 820301 NIH-CA-13410 and
NSF-DCB-9105594.
Received 12 November 1993; accepted 16 February 1994.
[Table ofContentsI [Full Aniclcj [Citation in PubMedl [Related Articles!
Last Update: August 14, 1998
CONCLUSIONS
Endosulfan should be banned as a compound in India for cashew plantation or
any other crop, just like all other organochlorine compounds. Organochlorines
are not adapted to local growing conditions or to local patterns of use.
Endosulfan’s high short-term toxicity in particular has alerted the plantation
corporations in Kerala against the using of endosulfan as a compound for
cashew plantation.
Decision-making cashew plantation pesticide use in parts of Kerala
should be more consultative, rather than remaining in the hands of PCK. It
needs to be more open and public so that other cashew planter and development
experts, other stakeholders and groups such as consumers’ unions and
environmental NGOs are actively involved. Integrated management of pests,
pesticides, pesticide resistance and crops requires an interdisciplinary and
participative approach that goes well beyond the technical level to include socio
economic, cultural and ecological considerations, as well as the preferences of
farmers, livestock herders and fishing communities. Personnel and consumers of
food crops from cashew growing areas in this areas.
The CSE project has made a small start by copying the already mixed
Australian experiences and West African with endosulfan use of cashew growing
conditions without adequate consideration of local conditions and patterns of '
pesticide use. The result should open up as soon as possible, and actively invite
other stakeholders to participate in the design, elaboration, execution, monitoring
and evaluation or strategies put in place to manage pests, pesticides, pesticide
resistance and crops.
18
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TITLE:
Bioaccumulative potential and toxicity of endosulfan insecticide to
non-target animals.
AUTHORS:
Naqvi SM; Vaishnavi C
AUTHOR
Department of Biology, Southern University, Baton Rouge, LA 70813.
AFFILIATION:
SOURCE:
SECONDARY
SOURCE ID:
ABSTRACT:
Comp Biochem Physiol C; VOL 105, ISS 3,1993, P347-61 (REF: 116)
TOXBIB/94/037942
1. Endosulfan insecticide is a polychlorinated compound used for
controlling a variety of insects; it is practically water-insoluble, but
readily adheres to clay particles and persists in soil and water for
several years. Its mode of action involves repetitive nerve-discharges
positively correlated to increase in temperature. This compound is
extremely toxic to most fish and can cause massive mortalities. In fish, it
causes marked changes in Na and K concentrations, decrease in blood
Ca(2+) and Mg levels and inhibits Na, K and Mg-dependent ATPase
(in brain). 2. Bioaccumulation of endosulfan is reported for marine
animals; however, freshwater animals (e.g., crayfish) accumulate it to
some extent, but they lose the compound rapidly during depuration.
Endosulfan is generally less toxic to aquatic invertebrates than fish.
However, it causes decreases in adenylate energy charge, oxygen
consumption, hemolymph amino acids, succinate dehydrogenase,
heart-beat (mussel) and altered osmoregulation. 3. Generally,
mammals are less susceptible to endosulfan’s toxicity than aquatic
animals. The majority of studies conducted on laboratory mammals can
be summarized, (a) Neurotoxicity: male rats are more sensitive than
females to endosulfan, which decreases brain and plasma
acetylcholinesterase activity. Endosulfan I (a metabolite) causes a
significant change in norepinephrine, 5-HT and GABA, (b) Renal
toxicity: inhibition of MFOs activity was noticed in rats; other effects
included changes in proximal convoluted tubules and necrosis of the
tubular epithelium, (c) Hepatotoxicity: chemically-induced
aminopyrine N-demethylase and aniline hydrolase were found in rat
liver, and reduction in the glycogen level occurred, (d) Hematologic
toxicity: endosulfan exposure resulted in a significant decrease in the
level occurred, (d) Hematologic toxicity: endosulfan exposure resulted
in a significant decrease in the erythrocyte glutathione reductase,
hemoglobin amount, RBC number and mean corpuscular volume. 4.
Respiratory toxicity: involved dyspnea, acute emphysema, cyanosis
and hemorrhages in teh interalveolar portions of rat’s lungs. 5.
Biochemical: in rats, endosulfan caused increased glucose-6-phosphate
CONCLUSIONS
Endosulfan should be banned as a compound in India for cashew plantation or
any other crop, just like all other organochlorine compounds. Organochlorines
are not adapted to local growing conditions or to local patterns of use.
Endosulfan’s high short-term toxicity in particular has alerted the plantation
corporations in Kerala against the using of endosulfan as a compound for
cashew plantation.
Decision-making cashew plantation pesticide use in parts of Kerala
should be more consultative, rather than remaining in the hands of PCK. It
needs to be more open and public so that other cashew planter and development
experts, other stakeholders and groups such as consumers’ unions and
environmental NGOs are actively involved. Integrated management of pests,
pesticides, pesticide resistance and crops requires an interdisciplinary and
participative approach that goes well beyond the technical level to include socio
economic, cultural and ecological considerations, as well as the preferences of
farmers, livestock herders and fishing communities. Personnel and consumers of
food crops from cashew growing areas in this areas.
The CSE project has made a small start by copying the already mixed
Australian experiences and West African with endosulfan use of cashew growing
conditions without adequate consideration of local conditions and patterns of '
pesticide use. The result should open up as soon as possible, and actively invite
other stakeholders to participate in the design, elaboration, execution, monitoring
and evaluation or strategies put in place to manage pests, pesticides, pesticide
resistance and crops.
18
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TITLE:
A sex-related difference in the neurobehavioral and hepatic effects
following chronic endosulfan treatment in rats.
AUTHORS:
Paul V; Balasubramaniam E; Jayakumar AR; Kazi M
Department of Pharmacology and Environmental Toxicology, Dr.
AUTHOR
AFFILIATION: A.L.M. Postgraduate Institute of Basic Medical Sciences, University of
Madras, India.
SOURCE:
Eur J Pharmacol; VOL 293, ISS 4,1995, P355-60
SECONDARY
SOURCE ID:
TOXBIB/96/352831
ABSTRACT:
The neurobehavioral and hepatic effects following chronic endosulfan
administration were studied in adult male and female rats. The
neurobehavioral effect was determined by testing spontaneous motor
activity, motor coordination and learning and memory processes in
rats of either sex, 30 days after treating the animal orally with
endosulfan (3.0 and 6.0 mg/kg per day). Mortality occurring during
the treatment and body weight gain at the termination of treatment
were also recorded. Liver weight and liver and serum concentrations
of glutamic oxaloacetic transaminase, glutamic pyruvic transaminase
and acetylcholinesterase were measured in order to determine the
hepatotoxic effect of endosulfan. Body weight gain, motor coordination
and acetylcholinesterase activity were unaltered in either sex.
Learning and memory processes were impaired in both groups
indistinguishably. Liver weight and liver and serum transaminases
concentrations were increased more markedly in female than in male
animals. A 30% mortality occurred in female group that received 6
mg/Kg of endosulfan. Endosulfan stimulated spontaneous motor
activity more markedly in male than in female animals. These findings
suggest that a sex-related difference seems to occur in the stimulation
of spontaneous motor activity, liver injury and mortality that result
from repeated exposure to sublethal doses of endosulfan in rats.
MAIN MESH
HEADINGS:
Endosulfan/*TOXICITY
Insecticides, Organochlorine/*TOXICITY
Liver/*DRUG EFFECTS
Liver Diseases/*CHEMICALLY INDUCED
Memory/*DRUG EFFECTS
Motor Activity/*DRUG EFFECTS
Acetylcholinesterase/BLOOD
Animal
Comparative Study
Female
Liver/ENZYMOLOGY
ADDITIONAL
MESH
HEADINGS:
CONCLUSIONS
Endosulfan should be banned as a compound in India for cashew plantation or
any other crop, just like all other organochlorine compounds. Organochlorines
are not adapted to local growing conditions or to local patterns of use.
Endosulfan's high short-term toxicity in particular has alerted the plantation
corporations in Kerala against the using of endosulfan as a compound for
cashew plantation.
Decision-making cashew plantation pesticide use in parts of Kerala
should be more consultative, rather than remaining in the hands of PCK. It
needs to be more open and public so that other cashew planter and development
experts, other stakeholders and groups such as consumers’ unions and
environmental NGOs are actively involved. Integrated management of pests,
pesticides, pesticide resistance and crops requires an interdisciplinary and
participative approach that goes well beyond the technical level to include socio
economic, cultural and ecological considerations, as well as the preferences of
farmers, livestock herders and fishing communities. Personnel and consumers of
food crops from cashew growing areas in this areas.
The CSE project has made a small start by copying the already mixed
Australian experiences and West African with endosulfan use of cashew growing
conditions without adequate consideration of local conditions and patterns of'
pesticide use. The result should open up as soon as possible, and actively invite
other stakeholders to participate in the design, elaboration, execution, monitoring
and evaluation or strategies put in place to manage pests, pesticides, pesticide
resistance and crops.
18
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TITLE:
Endosulfan-induced biochemical changes in the testis of rats.
AUTHORS:
Sinha N; Narayan R; Shanker R; Saxena DK
AUTHOR
Industrial Toxicology Research Centre* Mahatma Gandhi Marg,
AFFILIATION: Lucknow, India.
SOURCE:
Vet Hum Toxicol; VOL 37, ISS 6,1995, P547-9
SECONDARY TOXBIB/96/160119
SOURCE ID:
ABSTRACT:
Adult male rats were exposed to 0,2.5, 5.0 or 10.0 mg endosulfan/kg
body weight through oral intubation for 70 d. Decreased sperm counts
m the cauda epididymis and reduced intratesticular spermatid counts
associated with elevation in the activities of specific testicular marker
enzymes (sorbitol dehydrogenase, lactic dehydrogenase, gamma
glutamyl transpeptidase, and glucose-6-phosphate dehydrogenase)
were seen in all the endosulfan-dosed groups. Endosulfan caused
impairment in testicular functions by altering activities of the enzymes
responsible for spermatogenesis, thereby influencing intratesticular
spermatid count and causing low sperm production and sperm
deformity.
MAIN MESH
HEADINGS:
Endosulfan/*TOXICITY
Insecticides, Organochlorine/*TOXICITY
Spermatogenesis/*DRUG EFFECTS
Testis/*DRUG EFFECTS
additional
gamina-Glutamyltransferase/METABOLISM
Administration, Oral
Animal
Dose-Response Relationship, Drug
Endosulfan/ADMINISTRATION & DOSAGE
Glucoscphosphatc Dehydrogcnasc/M ETA HOLISM
Iditol Dehydrogenase/METABOL1SM
Insecticides, Organochlorine/ADMINISTRATION & DOSAGE
Lactate Dehydrogenase/METABOLISM
Male
Rats
Sperm Count/DRUG EFFECTS
Sperm Motility/DRUG EFFECTS
Support, Non-U.S. Gov't
Testis/ENZYMOLOGY
Testis/PATHOLOGY
PUBLICATION JOURNAL ARTICLE
TYPES:
MESH
HEADINGS:
CONCLUSIONS
Endosulfan should be banned as a compound i,n India for cashew plantation or
any other crop, just like all other organochlorine compounds. Organochlorines
are not adapted to local growing conditions or to local patterns of use.
Endosulfan’s high short-term toxicity in particular has alerted the plantation
corporations in Kerala against the using of endosulfan as a compound for
cashew plantation.
Decision-making cashew plantation pesticide use in parts of Kerala
should be more consultative, rather than remaining in the hands of PCK. It
needs to be more open and public so that other cashew planter and development
experts, other stakeholders and groups such as consumers’ unions and
environmental NGOs are actively involved. Integrated management of pests,
pesticides, pesticide resistance and crops requires an interdisciplinary and
participative approach that goes well beyond the technical level to include socio
economic, cultural and ecological considerations, as well as the preferences of
farmers, livestock herders and fishing communities. Personnel and consumers of
food crops from cashew growing areas in this areas.
The CSE project has made a small start by copying the already mixed
Australian experiences and West African with endosulfan use of cashew growing
conditions without adequate consideration of local conditions and patterns of '
pesticide use. The result should open up as soon as possible, and actively invite
other stakeholders to participate in the design, elaboration, execution, monitoring
and evaluation or strategies put in place to manage pests, pesticides, pesticide
resistance and crops.
18
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---------------- ----------- ----------—™.—
___________ __
TITLE:
Endosulfan-induced biochemical changes in the testis of rats.
AUTHORS:
Sinha N; Narayan R; Shanker R; Saxena DK
AUTHOR
Industrial Toxicology Research Centre, Mahatma Gandhi Marg,
AFFILIATION: Lucknow, India.
SOURCE:
Vet Hum Toxicol; VOL 37, ISS 6, 1995, P547-9
SECONDARY TOXBIB/96/160119
SOURCE ID:
ABSTRACT:
Adult male rats were exposed to 0, 2.5, 5.0 or 10.0 mg endosulfan/kg
body weight through ora! intubation for 70 d. Decreased sperm counts
in the cauda epididymis and reduced intratesticular spermatid counts
associated with elevation in the activities of specific testicular marker
enzymes (sorbitol dehydrogenase, lactic dehydrogenase, gamma
glutamyl transpeptidase, and glucose-6-phosphate dehydrogenase)
were seen in all the endosulfan-dosed groups. Endosulfan caused
impairment in testicular functions by altering activities of the enzymes
responsible for spermatogenesis, thereby influencing intratesticular
spermatid count and causing low sperm production and sperm
deformity.
MAIN MESH
HEADINGS:
Endosulfan/*TOXICITY
Insecticides, Organochlorine/*TOXICITY
Spermatogenesis/*DRUG EFFECTS
Testis/*DRUG EFFECTS
additional
1
gamma-Glutamyltransferase/METABOLISM
Administration, Oral
Animal
Dose-Response Relationship, Drug
Endosiilfan/ADMINISTRATION & DOSAGE
Glucosephosphate Dehydrogenase/METABOLISM
Iditol Dehydrogenase/METABOLISM,
Insecticides, Organochlorine/ADMINISTRATION & DOSAGE
Lactate Dehydrogenase/METABOLISM
Male
Rats
Sperm Count/DRUG EFFECTS
Sperm Motility/DRUG EFFECTS
Support, Non-U.S. Gov't
Testis/ENZYMOLOGY
Testis/PATHOLOGY
PUBLICATION JOURNAL ARTICLE
TYPES:
MESH
HEADINGS:
CONCLUSIONS
Endosulfan should be banned as a compound in India for cashew plantation or
any other crop, just like all other organochlorine compounds. Organochlorines
are not adapted to local growing conditions or to local patterns of use.
Endosulfan’s high short-term toxicity in particular has alerted the plantation
corporations in Kerala against the using of endosulfan as a compound for
cashew plantation.
Decision-making cashew plantation pesticide use in parts of Kerala
should be more consultative, rather than remaining in the hands of PCK. It
needs to be more open and public so that other cashew planter and development
experts, other stakeholders and groups such as consumers’ unions and
environmental NGOs are actively involved. Integrated management of pests,
pesticides, pesticide resistance and crops requires an interdisciplinary and
participative approach that goes well beyond the technical level to include socio
economic, cultural and ecological considerations, as well as the preferences of
farmers, livestock herders and fishing communities. Personnel and consumers of
food crops from cashew growing areas in this areas.
The CSE project has made a small start by copying the already mixed
Australian experiences and West African with endosulfan use of cashew growing
conditions without adequate consideration of local conditions and patterns of'
pesticide use. The result should open up as soon as possible, and actively invite
other stakeholders to participate in the design, elaboration, execution, monitoring
and evaluation or strategies put in place to manage pests, pesticides, pesticide
resistance and crops.
18
<
Pestic. Sci. 1997, 50, 21-27
THANAL
147
PO'»T tc:
• C
KAV/01 *Q.T Ml ‘ U v -
itive
Ina/.
keralam.
tnde
I
•
and *
owth ’
1994) ?
Plam
fork, .
lerbi- J
L. J. f
1 cell |
nt., 7 I
S-’F” 5
Plant I
icular ■
sther- ;
Ethyb
2
e and
Pi ;
Fate of Endosulfan in Cotton Soil under
Sub-tropical Conditions of Northern India*
the
zing
72
/era. U.,
issay
d. T.
linar
1986,
’
O'. 5
’•,■1
Trilochan S. Kathpal,: Attar Singh, Jagbir S. Dhankhar & Gulab Singh
Centre of Environmental Studies, CCS Haryana Agricultural University, Hisar-125004, India
(Received 20 February 1996; revised version received 30 September 1996; accepted 23 December, 1996)
Jerre/tna fie d studies were conducted with endosulfan during the
1989 90 Kharf season in bare cotton soil, to investigate the fate of endosulfan
and its downward movement under sub-tropical conditions of northern India.
Field experiments consisted of spray application of endosulfan at 875 g ha~l 42
and 63 days after the assumed date of sowing in two separate treatments. Soil
samples drawn periodically from different depths were analysed by GC-ECD
(Ni ) for endosulfan and its breakdown products.
Dissipation of the total endosulfan residues occurred to an extent of 92-97%
jn the first four-week penod and by about 99% in 238 days7ntwJ distinct phSs
in first-order kinetics. Residue half life
varied from 39 to 42 days. The
parent compound metabolized to endosulfan-diol and endosulfan sulfate
Endosulfan-diol remained confined in the upper 5-cm layer and dissipated com
pletely in 28 days whereas endosulfan sulfate was first detectable seven days after
treatment and persisted until the end of the experiment, remaining confined in
the upper 0-10 cm soil layer. The ^-isomer also did not leach down beyond
10 cm depth.
Key words: endosulfan, dissipation, persistence, metabolites. residue half life
sub-tropical conditions
Singh,
Itiples
senesr. Cell
1 INTRODUCTION
tersen,
For about the last three decades endosulfan [(1, 4, 5, 6,
y von
6-34.
tnethv^?1?!0'8’ 9’ 10-trinorbom-5-en-2, 3-ylenebiscumU'
differ^ ene?sulfiteJ has been widely used for controlling
,
1cotton0 JnSi!ct pests of field crops such as Paddy,
nologs
(1992)
crons nn/2 Unt’ oilseeds’ P^ses, vegetables and fruit
$ ■: ^-^tton™- SU^t1r°Pical conditions of India. In the
es tbci' • V^^ommended Sf 61 °f nordlern India the compound is
ootini
^fbollworm
controIlinS hairy caterpillar, spotted
- Whas b^n
u°fPer’ etC’ 011 ^^n.1 In recent years,
&titernativr
^°r controHing termites in soil as an
“orS
Indian m° 1 nn’ w^cb bas keen withdrawn from
^^hjer^tence
SinCC December 1993 due to its high
amb*
/tob£
Work w
Intem^io^rtCd
3
^hth
a poster
poster session
session of
of the
the Ei
Eighth
san'n^
DC Irca °n?e^ o^Pestlcide Chemistry held in
whom
USA/
n 4-9
1994.
on
4-9 ^ly.
July, 1994.
“^Pondence should be addressed.
*
a
T'Y
. •
•
«
—
'**’••*••••••*** T
AAV1U
111
Soil serves as a major sink for plant protection
chemicals applied directly to soil or entering indirectly
during plant protection operations or through crop
residues of treated plants. Xenobiotics present in soil
may be absorbed by plants or may dissipate by chemi
cal, microbial degradation, downward leaching or vola
tilization. Additionally, some portion of the chemical
may become part of soil system in the form of bound
residues. The dissipation pattern of endosulfan has been’
extensively documented on different crops2-6 under
sub-tropical conditions but very little information is
available on its fate and dissipation behaviour in cotton
soils. Under northern Indian conditions, dissipation of
endosulfan residues was observed to be about 63% in
two months under .cover of sorghum in alluvial soils.3
The sandy loam character of the cotton soil enhances
the chances for downward movement of pesticides
which may result in the contamination of ground water.
It was thought imperative to undertake investigations
21
-613X/97/S17.50 f 1997 SCI. Pri:
inted in Great Britain
22
Trilochan S. Kathpal et al.
TABLE 1
Sampling Schedule Followed forT1 and T2
to study the fate, movement and dissipation of endo
sulfan in cotton soil without a growing crop under sub
tropical condition of Hisar, India, focusing on its
potential for contaminating ground water.
2
2.1
-1
0
7
14
28
70
154
238
MATERIALS AND METHODS
Chemicals
Endosulfan 357 g litre-1 EC (‘Thiodan’ 35) and refer
ence standards of endosulfan isomers, endosulfan-diol
and sulfate were obtained through courtesy of Hoechst
Schering AgrEvo Ltd, Bombay; the derivatizing
reagent, N-methyl-N-trimethylsilyl-trifluoroacetamide
(MSTFA) was procured by courtesy of M/s Hoechst
Schering AgrEvo Ltd, Frankfurt, Germany. All reagents
used for extraction, clean-up and other purposes were of
analytical grade.
2.2
Sampling interval (DAT/
Field metabolism and movement experiment
The field experiment was conducted during May 1989—
April 1990 at the Research Farm of CCS Haryana Agri
cultural University, Hisar, India. The soil was sandy
loam having 67-3% sand, 13-8% silt, 18-6% clay, pH
measured with KC1 (1:2) 8-10; CEC [c mol (P + t)
kg-1] 11-45; C + N, 11 + 1; organic matter 0-5%;
saturation, 33-40% and bulk density 1-46 Mg m-3.,Out
of 0-40 ha area prepared for field studies, three plots
each measuring 500 m2 were demarcated for three treat
ments (T), leaving a border area of 2-5 to 6 m around
the experimental plots. In the centre of each plot an
area of 15 x 15 m was marked as sampling area.
In Tj and T2 endosulfan EC was applied at 875 g Al
ha-1 in 375 litre water 42 and 63 days after the
assumed date of sowing, i.e. 21 June 1989; T3 was kept
as the untreated control plot. To ensure uniform cover
age of the field endosulfan emulsion was sprayed in
cross directions with a knapsack sprayer.
Throughout the experiment, the plots were kept free
of weeds by hand hoeing, taking care not to disturb the
upper layer of soil. The plots were irrigated six times.
The first irrigation was given 28 days after the assumed
date of sowing at 100 litre m-2, second at 75 litre m-2
and thereafter at 50 litre m-2 at a 21-day intervals.
This schedule was selected as if irrigation would have
been carried out under normal cropping conditions. On
the assumed date of sowing 30 kg ha-1 each of nitro
gen and P2O5 were applied during field preparations.
An additional 30 kg ha-1 of nitrogen was given prior
to the second irrigation.
In order to observe the fate and downward move
ment of endosulfan and its metabolites, soil samples
were drawn at eight time intervals (—1 to 238 days) at
four different depths (Table 1). Soil samples were drawn
Depth of sampling*
dp d2, d3, d4
dx
dpd2
dp d2, d3
dp d2, d3, d4
dp d2, d3, d4
dp d2, d3, d4
a DAT = Days after treatment.
b dj = 0-5 cm; d2 = 5-10 cm; d 3 = 10-15 cm; d4 = 15-30
cm.
randomly with the help of a tube anger (dia 2-5 cm) on
each date from 40 different places in a marked
15 x 15 m area. All core samples of different depths
were mixed separately and, after quartering, two com
posite samples were drawn from each depth and tn
ment. Samples were packed in polyethylene boxes lined
with aluminium foil and stored in a deep freeze at a
temperature below — 30°C until the analysis, which was
carried out within one to three months of sampling.
Meteorological conditions except rainfall prevailing
during the experiment were quite normal compared to
the climatic conditions of the last ten years. The
maximum, minimum temperatures, pan evaporation
rate and rainfall during the experimental period as well
as long-term values are depicted in Fig. 1.
23
Extraction and clean-up
Soil samples were air dried, passed through a 2-mm ;
sieve and quartered to obtain a representative 50-g .
sample after homogenization. Acetone extraction was
carried out according to the method of Werner et al.1
The acetone extract was diluted with aqueous sodiv
‘
chloride solution (40 g litre-1; 600 ml) and residues ‘
partitioned to hexane (3 x 50 ml). The combined
hexane phases were evaporated to about 35 ml on a
rotary flash evaporator at 40-45°C. The hexane extract
was cleaned up with an improved technique8 using ‘
Darco-G-60 as adsorbent and hexane + toluene (95 + 5
by volume) as eluant. The eluates collected were evapo
rated to a volume of 10 ml on a flash evaporator.
2.4
Derivatization of endosulfan and its metabolites
From the cleaned extract (10 ml) an aliquot (0-02 ml)
was taken in a graduated injection bottle and diluted to
0-1 ml with toluene. The silylation7 was done with
0-04 ml MSTFA in a capped injection bottle by heating
at 70-80°C for 15 min. After cooling of solution toluene
was added up to a final volume of 1 ml.
23
ate of endosulfan in cotton soil in northern India
MAX (EXPT. PERIOD)
MAX (10 YRS. AV )
MIN (EXPT. PERIOD)
(a)
MIN (10YRS. AV.)
S
50
UJ
5
j
£3
40
30
£
si I
20
10
0
3
I
(b)
30
■I PAN EVAP RATE (EXPT. PERIOD)
E3 PAN EVAP RATE (10 YRS. AV.)
I
I
20
10
I
0
J
J
A
S
0
1 mC
N
D
fl
J
F
M
A
(c)
130
120
110
100
CZ) RAIN FALL (EXPT. PERDD)
90
■I RAIN FALL (DYRS AV.)
80
-J
5
z
<
70
60
50
r
40
30
20
10
0
i
Ill
j
j
A
S
0
N
D
J
F
M
A
Fig. 1. Meteorological observations at the experimental site:
(a) air temperature (b) pan evaporation rate and (c) rainfall
(monthly averages) of experimental period (June 1989 to April
1990) and of last 10 years.
The derivatized residues were determined by in
jecting 1-3 fii of toluene solution into a gas liquid
chromatograph (GLC, HP 5890A), equipped with Ni63
detector and a HP-1 (methyl silicone gum)
’0m x 0-53 mm x 2-65 /rm film thickness column. The
ejection port and detector temperatures were 265°C
and 270°C, respectively. The column temperature was
set to 200°C (1 min)—3°C min'1 to 215°C (2 min)—
20°C min"1 to 260°C (2 min). The gas flow (N2) was set
to 15 ml through column and 55 ml make-up through
detector. The retention times (Rt) observed under these
conditions were: endosulfan-a, 3-20 min; endosulfan p;
4-03 min; endosulfan sulfate, 4-95 min, endosulfan diol
3-75 min.
2.5
RESULTS AND DISCUSSION
3.1 Environmental fate and persistence behaviour of
endosulfan in soil
H-
UJ
endosulfan sulfate and endosulfan-diol were 98%,
106%, 95% and 95%, respectively.
The limits of detection were 0-01 j2g g'1 for each of
the endosulfan isomers and breakdown products.
Recovery experiments
Before starting the analysis of test samples, recovery
experiments were conducted with soil samples from the
control plot fortified at levels of 0-1 and 0-5 mg kg-1.
Each fortification level was prepared in three replicates.
Recoveries observed for a- and /Tisomers of endosulfan,
In both treatments, endosulfan was detected in the form
of a- and ^-isomers on the day of application (Tables 2,
3). In seven days endosulfan was converted to endo
sulfan sulfate in Ti as well as in T2. The formation of
endosulfan-diol was observed in Tt only.
The endosulfan a-isomer persisted up to 14 days in
Tj and 28 days in T2. The endosulfan ^-isomer was
relatively more persistent than the a-isomer. Its residues
persisted up to 70 days in Tj and 238 days in T2 in
detectable amounts. These results confirm observations
of Kimber et al.9 with endosulfan in cotton soils of Aus
tralia, that, although the endosulfan a-isomer is 70% of
the active ingredient in commercial formulations,
because of its high volatility it is found in soils at appre
ciable levels only immediately after spraying.
The endosulfan-diol persisted up to 14 days. The
endosulfan sulfate residues in the soil samples were
highest on day 7 in T| and day 14 in T2 with
0-666 mg kg'1 and 0-143 mg kg"1, respectively. Endo
sulfan sulfate persisted until the termination of the
experiment in both treatments, always being around
four times higher in Tj than in T2 (Tables 2 & 3). This
observation is in accordance with findings on environ
mental fate of endosulfan in Australian cotton soils,9
where also endosulfan sulfate was the main breakdown
product followed by endosulfan-diol.
Dissipation of endosulfan occurred in two phases in
first-order kinetics (Table 4; Fig. 2). Residue half-life
(Ti/2) values varied from 5-4 to 7-3 days in the first .
phase, 78-6 to 115-3 days in the second phase and from
39-5 to 42-1 days for overall period. Residue half-life of
15 days for endosulfan has been reported in Australian
black soil10 when incubated at 30°C at field capacity
moisture level.
In the first phase (28 days after treatment) the rate of
dissipation was slightly faster in Tj (32-95%) than T2
(27-92%) whereas in the second phase (28-238 days) the
rate of dissipation was similar in both treatments.
3.2
Movement of endosulfan and its metabolites
As evident from the data given in Tables 2 and 3 endo
sulfan and its breakdown products did not move
beyond 10 cm depth (Fig. 3). a-Endosulfan remained
confined in 0-5 cm in Tj but moved down to 10 cm in
T2. The ^-endosulfan leached down to 10 cm, both in
Trilochan S. Kathpal ct al.
24
TABLE 2
Dissipation of Endosulfan in Cotton Soil in Tj (Treatment given 42 Days after Assumed Date of Sowing)
Endosulfan residues (nuj kg~l)a
DAT
Depth (cm)’
a-isomer
fi-isomer
Endodiol
Endosulfate
L Endosulfan
-1
0(1 h)
7
14
0-30
0-5
0-5
0-5
5-10
BDl?
2-350
0-996
0-243
BDL
BDL
0-676
0-273
0-129
0-036
BDL
BDL
0-134
0-096
BDL
BDL
BDL
0-666
0-107
BDL
28
0-5
5-10
10-15
BDL
BDL
BDL
0-034
0-002
BDL
BDL
BDL
BDL
0-109
BDL
BDL
70
0-5
5-10
10-15
15-30
BDL
BDL
BDL
BDL
0-009
BDL
BDL
BDL
BDL
BDL
BDL
BDL
0-058
BDL
BDL
BDL
0-5
5-10
10-15
15-30
BDL
BDL
BDL
BDL
BDL
BDL
BDL
BDL
BDL
BDL
BDL
BDL
0-040
BDL
BDL
BDL
0-5
5-10
10-15
15-30
BDL
BDL
BDL
BDL
BDL
BDL
BDL
BDL
BDL
BDL
BDL
BDL
0-034
BDL
BDL
BDL
BDL
3-026
2-069
0-575
0-036
0-611
0-143
0-002
BDL
0145
0-067
BDL
BDL
BDL
0-067
0-040
BDL
BDL
BDL
0-040
0-034
BDL
BDL
BDL
0-034
154
238
Dissipation (%)
31-62
79-81
95-21
97-78
98-68
98-88
a Mean of two replicates.
b BDL - Below detectable level.
Tj and
until 28 days of experimentation. The
zmount
in the 5 U) an hfer v/'dt ^ig/hliaintly
working on the environmental fate of endosulfan
lower than in the 0-5 cm layer. Endosulfan-diol, which
was detected only in T,, did not leach beyond 5 cm.
Likewise endosulfan sulfate mainly remained confined
in upper 5-cm layer up to the termination of the experi
ment except on day 154 in T2 when residues to a level
of 0-10 mg kg-1 were found in 5-10 cm depth. Similar
observations have been made by Kimber et al.9 while
50
**0
‘
TREATMENT 1
5.0
TREATMENT 2
3 3.0 -
3 3.0
I 20£ i.o •
§ oL
g 2.0
3
18
1.0
-J
35
70
105
TIME
140
175 210 245
(DAYS)
0
0
35
70
05
TIME
140 175 20
245
(DAYS)
Fig. 2. Dissipation of endosulfan applied at 875 g Al ha" 1 in cotton soil.
T1/2 values
T’i
Phase I
Phase II
Overall period
5-4 DAYS
115-3 DAYS
42 1 DAYS
T2
7-3 DAYS
78-3 DAYS
39-5 DAYS
i
i
'Tw 4.0
'G 4 0 ‘
0
1)^ bulk of
7/^/
pesticide remained in top 5-cm layer in cotton-growing
soils of Australia. Probably adsorption of endosulfan
and its metabolites was strong on soil particles due to
their polar character, resulting in negligible downwr
movement with irrigation and rain. Also low water
solubilrty can be another reason for negligible downward mobility.
25
ate of endosulfan in cotton soil in northern India
TABLE 3
Dissipation of Endosulfan in Cotton Soil in T2 (Treatment given 63 Days after Assumed Date of Sowing)
Endosulfan residues (mg kg ~1 )a
DAT
Depth (cm)
a-isomer
fl-isomer
Endodiol
Endosulfate
E Endosulfan
-1
0(1 h)
7
14
0-30
0-5
0-5
0-5
5-10
BDL?
2-225
1-409
0-490
0-081
BDL
0-575
0-500
0-124
0-032
BDL
BDL
BDL
BDL
BDL
BDL
BDL
0-125
0 143
BDL
0-5
5-10
10-15
0-042
BDL
BDL
0-070
BDL
BDL
0-5
5-10
10-15
15-30
BDL
BDL
BDL
BDL
BDL
2-800
2-034
0-757
0-113
0-870
0-216
BDL
BDL
0-216
0-071
BDL
BDL
BDL
0-071
0-075
0-010
BDL
BDL
0-085
0-023
BDL
BDL
BDL
0-023
28
X
70
0-014
BDL
BDL
BDL
0-104
BDL
BDL
BDL
BDL
BDL
BDL
' BDL
BDL
BDL -
0-057
BDL
BDL
BDL
154
0-5
5-10
10-15
15-30
BDL
BDL
BDL
BDL
0-027
BDL
BDL
BDL
BDL
BDL
BDL
BDL
0-048
0-010
BDL
BDL
238
0-5
5-10
10-15
15-30
BDL
BDL
BDL
BDL
0-014
BDL
BDL
BDL
BDL
BDL
BDL
BDL
0-009
BDL
BDL
BDL
Dissipation (%)
27-36
r
1 :■
: »
■
6S-93
92-29
97-46
96-96
99-18
■
“ Mean of two replicates.
* BDL = Below detectable level.
1
i
Low vertical mobility of four organochlorine insecti
cides. i.e., aldrin, HCH, chlordane and heptachlor was
demonstrated in sandy loam soil in a long-term experi
ment covering ten crop seasons.11 It was noticed that
highest residue concentrations were present in the
surface (0-10 cm) of the fallow plots but in the 102u cm layer of the cropped soils.
, ,,
There are many variables such as fertilizer applica
tion, irrigation, cropping pattern and other agronomical
practices, which influence dissipation of pesticides under
■!
TABLE 4
First-Order Kinetics of Endosulfan Dissipation in Cotton Soil
s
4
1p
5-4
115-3
42-1
0-129
0-006
0-016
Treatment 2
-0-99
Y = 3-51 —0-041 X
-0-89
Y - 2-34 - 0-004 X
— 0-87
Y - 3-009 - 0-008 X
7-3
78-6
39-6
0-095
0-009
0-016
Regression equation*
First
Second
Overall
First
Second
Overall
;1
i
Treatment 1
-0-99
y = 3-58 - 0-056 X
— 0-91
Y = 2-11 - 0-003 X
-0-81
Y = 2-92 - 0-007 X
Phase0
i
t
(days)
Rate
constant
(K)
Correlation
coefficient
(r)
0 First phase: 0-28 DAT; second phase: 28-238 DAT.
b Y = Log [Residues ,x 103]; X = Interval (days)’after treatment.
?
26
Trilochan S. Kathpal cA al.
6.0
/
TREATMENT 1
5.0
4.0 -
Ten
5 3.0 DI
UJ
3
£ 2.0 s
02
03
1.0 -
0
0
7
14
26
70
154
236
(DAYS)
TIME
50
TREATMENT 2
4.0
3.o-
5
01
to
g 20-
02
E
03
1.0 -
0
0
7
14
28
TIME
70
154,
236
(DAYS)
Fig. 3. Downward movement in soil of endosulfan applied at 875 g Al ha-‘‘42 daysfTJ and 63 days (T.) after assumed date of
sowing. D, =0-5 cm-‘;D2 = 5-10 cm; D3 = 10-15 cm;D4 = 15-30 cm.
field conditions. In the current studies, the following
processes can be considered to have operated in the dis
sipation of endosulfan (1) volatilization due to fallow
plots (2) hydrolysis of endosulfan and metabolization
because of alkaline pH (8’1) of soil and irrigation water
(8-2) (3) photochemical and microbial decomposition.
According to various researchers12,13 microbial and
chemical degradation are minor routes of dissipation of
pesticides from soil but most are lost in significant
amounts through volatilization.14,15 In the light of
these findings, in our studies volatilization was probably
the dominant factor in the dissipation of endosulfan and
its metabolites which was probably favoured by a rela
tively high temperature coupled with low rainfall as
compared to the ten-year average values, particularly in
the post-application stages both in Tj and T2 (Fig. 1).
From these investigations, the conclusions can be
drawn that under sub-tropical conditions (i) endosulfan
was converted to endosulfan sulfate and diol in sandy
loam soil (ii) endosulfan sulfate persisted in measurable
amounts up to 238 days whereas diol dissipated almost
completely within 28 days (iii) major quantities of resi-
dues remained confined in the upper (0-5 cm) layer;
however, very small amounts moved down to 10 cm
depth, (iv) dissipation of total endosulfan was fairb’
rapid. Hence endosulfan can be considered an enviroi.
mentally sound insecticide for the use in cotton under
sub-tropical conditions of northern India.
ACKNOWLEDGEMENT
The authors express their sincere thanks to the Director
of Research, Head, Department of Chemistry and Bio
chemistry for laboratory facilities and Head, Depart
ment of Soil Science, CCS Haryana Agricultural
University, Hisar for field facilities. Financial assistance
provided by M/s Hoechst Schering AgrEvo Ltd,
Bombay, is sincerely acknowledged.
REFERENCES
1. Anonymous, Package of Practices for kharif crops.
Haryana Agricultural University, Hisar, India 1989, pp.
33-66.
ate of endosulfan in cotton soil in northern India
27
'
!
I
I
{I
Kathpa1’ T- S- & Srivastava, B. P„ Persistence of
endosulfan residues in and on bhindi (Abelmoschus esculentus Moench) fruits. Indian J. Pl. Prot., 2 (1973) 45-53
3. Kathpal, T. S. & Dewan, R. S., Endosulfan residues in/on
sorghum under different agro-climatic conditions of India
Indian J Agric. Sci., 46 (1976) 354-8.
4. Kathpal, T. S Bhatnagar. V. S., Gupta, H. C. L. & SrivaslaVA T R’ Res,duesjof endosulfan in/on ber (Zizyphus
jujuba Lamk) fruits and leaves. Pesticides, 21 (1977) 37-Q
5. £adav» G-S., Kathpal, T. S., Sharma, P. D. & Singh, G.,
Relative efficiency of some synthetic pyrethroids and
endosulfan against bollworm pests of cotton and their
residues in cotton seed. J. Insect Sci., 6 (1993) 92-6.
6. ^nnual Report, Endosulfan dissipation on cowpeas. All
India Coordinated Research Project on Pesticide Resi
dues, New Delhi, 199I-93 pp. 12-13.
7. Werner, H J., Klante, G. & Merz, H. D., Residue determina ion of the active ingredient and endosulfan sulfate in
soil, water urine and plant material as well as of
endosulfan-diol and endosulfan-lactone. Hoechst (AG)
Documentation No. A. 34468, 1986, pp. 1-21.
8. Kathpal, T S. & Dewan, R. S., An improved clean-up
technique for the estimation of endosulfan and endrin
residues. J Assoc, off Anal. Chem., 58 (1975) 1076-8.
9. prober, S W. L., Coleman, S., Coldwell, R. L. &
Kennedy, I. R., The environmental fate of endosulfan
2’
10. donthofn’pSaK' fr Kenned>': L R- Studies on the degrada-
growing regions oTN^hX^sSwa^s fW
cropped and uncropped soil. Envir. Poll., 70 (1991). 21912. Edwards, C. A., Occurrence and
m the physical environment, in pJrsisX' PeltlcidesZ
fondOonmie970 pp nS"0 SCienCe SerieS' Butterworth-
13.
135-6h0°ate and P'Vr01an‘ Ecotoxico1- Em- Safe<y- 5 (1981)
V’ IgUe' K’ Spencer- W' F- & Martin, J. P„
Volatility of organochlonne insecticides.from soil: Effects
of concentration temperature, air flow rates and vapour
pressure. Soil Sci. Soc. Amer. Proc., 36 (1972) 443-7
15. Spencer, W. F., Farmer, W. J. & Claith, M. M., Pesticide
volatilization. Res. Rev., 49 (1973) 1-47.
14'
r
Tl-I AN AL
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KAV/O1^'
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KERALAM.
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POST ECX No. 815
’ »• ,V/DI ^R.THIQOV
j
KERALAM.
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NTH -Pc0
Pi'. :6950t
Fox
B-sidues of Pesticides and Other
a Chemicals in Foods and Feeds
t..-.
u7
RUCKSTANDS-BERICHTE
Riickstande von Pesticides und anderen
Fremdstoffen in Nahrungs- und Futtermitteln
I
f
Edited by
FRANCIS A. GUNTHER
t
Riverside, California
ADVISORY BOARD
EIBW S ^eTny ’ UBao-^SMUSSEN, Copenhagen, Denmark
J.
. Coos^ Washington, D.C. . D. G. CROSBY, Davis, California
C L Dunn wf PORMA-V;AN DEN Bkusl. Bruxelles, Belgium
T
B AT L H- FREHSE- ^erkusen-Bayerwerk, Ge^ny
JS A
n ’^n8 andJ ’ IL G21s5BiiHE®. Basel, Swiue/laH
T vv
' b‘lavllle- Maryland • T. H. Harris, Bethesdi Marv'^rd
O T&A^™NRFaI!SrhUr<:h’ VirSiQia ’ H' HURTIG’ O"*™. Canada
h
I
I
I
H. rLlSXJS'
SuXkV:
N. N^M
, M
, U.S.S.K. • R. M™®MXeiher“ -^7
J
ebnxkov
oscow
r
P. DE Pibtri-Tonblli, Mdano, Italy • R. Truhaut, Paris, France
VOLUME 22
i
x°
.
gS>!i
i°
UU’Lj
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)*'
SPRINGER-VERLAG
BERLIN ■ HEIDELBERG ’ NEW YORK
1968
.1
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Preface
are of con™ to
"f°reign'' Chemica!s in fccds^
or concern to everyone everywhere is amply attested by the receot'on
accorded previous volumes of "Residue Reviews" and by the ^ifv^ ea
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control sotj of Xj pe^ZS foZXZdtb™^
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LY34Jr^-'Kjjl.l
<
These matters are also of genuine concern
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hese chemicals have resulted in a few mishaps from imp-/vo-■ .d,
■ for some of
’
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safety-in-use evaluations of any of these chemiralsA " ■
Adequate
stuffs are not simple matters, and they incorporate th^X- A/'-0 °T
of many individuals highly trained in a
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yariety of complex bi -logical, chemicjlint0'1 teChnOlOgicaI- medical- Pharmacological, and
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'
L
'Residue Reviews” attempts to provide concise, critical reviews of timely
advances, philosophy, and significant areas of accomplished or needed en
deavor in the total field of residues of these chemicals in foods, in feeds, and
in transformed food products. These reviews are either general or specific, but
properly they may lie in the domains of analytical chemistry and its method
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physiology, regulation, and' toxicology; certain affairs in the realm of food
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crops. Added plant or animal pest-control chemicals or their metabolites that
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Department of Entomology
University of California
Riverside, California
January 27, 1968
1 able of Contents
’roperties, effect, residues and analytics of the insecticide endosulfan
By H. Maier-Bode .
!■
Einfluss von Nacherntefaktoren auf die Riickstiinde von Pfianzcnschutzmitteln in Obst, Gemuse und einigcn Sonderkulcurcn
By H. Siobwasser, B. Rademacher and E. Lange
Subject index .
I
F.A.G
?■
Manuscripts in Press
45
113
120
I
II
J
I
I
Properties, effect, residues and analytics of the
I
I
insecticide endosulfan
!
By
Hans Maier-Bode*
f
Contents
I
I
II
I. The active principle endosulfan
a) History and properties
b) Formulations
c) Transformation products
II. Action ...
a) Effect on plants
b) Effect on warm-blooded animals
c) Effect on arthropods
d) Side reactions .
III. Behaviour in the organism
a) Behaviour on the surface of plants
b) Behaviour in warm-blooded animals
c) Behaviour in arthropods
IV. Residues
...
2) Residues on fruit
b) Residues on vegetables
c) Residues on fodder plants
d) Residues on tobacco
V. Tolerances and time limitations
VI. Analysis
a) Identification .
b) Detection
c) Quantitative determination
d) The analysis of-endosulfan metabolites
nummary
..................................
A
•
.
WA C
Instirut
■J|O (g
i j A*<
.
L
<
>
>
p<
not**''
2
2
4
4
6
6
6
7
8
11
11
12
15
17
22
22
23
23
23
24
24
24
27
34
36
38
39
der Rheinischen Friedrich-WUhelms-Universitat Bona,
a) Hisiory and properlies
r
Endosulfan (CgH^OaClcS) is the common name of th
isccticide
6,7',#,9,10,10 - hexachloro - l,5,5a,6,9,9a - hexahydro - 6,9 - methano - 2.4,3. Joenzodioxathicpine - 3 - oxide, or a,Q - 1,2,3,4,7,7 - hexachlorobicyclo - (2,2,
1) - heptene - (2) - bis-hydroxymethylene - (5,6) - sulfite, or 5 - norbornene2.3 - dimethanol - 1,4,5,6,7,7 - hexachloroc}rclic sulfite (Chemical Abstracts).
CLX'
0=S^
|
Formula 2
CI
Cl
ch2—0
Cl
1;
ClCCl
Cl
0
Cl
i
ch2---- 0
s
t
CL
Formula 3
Formula 1
These isomers differ in their chemical, physical, and toxicological properties.
In the solid state /^-endosulfan exists in two modifications as shown by infra
red spectra in potassium bromide tablets, one with a highly symmetrical
crystal form (I) and one with a low symmetrical crystal form (II). Modifica
tion I is formed mainly during me crystallization of /?-endosulfan from
I;
petroieum ether, modification II during the crystallization from methanol.
The SO band in the infrared spectrum of I is at 1192 cm.’1, that of II at
t
1180 cm/1 (GORBACH et al. 1966). In technical endosulfan the a- and /?isomers are contained in an approximate ratio of 70:30. It is a 90 to 95 per
cent pure mixture of isomers and forms cream to brown-coloured fiakes with
a terpene-like odour, specific gravity (D20) 1.745, vapour pressure 9 x 10’3
mm. of Hg at S0°C. It melts between 80c and 90°C. It is prittically insoluble
in water. At 20 C. the solubility in acetone is 33 percent, in benzene 37 per
cent, in xylene 45 percent, in carbon tetrachloride 29 percent, in chloroform
50 percent, in ethanol five percent, in methanol 11 percent, and in kerosene
20 percent.
Under normal conditions endosulfan is stable in storage. It is non-flam
mable. It is hydrolyzed slowly by aqueous alkalis and acids. In investigations
on the persistence of endosulfan in natural waters, no endosulfan was detecti.;
scl- m- Pond with a water content of 350 cu. m. 21 days after
a S?fay mixmre. contai‘ning 672 g. of endosulfan (sensitivity
j
O^fzA1^<^^^0.03 p.p.m.; endosulfan content of the water three days after
b
< ^eatmentyQ.^p.m.). In arable soil nothing was detectable from 0.55 ppm
k, tA f
SEAL
\
'
1
Endosulfan is usually named in the literature on crop protection chemicals
among the "chlorinated hydrocarbons of the cyclodiene group” (e.g., MARTIN
1964, miller 1965). As a sulfurous acid ester of a cyclic diol, however, it
differs so markedly from the insecticides of this group (e.g., aldrin, dieldrin,
endrin) in chemical properties, physiological effects, and behaviour on the
surface of live plants and in the animal organism that it cannot be counted
among them (maier-bode 1966 and 1967). Recent investigational results
have been compiled in this report which are important for the toxicological
appraisal of endosulfan and the residues formed in practical application on
plant material.
Endosulfan was developed by Tarbwerke Hoechst AG. (FRENSCH et al.
1954 and 1954 a) and introduced by this firm under the registered trademark
of THIODAN @. It is an insecticide that is not dangerous to the honey-bee
or only slightly so and in many cases has a selective action (FINKENBRINK
1956, 1958, and I960).
Endosulfan that is formed as a colourless, crystalline product by the
reaction of thionylchloride on the addition product from hexachlorocyclopentadiene and czr-butene-diol-1,4 is a mixture of two isomers (FRENSCH 1958)
which possess the following configuration according to the results of infrared
and NMR-spectroscopic examinations (FORMAN et al. 1965):
i
W ( * ntNGA.R
| \
NOTArY J
/
1
.. ?
4
I
Hz\ns Maier-Bode
of endosulfan after 101 days, nor was transportation in seepage water through
a layer of soil detectable (sandy clay, soil number 80, thickness of layer 50
cm. diam. 25 cm.) {FARBWERKE HOECHST AG. 1964).
b} Formnlations
Endosulfan formulations are sold under various names (THIODAN,
CYCLODAN, THIMOL, THIOFAP., MALIX), for exampie as:
THIODAN wettable powder with 17.5, 35, and 50% active principle con
tent (technical grade)
THIODAN emulsifiable with 17.5 and 35% active principle content (tech
nical grade)
THICDAN dust with 1, 3, 4, and 5% active principle concent (technical
grade)
THIODAN granules with 5% active principle content (technical grade),
and also as emulsion concentrates and nebulizing products containing
mineral oil
i
I
s
Endosulfan
Cl
ch2----- 0
Cl
so2
CICCL
Cl
CH,----- -0
Cl
Formula 6
J
In contrast to the sulfurous acid ester (endosulfan), there is Giily one form
of the sulfate and not a- and ^-isomers.
c) Transformation 'products
to occur on plan-: surfaces or in the animal organism:
.OH
Cl
The following transformation products of endosulfan have been known
j
Cl
CL C CL
Cl
■ch2ch
Cl
CICCL
Cl
I
■ch2ch
Cl
Formula 7
This ether is soluble in benzene, chloroform, acetone, and methanol; it is
slightly soluble in hexane and carbon tetrachloride.
I
Formula 4
This diol is soluble in acetone and methanol but is sparingly soluble in carbon
tetrachloride.
!
0
Cl
h2
Cl
C cc
0
0
Cl
c
h2
Cl
Formula 8
Formula 5
This ether is soluble in hexane, benzene, chloroform, and methanol.
r
) This lactone is soluble in benzene,, chloroform,,acetone, and methanol; it-ds) slightly soluble in hexane and carbon tetrachloride.
IF
..o’
6
Mans jMaier-Bode
Endosulfan
II. Action
a) Effect on plants
!
In practical application under the most varied climatic conditions plants
have an extensive tolerance to endosulfan. In the spraying of greenhouse
cucumoers with endosulfan, an overdosage occasionally caused light spots and
burns on the leaves; on decorative plants of the genera Saintpaulia and bnpatiens under glass at high atmospheric humidity it caused discoloration of the
blossoms. When endosulfan was sprayed into apple blossoms in field trials a
slight impairment of pollen germination was observed which, however, did
not have an unfavourable effect on the subsequent formation of fruit (DHURIA
ct al. 1965). The taste of harvested crops, including potatoes, was not infiuenced by soil treatment with 1.5 to 4 kg./ha. of endosulfan (FINKENBRINK
1957 and 1958, Farbwerke Hoechst AG I960).
I
f
f
b) Effect on warm-blooded animals
Tne oral LD50 of the isomer mixture for white rats is approximately 100
(30 to 220) mg./kg. body weight (LINDQUIST and DAHM 1957, CZECH 1958,
Hazleton Laboratories 1958 and 1958a, KERR and’ BROGDON 1959, MAIERbode 1965). that of G-endcsulfan 76 mg./kg. and that of /?-endosulfan
240 mg./kg. (Farbwerke Hoechst AG 1967). The symptoms of incipient
poisoning in dogs after oral application of 200 and 500 mg. of endo
sulfan in gelatine capsules/kg. bod}- weight were increased saliva formation,
vomiting, and tonic and clonic cramps. The animals which did not vomit
during these tests died (Hazleton Laboratories 1967 c).
undiluted endosulfan is slowly and incompletely absorbed in the digestive
tract of warm-blooded animals. Absorption is more rapid in the presence of
alcohols, oils, and emulsifiers. The same substances also accelerate its absorption
by the skin. With intraperitoneal administration the acute LD50 of endosulfan
dissolved in ethyl or isopropyl alcohol is eight mg./kg. body weight in rats
(lendle 1956). According to investigations of Hazleton Laboratories
(1967, 1967a and b) the acute dermal LD;-o of endosulfan, in a suspen
sion with cotton seed oil, is 681 mg./kg. for rats, 147 mg./kg. for rabbits, and
over 1,000 mg./kg. for guinea pigs. The percutaneous LD-,o for rabbits is 360
mg./kg. (KLIMMER 1964).
On the conjunctiva of the rabbit eye endosulfan dilutions, as from 1:1,000,
neither cause p^in,nor_suhjequent inflammations, apparently because the in
stilled susppn^io'fiVYf
removed by the lacrimal fluid (Farbwerke
Hoechst
irritation of the mucosa of the nose and
eyes
no^^ijiibirdtpy'symptoms of poisoning after several hours’
grazint//^fpast^^^Aha^
sprayed with ’Thiodan emulsifiable”
(17.5%^:(i^ ^l-ed^K content, ■technical grade) even after a four- to five
fold ovArdo^ge (V& !'£■$&.)) (CZECH 1958). On the other hand, owing to
gross negligence of ^e necessary precautions, some losses in cattle resulted
when rape pests were controlled with endosulfan from the air by pasture land
being used as landing strips and loading places for aircraft, and "spraying
equipment” was tested from parked aircraft on grass land areas onto which
cattle could move subsequently (Pffanzenschutzamt des Landes Schleswig
Holstem 1961). The intoxication symptoms were similar to those known
from experiments with rats: unsure gait, disturbance of balance, vomiting,
and cramps; they mostly disappeared with a fevt days. No changes were
detectable in the blood picture of treated animals. (LENDLE 1956).
Chronic feeding trials with rats and dogs revealed the following picture
on daily administration of ten and 30 p.p.m. endosulfan with the feed ever a
period of two years in rats neither significant macroscopic nor microscopic
changes of the organs were detectable. With concentrations of 100 p.p.m. in
the daily feed, changes in the kidneys and liver were detectable histologically.
The tumor rate was not increased at any dosage (10, 30, and 100 p.p.m.).
According to the Hazleton Laboratories report of a two years feeding in
rat the no effect level is 30 p.p.m. In 20 months’ feeding trials on dogs
with 3, 10, and 30 p.p.m. endosulfan in feed there was no evidence of in
toxication (Food Machinery Corporation. Niagara Chemical Division 1967).
Inquiries in Belgium, Denmark, France, Great Britain, Italy, and The Nether
lands showed that, like in West Germany, no symptoms of intoxication or
allergic manifestations that might be connected with the application of endo
sulfan have become known with regard to human beings (Farbwerke
Hoechst AG 1966).
c) Effect on arthropods
r
r
r
f
7
Endosulfan acts as a contact poison on eating and sucking arthropods;
in many cases (e.g., on Leptlnotarsa decemlineata Lay, and Periplaneta americana L.) it also acts as a poison ingested by eating. Under outdoor conditions
it hardly acts as a respiratory poison; thus, its toxic effect is at times slower
than that of insecticides with a high vapour pressure which are conveyed more
rapidly through the tracheae to the site of action in the organism. After its
absorption by the body of the arthropod, according to experiments with radioactively labelled endosulfan on Periplaneta americana L., it seems probable
(SCHULZE 1965 ) that it is distributed by means of the haemolymph. Absorp
tion and speed of action of a- and ^-endosulfan, also the technical active prin
ciple, are promoted by raising the temperature and even more sc by increasing
atmospheric humidity (ROMER 1957, CZECH 1958, KLEE I960, SCHULZE 1965
and 1967).
The insecticidal effectiveness of the two isomers, of technical endosulfan,
and of endosulfan sulfate formed therefrom by oxidation, is of similar magni
tude. Table I shows the LD50 values which BARNES and WARE (1965) deter
mined after topical administration of these compounds and of endosulfan diol
and ether in acetone solution on the mesosternum of normally sensitive house
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V
Table II. LD50 values of various organocblorine insecticides for wild birds (DEWITT et al. 1963)
Species
Bobwhite
(Cplinus rirginianus)
Ring-necked pheasants
(Phastan ns
colchicus torqiiatiis)
Mallards
(A iias plalyrhynchos)
No. of days
to reach
LDso
Aldrin
Chlordane
Dieldrin
Endrin
Young
birds
up to 10
4.5
700
10
12
270
45
500
10 to 100
9.5
500
47
8
380
>160
1500
Adult
birds
up to 10
3.5
90
4.2
1
10 to 100
6.5
730
40
10
>2600
90
>2100
Young
birds
up to 10
6.5
550
90
3
620
305
300
10 to 100
11.5
170
35
>1400
140
450
Adult
birds
up to 10
4.3
10 to 100
18
^'ou ng
birds
up to 10
190
10 to 100
540
Age
group
Adult
birds
LDno, (mg./kg.)o
up to 10
105
10 10 100 |
285
Endosulfan Heptachlor Toxaphene
55
7
340
>200
75
21
850
180
> 600
40
25
200
590
2000
425
420
> 750
200
310
410
a LD..o (mg./kg.) means the average total insecticide (mg.) which was eaten by the birds (per kg. of body weight) within that time during which 50% died. Figures marked with the sign > signify that a 50% mortality of the birds was not reached at the stated amount of insecticidc (mg./kg. body weight) within the time given in column 3 of the table.
I
Table III. Toxicity of various organochlorine insecticides to sweet-water animals at a concentration of 0.1 mg./I. of water
p.p.m.) (LUDEMANN and NEUMANN I960)
Toxicity"
Test
duration
(hours)
Species
0.1
Aldrin
Tub!Iex tubifex
%
Dreisscna polymorpha
96
Cyclops siren uus
24
Gam marus (Carinogam marus}
roeselii
24
(-4-)
Daphnia magna
24
(-I-)
Asellus aqtiallcus
24
(+)
Cambarus afjinis
24
Corethra (Cbaoborus)
plumicornis, larvae
24
Bufo bufoy larvae
48
Cyprinus carpio
48
DDT
Chlordane
Dieldrin
Hndrin Endosulfan I Hcptachlor
Lindane Toxaphene
(-I-)
CO
(+)
(+)
+
+
(+)
(4-)
(+)
(+)
(4-)
( +)
+
(+)
(4-)
+
+
(+)
(-{-)
H4-
(-I-)
(4-)
(4-)
(4-)
(+)
(+)
+
4-
4-
4-
+
+
(+)
(+)
+
+
(+)
<+)
4-
I
(+)
( +)
gu
(+)
(4-)
(4-)
4-
+
o4-:==an test animals were killed; (d-)” some of the test animals were damaged or killed; —
tests: 24 to 96 hours (see table), subsequent observation time: 24 to 72 hours.
no detectable damage. Duration of
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Hans Maier-Bode
12
13
Endosulfan
Table IV. The degradation of endosulfan on fodder grass (drift from cockchafer ,
control with ‘’Thiodan emulsified” (MAIER-BODE 1962 and 1966)
i
Content (p.p.m.) in the grass of
Days
Ratio a-endosulfan to pafter
treatment : a-Endosulfan 8-Endosulfan a 4- /3-Endosuifan endosulfan in residue
0
1.3
0.5
1.8
2.6 : 1
7
0.15
0.12
0.3
1.3 : 1
14
0.04
0.07
0.1
0.6 : 1
■
A
I
Apart from the peaks characteristic of a- and (3-endosulfan, a third peak is
found in the gas chromatography of extracts of endosulfan residues, e.g., on
tree leaves, spinach, cqlery, alfalfa, grass, and also fruit. This peak, which is
not present immediately after application of the insecticide or is only indicated,
reaches a maximum approximately 10 to 15 days later and then recedes again
(Fig. 1) (MAIER-BODE 1962, Food Machinery Corporation, Niagara Chemical
Division 1963, HARRISON et al. 1963). This third peak in the gas chromato
gram indicates the presence of a transformation product formed by oxidation
on the surface of the plant. The substance was subsequently identified as endo
sulfan sulfate (CASSIL and DRUMMOND 1965, FOPMAN et al. 1965). Endosul
fan was detected on harvested crops in amounts up to 0.3 p.p.m., but mostly
under 0.1 p.p.m. In its toxicity to warm-blooded animals (rat) and insects
endosulfan sulfate is largely similar to technical endosulfan (CASSIL and
DRUMMOND 1965). The endosulfan sulfate determined analytically in endo:
sulfan residues, together with endosulfan as such, therefore has a toxicological
foundation. HARRISON et al. (1967) were able to reproduce the oxidation of
endosulfan to endosulfan sulfate in vitro when they irradiated with ultraviolet
light a solution of rhe insecticide in glycerin in a thin layer.
n
i
B
I
b) Behaviour in warm-blooded animals
RAHN (1963) did not find any unchanged endosulfan in the urine of rats
after intraperitoneal application of 20 mg. of technical endosulfan/kg. in an
oily solution but found endosulfan diol and an unknown compound, both as
water-soluble conjugation products. According to BALLSCHMITER and TOLG
(1967) endosulfan is net excreted in rat urine as endosulfan diol but as endosulfan-a-hydroxy ether, deema et al. (1966) observed transient amounts oI/zq^
endosulfan and endosulfan sulfate in the body fat and liver of mice aft^Z^ /“
administration of Ci4-labelled endosulfan; they detected endosulfan metaj^S^/
litess in the feces.
teces.
nu, ;
According to Food Maebi^ery G&rporation. Niagara Chemical DavivifSh yS.
(1963), dogs excrete in the feces 13 to 25 percent of the a- and /3-endosuna^x
that was administered orally on 28 consecutive days in amounts of 0.35
.f
Fig. 1. Gas chromatograms of benzene extracts of grass after spraying at time of
sprouting ("Thiodan Ol”, Mar. 1962). Electron-capture detector, 600-cm. steel
column, 2.5% silicone grease BR 4-0.25% Epicore on silaceous earth. 185° C., N2
O \x pressure 0.45 kg./cm.2 gauge, chart speed 10 mm./min. I = a-endosulfan, H — /?endosulfan, III — endosulfan sulfate. A — 0 day after treatment, with 5 /-I. of extract
\'
\‘t equivalent to 2.5 mg. of grass; B= 3 days after treatment, with 10 ?-l. of extra.: equivl
halent to 5 mg. of grass; andC= 10 days after treatment, with 10 gl. of extract equivato 10 mg. of grass (MAIER-BODE 1962)
'5/UF'? /
14
Hans Mater-Bode
’
15
1.75 rng./kg./day, respectively. Only very small amounts of endos an were
detectable in the urine (0.02 to 0.1 p.p.m.). Endosulfan could not be detected
in the muscle, liver, and fat of the dogs but a maximum of 10 p.p.m. of endo
sulfan sulfate was found in the fat. The brain, blood, and kidneys were residuefree. No metabolites other than the sulfate were found.
GORBACH (1965 and 1966a) compared the behaviour of the insecticides
endosulfan and dieldrin in the metabolism of milk sheep. They were given
a daily oral dose of 15 mg. of endosulfan and dieldrin, respectively, on 28
consecutive days. During the test period approximately 20 percent of the
endosulfan administered was excreted unchanged in the feces, with a smaller
portion in the urine as water-soluble transformation products, among them
probably endosulfan diol. In the miLk of the animals no a- or ^-endosulfan
could be detected, whereas endosulfan sulfate was found, mostly in amounts
between 0.02 and 0.1 p.p.m. Twenty days after commencement of the admin
istration of insecticide neither endosulfan nor any of its transformation prod
ucts was detectable in the organs of the slaughtered animals. An average of
0.1 p.p.m. of endosulfan sulfate was found in the renal and intestinal fat, but
no endosulfan. Table V shows that in contrast thereto the insecticide content
of the lipid-containing organs and the fat and milk was much higher in the
corresponding feeding tests with dieldrin, viz. 0.1 and 13.7 p.p.m. on average.
When the endosulfan administration is discontinued, the endosulfan con
tent of the milk falls rapidly (KLOSS et al. 1966). After a single application
of 14 mg. of (AMabelled endosulfan/kg. of sheep, the highest endosulfan con
tent of the milk calculated from the radioactivity was 0.25 p.p.m. six to 24
hours after application. Three days later it was 0.04 p.p.m. and after 11 days
it was below 0.01 p.p.m. The half-life of the radio-activity in the feces and
urine was about two days. In an animal slaughtered 40 days after commence
ment of the test, C14-residues were detectable only in the liver; they correspond
to less than 0.05 p.p.m. of endosulfan.
The Pood Machinery Corporation, Niagara Chemical Division (1965)
detected between 0.1 and 0.2 p.p.m. of endosulfan sulfate in die milk of cows
that had been given 2.5 p.p.m. of a-endosulfan. 2.5 p.p.m. of ^-endosulfan,
and 5 p.p.m. of endosulfan sulfate in the feed on 30 consecutive davs; 20 days
after rhe conclusion of the administration of the insecticides less than 0.005
p.p.m. of endosulfan sulfate was detected. BECK ct al. (1966) could not detect
any residues of insecticide in the milk of cows which had been fed for 21
consecutive days on silage containing 0.41, 0.70, and 2.35 p.p.m. of endosulfan.
It was proved (MAIER-BODE 1966), in contrast to DDT and other insecti
cides from the series of organochlorine compounds, that endosulfan is only
slightly persistent in warm-blooded animals, by adding tw-o p.p.m. of endo
sulfan and seven p.p.m. of DDT, respectively, to the daily feed of female pigs
weighing approximately 35 kg. on 27, 54, and 81 consecutive days, respec
tively, corresponding to the U.S. tolerances. Twenty-four hours after the last
feeding with insecticide the animals were slaughtered. No insecticide was de
tectable in the blood of the endosulfan animals but 0.003 to 0.004 p.p.m. v.-as
found in that of the DDT animals. The body fat of the pigs fed with DDT
contained .8 to 10 p.p.m. of insecticide, that of the endosulfan-fed animals less
than 0.1 p.p.m. In the muscle and liver 0.6 p.p.m. of DDT but no (<0.01
p.p.m.) endosulfan was found, nor was endosulfan detectable in die kidneys,
bile, spleen, lung, heart, pancreas, brain, spinal cord, and ovaries, whilst the
DDT content was between 0.02 and 0.3 p.p.m. Details of the results of these
experiments are shown in Table VI.
In another test series no traces of the insecticide were detectable in the
body fat of pigs of varying weights 11, 27, and 55 days after the last of 30
consecutive daily additions of two p.p.m. each of endosulfan to the feed
( MAIER-BODE 1967 ) .
!
I•
Table V. Contents oj endosulfan, its metabolites, and dieldrtn in the organs, fat,
and milk of milk sheep in a 28-day feeding test using 15 mg. of insecticide/
animal/day (GORBACH 1965 and 1966a)
Endosulfan0 a
h ' Endosulfan0 metabolites
(p.p.m.)
(p.p.m.)‘
On day 20c
Min. Max. : Av.
Dieldrina--b (p.p.m.)
Min. : Max.
Av.
Min. ! Max. i
Av.
Muscle
n.d.
n.d.
n.d.
n.d.
n.d.
n.d.
1.0
0.5
0.8
Liver
n.d.
n.d.
n.d. !
n.d.
n.d.
n.d.
0.5
0.5
0.5
n.d.
n.d.
0.1
0.1
0.1
Kidneys
n.d.
n.d. |
n.d. i
n.d.
Brain
Renal and
intestinal fat
Dars I-2S
Milk
n.d.
n.d.
n.d.
n.d.
n.d.
n.d.
n.d.
n.d. | n.d. !
n.d.
0.3
0.1d
9
20
13.7
n.d.
n.d. !
0.3
0.0/d
n.d.
6.0
3.1
n.d.
n.d.
t
r
I
c) Behaviour in arthropods
1
and endosulfan sulfau
0 n.d.=not detectable (for endosulfan, endosulfan diol,
<
< 0.01 to < 0.05 p.p.m., for dieldrin < 0.06 p.p.m.).
o — = not examined.
c On slaughtered animals.
d Endosulfan sulfate.
:io (s
•I (
Technical endosulfan dissolved in acetone applied to the mesosternum of
..
house flies (Alkr^ don?estica) slowly penetrates into the body of the anima Is
Cl VApproximately 24 hours after application part of the insecticide is still de)
Vtectable on the surface of the body. a-Endosulfan is absorbed faster than
) M The /?-isomer. Thirty minutes after application endosulfan was detected in
^extracts from homogenized dies, regardless of whether the animals were nor• Z'
z
16
I
Hans Maier-Bode
1 able '.’ j. Entiosulfan and DDT content of pigs after administration of 2 p.p.m.
of endosulfan or 7 p.p.m. of DDT in the feed (MAIER-BODE 1966)
54
81
27
Endosulfan5
(p.p.m.)d
Tissue or organ0
54
81
DDTc
(p.p.m.)*
Blood
n.d.
n.d.
n.d.
0.004
0.004
0.003
Fatty tissue
0.07
0.09
0.04
8.5
9-1
9.7
Muscle ( neck)
n.d.
n.d.
n.d.
0.36
0.64
0.71
Liver
n.d.
n.d.
n.d.
0.61
0.57
0.64
Kidney
n.d.
n.d.
n.d.
0.15
0.18
0.20
Bile
n.d.
n.d.
n.d.
0.03
0.03
0.04
Spleen
n.d.
n.d.
n.d.
0.09
0.12
0.16
Lung
n.d.
n.d.
n.d.
0.05
0.06
0.08
Heart
n.d.
n.d.
n.d.
0.13
0.20
0.25
IV. Residues
“r T
Pancreas
n.d.
n.d.
n.d.
0.25
0.33
0.28
Brain
n.d.
n.d.
n.d.
0.13
0.14
0.19
Spinal cord
n.d.
n.d.
n.d.
0.25
0.23
0.40
1.0 h
0.80 0.60 -
Ovary
n.d.
n.d.
n.d.
0.02
0.22
0.20
0.40 —
E
° Mean
j
_
_ neck,
of the active ingredient
contents determined _in___
the__fat of the back,
abdominal muscle, intestines, and kidney, calculated
fat. All X....re
other
- on
-- extractable
-------------- —
sults are calculated on the total organ weight.
6 a- and jS-endosulfsn, endosulfan sulfate.
c DDT 4- DDE.
d n.d. = not detectable, i.e., in the a- and /3-endosulfan <0.01 p.p.m., in endo
sulfan sulfate <0.02 p.p.m., in DDT and DDE < 0.03 p.p.m.
mally sensitive or resistant to the insecticide. No endosulfan sulfate was found
in the eces but small amounts of a- and /^-endosulfan and two transformation
products of the insecticide that have not been identified so far were found
(BARNE3 and WARE 1965). BALLSCHMITER and tolg (1966 and 1967) de
tected mdosulian sulfate, endosulfan ether, endosulfan-a-hydroxy ether anti. - - endosui. :. .1. lactone alongside one another as transformation products of
~
sulfan after peroral, cutaneous, and subcutaneous administration
imagines of the migratory locust Pachytilus niigratorius rnigrraorioid^^Tto
seven days after discontinuing the administration of endosulfan-(Afa{ning^ci
feed, no unchanged endosulfan was detectable in the bodies of the
were any of the transformation products found.
<1^
17
Table VII contains a selection of results from investigations on different
kinds of fruit, vegetables, and fodder plants for their endosulfan content after
application of the insecticide as a spray or dusting powder. The analysis
results from the United States are from tire laboratories of Food Machinery
Corporation, Niagara Chemical Division. The residues determined up to 1962
comprise the a- and ^-endosulfan contents of the tested plant materials. The
residues incorporated in Table >711 relating to 1963 and after, in addition
to the a- and ^-endosulfan content, also include the endosulfan sulfate content;
these analyses are reproduced in italics in the table.
Figure 2 demonstrates by means of two examples from Table VII (apples
1963, three sprayings; alfalfa 1964, one spraying) the distribution in'each
case of a-endosulfan, ^-endosulfan, and endosulfan sulfate in the residues.
In both cases less than 0.2 p.p.m. of endosulfan sulfate is contained in the
analyzed material 15 days after the treatment.
Feeding period (days)
27
Endosulfan
I
cL 0.20Q.
T
T
I
1
\
>x-
/\\
\
/
I
I
0.10 — I1
0.08
I ,
LS
0.06
■o
X ""
x
0.04 - !
I
I
o:o2
/
/
•0.01 y_____ 1
0
6
I
12
J____ I
18
24
Days
I
30
I
36
42
A'.
\ dt b
f
Fig. 2. Residues of endosulfan and endosulfan sulfate on apples (three opuya
wliu
sprays vzith
Thiodan V/P, 2.2 Ib./acre each) and on alfalfa (one sprav with Thiodan EC 0 25
lb., acre) according to .^SSIL
CASSIL (1963) and HOLSING (1964)'
(1964) {Food Machinery Corp.
Corporation, Niagara Chemical Division)') x
— x apples, a- and P-endosulfan; o---------- eapples, endosulfan sulfate; x—• alfalfa, a- and (3-endosulfan; o—-o alfalfa, endosulfan
sulfate
Tabic VII. Endosulfan residues under practical conditions of applicatio.'H
Crop
j Location
__ ____
Apple
USA, Calif.
USA, Calif.
USA, Calif.
USA, Calif.
I960
1960
1963
1963
VI, VII
VI, VII
V, VI, VII
V, VI, VII
3
i960
V, VI, VJI
1
2
1958
1963
IX
V, VI
USA, Calif.
USA, Oreg.
2
1
I960'
1960
V, VI
VI
USA, Calif.
USA, Calif.
1
1
1958
1958
V
V
\VP
1
1961
WP
1
1961
2
1
1960
1959
VII
VII
1
1961
IV
Pear
USA, Calif.
USA, Calif.
USA, Calif.
Strawberry
Raspberry
WP
EC
WP
WP
Netherland
Netherland
Grape
USA, Calif.
USA, Calif.
Spinach
month
2
2
3
3
Peaches
Cherry
year
WP
Dust
USA, Va.
Residues (p.p.m.)d
Act.
ingre
Anal.
dient
(Ib./acrc) method6
Time of application
No. of
Formu appli
lation'1 cations
Week.': after last application
J,it/!
0
0.5
I
1
2< -r
1 4 -!
3
3
2.2
2.2
GC
GC
GC
GC.
c
c
C
c
3.5
GC
C
0.5
1.4, 2.2
Col.
GC
c
c
6.0
3.9
3.0
1.7
1.0
1.2
2.25
I
GC
GC
C
C
15
4.6
2.1
1.5
0.7
0.4
0.3 !
0.15 | --
4
2
Col.
Col.
c
c
9
5.7
1.2
0.6
0.8
0.5
0.4
0.2
V
GC
W
2.4
0.9 j 0.6
V
GC
w
0.5
1.05
GC
Col.
C
C
1
GC
2.7
2.0
1.7
1.4
o.'>
0.6
0.3
0.7
1.3
0.8
1.2
0.7
0.8
1.3
1.2
5
1
I 0.3 I —
I1 n0.29 1 __
... I 0.5
j 0.7
0.
0.5 I 0.5
i Q-2 :
i 0.4
I
!
j
0.1 1 0.06
1.2
0.8
0.4
0.05
0.1
0.05
0.1
21
4.7
0.7
0.23
<0.C
*
co
tn
2(
X -ttV
Q qTUj rn
*;
73
V
1 x-B
r* ) rn >
Table VII. (continued)
I
j
, Crop
Local ion
No. of
Formu- applilation'7; cations
Chard
USA, Wash.
Spray
2
Collard
USA, Wash.
Spray
4
Cauliflower
USA, N.Y.
Water cress
Green pea
Green bean
month
1
Col.
0.75
Col.
Residues (p.p.m.)fi
Weeks after last application
Lit.0 |
M
-0— L°2_-
1
2
57
—
6.8
2.3
39
—
| io.i
•
1964
VIT, VIII, IX
0.75
GC
PC
15
1964
VJI, VIII, IX, X
0.75
GC
Spray
2
I
1
2
1
1958
1958
1966
1966
VI
VI
VI, VII
VII
1
1
3
US.A, Hawaii
USA, Hawaii
Col.
Col.
Col.
GC
GC
2
1
1961
1960
<0.05fi <0.05° | <0.05° I <0.05^
8.3/
4.5/
3.3/ j 3.8/
II
0.5(1 j 0.1
0.1°
0.1
2.6/
0.2/
0.3/
0.45/
60
M
■ 8
!
I
1.6
C
59
9.5 j 2.7 I 0.1
! 14
I 0.3
c
c I 3
I E3 i 0.2
C I H
2.3 j 0.2
V, VI
XII
1
0.5
GC
C
USA, Miss.
W. Germany
3
1
1959
1962
VII
VII
1.5
0.25
Col.
GC
1
1960
w IX
1
GC
2
2
2
C
I
1.24<i <0.05^ I <0.05f/1 — j
<O.O5i7 <0.05M<0.05id
0.8/
—
0.06/ ! 0.05/ .
1.4
0.06
— i
_
1965
1964
1965
IX
VII, VIII
VII
1
0.5
0.25
GC
GC
GC
H
C
C
O.9o
1.2o
VI
VII, VIII
2.5
0.5
GC
GC
II
II
VII, VIII
1.0
GC
II
USA, Wash.
USA, Calif.
USA, Calif.
USA, Calif.
USA, Calif.
EC
EC
EC
USA, N.Y.
USA, Calif.
USA, Calif.
USA, Miss.
USA, N.Y.
USA, N.Y.
EC
EC
EC
1
WP
WP
3
1958
1965
1964
i
1
II
i133
H
MB
9.2
16
1.3
2.3i
5.0/
2.9i
87.5/ j
0.5
r:.
|I
0.05 i
...
0.2
r
2.9
8
French bean USA, Orc.
Red kidney
bean
year
Act.
ingre
dient
Anal,
(Ib./acrc) met hod &
EC
USA, N.Y.
Lettuce
Time of application .
.— i
b
__ I
0.02 I — ' —
i-
0.0Sl‘
0.3<1
0.1 o
0.2
!
I -
().05o
0.07 j
O.IJi
0-3'■
0.09! 0.05!
4.1/
1.2/
0.2i
O.OO1
5.0/ 3.0/
—
—
—
Tabic VII. (continued)
Location
Crop
ikry
jmato
USA, N.Y.
USA, N.Y.
USA, Fla.
No. of
Formu appli
lation0 cations
EC
EC
EC
USA, Miss.
USA, Ohio
Watermelon USA, Fia.
USA, Calif. I —
Time of application
year
month
1964
Act.
ingre
Anal.
dient
(lb./acre) method6
Residues (p.p.m.)d
Weeks after last application
Lit\
0
0.5
2
9
1964
1964/65
VII, VIII
VII, VIII
XI, XII, I
0.5
1
0.5
GC
GC
GC
H
II
II
1.8
3.0
1.91
6
1
1959
1959
V, VI
XI
0.5
0.8
GC
GC
II
II
0.07
1.2
1
1
1959
1961
V
IX
4.2
I
Col.
GC
II
C
0.5
5
1958
VII, VIII, IX
0.625
Col.
II
2
3 '
4
I__ 5__
0.9
1.8
1.0/
0.7
1.3
0.71
0.4
0.7
0.4j
—
—
—
—
—
_
__
—
0
0.5
0.05
0.03
0
0
ju ash
USA, N.Y.
rtichoke
USA, Calif.
USA, Calif.
USA, Calif.
Dust
EC
WP
I
4
4
1959
1966
1966
X
VI, VII, VIII
VI, VII, VIII
1.2
0.75
0.75
G(
GC
GC
C
0.6
1.7
3.0
nrot
USA, Calif.
EC
2
1965
IV, V
1.0
GC
C
Haifa
LjSA, Ohio
USA, N.Y.
EC
1
1
1961
1964
IV
V
0.25
0.25
GC
GC
USA, Ohio
EC
1
1963
IV
0.25
ikSA, N.Y.
EC
1
1964
V
EC
1
1964
EC
Thiodan-01
Dust
1
1
1
ed clover
1
0.1
0.3
0.8
0.02
13.9'
0.21'5.6'
3.0f
0.03k
l.Oi
1.6t 2.4/ 1.3f
0.0V- 0.03k 0.01*
0.31 0.7' 0.41
I-I
c
14.5
2.7
2.4
1.0
0.2
0.1
0.05
0.1
GC
H
11
2.0
0.3
0.06
0.25
GC
H
8.2
2.2
0.6
0.3
0.2
0.45vl
V
0.25
GC
II
6.8
1.0
0.7
0.6
0.3
2.3m
1962
1962
V
IV
0.21
0.6
GC
GC
MB
MB
1.8
55
0.3
0.1
2.0
1962
V
1.8
GC
MB
1.2
0.2
0.1
0.2 M
c
c
0/1
0.01
0.09
0.24"1
n.cl.
CP
) if
)m
-
fr^sfebf-.
trefoil*
odder Grass \V. Germany
W. Germany
W. Germany
20
a -£C = enHdSion concentrate, WP —wettable powder.
6 Col.
dolorimetric method, GC —gas chromatographic method.
t-C = CASSiL (1958/66), Il=
-—HOLSING
not----- (1958/65),
-------- ... M = MAITL1-N and WALKER (1963), MB ~ MAIER-BODE (1965 and 1967),
V --wrr (W66 b).
dThe residue data printed in italics comprise the content of a- and ^-endosulfan and endosulfan sulfate in the tested materials, the data
n normal print refer only to a- and ^-endosulfan.
e In tire heads.
f In the leaves.
u In the pods with seeds.
7‘ Podded.
' In the pods.
■' Trimmed for the market.
In the roots.
‘ In the entire plant.
m In hay.
Hans Maier-Bode
•
’
Iiadosulfan
a) Red-dues on jruit
23
c) Residues on fodder plants
Table VII, in the case of apples, pears, peaches, cherries, strawberries, and
grapes shovzs that the residues do not exceed 0.5 p.p.m. three weeks after
treatment; the only exception are apples at 0.7 p.p.m. In most cases an over
dose was applied, as endosulfan is recommended at 0.2 to 1.5 Ib./acre. The
results are preponderantly from California.
In Dutch tests with raspberries (wit 1966 a), on one occasion 0.6 p.p.m.
and on another 0.06 p.p.m. of endosulfan were found four weeks after treat
ment. It is possible that a large overdose was applied in the first case; there
are no details in the report as to the amount of active ingredient applied/unit
area. About 0.1 p.p.m. of endosulfan was found in the cold-pressed juice of
black currants, pasteurized for 20 minutes at 85° C., which had been sprayed
with endosulfan at the commencement of blossoming, during full bloom, and
for a third time nine days before harvesting [amounts applied: 0.3 percent
Thiodan wetrable powder vzith 17.5 percent endosulfan, 0,2 gal./bush
( MAIER-BODE 1967 ) ].
On alfalfa, clover, and grass, endosulfan residues fall to about 0.5 p.p.m.
or further within two or three weeks of treatment in the warmer season, above
all also because of the rapid increase of the plant mass. At lower temperatures
and slow plant growth when, for example, the insecticide drifts from pwblossom sprayings in orchards onto grassland, degradation may be slower
(MAIER-BODE 1965). In the manufacture of silage fodder'any endosulfan
residues possibly present on the plant material are only degraded slightly
(BECK et al. 1966), also in the drying of grass, clover, or alfalfa to make hay.
Here, the endosulfan content of the plant material virtually increases to rhe
same extent as the water content decreases. Table VII contains examples of
this on alfalfa, clover, and grass. Provision must therefore be made in advance
for a low insecticide content of harvested products destined for the prepara
tion of silage feed or hay, by adhering to the directions relating to dosage
and waiting period.
f
!
r
d) Residues on tobacco
I
I
b) Residues on vegetables
lable A II reveals that the endosulfan residues in fast-growing leaf vege
tables (spinach. lettuce, vzater-cress) are usually belovz 0.5 p.p.m. tw’o to
three vzeeks after application. In contrast, MAITLEN et al. (1963), in the case
of chard, collards, and lettuce, with a high initial dose (on day zero between
39 and 69 p.p.m.) detected between 1.6 and 3 p.p.m. of residues two weeks
after treatment with endosulfan spray mixture. After spraying cauliflower
with endosulfan several weeks before the harvest, the insecticide is mainly
found in the leaves and to a lesser extent on the flower. Two weeks after the
last of eight sprayings the initial endosulfan content of the cauliflower leaves
was still 3.8 p.p.m., and the flower contained less than 0.05 p.p.m. One week
after treatment of the plants, traces up to 0.3 p.p.m. of endosulfan were de
tected on the s^eds and pods of peas and beans. In contrast, the foliage of the
bean plants still contained 4.1 and 5 p.p.m., respectively, three weeks after
treatment. One week after treatment of the plants with endosulfan spray
mixture, 0.05 p.p.m. residues were detected in carrot roots and three p.p.m.
at the same time on the carrot leaves. These analytical results on cauliflower,
peas, beans, and carrots confirm that endosulfan does not penetrate the interior
of the plants and cannot therefore act as a systemic insecticide. Existing analytical results shew that only slight endosulfan residues are detectable a short
time after application of the insecticide on tomatoes, melons, squash, and
artichokes.
After drying, tobacco leaves treated in rhe held vzith endosulfan still con
tained 16 percent of the insecticidal residues determined on the green leaves.
Three percent of the originally present endosulfan residues was still detected
in the smoke of cigarettes made from this tobacco (GUTHRIE and BOWERY
I.
1962.
E
V. lolerances and time limitations
Table Vj.II gives a survey of the tolerances laid down at present in various
countries tor endosulfan. They are between zero and two p.p.m. The zero
tolerance for meat and milk is founded on the low persistence of endosulfan
and its metabolites in vzarm-blooded animals end its lack of accumulation in
the fat and lipoids of the animal organism (see section III b).
The waiting period between the last appheation of endosulfan and the
harvest recommended and stipulated for the avoidance of exceeding the toler
ance vary in the individual countries, depending on the agriculturafconditions
and are, for example:
42 days in Denmark and Great Britain
35 d;.ys in Austria
X
30 days in CSSR, Germany (Fed. Rep. and Dem. Rep.), Hungary, Poland,
. Sweden
Xx 28 days in Angola, Belgium, Benelux, Finland, Holland
days in Italy, Norway, Spain.
die United Stares the waiting periods arei between "no time limitations”
eal
^^yh30 days: for example, "no time limitations on cucumbers and melons, one
d° )S. SU1&ARARAJAk May Von tomatoes, four days on strawberries, »seven days on broccoli, cabbage,
/£gTes’ and plums, 14 davs on lettuce, 21 davs
IYENGAR
. 5 on cherries, and one to 30 days
~
Jen Apples,
peaches,
and1 pears.
’
•
4
>
)TARY j
,
1
Hans Maier-Bode
24
Endosulfan
Table VIII. Tolerances for endosulfan
I
Tolerance
(p.p.m.)
Country
2
United States
Range of validity
Fruits (e.g., apples, apricots, cherries, grapes, pears,
plums, strawberries)
Vegetables (e.g.,
melons, tomatoes)
2
Canada
broccoli,
cabbage,
cucumbers,
Fruits (e.g., apples, apricots, cherries, pears, plums)
Vegetables (e.g., broccoli, cabbage, spinach)
1
Canada
Fruits (e.g., grapes, strawberries)
Vegetables
tomatoes)
(e.g., cauliflower, cucumbers, melons,
0.5
Switzerland
Strawberries
0.5
Holland,
Benelux
Fruits and vegetables
0.5
Germany
(Fed. Rep.)
Leaf vegetables .-.ad other sproutmg vegetables, fruit
vegetables, legumes, fruit without grapes
Zero
United States
Meat and milk
VI. Analysis
a) Identification
The most recent publication on the identification of endosulfan by means
of the infrared spectrum and the nuclear magnetic resonance spectrum is that
of FORMAN et al. (1965). It is mainly concerned with the clarification of its
isomers. Infrared spectra have been used for identification and also for quan
titative determination by several authors (LINDQUIST and DAHM 1957, ZWEIG
and archer I960, paulig 1961, blinn and gunther 1962, morris and
HAENNI 1963).
b) Detection
Particularly suitable for qualitative detection are the colour reactions
which can be carried out on a chromatogram after paper chromatographic
Cr—
or thin-layer chromatographic separation. LINDQUIST and DAHM (1957^7^^
separated the endosulfan isomers and impurities by reversed-phase pap^/^
chromatography using the system silicone-oil/watcr-ethanol. RAHN (1963[|Ll- (
I
25
preferred the same technique in his metabolic studies on endosulfan. He
worked successfully with the system dimethylformamid as stationary phase
and benzene as mobile phase. Mineral oil as stationary phase and 65 percent
methyl-Cellosolve in water as mobile phase served TERRANOVA and WARE
(1963) as developing system in his studies on the metabolic fate of endo
sulfan in bean plants. Further work on paper chromatography was done
by Evans (1962).
In 1962, YAMAMURA and NIWAGUCHI (1962 and 1962 a) studied the
separation of aldrin, dieldrin, endrin, and endosulfan on starch-bound silica
gel chromatoplates mainly developed with mixtures of hexane or cyclohexane
and acetone. WALKER and BEROZA (1963) used silica gel G plates and de
veloped the plates with hexane acetone (9 —1) and hexane-ethylacetate
(9 -p 1). ABBOTT et al. (1964) recommended a mixture of petroleum ether
(b.p. 40° to 60° C.), liquid paraffin, and dioxane (94 4- 5 -f- 1) as de
veloping agent for separation of endosulfan from several other chlorinecontaining insecticides such as DDT, BHC, dieldrin, endrin, heptachlor,
methoxychlor, heptachlorepoxide, and some other compounds. Some selected
data given by WALKER and BEROZA (1963) are shown in Table IX.
More recently, KOVACS (1966) developed a thin-layer chromatographic
technique on micro slides, coated with either aluminum oxide G or MN silica
gel G-HR. Developing agents have been w-heptane with one percent acetone
and w-heptane with 25 percent dimethylformamide. The technique in gen
eral has been reviewed by ABBOTT and THOMSON (1965) and will not be
further described here with the exception of those visualization techniques
which are especially useful for the detection of endosulfan. One of the
most common chromogenic reagents was described by MITCHELL (1958),
i.e., silver nitrate and 2-phenoxyethanol in acetonic solution with subsequent
irradiation with ultraviolet light. The reagent has been adopted (walker
and BEROZA 1963) for similar purposes on thin layers. On silica gel or
alumina plates, however, one obtains dark backgrounds which limit its
sensitivity. RAHN (1963), using barium chloride and sodium rhodizonate
for the detection of endosulfan on paper chromatograms, obtained white
spots on pink background. Again, walker and BEROZA (1963) recom
mended the use of fluorescein and silver nitrate after a treatment with iodine
or bromine and irradiation with ultraviolet light to visualize endosulfan.
This leads to the vast field of fluorescent substances as chromogenic agents.
BALLSCHMlTER and TOLG (1966 and 1966 a) selected the following reagents
out of many, to detect even as little as 20 ng. of endosulfan on silica gel G
or aluminum oxide G chromatoplates in acetone and water as solvents, for
example:
4,4'-bis-diethylamino-biphenyl
3-dimethylamino-fluoranthen
\*?'\
9-methyl-carbazole
'' ' -x \»
^-amino-pyrene
)' IJ
Rhodamine B or Resorufin
■■
26
Hans Maier-Bode
Endosulfan
J abw IX. Rz values of some pesticides on silica gel G thin layers (WICKER and
BEROZA 1963)
Hexane -4- ethylacetate
_________ (9-4-1)
Trichlorfon
Phosphamidon
Schradan
Carbaryl
.' zinphos-methyl
Captan
Malathic-n
p-r.::dGsrt'ljan
Meth y J pa rath ic n
Binapacryl
Su Ifotep
Parathion
Mctho.xychlor
Ethion
Endrin
Dieldrin
Din neap
Lindane
o,p'-DDT
£.<-DDT
Dicofol
Heptachlor epoxide
Tetradifon
TDE
Ethion
Phorate
Toxaphene
G.-Ej:dcsulfan
«,p'-DDE
Chlordane
Hepta chlor
Toxaphene
Aldrin
Chlordane
0
0
0
0.02
0.03
0.05
0.06
0.10
0.11
0.14
0.15
0.17
0.20
0.21
0.22
0.27
0.29
0.31
0.32
0.34
0.35
0.36
0.37
0.37
0.37
0.3S
0.38
0.38
0.40
0.40
0.40
0.42
0.43
0.44
0.46
0.46
0.48
0.48
0.49
0.50
0.52
0.54
0.54
0.54
0.54
0.55
0.55
0.56
0.57
0.57
0.62
0.64
0.65
0.65
0.67
0.67
27
£p«S£Pte te
ll a » U
Hexane + acetone
______ (9-p 1)____
Trichlorfon
Phosphamidon
Schradan
the low concentration of tb fluon
4
“ “ CaUSed primarii-v bv
10-4- to 10^ v,/v.
Ascent mdteator which should not exceed
c) Quantitative d-etcrriiination
Carbaryl
Azinphos-methyl
fon-ned is SdUodoXSS'
and dl£ sodiu“
very fast and
X
TX “
™s
is
routine method if the saparX dX ^^ X
1964 as a
quired. The method is us-d nd L rinmarion of the two isomers is not re
analysis of endosulfan in hs v'^ouslor^] T
C°ntro1 and rou^e
products. The
The decomPOsinon of endosulfan in these MrZ -formulated P
can be determined. The
Captan
Malathion
Methyl parathion
fi-Endosulfan
Parathion
Methoxychlor
Di cofol
2,““”'” “ ’
•«d ARCHER <1»>
Binapacryl
material and in
" h>-
Xr„;G £““,2;;
Sulforep
chromatographic separation >> r^r- a
advantageously if a column
derermination, as pXosed '
cXXX i % X sPeOT0P!-ctc°e:ric
chromatographv is carried or- -n ? 5 AC
,Jlod for endosulfan. This
It has been proved dTX^XT^Xdo^ol
“4
Tetrad i fan
Lindane
Ethion
Dinocap
tsomers If aluminum oxide having the activmz X- 1T
4 “““
phase the recovery of endosulfan is oriv 7$ XTiT “
Dieldrin
Phorate
I
Ethion
p,p'-DDT
Endrin
Toxaphene
a-Endosuljan
Heptachlorepoxide
Chlordane
o^'-DDT
p,y-DDE
Chlordane
Heptachlor
Aldrin
Toxaphene
,s
LUdWigXwKhZh STAHL ’and this
I
isomers prior
seP-ation of the two
(1964). Ii2e silicaCOLAS “ <lme recommendations given in FAO v-IethoTl^fo
aCC0rdance wi*
^07%
mU“ d£Press“S agent. A single polaro^ST^aiT" g
? “T’
ipp j5,
'
V
f’
)’* ‘I960). This may be done in
y ^sample-to-solvent ratio depends hrgely
A
c/ (zweig and archek
J
la
I
H
Endosulfan
Hans Maier-Bodb
28
fruit the ratio of one mi. of solvent for four g of sample is
For more leafy crops the amounts of solvent s ou.
c
r
extracapchfr i960). Several solvent mixtures are recommenciud for
tion
"diethvl ether and mixed hexanes (LINDQUIST et al. 1^9),
and’subsequent extraction of the acetone/water solution
(Boots Pure Drug Co., Ltd. 1959), or carbon tetrachloride (pAULIG 1901)
S alcohol/hexane mixtures (Pood Machinery Corforatt°n’^S^
cal Division I960. ZWEIG and ARCHER I960, BURKE and M.LLS i9fo)■
iropanol-hexane mixture is the most used extraction solven. anu r
recommended. A suitable mixture consists of two g. of hexane
;
isopropanol/c. of sample. This mixture is appropriate not only for the
S. =1
J !»(,
ta 1.^1 te
“““
well For this purpose the tissues are minced and mixed with sodium sulfate
foJtveral minutes; isopropanol is added and dre entire
for an additional five co ten minutes. Even. fatty^ material cm
by this method {Rood Machinery Corporation, Niagara Chemical D ,
1960 1963). Instead of hexane benzene may be used as we^.
A rapid method to be used for chlorinated pesticides in fluid mwe w
published by ONLEY (1964), in which endosulfan is extracted direcdy from
whole milk The extraction solvent is a mixture of acetonitrile, ethyl e.ne ,
diox?ne and acetone (15 + 5 + 5 + 5 v./v).
...
If pure solvents am used the extract is contaminated with watery suspensions and small particles. These interferences are eliminated by stirring i
extract with anhydrous sodium sulfate and filtering through a soft fiber paper (
or glass wool. Extracts with alcohol-hexane mixtures are freed from the alcohol
component by shaking with water. After separation of the orgamc ph.,
■ from the water phase the former is dried with anhydrous sodium sulf.te and
I
-
I
i
i
^Cfeas^^ending on the ultimate determination method chosen there
Endosilfan+iponified with ethanolic potassium hydroxide solution and
the split-off sulfur dioxide is separated by steam distillation after acidification
of rhe alkaline solution with p-toluenesulfonic acid The sulfur dioxide is
determined colorimetrically. Alternatively, the endosulfan residue
altered chemically but is purified by suitable separation methods to a certain
decree so that it is possible to determine it specificahy.
In aff cases where the extraction is carried out with acetone or some
other solvent miscible with water the extract can be shaken out with a
convenient solvent as benzene, hexane, or methylene ch.oride after e g
diluted with much water. Fat-containing extracts (normally hexane extrac
are subjected to the so-called acetonitrile-hexane-distribution (mills e. a..
-963). During this process the fat is dissolved in the hexane phase while
the ^Hdosulfan remaihTffrrtre acetonitrtle-phase. The acetonitrile phase,
containing the endosulfan residue, can be either concentrated by evapora-
I
29
tion or shaken out with petroleum ether or another suitable solvent as
mentioned above after dilution with a large amount of water (FoorZ Machin
ery Corporation, Niagara Chemical Division I960, GORBACH 1966). A more
systematic investigation of the distribution behaviour of endosulfan among 25
other insecticides in 19 binary solvent systems has been carried out by
BEROZA and BOWNLVN (1965 and 1965 a). By means ot the tabulated
"p”-values (p = fractional amount in the upper phase) it is possible to
select the most promising binary solvent system to separate endosulfan from
unwanted material. If any interfering substance from a sample appears to
have a great affinity for the upper phase a system giving a low insecticide
"p”-value is to be preferred. For example, endosulfan has low p -value (0.15
a-endosulfan, 0.05 /3-endosulfan) in the system isooctane/85 percent di
methylformamide, but butterfat distributes readily into the isooctane phase.
The superiority of the isooctane-dimethylrcrmamide system is therefore
clear. The separation efficiency is enlarged if the Craig counter-current
distribution technique is used.
Column chromatography and thin layer chromatography have been used
extensively as cleanup technique. Both have been reviewed in connection
with their use for endosulfan extracts in Residue Reviews (ABBOTT and
THOMSON 1965, MORLEY 1965). Both are used mainly for the analysis
of formulations. Florisil is widely used for cleaning up solutions m residue
work. BURKE and MIILS (1963) recommended columns of preactivated
Florisil. The endosulfan-containing extract is transferred to the column with
a minimum of petroleum ether. The ffist elution step is performed with
a ((5_j_ 94) mixture of ethyl ether and petroleum ether. This eluate con
tains DDT and several other chlorinated pesticides. The endosulfan is
eluted with a (30 + 70) mixture of the afore-mentioned ethers. However,
this procedure does not eliminate all unwanted materials, so BURKE and
mills (1963) propose to cleanup the (30 + /0) eluate with the AOAC
cleanup mixture (10 parts anhydrous sodium sulfate, five parts Attapulgus
clay, five parts Celite 545, and tv/o parts Nuchar 190-N) in a second
column procedure. Chromatography on carbon-Celite mixtures has been
carried out by MOATS (1964).
In routine residue analysis it has been proved {Rood Machinery Corpora
tion, Niagara Chemical Division I960, GORBACH 1966) that a single treat
ment of benzene extracts with the carbon-Attapulgus-clay mixture in a
separatory funnel gives a sufficient cleanup in most cases. Pure charcoal
(e.g., Norite A, Nuchar C 115n) as a batch has also been used (GRAHAM
et al. 1964). As a further adsorbent, magnesium oxide may be used (MAITLEN
thin layer chromatographic plate? as an open chromatographic column
k\has befcjn 'used in routine work, too (( GORBxA.cn 1966). The layers (silica gel
Darmstadt) have a thickness of about one mm. and the extract
3^^vpnt' o)i%i^plate as a 10 to 15 cm. long streak. A test spot near the edge
V
30
Hans Maier-Bode
Endosulfan
*of the plate permits detection of the position of the wantcu *esidue on the
plate after development with benzene/acetone (9 -r 1)- The gel is scratched
off and eluted with benzene or chloroform.
»
>
Methods of determination.
Photometric determination. In an alkaline medium, endosulfan when
heated splits off sulphur dioxide with which ^-rosaniline and formaldehyde
in solution produce a red colour whose absorption at 570 nm is measured.
This method is to be recommended if there is no possibility’ of carrying out
the final determination gas-chromatographically (GRAHAM et al. 1964). The
colorimetric determination of endosulfan with pyridine and methanolic
potassium hydroxide solution has been recommended as an alterna
tive method (BUTLER et al. 1962). The hexane extracts, concentrated by
evaporation, may be used for this colour determination without cleanup. Of
45 insecticides tested, only captan, chlordan and heptachlor interfere. Endo
sulfan diol is also determined by this method. An infrared method has been
developed by ZWEIG et al. (I960).
Gas chromatographic determination. Gas chromatographic techniques
are common for the detection of residues of endosulfan and its metabolites.
Stainless steel, aluminum (CASSIL 1962, BURKE and MILLS 196^) and quartz
(CASSIL and DRUMMOND 1965) have found approval as material for separa
tion columns. The column material has some influence on the stability of
endosulfan during the separation process. There are numerous prescriptions
which state how the solid support and the stationary phases should be. It
seems to be clarified that the pretreatment of the solid support is mainly
responsible for the stability of endosulfan on the column. Chromosoro Tv
washed with hot hydrochloric acid in a glass column and coated with the
stationary phase in the same column is a recommended solid support (CASSIL
1962). Purified silicone grease (CASSIL 1962), Dow Corning 200 (burke
and HOLSWADE 1964), Dow Corning 11 (ZWEIG et al. I960), and the fluoro
silicon rubber QF 1 (HENLY et al. 1966) have been used as stationary
phases. Mixtures of DC 200 and QF 1 have been preferred by burke and
HOLSWADE (1966). As an example, some selected data given by these
authors are listed in Table X.
The microcoulometric detector. Originated by COULSON et al. (I960),
this apparatus is now manufactured by7 the Dohrman Instruments Company.
A first review of this technique was given by CASSIL (1962) in this journal.
Several other authors used this detector for the determination of endosulfan
(BURKE and MILLS 1963, BURKE and HOLSWADE 1964, CHALLACOMBE et al.
1964). Microcoulometry7 pvviuvj
provides U4XX
an absolute and stoichiometric
measure----of
- ----------------------------------------------------chlorine and sulfur in pesticides. The detection limit for endosulfan with
this detector is about five to 10 ng. The coulometric method applied to thj/^
determination of endosulfan is superior to other methods if the sulfur
and the chlorine cell are used side-by-side. The interferences by chlorinqYa^ '
but non sulfur-free pesticides can be eliminated by using the sulfur '££5 ) S.
R
31
Table X. ReL
rcteni^n times of pesticides and related compounds with elec
tro..-capture detection (BURKE and HOLSWADE 1066). Olumu ■ Mixture of
<ln-,00° eX,)
80/1(10
Chrorn O and 10% DC
2iood- ■
°n 8!J'd°i GaS Chr°m Q1
0
Codwtw
^.00 0., section temp. 225 C.; £as fiote rate 120 ml. N^mim Detector: electrcL
capture, concentric type, tritium source
I.
Retention time rei.
to aldrin*1
Pesticide
. $
I
i
THE
qt-Lv
5 L
T“
Djchlorvos
Simazine
Atrazine
Propazine
Mevinphos
Chloranil
Tecnazene
Chlorpropham
2.4- D-raethylester
DDT (tech.)
Phorate
BHC (tech.)
a-BHC
Vegadex
Methoxychlor (tech.)
Tetraiodoethylene&
2.4- p-isopropylester
Diazinon®
Dicofol (tech.)
Lindane
B-BHC
Quintozene
Dioxathion
7-BHC
Heptachlor
Dimite
2,4,5-T-isopropyiester
Dichlone
Dimethoate
Fenchlorphos
Aldrin
Isobenzan
o,/?'-TDE olefin
Isodrin
Perthane olefin
h,//-Dicofol
Chlorobenzilate
Methyl parathion5
o^'-DDE
Heptachlorepoxide
Malathion6
£,//-TDE olefin
- ..
Chlorbenside
Dacthal
\> o,//-Dichlorodiphenylmonochloroethane
•x X ^-Chlordane
) . Qxydemeton-methyl
/
0.14
0.26, 0.54
0.26, 0.55
0.26, 0.56
0.31
0.37, 1.52, 1.73
0.38
0.41
0.42
0.39, 1.88, 2.48, 2.70, 3.23
0.45
0.-16, 0.58, 0.68
0.46
0.46
0-51, 3.23,4.6
0.51
0.55
0.56
0.58, 0.74, 1.09, 1.31, 1.86. 2.21, 2 37
0.58
0.60
0.61
0.66, 1.13, 14.27
0.68
0.81
0.82, 1.31
0.84
0.86, 2.04
0.97
0.97
1.00
1.14
1.21
1.25
1.31
1.31
1.33, 2.93
1.42
1.46
1.47
1.48
1.50
1.51
1.52
1.53
1.57
1.69
1.70
!
!
32
Endosulfan
Table X. (continued)
instead of the chlorine cell. In general, microcoulometric detection is. much
more insensitive to interferences which are encountered in ionization
Retention time rel.
to aldrin®
Pesticide
r
33
HANS MAIER-BODB
^-Chlordane
p,p'-DDE
Parathion®
a-Endosulfan
£,p'-DichIorodiphenyimonochloroethane
Perthane
Folpet
o,p'-TDE
Captan
Dieldrin
Paraoxon6
Dyrene
Hydroxy propazine6
' '
o. p'-DDT
Endrin
Sulphenone
Kepone
^.p'-TDE
Chlorfensone
^■Endosulfan
^,p'-Methoxychlor olefin
Ethion
p, p'-DDT
Carbophenothion
Endrin alcohol
Endrin aldehyde
£,p'-Methoxychlor
Prolan
Dilan
Mi rex
Bulan
Delta Keto 153 (endrin product)
Imidan
Tetradifon
Azinphos-methyl6
Co-Ral
Chlordane (tech.)
Toxaphene
Strobane
i
1.73
1.88
1.88
1.89
1.94
2.02, 2.60
2.03
2.04
2.10
2.22
2.25
2.29
2.46
2.48
2.55
2.62
2.67
2.70
2.78
2.92
3.00
3.23
3.28
3.33
3.45
3.98
4.80
4.90
4.40, 4.90, 5.70
5.15
5.70
6.05
7.54
8.75
9.3
?3 5
6 "2, 0.S1, 1.07c, 1.55, 1.72, 2.78
1.70, 2.25, 2.37c, 2.55, 3.03, 3-66, 4.10, 4.70 5.8
1.09, 1.38, 1.53, 1.69c, 2.16, 2.52, 3.01, 3.56, 4.57
detectors: interfering peaks are mostly eliminated. Solvents that are more
volatile and less stable, e.g., acetonitrile, can be used.
The electron-affinity detector. The electron-affinity detector is probably
tire most widely used detector for residue analysis. A review of this technique
has been given by CLARK (1964) in Residue Reviezus. There are two main
types of electron-capture detectors: the concentric type and the parallel plate
type. Endosulfan is detected very sensitively by both types. The limit of
detection is 50 to 100 pg. References to the use of the electron-afinity
detector for the detection and determination of endosulfan are numerous:
GUTENMANN and LISK (1963), TERRANOVA and WARE (1963), BONELLI
et al. (1964), BURKE and GIUFFRIDA (1964), ONLEY (1964), BARNES and
1
WARE (1965), and BEYERS (1965).
Total chloride methods. Total chloride methods were used by PHILLIPS
and DeBenedictis (1954) as the sodium reduction technique, by LISK
(1962) as oxygen flask combustion, and by EGAN and EVA.NS (I960).
1
d) The analysis of endosulfan metabolites
■
The analytical behaviour of the endosulfan metabolites is similar to
endosulfan. For their extraction, benzene or benzene/isoproponal are suit
able. Paper chromatography (TERRANOVA and WARE 196n, BARNES and
WARE 1965) and thin-layer chromatography (BALLSCHMITER and TOLG
1966 and 1966 a) were applied for the separation of the metabolites. On
aluminum oxide G plates the visualization is achieved by spraying with the
Rhodamin reagent. In Table XI are reproduced the R/ values that have been
determined.
Table XI. R; values of endosulfan metabolites
Metabolite
a-Endosulfan
a When more than one peak is present, the major peak(s) is italicized. All reten
tion times measured from leading edge of solvent peak. Aldrin reference, retention time
approximately 3.5 min.
0 Not chlorinated.
o Other smaller peaks not included.
V-0
Methanol
0.75
0.91
0.26
0.91
Endosulfan sulfate
0.15
0.91
Endosulfan diol
0.05
0.82
Endosulfan ether
0.60
0.91
Endosulfan-a-hydroxyether
0.08
0.91
Endosulfan lactone
0.00
0.12
^-Endosulfan
The
phase varies from five to 20 percent, the length,
of.^^ktTirfi'frb^'^y0 three m., and column diameters from four t^„
Acetone
and w-hexane
(1:6)
____
34
Lans 31 air;;.bqpe
Endosulfan
y The gas chromatographic retention tiroes on three columns with -n
tionary phases of different polarity have
“=" "f”™ b>- “™»r„
the
insec« is approximately
endosulfan as applied in prarricp \ • artnroE°^s5 including the honey-bee,
holds good forCTbWH v 1 mn™ Of or litde d“ger. The same
is a fist poison
On
hand, endosulfan
Tabic All. RetcnlioK times of c^osulfan metabolites
Column'1
Metabolite
I
II
III
a-Endosulfan
1.
>■ -Endosulfan
1.
1.
2.16
2.70
1.34
4.83
6.02
1.70
0.34
0.47
0.43
1.09
0.67
2.31
0.71
Endosulfan sulfate
Endosulfan ether
Endosulfan-a-hydroj.jether
I
I
Endosulfan lactone
0.73
those of DDT, aldrin^ ottexapbe^"
surfaces more quickly’ than P endosT'0^11
oa
Plai« surfaces than
dlsapPears from the plant
as transformation product of the
if
w! •
d °n eaves and fruits>
to technical endosulfan Other m-tabnFr'
roxicolo^:'caIIy equivalent
ether) could be detected oSsLoVn
(endosulfai\ ^ol, endosulfan
i
i
for human consumption.
........ '
nts»Qot in crops-intended-
i-
a Columns: 1 = 2%
2;; QF-i
;
on •■Anakrcm
'
ABS, 110-120 mesh; 11 = 272
2% 322-62
XE-60
on Anakrom ABS, 110-120
— ._J mesh; 1-T
III = 5% SE-30 on
©iacopert PAW, 6®-80 mesh'.
■■
revealed only traces of endosulfan sulfate (0 02.C°WS
i . .
.u- lo u.z p.p.m.); on internoting the administration
of ku
endosulfan
limits of analytical detection. In c . .......... 1 tlhese rapidly decreased below the
n°t-±tE£d in the
or lipoids ofC2n^st.to DDT or dieldrin, endosulfan is
a warm-blooded
organism. After addition
of two p.p.rn. of endosulfan" or seven
■
-n
p.p.m.
of
DDT
(United States tolerI
-ces) to the daily feed of swine oveb
periods
of 27, 54. and 81 days the
body fat of-the animals contained .■.t
8 to'
10
19 p.p.m. of DDT, but less than
0.1. p.p.m. of endosulfan.
Endosulfan sulfate, endosulfan
ether, endosulfan-a-1■hydroxy
.
, ether, and
: endosulfan lactone were found
as metabolites of endosulfan
in insect
----- -m
organisms.
Two to three weeks after normal
.
number of fruit, vegetable, and fodder application of endosulfan to
to a large
plants
in
the
field
less
than
0.5
of residues (including endosulfan sulfate)
- J p.p.m.
■ ) were found. With higher7oses
up to two p.p.m. and occasionally up to
ot 0.3 p.p.m. endosulfan in cauliflower le,three p.p.m. were found. A content
•aves was accompanied by a content
of less than 0.05 p.p.m. in the flower-head
nnn. in
• the
u co
' a contenr of three p.pm in
carrot leaves by 0.03 P-p.m.
p.p.m.
m the corresponding tubers.
1 "
During the preparation of silage
the endosulfan residues
present on the
plants were only decomposed co a'small
” extent, likewise on drying of grass,
Cl0^r’ and aI^a to hay.
endosulfan nn r
/ \\ . , Tlie tolerances
;•
— for cuausui
osulh n on Q
ops ana
of...plant
crops
and toodstuffs
foodstuffs of
plant origin
:
d°Wn m various countries
y ^'Ot recommended intervals 'iXvX £
2nd
P-PfuTh
prescribed
. .
,
P-p-m. Thes prescribed
l ’ iX
the
last
apphcatW-of
endosulfaff
and
°f endos”lfan and
" ) harvesting range between "no time
«me Immarmns" and 42 days. Meat and milk
n
*1 Jmted StateS ,m7 not
any endosulfan
.
JkJ / Th!S report
report concludes
concludes with
with a review of rhe
I (zero tolerance). ■
a
With methodS Of ;“ng and assaying ihe inZct cX “T"’ ""-I '
q\ . ' °
msecucide m commercial
)
I
Summary
The insecticide endosulfan
go rained by the action of thionyl chloride
on the addition compound of hexacifforccyclopentadiene and c'/j-butene-2diol-1,4 and is a mixture of
two isomers^ the lower melting isomer being
dcui^naLCu a-endosulian and toe higher /3-endosulfan. m me literature on
•
- In the literature
o'X1^5!61?005"1^
usually incMed
included am°^ '’Urinated hydrocarbons
ox the cyclodtene grcr.p”. As sulfite
ester of
he ester
of a ct-clic diol it neverth'Xs differs
--dTS^5’
t £he ^^ctlcides of this group, such as aldrin, diddL
I
^“e\P^sielogic2l effects, and behaviour'
I
.
3o p.p.rn. of endosulfan in the feed occasioned no microscopic and =
cop.c symptoms m rars. The incidence of rumours was not ina ased byTndo’
sulfan m the rat fed. Dogs tolerated 30 P.P.m. of endosulfan in the feed for
?d for two
Ldication10Uf reaCri°n- Qllesn°nn2)reS in seven countries did not yield
■
anyho
utable to A
(
sor
35
- ””
•\
<
Vug
'■T.
' ■
*»
36
Hans Maier-Bodb
formulations and in residues from its application in crop protection.^ Concern
ing the analysis of residues, the processes of extraction, cleanup, the photo
metric and gas chromatographic methods are discussed in detail.
I
Endosulfan
Resume*
L’insecticide endosulfan cst obtenu par Taction du chlorine de thionyle
sur le compose d’addition de Thexachlorocyclopentadiene et du cis-butene2-diol-1,4. Il est un melange de deux isomeres, Ta-endosulfan, qui possede
le point de fusion le plus bas, et le (3-endosulfan. Dans la litterature sur les
pesticides, Tendosulfan est habituellement compris dans les hydrocarburcs
chlores du groupe cyclodiene”. En tant qu’ester sulfone d un diol cyclique,
il se distingue neanmoins si nettement des insecticides de ce groupe, tels que
Taldrine, la dieldrine et Tendrine, par ses proprietes chimiques, ses effets
physiologiques et son coipportement a la surface des plantes vivantes et dans
Torganisme animal, qu’il ne neut etre reconnu comme membre du groupe en
question.
L’endosulfan est bicn tolere par les plants cultivees, a peu d exceptions
pres comme, par exemple, les concombres sous verre soumis a de forts,,
surdosages. La DL50 aigue par voie orale chez le rat est de 76 mg/kg de
poids vif pour T^-endosulfan, de 240 mg/kg pour le /3-endosulfan et de 100
mg/kg pour le melange technique des isomeres. La DL.-o aigue par voie
dermique d’une suspension d’endosulfan technique dans 1 huile de coton est
de 681 mg/kg de poids vif chez le rat, de 147 mg/kg chez le lapin et de .
plus de 1000 mg/kg chez le cobaye. Dans une experience d’une duree de
deux ans, 1’adjonction de 30 ppm d’endosulfan a la nourriture na donne
lieu a aucun symptome microscopique ou macroscopique chez le rat. Ladjonction d’endosulfan a la nourriture du rat n’a entraine aucune augmentation
de la frequence des tumeurs. Des chiens ont tolere 30 ppm d’endosulfan dans
la nourriture durant deux ans sans manifester de reaction. Des interrogatoires
pratiques dans sept pays n’ont revele aucune indication de symptomes de
toxicite ou de reactions allergiques chez 1’homme attribuables a 1 usage de
Tendosulfan.
La toxicite des deux isomeres de Tendosulfan a Tegard des insectes est
approximativement la meme. Pour un certain nombre d arthropodes utiles,
comprenant Tabeille, Tendosulfan, tel qu’il est applique en pratique, est
inoffensif ou peu dangereux. Il en est de meme pour les animaux sauvages
a sang chaud. Au contraire, Tendosulfan est un poison pour le poisson.
Les residus d’endosulfan sont moins persistants sur la surface des plantes
que les residus da-DDfT, d’aldrine ou de toxaphene. L a-endosulfan disparait
plus rapic}^§^B£kM$^Ce
plantes que le /3-endosulfan. Des residus
de sulf^^9|gdo3gtfeg<^^yant 0,3 ppm, mais generalement inferieurs
I*)*
ERUEL-
I
I
I
■
I
37
a 0 1 ppm, ont ete trouves sur les feuilles et les fruits comme produits de
transformation de Tendosulfan. D’autres metabolites (diol et ether d endo
sulfan) pourraient etre deceles occasionnellement dans les plantes, mais non
dans les recoltes destinees a la consommation humaine.
Apres ingestion d’endosulfan par les animaux a sang chaud. une partie de
l’insecticide se retrouve inchangee dans les feces; les metabolitesJiydrosolubles (diol, a-hydroxy-ether et sulfate d’endosulfan) doivent etre recherches dans Turine. Lors des tests d’ingestion, on ne decele que des traces
d’endosulfan (0,02 a 0,2 ppm) dans le hit des moutons et des vaches.
Lorsque Tadministration du produit est interrompue, ces quantites decroissent
rapidement en dessous des limites de detection analytique. A Tinverse du
DDT ou de Taldrine, Tendosulfan n’est pas emmagasine dans la graisse ou les
lipides des organismes a sang chaud. Apres addition de 2 ppm cendosu an
ou de 7 ppm de DDT (tolerances des U.S.A.) au regime quotidien du pore
durant des periodes de 27, 54 et 81 jours, les tissus adipeux des ammamr
contenaient 8 a 10 ppm de DDT, jnais moins de 0,1 ppm d’endosuuan.
Le sulfate, Tether, Ta-hydroxyether et le lactone d endosulran one e-.e
retrouves comme metabolites de Tendosulfan dans lorgamsme^des insectes.
Deux a trois semaines apres Tapplication normale d enaosuiran a un gran
nombre de fruits, de legumes et de plantes fourrageres dans les champs, les
residus etaient inferieurs a 0,5 ppm (y compris le sulfate d’endosulran).
Avec des doses plus elevees, on a trouve dans certains cas des residus
atteignant 2 ppm et occasionnellement 3 ppm. Une teneur ce 3,8 ppm
d’endosulfan dans les feuilles de choux-fleurs s’accompaignait d’une teneur
inferieure a 0,05 ppm dans les teres, tandis cue dans les carottes, on relevait
respectivement 3 ppm dans les feuilles et 0,03 ppm dans les racines correspondantes.
Durant la preparation de Tensilage, les residus d’endosulfan presents sur
les plantes ne furent decomposes que dans une faible mesure; il en fur. e
meme lors du sechage de 1’herbe, du trefle et de la luzernc- pour la preparation
du foin.
.
.
Les tolerances etablies dans differents pays pour Tendosulran clans les
recoltes et les denrees alimentaires d’origine vegerale sont de 0,5, 1 et 2 ppm.
Les intervalles entre la derniere application du produit et la recolte, prescrits
ou recommandes, se tangent entre “pas de limitation’’ et 42 joins. Aux
U.S.A., la viande et le hit ne peuvent pas contenir d’endosulfan (tolerance
zero).
Le rapport presente en conclusion un examen de Tanalysc de 1 endosultan
qui traite des methodes d’identification et de dosage de l’insecticide dans
les formulations commerciales et les residus provenant de 1 application da
produit dans la protection des recoltes. En ce qui concerne Tanalyse des
residus, on discute en detail les precedes d’extraction, h purmcation, les
methodes phoromemques-ec par chromatographie_gazeuse.
Hans ia • er -Bode
58
*
Endosulfan
• Ubersent vom Autcr.
wasserlosliche Meu._jliten nachweisen (Endosulfandiol, Endosulfan-a-hydroxyather, Endosulfansulfat). In dcr Milch von Schafen und Kiihen wurden
bei Fiitterimgsversuchen mit Endosulfan nur geringe Mengen (0,02 bis 0,2
ppm) Endosulfansulfat gefunden. Sic sanken nach Absetzung der EndosulfanVerabreichung schnell unter die analytische Erfassungsgrenze. Im Gegensatz
zu DDT oder Dieldrin wird Endosulfan in Fett und Lipoiden des Wcrmbliiter-Organismus niche gespeichert. Nach Zusatz von 2 ppm Endosulfan
bzw. 7 ppm DDT (USA-Toleranzen) zum taglichen Putter von Schwcinen
wiihrend 27, 54 und 81 Tagen enthielt das Korperfett dcr Ticre 8-10 ppm
DDT. aber weniger als 0,1 ppm Endosulfan.
Als Umwandiungsprodukte von Endosulfan wurden im Organismus von
Insekten Endosulfansulfat, Endosulfanather, Endosulfan-u-hydroxyather und
Endosulfanlacton gefunden.
An einer grossen Zahl von Obst-, Gemusearten und Futterpflanzen
wurden zwei bis drei Wochen nach praxisublicher Endosulfan-Anwendung
weniger als 0,5 ppm Insektizidriickstand (einsschliesslich Endosulfansulfat)
gefunden, bei hoheren Dosierungen in manchen Fallen bis etwa 2, gelegentlich
auch bis 3 ppm. Bei einem Gehalt von Blumenkohlblattern an 3,8 ppm
Endosulfan enthielten die Blumen weniger als 0,05 ppm des Insektizids, bei
einem Gehalt von Mohrenlaub an 3 ppm Endosulfan waren in den
zugehorigen Mohrenwurzeln 0,03 ppm des Insektizids nachzuweisen.
Wahrend der Herstellung von Silagefutter werden auf dem Pflanzenmateriai
vorhandene Endosulfan-Riickstande nur in geringem Masse abgebaut ebenso
beim Trocknen von Gras, Klee und Luzerne zu Heu.
Die in verschiedcnen Liindern festgelegten Toleranzen fiir Endosulfan
auf pflanzlichen Ernteprodukten und Lebensmitteln pEanzlicher Herkunft
liegen bei 0,5, 1 und 2 ppm, die vorgeschriebenen oder empfohlenen
Wartezeiten von der letzten Endosulfan-Anwendung bis zur Ernte zwischen
"no time limitations” und 42 Tagen. Fleisch und Milch diirfen in den USA
kein Endosulfan enthalten (Zero-Toleranz).
* Der Bericht schliesst mit einem Ueberblick uber die Analytik des Endo
sulfan. Behandelt werden die Identifizierungs- und Bestimmungsmethoden
fiir das Insektizid in Handelsformulierungen und Riickstanden aus seiner
Anwrendung im Pdanzenschutz. Bei der Riickstandsanalyse werden die Verfahren der Extraktion, der Extrakt-Vorreinigung ("clean up”), die bekannt
gewordenen photometrischen und gaschromatographische. Analysenmethoden im einzelnen besprochen.
Zusammenfassiing*
Das Insektizid Endosulf.m entsteht bei der Einwirkung von Thionylchlorid
auf das Addukt aus I-Iexachlcrcyclopentadien und cis-Buten-2-diol-l,4 und
ist ein Gemisch zweier Isomerer, von denen das niedriger schmelzende als
a-Endosulfan, das hoh „r schmelzende als ^’-Endosulfan bezeichnet wird. In der
Pdanzenschutzmittel-Literarur wird Endosulfan gewohnlich unter ' Chlorierte
Kohlcnwasserstafle der Cyclodiengmppe” genannt. Als Schwefligsaureester
eines cyclischcn Diols unterscheidet es sich indessen von den Insektiziden
dieser Gruppe. z.B. Aldrin, Dieldrin, Endrin, in den chemischen Eigenschaften,
in den physiologischen Wirkungen und im Verhalten auf der Oberflache
lebender PEanzcn und im tierischen Organismus so wesentlich, dass es nicht
zu ihnen gcrechnet werden harm.
Von Nutzpfianzen. wird Endosuifan mit wenigen Ausnahmen, z.B. Gurken unter Gias bei starker Ueberdosierung, gut vertragen. Die akute orale
LDgo fur Ratten betragv bei a-Endosulfan 76, bei ^-Endosulfan 240 und beim
technischen Isomerengemisch etwa 100 mg/kg Korpergewicht. Die akute
dermale LD-n des in Baumwollsaatol aufgeschlammten technischen Endo
sulfan betragt fiir Ratten 681, fiir Kaninchen 147 und fiir Meerschweinchen
liber 1000 mg,, kg. Im 2Jahres-Fiitterungsversuch verursachren 30 ppm
Endosulfan in der Nahrung von Ratten weder makroskopisch noch mikroskopisch erkennbare Schaden. Die Tumorrate wurde dutch Endosulfan
im Rattenfutter nicht erhoht. Hunde vertrugen im Futter 30 ppm
Endosulfan im 2Jahres-Fiitterungsversuch reaktionslos. Pnindfragen in 7
Laadern ergaben in keinem Fall Hinweise auf Vergiftungssymptome oder
ailergische Reaktionen an Menschen im Zusammenhang mit EndosulfanAnwendung.
Gegenuber Insekten 1st die Toxizitat der beiden Endosulfan-Isomeren
etwa gleich. Fiir eine A.nzahi niitzlicher Arthropoden, auch die Honigbiene,
ist Endosulfan unter praktischen Anwendungsbedingungen ungefarlich
oder mindergefahrlich, desgleichen fiir warmbliitige Wildtiere. Dagegen ist
Endosulfan ein Fischgift.
Auf PEanzenoberflachc-n sind Riickstande von Endosulfan weniger
persistent als solche von DDT, Aldrin oder Toxaphen. a-Endosulfan verschwindet von den Pflanzenoberfachen schneller als ^-Endosulfan. Als
Umwandlungsprodukt des Endosulfan auf Blattern und Fruchten wurden
bis 0.3 ppm, meist unter 0,1 ppm, Endosulfansulfat gefunden. Dieses ist
toxikologisch wic technisches Endosulfan zu bewerten. Andere Metaboliten
(Endosulfandiol, Endosulfanather) konnten an Pfianzen zwar gelegentlich
nachgewiesen werden, nicht aber in Ernteprodukten, die fiir die menschliche
Ernahrung bestimmt sind.
Nach Verfiitterung von Endosulfan an Warmbliiter wird ein TeilzZ&r
Insektizids unveriindert in den Faeces wiedergefunden; im Urin liesse^g<my
4
39
i
5
!
i
I
I
I
References
..
SiJi1
'
-V’ V.
■sVP
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(1963)'
BUTLER, L. L, J. C. M5r
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'|U- ( .
i
I
(1965).
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Farbwerke Hoechst AG.. Pflanzenschutz-Forschung: Unpublished laboratory reports
■
I
j
/dV
^AHEY: Microdeterminatioi^Jc^ Thiodan >
..
41
’1
/
1
(1955-1967).
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42
Hans Maier-Bode
Endosulfan
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(Tbiodan) der
der Farb’^rkc^ 1'
j
43
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I
I
I
s
i
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I
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'I^'(
"
’
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V
^'1 /. /
1
f\s
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■. ,
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b
—+
44
Hans Maier-Bode
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n
u
• i
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J „
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,
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-------- Identification of organic chlorinated pesticides by plate chromatography. Proc.
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■•truELwL's,lno
| l
-A/
A° A
F/oun^>^,,
A,
mitteln in Obst, Gemuse und einigen Sonderkulturen
Von
H. Stobwasser*, B. Rademacher* und E. Lange*
Inhalt
■
I
I. Einleitung
II. Lagern und Tiefkuhlen
a) Obst........................................................................................
b) Gemuse
III. Reinigen, Waschen und Schalen
a) Obst
b) Gemuse
IV. Verarbeitung
a) Obst
b) Gemuse
c) Sonderkulturen
•
V. Ubersicht uber untersuchte Kulturen und Pflanzenscmtzm:::,ei
VI. Toleranzen der aufgefuhrten Pfianzenschutzmittel (U.S.A.,. Niederknde,
Deutschland) und deren chemische Bezeichnungcn
VII. Besprechung der Ergebnisse und Schlussbetrachrung
Zusammenfassung . .
Resume
Summary
Literatur
45
47
47
52
58
58
64
70
70
73
86
90
93
93
103
105
106
108
I. Einleitung
Die Anwendung chemischer Pfianzenschutzmittel- gegen Krankheiten
und Schadlinge der Kulturpflanzen und gegen Unkrnuter bin ter lass. Riickstande. Ihre Haltbarkeir auf und in den Pflanzen ist schr verschieden und
abhiingig von den chemischen und physikalischen Eigenschaften der
Wirkstoffe, ihrer Formulierung und Anwendungsform, von der Arc der
Pfianze und der Beschaffenheit ihrer Oberflache, von den physiologischen
Umwandlungen in den Pflanzen und von Umwelcseinflussen wie Ternperatur,
• Institutliir Pflanzenschutz der Universitiit (Landv.-inschaftlichen Hochschule),
Stuttgart-Hohenheim, Deutschland.
1 Chemische Bezeichnungen der P;.-stizide vergl. rabclie XKXIL
45
■
A WHITE PAPER
ON THE
REPORT ON THE VISIT OF THE EXPERT TEAM
CONSTITUTED BY THE
KERALA AGRICULTURE UNIVERSITY
FOR INVESTIGATING
THE ENVIRONMENTAL EFFECTS OF
AERIAL SPRAYED ENDOSULFAN ON
CASHEW PLANTATIONS IN PERLA AREA OF
KASARAGOD DISTRICT
September 2001
i
€
ENDOSULFAN SPRAY PROTEST ACTION COMMITTEE ( ESPAC)
Perla - Padre - 671552 Kasaragod , Kerala
0
acknowledgement
ESPAC acknowledges participation of our villages and the people,
members of the steering committee and public-interest scientists,
who provided information which was useful in preparing this white
paper. We also acknowledge the technical assistance from Thanal
Conservation Action and Information Network in preparing this
document.
For any further information^ please do contact
Endosulfan Spray Protest Action Committee (ESPAC)
c/o Kajampady Nursing Home,
P.O Perla, Kasaragod - 671 552
Phone : 895OSS
contents
background.
3
the critique.
5
attachment— 1 (letter from ESPAC to the Vice-Chancellor, KAU).
19
attachment-2 (endosulfan - regulations and violations).
21
attachment — 3 (world wide regulatory status of endosulfan).
23
attachment — 4 (endosulfan - a short summary ).
24
references
30
2
f)
A WHITE PAPER
ON THE
KAU REPORT ON THE VISIT OF THE EXPERT TEAM CONSTITUTED FOR
INVESTIGATING THE ENVIRONMENTAL EFFECTS OF AERIAL SPRAYED
ENDOSULFAN ON CASHEW PLANTATIONS IN PERLA AREA OF KASARAGOD
DISTRICT
Background
The people of Kasaragod, mostly from Cheemeni, Periya-Pullur, Rajapuram,
Panathadi, Muliyar, Perla have been complaining against aerial spraying of
endosulfan by the PCK in their cashew plantations for the last 20 years. Reports
have come in the media right from 1979 pointing out the hazards of the use of
pesticides and aerial spraying of the same. None of the concerned authorities
nor the scientists have ever thought it necessary to look into the environmental
and health problems. Court cases against the spraying have been filed from
Periya-Pullur from 1998 onwards and the PCK only responded by wTiting to the
companies producing and supplying endosulfan to give them information which
will help in continuing its use.
From December 2000, the media had played an important role in highlighting
this issue and more importantly in waking up the authorities who were feigning
a slumber. For the first time, the hue and cry was loud enough for authorities
and the scientists to hear. Now they say that the media, the voluntary
organisations and environmentalists are sensationalizing the issue. Who is
responsible for this? Now they are saying that this sensationalizing will affect
cashew export prospects. Who is responsible for this ? Children with
congenital anomalies, skin diseases, cerebral palsy, hydrocephalus were forced
to parade before the media, not because they wanted to sensationalize this
issue. They did it to make these authorities and scientists open their eyes and
ears.
In January 2001, the Centre for Science and Environment collected 25 samples
of blood, fat, milk, vegetables, cashew, leaves, soil, water etc from Enmakaje
village. There were prominent scientists who guided this study. Prof. M K
Prasad and Dr. Raghunandhan guided the sample collection and Dr. Padma
Vankar of IIT, Kanpur did the analysis at the State of art lab at CSE. All
samples had very high levels of endosulfan. This was the first evidence that
endosulfan was in the environment and human beings. The persistence of
endosulfan ( half-life of 2-7 days in plants and upto 800 days in soil) was a
known fact and we realised that our exposure to endosulfan was not just at the
time of spray but through out the year as well. We also knew very well from
literature that endosulfan could harm in many possible ways - reproductive
system, endocrine system, central nervous system, skin, kidneys and liver
disorders and cancer to name a few.
On January 16th, ESPAC sent a letter to the then Vice-Chancellor of KAU asking
for clarification on a reported recommendation that they had given on
endosulfan use and requesting the VC to withdraw the certification issued, if
any. There was no reply to this letter. Later we understood that an expert team
of agriculture scientists was set up to study the issue and on the 19-h of
February they visited the area to do a preliminary investigation into the
problems due to aerial spraying of endosulfan. These scientists, many of whom
already knew the problem and had taken a position that endosulfan was a safe
and harmless chemical, came, visited some houses in our area, collected
3
samples and left. Inspite of the fact that they were 20 years late, we welcomed
them in hope that they would see the intensity of the impact and report to the
University and other authorities. Events that followed proved that they had not
come here with a clean heart and an open mind. The result was a series of
happenings which have turned out to be humiliating to the Kerala Agricultural
University, other fellow scientists and the State.
The results of the CSE analysis was released on February 21st and was
nationally covered by all the media. This must have innerved the KAU. On 28th
of February, the deadline set by the University for submitting the report, this
expert committee of the Kerala Agriculture University released a letter through
the official email of the College of Agriculture, Padanakkad- kaupad@vsnl.com
saving that the CSE study was exaggerated and sensational. The team member
who authored the letter requested that maximum publicity be given to this
opinion. Even the methodology of the CSE study was questioned in the email
letter. But the expert team did the most untimely and silly thing. They
challenged the CSE results on frivolous grounds and that too even before their
own analysis was done. Expectedly enough, on April 10th a member of the
expert team called up ESPAC and said that none of the samples that they had
collected had endosulfan contamination and some samples had only traces
which were very much below the tolerable levels. These results were also
released “unofficially* from the official email of the College of Agriculture,
Padanakkad.
While the CSE had followed very meticulous, transparent and scientific
procedures for the sample collection - taking the utmost care to collect in
sampling bottles, packing in ice boxes and sealed containers - the KAU team
came with empty hands, collected the samples and took them back in polythene
covers. Later, we understood that the expert committee had submitted a report
to the Vice-Chancellor of KAU and had also distributed a Thought paper among
the scientists in the KAU. While we were not given these reports, the PCK
General Manager and the Managing Director were quoting these results and the
report in the media. We then got a copy of this report unofficially and found that
the report was baseless, unscientific and an insult to the already beleaguered
people of Kasaragod. We discussed this report with prominent scientists, media
persons and leaders of the community and we are sorry to state that this report
demonstrates the pathetic state of affairs of research and knowledge levels of
this team of scientists of the Kerala Agriculture University. These scientists
have all proven to harbor a clear bias and we are forced to realize the vested
interest that led the scientists to submit such a poor report.
Hence, ESPAC has decided to produce a white paper of the report with the
good intention and moral responsibility to point out before the Vicechancellor of the KAU and others of concern in the State what actually
happened during the expert teams fact-finding visit. We are doing this
because we know that neither the Kerala Agriculture University nor the
esteemed scientists in the University who have been contributing their
best to science and society would approve of such wrong and mean ways of
some of their fellow scientists. We also hope that this white paper on the
report will start a serious introspection among the Agriculture Scientists
about their state of research, understanding of issues and credibility.
Note to the Critique : The Original Report of the KAU is fully
reproduced below in small italics and it is interspersed at relevant
! points with our critical comments in boxes.
4
o
REPORT ON THE VISIT OF THE EXPERT TEAM CONSTITUTED FOR INVESTIGATING THE
ENVIRONMENTAL EFFECTS OF AERIAL SPRAYED ENDOSULFAN IN PERLA AREA OF
KASARAGOD DISTRICT
Kerala Agricultural University
Cashew Research Station Madakkathara 680651
As per order DO. No. DR. 70/2001 dt 13.22001 of the Director ofResearch Kerala Agricultural
University, an expert committee was constituted with the following members to study the environmental
effects ofaerial sprayed endosulfan spray on cashew plantations ofKasaragod district
1.
2.
3.
4.
5.
Dr. M. Abdul Salam
Associate Professor and Head, CRS Madakkathara, Thrissur
Convenor
Dr. 8 Nazeema Beevi
Associate Professor and Head,
A.I.C.R.P. on pesticide residues. College ofAgriculture Vellayani, Trivandrum
Member
Dr. A.M. Ranjith
Associate Professor, Dept ofEntomology,
College ofHorticulture, Vellanikkara, Thrissur
Member
Dr. Samuel Mathew
Associate Professor (Ag. Chem), AMPRS, Odakkali
Member
Dr. KM. Sreekumar
Assistant Professor (Entomology), College ofAgriculture, Padannakkad
Member
The study was ordered at the instance ofa complaintfiled by Mr. Aravinda, Chairman, Endosulfan
Spray Protest Action Committee, Padre to theVice-Chancellor, Kerala Agriculture University. It was
directed by the University to submit a preliminary report before 28th Feb. 2001. Accordingly, the members
ofthe above committee (excepting Dr. Nazeema Beevi) visited the problem area on 19th Feb 2001. The
following members were also present
1. Dr. B. Jayaprakash Naik, Associate Professor RARS, Pilicode.
2. Sri. M. Bhaskaran, Dy. Director, Dept, ofAgriculture, Kasaragod
1.
2.
3.
4.
5.
6.
The following
activists also accompanied us.
... environmental
?
Dr. Sripadi Kajampadi
Sri Ganapathi Bhatt, Pattadka House (P.O) Vani Nagar
Narayana Sasthri, Kollengala
Rajagopal Sharma
Venkita Ramana Bhatt, Edamala
K. Srinivasa Naik, Ward Member
The study was not ordered at the instance of a complaint filed by Mr. Aravinda
of ESPAC. The PCK had reportedly released a press statement saying that "In
Kasaragod since 1976 , endosulfan is being aerially sprayed and that Agri
University has certified that there is no much harm by this sort of spray (as
reported in Janavahini t A Kannada daily , dtd .January 9.2001). ESPAC had sent
a letter to the VC of KAU seeking clarification in the light of the above
statement. This clarification has not been answered till date. Copy of this letter
is in attachement-L
About 25 people accompanied the team of experts and none of them are
"environmental activists*. The six names listed above are members of ESPAC. Dr
Sripathy Kqjampady is a Local Medical Practitioner at Perla and ICSrinivasa Naik
is the Panchayath Member of Ward 6Z which the team has visited. The others
are farmers and affected people. KAU expert team has unnecessarily alleged
that they are *environmental activists' to create a ground for further argument
that the issue is sensationalised by environmental organisations.
5
Recently, a large number ofreports have appeared in the mass metho, both print and electronic,
on the alleged effects ofendosulfan on the environmentfollowing aerial applications ofthis insecticide on
cashew plantations in Kasaragod district.
About Endosulfan
The committee has made an attempt to gather sufficient information from various sources to make
an assessment ofthe toxicological and environmental aspects ofendosulfan. The toxicological data are
presented in Annexure 1. Critical information on the subject is abstracted below.
1.
Endosulfan is a neuro toxic insecticide belonging to the group ofcyclodienes. Some ofthe related
insecticides ofthe same groups viz., Chlordane, Heptachlor, Aldrin, endrin and Dieldrin were
bannedfor use in agriculture because oflong persistence oftheir toxic residues in the
environment.
Endosulfan is a neurotoxic insecticide belonging to the group orgonochlorine and
the sub-group cyclodienes. All the related insecticides in this sub-group viz
Chlordane, Heptachlor, Aldrin, Endrin, Dieldrin and Mirex has been banned in
India and is slated for a global phase out by the Stockholm Convention.
Endosulfan is chemically very close to Dieldrin, substituting a heterocyclic sulfur
in place of the saturated bicyclic ring system.
2.
It is reported that Endosulfan is not likely to cause reproductive effects in humans at expected
exposure levels.
It is impossible to conclude that Endosulfan is not likely to cause harm to
reproductive system in human beings, because no experiments have ever been
conducted on the reproductive system effects on human beings and it is also
impossible, dangerous and unethical to do so. The only experiments we know about
the reproductive system effects are studies on aquatic organisms and mammals
(rats, rabbits etc). A large number of studies done on fish, rats, mice and
rabbits prove that endosulfan is an insecticide which can affect the reproductive
system. (Barry et al., 1995: Barry, 1996; Chakravorty et al., 1992; Kulshrestha &
Arora, 1984; Pandy, 1988; Wilson & LeBlac, 1998; Sinha et al., 1997; Singh &
Pandey, 1989; 1990; Gupta & Chandra, 1977; Gupta et al., 1978). The National
Institute for Occupational Safety & Health (NIOSH) states that the
Reproductive System is a target organ of endosulfan poisoning.
3.
It is also reported that endosulfan does not appear to be carcinogenic.
It is dangerous, especially by agricultural scientists, to make statements like
"does not appear to be carcinogenic* about a chemical which many studies have
proven to display carcinogenic properties. Most of the studies reviewed by the
WHO, were studies done by scientists affiliated to Hoechst, the patent holder
of endosulfan, and no wonder they did not prove conclusively that endosulfan is
carcinogenic, mainly due to high mortality of the experimental animals.
Furthermore, there are other studies which show that endosulfan can cause
cancer (Reuber, 1981; Fransson-Steen, 1992 ). The second study also showed
that endosulfan is a potential liver tumour promoter.
6
u
Moreover, Endosulfan has been proven to be Mutagenic, Clastogenic and
Genotoxic in many in vitro and in vivo assay studies (Syliangco, 1978; Adams,
1978; Naqvi 4 Vaishnavi, 1993; Yadav et al., 1982; Me Gregor et al., 1988;Dubois
et al., 1996; bzwonkowska 4 Hubner, 1986; Dhouib et al, 1995; Velazquez et al.,
1984; Pandey et al., 1990a ). Studies done on human cells both in vitro and in vivo
also showed that endosulfan is mutagenic and genotoxic (Sobti et al., 1983;
Dulout et al., 1985; Yuquan et al., 2000)
Cytotoxic effects of endosulfan and cell structure damage was shown in many
studies (Bain 4 LeBlanc, 1996; Huang 4 Casida, 1996; Rosa et al., 1996; Dubey et
al., 1984; Yamano 4 Morita, 1995). Daniel et al (1986) showed that even at a
concentration of 0.001 microgram/ml (1 ppb) endosulfan was found to damage
human red blood cell membranes.
4.
Endosulfan rapidly degraded mainly into water-soluble compounds and eliminated in mammals
with very little absorption from the gastro-intestinal tract.
This is an unscientific, vague and too simplified a statement. The fate and
degradation of endosulfan is dependent on the fate and degradation of each of
its isomers and also its metabolites. This is different in different medium.
It is known that endosulfan ( both alpha and beta isomers ) are metabolized in
the mammalian system, but it is not known how much of it is absorbed and how
much is eliminated and over what time. We now know that it induces toxic effects
in kidneys, liver, the CNS and Reproductive systems (NIOSH, 1997). Studies
also show that the alpha-isomer is known to persist longer than the beta-isomer,
particularly in brain tissue and plasma (Gupta, 1978). Ceron et al (1995) detected
alpha-endosulfan in liver and brain tissues in rabbits exposed to endosulfan.
5.
It is moderately persistent in the soil environment with reported a^-erage half-life of50 davs. It
has a moderate capacity to adhere to soils. Owing to low water solubility and immobility in soils,
it is not likely to cause threat to ground water.
This statement is summarily wrong, because it is not possible to be so accurate
and single-numbered in talking about its fate and degradation in soil. Endosulfan
isomers show different rates of dissipation from soil (Stewart and Cairns, 1974).
The study found that half-life of alpha-endosulfan is 60 days and beta
endosulfan is 800 days. In another report, the half-lives were estimated as 35
and 150 days respectively (EXTOXNET, 1996). The major products of
degradation of endosulfan in soil are endosulfan diol and endosulfan sulfate
(^art^nsf 1976; El Beit et al., 1981). The metabolite endosulfan sulfate is more
persistent than the parent compound. (Stewart and Cairns, 1974). So even if
endosulfan disappears from soil, its metabolites which are much more stable and
toxic compounds could be there for years.
Even if endosulfan is immobile in soil, the top soil (upto 15 cm) where 90% of
endosulfan residue may be found (Stewart and Cairns, 1974) may itself be mobile
and can contaminate water sources like streams and ponds.
7
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6.
It is relatively toxic to fish, hut comparatively safe to honey bees
The Annexure I in this KAU report itself soys that endosulfan is extremely toxic
to fish, but in this abstract it has become "relatively toxic*. This is the best
example of a casual approach or intentional misleading. Every document and
research all over the world says that endosulfan is extremely toxic to aquatic
organisms. Even very low concentrations of endosulfan use has resulted in fish
kills. For example, in June 1969 itself, a massive fish kill in the Rhine River was
associated with a maximum endosulfan concentration of 0.7 micro-gram/L (Greve
4 Wit, 1971) Many countries all over the world has banned or severely restricted
endosulfan mostly for its aquatic toxicity. This was recognized in 1991 itself by
the Dr. Banerjee Committee appointed by the Central Insecticides Bureau and
later by the Dr. R B Singh Committee in 1999. They had recommended that
endosulfan should not be used near waterbodies. The Agriculture University and
the Department has been recommending endosulfan in Kerala, ignorant of this.
Media has already raised doubts as to whether this has been intentional (to
promote the industry ?)
Endosulfan is acutely toxic to honeybees. In our area, one of the most significant
environmental impact was the total death of bees. Farmers who had more than
40 nests of bees have totally lost all their bees, over the years. The US National
Wildlife Federation says that endosulfan is extremely toxic to wildlife and
acutely toxic to bees. (NWF, 1987). The HIL (Hindustan Insecticides Limited )
has themselves in their document on endosulfan said that "Endosulfan is toxic to
honey bees in the laboratory*. But they also add that it "appears* to be "without
significant impact" in the field. While this is a highly ambiguous statement, the
KAU has gone one step ahead and stated that endosulfan is comparatively safe to
honeybees.
7.
It is permitted to be used as sprayfrom helicopter (aerial spray) at 2 to 3 meters heightfrom crop
canopy.
This permission is as old as 1983, when endosulfan along with other banned
chemicals like BHC, Toxaphene was also allowed for aerial spray. The Central
Insecticides Bureau has not been giving permission for aerial spray since 1993.
From the expert committee report it is shocking to note that even the
Agriculture University is ignorant of these facts. The Hindustan Insecticides
Limited, the company from which PCK buys endosulfan (Hildan) itself says as
precautions that "Do not apply under meteorological conditions or from spraying
equipment which could be executed to cause spray to drift into wetlands and
waterbodies*. They had also warned that contamination is possible through
"Drift, Volatilization and Particle Transport*.
The KAU experts should also have enquired why and how aerial spraying was
done from 1976 onwards, but the concentration and method of spray was only
standardized in 1997 ( by NRCC).
8
Details ofSpot Inspection
The team visited the Perla. Swagha, Penaladka, Kollengal, Galigopura, areas of Kasaragod Taluk
and interviewed a random sample of 10 families ofthe area. . Iccording to Mr. . [ravinda there are 156
cases ofCentral Nervous System (CNS) and related disorders in Padre Tillage as detailed below.
Cancer (living)
:
3
Cancer (Dead)
•
:
46
Mental retardation
23
Psychic cases
43
Epilepsy
:
23
Porn handicapped
:
9
Suicides
:
9
The team did not do any random sampling as they have stated. They only went to
those houses we took them to.
During the investigation, we come across three groups ofpeople with following views.
m
J group ofpeople strongly arguing that the CNS related abnormalities are due to aerial spray of
endosulfan. These persons stay in the adjoining areas ofplantation within 3 to 4 kilometers with .
some sharing boundaries with PCK. These people also reported that the minimum precautions
prescribedfor aerial spraying were seldom obser\'ed. The details offive families inspected are
given below.
There was no such group and all these people mentioned below are staying within
SCO metres from the plantation and some on the border. Why has the University
team hidden the details they have collected ? Why are they trying to down play
the toxicity and health hazards of endosulfan ? The actual health problem seen in
each of these houses is described in the boxes here.
1.
Korangpappa Rai, Padre, Enmakaje Panchayath (House wife sufferingfrom
Neurological complaints and bedridden for last 2 years.)
Kcragappa Rai, 73 years old - was almost bed ridden for the last two years for
backache and numbness.
Lekshmi, wife - was suffering from Parkinson's Disease for the last two years (
neurological disease ) and died after the team visited.
Ramanna Rai, second son, married for the last 18 years and issueless. Indravathi,
his wife is anaemic and weak.
Kamala, daughter, born handicapped. She suffered from a disease whose
symptoms were like jaundice. She died of liver cancer at the age of 25.
Leela, second daughter had multiple abortions and issueless for long time. Now
has a son who suffers from asthma.
Yamuna, third daughter suffering from some neuro-muscular complaint- swelling
joints and pain undiagnosed. She also has a girl with chronic ailment.
The KAU team had seen the suranga outlet and the small pond covered with a
fertiliser bag supplied by the PCK. They saw the family using this suranga water
and Dr Abdul Salam even observed that endosulfan could be smelt even after two
months of spraying.
This house is almost on the border of the plantation and Koragappa said that
endosulfan drizzles down on them during the helicopter spray. Their 10 month
old cow has stunted growth. Koragappa complains that such cows do not milk in
time and even if it does ( usually as late as 3-4 years ) gives only very little milk.
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2.
Govt. H.S.S. Padre, P.O. Vaninagar, Enmakaje Panchayath- Explained by C.
Narayanan, Assistant Headmaster (9 mentally andphysically retarded students out of 153
in the lower primary section)
1.
Udayakumar
14 Years
2.
Rohini
10 Years
3.
Mahesh Babu
14 Years
4.
Jayakumari
12 Years
5.
Nalini
12 Years
The Govt. Higher Secondary School has a total strength of 622 students. Of
this there are 153 students in the lower primary section. Mr. C Narayanan is an
Asst. Teacher, and not the Asst. Headmaster.
Nine children in the LP section is mentally and physically retarded and 21 others
are of low/very low IQ. The list of these 30 students in the LP section with
scholastic backwardness has been submitted to the Block Resource Centre,
Badhiadukka and to all the enquiry committees. The list does not have Nalini.
There is one girl Nalini in the school who is neither mentally nor physically
retarded, but she is suffering from skin disease. A number of such children are
suffering from various other ailments like asthma, fits and epilepsy, handicap,
frequent ear oozing and problems with eye sight.
The School Resource Group Meeting of 3rd January 2000 had noted that *40
children coming from the west side (back side) of the school are found to have
mental and physical weakness. Most of them are frequently ill. Their learning
capabilities are very low. What may be the reason ?* This observation was made
even before the local doctors identified endosulfan to be cause for the many
ailments in Padre. The PCK plantations are at the west side of the school. Many
children coming to school during the spraying season have headache, vomiting,
stomach ache, itching and are rushed to the hospital or doctors.
3.
Sheena Shetty, 59 years, Periyaladkam (Daughter 23 Years old married and healthy,
Elder son 21 Years is mentally retarded and the younger son 16years is also with low IQ)
Sheena Shetty , 59 years, NayarBalike ( not Periyalaa'ukam)
Wife : Mukthaka Shetty, 52 years whose blood showed 196.47 ppm of total
endosulfan in CSE test. Lakshmi, their eldest daughter, born normal, became
epileptic at the age of 15, died after falling and injuring her head at the age of
22,10 years ago. Saraswathi, their second daughter, born normal, aged 25 now is
married. Kittanna, 21 years was born cerebral palsy ( and not just mentally
retarded as reported by KAU scientists). He needs help for everything. CSE
tests showed 109.5 ppm of endosulfan in his blood. Shreedhara, 17 years is
mentally retarded ( not just low-IQ) and studies in the 6th standard. Their house
is on the banks of the Kodenkeri stream and very near the plantation borders.
This case was widely reported in the media. Were the KAU scientists that hard
hearted to even misreport these cases in the most casual way or was it
intentional?
Mukthaka regularly goes to collect cashew and firewood from the plantation.
Their cow which was carrying was grazing in the plantation at the time of spray
in December 2000. They let her as usual for grazing, as PCK had not informed
about the spray. The cow returned bleeding and vomiting and had a fatal
haemorrhage and died in 8 days.
10
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4.
Sai Pangalu Kukkunadi Narayana Bhatt, Kollegal P.O. Padre
5ai Pangalu Kukkanadi Narayana Bhatt, age 47
His father, Vishnu Bhatt died of abdominal cancer 6 years ago
His mother also died of cancer soon after.
His sister Girija, age 35 suffers from epilepsy for the last 17 years and is now
very weak
His nephew (one sisters son) , Vishnu Bhatt (age 22) was born mentally retarded
and suffers from fits ( congenital)
Another nephew(another sisters son ) Vishnu Kulkarni ( 18 years) suffers from
the same problem. He also has gynaecomastia (breast enlargement). His blood
showed 108.9 ppm of endosulfan in the CSE analysis. Both the boys are mentally
challenged and are living with Narayana Bhatt as both his sisters have left them
in his custody and live elsewhere.
This house is on the border of the plantation. The team visited the house but
has not reported any of these problems. Why ?
This case also shows a social problem. What is going to happen to all these
children once their guardians are not any more able to look after them.
5.
Sri Hari Sajjangade Bhatt, Periyaladkam (House wife is a lucoderma and asthma patient.
However disease symptoms developed only 2 years back, otherfamily members are not
affected.)
There is a mistake here. Even though Srihari Sajjangade Bhatt accompanied the
team,.his family was neither visited nor information collected.
From what is little described this case looks like that of Kollengana Narayana
Shasthri, 56 years. He has a chronic back problem and recently developed
diabetes. His wife Prabha N Sasthri is a leucoderma and asthma patient, age 47.
She developed asthma and leucoderma some time in 1986 only after coming to
Padre to stay after her marriage. She is mildly diabetic and has been recently
diagnosed for endometriosis. Her blood showed 114.13 ppm of endosulfan in the
CSE tests.
His brother - Kripanithi, age 43 developed skin disease 20 years ago. He spent
nearly Rs. 50,000 on various treatment and over the last one and half year is
controlled. His son also has skin disease. All of them live in the same house.
This house is also very near the plantation and the Kodenkeri stream.
Their cow died due to liver problem after delivery. A buffalo also had liver
problems but could be treated.
Although persons with CAS related disorders were present in these families, no evidence was
available to confirm the involvement ofendosulfan.
What is the kind of evidence that will confirm the involvement of endosulfan ?
The team confirms that they found CNS related disorders, do they recognise
that CNS related diseases can be caused by endosulfan ? What kind of evidence
did the team look for in a fact-finding visit which just lasted some hours ? Did
the KAU experts expect that the ordinary, uneducated, affected people should
also give them evidences to prove that the CNS and other diseases are due to
endosulfan ?
11
u
a.
A group offollowing persons living in the adjoining area ofthe plantation who believed that they
were not affected by the aerial spraying.
The KAU report says that this “group* is living adjoining the plantation. But they
say the first group earlier listed lived within 3-4 km. This is done with a clear
malintention. All these people are living very near the plantation, some adjoining
and the experts are manipulating and misleading with words.
I.
Baire, farm labourer, Periyaladkam. (11 memberfamily all are healthy)
Baire, is around age 60.
One of his daughters is of age 25, is retarded in growth and looks the size of
about 15 years.
His grandson in another daughter, Ravi, is physically and mentally retarded.
The expert team had visited Baire's house, but only casual enquiries were made
with him.
2.
Janaki 50 years (house wife) Periyaladkam, Son Janardhana, 18 years (both did not
complain about any health problem)
This case is true, though no house visit was made and is a casual finding on the
way. We do not know if there are any health problems in the family.
3.
Rama Bhatt, 35 years, Periyaladkam (hisfather 60 years de\'eloped paralysis 8 months
back, his paternal uncle 62 years was bom handicapped). No CNS relateddisorders
were reported in theirfamilies.
There is a serious mistake in this case. There is no such person as Rama Bhatt
who suites this description.
Did the team make a mistake or did they actually cook up a name. We wonder
because while they have taken care not to mention the many cases in the family
of the earlier samples, the expert team seems to purposefully mention about a
parental uncle who was born handicapped to show that the many cases of
congenital handicaps found in Padre need not be because of endosulfan.
We are also not claiming that. All we are saying is that there are a lot of health
problems and endosulfan is the primary possible agent that can cause this. There
are no other agents in the area that can cause it and so endosulfan is suspected.
The scientists on the other hand want to prove that there is some other agent
and endosulfan is not the agent causing these diseases. This is a very narrow
minded and unscientific approach.
In this case the person they have mentioned here does not exist at all.
12
in.
A group ofpersons who are employees ofPCK and staying inside the aerial sprayed plantations
who argued that aerial spraying did not cause any adverse effect on their health as highlighted
recently in the media.
It is quite true that the PCK employees have been "arguing* that aerial spraying
did not cause any adverse effects. The workers usually handspray or use rocker
sprayers, without any safety measures and clothing. They spray endosulfan,
carbaryl, quinalphos etc and compared to ground spraying, aerial spraying is safer
for the employees health. They would only be as affected as the rest of the
people in the locality. But, this argument has been twisted by the scientists to
show that the aerial spraying has not caused any adverse effects.
Moreover, it cannot be expected from workers working under a repressive
management as the PCK to come out and talk about their problems. Did the team
ask them about the safety measures provided to them during spraying ? Did the
team ask them how many times in the last 26 years they have been medically
checked up for their blood levels for acetyl cholinesterase ? Did the team find
out the concentrations at which endosulfan was used in Kasaragod ? These are
the crucial matters and nothing of this is mentioned in the report.
1.
Mr. Manapattali (52 years, field supervisor, PCK Estate, Vani nagar)
Mr. Mana Pattali is a chronic alcoholic and was under intoxication when talking to
the scientists. His wife has psychiatric problems and was recently admitted for
treatment. All his children are underweight and anaemic.
2.
Mr. Moitheen kutty, 47 years, PCK estate, Padre.
The workers of the plantation are not just victims of the chemical but their own
silence as well. Mr. Moideenkutty asks "My father also died of cancer, do you
mean to say that it is due to endosulfan ?"
The workers of the plantation are our own people and we are concerned about
their health and welfare. We understand that they are not in a position to come
out and talk about this issue and their health problems. The workers are not
even able to complain to anybody that they are not being given the mandatory
safety equipments for spraying.
Here also no CNS related disorders was reportedfrom their families.
The unfortunate workers of the plantation have not even been paid their salaries
regularly, and have been subject to the worst human rights violation and their
voices are gagged by the authorities, threatening disciplinary action, which
underpaid people like this cannot afford to face.
How many worker's families did the team visit ? In Perla Division alone there are
56 workers and families in PCK ? We know that many families of workers in this
division alone have CNS and other diseases.
13
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Samples collectedfor Residue Analysis
For undertaking ofa preliminary study on endosulfan residues ue have collected thefollowing
samplesfrom the sprayed plantations as well as from the adjoining environment.
1.
Soil samples
.2.
Plant samples
3.
Well water samples
4.
Rivulet water samples
5.
Black pepper samples
6.
Betel leafsamples
7.
Butter samples
The residue analysis is proposed to be conducted simultaneously at two ofour laboratories, viz.
AMPRS, Odakkali, andMCRPon Pesticide Residues Laboratory, College ofAgriculture Vellayani for
confirmation ofresults.
Scientists and other employees working in the above mentioned labs have
confirmed in private conversations that the labs cannot do proper testing,
because they do not have the necessary standards to do the testing. The
standards with which they have tested are nearly 2-3 years old and since it is
costly to buy new standards for endosulfan and metabolites, they had to do it
with the outdated standards. This speaks very badly of the University, which we
think should have been equipped.
Moreover, ore the scientists going to prove that endosulfan is not the cause of
the health problems, simply by doing a residue analysis ? Even a layman knows
that a residue analysis only shows how much of endosulfan remains in these
samples after a period of time. It cannot be used to prove that sprayed
endosulfan is "safe* and "harmless* as the scientists have been claiming.
Moreover, the samples were collected nearly two months after the last spray.
An Important Observation
The PCK plantations of the area are randomly distributed in hilltops with deep valleys and a
number of water bodies in between. The cashew tree population ofthis plantation is sparse. There exist a
large number ofother trees also in-between. The topographical lie ofthe land and a high degree of
inhabitation make it very difficult to satisfy the following precautionary measures that are essentialfor
undertaking aerial spraying.
Regulating the height ofthe helicopter at a specified level (2 to 3 meters) from the crop
1.
canopy to avoid drift.
2.
Minimizing drift to the inhabited area by stopping spraying 10 meter ahead ofthe
borders.
Effective covering ofthe water bodies existing in large numbers.
3.
As such there is a necessity to prevent PCKfrom aerial spraying in this area, to avoid
contamination ofthe inhabited environment.
The National Research Centre for Cashew (NRCC) is located at Puttur, which is
near the PCK plantation borders ( about 20-30 km by road). The College of
Agriculture at Padanakkad is also very near the PCK plantations. The Directorate
of Agriculture has a Regional office at Kasaragod. The people have been
complaining for the last 20 years. What were these agencies doing for the last
20 years ? Now, the scientists are saying the topography is not suitable for
aerial spraying ? They have “discovered* that it is difficult to satisfy the
precautionary measures for aerial spraying. But many scientific studies have
been done at the Cashew Research Station of KAU and why did they not discover
these earlier itself, even when people complained ?
14
He were facing the following difficulties during the course of the investigation.
J.
To deal with a pcnic stricken and emotional group ofvillagers who were agitated due to the
alleged involvement ofaerial sprayed endosulfan in creating various health hazards among the
local people.
The people are panic-strikeri and emotional because families have been living with
abnormally born children and more and more children are being born with
congenital anomalies. Our own assessment of Cancer related deaths show a near
doubling of number of deaths in the last decade. On one hand scientists were
saying that endosulfan is a "harmless" pesticide. On the other hand all the
documents we had referred to say that endosulfan is an extremely hazardous
neurotoxicant with carcinogenic, genotoxic, mutagenic and endocrine disruption
properties. Endosulfan can affect reproductive systems. There are so many
people with infertility problems, miscarriages, still-births. Would the team
members which came to study not panic or be emotional if their own children and
families were being affected like this ?
The people were also finding it difficult to convey this message to the
emotionless scientists, who showed a lot of sympathy. This report proves that all
the sympathy they showed was only to extract from us the needed information
about our problems and write a report like this quite contrary to the reality biased, narrow and insulting.
Non-availability ofthe quick and reliable method to assess the level ofendosulfan contamination
in the environmental samples such as soil, plant tissues, drinking water, animal samples and
human samples.
If the expert team did not have a quick and reliable method, why did they collect
samples ? How will they do analysis ?
It is understood that there are very reliable methods of residue and
contamination analysis like in the study done by Centre for Science and
Environment, NewDelhi.
The expert team scientists have claimed that they will do analysis in two of their
labs and at the same time they also say that "quick and reliable" methods are not
available. With neither expertise nor infrastructure they also keep repeating
that endosulfan will not cause health problems.
3.
Continuous sensationalisation ofthis issue both in the print and electronic media even at national
level.
No village would like to be in the glare of the media and be sensationalized for
the most devastat:rg of things like this. If anybody has to be responsible for
this, it is the PCK, the KAU, the NRCC, the CPCRI, the Agriculture Department
and the Central Insecticides Bureau for playing their own parts in failing to
protect the people’s health and future and conniving with the industry and
Pesticide Manufacturers (and PMFAI).
Involvement of * arious environmental and voluntary organisations to sensitionaUse the issue in a
big way.
15
0
When affected villagers come out to voice about a human right violation that
they have been subjected to, it is natural that the scientists, who have silently
watched this go on and sometimes even been party to this, blame voluntary and
environmental organisations for this. In this case, the affected villagers, the
doctors, panchayath representatives have also been branded as environmentalists
in the report. This issue has been aired since 1980 mostly by elected
representatives of the people. Enmakaje and Kumbadaje panchayath has been
passing resolutions since mid-80’s asking stopping of aerial spraying.
5.
The incidence of a number ofhealth hazards in the area (most ofthem CNS related disorders)
whose causes cannot be clearly traced in a short time.
Even though the expert team found it difficult to “clearly trace* the causes in a
short time, they could trace that endosulfan is not a cause. Nowhere in this
report have they raised the doubt that endosulfan could also be a suspect, when .
people were blaming endosulfan and available literature was also pointing to
endosulfan being a possible agent.
Spraying of endosulfan has been going on in atleast 9 panchayaths in Kasaragod,
where the people have been directly exposed to the pesticide. All these
panchayaths have reported similar health problems. All the health problems in
this area have occurred only after spraying was started in the plantation. Any
body with a scientific approach and simple logic can easily find that there is
endosulfan as the only common link. So it is not the lack of "time* which is the
difficulty but the lack of an open and unbiased mind.
6.
The probable damage on the export prospects ofcashew would be unpredictable ifthe issue is
aired in a big way in the international media.
Many of the villagers affected are also cashew growers and we have much more
stakes in the fall and rise of cashew price and exports than the scientists who
have aired this concern. None of us use endosulfan in cashew and now our
economy is getting affected. These scientists actually have nothing to lose,
because they can still continue their research (into why exports fell ?, why price
went down ?, what is wrong with CSE ?, who is the anti-cashew lobby ?, then get
lots of funds for research and keep their lives brimming) and survive. When
Cashew plantations all over the world are going organic, and when the Cashew
Export Promotion Council was the first one to take up this issue and request
stopping of endosulfan use and aerial spraying, how can the scientists air such a
concern. It is the use of such chemicals in export crops that is going to
ultimately affect export prospects as has been seen in many other cases. Also, in
a discussion with E5PAC, Smt. Gowri Amma, the Agriculture Minister had
indicated that the State’s preferences would be to move to sustainable
cultivation. Agenda 21 document prepared by the Ministry of Agriculture of the
Government of India outlays a vision to move away from pesticide use. These are
progressive steps towards protecting the export prospects of cashew.
We also understand that the convener of the expert team. Dr. Abdul Salam,
himself is a cashew grower. We would like to know whether he has used
endosulfan in his plants in the last two decades to contain the TMB. If not, why ?
16
However considering all the above aspects, an attempt is made to analyze the issue objectively
giving due consideration to social, environmental and national interests.
Recommendations
1.
From the short visit made and information gathered it is difficult to make any conclusion either in
favour or against the argument that endosulfan causes health problems. In view ofthe above it is
essential that a multi-disciplinary expert group (medical, agricultural, environmental scientists)
investigates on the various aspects ofthe health and environment related problems ofthe area.
2.
In view ofthe topographical disadvantages and high degree ofinhabitation in the adjoining areas
ofcashew plantations, the Government may be requested to stop PCKfrom the aerial spraving in
this area with immediate effect. The Director, NRCC Puthur has indicated this view as well.
3.
The PCK should be advised to rationalize the plant protection operations in cashew on more
scientific grounds. The current practice ofscheduled spraying should be replaced with a need
based application following insecticide rotation.
4.
During the last year the country earnedforeign exchange to the tune ofRs. 2500 Crores through
the export ofcashew kernels. Ifthe present level ofpropaganda regarding the use ofpesticide on
an export crop like cashew is aired internationally, it may drastically damage the export prospects
ofcashew. This ultimately will affect the farmer himself.
5.
Necessary technical andfinancial sanctions may kindly be accorded to the Heads ofANIPRS,
Odakkali and AICRP on Pesticide Residues Laboratory, College ofAgriculture Vellayani to
complete the analysis ofenvironmental samples collected on a time bound basis
Dr. M. Abdul Salam
Dr. A.M Ranjith
Dr. Samuel Mathew
Dr. K. M. Sreekumar
Nileswar
20-1-2001.
Annexure-I
Toxicological information on Endosulfan
1.
Acceptable daily intake (ADI) is 0.0075 mg/Kg. ffVHO,1975). ADI is the daily maximum dose ofa
chemical which, during an entire life time, appears to be without appreciable risk on the basis of
all the facts known at that time. Without appreciable risk is taken to mean the practical certainty
that injury will not result even after a life time ofexposure. It is worked out toxicological
investigation on test animals like rabbits.
2,
Mammalian Safety Ratio (MSR) is 2.81 showing that the chemical is only slightly selective. It is
toxic to mammals as well as insects.
3.
Insecticide suitability rating ofthe insecticide (ISR:39) is ‘Fairly acceptable ’ (Ranging: 30-44)
This is worked out taking into consideration the toxicity to target insects, safety to beneficial
insects and mammals, Mammalian Safety Ratio and the costfactor.
4.
LD5o (Median lethal dose) for honey bees is 275 mg/Kg body weight
5.
LD5q (Oralfor rats) is 18-43 mg/kg body weight.
6.
LD5o (Dermalfor rats) is 74-130 mg/kg body weight
7.
LC5o (Median lethal Concentration) forfish is 0.001 ppm. So the insecticide is extremely toxic to
fish when compared to mammals and other higher animals.
8.
The insecticide can be excreted in stools orfeces.
9.
On fruits and vegetables, the tolerance limit is 2 ppm (B7{0-1985). (Tolerance limit is the legally
permitted concentration ofa residue in or on afood, derived taking into account both the range of
the residues actually remaining when the food isfirst offeredfor consumption following good
agricultural practices, it is also known as Maximum Residue Level)
10.
At a rate 0.1 % application the insecticide degraded to 0.88 ppm. on brinjal and to 0.98 ppm. on
bhendi within a period of 7 days.
11.
Maximum waiting period before consumption ofthe treatedfood material isfixed at 6-9 days
(FAOAlHO-l985). Waiting periodfor some crops are asfolioivr.y;
a.
Cowpea, Cauliflower, Cabbage
:
10 days
b.
Tomato
8 days
c.
Bhendi and Brinjal
:
7 days
d.
Pigeon pea /redgram
:
7 days
12.
Pest management ratingfor different organismsfor an insecticide is asfollows:
a.
Mammals
4
b.
Fish
4
c.
Birds
4
17
Bees
:
2
Persistence
:
3
Overall rating : 9.7 means that it can be usedfor pest management purposes under skillful
supervision. It was thusfound to be comparatively safe to honey bees and natural enemies (parasitoids and
predators) ofthe ecosystem at the applied doses.
Environmental persistence of the insecticide is rated as 3 (that is moderately persistent) It was
13.
also observed in the tropical climatic conditions the insecticides degradesfaster than that in
temperate conditions (Nearly 4 to 12 months in tropics).
14.
Instances ofpoisoning - Not available
The chemical is still recommendedfor pest management on a variety offield and plantation crops
15.
like cereals, pulses, cotton, fruits, vegetables, tea, coffee, cashew etc.
d.
e.
Acknowledgement
The committee wishes to place on record their appreciation and thanks to
Sri. Id. Bhaskaran Deputy Director, Dept, ofAgriculture, Kasaragod District for the excellent
arrangements at Kasaragod and alsofor accompanying the team throughout.
Dr. B. Jayaprakash Naik, Associate Professor, RARS, Pilicode for serving as the tongue ofthe
2.
team, to interview the respondents in Kannada and Tulu Languages.
The Associate Dean, College ofAgriculture, Padannakkadfor providing computerfacilities and
3.
infrastructure support and
4.
The Associate Director, RARS Pilicodefor the help rendered.
Convenor
Expert Committee.
I.
News paper cuttings attached
1.
2.
3.
4.
5.
“Aerial spray ofpesticides makes life cheaper than Cashew ”, The Evidence Weekly Dec 25-31,
1981
“Pesticides turn pests - Polluted crabs spell dread diseases in Karnataka Village ” Sri Padre,
“Where a cashew pesticide is turning homicide ”, The Hindu Business Line 17-1-2001
“Insecticide blamedfor making Swarga a hell”, Indian Express, 5-01-2001
“Health hazards ofpesticide spray", panic grips hamlet”, The Hindu, 5-02-2001
We do not wish to comment on the recommendations as the expert team has the
freedom to make observations based on their own learning and understanding of
the issues and their knowledge base.
We did not wake up one fine morning to say that endosulfan is the cause of all our
health problems. In the last two and half decades we have been living and seeing
the growing health crisis in our families. We have been suspecting various
possible causes. The search also took us to the nearby panchayaths. We found
similar health problems in more than ten panchayaths in our district. And all
these panchayaths had only one common factor - endosulfan.
We did a thorough review of literature on endosulfan and shortlisted the possible
health problems it can cause or induce. To our shock, it matched with the list of
diseases that we shortlisted as common in the affected panchayaths. So, after a
26 year trial in our community and villages we are convinced that endosulfan is
the culprit.
Rachel Carson wrote in Silent Spring
a public "fed little tranquilizing pills of
half-truths. We urgently need an end to these false assurances to the
sugarcoating of unpallatable facts.* This was in 1962. We wish to ask the same
to all who were responsible for this tragedy of our villages and to all who are
desperate to cover up or “sugarcoat* the truth about this poison.
18
c
Attachment - 1
Copy of letter from ESPAC to the Vice-Chancellor, KAU
REGISTERED MAIL
16th January 2001
From :
Aravinda .¥
Chairman ,
Endosulfan Spray Protest Action Committee -Padre ,
Yedamale ,
Post : Padre ,Via Perla 671552
Kasaragod
To :
Dr.K.N.Shyamasundaran Nayar
Vice-Chancellor
Kerala Agri University (KAU)
Vellanikkara
Thrissur,Kerala
Sir ,
Sub : Endosulfan aerial spray by PCK suspected to be the reason
behind veiy high incidence of dreaded diseases in our village Clarification about your reported certification of endosulfan as
’harmless’ - sought .
In our village , we have veiy recently realised that there is a veiy high incidence of CNSrelated diseases like Cancer , Mental Retardation , Psychiatry' , Epilepsy and a host of
other diseases like Asthma , Skin diseases like Psoriasis etc .Results of an informal
Survey conducted by Dr. YS Mohankumar ,MBBS, practicing in our area since the last
19 years is as follows: (Statistics collected upto 5th Jan 2001)
Cancer - living
Cancer - dead
Mentally Retarded
Psychiatric Cases
Epilepsy
3
46
23
43
23
138
Congenital anomaly
(Bom handicapped ) 9
Suicide cases
9
18
156
( This in about 4 sq.km area of Padre village, Enmakaje Panchayath,Kasaragod
Dt.,Kerala,India, from among an estimated population of 2,000 people, from
approximately 200 houses. )
There is no polluting industry in and around . We strongly suspect this to be an ill-effect
of endosulfan being aerially sprayed at the nearby hilltops by PCK (Plantation
Corporation of Kerala). Latest toxicology' literature also point out towards this .
19
0
The PCK has reportedly released a press statement saying that " In Kasaragod since
1976 , endosulfan is being aerially sprayed and that Agri University has certified that
there is no much harm by this sort of spray (as reported in Janavahini , A Kannada
daily , dtd .January 9,2001, xerox copy enclosed)
The above statement wherein your certifying the insecticide as ’causing no much harm *
is very vague and misleading . In the light of the above , we request you to kindly clarify
the following aspects to us , in the interest of public health.
(1) Have you conducted field trials of aerial spray of endosulfan ? If yes,in which year
this trial was conducted and what was the concentration and type of endosulfan
then
used ? Was the long time effect studied ?
(2) What are the precautionary measures suggested by you ?
(3) You must be aware that in the recent decades lot of toxological studies have been
conducted and lot of information on possible ill-effects of endosulfan are available .
Just to quote one , ” Endosulphan has a proven toxic effect on the human foetus
(and on mammalian fetus) and produces mutations. Organochlorines in general
have the whole range of possible toxic effects on liver, kidney, bonemarrow, blood,
brain (loss of intellectual functions and psy chiatric illness), carcinogenicity, damage
to reproductive system and to foetus/embiyo. Organochlorides differ in their most
prominent of toxic effects, in the amount needed to trigger short-term poisoning
symptoms and long-term poisoning, and the most easy route of
ingestion/absorption into the body." (Source :a German publication from
1988:Gefahrdungen der Gesundheit durch Pestizide - to be translated as "Health
dangers arising from pesticides" - by a team of authors.Irene Witte, Ruth Jahne, Rolf
Weinert, Kilian Kobrich, Heike Jacobi )(Frankfurt, Germany, 88)
(4) We understand that all the prescribed precautionary measures and including the
maximum allowed concentration of endosulfan is not being followed by PCK . Under
this circumstances , and in view of the latest findings about ill-effects of endosulfan
, don’t you think summarily endorsing endosulfan as 'not causing much harm’ is
unfair and would bring a bad name to your esteemed institution's reputation ?
We , therefore , request your goodself to kindly clarify the above points and in view of
the co-relation to the endosulfan spray that seems to exist with the very high incidence
of diseases in our area , to conduct a fresh field trial about short term and long term
and long term toxicity of the above insecticide in our field conditions . Until such a
thorough study is conducted , in the interest of public health and humanity , we
request you to withdraw the certificate issued by you to the PCK .
Well appreciate a prompt reply from you , considering the urgency of the situation .
Respectfully yours.
Aravinda Yedamale
20
0
Attachment - 2
Endosulfan - Regulations and Violations
(A note on the regulation in India and how it was violated in
the PCK owned plantations of Kasaragod )
The Central Insecticides Bureau
The Central Insecticides Bureau (CIB) is the Central Govt. Agency, which regulates
pesticide use in India. They have periodical reviews of use of pesticides and is the
agency for registering its manufacture, sale and use.
The Designated Licensing officer in the States
stocking and use of pesticides.
issue licenses for manufacture, sale,
Aerial spraying of Endosulfan
Among other conditions like giving prior information to the people in the area advising
them to keep away from the area of application for a period of 20 days, covering all the
water sources during spraying etc as stipulated by the Insecticides Act 1968, the CIB
prescribed that the spraying of endosulfan should be undertaken at a height of not
more than 2 to 3 metres above the foliage. This was always violated in the PCK
plantations.
It has also come to light now that aerial spraying of endosulfan was never allowed by
the CIB from 1993. The CIB had given approval for aerial spraying of endosulfan only
till December 1992. But the PCK, the Department of Agriculture in Kerala and the
District Collector has been issuing aerial spraying orders even after 1993 up to the last
season, without the approval of the CIB.
General Use of Endosulfan
Dr. Banerjee committee -1991
In 1991 the CEB appointed a committee under the chairmanship of Dr. Baneijee to
review whether some pesticides, including endosulfan should be continued to be used in
India. Among other recommendations this expert committee concluded
1. That the use of endosulfan be continued
2. That the registration committee should not allouj the use of endosulfan near rivers,
lakes, sea and ponds, which are expected to be polluted.
The committee also
recommended putting this in the certificate of registration as a condition and a
warning on the labels and leaflets in the containers.
Dr. R B Singh committee - 1999
In 1999, the CIB appointed an expert committee under the chairmanship of Dr. R B
Singh to review the continued use of some pesticides including endosulfan.
This Committee also recommended the continued use of endosulfan and among others
it recommended that
Labeling should be made mandatory in bold letters to avoid use of endosulfan near
water sources.
The Registration Committee meeting
The 195th Registration Committee (of the CIB) meeting held on 14th December 1999
agreed for the continued use of endosulfan and suggested to incorporate a warning
statement on the labels and leaflets indicating that endosulfan should not be used near
water sources.
21
0
Inter-ministerial Committee
The 10th meeting of the Inter-Ministerial Committee to review the use of insecticides and
hazardous chemicals held on 29-12-1999 also recommended among others that
1. the continued use of endosulfan in the country
2. incorporating the warning in the labels and leaflets that endosulfan should not be
used near the water resources
The Central Insecticides Bureau and the Ministry of Agriculture has not yet
implemented the restrictions suggested by the various committees, while always
approving the continued use of endosulfan.
Endosulfan has been aerially sprayed in 4600 ha of cashew plantations owned by the
Plantation Corporation of Kerala for nearly 25 years now. It is quite evident as per the
recommendations that
it has been officially recognized that endosulfan is highly toxic to aquatic beings
especially fish and contaminates water
and that it cannot be used anywhere in Kerala where water bodies are plenty in the
form of sea, rivers, lakes, backwaters, rivulets, streams, surangams, ponds, wells
etc.
In this context had the recommendations been implemented in 1991 the miseries and
the toxic burden of the villagers of Kasaragod could have been avoided. Even today, the
recommendations are kept aside for reasons unknown and the use of this highly toxic
chemical continues to steal the future of many many innocent children of Kasaragod
and elsewhere.
In this context the State Government had taken the precautionary measure of
suspending all use of endosulfan in Kerala. But the chemical should be suspended
from use permanently.
i
22
c
Attachment - 3
World wide regulatory status of Endosulfan
The last decade (1990-2000) has been a period when countries all over the world has
taken a very progressive and precautionary look at pesticide use. In our knowledge
there are so many countries that have banned/ severely-restricted endosulfan for farm
and agriculture use.
Columbia is the latest to ban endosulfan in all its crops in March 2001. The State
Council (Consejo de Estado) the supreme administrative court of Columbia in a
landmark judgement banned all use of endosulfan. The court originally considered a
ban on use in coffee but after considering its toxicity and risk to human health, it
ordered a ban of endosulfan use in all crops.
Severely Restricted
Africa
(1 country)
Asia Pacific
(16 countries)
Europe
(12 countries)
Belize
Singapore
Bangladesh (Ban in Rice)
Tonga
Syria
Indonesia
Cambodia________________
Japan____________________
Korea ( Ban in Rice)______
Kh asakisthan____________
Kuwait
Germany
Yugoslavia_____
Netherlands
Finland_________
United Kingdom
Ru ssia_________
Venezuela
Brazilian State of
Rondonia
Dominica
United States
Canada______
Australia
22
Colombia
North America
(2 countries)
Australia_____
Total
Pakistan
Philippines (allowed only
for Pineapple)____________
Lithuania_________________
Sri Lanka_________________
Taiwan___________________
Thailand (Ban in Rice)
Luxembourg
Denmark
Sweden
Norway
South, and Central
America
( 4 countries)
Priority for
re-evaluation
10
Portugal
Spain
4
Most of the countries have banned/severely-restricted endosulfan due to its toxicity to
aquatic organisms and mammals. A developing country like Syria follow very practical
and scientific criteria based on the precautionary principle for canceling the registration
of a pesticide. A pesticide is banned in Syria
if the pesticide was unhealthy
if it is banned in the source country or in two other developed countries
If it is banned by a resolution issued by any international organisation
If there are available excuses for any pesticide registering committee to cancel it
depending on scientific researches and reports carried out by any Arabian or
international side.
23
Attachment - 4
ENDOSULFAN - A SHORT SUMMARY
Endosulfan is an organochlorine insecticide of the cyclodiene subgroup.
It acts as a poison to a wide variety of insects and mites on contact and
as a stomach acaricide.
Uses
It is used as an insecticide for vegetable crops; control of aphids; thrips,
beetles, cutworms, bollworms, foliar feeding larvae, mites, bugs, borers,
whiteflies, slugs and leaf hoppers in citrus deciduous and small fruit
fibre crops, forage crops, oil crops, grains, coffee, tea, forestry, tobacco
and ornamentals. It is used to control tse-tse flies and termites and is
also used in rice and legumes in India.
Formulations of endosulfan include emulsifiable concentrate, wettable
powder, ultra-low volume (ULV) liquid, granules and dust.
Production and Status
Endosulfan is produced by the reaction of hexachlorocyclopentadiene
and cis-butene- 1,4-diol in xylene, followed by hydrolysis of the adduct to
the cis-diol or dialcohol. Endosulfan is then produced by treating this
bicyclic dialcohol with thionyl chloride. Technical endosulfan is made up
of a mixture (7:3) of two molecular forms (isomers) of endosulfan, the
alpha- and beta-isomers. Technical grade endosulfan contains at least 94
per cent of the alpha- and beta- isomers. It may also contain up to two
per cent endosulfan alcohol and one per cent endosulfan ether as well as
endosulfan sulfate. Of these the alpha-isomer is more toxic than the
beta-isomer, while the beta-isomer is the more stable and persistent
isomer.
Endosulfan is sold in India in various trade names, some of them are
Agrosulfan, Aginarosulfan, Banagesulfan, Seosulfan, Endocel, Endoson,
Endonit, Endomil, Endosol, Endostar, Endodaf, Endosulfer, E-sulfan,
Endorifan, Hildan, Chemusulfan, Kilex-endosulfan.
Characteristics and Toxicity
Endosulfan is chemically very close to Dieldrin, substituting a
heterocyclic sulfur in place of the saturated bicyclic ring system. The
other well known chemicals in cyclodiene sub-group are Aldrin, Endrin,
Dieldrin, Heptachlor, Chlordane and Mirex. All these cyclodienes, except
endosulfan are already banned in India and is going to be globally
phased out by the Stockholm Convention signed by World Countries in
May 2001 under the auspices of the UNEP. Of the 12 chemicals ( Dirty
Dozen ) to be initially phased out, nine are pesticides of which six of them
belong to the Cyclodiene sub-group.
Endosulfan is considered to be highly toxic. It can adversely affect
human and wildlife exposed to it. It has been shown to cause damage to
the nervous system, as well as other parts of the body, with the liver and
kidney being target organs for chronic exposure in mammals. Endosulfan
is proven to show carcinogenicity and is a liver tumor promoter.
24
u
Endosulfan is genotoxic, mutagenic and cytotoxic. It is suspected to be
teratogenic, it is shown to affect the reproductive system and disrupts
the endocrine system. Its teratogenicity could not be reliably proven due
to the maternal toxicity it showed on the experimented animals. Its
effects particularly, estrogenic properties can have wide and disturbing
effects on the human and wildlife health. Endosulfan is extremely toxic
to Fish and many other aquatic organisms. It is toxic to insects and also
to mammals. It is toxic to honey bees.
Physical and Chemical Properties
Chemical name: 6,7,8,9,10,10-Hexachloro-l,5,5a,6,9,9a-hexahydro-6,9met±iano-2,4,3-benzodioxathiopin-3-oxide
Chemical formula: CgHeCleOsS
Chemical Structure:
Cl
cLci
o—8=0
Cl
Cl
^0
Cl
Melting point:
Pure (100%): 106°C
Technical (90%-95% pure): 70°- 100°C
Odour: Slight odour of sulfur dioxide
Solubility in water at 22°C: 0.16-0.15 mg/L
Partition coefficients:
Log Kow: 3.55 and 3.62
Log Koc:.* 3.5
Vapour pressure at 25°C: l*10’5 mmHg
Vapour pressure at 80°C: 9*IO-3 mmHg
Henry’s law constant at 25°C: 1 * IO-5 atm m3/mol
Bioaccumulation factor (BCF): <3000
Classification
Endosulfan is classified in India as an “Extremely Hazardous” pesticide
(ITRC,1989). Endosulfan is classified as a “Moderately Hazardous”
chemical by WHO (Class-II). The European Union and the U.S
Environmental Protection Agency ( USEPA) have classified Endosulfan as
Class lb (Highly Hazardous) . The USEPA has listed the compound in the
Extremely Hazardous Substances List under the Environmental
Standards. Endosulfan is classified as a “highly toxic” substance as per
many other agencies(EXTOXNET, 1998). The classification of WHO was
found to be inappropriate considering the classification followed in
countries all over the world. It is alleged that the WHO has classified
endosulfan as a Class II or “Moderately hazardous” pesticide based
mainly on LD50 value taken from company generated acute toxicity data
(Quijano R.F, 2000).
25
0
Fate and Degradation in the Environment
The two isomers of endosulfan have different fates in the environment,
beta-endosulfan is more persistent than alpha-endosulfan (NRCC, 1975).
Endosulfan sulfate is the main degradation product of both isomers, and
is itself persistent in the environment (NRCC, 1975). Whereas,
endosulfan diol is their hydrolysis product which tends to form in
alkaline aquatic environments (NRCC, 1975).
Drift from aerial applications and volatilization from water and plant
surfaces are the primary ways of endosulfan entry into the atmosphere. It
has been found that some of the endosulfan sprayed on crops and water
will volatilize to the air (Simonich and Hites, 1995;Terranova and Ware,
1963). The volatilization half-life from surface water varies from 1 Idays
to one year and from plant surfaces from two to three days (Callahan et
al., 1979). In air, endosulfan is carried over long distances. Traces of
endosulfan have been found in Arctic air as well as snow samples (Gregor
and Gummer, 1989).
In water, endosulfan undergoes hydrolysis and microbial degradation.
The rate of hydrolysis is influenced by pH. The hydrolytic half-life can
range from five weeks at pH 7 to five month at pH 5.5 (Greve and Wit,
1971; Schoetteger, 1970). Microbial degradation products of endosulfan
in water include endosulfan sulfate and endosulfan diol (NRCC, 1975).
The half-life of endosulfan in water varies from three to seven days to
about five months, depending on the dissolved oxygen content and pH of
the water as well as the degree to which the water is polluted (NRCC,
1975).
In soil, endosulfan binds strongly to soil particles and is not readily
leached out to ground water. The bulk of endosulfan residues is bound to
the top 15 cm of soil surface layers. In experimental conditions, 90 per
cent of the endosulfan residues were found in the top 15 cm horizon of
the soil surface, nine per cent at a depth of 15-30 cm, and only one per
cent was found at the depth of 30-45 cm after 503-828 days (Stewart and
Cairns, 1974).
In soil, endosulfan is subject to photolysis, hydrolysis or biodegradation.
Major products of degradation processes in soil are endosulfan diol and
endosulfan sulfate (Martens, 1976; El Beit et al., 1981). Endosulfan
isomers show different rates of dissipation from soil. Endosulfan sulfate
is more persistent than the parent compound (Stewart and Cairns, 1974).
In experimental applications of endosulfan 50 per cent of a-endosulfan
disappeared within 60 days, versus 800 days for p-endosulfan. In
another report, the half-lives of a- and (J-endosulfan were estimated as
35 and 150 days, respectively (EXTOXNET, 1996).
Endosulfan is less persistent on plant surfaces and rapidly degrades to
endosulfan sulfate and endosulfan diol. The estimated half-life of
endosulfan on plants ranges from 1.95 to 2.74 days.
26
I'
Residues
Endosulfan is released to the environment mainly as a result of its use as
an insecticide.
High concentrations of endosulfan, as alpha-endosulfan, beta
endosulfan and endosulfan sulfate, have been detected in tree bark
samples throughout the world, particularly in India and the Pacific Rim
(Simonich and Hites, 1995). It was speculated that the high
concentrations of endosulfan in these areas were due to its use on rice.
In aquatic ecosystems, endosulfan partitions to plants and animals and
also accumulates in sediment. Both endosulfan and endosulfan sulfate
have a longer half-life in sediment. Concentrations of endosulfan in
sediment have been reported to be 32,000 times higher than in the water
column (NRCC, 1975).
Although generally low concentrations of endosulfan have been found in
surface water, lethal concentrations may be found in ponds and streams
in the vicinities of spraying areas. A study using water containers
indicated that drift from aerial agricultural spraying could produce
concentrations lethal to fish in shallow exposed water bodies 200 m away
from the target spray area. Levels of 1.7 mg/L and 0.04 mg/L were found
in water containers in the vicinities of the spraying areas and 200 m
away. These levels are found to be lethal to fish (Ernst et al., 1991). This
experiment confirms that the agricultural practice of applying endosulfan
aerially may lead to increased pesticide concentrations in waters off-site,
which could result in fish kills in unexpected areas.
Globally, endosulfan is one of the most commonly identified chemical in
any residue analysis in fruits and vegetables, for which it is mostly used.
In a study sponsored by Indian Council of Agriculture Research (ICAR) the All India Coordinated Research Project (AICRP) on Pesticides
Residues in 1999 -out of 422 farm-gate vegetables tested for residue of
endosulfan 322 (79%) were found to be contaminated. The residue
levels ranged upto 18.63 mg/kg (the second most contaminating after
residues of copper, upto 75 mg/kg, which is a metal and does not
undergo degradation). The allowable Maximum Residue levels of
endosulfan in food is 0.5 to 2 mg/kg. Moreover, the contamination
percentage of endosulfan (79%) was second only to Lindane
(96%).(Toxics Link, 2000)
Exposure
Human Beings may be exposed to endosulfan from
•
breathing air near where it has been sprayed
•
drinking water contaminated with it, from direct application, spray
drifts or runoffs;
•
eating contaminated food;
•
touching contaminated soil;
•
smoking cigarettes made from tobacco with endosulfan residues,
•
working in an industry where it is used or living near its vicinity.
Wildlife may be exposed to endosulfan in the environment by consuming
plants that have been sprayed with endosulfan, ingestion of soil or
dermal contact with soil. Additional exposure can occur through
27
inhalation of air in the area of agricultural application. Exposures in
aquatic environments may occur due to surface runoff following
agricultural application, or upon deposition of endosulfan following longrange transport in the atmosphere. Fish have been exposed to sufficient
quantities of endosulfan in agricultural run-off to cause mortality (Frank
et al., 1990).
In the mammalian system, the alpha-isomer of endosulfan persists in the
body longer than beta-endosulfan, particularly, in brain tissue and
plasma. Male rats fed with technical-grade endosulfan had detectable
levels of alpha-endosulfan in brain tissue and plasma, with less beta
endosulfan, and almost no endosulfan sulfate detected (Gupta, 1978).
Similarly, in rabbits, which died following acute exposure, alpha
endosulfan residues were also detected in liver and brain tissue (Ceron et
al., 1995), but no residual beta-endosulfan or endosulfan sulfate was
found.
Acute toxicity
Endosulfan is classified as a highly toxic substance. It is acutely toxic to
birds, marine and freshwater fish, and mammals. Like other chlorinated
cyclodienes, endosulfan is a neurotoxin affecting the central nervous
system (CNS) of aquatic organisms as well as mammals.
People who are occupationally exposed to endosulfan are advised to avoid
eye and skin contact as well as inhalation exposure. Symptoms of acute
toxicity in humans are restlessness, irritability and hyperexcitability',
followed by headache, dizziness, nausea and vomiting, blurred vision,
unconsciousness, insomnia, lack of appetite, loss of memory,
albuminuria, haematuria and in some cases, confusion.
Chronic toxicity
Chronic exposure to endosulfan may result in general toxicity s^miptoms
such as liver and kidney damage as well as effects on the CNS, immune
system and the reproductive system.
Neurotoxicity
Endosulfan may have adverse effects on the CNS of aquatic organisms,
birds and mammals. The main mechanism of action of endosulfan in the
CNS is inhibition of brain acetylcholinesterase, causing uncontrolled
discharges of acetylcholine. Abnormal behaviour has been observed in
fish and mammals being chronically exposed to endosulfan.
Carcinogenicity
Even though, endosulfan was not classifiable as to its carcinogenicity
(due to lack of sufficient data), studies have shown that it can be
carcinogenic. Reuber, 1981 showed that endosulfan was carcinogenic in
male and female rats at all sites examined. It also induced liver tumours
in female mice. Another study(Fransson-Steen, 1992) found that
endosulfan promoted the growth of altered hepatic foci in rats in a
similar manner as the structurally related chlorinated insecticides,
chlordane, aldrin and hcptachlor did, indicating that endosulfan is a
potential liver tumour promoter.
28
G
Immune System
Endosulfan is also known to affect the immune system. Target organs are
the kidneys and liver. A number of studies have shown endosulfan to
hepatotoxic. Endosulfan inhibits leukocyte and macrophage migration
causing adverse effects on the humoral and cell mediated immune
system.
Reproductive Effects
A number of studies have shown a potential for adverse effects of
endosulfan in the reproductive system of aquatic organisms and
mammals. Histological changes in reproductive organs were seen in
aquatic organisms following exposure to endosulfan at concentrations as
low as 0.00075 mg/L (0.75 pg/L). Endosulfan treatment in male rats was
reported to cause a dose-dependent reduction in sperm counts, sperm
abnormalities and decreased daily sperm production as well as decreased
testis weight.
Endocrine disruptive action
In vitro studies show endosulfan is estrogenic (in the E-SCREEN assay).
Endosulfan I competes with [3H] 17p-estradiol for binding to the estrogen
receptor. Endosulfan sulfate inhibited binding of [3H]R5020 to the
progesterone receptor by 40-50 per cent. Low levels of endosulfan (1 nM,
0.41 ppb) can inhibit the human sperm acrosome reaction, initiated by
progesterone and glycine, but the inhibition is not complete. Endosulfan
II and endosulfan sulfate decreased p-galactosidase activity of
progesterone (Jin et aZ.,1997).
In vivo studies showed that Endosulfan decreased plasma vitellogenin
levels in catfish (Chakravorty et al., 1992). Endosulfan also decreased the
number and size of oocytes in fresh water teleost fish, and increased the
number of deformed oocytes, damaged yolk vesicles, and dilated
gonadosomatic index. It caused a dose-dependent reduction in sperm
counts in rats, reduced the number of spermatids, caused sperm
abnormalities and decreased daily sperm production.
Genotoxicity and Mutagenicity
Several independent studies have shown that endosulfan is genotoxic.
Data from in vitro and in vivo mutagenicity studies generally provide
evidence that endosulfan is mutagenic, clastogenic and induces effects
on cell cycle kinetics. (Syliangco, 1978; Adams, 1978; Yadav et al., 1982).
Endosulfan was also found to cause chromosomal aberrations in
hamster and mouse, sex-linked recessive mutations in Drosophilia, and
dominant lethal mutations in mice(Velasquez et al., 1984; Naqvi and
Vaishnair, 1993). Studies in human cells both in vitro and in vivo also
showed that endosulfan caused the occurrence of sister chromatid
exchanges indicating chromosomal damage(Sobti et al., 1983; Dulout et
al., 1985). Very recently, a team of researchers in Japan found further
evidence of endosulfan genotoxicity using sister chromatid exchanges,
micronuclei, and DNA strand breaks as detected by single cell gel
electrophoresis as biomarkers (Yuquan Lu et al., 2000).
29
0
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35
4
Q
3^3-
The issue
I.
If what is chronicled in the Silent Spring could shock the world awake off
the suicidal path that pesticide use would lead humanity to, then here in
these villages one can see the most horrid reality of Rachel Carson’s fears
come true.
Today villages in Kasaragod District are complaining from peculiar and
complex variety of diseases unprecedented in this part of the country.
All these villages lie in the mid-lands and laterite hill area of Kasaragod
District, the northernmost district of the Kerala State. None of these
diseases were known to the people of the area about two decades ago.
These diseases are uniform in nature in almost all these villages and
there seems to be no section of the people who have been Spared from
being affected. The peculiar set of diseases has affected atleast 15
panchayaths in the District. The aerial spraying of endosulfan - a highly
toxic organochlorine pesticide is being blamed as the cause for these
diseases. The spraying is done by the Plantation Corporation of Kerala
(PCK), a Government of Kerala undertaking, in the cashew plantations
which lies in or borders these panchayaths. The PCK has been
undertaking the aerial spraying ritually for the last 26 years in their 4600
ha of cashew plantations.
Incidence of increased number of children born with congenital
anomalies, mental retardation, physical deformities, cerebral palsy and
mental ailments like epilepsy are reported from many families across
panchayaths. Many reports in all the prominent dailies and magazines
were showing children with congenital physical deformities, stunted
growth, mental retardation and cerebral palsy. Cases with
hydrocephalus was also reported. Psychiatric problems are also on the
increase and many young and old are succumbing to suicidal tendencies
with apparently no reasons as such. Doctors have recorded many cases
of cancer, especially of the liver and blood. Informal survey’s have also
revealed increased rate of breast, throat and intestinal cancer. Cancer
among men is almost double that of women. Men are also suffering from
infertility and undescended testis. Miscarriages and hormonal
irregularities are being reported among women. More and more people
are falling ill to rheumatic complaints. Paralysis is very common.
Parkinson’s Disease is also being reported. Endometriosis, a serious
illness affecting the uterus has been diagnosed and is causing serious
concern.
Many complain of Skin disorders like Psoriasis, Eczema, Leucoderma and
other forms of dermatitis. Very pathetic cases were also found where a
chronically affected person was scratching his wound with stone to stop
the itching. Children have become susceptible to frequent illness,
showing a deterioration of the immune systems. Doctors are forced to
give high doses of antibiotics even to contain minor fevers. People were
i
5
also complaining of hearing and vision loss. Asthma and breathing
complaints were too common.
Since the middle of the nineteen seventies, nature has been sending
warning signals of impending danger to people in these villages. It came
in the form of mass death of honeybees, fishes, frogs and birds. Cows
and chicken also started dying of sudden and mysterious reasons. Over
some time, fox population started dwindling and there was many a mind
that silently worried at these warning signals. In 1979, a farmer in Padre
realised that reason for three of his calves born with deformed limbs and
having stunted growth could not be just attributed to his fate. Moreover,
he had just read that pesticides like Endrin ( Referring to the The
Handigodu Syndrome which was very much in the news then) could
actually cause such effects. The evidence towards such an hypothesis
was lacking then, but still he reported it to a local journalist Shree Padre
who wrote the first article “Life cheaper than Cashew” in “The Evidence”
(dec. 1981) and raised a doubt that Endosulfan, which was being aerially
sprayed in the plantations in his village was the cause for such
environmental problems. The first warnings were already there. The
people started complaining. In 1984, two panchayaths passed
resolution not to spray pesticide by air as there is large-scale drift and
problems caused for cattle and people. When the local MLA Sri. Subba
Rao becomes Minister he ordered the suspension of the aerial spraying.
The aerial spraying in some areas was suspended for nearly two years. In
1988, the PCK wrote to National Research Centre for Cashew (NRCC) for
advise on the crop protection against the Tea Mosquito Bug which was
affecting their plantation. The NRCC recommended endosulfan use at
0.05% concentration. All through these years aerial spraying of
endosulfan was continuing. But it is now learnt that this
recommendation was never followed as it was found to be ineffective to
control the bug. More and more news of health problems started being
reported from all other places in Kasaragod as well. Local sports and
arts clubs, cultural clubs and community organisations were taking
serious view of these problems. Many of them passed resolutions and
also complained to the District Collector, who is the authority to permit
aerial spraying. In 1994, the Kerala Sastra Sahithya Parishad (KSSP)
alleged that the problem is caused by insecticide and asked for stricter
regulations in the aerial spraying. By this time, the local print media
including the major dailies started reporting the issue of health problems
and spread of strange diseases and health disorders. The people also
started agitating. Surprisingly, in 1997, Dr. EW Bhaskara Rao, the
Director of NRCC recommended aerial spraying at 1% concentration of
Endosulfan 35EC. He added that “ In this connection I am also to
mention that aerial spraying trials were conducted in the PCK orchards
and the spraying method was standardised for the first time in the
country”. (Letter No. F. PA (TECH.ADV)/97 dated 26 December 1997 to
the Manager, PCK Ltd ). It is indeed appalling that aerial spraying of
endosulfan was going on for more than 20 years before it was
standardised.
6
At the same time, Dr. Mohankumar, a local medical practitioner of
Enmakaje, concerned with the large number of strange diseases wrote to
IMA and other psychiatric specialists drawing their attention to the
mysterious nature of the problems there. He felt the root of the problem
lies in the water in the area. Dr. Mohankumar reported that there were
abnormally high numbers of psychiatric and epileptic cases in his village.
Almost at the same time Leelakumari a mother of two children and
Agriculture Assistant working in the Periya Krishi Bhavan, who had
moved to her new home in Periya village, realized that her son who is a
good singer is loosing his voice and suffers from depression. Her
daughter also developed some hormone problems and she put her up in
a hostel outside the area till the spray drift recovers. She found that she
herself was suffering from loss of voice and hormonal problems. She
appealed to the PCK, the District Collector and all the authorities to stop
poisoning their fields and wells. The Kerala State Pollution Control
Board collected water from their well and reported that the well was not
contaminated, but the procedure they followed in testing and their very
lackadaisical attitude in monitoring and controlling pollution was later
criticized in various forums. The KSPCB Chairman also made a
statement in a prominent magazine that they lacked information about
endosulfan. Leelakumari along with Kottan, a farmer and local
politician and others appealed to the Munsif Court for stay of spraying in
1998. The Hon’ble Munsiff, while issuing the stay order observed that
<rThe Stand taken by the respondents ( the PCK ) is that of a heartless
industrialist. They say that use of insecticides would bring more profit
and more foreign exchange. But it cannot be at the cost of human
lives.... Certainly we have power to destroy nature, but the question is
whether we have the wisdom to preserve it...” . Many local environmental
groups, led by the Society for Environmental Education in Kerala (SEEK)
also joined in support of the struggle of the people and filed separate
petition in the High Court asking for stopping aerial spraying in Periya
Division. Two separate fact finding teams, one led by SEEK and later one
by Thanal reported incidence of similar diseases in all the panchayaths
that have plantations or are close to them. The survey also found that
PCK has violated the Insecticides Act in precautionary and safety
measures and even in concentrations of the chemical sprayed. In many
places the PCK workers themselves reported health disorders but
requested anonymity out of fear of the management. Soon after, Thanal,
supported by SEEK and many community and local groups decided to
conduct a long term monitoring of the area to study the endosulfan
caused problems. This was launched in October 1999. A preliminary
report was submitted to the District Collector.
In December 1999, inspite of all the hue and cry over the unmindful
spraying of endosulfan over the plantations and the people’s dwellings
and waterbodies, the PCK was getting ready for the next round of
spraying. The environmental groups - SEEK, INTACH(Natural Heritage),
NAPM, Earth Society, KPSS, and Thanal - named PCK as the worst
polluter of the State and declared the area as a silent Bhopal caused by
PCK while remembering the 15th Anniversary of the Bhopal disaster.
7
They also released ‘The chemical free century - Declaring a toxic free
future” on this occasion.
In January 2000, the School Resource Group meeting in the Govt. High
School in Vaninagar in Enmakaje observed that students coming from
the backside of the school was generally found to be mentally and
physically backward and their learning capabilities were also poor. The
SRG wondered why this was happening. Later it was realsied that the
plantation was in the backside of the school. LP section of the school has
about 152 students, 40 of those who come from the back side is suffering
from some sort of congenital anomaly, mental retardation, physical
deformity. Many other are frequently taken ill.
In October, 2000 the Munsif Court of Hosdurg ordered permanent
prohibition of use of any insecticide by air. The court also restrained PCK
from using other methods which may cause harm to others properties.
This order was on a case filed in Periya Plantation area only and was not
operational to other areas. The PCK, inspite of massive and widespread
protests from other areas, especially Muliyar and Perla plantation area,
restored to aerial spraying of endosulfan, after arresting hundreds of
people who were asking for their wells and other waterbodies to be
covered, as per the Insecticides Act and the directions of the District
Collector.
It was soon after this that Sports and Arts groups, cultural groups,
panchayaths and environmental groups came together and formed a
larger network to protest against the endosulfan use and aerial spraying
and to find an alternate solution to this issue. All these groups
recognised that information about toxicity of endosulfan and the
problems it created was lacking. Information from various national and
international sources was collected and their worst fears were confirmed.
The people realised that they were exposed to a chemical which has been
classified as an “extremely hazardous” pesticide affecting the Central
Nervous system, Reproductive system, Immune System, Liver, Kidneys
and Skin. The Government machinery and the Insecticides Act could do
nothing to protect them from being poisoned. The Scientists at the KAU
were still asking for evidence of contamination and were terming this
pesticide as a “safe” pesticide, pointing out to its use in IPM. Separate
surveys by Thanal, Dr Mohankumar and Link-Trada revealed that there
is matching of the diseases in the panchayaths and the possible diseases
that could be caused by endosulfan. Central nervous system disorders psychiatric cases, Parkinson’s disease, epilepsy, cerebral palsy, mental
retardation, congenital anomalies, Reproductive system disorders,
infertility, hormonal disturbances, asthma and respiratory problems,
skin diseases, gynecological problems, cancer of the liver, throat, blood
and uterus were just some of them. The people then approached the
NRCC and KAU enquiring whether they had done any study of long term
efficacy of endosulfan on the pests, long term toxicity studies on the
people and environment. Both had never done any studies and
maintained a silence on these queries. The truth was that PCK had also
8
never in the last 26 years done even the mandatory medical examination
of the workers.
The groups then tried to get in touch with other scientific labs in the
country to find out whether it was possible to find out if the area was
contaminated.
The Centre for Science and Environment finally responded and sent their
researchers to collect the samples and analyze at CSE lab. The whole
process was done by a team led by Dr. Padma S Vankar Senior scientist
in charge of the Facility for Ecological and Analytical Testing at the I IT,
Kanpur. Retd. PVC and Coordinator of the Environment Centre of the
KSSP, Prof. M.K.Prasad , And Dr. Raghunandan, Associate Professor
and Veterinary Toxicologist from IRTC ( On deputation from KAU)
supervised the sampling. 25 samples were picked from the village. The
CSE found alarming level of endosulfan in all the samples. They publicly
released the report in February 2001. Not only was this a shocking
revelation, but the CSE also showed what public-interest science was all
about - transparency and responsibility.
Several cases were now filed at different courts including Munsif Court
and High court. The Munsif Court of Kasargod stayed all pesticide
applications in Kasargod taluk in February 2001. The CSE report, which
was only an exercise to find evidence and alert the public, succeeded in
bringing a lot of national and international attention to the problem.
The Cashew Export Promotion Council immediately responded and wrote
to the Directorate of Cashew and Cocoa and they in consultation with
NRCC advised PCK to refrain from aerial spraying. The NRCC then sent a
notification to all the Cashew growing agencies in the country
withdrawing the recommendation for endosulfan use in Cashew.
Soon after, a KAU team of experts rushed to the field, collected samples
and visited a number of families affected by the diseases. They alleged
that the CSE study is not scientific. The report of the KAU study has also
not been published, even after 6 months.
The Kerala Government has meanwhile upheld the precautionary
principle and responded to the issue by banning endosulfan use in the
State.
Meanwhile, FIPPAT, a private lab near Chennai was commissioned by the
PCK to study the problem. The report was released in a press conferences
by the Pesticide Manufacturers and Formulators Association of India
(PMFAI). This has clearly sent the signals to the people and have made
them all the more clear of the unholy liaison between the PCK and the
pesticide industry. The Enmakaje Panchayath has already disowned the
FIPPAT study for all the secrecy, which shrouded the study and the
panchayath not being informed of the study.
The demand from the PCK and the industry is that they be allowed to
continue the use of endosulfan and that the Government do a thorough
9
study of the reported health problems in Kasaragod and identify the
cause of them. At the same time the scientists of the KAU and the NRCC
have openly stated their position that it is not fair to blame endosulfan
and punish the culprit without scientific evidence. This position is
contradictory to the precautionary principle which India is bound to
follow as a signatory of the Rio Declaration. The Precautionary principle
clearly states that uIn order to protect the environment, the precautionary
approach shall be widely applied by States according to their capabilities.
Where there are threats of serious or irreversible damage, lack offull
scientific certainty shall not be used as a reason forpostponing costeffective measures to prevent environmental degradation^ . The Agenda
21 document prepared by the Ministry of Agriculture of the Government
of India also outlays a vision to move away from pesticide use.
Hypothesis
The primary aim of a hypothesis is to start at an “educated guess” or a
“tentative assumption” and this should be guided by the most probable/
possible / plausible option from a set of answers or in this case causative
factors for a problem of this nature.
Hence on the onset, we ask the question - Why did the people conclude
that endosulfan was the cause for their ailments ?
Most families in many of these villages once believed that the health
disorders that they were suffering from was because the local god was
angry with them for some unknown reason. For example, in Enmakaje,
the people believed that Jadathari ( the Lord Shiva ) was angry with them
and people conducted special pooja’s and rituals like theyyam for
appeasing him. People like Dr. Mohankumar believed that there must be
something in the water that they use, from the stream nearby that must
be contaminated by radiation or heavy metal. But slowly, as time
passed by and the ailments were mounting to threatening proportions,
the evidence were all pointing towards one possible chemical whose
presence was there in abundance in their midst atleast three times every
year. Endosulfan was the only chemical, or rather the only pollutant
externally introduced into their lives for the last 26 years. So, why did
the people conclude that endosulfan was the causative factor ? primarily because there was no other source of pollution or possible
poisoning other than this chemical.
Added to this are other reasons -The people have been seeing this kind of
strange diseases in their families only since the middle of nineteen
seventies and early nineteen eighties. There was no such incidence of
congenital anomalies among the people born before the nineteen eighties.
Many other villages in Kasaragod have also reported such health
problems at various times in the last decade and the only common factor
to which all these villages were exposed, invariably happened to be
10
endosulfan and nothing else. Members of the same family but living in
various villages find that the diseased are only in the villages which are
close to the PCK plantations. This again shows that the problem is not of
genetic and familial nature.
In this context, it would be interesting to point out a matter that occurred
in 1998. During an earlier study of the Grasim factory and its pollution
which caused Cancer in a number of homes in Vazhakkad and
surrounding villages, a Health Inspector working at Vazhakkad observed
in one of his talks with our researcher that “cancer incidence was not
very high in Vazhakkad, and was only comparable to those in Panathadi
panchayath” where he used to work before being transferred to
Vazhakkad. This anecdote is pointed out here, because Panathadi
panchayath is in Kasaragod and one of the most affected area, and has
been exposed to endosulfan spray and if one is to give due weightage to a
Health Inspectors observation, though unofficial and passing, the
semblance is indeed worth pursuing. Moreover, Panathadi has no such
hazardous / chemical industries, like in Mavoor.
In the preliminary survey itself it was found that the people were
complaining about the acute health problems which resulted soon after
the spraying. Irritation to the skin, convulsions, vomiting tendencies,
sickness, dizziness etc were common to many of the exposed people. The
school children were the worst affected, especially because they had to go
to school, many a time through the shortcuts via the plantation area and
soon after they reached school had to be taken to a doctor. But, it was
learnt that soon after the aerial spray many of the chronic cases
underwent a resurgence and sometimes these then had to be treated
anew. Skin diseases, descending of the testis, swelling of the testis,
disruptions in menstrual cycles, sudden changes in blood sugar levels,
frequent fever among children, asthma, breathing difficulties increased
among the chronically ill people during and after spraying season.
Swelling of lymph glands and scrotum was reported soon after spraying.
One girl in Periya reported that her periods stop soon after the spraying
and she suffers from a lot of hormonal problems and weakness for the
ensuing 3-4 months, after which her periods reoccur. Evidently, it is
clear that endosulfan spraying is linked to the triggering of the chronic
problems as well.
The local doctors whom our researchers interviewed also corroborate
these findings. The veterinary doctors in many panchayaths also report
of diseases to cattle and to domestic animals. In Padre, the spraying this
year caused serious diseases among the cattle. Many cows miscarried,
soon after the spray and some had very violent deaths. People reported
that this was very common especially among the cows, which graze in the
plantation.
Local people and panchayath representatives also revealed that the
health effects were most prominent in villages which have the PCK
plantations lying within it or borders it. Villages close by the plantation
11
had markedly reduced incidence of diseases and villages which were
distant from the plantations were not affected by these kind of health
problems. This again supported the hypothesis that endosulfan is the
primary causative factor. Moreover, the similarity in complaints as
stated by the families in various villages - up north in Enmakaje and
Bellur and down south in Cheemeni area were largely similar in nature.
It was also observed that most of the employees of the PCK and their
families were also affected, though only comparable with the non
employees living in the same area. This must have been primarily
because of aerial spraying, which did not discriminate between
employees and non-employees. Adding to this observation was the fact
that some of the workers were suffering from very serious chronic illness,
like throat cancer and chronic skin diseases. But, these workers
revealed that they were directly involved in the spraying many a time as
mixers or applicators. The researchers also observed endosulfan spraying
in new saplings of cashew using hand-sprayers. The employees also
reported that they were not given any protective clothing or gear during
such spraying which is mandatory under the Insecticides Act.
All these singularly points to the fact that the health disorders were very
much linked to the proximity of the villages with the PCK owned cashew
plantations. The plantations have been consistently sprayed with
endosulfan, aerially for the last 26 years, 3 times every year, violating all
the precautionary measures ( many a time because it would be
impossible to take precautionary measures in an area like Kasaragod, as
noted by the KAU scientists and the NRCC) and the rules of pest control.
And hence it is concluded that the use of endosulfan in the plantations
must be the primary suspect for all these health disorders caused in the
villages in Kasaragod.
Nevertheless, it is felt that the study must also consider other possible
causative factors as well. The causative factors must either be due to
some human-induced activity or due to some natural phenomenon.
Health and Environmental problems of this nature can also be caused by
human-induced activity which involves industrial processes especially of
hazardous nature related to radio active substances, heavy metals or
chemically hazardous substances. Fortunately, no such activity can be
found anywhere in Kasaragod District. Hence there is no possibility of
any other human-induced activity, other than endosulfan exposure to be
the causative factor. Moreover, there were also no possible sources of
contamination of air or water from across the borders of the State from
Karnataka.
The other possible causative factor raised by many scientists in the KAU
and also suspected by Dr. Mohankumar in 1997 ( though he does not
endorse it now) is the possibility of a background natural radiation or
heavy metal release. But the problem that has been identified have a
maximum history of only 26 years and not more than that. This is an
12
important matter that needs to be kept in mind while spelling out the
causative factors. It is very difficult to believe that background radiation
or heavy metal contamination can occur suddenly, out of the blue, 26
years ago, from the surrounding hills and water sources. The only
activity, which can possibly trigger such radiation or heavy metal
contamination, is a large scale mining operation as in the UCIL in
Jarkhand, where large-scale mining for Uranium ( a radio-active
substance) has triggered an unprecedented health crisis among the
surrounding communities. Moreover, there is always the possibility that
the background natural radiation/ heavy metal exodus, if any, may not
have been noticed or recorded earlier. If so atleast its effects must
surely have been felt earlier itself. In this case, no such effects has been
reported before 1979. Hence it is impossible that any sources of
radiation or heavy metal contamination is a possible causative factor.
Health impacts
The next important logical step is to ask the question- Are the aberrant
health problems seen in the villages in Kasaragod related to endosulfan ?
For establishing this crucial link, it is important to find out what acute
health problems were caused when endosulfan was aerially sprayed and
what are the aberrant health problems seen and reported from the
suspected areas.
Acute effects during and immediately after the spraying
The following acute effects were reported from places exposed to
endosulfan aerial spray
A Noxious smell fills the air and people find it difficult to breath.
The whole area carries a smoggy look.
Eye irritation, itching , sometimes with tears in the eye
Headaches and dizziness.
Suffocation and choking feeling.
Coarse feeling in the throat.
Skin itches, with swelling when scratched.
Seizures among grazing animals, sometimes leading to death.
Bleeding leading to abortion and sometimes death if the animal (cow,
dogs) were pregnant.
General issues of health.
People were found to be generally weak, getting tired quickly. Most of
the people were laborers or were involved in work mostly of physical
nature. They complained that they are not able to work as they used
to some years back. Earlier where they used to work for more than 8
hours, today they are not able to work for more than 2 or 3 hours.
13
Many people, including women and children were found to be anemic
and ailing from frequent fevers and diseases, indicating effects on the
immune system.
People, especially women look over aged.
Men, especially young men who were under grown, physically. 25 to
35 year old men looked only in their teens or early twenties.
People disclosed about many cases of infertility, which was high
among men. The local doctors also confirmed that infertility cases
were high.
Many people were being treated with hormones for a variety of
problems. The doctor also mentioned about cases of breast
enlargement in boys (gynaecomastia) which was an alarming
revelation.
Women were suffering from serious gynecological problems. Many of
them have had problems that have resulted in their Uterus removed.
A large number of women disclosed to the women members of our
team that they have menstrual problems.
There were cases of women taking hormonal treatment to correct their
hormonal cycles before their marriages
The ailing people approach the local doctors who find it difficult to
cure many of these chronic ailments and refer them to specialists at
Kanhangad or Mangalore. If their disease is complicated and need
special treatment or surgery they usually go to Mangalore.
Many of the ailments have not found a proper cure and now people
know that diverse unknown diseases are inflicting them. They even
know that the doctors are not able to diagnose their problems. So
they simply continue taking the high doses of medicines that are
being given.
Problems affecting the Skin
A number of people have skin problems ranging from small, frequent
itches to chronic cases like Psoriasis and Eczema . Many of them are
being locally treated as allergies and the doctors are generally not
inclined in finding the cause.
Rashes are found in the hands and the inner palms, with itching
which turns to septic boils.
Discolored patches appear on the skin with itching sensation.
Swelling of legs and hands, darkening of the skin. The swelling is
specifically reported by many of the plantation workers who are
directly in contact with the pesticide mixing and spraying operations.
One ex-worker disclosed that most of the plantation workers have
some sort of skin diseases or other. His daughter complained of
frequent swelling of the body and getting tired very quickly. She
disclosed of having gynecological problems as well. She revealed that
her periods stop soon after the spraying season and resume only after
3-4 months, during which time her blood sugar level also goes down
and she suffers from a variety of problems.
Some women reported frequent swelling of the whole body.
14
Problems affecting the Lungs, Throat etc.
A number of people were suffering from Cancer of the throat. Some of
them could not be interviewed as they had been hospitalised. One
case had only recently been diagnosed and their relatives asked us not
to meet him as he did not yet know he had cancer.
There were multiple cases of people, mostly men, who gradually lost
their voice and finally when pain set in, the disease was diagnosed as
Cancer of the throat or larynx.
Many men suffered from pain in the throat.
A very large percentage of the children were suffering from difficulty in
breathing, asthma etc. Children seem to have been the most affected
by this. They also get very frequent fevers, which sometimes last for a
month. We found one infant ( 6 months) suffering from a mild cold,
but administered with Amoxicillin tablets.
Many complained that soon after the spraying, they have throat
problems and some complained of loss of voice. Many have difficulty
raising their voice when speaking.
Problems affecting the Eye
Generally, people complained of itchiness and watery eye during the
spraying. The irritation sometimes continues for atleast three days,
during which the whole area bears a foggy look with visibility much
reduced.
a large number of people had problems related to vision, though it is
not known whether it is directly due to spraying. But it is now known
that long-term exposure to organochlorines can affect the nervous
system affecting hearing and vision.
Some plantation workers disclosed, on promise of anonymity, that
almost all the workers suffer from eye itching, burns, chronic
headache and sometimes loss of vision also.
Problems affecting the Stomach and Gastro-Intestinal system.
A good number of people, especially men get frequent stomach ache’s.
Sometimes vomiting accompanies such ache’s especially in children
The Staff Nurse at Navodaya Vidyalaya school at Periya reported that
in 1988 she had conducted a health survey of the locality with
participation from her school children. The report is unfortunately
misplaced now, but she remembers having seen a lot of cases of
stomach and intestinal problems.
Even though a number of such disorders were reported, some of the
aberrant diseases which had reached alarming proportions and are of
concern were also identified. It is felt that these have to be discussed
separately, due to its fatal and threatening nature.
15
Cancer
Survey conducted in Periya-Pullur , Muliyar, Cheemeni and Rajapuram
reported that a number of people were suffering from Oral cancer, cancer
of the throat and stomach, prostrate cancer and intestinal cancer. Local
doctors and the doctor at the Public Health Centre at Periya also said
that incidence of cancer especially the ones mentioned above was high.
Women at the same time seem to be affected more with breast cancer.
The comment by the Health Inspector of Vazhakkad who found that
cancer cases in Pananthadi (Kasaragod) were as common as in
Vazhakkad (Calicut, affected by the pollution from Grasim Industry )
corroborates the findings. Dr. Mohankumar, a doctor practicing in
Enmakaje has found from his observations of his patients that there were
51 cancer deaths in just 126 houses near the Kodenkeri Stream at
Enmakaje Panchayath. He enlisted 4 living cancer cases now in these
houses. Many of these cases, the doctor remembered were cancer of the
liver and blood. A survey done by Link-Trada of Mangalore also identified
11 cancer deaths in just 52 families in the last 5 years.
An analysis of the death records of some of the panchayaths also
suggested an increasing pattern of cancer deaths over the years. For
example, cancer deaths recorded in Enmakaje panchayath alone have
increased from 37 (1982-87) to 49(1988-93) and to 71 (1994-99). This
means an increase of 33% in just 6 years and 92% in 12 years.
Incidentally, this data does not include the deaths in the panchayath
which could have got recorded at Kasaragod Municipality, Mangalore,
Kanhangad or elsewhere were many of the patients die in hospitals.
Considering this also would only add to the already alarming percentage
of increase.
Comparatively, Meenja Panchayath which is an unexposed area away
from the PCK plantations did not show any significant increase in cancer
deaths over the same period. The recorded cancer deaths were 40 (198287), 32(1988-93) and 47(1994-99).
Reproductive System ailments
Almost all the families that had participated in the surveys and the
informal interviews revealed some sort of gynecological problem or other
in most women living near, in and around the plantations. Most of the
women at Periya, Cheemeni, Muliyar, Rajapuram were found suffering
from irregular periods, sometimes even twice or thrice a month, showing
a clear case of hormonal disruption, much possible with organochlorine
induced chronic toxicity effects. Many of them were suffering from
profuse bleeding during the periods and were in acute pain. There are
cases of periods getting stopped much before the menopause age. One
girl complained that soon after the spraying, her periods get stopped and
she suffers from hormonal problems. The periods then reoccur 3-4
months after the spraying season. Most of the married women with
children have gynecological problems, leading to the uterus being
16
removed. Many young women have irregular periods and other related
problems like pain, headache’s, dizziness, weakening of the body etc.
Women around the age of 30 looked beyond their age. They were also
found tired and weak, unable to do the work that their age should be
allowing them to do. It was understood from them that women take
hormonal treatment to correct their menstrual cycles, so they would not
have marital problems. Infertility and Miscarriages were also high.
Some cases of endometriosis have also been reported. Organochlorine
pesticides are known and proven to cause endometriosis and breast
cancer.
Men were found to be more elusive in talking about their reproductive
health problems. But some of them disclosed that they were suffering
from undescended testis. Infertility was also high in the area, especially
among men. It was learnt, with shock that boys had retarded sexual
growth and this was also leading to some sort of desperation. But social
ostracism was feared, especially related to reproductive health and it was
understandable that young boys and girls of age would not wish or be
allowed to disclose their sexual growth and reproductive health related
problems.
Central Nervous System related problems
The many surveys by the panchayaths along with local groups, especially
at Belur, Enmakaje and Muliyar and the survey done by SEEK and
Thanal in other villages revealed the presence of diseases which could be
connected to some form of Central Nervous System disorders. There
were too many cases of congenital anomalies with brain disorders like
cerebral palsy, retardation of mental growth, epilepsy, physical
deformities like stag horn limbs, deformed or part grown limbs.
Psychiatric problems, which is traditionally considered a mental health
problem is also on the increase. Today modern science do not consider
psychiatric problems as just a mental health problem, but also as a
nervous system problem which can be caused by neurotoxins. There is
growing evidence that suicides and suicidal tendencies may also be
caused by prolonged exposure to neurotoxins. Dr. Mohankumar in his
study has revealed that there are 38 cases of mental retardation, 49
psychiatric cases, 33 epilepsy cases and 11 suicidal cases in just 126
houses he surveyed. Similar cases have been reported from other
villages like Kumbadaje, Muliyar, Bellur also.
The deaths due to Rheumatism, Paralysis and arthritis are also on the
increase. Data from death records of Enmakaje Panchayath reveal a
nearly five fold ( 488%) increase of deaths due to rheumatic complaints,
arthritis, paralysis etc in the last 12 years. These are also linked to
weakening of the CNS as well.
While discussing congenital anomalies it is important to note that many
of the conventional understanding of toxicity and effects being related to
17
exposure levels and applied concentrations are being questioned and
have been rendered meaningless with newer findings.
A study “ A case-control study of pesticides and foetal death due to
congenital anomalies” reported recently in the journal Epidemiology
(12:148-156) by Bell EM, Hertz-Picciotto and JJ Beaumont have revealed
that there is “ a strong association between exposure to commercially
applied agricultural pesticides during a crucial period in foetal
development and the likelihood of foetal death due to congenital defects”
The study revealed that foetal death is more likely among mothers who
are living within a 9-square mile area in which commercial pesticide
spraying takes place during pregnancy. It was also discovered that risk of
foetal death is greater for exposures in week 3-8 compared to week 1-20.
This 3-8 weeks period is considered as the most vulnerable period in
human development (the period of “organogenesis”)
The exposure of organochlorine pesticides which are endocrine
disruptors can cause a variety of health ailments which may not be
directly linked to the causal substance. The endocrine disruption during
early development stages, even at insignificant levels can trigger
malfunctioning of thyroid gland and leading to failure in brain
development and complex development disorders in the foetus. In “Our
Stolen Future”, Theo Colborn et al concludes a chapter- Altered Destiny
saying e(As we wrestle with the question how much chemical contaminants
are contributing to the trends and societalpatterns we see - in breast
cancer, prostrate cancer, infertility, and learning disabilities - it is
important to keep one thing in mind. Scientists keep finding significant,
often permanent effects at surprisingly low doses. The danger we face is
not simply death and disease. By disrupting hormones and development,
these synthetic chemicals may be changing who we become. They may be
altering our destinies.99
A deeper and better understanding of the issue at Kasaragod is called for
and one needs to explore whether the problems like congenital anomalies
found in Kasaragod are just the direct effects on the CNS and the
endocrine systems or whether they are related to such complex problems
as developmental stage exposures.
A literature survey of health effects that endosulfan can cause
Now the question that has to be answered is whether toxicological,
epidemiological or medical studies have shown that endosulfan can
cause these aberrant diseases.
Endosulfan is an organochlorine insecticide of the cyclodiene subgroup.
It acts as a poison to a wide variety of insects and mites on contact and
as a stomach acaricide.
Human Beings may be exposed to endosulfan from
breathing air near where it has been sprayed
18
drinking water contaminated with it, from direct application, spray
drifts or runoffs;
eating contaminated food;
touching contaminated soil;
smoking cigarettes made from tobacco with endosulfan residues;
working in an industry where it is used or living near its vicinity.
Acute toxicity
Endosulfan is classified as a highly toxic substance. It is acutely toxic to
birds, marine and freshwater fish, and mammals. Like other chlorinated
cyclodienes, endosulfan is a neurotoxin affecting the central nervous
system (CNS) of aquatic organisms as well as mammals.
People who are occupationally exposed to endosulfan are advised to avoid
eye and skin contact as well as inhalation exposure. Symptoms of acute
toxicity in humans are restlessness, irritability and hyperexcitability,
followed by headache, dizziness, nausea and vomiting, blurred vision,
unconsciousness, insomnia, lack of appetite, loss of memory,
albuminuria, haematuria and in some cases, confusion.
Chronic toxicity
Chronic exposure to endosulfan may result in general toxicity symptoms
such as liver and kidney damage as well as effects on the CNS, immune
system and the reproductive system.
Neurotoxicity
Endosulfan may have adverse effects on the CNS of aquatic organisms,
birds and mammals. The main mechanism of action of endosulfan in the
CNS is inhibition of brain acetylcholinesterase, causing uncontrolled
discharges of acetylcholine. Abnormal behaviour has been observed in
fish and mammals being chronically exposed to endosulfan.
Carcinogen icity
Even though, endosulfan was not classifiable as to its carcinogenicity
(due to lack of sufficient data), studies have shown that it can be
carcinogenic. Reuber, 1981 showed that endosulfan was carcinogenic in
male and female rats at all sites examined. It also induced liver tumours
in female mice. Another study(Fransson-Steen, 1992) found that
endosulfan promoted the growth of altered hepatic foci in rats in a
similar manner as the structurally related chlorinated insecticides,
chlordane, aldrin and heptachlor did, indicating that endosulfan is a
potential liver tumour promoter.
Immune System
Endosulfan is also known to affect the immune system. Target organs are
the kidneys and liver. A number of studies have shown endosulfan to
hepatotoxic. Endosulfan inhibits leukocyte and macrophage migration
causing adverse effects on the humoral and cell mediated immune
system.
19
r
Reproductive Effects
K number of studies have shown a potential for adverse effects of
endosulfan in the reproductive system of aquatic organisms and
mammals. Histological changes in reproductive organs were seen in
aquatic organisms following exposure to endosulfan at concentrations as
low as 0.00075 mg/L (0.75 g/L). Endosulfan treatment in male rats was
reported to cause a dose-dependent reduction in sperm counts, sperm
abnormalities and decreased daily sperm production as well as decreased
testis weight.
Endocrine disruptive action
In vitro studies show endosulfan is estrogenic (in the E-SCREEN assay).
Endosulfan I competes with [3H] 17 -estradiol for binding to the estrogen
receptor. Endosulfan sulfate inhibited binding of [3H]R5020 to the
progesterone receptor by 40-50 per cent. Low levels of endosulfan (1 nM,
0.41 ppb) can inhibit the human sperm acrosome reaction, initiated by
progesterone and glycine, but the inhibition is not complete. Endosulfan
II and endosulfan sulfate decreased -galactosidase activity of
progesterone (Jin et al, 1997).
In vivo studies showed that Endosulfan decreased plasma vitellogenin
levels in catfish (Chakravorty et al, 1992). Endosulfan also decreased the
number and size of oocytes in fresh water teleost fish, and increased the
number of deformed oocytes, damaged yolk vesicles, and dilated
gonadosomatic index. It caused a dose-dependent reduction in sperm
counts in rats, reduced the number of spermatids, caused sperm
abnormalities and decreased daily sperm production.
Genotoxicity and Mutagenicity
Several independent studies have shown that endosulfan is genotoxic.
Data from in vitro and in vivo mutagenicity studies generally provide
evidence that endosulfan is mutagenic, clastogenic and induces effects
on cell cycle kinetics. (Syliangco, 1978; Adams, 1978; Yadav et al., 1982).
Endosulfan was also found to cause chromosomal aberrations in
hamster and mouse, sex-linked recessive mutations in Drosophilia, and
dominant lethal mutations in mice(Velasquez et al., 1984; Naqvi and
Vaishnair, 1993). Studies in human cells both in vitro and in vivo also
showed that endosulfan caused the occurrence of sister chromatid
exchanges indicating chromosomal damage(Sobti et al., 1983; Dulout et
al., 1985). Very recently, a team of researchers in Japan found further
evidence of endosulfan genotoxicity using sister chromatid exchanges,
micronuclei, and DNA strand breaks as detected by single cell gel
electrophoresis as biomarkers (Yuquan Lu et al., 2000).
Comments
From literature and the studies available from all over the world one
recognises that endosulfan is a highly toxic chemical, used widely as a
pesticide but with toxicological properties comparable with the likes of
20
DDT and Dieldrin, which have been banned in the country and is slated
for a global phaseout.
Endosulfan has been recognised as a chemical which can cause
endocrine disruptions, reproductive system disorders, central nervous
system disorders, liver and kidney dysfunctions in many studies on
animals and human beings - in vitro and in vivo. It has been shown to
display genotoxic, mutagenic and carcinogenic effects.
The health problems seen in the villages adjoining the PCK plantations in
Kasaragod have much in similarity to the kind of effects that can be
perpetuated by the prolonged exposure to endosulfan. The presence of
endosulfan in the environment is confirmed not only because CSE
studies established the same but primarily because endosulfan was
sprayed for more than 20 years, three times every year and its
cumulative presence in the environment is a non-negotiable reality. The
presence of these aberrant health issues and the various studies
confirming the toxicological and health effects of endosulfan are equally
non-negotiable realities.
The hypothesis of the people in the villages, suspecting endosulfan as the
causative factor for their various health problems is indeed true and is
supported by scientific studies on health effects of endosulfan exposure.
In these circumstances, there is a primary responsibility to acknowledge
that there is a problem existing suspected to be caused by endosulfan
exposure. It is now a proven fact that endosulfan is capable of causing
the health problems as seen in the villages in Kasaragod. It is extremely
sad to note the attempts from industry and associated scientists to label
endosulfan as a “safe” and “soft” chemical by alienating themselves from
new scientific findings and the realities.
What one needs to explore is
> what were the overall and specific conditions that led to such a
homicidal exposure to endosulfan
> what were the specific and overall mechanism that failed in
preventing such an exposure and consequent health issues
> who were responsible, to what extent and how such exposures and
poisoning can be avoided in future
> how such a chemical banned/restricted in many countries and
also recommended for restriction in India continued to be so
recklessly used
> what are the health problems that need to be remediated and
compensated and what is the mechanism for the same
> what are the environmental problems that endosulfan use has
triggered and the mechanism for remediation
21
e-
Household Survey to Assess
the Health and Environmental Impact
of Aerial Spraying of Endosulfan
in PCK Cashew Plantation
of Kasargode District
Kasargode District Committee
Kerala Sastra Sahitya Parishad
August 2001
Background
Padre village in Kasargocie district has become the focus of international attention recently. A
large number of inhabitants in the village are said to have physical deformities, disorder.-, of
the central nervous system and a various other diseases. A local doctor and journalist were
the ones who focused attention on the problem. They believed that the spraying of the
I
pesticide Endosulfan by the Plantation Corporation of Kerala was the cause.
I
Plantation Corporation of Kerala maintains a 2200 hectare Cashew estate that abuts 7
Panchayaths of the district. Aerial spraying of Endosulfan by helicopters has been going on
or nearly two decades to counter the pest
„„sqMo
■ (HdopelM ammi! S) The
estate ts s,mated amongst a heavily popdated area and people live even w,ihi„ 100 meters of
its borders.
Endosulfan is an organochlorine chemical. It is r
a cream-to-brown-colored solid that may be
in crystals or flakes and smells like turpentine and is an
insecticide used to control insects on
grains, tea, fruits, vegetables, tobacco, and cotton.. Sold
as a mixture ol two different forms
of the same chemical (alpha- and beta-endosulfan)
, it degrades into the sulfate form in the
soil.
Endosulfan enters the environmenj primarily through spraying
f„rm crops „ d„cs
dissolve easily i„ water. In soil, some endosulfan evaporates into air and some breaks down.
It may stay m soil for several years before it all breaks down. |, may aee.mmla.e in lire bodies
Offish and oilier organisms dial live in endosulfan-conlaminated waler.
Endosulfan mainly affects the central nervous system. Aeeidenlal ingestion and breathing of
ugh levels of endosulfan results in convulsions and death. Hyperactivity, tremors, decreased
resprratron, and sal.vation have also been noted in people who ingested high levels of i,
These levels are many thousands of limes higher than the average exposure. We don't know
t >e effects from long-term exposure to low levels of endosulfan. Animal studies have shown
effects on ,he kidneys, icsles. developing fems. „„d liver from tonger.tcrrll CX|)ost|K
evels of endosulfan. The abilily of animals to light infection was also lowered. It is also now
mown to be an endocrine disrupting chemical with estrogen like actions
Kerala Sasrra S.hi.ya Parish.d (KSSP) is a People's Science Movement with grassroots
workers in all districts of the State. We. the KSSP district committee of Kasargode
considered this a serious issue tbal needed a seiemilic study. We fel, ihat chronic low dose
toxicity in humans though not documented in scientific literature is plausible in this case,
given the peculiarities of terrain and habitat as well as continued aerial spraying with
inadequate precautions over a long period. It is difficult to establish cause-effect iclalionships
by chemical measurements in low-level exposures, particularly lor birth defects, mental
retardation etc. For this reason we felt that a household survey for measuring disability and
morbidity and comparison with the population of the state (for which data exists) would be
invaluable. The survey was designed and conducted with the help of the KSSP Environment
center, Thrissur.
Objectives
To assess
1. Whether proper safety precautions were observed during aerial spraying of
Endosulfan by the PCK plantations
2. The impact of the pesticide spraying on the environment around the PCK plantations
3. The impact on human health particularly in relation to the rates of disability, chronic
morbidity and reproductive health
Methods
Household survey was conducted in 7 panchayats surrounding the Plantation area. The
households situated within 500 meters of the plantation border were the ones surveyed. .
Questionnaire was prepared by the Environment sub-committee of the Kerala Sastra Sahitya
Parishad. The volunteers for the household survey were given one day training held at
Cheemeni, Chalinkal, Panathadi, Rajapuram, Mooliar, and Badiyadukka.
A total of 747 househols having 4102 inhabitants were surveyed. The breakup of household
according to the Panchayats is given below.
Table 1
Distribution of the sample
[ Pan chav a t/B lock (PCK)
Number of households
Aren A
288
Cheemeni
----- --------Panathur
43
126
Kajapuram
33
Periya
70
Kottur
34
Mooliyar
A rea B
153
Enmakaje
747
Total-
Results
Demographic and household details
are similar in the two
Tables 2 and 3 show relevant demograph ic details. Consanguinity rates
ion of childless couples is about three times higher in Enmakaje
study areas. The proportion
areas. In both areas the vast majority have been in residence
(Area B) compared to the other
for more than 10 years.
There is a sinking difference in .he main source of «er in .he two areas. (Table 4).
Eunial.aje more than one ihod the popnia.ion depends n.ainiy on Sn.angan.s to n.ee. .hen
water needs.
Tabic 2
Some demographic features in the sample
Pa ra meter
Area A
Area B
AH
■3692’’
'1010^
4T02
TTT”
6.6
5.49
6.3
7.4
C6”
Sample size
Family size
Consanguinity rate (per 1000)
Childless couples (per 1000)
6.6
2
____
Table 3
Years of residence in the area (% of families)
Area
5 years
5-10 years
10 years
Area /\-
10.8
118
76.4
Area B (Enmakaje)
8.5
7.8
83.7
All
10.3
11.8
77.9
Table 4
Main water source of the households (%)
Area
Well
Tube well
Su ran gam
Other
Area A
87.9
6.1
52
0.8
Area B (Enmakaje)
54.2
0.6
36.6
8.5
All
81.0
5.0
11.6
2.4
Tables
Answers to questions asked to assess observance of safety precautions by the company
and people (% of families)
Area A
Area B
All
Company informs us prior to spraying
51.9
18.3
45.0
Company supplies material to cover waler bodies
36.4
3.3
29.6
Spraying done only during stipulated time
29.2
11.8
25.6
Wells are covered during time of spraying
47.6
9.2
39.8
Keep indoors during spraying time
25.4
18.3
24.0
Pesticide falls in the compound
66.7
75.5
68.4
Pesticide falls on body of family members
53.0
75.2
68.4
Response
Obsevance of safety regulations
Data in Table 5 shows that safety precautions are not practiced satisfactorily by the company
and the majority of people. This is more strikingly so in Enmakaje. (The somewhat better
figures in the rest of the areas arc mainly due to the data from 288 households in Chccmeni
Panchayath where there were some protests in the early 1990s.)
Majority in both areas testified that spraying is done throughout the day and not merely in the
stipulated time.
Further it was unanimously claimed that the height from which spraying was done is much
mor e than the mandated 5 meters.
Environmental impact
In both areas (more in Enmakaje) a majority of observants felt that there has been a reduction
of small animals like fish and frogs in the area in recent years after the spraying of pesticides
started. Fish kills with floating dead fish is said to be common occurrence. Bee rearing was a
common practice previously. Now most people have given it up because bees do not return
after flying off to gather honey. Putting the soil from the area into river water often resulted
in fish kills.
Birds arc strikingly few in Padre (Enmakaje Panchayath). So are frogs and fish according to
residents. Squirrels have virtually disappeared. People in all areas said that animals dying
after spraying was common. Snake deaths are reported from Periya.
Infertility in cattle was reportedly ver}' high in Enmakaje.
Tabic 6
Answers to questions asked to assess environmental impact ( % of families)
Area A
Area B
All
Yes
6.3
42.5
18.1
Yes
4.8
6.3
5.3
Do you feel that there has been a
Yes
40.2
79.7
48.3
reduction of small animals like frogs, fish
No
14.4
9.8
13.7
and bees in recent years ?
Don’t know
39.2
10.5
333
Is it common to find dead fish, frogs etc.
Yes
37.5
74.5
45.1
in the aftermath of spraying?
No
14.8
15.7
15.0
Don’t know
48.8
7.8
40.4
Question
Response
Are there infertile cattle in you house?*
Are there cattle with birth defects in your
house?*
* denominator is households owning cattle
i
Kcrala accordmg to the
Disability and Chronic Morbidity
Disability
« 73 % ",sher ti"mak’,C “a'by Kerala Sasir. Sahiiya rarisbad in 1
"
Xe levei bd-oK b.* snrvey eanduoa by U
by ,M%.
L«»r disabiW and a,„ compared l0 Karaia in .be KW
Ltoyise Chronic morbidity is b,Eber y
study-Both total disability and chronic morb'd
ditfoent ,n Area
,
Ln compared to the State figures. (Tab
Table 7 „
Disability rates (per 100000)
Area A
Area B
All
(K'SSP)
Disability'
693
614
■495"
Locomotor
634
■5267
Visual
TTT
rTTFuTTFicm
T132
■ITT
7079
"^3fF
TsF”
244^
'tm'
Hearing
Kerala 1996
■7365
7"
133...
1
244
T
I
TtT
Pfotal
Tab'e 8
• n and Arthritis)
1)i(lity1,tr1»00(eseludingDmbe-'”'’'r‘CnS‘’ '
Chronic morbidity I
Rate
Sample
__
Area A
___
pkrea B
fTT
21
Wera7T996 (KSSP^
°::z..
'mF’
Tot'
TsTT
"77.6
.................. .. ......... -
In all areas surveyed, it is abundantly clear that the proper precautions were ignored and rules
flouted by the company. Aerial spraying is practiced in countries like Australia and the US
where there are vast stretches of farmland on Hat terrain. Here, on the other hand, is an
undulating terrain heavily admixed with human habitation. It is impossible to spray from a
height of less than 5 meters, and frequently the spraying was done above a height of 10
meters or more, thus increasing the chance of drift into the surrounding houses and water
bodies.
The Environmental impact was also seen in all areas studied. Though higher in Padre village
of Enmakaje, none of the other areas were exempt. The human health indicators however
showed a difference. In Enmakaje - focus of the controversy - the disability rates were nearly
twice that of the State average. Chronic morbidity was also significantly higher. There was no
significantly high level of consanguinity. Moreover, the problems were mostly seen in the
young, and according to the residents, was not known a generation ago.
In the other areas, disability and morbidity indicators were not significantly higher than the
state average and hence the environmental assault is of a lesser magnitude. The reasons for
this difference has to be studied. One possible reason relates to the water source in the two
areas. In Padre, large number of families depend exclusively on Surangams. d hey are tunnels
cut through rock that collects rainwater from the hilly catchment above. In case of Padre,
polluted water from the plantation in the hills above. Continuous consumption of this water
for a long time can mimic health effects produced in animal studies. Exposure to expectant
mothers could result in birth defects to the fetus and the estrogenic effects could result in
reproductive failure in adults.
This study does not furnish absolute and final proof that Endosulfan has produced all the
health problems in Padre or Eco-damage in the whole region. But such proof cannot by
obtained by any kind of study. There is however, sufficient reason to suspect it as the most
likely contributing cause.
The burden in such cases - especially when human life and health is in peril - should not be
to prove the cause-effect relationship, but rather to disprove it.
There is sufficient reason to discontinue the use of Endosulfan in the Cashew plantations of
Kasargode district and seek alternate pest control measures. Any Economic or ‘cost-benefit'
arguments to the contrary would be callous, unethical and a gross human rights violation.
r\
References
.
ATSDR. 1993. Toxicological profile for endosulfan United S'ates Agency for Toxic
Substances and Disease Registry, Atlanta. GA. Available from NT1S, Spungfield.
.
AravinTan KP^Kunhikannan TP (eds) Health transition in rural Kerala 1987-1996.
Kerala Sastra Sahitya Parishad. Kochi 2000.
A
WWF
November 12, 2001
Public Information and Record Integrity Branch
Information Resources and Services Division (7502C)
Office of Pesticide Programs
Environmental Protection Agency
1200 Pennsylvania Ave., NW.
Washington, DC 20460
RE: docket control number OPP-34242: Endosulfan
World Wildlife Fund (WWF) submits the following comments regarding EPA’s risk assessment
of endosulfan. WWF is a non-profit organization with over 1 2 million members in the U.S.
WWF is dedicated to using the best available scientific knowledge to preserve the diversity and
abundance of life on Earth by conserving endangered spaces, safeguarding endangered species,
and addressing global threats to the planet’s web of life.
Endosulfan is a broad spectrum organochlorine insecticide that has been used since the 1950s on
a wide variety of crops in the U.S. and globally. An estimated 1.4 million to 2.2 million pounds
of endosulfan are applied annually in the U.S.. Endosulfan is used in most states, especially in
Arizona, California, the Pacific Northwest, Texas, the Southeast, Maine, and in states located
between Delaware and New York west to Indiana and Michigan. Use on New York apples,
Mississippi cotton, Tennessee lettuce, Georgia pecans, Maine potatoes. North Carolina tobacco,
and Florida tomatoes represents ~ 70% of the total amount of endosulfan used. Technical
endosulfan is composed of a mixture of the a-endosulfan (-70%) and 0-endosulfan (-30%)
isomers.
EPA considers endosulfan a very persistent and highly toxic pollutant. For these reasons EPA
has proposed endosulfan as a candidate for the development of National Action Plans under the
PBT (Persistent, Bioaccumulative, Toxic) Initiative. Currently the data regarding endosulfan
bioaccumulation are mixed in terms of environmental fate. This insecticide has a relatively high
octanol/water partition coefficient (K0W= 55500-61400) and bioaccumulation factors up to
2429X for edible tissue, although its depuration rate from fish hinders further bioaccumulation in
the food web. Because the studies generating the above data do not follow current guidelines,
EPA has requested a new bioaccumulation study to clarify the actual extent of bioaccumulation
and the rate of depuration of endosulfan and/or its transformation products in fish. We concur
that better data are needed to fully evaluate this pesticide’s fate in the food chain.
World Wildlife Fund
1250 Twenty-Fourth St., NW Washington, DC 20037-1132 USA
Tel: 202.293.4800 Fax: 202.887.5293
www.vvorldwtldlife.org
Affiliated with World Wide Fundfor Nature
Endosulfan is also a semivolatile compound that can be detected in places where it has never
been directly applied, such as the Arctic and national parks. The primary endosulfan metabolite
of toxicological concern in plants, animals and the environment is endosulfan sulfate, which is
considered to be of equal toxicity to endosulfan, although it is more persistent than the parent
compound. For the purposes of endosulfan risk assessment the a- and p-isomers and endosulfan
sulfate are considered to be of equal toxicity.
Endosulfan’s predominant toxicological effect is over stimulation of the central nervous system
due to inhibition of Ca?^, Mg2< - ATPase and antagonization of chloride ion transport in gammaaminobutyric acid (GABA) receptors. Both endosulfan isomers, along with dieldrin, ketoendrin,
toxaphene and hepatochlor epoxide have been shown to competitively bind with GABA
receptors. Neurological effects characteristic of endosulfan exposure include hyperactivity, tonic
contractions, involuntary muscle movements, pronounced sensitivity to noise and light,
incoordination, seizures, and convulsions. In addition, endosulfan is considered to be an
endocrine disruptor impacting estrogen, androgen and thyroid hormone systems (Table 1). With
respect to wildlife species endosulfan is moderately toxic to honey bees (LD50 = 4.5 ppm),
highly toxic to birds (mallard duck LD50 = 28 ppm) and mammals (laboratory rat LD50 =10
ppm) and very highly toxic to freshwater and esturarine/marine fish and invertebrates. It is not
surprising that endosulfan is one of the most frequently reported (5% of reported incidents)
causes of aquatic incidence reports; only organophosphate pesticides and carbofuran are higher.
MAIN CONCLUSIONS
We believe the conclusions in the endosulfan Environmental Fate and Effects Division
(EFED) chapter do not support the re-registration of endosulfan. The risk assessment
greatly underestimates risk to wildlife by failing to consider endosulfan sulfate exposures.
Even with this significant omission, the EFED assessment shows that endosulfan use will
result in serious harm to wildlife. For example, for tomato use alone (considered to be a
vulnerable crop) it was estimated that there is a 90% probability that approximately 60%
of all aquatic species will suffer 50% mortality. Even for a less vulnerable crop like apples,
EPA estimates that there is a 10% probability that 10% of all aquatic species will suffer
50% mortality. We believe the high acute and chronic risks to wildlife, including
endangered species, warrant regulatory action.
IS EPA nevertheless chooses to reregister endosulfan, we believe at least the full 10X FQPA
safety factor should be applied to take into account evidence of 1) increased qualitative
susceptibility to developing organisms, 2) evidence of endocrine disruption and 3)
developmental neurotoxicological data gaps.
COMMENTS ON THE ENVIRONMENTAL FATE AND EFFECTS DIVISION
(EFED) RISK ASSESSMENT
We present the following specific comments to emphasize our position that the EFED
assessment does not support, endosulfan re-registration. EPA’s refined assessment uses non
conservative assumptions, “typical” application rates and the assumption of a 300-foot spray
drift buffer, yet 88% of crops modeled are predicted to exceed acute high risk levels of concern
2
(LOCs) more than 99% of the time to aquatic organisms. Similarly, chronic effects are also
expected for endosulfan with risk quotients (RQ) calculated to be as high at 487. It is worth re
emphasizing that this assessment does not use particularly conservative assumptions and does
not include risk due to endosulfan sulfate, the primary degradation product, which is considered
equal to the toxicity of endosulfan and more persistent than the parent compound.
Chronic LOCs were exceeded for birds and mammals while acute high risk, restricted use and
endangered species LOCs are exceeded for freshwater and estuarine/marine fish and
invertebrates. The chronic RQs for freshwater and estuarine/marine fish and invertebrates range
from 2.2 to 487. The EFED assessment states that “ In general, the magnitude of the aquatic RQ
values is high enough that reduced application rates and the use of buffers does not reduce the
likelihood of exceeding either acute or chronic LOCs” (p. 23). The labeled single appl ication rate
for endosulfan on pecans is 1.5 Ib/A. In order to avoid exceeding acute LOCs for the striped
bass, the maximum application rate would have to be reduced to 0.007 lbs a.i./A.
The inclusion of endosulfan sulfate in the assessment would only increase risk associated with
endosulfan use.
The Calculated Risk Quotients (RQs) are underestimates of endosulfan toxicity
Failure to include endosulfan sulfate in surface and groundwater Estimated Environmental
Concentrations (EECs)
It is unclear why EPA chose to combine residues of a-endosulfan, p-endosulfan and endosulfan
sulfate in the HED assessment, but not in the EFED assessment. Combined residues presented in
the HED assessment for surface water are 8.1 pg/L (peak) and 1.3 p.g/L (chronic) while the
combined residue for ground water is 0.012 pg/L (p. 8). These combined residue values appear
to be simply the sum of total endosulfan (comprised of a-endosulfan and p-endosulfan isomers)
and endosulfan sulfate presented in the EFED assessment. In contrast, the EFED assessment
only considers endosulfan EECs when conducting crop specific RQs, although EECs for
endosulfan and endosulfan sulfate residues appear to be available as they are presented in various
tables throughout the EFED assessment. Given that endosulfan and endosulfan sulfate are
considered to be similar in toxicity, use of the same combined residues in the EFED assessment
as is used in the HED assessment would only further increase RQ values that already indicate
very high risk to aquatic organisms. We suggest EPA recalculate EEC using the combined
residue measurement to present a more accurate representation of risk to wildlife species.
Chronic risk to freshwater invertebrates is based on an inappropriate extrapolation
Chronic risk to the most sensitive freshwater species (rainbow trout and the invertebrate
crustacean scud) were estimated based on the observed ratio chronic to acute toxicity of 0.1 from
fathead minnow data. However the EFED assessment recognizes this as a nonconservative
extrapolation because a similar chronic/acute ratio calculated for invertebrates result in a value of
0.01. Thus, the EFED assessment chose to use a ratio of 0.1 based on the fathead minnow to
extrapolate from acute to chronicYisk for the invertebrate crustacean scud, despite calculating a
ratio of 0.01 based on invertebrate data.
3
In addition to these specific comments on the endosu'tan spec''^
general characteristics of EFED assessments that underestimate risk
Chronic risks are based on a
wild
species
.p
NOF.C while acute risk arej2asgd oiLLQll^-1^0
There is internal inconsistency regarding risk assessmem
scenarios. Chronic risks are based on t e no o serve
^Xn^NOEC), while acute
mortaiitv (LC50 or LD50). 11 seems
species where short-tene exposures
I
tta
, 0| LC, () which wou|d be
reproduction. A justification for
insisted with the NOEC used in chronic risk assessment, would be a useful addition to
more c~--------the EFED assessment.
Risk quotients are calculated in a crop“Specific niajinei.
Risks to wildlife species are presented on a crop by crop basis. FaiHng to consider a^egate risk
assessments (risks from all crop treatments simultaneously) a practicej4.’ren
aggregate risk assessment ofHED further underestimates risk to wildlife species.
COMMENTS ON THE HEALTH EFFECTS DIVISION (HED) RISK ASSESSMENT
The full 10X FQPA Safety factor should be applied to endosulfan because of evidence of
increased developmental susceptibility and significant data gaps, including endocrine
disruption
We stronidv encourage EPA to telain at least a I0X safety factor lor endosulfan We believe the
definition°of “increased susceptibility” adopted by the FQPA Safety Factor committee is. narrow
d
ores evidence of qualitative susceptibility In addition, die committee choses 0 overlook
significance of endocrine dismptor data gaps tor embryos, fetuses, infants and children
Evidence on developmental susceptibility
The FOPA Safety Factor Committee determined that there was no evidence of increased
auanfnative susceptibility based on developmental rat and rabbit studies and m a rat reproduction
studv However m the rat reproduction study increased pituitary and uterine weights were
observed in developmentally exposed females. These endpoints could be interpreted'ev.den
ofqXdve increased susceptibility because they are considered more severe than effetfs
observed in parental animals (decreased body weight). The committee instead chose to focus o
:Xce ofquXive susceptibility. I e a simple comparison ofihe*“eiXIX
adult and developmentally exposed animals. We also found it troubling tl
the effects
Committee questioned the significance of the pituitary and uterine effects becaus the efiec s
were not consistent between generations and the target organ toxicity was not seen my
study. To the contrary, we believe these findings only strengthen the widely articulated
4
argument that functional developmental effects may not be accurately predicted based on adult
exposure and/or developmental studies that focus on structural teratology assessed at birth.
We also note that there is evidence of increased quantitative response to endosulfan in young iats
compared to older animals (Kiran, 1990). Oral administration of 12.5 mg endosulfan per kg body
weight for four days inhibited erythrocyte membrane Na . K -Al Pase and Mg -A Pase k <
greater extent in animals initially exposed at 1 5 days compared with animals exposed at 30, 70
and 365 days of age. The percent inhibition of'Na' K -ATPase activity was 34/o tn 1-> day u.
rats and 117% in 365 day old rats. Similarly, Mg -ATPase activity was inhibited 35.3 /o in .
day old rats and 17.6% in 365 day old rats. In both these cases, percent inhibition decreased
consistently as animals aged.
Developmental neurotoxicity and endocrine disruptor data gaps
The FQPA Safety Factor Committee has applied a 3X safety factor to endosulfan due to the
developmental neurotoxicity study. However, it sidesteps discussion of the potential for
endocrine disruption in embryos, fetuses, infants and children because endocrine screens and
assays have not been finalized. Subjecting endosulfan in the future to finalized screens and
assays is likely to only confirm what EPA already knows - that endosulfan is an endocrine
disrupting chemical in mammals and fish. It is also worth reiterating that the endpoints
suggestive of qualitative increased susceptibility are endocrine related (increased pituitary am
uterine weight in developmental exposed female rats). The FQPA Safety Factor represents one
available mechanism to account for endocrine disrupting effects until appropriate screens and
assays can be developed. In addition, we note that the endosulfan rat reproduction study (the
“gold standard” for evaluating endocrine disrupting effects) described in the draft assessment
was conducted in 1984, before 1996 guideline changes which added additional endpoints
responsive to estrogenic and/or androgenic endocrine disruption. (Table 2, summarized from
Federal Register: October 31, 1996; Vol 61, No 212; Pp 56273-56322). EPA faces an unenviable
struggle with consistent application of the FQPA safety factor, but it must not discount endocrine
disruption simply for the sake of consistency with prior tolerance decisions, particularly if doing
so ignores areas of science especially relevant to embryos, fetuses, infants and childien.
To date, much of the discussion of endosulfan’s endocrine disrupting properties has focused on
interference with estrogen interaction and reproductive effects. However, endosulfan has also
been demonstrated to have effects on thyroid hormone in fish (Table 1). These effects include
thyroid histopathology and altered thyroid hormone levels. More specifically, endosulfan has
been shown to increase T4 (considered to be the biologically inactive precursor to T3) and
decrease T3 levels (considered to be the thyroid hormone that is biologically active at the tissue
level) and decrease T3/T4 ratio (S-inha,1991). The effects of endosulfan on thyroid hormone
levels in mammals do not appear to have been studied, although parathyroid hyperplasia and
thyroid follicular damage has been reported in rats (Table 1). Potential effects of thyroid
disruption on developing organisms should also be considered in the risk assessment. Maternal
hypothyroidism (increased TSH, usually associated with decreased T4 and/or T3) is well known
to have detrimental effects on cognitive and psychomotor development of the offspring
(Haddow,1999, Morreale de Escobar,2000, Pop, 1999). A recent study found the odds ratio for
children having an IQ more than 1 standard deviation below the mean was 4.7 (95%CI 1.5 to
5
14) for women with a 17 week gestation TSH value equal to or greater than the 99.85"’ percentile
those already at risk for congenital hypothyroidism (estimated to be 1 in 4,000 by the lh\K
Foundation of America). The potential for endosulfan to induce developmental hypothyroidism
is yet. another justification for applying at least a 10X safety factor.
The selection of a safety factor has great implications for estimating endosulfan dietary risks.
OPP estimates that acute dietary risks for children 1-6 years of age are 70/o and 51 /o of the acute
Population Adjusted Dose or aPAD (0.005 mg/kg/d), depending upon whether weighted or
unweighted FDA data are used to estimate dietary exposure. Application of the frill 10X sa y
factor would result in the acute dietary exposure for this group at the 99.9 percentile to be 234/o
(0 003511 mg/kg/d; without using weighted FDA data) and 170% (0.002552 mg/kg/d, using
weighted FDA data) of the aPAD (0.0015 based on a 10X safety factor). Similarly the chronic
dietary food risk to children 1-6 would also increase to approximately 20% of the chronic
Population Adjusted Dose or cPAD based on weighted and without using weighted FDA data.
These findings are particularly relevant to farmworker children who are likely to have increased
levels of exposure and for whom EPA has not conducted a dietary risk assessment.
Update of endocrine table
Appendix A of the toxicology chapter on endosulfan summarizes key endocrine-related effects
resulting from endosulfan exposure
http://www.epa.gov/pesticides/reregistration/endosulfan/toxendosuLJLPQE) Th18 appendix is
well organized and thorough, although we note that additional endocrine related findings in
wildlife species should be included. Studies described in Appendix A are presented m Table I
along with additional endocrine-related studies not originally presented in Appendix A.
In summary, we believe endosulfan’s high potential to adversely affect wildlife species,
especially aquatic organisms does not support its re-registration. Should EPA nevertheless opt to
register endosulfan, it should retain the 10X safety factor to protect embryos, fetuses, in ants anc
children.
r'0-
6
We appreciate the opportunity to provide these comments in response to the endosulfan HED
and EFED assessments.
Sincerely.
Theo Colborn, PhD
Senior Program Scientist and Director
Wildlife and Contaminants Program
(202) 778-9643
Kristina Thayer, PhD
Program Scientist
Wildlife and Contaminants Program
(202) 822-3473
kristina.thayer@wwfus.org
Sarah Lynch, PhD
Senior Program Officer
Center for Conservation Innovation
(202) 778-9781
lynch@wwfus.org
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Bhattacharya L. Histological and histochemical alterations in the thyroid activity of endosulfan
treated Oreochromis mossambicus. Journal of Environmental Biology 16:347-351(1995)
Brieske J, Mousa M, Madhukar B, Boyd S, Chou K. Anti-androgenic potential of endosulfan and
its microbial transformation products. Organohalogen Compound 34:357-359(1997).
Cerkezkayabekir A, Aktac T. The histopathologic effects of endosulfan on the mouse thyroid
gland. Turkish Journal of Biology 21:439-444(1997).
Chakravorty S, Lal B, Singh TP. Effect of endosulfan (Thiodan) on vitellogenesis and its
modulation by different hormones in the vitellogenic catfish Clarias batrachus.
Toxicology 75:191-198(1992).
Edwards J A, al e. Effect of endosulfan-techincial (code 02671 01 AT209) on reproductive
function in the rat. Hoeschst Aktien-gesellschaft Huntingdon Research Centre, Study//
HST204/83 768(1984).
Gill TS, Pande J, Tewari H. Effects of endosulfan on the blood and organ chemistry of
freshwater fish, Barbus conchonius Hamilton. Ecotoxicology & Environmental Safety
21:80-91(1991).
Gimeno L, Ferrando MD, Sanchez S, Andreu E. Endosulfan effects on liver and blood of the eel,
Anguilla Comparative Biochemistry & Physiology C 108:343-348(1994).
7
Haddow JE Palomaki GE, Allan WC, Williams JR, Knight GJ, Gagnon J, O'Heir CE, Mitchell
ML, Hermos RJ, Waisbren SE, Faix JD, Klein RZ. Maternal thyroid deficiency during
pregnancy and subsequent neuropsychological development of the child. N Engl J Med
341:549-55.(1999).
Hemmer MJ, Hemmer BL, Bowman CJ, Kroll KJ, Folmar LC, Marcovich D, Hoglund MD,
Dens’low ND. Effects of p-nonylphenol, methoxychlor, and endosulfan on vitellogenin
induction and expression in sheepshead minnow (Cyprinodon varieyatus). Environmental
Toxicology & Chemistry 20:336-343(2001).
Hodges LC, Bergerson JS, Hunter DS, Walker CL. Estrogenic effects of organochlorine
pesticides on uterine leiomyoma cells in vitro. Toxicological Sciences 54.355-364(2000).
Kiran R, Varma MN. Age related toxic effects of endosulfan on certain enzymes of rat
erythrocytes. Indian Journal of Experimental Biology 28:69?-696(1990).
Morreale de Escobar G, Obregon MJ, Escobar del Rey F. Is neuropsychological development
related to maternal hypothyroidism or to maternal hypothyroxinemia? J Clin Endocrinol
Metab 85:3975-87.(2000).
NCI. Biassay of endosulfan for possible carcinogenicity (CAS# 115-29-7) and NC1-CG- FR-62.
Report. Hazelton Lab. Inc., Vienna:DREW Publ# (NIH) 78-1312. NCI Technical Report
No. 62, 1978. MRID# 00004256(1978).
Newbold RR, Jefferson WN, Padilla-Banks E, Walker VR, Pena DS. Cell response endpoints
enhance sensitivity of the immature mouse uterotropic assay. Reprod Toxicol 15.24552.(2001).
Park D, Hempieman SC, Propper CR Endosulfan exposure disrupts pheromonal systems in the
red-spotted newt: a mechanism for subtle effects of environmental chemicals.
Environmental Health Perspectives 109.669-673(2001).
Petit F, Le Goff P, Cravedi JP, Valotaire Y, Pakdel F. Two complementary bioassays for
screening the estrogenic potency ofxenobiotics: recombinant yeast fortrout estrogen
receptor and trout hepatocyte cultures. Journal of Molecular Endocrinology 19.321335(1997).
Pop VJ, Kuijpens JL, van Baar AL, Verkerk G, van Son MM, de Vijlder JJ, Vulsma T,
Wiersinga WM, Drexhage HA, Vader HL. Low maternal free thyroxine concentrations
during early pregnancy are associated with impaired psychomotor development in
infancy. Clin Endocrinol (Oxf) 50:149-55.(1999).
Rambabu JP, Rao MB. Effect of an organochlorine and three organophosphate pesticides on
glucose, glycogen, lipid, and protein contents in tissues of the freshwater snail Bellamya
dissimihs (Mueller). Bulletin of Environmental Contamination & Toxicology 53:142148(1994).
8
Rastogi A, Kulshrestha SK. Effect of sublethal doses of three pesticides on the ovary of a carp
minnow (Rasbora dan icon ins'). Bulletin of Environmental Contamination & Toxicology
45:742-747(1990).
Shelby MD, Newbold RR, Tully DB, Chae K, Davis VL. Assessing environmental chemicals for
estrogenicity using a combination of in vitro and in vivo assays. Environmental Health
Perspectives 104:1296-1300( 1996).
Singh SK, Pandey RS. Effect of sub-chronic endosulfan exposure on plasma gonadotropins,
testosterone, testicular testosterone and enzymes of androgen biosynthesis in rats. Indian
Journal of Experimental Biology 28:953-956(1990).
Sinha N, Lal B, Singh TP. Effect of endosulfan on thyroid physiology in the freshwater catfish,
Clarias batrachus. Toxicology 67:187-197( 1991).
Sinha N, Lal B, Singh TP. Pesticide induced changes in circulating thyroid hormones in the
freshwater catfish Clarias batrachus. Comparative Biochemistry & Physiology C
100:107-110(1991).
Sinha N, Narayan R, Shanker R, Saxena DK. Endosulfan-induced biochemical changes in the
testis of rats. Veterinary & Human Toxicology 37:547-549(1995)
Soto AM, Chung KL, Sonnenschein C. The pesticides endosulfan, toxaphene and dieldrin have
estrogenic properties in human estrogen-sensitive cells. Environmental Health
Perspectives 102:380-383( 1994).
Soto AM, Sonnenschein C, Chung KL, Fernandez MF, Olea N, Serrano FO. The E-SCREEN
assay as a tool to identify estrogens: an update on estrogenic environmental pollutants.
Environ Health Perspect 103:1 13-22.( 1995).
Turner KO, Syvanen M, Meizel S. The human acrosome reaction is highly sensitive to inhibition
by cyclodiene insecticides. J Androl 18:571-5.(1997).
Vonier PM, Crain DA, McLachlan J A, Guillette LJJ, Arnold SF. Interaction of environmental
chemicals with the estrogen and progesterone receptors from (he oviduct of the American
alligator. Environmental Health Perspectives 104:1318-1322(1996).
Zou E, Fingerman M. Effects of estrogenic agents on chitobiase activity in the epidermis and
hepatopancreas of the fiddler crab, Uca pugilator. Ecotoxicology & Environmental
Safety 42:185-190(1999).
9
TABLE 1. ENDOSULFAN ENDOCRINE-RELATED STUDIES
in vivo studies
study design/reference
acute
1 injection - PND17 or
injection daily PND 17-19
(Newbold,2001)
acute PND 17-19
(Shelby, 1996)
dose
0.1-1,000,000
gg/kg
3 day exposure to
immature rats
(Ashby, 1997)
two-generation
(Edwards, 1984)
5-100 mg/kg
not uterotropic-
6.18 mg/kg'd
increased uterine weight (female pups in the Fib generation)
increased pituitary weight (female pups in the F0 generation)
rat
chronic
(NCI, 1978)
20.8 mg/kg/d
rat
chronic
[Singh. 1989 #12]
15 and 30 day
(Singh, 1990)
species
mouse
mouse
rat
rat
rat
1-1,000,000
H&/kg
70 day study
(Sinha, 1995)
2.5 mg/kg/d
mouse
acute
(Cerkezkayabekir, 1997)
20 days
(Bhattacharya, 1995)
4.16 mg/kg/d
96 hours
(Sinha. 1991)
0.008 mg/L
freshwater catfish
CClarias batrachus
•
7.5 and 10
mg/kg/d
rat
Mozambique tilapia
(Oreochromis
mossambicus)
____________________ endocrine-related effects_____________________
exposure to endosulfan stimulated epithelial cell height, epithelial and stromal
cell proliferation, endometrial gland number as well as induction of
estrogen-responsive proteins lactofenin and complement C3.
uterine weight/BW was not significantly increased with endosulfan exposure,
not uterotropic
0.001 ppm
«
testicular atrophy characterized by degeneration and necrosis of the germinal
cells lining of the seminiferous tubules, multi-nucleated cells (fusion bodies), and
calcium deposition resulting in aspermatogenesis
parathyroid hyperplasia______________________________________________
inhibitory effect on enzymes involved in androgen biotransformation
inhibition of testicular androgen biosynthesis without affecting testicular weight
(decreased plasma and testicular testosterone levels)
decreased LH, FSH levels____________________________________________
decreased sperm counts in the cauda epididymis and reduced intra testicular
spermatid counts associated with elevation in the activities of specific testicular
marker enzy mes (sorbitol dehydrogenase, lactic dehydrogenase, gamma glutamyl
transpeptidase, and glucose-6- phosphate dehydrogenase)___________________
thyroid follicle damage
accolloidal and atrophied thyroid follicles, goitrogenesis, hyperplastic thyroid
follicles, increased follicular diameter, increased nuclear diameter, increased
ratio of thyroid epithelial height/thyroid follicle diameter, increased percentage
of inactive thyroid follicles__________________________________________
increased semmT4. decreased serum and T3/T4 ratio, decreased percent of T4
converted to T3
10
TABLE 1. EM)OSU
LEAN ENDOCRINE-RELATED STIDIES in vivo studies continued
endocrine-related effects
TncrMd W inTitellogemc and post-vitellogenic phase, decreased T3 tn
vitelfeenic and post-vitellogenic phase, decreased T3/T4 ratio in vitellogen
______ species_____
freshwater catfish
(Clari as batrachus)
study design/reference
96 hours
(Sinha, 1991)
dose
0.008 mg/L
.
freshwater catfish
(Clari as batrachus)
16 day exposure
(Chakravorty ,1992)
0.0015 mg/L
and »tt-vitellogenicphas^__---- --------------------- —--------- -------- ^“-7
; ^dectoin plasma vitellogcmn protein following 16 hours of
maxii
deciBiin plasma viteUogenin protein from 48 hours through 16 days.
. addhh of E2 and LHRH or E2 and T3 to endosulfan treatment returned plasma
sheepshead minnow
(Cyprinodon
variegatus)
carp minnow ,
(Rasbora daniconius)
Red-spotted newt
(Notophthalmus
viridescensj
2-42 day exposure
(Hemmer,2001)
15.9 - 788 ng<L
75 day exposure
(Rastogi,1990)
0.001 mg/L
Female red-spotted newts
were treated for 4 days.
(Park, 2001)
vitelkenin production to normal levels------------------------ ---------- —-----------no doable hepatic vitellogenin mRNA or serum vitellogenin protein in male
fishmipled periodically over 2-42 days of exposure
.
percuage of immature oocytes increased, while the percentage of mature
.
S gTmXXatTmdi°ces across the exposure period (0 to 75 days) relative
.
caXhe rupture of oocyte walls as well as the disintegration of cortical alveoli
and ilk granules relative to controls
__ —------ ----------- —— ulHI-ied males selected water containing odor from endosulfan-treated females
less idn water from untreated females, lower mating success, decreased luminal
areaftpheromone gland, decreased olfactory response m untreated males
exped to odor sources from endosulfan-treated females
5 ppb
10 ppb
.
.
fiddler crab, Uca
pugilaior
3 and 7 days exposure
(Zou,1999)
0.05-0.20 mg/L
.
.
lowemaung success, decreased alveolar area of pheromone gland, ^“sed
olfaoty response in untreated males exposed to odor sources from endosulfan
treatfcfemales
,
•
Mecnscd luminal area of pheromone gland not observed; no difference in
____
——and 0.20 mg/L inhibited chitobiase activity (enzy me
necsarv' for molting) m the epidermis and the hepatopancreas.
with days exposure, chitobiase activifr in the epidermis and hepatopancrease
contiiBd to be inhibited at the same doses.--------- —----- --------------------
olfaotv mate selection
11
EDIES in vivo studies continued------- i n-Z
T kl31F 1 ENDOSULFA^ENPQP^^b-relateds:;
1---------- st„(|v design/rdercice^y
species
1-4 weeks exposure
rosy barb
(Gill, 1991)
(Barbus conchonius)
dose______ .
6.72 ppb
“1
c““r°‘
a',!
"esKrol * ““I
eel (Anguilla
anguilla)
freshwater snail
Bellamya dissimilis
climbing perch
(Anabas scandens)
12- to 96-hour exposure
(Gimeno,1994)
"«^’,“g,,72h0"re
4.1 and 8.2 |ig/L
exposure
at 24‘and 96-haur
.t
24^id964iour exposure
jRambabu, 1994)
21 day exposure
(Yasmeen 1991)
0.18:and
1.8 m^'L
6 ppb
.
glucose, glycogen and to
ip
ttaeiointsasmeasure^^
12
antie and foot tissues
FABLE 1. ENDOSULFAN ENDOCRINE-RELATED STUDIES
in vitro studies
endocrine-related effects
cell type/reference
human breast cancer cells
(MCF-7)
(Soto, 1995)
concentration
10 |jM
'thereiative proliferation potency (RPP) of endosulfan compared estradiol is 0.0001%
maximal endosulfan cell yield is 81.25% of the maximal estradiol cell yield
relath e binding affinity1 of p-endosulfan is 0.00024 (IC50 = 631.0 ± 88 pM)
7
•
•
1 and 10 piM
human breast cancer cells
(MCF-7) •
(Soto, 1994)
10 |jM
yeast and
trout hepatocytes
(Petit, 1997)
10 s to 10'4M
(Shelby, 1996)
10 9 to TO'6 M
alligator oviduct tissue
extract
(Vonier,1996)
50 pM
(Tunner 1997)
rat leiomyoma cells
(Hodges,2000)
increased progesterone receptor (PR) levels 9 to 17 fold over no hormone control treatment and
increase was 46 and 89% that of InM E2
E2 decreased estrogen receptor (ER) levels compared to no hpnnpne conffi)!, but endosulfan didnot
Ablative proliferation potency (RPP) of endosulfan and p-endosulfan compared estradiol is
0.0001%
maximal p-endosulfan cell yield is 78.26% of the maximal estradiol cell yield
traximunipi-galactoside activity in yeast for a-endosulfan and P-endosulfan was 25.87% and 20.72%
maXmn vitdlogemn induction in trout hepatocytes for a-endosulfan and P-endosulfan was 42.9%
and 51.0% compared to estradiol
______________________________ —no ex idence of competitive binding, no evidence of transcriptional activation in ER transfected HeLa
competitn e binding to estrogen receptor -a by endosulfan 1 and endosulfan sulfate; these compounds
were insoluble at concentration necessary to achieve 50% inhibition.
30 |jM
1 nM
MOOV-M
•
.
rat prostate tissue extract
(Brieske,1997)
«
competitive inhibition of progesterone by endosulfan sulfate by 40250%-------inhibi ted progesterone initiated acrosome reaction
endosulfan-a (10 pM) stimulated cell proliferation with 6 and 7 days exposure. while endosulfan-p
(10 pM) inliibited cell proliferation at the same timepoints.
cell proliferation stimulated by endosulfan-a (10 pM) was blocked by an antiestrogen (ICIl 82.78 )
after 6 davs exposure.
both endosulfan-a and -0 (10 pM each, separately) induced a vitellogenin reporter gene (an .\F-2
requiring estrogen-inducible gene, after 24 hr exposure.
both endosulfan-a and -p (5 pM each, separately) induced progesterone receptor mRNA (another
estrogen-inducible gene, after 24-hr exposure. ------------- ------------------------------ ----- —
decreased binding of androgen to the androgen receptor (endosulfan lactone > a-endosulfan .
endosulfan sulfate)y-—
13
TABLE 2. Comparison of Pre- and Post-1996 Multigenerationai Study Guidelines
•
•
post-1996_____
FO pre-breed exposure
pre-1996________
FO pre-breed exposure
no vaginal smears specified_________
Fl and F2 weaning necropsy
organ weights not specified
estrous cyclicity
Fl pre-breed exposure
no vaginal smejirs specified
no measures of sexual maturity specified
FO and Fl parental necropsy
organ weights not specified
reproductive organs retained for histopathology
•
•
•
FO and Fl male reproductive assessment
no sperm assessments specified
no spermatid head counts specified
no details of examination of testis and epididymides
FO and Fl female reproductive assessment
stages of estrous at necropsy not specified
no details of examination of ovaries
Triggers
AGD of F2 newborns not specified
histopathology of weanling organs not specified
histopathology of reproductive organs based on
estrous cyclicity or sperm measures not specified
•
•
•
•
•
•
•
•
•
Fl and F2 weaning necropsy
special attention to reproductive organs, organ weights of brain, fiver, thymus
retain gross lesions and target organs________________________________
Fl pre-breed exposure
age of vaginal patency
preputial separation
estrous cyclicity7
FO and Fl parental necropsy
gross necropsy; special attention to reproductive organs
absolute and relative organ weights:
uterus, ovaries, testes, epididymides (total and cauda), prostate, seminal vesicles (with
coagulating glands and their fluids), brain, liver, kidney, adrenal glands, spleen, known
target organs
retained for histopathology:
vagina, uterus with cervix, ovaries with oviducts, testes, epididymides, prostate, seminal
vesicles, coagulating glands, known target organs and gross lesions
FO and Fl male reproductive assessment
cauda epididymides (or vas deferens for motility and morphology), sperm number, sperm
motility, sperm morphology, testes (homogenization resistant spermatids)
retained for histopathology:
testis - atrophy , tumors, retained spermatids, missing germ cell layers or types,
multi nucleated giant cells, sloughing off of spermatogenic cells into lumen
epididymis - caput corpus, longitudinal section, sperm granulomas, leukocyte infiltration
(inflammation), aberrant cell types in lumen, absence of clear cells in cauda epithelium
FO and Fl female reproductive assessment
vaginal smears for estrous cyclicity
identification of estrous at time of termination
post-lactational ovary- - five ovarian sections should be taken at least 100pm apart from
inner third of each ovary, total number of primordial follicles from those 10 sections,
presence or absence of growing follicles and corpora lutea__________________________
T riggers
if treatment -related effects on F1 sex ratio or sexual maturation, AGD measured in F2
offspring on PND 0
histopathology of gross lesions; if effects observed in high dose animals, histopathology of
target organs in mid or low dose levels
if treatment-related effects are observed in fertility, cyclicity or sperm measures,
histopathology of reproductive organs in low and mid dose animals
if treatment-related effects observed in gross pathology or organ weight dam, histology ot
weanling organs
14
THANAL
POST fCX » o. CIS
^'WDI
ENDOSULFAN
KERALAM.
■•■J
<8
-IFH Puk-I
2>. I 6
187
Pi
5. POTENTIAL FOR HUMAN EXPOSURE
5.1
OVERVIEW
Endosulfan is released to the environment mainly as the result ol its use as an insecticide. Significant
contamination is limited to areas where endosulfan is manufactured, formulated, applied, or disposed ol.
The compound partitions to the atmosphere and to soils and sediments. Endosulfan can be transported
over long distances in the atmosphere, but the compound is relatively immobile in soils. It is transloimed
by hydrolysis to the diol and by microorganisms to a number of different metabolites. It is
bioconcentrated only to low levels and does not biomagnify in terrestrial or aquatic food chains.
The most important routes of exposure to endosulfan for the general population are ingestion ol food and
the use of tobacco products with endosulfan residues remaining alter treatment. Farmers, pesticide
applicators, and individuals living in the vicinity ol hazardous waste disposal sites contaminated with
endosulfan may receive additional exposure through dermal contact and inhalation.
Endosulfan has been identified in at least 164 of the 1,577 hazardous waste sites that have been proposed
for inclusion on the EPA National Priorities List (NPL) (Haz.Dat 2000). However, the number of sites
evaluated for endosulfan is not known. The frequency ol these sites can be seen in Figure 5-1. Of these
sites, 87 are located in the United States, one is located in Guam, and one is located in the Virgin Islands
(not shown).
5.2 RELEASES TO THE ENVIRONMENT
Endosulfan (one or both of its isomers) has been identified in a variety ol environmental media (air,
surface water, groundwater, soil, and sediment) collected at 164 ol the 1,577 NPL hazardous waste sites
(HazDat 2000).
Endosulfan has been released to the environment mainly as a result of its use as an insecticide. There are
no known natural sources of the compound. Endosulfan and endosulfan sulfate are not contained in the
list of chemicals for which releases arc required to be reported to EPA for the SARA Section 3I3 Toxic-
Release Inventory (TRI) (EPA 1997a).
Figure 5-1. Frequency of NFL Sites with Endosulfan Contamination
m
z
o
O
>
z
T
o
m
z
r-
o
X
X
c
>z
m
x
T
O
co
c
X
Frequency of
NPL Sites
m
Derived from HazDat 2000
§
ENDOSULFAN
189
5. POTENTIAL FOR HUMAN EXPOSURE
The TRI data should be used with caution because only certain types of facilities are
required to report.
This is not an exhaustive list.
5.2.1
Air
Endosulfan (one or both of its isomers) has been identified
164 NPL hazardous waste sites where it was detected in
in air samples collected at only 4 of the
some environmental media (IlazDat 2000).
As a result of its use as an insecticide on fruit trees, vegetables, and other crops, endosulfan is released
directly to the atmosphere during application. The compound is applied principally by air-blast
equipment or boom sprayers (WHO 1984). No information was found in the available literature
regardmg atmospheric releases from manufacturing or formulation operations, or occurrence of the
compound in air samples collected at NPL sites.
5.2.2 Water
BiXtair.,, (one or bo4 of«
samples epHeoM f„m
bls be<!n
NPL hazard
ib 24 suir,cc
it w„
,n<1 ,
in
media (IlazDat 2000).
Effluents from manufacturing and formulating facilities and surface runoff from treated croplands are
sources of releases of the compound to surface waters. Endosulfan has been detected in rivers draining
.ndustrtal areas where manufacturers or formulators of the compound are located (WHO I984) and in "
streams adjacent to treated fields (NRCC 1975). For example, about 0.6% of the 5.6 kg/hectare
ol endosulfan applied to soybean fields in Mississippi was lost from the fields in runoff. Endosulfan
residues were detected up to 3.5 kilometers (km) downstream from the treatment area for about 3 weeks
oilowing the last application of the compound (Willis et al. 1987).
The TRI data should be used with caution because only certain types of facilities arc
This is not an exhaustive list.
required to report.
190
ENDOSULFAN
5. POTENTIAL FOR HUMAN EXPOSURE
5.2.3 Soil
Endosulfan has been identified in 162 soil and 45 sediment samples collected at Bl of the 164 NPL
hazardous waste sites where it was detected in some environmental media (HazDat 2000).
The main routes of release of endosulfan to soils arc application of the compound to crops and land
disposal of unused formulated pesticide products containing the compound.
The TRI data should be used with caution because only certain types ol facilities arc required io repoit
This is not an exhaustive list.
5.3
5.3.1
ENVIRONMENTAL FATE
Transport and Partitioning
Spray drift from aerial application of endosulfan is often the source of contamination of adjacent
untreated croplands and streams (NRCC 1975). However, endosulfan released to the atmosphere may
also be transported for long distances before being removed in wet and dry deposition. For example,
endosulfan was detected in rainfall samples collected in 1976 and 1977 in Canada at sites inland from the
Great Lakes and remote from any nearby industrial or urban contamination. Mean rainfall concentrations
of I-2 ng/L for the a-isomer and 4-5 ng/L for the [i-isomcr were associated with particulate deposition
during rainfall events. A seasonal pattern was observed in the rainfall concentrations; endosulfan was
detected in spring and summer rainfall samples but not in fall and winter samples (Strachan cl al. 1980).
a-Endosulfan was detected at concentrations of 0.1-1.34 ng/L in snowpack samples collected from
12 sites widely distributed throughout the Canadian Arctic in the spring of 1986 (Gregor and Gummer
1989). The source of the contamination was reported to be long-range atmospheric transport and
subsequent deposition in snowfall The environmental distribution of organic chemicals in air has been
characterized in terms of persistence and spatial range (Scheringer 1997). The model shows endosulfan
to have a limited spatial range (approximately 15% of the earth’s perimeter) and a persistence of less than
10 days. Spatial range is predicted to increase with increased sorption of the compound to particulate
matter, a condition hypothesized to preclude the fast reaction of scmivolatilc compounds with OH
radicals.
191
ENDOSULFAN
5. POTENTIAL FOR HUMAN EXPOSURE
Endosulfan is also released to the atmosphere as the result of volatilization from treated plant surfaces and
surface waters. The volatilization hall-life from surface walers is greater than I I days and possibly
greater than I year (EPA 1979). The vapor pressure (1 x 10'5 mmlIg at 25 • €; 0.83 mPa at 20* C) and
Henry's law constant (Ixl0'5-2.6xI0 5 atm mVmol at 25 •€) values lor endosulfan isomers and
endosulfan sulfate presented in Tables 3-5 through 3-8 also suggest limited volatilization from surface
waters. However, it has been reported that substantial volatilization losses from aqueous surfaces in
seawater/sediment microcosm tests occur (Cotham and Bidleman 1989). The a-isomer volatilized to a
much greater extent than the p-isomer during the initial 72 hours following introduction ol the
compounds to the test chambers. Air/water partitioning of endosulfan has a major influence on the fate ol
the material in the atmospheric compartment. The air/water distribution of the endosulfan isomers was
determined using a wetted-wall-column apparatus.
When pure p-endosulfan was allowed to equilibrate in the apparatus, the ratio of the 0-isomer to the
a-isomer in the gas phase became 8:92 at 20 • C, suggesting that the p-isomer converts to the a-isomcr
(Rice et al. 1997). Several investigators have reported rapid initial losses of endosulfan residues from
treated plant surfaces due to volatilization (Archer 1973; Terranova and Ware 1963; Ware 1967). One
research group (Willis et al. 1987) attributed the limited runoff losses found in soybean Helds treated with
endosulfan to early losses of the compound during application and to volatilization/degradation ol the
compound from plant surfaces. Air sampling performed in a wind tunnel under defined conditions
(20 • C; air velocity I m/sec; relative humidity 40-60%) showed that 60% of the initial dose of endosulfan
is volatilized from French bean surfaces after 24 hours (Rudcl 1997). Influences ol various pesticide
application formulations were not tested.
The results of several laboratory and greenhouse studies indicate that a- and p-endosulfan are strongly
adsorbed to soil. In standard glass-column elution tests, both isomers were found to adsorb tightly to
loamy sand, sandy loam, sandy clay loam, and sandy clay soils (Bowman et al. 1965; El Beit et
al. I98lc). In model soil evaporation beds constructed to test the feasibility ol treating pesticide wastes,
endosulfan exhibited no movement in loamy sand soil beds up to 54 weeks after the start ol the tests
(Hodapp and Winterlin 1989). In air sampling studies done in a wind tunnel, 12% of the initial
endosulfan application volatilized from a silty sand soil alter 24 hours, as compared to 60% from plant
surfaces in 24 hours (Rudel 1997). Endosulfan did not leach from sandy loam soil following
incorporation of 6.7 kg/hectare of the compound (Stewart and Cairns 1974). After sampling periods of
503-828 days, 90% of the residues were found in the top 0-15 cm of soil, 9% at 15-30 cm, and I % at
30—45 cm. In one report, an estimated Koc of 2000 was determined for endosulfan suggesting that
192
endosulfan
5. POTENTIAL FOR HUMAN EXPOSURE
„„M,.y .. »l IP
<S..re of Clrmrn,.
Tbe
i-—
mrioo .orl-oni w measororl to be 3.S«> ««l IWS3, renpo-ve y
aojanol/water
L.- ....
a
« » -> p— “ — Ze
partition coefficient. Kw and K... Using a regress
(1990) and the reported log KIW values found >n Tables 3-6 and
.. ...
.
Indosulfan can be estimated to be 2,887 and 1,958, respectively.
——- “•* s2-“ z: zxX'
—
L ..nples — <n-
'
(Greve and Wit 1971).
L„,^—
L^™.r^ofr. »generally pea £-7. *
*
endosulfan. Maximum bioconcentration factors (
elimlnated w.th.n 2 weeks of t— Co clean water (NRCC .975
.......... ...... .............. „
A — BCF o f.
,■eported for (I-endosu)fan in musse) tissue (Ernst 1977). In a similar study, endosul
., t nrr nf
specified, had a measured
5 in mussel tissue (Roberts 1972). Tissue concentrations of
lpr fnr example a depuration half-
x*«- x™
:xz:
o- \ \ > a RCF of 2 6<>0 was obtained for zebra hsn
were transferred to uncontaminated seawater. Sum ar y,
- exposed to 0 3 pg/L of endosulfan for 2! days in a Gow-through apuanum (To.edo and Jo ss
Zofon «W“--*m'“*“ T “»
:, ”Z -in >20 hou»
,0 takw.„
» «« .................. - o>...... -..... .. “
—«>». ...... > Z2«“
................ ....... ........................................................................................................—'
,6 K
C—.VL for 24 boors.
,
ro 2 wrssb-.H-r — for 7 ^s «» .« „<■—c„tal«L.
catfish were 61.3
(a-isomer) following 7 days of exposure
■ W,
A^-oorsof^-f^——
0.145 pg/kg a-isomer, 0.138 gg/kg tor the p-.somcr, and 0.1 17 pg/ g
Ahmad 1989).
ENDOSULFAN
193
5. POTENTIAL FOR HUMAN EXPOSURE
Plant tissue residues are usually the result of surface deposition of the compound (EPA 1992c). Veiy
limited data indicate (hat endosulfan and its metabolites arc translocated in plants. In one study, the
above-soil portion of bean and sugar beet plants were immersed in a water solution containing endosulfan
and then allowed to diy under both laboratory controlled and semi-controlled greenhouse conditions
(Beard and Ware 1969). Both a- and 0-endosulfan and its metabolites (endosulfan diol, ether, and
sulfate) were found to penetrate plant tissue and were translocated from the leaves to the roots of both
bean and sugar beet plants. Translocation occurred at a higher rate in greenhouse plants (han in
laboratory plants. Under semi-controlled greenhouse conditions for both beets and beans, the highest
residues were found in the plant extracts (indicating penetration of the material), with lower
concentrations deposited on leaves, and with the lowest levels in the roots. The residue levels on both the
plant surface and in tissue extracts decreased during the course of the experiment, while the levels in the
roots increased. In bean plant roots, translocation (day 4) was as follows: isomer p (0.28 ppm) > ether
(0.18 ppm) > sulfate (0.08 ppm). No residue of the a-isomer or the diol appeared in bean roots by day 4.
In sugar beet roots, residue levels were as follows: a-isomer (2.8 ppm) > p-isomer (0.5 ppm) > ether
(0.1 ppm), sulfate (0.1 ppm) > diol (0 ppm) (Beard and Ware 1969).
The results of metabolism studies with laboratory animals and livestock indicate that endosulfan does not
bioconcentrate in tatty tissues and milk. Lactating sheep administered radiolabeled endosulfan produced
milk containing less than 2% of the label. Endosulfan sulfate was the major metabolite in milk (Gorbach
et al. 1968). A half-life of about 4 days was reported for endosulfan metabolites in milk from survivors of
a dairy herd accidentally exposed to acutely toxic concentrations of endosulfan; endosulfan sulfate
accounted for the bulk of the residues detected in the milk (Braun and Lobb 1976). No endosulfan
residues were detected in the tatty tissue of beef cattle grazed on endosulfan-treated pastures for
31-36 days (detection limits of 10 ppm for endosulfan, 40 ppm for endosulfan diol); the animals began
grazing 7 days after treatment of the pastures. Some residues were detected in the fatty tissue of one
animal administered 1.1 mg/kg/day of endosulfan in the diet for 60 days. No endosulfan residues were
detected in milk from cows fed silage containing 0.41-2.35 ppm endosulfan for 21 days (Beck et
al. 1966).
In field trials following multiple aerial applications of endosulfan for tsetse fly control in Africa over a
3-month period, residues ol the compound in fish tissues decreased to low concentrations within 3 months
alter spraying. The fish tissue residues were still detectable after 12 months. Residue concentrations in
fish-eating birds and crocodiles were similar to fish tissue residue levels; endosulfan did not biomagnify
in the food chain (HSDB 1999).
ENDOSULFAN
194
5. POTENTIAL FOR HUMAN EXPOSURE
5.3.2 Transformation and Degradation
5.3.2.1 Air
The a- and p-isomers of endosulfan undergo photolysis in laboratory tests after irradiation in polar
solvents and upon exposure to sunlight on plant leaves. The a-isomer also undergoes isomerization to the
p-isomer, which is relatively more stable (Dureja and Mukerjee 1982). A photolytic half-life ofabout
7 days was reported for endosulfan by EPA (1982c). The primaty photolysis product is endosulfan diol,
which is subsequently photodegraded to endosulfan a-hydroxyether. Endosulfan sulfate is stable to direct
photolysis at light wavelengths of >300 nm; however, the compound reacts with hydroxy radicals, with
an estimated atmospheric half-life of 1.23 hours (HSDB 1999).
5.3.2.2 Water
Endosulfan undergoes hydrolysis to endosulfan diol in surface water and groundwater. The rate of
hydrolysis is inlluenced by pH. Half-life values reported in the literature vaty somewhat. The chemical
degradation of a- and P-endosulfan was studied under both anaerobic and aerobic environments. Under
aerobic conditions, both hydrolysis and oxidation of endosulfan can occur, while under anaerobic
conditions, only hydrolysis can occur. The hydrolytic half-lives for a- and P-endosu)fan under anaerobic
condmons at pl I 7 were 35 and 37 days, respectively (Greve and Wit 1971). At pl I 5.5 the half-lives
were I5I and 187 days, respectively. Under aerobic conditions, the half-lives decreased. At pH 7, the
half-lives of the chemical degradation (hydrolysis and oxidation) of both a- and P-endosulfan were 23 and
25 days, respectively, while at pH 5, the half-lives were 54 and 51 days, respectively. Al T=20 • C and
pHs of 5.5 and 8.0, the half-lives of a-endosulfan in distilled water were 11.3 and 5.3 days, respectively
(Kaur et al. 1998). The half-lives at pH 7.23 and 69.5 • C for a- and P-endosulfan were 1.2 and
0.96 hours, respectively (EPA 19871). Losses of endosulfan, at an initial concentration of 0.5 mg/L, from
natural lake water and tap water were 89 and 69%, respectively (Ferrando et a). 1992). The natural water
was more alkaline than the tap water; this finding is in agreement with other studies. The half-life of the
pesticide in the tap water was approximately 68 hours.
Endosulfan in aqueous solutions is also expected to undergo biodegradation. In laborato.y tests at pH 7
and 20 -C, Pseudomonas bacteria degraded endosulfan (isomers not specified) under aerobic conditions
With a half-life ofabout I week (Greve and Wit I97I). Biotic and abiotic transformations of endosulfan
m seawatcr/sedunent microcosms have been reported (Gotham and Bidleman 1989). In biotic tests. Kalf-
ENDOSULFAN
195
5. POTENTIAL FOR HUMAN EXPOSURE
lives for the a- and p-isomers in seawater-only microcosms (pl I- R)
were about 5 and 2 days, respectively,
oondlriobs st . pH of d oe h.ghe,-. the b.tr-ldo foe the Mto,
higher, the hall-life lor the a-isomer
2-3 dsys. Mtorhe b.IMfe for „ p.is„mer „
d!,ys. H.,r.,iyes „,c
rn .«„»!y MM, u„der
sod,m« microcosms. possiMy because of th. lower pH. <73-7.7) i„ these test systems; h.lMyes wero
- and S3 day. for the
.„d pdsoment. rcpealeely. Eudosuirau diol was the main metabolite
identified.
5.3.2.3 Sediment and Soil
Endosulfan released to so,I is most likely subjected to photolysis (on soil surfaces), hydrolysis (under
a kalme cond.t.ons), or biodegradation. Endosulfan has been shown to be biodegraded by a wide variety
o sod m.croorgan.sms in numerous studies. Sixteen of 28 species of fungi, 15 of 49 species of soil
actena, and 3 of 10 species of actinomycetes mctabol.zed radiolabeled endosulfan in a iaborato^ study
under aerobic condnions (Martens 1976). Endosulfan sulfate was the major product ofthe fwgal
ntctabobsm, whereas the bacteria! transforation produced endosudan diol. Degradat.on ofendosuHan
y soi lung, and bactena has also been reported (El Beit et al. 1981b). Biotransformation occurs under
ol aerob,c and anaerobic conditions. Aerobic incubation of soil with endosulfan yielded mainly
endosulfan sulfate (30-60%), some endosulfan diol (2.6%), and endosulfan lactone (I 2%) (Martens
1977) Fiooded (anaerobic) incubation produced mainly endosulfan dio. (2-18%), endosulfan sulfate
- A), and endosulfan hydroxyether (2-4%). In aqueous nutrient media (20-C) containmg a mixed
culture of m,croorganisms isolated from a sandy loam so,., endosu.fan was reported to be transPirmed to
cn osulfan d,ol w,th half-bves of about 1.1 and 2.2 weeks for the a- and P-isomers, respectively (Miles
and Moy 1979).
iwo-memberri bMen.l c„c„llure „ f„„d
,mMca||y degradc a
MM, .ny of te ^bohre,. Ho„v„. .he ^..d.r.on .rsorbbo.nd c„„„sil,r<n „s
by 4.lold lta„ in eullu„ m|i.; on,y m%
raucria| (.a.
A fcld sludy „„„„ aaW lhal ei)d0!ulfan m
«=b. (A^rbi or .t
X
’f6-7
mj. The beif-r™ r„, rhe
lnd
»f ■*
lo be 6l) an(l gM dw
were
„^l990
e„dosa|fm
„„„„
ey^rbod (Kadtp., aal. | W „ „„ f„„d
w
i«0 -by ,«.m „„ (Slew,r, ,„d c,irB,
hm been repo« , toMItotoM. ..
or roomere r« e„d„ulf.„ a|Cdb„,
study oonduoted
a[ m
(U g
Hnd bl„dce„lle
196
ENDOSULFAN
5. POTENTIAL FOR HUMAN EXPOSURE.
two different soil plots, while p-endosulfan could be detected up to 70 and 238 days. An overall half-life
for endosulfan degradation ranged from 39.5 to 42.1 days. Endosulfan residues dissipated to an extent of
92-97% in the first 4-week period of application and by about 99% in 238 days. A residue half-life of
15 days for endosulfan (unspecified isomer) has been reported in Australian black soil when incubated at
30 • C at field capacity moisture level (Kathpal et al. 1997). Fate and movement of endosulfan isomers
and endosulfan sulfate under field application conditions have been studied (Antonious and Byers 1997).
New modes of cultivation showed reduced runoff water and sediment loss and reduced endosulfan
movement from the site of application to the surface water runoff. Results indicated vertical movement of
the pesticide through the vadose zone at a concentration of 0.63 pg/L. Soil core dala shows endosulfan
leaches from 23 to 46 cm into the soil (Antonious and Byers 1997).
On plant surfaces, as in soils, numerous studies have demonstrated that endosulfan is oxidized to
endosulfan sulfate. Initial residues of endosulfan on treated vegetables generally range from I. to
100 mg/kg. However, residue levels typically decrease to less than 20% of initial levels within I week
after treatment (NRCC 1975). Residues of endosulfan isomers arc generally negligible after 2-3 weeks;
the a-isomer is much less persistent than the p-isomer. In most plant residue studies, endosulfan sulfate
residue levels tend to increase relative to the parent isomers and other metabolites and appear to be very
persistent (Coleman and Doiinger 1982).
5.4
LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT
Reliable evaluation of the potential for human exposure to endosulfan depends in part on the reliability of
supporting analytical data from environmental samples and biological specimens. In reviewing data on
endosulfan levels monitored or estimated in the environment, it should also be noted that the amount of
chemical identified analytically is not necessarily equivalent to the amount that is bioavailable.
5.4.1
Air
Endosulfan has been detected in only a limited number of ambient air samples taken in the United States.
As part of EPA's National Pesticide Monitoring Program conducted between 1970 and 1972, in 1970,
only 6.6 and 1% of the ambient air samples collected at selected sites in 14 states contained a- and
p-endosulfan, respectively. Mean concentrations for the positive samples were I 1 2 ng/m’ for the
a-isomcr (maximum 2,257 ng/m3) and 22 ng/m3 lor the P-isomer (maximum 55 ng/m3) Sampling sites
were selected tor their potentially high concentrations of pesticides in ambient air. Endosulfan was not
ENDOSULFAN
197
5. POTENTIAL FOR HUMAN EXPOSURE
detected in any ofthe ambient air samples collected from sites in Estates in 1971 or 1972 (Kutz ct a).
1976). a-Endosulfan was detected at a mean concentration of 0.078 ng/m’ in ambient air samples
collected in Columbia, South Carolina from June to mid-August 1978 (Bidleman 1981). Air samples
obtamed ata rural site near Egbert, Ontario, Canada in 1988-1989 contained an average of3.7 ng/m1 of
the local and regionally used pesticide, endosulfan (Ilofl'ct al. 1992). The average air concentration of
a-endosulfan over a 14-month period in 1991-1992 in Bloomington, Indiana, was 86 pg/m' (0.086 ng/m')
(Buigoyne 1993). Dmrnal vacations in ambient air concentrations of endosulfan were noted for samples
taken in September 1994 near Bloomington, Indiana (Wallace and Hites 1996). Air samples taken over a
6-hour penod in the morning had twice the concentration (0.031 ng/m’) than those collected at midnight.
Rainfall samples collected in the Great Lakes area of Canada in 1976 and 1977 contained mean
concentrations of 1-2 ng/L (parts per trillion) a-cndosulfan and 4-5 ng/L P-cndosulfan. Endosulfan was
detected in spring and summer rainfall samples but not in samples collected during the fall and'winter
(Strachan et al. 1980). a-Endosulfan has also been detected in snowpack samples obtained from widely
d.strtbuted sites in the Canadian Arctic. Endosulfan concentrations in samples collected in (he spring of
1986 ranged from 0.1 to 1.34 ng/L (Gregor and Gummer 1989).
5.4.2 Water
Although endosulfan and endosulfan sulfate have bee,, found at low coneentrations in a few surface water
and groundwater samples collected at hazardous waste sites (see Section 5.2.2), no information was found
>n the available literature regarding current concentrations of endosulfan or endosulfan sulfate in domestic
surface waters not associated with these sites. The World Health Organization (WHO) reported that
although endosulfan has been detected in agricultura) runoff and in surface waters draining industriahzed
areas, contammatton of surface waters with this compound docs not appear to be widespread (WI IO
1984). EPA (1982c) stated that endosulfan concentrations in surface water are generally
I» .
orslrcams i„ He
h-om ! 96S „ , 97!. endoa.dta
eoneen«„„ „f „.„2
UniW SMe, c„„ducM by
b s &o|og]oa|
deleted !„ <„ly , „r lte 5« s„rtee „a.e. aampfea e„lkc,ed
(EPA
tea, ln»er Harder Navigalion Cana! of Lake
dd a“ l'V"S
..de) (MeF.!! e. a!. ! ,S5).
I ppb.
(N„ Odea,,,. Lnnra!.™,. A, edb.nd
PP‘ ’' 5 ” 'b'’ “e>' “ PP‘ ‘' 5 ■”
■’«»"“ ”■
«e microlayer and .U!pe„ded ardlda U 3 of 5 a„iona along He N»Em River in ! 9S!
!,,.).
,
198
ENDOSULFAN
5. POTENTIAL FOR HUMAN EXPOSURE
ranging from 0 to 0.0204 pg/L and from 0 to 0.025 mg/kg, respectively (level of detection ,0.000 I [Ig/L
in water and 0.00I mg/kg in suspended solids) (Maguire et al. 1983). a-Endosulfan was not detected in
subsurface water at any of the stations. Concentrations of ^-endosulfan in the surface microlayer,
subsurface water, and suspended solids were below the detection limits, except at one station where
P-endosulfan was found ata level of 0.02I mg/kg in suspended solids (Maguire et al. 1983).
Rain samples collected from around the Great Lakes contained both a- and (J-endosulfan (Strachan and
Huneault 1979). Mean concentrations of a-endosulfan in ram samples from the Great Lakes ranged from
0.1 ng/L (n=13) to 3.8 ng/L (n=16). Mean concentrations of [Lendosulfan in rain samples ranged from
I (n= 14) to 12 ng/L (n=l 6). The endosulfans were not found to any significant extent in snow-core
samples (Strachan and Huneault 1979). Detection limits were not reported.
Runoff waters from agricultural areas have been found to contain low concentrations ol endosulfan in the
aqueous phase and higher concentrations in the particulate phase of the runoff. For example, runof I from
a soybean field in Mississippi treated with 5.6 kg endosulfan/hcctare was reported to contain maximum
concentrations of 0.019 mg/L and 8.7 mg/kg (<i- and [J-isomers) in the aqueous and suspended sediment
phases, respectively (Willis et al. 1987). The samples were collected within 3 weeks ol the last
application of the compound. Samples taken from runoff ditches from an agricultural area near Lake Erie
in Ontario, Canada, contained endosulfan residue (unspecified isomcr/sulfatc content) concentrations ol
<0.002-0.18 pg/L in runoff water and 1-62 pg/kg in bottom mud. Soils from a farm located near the
runoff ditch contained 640 pg endosulfan residucs/kg (Miles and Harns 1971). Endosulfan was detected
in stream waters collected from 11 agricultural watersheds in Ontario from 1975 to 1977 (Frank et al.
1982). The overall mean for all 11 watersheds was 3.7 ng/L in 1975-1976 and 2.0 ng/L in 1976- 1977.
Detection limits were not reported. Endosulfan exceeded the water quality criteria of 3.0 ng/L established
by the International Joint Commission for lake and stream waters entering the Great Lakes in 14% ol the
samples. Endosulfan appeared in water samples throughout the year (outside the spray season); it cnteied
water with storm runoff throughout the season because of its persistence in soil (Frank et al. 1982). In the
early 1990s, endosulfan was found in the waters and sediment of'the canals ol South Honda (Miles and
I’feuffer 1997). a-Endosulfan and endosulfan sulfate residues as high as 0.22 and 0.15 pg/L, respectively,
were observed in confined surface waters in the Homestead area. Such values exceed the Florida water
quality criterion.
From February 1995 to June 1997, endosulfan concentrations (isomers not spccihcd) m river, well,
lagoon, and spring water samples wqre studied from the greater Cholutecan River Basin of Honduras
199
ENDOSULFAN
5. POTENTIAL FOR HUMAN EXPOSURE
(Kammerbauer and Moncada 1998). Endosulfan was found predominantly in Choluteca well water and
in Yeguare river water at approximately 0.06 mg/kg. It was also found in Choluteca river water,
Zamorano well/lagoon water, and La Lima well/lagoon water at concentrations ranging from 0.01 to
0.02 mg/kg. In a study of water samples collected from the Segre river basin in Spain from May-June
1995, endosulfan (isomers not specified) was detected in four of six samples at approximately 0.01 pg/L
(Planasctal. 1997).
Three out of nine groundwater samples extracted from Dobrich in northeastern Bulgaria contained
endosulfan (isomers not specified) ranging from 0.020 to 0.025 gg/L in March 1996 (Pulido-Bosch et al.
1999). The suspected source of this pollution was from agricultural practices in the region.
5.4.3 Sediment and Soil
Endosulfan has been detected in only a limited number of urban and agricultural soils in the United
States. The National Soils Monitoring Program conducted in 1972 included the collection of 1,483 soil
samples from 37 states. The a- and p-isomers of endosulfan and endosulfan sulfate were each detected in
only one sample at <0.01 ppm (Carey et al. 1979a). Endosulfan was not detected (method detection limit
of 1 gg/kg) in sediments collected from the Central Columbia plateau of the United States (Munn and
Gruber 1997). In soil samples collected from five metropolitan areas in the United States as part ot the
Urban Soils Monitoring Program, endosulfan sulfate was detected in samples from two cities: Macon,
Georgia (in 1 of 43 samples) and Baltimore, Maryland (in 1 of 156 samples) at concentrations of
<0.01 ppm (Carey et al. 1979b). Surveys of agricultural soils in North America have determined that
endosulfan residue levels (a- and p-isomers and endosulfan sulfate) arc typically less than 1 mg/kg (WHO
1984).
From February 1995 to June 1997, endosulfan concentrations (isomers not specified) in soil samples were
studied from the greater Cholutecan River Basin of Honduras (Kammerbauer and Moncada 1998).
Endosulfan was found in Choluteca and La Lima soil at concentrations ranging from 0.01 to 0.02 mg/kg.
Soils sampled at two sites in creek beds and drainage ditches in an agricultural area in the Point Mugu
watershed near Oxnard, California, contained endosulfan at concentrations between 20 and 30 ppm. The
majority of the other sites had much lower concentrations (Leung et al. 1998).
ENDOSULFAN
200
5. POTENTIAL FOR HUMAN EXPOSURE
5.4.4 Other Environmental Media
Levels oi endosulfan and endosulfan sulfate in domestic foodstuffs have been determined as part of
FDA's Total Diet Studies series. The FDA’s 1995 pesticide residue monitoring program found
81 instances of detection of endosulfan in 3 market baskets consisting of 783 items (FDA 1995). In the
1980-1982 survey of 27 cities (Gartrcll ctal. 1986), individual food items were separated into food
groups, and foods in each group were blended in amounts proportional to weights consumed to yield
homogeneous composites. a-Endosulfan, p-endosulfan, and endosulfan sulfate were detected only in the
leafy vegetable, garden fruit, and fruit food groups. The isomers and the breakdown product were not
found in the following food groups included in the survey: dairy products; meat, fish, and poultry; grain
and cereal products; potatoes (a- and p-isomers); legume vegetables; root vegetables; oils and fats; sugar
and adjuncts; or beverages.
Domestic and imported pears and tomatoes were collected and analyzed for pesticide residues from July
1992-July 1993 (Roy et al 1995). Endosulfan (both isomers) was found in 471 of 1,219 domestic tomato
samples at a maximum concentration of 0.2 mg/kg and in 80 of 144 imported tomato samples at a
maximum concentration of 0.55 mg/kg. In pears, endosulfan was found in 144 of 710 domestic samples
at a maximum concentration of 1.1 mg/kg, and in 4 of 949 imported samples at a maximum concentration
of 0.13 mg/kg.
Studies of carrot and tomato crops sprayed with endosulfan 2 to 8 days prior to harvest showed that more
pesticide remains in the pulp than in the juices of these vegetables. Washing and peeling the vegetables
lowered the endosulfan concentration considerably (Burchat et al. 1998).
Neither endosulfan nor endosulfan sulfate was detected in surveys of the milk supply of the southern
region of Ontario, Canada conducted in 1970—1971 and 1973 (Frank et al. 1975). In Burley tobacco,
when the crop was harvested immediately after treatment with 0.5 pound/acrc of endosulfan, the total
endosulfan residue levels (isomers and sulfate) were reported to average 23.2 ppm after curing for
4 months. Average total residues decreased to 2.2 ppm when the time between treatment and harvest was
increased to 28 days (Dorough et al. 1973).
ENDOSULFAN
201
5. POTENTIAL FOR HUMAN EXPOSURE
5.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE
The main loute of exposure to endosulfan for the genera) population is ingestion of food containing
residues ot endosulfan as a result of application or bioconcentration. Levels of endosulfan and
endosulfan sulfate in domestic foodstuffs have been determined as part of FDA’s Total Diet Studies
series. The FDA’s 1995 pesticide residue monitoring program found 81 instances of detection of
endosulfan in 3 market baskets consisting of 783 items (FDA 1995). A total diet study conducted by the
FDA from June 1984 to April 1986 studied the dietary intake of various pesticides by different age
gioups in the population (Gunderson 1995b). The mean daily intakes per unit of body weight (mg/kg
body weight/day) for a-endosulfan were 1.3x 1 O'6 for ages 14-16 years, 1.8x1 O’6 for ages 25-30 years and
2.Ox 106 for ages 60-65 years while for p-endosulfan, the mean daily intakes were 2.1 xl O’6 for ages
14—16 years, 2.5x 10 for ages 25—30 years, and 2.9x 1 O'6 for ages 60—65. In the same type of study
conducted from July 1986 to April 1991, the mean daily intakes per unit body weight (mg/kg body
weight/day) for a-endosulfan were 2.3x 1 O’6 for ages 14-16 years, 3.Ox 10'6 for ages 25-30 years, and
3.8x106 for ages 60-65 years, while for P-endosulfan, the mean daily intakes were 6.5x I O’6 for ages
14-16 years, 6.8x 1 O'6 for ages 25-30 years, and 9.9x 10'6 for ages 60-65 years (Gunderson 1995a).
Studies of foods in India have identified endosulfan in okra at an average concentration of 0.22 pg/g
(Mukherjee and Gopal 1996). Dietary characterization of food and beverages were made during a study
of human exposure in the lower Rio Grande valley (Berry et al. 1997). A total of 30 different pesticides
were detected in 54 local food samples; endosulfan was one of the most commonly found residues.
Endosulfan sulfate, a-endosulfan, and p-endosulfan residues were found in 4-6 foods sampled in the
spring at concentrations ranging from 0.005 to 0.072, 0.007 to 0.050, and 0.002 to 0.095 pg/g,
respectively (Berry et al. 1997). Howard (1991) has estimated an average daily intake of endosulfan via
via
food at 1.18 pg by averaging the average daily intake values for the years 1971-1976.
In Hsinchu, Taiwan, the dietary intake of a- and p-endosulfan was studied from June 1996 to April 1997
(Doong and Lee 1999). p-Endosulfan was not detected in any of the 14 different foods studied, including
fruits, meats, seafood, and cereal, and a-endosulfan, by contrast, was found in 78 of 149 samples at an
average concentration of 2.76 ng/g wet weight. Based on the average Taiwanese diet, the estimated daily
intake of a-endosulfan was 6.24x1 O’4 mg body weight/day.
Exposure to endosulfan residues in tobacco products could be another important source of general
population exposure. Endosulfan residues in tobacco leaves and finished tobacco products were reviewed
by EPA (1982a). For example, auction market tobacco had a mean residue of <0.2-14 ppm endosulfan
202
ENDOSULFAN
5. POTENTIAL FOR HUMAN EXPOSURE
and endosulfan sulfate in the early 1970s, and cigarettes sold in 1973 contained a mean residue of
0.83 ppm endosulfan. No information was found in the available literature regarding endosulfan
concentrations in cigarette smoke.
In occupational settings, exposure to endosulfan is mainly via the dermal and inhalation routes. Although
workers involved in the manufacture and formulation of pesticide products containing endosulfan are
potentially exposed to high concentrations of the compound, actual exposure is probably limited by the
use of engineering controls and personal protection equipment. The highest documented dermal and
inhalation exposures have been reported for agricultural workers involved in the spray application ol
endosulfan products. Among these individuals, mixers and applicators have the highest potential for
direct exposure. For example, during spray application of endosulfan on fruit orchards using air-blast
equipment, a mean dermal exposure of 24.7 mg/hour (range, 0.6-95.3 mg/hour) and a mean inhalation
exposure of 0.02 ng/hour (range, 0.01-0.05 ng/hour) were estimated in one study (Wolfe et al. 1972). In
another study in which endosulfan was applied to fruit orchards using air blast equipment, total exposures
of 0.27-2.2 mg/hour were reported during mixing operations, and 4.1-9.3 pg/hour were reported during
spraying operations (Oudbier et al. 1974). Estimates ol mean dermal exposure ol workers who apply
endosulfan to fields of tobacco in Kentucky have been made (Lonsway et al. 1997). The mean dermal
exposures to mixers and sprayers of endosulfan via a tractor mounted boom sprayer and highboy were
16.18 and 8.06 mg/kg/day, respectively. Not using protective measures when spraying endosulfan can
lead to poisoning. In the Punjab area, 8.6% of poisonings of all types admitted to the hospital in 1989
were due to endosulfan (Singh el al. 1992). Singh cautions that applications of oil to body surfaces before
beginning work in the fields will increase the absorption of endosulfan. Furthermore, the presence of cuts
on the legs or hands facilitates entry of pesticides to the body’s circulatory system. Studies of pesticide
penetration through protective clothing (Archibald et al. 1994a) indicated that rubber or tyvek provided
the best protection.
In one study, the exposure of an individual involved in spraying the compound, while wearing protective
overalls, gloves and breathing mask, was examined (Arrebola et al. 1999). The individual applied 300L
of an endosulfan mixture to plants and later gave 10 urine samples over the course of 3 days. The study
found that the highest concentrations occurred 4.3 hours after exposure with concentrations for a- and
p-endosulfan reaching 4,289 and 1,079 pg/mL, respectively. The half-lives for the excretion of a- and
p-endosulfan were determined to be 23 and 27 hours, respectively. Between October 1995 and
September 1997, 1 8 cases of endosulfan poisoning by accidental overexposure during spray applications
were reported at the medical center in Haryana, India (Chugh et al. 1998). Ten fatal cases of endosulfan
ENDOSULFAN
203
5. POTENTIAL FOR HUMAN EXPOSURE
exposure were reported in a survey of pesticide poisoning incidents in Spain from 1991 to 1996 (Garcia.
Repettoetal. 1998).
Endosulfan is a popular pesticide with greenhouse chrysanthemum producers. Surveys of usage patterns
and potential exposure were conducted in Ontario (Archibald et al. 1994b). Collection and analysis ofctand p-endosulfan and endosulfan sulfate in greenhouse air have been described (Vidal et al. 1997).
Results indicate that 7.5% of the initial concentration of endosulfan remained in the greenhouse
atmosphere 24 hours after application.
The National Occupational Exposure Survey (NOES), conducted by NIOSH from 1980 to 1983,
estimated that 3,205 workers in the agricultural services .industry were exposed to endosulfan in the
workplace in 1980 (NIOSH 1984). The NOES database does not contain information on the frequency,
concentration, or duration of exposure of workers to any chemicals; the survey provides only estimates of
the number of workers potentially exposed to chemicals in the workplace.
5.6
EXPOSURES OF CHILDREN
This section focuses on exposures from conception to maturity at 18 years in humans. Differences from
adults in susceptibility to hazardous substances are discussed in 2.7 Children’s Susceptibility.
Children are not small adults. A child’s exposure may differ from an adult’s exposure in many ways.
Children drink more fluids, eat more food, breathe more air per kilogram of body weight, and have a
larger skin surface in proportion to their body volume. A child’s diet often differs from that of adults.
The developing human’s source of nutrition changes with age: from placental nourishment to breast milk
or formula to the diet of older children who eat more of certain types of foods than adults. A child’s
behavior and lifestyle also influence exposure. Children crawl on the floor, pul things in their mouths,
sometimes eat inappropriate things (such as dirt or paint chips), and spend more time outdoors. Children
also are closer to the ground, and they do not use the judgment of adults to avoid hazards (NRC 1993).
Infants are particularly sensitive to endosulfan due to their higher intestinal permeability and immature
detoxification system. In a study of human breast milk conducted in the countiy of Kazakhstan in 1994,
the concentration of various contaminants, including endosulfan, were determined (Luttcr et al. 1998). Of
the 91 samples ofbreast milk analyzed, only 2 had detectable quantities of endosulfan (concentrations not
specified). In another study, the transfer of endosulfan and its metabolites were studied in breast milk of
204
ENDOSULFAN
5. POTENTIAL FOR HUMAN EXPOSURE
lactating goats (Indraningsih et al. 1993). Endosultan residues in milk of goats administcied a daily dose
of 1 mg/kg for 28 days reached 0.02 mg/kg on day 1. However, by day 8, no residues or metabolites
could be detected. Likewise, no endosulfan residues could be detected in the tissues ol kids except for
a-endosulfan in the liver at a concentration of 0.0011 mg/kg. Analysis of milk from cows which ingested
potentially poisonous amounts of endosulfan revealed a level ol >1 ppm endosulfan immediately
following the intoxication (Braun and Lobb 1976). This level decreased to I ppb at the end ol 35 days
with a half-life of about 4 days in milk. No endosulfan residues were detected (detection limit=
0.01 mg/L) in milk from cows fed silage containing 0.41-2.35 ppm endosulfan lor 21 days (Beck et al.
1966).
The FDA pesticide residue monitoring program analyzes selected baby foods lor endosulfan under its
Total Diet Study. In the period 1991-1995, 29 incidences of detectable amounts of endosulfan were
reported from analyses of 276 items purchased in 12 separate collections (FDA 1995).
A total diet study conducted by the FDA from June 1984 to April 1986 studied the dietary intake ol
various pesticides by different age groups (Gunderson 1995b). The mean daily intakes per unit ol body
weight (mg/kg body weight/day) for a-endosulfan were 2.6x 1 O’6 for children 6-1 1 months ol age and
4.5x10'6 for children 2 years of age, while for p-endosulfan the mean daily intakes were 5.4x 106 for
children 6-11 months of age and 8.1 x 10‘6 for children 2 years of age. In the same type of study
conducted from July 1986 to April 1991, the mean daily intakes per unit body weight (mg/kg body
weight/day) for a-endosulfan were 3.2x I O'6 for children 6-11 months of age and 7.6x 10'6 lor children
2 years of age, while for p-endosulfan, the mean daily intakes were 1.69x 10 s for children 6-1 1 months of
age and 2.38x10‘5 for children 2 years of age (Gunderson 1995a). From October 1984 through September
1991,27 market basket samples of foods eaten by infants and children were collected and analyzed for
pesticide residues (Yess et al. 1993). These foods included fruits/fruit juices, baked goods, cereals,
combination mcat/poultry dinners, desserts, infant formulas, and vegetables. Concentrations of
endosulfan (both isomers) found in foods eaten by infants were 0.001 mg/kg in I sample of desserts;
0.004 mg/kg (maximum) in 5 samples of applesauce; 0.0007 mg/kg in 1 sample of strained orange/orange
pineapple juice; 0.010 mg/kg (maximum) in 3 samples of peaches; 0.053 mg/kg (maximum) in
20 samples of pears/pineapplcs; 0.002 mg/kg in 1 sample of prunes/plums; and 0.004 mg/kg (maximum)
in 20 samples of raw pears.
205
ENDOSULFAN
5. POTENTIAL FOR HUMAN EXPOSURE
A similar survey conducted in 1977-1978 in 10 cities focused on infant and toddler diets (Podrebaiac
1984a). Of 11 food groups included in that survey, 0-endosulfan was found in the vegetables and fruit/
I
fruit juices food groups for the toddler diet at 0.001-0.004 ppm. Endosulfan sulfate was found in the
potato and sugar and adjunct groups in the infant diet at 0.001-0.004 ppm and in the vegetaMc and potato
groups in the toddler diet at 0.004-0.005 ppm. The compounds were not detected in the following food
groups included in the survey: drinking water; fresh whole milk; other dairy products; meat, fish and
poultry; grain and cereal products; oils and fats; or beverages. In a total of 98 infant diet composite
samples, [l-endosulfan was detected in 1 composite and endosulfan sulfate was found in 2 composites.
Out of a total of 110 toddler diet composite samples, the u-isomcr, fl-isomer, and sulfate forms were
detected in 1,2, and 2 composites, respectively.
Although child exposure to endosulfan through inhalation has not been studied, it is anticipated that
exposure through this route is extremely low. The vapor pressure of endosulfan is negligible
(1 .Ox 1 O'5 mmHg at 25 • C) (Coleman and Dolinger 1982), suggesting that an extremely small amount is
expected to exist in the vapor phase at environmental conditions (Bidleman 1988). Although the vapor
density is reported as 14 (HCDB 1986), suggesting that vapor-phase endosulfan is heavier than air.
inhalation exposure is not expected to be significant to children due to the extremely small amount of
endosulfan that will exist in the vapor-phase at environmental conditions.
Since young children spend more time outdoors and have a tendency to ingest soil, it is important to
examine child exposure through ingestion. Although no studies have been conducted concerning this
subject, exposure through ingestion of soil is not expected to be significant. Endosulfan undergoes many
degradative processes in the environment, such as hydrolysis, photolysis, oxidation, and biodegradation,
that will reduce its concentration in soil. Degradation half-lives for the combined effects ol hydrolysis
and oxidation in moist soils range from 23 to 54 days depending on pH (Greve and Wit 1971). Photolysis
on soil surfaces is expected to occur as well. The photolytic half-life of endosulfan on plant leaves was
reported to be 7 days (EPA 1982a). Endosulfan has also been shown to be biodegraded by both bacteria
and fungi in the soil environment (El Beit et al. 1981b; Martens 1976). Both abiotic and biotic processes
are therefore expected to decrease endosulfan concentrations in soil environments. However, children
may potentially be exposed to endosulfan from oral/dermal exposure if they play in the soil ot
contaminated areas such as hazardous waste sites. Based on degradation ol endosulfan in the
environment, child exposures to endosulfan through soil ingestion is not expected to be very significant.
endosulfan
5. POTENTIAL FOR
human exposure
. re of children to endosulfan after household use by parents.
children whose parents) work
No studies coudd be located discussing exposu
Ukew.se, no exposure studies could be
with endosulfan on a daily basis. However; many .
malcrials (N1OS! I 1995).
can be brought home through contaminate c o mg,
endosulfan used in a work
ofendosulto «— a
AKhongh no doeomoiried eases vM bo loeMrt .
soiling may be broughl home by working parenia- I1 ls unLL
Child may encounter under these situations.
POPULAT.ONS WITH POTENTIALLY H.GH EXPOSURES
5.7
FormeAS...1poa.o.denPPke.l»m»-ndo-...7o:.m>:Z;3
l„.,c molude po^.n ^g
wmkeis oimemly «P«sed » P»^ *
population with potentially high exposure to en o
the 162'NPL sites currently known to be contaminated w. h the^
population to higher
contaminated hazardous waste site media,
concentrations of endosulfan in the contaminated media
o(.
gcneral
Qf
le would potentially be
ex'posed have not been adequately characterized.
.ddiiinn io ...disidn.,. who am ooenp.imn.ik,
several groups
<1»> genorai population
h^und .ovels) to
^id^s living in prommuy io siles
„f, ...........
-»
X'XXZL w.s.0 si'ios Whom eudosiiiran has bee,, . ...................
. ............ on a
media (HazDat 2000).
5.8
adequacy of the database
led directs the Administrator of ATSDR (in consultation with the
Section 104(i)(5) of CERCLA, as amended,
whelhcr
Administrator of ERA and agencies and proems of
adequate information on the health effects °
available, ATSDR, in conjunction with the a ion
inliiaiion of « program of research designed to avn”'
med,nds io dnionnioc
' offeoW of eodosdU.o.
program (NTP), is required to assure the
techniqucs for dcvelopihg
207
ENDOSULFAN
5. POTENTIAL FOR HUMAN EXPOSURE
The following categories of possible data needs have been identified by a joint team of scientists from
ATSDR, NTP, and EPA. They are defined as substance-specific informational needs that if met would
reduce the uncertainties of human health assessment. This definition should not be interpreted to mean
that all data needs discussed in this section must be filled. In the future, the identified data needs will be
evaluated and prioritized, and a substance-specific research agenda will be proposed.
5.8.1
Identification of Data Needs
Physical and Chemical Properties.
The physical/chemical properties ol endosulfan are
sufficiently well characterized to enable assessment of the environmental fate of the compound (Budavan
1996; Coleman and Dolingcr 1982; EPA 1982c, 1987b; Hansch and Leo 1995; HSDB 1999; Metcalf
1995;NIOSH 1997; Sittig 1980; Suntio et al. 1988; Tomlin 1994). The relative persistence of the two
isomers and the potential for conversion from one isomer to another may also deserve further study.
Production, Import/Export, Use, Release, and Disposal.
Endosulfan is distributed in the
environment as a result of its use as an insecticide (Gregor and Gummer 1989; NRCC 1975; Strachan et
al. 1980). Humans may be exposed through the ingestion or use of contaminated food (Gartrell et al.
1986; Podrebarac 1984a) or tobacco products (EPA 1982a), contact with media from contaminated
hazardous waste sites (principally soils), or insecticide application (Oudbier et al. 1974; Wolfe et al.
1972).
Although endosulfan is currently produced for use as an insecticide, information on the current
production, import, and export of endosulfan by the United States is limited. Annual production volumes
in the United States were 3 million pounds in 1980 (Sittig 1980), and 10,000 metric tons (approximately
22 million pounds) worldwide were reported in 1984 (WHO 1984). However, as of 1982, endosulfan was
no longer produced in the United States (HSDB 1999). Although U.S. imports of endosulfan are
reportedly substantial, the most recent import information (182,000 kg) was lor the year 1982 (HSDB
1999). Additional information on the production/formulation, import, and export volumes for endosulfan
would be useful in assessing the extent to which, and conditions under which, humans may be exposed to
endosulfan or endosulfan sulfate.
Releases of the compound as an insecticide are typically to the atmosphere and land (WHO 1984). The
medium of most importance to human exposure appears to be contaminated foods (Gartrell et al. 1986).
208
ENDOSULFAN
5. POTENTIAL FOR HUMAN EXPOSURE
Methods suggested for the disposal of endosulfan, or more generally, pesticides, their residues and
spillage, and contaminated containers include ground surface disposal, incineration, lagooning, and
disposal in deep wells, sanitary landfills, and disposal pits (EPA 1974; FAO/WIIO 1975a; Working
Group on Pesticides 1970). However, no data on the amounts disposed of by each method were
available. Regulations pertaining to the disposal of endosulfan include the requirement that containers
contaminated with endosulfan residues be emptied, decontaminated, and cither recycled or disposed of in
landfills, depending on their condition (EPA 1974; FAO/WIIO 1975a; IISDB 1999). Current information
on disposal practices for endosulfan would be useful in evaluating (he potential lor exposure to
endosulfan and endosulfan sulfate.
According to the Emergency Planning and Community Right-to-Know Act of 1986, 42 U.S.C.
Section 11023, industries are required to submit chemical release and off-site transfer information to the
EPA. The Toxics Release Inventory (TRI), which contains this information for 1993, became available in
May of 1995. This database will be updated yearly and should provide a list of industrial production
facilities and emissions.
Environmental Fate.
Endosulfan partitions to the atmosphere and soils and sediments. It is
transported in the atmosphere (Gregor and Gummer 1989; Strachan et al. 1980), but it is immobile in soils
(Bowman et al. 1965; El Beit et al. 1981c; Hodapp and Winterlin 1989; Stewart and Cairns 1974). It is
transformed in surface waters and soils via hydrolysis (Greve and Wit 1971; Schoetteger 1970) and
biodegradation (Cotham and Bidleman 1989; El Beit et al. 1981c; Greve and Wit 1971; Martens 1976;
Miles and Moy 1979; Stewart and Cairns 1974). Endosulfan sulfate persists in soils (Coleman and
Dolinger 1982). Additional information is needed on the extent to which the compound undergoes
photochemical oxidation in the atmosphere. This information would be helpful in establishing the
atmospheric half-life of the compound.
Bioavailability from Environmental Media.
Endosulfan can he absorbed following inhalation of
contaminated workplace air and ingestion of insecticide-contaminated food (Ely et al. 1967). Dermal
contact with or ingestion of endosulfan that is tightly bound to soil particles is an exposure route of
concern at hazardous waste sites. No information is available on the absorption of endosulfan in either
adults or children following ingestion or dermal contact with contaminated soils. Therefore, additional
information is needed on the uptake of endosulfan from contaminated soil following ingestion or dermal
contact. This information would be useful in determining the bioavailability of soil-bound endosulfan.
209
ENDOSULFAN
5. POTENTIAL FOR HUMAN EXPOSURE
Food Chain Bioaccumulation.
Endosulfan is bioconcentratcd by aquatic organisms (Ernst 1977;
Novak and Ahmad 1989; NRCC 1975; Roberts 1972; Schimmel ct al. 1977) but not by plants or animals
(EPA 1982a). The compound is metabolized by terrestrial (Coleman and Dolinger 1982; El Beit ct al.
1981c; Martens 1977; NRCC 1975) and aquatic organisms (Cotham and Bidleman 1989), and it does not
biomagnify to any great extent in terrestrial or aquatic food chains (FISDB 1999). No additional
information on the bioaccumulation of endosulfan is needed at this time.
Exposure Levels in Environmental Media.
Endosulfan and endosulfan sulfate have been detected
in ambient air (Bidleman 1981; Kutz et al. 1976), surface water (EPA 1980b, 1982c; Frank et al. 1982b;
Maguire et al. 1983; McFall et al. 1985; Miles and Harris J 971; Willis et al. 1987), rain water (Strachan
and Huneault 1979), cropland soils (Carey ct al. 1979a, 1979b), and some foodstuffs (Gartrell et al. 1986;
Podrebarac 1984a). However, with the exception of the food concentrations, the data arc not current.
Estimates of human intake of endosulfan or endosulfan sulfate are limited to ingestion of contaminated
foodstuffs. Additional information is needed on the current levels of these compounds in ambient air,
surface water, and soils, particularly at the 162 NPL hazardous waste sites known to be contaminated with
these compounds. This information would be helpful in estimating human exposure to these compounds
via contact with contaminated media.
Reliable monitoring data for the levels of endosulfan in contaminated media at hazardous waste sites arc
needed. This information could be used in combination with the known body burdens of endosulfan to
assess the potential risk of adverse health effects in populations living in the vicinity of hazardous waste
sites.
Exposure Levels in Humans.
Endosulfan and endosulfan sulfate can be measured in human blood,
urine, and tissues following exposure to high levels in workplace environments or following accidental or
intentional ingestion of insecticides containing endosulfan (Coutselinis et al. 1978; Demeter and
Heyndrickx 1978; Demeter et al. 1977). However, no monitoring studies are available in which human
fluids or tissues were used to assess occupational or general population exposure to endosulfan.
Additional data on levels in human blood and urine are needed following occupational and general
population exposure, particularly exposure at hazardous waste sites, in order to correlate concentrations in
these media with those in environmental media and the subsequent development of health effects, if any.
This information is necessary for assessing the need to conduct health studies on these populations.
210
ENDOSULFAN
5. POTENTIAL FOR HUMAN EXPOSURE
Exposures of Children.
Data need to be developed to properly assess the exposure ol infants who
eat processed baby foods containing residues of pesticides such as endosulfan. Several studies have
estimated exposure based on endosulfan concentration found in foods typically eaten by infants; however,
no studies that directly studied infant exposure could be located. Attention should also be given to infant
formulas and to the tap water used to prepare infant formulas from condensed or powdered forms. More
data arc also required to properly assess endosulfan exposure to children who live, play, or attend school
near fanulands that are treated with endosulfan. Maps that catalog endosulfan use on crops and present
average application rates would better allow an assessment ol the potential for childicn in (aiming
communities to be exposed. The possibility that fanning parents’ work clothes and shoes may carry
endosulfan residues into the home also should be studied. In addition, home use ol endosulfan, which
may result in exposure of children, needs to be investigated.
Child health data needs relating to susceptibility are discussed in 2.1.2.2 Identification of Data Needs:
Children’s Susceptibility.
Exposure Registries.
No exposure registries for endosulfan were located. This substance is not
currently one of the compounds for which a subregistiy has been established in the National Exposure
Registry. The substance will be considered in the future when chemical selection is made loi
subregistries to be established. The information that is amassed in the National Exposure Registry
facilitates the epidemiological research needed to assess adverse health outcomes that may be related to
exposure to this substance.
The compound will be considered in the future when chemical selection is made lor subrcgistrics to be
established. The information that is amassed in the National Exposure Registry facilitates the
epidemiological research needed to assess adverse health outcomes that may be related to the exposuie to
this compound.
Information is particularly needed on the size of the populations potentially exposed to endosulfan
through contact with contaminated media in the vicinity of hazardous waste sites. The development of an
exposure registry would provide a useful reference too) in assessing exposure levels and frequencies. It
would also facilitate the conduct of epidemiological or health studies to assess any adverse health effects
resulting from exposure to endosulfan. In addition, a registry developed on the basis of exposure sources
would allow an assessment of the variations in exposure levels from one source to another and the cl feet
of geographical, seasonal, and regulatory action on the level of exposure within a certain source. These
211
IDOSULFAN
5. POTENTIAL FOR HUMAN EXPOSURE
assessments, in turn, would provide a better understanding of the needs for research oi data acquisition on
the current exposure levels.
5.8.2 Ongoing Studies
No ongoing studies regarding release, bioavailability, bioaccumulation or exposure registries were
located. However, several ongoing studies regarding the fate and transport, disposal, and human
exposure of endosulfan were located. Researchers from the University of Nevada arc examining the
atmospheric transport and deposition ol endosulfan and its input to the Sierra Nevada mountains
(FEDRIP 1999). At the University of California at Davis, researchers are examining an integrated
approach to the bioremediation of pesticides at hazardous waste sites (FEDRIP 1999). I his appioach
involves the use of flooded plots and rice plants to enhance degradation. Tn another study, researchers
from Kentucky State University arc analyzing the fate of endosulfan under Held conditions in an artificial
wetlands environment (FEDRIP 1999). They are studying the influence of landscape features and soil
amendments on runoff and infiltration of water quality as well as the late ol pesticides found along the
edge of fields. In New South Wales, a group of researchers arc examining the impact of endosulfan on
natural water systems as a result of industrial activity (FEDRIP 1999). At the Beltsville Agricultural
Research Center, the atmospheric and surface interactions of endosulfan and its fate and transport aic
being studied (FEDRIP 1999).
c- °;
___ -
5’
I
ENDOSULFAN
A REVIEW OF ITS
TOXICITY AND ITS EFFECTS ON THE
ENDOCRINE SYSTEM
Susan Sang, Ph.D.
and
Sanya Petrovic, M.Sc.
<8>
WWF
World Wildlife Fund Canada
October 1999
Endosulfan - A Review ofits Toxicity and its Effects on the Endocrine System
i H AA’
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WWF’s WILDLIFE TOXICOLOGY PROGRAM
World Wildlife Fund’s Toxicology Program is dedicated to protecting wildlife and their habitat
from harm caused by toxic chemicals.
Efforts include reducing pesticide use, reducing exposure to endocrine disrupting chemicals,
banning the use of lead shot and sinkers, and introducing pollution prevention for all direct and
indirect dischargers. WWF also undertakes practical projects to reduce reliance on pesticides and
other industrial chemicals.
ACKNOWLEDGEMENTS
WWF' would like to thank Dr. Michael Berrill (Trent University), Dr. Bill Frnest
(Toxic Substances and Pesticides Control Section, Environment Canada) and
Dr. Bruce Pauli (Canadian Wildlife Service) for their assistance in reviewing this report.
Special thanks to the Weston Foundation tor their support of our Wildlife Toxicology Research
Program.
This report is based on materials available up to and including those published in 1998.
Views expressed in this report are those of WWF and not necessarily those of the reviewers.
For more information or to order more reports contact:
Jarmila Becka
Wildlife Toxicology Program
World Wildlife Fund Canada
245 Eglinton Avenue East, Suite 410
Toronto, ON M4P 3JI
tel: (416) 489-4567 ext. 287
fax: (416) 489-3611
email: jbecka@wwfcanada.org
I his report is also available on our website: www.wwf.ca/hornione-disruptors/.
Endosulfan - A Review of its Toxicity and its Effects on the Endocrine System
I
TABLE OF CONTENTS
PAGE
EXECUTIVE SUMMARY
3
1.0
INTRODUCTION
6
2.0
CHEMICAL IDENTIFICATION
2.1 Chemical Profile
2.2 Trade Names
2.3 Physical and Chemical Properties
2.4 Mode of Action
2.5 Production and Use
6
6
7
7
7
8
3.0
ENVIRONMENTAL FATE AND DEGRADATION
3.1 Fate and Degradation in the Atmosphere
3.2 Fate and Degradation in Water
3.3 Fate and Degradation in Soil
3.4 Fate and Degradation in Plants
3.5 Bioaccumulation
3.6 Residues
3.6.1 Residues in Air
3.6.2 Residues in Aquatic Ecosystems
3.7
Exposure
9
9
10
10
10
11
11
11
12
13
4.0
TOXICOLOGICAL PROFILE
4.1 Acute Toxicity
4.1.1 Birds
4.1.2 Aquatic Organisms
4.1.3 Amphibians
4.1.4 Mammals
4.1.5 Microorganisms
4.2 Chronic/Subchronic Toxicity
4.2.1 Effects on the Central Nervous System (CNS)
4.2.2 Effects on the Immune System
4.2.3 Effects on the Reproductive System
4.2.4 Carcinogenicity
4.2.5 Mutagenicity
4.3 In Vitro Studies
4.3.1 Neuronal Cells
4.3.2 Liver Cells
4.3.3 Estrogenic Activity
4.3.4 Synergism
16
16
16
16
19
19
20
20
21
22
24
27
27
28
28
29
29
30
5.0
REGULATORY STATUS
31
Endosulfan - A Review ofits Toxicity and its Effects on the Endocrine System
1
5.5 World Health Organization and Food and Agriculture Organization
31
32
33
33
33
6.0
ALTERNATIVES
6.1 Integrated Pest Management (1PM)
6.2 Chemical Alternatives
34
34
34
7.0
CONCLUSIONS
35
8.0
RECOMMENDATIONS
36
9.0
REFERENCES
38
5.1
5.2
5.3
5.4
North America
Europe
Australia
Others
TABLES
Table 1: Estimated Annual Agricultural Use of Endosulfan in United States (1992)
Table 2: Total Use/Sale of Endosulfan in Canadian Provinces (1995-1997)
Table 3: Endosulfan Concentrations in Snowpack Samples from Amituk Lake
Table 4: Summary of Endosulfan Concentrations (pg/m3) in the Arctic Atmosphere
Table 5: Maximum Residue Limits (MRLs) in Vegetables arid Fruits in Canada
Table 6: Endosulfan Residues in Vegetables and Fruits Grown in Canada
Table 7: Acute Toxicity Values of Endosulfan
Table 8: Action and Advisory Levels for Endosulfan in the United States
Table 9: Endosulfan Maximum Residue Levels in Crops, Food, and Feeding Stuffs
Table 10: Codex Alimentarius Commission’s Maximum Residue Limits
8
9
12
12
14
15
18
32
32
33
Endosulfan - A Review ofits Toxicity and its Effects on the Endocrine System
3
EXECUTIVE SUMMARY
Endosulfan is a highly toxic chlorinated hydrocarbon pesticide which acts as a contact poison to a
variety of insects and mites.
Uses
Endosulfan is used extensively as an insecticide on food crops such as grains, fruits, tea and
vegetables, non-food crops such as cotton and tobacco, and on forage crops such as alfalfa. It is
also used as a wood preservative.
Release to the environment
Endosulfan is found in various compartments of the environment including air, water, and soil.
The most contaminated areas are located where endosulfan is formulated, used or disposed of. In
Canada, endosulfan is usually applied by aerial or ground spray techniques at rates of 0.25-0.1 g/L
of water or 0.22-4.4 kg/ha. Endosulfan residues have been found in fruits and vegetables as well
as meat, milk products, fish and other seafood.
Fate and exposure
In water, endosulfan has a relatively short resident time and normally disappears within two
weeks. It breaks down in water to endosulfan sulfate and endosulfan diol. Both endosulfan and
endosulfan sulfate have a longer half-life in sediment. Concentrations of endosulfan in sediment
have been reported to be 32,000 times higher than in the water column.
In soil, endosulfan readily binds to the soil particles and the majority stays within the first five
centimetres of the soil surface. Endosulfan isomers (ex and B) show different rates of dissipation
from soil. In experimental applications of endosulfan, at a simulated rate of 6.7 kg/ha, 50 per cent
of (x-cndosulfan disappeared within 60 days, versus 800 days for B-endosulfan.
In air, endosulfan is carried over long distances. Traces of endosulfan have been found in Arctic
air as well as snow samples.
Endosulfan is less persistent on plant surfaces and rapidly degrades to endosulfan sulfate and
endosulfan diol. The estimated half-life of endosulfan on plants ranges from 1.95 to 2.74 days.
Endosulfan does not accumulate in aquatic organisms. Up to 99 per cent of endosulfan disappears
from the system two weeks after exposure. Similarly, mammals and birds do not accumulate large
quantities of endosulfan or endosulfan sulfate in their bodies.
Human exposure
The most important routes of human exposure to endosulfan are ingestion of food and use of
tobacco products with endosulfan residues. Farmers, pesticide applicators, and individuals living
in the vicinity of hazardous waste disposal sites contaminated with endosulfan may receive
additional exposure through dermal contact and inhalation. Infants are also exposed to endosulfan
through ingestion of their mother’s milk.
Endosulfan - A Review of its Toxicity and its Effects on the Endocrine System
4
Acute toxicity
Endosulfan is classified as a highly toxic substance. It is acutely toxic to birds, marine and
freshwater fish, and mammals. Like other chlorinated cyclodienes, endosulfan is a neurotoxin
affecting the central nervous system (CNS) of aquatic organisms as well as mammals.
People who are occupationally exposed to endosulfan are advised to avoid eye and skin contact as
well as inhalation exposure. Symptoms of acute toxicity in humans are restlessness, irritability and
hyperexcitability, followed by headache, dizziness, nausea and vomiting, blurred vision,
unconsciousness, insomnia, lack of appetite, loss of memory, albuminuria, haematuria and in some
cases, confusion.
Chronic toxicity
Chronic exposure to endosulfan may result in general toxicity symptoms such as liver and kidney
damage as well as effects on the CNS, immune system and the reproductive system.
Neurotoxicity
Endosulfan may have adverse effects on the CNS of aquatic organisms, birds and mammals. The
main mechanism of action of endosulfan in the CNS is inhibition of brain acetylcholinesterase,
causing uncontrolled discharges of acetylcholine. Abnormal behaviour has been observed in fish
and mammals being chronically exposed to endosulfan.
Immune System
Endosulfan is also known to affect the immune system. Target organs are the kidneys and liver.
Endosulfan inhibits leukocyte and macrophage migration causing adverse effects on the humoral
and cell mediated immune system.
Reproductive Effects
Some studies have shown a potential for adverse effects of endosulfan in the reproductive system
of aquatic organisms and mammals. Histological changes in reproductive organs were seen in
aquatic organisms following exposure to endosulfan at concentrations as low as 0.00075 mg/L
(0.75 |ig/L). Endosulfan treatment in male rats was reported to cause a dose-dependent reduction
in sperm counts, sperm abnormalities and decreased daily sperm production as well as decreased
testis weight.
In vitro evidence for an endocrine disruptive action
Endosulfan is estrogenic in the E-SCREEN assay. Endosulfan I competes with [3H]17p-estradiol
for binding to the estrogen receptor. Endosulfan sulfate inhibited binding of [JH]R5020 to the
progesterone receptor by 40-50 per cent. Low levels of endosulfan (1 nM, 0.41 ppb) can inhibit
the human sperm acrosome reaction, initiated by progesterone and glycine, but the inhibition is
not complete. Endosulfan II and endosulfan sulfate decreased p-galactosidase activity of
progesterone (Jin et al.,1997).
Endosulfan - A Review ofits Toxicity and its Effects on the Endocrine System
5
In vivo evidence for endocrine disruption action
1. Endosulfan decreased plasma vitellogenin levels in catfish (Chakravorty et al., 1992).
2. Endosulfan decreased the number and size of oocytes in fresh water teleost fish, and increased
the number of deformed oocytes, damaged yolk vesicles, and dilated gonadosomatic index.
3. Endosulfan caused a dose-dependent reduction in sperm counts in rats, reduced the number of
spermatids, caused sperm abnormalities and decreased daily sperm production.
Regulatory status
Endosulfan is a restricted use pesticide in the United States of America and is banned in Norway
and Sweden. In Indonesia, the government is banning 28 pesticides including endosulfan due to
their impact on human health.
Endosulfan - /I Review ofits Toxicity and its Effects on the Endocrine System
6
1.0
INTRODUCTION
Endosulfan is an organochlorine pesticide used to control a wide range of insects and other
invertebrate pests. It is available as granules, dusts, wetable powders and emulsifiable
concentrates. Endosulfan is used as an insecticide on food crops such as grains, fruits, tea and
vegetables, non-food crops such as cotton and tobacco and on forage crops such as alfalfa. It is
also used in forestry practices as a wood preservative to control termites in logs.
A variety of insects are controlled by endosulfan, including aphids, beetles, bollworms,
spittlebugs, termites, tsetse flies, leafhoppers, pear psylla, fleabeetles, stemborers, stinkbugs, boll
weevils, loopers, corn earworms, peach twig borers, armyworms, cyclamen mites, mosquito
pupae, and many other insects.
Endosulfan is considered to be highly toxic. It can adversely affect human and wildlife exposed to
it. It has been shown to cause damage to the nervous system, as well as other parts of the body,
with the liver and kidney being target organs for chronic exposure in mammals. Fish are
particularly sensitive to endosulfan and fish kills have been reported following agricultural use of
endosulfan in Canada and in other areas. Recently, endosulfan has been implicated as a
xenoestrogen.
This paper reviews the toxicity of endosulfan, with particular emphasis on its ability to disrupt the
endocrine system, evidence of which has emerged since 1990. This is not an exhaustive review of
the literature available on endosulfan toxicity, as several other studies have extensively reviewed
the general toxicity of this pesticide (WHO, 1984; ATSDR, 1993; WHO/FAO, 1990; Ernst el al.,
1996; Environment Canada, 1990). Most of the information reviewed regarding the effects of
endosulfan on the reproductive system is from literature published post-1990.
2.0
CHEMICAL IDENTIFICATION
2.1
Chemical Profile
Endosulfan is produced by the reaction of hexachlorocyclorocyclopentadiene and cis-butene-1,4diol in xylene, followed by hydrolysis of the adduct to the cis-diol or dialcohol. Endosulfan is then
produced by treating this bicyclic dialcohol with thionyl chloride. Technical grade endosulfan
consists mainly of two different isomers, a and p, in approximately a 7:3 ratio. Technical grade
endosulfan contains at least 94 per cent of the a and p isomers. It may also contain up to two per
cent endosulfan alcohol and one per cent endosulfan ether as well as endosulfan sulfate (ATSDR,
1993).
Endosulfan - A Review ofits Toxicity and its Effects on the Endocrine System
7
2.2
Trade Names
Endosulfan is currently sold in Canada under the trade names: Thiodan (Hoechst Canada Inc.),
Endosulfan 400 (Pfizer C&G Inc.) and Wilson’s Endosulfan (Wilson Laboratories Ltd.). Other
common names for endosulfan containing products include Endocide, Beosit, Cyclodan, Malix,
Thimul and Thifor.
2.3
Physical and Chemical Properties
Chemical name: (\7,8,9,10,10-1 lexachloio-1,5,5a,6,9,9a-hcxahydro-6,9-inethano-2,4,3benzodioxatliiopin-3-oxide
Chemical formula: C9I UCf.OsS
Chemical Structure:
Cl
Cl
Cl
o —/S=O
Cl
Cl
O
Cl
Melting point:
Pure (100%): 106°C
Technical (90%-95% pure): 70°- 100°C
Odour: Slight odour of sulfur dioxide
Solubility in water at 22°C: 0.16-0.15 mg/L
Partition coefficients:
Log Kow: 3.55 and 3.62
Log Koc:: 3.5
Vapour pressure at 25°C: 1 * 10'5 mmHg
Vapour pressure at 80°C: 9*10’3 mmHg
Henry’s law constant at 25 °C: 1 * 10'5 atm m3/mol
Bioaccumulation factor (BCF): <3000
2.4
Mode of Action
Endosulfan is a neurotoxicant which disrupts the release of acetylcholine from presynaptic
vesicles. In fish, this results initially in hyperexcitability and increased respiration, fo|lpwed by loss
of equilibrium, .convulsions, irregular opercular movements and death. Other secondary actions
include biochemical changes in enzymatic activities, estrogen metabolisms, as well as in
carbohydrate, lipid and protein metabolism (Ernest e! a!1996).
I'.m/osiilfan - A Review oj its Toxicity and its R/fects on the Rndocrine System
8
2.5
Production and Use
Endosulfan, as an insecticide, was first introduced by ArgEvo (formerly Hoechst) in the 1950s. In
1984, the World Health Organization (WHO) estimated the worldwide production of endosulfan
at 10,000 tonnes (WHO, 1984). More recently, Barrie at al. (1992) estimated that the global
cumulative usage of endosulfan as 57,000 tonnes per year (based on sales figures).
Endosulfan was first registered in the United States (US) in 1954 by Farbwerke Hoechst AG.
Annual production was estimated at 1,368 million tonnes in 1984. Endosulfan has not been
produced in the US since 1982, however, it is still used in chemical formulations throughout the
country (ATSDR, 1993). In 1992, 817 tonnes of endosulfan were used in the US on various
crops, including cotton, vegetables and fruits, as outlined in Table I below.
Table 1: Annual Agricultural Use of Endosulfan in the United States in 1992
CROPS
Cotton
Apples
Tomatoes
Potatoes
Pecans
Pears
Lettuce
Grapes
Squash
Peaches
TOTAL / CROP (KG)
334,219 '
104,369
102,379
88,549
59,264
33,961
27,696
25,713
19,284
18,083
% OF TOTAL
35.26
11.01
10.80
9.34
6.25
3.58
2.92
2.71
2.03
1.91
Total
813,518
(USGS - Pesticide National Synthesis Project)
Endosulfan was first registered in Canada in 1958. Currently, there arc I 1 products in Canada
containing endosulfan which are registered for domestic, industrial and agricultural use. Sales of
endosulfan doubled between 1968 and 1974, reaching 92,569 kg in 1974 (Environment Canada,
1990). The use pattern of endosulfan in Canada is not well known. Estimated annual endosulfan
use in the Great Lakes region (US and Canada) is 72,338 kg or 159,476 pounds (Hoppin el al.,
1997). In Prince Edward Island (PEI), it has been used extensively on potato crops, with an
estimated 50-60 per cent of the 30,000 ha of potato fields being treated annually with an
endosulfan formulation, Thiodan. Table 2 is a summary of the total sale/use of endosulfan in
various Canadian provinces (based on personal communications with appropriate government
personnel). Endosulfan is not manufactured in Canada; the major suppliers in Canada are
PFIZER., C. & C. Inc., United Agr. Products, Wilbur-Ellis Co., Yellow Stone Agri. Products and
Makhteshim Agn N. A. Endosulfan is used on a number of different fruits and vegetables in
Canada, with maximum residue limits shown in Section 3.7.
Endosulfan - A lleview ofits Toxicity and its Effects on the Endocrine System
9
Table 2: Total Use/Sale of Endosulfan in Canadian Provinces (1995-1997)
PROVINCE_______
Prince Edward
Island
Ontario
British Columbia
Alberta
Quebec
Newfoundland
New Brunswick
Nova Scotia
Saskatchewan
North West
Territories
| Yukon __________
TOTAL KG
10,000-50,000
24,668
6,857
822
N/A
N/A
N/A
N/A
N/A
N/A
N/A
N/A = data not available
3.0
ENVIRONMENTAL FATE AND DEGRADATION
The two isomers of endosulfan which are used in commercial formulations have different tales in
the environment, as p-endosulfan is more persistent than oc-endosulfan (NRCC, 1975).
Endosulfan sulfate is the main degradation product of both isomers, and is itself persistent m t le
environment (NRCC, 1975). Whereas, endosulfan diol is their hydrolysis product which tends to
form in alkaline aquatic environments (NRCC, 1975).
3.1 Fate and Degradation in the atmosphere
Drift from aerial applications and volatilization from water and plant surfaces are the piimary
ways of endosulfan entry into the atmosphere. Although less volatile than many other
organochlorine compounds, some of the endosulfan sprayed on crops and in the water will
volatilize to the air (Simonich and Hites, 1995;Terranova and Ware, 1963). The volatilization
half-life from surface water varies from 1 Idays to one year and from plant surfaces from two to
three days (Callahan el al., 1979).
Endosulfan can be transported over long distances in air before being removed by dry and wet
deposition. Traces of endosulfan have been found in places were endosulfan has never been used.
For instance, endosulfan has been found in Canadian rainfall samples from remote areas, away
from the source of contamination, and in snowpack samples collected from the Arctic (Gregor
and Gummer, 1989).
While in the air, endosulfan undergoes photolysis mainly to endosulfan diol, a-endosulfan also
transforms to P-endosulfan, which is a more stable form (Dureja and Mukerjee, 1982). The EPA
estimated a photolytic half-life of seven days for endosulfan (EPA, 1982).
Endosulfan - /I Review ofits Toxicity and its Effects on Ihe Endocrine System
10
3.2 Fate and Degradation in Water
Manufacturing and formulating facilities, atmospheric deposition and runoff from treated
croplands are the major sources of endosulfan contamination of surface and ground water
(NRCC, 1975).
In water, endosulfan undergoes hydrolysis and microbial degradation. The rate of hydrolysis is
influenced by pH. The hydrolytic half-life can range from five weeks at pH 7 to five month a p
5.5 (Greve and Wit, 1971; Schoetteger, 1970).
Microbial degradation products of endosulfan in water include endosulfan sulfate and endosulfan
diol (NR.CC 1975) The half-life of endosulfan in water varies from three to seven days to about
five months,’depending on the dissolved oxygen content and pH of the water as well as the degree
to which the water is polluted (NRCC, 1975). For instance, 95 per cent of 10 (ig/L endosulfan in
raw river water at normal temperatures will disappear afler two weeks. The estimated half-hfe of
technical endosulfan in lake water is 50.3 hours (Ferrando el al., 1992). However, the degradat
half-life is much longer in sediment (NRCC, 1975).
3.3 Fate and Degradation in Soil
In soil endosulfan binds strongly to soil particles and is not readily leached out to ground water
The bulk of endosulfan residues is bound to the top 15 cm of soil surface layers^ In expenmenta
conditions, 90 per cent of the endosulfan residues were found in the top 15 cm horizon o> thei sod
surface, nine per cent at a depth of 15-30 cm, and only one per cent was found at the depth of 30-
45 cm after 503-828 days (Stewart and Cairns, 1974).
In soil, endosulfan is subject to photolysis, hydrolysis or biodegradation. Major product5 of
degradation processes in soil are endosulfan diol and endosulfan sulfate (Martens, !976, EIBe.t
ctl 1981). Endosulfan isomers show different rates of dissipation from soil. Endosulfan sulfate
more persistent than the parent compound (Stewart and Cairns, 1974). In expenmenta
applications of endosulfan, at a simulated rate of 6.7 kg/ha. 50 per cent of rt-cndosul an
disappeared within 60 days, versus 800 days for ji-endosulfan. In ai;ot‘ie"eP°Jl’lia‘‘’'1VCS °
a- and p-endosulfan were estimated as 35 and 150 days, respect.vely (EXTOXNET, 1936).
3.4 Fate and Degradation in Plants
On plant surfaces, residues of endosulfan isomers (a and p) rapidly degrade to endosulfan
metabolites with a half-life of 1.95 to 2.74 days. In pigeonpea pulse crop and on tomatoes,
endosulfan concentrations declined 62 to 64 per cent in the 48 hours
S72
application. Similarly, endosulfan residues on jute and grape crops fell 72 to 89 per centu.the
hours after treatment. The volatilization rate of endosulfan from plant surfaces is
than from soil surfaces. When French beans were sprayed with endosulfan (1 hmdan EC35)iu
controlled conditions, 60 per cent of endosulfan volatilized from plant surfaces within 24 hours.
Endosulfan - A Review of its Toxicity and its Effects on the Endocrine System
11
whereas the volatilization rate of endosulfan from soil surfaces was only 12 per cent after 24
hours (Rudel, 1997).
In plants sprayed with endosulfan, residues are reported to be initially as high as 100 mg/kg, and
decrease by up to 90 per cent in the span of a few weeks (NRCC, 1975). Some of the endosulfan
volatilizes to the air (Terranova and Ware, 1963), and of that which remains on the plants, most is
degraded Io endosulfan sulfale and endosulfan diol, and Io a lesser extent to cndosullan ether,
endosulfan cx-hydroxyether and endosulfan lactone (Archer,* 1973). Formation of endosulfan
sulfate depends on temperature, with less formed at temperatures below 16-18°C (Cassil and
Drummond, 1965).
3.5
Bioaccumulation
Endosulfan does not bioaccumulate in high concentrations in terrestrial animals or in plants or
biomagnify in terrestrial or aquatic food chains. However, it bioconcentrates to some extent in
aquatic organisms with a maximum bioconcentration factor (BCF) of approximately 3,000
(NRCC, 1975; Schimmel el al., 1977).
Mammals and birds do not accumulate large quantities of endosulfan or endosultan sulfate, with
BCFs of less than one (NRCC, 1975). This was confirmed in a recent study by a lack of
endosulfan residues in tissues of rabbits 35 days following a single oral dose of 15.13 mg
endosulfan/kg body weight (Ceron el al., 1995). The reason could be that most endosulfan is
metabolized in the body to hydrophilic compounds which are readily excreted (Smith, 1991b).
3.6 Residues
Endosulfan is released to the environment mainly as a result of its use as an insecticide. 3 he most
contaminated areas are locations where endosulfan is formulated, used or disposed. In Canada,
endosulfan is usually applied by aerial or ground spray techniques at rates of 0.25-0.1 g/L of
water or 0.22-4.4 kg/ha (Environment Canada, 1990).
High concentrations of endosulfan, as oc-endosulfan, p-endosulfan and endosulfan sulfate, have
been detected in tree bark samples throughout the world, particularly in India and the Pacific Rim
(Simonich and Hites, 1995). It was speculated that the high concentrations of endosulfan in these
areas were due to its use on rice.
3.6.1 Residues in air
Endosulfan residues have been found in snow samples in the Arctic, with levels measured at 410
pg/L (Gregor and Gummer, 1989) which is reflective of atmospheric deposition of endosulfan
distant from the area of use. In a more recent study, endosulfan residues were found in both
shallow and deep parts of snowpack collected from Amituk Lake. These levels are shown in I able
3.
Endosulfan - /I Review ofits Toxicity and its Effects on the Endocrine System
12
Table 3: Endosulfan Concentrations in Snowpack Samples from Amituk Lake
YEAR
CONCENTRATION (pg/L)
SHALLOW
135
95
217
1992
1993
1994
CONCENTRATION (pg/L)
________ DEEP________
466
734
605
(CACAR Report, 1997)
As noted above, endosulfan can be transported long distances in the atmosphere. In a recent study
at Resolute Bay in the North West Territories, a-endosulfan concentrations of 3.7 to 4.1 pg/m3
were measured in the air (Bidleman et al., 1995). The authors suggested that levels may actually
be higher than this, as recovery for endosulfan was not conducted during analysis. In an earlier
study, a-endosulfan levels of 1.8 to 9.7 pg/m' were measured in air at Ice Island in 1986-87
(Patton et a!., 1989). Endosulfan was also found in air samples collected, using high-volume air
samplers, in the western Arctic and Russia (CACAR, 1997). Table 4 is a summary of mean
concentrations of endosulfan found in Arctic air in 1993/1994.
Table 4: Summary of Endosulfan Concentrations (pg/m3) in the Arctic
Atmosphere
REGION
Alert (NWT)
Tagish (Yukon)
Dunay Island (Russia)
1993 MEAN
CONCENTRATION
(RANGE)
3.60 (0.02-9.42)
5.76 (0.08-15.30)
2.99 (0.05-7.18)
1994 MEAN
CONCENTRATION
_______ (RANGE)
4.89 (0.07-16.2)
6.58 (0.08-13.90)
(CACAR Report, 1997)
In the Great Lakes region, endosulfan levels in air are present at pg/m3 levels. Endosulfan
concentrations in air were reported to decrease in this area from the late 1980s to the early 1990s,
with 350 pg/m3 measured in 1988-89, and 89 pg/m3 measured in 1991-92 (Hoflfe/«/., 1992,
Burgoyne and Hites, 1993).
3.6.2 Residues in aquatic ecosystems
In aquatic ecosystems, endosulfan partitions to plants and animals and also accumulates in
sediment (NRCC, 1975). Concentrations of endosulfan in sediments were estimated to be up to
32,000 times the concentrations measured in the water column (NRCC, 1975). In sediments in
Jamaica, endosulfan levels were reported to range from below detection to 5,961 (tg/kg
(Mansingh et a!., 1997). Whereas, endosulfan levels in surface water in Jamaica ranged from
below detection to 3 I 8 pg/L (Mansingh et a!., 1997).
Endosulfan - /I Review of its Toxicity and its Effects on the Endocrine System
13
Shrimp and fish collected in Jamaica were reported to have residues of up to 15.9 ng/g wet weight
(x-endosulfan, 11.1 ng/g p-endosulfan, and 10.2 ng/g endosulfan sulfate (Mansingh et al., 1997).
Although generally low concentrations of endosulfan have been found in surface water, lethal
concentrations may be found in ponds and streams in the vicinities of spraying areas. A study
using water containers indicated that drift from aerial agricultural spraying could produce
concentrations lethal to fish in shallow exposed water bodies 200 m away from the target spray
area. Levels of 1.7 mg/L and 0.04 mg/L were found in water containers in the vicinities of the
spraying areas and 200 m away. These levels are found to be lethal to fish (Ernst et al., 1991).
This experiment confirms that the agricultural practice of applying endosulfan aerially may lead to
increased pesticide concentrations in waters olf-sitc, which could result in fish kills in unexpected
areas.
3.7 Exposure
Farmers, pesticide applicators, and individuals living in the vicinity of hazardous waste disposal
sites contaminated with endosulfan may receive exposure through dermal contact and inhalation
(Al SDK, 1993). Woikers who mix or spray endosulfan on tobacco were reported to receive
most of the exposure dermally, with minimal respiratory exposure. One study revealed a dermal
exposure of 16.18 mg/kg body weight/day for mixers and 8.06 mg/kg body wcighl/day for
sprayers (Lonsway et a/., 1997). The authors compared these values to a no-observed-adverseeffect-level (NOAEL) of 3 mg/kg body weight/day and a dermal LD5() of 359 mg/kg for
endosulfan, fherefore, pesticide applicators may be exposed to endosulfan levels above the
estimated NOAEL if they do not take appropriate precautions. Further it is recognized that these
workers were exposed to levels much higher than the acceptable daily intake (ADI) for endosulfan
of 6 pg/kg-day (0.006 mg/kg body weight-day) derived by the World Health Organization
(EXTOXNET, 1998). The ADI is derived by applying safety factors to a NOAEL to account for
intraspecies and interspecies sensitivity.
J he most important routes of endosulfan exposure for the general public are ingestion of food and
use of tobacco products with endosulfan residues. Generally, minimal exposures occur via
inhalation. Safe (1995) estimated the potential exposure of the general public to endosulfan from
food. Ingestion rates of endosulfan were estimated for infants, teenagers and elderly members of
the population. It is important to estimate the potential endosulfan intake of infants and teenagers,
as they consume a large amount of food compared with body weight, and therefore arc
considered sensitive populations. Endosulfan intake was reported to be 0.0274 pg/kg bw/day for
ages 6-11 months, 0.0135 gg/kg bw/day for 14-16 years, and 0.0210 pg/kg bw/day for people
aged 60-65 years. Therefore, although infants receive the most exposure, all of these exposure
levels are below the ADI for endosulfan of 6 pg/kg body weight/day established by WI IO
(EXTOXNET, 1998).
In human milk samples of women living in Egypt, a-endosulfan residues ranged from 0 to 61.80 p
g/L, with a mean concentration of 4.84 pg/L for all samples (Saleh et al., 1996). Concentrations
hidosulfan - J Review ofits Toxicity and its Effects on the Endocrine System
14
of a-endosulfan in breast milk were higher in women living in agricultural areas. Saleh el al.
(1996) assumed that infants would have a mean intake of 0.8 L milk/day and a body weight of 5
kg. Assuming an endosulfan concentration of 4.84 |lg/L in milk, the mean intake of endosulfan by
infants would be 0.774 ftg/kg body weight/day, or 7.74x1 O'4 mg/kg body weight/day, which is
lower than the ADI of 6xlO'J mg/kg body weight/day derived by WHO (EXTOXNET, 1998).
Therefore, the mean residues of endosulfan in mothers’ milk in Egypt do not surpass the
acceptable daily intake of endosulfan for their infants. No information was found in the literature
reviewed for this report relevant to recent endosulfan concentrations in human milk of Canadian
women.
Endosulfan exposures from food come from a variety of sources, including vegetables, fruits,
meat, milk and fish. Some of the residue levels reported in these foods and allowable residue
limits for specific foods are discussed below. Monitoring for pesticides has shown residual
endosulfan in vegetables (0.0005-0.013 mg/kg), seafood (0.2 ng/kg-1.7 |ig/kg), milk and tobacco
(EXTOXNET, 1996). Australian maximum residue limits (MRL) in cattle meat are 0.2 mg/kg and
0.3 mg/kg for stock feeds such as hay, silage fodder crops and pastures. The International
(Codex) MRL for endosulfan in meat is 0.1 mg/kg ( NSW Agriculture, 1997). The US ERA
allows 0.1-2 mg/kg endosulfan in food, and the US FDA allows up to 24 mg/kg endosulfan in
dried tea (ATSDR, 1998). In Canada, MRLs for endosulfan have been set for a variety of foods,
as shown in Table 5 (Health Canada, 1995). Table 6 provides a recent indication of endosulfan
residues found in fresh fruits and vegetables grown domestically (Health Canada, 1997).
Table 5: Maximum Residue Limits (MRLs) in Vegetables and Fruits in Canada1
FOOD
apples, apricots, broccoli, brussel sprouts, cabbage, cherries,
lettuce, peaches, pears, plums, spinach___________________
artichokes, beans, cauliflower, celery, cucumber, eggplant,
grapes, melons, peppers, pumpkins, squash, strawberries,
tomatoes, watercress__________________________________
peas________________________________________________
butter, cheese, milk, dairy products, meat and meat by-products
of cattle, goats, sheep, hogs, poultry and sheep_____________
MAXIMUM
RESIDUE LIMIT
(mg/kg)
2.0
1.0
0.5
0.1
(Health Canada, 1995)
1) Note that the maximum residue limits in Canada for fruits and vegetables are based on toxicological
information provided by industry and assessed by Health Canada.
Endosulfan - /I Review ofits Toxicity and its Effects on the Endocrine System
15
Table 6: Endosulfan Residues in Vegetables and Fruits Grown in Canada
FOOD
NO. OF
SAMPLES
4
1
14
1
8
4
26
MEAN
(mg/kg)
0.186
0.20
0.134
0.05
0.24
0.23
0.102
Apple
Beets
Brussels sprouts
Carrot
Celery
Cucumber
Greenhouse
Cucumber
0.855
Leaf lettuce
4
Fresh lettuce
0.602
3
8
0.134
Peach
1.278
Sweet pepper
11
0.062
Plum
5
Spinach
1
53.0
Squash
0.05
1
Tomato
0.233
3
Greenhouse tomato
0.775
2
(Health Canada, Food Inspection Directorate, 1997)
1) MRLs = maximum residue limits
MRLS1
RANGE
(mg/kg)
0.04-0.63
0.2-0.20
0.07-0.30
0.05-0.05
0.02-1.0
0.03-0.60
0.01-0.50
(mg/kg)
2.0
1.0
2.0
1.0
1.0
1.0
1.0
0.03-1.80
0.196-0.830
0.05-0.2
0.05-5.84
0.03-0.13
53.0
0.05
0.04-0.35
0.71-0.84
2.0
2.0
2.0
1.0
2.0
1.0
1.0
1.0
1.0
Wildlife may be exposed to endosulfan in the environment by consuming plants which have been
sprayed with endosulfan, ingestion of soil or dermal contact with soil. Additional exposure can
occur through inhalation of air in the area of agricultural application. Exposures in aquatic
environments may occur due to surface runoff following agricultural application, or upon
deposition of endosulfan following long-range transport in the atmosphere. Fish have been
exposed to sufficient quantities of endosulfan in agricultural run-off to cause mortality (Frank et
al., 1990).
In the mammalian system, the a-isomer of endosulfan persists in the body longer than [)endosulfan, particularly, in brain tissue and plasma. Male rats, given technical grade endosulfan by
gavage at 0, 5 or 10 mg/kg for 15 days, had detectable levels of a-endosulfan in brain tissue and
plasma, with less [3-endosulfan, and almost no endosulfan sulfate detected (Gupta, 1978).
Similarly, in rabbits, which died following acute exposure, a-endosulfan residues were also
detected in liver and brain tissue (Ceron et al., 1995), but no residual (3-endosulfan or endosulfan
sulfate was found.
Endosulfan - A Review of its Toxicity and its Effects on the Endocrine System
16
4.0
TOXICOLOGICAL PROFILE
4.1
Acute Toxicity
Endosulfan is classified as a “highly toxic” substance (EXTOXNET, 1998). People who use
endosulfan as a pesticide are advised to avoid eye and skin contact, as well as inhalation exposure.
The acute oral toxicity is higher than dermal toxicity (NRCC, 1975). Technical endosulfan has
been reported to be more toxic than endosulfan sulfate, endosulfan diol, endosulfan hydroxyether
and endosulfan lactone (Dorough et al., 1978).
Endosulfan, like other chlorinated cyclodienes is a central nervous system stimulant. The early
symptoms of acute toxicity in humans arc restlessness, irritability and hypcrexcitability, followed
by headache, dizziness, nausea and vomiting, blurred vision, unconsciousness, insomnia, lack of
appetite, loss of memory, albuminuria, haematuria and in some cases, confusion (Smith, 1991a,
b). Exposure of humans to high levels of endosulfan may cause permanent neurological disorder
and brain damage or death (Smith, 1991b). Occupational exposure was reported to result in
convulsions, dizziness, nausea, vomiting, and confusion in workers exposed to Thiodan during
bagging and in one case during cleaning vats containing endosulfan residues (Ely et al., 1967). In
a case-report of human acute toxicity from endosulfan, Aleksandrowicz (1979) reported that twoyears following recovery from acute endosulfan poisoning characterized by convulsions and
impaired consciousness, chronic neurological effects appeared to persist in a patient, including
effects on cognitive and emotional deterioration, impaired memory, and impaired visual-motor
coordination. However, it is noted that these people were exposed to large doses of endosulfan,
which were much higher than that experienced by the general public.
Variable acute toxicity values have been obtained for birds, aquatic organisms and mammals. A
summary of some acute toxicity values is shown in Table 7. The oral LD5o is the ingested value
that is required for 50 per cent mortality of the exposed organisms. Similarly, the dermal LD50 is
the amount of endosulfan applied on the skin which results in 50 per cent mortality, and the
inhalation LC50 is the inhaled concentration that causes the same endpoint. The LC50 for aquatic
organisms is the concentration of endosulfan in water that causes 50 per cent mortality in the test.
4.1.1 Birds
Endosulfan is acutely toxic to birds under laboratory conditions. It is extremely toxic to mallards
and starlings (LD50 < 40 mg/kg) and highly toxic to quail and pheasant (LD50 of 41 to 200 mg/kg)
(Smith, 1987). The toxicity of endosulfan to birds was reported to be higher in juveniles
compared to adults, with oral LD5o values as low as .33 mg/kg body weight for juvenile mallards
(NRCC, 1975).
4.1.2 Aquatic Organisms
Endosulfan is highly toxic to fish. Incidents of fish mortality have been associated with the
agricultural use of endosulfan in Canada (NRCC, 1975; Frank el al., 1990). Direct aerial
applications of endosulfan to water at low rates can kill fish. Significant numbers of fish have died
Kndosulfan .1 Review oj its Toxicity and its Effects on the Endocrine System
17
in endosulfan-contaminated rivers in Canada and Europe (NRCC, 1975). For example, in June
1969, a massive fish kill in the Rhine River was associated with a maximum endosulfan
concentration of 0.7 pg/L (Greve and Wit, 1971).
In 1975, an accidental spill of endosulfan caused a major fish kill in North Brook, a tributary of
the Dunk River in eastern Prince County of Prince Edward Island (PEI). Researchers from the
Biology Department of the University of Prince Edward Island, who had been monitoring fish
populations in a 905 m section of North Brook, found that brook trout populations in the area
reduced to 45-246 from 2,227-4,147. (PEI Department of Technology and Environment, 1999).
In August 1995, although endosulfan was sprayed according to label instructions, contaminated
runoff from cotton fields resulted in the death of more than 240,000 fish along a 25 km stretch of
a river in Alabama, USA (PANUPS, 1996).
The toxicity of endosulfan to aquatic organisms was reported to be in the order of
fish>insects>crabs>snails>worms (NRCC, 1975). No eflects were reported in algae at levels as
high as 1 mg/L (NRCC, 1975). Endosulfan and endosulfan sulfate were much more toxic to
aquatic organisms as compared with the diol and other breakdown products (NRCC, 1975).
In an acute toxicity study, Barry el al. (1995) exposed Daphnia carinala to technical grade
endosulfan, a- and p-endosulfan, endosulfan sulfate and a 50:50 mixture of a- and P-endosuIfan.
They reported LC50 values of 478 |lg/L technical endosulfan, 756 pg/L endosulfan sulfate, 249 p
g/L oc-endosulfan, 205 pg/L p-endosulfan, and 234 pg/L for the endosulfan mixture.
Endosulfan - A Review ofits Toxicity and its Effects on the Endocrine System
18
Table 7: Acute Toxicity Values of Endosulfan
SPECIES
ORAL
LDSo
(mg/kg)
Mammals
19-220
rats
10-23
female rats
40-125
male rats
7.36
mice
hamsters
118
cats
2
76.7
dogs
rabbits____________
Birds
young ducks
33
mature mallards
205-243
bobwhite quail
805
ring-neck
1275
pheasants_________
Aquatic Organisms
toad larvae
daphnia
crab
crab larvae
DERMAL
LD60
LCbo
(ng/L)
INHALATION
LC5o(mg/m3)
REFERENCES
(mg/kg)
8
12.6
34.5
74
200-359
EXTOXNET, 1996
Hoechst, 1983a, 1990
Hoechst, 1983a, 1990
EXTOXNET, 1996
EXTOXNET, 1996
EXTOXNET, 1996
EXTOXNET, 1996
EXTOXNET, 1996
EXTOXNET, 1996
EXTOXNET, 1996
EXTOXNET, 1996
EXTOXNET, 1996
123
0.3-740
620017780
31
freshwater prawn
0.16-4.1
freshwater snail
1800
pink shrimp
grass shrimp
pinfish
striped mullet
bluegill
rainbow trout
freshwater catfish
spot
marine fish
freshwater fish
0.04
1.3
0.3
0.38
1.2
1.4
14
0.09
0.63
3.9
Vardia et al., 1984
Magdza, 1983; Lemke,
1980; Barry et al., 1995
Reddy et al., 1995;
Radhakrishnaiah et
al, 1995
Selvakumar et al.,
1996
Shukla and Omkar,
1984; Omkar and
Murthi, 1985; Bhavan
et al, 1997
Jonnalagadda & Rao,
1996; Rambabu and
Rao, 1994
Schimmel et al., 1977
Schimmel et al., 1977
Schimmel et al., 1977
Schimmel et al., 1977
EXTOXNET, 1998
EXTOXNET, 1998
Sinha et al., 1991b
Schimmel et al., 1977
Ernst et al., 1996
Ernst et al., 1996
In addition to the variable toxicity of different endosulfan isomers and metabolites, species and
strains of aquatic organisms have variable susceptibilities to endosulfan. For instance, the 24-hr
Endosulfan - J Review ofits Toxicity and its Effects on the Endocrine System
19
LC5o concentrations for three different strains of Spanish brine shrimp {Artemia nauplii) exposed
to endosulfan were 2.83, 9.23 and 1.99 mg/L for a bisexual strain (A. salina), a parthenogenetic
strain (A parthenogenetica), and a parthenogenetic tetrapioid strain, respectively (Varo et al
1997). Exposure of these organisms to endosulfan at l/5th the LC50 concentrations (7.83, 9.23 and
1 99 mg/L) did not affect the rate of oxygen consumption. Although it was noted that the lack ot
effect on this endpoint may have resulted from an insufficient concentration of endosulfan (Varo
el al., 1997).
In addition to extreme acute toxicity of endosulfan to aquatic organisms, sublethal effects are seen
at concentrations that do not cause mortality. Sublethal effects, including necrosis of the gill
epithelium were noted after exposure of freshwater fish to concentrations as low as 3 pg/L
(Bhatnagar el al., 1992). Australian freshwater catfish exposed to endosulfan at 0.1 or 1.0 pg/L
for 24 hours were reported to have endosulfan residues in liver of 1 to 82 pg/kg, as well as
histopathological changes in liver cells (Nowak, 1996). In freshwater crabs exposed to 6.2 mg/L
endosulfan (35 per cent) for one day, sublethal effects included a decrease in protein content of
hepatopancreas and muscle tissue. Free amino acid and protease activity increased in these tissues,
as did the activities of alanine aminotransferase (Al AT), aspartate aminotransferase (AA f) and
glutamate dehydrogenase (GDI !) (Radhakrishnaiah el a!., 1995).
Snails (Bellamya dissimilis Muller) exposed to 0.18 or 1.8 mg/L endosulfan were reported to
have decreased glucose, glycogen, total lipid and protein concentrations in the visceral, mantle
and foot tissues (Rambabu and Rao, 1994). The authors suggested that this decrease in
biochemical parameters in various tissues may have an adverse effect on growth and reproduction.
In another study, adult snails exposed to 1.8 mg/L endosulfan had histopathological effects on the
digestive gland tubule, central connective tissue and columnar muscle fibres (Jonnalagadda and
Rao, 1996).
In summary, levels of endosulfan as low as 0.7 |_ig/L have been associated with fish mortality
(Greve and Wit, 1971), and levels as low as 0.1 pg/L have resulted in sublethal hepatic effects
(Nowak, 1996).
4.1.3 Amphibians
The current toxicity database for endosulfan-exposed amphibians is small. Two Indian studies
examining sensitivity of frogs to endosulfan, have found that in 96 hour static bioassays, tadpoles
of the frog Rana Ugrina and toad larvae {Rufo melanostictus) were more sensitive to endosulfan
than juvenile catfish or damsel fly nymphs (Gopal el al., 1981; Vardia el al., 1984). Based on
available toxicity data, the EPA concluded that there is sufficient information to characterize
endosulfan as highly toxic to amphibians. In a recent study, BCrrill el al. (1998) found that frogs
are affected by concentrations of endosulfan far less than previously anticipated.
4.1.4 Mammals
Mammals are also sensitive to endosulfan. Sensitivity can be partially dependent on the nutritional
status of the animal. Greater toxicity was seen in animals with lower protein intake (Boyd and
Endosulfan - A Review of its Toxicity and its Effects on the Endocrine System
20
Dobos, 1969; Boyd el al., 1970). Endosulfan was reported to have greater acute toxicity in male
albino rats fed low protein diets for 28 days prior to exposure^Boyd el a/., 1970). Acute oral
LD50 values in rats fed different levels of protein in the diet ranged from 5.1 to 102 mg/kg
endosulfan. Acute toxicity was characterized by effects on the central nervous system, including
tremors, tachypnea and convulsions, with deaths due to respiratory failure. Autopsies of the
treated animals revealed effects in brain and liver tissues, as well as some gastrointestinal
inflammation. In rats, cx-endosulfan is more toxic than p-endosulfan, with acute oral LD50 values
of 76 mg/kg for a-endosulfan and 240 mg/kg for p-endosulfan (Hoechst, 1990). In rats, acute
inhalation of endosulfan at a concentration of 3.6 mg/m3 for four hours was reported to result in
dyspnea, trembling and ataxia (Hoechst, 1983).
Endosulfan was acutely toxic to male rabbits at a level of 15.13 mg/kg body weight administered
once orally, with lethal effects in five out of seven animals, within hours of administration (Ceron
et al., 1995). Prior to death, symptoms included tremors, convulsions and depression. In surviving
rabbits, symptoms included prostration, diarrhea and anorexia for several days, with decreased
feed intake and weight gain observed when compared with controls.
ATSDR (1993) reported that systemic toxicity following acute exposure is likely to involve the
respiratory, cardiovascular, gastrointestinal, hematological, hepatic and renal systems (Garg el al.,
1980; Barooah el al., 1980; Kiran and Varma, 1988; Terziev el al., 1974; Hoechst, 1966ab, 1970,
1975, 1984a, 1988; EMC, 1959, 1981; Raymond el al., 1995). Chronic exposures to lower levels
of endosulfan are more likely to have effects on the renal and hepatic organs.
4.1.5 Microorganisms
Endosulfan in soil may be toxic to some soil microorganisms. Growth inhibition of several types
of bacteria and yeast-mold occurred in endosulfan-treated media (Digrak and Ozcelik, 1998).
In another study, endosulfan was toxic to microorganisms in three microbial test systems:
MicrotoxIM, the Motility test and the Growth Zone Inhibition test. Thiodan was very toxic to the
luminescent bacteria Pholobacteriumphosphoreum in the Microtox test, with an EC50 of 28 mg/L
at 15°C. In the motility test, a concentration of 32 mg/L inhibited motility of Spirillum voulans
after 60 minutes, and in the third test, the growth of Bacillus cereus was inhibited at low levels of
Thiodan (30 mg/L) (Ghosh el al., 1997). It is noted that these endosulfan levels are high
compared with levels that arc toxic to fish.
Endosulfan - A Review of its Toxicity and its Effects on the Endocrine System
21
4.2
Chroiiic/Siibchroiiic Toxicity
Chronic and subchronic exposure to endosulfan has been reported to cause general toxicities such
as liver and kidney damage, as well as effects on the central nervous system, the endocrine system
including histopathological changes in the reproductive tract, effects on the immune system, liver
and kidney being the main target organs, and effects on thyroid function. A number of recent
studies, which provide a summary of some toxicity data for endosulfan in laboratory studies, arc
discussed below.
4.2.1 Effects on central nervous system (CNS)
Endosulfan has been shown to have effects on the central nervous system (CNS) of both aquatic
organisms and mammals. The main mechanism of endosulfan action in the CNS is inhibition of
brain acetylcholinesterase (a key enzyme in the nervous system), increased binding of serotonin
(an important neurotransmitter in the brain, regulating functions related to mood, sleep and
appetite) by increasing the receptor’s affinity for the neurotransmitter, and effects on
monoamines.
Behavioral changes were observed in freshwater percoid fish (Colisa fasciatus) after exposure to
1 mg/L endosulfan solution (1 ppm Thiodan EC35) for 30 days. This included excitation, rapid
swimming behaviour, increased surfacing (since this fish is an air-breather), jerky movements, and
increased mucus secretion (Pandy, 1988).
Endosulfan has been shown to have adverse effects on the CNS of mammals, which is consistent
with CNS effects seen in aquatic organisms. Behavioural changes and neurological effects have
been observed in female rats aged 15, 30, 70, or 365 days after being exposed to 12.5 mg
cndosulfan/kg body weight per day for four days. Effects included body tremors, as well as foot
fighting. Endosulfan toxicity and neurotoxicity were reported to be age dependent with the largest
effects in the 365 day old (adult) rat group, with no significant effects in rats aged 15 days.
However, rats aged 15 days were reported to show more effects on Na', K -ATPase activity in
erythrocyte membranes (Kiran and Varma, 1988).
Behavioral changes were also observed in rat pups treated intraperitoneally (e.g. injection into the
abdomen) with endosulfan at levels of 0, 0.5 or 1.0 mg/kg body weight for three to five weeks.
The high dose group exhibited increased aggressive behaviour induced by foot-shock treatment,
whereas animals in the low dose group did not show effects on either of these parameters. The
effects on neonates were reported to be stronger than in adults who do not have effects on these
parameters at this dose (Zaidi el al., 1985).
Male and female rat pups were treated with 0 or 6 mg technical grade endosulfan/kg body weightday by gavage from days 2 through 25. I hc brain activity of several chemicals was studied in
these animals on days 10 and 25 to identify potential effects on the developing rat brain. In these
animals, there were no effects on the brain or body weights; however, there were cficcts on
I' lKlosidlun - .1 A’cv/ch1 of its Toxicity and its I'.JJccts on the I'.ndocrinc System
n
monoamines in different parts of the CNS. The authors reported increased levels of noradrenaline,
decreased levels of dopamine, and variable concentrations of serotonin in different brain regions.
No effects were reported in acetylcholinesterase activity of treated rats. Behavioural testing in the
treated rats suggested that there were adverse effects on memory, as observed through operant
conditioning (Lakshmana and Raju, 1994).
Mice have also e,xhibited signs of CNS toxicity following exposure to endosulfan. In a 13-week
feeding study, mice were given endosulfan in their diet at levels of 0, 2, 6, 18 or 54 mg/kg. This
was reported to result in increased mortality in males and females at the highest dose, with
symptoms of convulsions and increased salivation (Hoechst, 1984b; Barnard et al., 1985).
Additionally, in females there was decreased glucose at 6 mg/kg and above, increased hemoglobin
and decreased mean corpuscular hemoglobin at all levels as compared with controls. Since there
were effects observed at all doses, a lowest effect level (LEL) of 2 mg/kg diet (0.27 mg/kg body
weight-day) was reported from this study (Hoechst, 1984b).
Effects on the CNS have also been seen in laboratory studies with dogs. Endosulfan fed at various
levels in the diet caused a loss or weakening of placing as well as righting reaction (Hoechst,
1989b). Also, the dogs showed increased sensitivity to stimuli, such as noise or optical stimuli,
increased tonic muscle reactions, and convulsive spasm (Hoechst, 1989c).
4.2.2
Effects on immune system
In addition to effects on the CNS in several animal species, endosulfan is also known to affect the
immune system. The target organs are kidneys and liver. The endosulfan inhibits leukocyte and
macrophage migration, causing adverse effects on humoral apd cell mediated immune system
function.
Effects of endosulfan on the immune system were seen in male rats fed 0, 5, 10, or 20 mg/kg
technical grade endosulfan in the diet for up to 22 weeks and then immunized with tetanus toxoid
(Banerjee and Hussain, 1986, 1987). In this study, immune effects were seen beginning at eight
weeks, including decreased antibody titre and depressed leukocyte migration inhibition and
macrophage migration inhibition factors in the two high doses. Additionally, there was a reduction
of antigen-induced serum globulin fraction and immunoglobin in animals exposed to 20 mg/kg for
more than 12 weeks. In this study, there was no overt toxicity at any of the dose levels, no
mortality, nor were there effects on feed intake, body weight or thymus weight. There was a
decrease in spleen weight observed in high dose animals exposed to endosulfan for 22 weeks, but
not prior to that time. Therefore, the NOAEL from this study is 5 mg/kg endosulfan in the diet of
rats (which is equivalent to 0.25 mg/kg bw-day).
In a later study, groups of male rats were fed technical grade endosulfan in the diet at levels of 0,
10, .30 or 50 mg/kg for six weeks. Similar to the above study, the animals were immunized with a
tetanus toxoid. I he authors reported a decrease in liver weight in rats exposed to the high dose of
endosulfan. In this study, there was a dose-dependent decrease in serum antibody titer to tetanus
toxoid. Additionally, there was a decrease in serum haemaglutination and IgG/IgM
immunoglobulin levels in high dose animals (Banerjee and I lussain, 1987)
I'.iKlosulfan - .1 A’cv/rw o/'its 'l’()\i( ilv <ind its /'.//rc/.v on the hndocrine System
23
In mice, immunological effects following exposure to endosulfan included decreased neutrophils
and spleen weight, with a NOAEL of 2.1 mg/kg body weight-day (Hoechst, 1984b).
fhe liver is one of the target organs associated with endosulfan toxicity in chronic exposure. Sexrelated differences in hepatotoxicity, stimulation of spontaneous motor activity and mortality were
seen in rats given endosulfan orally for 30 days (Paul el al., 1995). Male and female adult rats
were fed technical grade endosulfan at 0, 3 or 6 mg/kg-day. Both male and female rats were
reported to have adverse effects on learning and memory, as observed from their escape response
upon exposure to shocks (e.g. CNS effects). Female rats were reported to have a greater increase
in serum and liver glutamic oxaloacetic transaminase and glutamic pyruvic transaminase
concentrations as well as liver alkaline phosphatase concentration. Serum alkaline phosphatase
concentrations were increased in both sexes. Alterations in liver enzymes are indicators of liver
toxicity, and the authors suggest that these data indicate that female rats are more susceptible to
endosulfan-induced liver toxicity. Females were also reported to experience greater mortality.
Both male and female rats were reported to have dose-related increases in liver weight, and
stimulation of motor activity (which was greater in males). There were no effects on liver and
serum acetylcholinesterase activity, motor coordination, or body weight gain in either sex.
Additionally, there were no convulsions reported in the rats at either dose.
Effects on the liver were also seen in another study, where male rats were fed 0, 360 or 720
mg/kg endosulfan for 30 days. Effects included increased liver weights at both levels, increased
kidney weights at the higher dose level as well as histopathological kidney effects in both
exposure groups. 'Hie kidney effects were reported to be reversible after cessation of exposure. In
this study, the EEL was 360 mg/kg (34 mg/kg body weight-day) (Hoechst, 1985a).
In a later study, rats fed 0, 10, 30, 60 or 360 mg/kg endosulfan for up to 90 days did not have any
increase in mortality, although decreased body weights were reported in high dose animals
(Hoechst, 1985b; Barnard elal.^ 1985). Additional observations in animals receiving endosulfan
at levels above 60 mg/kg included decreased red blood cell levels, increased kidney weights and
discoloration in the kidneys (which was suggested to be due to temporary storage ol endosulfan).
Therefore, although the kidney is a target organ for endosulfan-induced toxicity, the histological
effects seen in this study were not thought to be related to toxicity.
Male rats exposed to 0, 5, or 10 mg/kg technical grade endosulfan by gavage for 15 days in a
subchronic study had increased mortality in the high dose group, but not in the low dose group
(Gupta el al., 1978). In the low dose group, there were no effects on body weight or the weights
of kidneys, lungs, testes, small intestine, brain or adrenals. There was however, an increase in liver
weight seen in this group. In the high dose group, effects included decreased body weight and
decreased testes weight. Histopathological effects were reported in the liver, kidneys, lungs and
testes of the treated animals. There were no effects on the brain, small intestine and adrenal tissues
of these animals.
In a two year dietary study in which mice were fed 0, 2, 6 or 18 mg/kg endosulfan, adverse effects
were observed only at the highest dose level. Effects included decreased survival and body weight
Endosulfan - A Review ofits Toxicity and its Effects on the Endocrine System
24
gain at 18 mg/kg (2.51 and 2.86 mg/kg body weight-day in males and females, respectively)
(Hack el al., 1995). No significant findings were observed at the next highest level on feed and
water intake, clinical chemistry, hematology, histopathological changes in organs, effects on
reproductive organs or clinical signs. The authors reported a no-observable-effects-level (NOEL)
of 6 mg/kg (0.84 and 0.97 mg/kg body weight-day for males and females, respectively) for
endosulfan in mice.
A lower no-observed-adverse-effect-level (NOAEL) of 15 mg/kg (0.6 and 0.7 mg/kg body
weight-day for males and females, respectively) was identified in rats from a two year feeding
study (Hack et al., 1995; Hoechst, 1989a). The rats were fed a diet containing 0, 3, 7.5, 15 or 75
mg/kg endosulfan. There were adverse effects noted at the highest dose used in the study (75
mg/kg), which included reduced body weight gain in both sexes. At this dose, males also had an
increased incidence of adverse kidney effects (enlarged kidneys, blood vessel aneurysms and
glomerulonephrosis). There were no significant adverse effects on hematology, clinical chemistry,
intake of feed and water, urinalysis, ophthalmology, clinical observations, effects on reproductive
organs or mortality at any of the dose levels. The US EPA (1997) derived an oral reference dose
(RfD) of 0.006 mg/kg bw-day for humans based on this study (as discussed in Section 5.1).
ATSDR (1993) determined the lowest NOAEL from studies of immunological effects was 0.25
mg/kg body weight-day (5 mg/kg in the diet). This level was used by ATSDR (1993) in the
derivation of the subchronic minimal risk level of 0.002 mg/kg body weight-day for humans, using
a safety factor of 100 to account for interspecies and intraspecies variability. It is noted that this
level (based on immunological effects) is lower than the RfD derived by the US EP A (1997).
7.2.3
Effects on reproductive system
Exposure of aquatic organisms to endosulfan may have adverse effects on reproduction. A
summary of some recent studies is provided below.
There were no significant effects on male differentiation, proportion of males and proportion of
broods of daphnids reported in Daphnia magna exposed to endosulfan (50, 100, or 150 pg/L) for
up to 40 days (Zou and Fingerman, 1997). In a study with another species. Daphnia carinata,
endosulfan at levels of 0, 40, 80, or 160 |ig/L had effects on different levels of biological
organization, including “allocation of resources to reproduction, growth and reproductive rates
and population dynamics” (Barry, 1996).
Exposure of daphnids to 0, 20, 40, 80, 160, or 320 pg/L endosulfan had no effect on mortality,
but there was a reduction in maturity, carapace length and in the number of eggs in the first brood
of high-dose daphnids (Barry et al., 1995). In this study, they also observed a decrease in the
carapace length in the second reproductive instar as well as a decrease in the number of eggs in
the second. Barry et al. (1995) reported that endosulfan toxicity to daphnids, as measured by
brood size, was greater from water-borne exposure as compared with food-borne or food and
water-borne exposures. No significant effects were reported on either length or age at maturity in
this experiment.
Endosulfan - A Review of its Toxicity and its Effects on the Endocrine System
THANAL
Po;r (ex r o 315
25
1
K-RALAM
,r •
• ',?’003
Groups of 10 male and female crayfish were exposed to 600 jig/L Thiodan for 20 weeks and then
mated. No significant dincrcncc was reported in the number of eggs produced by control or
treated crayfish (Naqvi t7 tz/., 1991). The authors also exposed juvenile crayfish to 2, 10 or 15
pg/L fhiodan for 9, 23 or 27 weeks, respectively. No significant differences were reported for
weight gain or length of treated or control hatchlings, although the molt ing frequency of treated
hatchlings was slightly greater than controls.
Anti-estrogenic effects were seen following exposure of freshwater catfish (C. batrachus) to
0.0015 mg/L (1.5 pg/L) commercial grade endosulfan for 16 days, due to a significant decrease
in plasma vitellogenin levels (Chakravorty et aL, 1992). Vitellogenin is formed in the liver of
females under the control of estrogens and is important for reproduction. In this study, the effects
of endosulfan could be reduced through exposure to hormones. Decreased vitellogenesis
following exposure to endosulfan is important, since vitellogenin is required for oocyte growth
and embryo nourishment. This is suggestive of an anti-estrogenic effect of endosulfan since
estrogens increase vitellogenin levels. The authors suggested that the decrease in vitellogenin
synthesis was likely due to interference of “the hormones regulating vitellogenin synthesis.” In
another study, there were no estrogenic effects on vitellogenin response on day 18 in juvenile
rainbow trout exposed to endosulfan and/or dieldrin via intraperitoneal injection at doses of
approximately 4 mmoles/kg (Bjerregaard et al., 1998). It is noted that the species and route of
exposure were different in these studies.
Freshwater teleost fish (Channel striatns) exposed to 0.00075 or 0.001 mg/L endosulfan
(fhiodan) for 2 to 30 days during spawning were reported to have dose-related effects on
oocytes, including a decreased number and size of oocytes, deformed oocytes, damaged yolk
vesicles, and dilated gonadosomatic index (Kulshrestha and Arora, 1984). Similarly, Shukla and
Pandey (1986) found effects on fish reproductive physiology in Sarotherodon mossanibicus
exposed to 0.001 mg/L endosulfan for 20 days. Histological changes were present in the pituitary
and ovaries of endosulfan-treated fish.
t
Adult female percoid fish (Colisa fasciatits) were exposed to 1 mg/L endosulfan (Thiodan EC35)
for 30 days to study the effects of endosulfan treatment on the pre-spawning phase of the ovarian
cycle (Pandy, 1988). There were effects reported on ovarian activity in treated fish as compared
with controls, as well as a thickening of the ovarian wall, decreased diameter of stage II and III
oocytes, altered percentage of oogonia at different stages, as well as damage to yolk in stage 111
oocytes. It is possible that these effects could influence reproduction.
In conclusion, some studies have shown a potential for adverse effects of endosulfan in the
reproductive organs of aquatic organisms, while others have shown no effect. This could be due
to differential susceptibilities of species to endosulfan, as well as routes of exposure and duration
of exposure. In summary, histological changes in reproductive organs were seen in aquatic
organisms following exposure to endosulfan at concentrations as low as 0.00075 mg/L (0.75
Pg/L).
Endosulfan did not have any adverse effects on several estrogenic parameters: uterine weight,
peroxidase activity or PR content in juvenile female Sprague Dawley rats administered endosulfan
I'.ndosiilfan - .1 Review ofits Toxicity and its Effects on the Endocrine Svsteni
26
and/or dieldrin via intraperitoneal injection for three days at a level of 0.1 mg/kg-day (Wade et al.,
1997). The uterus of these animals was analyzed for effects of pesticide treatment and compared
with controls. Treatment of the rats with pesticides did not result in increased signs of toxicity,
nor were there adverse effects on body weight, liver weight, uterine weight, circulating estradiol,
uterine progesterone receptors, uterine cytosolic estrogen receptor levels, or uterine peroxidase
activity. Similarly, no adverse effects on the pituitary, which is important for endocrine function,
were observed, with no effects on circulating thyroxine levels, gross pituitary weight, pituitary
content of GH, FSH, LH, TSH or pituitary prolactin levels. •
In another recent study, there were no endocrine disruption effects in mice fed endosulfan and
monitored for effects on steroid hormone metabolism (Wilson and LeBlanc, 1998). Endosulfan
treatment resulted in an increase in testosterone elimination, but did not significantly alter the
homeostasis of testosterone, as measured in serum. There was an increase in total testosterone
hydroxyl metabolite production in female mice exposed to endosulfan, particularly in
concentrations of 16b, 6a and 16a-hydroxytestosterone. In this study, male and female mice were
fed endosulfan for seven days at levels ofO, 3.8, 7.5 or 15 mg/kg-day. In this study, the authors
reported greater toxicity in male mice and less metabolization of testosterone. Decreased body
weight was reported in both male and female mice at the high dose.
Endosulfan treatment was reported to cause a dose-dependent reduction in sperm counts in rats
given endosulfan at levels of 0, 2.5, 5, or 10 mg/kg-day, five days per week from the time of
weaning to 90 days of age (Sinha et al., 1997). Additionally, there were effects on
spermatogenesis, including a reduced number of spermatids, sperm abnormalities and decreased
daily sperm production. There were no significant effects on mortality, body weight or testis
weight in the treated animals. The authors reported increased activity of testicular marker
enzymes in the testis including lactate dehydrogenase, gammfi glutamyl transpeptidase and
glucose-6-phosphate dehydrogenase, and a decrease in sorbitol dehydrogenase (which are
indicators of spermatogenesis). The LEL for this study was 2.5 mg/kg-day, since effects were
seen at all dose levels. Other studies have shown that endosulfan can have effects on the
spermatogenic and steroidogenic cycle of adult rats (Sinha et al., 1995; Singh and Pandey, 1989,
1990). Additionally, Gupta and Chandra (1977) found decreased testis weights and
histopathological effects in the testis of rats treated orally with endosulfan for 15 days.
A NOAEL of 6 mg/kg body weight-day was identified from a study in which pregnant rats were
orally administered endosulfan during gestation days 6-18 (FMC, 1980b). In other studies,
increased maternal toxicity was reported in pregnant rats administered 5 or 10 mg endosulfan/kg
body weight-day orally on days 6-14 or 6-19 of gestation (FMC, 1980a; Gupta et al., 1978). In
the offspring, increased resorptions, skeletal variations and decreased birth weight and length
were reported at levels that caused maternal toxicity.
Endosulfan given to rabbits orally by gavage on days 6-28 of gestation at levels of 0, 0.3, 0.7 or
1.8 mg/kg-day was not reported to have teratogenic effects (FMC, 1981). It is noted that there
was maternal toxicity at the high dose, as evidenced by noisy, rapid breathing, hyperactivity and
convulsions. The US EPA (1997) suggested a NOEL for maternal toxicity of 0.7 mg/kg-day, and
a NOEL for developmental toxicity of greater than 1.8 mg/kg-day.
I'.iidosulfan - / I !’■ ‘
o/ its '/'oxicity aiid its Hffects on the I'Jidocrine System
T1
Female rats were given 0, 5 or 10 mg/kg body weight technical grade endosulfan by gavage from
days 6 through 14 of gestation and sacrificed at day 21 of gestation (Gupta el al., 1978).
Increased maternal toxicity was observed at both doses, including increased mortality, although
there were no changes in behaviour or appearance of the treated animals. The authors reported
that there was an increase in fetal mortality and resorption, no malformations, but some skeletal
abnormalities. However, the authors indicated that these results could not be interpreted as
teratogenic effects due to the observed maternal toxicity.
In summary, no endocrine disruption or estrogenic effects were seen in mammals exposed to
endosulfan, but there were adverse effects on the sperm of males treated with endosulfan. There
were no adverse effects on reproduction, including a two generation study in rats (WHO/FAO,
1990; US EPA, 1997; ATSDR, 1993), and no teratogenic effects were reported in hen or quail
eggs injected with endosulfan; however, sterility was reported (NRCC, 1975). The studies
reviewed for this assessment indicate that endosulfan does not appear to be a teratogen, with
effects in offspring seen only at maternally toxic doses, and therefore teratogenicity cannot be
adequately assessed.
4.2.4
('arcino^enicity
In the literature reviewed for this assessment, no studies were identified which suggest
carcinogenic activity for endosulfan. This includes a two year feeding study with endosulfan in
rats and mice at levels up to 75 and 18 mg/kg, respectively, in which there were no significant
increases in tumors when compared with controls (Hack el al., 1995). Earlier studies with
endosulfan precluded assessment of carcinogenicity due to increased mortality. Further to this, the
US EPA (1997) indicated that endosulfan is “not classifiable as to it’s carcinogenicity ”
4.2.5 Mutaget iicily
Endosulfan has been shown to have both positive and negative effects in both /// vitro and in vivo
mutagenicity and genotoxicity assays. It is noted however, that endosulfan is not known to be a
carcinogen in long-term animal studies. A summary of some studies is provided below.
Negative results for endosulfan were obtained in the Ames test with Salmonella lyphimurium
strains TA97a, TA98 and TAI00, with and without metabolic activation (Pednekar el al., 1987).
Negative results were also found with strains TA97a, TA98, TA 100 and TA 102; however, there
was a weak mutagenic response with TA98a, with and without metabolic activation in a modified
test which was more sensitive than the standard Ames test (Pandey el al., 1990b).
Positive results for genotoxicity were reported in a yeast gene conversion/DNA repair test with
Saccharomyces cerevisiae, with increased frequency of mitotic gene conversion and reverse
mutation (Yadav el
1982). Positive results were also obtained for endosulfan in an in vino
forward mutation assay with L51786 TK+ mouse lymphoma cells (McGregor el al., 1988).
Endosulfan (99 per cent pure) was reported to be positive for genotoxic activity in mammalian
Endosulfan - A Review ofits Toxicity and its Effects on the Endocrine System
28
hepatic and hepatoma cells, with increased DNA-adduct formation (Dubois et al., 1996). No
increase in DNA adduct formation was observed in bird cultured hepatic cells in this study.
In an in vivo micronucleus test with male Swiss albino mice exposed to 43.3 mg/kg endosulfan,
endosulfan was negative for mutagenicity with no statistically significant difference in the
incidence of bone marrow erythrocyte micronuclei in treated versus control mice (Usha Rani et
al., 1980). Similarly, endosulfan was reported to be negative in an in vivo cytogenicity assay in
which groups of eight male rats were exposed to 0, 11, 22, 36.6 or 55 mg/kg endosulfan in peanut
oil by gavage (Dikshith and Datta, 1978). Endosulfan levels of 22, 36.6 and 55 mg/kg were
reported to be toxic to the rats. Some chromatid breaks were reported in bone marrow cells, but
rats exposed to endosulfan did not have a significantly greater incidence of chromosomal
aberrations in bone marrow (somatic) or spermatogonial (germinal) cells. Positive results were
found in another assay for chromosomal aberrations in bone marrow cells of the Syrian hamster
treated in vivo with endosulfan (Dzwonkowska and Hubner, 1986).
In an in vivo study in which endosulfan was administered via intraperitoneal injection in rats,
Dhouib et al. (1995) reported that there was an increase in liver DNA adducts in controls;
however, there was no increase in kidney DNA adducts in treated rats.
Endosulfan had mutagenic activity in an in vivo study with Drosophila melangaster, with positive
results for induction of sex-linked recessive lethal mutation and increased sex-chromosome losses
(Velazquez et al., 1984).
Technical grade endosulfan had genotoxic effects in germ cells in two in vivo tests, the dominant
lethal test and the sperm abnormality test in mice (Pandey et al., 1990a). Male mice were
administered endosulfan via intraperitoneal injection at 9.8, 12.7 and 16.6 mg/kg bw-day for five
days, then mated with female mice. Positive results were found in the dominant lethal test at the
high dose only. This test measured the pre- and post-implantation loss of embryos and the results
indicate that at the high dose, endosulfan may have caused chromosomal aberrations in germ cells,
resulting in increased embryonic death. In the sperm abnormality test, mice were administered 9.8,
12.7, 16.6 and 21.6 mg/kg-day endosulfan for five days. Sperm abnormalities, decreased tests
weight and decreased sperm count were observed at 16.6 and 21.6 mg/kg-day. No effects in
sperm motility were seen in this study.
4.3.
In Vitro Studies
Endosulfan can be transported into cells, as evidenced by Bain and LeBlanc (1996) who reported
that oc-endosulfan is capable of binding p-glycoprotein and can be transported by p-glycoprotein
in vitro in B16/F10 murine melanoma cells transfected with the human MDR1 gene. This gene
codes for p-glycoprotein, which is responsible for transport of chemicals out of cells. MDR1 is
found in organs that produce hormones as well as organs which eliminate substances.
Endosulfan - A Review ofits Toxicity and its Effects on the Endocrine System
29
4.3.1 Neuronal Cells
In an in vitro neuronal model, a-endosulfan inhibited GABA (gamma amino butyric acid)stimulatcd influx of chloride ions in cerebellar granule neurons (Huang and Casida, 1996). This
was due to effects of endosulfan on the GABA-gated chloride channel in these cells. The acndosulfan inhibitory potency for [3H]ethylbicycloorthobenzoate binding in cerebellar granule
neurons and tissue in vitro is 17 and 12 nM, respectively, indicating that it is potent in these cells
(Huang and Casida, 1996). In another study with primary neuronal cultures of cerebellar granule
cells, a-endosulfan had small cytotoxicity effects, increased mitochondrial transmembrane
potential and increased intracellular free calcium after incubation (Rosa et al., 1996). In this
system, a-endosulfan did not generate oxygen free radicals.
In a study with rat mitochondria, Dubey et al. (1984) reported that endosulfan has effects on
mitochondrial transmembrane potential. The authors report that our results suggest that
endosulfan possesses dual properties, that of an uncoupler of oxidative phosphorylation and of an
inhibitor of the electron transport chain.” The cytotoxicity of endosulfan to neuronal cells was
studied in vitro in order to identify the effects at a cellular level. Mitochondrial transmembrane
potential was used as an endpoint of the status of the cells following exposure to endosulfan.
Rosa et al. (1996) suggested that this increase in transmembrane potential could be a result of cell
detoxification.
4.3.2
Liver Cells
In isolated rat hepatocytes, exposure of mitochondria and microsomes 11 to a-endosulfan caused
the depletion of cellular non-protein sulfhydryl content at a concentration of 10‘3 M, but not at
10'4 or 10’5 M. Additionally, a-endosulfan had an inhibitory effect on mitochondrial respiration
(Yamano and Morita, 1995). There were no significant effects with p-endosulfan at a
concentration of IO'3 M.
1.3.3
Nstro^enic A cli i 'Uy
Several recent in vitro studies have been conducted in an attempt to determine the potential
endocrine disrupting effects of endosulfan. A summary of some recent publications is provided
below.
Jin el al. (1997) studied the effects of oc-endosulfan, p-endosulfan and endosulfan sulfate in a
yeast system which expressed the human progesterone receptor B-form and a progesterone
sensitive receptor, p-endosulfan and endosulfan sulfate decreased p-galactosidase activity of
progesterone in this system, whereas a-endosulfan did not. The IC50 values for P-endosulfan and
endosulfan sulfate are 2.5 and 5 pM, respectively. Neither p-endosulfan nor endosulfan sulfate
inhibited progesterone binding. The authors suggested that the decrease in activity was due to
interaction of the chemicals with another site or via another mechanism.
Endosulfan - A Review of its Toxicity and its Effects on the Endocrine System
30
Fertilization of a mammalian egg depends on a sperm acrosome reaction, and it can be initiated by
the egg zona pellucida or progesterone. GABA receptor/chloride channels are involved in this
process, and there is some concern that insecticides which are blockers of the GABA-gated
channel may affect the sperm acrosome reaction, and thereby affect mammalian fertilization.
Turner et al. (1997) found that low levels of endosulfan (1 nM, 0.41 ppb) can inhibit the human
sperm acrosome reaction in vitro initiated by progesterone and glycine, but the inhibition is not
complete. Higher concentrations of endosulfan (500 nM) did not inhibit the reaction in vitro
initiated by inomycin, which “supports the view that these insecticides are antagonists of sperm
amino acid neurotransmitter receptor/chloride channels.”
Vonier et al. (1996) studied the binding activity of oc-endosulfan, P-endosultan and endosulfan
sulfate on the estrogen receptor and progesterone receptor in alligator oviduct protein extract, ocendosulfan “competed with [?H]17p-estradiol for binding to the estrogen receptor,” while pendosulfan had no “appreciable interaction with the estrogen receptor.” Endosulfan sulfate
inhibited binding of the synthetic progestin [3H]R5020 to the progesterone receptor by 40-50 per
cent, whereas neither oc-endosulfan nor P-endosulfan had effects. This suggests that endosulfan
may “interact with steroid hormone receptors.” Vonier et al. (1996) indicated that it is not known
whether endosulfan has effects as a progestin or antiprogestin.
Petit et al. (1997) studied the estrogenic effects of oc-endosulfan and p-endosulfan in a yeast
recombinant in vivo system which expresses the rainbow trout estrogen receptor, and also in an in
vitro test with rainbow trout hepatocyte culture vitellogenin gene expression (which depends on
estradiol). Both isomers of endosulfan had effects on p-galactosidase activity in yeast, but were
not able to displace pHJEi bound to rainbow trout estrogen receptor in the yeast system at the
highest concentration used. Both isomers had the ability to cause vitellogenin induction in
hepatocyte culture. Endosulfan potency was reported to be stronger in the hepatocyte culture than
the yeast system. Petit et al. (1997) suggested that these results are consistent with those reported
by Soto et al. (1994) and Arnold et al. (1996). It is noted that Petit et al. (1997) did not observe
synergistic activity with mixtures, as compared to the synergism of endosulfan and dieldrin seen in
MCF-7 cells (Soto et al., 1994) and in a yeast system (Arnold et al., 1996). Petit et al. (1997)
suggested that the endosulfan likely had effects on the hormones which regulate the synthesis of
vitellogenin, which resulted in a decrease in vitellogenin metabolism.
Endosulfan at a concentration of 10’4 M was reported to have some estrogenic activity since this
concentration caused a 2000-fold increase in p-galactosidase activity in a yeast system which had
been transformed with the human estrogen receptor (Ramamoorthy et al., 1997). Additionally, the
authors reported that endosulfan was weakly estrogenic in another assay, with a concentration of
2.5x1 O’5 M causing a four-fold increase in p-galactosidase activity in a yeast system transformed
with the mouse estrogen receptor. The induction of p-galactosidase activity was conducted in an
estrogen-responsive reporter system in yeast expressing” mouse or human estrogen receptors.
Endosulfan - A Review ofits Toxicity and its Effects on the Endocrine System
31
4.3.4 Synergism
Mixed results have been reported in assays which measured the synergistic activity of endosulfan
with other chemicals. Soto el al. (1994) found estrogenic activity with mixtures of chemicals,
including endosulfan, in human breast cancer estrogen-sensitive MCF-7 cells; however, none of
the chemicals were reported to have significant estrogenic activity on their own. In a later study,
Soto et al. (1995) found endosulfan to be estrogenic in human breast cancer estrogen-sensitive
MCF-7 cells and by the E-SCREEN assay. Petit el al. (1997) did not observe synergistic activity
with mixtures, as compared to the synergism of endosulfan and dieldrin seen in MCF-7 cells (Soto
el al., 1994) and in a yeast system (Arnold el a/., 1996).
Synergistic effects of endosulfan/DDT/chlordane mixtures were reported in human breast MCF-7
cells in vino (Verma el al., 1997). Arnold el al. (1996) reported that mixtures of endosulfan and
dieldrin were 1000 times more potent for estrogenic-induced activity in vitro in a simple yeast
estrogen system which expressed human estrogen receptor than either chemical alone. In this
study, individual chemicals had only weak inhibitory effects on the binding of [ HJ] 17p-estradiol
to the human estrogen receptor. However, these synergistic eftects have not been substantiated in
later studies. Ashby el al. (1997) reported negative results for estrogenic activity for mixtures of
endosulfan and dieldrin. Similarly, Shelby el al. (1996) found negative results for estrogenic
activity of endosulfan using in vitro and in vivo assays. Kaiser (1997) commented on the results of
the study of Arnold el al. (1996) and suggested that more research is required on this topic.
Endosulfan and dieldrin did not exhibit synergistic activity when administered together in either in
vivo or in vitro studies (Wade el al., 1997). Additive effects of the two pesticides were reported
in the in vitro studies.
In vitro studies with human breast cancer cells MCF-7 E3 were conducted with endosulfan and
dieldrin to identify effects on estrogen receptor activity (Wade et al., 1997). In this study, there
was a dose-related increase in cell proliferation with exposure to endosulfan. Exposure of the cells
to a mixture of endosulfan and dieldrin resulted in “a slight but significant increase in cell
proliferation over the effects of either pesticide alone.”
In an in vitro estrogen receptor competitive binding assay, endosulfan and dieldrin were tested
with uterine homogenates for evaluation of the degree of inhibition off Il| E2 binding from rat
uterine estrogen receptors (Wade et al., 1997). 1 he authors reported that there was a significant
inhibition of [3H] E2 binding but only at the highest dose tested (10 ^iM).” The authors reported
that there was additive but no synergistic activity with the two pesticides in this assay.
As reported in the above section, endosulfan was weakly estrogenic in yeast assays; however,
there was no synergistic activity with mixtures of endosulfan and either dieldrin, chlordane or
toxaphene in two yeast assays which had been transformed with either the human or mouse
estrogen receptor (Ramamoorthy et al., 1997). In these assays, the level of p-galactosidase
activity was monitored in the yeast culture system following exposure to the pesticide mixtures.
Kmlosulfan - /i Review of its Toxicity and its Kffe.cls on the Endocrine System
32
In summary, mixed results have been found for estrogenic activity of endosulfan in vitro, and
further studies are required to determine the estrogenic potential of endosulfan.
5.0
REGULATORY STATUS
5.1
North America
The US EPA (I997) provide an oral reference dose (RfD) for humans exposed to endosulfan
based on the results from a chronic feeding study in laboratory animals (Hoechst, 1989a). An RID
is a value which is considered to be a “safe” exposure level to a non-carcinogenic chemical. The
RfD is based on a toxicological study from which a NOAEL has been reported for health efTects.
A safety factor of 100 has been applied to the NOAEL to account for uncertainty in extrapolation
from animals to humans. Administration of endosulfan at levels of 0, 3, 7.5, 15 and 75 mg/kg in
the diet of male and female Sprague Dawley rats for two years resulted in adverse effects at the
highest dose level. Effects included decreased body weight gain in both sexes and, in male rats,
effects on the kidneys and increased incidence of blood vessel aneurysms. The US EPA derived an
oral RID of 6x1 O ' mg/kg body weight-day based on the NOAEL of 15 mg/kg diet (0.6 mg/kg
body weight-day in male rats) from this study.
AI SDR. (1993) cite (EPA, 1980 and Sittig, 1980) regarding criteria for protection of human
health and aquatic life in the United States, which are summarized in the Table 8.
Table 8: Action and Advisory Levels for Endosulfan in the United States
CRITERIA
Protection of human health for ingestion of water and aquatic
organisms
Protection of human health for ingestion of aquatic organisms
Protection of freshwater aquatic life - 24 hour average, chronic
Protection of freshwater aquatic life - ceiling, acute
Protection of saltwater aquatic life - 24 hour average, chronic
Protection of saltwater aquatic life - ceiling, acute
CONCENTRATION
IN WATER
75 pg/L
159 pg/L
0.056 pg/L
0.22 pg/L
0.0087 pg/L
0.034 pg/L
1‘jidosulfan - /I Review of its Toxicity and its Effects on the Endocrine System
33
5.2
Europe
Use of endosulfan is banned in Norway and Sweden due to its high toxicity. In the United
Kingdom (UK), the pesticides maximum residue levels (MRUs) in crops, food and feeding stuffs
for endosulfan, as well as other pesticides, has been recently amended to the Statutory Instrument
1997 No. 567. Table 9 is a summary of MRUs in various food commodities in the UK.
Table 9: Endosulfan Maximum Residue Levels in Crops, Food and Feeding Stuffs
in the United Kingdom
COMMODITY
Citrus fruits (grapefruit, lemons, limes, oranges, pomelos, others)
Tree nuts (almonds, brazil nuts, cashew nuts, chestnuts,
coconuts, others)_______________________________
Pome fruits (apples, pears, quinces, others)_________________
Berries and small fruits (table and wine grapes, raspberries)
Dewberries, loganberries, bilberries, cranberries, currant,
gooseberries, others_________________________
Stone fruits (apricots, cherries, peaches) __________________
Other fruits (avocados, bananas, dates, figs, pineapples, others)
Olives_______________________________ _______________
Kiwi fruit
5.3
MRL
(mg/kg)
1.00
0.10
1.00
1.00
0.05
1.00
0.05
1.00
1.00
Australia
In Australia, the MRL of endosulfan for meat fat is 0.2 mg/kg. The MRL for stock feeds such as
hay, silage fodder crops and pasture is 0.3 mg/kg. The critical level of endosulfan in the total diet
of cattle is 0.5 mg/kg (The Tamworth Centre for Crop Improvement).
5.4
Others
The Indonesian government is banning 28 pesticides, including endosulfan, according to a June,
1996 statement by the Minister of Agriculture. The reason for the ban is due to concerns about
the impacts of these pesticides on human health.
5.5
World Health Organization and Food and Agriculture Organization
In 1989, the World Health Organization (WHO) and the Food and Agriculture Organization
(FAO), through the Codex Alimentarius Commission, jointly established an acceptable daily
intake (ADI) of 0.006 mg/kg body weight-day of endosulfan (EXTOXNET, 1998). This value is
the same as the RfD derived by the US EP A (1997) in the United States. Maximum residue limits
in foods were also established and are reported as 2 mg/kg in most fruits and vegetables, 1 mg/kg
in cottortseed, 0.5 mg/kg in cottonseed oil, 0.004 mg/kg in milk and milk products, 0.2 mg/kg in
carrots, potatoes, sweet potatoes bulb onions, and meat fat, and 0.1 mg/kg in rice husk
(FAO/WHO, 1975). Table 10 lists the MRLs of various food commodities, established by the
Codex Alimentarius Commission in 1989.
Table 10: Codex Alimentarius Commission’s Maximum Residue Limits
COMMODITY
Cabbage (savoy), celery, spinach, pineapple, most fruits and
vegetables_________________ ________________________
Alfalfa forage, cabbage (head), cherries, clover, cotton seed,
grapes, kale, lettuce, peaches, plums, pome fruits, soya beans
(dry), sugar beets (leaves), sunflower seeds, trefoil
Board and common beans, broccoli, cauliflower, cotton seed oil,
cucumber, green pea, melons, rape seed, summer squash,
tomato_________ ___________ ____________ ________ ____
Carrot, onion (bulb), potato, sweet potato, wheat
Cacao beans, coffee beans, maize, meat (fat, not including
marine mammals), rice, sugar beet
_
Milk___________
T
Tea (green, black)_________________ __________________ __L
MRL
(mg/kg)
2.00
1.00
0.50
0.20
0.10
0.004
30.00
1) Note that MRLs are the sum of a-, [J-endosulfan and endosulfan sulphate
6.0
ALTERNATIVES
Due to concerns about the potential endocrine disrupting effects of endosulfan, it is prudent to
identify alternatives which can be used instead of endosulfan. Additionally, future potential insect
resistance to endosulfan (Brun el a/., 1995) may require that other pesticide alternatives be used.
.6.1
Integrated Pest Management (1PM)
Farmers traditionally rely on chemical pesticides to control pest populations in agriculture In
recent years, it has become more evident that intensive use of chemical pesticides often fails to
manage pests effectively; it is costly and pests are showing resistance to some pesticides. An
alternative approach to extensive chemical pesticide use, Integrated Pest Management (1PM), has
been recognized by experts in the field. The 1PM method relies primarily on biological and
ecological interventions such as using pests’ natural enemies, crop rotations banding of pesticides
(spraying of crop rows only, not the soil between them), scouting for pests (measuring pes
populations and spraying when their levels exceed a certain threshold) and reducing the volume of
pesticides applied.
Kruloxiilfan - - I Review of its Toxicily and its Effects on Ihc I'.ndocrine System
1
35
6.2
Chemical Alternatives
In Australia, concerns about the use of endosulfan led to suggestions of alternative pesticides
(NSW Agriculture, 1998). These include nicthomyl, cypcnncthrin, alpha cypermethrin,
deltamethrin, esfenvalerate, beta cyfluithrin and lambda cyhalothrin.
Endosulfan - A Review ofits Toxicity and its Effects on the Endocrine System
36
7.0
CONCLUSIONS
Endosulfan is a pesticide which is found in many products in Canada, with mean levels generally
below the maximum residue limits set by Health Canada. It persists for some time in soils and
sediment, but not in surface water. In the body, endosulfan is readily metabolized and does not
bioaccumulate. It is a central nervous system stimulant, and is acutely toxic to aquatic organisms,
birds, animals and humans. In humans, chronic exposure to low levels of endosulfan are not
known. Subchronic efTects in aquatic organisms include effects on thyroid hormones and
physiology, and on measures of metabolic function at low levels. In mammals, chronic/subchronic
exposure to endosulfan has been reported to have adverse effects on the central nervous system,
immune system, liver and kidneys, as well as body weight gain and survival. In mutagenicity
assays, endosulfan was shown to have both positive and negative effects; however, it has not been
shown to be carcinogenic in chronic studies. Hack el a/. (1995), and the US ERA (1997) indicate
that endosulfan is “not classifiable as to it’s carcinogenicity.”
The oral ADI and RfD for endosulfan are 0.006 mg/kg body weight-day (EXTOXNET, 1998; US
ERA, 1997). The ATSDR (1993) provided a lower minimal risk level of 0.002 mg/kg body
weight-day based on the immunological effects of endosulfan.
Endosulfan has been reported to be a xenoestrogen and has been associated with effects on
reproduction and the endocrine system (De Rosa et al., 1998; Davis and Bradlow, 1995). Studies
designed to examine the endocrine disrupting effects of endosulfan in vivo have reported both
positive and negative results. No estrogenic or endocrine disrupting effects were reported in
studies of testosterone homeostasis or uterus effects in mammals, but there were adverse effects
on the spermatogenesis of mammals. In aquatic organisms, endosulfan has been shown to affect
reproductive endpoints and vitellogenesis in some studies, but not others. In vitro studies
conducted to determine the potential endocrine disrupting effects of endosulfan have also shown
mixed results.
In summary, studies of potential environmental estrogens, including endosulfan, have been shown
to have conflicting results in different assays. Petit et al. (1997) suggested that there are several
potential reasons for the variability in response, which may include: i) cell membranes of different
cultures have different permeabilities; ii) variable metabolism in biological systems; iii) variable
toxicity in biological systems; iv) different gene activation pathways in different systems; v)
variable transcriptional activation in different systems; and, vi) different signaling pathways.
Further research is required to determine the endocrine disrupting effects of endosulfan in the
environment.
Endosulfan - A Review of its Toxicity and its Effects on the Endocrine System
IH a j A'
ro;r
fRAL A 1
r
. rar
37
8.0 RECOMMENDATIONS
Recommendation #1: Reduce the risk of public exposure to endosulfan by restricting use to
the early stages of the growing season.
I he general public is exposed to endosulfan through the diet or in air. Some vegetables and fruits
are contaminated with endosulfan residues. To reduce the risk of exposure, endosulfan use on
vegetables and fruits should be restricted to the early stages of the growing season and should not
be used close to the harvesting period.
*
Recommendation #2: Protective clothing and equipment should be used during the
spraying and manufacture of endosulfan to reduce the risk of workers’ exposure.
Workers in manufacturing and mixing facilities, farmers and sprayers are exposed to much higher
levels of endosulfan than the general public. Therefore, they should use protective equipment and
clothing to minimize the risks of exposure.
Recommendation #3: Restrict the use of endosulfan in areas where wildlife may come into
contact with contaminated vegetables, soils and water.
Wildlife can potentially be exposed to endosulfan in the environment through the ingestion of
plants sprayed with endosulfan, contaminated soil, as well as spray drift and surface water runoff
contaminating surface waters. Care should be taken to eliminate the use of endosulfan in the
vicinities of open waters and in areas that may facilitate wildlife exposure.
Recommendation #4: Ban aerial spraying of endosulfan to reduce wildlife exposure.
Endosulfan is extremely toxic to aquatic organisms. Endosulfan has entered the aquatic
environment on a number of occasions, resulting in fish mortality. Aerial spraying of endosulfan
should be banned to minimize the potential for spray drift to contaminate surface waters.
Recommendation #5: Caution must be taken to avoid adverse impact on ecosystems and
biodiversity.
Biodiversity may decrease in benthic organisms exposed to endosulfan in the sediment. Careful
examination of biological and management methods are needed to reduce conservation impact as
a result of endosulfan use.
Recommendation //6: Collaborative research should be conducted to further study the
cndociine disrupting eflccts ol endosulfan, as well as the hazards of chronic exposure to low
levels.
While further research is necessary to elucidate the endocrine disruption effects of endosulfan, we
are concerned that endosulfan may be entering the environment at levels which may have lethal or
Endosulfan - A Review ofits Toxicity and its Effect.f.v on the Endocrine System
38
sublethal effects on wildlife. Further research is needed to establish the hazards of low level
chronic exposure to endosulfan.
Endosulfan - A Review ofits Toxicity and its Effects on the Endocrine System
39
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Endosulfan - A Review of its Toxicity and its Effects on the Endocrine System
To
The Editor
Down To Earth
Dear Ms Sunita Narain,
I found your article on the endosulphan very comprehensive and well
investigated. Since you mentioned the visit of Mr Ganesan to CHC I would like to add
something more from that interaction. The conversation was basically around the industries
concern about the 'misinformed activists’ campaign against endosulphan, which was a ‘relatively
safe pesticide alternative’ today. As a health training and policy action group committed to
community health concerns and action initiatives, I informed him that we were neither anti
industry or anti-pesticide per se but pro people’s health and our concerns and interests were
around ‘evidence’ of dangers to community health of any nature. Also as an Occupational Health
consultant I have been interested in this issue ever since I did a large ICMR study on
Occupational Health hazards of tea plantation workers including pesticide hazard.
I requested him to provide us with all the information the association/industry had about
endosulphan, which he promptly gave me in a note with questions and answers on endosulphan.
Over the last few months two of our younger team members Dr Anur Praveen and Dr Rajkumar
Natarajan have done a detailed literature review. I am sending this io you as our commitment to
public education so that your readers can decide whether this is ignorance of an industry or a
deliberate misinformation campaign.
At the end of last month we iacilitated a very interesting three day Community Health
Environment Skill Share (CHESS), where over 100
]
professionals and activists gathered from all
over the country to share their concerns about pesticides, mines, industrial hazards and other
environmental hazards and explore ways and means of studying them and collecting health
evidence. We had the unique privilege of a presentation by Dr Sayed, Director of National
Institute of Occupational Health who summarised the findings of their study on endosulphan in
Kasargod, which has been submitted to the National Human Rights Commission. The findings
not only substantiate the literature review we have compiled in CHC but is a sound, scientific,
evidence based contribution to the controversy. As a contribution to people’s science I think
Down fo Earth should formally write to NHRC and N1OH (on behalf of your readers and the
affected victims of the endosulfan disaster) to release this report and make it a public document
to support the right of information.
ICMP, ethical guidelines published last year clearly states that one of the ethical principles are
Regards,
Dr Ravi Narayan
Community Health Cell Adviser, CHC, Bangalore
sochara @vsnl. com
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INDUSTRY VERSUS SCIENCE - IGNORANCE OR MISINFORMATION
Compiled by Dr Anur Praveen and Dr Rajkumar Nalarajan ( CHC)
Questions
Answers
( What the Industry provided us*)
What is
Endosulfan?
What we have to say
(The actual facts)
- Endosulphan is an organochlorine
Endosulfan is a popular insecticide
pesticide belonging to the same family
used worldwide in more than 60
countries including USA, Japan, many (cylodicnc sub group) as Aldrin, Endrin,
Dieldrin, Heptachlor, Chlordane and
European and Asian countries. It is
Mirex all of which are Persistent Organic
recommended for control of insect
pests in a variety of field and----------- rT\>Htttants(P(JPs)andbamiedbythe-------- 1
International POPs Convention Treaty.
plantation crops such as Cotton,
(Quijano. R. F., International Journal of
Vegetables, Wheat, Paddy, Mango,
Occupational Health, 2000)
Cashew, Tobacco, Coffee, Tea,
- Endosulfan itself is banned in Germany,
Sugarcane, Spices, etc.,
Singapore, Norway, Sweden and Belize.
Agricultural scientists call Endosulfan Its use in rice fields is not allowed in
Bangladesh, Indonesia, Korea and
as a “selective insecticide” as it has a
Thailand.
very low toxicity towards beneficial
insects such as honeybees and insect
- Its use is severely restricted in USA, UK,
predators/parasites and crop pests. It is Japan, Russia, Australia, Great Britain,
therefore considered to be the most
Finland, Netherlands, Denmark, Sri lanka,
Thailand, and Kuwait. (Hoeshcst, 1991:
ideal insecticide for use in IPM
(Integrated Pest Management) systems. IRPTC, 1993; PRC, 1994)
- Latest data reveal it is highly toxic to
I
bees, aquatic animals and other wildlife. It
is moderately to highly toxic according to
scale of Hodge and Stemer(1956).
- It is easily absorbed in the body
following ingestion, inhalation and skin
contact. (IPCS, WHO-EHC 40, 1984.)
- There is no authority or reference
quoting endosulfan as a selective or ideal
insecticide.
- Acute intoxication or systemic toxicity
causes neurological manifestaitions like
irritability, restlessness, muscular
* Note provided by Nir Ganesan of
twithieng, seizures, cyanosis, pulmonary
Pesticide Manufacturers Association
oedema and death. (IPCS, WHO-EHC 40,
1984 and
Gosselin. R. Et al, Toxicoloogy of
r
Commerical Products, 1984.)
2. Does
endosulfan
belong to the
insecticide
group i
Chlorinated
Hydorcatbotis”
| siinilai to
DDT?
3. How does
WHO rank
endosulfan for
its toxicity?
No.
Insecticides of Organo chlorine group
contain mainly the elements Carbon,
Hydrogen and Chlorine. Whereas,
Endosulfan additionally contains
oxygen and sulphur in a functional
sulphite group. Hence, in 1986, WHO
reclassified Endosulfan as sulfurous—
ester of a chlorinated cyclic diol. In he
handbook of International Union of
Pure and Applied Chemistry (1UPAC),
Endosulfan is designated as sulphite.
The UN body WHO has classify
pesticides as folloiw.
Class la : Extemely Hazardous
Class lb : Highly Hazardous
Class TT : Moderately Hazardous
Class III: Slightly Hazardous
1 Endosulfan conies under the Class H
“Moderately Hazardous” pesticide.
Endosulfan is a Persistent Organic
Pollutant belonging to the organocholrine
group and cyclodiene sub group. It
belongs to the same family as Aldrin,
Endrin, Dieldrin, Heptachlor, Chlordane
and Mirex all of which are Persistent
Organic Pollutants (POPs) and banned by
the Inlei national POPs Convenlion Treaty;
(Quijano. R. F., International Journal of
Occupational Health, 2000)
Although endosulfan is classified as
sulphurous acid ester of chlorinated cyclic
diol by WHO, it is still an organochlorine
and its degenerated product endosulfan
sulfate is very persistent and as toxic as
the parent compound.(ASTDR, US Dept
of health & human Services, 1993)
WHO basis for Class II (moderately
hazardous) is based on LD 50 value taken
from company generated* acute toxicity
rate . (Quijano. R. F., International Journal
of Occupational Health, 2000)
*This data was challenged because the
lab that did theses tests was charged with I
fraudulent practice.
1
In India, endosulfan is classified as an
"extremely hazardous" pesticide (ITRC
1989)
According to USEPA, endosulfan is
classified as “extremely hazardous” class I b (US Environmental Protection
Agency, Consolidated Chemicals List, 2”*1
February, 1990)
EXTONET classified it as a highly toxic
chemical. (European union, 1998)
Fate in EnvironmentIn soil4. What is the Degradation and dissipation of
The time taken for the concentration of
Endosulfan is rather fast from all
_fate
____
of
endosulfan sulfate to reduce to half us
endosulfan in—compartments of the environment
concentration in soil is 60- 800 days
(soil, water, air and organisms). Tn
the
(Stewart and Cairns, Journal of
Indian conditions, dissipation of total
environment?
Agricultural Food Chemicals, 1974)
Endosulfan residues occurs to the
&
Endosulfan was found in soil after 3 years
extent of 95% within 28 days after
5. Is use of
of usage. (Rao DMR, Murthy AS, Journal
application. On most fruits and
endosulfan
vegetables 50% of Endosulfan residues of Agricultural Food Chemicals, 1974)
safe for man
Concentration of endosulfan in sediment
is lost within 3-7 days after
and
is 32,000 times greater than in the water
application. In soil, it is degraded by
environment?
column. (NRCC, 1975)
microorganisms. It is practically
insoluble in water. The half line of
Endosulfan in water is estimated to be In watcrThe time taken for the concentration of
4 days.
endosulfan to reduce to half its
concentration in water in 3-days - 5
At the recommended rate/s and
method/s of application, Endosulfan is months depending upon pH of water, 02
(dissolved in water) and pollution in
safe to man and environment and is
water.
unlikely to lead to any user or public
(NRCC, 1975)
! health problems.
Endosulfan has been found in
Studies and reviews by WHO/FAO
and US show that Endosulfan does not groundwater at deep soil layers upto 20
days after spraying. (Paningbatan EP et al,
have carcinogenic/mutagenic
The Phillipine Agriculturist, 1991.)
/teratogenic effects. Endosulfan does
Endosulfan is lethal to fish, even at
not cause endocrine disruption.
acceptable levels in water bodies. (IPCS,
Endosulfan enjoys good user safety
WHO-EHC
40,1984)
record, though used in a variety of
situations worldwide.
In air
Endosulfan has been carried over long
distances and found in air and snow
samples in Arctic regions.
(Gregor and Grummer, 1989)
i
Endosulfan bioaccumulates in aquatic
species like fishes, (Naquvi SM,
Vaishnavi C, Comp Biochem Physiol C,
1993; Fernandez Casalderrey A, et al,
Comp Biochem Physiol C, 1991; IPCS,
WHO-EHC 40, 1984) Kingfishers that fed
on fish which were killed or incapacitated
by endosulfan aerial spray died.
(Douthwaite, 1982)
Endosulfan and its residues have been
found in foods like vegetables, crops and
infant foods. (Pordrebarac DS, 1984,
Bureau of Plant Industry Philippines,----1995)
Safety of endosulfan for man and
environmentNo chemical pesticide is completely safe!!
There has been no studies on to prove the
toxicity of endosulphan as it is ethically
and legally not permissible to perform
tests on humans with pesticides. However,
sufficient proof is available on the
mutagenic , carcinogenic, teratogenic and
geno toxic effects on animals. Naturally,
these studies are used to predict the
possible effects on human beings.
Endocrine disruptionEndosulfan has reproductive and
endocrine disrutping effects leading to
reproductive toxicity and changes in
reproductive organs. (Soto A, Colborn. T,
Van Saal F. S., Environmental Health
Perspectives, 1994)
Mutagenicity (Cancer causing)
A 1992 study concluded that endoulfan
could act as a tumour promoter.
(Fransson-Steen R, et al. Carcinogenesis,
1992)
It has produced high rates of
lymphosarcoma (cancer of lymph
nodes)(Industrial Biotest, 1965)
Genetic defects (genotoxicity)
Endosulfan has caused damaged to genes,
chromosomes and cell cycle kinetics.
(Yaquan Lu, et al, Environmental Health
Perspectives, 2000; ASTDR, 1993)
Birth defects
Low birth weieht and adverse behavioral
effects have been noted on the offspring
of exposed rats. Endosulfan may produce
both maternal and developmental toxicity
in humans. (ASTDR, 1993)-----------------
Nervous system;
Acute intoxication or systemic toxicity
causes neurological manifestations like
irritability, restlessness, muscular
twitching, seizures. Long term effects of
exposure to endosulfan have caused
seizures and mental retardation (ASTDR,
1993)
ImmunotoxicitvThis is the most sensitive endpoint of
endosulfan toxcity and humans are at risk
of adverse immune effects. . (ASTDR,
1993)
Tn environment-
Endosulfan is lethal to fish, even at
acceptable levels in both fresh water and
sea water. (IPCS, WHO-EHC 40, 1984)
Endosulfan has been proven toxic for
terrestrial birds and organisms like
beetles, mallards, kingfishers. (IPCS,
WHO -EHC 40,1984, Hudson et al, 1972)
The National Wildlife Federation US
states that endosulfan is extremely toxic to
wildlife and acutely toxic to bees. (NWF,
1987)
The Danish government has classified
endosulfan as acutely toxic to birds.
(Hanson OC, Ecotoxicological
Evaluation of Endosulfan. 1993)
Toxicity of endosulfan in roots and leaves
have been reported. (IPCS, WHO-EHC
40, 1984)
Released by §HC, Bangalore in public interest to support the campaign against
hazardous usk ofpesticides.
WHOEHC: World Health organization Environmental Health Criteria
IPCS:
International Program on Chemical Safety
ATSDR: Agency for Toxic Substances and Disease Register, Atlanta
ITRC:
Industrial Toxicology Research Centre
» COVER STORY
•.•ckwe’tt '^fc'^mjwwMsi
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The inside story of
H
H
how the pesticide
industry connived with
KV
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i
■
V
officials andscienti^t;
to mask the truth
about a<^2>o2
July 15,2002 • IJoww Ta .^rth} 25 |
J-SSl*'
a
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■■i
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Il was in February 2001 that Down To Earth broke the story.
I )<>wn lolm |h
BlIliP
iffll
A link was established belwcea the unusually high incidence of dclortnities and diseases in Padre •
a village in Kerala's Kasaragad district — and endosulfan, an organochlorhie pesticide, The ,
Plantation Corporation of Kerala (PCK) had been spraying endosulfan since the mid-1970s on its i
cashew plantations. The people of Padre had long been waging a lonely battle against the spraying ’
of the pesticide. Laboratory analysis conducted by the Centre for Science and Environment (CSE),
New Delhi, revealed that all samples collected from the village contained very high levels of the j
pesticide that has ironically been either banned or restricted in many countries.
As the news was splashed in the national media, public pressure forced a number of decisions. ]
The National Human Rights Commission asked government agencies, including the Indian j
Council of Medical Research (ICMR), to act. A study by the National Institute of Occupational '!
Health (NIOH) got underway. The Kerala government too set up a committee headed by eminent ?
engineer A Achyuthan to probe the matter. Both the Union and state governments banned aerial ’
spraying of endosulfan. The crusade seemed headed towards its logical conclusion.
Instead, the pesticide lobby opened up a new front as it launched an offensive to fight.for its ;
exhtemc. At stake was the fate of an Industry worth Rs 4,100 erurti Thus began a virulent cam- ;
puign that involved top scientists, ugrhulturalists and officials, The agenda was two fold; to dis- ;
credit CSKs study and prove that tmdasulfan was safe mid harmlesa, The eampaign straw bml
three components: disinformation, manufacturing data and influencing govermnent agencies to J
lift the ban.
Soon articles, interviews and advertisements began appearing in the media painting endosul- ’
fan as a safe pesticide. Meanwhile, an industry-sponsored report was being concocted — PCK had j
commissioned the Fredrick Institute of Plant Protection and Toxicology (FIPPAT) in j
Kancheepuram, Tamil Nadu, to conduct a study. Not surprisingly, the results completely absolved j
endosulfan. Activists opposing endosulfan were threatened with legal action. And this was just the *
beginning. From hobnobbing with scientists and organising five-star parties to sending emissaries 1
or accompanying officials to meetings, the pesticide lobby used every rule in the book and outside ’
it to kill a people's campaign.
In many ways, the endosulfan battle is a litmus test for the industry — a defeat here could not
only hurl profits, but also encourage more communities to come out in the open and more pesti
cides being pul on the hi! list. For now it seems that their strategy Is working, In March this year. 1
(he ban on endosulfan was lifted under mysterious circumstances. This, when the confidential
NIOH report — that Down lb Earth is in possession of — clearly implicates endosulfan as the
causal agent for the diseases. Clearly, the silent screams of Padre's residents for environmental ■
justice have fallen on deaf ears.
KUSHAL P S YADAV, who went under cover to dig out the dirt, and S S JEEVAN track the |
murky ways of an industry that prefers to profit over people's health
H t was a veiled threat that Padma S Vankar was least expectI in8- As advisor to cse’s pollution monitoring laboratory,
I she had supervised the testing of samples collected from
I Padre. Vankar is also in charge of the Facility, for Ecological
v
and Analytical Testing at the Indian Institute of Technology
(llT), Kanpur. The threat came in the form of an unexpected
visitor at iit in September 2001, Meet M Raghavendcr.
Raghavendcr is with emfa (Endosulfan Manufacturers and
Formulators Association). He had come to iit with a clear
agenda: to ask iit to distance itself from CSE s study and to
make Vankar admit that her findings were flawed. In short to
undermine the credibility of the study. “He ‘advised’ me to
1
| 26 | Down To Earth • July 15, 2002
keep away from controversies as I was a woman,” says Vankar.
He failed on both counts. But Raghavendcr was just a small
pawn in a well-orchestrated campaign that had already been
launched nationwide. The powerful pesticide industry was
faced with its toughest challenge yet.
Ths might of an Mmrtry
The pesticide industry in India is the fourth largest In the
world and second largest in the Asia-Pacific region, only after
China. Estimates of its total market value vary between1 Rs
3,800 and Rs 4,100 crore. According to the Pesticides
Manufacturers and Formulators Association of India (pmfai),
MUNkaj..
COVER STORY
1
/ U,.
there are around 55 basic produ
and 300 pesticide formulators. Besides, there are a number of small-scale players.
Around 200-odd generic products are manufactured in India.
Insecticides alone account for around 75 per cent of this mar
ket and the cotton crop consumes almost half the pesticides
produced in the country. Pesticides exports stood at Rs 1,600
crore in 2000-2001 and the industry is confident that it will
reach Rs 1,800 crore during this financial year.
India is the largest producer of endosulfan in the world,
according to emfa. Three major companies produce endosul
fan in India — Excel Industries, Hindustan Insecticides
Limited (HII.) and Ell) Parry. Of these, Excel is the market
leader as far as endosulfan is concerned (see box: Endosulfan
peddlers). Therefore, it is not surprising that many of its
officials have been visiting Kerala for the past one year trying
to get the state government to lift the ban. “S Ganesan and
other officials of Excel Industries have been spending a lot
of time in Kerala meeting senior government officials and
scientists,” says Sridhar R, an activist working with Thanal
Conservation Action and Information Network, a
Thiruvananthapuram-based ngo.
The managing director of the Excel Industries, Ashwin C
Shroff, refused to speak to Down To Earth saying that the mag
azine had a certain viewpoint. But he cannot deny that endo
sulfan dictates his company’s business interests. “We are
acutely aware of our dependence on endosulfan. That is why
in the last 6-7 years from a very high dependence of over 60-65
per cent, we have come to a level of less than 40 per cent. But
it is like a flagship product,” he told Business Line (January 21,
2001). Profits had to be protected at all costs. And thus began
the campaign.
A clarification
on Endosulfan
A taction of th« prtu had rocontty carried rtporlt
originating from one particular village in Kerala about
certain health problemi allegedly arlaing out of aerial
application of IndoiuHan. Thlt prett release brlngt a few
important facte to light In fhle connection.
• Ail peilKide* undergo e«tcns<ve solely testing before they oie
registered lor cdmmercial use When used as recommended,
registered pesticides do not pose on adverse impact on the
environment and people
• Endosulfan has been registered for commercial use in over 60
countries including USA, Japan and several European countries
Kienfilie lind<r.y» ol WHO/FAO •xport* and other regulatory
authorities do not suggest that use of Endosulfan causes diverse
health problems as alleged in the medio.
Thh clarification It leeued for the benefit of uten and
general public and to clarify the Incorrect impression
created by the media reports.
e
PMFAI
h>o«d by fSa.I^xp Oo»«,
PeeHdde Manufacturers and Fermufaters Asseciatien ef India
B 4, Anond Co op Hiy Society ltd , Sdioden lemple Rood. Malum.
Mumbai 400 016 Phone (022) 4375279 fa. (022)43/6856
[ moil pmlorf'i.lK>m4 vml nel In
was being used in over bU countries. Environmentalists in
Kerala question the motive behind organising so many press
conferences within a short period of time. “This was clearly to
mislead the people,” says Jayakumar C, coordinator of Thanal.
In June, articles taking up the cause of endosulfan
appeared in magazines like Agriculture Today. One such article
by It V V Bhaskara Rao, director, National Research Centre for
Cashew in Puttur, Karnataka, said: “First convict the suspect
TIm art of dMiformatton
then conduct the trial.” Obviously referring to the CSE study.
In May 2001, an innocuous-looking advertisement appeared
This quote became the most preferred quote for the pesticide
in a Bangalore-based daily, bmfai had issued “a clarification on
lobby. Ganesan became his biggest fan and wrote a letter
endosulfan” (see advertisement). The health problems in
showering praises: “Il’s a masterpiece, a perfect blend of scien
Kusaragod district were not due to endosulfan and that endo
tific information and literary skill.” (see p28-29) In another
sulfan was a ’registered’ and sale pesticide, it said. This clarifi
article, S K Handa, former head of the division of agricultural
cation was issued for the “benefit of users and general public
chemistry at icmr, alleged that cse’s study was “questionable”
and to clarify the incorrect impression created by the media
and “pseudoscientific”. It is another matter that these experts
reports”.
could not find any scientific inaccuracy in cse’s study (see
The advertisement was a damage control exercise. Every
‘Pesticide Plot’, Down To Earth, Vol 10, No 10).
newspaper and television channel worth its name had exten
Dave lapped up whatever Handa had to say. Speaking to
sively covered the endosulfan tragedy in Padre. The plight of
Business Standard, Dave said that
Padre villagers with cases of cere
M
^ie endosulfan issue has been
bral palsy, mental retardation,
P
V
”
T
exaggerated.
” One I’Mi Al member
cancer and other diseases cap
went on to blame the cause for the
tured the public imagination.
“strange diseases” on inbreeding
Excel Industries
Endosulfan was becoming a bad
—
“many of those affected by
Managing
director:
Ashwin
C
Shroff
word for everyone. “The adver
these
maladies are reported to be
Installed
capacity:
6,000
metric
tonnes
tisement was given in the newspa
related to each other”. On back
pers to educate the people (sic).
ground radiation, this association
We were not concerned about the
Hindustan Insecticides Limited (HIL)
offered many explanations, “it
reports for the first three months.
Chairperson and MD: Rajendra Mohan
could be microbial contamination
Later we realized that we had to
Installed capacity: 1,600 metric tonnes
of water in streams. Or heavy
intervene as this was wrong,”
metal contamination. Or poor
argues PMFAI president Pradeep P
EID
Parry
nutritional levels.” In other words,
Dave. The association organised a
Executive chairperson: M V Subbiah
anything else under the sun. But
number of press conferences in
Installed capacity: Data not provided
not endosulfan.
Kerala claiming that endosulfan
July 15, 2002 • Down To Earth | 27 |
. .. .
Jr
COVER STORY
■-
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:
PRADEEP P DAVE
i
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,
S
,
■ President, P0StiM0 Manufacturer!) and
FomulatonAaaoclutlon oflndla ,
The mastermind behind th
> THE
,
The disinformation campaign brought only limited dividends
for the pesticide lobby. They still needed a “scientific” study th
I
II
Conner Ihc cw study, And ihry didn't h«ve to wait long. In
fB
■A
The science of manufncturlno date
Pebnirtty 200L a Kerala Agrlcidtiihd thilvpislly (KAO) teain,
headed by M Alnlnl Nidritn, rtssoclrtle deatb College of
Agthulnue, Keirtln Agikuliuie Unlvetshy, toiidliiled rt Nludy
In Knsrtirtgod. The icwdls weir nstunlhhlng. No significant
residues of endosulfan were found in any of the samples. The
industry couldn't have asked for more. And they went to town
with the findings. But there were only a few takers.
I he kau study has become somewhat of a joke among
learned circles. Differences within the kau team have cast a
shadow over its credibility. Thomas George, who did the
residue analysis, has washed off his hands as far as the sampling
process is concerned. “I never visited that place (Kasaragod), so
I do not know how the samples were collected and from where
they were collected. I simply did the residue analysis for the
team,” says George. He is also quick to point out that he was
only involved with the kau team in the first round of analysis. “I
was not involved the second time,” he says. But other scientists
in the team swear that (ieorgc was involved in both thclmnlysis
— the papers clearly mention hh name In both the teams.
Activists allege that Salam and Samuel Mathew, another
member of the kau team, were hobnobbing with industry rep
resentatives. “I met them only to get the scientific studies on
endosulfan,” defends Mathew. Mathew’s situation is akin to a
judge asking the accused for evidence to save him. Salam says
that he was not influenced by anyone. Moreover, even the KAU
team admitted the problems faced during their investigation
in their report: “Non-availability of quick and reliable meth
ods to assess the level of endosulfan contamination in the
environmental, animal and human samples.”
Activists and people’s groups in Kerala have reject
MUTUAL ADM!
ed the kau study.
Ganesan’s letterg
The endosulfan conspiracy took a new turn
FAJT
when the pck commissioned the Fredrick Institute
of Plant Protection and Toxicology (pippat) in
• OMM
Kancheepuram, Tamil Nadu, to conduct a study at a
ft Iw MwUn Rm
0«M>M.N»CC.tw»«
cost of Rs 7 lakh, according to pck. Controversy has
OaarftlkMtanlM.
trailed this study from the onset. Villagers of Padre
Al (*
. mm* a, **do hr
MM> M -HrW CMMM TW (
.
•
M*e< UMd *1
UM*
:
and other areas refused to cooperate with this team
tM^'MMHMklrM.nt. WM0'/
•MMMM a aU. IM| MM
to collect samples as they knew that it was an'indus-rty >•«*. «M Mmr
try-sponsored study. “We did not even know when
""****■ J 7*“,jl<>*T '
they collected the samples,” says Shree Padre, a jourI ^...R Ml n tMM ^IiM. '
nalist-farmer who along with Mohana Kumar Y S, a
doctor in Padre, have been protesting against the
!■
I N S I DI R’
former vIce-preMant, Pest &ntml India Umltecl
'Mndu.try’«lobt>ywnhthB8Ov<,rnmontte»<>»tron0,
I
'
"RvusstratronofpBRttelclMlnlndlalRttbiota/rKiR^
i
mm
i
mm
........ .. **Ka’iBl
iSb^sgplfcr
nMwMnMMMwte.v. .
-7.:............................ iji'-Fma/ance loMa
W®..., -
I’1
.. ....
c " '' - ®|||
.,,
.,
JAYAKUMAR C
: ■',
Coordinator. Thanal ’
Hte^Owarh^theflohta^lnstth.
MIHBNSIMK? indu#t'v'"K8rala
I 28 I Down To Earth • July 15, 2002
4BMMK
SiL
J
•
I
spraying for many years. “Later we came to know
that the samples were collected from young pck
workers, and not from the villagers,” says Sripathy
Kajampady, a doctor in Kasaragod who has been
fighting for the victims. FIPPAT director
Balakrishnamurthy refutes these allegations: “We
did a scientific collection with the help of proper
authorities.” Members of the Achyuthan committee
■
U. «. < MMt
m A. *Mk VMW, Rk Mr
¥if «
nt a. MM>
•* A. MM. «
*kd.M*w«r*M«**IM<MMryU .UM M. ft HMten Rm, I m> mI '■
•• H* M«, UM« Vm m.
i
I
COVER STORY
r
I
!
— comililiilcd by the shite govern
meni
are however, hu from Nath
tied. They have criticised the report
for improper sampling and also the
22. Comments on SEC report by the Project Co-ofdlnator, AICRP in Pesticide Residue.
lack of cross checking the findings at a
SARK New Delhi dt. 6.11.2001.
, I
different lab.
The pesticide lobby was quick to
question cse’s study saying that it had
ANNEXURE X2
used concentrated sulphuric acid and
so it should be verified by an inde
CoitiiiioiKs on the report prepared by A NOO 'Centre fbr
pendent residue expert, ft is another
Science and Environment’ and submitted to the Director,
matter that while the cse study did
I.A.R.I., New Delhi by
not use sulphuric acid on blood sam
- ----------------------------- vide their letter No.
ples, the fippat study, which the
MFAI/ENDU/01-02 dated 22/10/2001
industry lapped up, did.
It is unbelievable. CSE collected
the samples a few days after the spraying and found high levels
The knack of Intimidation
of endosulfan in all the samples. “T he fippat study, though
The industry’s next target was scientists and officials who were
started one month later than CSE, shows just the opposite
on committees that could decide the fate of endosulfan.
results, that is, complete absence of endosulfan residues in
Almost all of them confessed to Down To Earth that they had
blood, cow milk and water samples,” says the nioh report.
been approached by the industry representatives and fed with
Moreover, nioh, which did its study almost 10 months
scientific literature about endosulfan. "Imhisliy tepwsenta
after the last spraying, found endosulfan residues in water sam
lives approached me many times with a lot of do< nmenls, nal
pies collected from Kasaragod. nioh also found residues in the
urally to influence me. But I made it clear that I will just
blood samples of children of Vaninagar school. “The detection
depend on scientific evidence. T he representatives came with
of endosulfan in the blood samples of children and water sam
their so-called scientists and doctors to prove that endosulfan
ples, 10 months after the last aerial spraying of endosulfan, sig
is harmless,” says Salam.
nifies a continuous exposure to endosulfan,” says the report
Ditto for A Achyuthan, Samuel Mathew (scientist with kau
(see box: What the report says on p31).
and member of Achyuthan committee), T homas George (who
Although the fippat study was commissioned by the pck, it
did the residue analysis for the kau team), C S Srinivasan (agri
was released by pmfai’s Dave at press conferences in
culture secretary) and L Sundaresan (former kau director and
Kozhikode and Thiruvananthapuram, where selective extracts
member of Achyuthan committee). A look at the industry’s
were reproduced for the press. “ This clearly points
dossier is predictable: only selective information about endo
ATION CLUB out the nexus between industry-PCK and fippat,” sulfan is enclosed. Says Achyuthan: "First they (industry repre
Bhaskara Rao
says Jayakumar. Activists in Kerala and people of
sentatives) came to my house. But I told them that I would
Kasaragod have branded the fippat study as a “wellhold discussions only in Kasaragod and not in my house.”
schemed industry effort”.
Industry, however, refutes these allegations. “We never
An interesting incident that proves the nexus
' KA My mi
approached the scientists. We only approached the agriculture
between the industry and private labs took place
department,”’ was Dave’s candid reply.
when the industry made a presentation before the
‘ It is amazing that the industry knew every move of the
Achyuthan committee, fippat scientist A Ramesh
Achyuthan committee well in advance,” says Jayakumar. Just
C UM TW TrW. k b a BMW
M ItastfalaiHMaal wtBaaMM
accompanied the industry team that included Dave
before the Achyuthan committee was to hold a public hearing
**
ZumZZm
and S Ganesan of Excel Industries. “Ironically, the
in Kasaragod on September 5-6, 2001, pmfai organised a press
fippat scientist did not accompany the pck team,
conference at Kochi on September 4. T hree doctors from
fbNrvoxMiiwuvte
• IM av«BMn
awW
which had commissioned the study,” says
k MM MBaaa M *aw W Ba
Mumbai spoke at the press conference and condemned the USE
a«M.
*a
<a*M aWW/>a.
Achyuthan. When Down To Earth asked fippat
study and Mohana Kumar. When grilled by newspersons, the
director as to what business did their scientist have
doctors admitted that they had not visited Kasaragod or met
by accompanying the industry team to a govern
the affected people.
ment committee, he said: “He might have gone in
On August 30, 2001, pmfai and Excel organised a dinner at
the same car, but was not with them.” When told
the South Park hotel in Thiruvananthapuram, which was
■ »«,**«;
inu ti
that Ramesh’s criticism of cse analysis was recorded
attended by senior government officials and kau scientists. One
in
the
committee
’
s
final
report,
he
gave
a
contradic
regional newspaper Madhyatnatn Dailyhad an interesting com
--raewnwam
tory reply: “It is not a big crime (accompanying the
ment to make on this gathering. “Pesticides manufacturers are
industry team). But we are not associated with any
trying to pull strings at the top to get the ban on endosulfan
industry.”
lifted. The pmfai and the Excel company has been trying to
influence the agricultural experts in the state to take a decision
in their favour. For this, they had arranged a dinner in a promi
nent five-star hotel in Thiruvananthapuram where experts and
government officials took part. It is learnt that people in the
higher ups, including agricultural experts had taken part.
The Achuythan committee's small 'mistakes’
i m
m
k
Inly IS, 2(10? • Down Io Enrlh | 29 |
i I
!
I
[ !
i
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COVER STORY
I
J
'■'o
I
'fe!
»
Manufacturers lobby is making all intensive effort to get the ban
lifted.” In another incident, a freelance filmmaker claims to
have accidentally spotted Ganesan, Dave, and '! homas George
(who did residue analysis for kau) at Chaithram hotel,
Thiruvananthapuram. George admits having gone to the hotel,
but only “to collect some documents regarding endosulfan”.
The pesticide lobby also tried to influence civil society
groups. Ganesan paid a visit to Ravi Narayan of the
Community Health Cell (cite), Bangalore, who was trying to
Investigate the health problems in Kasaragod. Ganesan is the
general manager with Excel Industries but was introduced to
Narayan as a scientific advisor to pmfai. “They wanted a
leisurely meeting with me at some five-star hotel on a
Sunday,” remembers Narayan. When he declined the offer,
Ganesan went to meet Narayan al his office in January.
Ganesan had an unbelievable incident to narrate, “csf chair
pet non Anil Agio Will admitted that their wits a mistake in csp’s
analysis of samples," Ganesan is said to have told Narayan.
"They can gel away by saying anything because Anil Is not
there to call their bluff," says Narayan.
If civil society activists could not be won over, the industry
tried to strangle their voices, 'fake the case of Madhumita
Dutta. As central coordinator of Toxics l ink, a New Delhi
based non governmental organisation, she had made a preset!
tation at a conference organised by the Confederation of
Indian Industry (cil) on Persistent Organic Pollutants (rot’s)
on March 6-7, 2002 in New Delhi. She spoke about the endo
sulfan problem in Kerala and how dangerous pesticides arc to
human health. This was enough for emfa’s Raghavcnder to
write a letter to cil wanting it to expunge her statements. He
also wrote to Dutta insisting, “We strongly advice you to
refrain from spreading further misinformation on the subject."
Such is the insecurity of the pesticide lobby.
The Achyuthan committee submitted its final report in
November 2001. “There is no evidence to
implicate or exonerate endosulfan as a
causative factor of the health problems,” it
said. But some glaring errors in the report
have come to light. The report quotes the
remarks made by the Indian Agricultural
Research Institute (lARl), New Delhi, to sup
port the cause of endosulfan. IARI, in fact,
made no such remarks. 'These notes were
actually prepared by the pmfai and submit
.^1ted to the iari (see p29). “We committed a
mistake," admits Achyuthan. This mistake
was one of the basis on which the committee
rejected the dsi' report, while accepting the
kau and I ippa I reports.
On the basis of the Achyuthan commit
tee’s findings, pmfai filed a writ petition in
| JO | Down To Earth • July 15, 2002
the Kerala High Court to lift the ban on endosulfan in the
stale. I hey also tried to use Section 27 <»l the Insecticides Act
of 1968. This act states that the state government can suspend
the use of a chemical only for certain period of time and can
not ban it completely. 'This power rests with the registration
committee of the Central Insecticides Board (cm), Faridabad,
i
I
■
Haryana.
It seems that the endosulfan conspirators have won, at least
for the time being. The Kerala government lifted the ban on
endosulfan on March 22, 2002, based on the recommendations
of the Achyuthan committee and the KAU study. It is surprising
because lifting the ban was never the mandate of the Achyuthan
committee. “We were not asked to comment on the issue of the
ban,” says Achyuthan. However, the ban on aerial spraying of
endosulfan remains. Perla division of pck (covering Padre and
Muliyar villages in Kasaragod district) have been given a pesti
cide holiday for five years. “When the bun was lifted, the entire
state government employees weie on strike. Il Is ((idle possible
that the iigikulluie secicliiiy who had Issued the order might
have had to type the order himself," alleges Jayakumar.
The agriculture secretary, C S Srinivasan, — who activists
allege is an industry person
also held the additional post of
director of agriculture depaitment (I'chiiiaty 28 Io Minch 18)
when the final decision was taken to lilt the ban. When I hnvn 7b
1'iirlh sought an appointment with Srinivasan, he refused. But
when the same reporter approached him ns n freelance journal
ist, he readily agreed for an interview. He said that he had just
received the NIOII report (it reached him three months ago), but
he didn’t have the time to go through it. Maybe Srinivasan just
wanted to keep the report out of the media’s reach.
'The role of the state’s chief minister, A K Antony, has been
quite bi/zarc. Some activists allege that he is a "dummy" —
someone who has been unable to take a principled stand. His
government has lifted the ban, even as it sits on the nioh
report, which clearly calls for stopping the
use of endosulfan. According to Section 27
of the insecticides act, the state govern
ment could have either extended the ban
or issued fresh orders to continue the ban.
Antony could have also taken up the mat
•J
ter with the Union government on the use
of endosulfan. But he did not do so. How
can the chief minister be so apathetic to the
sufferings of children.
__________ _____________
The order itself to lift the ban was a
hushed up affair. Even today most people
in Kerala are unaware that the ban has
MmwiMMiiai
been lifted. And to add salt to Injury, a
fresh batch of endosulfan reached all
KrishibhavtiHs in Kerala this month.
Kerala’s residents are terrified.
I
I
j
*
:
1
COVER STORY
FBWsli I iWarn I
sKS
In August 2001, the National Human Rights Commission
(NHRC) asked the Indian Council of Medical Research
(ICMR) to submit a report on the health hazards due to the
spraying of endosulfan in cashew plantations in Kasaragod
district within four months. ICMR In turn asked the National
Institute of Occupational Health (NIOH), Ahmedabad, to send
a team to Kerala.
A three-member NIOH team — comprising NIOH director
H N Saiyed, deputy director Aruna Dewan and H R Rajmohan
of the Regional Occupational Health Centro (ROHC),
Bangalore — visited the district on August 9-11 and then
again In September. They had a clear mandate: a crosssectional environmental epidemiological study to Investigate
the disease pattern in the affected villages and a control
ItKini /
.* w 18al Ju mA?Tfi ■ m
few copies are available. Most activists and the media don't
have any clue about the findings. "Has this damning report
been kept secret because it clearly implicates the pesticide
industry,” asks Jayakumar C of Thanal, a Thiruvananthapuram- based non-governmental organisation.
WHAT THE REPORT SAYS
Two months after the spraying, FIPPAT study did not
find endosulfan residues. This Is what NIOH found 10
months later. Even months after the spraying, blood
samples of young children had deadly endosulfan
1
residues. Remember, there Is no standard for this
pesticide in blood because there is no safe level.
Totat andotulfnn rvaktua
(In parts per biUlon (ppb))
MM
Water In pond naar Kodanklri atraam
0.0687
Well water naar *01)001
0.02011
Wall wntor near bouo*
0.0204
f
Blood samples of children from Vaninagar school
I*'-A
Cods 1
I
if
,
78.74
Coda 4
28.44
Codes
48.00
Code 104
33.57
congenital abnormalities: Significantly higher in the
exposed group of females as compared to the control
group. Congenital heart and skeletal abnormalities were
also high. Exposure linked to genotoxic agent, which
could be endosulfan in this case.
y.-'^‘7.-”'..'
■
ILLUS1RATIONS AKKI
Congenial abnormalities
I
I
population. The team was headed by Saiyed and comprised
members from NIOH, ROHC and the department of pedi
atrics, Kasturba Medical College, Mangalore. The field study
was conducted from September 24 to October 7. In the first
phase, blood samples of 262 schoolchildren (170 exposed
and 92 control) were collected for detecting endosulfan
residues, hormonnl analysis, thyroid hormones, sex hor
mones and cytogenetic studies.
It is significant that the NIOH team decided to select a
control group. A control group is comparable with the
exposed group in all respects, except for the exposure,
which in this particular study was endosulfan.
The NIOH report indicates that endosulfan is the cause
for a number of health problems among schoolchildren living
in the exposed area. Those children had significantly lower
intelligence level then the control group. They also had a very
high incidence of various sexual disorders when compared
to control group (see box: What the report says).
The report was finalised In March 2002, but has been
kept confidential. Only a few are privy to the findings. Down
To Earth managed to get hold of the report, of which only a
Contrrtt (% of people
affected tn the group)
Exposed (% of peorrle
affected in the group)
1.08
5.8
neurological problems: Significantly higher prevalence of
learning disabilities, low IQ and scholastic backwardness
were found. Exposure to some neurotoxic agent, possi
bly endosulfan, during development stages.
Control (% of people
effected in the (pcnrp)
Exposed (% of people
effected In Hh> group)
Leeming disability
2.60
10.7
Retained In same class
13.50
20.40
ABNORMAtrnEs 4N reproductive system: Findings are strik
ing and point to exposure to an endocrine disruptor. Girls
attain menarche early, menstrual disorders frequent.
Boys’ puberty delayed. Signify exposure to oestrogenic
substances and endosulfan is experimentally shown to
have oestrogenic effects.
Menstrual disorders
Control (% of people
effected In the group)
Exposed (% of people
affected in tt»e group.)
4
21.80
Inly I'., 'lid ‘ • howii Io I .iilh | I I
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■
COVER STORY
icauni
I
THE BUSNESS OF POISOfUIIVG
I
Endosulfan constitutes only a small share of the pesticide market.
So why is the pesticide industry paranoid?
he protest against endosulfan in Kerala has become a
symbol of struggle against pesticides in India. The
pesticide industry is worried about endosulfan as
much as it is of its other products. As Dave proudly
puts it, I do not defend just one molecule. I am the president
for 200 molecules. We will not ban anything just on the basis
that il is banned in other countries.” If
endosulfan is banned in Kerala, it
could have a cascading effect in the rest
of the country. A successful campaign
for banning a particular pesticide will
F'
fuel the fire for other movements as
well in India. More pesticides would be
under scrutiny. More communities
would feel encouraged to protest. And
more pesticides would be on the hit
list. That is something the industry
; 1 ' X'-
Governments are buckling under the pressure from the civil
society groups to ban harmful chemicals and pesticides. Last
year, Columbia banned endosulfan. The Philippines rein
stated the ban on endosulfan after a long-drawn battle with
the industry (see box: Threats and a ban). Other countries are
cither restricting the use of this pesticide or banning it com
I
■
I
a
cannot afford to lose out on.
There are already reports of a
similar problem in Karnataka. The
Karnataka Cashew Development
Corporation had been spraying endo
sulfan on its plantations in Dakshina
Kannada and Udipi districts since 1987. People in these areas
are also suffering from strange diseases (sec ‘Double Trouble’,
Down To Earth, Vol 10, No 11).
1
A laroor game plan
I In iilin ill lli< liiilii'ili yS i ampalgn
i
I...
n, In latl, nm< li laigri If
lb l«l blldllglc dll (he VuIllU llldt diC Cdllillg l<Hr a ban on pesti
cide products. Worldwide, awareness about harmful effects of
pesticides on humans as well as the environment is increasing.
The Philippines banned endosulfan In
1992. The Industry led by Hoechst of
Germany launched an offensive. It filed
contempt proceedings against the
Philippine Fertilizer and Pesticide
Authority’s (FPA), which Imposed the
ban. It also harassed field workers who
came forward with their personal expe
riences about exposure to endosulfan.
The ban was successfully challenged
by the industry.
In 1993, a subsidiary of Hoechst,
AG, of Germany, filed another lawsuit
against a news agency, Philippine
News and Features, that ran a story on
| 32 | Down To Earth • July 15, 2002
1
pletely. The industry is feeling the heal
for more than one reason. Recently,
India
signed
the
Stockholm
Convention, a global treaty to protect
human health and the environment
from persistent organic pollutants
(pops), pops are chemicals that remain
in the environment over long periods.
By implementing the Convention,
governments will eliminate or reduce
the release of pops into the environ
ment. In the first phase, 12 pops have
been identified for phase out.
Endosulfan is not yet on this list, but
has all the ingredients to make it in the
next round.
As consumer pressure is increasing, corporate bodies are voluntarily moving away from pestitides. “Industry representatives told me that endosulfan for
cashewnut plantations is just a small market. They are more
concerned about endosulfan being used in cotton and in other
'.lalci, IhcyNuid il it In b.mncd in Kcral.i, it will hnvr rcpcriusU'hi* all over India," hays Salam. When have was asked
whether they lelt threatened by such campaigns (like the one
on Kerala) he replied: "It’s just that we have to protect our
interests and present our side of the story.”
the possible carcinogenic nature of
the insecticide, Thiodan (Hoechst’s
trade name for endosulfan formula
tion). Even a scientist quoted in the
story, Romeo Quijano, was sued for
over US $814,800, according to
Pesticide Action Network (PAN), a
global antl-pestlclde body.
Citizen and farmers groups got
together to fight back. They were out
raged that anyone coming out in the
open about the effects of pesticides
was slapped with a lawsuit. Activists
were also disturbed by media offensive
Initiated by Hoechst’s regional sub-
■-J
sldlary that portrayed pesticide prod
ucts as safe.
In March 1994, the Philippine
government ordered Hoechst to with
draw Its television advertisement on
Thiodan calling It “false, misleading
and deceptive’’. On June 1, 1994, the
government reinstated Its restrictions
on endosulfan sales and banned trlphenyltln acetate, despite threats by
Hoechst that It would pull out of the
country If the decision were not
reversed. The ban etill holde on th© ub©
of endosulfan, except for use In
pineapple farms.
MS
i
COVER STORY
*■*>
I-' z
1
? 0T Ta
' ...1
'
^4®
A
RKS MB BMGfiBES
Pesticide regulations in India are lax. The industry has exploited the loopholes to
corrupt the system. And the government has turned a blind eye to the problem
esticides arc regulated under the Insecticides Act of
1968 and Insecticides Rules of 1971. In May 2000, the
Insecticide (Amendment) Bill 2000, was passed under
the shadow of suicide deaths of farmers because of
spurious pesticides. This amendment made the punishment
for adulterated pesticides more stringent. But it did little to
clean up the regulations to register pesticides and to monitor
this poison industry. The insecticide act regulates the import,
manufacture, sale, transport, distribution and the use of insec
ticides to prevent any risk to people and animals. The registra
tion committee, constituted under Section 5 of the act,
registers an insecticide after verifying its efficacy and safety
to human beings, animals and the environment. The
Central Insecticides Board (gib) based in Faridabad, Haryana,
advises the Union and state governments on technical
matters. In 2001, a total of 2,718 applications were received
for registration, of which 1,439 were approved, according to
the government.
Basically, there arc two types of registration under Section
9 of the Insecticides Act — primary and secondary. When a
new molecule is registered in India it gets a primary registra
tion. Subsequent applications for the same molecule get the
secondary registration. Registering a new molecule requires
the generation of studies — environment dependent data
conducted under Indian agro-climatic conditions and envi
ronment independent data.
Environment independent data can be straightaway lifted
from existing data elsewhere in the world. But generating
environment-dependent data usually takes around 4-5 years.
Data sets on various subjects including toxicology and phyto
toxicology need to be generated to register any new molecule.
Once a primary registrant exists, others applying for fresh
registration are given a secondary registration.
Of course, these are just rules prescribed by the govern
ment. These arc rarely followed.
Post-lnfestod system
I he first step to register a new pesticide is the generation of
data. This is also the first step where corruption can creep in.
A company has the option of either going to a government lab
July IS, 2(102 • Down To Earth | 33 |
COVER STORY
|
I
Asnwscm
KNDOCCL
BHSBfflg
iff be tl^<B!f6aflWents mW pMiJSWIe^ health abova
anything else. Otherwise, this industry of death will become even more
deadly In thenars to come
_________
■SP®
or a government-approved pri
vate commercial labs. "Com
panies usually prefer govern
ment-approved commercial labs
as they can generate the desired
iSCThctfj^.
rl
results. And quickly. Bureau
cratic hurdles in government
labs can cause long delays,” says
N G Waghle, former vice-presi
J
MMjjl
dent, Pest Control India Limited.
!
Private labs are primed to cater
to the industry’s demands, he
adds. Where everything comes at
■ g=|^t?^'3I’S?=wS5
r
a price.
"Indian registration proce
nssL.*xSiCTir*-- — — — *-,/3^^^ixim'sea*~*’,K»
dures arc hopelcNN, It Is a big
----i
tamasha," says P D Deshmukh, a
I
senior pesticide industry insider.
Farmer education: try
With an experience of 30 years
reading the fine print
with the industry, Deshmukh has
amazing tales to narrate. "I know
of one lab which promised to generate toxicological data for a
fe . H
MiMi
product within a day. Generating this data usually takes one to
one and a half years. The head of the lab told me that he would
propone the exchange of letters by one year —- making it look as
if the application was filed a year ago. Many multinational and
Indian companies are a part of this racket,” alleges Deshmukh.
It is scary to imagine how many dangerous pesticides would
have made it to the farms without proper testing,” fears Waghle.
Recounting his 35 years of experience in the industry,
'■:
■■■'5
.
touch with the company. The company pays the agent for all the
dirty work,” he adds. Waghle has given Down To Earth names of
a few of the legendary agents and their clients.
The laws itself arc geared to protect the industry. The
endosulfan establishment has used these loopholes to great
advantage. For example, the pck violated many regulations
while conducting aerial spraying. The insecticides act makes it
I
mandatory for a company to inform people about aerial
spraying of pesticides. All waterbodies in the area must also be
covered during spraying. But this was not done by the pck.
* I he cib has prescribed that the endosulfan spraying should
be undertaken at a height of not more than 2-3 metres above
the foliage. But even this was always violated in the pck planta
tions,” says L Sundaresan, former director, department of
agriculture, Kerala,
"Aerial fepraying <»l riidmiulfiiii wan never allowed by the
cib alter 1993. The cib had given approval for aerial spraying
of endosulfan to the pck only till December 1992. But the
department of agriculture in Kerala and the district collector
have been issuing aerial spraying directives even till January
2001,” alleges Jayakumar.
The Union government made some tired efforts to make
pesticide use "safe”. It appointed committees. These commit
tees allowed the use of endosulfan with a word of caution:
pesticides must be used very carefully and specified areas
where they must not be used. In 1991, the Union government
appointed a committee headed by S N Banerjee, former plant
protection advisor to the government, to review whether some
pesticides, including endosulfan, should be used in India. The
committee said that the registration committee of cib should
Waghle, recounts shocking tales of how companies have cor
not allow the use of endosulfan near rivers, lakes, sea and ponds.
rupted even top officials in pesticide registration bodies.
The committee also recommended a warning must be displayed
'Companies are wary of directly approaching cib officials, so
on all labels and leaflets of containers. As far as other warnings
they use the services of a broker,” he says. Agents act as a liaiare concerned, companies display them in such small point size
.on between the indu.try and cm. Bribing of Junior and senior that it i» unreadable\See FnwwV'ednenrion
------- ---- ------- 1 on this page).
of 1 iciais at CIB takes place through these designated agents. The
Another committee headed by R B Singh, made similar
industry has developed the bribing of officials into an art
recommendations in 1999. It reinforced the fact that labelling
form. And the agent is an integral part of this racket.
should be made mandatory in bold letters to avoid use of
endosulfan near water sources. 1 he 195th meeting of registra
Ugly Interface
tion committee of cib, held in December 1999, agreed to
The broker is usually a regular face at the cm, says Waghle. So
implement the recommendations. But they were never
even officials feel comfortable inleractinf; with him. Industry
actually implemented, The cm has chosen to sit on these rec
pays this agent for all the dirty work that they want to get done
ommendations. Endosulfan is still used indiscriminately, as
— registration of a new molecule or stealing data for already
the Kasaragod tragedy shows.
registeied molecule or even bribing the registration commit
The pesticide industry does not like the regulations of the
tee members to influence decision-making at the top level. But
insecticide act saying that the cumbersome procedures for reg
the bribe is not always money.
istration are strangling growth. But, seeing the way the indus
Many top cib officials, including the registration committee
try has sidestepped, indeed, trampled over all procedures and
members, regularly receive junket invitations, says Waghle. The
norms of decency in the endosulfan case, it is clear that this
company pays for all the expenses — air tickets, five-star hotel
"dirty" business needs more, not less, controls. But this time
accommodation and even shopping expenses. Again there is no
it needs monitors who will have public accountability.
direct involvement of the industry. It is done through the agent.
Otherwise, this industry of death will become even more
“'I’hc official simply has to inform the agent, who then gets in
deadly in the years to come. ■
| 34 | Down To Earth • July 15, 2002
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