India - Pesticides and Health Meeting 8th to 10th October 2002 Indian Social Institute, Bangalore · Community Health

India - Pesticides and Health Meeting 8th to 10th October 2002 Indian Social Institute, Bangalore

Item

Title: India - Pesticides and Health Meeting
8th to 10th October 2002
Indian Social Institute, Bangalore
extracted text: India - Pesticides and Health Meeting
8th to 10th October 2002
Indian Social Institute, Bangalore

Collectively organised by

Community Health Cell, Bangalore
Community for Resource Education, Hyderabad
Corpwatch India
Greenpeace India
Institute for Cultural Research and Action (ICRA), Bangalore
Paryavaran Suraksha Samithi, Gujarath
Pesticide Action Network- Asia Pacific
Thanal Conservation Action Information Network, Trivandrum
ToxicLink- Chennai

"A healthy farm culture can be based only upon familiarity and
can grow only among a people soundly established upon the
land; it nourishes and safeguards human intelligence of the
earth that no amount of technology can satisfactorily replace.
The growth of such a culture was once a strong possibility in
the farm communities of this country. We now have only the
sad remnants of those communities. If we allow another
generation to pass without doing what is necessary to enhance
and embolden the possibility now perishing with them, we will
lose it altogether. And then we will not only invoke calamity we will deserve it."

Wendell Berry

This dossier contains
1. Pesticides - Killers in our midst

Dr. Marion Moses

[Article from "Warning Pesticides are dangerous to your health!" - Stop endocrine
dirupting Chemicals report by Pesticide Action Network Asia Pacific]

2. Endocrine Disruption : New threats from old chemicals
Smolen

1
Dr. Michael

[Article from 'Warning Pesticides are dangerous to your health!" - Stop endocrine
dirupting Chemicals report by Pesticide Action Network Asia Pacific]

9

3. Acute Effects of Pesticide Exposure
[Article from "Pesticides and Human Health" A Resource for Health Care
Professionals by Physicians for Social Responsibility and Californians for pesticide
Reforms]

20

4. Dermatologic effects of pesticide exposure
[Article from "Pesticides and Human Health" A Resource for Health Care
Professionals by Physicians for Social Responsibility and Californians for pesticide
Reforms]

24

5. Pesticides and Cancer
[Article from "Pesticides and Human Health" A Resource for Health Care
Professionals by Physicians for Social Responsibility and Californians for pesticide
Reforms]

26
6. Pesticides and respiratory Disease
[Article from "Pesticides and Human Health" A Resource for Health Care
Professionals by Physicians for Social Responsibility and Californians for pesticide
Reforms]

32

7. Neurological and Behavioral effects of Pesticides
[Article from "Pesticides and Human Health" A Resource for Health Care
Professionals by Physicians for Social Responsibility and Californians for pesticide
Reforms]

34

8. Reproductive and Developmental effects of Pesticides
[Article from "Pesticides and Human Health" A Resource for Health Care
Professionals by Physicians for Social Responsibility and Californians for pesticide
Reforms]

37
9. Effects of Pesticides on the Immune system
[Article from "Pesticides and Human Health" A Resource for Health Care
Professionals by Physicians for Social Responsibility and Californians for pesticide
Reforms]

41

Contd

10.

11.

12.

Hidden dimensions of damage : Pesticides and Health
Monica Moore
[Article from Fatal Harvest The Tragedy of Industrial Agriculture edited
by Andrew Kimbrell 2002]

43
DDT and other chemicals used in vector management programmes
[ First part of Chapter IHazards and Exposures Associated with DDT
and Synthetic Pyrethroids Used for Vector Control by WWF)
58
Inadequate Testing of Pesticides Warren Portel et al
[Article from "Warning Pesticides are dangerous to your health! " - Stop
endocrine dirupting Chemicals report by Pesticide Action Network Asia Pacific]

65
13.

Recommendations : Protecting farm workers from pesticides
[Chapter 5 of "Fields of poison" by California Farmworkers and
Pesticides]

14.

IG Farben : Participating in State sponsored Human Rights
Atrocities
[Article from www.bhopal.net ]

68

72

15.

Globalization : Free trade in toxic products, technologies and
wastes
[Article from www.bhopal.net ]

16.

Impact of Corporate Control - The Pesticide TNCs
Barbara Dinham

75
[Article from 'Warning Pesticides are dangerous to your health! " - Stop
endocrine dirupting Chemicals report by Pesticide Action Network Asia Pacific]

79

17.

End Note by Nityanand Jayaraman
• •■■84

Please turn over

What follows is a collection of papers on die topic "pesticides and
health". India is world leader in pesticide contamination matching with
some of the most contaminated countries. But for us who lived in the
richness of biodiversity and culture the introduction of the registered
poisons - the product of corporate indulgence on natural systems for
private profits is relatively a strange thing. So it took time to understand
and respond and sadly we have paid heavy toll by impairing our
communities.
The village communities and the public interest groups always used to
respond to criminal acts against the collective good. The shift from
peasant sciences of survival and wisdom to the information and market
driven world, and we are once again lost. Current attempts by the
individuals and groups are to rediscover where we are and then position
ourselves in the struggle for our survival. Many communities are putting
efforts to network and join together. The struggle for justice in Bhopal
is declaration by all of us that we will not surrender and in the 18th year
with more meaning and purpose we continue.
We hope that this meeting on pesticides will be one of such steps to
understand where we are in terms of dis-information and illusions and in
which direction we have our future and also to reinvent die hope of
being in a poison free world of ours.

We have only poisons to lose.
Jayakumar C.

October 8, 2002.

Pesticides - Killers in Our Midst
byDr. Marion Moses

Introduction
esticides are toxic chemicals delib
erately added to our environment.
They are poisons by design whose
purpose is to kill or harm living things. They
can kill or harm human beings as well.
Many of the pesticides being used in
farms, orchards, plantations and rural rice
fields around the world are highly toxic.
Farmers and agricultural workers are heavily
exposed to pesticides known to damage the
brain and nervous system or that cause can
cers, birth defects, miscarriages and still
births. Many of the pesticides they are ex
posed to are banned or severely restricted in
other countries. (See Box: Banned Pesticides
are Still Traded).
In rural Asia for example, the use of pes
ticides has permeated even the remotest vil
lage. The availability of highly toxic pesti
cides, lack of information and knowledge of
their hazards, aggressive marketing by the A farmer in North Sumatra, Indonesia, spraying while
walking through pesticide sprayed fields, with no protec
industry as well as poverty, illiteracy, and lack
tive clothing. Photo: PAN North Sumatra.
of health facilities ensure that pesticides are
a major cause of poisoning in rural farming com
pour them into the spray containers which is an
munities. Impacts on the health of women and
even more serious health risk since they are han
children are of a particular concern.
dling the concentrated products. Often, the women
The severity and extent of the problems de
do not even know the names or hazards of the pes
scribed by women working in rural farms and plan
ticides they are mixing and applying. They receive
tations in Asia are shocking. Pesticide exposure is
no education or training in how to use them prop
a likely source of many of the health problems
erly
or how to protect themselves and their chil
documented by groups like PAN Asia and the Pa
dren. Even if they were provided full protective
cific. Unlike other parts of the world, women in
equipment and clothing appropriate for pesticides
Asia have more direct and heavier exposure to
they are working with, they would still be at risk
pesticides than their sisters in other regions.
from heat stress and even death from heat stroke.
The majority of workers who apply pesticides
This is especially true since they do not have
in plantations, in countries like Malaysia for ex
enough water (or sometimes not any water) to drink
ample, are women. They also mix pesticides and

P

India - Pesticides and Health Meeting, October, 2002

1

d:

-

.. -

---------------

Banned Pesticides are Still Traded
hough several highly hazardous pesticides are banned in many countries, they are
still being produced and exported, and finding their way to many other countries. Many of these are
amongst the "dirty dozen" pesticides—in reality 18 pesticides including chlordane, parathion and lindane that
were the subject of a decade long campaign by the Pesticide Action Network.
During 1995 and 1996 for example, the U.S. exported highly toxic pesticides including chlordane, hep
tachlor. parathion and lindane, to countries which had banned them. Chlordane was exported to Brazil, Singapore
and the Netherlands; heptachlor to Brazil and the Netherlands; aldicarb (an “extremely hazardous" pesticide)
to Argentina and paraquat (another highly toxic pesticide) to the Dominican Republic. Other hazardous chemi
cals exported include pentachlorophenol to Thailand and EDB to Belgium.
According to Greenpeace, India, which has emerged as a major centre of pesticide production in Asia
(the other being China) exports hazardous pesticides including aldrin, chlordane, heptachlor, DDT and BHC to
several countries, “including countries where their use has long since been banned”.
“Reports indicate that clandestine manufacturing of several POP (persistent organic pollutant) pesticides
may be contributing to illegal exports to Bangladesh and Nepal. As far as many Bangladeshi and Nepali
activists are concerned, India is to South Asia what the U.S is to the world—a “toxic imperialist”.
For instance, during 1997 India exported DDT to Bangladesh, Japan, Nepal, New Zealand, Sri Lanka,
Switzerland and United Arab Emirates, and aldrin to 20 other countries including Australia, the Netherlands
and the U.S. “However, officials from the Netherlands and Australia report that their records do not reflect
these findings."
Despite aldrin's registration being withdrawn in 1996, Greenpeace's research found that aldrin formula
tions were being sold in shops in New Delhi. A shopkeeper said several manufacturers continued to supply
aldrin as “this is the best for killing termites..., it is poisonous only if you drink it".

T

Source: "Toxic Legacies; Poisoned Futures -Persistent Organic Pollutants in Asia", by Von Hernandez and Nityanand
Jayaraman, Greenpeace International, Amsterdam, 1998; and Global Pesticide Campaigner, Volume 9, Number 1, PAN
North America, April 1999.

in order to flush out these loxins. Many women
are working with pesticides that are so dangerous
they cannot be used safely under any conditions
of agricultural practice. Even those who do not

spray are exposed to pesticides through agricul
tural activities involving contact with heavily
sprayed crops.
The purpose of this article is to briefly summa
rize the human health effects of pesticides. The
discussion is in two parts:
/. The three major factors contributing to the im
pact of pesticides on human beings.
2. The three major ways that pesticides affect hu
man health.
A special effort has been made to highlight par
ticular concerns women and children face from
exposure.

Factors Contributing to the Impact of
Pesticides on Human Beings
There are three major factors in the impact of
pesticides on human beings - how hazardous or
poisonous they are, how they get into the body,
and how long they slay there.

7. How Hazardous or Poisonous a Pesticide is

Illustration by Allan Woong, based on illustrations
in ’Harvest of Sorrow- Farm Workers and Pesti
cides', Part I, by Dr. Marion Moses.

The U.S. Environmental Protection Agency
(EPA) and the World Health Organization (WHO)
classify each pesticide into one of four categories;
depending on how much it takes for the pesticide
to kill a laboratory rat or mouse. The less it takes
to kill the animal the more toxic it is. The most
dangerous pesticides are in EPA Category I, and
WHO Category IA and IB. These categories do

India - Pesticides and Health Meeting, October, 2002

2

Table 1

Highly Toxic Pesticides
EPA Category I - WHO Category IA and IB

LDm or MLD' (in milligrams/kifogram of body weight In rats)
Use2

LDJ0
MLD1

Pesticide (brand name)

Acrolein (Magnacide H)

H

29

Aldicarb (Temik)

I

1

Azinpbos-ethyl (Gusathion A,)

l

Azinphos-m ethyl (Guthion, Gusathion)

Pesticide (brand name)

Use2

LDJ0
MLD’

Isofenphos (Oftanol)

1

20

Isolane

1

11

12

Mephosfolan (Cytrolane)

1

8.9

l

4

Mecarbam (Afos)

1

36
25

Bornyl

l

31

MEMA (Organic Mercury Compound)

Fn

Calcium cyanide

Fm

10

MEMC (Organic Mercury Compound)

Fn

22

Carbofuran (Furadan)

I

15-26

Methamidopbos (Monitor, Tamaron)

1

20

Chloethocarb (Lance)

I

35.4

Methidathion (Supracide)

1

44

Chlormephos (Dolan)

I

7

Methiocarb (Mesurol)

1

20

Cydoheximide

FrVPGR

2

Methomyl (Lannale, Nudrin)

1

17

Demeton (Systox)

I

2.5-6

Methyl paralhion (Folidol-M)

1

20

3

Demeton methyl (Metasystox)

I

30

Mevinphos (Phosdrin)

1

Dieldrin

I

37

Mexacarabate (Zectran)

1

24

Dimefox (Hanane)

I

5

Monocrotophos (Azodrin. Nuvacron)

1

8-23

Dinitro-ortho-cresol (DNOC)

Fn/H/I

20

Omethoate (Folimat)

1

25

D'rlirophenol (DNP)

l/Fn

30

Oxamyl (Vydate)

1

5.4

Dinoseb (DNBP)

H

40

Oxydemeton methyl (Melasystox-R)

1

30

Dioxathion (Delnav)

I

45

Oxydifulfuton (DiSyston S)

1

3.5

Disulfuton (DiSyslon)

I

4

Parathion (Ethyl parathion. Folidol)

1

2

Endrin

I

7-15

Phorate (Thimel)

1

2-4

E thion

I

21

Prothoate

1

8

Fenamipbos (Nemacur)

N

5

Schrad an

1

9

Fensulfothion (Danasit)

I

5

Sodium arsenite (Pamol)

Fn/H/I

10

Fluenethyl (Lambrol)

I

3-8

Sodium cyanide

Fm

6.4

Fonofos (Dyfonate)

I

6-17

Sutfotepp (Bladafume)

1

10

Formetanate HCI (Carzol)

I

20

Terbuphos (Counter)

1

1.3

Fumiloxin (Phostoxin)

Fm

0.3

Thallium sulfate

R

16

Isazofos (Triumph)

I

40

Zinc phosphide

Fm

45.7

1. Lethal Dose 50. Median Lethal Dose-the lower this number the more toxic the pesticide.

2 /=insecticide. Fm=fumigant. Fn=fungicide. H=herbicide. N=nematicide. R=rodenticide. PGR=plant growth regulator.
Compiled by Dr. Marion Moses, Pesticide Education Center, San Francisco CA, 1999.

not include long term effects. (See Table 1 for a
list of the most dangerous pesticides).
2. How Pesticides Get Into the Body
There are four ways that pesticides get into the
body - by breathing them in, by swallowing them,
through the skin and through the eyes in cases of
splashes or spills. Most workers think that breath
ing in the vapors is the major way that pesticides
get into the body. This is not so. The major route
of pesticide absorption into the body is through
the skin. Some parts of the skin however absorb
pesticides more easily than others. The genital area
is an area of high absorption, as is the face and
neck, followed by the back of the hand, and the
armpits and lower forearm. If the skin is damp or
wet, or if there is a cut or rash or even minor irrita

tion of the skin, pesticides will go through the skin
faster and in larger amounts.
Children will absorb more pesticides than an
adult at the same level of exposure. This is be
cause they have a lot more skin surface for their
size than adults, and also take in more breaths per
minute. (See Box: Infants and Children Face
Greater Risks! on page 14).
Women have thinner skin than men and may
likewise absorb more under similar levels of ex
posure. If a woman is pregnant, once pesticides
get into the blood stream they can cross the pla
centa and affect the developing foetus.

How Long Pesticides Stay in the Body
A lot of the older pesticides such as DDT, di
eldrin, lindane, heptachlor, and chlordane break

3.

india - Pesticides and Health Meeting, October, 2002

Absorption of Pesticides Through the Skin

Order of absorption highest to lowest:
1.
2.
3.
4.
5.
6.

Scrotum
Armpit
Ear canal
Forehead
Behind ear and jaw
Scalp

7. Top of hand
8. Abdomen
9. Ball of foot
10. Palm of hand
11. Forearm

7

Illustration by Allan Woong, based on illustra
tions in 'Harvest of Sorrow- Farm Workers and
Pesticides', Part II, by Dr. Marion Moses.

down very slowly. Children do not handle toxic
chemicals in lheir bodies as well as adults. This is
because lheir liver enzymes and their immune sys
tems are less mature. Women also may have less
efficient detoxifying mechanisms, especially dur
ing pregnancy and lactation.
The DDT type of pesticides are also known as
persistent organic pollutants, meaning that they are
persistent in the environment and resist breakdown
by natural processes for long periods of time. Be
cause they are fat-soluble and resist breakdown,
these chemicals are stored in fatty tissues and can
stay in the body for many years. Since women have
a higher percentage of body fat than men, they
store more pesticides in their body. Human breast
milk is also high in fat and pesticides have been
found in human milk in several countries.
Most of the pesticides in use today do not stay
in the body for more than two or three days. They
are eliminated from the body through the urine.
This is why it is very important for workers exposed
to pesticides to drink lots of water. Women espe
cially must drink lots of water since their renal func
tion compared to men, is slightly less efficient, es
pecially during pregnancy.

The Major Ways Pesticides Affect
Human Health
Pesticides affect human health in three major
ways - causing immediate health effects, causing
long term effects, and worsening pre-existing con
ditions.

7.

Immediate Effects
Reactions to pesticides that occur within a very
short time after exposure are called acute effects.
They can appear within minutes or hours, some
times days of exposure. The most common acute
effects are irritation of the eyes, nose and throat,
such as tearing, stinging, burning and coughs. Skin
rashes and itching are also common. Nose bleeds
are less common. These local effects are due to
direct contact with the pesticide.
Some pesticides can cause allergic dermatitis.
Plants such as poison oak, poison ivy and many
others that workers are exposed to can also cause
allergic dermatitis. It may be difficult to find out
whether it is a pesticide or not without doing spe
cial skin tests. Pesticides reported to cause aller
gic dermatitis include anilizine, benomyl, captan,
chlorothalonil, dazomet, dichlorvos, malathion,
maneb, naled, and PCNB.
After pesticides go through the skin they get
into the blood stream and go throughout the body.

India - Pesticides and Health Meeting, October, 2002

4

Table 2

T

Pesticide Chemicals Classified by US EPA as Known,
. • Probable or PcsslbteHumanCarcInogens
Group A - Known Human Carcinogens

Arsenic, inorganic
Chromium VI
Ethylene Oxide Group I

Group 81 - Probable Human Carcinogens
,'wth kmiod human evidonco)
Acrylonitrile
1 Cadmium
' Creosote
Ethylene Oxide
, Formaldehyde

Group 82 - Probable Human Carcinogens
*
(wrfft sutfKxnt evidence in animals and
inadequate Cf no evidence in humans)
I Acetochlor
! Acifturofen. sodium salt
Amitroie
' Cacodylic Acid
■ Captafoi
Captan
; Chlordimeform
I Chtoroanilino
Cyproconazole
Daminozide (Alar)
1.2-Dichloropropene (Telono)
1.1-Dimethyl hydrazine (UDMH)
Dipropyl isocinchomeronato (MGK 326)
F en oxycarb
Folpet
Furmecydox
Haloxyf op-m ethyl
Lactofen
Mancozeb
Maneb
Met am Sodium
Orthoph enylphcnol
Oxythioquinox
* Procymidone
[ Pronamide
1 Propargile
; Propoxur(Baygon)
I Propylene Oxide
1 Tenazole
i Thlodicarb
1 Triphonyltin hydroxide

’ Group 82 - Probable Human Carcinogens —
(with sufficient evidence in animals and
inadequate or no evidence in humans)
\ Acetaldehyde
j Aramite
i Azobenzene
Bis(chloroethy1) other
Carbon Tetrachloride
Chlordane
Chloroform
1.2-Dibrcmo-3-chloropropane (DBCP)
Dibromoelhane. 1,2 (EDB) -ethylene
dibromide]
Dichloro diphenyl tnchloroethane (DDT)
1.2 - Dichloroethano
Didoromethane
Dieldrin
Di(2-ethylhexyl)phlhalato
Epichlorohydrin
Ethylene thiourea
Heptachlor
Heptachlor epoxide
Hexachlorobenzene
Haxachlorocydohexane, tech
Lindane
Methylene chloride (see dichloromethane)
Mirex
Pentachlorophenol
Perchloroethylene
Polychlorinated biphenyls (contaminants
Propiolactone
Toxaphene
Trichloroethyl eno
Trichlorophenol 2,4,6

Group C • Possible Human Carcinogens

Amilrnz
Asulam
Atrazine
Bcnomyl
Bifcnthrin
Bromacil
Bromoxynil
Calcium Cyanamide
Carbaryl
Clofontozine
Cyanazine
Cypormethrin
Dacthal
Dichlobenil
Dichlorvos (DDVP)
Didofop-mothyl
Dlcofol
Difonoconazolo
Dimelhonamid (SAN 682H)
Dimothipin (Harvado)
Dimethoate
Dinoseb
Ethalfluralin
Elhofonprox
Fenbuconazolo
Fipronil
Fluometuron
Fomosafen
Hoxaconazolo
Hexythiazox (Savoy)
Hydramothylnon (Amdro)
Hydrogen cyanamide
Imazalil
Isoxaben
Llnuron
2-Mercapto benzothiazole
Methidathion
Methyl 2-bonzimidazolo carbamate (MBC)
Motolachlor
MolinaloNitrofen
Norflurazon
N-Octyl blcyclohepleno dicarboximido
(MGK-264)
Oryzaiin
Oxadiazon
Oxadixyl
Oxyfluorfen
Paradichlorobonzeno
Parathion
Pendimethalin
Pontachloronitrobenzene
Permethrin
Phosmot
Phosphamidon
Piperonyl butoxide
Prochloraz

Prodiamine
Propazine
Propiconazole
4-Pyridazino carboxylic add,
2-(4-chlorophenyi)-3-ethy12.5-dihydro-5-oxo-,potassium salt (MON
21200)-post FQPA
Pyrithiobac-sodium
Sim azine
Tebucon azole
Terbutryn
2-(Thiocyanomelhytthio) benzothiazole
(TOMB)
Triadimefon
Triadimenol
Triallale
Tribenuron methyl
Tridiphane
Trifluralin
Triflusulfuron-methyl
Uniconazole
Vindozolin

• Classified by the Office of Pesticide Programs •• Not Classified by the Office ofPesticide Programs
Source: US. Environmental Protection Agency. Pesticidal Chemicals Classified as Known,
Probable or Possible Human Carcinogens. Office of Pesticide Programs. Washington, D.C. 1998.

Compiled by Dr. Marion Moses, Pesticide Education Center, San Francisco CA., 1999.

Once pesticides get into the system they
can cause poisoning, Signs and symp
toms of systemic poisoning include head
aches, dizziness, nausea, vomiting,
( lamping, breathing difficulties and
blurred vision. If tire poisoning is severe
and proper treatment is not avail.ible,
death can occur. Most serious poison
ings and deaths from pesticides occur in
developing countries.
2. Delayed Effects
Pesticides can cause delayed or long
term effects which occur months or years
after exposure. These are called chronic
effects. They can result from low levels
of exposure over a long period of lime.
They can occur even if there has never
been any apparent health problems dur
ing the time of exposure to pestic ides.
The three major chronic effects from pes
ticides are cancer, neurological damage
and adverse effects on the reproductive
system.
CANCER: Many pesticides are
known or suspected to cause cancer in
laboratory animals. The U.S. EPA clas
sifies pesticides into groups of known,
probable, or possible causes of cancer
in humans. (Table 2 lists the pesticides
in these different categories).
There is now a large body of evi
dence that pesticide exposure is a risk
factor for cancer in humans, especially
children. Studies done in the United
Stales, several European countries, Bra
zil, and China show that children whose
parents are occupationally exposed to
pesticides or whose parents use pesti
cides in and around the home are more
likely to get leukemia, brain cancer, non
Hodgkin lymphoma, soft tissue sarcoma,
and Wilm's tumour. There are many
studies done throughout the world on
farmers, pesticide sprayers and factory
workers exposed to pesticides that link
cancer in adults to pesticide exposures.
The kinds of cancer that have been found
include: non-Hodgkin lymphoma, brain
cancer, leukemia, soft tissue sarcoma,
pancreatic, testicular and prostate can
cer among others.
NEUROLOGICAL EFFECTS: There
is abundant evidence from laboratory
animals that pesticides can cause per
manent damage to the brain and nervous
system. Low levels of exposure to neu-

India - Pesticides and Health Meeting, October, 2002

5

,Tabfe3
'
T' •
roloxic pesticides to the developing
Pesticides that are Endocrine Disruptors
.. ■>
brain can potentially affect brain de
velopment in complex and subtle
Fenchlorfos
AJachlor
Fenitrothion
Aldicarb
ways that are difficult to observe and mea
Fenvalerate
Aldrin
sure.
Fipronil
Amitrole
Flucythrinate
Atrazine
Such potential effects include ef
Heptachlor
Benomyl
fects on memory, judgement and in
Hexachlorobenzene
Bifenthrin
Hexachlorocyclohexane
oxynil
Bromoxynil
telligence as well as personality, moods
Lindane
Cadmium
and behaviour. There are human stud
Malathion
Carbaryl
ies that show permanent effects on the
Mancozeb
Carbofuran
Maneb
Chlordane
btain and nervous system years after
Mercury
Chlordecone (Kepone)
apparent complete recovery from pes
Methomyl
Chlorpyrifos
Methoxychlor
lambda-Cyhalo th rin
ticide poisoning. There are many in
Methyl parathion
Cypermethrin
dividual reports of permanent changes
Metiram
2,4-D
Mirex
DBCP
in behavior and personality in work
Nabam
DDE
ers and others seriously poisoned by
Nitrophen (TOK)
DDT
Ortho-phenyphenol
Deltameth rin
pesticides.
Parathion
Dichlorvos (DDVP)
There are very few studies of highly
Pentachlorobenzene
Dicofol
Permethrin
Dieldrin
susceptible groups such as pregnant
Pidoram
Dienochlor
women and children. Recent data
Pyrethrins
Dimethoate
Dinitrophenol
Simazine
show that endocrine disruptor pesti
2,4,5-T
Dinoseb
cides can affect hormone levels at criti
Endosulfan (thiodan)
Toxaphene
Tributyltin
Endrin
cal periods of development of the brain
Esfenvalerate
Trifluralin
at very low levels of exposure that
Ethafluralin
Triphenyltin
Vinclozolin
were previously thought to be not
Zineb
harmful. (See Table 3 for a list of pes
____________________________________
ticides which are endocrine
Source; Based on data found In U.S.EPA (Environmental Protection Agency) Fact Sheets,-^
RED (Registration Eligibility Documents), and CalEPA (California Environmental^^.::
disruptors).
Protection Agency) Toxicology Summaries of selected pesticides.
Pesticide exposure can increase
Compiled by Dr. Marion Moses, Pesticide Education Center,San Francisco CA./7999.
the risk of Parkinson's disease, espe
cially in younger people. Pesticides
may also be implicated in amyotrophic lateral scle
logical diseases. The percentage of people poi
rosis (ALS, Lou Gehrig's Disease) and other neuro
soned by pesticides who develop changes in brain

I

DBCP and the Banana Workers

In 1997, four chemical corporations that produced dibromochloropropane or DBCP—Amvac, |
, Dow, Occidental and Shell—reached an out-of-court settlement of over US$45 million dollars with ,
thousands of banana workers from 11 countries. More than 6,000 of the claimants were Philippine
I farmers who worked in the banana plantations in Mindanao. The rest of the claimants came from I
| Costa Rica, Honduras, Guatemala, El Salvador, Nicaragua and Ivory Coast
|
The workers' lawsuits had demanded compensation for permanent sterility linked to DBCP |
I exposure while they were working on the banana plantations. DBCP, an extremely toxic nemati- .
l cide with severe acute and chronic health effects, is one of the 'Dirty Dozen' targeted by the I
I Pesticide Action Network (PAN) for elimination. The first known human sterility cases linked to I
| DBCP were identified in California in 1977. The companies knew that the product caused male |
| sterility in rats as early as in the 1960's, but concealed this information. U.S. exports of DBCP i
never the less continued after the California cases came to light; after the fumigant was banned in
I the U.S. in 1979.
1
In the Philippines, DBCP was used in the 1970s and 80s. Tests conducted showed that the |
| farmers were not adequately warned, or were not warned at all of the harmful effects of DBCP. |
I Aside from sterility, the affected farmers also complained of impotence and cancers.
According to lawyers representing the banana workers made sterile by DBCP use in the '
I 1970s and 80s, the vast majority of the 26,000 claimants had accepted the deal with the chemical I
| companies. However, organizations representing male victims state that no amount of money |
| could compensate for the suffering caused by the indiscriminate use of DBCP on banana planta- i
. lions for 15 years. Not surprisingly, some had not welcomed the offer. The payments the individual
' workers would receive after deducting costs would be minimal. Although legal action is still '
I continuing against banana multinational companies such as Chiquita, Dole, Del Monte and Stan- I
| dard Fruit, there are fears that these companies will also settle out of court for lesser amounts. |
Source:

Global Pesticide Campaigner, Vol. 8 No. 1, March 1998; and Philippine Daily Inquirer, June 25, 1997.

India - Pesticides and Health Meeting, October, 2002

6

j

Infants and Children Face Greater Risks!
Infants and children face greater risk from pesticides and other environmental toxins because they have
greater exposure, and less ability to get rid of toxic chemicals from their bodies.
Greater Exposure: Infants and children absorb more into their bodies than adults. The major
reasons for this are:
. They have much more skin surface for their size. 2). They take in more breaths per minute.
1)
3). They eat and drink much more for their weight.
4). They are much more likely to come in contract
with contaminated surfaces and objects.
The “job” of children is to explore. Their crawling, toddling, play and other activities put them in direct contact
with contaminated soil, floors, furniture, toys, and carpets. They put everything in their mouths. They often
wear less clothing therefore have more exposed skin surface. Children living on farms or near agricultural
areas risk even greater exposures from drift and contamination of air, soil, food, and water by chemical
pesticides.
Less Ability to Get Rid of Chemicals: Once pesticides get into the bodies of Infants and children,
they are more vulnerable to toxic effects. The major reasons for this are:
. Infants and children have less mature mechanisms in their body to break down chemicals into less
1)
harmful substances.
. Infants and children have less mature mechanisms in their bodies to get rid of toxic chemicals from their
2)
bodies.
»
.
3)
Infants and children have less mature immune systems to protect them from toxic chemicals.
.
4)
Infants and children are growing and developing and at a rapid rate putting many body cells and tissues
at risk - especially the brain and nervous system, and the blood and immune system.
This puts children at greater risk of cancer and other chronic diseases.
Brain Cancer: Studies done in the United States, Canada, France and Norway show that children
whose parents are farmers or who live on farms have a three to seven fold increased risk for brain cancer.
Two United States studies found that pesticide use in the home increased the risk of brain cancer in children
six to eleven fold.
Leukemia: Studies done in the United States, Canada, and China show that children whose par
ents work with pesticides on farms have a two to eleven fold increased risk for leukemia. Studies done in the
United States and German found that pesticide use in the home increased the risk of leukemia in three to
nine-fold. Other studies also found children to be at increased risk for non-Hodgkin lymphoma, Wilm's tu
mor, and soft tissue sarcoma.
Source: Dr. Marion Moses, Cancer in Children and Exposure to Pesticides, Summary of Selected
Studies, Pesticide Education Center, San Francisco CA. May 5, 1999.

function is however not known.
REPRODUCTIVE EFFECTS: Many widely used
pesticides are known to cause birth defects, steril
ity and foetal death in laboratory animals (see Table
4). Occupational exposure to the pesticide DBCP
(dibromochloropropane) is a proven cause of ste
rility in human males. (See Box: DBCP and the
Banana Workers).
Human studies have found increases in spon
taneous abortion, stillbirth, infertility, and birth
defects in exposed workers. The highest risk is in
women who work and live on farms or in agricul
tural areas or who have come into direct contact
with pesticides during pregnancy.
Studies often do not find an increase in birth
defects associated with pesticide exposure. This
may be due to direct toxicity to the embryo and
foetus while still in the womb, leading to an early
spontaneous abortion.
Effects on Existing Conditions
People with asthma and allergies, especially
children can react to low levels of pesticides that
3.

do not affect those without them. The pesticides
most likely to percipitate or aggravate asthma are
the pyrethrins and pyrethroid classes of pesticides,
and the organophosphates and methyl carbamates.
However, any pesticide or inert ingredient can still
be a potential problem. The only effective treat
ment is to avoid exposure to the pesticide.
Pesticides can also cause irregular heart
rhythms, and people with heart disease may have
a worsening of their condition when exposed.
Pesticide exposure can also weaken the im
mune system. The most susceptible to such ef
fects are children, pregnant women, those with
chronic medical illnesses, and cancer survivors.

Countering the Toxic Legacy
Pesticides are used in ways that maximize op
portunities for human exposure and environmen
tal contamination. Most regulations are not strong
enough to protect workers from the adverse health
effects of pesticides, especially women and chil
dren. Many workers are poisoned even when all
rules and regulations have been followed.

India - Pesticides and Health Meeting, October, 2002

7

Just because a pesti
Table 4
Pesticides That Are Teratogenic (cause Structural
cide is used according to
Birth Defects) in Laboratory Animals
label directions, it does
not mean that potential
Fenarimol
Acrolein
harmful effects are not oc
Fenoxaprop ethyl
Abarmectin
curring, The effects may
Fluazifop-butyl
Bacquacil
not show up until many
Folpet
Bitertanol
years later. There is often
Hexachlorobenzene
Benazolin-ethyl
a false sense of security if
Kinoprene
Benomyl
there is no apparent im
Maleic hydrazide
Bentazon
mediate illness or acute
Mancozeb
Bromoxynil
effects.
Methyl parathion
Cacodylic acid
Methoprene
Captafol
One of the most im
Captan
Mirex
portant concerns not ad
Fenamiphos (Nemacur)
Carbaryl (Sevin)
dressed by current pesti
Nitrofen (TOK)
Chloramben
cide laws and regulations
Ortho-phenylphenol
Chlordimeform
is the effect of multiple
Paclobutrazol
Chlorpropham
exposure. All workers are
PCNB
Copper sulfate
exposed to many different
Cyanazine
Phosmet
pesticides in the course of
Picloram
Cydoheximide
their working life. The
Cyromazine
Propargite (Omite)
combination of low level
Sodium arsenate
2,4-D
exposures to many differ
Sodium arsenite
Dichlobenil
ent pesticides add up to a
Sodium omadine
Dichlorophene
large toxic burden, espe
DMF
2,4,5-T
Terrazole
2,4-DP (Dichlorprop)
cially for the embryo and
Triadimefon
Dinocap (Karathane)
foetus developing inside
Tributyltin oxide
Dinoseb
the womb. The possible
Trichlorfon
Diquat
synergistic effects of these
Trifluralin
Endosulfan
combined and mixed ex
Triphenyltin fluoride
Endothall
posures have not been
Triphenyltin acetate
Ethion
studied. The laws that
Triphenyltin hydroxide
2-Ethyl 1,3-hexanediol
regulate pesticides do not
Vinyzene
Ethylene dichloride
require these kinds of tests
Warfarin
to be done. The younger
Sources: U.S. Environmental Protection Agency. Teratogenic Pesticides (as of June 1988),
the individual the greater
Office ofPesticide Programs, Washington, D.C. 1998. California Environmental Protection
Agency, ‘Chemicals Known to the State to Cause Reproductive Toxicity’, Office of
the risk of adverse effects
Environmental Health Hazard Assessment, Sacramento, CA December 26,1997.
from toxic exposures.
Compiled by Dr. Marion Moses, Pesticide Education Center, San Francisco CA., 1999
Some pesticides are
so toxic that they cannot
be used safely under any conditions of agricultural
practice. Once we release these toxic chemicals
Dr. Marion Moses is President of the Pesticide Educa
we cannot take them back. The only way to elimi
tion Center (PEC) in San Francisco, California. A physi
nate the health risks from toxic pesticides is to elimi
cian, certified in Public Health and Preventive Medicine
nate the exposures; beginning with the most highly
(specializing in Environmental and Occupational Medi
toxic pesticides and those that cause cancers and
cine), Dr. Moses interest in pesticides began in the
birth defects.
1960s with her work with the United Farm Workers of
America, affiliated to the American Federation of LabourFuture generations will no doubt look back on
Congress of Industrial Organizations (AFL-CIO), in one
the twentieth century use of toxic pesticides in food
of the largest agricultural areas in the world. She has
production as one of the more bizarre practices of
many years experience investigating and documenting
their ancestors. The public health community must
pesticide related illnesses in farm workers both short
work together with workers and their advocates to
and long term. She has published widely on the ad
promote safer alternatives to toxic pesticides that
verse health effects ofpesticide in humans, and is a con
do not threaten the health of people and the envi
sulting editor for the American Journal of Industrial Medi
ronment.
cine, and the Archives of Environmental Health.
India - Pesticides and Health Meeting. October, 2002

8

Endocrine Disruption: New Threats
From Old Chemicals
byDr. MichaelSniolen

^hrough a series ofaccidental discover
ies, researchers stumbled on the fact that
some widespread, man-made chemicals,
called "endocrine disruptors", can interfere with
the body's own hormones andjeopardize health.
In the past five years, the scientific investigation
of this problem has intensified and provided
steadilygrowing evidence Unking these synthetic
endocrine-disrupting compounds to impaired
health in wildlife and people. The exploration is
ongoing and far from complete...
"Chemicals that compromise life A call to action", World Wildlife Fund.

7

Reports of disturbing global trends in human
health are appearing regularly in government re
ports, scientific papers, and even the news media.
During the past few decades, increases have been
recorded in the incidence of prostate, testicular and
breast cancers
developmental problems such
as hypospadias and undescended testicles121-forms
of genital malformations, and reported global de
clines in sperm quality and quantity13-'". Scientists

now have an explanation that could account for
many of these problems: disruptions to the devel
oping endocrine system.
Discussion of this hypothesis has previously
been confined to scientific literature, and only in
the last few years has it seeped into the policy and
public arenas. This visibility has been greatly in
creased with the publication of a book, "Our Sto
len Future: Are we threatening our fertility, intelli
gence and survival?", written by Theo Colborn,
Dianne Dumanoski, and John Peterson Myers. This
book presents the scientific evidence supporting
concern for the endocrine-disrupting effects of
some man-made chemicals. Written specifically
for the general public, it has already sparked much
debate.

The Endocrine System and Endocrine
Disruption
The endocrine system is the body's chemical
"messenger system" of hormones and other spe
cial messengers, which help communication be-

What Are Hormones?
Hormones are naturally-occurring chemicals that circulate at very low levels in the blood
stream of all vertebrate animals including reptiles, amphibians, fish, birds and mammals.
(Vertebrates are animals with a backbone.) In all vertebrate species, hormones act as chemi
cal messengers and as switches, turning on and off bodily systems that control growth, devel
opment, learning and behayiour. Hormones start affecting every animal shortly after it begins
life as a fertilized egg. Hormones control growth and development prior to birth or hatching,
and hormones continue to influence behaviour throughout life. Hormones tell bears when to
hibernate, tell salmon when to return to their spawning grounds, and cause women to men
struate every 28 days or so. Hormones profoundly affect the nervous system, the reproduc
tive system, and the immune system. Naturally-occurring hormones are also implicated in
some forms of cancer, such as female breast cancer which is widely believed to be linked to a
woman's lifetime exposure to estradiol (estrogen), the main female sex hormone.
Source: ‘Hormonally Active Agents In The Environment', Ernst Knobil and others, Wash
ington, D.C.: National Academy Press, July 1999'. Page 197.

India - Pesticides and Health Meeting, October, 2002

9

Illustration by Allan Woong based on illustration in 'Our Stolen Future- Are We Threatening Our
Fertility, Intelligence, and Survival?-A Scientific Detective Story, Dutton U.S., 1996.

tween the various parts of the body. The system
involves a variety of organs, called endocrine
glands (the thyroid, thymus, pituitary, adrenal, the

Diagram 2: The Lock-and-Key model of hormone-receptor interaction necessary for a hor
mone to trigger biochemical activity in a cell

Occupied receptor activates en
zyme, which in turn triggers
chemical reaction

Illustration by Allan Woong based on illustration from
'Generations at Risk: How Environmental Toxicants May
Affect Reproductive Health in California', A Report by
Physicians for Social Responsibility (L.A. and San Fran
cisco), and The California Public Interest Research Group
Charitable Trust, 1999.

testicles, ovaries, etc) that release the hormones to
be carried in the bloodstream to specific target sites
(cells) in the body. (See Box: What are Hormones?)
Latching on to unique "receptors" at the target
site, the hormones signal and govern various pro
cesses and functions such as growth and develop
ment (including brain development), metabolism,
reproduction, immune system, etc. (See Diagrams
1 and 2).
Distantly related groups of living things like
birds, mammals and humans share almost identi
cal hormone and receptor systems, and similar bio
logical responses. Disruption of this finely balanced
endocrine system occurs when biologically active
foreign chemicals interfere with the body's mes
senger system of hormones, and this can lead to
developmental, reproductive, behavioural, immu
nological (i.e. effecting the immune system) and
physiological changes.
However, chemicals have always been as
sessed for safety based only on whether they cause
cancer, poison people outright or produce obvi
ous developmental abnormalities151. Toxicologists
use high doses of chemicals to assess their effects
and, when no effects appear, the chemicals are con
sidered safe until proven otherwise. Examples of
the effects of foreign chemicals on the endocrine
system have always-been portrayed as novelties or
rarities of nature. '
Thus when fleas, which were living on rabbits,

India - Pesticides and Health Meeting, October, 2002

10

DES and Vaginal Cancer
From 1950 - 1971 diethylstilbestrol (DES), a syn
thetic estrogen with a chemical structure considerably
different from naturally-occurring estrogen, was used
in an attempt to prevent spontaneous abortions in
women. An estimated 5-10 million Americans were
exposed to DES during pregnancy (DES mothers) or
in the uterus (DES daughters or sons).’’’
No harmful effects of DES exposure were sus
pected until 1970 when a rare form of vaginal cancer
was reported in six young women, ages 14-21, who
had been exposed to DES in the uterus.'2’ Previously,
this disease had occurred almost exclusively in older
women, but it is now know to be caused in younger
women by exposure of the developing foetus to DES.
The risk for developing vaginal cancer from birth to age
34 is estimated to be 1 in 1000 to 1 in 10,000 for women
exposed in the uterus - accounting for thousands of
cases in the U.S. alone.
Later studies demonstrated that DES daughters
often have abnormalities of their reproductive organs,
reduced fertility, and unfavourable pregnancy outcomes
including ectopic pregnancies, miscarriages, and pre
mature birth, as well as immune system disorders. DES
sons are more likely to have small and undescended
testicles, abnormal semen, and hypospadias.131 DES
mothers have a breast cancer risk about 35 per cent
greater than those not exposed.’4’ Animal studies in
mice and monkeys show that prenatal DES exposure
may result in masculinization of parts of the female brain
and feminization in males.151 Several studies in humans
suggests similar results.'6’
Some DES daughters and sons are now in their
mid-20’s. Many do not know that they were exposed in
the uterus. Their health status require careful atten

were discovered to use the hormones in rabbits to
signal their own reproductive cycle, that was an
amazing fact of natural history. When DES (dieth
ylstilbestrol), an estrogen-like synthetic molecule
given to pregnant women to guard against miscar
riages, was found to alter the development of their
offspring161, that was considered an unfortunate side
effect of a drug. (See Box: DES and Vaginal Can
cer). When sheep and cows developed reproduc
tive problems after eating plants rich in plant es
trogens, that was a problem in animal husbandry.
But disruptions to the endocrine systems are
not isolated or rare events. Today there is concern
that animals and people are experiencing disrup
tions to their endocrine systems, leading to the
changes mentioned earlier. (See Box: Wildlife
Health Effects). Although a number of natural
chemicals in plants (i.e. phytoestrogens like
genistein, daidzein, and coumestrol) can also in
terfere with the endocrine system in vertebrates,
the main concern now is with man-made chemi
cals which our bodies had never before encoun

tion. As yet there is no definite evidence for adverse
health effects in the offspring of those who themselves
were exposed to DES in the uterus (DES grandchil
dren). However, since many are still young, it is too
early to draw final conclusions and the issue is not
resolved.
DES is an example of an estrogenic chemical
which causes reproductive and developmental
abnormalites, immune system malfunction, and can
cer in some people exposed as foetuses.

References:
1.
GuistiR.M., Iwanmoto K., Hatch E.E., ‘Diethylstilbeslerol revisited:
A review of the long-term health effects, Ann Ini Med 122 (10):778788,1995.
2.
Herbst A.L., Scully RE., Adenocarcinoma of the vagina in adoles
cence: a report of 7 cases including 6 clear-cell carcinomas (so-called
mesonephromas), Cancer25:745-747,170.
3.
Gill W.B., Schumacher G.F.B., Bibbo M., el al., Association of
diethylstilbesterol exposure in utero with cryptorchidism, testicular hy
poplasia, and semen abnormalities, J. Urol 122:36-39,1979.
4.
Colton T, Greenberg E.R., NollerK., el al., Breast Cancer in moth
ers prescribed diethylstilbesterol in pregnancy, Further Follow-up. JAMA
269 (16): 2096-2100,1993.
5.
Tarttelin M.F., Gorski R.A., Postnatal influence of diethylslilbesterol
on the differentiation of sexually dimorphic nucleus in the ral is as ef
fective as perinatal treatment, Brain Res 456:271-274,1988.
6.
RemischJ.M , Zienba-Davis M.. Sanders S.A.. Hormonal Contribu
tions to Sexually Dimorphic Behavior in Humans.
Psychoneuroendocrinology 16(1-3): 213-278, 1991

Source: Generations at Risk: How Environmental Toxi
cants May Affect Reproductive Health in California, A
Report by Physicians for Social Responsibility (L.A. and
San Francisco), and The California Public Interest Re
search Group Charitable Trust, 1999.

For more information visit the following websites: http:/
/www.igc.apc.org/psr/index.html or http://www.pirg.org/

Pirg
tered. And this concern is not limited only to per
sistent chemicals that build up to high concentra
tions in the body but also to many short-lived ones
which, while they are in the body, can disrupt the
endocrine system.
So in 1992, a group of scientists with expertise
in varied fields (from anthropology, endocrinology,
medicine, immunology reproductive physiology,
and histopathology) met to explore the potential
for endocrine system disruption in humans and
wildlife. They concluded that: "A large number of
man-made chemicals that have been released into
the environment, as well as a few natural ones,
have the potential to disrupt the endocrine system
of animals, including humans"’71. These chemicals
include a variety of pesticides and industrial chemi
cals. Published research convinced the scientists
that wildlife populations have been affected, ex
amples of which included:
•
"thyroid dysfunction in birds and fish;
•
decreased fertility in birds, fish, shellfish, and
mammals;

India - Pesticides and Health Meeting, October, 2002

11

Diagram 3: Receptor Effects of
Synthetic Chemicals

•
•
•
•

•
•

gross birth deformities in birds, fish, and turtles;
metabolic abnormalities in birds, fish, and
mammals;
behavioural abnormalities in birds;
demasculinization and feminization of male
fish, birds, and mammals;
defeminization and masculinization of female
fish and birds;
and compromised immune systems in birds
and mammals" ‘.

Man-made chemicals can interfere with the en
docrine system in a number of ways. The hormones
or messengers in the body have a complex feed
back system, which closely controls their release
and persistence in the body. Some man-made
chemicals can mimic the natural hormone and
activate biological processes (some can even super-activate the processes). Others can merely bind
to and block the receptors so that the natural sys
tem can no longer be turned on. Yet others may
react directly or indirectly with natural hormones
or alter natural patterns of hormone synthesis. (See
Diagram 3).
Illustration by Allan Woong based on illustration
in 'Our Stolen Future- Are We Threatening Our
Fertility, Intelligence, and Survival?-A Scientific
Detective Story, Dutton U.S., 1996.

Problems for the Unborn
Reports of endocrine system disruptions involve
development of a baby can thus have pronounced

Wildlife Health Effects
A variety of invertebrates, reptiles, birds, fish and mammals
have been adversely affected by Endocrine Disruptors (EDs).
The following examples illustrate the diversity of health ef
fects:

v

❖

Various types of snails exposed to environmental levels
of tributyl-tin, an anti-fouling additive used in marine
painton ships, develop a condition called imposex in
which affected female snails have irreversibly superim
posed male sex characteristics.
Hermaphroditic (having both the male and female sex)
fish are found in rivers below sewage treatment plants
in Great Britian. Vitellogenin, a protein normally syn
thesized by female fish in response to estrogen, is uti
lized as a yolk protein to nourish the developing fish.
Male fish have vitellogenin levels similar to gravid fe
males in some rivers. Laboratory tests show that
nonyiphend, an alkyiphenol used in detergents and sur
factants and found in effluent; behaves as an estrogen
mimic and induces vitellogenin formation and testicular
inhibition in male trout. However, it is not entirely dear
which chemical or combination of chemicals in the sew
age effluent mixture is responsible for the observations
in river fish. Some investigators believe that estrogens
from the urine of women taking birth control pills also

contribute.

❖

Alligators and red-eared turtles in LakeApopka in Florida
are demasculinized after exposure to a mixture of chemi
cal contaminants induding the pestidde, dicofol. There
are no normal male turtles in Lake Apopka. All
hatchlings have either normal appearing ovaries or are

intersex.

v

Gulls breeding in the Puget Sound and Great Lakes re
gions show evidence of eggshell thinning and reproduc
tive tract abnormalities with feminization of male em
bryos. In some instances, populations have declined
and sex-ratios are skewed. These areas are contami
nated with mixtures of DDT, PCBs, and pofycydic aro
matic hydrocarbons, each of which may cause the ob
served effects. Birds from these areas and from loca
tions far more remote from industrial activity show el
evated tissue levels of contaminants.
Great Lakes gulls and terns, as well as some western
gulls, have, within the past several decades, shown su
pernormal egg dutches and female-female paring. Gulls
in these colonies also show excessive chide mortality,
birth defects, and skewed sex ratios, with an excess of
females. These effects correlate with levels of persis

•I’

tent organic pollutants like PCBs and DDT.
Seal populations have markedly dedined in portions of
the Wadden Sea in the Netherlands. Fish from the area
of dedine are contaminated with higher levels of PCBs
and pestiddes than those from other areas. Captive
seals fed fish exdusivety from the contaminated areas
were less able to reproduce and had altered estrogen
levels compared to seals fed less contaminated fish over

a two year period.
Source: Generations at Risk: How Environmental Toxi
cants May Affect Reproductive Health in California, A
Report by Physicians for Social Responsibility (L.A. and
San Francisco), and The California Public Interest Re
search Group Charitable Trust, 1999.
See also the following websites: http://www.igc.apc.org/
psr/index.html or http://www.pirg.org/pirg

India - Pesticides and Health Meeting, October, 2002

12

Pesticide Exposure May Impair Children's Brain Function
Dramatic deficits in brain function are seen in rural chil
dren with long-term exposure to pesticides compared with
children not similarly exposed, according to a recent study in
"Environmental Health Perspectives." The study compared
two groups of four-and-five-year old children in the Yaqui Val
ley of Sonora, Mexico, who are very similar except in their
levels of pesticide exposure. The children share a common
genetic and cultural background, eat the same foodsand drink
the same water. The major difference was in their exposure
to pesticides.
Thirty-three of those studied lived in the valley, a farming
area where pesticide use was relatively intense. Farmers re
ported that two crops a year may be planted with up to 45

DDT to combat malaria (this programme was also carried out
in the valley).
The researchers developed and used a Rapid Assessment
Tool to measure the growth and development of these two
groups of children. Although the groups were similar in physi
cal growth, a comparison of their functional abilities showed
some marked differences.
The valley children showed: less stamina (or physical en
durance, measured by making the child jump in place foras
long as possible); lower motor or hand-eye co-ordination (abil
ity to catch a large ball from a distance) and even lower fine
eye-hand co-ordination (ability to drop a raisin into a bottle
cap); and poorer short-term memory.

pesticide applications per crop. Organophosphates, organochlorines and pyrethroids were among the chemicals used.
In addition, household insecticides were usually applied each
day throughout the year. Contamination of the local popula
tion had been documented, with women's breast milk con
taining concentrations of lindane, heptachlor, benzene
hexachloride, aldrin and endrin all above limits established by
the UN Food and Agricultural Organization.
The second study group (17 children) lived in the foot
hills, where most families were involved in ranching and pes
ticide use was minimal. Foothill residents used traditional meth
ods of intercropping for pest control in gardens and rarely
used insecticides indoors. Residents stated that their only
exposure to pesticides was annual government spraying of

One ofthe most striking differences between the two
groups was the ability to draw a person. The valley children
showed much less ability to draw a person than the foothill
children (see drawings); even while looking at a person and
drawing, the valley children "continued to draw meaningless
circles". Some of the valley mothers later told the researchers
about their frustration in trying to teach their children how to
draw. The decreased eye-hand co-ordination and ability to
draw could indicate impairment of brain function among the
pesticide-exposed valley children, say the researchers.
Source: Environmental Health Perspectives, Volume 106 Num
ber 6, June 1998; and Global Pesticide Campaigner, Pesticide
Action Network (PAN) North America, September 1998.

India - Pesticides and Health Meeting, October, 2002

13

velopment and causes po
tentially serious problems.
For example, crossed mes
sages signalling the devel
opment of parts of both
sexes can cause "feminiza
tion" and "demasculiniza
tion"
of
males
or
"defeminization" and
"masculinization" of fe
males, the offspring acquir
ing an intermediate or "in
tersex" design compared to
what was to be by genetic
inheritance alone. (See
Box: Edocrine Disruptors
and Genital Birth Defects)
Similarly, disturbance
to thyroid, estrogen,
testesterone and other
harmone systems can
cause reduced growth,
birth defects, functional ab
normalities,
altered
behaviour, reduced fertility,
learning disabilities (See
Box: Pesticide Exposure
A negative feedback loop in hypothalamic-pituitary-gonadal (HPG) hormonal
May Impair Children's
communications tends to keep sex hormons at constant levels. In males, the
Brain Function), lower in
feedback loop is always negative. In females, it fluctuates between negative
telligence and greater sus
and positive. Illustration by Allan Woong based on illustration from 'Genera
tions at Risk: How environmental Toxicants May Affect Reproductive Health in
ceptibility to diseases.
California', A Report by Physicians for Social Responsibility (L.A. and San Fran
Of all these endocrinecisco), and The California Public Interest Research Group Charitable Trust, 1999.
disruption effects, the most
serious arise from changes
the more familiar thyroid, estrogen and testoster
occurring during development. Endocrine disrup
one hormones as well as less well understood de
tion can occur in adults, but these typically require
velopmental messengers. One such specialized
higher concentrations of the chemicals, and when
developmental messenger (Mullerian inhibiting
these chemicals are removed from the system, the
substance) is released in the developing male foe
effects may disappear. The threat to the develop
tus to signal the resorption of the embryonic tissue
ing foetus is more severe in that the changes caused
that would otherwise produce a female reproduc
during this stage cannot be undone later. These
tive system. All embryos have the potential to be
effects are typically irreversible and permanent18’.
come either male or female, and simultaneously
(See Box: Suffer the Little Children...)
develop two separate kinds of tissues, one that will
give rise to male and the other to female reproduc
Concern for Women
tive systems.
Early in life, a developmental switch is thrown
This is a cause for special concern for women
(under the direction of the sex chromosomes) sig
who use, mix or spray pesticides. Chemicals are
nalling the right set of tissues to develop the ap
readily adsorbed into the body and can be easily
propriate reproductive organs while tissues fated
passed on through the bloodstream to the foetus or
for the opposite sex are signalled to self-destruct.
to breast tissue from where it can pass into breast
The switch sets in motion specific activities along
milk and to suckling babies. Pesticides are de
a number of endocrine pathways, and the result
signed to be biologically active in order to kill pests,
ing chorus of messengers directs the further
and many of them have been discovered to affect
constuction of the anatomy, physiology and
the developing endocrine, reproductive, neural and
behavioural traits relevant to that sex. Disturbance
immune systems. Exposures to endocrine disruptor
to these hormonal ebbs and flows confounds de
chemicals during the critical stages of growth and
India - Pesticides and Health Meeting, October, 2002

14

Edocrine Disruptors and Genital Birth Defects
In 1997, a group of researchers at the U.S.
Centre for Disease Control and Prevention, lead by
Len Paulozzi, reported that cases of male genital
birth defects (known as hypospadias) among boys
in the US was increasing, and had doubled between
1970 and 1993 - from 20 cases per 10,000 births
in 1970 to 40 cases in 1993 (see chart below). Ris

Patients with Hypospadias
Doubling in the U.S.

ing rates of hypospadias have also been reported
from European countries.
Hypospadias is a genital defect in males where
the urinary opening is misplaced on
the underside of the penis instead
of at the end or, in some cases, lo
cated in the scrotum. This condi
tion has been linked to the inad
equate release of the male hormone
testosterone during a critical period
of foetal development - between the
56th and the 80th day after con
ception when the urogenital tract
develops in the foetus. This leads
to the “incomplete masculinization"
of the male genitals.
"As you block the foetus' own
testesterone, the foetus cannot
masculinize itself, and you end up
getting these various states of femi
nization of the foetus, of which hy
pospadias is a mild form", says
Paulozzi. Undescended testicles, where the testes
do not descend into the scrotum and are retained
within the abdomen, vaginal pouches where the pe
nis is covered with a layer of fat, cleft penis, re
duced seminal vescicles, etc are among the other
features of this incomplete masculinization or
“feminization" of the male genitals. Also cases of
such genital defects seem to be increasing accord
ing to various reports. Such defects have also been
found to occur in animal studies using pesticides
such as DDT (and its breakdown product DDE) and
vinclozolin, a fungicide used commonly on fruits and
vegetables.
Similarly, cancer of the testicles in men has

been found to be increasing in several countries and
the incidence of testicular cancer has been found
to be higher among men with developmental defects
such as hypospadias and undescended testicles. Re
searchers say that this indicates that the higher
rates of testicular cancer have something to do with
events in early life or in the womb itself. Here again,
laboratory studies with animals have indi
cated that estrogens may have a major role
in promoting testicular cancer.
Meanwhile, studies done by Frederick
vom Saal at the University of Missouri, USA,
have shown that mouse foetuses exposed to
very small doses of estrogen-like chemicals
developed enlarged prostates and the mice
later had declined sperm counts.
Decline in sperm counts in men has also
been found in studies of semen samples from
various regions of the world. In 1992, Dan
ish endocrinologist, Niels Skakkebaek and his
colleagues analyzed various studies of semen
quality (covering 15,000 men from 20 coun
tries) published over the previous 50 years
and found that the mean sperm count had
declined nearly 50 percent worldwide over
that period - from 130 million/mL in 1940 to
66 million/mL in 1990. This study turned out to be
very controversial: while some smaller scale and lo
calized studies of semen quality that followed found

a decline in sperm count, a few others did not.
However, in 1997, Shanna Swan and her group
at the California Department of Health Services,
USA, reviewed and re-analyzed Skakkebaek's data
for sperm count, taking into account regional varia
tions in sperm count, and came to the conclusion that
there was indeed a sharp drop in sperm count world
wide; if anything, they found, the drop could be
sharper than what was estimated by Skakkebaek.

Source: K. Prabhakar Nair, varied researched
references, 1999. Graphs taken from Japan Off
spring Fund (JOF) information posters for their
Endocrine Disruptors Campaign.

India - Pesticides and Health Meeting, October, 2002

15

Suffer the Little Children...
Theo Colborn, a researcher at the World Wild
life Fund (WWF), has been closely following
and synthesizing research on endocrine-dis
rupting chemicals around the world for years.
She put together, for the first time the mount
ing evidence, collected from all over the world,
for the endocrine-disrupting effects of synthetic
chemicals, including pesticides and industrial
chemicals, in her book, “Our Stolen Future".
In this extract here, taken from her interview
with “Mother Jones", a U.S. magazine, she
talks about the implications of these endocrinedisrupting effects of synthetic chemicals. She
says:
“We are neutering the population (as a result
of the interference of some organic pollutants
and industrial chemicals which act like hor
mones); we are making females more mas
culine and males more feminine.

Up until the 56th day from the day of concep
tion, you can’t tell the sex of the foetus. The
tissue that is there is going to eventually pro
duce testicles or ovaries. It takes just a slight
tweak of a hormone to make it grow into a
male tissue and become a testicle; a tweak in
the other direction, and it will become female
tissue.

What we are finding in fish and birds and even
mammals now are ovotestes, or testes that
have ovarian tissues in them. We have un
covered a new series of subtle effects, which
probably take place during embryonic and foe
tal development and which have long-term
effects that keep an individual from reaching
his or her full development.
We are seeing an increase in hypospadias in
boys. Hypospadia is a condition where the
urethra doesn’t come out at the end of the
penis. This particular developmental process
starts on day 56 in the womb and ends on day
84. Hypospadia has nothing to do with ge
netic pre-disposition. But what can cause this
condition is dioxin and DDT. And it is not just
this type of hypospadias that is increasing but

also the more severe form, where the end of
the urethra actually comes out of the scrotum.
It is almost impossible to repair this surgically.
Hypospadias and undescended testicles - an
other condition that results from males not fully
developing in the womb - put young men at
greater risk of developing testicular cancer,
which is one of the fastest-growing cancers in
the world, and is occuring in younger and
younger men.
Finally, males with hypospadias and unde
scended testicles always produce less sperm,
which means they are more likely to have re
productive problems...
During embryonic and foetal development, the
brain isn’t developed yet, so you have got an
individual that has no feedback mechanism to
protect itself. The foetus is still growing new
tissue, constructing its nervous system, con
structing elements of its immune system and
the reproductive tract. When all your organs
are formed and fully functioning, it takes a lot
more to blow them away.
But we are never going to be able to prove a
causal relationship of anything in a human be
ing because we can’t feed chemicals to hu
man beings and wait for them to grow up.
In the case of a developmental problem such
as attention deficit hyperactivity syndrome
(ADHD) in children, for example (this is in an
swer to the interviewer’s question on ADHD—
ed.), it is very difficult (to prove a causal rela
tionship) because the syndrome is probably
precipitated pre-natally or in early infancy
through something that interfered with the de
velopment of the brain. And the presence of
the chemical in that individual later on in life
may not indicate that it was the cause.

Despite the fact that there are a lot of misdiag
nosed kids, I still think ADHD is on the increase.
And the evidence is almost overwhelming that
these chemicals are involved."

India - Pesticides and Health Meeting, October, 2002

16

Common Pesticides as Endocrine Disruptor
Endocrine-disrupting pesticides vary in their effects since they may involve different receptors and target cells,
accumulate at different rates, and have different binding affinities. Consider, for example, vindozolin, a com
monly used fungidde (which has been shown to strongly block the receptors for the male hormone androgen
when given to pregnant rats)(1). When vindozolin was present during critical periods of foetal development,
genital malformations were common and these would affect reproduction later in life. Sdentists had difficulty
identifying the male offspring at birth because they had genitals that were feminized: i.e., undescended testes,
vaginal pouches, reduced seminal vesides and prostate glands and deft phalli. The vindozolin molecule itself
is not the culprit but it is broken down in the body into two products which are endocrine disruptors. This
provides a dassical example of the body’s natural chemical detoxification system producing more dangerous
chemicals.
Another example is the old DDT. Concerns about the effects of DDT and its metabolites on the health of wildlife
and humans have a long history. A variety of abnormalities seen in male sexual development have been linked
to DDT. It was earlier thought that these effects (as also the well-documented eggshell thinning) were in part
due to DDT's interference with estrogen receptors but recently it has been shown that the primary metabolite
(breakdown product) of DDT, p,p'-DDE, blocks androgen receptors. Like vindozolin, it also binds to the andro
gen receptor, blocking a switch critical for the development of normal males.(2)

Eggshell thinning is another effect seen in birds exposed to DDT. Scientists had long suspected that this was
the result of estrogen-mimicking. However, recent work reveals thatthe effect isalso instigated by DDE which
acts to inhibit the production of another hormone, called prostaglandins, which are critical to calcium balance
and deposition of calcium in eggshells. This is a very important example that endocrine disruption does not only
occur through the receptors that hormones usually signal cells in the body. Many hormones have other
specialized ways of communicating other messages that are critical for many other processes.
Theseareonly two examples of endocrine-disrupting behaviours of commonly used pesticides.

Other Offending Pesticides
Herbicides:

2,4,5,-T
AJachlor
Amitrole
Atrazine
Metribuzin
Nitrofen
Trifiuralin
Fungicides:
Benomyl
Ethylene thiourea
Fenarimol
Hexachlorobenzene
Mancozeb
Maneb
Meti ram-complex
Tri-butyi-lin
Zineb
Ziram

Insecticides:
beta-HCH
Carbaryl
Chlordane
Chlordecone
Dicofol
Dieldrin
Endosulfan
Heptachlor / H-epoxide
Lindane (gamma-HCH)
Malathion
Methomyi
Methoxychlor
Oxychlordane
Parathion
Synthetic pyrethroids
Transnonachlor
Toxaphene

Nematocides:
Aldicarb
DBCP

References:
1. Gray Jr, L.E., J.S. Ostby and W.R. Kelce, 1994, Developmental effects of an environmental antiandrogen: the fungicide
vindozolin alters sex differentiation of the male rat, Toxicology and Applied Pharmacology, 129:46-52.
2. Kelce W.R., C.R. Stone, S.C. Laws, L.E. Gray, J. A. Kemppainen and E. M. Wilson, 1995, Persistent DDT metabolite p,p'DDE is a potent androgen receptor antagonist Nature, 375:581-585.
Source: Dr. Michael Smoien, World Wildlife Fund, USA.

India - Pesticides and Health Meeting, October, 2002

17

DDT Can Reduce Breast Milk
Besides the numerous health effects of DDT, the presence of DDT and DDE (a breakdown product of DDT)
in breast milk can lead to a decrease in breast milk and shorten the period of lactation, according to some
studies. This is significant in that breast milk is the main source of healthy food and nutrition for infants in
developing countries, and it is in these countries that DDT is still being heavily used.
Studies of the implications of DDT and DDE in mothers’ milk done in Mexico and the U.S. have
shown that higher levels of DDE in breast milk are associated with shorter periods of lactation. (,) A fall in
estrogen levels partly leads to lactation after child birth, but the presence of estrogen mimics like DDT or
DDE in these mothers inhibits full lactation, it is said.
But whether it is as a source of contamination of breastmilk, or as a cause of a reduction in
breastmilk and shortening of the period of lactation, it is clear that it is the use of pesticides that need to
stop, and not the act of breastfeeding itself. Very often contamination and problems with breastmilk are
used as a deterrent to women who want to breastfeed their babies. Breastfeeding is very important to the
wellbeing and nutrition of the baby.
Source: Global Pesticide Campaigner, September 1998; and additional comments on breastfeeding
from the International Baby Food Action Network, November,!999.

Reference:
1. Gladen. B.C., WJ. Rogan. 1995, “DDE and shortened duration of lactation in a northern Mexican town", American Journal of Public
Health. 85 (4) Rogan W.J., B.C. Gladen. etaf. 1987. "PCBsand DDE in human milk: effects on growth morbidity and duration of lactation",
American Journal of Public Health, 77(10)

effects on its health later in life.
For example, changes in the developing brain
can alter neural pathways leading to altered adult
behaviour or alter the functions of many endocrine
systems. (See also Article: Pesticides and Aggres
sion, in page 37). Changes to the thymus and bone
marrow cells can lead to immune suppression.
Changes to the testis or ovary can reduce sperm or
egg quality and quantity.
Scientists studying cancer are also concerned
that subtle changes in early development can pre
dispose individuals to certain types of cancer later
in life, such as prostate or breast cancers. There
fore, the presence of endocrine disrupting chemi
cals is particularly serious in pregnant or nursing
women, and in developing foetuses or infants. (See
also Article: Pesticides, Organoch/orines and
Breast Cancer, in this Section).
We must therefore assess to what extent pesti
cides are involved in endocrine disruption, spe
cially those pesticides which are produced in large
quantities, widely dispersed and frequently trans
ported over long distances over water or through
the air. Many pesticides and other synthetic chemi
cals do not degrade and persist in the environment.
Some breakdown in the body into different chemi
cals that are more biologically active, and inter
fere with the function of the normal endocrine sys
tems. Many can accumulate in the fat of animals
and are passed through the predator-prey food
chain.
Preliminary studies have identified pesticides
such as endosulfan, methoxychlor, dicofol, lindane,
DDT and its metabolites, vinclozolin, chlordecone,
toxaphene, 2,4-D, 2,4,5-T, atrazine, carbaryl, di

eldrin, heptachlor, mirex, malathion and chlordane
as endocrine-disruptors. There is no battery of tests
yet available that can ascertain that specific chemi
cals are either endocrine-disruptors or are safe.
Such screening tests are currently being evaluated
but until such tests become available, every chemi
cal, especially pesticides, must be considered po
tentially disruptive.
Exposure to commonly used pesticides is not
restricted only to applicators but consumers too.
Vinclozolin residues for instance, can be found in
many foods, including beans, peas, and onions191.
DDE (a breakdown product of DDT) may be a more
serious concern since it dissolves in body fat, re
sists degradation, persists in the body for decades
and, transferring through the food chain, gets con
centrated to high levels in fish, wildlife and hu
mans worldwide. Even when dietary or occupa
tional exposures to the chemical are low on a daily
basis, the concentrations in body tissues increase
over the years, and by the time a female reaches
reproductive age, the concentrations of chemicals
such as p,p'-DDE can be substantial. (See Box:
Common Pesticides as Endocrine Disruptors).

A Sensitive Target
As mentioned earlier, the developing offspring
is the most sensitive target of endocrine disruption.
Many man-made chemicals can cross the placen
tal barrier in the womb and diffuse from the
mother's body into the developing offspring. Fur
ther, fat-loving chemicals lodged in the fat-rich
breast milk are passed on to suckling infants. Thus
the exposure to concentrated doses of these chemi
cals in the womb and in early childhood can be

India - Pesticides and Health Meeting, October, 2002

18

the highest. This is a matter of much concern. This
is because much of the development of the ner
vous, reproductive and immune systems contin
ues long after birth, and exposure to chemicals such
as DDT and its metabolites in the early phase of
life can have a wide range of effects on this devel
opment. Besides the well-known consequences,
there may be other, more cryptic, effects arising
from a soup of endocrine disruptors. It has been,
for example, reported"01 that higher levels of DDE
in women shortens the period of lactation; DDE as
a contributing factor in lactation failure is a phe
nomenon that is being noticed throughout the
world. (See Box: DDT Can Reduce Breast Milk).

What Should We Do?
We must begin by recognizing that man-made
chemicals have the potential to disrupt the natural
endocrine systems of animals, and because the
endocrine system is interwoven throughout the life
of every animal, effects may vary in site and sever
ity. Disturbances instigated in the developing off
spring may not be seen until adulthood, far re
moved from the early endocrine disruption. Like
wise, we cannot assume that processes common
Io insects, fish, shellfish, amphibians, reptiles, birds
and mammals are different from the cellular and
molecular processes in humans.
We must realize that we are literally awash in
man-made chemicals that have not been rigorously
tested for their ability to disrupt endocrine systems,
and that we can no longer afford to assume that
they are inert baggage that we acquire through life.
We must assume that man-made chemicals can
be endocrine disruptors, and until tests are imple
mented to screen and test these chemicals, we must
be prudent and adopt the precautionary actions
necessary to safeguard our survival.

Dr. Michael Smolen of the. World Wildlife Fund (WWF)
U.S; is part of the team of scientists who have under
taken extensive work and research on environmental
contaminants, a major part of which include pesticides,
their impacts - particularly on the human endocrine
system - and the serious human health and environ

mental implications of exposure to such contaminants.

References:
I. Davis D.L., A. Blair and D. Hoel, 1992, 'Agricultural
Exposures and Cancer Trends in Developed Countries',
Environmental Health Perspectives, 100:39-44.

2. Giwercman A., E. Carlsen, N. Keiding, and N.E.
Skakkebaek, 1993, 'Evidence for increasing incidence
of abnormalities of the human testis: A review'm, Envi
ronmental Health Perspectives 101, (Supplement 2):6571.
3. Carlsen, E., A. Giwercman, N. Keiding and N.E.
Skakkebaek, 1995, 'Declining semen quality and in
creasing incidence of testicular cancer: Is there a com
mon cause?', Environmental Health Perspectives,
1 (^Supplement 7):137-139.

4. Auger, J., J.M. Kunstmann, F. Czyglik, P. Jouannet,
1995, 'Decline in semen quality among fertile men in
Paris during the past 20 years', New England Journal of
Medicine, 332(2):281-285.
5. Colborn T., 1995, 'Pesticides - How research has
succeeded and failed to translate science into policy:
Endocrinological effects on wildlife', Environmental
Health Perspectives, 103(Supplement 6):81 -85.
6. Bern, H.A., 1992, 'Diethylstilbeslrol (DES) syndrome:
present status of animal and human studies', in: Hor
monal Carcinogenesis, (). Li, S. Nandi, and S.A. Li, eds.).
Springer-Verlag, New York, 392p.

7. Colborn, T. and C. Clement, 1992, 'Chemically-in
duced alterations in sexual and functional development:
The wildlife/human connection', Princeton Scientific
Publishing, Princeton, New Jersey.

8. Bern, H„ 1992, "The fragile fetus", in: 'Chemicallyinduced alterations in sexual and functional develop
ment: The wildlife/human connection', (Colborn, T. and
C. Clement, eds.), Princeton Scientific Publishing,
Princeton, New Jersey.
9. The Pesticide Register, 1991, Joint publication of
MAFF and HSE, .Issue 3, March 1991. London.
10. Gladen B.C. and W.J. Rogan, 1995, "DDE and short
ened duration of lactation in a northern Mexican town",
American Journal of Public Health, 85(4):504-508.

India - Pesticides and Health Meeting, October, 2002

19

2 i Acute Effects of
I Pesticide Exposure

J

Three farmworkers were transported to the emergency room by their supervisor They hud
been working in a vineyard when a nearby cotton field was aerially sprayed with pesticides.
7 he spray had drifted downwind into the vineyard where about a dozen people were
working Many of the workers began to complain ofa variety ofsymptoms, inc hiding
difficiiliy breathing, irritation «/ the eyes and throat, and nausea. The sickest workers were
taken to the emergency room, while others were being seen in a load clinic. There was no
information available yet about what the workers were exposed to.

'
•:
i
;
1
‘
’
’
I
i
•
;

Cute pesticide poisonings present with rapid onset of symptoms—such as those in the
case above—stemming from exposures generally within the past several hours or days.
Acute pesticide poisonings are the pesticide-related health effect that practitioners are most
likely o recognize and treat. However, large numbers of acute pesticide poisonings each
year go undiagnosed and unreported, according to pesticide researchers.' The available
reporting data indicate that each year between 2000 and 5000 individuals require hospitali/ation as a result of pesticide poisoning in the United States.2 Children under six years of
age represent more than half of acute reported pesticide poisoning incidents, usually via
accidental ingestion or dermal exposure? An estimated 10,000-20,000 farmworkers in rhe
United States suffer from acute pesticide poisonings each year.' In California the state’s
Pesticide Illness Surveillance Program reported nearly 4000 farmworker pesticide poisonmgs from 1991 to 1996?

;
»
?
i
’•
i
’’
•

,

Physicians should be aware of the pesticide poisoning reporting requirements under the
California Health and Safety Code.6The state Pesticide Illness Surveillance Program (PISP)
requires that “any physician or surgeon who knows, or has reasonable cause to believe, that
a pai icni is suffering from pesticide poisoning or any disease or condition caused by a
pesticide shall promptly report that fact to the local health officer by telephone within 24
hours and by a copy of the report within seven days?’ failure to report can result in civil
penalties of up to $250. County health officers must then report to county agricultural
< nmnissioners, who determine whether the cases arc potentially related to pesticides. I'hc
>t.nc 1 Ocpartmcm of Pesticide Regulation (DPR) administers the program. Pesticide illness
records arc useful for assessing the public health implications of pesticide use and the
dfck livmcss of current regulations. DPR reports, however, that most pesticide illness data
aie obtained from workers compensation reports rather than through the PISP.

’.
s
'.
ji

( archil diagnosis is critical. An I'.PA model screening protocol is included in the appendix
of this resource kit. for a comprehensive guide to protocols for diagnosis, treatment, and
follow-up of acute pesticide poisoning, refer to the U.S. I’.PA handbook on Recognition
and Management of Pesticide Poisonings?

;
■

(Organophosphate and carbamate pesticides arc among the most common causes of
pesiicidc poisonings and hospitalizations in the United States.”

:•
?
;
i

( Organophosphate (OP) insecticides irreversibly deactivate the enzyme acetylcholinesterase,
thereby destabilizing ncurotransmission ai synaptic junctions. This leads to overstimulation
of boih ihc sympathetic and parasympathetic nervous systems.1" " Specific antidotes and
ihcr.ipcuik protocols arc available for organophosphate and carbamate poisonings.

•

< One ol die most frequently used (OP pesticides is chlorpyrifos (Dursban or l.orsban) It is
widely used io kill insects in agriculture, as well as in home insect sprays and in dips to kill
Hc.r., ( Oilier common OP insecticides include malathion, azinphos-mcthyl (( million).

I

j

Overview

■

Acute
Organophosphate
and n-methylCarbamate
Toxicity

India - Pesticides and Health Meeting, October, 2002

20

methyl parathion, diazinon, demeton, and phosmet. These pesticides arc often used in
agriculture, homes and gardens.
The N-mcthyl-carbamate insecticides also deactivate acetylcholinesterase, but the inhibi
tion is reversible rather than permanent. Thus, while the symptoms of carbamate and
organophosphate poisoning are identical anti may be equally severe, carbamate poisoning
generally runs a shorter course.12 Common N-methyl-carbamate pesticides include carbaryl
(Sevin), aldicarb (Temik), fenoxycarb, propoxur, and mcthomyl.
Signs and Symptoms

The symptoms of OP or carbamate poisoning include bradycardia, dyspnea, wheezing,
nausea, vomiting, diarrhea, ocular meiosis, fasciculations, muscle weakness, and hyperse
cretion, (e.g., lacrimation, perspiration, rhinorrhea, and salivation). Central nervous system
signs anil symptoms are also prominent, including headache, dizziness, restlessness, and
anxiety. Severe intoxication may result in psychosis, seizures, and coma.”
Children may present with a different clinical picture from adults. Hypotonia, lethargy.
seizures, and coma were more common presenting symptoms in children than in adults,
and children rarely present with the classic cholinergic signs of salivation, lacrimation,
diaphoresis, bradycardia, or fasciculations.1''

Theoretically, acme symptoms of organophosphate or carbamate poisoning are classic and
easily recognized, but in practice diagnosis can be difficult. Pesticide poisoning can easily
be misdiagnosed as gastroenteritis, influenza, bronchitis, or a wide range of other illnesses.
Even severe pesticide poisoning requiring intensive care unit admission was misdiagnosed
80% of the time in one series, with diagnoses including pneumonia, meningitis, and
epilepsy.”

The only way to be sure to correctly diagnose acute pesticide poisoning is to maintain a
high index of suspicion and take a screening occupational and environmental history from
any patient that presents with suggestive symptoms. Brief questions about occupation,
household exposures, and any other potential exposures to fumes, dusts, or gases will allow
a rapid assessment of the likelihood that an illness could be related to pesticides or other
toxic chemicals.
Diagnosis and
Treatment

Plasma or red blood cell cholinesterase levels can be useful in OP or carbamate poisoning,
and are readily available through most labs. However, treatment should not be delayed
pending results of the laboratory test. Baseline cholinesterase levels, particularly in plasma,
are subject to wide variability. As a result, interpretation of the results can be difficult
without a baseline for the individual, and a result within the normal range may still
represent clinically-significant suppression of cholinesterase for a particular individual.16
Urinary alkyl phosphates and phenols can be useful for documenting exposure within the
first 48 hours, and arc more sensitive to low-level exposure than cholinesterase levels.
Therapy for any pesticide poisoning begins with removal of all potential sources of
ongoing exposure including gloves and clothing (every effort should be made to ensure
privacy when removing clothes in field situations). If residues may be on skin or hair, the
patient should be decontaminated with ample soap and water. Supportive care, including
continuous cardiac monitoring, oxygenation, airway preservation and aggressive hydration,
are all generally indicated.17

For many ingested pesticides gastric lavage and cathartics may be indicated. Be aware,
however, that gastric lavage is contraindicated with hydrocarbon ingestion (a common
vehicle in pesticide preparations), and cathartics may not be needed after ingestion of
pesticides such as the OPs and carbamates, which often result in diarrhea.'8 Consultation
with a Poison Control Center is highly advisable at this stage.”
Atropine sulfate TV or IM is used to control muscarinic symptoms of OP or carbamate
poisoning, including lacrimation, salivation, vomiting, diarrhea, and bronchorrhea. This
treatment does not affect nicotinic symptoms such as muscle weakness, fasciculations, and

India - Pesticides and Health Meeting, October, 2002

21

respiratory depression. An atropine challenge can be useful for diagnostic purposes.
Atropine is generally administered in repeated doses of 2-4 mg q 15 minutes in adults, or
0.05-0.1 mg/kg q 15 minutes in children until secretory symptoms have reversed. Consult
a Poison Control Center or EPA’s Recognition and Management of Pesticide Poisonings
for current treatment protocols. Repeated doses may be needed for hours, particularly in
the case of OP poisoning, and severe poisoning can require very large doses, up to 300 mg/
day.20
Pralidoxime IV is used to reactivate cholinesterase only in severe cases of OP poisoning. A
blood sample for cholinesterase must be drawn prior to administration of pralidoxime.
This medication is generally contraindicated in carbamate poisoning. The adult dose of
pralidoxime is up to two grams in a slow IV drip, while for children the dose should nor
exceed 50 mg/kg. Blood pressure and heart rate must be carefully monitored during
dosing.21

Other Pesticides
Associated with
Acute Poisoning

Acute symptoms associated with other major pesticide categories are presented in 'fable 21. It is noteworthy that clinical manifestations of acute poisoning have only been studied
for a small fraction of pesticides in current use.
Patients who have suffered acute pesticide poisoning require close medical follow-up
because certain health effects, particularly neurological impairment, can emerge after
apparently successful treatment and recovery.22

Preventing
Acute Pesticide
Poisoning
Advice for Patients

• Avoid using pesticides unless absolutely necessary. Select less toxic alternatives whenever
possible. For example, insect baits and traps are almost always safer than broadcast
sprays, and non-pesticide alternatives include sealing cracks, cleaning up food scraps, and
using soap products to eradicate scents.
• If there are children in the home, make sure that all pesticides are stored out of reach. Do
nor store any highly toxic pesticides in the home, especially agricultural pesticides or OP
pesticides.
• Never store pesticides in containers other than the original, labeled container. In particu
lar, never store pesticides in soft-drink bottles or other food containers.
• If any object, including clothing, containers, or equipment, becomes contaminated with
pesticides, discard it or clean it thoroughly and separately. Do not leave any pesticidecontaminated objects in areas where children might come into contact with them.

• Never apply pesticides without following label directions. Always wear protective gloves,
long sleeves, and protective clothing. Do not re-enter an area where pesticides were
applied until well after any time interval specified on the label.
• If you suspect pesticide poisoning, seek emergency medical care as quickly as possible.
Bring along any containers associated with the incident.

India - Pesticides and Health Meeting, October, 2002

22

Table 2-1: Acute Symptoms Associated With Some Major Pesticide Categories
i

1

|

1
1
i
|

Pesticide Category

Chemical Examples

Physiological Target

Acute Symptoms

Diagnosis/Treatment
Cholinesterase levels/
Supportive care, atropine,
pralidoximc

Organophosphates

Chlorpyrifos, diazinon,
methyl parathion,
malathion, azinphos-methyl,
naled

Irreversibly inhibits
acetylcholinesterase resulting
in muscarinic and nicotinic
effects

Vomiting, diarrhea,
hypersecretion,
bronchoconsrricnon, headache,
weakness

n-methyl Carbamates

Carbaryl, aldicarb, fcnoxycarb,
tncthomyl. bendiocarb

Reversibly inhibits
acetylcholinesterase resulting
in muscarinic and nicotinic
effects

Vomiting, diarrhea,
hypersecretion,
bronchoconstriction, headache,
weakness

Cholinesterase levels/
Supportive care, atropine

Pyrethnns

Pyrethrum

Neuronal paralysis,
sensitization

Allergic reactions, anaphylaxis.
Tremor, ataxia at very high
doses

No diagnostic test/
Treat allergic reactions with
antihistamines or steroids, as
needed

Pyrethroids
Type I

Allethrin, permethrin,
tetramethrin

Interference with sodium
channel in
neuronal cell
membranes — repetitive
neuronal discharge

Dizziness, irritability to sound
or touch, headache, vomiting,
diarrhea

No diagnostic test/
Decontamination,
supportive care,
symptomatic treatment

Tvpc II
< cy a no- pyrct hroids)

Dcltamcthrin, cypcrmcthrin,
fenvalcrate

Interference with sodium
channel and inhibition of
gamma-aminobutyric acid
(GABA)

Seizures, dizziness, irritability to
sound or touch, headache.
vomiting, diarrhea

Note: Skin contact may cause
highly unpleasant, temporary
paresthesias, best treated with
Vitamin E oil preparations

Organochlorines

Lindane, endosulfan, dicofol,
methoxychlor

Blockade of chloride channel
m the GABA receptor complex

Incoordination, tremors,
paresthesia, hyperesthesia.
headache, dizziness, nausea.
seizures

Detectable in blood/
Decontamination, supportive
care, cholestyramine to clear
entcrohcpatic recirculation

Chlorophcnoxy
compounds

2,4-Dichlorophenoxyacctic acid
(2.4-Dy 2.4-DB, 2,4-DP

Peripheral neuropathy,
myopathy, metabolic acidosis.
skin and mucus membrane
irritant, uncoupler of oxidative
phosphorylation

Nausea and vomiting.
headache, confusion, myotonia.
low fever, acidosis, EKG
changes. CI’K elevation,
myoglobinuria

Detectable in urine and blood/
Decontamination, hydration.
forced alkaline diuresis

Dipyridyi compounds

Paraquat, diquat

Corrosive, free radical
formation, lipid peroxidation,
selective damage to
pneumatocytes

Pain, diarrhea, headache,
myalgias, acute tubular
necrosis, delayed pulmonary
edema.
Neurologic toxicity from
diquat

Urine dithionitc test
(colorimetric), detectable in
urine and blood/
Decontamination, do
not administer oxygen,
aggressive hydration.
hemoperfusion

Anticoagulant
*
Rodenticide

Warfarin, brodifacoum,
difcn-acoum, coumachlor,
bromadiolonc

Antagonize vitamin K,
inhibition ofclotting factors

Nosebleeds, hematuria, rnelena.
ecchymoscs

Elevated PT and I NR/
Vitamin K
administration

Chlorophenols

Pentachlorophenol (PCP, Penta)

Uncouples oxidative
phosphorylation, skin and
mucus membrane irritant

Fever, tremor thirst, sweating,
tachycardia, hypercapnia, chest
constriction, abdominal pain

Detectable in blood anil urine/
Decontaminalion, support ive
care, control hyperthermia

Dinocap

Uncouplcr of oxidative
phosphorylation

Hyperthermia, tachycardia,
anxiety, confusion, headache,
diaphoresis

Detectable in scrum, bright
yellow staining of skin and
urine/
Supportive care, control
hyperthermia

Methyl bromide

Irritant, inhibits sulfhydryl
enzymes and reversibly breaks
down ATP

Headache, ataxia, tremor,
agitation, visual disturbances.
vomiting, seizures, pulmonary
edema

Blood or urine bromide levels/
Supportive care.
benzodiazipines. dimercapiul

Mctam sodium

Decomposes in water to
methyl isothiocyanate,
severely irritant gas

Mucus membrane irritation,
pulmonary edema

No diagnostic test/
Supportive care

Nitrophenols and
Nitrocreosols

i
I

fumigants

Fumigants

>ourc J.R. Rcig.irt and J.R. Roberts. Recognition and Management oj Pesticide Poisonings. Fifth Ed. U.S. Environmental Protection Agency, EPA T35-R-9S-OO3. 1999 Online .it httpU
www cp.i.gov/pi->iicidcs/s.ilrty/healrhcarc

India - Pesticides and Health Meeting, October, 2002

23

j

3

Dermatologic Effects of
Pesticide Exposure
An agricultural worker comes in with a rash on her hands and arms. It appeared three days
ago, the day after she went into some recently sprayed strawberryfields to pickfruit. She
reports that many co-workers have similar rashes but have not sought medical attention:
Theyfear losing theirjobs ifthey report the problem. She does not know the name ofthe
pesticide sprayed, but thinks it is used to control mold. She mentions that she is pregnant and
wonders whether the chemical could harm her baby.

Overview

Many pesticides penetrate the skin and cause systemic exposure.1 Acute illness and death
have been reported from percutaneous absorption of pesticides, particularly through
damaged skin.2
Dermatitis is the second most common occupational disease. Rates in the agricultural
industry are the highest of any industrial sector? In California, pesticide-related skin
conditions represent between 15% and 25% of pesticide illness reports.4
Skin reactions can involve any skin area, including areas covered by clothing, particularly if
the pesticide contacts the clothing and soaks through. However, exposed areas, such as
arms, hands, face, and neck, are most commonly affected?

Pesticides are reported to cause irritant dermatitis, allergic contact dermatitis, and other
skin conditions, including photodermatitis, porphyria cutanea tarda, and chloracne.6
Plants alone can also cause dermatitis. Strawberries, mangoes, and some nursery plants are
common causes of allergic contact dermatitis. Parsley and limes can cause
photodermatitis.7'8

Irritant
Dermititis

• Soil fumigators can get irritant dermatitis and chemical burns of tire lower extremities
from methyl bromide, dichloropropene (Telone), and metam sodium. These can be
prevented by use of chemical-resistant boots.9,10
• Other pesticides frequendy associated with irritant dermatitis include the herbicides
paraquat and diquat, the miticide propargite, and the fungicides sulfur, ziram, benomyl,
and captan. Reactions are generally more severe in the setting of pre-existing skin
abrasions, such as those produced by picking or weeding prickly or rough crops."

Allergic
Dermititis

• Fungicides are particularly known as potential skin sensitizers. The ethylene
bisdithiocarbamate (EBDC) fungicides such as maneb, mancozeb, zineb, and ziram
break down to ethylene thiourea, a known sensitizer.12,13,14

• Sulfur is one of the most commonly reported causes of skin reactions among agricultural
workers. This compound is a skin irritant, but can also cause allergic dermatitis.15,16

Source: MA O'Malley, Skin reactions to pesticides, Occup Med State Art Rev 12
((1997J2): 327-45.

India - Pesticides and Health Meeting, October, 2002

24

• The organic pesticide Bacillus thuringiensis has recently been shown to induce skin
sensitization in exposed workers,17 as have the fungicide triforine and the organophos
phate insecticide dichlorvos (DDVP).18
• Patch testing with standardized concentrations of certain pesticides can be used to
confirm sensitization.15

Other Skin
Manifestations
of Pesticide
Exposure

• Paraquat and diquat, herbicides that can cause skin burns, are also known ro severely
damage fingernails.20,21
• Various herbicides have been associated with chloracne, potentially due to contamina
tion with dioxins. The principal herbicide that has been associated with chloracne is
2,4,5-trichlorophenoxyacetic acid (2,4,5-T), the now-banned primary constituent of
Agent Orange. Other herbicides potentially associated with chloracne include 2,4-D,
diuron, and linuron.22
• Porphyria cutanea tarda has been reported following exposure to hexachlorobenzene and
diazinon.23

Chapter 3 Notes

1

R.C. Wester, D. Quan, and H.I. Maibach, In vitro percutaneous absorption of model compounds glyphosate
and malathion from cotton fabric into and through human skin, Food Chem Toxicol'S^ (1996)8:731-35.'

2

F. Jaros, Acute percutaneous paraquat poisoning, Lancet 1 (1978): 275.

3

MA O’Malley, Skin reactions to pesticides, Occup Med State Art Rev 12 (1997)2: 327-45.

4

Ibid.

5

Ibid.

6

Ibid.

7

Ibid.

8

E. Paulsen, Occupational dermatitis in Danish gardeners and greenhouse workers (II): Etiological factors, Contact
Dermatitis 38 (1998)1: 14—19.

9

M. Hezemans-Boer, J. Toonstra, J. Meulenbelt, et al.. Skin lesions due to exposure to methyl bromide, Arch
Dermatol 124 (1988): 917-21.

10

D. Koo, L Goldman, and R. Baron, Irritant dermatitis among workers cleaning up a pesticide spill: California
1991, AmJIndMed27 (1995)4: 545-53.

11

See note 3 above.

12

M. Bruze and S. Fregert, Allergic contact dermadtis from ethylene thiourea, Contact *Dermatitis
)
12.

13

M. Johnsson, M. Buhagen, H.L. Leira, and S. Solvang, Fungicide-induced contact dermatitis, Contact Dermatitis
9 (1983): 285-88.

14

P. Koch, Occupational allergic contact dermatitis and airborne contact dermatitis from 5 fungicides in a vineyard
worker; Cross-reactions between fungicides of the dithiocarbamate group, Contact Dermatitis ?A (1996)5:324—
29.

15

D.S. Wilkinson, Sulphur sensitivity, Contact Dermatitis 1 (1975): 58.

16

See note 3 above

(1983): 208-

17

l.L Bernstein, JA Bernstein, M. Miller, et al. Immune responses in farm workers after exposure to Bacillus
thuringiensis pesticides, Env Hlth Persp 107 (1999)7:575-82.

18

A Ueda, K. Aoyama, F Manda, et al., Delayed-type allergenicity of triforine (Saprol), Contact Dermatitis 31
(1994)3:140-45.

19

KA Mark, R.R. Brancaccio, NA Sorer, and D.E. Cohen, Allergic contact and photoallergic contact dermatitis
to plant and pesticide allergen, /W? Dermatol 135 (1999) 1:67-70.

20

R.L Baran, Nail damage caused by weed killers and insecticides, Arch Dermatol 110 (1974): 467.

21

C.E. Hearn and W Keir, Nail damage in spray operators exposed to paraquat, BrJIndMedTS (1971): 399—
403.

22

AJ. McDonagh, DJ. Gawkrodger, and AE. Walker, Chloracne—study of an outbreak with new clinical
observations, Clin Exp DermatoliH (1993): 523-25.

23

AG. Collins, AW Nichol, and S. Elsbury, Porphyria cutanea tarda and agricultural pesticides, Australia J
Dermatol23 W&2)-.7t>-75.

India - Pesticides and Health Meeting, October, 2002

25

4

Pesticides and Cancer
A til-year-oldfarmworker comes into your office complaining offatigue and bone pain.
Since teenagers, he and his sister have worked in fields harvesting crops and mixing pesti
cides. His work-up reveals multiple lytic bone lesions, pancytopenia, and a monoclonal
immunoglobulin spike. A bone marrow aspirate confirms a diagnosis ofmultiple myeloma.
He responds well to treatment. He later tells you that his sister was treatedfor a soft-tissue
sarcoma a few years ago at age 36. Both siblings are motivated to encourage co-workers to
participate in a study offarmworker health that is being proposed by the Public Health
Department. They ask iftheir diseases could be related to pesticide exposure. How do you
respond?

Overview

A wealth of research explores connections between pesticide exposure and neoplasia.
Collected clues from the fields of molecular biology, toxicology, biochemistry, and epide
miology may help us chart a course for cancer prevention.

Numerous pesticides are implicated in causing or promoting many types of cancers,
leukemias, and lymphomas. Some of these diseases are relatively common, others quite
rare. Many of the neoplasms for which association with pesticides is most well-established
are among those cancers increasing in incidence in industrialized countries. It is unclear
whether exposure to pesticides is causally related to the rising rates of these cancers.
The mechanisms by which pesticides contribute to cancer causation vary, and one pesticide
may operate by more than one of the major mechanisms, which include
• Genotoxic effects—producing direct changes in DNA.
• Promotion—causing fixation and proliferation of abnormal clones. This process
includes endocrine effects that may stimulate otherwise quiescent but hormon
ally sensitive cells to carcinogenesis.
• Immunotoxic effects—disturbing the body’s normal cancer surveillance
mechanisms.

Whereas the usual concept of toxicity follows the principle that “the dose makes the
poison,” genotoxic chemicals and hormone disruptors may have effects at very low doses
without a true threshold below which no risk exists (the stochastic or probabilistic model).
Current understanding of carcinogenesis favors the conclusion that even a tiny dose of a
genotoxic agent can initiate the process of converting a normal cell to a malignant one.1,2’3''1'5

In the field of endocrine disruption, some scientists argue that because background levels of
endogenous hormones such as estrogen are known to promote cancer, any additional
external hormonally active agents add to an already established risk.6 For these reasons, at
least in theory, even rather low-dose exposure to certain carcinogens may pose a health risk.
Three major lines of evidence relate cancer to pesticide exposure:

1. Cell-culture studies that demonstrate effects such as chromosomal damage or
estrogenic! ty.
2.

Laboratory animal studies (see Table 4-1).

3.

Human epidemiological investigations.

This section focuses primarily on human epidemiological evidence linking pesticide
exposure and cancer.

Overview of the
Epidemiological
Evidence

Abundant in vitro and animal research on the potential carcinogenic effects of pesticides is
available and often leads to important advances in understanding human carcinogenesis.
However, to eliminate the variable of cross-species interpretation of tests, we confine

India - Pesticides and Health Meeting, October, 2002

26

discussion to the study of exposed humans. In the case of pesticides, a number of occupa
tional, home, and other environmental studies illustrate rhe risks of exposure.

For many human studies of pesticides and cancer, the pesticide specifically responsible for
carcinogenesis has not been determined. Because occupations in agriculture involve use of
multiple agents (including non-pesticidal chemicals), it is often difficult to determine what
agent is linked to a specific endpoint. The same problem occurs with home and environ
mental exposures, where multiple products may be used, their doses unmeasured, their
names long forgotten by those exposed. In this document, whenever studies are specific
enough, the class or type of implicated pesticide will be provided.
It is scientifically difficult to prove that something causes cancer. For example, it took a
decade of research to confirm the causative link between cigarettes and lung cancer, despite
the fact that smoking causes more than 90% of all lung cancers and one third of all
cancers in the U.S.5

When we refer to the risk of developing various cancers, it should be understood that
pesticides are not the only possible cause of any given disease (e.g„ leukemia may be caused
by some pesticides and also by other chemicals such as benzene). It is usually not possible
to know, on an individual basis, all factors that have contributed to carcinogenesis. The
following information summarizes those substances that should stimulate suspicion and
rigorous study if we are ro progress toward prevention.

Pesticides and
Cancers of
Adulthood
Hematological
Malignancies
Non-Hodgkins
Lymphoma (NHL)

Sometimes called the “silent epidemic,” over the last several decades Non-Hodgkins
Lymphoma (NHL) incidence has been increasing by 3-4% per year throughout most of
the world.'1'10 In some studies annual increases in incidence are as high as 4.2-8.0%." 12''
These reported increases are corrected for known viral causes of NHL, such as human
immunodeficiency virus (HIV), and therefore largely exclude AIDS-related lymphomas.1'1'15 Some research on pesticide workers demonstrates associations between occupa
tional exposures (in agriculture or exterminator work) and NHL.16'1 JSA large number of
studies find more specific correlation, especially to phenoxy herbicides such as 2.4dichlorophenoxyacetic acid (2,4-D).19,2"'21'22 Other research on pesticide workers implicates
furan and dioxin contaminants (2,3,7,8-tetrachlorodibenzo-p-dioxin) of the phenoxy
herbicides.23 Although the phenoxy herbicides and rheir contaminants are the most
consistently NHL-associated chemicals, investigators raise concern about other pesticides,
including lindane (used in some head and body lice-treatments),2'1 organophosphate
pesticides,23 and a variety of others, such as carbaryl, chlordane,
dichlorodiphenyltrichlorethane (DDT), diazinon, dichlorvos, malathion, nicotine, and
toxaphene.26 Evidence shows that some fungicides may also be lymphomagens.2

Other epidemiologists have studied exposure of persons who are not pesticide workers but
live in areas of pesticide use or drift. Herbicide spraying doubled the risk of fatal NHL in a
study of persons living in agricultural regions in Canada.25 The phenoxy herbicides were
associated with increased risk of NHL among residents of rice-growing areas in northern
Italy.29 In the U.S., a cluster of NHL and other B cell malignancies has been reported in a
Midwestern farming community.30
Humans and their dogs live in close proximity, and a study of canine cancer reinforces the
above data. Increased risk of canine malignant lymphoma has been associated with pets’
exposure to 2,4-D on lawns.31
Multiple Myeloma |MM)

Multiple Myeloma (MM) is another hematological malignancy for which age-adjusted
incidence seems to have increased during rhe last several decades. Rates vary, even among
industrialized countries: U.S. investigators found an increased incidence of 4% per year
from the late 1940s to the early 1980s among white men and.women.32 In contrast,
epidemiologists in Spain observed a greater than 10% annual rise from the 1960s to the

India - Pesticides and Health Meeting, October, 2002

27

mid-1980s." A number of reports cite intermediate increases in several other nations.14
Many epidemiological studies reveal an association between employment in farming and
the chance of contracting MM, with risks as high as 5-fold.'5•
Some investigators have more specifically identified possible causative agents. One study of
herbicide applicators reports an 8-fold increase in risk of succumbing to MM."’The
phenoxy herbicides are implicated in this excess risk,41 an association that should not be
surprising since the malignancy is closely related to lymphoma. Chlorinated insecticides are
also associated with increased risk for MM in another study.’’
Hairy Cell
leukemia (HCL)

Increased occurrence of a rare disease is often more obvious to researchers than a similar
rise in the rate of a common illness. The latter tends to get "washed out” among the large
numbers of expected cases. Hairy Cell Leukemia (HCL) is so rare that multiple recent
reports linking it with pesticide exposure raise great interest. '3,44 One study specifically
associates organophosphates with HCL.45

Myelodysplastic
Syndrome (MDS)

Myeloid leukemia and Myelodysplastic Syndrome (MDS) have been associated with
occupational exposure to pesticides.46'4’ One case-control study finds significant associa
tions between occupational exposure to pesticides and both acute myeloid and lymphoid
leukemia.48 Review of recent Cancer Registry of Central California data shows correlation
of the herbicides 2,4-D and atrazine and the pesticide captan with leukemia among
Hispanic males.'4 One cohort study of a group of gardeners known to have been highly
exposed to pesticides reveals a nearly 3-fold increased risk for chronic lymphocytic leuke
mia,'" an illness for which few possible causes have been proposed.

Soft Tissue Sarcomas
(STS) in Adults

As with NHL, development of Soft Tissue Sarcomas (STS) as a function of pesticide
exposure is widely studied and frequently correlated. While some studies reveal a simple
association with gardening or farming,5152 many show a more specific association with rhe
phenoxy herbicides'3 54 or with a combination of exposure to phenoxy herbicides and the
pesticide contaminant TCDD.'5
Occupational exposure to phenoxy herbicides and/or chlorophenol is repeatedly linked to
STS.'6 ' 58 in one of the most detailed investigations of any tumor/pesticide association,
one case-control study of workers with STS derived odds ratios for exposure to three major
pesticide-classes—phenoxy herbicides, chlorophenols, and dioxins. The odds of contract
ing STS after exposure to any phenoxy herbicide was approximately ten times higher than
for non-exposed controls; to the class comprising 2,4-dichlorophenoxyacetic acid, 2,4,5trichlorophenoxyaceric acid, and 4-chloro-2-methylphenoxyacetic acid and to any chlori
nated dibenzodioxin or furan, nearly six; and to 2,3,7,8-retrachlorodibenzo-p-dioxin.
greater than five.'4

Carcinomas and
Central Nervous
System (CNS)
Malignancies in
Adults
Skin Cancer and Cancer
of the Lip
Brain Tumors

While elevated risk for skin cancer and cancer of the lip is repeatedly associated with
farming,60<’l,<’2'63 ultraviolet light exposure may be a more likely causative factor than
pesticides. Therefore, observation of an association between one specific type of skin
cancer—Bowen’s disease—and the manufacture of paraquat64 is of interest because the
paraquat-associated skin cancers demonstrate DNA abnormalities which differ from
sunlight-induced skin cancers.

The age-adjusted incidence of primary tumors of the Central Nervous System (CNS)
(particularly astrocytomas, including the rapidly progressive glioblastoma multiforme as
well as the benign meningiomas) appears to have increased by 50-100% over the past
several decades, with greatest increase among the elderly.6'-66-6” Studies also show increased
occurrence of high-grade neuroepithelial tumors, lymphoma, and other primary CNS
tumors of 5-13%68'6’ per annum in rhe elderly. Some observers attribute the apparent
increase to the availability of computerized tomography,70 but disproportionate increase in
certain histologic types,71 parallel increases in mortality,72 and studies that show diagnostic

India - Pesticides and Health Meeting, October, 2002

28

imaging only contributes about 20% to case ascertainment all suggest the rise is probably
real.73
Several studies of workers in farming,74 gardening and orchard work,75 pesticide applica
tion,76 and golf-course superintendence77 show increased risk for primary tumors of the
brain. Research analyzing risk of brain cancer among many occupational groups indicates
that workers in occupations likely to involve pesticide exposure heighten their liability to
brain tumors.78,7’ No studies yet connect specific pesticides to these observed increases.
Respiratory Tract Cancer

Modest increase in cancers of the nose and nasal cavity is reported among workers exposed
to phenoxy herbicides and chlorophenols.80,81 A greater than 2-fold increase in lung cancer
(adjusted for smoking) has been observed among structural pest-control workers.82 Excess
cancer of the sinonasal cavities and lungs has been found among women working in
agricultural settings.83

Gastrointestinal Cancers

Gastric cancer has been associated with work as a farmer,84 as has colorectal cancer.85,86 In
one retrospective cohort study, colorectal cancer specifically correlated with working in a
plant that manufactured the herbicide alachlor. For all exposed workers, risk for developing
leukemia or colorectal cancer was 50% higher than for a comparable non-exposed popula
tion, while incidence of colorectal cancer among workers with five or more years of the
highest alachlor exposure was more than five times greater.87
One study finds that biliary and liver cancer correlate highly with work as a pesticide
applicator.88,89 Another study strongly implicates exposure to DDT.90 Research on workers
in plants that manufacture organochlorines shows a nearly 4-fold increased risk from
exposure to chlordane, heptachlor, endrin, aldrin, and dieldrin.” These pesticides are no
longer used in the U.S., but persist in the environment—including termite-protected
homes—so exposure may still occur.

A number of studies implicate pesticides in pancreatic cancer. They show that occupational
pesticide-exposure increases the risk of pancreatic cancer.92,93,94 Workers exposed to DDT
and related compounds suffer more than a 7-fold increased incidence of pancreatic cancer
compared with non-exposed workers.95 In short, organochlorine exposure appears to be
consistently linked with a variety of gastrointestinal malignancies.
Urinary Tract Cancer

The U.S. has recently experienced increased incidence of and mortality from renal cancers.
According to the Surveillance, Epidemiology and End Results (SEER) national cancer
monitoring program, the last 25 years have witnessed dramatic increases in disease and
death from kidney cancer among black and white Americans of both sexes. During the last
20 years, all white men saw increased incidence at 3.1% per year; white women at 3.9%;
and African-American men and women, the steepest at 3.9% and 4.3%.96 Such rates over
a 20-year period cannot be explained by early detection, especially given that screening
tests are not routinely employed. An environmental cause is likely.

Occupational exposure to pesticides (work in agriculture) has been correlated with in
creased risk for kidney cancer (or hypernephroma).’7,,8,” One study shows specific risk
associated with pentachlorophenol.100 Among women occupationally exposed to pesticides,
one study observed increased incidence of bladder cancer.'01
Testicular Cancer

Testicular cancer is another malignancy rising in occurrence for the last several decades in
virtually all developed nations. Annual incidence increases range from 2.3% to 5.2% in
Europe since the 1940s.102 In Miyagi, Japan, growth is among the highest, with 6.6% per
annum.103 U.S. data suggest similar trends: The nations oldest on-going statewide tumor
registry finds a mean annual increase in testicular cancer incidence of more than 5.5% over
the last 60 years.104
Studies of offspring of parents who work in agricultural activities reveal higher rates of
testicular cancer, with occurrence manifesting in childhood as well as young adulthood.105

India - Pesticides and Health Meeting, October, 2002

29

Another study shows excess risk of testicular cancer among workers exposed to phenoxy
herbicides and chlorophenols.106
Prostate Cancer

Numerous studies demonstrate small but significant correlations between prostate cancer
and occupational settings likely to lead to pesticide exposure,l07,loa as well as jobs involving
direct pesticide or herbicide application.109

Breast Cancer

Age-adjusted incidence of breast cancer in industrialized countries has increased 1-2% per
year for several decades, both before and after introduction of mammography."01" This
observation suggests environmental factors may play a role in this common disease.

Recent years have witnessed great controversy over the possibility of attributing increased
breast cancer incidence to hormonally active environmental contaminants, including some
pesticides. The organochlorines have received special attention due to their estrogenic
effects in vitro, lab animals, and wildlife. While we cite studies that seem to support that
some pesticides contribute to breast cancer causation, it should be noted that there are
negative findings as well, so the precise contribution of pesticides to breast carcinogenesis is
not settled.
A case-control study of postmenopausal breast cancer measured serum levels of certain
organochlorine compounds (DDE, hexachlorobenzene, mirex, and several polychlorinated
biphenyls or PCBs). Some increased risk appeared for women with certain types of PCBs
and mirex detectable in their serum, but this effect was predominantly restricted to
postmenopausal women who had never breast-fed."2 It should be observed that PCBs,
although organochlorines, are not expected pesticide-components.
Another case-control study analyzed breast tissue from patients with invasive cancer for the
presence of organochlorines and compared it with control measurements from women
with benign breast biopsies. Some, but not all, classes of PCBs were associated with breast
cancer, especially among postmenopausal women with estrogen-receptor positive tumors.
Hexachlorobenzene levels were also associated with increased risk of malignancy."1

Case-control research from Colombia showed an association between serum
dichlorodiphenyl-dichloroethane (DDE, a metabolite of DDT) levels and risk for breast
cancer."4 Another study found serum dieldrin levels associated with dose-related, signifi
cantly elevated risk of breast cancer, but other organochlorines appeared nor to affect
risk."5
In an ecological study of breast cancer incidence in an agricultural district heavily contami
nated with organochlorine and triazine herbicides, a very modest but statistically significant
increased risk of breast cancer is evident."6

In summary, organochlorine pesticides may disrupt some actions of estrogens. However,
the actual effect on breast cancer risk is likely to vary from compound to compound and
even change with different endocrine states of the host."7
Thyroid

A large cohort study of workers exposed to phenoxy herbicides and chlorophenols reveals
increased risk of thyroid cancer among exposed persons."8

In a community exposed to unusually high levels of the organochlorine
hexachlorobenzene, excess incidence of thyroid cancer was observed."’An agricultural
region of Minnesota with heavy use of ethylene bis-dithiocarbamate fungicides (such as
maneb, mancozeb, and zineb) suffered a nearly 3-fold increased risk. These fungicides are
metabolized to ethylene thiourea, a known thyroid carcinogen in animals.12"

Pesticides and
Childhood
Malignancies

Every year approximately 8000 children under age fifteen are diagnosed with a malignant
disease, most frequendy leukemia and brain tumors. Environmental exposure such as to
ionizing radiation, hormones, and antineoplastic agents are accepted to be contributors to
these diseases. Some childhood tumors such as gliomas, leukemia, and Wilms’ tumor seem

India - Pesticides and Health Meeting, October, 2002

30

to be increasing in incidence, but the cause
for most of these illnesses remains un
known.121 The clues pertaining to pesticides
and. children should be treated seriously
given pesticides’ ubiquitous presence, the
tendency of children (especially toddlers) to
experience their world by tasting it, and the
possible increased sensitivity of children to
carcinogens.
Childhood leukemia

Non-Hodgkin's
lymphoma

Brain and Nervous
SysfemTumors

Sarcomas

Wilms' Tumor

Chapter 4 Notes

Table 4-1: Carcinogenic Pesticides
Chemical Name

Chemical Use

Arsenic acid

Herbicide

Arsenic pentoxide

Insecticide,
wood preservative

Arsenic crioxide

Rodenticide

Cacodyl ic acid

Herbicide, defoliant

Capcan

Fungicide

Chlorothalonil

Fungicide

Parental occupational exposure ro pesticides
as well as home and garden pesticide use
may increase risk of childhood leuke
mia. 122,123'124 Home use of pest strips has
been strongly associated with risk.125

Chromic acid

Wood preservative

Creosote

Wood preservative

Daminozidc

Plant growth regulator

Ddvp

Insecticide

Di propyl
isocinchomcronate

Insecticide

Pesticides have been linked to childhood
NHL.126 Children of parents engaged in
agricultural work show higher than
expected risk.127

Diuron

Herbicide

Ethoprop

Insecticide

Ethylene sodium

Fumigant

Fenoxycarb

Insecticide

Folpet

Fungicide

A multicenter case-control study finds
home use of pesticides increases risk of
childhood brain cancers.128 Other research
on home pesticide deployment demon
strates highly significant correlation
between pediatric brain tumors and use of
sprays or foggers to dispense flea and/or
tick pet-treatments.12" Other pesticides
implicated include pest strips, termite
control pesticides, lindane shampoo, flea
collars, yard and orchard herbicides, home
pesticide bombs, and carbaryl for outdoor
use.13,1 Occupational pesticide use by
parents has been associated with increased
risk of childhood neuroblastoma.131

Formaldehyde

Microbiocidc

Iprodionc

Fungicide

Lindane

Insecticide

Mancozcb

Fungicide

Maneb

Fungicide

Metam-sodium

Fumigant

A study of parental occupation and
childhood cancer shows a strong association
between fathers’ employment in agricul
tural work (from six months prior to
conception up to rhe time of diagnosis) and
Ewings’ sarcoma in offspring.132 Yard
pesticide treatments have been linked to an
increased rate of childhood soft-tissue
sarcomas.133
Paternal employment in agriculture has
been associated with increased risk of
Wilms’ tumor.134 In other studies, both
paternal and maternal exposures to pesti
cides correlates with increased risk.135,136

Metiram

Fungicide

Ortho-phcnylphenol

Microbiocidc

Ortho-phenylphcnol,
Sodium salt

Microbiocide

Oxadiazon

Herbicide

Oxythioquinox

Insecticide, fungicide,
fumigant

Para-dichlorobenzenc

Insecticide

Pcntachlorophenol

Wood preservative

Potassium dichromate

Wood preservative

Propargice

Insecticide

Propoxur

Insecticide

Propylene oxide

Fumigant

Propyzamide

Herbicide

Pyrethrins

Insecticide

S,S,S-tributyl
phosphorotrithioace

Defoliant

Silica aeroge

Insecticide

Sodium dichromace

Wood preservative

Thiodicarb

Insecticide

Thiophanate-methyl

Fungicide

Trichlorfon

Insecticide

Vinclozolin

Fungicide

Source; Pesticides listed as known, likely, or probable carcinogens
by U.S. EPA Office of Pesticides Programs as of August 1999. or
by the state of California under Proposition 65 and the Sale
Drinking W.ucr and Toxic Enforcement Act of 1986.

1

K.S. Crump, An improved procedure For low-dose carcinogenic risk assessment from animal data,/ Env Path
Toxicol 5 (1980): 675-84.

2

C.C. Brown, Learning about toxicity in humans: Some studies in animals, Chontech 13 (1983): 350-58.

3

E.L. Anderson, The Carcinogen Assessment Group of the U.S. Environmental Protection Agency, Risk Anitlysis 4
(1983): 277-95.

India - Pesticides and Health Meeting, October, 2002

5

Pesticides and
Respiratory Disease
A 24-year-old man comes into an occupational health clinic with a three year history ofchest
tightness, wheezing, and episodic dyspnea. The patient works in a chemicalplant that
manufactures pesticides. His symptoms began shortly after his transfer to a captafolproduc
tion line, are worst in the evening and at night, but resolve on weekends and vacations.
There is no personal orfamily history ofallergies or asthma. Review ofsystems reveals rashes
on his wrists above his gloves, chronic burning eyes, and rhinitis. Specific bronchial challenge
testing reveals a marked andpersistentfall in FEV1.'

Overview

Acute organophosphate or N-methyl carbamate overexposure is well known to cause
cholinesterase inhibition, resulting in bronchoconstriction, increased airway secretions, and
respiratory distress.2
A few pesticides are known sensitizers and can result in allergic reactions including
asthma.3''1 An association between low-level pesticide exposure and asthma is controversial,
and confounded by the fact that animal, plant, and odier antigens cannot be completely
ruled out.
A few studies report other respiratory effects from pesticides, including pulmonary
hemosiderosis, pneumonia-like infiltrates, chronic bronchitis, pulmonary fibrosis,
Wegener’s granulomatosis, and respiratory muscle impairment.5,6,7,8'9
The main target organ for the herbicide paraquat is the lung. This pesticide is selectively
taken up by the lung from peripheral blood, and causes oxidative damage presenting as
acute pulmonary edema and hemorrhage or as delayed pulmonary fibrosis. Respiratory
failure has occurred following exclusively dermal exposure to this chemical.10

Pesticides and
Asthma

• Case reports and specific bronchial-challenge testing link several pesticides with occupa
tional asthma. These pesticides include captafol,” sulfur,12 pyrethrins and pyrethroids,13
tetrachloroisophthalonitrile,1'1 and several organophosphate and N-methyl carbamate
insecticides that appear to have a methacholine-like effect on the lung.15,16
• A cross-sectional study of nearly two thousand farmers in Saskatchewan revealed a
significant association between physician diagnosed asthma and reported use of cho
linesterase inhibiting pesticides. Potential confounding from exposure to fungi and
pollen cannot be completely ruled out.17

• Plantation workers in India showed a potential association between pesticide exposure
and respiratory impairment. Although overall prevalence of asthma was lower among
workers than among controls (perhaps due to the well known “healthy worker effect,” in
which the working population, on average, enjoys a better health status than the overall
population),18 the pesticide exposed workers revealed an exposure-related increase in
both obstructive and restrictive deficits on pulmonary function testing.19
• Vineyard and orchard workers in Eastern Europe had significantly higher overall
prevalence of dyspnea, chest tightness, chronic cough, and chronic phlegm compared
with non-pesticide-exposed controls. Among both smoking and non-smoking workers
employed for greater than ten years, FEV,, FEF25, and FEF50 were significantly reduced.
Exposed workers also had significantly reduced FVC compared to controls. It was not
possible to determine whether findings were due to pesticide exposure or to occupational
exposure to dust, pollen, or mold. However, the workers were exposed to a variety of
organochlorines, organophosphates, sulfur, and inorganic copper compounds.20

India - Pesticides and Health Meeting, October, 2002

32

• Worldwide population trends indicate that the prevalence of asthma is increasing in the
general population, particularly among children and young adults. Severity of asthma, as
measured by emergency room visits, hospitalizations, and deaths, is also increasing
despite treatment advances.21 Causes of these trends are not well understood, but it is
possible that increasing exposure to pesticides may play a role.22
• Children are more susceptible to airborne health hazards than adults for several reasons,
such as more rapid respiratory rate and greater volume per unit of body weight, and
greater average activity level with faster respiratory rates. Furthermore, very young
children are naturally closer to the ground or floor, where chemicals denser than air tend
to accumulate. The fact that terminal airways of the lung are not fully developed until
several years after birth is also significant.23

Other
Respiratory
Diseases
Related to
Pesticide
Exposure

• An interesting case report describes a young woman who developed diffuse pulmonary
hemosiderosis four days after she applied a combination of three synthetic pyrethroids
(delramethrin, cyhalothrin, and bensultap) to a strawberry field. The patient developed
sudden onset of dyspnea and severe hemoptysis requiring transfusion. Her chest x-ray
showed bilateral cloudy infiltrates, and bronchoalveolar lavage revealed hemosiderinloaded macrophages. All antibodies were negative. The syndrome responded well to
cyclophosphamide.24
• One group of researchers proposes the existence of a “biocide lung” following prolonged
exposure to pesticides. This syndrome is characterized by intermittent pulmonary
infiltrates followed by chronic progressive fibrosis.25
“ In a survey of about 200 Danish fruit-growers, individuals reported using an average of
13 different pesticides. The most commonly used pesticides comprised captan, paraquat,
parathion, azinphos-methyl, diquat, amitrol, benomyl, and simazine. Approximately
40% of the growers reported at least one significant respiratory symptom in connection
with pesticide spraying, and nearly 20% had diminished peak flow. These findings were
more common among workers who did not wear respiratory protection when applying
pesticides. X-ray revealed pulmonary infiltrates or fibrotic changes in nearly one quarter
of the subjects.26

• A case-control study of 101 patients with Wegener’s granulomatosis found that cases
reported significantly greater occupational exposure to pesticides compared with both
healthy controls and controls with other pulmonary diseases.27

• A study questionnaire administered to 54 workers in an Eastern European pesticide
plant revealed a 50% prevalence of chronic bronchitis. Approximately two-thirds of the
workers had significandy decreased peak expiratory flow. Exposed workers also showed
significantly diminished maximum inspiratory and expiratory pressures, potentially
indicating respiratory muscle weakness.28

India - Pesticides and Health Meeting, October, 2002

6

Neurological and
Behavioral Effects of
Pesticides
A 52-year-old patient draws your attention to a tremor that has become increasingly
bothersome over the pastyear. On examination, the tremor is pill-rolling and resolves with
intention; the patient also has a positive Romberg Sign and an unstable tandem gait. You
make a preliminary diagnosis ofearly Parkinson’s Disease. The patient’s wife mentions that
she recently read in the newspaper that most Parkinson's isfrom environmental causes, and
asks ifthefact that her husband is a farmer and has usedpesticidesforyears could be related
to his early-onset disease.

Overview

Pesticides have been shown to affect both the central nervous system (CNS), and the
peripheral nervous system (PNS) in animals and humans via a variety of mechanisms.
The effects of neurotoxic pesticides can be assessed by measuring changes in neurochemis
try, neuropathology, and behavior, including subtle effects on visuospatial function,
concentration, reaction-time, learning, and short-term memory.1,2

Certain pesticides, for example, the organophosphates and N-mcrhyl carbamates, are
designed specifically to damage neurological function in insects and are neurotoxic in
humans because of similarities in nervous system function between insects and humans.

Human neurotoxic effects may be acute, may represent the chronic sequelae of an acute
poisoning, or may result from chronic exposures in the absence of an acute episode of
poisoning? This section focuses on the chronic neurotoxic effects of pesticide exposure.

Pesticides and
Parkinson's
Disease (PD)

There is increasing evidence that a high proportion of Parkinsons Disease (PD) may be
associated with environmental factors?

• Specific pesticides and pesticide classes implicated in PD include paraquat, the organo
phosphates, dieldrin, and the manganese-based fungicides maneb and mancozeb.5,6,7
• The designer heroin-like drug MPTP, known to cause a Parkinsonian syndrome in
addicts via the neurotoxic effect of its major metabolite, is chemically related to the
herbicide paraquat.8
• Numerous studies identify a higher incidence of PD in industrialized countries. Within
these countries, people who live in rural areas, live or work on farms, or report a history
of pesticide use have the highest risk.9,10
• Several population-based case control studies identify a 4-fold increased likelihood of
past herbicide exposure among patients with PD, and a 3—4-fold increased likelihood of
prior exposure to insecticides.11,12

• Several recent studies indicate a possible role for gene-pesticide interactions in the
etiology of PD. In particular, higher than expected rates of certain glutathione transferase
polymorphisms, the slow acetylator genotype of N-acetyltransferase-2, and the slow 4hydroxylation of debrisoquine (the CYP 2D6 29B+ allele) have all been reported in
patients with PD.l3,14,15These genetic variants may increase risk from environmental
exposure by slowing detoxification of exogenous compounds.16

Peripheral
Neurotoxicity

• The cholinesterase inhibiting pesticides (organophosphates and N- methyl carbamates)
interfere with impulse transmission in the PNS. Chronic effects of exposure can include
sensory, motor, and autonomic neuropathies.17

India - Pesticides and Health Meeting, October, 2002

34

• Organophosphate pesticides can rarely cause a distinct syndrome known as organophos
phate-induced delayed polyneuropathy (OPIDP), which occurs within five weeks after
an acute intoxication.18 OPIDP is characterized by axonal degeneration and secondary
demyelination of long tract neurons.19 Symptoms of OPIDP include paresthesias of the
limbs, leg cramping, motor weakness of the wrist and ankle, and, in severe cases,
paralysis.20 Permanent residua include weakness, loss of reflexes, and sensory impair
ment.21

• In some cases, a so-called “intermediate syndrome” may develop 24 to 96 hours follow
ing acute organophosphate pesticide poisoning. The main symptoms consist of proximal
muscle weakness, profound weakness of the neck flexors, and weakness or paralysis of the
muscles involved in respiration.22 Sensory function is completely spared.23 This syn
drome may or may not be followed by OPIDP24 Neither OPIDP nor the intermediate
syndrome respond to therapy with atropine or pralidoxime.25

• PNS impairment may also occur following chronic occupational exposure to pesticide
mixtures, even in the absence of acute poisoning or frank OPIDP. Several studies report
an increased prevalence of neurological abnormalities in exposed workers compared with
controls. Abnormalities include hyporeflexia, dysequilibrium, reduced vibration sensitiv
ity, and nerve conduction delays.26,27 Other studies fail to find peripheral nerve conduc
tion delays in workers who have not suffered high level exposure.28
• Workers exposed to mixed pesticides, particularly to the dirhiocarbamate fungicides
maneb and zineb, have been shown to have slowed peripheral nerve conduction. Motor
and sensory conduction were affected equally, with some indication of autonomic
dysfunction as measured by reduced respiratory variability.29

Neurocognitive
Effects of
Pesticide
Exposure

• Many pesticides are able to penetrate the blood brain barrier, while others exert indirect
effects on the brain via disruption of oxygen supply, nutrients, hormones, or neurotrans
mitters.30
• Areas of the brain most commonly affected by pesticides include the limbic system,
hippocampus, basal ganglia, and cerebellum.31
• Evidence of pesticide-associated neuropsychological deficits is based primarily on studies
of workers acutely or chronically exposed to organophosphate pesticides, although some
case reports also implicate N-methyl carbamate pesticides in the appearance of similar
effects.32
• Cognitive symptoms in these populations include impairment of memory and psycho
motor speed, and affective symptoms such as anxiety, irritability, and depression.33
Visuospatial deficits have also been linked to organophosphate exposure.34 Standardized
neuropsychiatric testing batteries confirm these deficits in exposed groups compared
with unexposed controls. Long-term memory and language abilities are generally
spared.35

• The fumigants methyl bromide, sulfuryl fluoride, and dichloropropene (Telone) have
been reported to cause personality changes and shortened attention span following
exposure. Methyl bromide exposure was related to decreased touch sensitivity and
reduced cognitive ability; Telone exposure, to increased depression and anxiety reflected
in standardized test batteries; and sulfuryl fluoride, to a range of behavioral and cognitive

deficits.36,37

Pesticides and
Seizures

• Many pesticides are known to increase CNS excitability and to produce seizures with
acute high-dose exposure.38
• Recent animal studies indicate that some pesticides can cause an electrical kindling
response after repeated sub-threshold dosing. Low doses repeated three times a week for
ten weeks of the pesticide lindane (used to treat head lice) resulted in enhanced myo

India - Pesticides and Health Meeting, October, 2002

35

clonic jerks and seizures ar normally subconvulsant doses. Odier organochlorine pesti
cides, such as endosulfan and dieldrin, are reported to have similar effects.'9

Effects of
Pesticides on
Neurological
Development in
Children

Neurological development in children is particularly vulnerable to disruption. Although
there is some plasticity inherent in the development of the nervous system, even low-level
exposure during the brain-growth spurt have been shown to exert subtle, permanent effects
on the structure and function of the brain.
• Animal studies have demonstrated periods of vulnerability, particularly to anticholinest
erases, during early life.'" Recent evidence supports the finding that acetylcholinesterase
may play a direct role in neuronal differentiation.41

• Children from a region in Mexico with intensive pesticide use were found to have a
variety of developmental delays compared with otherwise similar children living where
fewer pesticides were used. Although the children were similar in growth and physical
development, significant delays were noted among the exposed children in physical
stamina, gross and fine hand-eye coordination, and short-term memory.42

Table 6-1: Chronic or Delayed Neurotoxic Effects of Pesticides■

Pesticide Category

Effects on Central
Nervous System

Effects on Peripheral
Nervous System

Organophosphates
c.g., malathion, chlorpyr’tfos

Cognitive, affective and
perceptive effects

OP1DP; sensorimotor neuropathy,
intermediate syndrome

Carbamates
c.g., carbaryl

Memory deficits; visual
impairment; lassitude

Sensorimotor neuropathy

Organochlorines
c.g., kepone

Impairment of cognitive function
and personality; seizure kindling

Tremor (Kepone shakes)

Metah
c.g.,monosodium methyl arsenate,
lead arsenate, zinc phosphide

Impaired visuospatial abilities;
deficits in short-term verbal
memory

Painful, burning dysesthesias

Fumigants
c.g., carbon disulfide,
dichloropropenc, methyl bromide

Cognitive impairment; mood
changes; difficulty concentrating;
pyramidal signs

Loss of reflexes and distal motor
strength

Fungicides
c.g., dithiocarbamates—zeneb,
maneb, mancozeb

Reduction of physiologic
respiratory arrhythmia; possibly
Parkinsons

Reduced nerve conduction

Pyrethroids
c.g., fenvalcratc, cypcrmcthrin

Reduction of spontaneous motor
activity; altered startle response

Cutaneous paresthesia; numbness

Rodenticides
c.g., vacor
(N-3-pyridylmcthyl-N-pnitrophcnyl urea)

Minimal data on cognitive
impairment

Autonomic incompetence

Sources: M C Kcifcr and R.K.Mahurin, Chronic neurologic effects of pesticide overexposure, Occup Med (Philadelphia)
12 (1997): 291-304; M.M. Amr, E.Z. Abbas, G.M. El-Samra, et al., Ncuropsychiatric syndromes and occupational
exposure to zinc phosphide in Egypt, Env RsrchTi (1997): 200-206; D.J. Echobichon and R.M. Joy, Pesticides and
neurological diseases, 2nd cd. (Boca Raton, FL: CRC Press, Inc., 1994); L Roscnstock, M. Kcifcr, WE. Daniell, ct al.,
Chronic central nervous system effects of acute organophosphate pesticide intoxication, Lancet 338 (1991): 223-’27.

Chapter 6 Notes

1

D.J. Echobichon and R.M. Joy, Pesticides and neurological diseases, 2nd ed. (Boca Raton, FL CRC Press, Inc.,
1994).

2

L.S. Engel, M.C. Keifer, H. Checkoway, et al., Neurophysiological function in Farmworkers exposed to
organophosphate pesticides, Arch Environ Hlth 53 (1998): 7-14.

3

A.M. Evangelista De Duffard and R Duflard, Behavioral toxicology, risk assessment, and chlorinated hydrocar
bons, Environ Hlth Persp 104 (1996): 353-60.

4

J.W Langston, Epidemiology versus genetics in Parkinsons disease: Progress in resolving an age-old debate, Ann
Neurol44 (1998)3 Suppl. I: S45-52.

5

L Fleming, J.B. Mann, J. Bean, et al., Parkinsons disease and brain levels of organochlorine pesticides, Ann of
Neurol%{\W}'.\^y

India - Pesticides and Health Meeting, October, 2002

36

Reproductive and
Developmental Effects
of Pesticides
A 32-year-oldnum comes in with concerns aboutfertility. He has been marriedfouryears
and his wife has not become pregnant despite regular attemptsfor the past severalyears. The
man reports that he works at a chemical company that manufactures pesticides and that
several other men are having similarproblems. The men complained to the union steward;
all would be coming in for medical evaluation over the nextfew weeks. Semen analysis
reveals azospermia.

Overview

Pesticides may affect human reproduction by direct toxicity to the reproductive organs or
by interference with hormonal function.1'2,3,4 Effects of pesticides on reproduction may
include menstrual abnormalities, male or female infertility, or hormonal disturbances.
The developing fetus and infant are disproportionately susceptible to the health effects of
pesticides.5 Developmental toxicity of pesticides may result in spontaneous abortion,
growth retardation, structural birth defects, or functional deficits.6

There is often a period of vulnerability to the effects of toxic chemicals—including
pesticides—during fetal development and early childhood. This vulnerability occurs
during the period of development of various organ systems. Permanent structural birth
defects or permanent functional changes may occur.

.Male Infertility: The Example of DBCP

.

;

The most thoroughly studied human epidemic of pesticide-induced' rcprodticuve d^functioh'began'ih the 1970s ' fx
• whenmen'at an Occidental chemical plant in Southern Calffor^sou^t medicak^eforlliffertilii^I^any^werejAJ.’; J-

sterile, and subsequent investi^tion found dmt a
(DBCP), "was responsible for effects qii spermatogenesis and for-.genn^cell’mutations ."hln many cases,.effects were ?
permanent. Rddent':studies.j5ac|oi^^^^des earlier found dramatic testicular tdxicityiin
- -t-:was disregarded until
"Although useof DBCP has beendiscontimied in me .U.S.,- it is-persistent.in.sdil and.s.t
./some parts of California. Thus there is potential for pngotng loiwlevel
.'such exposures over"the reproductive'life-spari afe.unkhpwn. DBCP. 'was still 'jis'ed.unti
f banana plantanons/tesultingin .eptd^fes of'stenlity. in agricultural worfcers;lJ?^^4j

Effects of
Pesticides on
Fertility

term effects of ■, T

Use of chlordecone (Kepone) was discontinued in the U.S. after incontrovertible evidence
that it causes decreased sperm mobility and viability, in addition to serious neurological
effects in workers.13
Exposure to carbaryl has been associated with increased frequency of morphologically
deformed sperm, but longitudinal studies have not been conducted to confirm adverse
reproductive outcomes.14
• The herbicide 2,4-Dichlorophenoxyacetic acid (2,4-D) is spermatotoxic in laboratory
animals. A correlation between increased exposure to 2,4-D and decreased sperm density
along with increased percentage of abnormal sperm was reported in agricultural pesticide
applicators.15

India - Pesticides and Health Meeting, October, 2002

37

• A study of over eight hundred couples undergoing in-vitro fertilization revealed that men
moderately or highly exposed to pesticides at work had significantly decreased fertiliza
tion rates compared with unexposed males, with only one-third the likelihood of
successful in-vitro fertilization. These effects persisted after adjustment for all other
known exposures, including smoking, alcohol, caffeine, and other chemical use."’
• Wives of male fruit growers in the Netherlands have shown an increased time-topregnancy, particularly during the spring and summer growing season when pesticides
are applied. During that season, time-to-pregnancy more than doubled. Twenty-eight
percent of farm couples sought medical attention for infertility, compared with only 8%
in rhe control (unexposed) population.17

i

* Increased time-to-pregnancy was also found to be significant in Canadian farm families.
During periods when both husbands and wives applied pesticides, fecundability dropped
to between 50% and 80% of expected, whereas when only the husband or neither
partner applied, fecundability was within normal ranges. There was no clear link to
particular pesticides or pesticide classes.18

Developmental
Abnormalities:
Growth
Retardation and
Spontaneous
Abortion

I

• Numerous studies report an increased rate of spontaneous abortions and stillbirths
among female agricultural workers. These studies are limited by potential recall bias, and
by difficulties in exposure assessment since workers are exposed to a complex mixture ol
chemicals and doses are unknown. Some studies of wives of agricultural workers also
show an increased risk of spontaneous abortion and stillbirth.K20,21,22,2’2''

I

• A California study demonstrated an association between pesticide exposure at work or in
the home and stillbirths, particularly those with congenital anomalies. Elevated risks
ranged from a 70% increased risk of stillbirth for home exposure to pesticides, to a
240% increased risk for occupational exposure.2'
• Higher levels of organochlorine pesticides have been found in abortuses and pre-term
infants than in full-term babies.26
• Women living in communities supplied with drinking water contaminated by a variety
of herbicides, including atrazine, cyanazine, and metolachlor, had an 80% increased risk
of intra-uterine growth retardation compared with similar communities with uncontaminated water.2
• Teachers working in day care centers in Germany where wood was treated with the
pesticides and wood preservatives pentachloropheno! and lindane were significantly
more likely to give birth to lower birthweight and smaller size infants. These preservatives
are known to volatilize off wood for years and become entrained in air or dust particles.26

Pesticides and
Birth Defects

Numerous epidemiological studies and case reports associate pesticide exposure at work or
home with increased risk of various types of congenital malformations.29
Particular birth defects associated with pesticides include

• Cleft lip and palate—a doubling of risk with exposure during the first trimes
ter.30-31^
• Limb defects—a 3-4-fold increased risk for garden or workplace exposure, and
greater than doubling of risk with household exposure, particularly if pesticides
were applied by a professional pest eradication service?3,3'1'35'36
• Cardiovascular malformations, particularly Total Anomalous Pulmonary
Venous Return—a 2-3-fold greater risk found in the Baltimore-Washington
Infant Study?7
• Spina bifida and hydrocephaly—a 2.7- and 3.5-fold increased risk respectively
in one study, and a 50% increased risk with residence within a quarter-mile of
an agricultural field in another.38,39

India - Pesticides and Health Meeting, October, 2002

38

• Cryptorchidism and hypospadias—2-3-fold greater rates of orchidopcxy in
highly agricultural areas: a 50% increase in hypospadias also reported.

• A California studv using the state birth defects monitoring program found that infants
with limb reduction defects along with other anomalies were 60% more likely to have
parents involved in agricultural work and 2.4 times more likely to live in an agricultural
county compared with unafflicted infants.'1'
• One Minnesota study of pesticide applicators revealed that their children were at higher
risk ofa variety of birth defects, including circulatory/respiratory anomalies, and
urogenital, musculoskelet.il, and integumental defects. These same trends and birth
defects, although less marked, were paralleled among the general population in heavily
agricultural regions of the state. Defects were most significantly associated with use of
Table 7-1. Developmental and Reproductive Toxins
Chemical Name

Chemical Use

1080
2,4-Db acid
Amitraz
Arsenic acid
Arsenic pentoxide

Rodenticide
Herbicide
Insecticide
Herbicide
Multiple uses, insecticide
wood treatment
Rodenticide
Fungicide
Herbicide
Herbicide
Herbicide
Herbicide
Herbicide
Herbicide

Arsenic trioxide
Benomyl
Bromacil. Lithium salt
Bromoxvnil octanoate
Chlorsulfuron
Cyanazine
Cycloate
Diclofop-methyl
Disoditim evanodithioimido
carbonate
Epic
Ethylene oxide
Fcnoxuprop ethyl
Fluazifop-bucyl
Hydramcchylnon
Linuron

Metam-sodium
Methyl bromide
Med ram
Myclobutanil
Nabam
Nicorinc
Nitrapyrin
Oxadiazon
Oxydemeton-mcchyl
Oxyrhioquinox

Potassium dimethyl dithio
carbamate
Propargitc
Resmethrin
Sodium dimethyl dithio
carbamate
Streptomycin sulfate
Tau-fluvalinate
Thiophanatc-methyl
Triadimcfon
Triburyltin methacrylate
Triforine
Vinciozolin
Warfarin

Microbiocide
Herbicide
Fumigant
Herbicide
Herbicide
Insecticide
Herbicide
Fumigant
Fumigant
Fungicide
Fungicide
Fungicide
Insecticide
Microbiocide
Herbicide
Insecticide
Insecticide, fungicide,

developmental
Toxin

Y
Y
Y
Y
Y
Y
Y
Y
Y

Y

Y

Y
Y
Y
Y
Y
Y
Y
Y
Y
Y
Y
Y
Y

Microbiocide

Y
Y
Y

Fungicide
Fungicide
Rodenticide

Y

Y
Y

Y

Microbiocide
Fungicide
Insecticide
Fungicide
Fungicide
Antifoulant, microbiocide

Male
Repro. Toxin

Y
Y

Y
Y
Y

fumigant

Insecticide
Insecticide

Female
Repro. Toxin

Y

Y

Y

Y

Y
Y

Y
Y

Y
Y
Y
Y
Y
Y
Y
Y

‘source; Proposition 65 List nt Chemical
*
Km wn in ihv Stare ol California to Cause Cancer and Reprodus. live Harin (Sacramento: Caliloinia < Mine
•ntory database
*
•nuronmental Health Hazard Assessment. 2’ December 1999). United State Environmental Protection \gencv To\k Release In

India - Pesticides and Health Meeting, October, 2002

39

2.4-0 and various fungicides. Risks for children of both pesticide applicators and the
general public in the agricultural region were greatest among those conceived in the
spring, a time of greater pesticide use."

• Communities in Iowa with elevated levels of the herbicide atrazine in their drinking
water showed a 2-3-fold increase in all birth defects—specifically, a 3-fold increase in
cardiac defects, a 3-4-fold increase in urogenital defects, and a nearly 7-fold increase in
limb reduction defects.'14
• Numerous case reports and case series present various combined severe congenital
anomalies following occupational or accidental exposure of pregnant women to pesticides.'"'’6'47
• Many pesticides are reported to cause birth defects in animals. Pesticides listed as
reproductive or developmcnt.il toxicants by the State of California or by U.S. EPA are
listed in Table 7-1.

Disruption of
Hormone
Function

Various pesticides mimic estrogen, while others block androgens or thyroid hormone.4"

• Estrogenic pesticides that have been studied in some detail include numerous banned
and still used organochlorine pesticides, such as DDT, chlordccone, dicofol, methoxy
chlor, endosulfan, and lindane.4'’ Fungicides such as vinclozolin and iprodione arc anti
androgens.’" In addition, some triazine herbicides such as atrazine interfere with estrogen
via indirect pathways.”

Table 7-2: Endocrine-Disrupting Pesticides
Chemical Name

Chemical Use

Alachlor

Herbicide

Aldicarb

Insecticide

Atrazine

Herbicide

Benomyl

Fungicide

Carbaryl

Insecticide

Chlorpyrifos

Insecticide

Cyanazine

Herbicide

Endosulfan

Insecticide

Lindane

Insecticide

Malathion

Insecticide

Mancozeb

Fungicide

Maneb

Fungicide

Mcthomyl

Insecticide

Methyl parathion

Insecticide

Metiram

Fungicide

Metolachlor

Herbicide

PCNB

Fungicide

PCP

Wood preservative

Pyrcthrins

Insecticide

Resmcthrin

Insecticide

Simazine

Herbicide

Tributykin methacrylate

Antifoulanr, Microbiocide

Tributyltin oxide

Antifoulant, Microbiocidc

Vinclozolin

Fungicide

Sources: L. Keith. Environmentalendocrine disruptors (New York: Wiley
Inrerscicnce. 1997): J. Licbman. Rising toxic tide (San Francisco:
Pesticide Action Network/Californians for Pesticide Reform. 1997):
Illinois EPA. Report on endocrine disrupting cl<e»ticaL (Illinois EPA.
1997) I Cnlborn. I > Dumanoski. and | P Myers. Our stolen future
(New York: Penguin Books. 1996). 25k ( M Benbrook. Growing
doubt: A printer on pesticides identified ,ts endocrine disruptors andJor
reproductive Toxicants (The National Campaign lor Pesticide Policy
Reform. September 1996)

• Penrachlorophcnol (PCP), a pesticidal wood preservative, binds to
human transthyretin and may directly reduce uptake of thyroxine
(T4) into the brain.’’" Other currently used pesticides, including
dicofol and bromoxynil, have similar effects on thyroxine binding, as
does dinoseb, now banned.’4

■ Health effects of endocrine disrupting pesticides in animals include
altered circulating hormone levels, hypospadias, nipple development
in males, cryptorchidism, decreased semen quality, altered time to
sexual maturity, and abnormal behavior.”56'57
• Male pesticide factoiy workers in China exposed to the organophos
phate pesticides ethyl parathion and methamidophos had significant
abnormalities in their reproductive hormone profiles. Increased
pesticide exposure correlated positively with serum LH and FSH
levels, and negatively with serum testosterone. In addition, workers
with higher exposure tended to show greater risk of abnormal semen
parameters.58
• Workers applying ethylene bisdithiocarbamate fungicides (such as
Maneb or Zineb) in Mexico developed elevated levels ofTSH
without changes in thyroid hormone levels. Although findings were
subclinical in these healthy adult males, they could be relevant to a
developing fetus were a pregnant woman exposed.’9

• In the ferus or neonate, disruption of endocrine homeostasis can
result in permanent alterations in sexual development, whereas
disturbance in adulthood is less likely to create lasting health ef
fects/"

India - Pesticides and Health Meeting, October, 2002

40

8

Effects of Pesticides on
the Immune System
A family comes into a local clinic because the state health department recently informed them
ofpesticide contamination in the well water in their small town. They want to know
whether their children’s persistent respiratory infections and skin rashes might be associated
with the water contamination problem. They are particularly concerned about immune
problems and want to have their immunefunctions tested. They also want to know whether
switching to bottled water is sufpcient to protect them.

Overview

I litre is limited evidence that exposure to certain pesticides may compromise the immune
system. Findings are based primarily on animal studies that demonstrate damage to
immune organs, suppression of immune-mediating cells, and increased susceptibility to
infectious disease.'-”3-4-5-6

The intrinsic variability of immune parameters between and within individuals makes
study of rhe effects of environmental or occupational exposure on human immune
function extremely difficult.

Pesticide exposure has been associated with

• Hypersensitivity reactions ranging from dermatitis to asthma or anaphylaxis.

• Suppression of immune function and consequent susceptibility to infectious
pathogens.
• Autoimmune responses.
• Cancers of immune cell lines (see Section 2. Pesticides and Cancer).

Allergic
Responses

• Some pesticides may cause immediate hypersensitivity symptoms such as rhinitis,
asthma, or anaphylaxis.7-" Pesticides reported to cause hypersensitivity reactions in
humans include atrazine, parathion, dichlorvos, captafol, folpet, captan, naled, maneb,
zineb, dithianone, and dinitrochlorobenzene.',l,)

Immune
Suppression

• Adults occupationally exposed to organophosphate or organochlorine pesticides were
found to have increased frequency and severity of respiratory infections such as tonsilli
tis, pharyngitis, and bronchitis. These workers also showed diminished neutrophil
response—related to duration of exposure to pesticides—including impaired phagocyto
sis, respiratory burst, and adhesion."12

• In humans, one now—banned organochlorine pesticide, chlordane, was associated with
abnormal T-cell and B-cell subsets, decreased proliferation response to mitogen, and
suppressed antibody-dependent cell cytotoxicity. These findings were statistically
significant among people whose homes were sprayed with this pesticide for termite
control.13
• A study of Nebraska farmers showed slight but significant reductions in serum comple
ment activity in the most highly pesticide-exposed group. No consistent differences in
total leukocyte count, mitogen-stimulation ofT-cell or B-cell proliferation, or scrum IgG
and IgM concentration among the groups were detected.1'1
• Women who consumed aldicarb contaminated groundwater in a potato farming area
had significantly decreased CD8 cell subsets when compared with women drinking
unconraminated groundwater."
• The environmentally persistent wood preservative pentachlorophenol (PCP) is consis
tently associated with a range of abnormal immune parameters, from increased levels of
serum IgM and increased immature leukocytes to greater incidence of infection and

India - Pesticides and Health Meeting, October, 2002

41

aplastic anemia. Proliferative responses to mitogen and antigen have been reported to be
significantly depressed in residents of log homes preserved with POP.16'1

Autoimmunity

• Metal-based pesticides such as arsenic and copper arc repeatedly associated with autoim
mune responses.18
• A small four year follow-up study of people overexposed to chlorpyrifos reveals persis
tently higher levels of antibiotic sensitivity, autoimmunity, and CD26 cells.1'1
• Other pesticides reported to be associated with indications of autoimmunity in humans
include chlordane/heptachlor, pentachlorophenol, and formaldehyde/"

Other Possible
Immune Effects

• Some researchers hypothesize that several controversial and poorly understood syn
dromes, including Multiple Chemical Sensitivity Syndrome, Chronic Fatigue Syndrome,
and Gulf War Syndrome, may be due to an immunotoxic response to pesticides and
other chemicals. Testing of immunologic parameters in these individuals yields conflict
ing results.21,22,23 24 At present, the etiology of these syndromes is unknown and the effects
on the immune system have not been established.

Table 8-1: Immunotoxicity of Pesticides
Pesticide
Organophosphates
Dichlorvos

Immune Effect
Inhibits complement
Interferes with lymphocyte DNA repair
Suppresses serum antibody titers to 5. typhi

Malathion

Stimulates macrophage respirator)' burst and phagocytosis
Suppresses humoral immunity

Parathion

Decreases resistance to viral and bacterial infection
Decreases T-cell proliferation
Delays antibody production

Chlorpyrifos

Increases CD26 cells, autoimmunity, and antibiotic sensitivity

Carbamates
Carbaryl
Carbofuran
Aldicarb

Decreases macrophage cytotoxicity
Inhibits T-cell activation to mitogen (worse with multiple low doses)
Decreases CD8 cells
Increases response to Candida antigen
Increases total lymphocytes'
*

Pentachlorophenol

Reduces humoral response
Decreases IL-2 production
Decreases CD4 cells
Increases immature leukocytes
Increases chronic cutaneous inflammation

Mecam sodium

Increases complement activity
Decreases NK cell activity

Organochlorines
Chlordane
Hcptachlor

Produces abnormal B- and T-cell subsets
Decreases mitogen response
Decreases antibody-dependent cytotoxicity
Increases autoantibody production
Delays macrophage activation

Aldrin
Dieldrin

Decreases resistance to viral infection suppress macrophage activity

Lindane
Benzene hexachloride

Decreases macrophage activation
Decreases resistance to giardia

Tributyl tin oxide

Decreases ability to resist bacterial and parasitic infection
Creates immune dysfunction at low dose levels4

Source: 1 VcxciJ. B . Blakley. I*. Brousseau, and M. Fournier. Immunoioxicicv ol pcMicides: A review, Toxicol bul lllib 15
(1999): 119-32. Notes: </’!’. Vi.il. B. Nicholas, and J. Descotes, Clinic.il iinmunoioxicity ol pesticides./ Toxicol Em- Hlth 48
(1996): 21 5 -29. b I’ A Botham. Are pesticides imniiinotoxic? zL/irnr Dru$ React Acute Rouon Ret 9 (1990): 91 - 101.

India - Pesticides and Health Meeting, October, 2002

42

HIDDEN DIMENSIONS OF DAMAGE
Pesticides and Health
MONICA MOORE

the idea that pesticides are dancerous is not controversial. After all, pesticides are cre

ated and released into the environment in order to kill organisms considered pests, be they insects,
weeds, bacteria, fish, snails, birds, rodents, or other forms of life. Yet most people do not realize
just how dangerous many pesticides are, either individually or in combination with one another,
or how far beyond their intended targets the harmful effects of pesticides actually reach. Ulti
mately, pesticides affect all members of an ecosystem, from the tiniest invertebrates to humans and
other large animals living at the top of their food chains.

A Ithough the true extent of pesticide-related damage has never been
-LJL (and may never be) fully quantified, enough is known to indicate

that these chemicals are very costly to the health of present and future
generations. The long list of known and suspected health problems linked

to pesticides grows steadily as new scientific discoveries reveal more of the

intricate systems in and around us that influence our health and develop
ment from the moment of conception until we die. Numerous studies

document disturbing levels of pesticide poisonings and other damage in
wealthy as well as poor countries, and knowledgeable sources agree that

these documented cases represent only a fraction of the actual total. And

of course human poisonings are only the beginning of a much larger story
of poisonings.

The fact that spreading billions of pounds of toxic pesticides throughout the
environment each year results in extensive harm should not be surprising to

policy makers, growers, or the general public. Yet somehow it remains not
just surprising, but eternally so. This never-ending lack of awareness of the

true scale of damage keeps people from challenging assumptions that societies
benefit more than they lose from continuing their dependence on pesticides.

Meanwhile, the true dimensions of pesticide damage to human health and the

environment remain among the best kept, least acted on secrets of agricul
tural, public health, development, and regulatory authorities around the globe.

India - Pesticides and Health Meeting, October, 2002

43

This article considers the extent of pesticide-caused damage to human health.

Because we humans are. an integral part of the environment, environmental
health impacts arc an important part of this discussion. Assessing pesticide.

damage requires pulling together information of many different types from

many sources, including acute and chronic effects of different kinds of pesti
cides; fate and transport of pesticides in the environment; pesticide poisonings

statistics: and information on pesticide use, sales, and markets. Some of this
information is reasonably easy to find, if you know where to look for it. Other

pieces of the puzzle exist only as educated guesses or closely guarded com
mercial secrets that require determined efforts, dumb luck, huge sums of

money, or all of the above to bring to light.

I nderstanding the true dimensions of pesticide health effects also requires
the eoiisidcration of factors that shield pesticide damage from public scrutiny

and outrage. For example, how is it that so many people have no idea either
of the scale of pesticide use in conventional agriculture or of the extent of

public health problems caused by these chemicals? Why is the public so

unaware of the unavoidable exposures to pesticides they endure daily through

their food, water, air, workplaces, and living environments? Most disturb
ingly why is agricultural reliance on pesticides growing despite often heroic
efforts of ecologically minded fanners to meet consumers' preferences for
organically produced food and libers?
Addressing these questions means examining both the biological mechanisms

of pesticide poisonings and pest resistance, and the mechanisms of powet

that operate, in corporate boardrooms and national Capitols. This means
looking directly al the. economic, social, and cultural contexts that grant

official invisibility to epidemic levels of poisonings and other forms of pesti
cide damages. Seen from this perspective, pesticides can be important
teachers that help us see interconnections among seemingly distant people,

places, and ecological communities. But insights into interconnections with
out actions to reduce pesticide use and promote safer, ecologically based

alternatives will not prevent further damage. Unfortunately, the lesson that
pesticides should be teaching us — that an ounce of prevention is much

better than a pound of cure, especially when the damage is avoidable and
no cure exists — has yet to be learned. For this reason, exposing the hidden

dimensions of pesticide damage remains an urgent public and environmen

tal health priority and a continuing challenge for the sustainable agriculture

movement.

HOW PESTICIDES DAMAGE HUMAN HEALTH
Pesticides can affect human health through acute (short-term) effects,
chronic (long-term) effects, or both. Chronic health effects can be delayed

erects from an individual exposure or the result of repeated low-level expo

India - Pesticides and Health Meeting, October, 2002

44

sures, whose impacts build up over time. Most pesticides have acute toxic
effects: many also present serious chronic hazards. Pesticide exposures can

also worsen existing illnesses and medical conditions, including asthma and

other respiratory illness, liver and kidney disease, and many others.
Acute Pesticide Poisoning. Symptoms of acute pesticide poisonings may

be local, causing irritation or damage to the skin or eyes. Some pesticides

can cause allergic reactions, another type of acute effect. Acutely toxic pesti
cides can also affect the body systemically, causing problems as they begin
moving through the blood. Many pesticides generate both local and systemic

effects. Specific symptoms vary according to the type of pesticide and also

within tvpes. The following section describes a range of acute poisoning
symptoms for several major types of pesticides, illustrating some of the
main wavs that pesticides affect human health.

Nerve Poison Pesticides. Two closely related types of nerve poison pesti

cides, the organophosphates and the methyl carbamates, are responsible for

most acute pesticide poisonings and deaths in the United States and world
wide. Both of these compounds kill insect pests by stopping a critical nerve

impulse-transmitting enzyme, from functioning normally. Unfortunately,
they block the same enzymes in the bodies of non-targcl insects, birds, fish,

reptiles, mollusks, amphibians, and mammals, including people. Mild sys
temic poisoning symptoms produced by these pesticides include blurry' vision,

headache, dizziness, fatigue, diarrhea, nausea and vomiting, heavy sweating,
and muscle or abdominal pain. As the level of poisoning increases, a victim’s

pupils shrink and he or she experiences difficulty walking, talking, and con
centrating. Twitching muscles and generalized weakness arc also symptoms.
Signs of severe poisoning include pinpoint pupils, convulsions, unconscious

ness, difficulty breathing, coma, and death. Organophosphate and carbamate
pesticides are widely produced and used throughout the world.

Organochlorine Pesticides. This category includes DDT, the world’s most
notorious pesticide, along with other less famous compounds. Organochlorincs

affect the brain and increase the sensitivity of neurons. While better known
for their chronic effects, many organochlorincs arc highly acutely toxic as

well. Convulsions are the classic acute poisoning symptom for this category,

India - Pesticides and Health Meeting, October, 2002

45

and may or mav not be accompanied by other symptoms, including head
ache, dizziness, nausea, vomiting, tremors, lack of coordination, and mental

confusion. Organochlorines can also cause local irritant effects, including
allergic reactions. Although some older organochlorine pesticides have been
widely banned, use of others remains common in the United States and

throughout the world.

Pyrethrins and Synthetic Pyrethroids. Pyrethrins are naturally occur
ring compounds derived from chrysanthemum flowers, and pyrethroids are

their synthetically manufactured chemical cousins. These compounds also

affect the brain and nervous system, although differently than do the two
pesticide types mentioned above. Acute poisoning symptoms produced by
these pesticides include local skin irritation, multiple allergic reactions,

dizziness, tremors, irritability to sound or touch, headache, vomiting, and
diarrhea. Because this class of insecticide tends to break down sooner in (he
environment than do many organochlorines, they are often substituted for

them, and are used widely in agriculture, as well as in homes and gardens.
Dipyridyl Pesticides. This category' includes the herbicides paraquat
and diquat, highly toxic compounds responsible for many acute poisonings
in the United States and internationally. These pesticides are very strong

irritants that can severely damage the skin, eyes, mouth, nose, and throat,

including causing blindness and fingernail loss. They destroy lung tissue
and cause failure of the kidneys, liver, and other organs. Symptoms of

poisoning by these pesticides include pain, vomiting, diarrhea, headache,

nosebleeds, loss of appetite, and death. Paraquat in particular is in wide

use throughout the world.
Chlorophenoxy Herbicides. This category of herbicides includes the wellknown weed killer 2,4-D and also 2,4,5-T, an ingredient of the Vietnam

War-era defoliant known as Agent Orange. Products containing 2,4-D are

big sellers in both agricultural and over-the-counter home and garden prod
ucts. While the long-term health effects of phenoxy herbicides are usually

considered more serious, acute poisoning symptoms can include skin irrita
tion, headache, nausea, vomiting, low fever, mental confusion, abdominal
pain, and temporary changes in heartbeat.
“Inert” Pesticide Ingredients. The already daunting task of evaluating

pesticide harm is made much more difficult by the unidentified “inert”

India - Pesticides and Health Meeting, October, 2002

46

ingredients found in all formulated pesticide products. These falsely named
ingredients include solvents, emulsifiers, and other substances added to a

pesticide product to make it easier to blend or apply or for any other reason
not directly related to killing a target pest. So-called “inert” ingredients may
have serious negative health effects, and some are even used as pesticides

in other products. Although they often make up over 95 percent of the for
mulated product, the true identity of “inert” ingredients is classified as

“confidential business information” and kept secret from both product users
and the public. The result is that no one has any idea of what chemical

combinations they are being exposed to when they come in contact with

pesticides.

CHRONIC HEALTH IMPACTS
Many pesticides are known to cause chronic effects in people, laboratory

animals, and/or wildlife. Such effects include many types of cancers, neuro
logical effects, reproductive and developmental illness, and disruption of the
endocrine system. Whether subtle or drastic, the pesticide origins of these

long-term health impacts are more difficult to prove than are acute poison
ings. While not comprehensive, this section presents summary information

about several types of chronic pesticide health effects.
Pesticides and Cancer. Many pesticides used in agriculture and in homes,

gardens, buildings, and public spaces are linked to different kinds of cancers.
According to the Environmental Protection Agency (EPA), 1 12 currently

registered pesticides arc known, probable, or suspected carcinogens. Pesti
cides can increase cancer causation through several mechanisms, including

by promoting abnormal cell proliferation, directly altering DNA, or disrupt

ing the immune system. Evidence linking pesticides to cancer comes from
three major sources: human epidemiological investigations, studies performed
on laboratory animals, and cell-culture studies. The following examples

emphasize epidemiological studies:

• The agricultural and home-use weed killer 2,4-D has been associ

ated with malignant melanoma in several studies. One study in the
Journal of the American Medical Association found that farmers
who mixed or applied 2,4-D more than 20 days per year had a
six times higher risk of non-Hodgkins lymphoma.

• Overall incidence of childhood leukemia in the United States

increased by 27 percent between 1973 and 1990. One National
Cancer Institute study found that in homes where pesticides were

used even just once a week, childrens risk of leukemia increased
400 percent. Other studies show that children whose fathers work
in jobs that expose them to pesticides have a threefold increased

risk of leukemia.
• Use of the pesticide lindane has been linked with aplastic anemia.

India - Pesticides and Health Meeting, October, 2002

47

One studv found that use of lindane shampoos to treat head lice

is associated with higher incidence of aplastic anemia in children.

Lindane has also been linked with lymphoma and breast cancer

in adults.
• Childhood brain cancer has increased by .33 percent in the past
20 years; risks of childhood brain cancer were found to be elevated

two- to sixfold in homes where pesticides arc used. One study in
Environmental Health Perspectives found brain cancer rates to be

five times higher in homes where “no-pest" strips were used and
six times higher in homes where pets wore flea collars.

Neurological and Behavioral Effects of Pesticides. As mentioned, pesti

cides that affect the nervous system cause more acute poisoning cases than

any other pesticide category'. But these pesticides also have serious long-term
effects on both the central and the peripheral nervous systems. Many years

after the fact, large numbers of people who have suffered serious acute organophospate poisoning have significantly impaired hearing, vision, intelligence,

coordination, reaction time, memory, and reasoning. Cognitive symptoms of

chronic damage, to the nervous system include personality changes, anxiety,
irritability, and depression. A growing body of evidence indicates that Park

inson's disease may be linked to exposures to certain pesticides and pesticide

classes, among other environmental factors. Specific chemicals implicated in
this particular type of damage include the herbicide paraquat, the organo
phosphates, dieldrin (an organochlorine), and the fungicides maneb and

mancozeb. Other herbicides and insecticides also appear to be associated with
development of Parkinson’s disease. Several fumigants, including methyl
bromide, Tclone, and sulfuryl floride, are linked with a range of behavioral

and cognitive effects. As they are with other health effects, children arc par

ticularly vulnerable to chronic neurotoxins, and exposures during key periods
of brain growth can result in permanent effects on the structure and func
tion of their brains.

Reproductive and Developmental Effects. Pesticides can damage men’s
and women’s fertility by affecting their reproductive organs directly or indi

rectly, or by disrupting the normal functioning of their hormones. Fertility

can be impaired by occupational exposure to pesticides, as indicated by
increased time-to-pregnancy documented in spouses of farmers and agricul

tural workers and other types of studies in North America and Europe. It
may even be destroyed forever, as hundreds of men exposed to the pesticide
DBCP in the United States, Central America, and Africa have learned to

their deep and lasting sorrow. Widely used pesticides that are known to be
reproductive toxins in men, women, or both include the herbicides 2,4-D
and chlorosulfuron, the rodenticide 1080, the insecticides oxydemeton-

methyl and hydramethylnon, and the fungicides benomyl, myclobutanil,
and triadimefon.

India - Pesticides and Health Meeting, October, 2002

48

Most pesticides can cross the placenta and enter the body of a fetus. Develop
mental effects of pesticides can include spontaneous abortion, stillbirth, birth
defects, low birth weight and smaller infants, and functional impairment.

Many studies show that mothers’ occupational exposure to pesticides increases

risks of congenital birth defects. Others demonstrate that increases in a
variety of birth defects are associated with fathers’ employment as pesticide
applicators. The timing of exposure can be critical: the periods of fetal devel
opment and early childhood, in which the body’s organ systems are formed,
are especially vulnerable times for this type of health effect

Endocrine Disrupting Pesticides. Many pesticides can disrupt normal
functioning of the endocrine system in people and other animals. Such pest

icides may strengthen or weaken, imitate or block the effect of naturally

occurring hormones, leading in turn to serious problems, including cancer,
reproductive illness, or developmental effects. Most pesticides have not yet

been studied for their potential to affect hormones or otherwise disrupt the

endocrine system, and the tests capable of detecting such effects are still

being developed. Pesticides that have been identified as having this type of
effect so far include the popidar weed killers atrazine, alachlor, cyanazine,

and simizine; the insecticides aldicarb, carbaryl, lindane, endosulfan, res-

methrin, and other synthetic pyrethroids; the fungicides vinclozalin, metiram,
benomyl, mancozeb, and maneb; and the wood preservative pcntachloro-

phcnol. Many pesticides that persist for long periods in the environment arc

known to be endocrine disruptors, including DDT, aldrin, endrin, dieldrin,
chlordane, heptachlor, and other organochlorine insecticides.

PESTICIDE POISONING AND CHILDREN
Children are more susceptible to the acute and chronic heath effects of pes
ticides than adults are for several reasons. Because their bodies and organs
arc still growing and developing, children’s bodies do not process these poi
sons as well as those of adults. Children are also more exposed to pesticides.

Pound for pound, children cat more food, drink more liquids and breathe.
in more air than adults, so they take, in more pesticides per unit of body

weight than adults do. Because they are smaller, children’s bodies have a
relatively greater surface area in contact with the world then adults do, and

most pesticide exposures occur through the skin. Children also have more

contact with pesticides and other environmental toxins because they crawl

around on all kinds of surfaces, often put their hands in their mouths, hug

pets more frequently, and generally are in more intimate physical contact
w'idt the world than are adults. Children in agricultural settings face partic

ularly liigh risks. Children ten years and older may work legally on farms,
and younger children of farmworkers often join older family members in
the fields out of economic necessity. As a result, farm kids often have much
higher exposures to pesticides than other children do.

India - Pesticides and Health Meeting, October, 2002

49

There is some evidence that acute poisoning of children tends to be noticed

and treated more readily than occupationally related poisonings, especially
when caused by swallowing a pesticide, a spill, or some other specific event

in the home. Reports from the national network of Poison Control Centers
show that more than 50 percent of pesticide poisoning emergencies reported

in the United States each year involve children less than six years old.
Poisonings that occur away from home are less likely to make it into the

official record.

U.S. AND GLOBAL POISONING ESTIMATES
Although acute pesticide health effects, which occur within moments or days
of exposure, arc more easily identified than chronic poisonings, most acute

agricultural poisonings go unrecognized or unreported. There are many rea
sons for this. Many symptoms of acute poisonings (e.g., headache, nausea,

dizziness, diarrhea, vomiting, and skin rashes) are also associated with other
common conditions, making accurate diagnoses difficult even when health
care professionals arc informed enough to consider pesticide poisoning as a

possibility. The fact that most of the world’s agricultural workers have no
access to health care obviously contributes to a lack of reliable, data on agri
culture pesticide poisonings. Furthermore, many farmworkers fear being

fired or getting labeled as troublemakers if they seek medical help or take

time off work to recover when poisoned bv pesticides on the job.

\\ here reliable numbers are unavailable, educated guesses become increasingly
important. In the United States, government estimates indicate more than
20,000 farmworkers out of an estimated population of 5 million workers in
this country suffer acute pesticide poisonings annually. Yet authorities also
acknowledge that their estimates are based on very little knowledge regard

ing the extent of actual pesticide exposures and resulting health effects. In
terms of chronic impacts, no serious effort to develop estimates of annual

cases has been attempted.
At the global level, the World Health Organization published an estimate
in 1990 that 3 million severe acute pesticide, poisonings occur in developing

countries each year, including some 220,000 fatalities. This figure is still widely

cited today, although another study by the same expert indicates it is a seri
ous underestimation. Based on hospital records in four Asian countries, this

expert concluded that between 2 and 7 percent of the. agricultural labor force
in developing countries is poisoned annually, which would revise his previous

estimate upwards to well over 25 million poisoning cases each year in devel
oping countries alone.
Another more in-depth field study of 228 farmers and pesticide sprayers in
Indonesia found that 21 percent of all pesticide applications over the study

India - Pesticides and Health Meeting, October, 2002

50

season resulted in symptoms that strongly indicated organophosphate pes

ticide poisoning. Asked if they remembered ever having been poisoned by

pesticides, 9 percent of the farmers reported at least one incident serious

enough that they sought medical attention. The study noted that the farmers
"tended to accept this level of illness as part of the work of farming.” Most

of the farmers also reported pesticide storage, disposal, and other practices

that put their family members at risk.
Translating these figures into a fictional nonagricultural setting helps to

highlight the social and economic assumptions that allow such astounding

rates of occupational hazard to persist without consequences to the suppliers
of the injurious product or adoption and enforcement of regulatory measures
sufficient to reduce the rate of injury. Consider the following: word proces

sors are basic tools for many firms and industries, and millions of people

rely on them for personal uses as well. Now imagine that 21 percent of the
time you, or anyone else, used a word processor at work you would receive

an electrical shock. That’s on average, so it wouldn’t be every time, and
the shock wouldn’t be enough to kill you — at least not most of the time.
I hen imagine that nearly 10 percent of the people using word processors

got shocked severely enough to require medical treatment at some point in

their careers and that their families were al risk from the word processors
that they kept al home.

Does it seem reasonable for you to be forced to accept being shocked
repeatedly as “part of the work of word processing”? Or that the computer

company whose products kept shocking you should be allowed to stay in
business?

THE BENEFITS OF CHRONIC UNCERTAINTY
In the early stages of learning about pesticide dangers, many people get
frightened or overwhelmed and don’t want to know more. This is easily

understandable. Professionals deeply familiar with pesticide health effects

also may numb themselves to the pain and suffering they encounter in

laboratory animals, wildlife, and men, women, and children exposed to

pesticides in order to stay focused on the task at hand. But overwhelmed
individuals and psychic numbing among experts should not prevent public

acknowledgement of massive, unnecessary proliferation of dangerous pesti
cides into the air, water, food, and public spaces we all share.

Chronic pesticide poisonings provide an instructive case in point in con
sidering factors that blunt public awareness of pesticide damages. No one
disputes that such poisonings occur, but the extent, frequency, significance,

and implications of these poisonings are endlessly controversial. From a
public health and welfare perspective, acting to reduce use of hazardous

India - Pesticides and Health Meeting, October, 2002

51

chemicals, getting them off the market, and replacing them with less or
non-hazardous alternatives is the obvious and most effective way to address

individually the damage — impossible to prove hut collectively very real —
caused by chronic pesticide poisonings. The same course of action Hows

easily from an environmental frame of reference.
But somehow, this is not what happens. Instead, industry scientists, regula

tors, pesticide users, and public interest groups all agree that chronic
pesticides are health hazards, but disagree on how hazardous and what

to do about it. This is where you start to see the qualifying phrases stack

up in both industry and government regulatory positions: yes, they arc
hazardous .

but they can be applied in a safe and harmless manner when

applied according to label instructions. But our research indicates that (his

product presents no significant hazard to the public. But by controlling the

exposure, we can control the risk, and the exposures arc at safe levels. But
alternatives are not available or cost effective. But we don’t know enough

about the extent of harm to justify taking "extreme measures” (code for
removing a product from (he market). But the harm done (to many) is

outweighed b\ the economic benefits (to increasingly few) of using the
pesticide.

Driven by such assertions, which are rarely if ever subject to open scrutiny.
scarce public funds and the greater resources of industry arc spent docu
menting that long latency periods, confounding exposures, and other factors

make it difficult to estimate individual and aggregate exposures or quantify

risks from chronic pesticides. This is true. Yet such “insights” do little to
prevent further damage or develop alternatives to more pesticide, use. In this

intentionally endless quest for greater knowledge, new studies arc designed

to better understand a pesticide’s mode of action, establish clearer causal
relationships, identify so-called “safe” exposure levels, quantify the extent
of harm more precisely, etc. Meanwhile, serious measures to reduce and

eliminate the source of harm never make it onto the list. As the wheels of
investigation grind on, uncertainty is “resolved” in favor of pesticide manu
facturers and users, who continue to develop their plans and project future

profits based on continuing use of chronic poisons.

PESTICIDES IN THE ENVIRONMENT
Ultimately, most pesticides in the environment degrade upon exposure to air,
sunlight, and water, or as they are broken down within plants, animals, and

microorganisms. How long this takes and how much damage is done in the.
meantime varies greatly from case to case, however. Different types of pesti
cides break down differently, and while the chemical breakdown products of

these processes are usually less harmful than the original material, some are

even more dangerous than the parent compound, as in the cases of the insec
ticides aldicarb, malathion, and ethyl parathion, and the herbicide atrazine.

India - Pesticides and Health Meeting, October, 2002

52

How pesticides break down in the environment is also influenced strongly
by temperature, moisture, presence or absence of other chemicals, and many
other factors. But predicting the environmental conditions of where a pesti
cide may end up is no simple matter. Pesticides are highly mobile and can

travel vast distances. Once released into the environment, they are like genies

let out of their bottles — impossible to put back in. Pesticides applied by
aircraft can drift many miles from their supposed targets, evaporating in and

out of a solid state within air currents, only to land, revolatilizc, and set off
again. Tiny pesticide droplets suspended in fog can be deposited onto birds,
wildlife, leaves, and any other living or nonliving surface touched bv the mist.
Ram, storms, and irrigation ditches routinely sweep huge loads of pesticides
into streams, lakes, wells, and rivers, with often devastating effects on fish.

amphibians, and aquatic invertebrates. Pesticides cross the seas on prevailing
currents to contaminate Arctic and Antarctic environments, native peoples,

and the animals they depend on for sustenance, thousands of miles from
the original application. They also move through aquifers and groundwater,

to the horror of those who depend on these sources for their drinking water.
Another way pesticides travel is through food chains. In this mode of trans
port, pesticides that are taken up within smaller organisms and not broken
down or excreted remain stored there until the organisms are eaten by
another creature, whose body burden of pesticides increases accordingly.

The same thing happens again when that creature becomes a meal for

another predator, and so on and so on. These pesticide body burdens travel
with their '’hosts,” and migratory animals such as marine mammals, birds,
and fish often carry pesticides over long distances before being eaten by

predators.
The continuing process of adding and passing on new loads of pesticides and
other toxins through the food chain is called bioaccumulation, and it is the

reason that top predators like birds, sharks, some whales, bears, and people
carry high concentrations of certain poisons in their bodies. Breast-feeding
infants of mammalian predators, including human babies, arc at the pinna
cle of the food chain, since large amounts of bioaccumulating chemicals

collect in breast milk and are passed into the infants’ bodies as they feed.

India - Pesticides and Health Meeting, October, 2002

53

PERSISTENT ORGANIC POLLUTANTS
One particular type of pesticide combines several characteristics that make

it a special threat to life. Persistent Organic Pollutant pesticides (POPs) —
such as DDT — are linked with serious chronic health effects; they last for

long periods without breaking down; they travel far and wide in the envi

ronment; and they build up to ever higher and more harmful levels in the

food chain. Since their widespread production and use began, less than 60
years ago, POPs pesticides and other POPs chemicals have moved through
out the global environment to threaten human health and ecosystems around
the world. All living organisms on earth now carry measurable levels of
POPs in their tissues, and evidence that exposure to even tiny amounts of
POPs during critical periods of development can cause irreversible damage

is strong and increasing. Effects of such exposures can take years to appear,
sometimes appearing first in the offspring of exposed parents. In this tragic
legacy of damage, children can end up suffering from a parent’s exposure

to a POPs chemical that occurred decades before they were born.

In an encouraging example of coordinated action to reduce chemical hazards,
nations around the world recently recognized and began addressing the extra
ordinary threat of POPs chemicals with an international treaty. The new
POPs treaty mandates global phase-outs of production and use of POPs

chemicals. This type of global approach to eliminating chemical damages
is both inspiring and much too rare.

WHAT LIES BENEATH
The fact that pesticides continue to be promoted and accepted as the most

efficient and desirable form of pest management is a symptom of a different

kind of chronic poisoning. Driven by economic policies that put short-term
profits and agricultural exports first, and address health and social concerns

only later, if at all, extractive, chemical-intensive industrial agricultural is

gaining ground despite our greenest intentions and desires.
The approximately S35-billion-a-year pesticide, business lies at the center of
these expansive lies. Dominated by ten corporate giants based in the United

India - Pesticides and Health Meeting, October, 2002

54

States atid Western Europe that control nearly 90 percent of the global pes

ticide market, this industry is directly (but not solely) responsible for the

release of several billion pounds of pesticides into the environment ever)'
year. And that’s just one piece of the agro-industrial complex. Increasing use
of pesticides and other harmful agrochemicals, despite their negative health

and environmental impacts and the sustained growth of the organic sector,
underscores the power of these industries to thwart attempts toward biologi
cally based pest management and ecological agriculture. Continuing public
confusion regarding the true extent of pesticide damages, weak national

regulatory and enforcement systems, and a pervasive lack of public invest
ment in already existing and promising new alternative pest management

approaches are additional symptoms of these industries’ poisonous influence.

Ironically, many people believe that agriculture is gradually giving up its
dependence on pesticides. Agrochemical and related industries’ investments
in marketing, public relations, and political campaigns help explain this

misperception. For example, most people mistakenly believe that when pes
ticide producers proclaim their environmental commitments, this means
they are reducing production of environmentally harmful materials. Many

people also believe that because organic agriculture is making such rapid
gains, levels of pesticide use must be falling as well — and national regula

tory authorities neither collect nor publish pesticide-use data showing that
exactly the opposite is true. People also assume that pesticides on the market

must be safe, or pesticide regulatory agencies would not allow manufac
turers to sell them, reflecting a widely held but dangerously inaccurate.
understanding of these agencies’ role. And of course psychic numbing and

feelings of being overwhelmed also help shield corporations and govern
ments from scrutiny.

REGAINING GROUND
Acknowledging such barriers and the power of corporate interests to main

tain them in no way implies that our societies can never awaken from the
health and environmental nightmares of conventional industrial extractive.
agriculture. Rather, it points directly to the need for multiple and reinforc

ing strategies of public education, analysis, and actions over time. To be
effective, these strategies must facilitate the development of new leadership

and other resources needed to transform agricultural policy and practice.

They must also address the social contexts in which massive unnecessary
pesticide damages arc considered “normal” and acceptable and in which

companies responsible for these damages are rewarded for inflicting them.
Changing how our societies deal with the uncertainty that surrounds the

hidden dimensions of pesticide damage is an important element of stem
ming the rising toxic tide of pesticides. When protecting people and the

environment from pesticide harm, it is not reasonable to require iron-clad

India - Pesticides and Health Meeting, October, 2002

55

scientific proof or multi-stakeholder consensus that a pesticide causes a

certain number of deaths or percentage of cancers or other types of health
effects before taking action to reduce harm Even where our knowledge of
the mechanisms and extent of damage is not complete, awareness of harm

should automatically trigger actions to protect the health of our families,
communities, and environment.

Protecting health in highly contaminated and otherwise compromised

environments is extremely difficult, and mitigating and healing damages
to health from such contamination is generally prohibitively expensive and

often impossible. That is why preventing the release of harmfid chemicals
and other forms of environmental contamination is the most effective,
economical, and morally justifiable approach to safeguarding people and

ccosvstems from costly and often irreversible damages, such as those
described here. Acceptance of this straightforward approach is guiding

efforts toward cleaner production in several industries and gaining credibil
ity in some nations, most notably in Scandinavia. Although increasing global
pesticide sales and marketing of new genetically engineered pesticides show

that the conventional agriculture industry has yet to embrace this precau
tionary approach, those of us convinced of the wisdom of moving toward

cleaner production in agriculture have much to work with.

Knowing that we need to move toward an agriculture capable of supplying
the foods and libers we need without destroying people’s health, environments,
and cultures in the process helps us target our efforts. Since preventing pest
problems is essential to healthy and successful agriculture, for example, we

know we must figure out much better wavs to do this than reflexively using
pesticides. Similarly, preventing pesticide-related damage to health implies

rapid elimination of pesticides known or suspected to cause such damage.
This means we need effective mechanisms for targeting major uses of haz

ardous pesticides, removing those products from the market, and replacing
them with safer alternative approaches.

Fortunately, many proven alternative methods and products are available to
reduce our current massive dependence on pesticides, and more arc becoming

available with time. Where such alternatives already exist, we must move far

more quickly to implement them. Wherever they arc not available, we need
to move urgently to apply the human creativity, financial resources, and

other support to ensure they are developed and implemented as rapidly

as possible.
Meanwhile, the secrecy and misinformation surrounding the true scale of pes
ticide use in agriculture remain a huge obstacle to the development of safer
pest management alternatives. Think of the billions of pounds of pesticides

being released into the environment each year as straws being loaded onto
camels’ backs. We and our families, communities, and environment are the

India - Pesticides and Health Meeting, October, 2002

56

camels. and the burdens we bear arc packed for us by experts \\ ho swear
they are essential to keeping us fed and are otherwise not a problem — and

who make a commission on every straw wc carry.
All of us have the right to know what pesticides wc are exposed to intention
ally or unintentionally, and to be heard in decision-making processes that

affect whether or not these exposures continue. In addition to ensuring our
right to know, public reporting and disclosure of pesticide use is also crucial
to creating effective demands for safer alternatives. The same corporate

advertising expertise that helped create chemically dependent agriculture

now chums out messages telling us about the greening of agriculture. These
messages are all the more easily swallowed because they are partially true —
despite industrial agriculture’s stalling tactics and thanks to the ceaseless

efforts of a small but growing number of farmers leading the way to more
ecologically and socially beneficial agricultural systems.
Separating agricultural fact from profitable fantasies requires more informa

tion than the public is presently allowed access to. Using new information
technologies, it could be easy for any man, woman, or child to find out
whether the use of specific pesticides on specific crops in specific places is
going up. down, or staving the same in their county, state, and country.

Other questions that should be easily answered include whether public and
piivate funds dedicated to research and extension programs designed to

reduce pesticide use arc increasing, and where, to find detailed information

about farm ownership and the ecological and labor conditions under which
food and libers arc grown and processed Without constant public tracking

of these and other indicators of progress toward ecologically based agricul
tural production, all wc have is assurances from people whose words wc
know from experience cannot be trusted without independent verification.

/Is the use ofpesticides increases, so does the rate of breast cancel'.

According to the National Cancer Institute, 50 to 60 percent higher
levels of organochlorine pesticides are found in the breast tissue
of women with breast cancer than in the tissue of health y women.

Yet the cancer-establishment has actively denied the connection to
pesticides, no doubt due to its own involvement in the petrochemical
industry. No wonder that surgery is considered a remedyfor cancer,

while reducing pesticide use is not.

India - Pesticides and Health Meeting, October, 2002

57

I.

DDT AND OTHER
CHEMICALS USED IN
VECTOR MANAGEMENT
PROGRAMS

A Brief History
DDT (dichlorodiphenyltrichloroethane) is an
organochlorine insecticide used mainly to
control mosquito-bome malaria. DDT’s
insecticidal properties were discovered in the
1930s by Swiss chemist Paul Muller.
Considered harmless to mammals this odorless,
tasteless, white crystalline chemical was used
during the Second World War for crop
protection as well as protection of troops from
malaria and typhus. DDT’s characteristics of
insolubility in water, persistence, long half-life
of 10-35 years and high-contact toxicity made it
appear to be the ideal insecticide. As a
consequence, Muller was awarded the Nobel
Prize in 1948. Only a few years later, Swiss
scientists confirmed the connection between
unborn and functionally-impaired calves whose
mothers had been grazing on pastures that had
been sprayed with DDT. Previously, U.S.
agricultural researchers had linked similar
severe impairments tn calves whose mothers
had been eating feed salted with DDT for pest
control (EEM on POPs, Annex II). Still others
had found that young roosters treated with
DDT had severely underdeveloped testes and
failed to grow the normal combs and wattles
roosters use for social display (Colborn et al.,
1996).

Regardless of these effects, DDT’s efficacy and
low-production costs made it the most widely
used agricultural insecticide in the world from
1946 to 1972. Total world production of DDT
during this period has been estimated from 2.8
million tonnes to more than 3 million tonnes
(IEM on POPs, Annex II).

The effects of DDT on wildlife reproduction
and its residues appearing in food products that
had been sprayed with DDT became evident in
the 1960s. Long term studies showed that DDT
was found at alarming levels in many animal
species including fish, birds, and mammals.
Many birds such as peregrine falcons,
California condors, and bald eagles with high
levels of DDT in their bodies began producing
weak eggshells, which were crushed upon
incubation. The result was a decline in the bird
populations and a threat to their very
existence. These findings led to DDT use
restrictions and bans in the U.S., Canada, and
most European countries in the early 1970s.
DDT is now banned in 34 countries and
severely restricted in 34 (EEM on POPs, Annex

n).
Insecticides Currently in Use
The World Health Organization (WHO)
approves use of DDT in controlling malaria,
provided several conditions are met, including
limiting its use to indoor spraying, taking
appropriate safety precautions, and using
materials that meet WHO specifications. Four
major groups of insecticides are available for
indoor spraying: organochlorine chemicals
(DDT), organophosphates, carbamates, and the
synthetic pyrethroids (Table 1-1). The
undesirable effects of DDT are widely known;
they have driven the restrictions on DDT that
have occurred to date and are responsible for
DDT being targeted in international POPs
negotiations. The organophosphates and
carbamates are acutely toxic to humans, and
pose a high hazard in particular to those who
work with them (Herath, 1995). The synthetic
pyrethroids are not as toxic as the carbamates
or organophosphates, and are widely used as an
alternative to DDT or used to impregnate
bednets. Because most reports of wide-scale
applications of pesticides for vector control
involve DDT or the synthetic pyrethroids, the
discussion that follows focuses mainly on these
pesticides.

India - Pesticides and Health Meeting, October, 2002

58

Table 1-1: Vector-Control Insecticides and Their Known Health Effects
Health effects modified from Lars et al. (1996), WHO Environmental Health Criteria or Health Safety Guides,
EXTOXNET-Extension Toxicology Network, Co-operative Extension Offices of Cornell University, The University of
California, Michigan State University, and Oregon State University. (Listing adapted from Chavasse and Yap, 1997)

Insecticide

Type

Indoor

Bendiocarb

C

+

Propoxur

C

+

Very high acute toxicity;
suspect carcinogen,
mutagen

DDT

OC

+

Possible carcinogen

Chlorpyrifos

OP

+

Medium-high oral toxicity,
dermal and inhalation;
delayed neurotoxin;
sterility and impotence

Fenitrothion

OP

+

Moderate - high acute
toxicity

Malathion

OP

+

Medium-high acute
toxicity; suspect mutagen;
delayed neurotoxin

Bifenthrin

SP1

Cyfluthrin

SP2

Cypermethrin
(includes a)
Deltamethrin

Bednets

Toxicity to
Humans/Mammals
High acute toxicity

+

Very high acute toxicity;
suspect carcinogen,
mutagen

+

+

High acute toxicity

SP2

+

+

Moderate-high toxicity

SP2

+

+

High acute toxicity

X-cyhalothrin

SP2

+

+

Permethrin

SP1

+

+

Environmental Toxicity
Moderate-high toxicity to fish,
birds, crustaceans; neither
bioaccumulative nor persistent
Moderately persistent; very
high acute toxicity to birds,
fish, bees, crustaceans; low
bioaccumulation
Highly toxic to fish and aquatic
species, moderately toxic to
birds and mammalian species;
eggshell thinning in birds; very
persistent and bioaccumulative
Moderately persistent in soil;
high-very high acute toxicity to
birds, molluscs, crustaceans,
bees; long-term effects on
reproduction/growth of fish;
bioaccumulative in aquatic
organisms
Moderately bioaccumulative;
high toxicity to some birds;
high toxicity to crustaceans;
not persistent
Not persistent;
high toxicity to birds, fish
crustaceans; highly toxic to
bees, amphibians
Moderately persistent; very
high acute toxicity to fish,
crustaceans, aquatic
invertebrates
Moderately bioaccumulative;
highly toxic to fish,
crustaceans, and bees
Highly toxic to aquatic
invertebrates and fish

Moderately bioaccumulative;
highly toxic to fish,
crustaceans, and molluscs
Highly bioaccumulative; highly
toxic to fish and crustaceans
Highly toxic to aquatic
arthropods and fish

Key: C = carbamate; OC = Organochlorine; OP = Organophosphate; SP = Synthetic Pyrethroid (Type 1 or Type 2)

India - Pesticides and Health Meeting, October, 2002

59

Chemical Properties
DDT is available in several different forms:
aerosol, dustable powder, emulsifiable
concentrate, granules, and wettable powder.
Technical grade DDT is actually a mixture of
three isomers of DDT, including the p,p’-DDT
isomer (85%) with the o,p’-DDT and o,o’-DDT
isomers present in much lesser amounts
(ATSDR, 1994). The content of these isomers
is important because the o,p’(ortha-para)
isomer is said to be five to nine times less toxic
in tests with rats than the p,p’(para-para)
isomers. While DDT is highly resistant to
degradation, some microbes can degrade DDT
into a variety of metabolites. Among the more
important of these is DDE and TDE (DDD).
The latter is also manufactured as a commercial
product (IEM on POPs, Annex H).

Persistence and Transport
Characteristics
At present, most of the millions of tonnes of
DDT that have been produced in the past
continue to be transformed and redistributed
throughout the environment. DDT and its
metabolites have been detected in virtually ail
media throughout the world. An extremely
stable chemical compound, 50 per cent of the
DDT sprayed on a field can remain in the soil
10 to 35 years after its last application. For

example, an Oregon (U.S.) orchard still had 40
per cent of the original DDT used 20 years
later. DDD has also been shown to be even
more persistent in soils, sediments, and waters,
lasting 190 years and longer (LEM on POPs,
Annex D).
These compounds do not remain in the soil,
but are transported into the general
environment by the processes of volatilization,
through wind and water erosion. Although
more than 20 years have passed since the last
applications of DDT, soils in the southern U.S.
cotton belt are estimated to be volatilizing 110
tonnes of DDT and its metabolites annually
into the atmosphere. These small particles are
transported long distances on air currents, and
are returned to the land surface by
precipitation.

DDT in the Arctic Food Web
There has been very little local use of DDT in
the high arctic, therefore the presence of DDT
in arctic biota is indicative of the global or
hemispherical transportation of this
compound. DDT has been found at various
concentrations in all trophic levels of the arctic
food chain. Table 1-2 is a summary of DDT
concentrations found in the lower trophic
levels of the arctic marine food web. Table 1-3
shows concentrations of DDT in the blubber
of arctic mammals.

Table 1-2: DDT Concentrations (ppb lipid wt.) in Marine Biota in Various Locations in High Arctic
(adapted from Canadian Arctic Contaminants Assessment Report, D1AND)
Biota

Region

Total DDT

Epontic Particles

Ice Island
Barrow Strait
ice Island
Barrow Strait

20-70
150-360
8-150
2-20

Ice Island
Barrow Strait
Arctic Ocean
Barrow Strait

<350
3-60
2,200-25,900
15-1,590

Zooplankton
Amphipods
Pelagic
Pelagic
Benthic
Benthic

India - Pesticides and Health Meeting, October, 2002

60

Biota

Region

Total DDT

Lancaster Sound
Barrow Strait
Cumberland Sound
Beaufort Sea
Wellington Bay
Cambridge Bay
Hall Beech

66-120
15-255
626-1,044
659-1,1251
93
1,225
135

Sanikiluaq
Manitounuk Sound

34
13

Fish

Arctic Cod
Turbot
Four-hom Sculpin

Bivalves
Clams
Septentrion sp

Table 1-3: Mean Concentrations (ppb wet wt.) of Total DDT in Blubber of Arctic Mammals
(adapted from Canadian Arctic Contaminants Assessment Report, DIAND)
Species

Female

Male

Ringed Seal
Harp Seal
Beluga Whale
Narwhal
Walrus
Adult Polar Bear (Bemhoft et al., 1997)

473
486
1,940
NA
744
372

959
NA
4,974
3,232
1,744
340

Water runoff provides another mode of
transportation. DDT sticks to soil particles by
the process of adsorption. These panicles are
transported to lakes and rivers and are the
principal route by which lakes and streams
become contaminated. In an experimental plot
of cotton, runoff waters transported 2.8 per
cent of the DDT applied in six months.

Under tropical conditions, residues continue to
be detected in major water bodies in the
Philippines despite DDT’s restricted-use status.
Fish, as well as duck eggs, from lake areas also
show residues (DEM on.POPs, Annex H).
While DDT will evaporate and photo-oxidize
from soil surfaces to a certain degree, it is a
robust and long-lived chemical compound.
Even when its use is banned globally, DDT
and its various metabolites will continue to
travel in the winds and waters and accumulate
in the bodies of the world’s organisms for
decades to come.

Bioaccumulation in Organisms
Bioaccumulation Potential
Bioaccumulation reflects the relationship
between how much is taken into an organism
by exposure versus how much is lost through
metabolism and excretion. The key in pesticide
exposure scenarios is whether the rates of
metabolism and excretion remove enough of
the substance to prevent a gradual increase in
the organism. If the rates of metabolism and
excretion are not rapid, an organism will
accumulate ever-increasing concentrations,
adding to the concern about chronic, low-dose
exposures.
Chemicals that are water soluble are more
easily excreted, as well as more easily mobilized
to sites responsible for metabolism of the
compound. On the other hand, a chemical
with high solubility in lipids (fats, oils, or
waxes) has bioaccumulation potential. Such
lipophilic chemicals easily move into cells and

India - Pesticides and Health Meeting, October, 2002

61

■are sequestered in fat where they can become
more persistent. DDE is an example of a
lipophilic chemical that resists enzymatic
degradation and, therefore, rapidly
bioaccumulates. DDT is also lipophilic,
however, it is more readily degraded and
excreted from the body.

America’s Great Lakes basin despite
restrictions on its use in the United States and
Canada. It appears that much of the DDT
currently being deposited in the basin is
atmospherically transported from Central and
South America.
Even though the concentration of DDT in
plankton is 1/100 part per million, the flesh ot
a fish-eating bird in the same lake system may
contain 630 times that concentration (Colborn
etal., 1990).

Bioaccumulation in the Great Lakes Food
Web
DDT continues to be deposited in North

Table 1-4: Bioaccumulation of DDT in Lake Ontario Food Web (Colborn et al, 1990)
Species

Concentration (ppm wet weight)

Plankton
Mysis
Pontoporeia
Sculpin
Smelt
Lake Trout
Herring Gull

0.01
0.03
0.10
0.40
0.40
1.10
6.30

Synthetic pyrethroids are also lipophilic
though they are more like the isomers of DDT
in that they can be metabolized to more water
soluble forms that can then be excreted.
Furthermore, the sites where they can be
metabolized are not limited to the liver and
therefore, metabolism is much quicker. For
example, the elimination half-life for
deltamethrin in plasma of the rat is 33 hours
(Anadon etal., 1996) with almost complete
elimination from the body by day 4 (Ruzo et
al., 1978). Cypermethrin is more resistant to
elimination; 90% is lost in the first four days,
however, total elimination may take as long as
17 to 26 days (WHO Working Group, 1992).
Synthetic pyrethroids (permethrin,
deltamethrin) are rapidly distributed in the
body (Anadon et al., 1991, 1996). The primary
sites of deposition are the central nervous and
peripheral nervous systems, which can have
concentrations of permethrin ranging from 1.5
to 7.5 times higher than those observed in
plasma. In another study, a single topical
application of deltamethrin (0.75%),

cypermethrin (10%), or cyhalothrin (4.5%) to
dairy cows was detectable in both the cows
blood and milk for 28 to 35 days (Bissacot et
al., 1997). In these situations, bioaccumulation
results in much lower peak concentrations
since the differences between exposure and
intake are not widely different from
metabolism and excretion. The concern would
be if the exposure is periodic, with a span
shorter than the rates of excretion. Chronic,
low-dose exposures may lead to slightly
increased concentrations in the body. There is
little known about the pharmacokinetics ol the
synthetic pyrethroids.

DDT Bioaccumulation in Humans
In surveys around the world of human blood,
fat tissue, and breast milk, DDT and its
metabolites are found in substantial quantities
(Thomas and Colborn, 1992; Jensen, 1990).
For example, Table 1-5 reviews concentrations
of two isomers that are known endocrine
disruptors. Since DDT is very lipophilic, it
accumulates in all fats, including the 3% fat

India - Pesticides and Health Meeting, October, 2002

62

found in breast milk (Rogan et al., 1986). The
quantity of DDT and DDE varies with the age
of the individuals with young individuals
having higher concentrations than older
individuals. This is probably the result of a
combination of a pesticide-rich food source

(breast milk) and a lower total body fat content
in the baby. As the baby matures, fat
accumulations increase the available pool
which in effect dilutes the DDT/DDE
enriched fetal fat reserve.

Table 1-5: Concentrations of o,p'-DDT or p,p'-DDE (endocrine-disrupting isomers of DDT) in
Breast Milk of Women (standardized to ppm fat)
Country
Canada
U.S.A, New York
Mexico, Veracruz
Mexico, Mexico-City
Germany
Spain, Madrid
Norway
United Kingdom
France
Slovakia
Yugoslavia,
Krk Island
Labin
Croatia
Nigeria
Nigeria, Benin
Kenya
New Guinea, Papua
Uganda
Zimbabwe, Kariba
Australia, Victoria
India
India
Jordan, Amman
Saudi Arabia
Turkey
Thailand, Bangkok
Vietnam

# Women

Year

497
7
43
50
150
51
20
193
20
50

1995
1985-87
1994-95
1994-95
1985-87
1991
1988
1989-91
1990-91
1994

33
20
50
10
35
68
41
143
39
60
60
25
15
115
104
3
7

1986-87
1986-87
1981-82
1987
1981-82
1983-85
1990
1992-93
1994
1995
1985-86
1988
1989-90
1995-96
1995-96
1985-87
1985-87

o,p'DDT
0.003
0.27
0.14
-

-

0.06

1.43

0.23
-

p,p'DDE
0.22
0.54
5.02
0.59
0.75
0.60
0.97
0.40
2.18
1.20

*
1.10
*0.55
1.90
0.99
1.1
1.73
0.45
2.35
13.60
0.96
7.28
2.00
2.04
2.01
3.61
6.70

X
DDT

6.44
0.93
0.66

-

-

0.89

25.26

3.31
0.27
2.36

Citation
Newsome et al., 1995
Schecter et al., 1989
Waliszewski et al., 1996
Torres-Arreola et al., 1998
Schecter et al., 1989
Hernandez et al., 1993
Skaare et al., 1988
Dwarka et al., 1995
Bordet et al., 1993
Prachar et al., 1996
Krauthacker, 1991
Krauthacker, 1991
Krauthacker et al., 1986
Atuma and Okor, 1987
Atuma and Vaz, 1986
Kanja et al., 1986
Spicer and Kereu, 1993
Ejobi et al., 1996
Chikuni et al., 1997
Quinsey et al., 1995
Zaidi et al., 1989
Tanabe et al., 1990
Alawi et al., 1992
Al-Saleh et al., 1998
Coketal., 1997
Schecter et al., 1989
Schecter et al., 1989

Note: Methodologies used to quantify isomers varied, however they allow for comparisons of geographical differences.
* Median

A breast feeding baby can acquire
concentrations of lipophilic chemicals at
extraordinary rates. Mes et al. (1984) estimated
that babies could acquire 1.8 micrograms of
p,p’-DDE per gram body fat (or 1.8 ppm) by
the 14th week of breast feeding from breast
milk alone. Furthermore, the infant’s DDT
levels could reach those of the mother in the
first three months of breast feeding. The levels

of DDT in the blood begin to decline at about
3 years of age, again probably reflecting the
shift in diet to a less contaminated food, and an
increase in new fats.
Based on observations in South Africa of DDT
(and DDT derivatives) in breast milk, Curtis
(1994) estimated that a baby fed entirely by
breast milk exceeds the allowable daily intake
(ADI) for DDT (0.02 mg/kg), as determined

India - Pesticides and Health Meeting, October, 2002

63

by FAO/WHO (1985), by 5 to 18 times.
Rogan and Ragan (1994) estimated that over a
nine-month period of breast feeding, an infant
can acquire 21.5 mg of DDE based on the 90lh
percentile level. Such estimates identify breast
feeding as a principal source of exposure to
DDT and DDE. It must be pointed out that
this exposure of the newborn coincides with
development of their brains (Eriksson, 1997),
so such exposure has implications for neural
development, behaviour, and susceptibility to
insecticides later in life (Johansson et al., 1996).
This concern for exposure during early
development will be discussed in more detail
later in the paper.
The DDT and DDE a nursing baby acquires
from breast milk come directly from the low
background exposures and accumulation over
the years in the mother. In one study, levels of
DDE were found to be 17% lower in women
who had breast fed previously as compared to
those who had not. This was confirmed in
studies of women who were followed through
two pregnancies, where there was a 23%
difference in DDE levels between their first
and second child.
The quantity also changes with the length of
the nursing period - declines in DDE in milk
of 20% at six months, and a 40% decline by the
18lh month of nursing (Rogan etal., 1986). The
amount of DDT and DDE in the bodies of the
women participating in this study was the
result of low background exposures beginning
early in their lives. It was not the result of
accidental or agricultural exposures.

Lactational transfer is not limited to DDT or
DDE. Any pesticide that enters the body can
be excreted in breast milk (Rogan and Ragan,
1994). Synthetic pyrethroids have also been
reported in the milk of dairy cows when
pesticides were applied as a pan of an
ectoparasite control program. Deltamethrin,
cypermethrin, or cyhalothrin were reponed in
milk within 24 hours of application (Bissacot
and Vassilieff, 1997), with concentrations of
0.51, 0.36, and 0.19 ppm, respectively. The
organophosphate pesticide, chlorfenvinphos,
another topical treatment for ectoparasites in
cattle, was recorded to vary from 1.18 to 10.40
ppb in milk from cows in Kenya (Kituyi et al.,
1997). Only recently has attention been
focused on the transfer of synthetic chemicals
in human or cow milk, and therefore, it is not
known what the magnitudes of transfer are for
commonly used pesticides.
The fact remains that this lactational transfer is
the rule ofpharmacokinetics ofsynthetic
chemicals, and not the exception. The concern
increases as the transfer rate and concentration
of the chemicals increases, which is related to
both the application rate, frequency, and the
bioaccumulation potential of the chemicals.

J)CT

</, -/Lz

h/of

mfr

CP tr-aJ'O-T-Af .

The persistence of lipophilic chemicals is cause
for concern because exposure to low
concentrations over an extended period of time
may lead to substantial burdens later in life. In
an analysis of DDT exposures associated with
indoor application of DDT for malaria control
in KwaZulu, Africa, Bouwman and colleagues
(1991, 1993, 1994) found that household
members in regions that used indoor pesticide
applications for vector control had significantly
higher DDT levels in their sera than those in
regions where no spraying occurred.

India - Pesticides and Health Meeting, October, 2002

oj

ppbr>
a^oxre.
PP1^-

4
Ah

fa

64

tdattj 4 .

Inadequate Testing of Pesticides

new study in the journal of Toxicology
and Industrial Health identifies signifi
cant shortcomings in toxicological test
ing protocols currently used terregister pesticides
in the United States. The five year study, released
in March 1999, suggests that combinations of com
monly used agricultural chemicals in concentra
tions that mirror levels found in groundwater can
significantly influence immune and endocrine sys
tems as well as neurological health.
"The single most important finding of the study
is that common mixtures, not the standard one-

A

chemical-at-a-time experiments, can show biologi
cal effects at current concentrations in groundwa
ter," said Warren Porter, lead author and Univer
sity of Wisconsin professor of zoology and envi
ronmental toxicology.
The experiments performed by Porter's group
suggest that children and the developing foetus are
most at risk from pesticide-fertilizer mixtures. Their
influence on developing neurological, endocrine
and immune systems portend change in the ability
to learn and in patterns of aggression. (See Box:
Household Pesticides and Childhood L eukaemia)

■ ■■
Chronic Effects in U.S. Farmworkers
Despite the fact that millions of farmworkers in the U.S. are exposed over extended periods of time to multiple
pesticides, few studies have addressed the relationship between exposure and subsequent illness in this popula
tion. Although very limited data are available, studies which have been conducted show disturbing evidence of
chronic effects of pesticide exposure among farmworkers. The following is a brief summary of some of the findings
of studies on farmworkers done in the U.S.
Cancer: One cancer study conducted in the USA in 1993 found that when compared to the general popula
tion, both farmers and farmworkers have increases in multiple myeloma and cancers of thestomach, prostate and
testis. In addition, farmworkers show unique increases in cancers of the mouth, pharynx, lungs and liver.
Birth defects and stillbirths: Although increased numbers of birth defects have been recorded among farm
area residents, very few studies have looked at birth defects among farmworkers. In one study of 990 single births,
limb reduction defects occurred among offspring of agricultural workers three to 14 times more frequently than
among the general U.S. population. The risk was greatest for mothers residing in countries with high agricultural
productivity (2.4 times) and high pesticide use (3.1 times). In another study, occupational exposure of pregnant
women to pesticides during the first and second trimesters increased the risk of stillbirths and early neonatal
deaths by 5.5 and 4.8 times respectively, compared to unexposed groups.
Developmental effects: Many pesticides are known to disrupt the human endocrine system. The endocrine
system is a complex array of glands, organs and tissues that secrete hormones (chemicals produced by the body)
into the bloodstream and regulate a range of physiological and neurological systems. Reproductive organs appear
to be at particular risk for development abnormalities when pregnant women are exposed to endocrine-disrupticy
chemicals (EDCs). In both sexes, the brain, thyroid, liver, kidney and the immune system are also potential targets
for EDCs. Since EDCs persist in body fat; they may also exert their effects long after exposure.
Thus even with limited data available a startling picture emerges of the dangers facing farmworkers.
Source: "Fields of Poison, California Farmworkers and Pesticides", by Margaret Reeves and Kristin Schafer
(Pesticide Action Network North America), Kate Hallward (United Farm Workers ofAmerica) and Anne Katten
(California Rural Legal Assistance Foundation), Californians for Pesticide Reform (CPR) Series, 1998.

India - Pesticides and Health Meeting, October, 2002

65

Household Pesticides and Childhood Leukemia
he use of pesticides in homes is generally increasing. They are used as indoor pest control
lers, on indoor plants and in home gardens. However, exposure to some of these pesticides,
particularly exposure before birth (foetal exposure) increases the risk of children developing leu
kemia, according to a recent study.
A comparative study of the pesticide exposure background of nearly 500 children with (acute
lymphoblastic) leukemia and a similar number of children without the disease by a group of re
searchers from McGill University in Montreal, Canada, has shown that “indoor use of some insecti
cides ... and pesticide use in the garden and on interior plants increased the risks up to several-fold".
The study was published in the journal, ‘Epidemiology1, in September,! 999.
Sourcing the paper in the journal, ‘The Sun', Malaysia, recently reported (1): “According to the
authors, the use of insecticides in the garden and inside the house, particularly frequent pre-natal
exposure, was associated with increased risks of leukemia. For example, foetal exposure to house
hold cockroach, ant and/or wasp-fighting compounds during pregnancy increased a child's risk of
developing leukemia by 79 per cent, the investigators report, compared with children without such
exposure. The researchers also noted that foetal exposure to moth-killer compounds was associ
ated with more than double the risk for childhood leukaemia. “Household insecticides used in the
study included compounds such as organophosphorus, chlorpyrifos, diazinon, dichlorvos, malathion,
cygon, propoxur, carbaryl and chlordane.”
The study also found that such cancer risks were much higher in children who possessed genes
linked to the activity of certain enzymes (P 450) which, they suggest, can activate the carcinogens in
the pesticides. However another researcher, writing in the same journal, said that these results must
be cosidered priliminary as the study was “one of the first, if not the first, to evaluate gene-environ
ment interactions for pesticides and childhood leukemia".
Source: The Sun, Malaysia, August 23, 1999.

T

Fertilizer and Pesticide Combinations
The study focused on three commonly used
farm chemicals: aldicarb, an insecticide; atrazine,
a herbicide; and nitrate, a chemical fertilizer. All
three chemicals are in wide use worldwide and
are the most ubiquitous contaminants of ground
water in the United States.
In a series of experiments, when mice were
given drinking water laced with combinations of
pesticides and nitrate, they exhibited altered im
mune, endocrine and nervous system functions.
Those changes, according to Porter, occurred at
concentrations currently found in groundwater.
Effects were most noticeable when a single pesti
cide was combined with nitrate fertilizer.
The apparent influence of pesticide and fertil
izer mixtures on the endocrine system, the system
of glands such as the thyroid that secretes hormones
into the bloodstream, may also result in changes
in the immune system and affect foetel brain de
velopment. "Thyroid disruption in humans has
multiple consequences", Porter said. Some of these
include effects on brain development, level of irri
tability, sensitivity to stimuli, ability or motivation
to learn and altered immune function.
A curious finding of the study is that animals
may be more vulnerable to the influence of such
chemicals depending on the time of year: "Our
current working hypothesis is that animals are sea

sonally vulnerable because of subtle modulation
of natural seasonal variation in hormone levels,"
according to Porter.

Need for New Testing Methods
This new study, Porter contends, adds to a
growing body of evidence that current testing meth
ods required for the registration and use of chemi
cal pesticides in the US are fundamentally flawed.
The study lists 6 important deficiencies in current
testing protocols.
• Current tests do not require chemicals to be
tested at low dose pulse exposure. Pulse doses
of low levels of pesticides at critical times when
developmental windows are open and body
defenses are unable to respond may lead to
permanent changes in a foetus. It is important
to remember that the embryo has almost no
defensive systems against chemicals and no
feedback systems to modulate chemical con
centrations early in its development.
• Toxicological tests have typically focused on
cancer and mutation endpoints and have not
looked at other critical concerns such as endo
crine and immune system effects that can oc
cur.
• Standard toxicological tests only evaluate one
route of exposure at a time, rather than all pos-

India - Pesticides and Health Meeting, October, 2002

66

Flyers Beware!

Pesticides on Aircraft

Airline passengers and crew can be exposed to hazardous pesticides without their knowl
edge, according to a report released by the Northwest Coalition for Alternatives to Pesticides
(NCAP), USA. The report, "Flyers Beware: Pesticide Use on International and Domestic Aircraft
and Flights" states that pesticides are commonly used on both cargo and passenger aircraft in
the U.S and in other countries. Some airlines spray voluntarily, while others spray to comply
with national regulations or requirements of other countries. Pesticides are used in occupied
and unoccupied passenger cabins, galleys, cockpits and cargo holds.
On flights to at least six countries (Trinidad and Tobago, Grenada, Madagascar, Kiribati,
India and Uruguay) passengers are directly sprayed with pesticides after landing while still
strapped in their seats. According to one airline attendant, passengers' clothing, skin and hair
may be soaked with the pesticide.
On flights to many other countries, passengers are exposed to pesticides sprayed prior to
boarding without their knowledge. This type of spraying leaves long-lasting insect-killing resi
dues in the passenger cabin. It is currently required on some or all flights to Australia, New
Zealand, Jamaica, Barbados, Panama, Fiji and Guam.
Passengers on U.S. domestic flights may also be exposed to insecticides residues sprayed
on aircraft.
Several insecticide active ingredients commonly used on aircraft, including permethrin,
cypermethrin and piperonyl butoxicide, are classified by the U.S Environmental Protection Agency
as possible human carcinogens. Others are classified as reproductive hazards or suspected
endocrine-disrupting chemicals.
NCAP says airlines should use non-toxic pest prevention and management practices, and
that governments should prohibit or discourage use of hazardous pesticides on aircraft.
Source: Northwest Coalition for Alternatives to Pesticides (NCAP) published in Global Pesticide
Campaigner, April 1999.

The full report on aircraft spraying js available on NCAP's website at www.efn.org/~ncap/
AirlineSpray.pdf. For further information contact: Northwest Coalition for Alternatives to Pes
ticides (NCAP), P.O. Box: 1393 Eugene, OR 97440. Tel: (541) 344 5044 Fax: (541) 344 6923.

sible routes i.e. oral, cutaneous and respiratory.
Most testing is clone with pure forms of pesti
cidal active ingredients rather than with com
mercial formulations. There are three types of
chemical additives missing from most testing
protocols; i.e. contaminants of manufacturing
processes, toxic waste deliberately added from
chemical reactor cleaning processes and "in
ert" ingredients.
• Current testing requirements do not evaluate ex
posure effects from chemical mixtures. While it
is impossible to examine all possible mixtures,
common combinations generated in specific
areas due to crop rotation and tillage practices
could be examined.
• Laboratory animals generally live in an envi
ronment where climate, nutrition and disease
are carefully controlled. Researchers know that
•

when additional stresses are present, toxic re
sponses to registered chemicals occur that may
not appear under current standard testing pro
cedures.
"Toxicology testing so far has been extremely
limited in scope and focused on mechanisms that
require extensive mutations or cell damage to show
any effects," said Porter. "They do not adequately
assess the potential for biological effects under real
world exposure scenarios." (See Box: Flyer Beware!
Pesticides on Aircraft)
Source: Global Pesticide Campaigner, Volume 9, No.
Z. PAN North America, April 1999, Original Source:
Warren Porter et a!., "Endocrine, Immune and
Behavioural Effects ofAldicarb (carbamate), Atrazine
(triazine) and Nitrate (fertilizer) mixtures at ground
water concentrations," Toxicology and Industrial
Health (1999), 15, 133-150, University of WisconsinMadison Press Release, March 15, 1999.

India - Pesticides and Health Meeting, October, 2002

67

5 Recommendations: Protectins
Farmworkers from Pesticides
"Pesticide exposure can cause serious acute illness among
farmworkers. In the incident described in this report, workers
entered a field well before the end of a label-specified re
stricted entry interval (REI) and incurred pesticide exposure
that resulted in a moderately severe illness. The incident dem
onstrates that 1) posted and oral warnings based on the REI
are necessary to prevent illness among workers performing
hand labor in fields recently treated with pesticides and 2)
failure to adhere to an REI can result in substantial morbidity
[illness] among exposed workers. Because this incident dem
onstrates that sole reliance on these control measures may be
inadequate, the substitution of safer, less toxic alternative pes
ticides should be adopted when feasible" (CDC 1999).

As demonstrated in the above excerpt from a
recent Center for Disease Control (CDC)
report, reliance on notification measures
alone is in many cases inadequate to prevent
farmworker poisoning by pesticides.
Farmworker experiences show that even pes
ticide applications which follow the letter of
the law can result in exposure or illness.

pesticide illnesses are also critical, as is access
to accurate information on pesticide use, vio
lations and illnesses for both farmworkers
and the general public. Below we explore
these recommendations in greater detail, in
cluding some of the specific steps needed to
reduce farmworker exposure to dangerous
pesticides.

The most important and urgently needed
step to reduce exposure is eliminating use of
pesticides which endanger the health and
well-being of farmworkers throughout the
state. Phasing out use of the most dangerous
pesticides—those that cause cancer or repro
ductive harm, or are extremely toxic to the
nervous system—would represent tremen
dous progress toward a more sustainable,
healthy and humane agricultural system.
Substituting safer alternatives for toxic mate
rials is a well-established first step in worker
protection as outlined in the widely accepted
principles of industrial hygiene (Soule 1991).
Specific steps needed to reach this goal and
effectively promote viable alternatives are out
lined in Recommendation #1 below.

1. Rapidly phase out use of the most
toxic pesticides and promote
healthy and sustainable alternatives.

To reduce the level of farmworker exposure
to those pesticides which remain registered,
we recommend outlawing several hazardous
use practices, improving protection from drift
and residue exposure, and significantly
strengthening the existing enforcement sys
tem. Improved reporting and treatment of

• California’s Department of Pesticide Regu
lation (DPR) should develop and imple
ment a plan to phase out use of pesticides
that cause cancer or reproductive harm or
are highly poisonous acute nerve toxins. In
addition, the agency should develop and
implement a plan for reducing use of all
pesticides, including setting annual goals
for total use reduction and ensuring, at the
same time, that toxicity is not increased.
• DPR should immediately prohibit use of
pesticides that are most hazardous to work
ers (highly acute nerve toxins, carcinogens
and pesticides that cause reproductive
harm) on labor-intensive crops.
• California Environmental Protection
Agency (CalEPA) should commit signifi
cant resources to organic agricultural re
search and programs to assist farmers in
pesticide use reduction and in rhe transi
tion to sustainable alternatives?7

India - Pesticides and Health Meeting, October, 2002

68

• CalEPA and California Department of
Food and Agriculture (CDFA) should in
crease their research and training budgets
in each of the following areas: organic agri
culture, biointensive and integrated pest
management programs and pesticide use
reduction programs. These expenditures
should be analyzed annually and compared
with expenditures in support of conven
tional agriculture. Results of this analysis
should be made public and widely avail
able.
2. Improve regulations to reduce
farmworker exposure.

• DPR should ban aerial spraying of agricul
tural pesticides, and prohibit use of back
pack spraying for all restricted use pesti
cides and acute systemic toxins.
• DPR should expand posting requirements
to apply to all agricultural pesticide appli
cations. Warnings should be required prior
to application along the perimeter of all
areas where application occurs in such a
manner that the warnings are highly visible
to workers and other people who might
enter the area. All posting signs should in
clude pesticide name and reentry date and
be written in the primary language(s) of
the farmworkers.
• DPR should require that employers notify
farmworkers 24 hours in advance of all
pesticide applications in fields they work in
or near.

• DPR should extend restricted entry inter
vals (REIs) to take into account multiple
pesticide exposure and prevention of
chronic health effects. Early reentry excep
tions should be eliminated, and DPR
should document and make public the sci
entific basis for REIs.
• DPR should establish and/or expand
worker buffer zones for all fumigants and
air-blast spraying.

• Growers should be required to provide
washing and laundry facilities for
farmworker use on any farm where pesti
cides are applied.

• Training requirements should be improved
and enforced for all pesticide applicators
and workers who enter fields or handle
crops.
• Agricultural workers should be covered by
OSHA’s Hazard Communication Stan
dard.
3. Strengthen enforcement of
existing laws.

• DPR should set minimum mandatory
penalties that county agricultural commis
sioners must issue for violations of pesticide
laws that could endanger the health and
safety of workers. The option of issuing
“Notices of Violations” and “Letters of
Warning" should be abolished.

• DPR should increase fine levels for moder
ate and serious violations and enforce the
automatic “serious” designation for repeat
"moderate” violations, as specified in pesti
cide regulations.
• DPR should require pesticide users to be
familiar with regulatory requirements. The
“ignorance excuse,” a policy of leniency
towards violators if they claim to be unfa
miliar with relevant requirements, should
be abolished. (The DPR Pesticide Policy
Manual currently recommends issuance of
a “Notice ofViolation” rather than a fine
for a violation that is a possible health and
safety hazard if the violator is judged unfa
miliar with pesticide regulatory require
ments.)

• An independent review board should be
established to annually evaluate the perfor
mance of each county agricultural commis
sioner, with participation from agricultural
workers. Elected county officials should
receive copies of all agricultural commis
sioner workplans and evaluations. DPR
should exercise its authority to withhold
Rinding from agricultural commissioners’
offices that inadequately enforce regula
tions.
• DPR should require that every county agri
cultural commissioner’s office have at least
one bilingual investigator on staff.

India - Pesticides and Health Meeting, October, 2002

69

• DPR should require special investigations
of all pesticide illnesses resulting from legal
use practices, rather than allowing agricul
tural commissioners to take no action in
cases where no specific violations are
found.

• Insurance companies should be required to
immediately forward copies of “Doctors
First Report of Occupational Illness or In
jury” involving pesticides to the Depart
ment of Health Services (DHS) and DPR
Worker Health and Safety Branch.

• Poisoning investigations should always in
volve the Department of Health Services'
Occupational Health Branch and/or
OSHA, in addition to DPR.

• DHS should establish and fund a program
to monitor long-term health impacts of
pesticide exposure among farmworkers.

• State agencies should assess stiff penalties
for employer retaliation against whistle
blowers and for interference with workers’
right to organize.
• Agricultural inspectors should enforce ex
isting law (CCR, Tide 8, Section 3457),
which mandates a minimum $750 fine for
inadequate sanitation facilities, as specified
in CalOSHA regulations.
• DPR should mandate that egregious viola
tors whose actions endanger workers shall
be referred for civil or criminal prosecution
and/or have pesticide use permits and li
censes revoked for a full growing season.
4. Improve reporting of pesticide
poisonings.

• Work “safety incentive” contests that pro
vide bonuses or prizes to work crews when
no injuries or illnesses are reported in a
given time period should be prohibited.

• DHS should expand its existing program
to train doctors about pesticide poisoning
diagnosis, treatment and reporting require
ments. Crop-sheets highlighting symptoms
of pesticide poisoning should be widely
distributed to migrant healdi clinics and
other physicians or health care providers.

• CalOSHA and the Medical Board of Cali
fornia should exercise their authority to
fine doctors who fail to report pesticide
poisonings promptly to the county health
authorities.
5. Improve farmworker access to
medical treatment.

• Failure of agricultural employers to provide
workers and doctors with full information
about chemicals involved in a possible ex
posure incident should constitute “interfer
ing with access to medical treatment” and
should be enforced aggressively. Regula
tions requiring employers to take exposed
workers promptly to a doctor should be
enforced.
• The federal government should increase
funding for migrant clinics and other
health care providers for farmworkers, in
cluding funding for free annual physicals to
screen for symptoms of pesticide exposure.
These free physical exams should be avail
able to all, regardless of immigration status.

• Agricultural employers should be required
to provide health insurance and/or estab
lish a fund to finance farmworker health
care costs.

DPR should expand posting requirements.

• DHS should expand cholinesterase moni
toring programs to include all field workers
who could be exposed to organophos
phates or carbamates during the course of
their work.

India - Pesticides and Health Meeting, October, 2002

70

6. Ensure farmworker and public
right-to-know.

• DPR should expand workers’ right-toknow to include posting of REIs and de
scriptions of acute and chronic health ef
fects associated with each chemical. The
information should be posted in a neutral
location on the farm in an understandable
format and language.
• The Office of Environmental Health Haz
ard Assessment should ensure that all
farmworkers are guaranteed “adequate
warning” about exposure to carcinogens
and reproductive toxins, as required under
Proposition 65.
• County agricultural commissioners should
document all drift inquiries; monitor, ana
lyze and publish trends in inquiries and
complaints; and institute mandatory site
visits in response to repeated inquiries and/
or complaints.

available to DHS and the public within.
three months of an investigation.

• DPR should release pesticide use and ill
ness data no later than six months after the
end of the year for which the information
is reported, and should produce an ana.vsis
of pesticide use trends and reported poi
sonings.
• DPR should establish a public database
with information on the amount ot pesti
cides used, violations reported, number ot
workers affected by the violations and
number of pesticide illnesses for each user
grower. This integrated database could be
an expansion of the Agricultural Civil Pen
alties database of pesticide enforcement
actions, and would be analogous to the na
tional Toxic Release Inventory and rhe
statewide Hot Spots database for air pollut
ing chemicals.

• County agricultural commissioners should
make the results of pesticide investigations

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India - Pesticides and Health Meeting, October, 2002

71

"Its bricks were... cemented by hate; hate and discord, like the Tower of Babel, and ....in it we hate
the insane dream of grandeur of our. masters, their contempt for God and men, for us men."
- Primo Levi describing the Carbide lower in the middle of the Auschwitz rubber plant, built by concentration camp inmates”
The relationship between government audiorities and corporate human rights abuses is a significant and sometimes confusing issue.
Governments cannot legally authorize corporations to violate human rights, but corporations often act as if government's permission or
encouragement will suffice. Perhaps the most notorious example of this relationship occurred under the Nazis’ genocidal rampage in Europe.
A cartel of chemical companies known as IG Farben took part in. and benefitted from, die Nazis' atrocities.
In 1925. Bayer. BASF Hoechst and other German companies joined forces to form the cartel — in German an Intetessegemeinsdiafi. or
"IG.' which they named "IG Farben.' This became the linchpin of Hitlers military/industnal complex, providing synthetic nitrates. fuel and
rubber"' The Nazis Dr. Josef Mengele conducted gruesome experiments on the inmates in the concentration camps at Auschwitz and else
where. IG Farben is alleged to have experimented on inmates against their will with drugs and other chemicals.

Except from "Victims No More," National Catholic
Reporter. John L. Allen Jr.
tiring the unwilling testing of new drugs on con
centration camp prisoners. Nazi Doctor Josef
Mengele favored experiments on twins because
twins have the same genetic code21. Eva Mozes Kor was
injected with unknown chemicals several times. After one
such set of injections. Eva developed an intense fever and
was sent to the prison infirmary. During the first two
weeks Eva was hospitalized, her twin sister Miriam was
put under constant SS guard. The guards were poised to
kill Miriam as soon as Eva died, so doctors could perform
comparative autopsies.
Kors lawyers say they have evidence of ampules of
drugs bearing the Bayer label found in Auschwitz, records
of doctors who were Bayer employees and who conducted
experiments in rhe camps; and correspondence suggesting
that Bayer officials knew about the experiments and col
lected results' ’. The lawsuits name specific people as IG
Farben employees., such as SS Dr. Helmut Vetter and Dr
Bruno Weber/' |Bayer denies rhe allegations.)
"In response to requests from Bayer, they experimented
with drugs Bayer was in the process of developing." Kors
lawyer Richard Shevitz said. “This was [research and
development] conducted in the context of the Holocaust"

Some previously published documents seem to buttress
parts of that argument One of the most sensational is a
Nov. 19, 1943. letter from an IG Farben official. Wilhelm
Mann, to Otmar von Verschucr, Mengele's mentor. In the
letter. Mann — director of pharmaceutical sales at
Leverkusen — thanks Verschuer for acquainting him with
Mengele. and says he found Mengele's demonstrations
“very impressive." He says he will take up the question of
funding, and refers to an enclosed “first check "t7
An Austrian association that maintains records from the
Matthausen Gusen camp system confirmed that Dr.
Helmut Vetter did inject inmates with drugs labeled
“Ruthenol" and “Praeparat 3582" in block 27 of the
Gusen camp.
Shevitz says he believes the concentration camp experi
ments helped Bayer develop products-that are in use today.
"We know they were used to develop conventional medi
cines. It's a matter of asking Bayer how much profit can be
traced to those experiments. Its a significant amount of
money.” he said.
As much as she wants — and believes she is owed —
financial compensation and an explanation of what was
done to her in Auschwitz. Kor believes her fight with
Bayer has broader significance too “Companies must treat
human beings with respect."
While in no way diminishing the incomparability of the
Holocaust, Michael Bazyler. a professor at the Whittier

India - Pesticides and Health Meeting, October, 2002

72

Law School in Costa Mesa. California said Kors lawsuit
and those of other survivors form a dramatic new front in
the broader fight to hold corporations accountable for
their conduct.'
*
“Obtaining compensation from bankers and industrial
ists who profit from human rights abuses sends a message
that they cannot hide behind the cloak of ‘business as
usual' when they become joint venturers with a dictatorial
regime.' he said

IG Farben was the only business to operate its own con
centration camp IG Farben erected the Monowitz camp.
with guard towers, barbed wire and gallows. The forced
labor of inmates was used to erect the chemical opera
tions Norbert Wollheim. a German Jew who was brought
with his wife and thrce-ycar-old son to Auschwitz in 1943.
testified after the war that he was separated from his wife
and child and taken to a camp.w There he was robbed of
all possessions, deloused, registered, and tattooed with the
number 107 984. The next day he was brought to a syn
thetic rubber plant being built for IG Farben’'1 by slave
labor of concentration camp inmates:
“As initiation, as was the general rule, we were
given only the hardest and most strenuous work.
such as transportation and excavation work I
came to the dreaded “murder detail 4." whose
task it was to unload cement bags or construction
steel. We had to unload the cement from arriving

1938-1943

1925

1933

Major German
chemical companies
form IG Farben.

First Nazi concentration IG Farben made profits of
camps builL
100-200 percent from stock
holdings in Degesch, the
manufacturer of Zyklon B.

Photo taken by Gary Cohen in Auschwitz Museum Source of original photo unknown.

Freight cars all day long
at a running pace.
Prisoners who broke
clown were beaten by
the German IG foremen
as well as by the kapos
until
they
cither
resumed their work or
were left there dead. I
saw such cases myself.
I also noticed repeat
edly, particularly dur
ing the time when the
SS accompanied our
labor unit themselves,
that the German IG
foremen tried to sur
pass the SS in brutali
ties/
Workers unable to keep
up with the pace were put to
death. Paul M Hebert, one
of the judges at the postwar
trial of IG Farben wrote: “It was Farbcn’s drive for speed in
the construction of Auschwitz which resulted indirectly in
thousands of inmates being selected for extermination by
the SS when they were rendered unfit for work..."31

IG Farben: A Human Rights Analysis
One thing the Farben case showed clearly was that the
chemical industry’s officials were capable of objectifying
humans, even to the extent of making their lives expend
able. And the industry’s technologies had rhe capacity for
large-scale killing. The atrocities of the era violated the
Right against Genocide.
Some Farben officials were ultimately prosecuted for
their part in the atrocities. At Nuremberg, twelve senior
executives were jailed for terms ranging from one to eight
years. The allies then split the company back into its orig
inal constituents: Hoechst Bayer and BASF. One of the
company's dominant figures, rhe scientist Fritz ter Meer.
got seven years When he ('merged from jail, he was imme
diately appointed chairman of Bayer. IG Farben proved
able to survive the political regimes with which it was inti
mately associated
Philosopher Hannah Arendt, in attempting to under
stand the Nazi era. has written that evil was not only com
mitted by fundamentalist zealots, but by people who were
simply doing their jobs - embodiments of rhe “banality of
evil." In this way. thousands of petty officials could fulfill
their small, seemingly innocuous jobs, connected together

1940

1943

The building of Auschwitz begins
with oversight by IG Farben officials,
and labor from concentration camps.

IG Farben official Wilhelm
Mann writes letter
expressing appreciation
of S.S. Dr. Mengele's
experiments.

1R

India - Pesticides and Health Meeting, October, 2002

73

in a vast machinery of brutality and injustice that sent mil
lions of people io their deaths.

Photos Courtesy of US Hoiocausi Memorial Museum Photo Archives

The Nazis' efficient technological and corporate struc
ture was an effective mechanism both for removing indi
vidual responsibility and in dehumanizing its victims.
Jews in transport trains to the death camps were called
“pieces". Train officials processed 15.000 pieces from
Hungary. 10.000 pieces from Greece, a million pieces from
Poland, etc.
The IG Farben case is the only one in which chemical
industry executives were prosecuted and convicted of
crimes against humanity. The activities of Farben were
undertaken on behalf of the most evil regime of the cen
tury. whereas the other case studies in this paper involve
more purely commercial endeavors.
After the Nazi era. the chemical corporations shifted to
justifying their most harmful activities not in terms of the
need for extermination of people, but in terms of accept
able risks and the need to advance their product lines and
profitability. Underlying both Nazi and corporate logic,
however, a similar dehumanization finds expression. A
certain group of human beings is made expendable, a cer
tain amount of destruction must be tolerated, in the name
of progress and profit
One result of the Nazis’ experimentation was the estab
lishment of the Nuremberg Code, which provides that
experimentation on human subjects shall not be commit
ted without willing participation of the subjects. While
that code was established in a medical context, the same
ethical rationale applies to the industry’s global experi
ment on involuntary humans. Yet. as far as we know, the
obvious connection has yet to be made in any courts.

sb
Zyklon-B, used to kill concentration camp inmates, was provided to

the Nazis by IG Farben. This is a Stockpile of Zyklon-B poison gas pel

lets found at Majdanek death camp in 1944 and close-up of the con
tainers and a gas mask. The containers hold Zyklon-B pellets (hydro

cyanic acid) that vaporize when exposed to air. Originally intended
as a disinfectant and insecticide, the Nazis discovered through

experimentation that the gas could be used to kill humans. Prisoners
were forced into air-tight chambers disguised by the Nazis to look
like shower rooms. The Zyklon pellets were dumped into the cham

bers via special air shafts or openings in the ceiling. The pellets
would vaporize, giving off a noticeable bitter almond odor. Upon
being breathed in, the vapors combined with red blood cells, depriv
ing the human body of oxygen, causing unconsciousness, and death

through oxygen starvation.

1944

1948

1953

1956

1995

The IG Farben industrial complex at
Auschwitz is bombed by the Allies.
Gassings end in November after
more than a million are dead.

Nuremberg trials convict twelve
Farben executives of human rights
violations, including Fritz ter Meer.

IGFarbeffs assets
divided between
Hoechst, BASF, Bayer
and other firms.

IG Farben executive
Fritz Ter Meet is
released from jail and
elected Chairman of
the Board of Bayer.

Ernest Krienke, chairman of IG
Farben Board, rejects demands
that the surviving IG Farben
slave laborers be paid repara
tions by the company.

India - Pesticides and Health Meeting, October, 2002

74

Thor employs a lol of casual labor..and when they become ill from the poisons they are fired
for carelessness.
-Eric Ncube, former shift leader atlhor Chemicals, South Africa.
a plant that received mercurg wastes from US and British manufacturers

Exporting Toxic Pesticides
Excerpt from "Human Rights Implications of the
Export of Banned Pesticides," by Beth Gammied3
disturbing pattern has emerged. A chemical company
' \ will spend large amounts of money to manufacture a
k
pesticide, and obtain its registration to be sold in the
United States. The pesticides harmful health and environ
mental effects then become apparent, either through incidents
of pesticide poisoning or further research. After a slow and
laborious process, the EPA eventually determines that the pes
ticide causes harm to human health or the environment, and
the pesticide is removed from the American market. However,
the chemical company continues to export the banned pesti
cide to foreign countries or transfers production out of the
United States. Thus a “circle of poison" is created: a pesticide
is manufactured in the United States, is exported, and returns
to the United States on pesticide-tainted fruits and vegetables.
The unfortunate reality is that corporations often know or
suspect the detrimental impacts of their products, but do
not act on what they know.
Early studies by Shell and Dow revealed that DBCP
caused sterility and precancerous lesions in lab animals3,1
I lowever. these results were not revealed to the workers in
the DBCP manufacturing plants nor to the agricultural
workers who were exposed to DBCP in the field.35
Widespread use of DBCP throughout the banana industry
was prevalent in all major banana plantations during the

1970's. The EPA suspended the sale of DBCP for most uses
in 1977 after Occidental workers brought suit for sterility in
California. The potential for profit and the drive to keep
businesses in operation too easily overrides the concerns
about health. While Dow, Occidental, and Shell ceased pro
duction of DBCP after California banned its use. a smaller
company. American Vanguard Corporation (Amvac), seized
the opportunity to fill the vacuum in the DBCP market by
manufacturing and exporting DBCP36 Amvac produced and

"[QJuite frankly, without DBCP, Amvac would go
bankrupt."
- Former Amvac executive
In a report to the U.S. Securities and Exchange
Commission, Amvac stated:

[Management believes that because of the extensive
publicity and notoriety that has arisen over the sterility
of workers and the suspected mutagenic and carcino
genic nature of DBCP, the principal manufacturers and
distributors of the product (Dow, Occidental, and Shell
Chemical) have, temporarily at least, decided to
remove themselves from the domestic marketplace
and possibly from the world marketplace.
Notwithstanding all the publicity and notoriety sur
rounding DBCP,... it was [our] opinion a vacuum existed
in the marketplace that [we] could temporarily occupy...
[we] further believed that with the additional DBCP,
sales might be sufficient to reach a profitable level.38

India - Pesticides and Health Meeting, October, 2002

75

sold DBCP for export. Dc.w also profited: although the com
pany no longer manufactured DBCP, it received a three per
cent royalty on all DBCP sold due to a patent agreement/7
Tlie effects of DBCP exports proved to be just what one
would expect based on the numerous studies on DBCP
exposure. DBCP sterilized many men. including those
working in factories where DBCP was manufactured and
those who applied DBCP in the field."’ As of 1992, approx
imately 15.000 male banana workers in 12 banana-growing
countries, i; riuding 12.000 in Costa Rica and the
Philippines alone, had been sterilized by their exposure to
DBCP in the field. ' These men. unable to father children.
suffer a wide-range of secondary effects, including depres
sion. impotence, and divorce as well as cancers possibly
linked to their exposure ’
Approximately 29% of all pesticides sold abroad are
either banned restricted, or unregistered in the United
States. Over a three-month period during 1990, an esti
mated 3 5 million pounds of banned, canceled, discon
tinued. or withdrawn compounds were exported, equal
ing almost a ton per hour.
These figures represent an enormous amount of exports
of illegal pesticides. The effect of this pesticide “dumping"
on foreign countries is considerable.
In 1990 it was estimated that 25 million people are
severely poisoned every year by agrichemicals. The World
Health Organization (WHO) estimated in 1985 that over
70,000 deaths resulted worldwide from accidental pesticide
poisoning. Some specific instances illustrate the devasta
tion of toxic chemical exports:
• DDT was sprayed heavily on cotton fields in
Guatemala. Researchers found that villagers living
near the fields had blood levels of DDT seven times
higher than those living in urban areas, and thirty-one
times higher than United States residents.11
• Residues of heptachlor have been found In the breast
milk of mothers in Perth, Australia, in amounts fifteen
times international standards.lj

• The WHO estimated approximately 37,000 cases of
cancer annually from pesticide exposure.10

Free Trade in Poisons: A Human Rights Analysis
Respect for human rights is seldom an obstacle to the glob
al trade in poisons. In our era of globalization, chemical
companies increasingly move around assets, products and
wastes on a global chessboard to maximize their profits and
minimize their costs. Asbestos, long banned in the U.S.
because of its devastating impacts on workers, is sold by
Canadian companies to “developing" countries. Waste
incinerators, discredited in the United States due to their
emission of dioxins and other pollutants, are being financed
by World Bank grants to more than 20 countries trying to
grapple with their burgeoning waste streams. The chemical
industry’s human
rights violations are
repeated in every
All persons have the right to freedom
corner of the Earth.
from pollution...and activities that
Chemicals that
adversely affect the environment,
.sterilize men or
threaten life, health, livelihood,
women, or other
well-being or sustainable development
wise endanger preg
within, across or outside national
nant women and the
health of the fetus in
boundaries.
utero, violate the
UN Commission on Human Rights47
right to family. The
Universal Declaration
of Human rights articulates this Right to Family: "men and
women of full age ... have the right to marry and found a
family."18 The U.N. recognized the Right to Family as
including the right of parents to decide when and whether
to bear children. *9 By taking away die opportunity to bear
children, the chemical industry’s involuntary sterilizations
of men and women violates this right.
The chemical industry's shifting of pollution and
products often constitutes a violation of the right against
discrimination, in this context often referred to as environ
mental racism. This is the discriminatory imposition of

India - Pesticides and Health Meeting, October, 2002

76

pollution on poor and minority ethnic populations/0 This
is frequently displayed in the movement of hazardous
wastes, products and production technologies from richer
to poorer locales. Waste disposal facilities and chemical
production clusters are notorious for their locations in
poor and ethnic minority neighborhoods. Wastes and
toxic substances run “downhill" in the direction of poor
countries and communities just as surely as water runs
down a mountain.
Cancer causing pesticides banned in the U.S. and
Europe have been freely exported to farmers in Asian,
African and Latin American countries for many years. But
pesticides exports are going through a transformation.
Increasingly, chemical corporations are moving pesticide
production facilities outside of traditional strongholds in
the U.S. and Europe, especially for older technologies/1
The Bhopal pesticide plant was an early example of this
tendency. Asia is seen as the choice region for expansion,
especially India and China.Jt Expansion in Latin America.
where many large facilities already exist, remains strong.53
In addition, transnationals are beginning to expand on a
very small base in Africa, and to explore new opportuni
ties in Eastern Europe.
Recently, the global trade in poisons has accelerated
under the banner of Free Trade, and a new international
agency called the World Trade Organization (WTO). Under
this new regime, global corporations are free to export dan
gerous products and technologies to 134 nations, as they
shop for the cheapest labor costs and weakest environmen-

tai and public
health protections.
When individual
nations try to
"In order to protect the
impose strict regu
environment, the precautionary
lations to defend
their citizens from
approach shall be widely
toxic exports, the
applied by States according
exporting nation
to their capabilities. Where
can appeal to the
there are threats of serious or
WTO to strike
irreversible damage, lack of
down those envi
ronmental laws as
full scientific certainty shall
an unfair restric
not be used as a reason for
tion of trade.
postponing cost-effective
In the course of
measures to prevent
enforcing its free
environmental degradation."
trade policies, the
WTO has ruled
Principle 15 of the Rio Declaration
against the ability
on the Environment and Development
of nations to apply
the Precautionary
Principle in their decisions to regulate product
imports. As Jim Puckett of the Asia Pacific
Environmental Network has written, the Precautionary
Principle is a common sense concept encapsulated in well
worn adages passed on from generation to generation
such as “a stitch in time saves nine", “look before you
leap“, “an ounce of prevention is worth a pound of cure,"

Precautionary Principle

Donna DeCesarc/Impact Visuals.

*

wt■
. Mm
Containers of hazardous waste in New Jersey bound for Asia, Greenpeace investigation.

India - Pesticides and Health Meeting, October, 2002

77

'fools rush in where angels fear to tread", "better safe than
sorry,' and “when in doubt, do without."'1 Put in the lan
guage of public polit y, the Precautionary Principle posits
that: where an activity raises serious or irreversible threats of
harm to the environment or human health, precautionary
measures should he taken even if some cause and effect rela
tionships are not fully established scientifically.
The relevance to the activities of the chemical industry is
clear. The industry over the last century has repeatedly
shown the dire results of a nonprecautionary approach. By
delaying action until there is scientific certainty, the public
and environment suffer enormous harm.
Yet the WTO made a decision in 1998 that limits the
ability of all governments that are party to the agreement
to apply the precautionary principle. The WTO struck
down a European Union ban on the sale of beef grown
with artificial growth hormones. The European countries
had adopted their ban based on studies that showed risks
of cancer and male sterility for consumers of the beef. The
issue is subject, as so many issues are. to continued sci
entific debate However, the precautionary approach
taken by the European countries was based on a conclu
sion that there was enough evidence to assert that the
synthetic hormones should be considered unsafe until
they are proven safe. Shockingly, the WTO barred this
approach. It requires that regulating nations provide
more scientific justification before acting. The WTO's
approach threatens to leave humanity helpless to inter
vene in the face of indications of harm The WTO has
endorsed the chemical industry's nonprecautionary
approach, under which scientific uncertainty becomes
an excuse for inaction. ' The rationale is cropping up in
opposition before the WTO of various nations' efforts
to keep toxic materials out of their economies and
environments. As Peter Montague has written:

international law. certain human rights including Rights
to life, rights against genocide and against the arbitrary
deprivation of life occupy a special status known as jus
cogens." These higher status rights are those for which
violations are deemed to "shock the conscience of
mankind” and thus are considered absolutely essential to
the maintenance of the international community. Any
treaty that contravenes a jus cogens norm is null and
void.50 Activities of trade organizations like the World
Trade Organization and of financial institutions like the
World Bank, in their prioritizing of economic interests
above the sanctity of life, have quickly moved to a point
of violating these jus cogens principles.
Unless human rights are enforced, we can expect global
chemical and biotech companies to accelerate movement of
their most harmful activities to th.e places where they can
experiment or sell their wares most freely. Hazardous tech
nologies and toxic substances may flow seamlessly across
boundaries of geography and state with little recourse to
those whose rights are irreparably harmed

France wants to ban asbestos, but is being chal
lenged by Canada on several grounds; one is that
there is no worldwide scientific consensus that a
ban is warranted. Denmark has announced its
intention to ban 200 lead compounds, but the
Clinton/Core administration is challenging this as
illegal because there are less trade-restrictive ways
to achieve the same public health objective. Mr.
Gore says. The European Union has said it wants
to ban lead, mercury and cadmium in electronic
devices, but the Clinton/Gore administration is
challenging this before the WTO.55 '

Current globalization trends erroneously allow prof
itability to trump health concerns, and corporate rights to
supersede human rights. Fortunately, international
human rights law may provide recourse against global
trade trends that undermine human rights. For instance.
the American law which authorizes the export of banned
pesticides, the federal Insecticide. Fungicide and
Rodenticide Act/7 could be challenged in US courts as
contravening human rights law/ Similarly, international
human rights law may override inconsistent activities
under international treaties, including trade treaties. In

India - Pesticides and Health Meeting, October, 2002

78

Impact of Corporate Control The Pesticide TNCs
byBarbara Dinbam

he challenge facing us is to achieve wider
acceptance of the understanding that
food security is about access to and dis
tribution of food, and not about production. In
dustry promotes the view that increasing produc
tion can eliminate hunger, and many decision
makers accept this perspective. The vision of food
security needs to be continually asserted against
the barrage of productionist propaganda from the
pesticide industry.
Agriculture is a complex sector. Unlike in
dustry, agriculture is a way of life, it involves steward

T

ship of the environment, it supports the rural so
cial structure, and the products of agriculture feed
the cities. In the forum of the World Trade Orga
nization, these facts are disputed, and under the de
velopment of Uruguay Round Agreement on ag
riculture, the outputs treated like any other product.
In the jargon of trade negotiations, this became re
duced to an argument about the 'multifunctional
nature of agriculture' - with pro-free traders refus
ing to acknowledge that protection was essential
to protect the way of life intrinsic to agricultural
production.

Top 10 Pesticide and Seed Companies
Market Dominance and Interlinking Shares (US$ million)

India - Pesticides and Health Meeting, October, 2002

79

The Chinese market is
particularly interesting:
China spends $6.7/ha
on pesticides, com
pared to $752/ha in Ja
pan, yet the Chinese
yield is second only to
Japan.1

The Seed
Companies

Part of the challenge to this view is continually
drawing attention to the role of the transnational
corporations that draw their profits from agricul
ture. Developments in this sector cut across the
global agenda of liberalization, but to expand the
companies constantly push for access to all mar
kets.

Concentration and Control in the
Pesticide Industry
In the last 50 years agriculture has been in
creasingly industrialized: first in Europe and North
America and then with the development of Green
Revolution techniques in developing countries.
Monocuitural production brought increasing use
of agrochemicals and by 1997, the global sales of
pesticides amounted to US$32 billion. The mar
ket is dominated by ten companies, which between
them take about 80 per cent of global sales. These
companies have elbowed out, or taken over, their
competitors that do not have the financial resources
to invest in the extensive research now needed to
stay in the business.
These companies dominate the market, but
there is also a growth of national pesticide indus
tries in developing countries (India, Taiwan, China,
South Korea, Mexico, Brazil) as well as a growth
in the 'generic' pesticide producers. There is also
an increase in the activities between the market
leaders and companies appointed to market their
older products.
The main markets for products remain in North
America and Europe as regions; though India is
now the second largest pesticide user in the world.
As these markets are 'saturated', the big growth
areas are targeted to be Asia and Latin America.

More recently,
concentration has be
gun to take place in
the $23 billion seeds
industry. Takeovers
and mergers escalated
throughout the 1990s
and are continuing
rapidly. In 1997, the sales of the top three compa
nies accounted for 1 7 per cent, and are continuing
rapidly. The companies were Pioneer Hi-Bred (20
per cent owned by DuPont), Monsanto and
Novartis - all leading agrochemical companies.
Changes in chemistry and economic, health and
environmental pressures led these companies to
develop a variety of strategies to continue extract
ing profits from agriculture.
The agricultural industries encourage
monoculture, an agricultural system which inher
ently reduces agrobiodiversity (the FAO says more
plant diversity has been lost to industrial agricul
ture than any other cause!), but which also in
creases pests attack and loss of beneficial animals
(including insects) and crops. Some scientists have
shown that reductions in biodiversity have led to
the evolution of aggressive pests and diseases which
are more difficult to control than those from which
they have been derived.2
The full impact of a consolidation of interests
is difficult to predict, but this trend now seems in
evitable. One industry analyst observed: 'The days
of seed companies selling commodity seed prod
ucts that will be sprayed with pesticides marketed
by a separate industry are clearly numbered. Seed
companies are now selling seed brands engineered
to express pest resistance genes or to be tolerant to
specific herbicides'.3
The gains for industry could be phenomenal.
Some industry analysts predict that the wave of ag
ricultural biotechnology: herbicide tolerance and
insect resistance traits could take the global
agrochemical market up to a US$100 billion a year
industry.4
Together the agrochemical and seed industries
are reinventing themselves, and no longer market

India - Pesticides and Health Meeting, October, 2002

80

1998 Top Ten Agrochemical Companies
Nearly all the major agrochemical companies increased sales in 1998,
according to Agrow: World Crop Protection News. DuPont's combined
agrochemical and biotechnology sales increased by over 25%, the high
est rate of increase for the top ten corporations. DuPont recently an
nounced that it had agreed to acquire the outstanding 80% stake in Pio
neer HiBred International that it did not already own. Pioneer, the world’s
largest seed company with sales of US$1,835 million in 1998, controls
about 42% of the U.S. maize seed market.
Monsanto's growth rate was a close second with combined agrochemi
cal and seed sales increasing by more than 23% in 1998. This was due to
a 25% increase in volume sales of the herbicide glyphosate (Roundup)
and a tripling of the area planted with Monsanto's genetically modified
crops
Novartis was the overall sales leader in 1998 with pesticide sales
reaching US$4,152 million and seed sales at US$1,005 million. Novartis,
as well as Cyanamid, DuPont, Rhone-Poulenc and Zeneca were all hit by
lower than expected herbicide sales in the U.S. due to low commodity
prices and weather conditions as well as other factors.
Agrochemical and seed sales in Asia, Eastern Europe and Latin America
were generally lower due in part to economic problems in these regions.
However, Cyanamid, Dow AgroSciences, Novartis, Rhone-Poulenc and
Zeneca all reported increased sales in Latin America. Cyanamid, Dow and
Novartis also had high sales in Asia.
Top ten agrochemical companies — 1998 sales
Company

*
Sales

% Change’

Novartis (Swiss)
Monsanto (U.S )
DuPont (U.S.)
Zeneca (U.K.)
AgrEvo (Ser)
Bayer (Ser)
Rhone-Poulenc(Fr)
Cyanamid (U.S.)
Dow Agro-Sci. (U.S.)
BASF (Ser)

$4,152
$4,032
$3,156
$2,897
$2,410
$2,273
$2,266
$2,194
$2,132
$1,945

-1.1%
23%
26%
8.3%
2.5%
0.2%
2.9%
3.5%.
11%
4.9%

” Millions of US$
” Since 1997
Sources: Agrow: World Crop Protection News, March 26, 1999 and Aprj!
16,1999. Kindly forwarded via PAN North America (panupdates@igc.apc.org)
May 7, 1999.

themselves as agrochemical and seeds companies,
but as the LIFE SCIENCES companies: playing with
lite through the manipulation of genes.

Corporate Strategies for Influence
The interest in expanding from the pesticide
market to other areas of profitability can probably
be traced back to the early 1980s, when environmental concerns began to influence the
agrochemical industry. This period began to see
the division between research-based agrochemical
companies and others; the cost of bringing new
products onto the market was a high but essential,
price to pay for staying in the game. Companies
opting for this route inevitably sought ways to cover
the cost of the research. With relatively flat sales

through the eighties, a range of
expansionary and defensive strat
egies were devised which kept the
industry in a dominant position.
Being a 'life science' company
implied heavy investment in re
search. So the underlying tactics
continue:
•
Expansion of sales of
older products, whose research
costs have been recouped. These
are cheaper and sell particularly
well in developing countries.
Most companies aim to increase
sales in developing countries, par
ticularly, but not exclusively, of
older products. The lucrative
Asian market has been a major
target.
•
Registration require
ments. Industry faces tighter reg
istration requirements. Its re
sponse is to promote'the 'science'
of risk management as the basis
for product acceptability. The
worker and consumer demand for
precedence of the precautionary
principle is undermined in the
face of widespread regulatory ac
ceptance of the infallibility of 'sci
ence', which puts regulators in a
defensive position. Speaking at
the British Crop Protection Coun
cil conference in 1997, B. Tho
mas of AgrEvo noted that data re
quirements on environmental fate
and ecotoxicology have in
creased in recent years, particu
larly in Europe, and that industry
is collecting data to lobby for a
relaxation of the criteria.

The Public Image
Aware of the poor image of pesticides triggered
by Rachel Carson's 'Silent Spring' and sustained
by publications such as 'A Growing Problem'and
the work of PAN, the agrochemical industry was
on the defensive for some time through the 1980s.
It is now more aggressively repackaging itself to
claim the moral high ground. Its approaches seek
to persuade decision-makers, and the public, that
the industry is benign and promotes the common
good through claims like:
•
Feed the world
•
Protect the environment
•
Can be used safely in developing countries
•
Are !PM friendly

India - Pesticides and Health Meeting, October, 2002

’i.;

Feeding the World
A key approach is the public relations strat
egy: winning hearts and minds by 'demonstrating'
that pesticides are essential in the battle to feed
the 'world's relentlessly increasing population'.
This public relations onslaught will continue as
companies seek to gain the moral high ground: con
vincing the public and decision makers that pesti
cides are needed because only by use of high in
put agriculture will a population of 8 billion (esti
mated global population in 2020) be fed. How
ever, food production in China has kept pace with
population growth, while meeting policy objectives
of maintaining reserves of 1 7 per cent of a year's
food needs.

Protecting the Environment
Companies argue that intensive agriculture will
prevent expansion onto wilderness areas, which
are an important residue of biodiversity.

Examples of advertising of pesticides by the ICI
company that drew heavy criticism from citizen
groups and the PAN Global Network. The poster
above came from a shop of an ICI distributor in
Quetzaltenango, Guatemala, 1992. The advert
below, stating that "paraquat works in harmony
with nature", was the focus of action by
Consumer groups in Malaysia in 1993.

Safe Use
Industry recognizes that pesticides have caused
health and environmental problems in developing
countries, and safe use campaigns are intended to
address bad press. This can be a cheap and effec
tive way of advertising. As one company spokes
man said: "If we teach farmers to use pesticides
correctly, there will be no lack of customers for
our products; indeed there might well be an in
creased demand for the safer and more sophisti
cated products which we are now making", David
McDonald - Novartis (Ciba Plant Protection Farmer
Support Team established in 1991)
Industry has invested mainly in only three safe
use projects under the Global Crop Protection Fed
eration (GCPF): in Kenya, Thailand and Guatemala.
These projects promote awareness of protective
clothing; pre-harvest intervals; labeling; good prac
tice on mixing and spraying, 'not decanting' pesti
cides, training distributors, improving registration,
raising formulation standards. The safe use pro
grammes provide an opportunity to promote pesti
cide use much more cheaply than through adver
tising, for example, children can be targeted
through the school curriculum: many companies
provide cartoon comic papers to schools. Further
more, government or development agency funds
can be sought to support safe use programmes, in
direct competition with funding alternatives. The
approaches learned from these countries are be
ing applied in other countries. Industry should
pursue safe use programmes, but real cost of pesti
cide use should be reflected in the products, and
not compete with the potential to train farmers in
Integrated Pest Management (IPM) alternatives
which will reduce or eliminate pesticide use.

India - Pesticides and Health Meeting, October, 2002

82

Corporate IPM
When presenting information at a global level,
industry asserts the importance of IPM and the
GCPF encourages all products to be marketed un
der an IPM umbrella. Some companies, notably
Novartis and Zeneca, have developed a small
number of flagship IPM projects. These have gen
erally been in areas where profound problems have
been identified as a result of pesticide overuse. The
industry approach to IPM is based on management
of pesticides, mainly to ensure that pests do not
develop resistance to pesticides. Their work un
dermines the work by the FAO, many other re
search institutes and NGOs which have developed
an approach to IPM based on no, or minimal, use
of pesticides. These alternatives draw on farmerparticipatory, knowledge-based strategies which
make full use of agricultural biodiversity, benefi
cial insects, understanding of economic loss, prin
ciples of rotation and other good farming practices.

•

•

•

•

•

What Industry Doesn't Like?
•
•
•
•

The precautionary principle
'Cradle to gra ve' responsibility for products
Economic instruments such as pesticide taxes
and subsidies for ecological agriculture
Regulation - instead "always opt for volun
tary controls. But codes are also important"

«
«

•

Strategies for a Sustainable Future
In spite of industry's assertions, most decision
makers recognize that access to food is as impor
tant as production. However most could not en
visage a pesticide-free agricultural strategy. In the
last 50 years, agrochemicals have become so much
part of production, that the way out of depend
ence will take some time, many strategies, and
struggles on different fronts. These could include
•
Documenting the continuing health and envi
ronmental costs of pesticides.
•
Demonstration of the continued environmen
tal threats of pesticides, which include, e.g.
loss of wild and 'free'food e.g. wild fruits, ber
ries and fish.
•
Water pollution: effect on health of humans
and animals.
•
The benefits of agricultural biodiversity.
•
Emerging knowledge: the impact and costs of
past ignorance: pesticides, POPs.
•
The importance of on farm inputs including
recycling of nutrients, preservation of
beneficials, and farming knowledge that de
bunks the myth that low input = low output.
Demonstration of successful IPM alternatives
should be emphasized.
•
Issues related to Food Security. Access is the

key word: i.e. access to food, to natural re
sources and land, access to education, water,
credit, seed supplies, technology; access for
women; and access to mechanisms of public
decision making.
Developing hunger maps and documenting
case studies of impacts: i.e. who are winners
and losers at regional/national and sub-national
level?
Asserting the multi-functional role of agricul
ture: i.e. it is about livelihoods, sustainability
and a way of life. Developing countries need
to push for recognition of the multi-functional
role of agriculture.
Governments to regulate TNC activities: point
to role of TNCs in global trade - it is absurd to
pretend that trade is merely between govern
ments.
Codes of conduct: government, industry and
civil society-with adequate monitoring.
Legally binding mechanisms: e.g. trade rules
with environment and social rights.
Trade rules which provide guidance, not to
increase or decrease trade.
Alliances with sympathetic stakeholders: the
public sector and non-corporate agricultural
research institutions; development agencies,
UN institutions, and academics.
Influencing the influences: e.g. World Bank,
development banks, and government policy
makers.

Barbara Dinham is International Projects Officer with
the Pesticides Trust, in the United Kingdom. This is an
edited version of the paper that was originally presented
to the Workshop on Transnational Corporations at the
Forum on Land, Food Security and Agriculture at the
Asia Pacific People's Assembly on APEC, November
1998.

References:
1). Grimes, Alison, Crop Production Opportunities in
China, AGROW, 1998
.
2)
RA Ennos, The influence of agriculture on genetic
biodiversity, BCPC, 1997. (Report in IPC Jan/Feb 1998).
. Beer, Andrew, 'Blurring the line between industries',
3)
AGROW Review of 1997, PBJ Publications Ltd., UK,
1998.
.
4)
Wood and Fairley, Chem Week, op. Cit.
.
5)
Biotech Crops Flourish, Chemical Week, 4-11 Feb
ruary 1998, p. 27.

India - Pesticides and Health Meeting, October, 2002

83

End note
- Nityanand jayaraman
At least 32 countries have banned its use. Endosulfan's irreparable and often fatal
damage to humans and animals is an established fact. Even in Kasaragod, villagers and
residents had suspected its role in the numerous health problems and deformities
observed in their cattle as early as in the early 1980s. In the year 2000, the extent of
the endosulfan disaster in Kasaragod became common knowledge. If that be the case,
why did it take more than two years to even temporarily ban it in Kerala? If that be the
case, why is aerial spraying banned in Kerala, while in the rest of the country, it
continues to be used with similarly devastating effects? And if that be the case, why
does the poison remain the most widely used pesticide in India? What engaged our
agricultural scientists in the conspiracy of silence, and what made others, including
regulators paid by taxpayers, mouth lines fed by the chemical industry?
The answer goes back to the access enjoyed by chemical industries to the corridors of
power and decision-making. For instance, at the 221st meeting of the Pesticides
Registration Committee held on 18 April 2002 to deliberate on the fate of Endosulfan in
the context of the Kasaragod's endosulfan disaster, five non-governmental entities were
invited — Plantation Corporation of Kerala; Excel Industries; Aventis Crop Protection
Ltd; Hindustan Insecticides Ltd; EID Parry Ltd. The first company is the accused in the
Endosulfan poisoning case; the others are chemical companies whose bottomlines
stand to be seriously affected if endosulfan is restricted or banned. None of those
affected by endosulfan or their appointees were granted access.

Chemical industries are no strangers to poisons and poisoning. Germany's Hoechst, the
original developer of endosulfan, has in its closets skeletons from the Nazi era, when as
part of IG Farben — a chemical industry cartel comprising Hoechst, Bayer and BASF —
it ran the research and development for the Nazis. Farben's numerous, usually fatal,
experiments on jewish prisoners yielded products including chemical pesticides and
pharmaceutical drugs that are still in use. Hoechst, now Aventis, was invited by our
government (see above) to present its views on whether its pesticide endosulfan ought to
be banned.

If chemical industries are getting away with murder, the blame lies squarely on our
regulators who are either in the pay of the industry or are desensitized into believing
that the numerous poisoning cases and deaths caused due to pesticide exposure are
actually an acceptable cost for food security. Surely, those killed or maimed or their
near and dear ones would not share our regulators' enthusiasm for "food security".
To an extent, the blame also lies with those working in the public interest for not having
been able to launch a concerted and well-strategised fight against chemical pesticides.
More and more, though, activists, NGOs and other public interest organisations are
coming together to correct this inadequacy. In this effort, they have to be able to equip
themselves with the skills necessary to assess, quantify and communicate health
damage by pesticides, and use such information in fighting for policies discouraging
pesticides. Key to this endeavor is a sound knowledge of the enemies — chemical
pesticides and the ways of their manufacturers — and the putting in place of the
infrastructure for pesticide-free agriculture.
Just as wars cannot be ended without strengthening peace, chemical pesticides cannot be
eliminated without strengthening natural agriculture.
*

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