UNSEEN POISONS Levels of Organochlorine Chemicals in Human Tissues
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UNSEEN
POISONS
Levels of
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UNSEEN
POISONS
Levels of
Organochlorine Chemicals
in Human Tissues
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GR£eN?£ACS‘
June
1998
Unseen Poisons
J
Levels of Organochlorine Chemicals
in Human Tissues
I
Global Review of Data on
12 Priority Persistent Organochlorine Pollutants
and
Some Other Organochlorines in HumanTissues
Authors: Michelle Allsopp, Ruth Stringer and Paul Johnston
Greenpeace Research Laboratories
Department of Biological Sciences, University of Exeter
Prince of Wales Road
Exeter EX4 4PS, UK
Special thanks are due to Wytze van der Naald of Greenpeace
International for reviewing the draft text of the report
The writing of this report was funded by Greenpeace International
ISBN: 90-73361-46X
This document is printed on 100% de-inked waste paper, no chlorine bleaching
LIST OF CONTENTS
1
SUMMARY
1.
INTRODUCTION
1.1
1.2
POPs in Human Tissue
Problems Comparing Human Tissue Levels of Organochlorines in Different
Countries
Relevance of Current Human Tissue Levels of Organochlorines to Human Health
1.3.1 Highly Exposed Members of the Population
1.3.2 Acceptable Daily Intakes of Organochlorines
1.3
2.
2.1
2.2
2.3
2.4
2.5
2.6
2.7
POLYCHLORINATED DIBENZO-P-DIOXINS (PCDDS),
POLYCHLORINATED DIBENZOFURANS (PCDFS) AND
POLYCHLORINATED BIPHENYLS (PCBS).......................
12
Introduction
Studies on Tissue Levels of PCDD/Fs in the General Population of Different
Countries
Studies on Tissue Levels of PCBs in the General Population of Different Countries
in the 1980/90s
Time Trends
Highly Exposed Populations
2.5.1 Nursing Infants
2.5.2 Arctic Regions
2.5.3 Residence in Contaminated Environments
2.5.4 Occupational Exposure
Relevance to Human Health
Polychlorinated diphenyl ethers (PCDEs) and polybrominated dibenzo-p-dioxins
and dibenzofurans (PBDD/Fs)
3.
DICHLORODIPHENYL TRICHLOROETHANE (DDT) AND
DICHLORODIPHENYL DICHLOROETHANE (DDE)....
3.1
3.2
3.3
3.4
Introduction
Levels in Breast Milk
Time Trends
Highly Exposed Populations
3.4.1 Nursing Infants
3.4.2 Occupational Exposure
Relevance to Human Health
3.5
7
28
4.
HEXACHLORBENZENE (HCB)
4.1
4.5
Introduction
Levels in Breast Milk
Time Trends
Highly Exposed Populations
4.4.1 Nursing Infants
4.4.2 Occupational Exposure
Relevance to Human Health
5.
HEXACHLOROCYCLOHEXANES
5.1
5.2
5.3
5.4
5.5
Introduction
Levels in Breast Milk
Time Trends
Highly Exposed Populations
5.4.1 Nursing Infants
5.4.2 Occupational Exposure
Relevance to Human Health
6.
DIELDRIN, ALDRIN AND ENDRIN
6.1
6.2
6.3
6.4
Introduction
Levels in Breast Milk
Time Trends
Highly Exposed Populations
6.4.1 Nursing Infants
7.
HEPTACHLOR AND HEPTACHLOR EPOXIDE
7.1
7.2
7.3
7.4
7.5
Introduction
Levels in Breast Milk
Time Trends
Highly Exposed Populations
7.4.1 Nursing Infants
7.4.2 Occupational Exposure
Relevance to Human Health
8.
CHLORDANE
8.1
8.2
8.3
8.4
Introduction
Levels in Breast Milk
Time Trends
Highly Exposed Populations
8.4.1 Nursing Infants
8.4.2 Occupational Exposure
4.2
4.3
4.4
.33
37
I
40
41
.43
a
9.
TOXAPHENE
9.1
9.2
9.3
9.4
Introduction
Levels in Breast Milk
Highly Exposed Populations
9.3.1 Nursing Infants
9.3.2 Other Groups
Relevance to Health
10.
MIREX
10.1
Introduction
Levels in Breast Milk
10.2
45
46
TABLES
,47
REFERENCES
.83
SUMMARY
I
Persistent organic pollutants (POPs) are a group of mainly synthetic chemicals which
have the property of being persistent in the environment. As a consequence of
anthropogenic activities, many POPs have become widespread pollutants throughout
the world in recent decades. Some POPs are known to bioaccumulate in the tissue of
animals and humans and are toxic to health.
There are numerous POPs which pollute the environment. Some of those which have
given rise for particular concern are persistent organochlorines. A previous meeting of
the UNEP’s governing Council in 1995, identified a list of 12 POPs as substances of
clear concern in accordance with the precautionary principle. These chemicals are all
organochlorines. They include dioxins and furans, which are produced as unwanted
by-products of several industrial processes, PCBs and HCB, which have several uses
and are also formed as unwanted by-products, and DDT, chlordane, heptachlor,
aldrin, dieldrin, eldrin, toxaphene and mirex which are pesticides.
The 12 POPs prioritised by UNEP have properties of being toxic to health. It is of
concern that all these chemicals have been detected in the tissues of humans from the
general population of various countries and in the tissues of many wildlife species. It
is also of note that even though there are many POPs, most of these chemicals have
not been assessed in human tissues.
Greenpeace has issued this report to highlight the levels of persistent organochlorines
found in human tissues throughout the world. Countries and populations in which
levels are particularly high are identified. Since these substances are toxic, the
relevance of current levels to human health is also briefly considered. One of the
greatest concerns with respect to health is the potential adverse effects that these
chemicals may have on the most vulnerable stages of life - the developing foetus in
the womb, and the nursing infant, since they are known to cross the placenta and are
present in breast milk.
Levels of POPs in Human Tissues
Most of the 12 POPs listed by the UNEP are widespread pollutants and they have
been found to commonly occur in human tissues world-wide. Levels in tissues are
most routinely determined in blood, breast milk or adipose tissue. This report focuses
mainly on levels of POPs in breast milk which have been documented in the scientific
literature over the past ten years.
a
The greatest number of studies on human tissue levels of organochlorines were
located for dioxins, furans and PCBs. Studies from many countries were found on
levels of DDT and HCB, but less research was available on other organochlorine
pesticides. Given the persistent and widespread nature of the 12 UNEP listed
chemicals, it is considered that there is a lack of data concerning their human tissue
levels for many countries, in particular for developing regions of the world. In
addition, studies regarding tissue levels of occupationally exposed individuals are also
limited.
A general observation from studies presented in this report is that levels of
organochlorine pesticides in human milk were highest in countries where these
chemicals are still in use, notably in developing countries. Another generalisation
which can be made is that levels of dioxins and furans were highest in industrialised
countries. This is synonymous with the fact they these compounds are produced as
by-products of many industrial processes, in particular processes involving chlorine.
There are however exceptions to these generalisations regarding levels of
organochlorine pesticides and dioxins/ftirans in human milk. Many POPs, including
PCBs and some organochlorine pesticides, appear to be transported long distances on
air currents from warm regions of the globe and subsequently deposited in colder
regions. This global fractionation process has resulted in particularly high levels of
POPs in Arctic areas. As a consequence, some indigenous people of Arctic regions
who rely on a traditional seafood diet have high tissue levels of PCBs and some
organochlorine pesticides.
Dioxins and PCBs
Dioxins, furans and PCBs are ubiquftftus in the global environment. Research has
shown that levels of dioxins and furans in human tissues are greater in industrialised
countries than in less industrialised countries. In the 1980s, studies showed that levels
of dioxins and furans in blood, adipose tissue and breast milk were considerably lower
in less industrialised countries, including Thailand, China, northern Vietnam,
Pakistan, Africa and Russia, compared to levels in some industrialised European
countries and the USA.
Research in the late 1980s and early 1990s showed that breast milk levels in many
industrialised countries were in the range of 10-20 ppt TEQ fat. The highest levels,
above 20 ppt TEQ, were found in some western European countries and one region in
Canada. The lowest levels were found in less industrialised regions, including
Pakistan, Russia, Albania, Hungary, Croatia and Norway. Comparatively low levels,
recorded in blood, were also evident in China, some other Asian countries and Gaza
in the Middle East. Most information on tissue levels of dioxins and furans is
available for European countries, USA and Canada. Fewer studies have been
conducted in Asia, and data in the scientific literature is very limited for Africa and
South America.
Studies show that individuals who were employed in the production chlorophenols
and phenoxyherbicides in the 1960s to 80s were highly exposed to dioxins. TCDD
levels in workers from trichlorophenol plants are still elevated by around 10-fold, two
decades after production ceased. Children bom to workers at a plant in Russia, who
are now adults, have levels 150-2000 times higher than the general population due to
placental/lactational transfer from their mothers. More recently, high exposures were
recorded at a pentachlorophenol plant in China, where blood levels of dioxins/furans
(total TEQ) are 50 to 400 times higher than the general population. There are several
other occupations where individuals may be exposed to higher than average levels of
dioxins/ftuans in many countries. Elevated tissue levels have been documented in
workers at municipal waste incinerators and in certain sectors of the metal industry.
Research on PCBs has revealed that similar levels in human milk are evident in many
European countries and Canada. Higher levels have been found in eastern Europe and
the former Soviet Union. Very high human tissue levels of PCBs are apparent in
2
*
populations in Arctic regions who consume a diet rich in seafood. For instance, blood
levels of Inuit in Arctic Quebec who rely on a traditional seafood diet were 15-fold
greater than residents of Southern Quebec.
Studies indicate that levels of dioxins and furans in human tissues in Western
countries have not increased in recent years. Levels in several European countries
appear to have declined somewhat in the past few years. There are difficulties in
comparing data for PCBs between studies, but relevant data shows that levels of PCBs
in human tissues have remained stable in recent years.
DDTandDDE
A summary of data compiled in this report on the levels of several organochlorine
pesticides in human milk from different countries is given in table 10.
DDT and its metabolite DDE are widespread contaminants in human tissues. DDE
has been detected in virtually all samples of breast milk taken from numerous
countries. By far the highest levels in human milk are evident in Asian, African and
South American countries where DDT is still used in agriculture or in sanitation
campaigns against malaria or tse-tse fly. Despite the undesirable properties of DDT, it
is used in developing countries primarily due to cost-benefit efficacy and broad
spectrum toxicity. However, given the continued usage of DDT, it can be considered
that there is a paucity of data on levels of DDT/DDE in human tissues from these
countries in the scientific literature.
Exceptionally high levels in human milk are reported for India (DDT and DDE > 10
ppm). Levels of DDE, (1 to 2 ppm), are found in eastern and some western European
countries, Russia and Australia. The lowest levels are found in some western and
northern European countries and the US. Levels of DDT is human tissues have
declined in recent years in countries where its use is banned, but no decline has been
recorded in other countries such as Mexico. Occupational exposure to DDT has been
studied in DDT sprayers in Mexico. Adipose tissue levels in the workers were 6-times
greater than the general population.
Hexachlorobenzene (HCB)
HCB is a widespread contaminant of human milk, being present in over 90% of milk
samples from most countries. Levels in the majority of countries were in the region of
0.05 to 0.2 ppm. Very high levels (>0.6 ppm) were evident in the Czech Republic and
Slovakia, possibly due to its formation during the manufacture of chlorinated solvents
and former agricultural use. Data from a few European countries show a decreasing
trend in levels in recent years. Occupational exposure has been reported to result in
elevated HCB levels in workers employed in hazardous waste incineration and from
processes formerly used for degassing aluminium.
Hexachlorocyclohexanes (HCH)
Gamma-HCH (lindane) and technical grade HCH, which consists of a number of
isomeric forms, are persistent pesticides which are not listed by the UNEP. However,
gamma and beta-HCH are both commonly detected in human tissues and studies have
listed levels in breast milk in several countries. Beta-HCH is the most persistent
isomer and it is widespread in breast milk throughout the world. The highest levels (4-
3
J
8 ppm) have been recorded in human milk from India and China. High levels (1.5-2.5
ppm) are also evident in Russia and Kazakstan.
Dieldrin, Aldrin and Endrin
Dieldrin is found in human milk of many countries, although the percentage of
samples in which it can be detected is variable. Levels for several countries are in the
range of 0.01 to 0.1 ppm. Very few studies have reported on the levels of aldrin and
endrin in human tissues.
Heptachlor and Heptachlor Epoxide
Data on levels of heptachlor and its breakdown product, heptachlor epoxide, in human
tissues are limited. The chemicals were reported in breast milk from several countries,
although the percentage of samples in which they are detected is variable. A previous
review noted the highest levels were evident in several western European countries,
Israel and Guatemala. In this review, the highest level (0.7 ppm) was recorded for
Jordan. Other countries had levels below 0.05 ppm, with the exception of Australia
and France.
Chlordane
Comparisons between studies of chlordane levels in human tissues are difficult,
because there is variation in the different isomeric forms and metabolites of chlordane
which are reported. It has been noted that the highest levels are present in the US,
reflecting its previous widespread use to control termites. There does not appear to be
a decreasing trend in the level of chlordane in human tissue.
Toxaphene
Few studies have monitored human tissue levels of toxaphene. It has been detected in
human milk from a few countries. Comparatively high levels were apparent in
Nicaragua.
Mirex and Other Organochlorine Pesticides
Very few studies have monitored levels of mirex in human tissues. In addition, there
are other persistent organochlorine pesticides which are still used, such as endosulfan,
which are present in human tissues, but are not often measured.
Acceptable Daily Intakes
Regulatory authorities use the process of risk assessment to estimate permissible
levels of contaminants in food which are deemed to be “safe”. These levels are known
as Acceptable Daily Intakes (ADI) orjolerable Daily Intakes (TDI).
Human milk contains various POPs which pass to a nursing infant, but unlike
foodstuffs, the levels it contains cannot be regulated. The applicability of ADIs to the
breast fed infant is questionable because ADIs are designed to prevent adverse health
effects over a whole lifetime exposure in a 70 kg adult. Nevertheless, given that an
infant is likely to be a more vulnerable lifestage than an adult to toxic insult from
chemicals, it has been proposed that ADIs should be lower for infants, and therefore,
current ADIs should not be exceeded by breast-fed infants.
4
It has previously been calculated that ADIs set by US EPA and WHO for
dioxins/furans are exceeded by breast-fed infants. In this report, estimates of whether
the current ADIs for organochlorine pesticides are exceeded are performed, based on
mean levels in breast milk recorded for different countries. Results show that
estimated infant intakes which exceed the ADIs are: DDT. in some African. Asian
and Latin American countries, and by over 6-fold in India and Zimbabwe; HCB. in
several countries, and by 6-8 fold in Czech and Slovak Republic; lindane, in two
countries, and in India by up to 12-fold; dieldrin, heptachlor and heptachlor epoxide
in several countries.
It is not favourable that current ADIs are exceeded by breast-fed infants, even though
the relevance of this to health is unknown. Indeed, it is questionable whether ADIs are
protective of human health in general. The process of risk assessment used in their
derivation involves many uncertainties. Furthermore, most of the 12 UNEP listed
chemicals have been identified as endocrine disrupters, and current endpoints in
toxicity tests may not be sensitive enough to detect adverse effects of such chemicals.
Research shows that these chemicals can have greater effects at lower rather than
higher doses. There is consequently a scientific opinion that there are no safe doses of
endocrine disrupters, just as there are no safe doses ofcarcinogens.
Relevance of Current Tissue Levels to Human Health
Persistent organochlorines have been reported to cause a wide range of adverse health
effects in experimental animals, and in humans as a result of occupational or
accidental exposure. Effects include toxicity to the liver, reproductive and nervous
systems, immune system abnormalities and cancer. There is evidence that some of
these chemicals, particularly dioxins and PCBs, have now reached levels in human
tissues which are near to, or within an order of magnitude of, levels that are known to
cause adverse effects in experimental animals. Highly exposed populations such as
Arctic Inuit who consume a seafood rich diet, occupationally exposed individuals, and
populations inhabiting contaminated environments could be more at risk. Studies on
infants from the general population of industrialised countries have suggested that
subtle effects on the nervous and immune system may already be occurring as a result
of placental and/or lactational exposure.
The Way Forward
POPs are a global problem. Some are detectable in human tissues world-wide and the
levels of many have not even been assessed. Many POPs, including those listed by the
UNEP, are potentially detrimental to the environment and human health.
To wait for scientific proof about the effects and risks posed by individual POPs
would take decades. There is only one clear way forward to overcome uncertainties
and safeguard the environment and human health - the adoption of the precautionary
principle and the implementation of zero discharge strategies. This requires
prevention of pollution at source, and implementation of clean production in industry
and agriculture. Such action needs to be enforced by legally binding international
agreements.
5
i
1.
INTRODUCTION
There are numerous chemicals that come under the category of persistent organic
pollutants (POPs). These chemicals resist breakdown by natural processes for long
periods of time, and are thus persistent in the environment. The UNEP's Governing
Council have listed 12 POPs of clear concern, in accordance with the precautionary
principle. They include dioxins and furans, PCBs, HCB, DDT, aldrin, endrin and
dieldrin, heptachlor, chlordane, toxaphene and mirex. These chemicals are all
organohalogens, specifically, organochlorines.
Many POPs, including some organochlorines, are not only persistent in the
environment, but are also soluble in fats (lipophilic). Consequently, they become
stored in the fatty tissues of animals and build up (bioaccumulate) as more of the
chemical is taken in. The levels of some of these chemicals increase (biomagnify) as
one animal eats another, so that the highest levels are found in animals at the top of
food chains, including humans. Many persistent organochlorines are also toxic to
wildlife and humans.
The 12 prioritised POPs listed by tlwUNEP have been produced or used in bulk
quantities in many countries. Dioxins, PCBs and HCB are still produced as unwanted
by-products in combustion and other industrial processes. The other chemicals are
pesticides. Most of these have been banned or have restricted use in many developed
countries. However, their use continqes in some developing countries.
Once released into the environment, many POPs, including some persistent
organochlorines, become airborne and may be transported for thousands of kilometres
in the atmosphere before condensing and falling back to the earth’s surface. As a
result of long-distance transport and their immense production and usage, many POPS
have become widespread global contaminants. There is evidence that some are carried
on air currents from warmer regions to polar regions. This process, known as “global
fractionation” is believed to be the reason why high concentrations of these chemicals
are now found in Arctic and Antarctic regions, where they have never even been used
(Wania and Mckay 1996).
i
Human exposure to many persistent organochlorines is unavoidable since these
chemicals are present in food. Due to their lipophilicity and bioaccumulative
properties, the highest levels are present in meat, fish and dairy products (Hall 1992).
Pesticide residues may also remain in some foods and low levels may occur in
drinking water (Culliney et al. 1992, HMSO 1995). Although food is the major
pathway of exposure to many persistent organochlorines for the general population,
exposure by inhalation or dermal contact is also possible.
1.1
POPs in Human Tissues
As a consequence of the persistent, lipophilic, bioaccumulative properties of many
POPS, and tendency of some to biomagnify within food chains, long-term exposure to
relatively small concentrations of these compounds leads to the accumulation of
considerable deposits in animal and human tissues. S.tudies which have monitored
levels of organochlorine POPs in human tissues provide scientific evidence that
humans are exposed to these chemicals. Indeed research from numerous countries has
6
demonstrated that measurable quantities of organochlorine pesticides, PCBs and
PCDD/Fs are present in human adipose tissue, blood and breast milk (Jensen and
Slorach 1991). Measuring levels of POPs in tissues is one of the most accurate and
precise ways of assessing human exposure to these environmental pollutants. This
information is also extremely useful for studying the relationship between human
exposure to POPs and health effects (Schecter 1998).
Levels of POPs in human tissue are most commonly assessed in blood, adipose tissue
or breast milk. Studies have shown that levels are generally similar in these three
media (Thomas and Colbom 1992). In the present report, emphasis is placed on levels
of organochlorines on the UN POPs list in human milk. Monitoring of human milk
concentrations may be used to assess both temporal and geographical variations in
human exposure to persistent, lipophilic contaminants (Dewailly et al. 1996). In this
report, studies from many different countries are considered, in order to provide an
indication of differences in world-wide levels of these compounds in humans. The
majority of these studies have reported on human tissue levels within a region of a
country rather than nation-wide levels, although tissue levels throughout countries are
often similar. Trends in the levels of organochlorines in human tissue with time over
the past few years are also discussed. However, information on trends has only been
published for a few countries where studies have monitored levels on a regular basis,
or where national programmes have been carried out and made available by
government health agencies (Mes 1994).
Information for the present report was located by performing searches of the scientific
literature over the past 10 years using BIDS ISI Science Citation Index data base
service. A greater number of studies on concentrations of organochlorines in human
milk were located in the literature compared to levels in blood and adipose tissue.
1.2
Problems Comparing Human Tissue Levels of Organochlorines in
Different Countries
There are several problems which can hinder comparisons between studies which
document the levels of organochlorines in human tissues. These problems arise from
differences in the scientific methods which are used to measure the concentrations of
contaminants. For example, differences between studies may occur in sample
collection, storage, preparation, the method used for chemical analysis, mathematical
analyses and data interpretation (Thomas and Colbom 1992). A difference in the
sensitivity of an analytical method for instance could affect whether or not a
compound is detected. Fortunately, analytical methods used in many recent studies
are similar, making comparisons between studies possible.
In the present report, comparisons of organochlorine pesticide concentrations in
human milk from different countries are made. There are however some discrepancies
in the sample collection methods used between these studies, which may cause
differences in the recorded levels of organochlorines in the milk. For instance, a
factor which is known to affect the contamination levels in breast milk is parity.
Primiparous women (first time pregnancy) can have higher levels of organochlorine
chemicals in breast milk than multiparous (second, third pregnancy etc.), because
lactation reduces the maternal body burden of organochlorines. Some studies have
accounted for the influence that parity can have on breast milk concentrations of
7
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organochlorines by only selecting primiparous women (eg. Dewailly et al. 1996).
However, many studies have not controlled for this factor and have analysed samples
from both primiparous and multiparous women.
Since a number of differences in the methodologies occur in studies from various
countries, results of these studies are not directly comparable. However, in the present
report, a comparison of such studies is made because this can at least give an
approximate indication of the variation in levels of organochlorine contaminants
between different countries.
Concentrations of environmental contaminants in human tissues are reported either on
a whole weight basis of the tissue concerned, or more often on the basis of
concentration in extractable fat (lipid) of the tissue. With regard to breast milk, the fat
content is highly variable between individuals, and the fat content influences the
concentration of fat soluble chemicals, such as organochlorines, in the milk. It is
therefore more favourable for organochlorine concentrations in breast milk to be
expressed on a milk fat basis since these chemicals are clearly associated with the
lipid fraction in milk (Quinsey et al. 1996).
In this report, organochlorine concentrations in human milk which have been reported
in the literature are given on a milk fat basis wherever possible. Unfortunately, data
on breast milk in studies from some countries is only reported on a whole weight
basis. These data are presented here in separate tables, because results on
wholeweight and lipid basis are not directly comparable.
13
Relevance of Current Human Tissue Levels of Organochlorines to
Human Health
Dioxins, PCBs and several organochlorine pesticides have been associated with
adverse health effects in humans and animals (eg. Allsopp et al. 1995, Allsopp et al.
1997). A wide array of effects have been documented including endocrine disruption,
neurotoxicity, immunotoxicity, reproductive disorders and cancer. In humans, such
effects have been reported following relatively high exposure to these chemicals as a
result of accidental or occupational exposure. However, studies also indicate that
some effects may occur at tissue levels which are at, or near to, those of the currently
found in general population as a consequence of unavoidable everyday human
exposure to these compounds.
Scientists have hypothesised that endocrine disruption - the disruption of hormone
systems in wildlife and humans - could be the mechanism by which some chemicals
cause many adverse effects on health. This has potentially implicated endocrinedisrupting chemicals in possible health effects on the general population such as
decreasing sperm counts, increases in reproductive problems, reduced intellectual
capacity and behavioural problems.
Chemicals which are known or suspected to disrupt the endocrine system based on
experimental evidence, include most of those POPs listed by the UNEP. These are
dioxins, PCBs, and the organochlorine pesticides DDT, DDE, chlordane, dieldrin,
hexachlorobenzene, mirex and toxaphene (Allsopp et alA997). The organochlorine
chemicals listed by the UNEP as priority POPs may also cause toxic effects through
mechanisms other than endocrine-disruption. For example, dioxins and certain PCBs
8
.1
appear to cause a broad range of health effects through their actions on a receptor in
the body, known as the Ah receptor.
It is difficult to predict the possible effects of current body burdens of organochlorines
on health in the general population. In a review of scientific data on dioxins, the US
EPA suggested that the potential for adverse impacts on human metabolism,
reproductive biology, and immune competence are at, or within one order of
magnitude of average background body burden levels in the general population. They
also noted that individuals at the high end of the general population range may be
experiencing some of these effects (US EPA 1994). Of perhaps the greatest concern is
the possible impact that organochlorines may have on the developing young. The
transplacental passage of organochlorines to the developing foetus has been well
documented and these chemicals may also pass to the infant via mother’s milk. There
is evidence which suggests that endocrine-disrupting chemicals, including some
organochlorines, may have reached Ipvels in the environment where they could cause
adverse effects on development in humans and animals. Such effects are subtle rather
than gross, representing a diminished potential, such as reduced fertility, reduced
intellectual capacity and weakened immune system (eg. Colbom et al. 1993, Colbom
1996). Recently, there has been concern among some scientific experts that impacts of
endocrine-disrupting chemicals on health could pose a long-term threat to world
biodiversity and to human society (Alieva et al. 1995).
1.3.1 Highly Exposed Members of the Population
The present report discusses human tissue concentrations of organochlorines found in
various countries. Individuals who are subjected to higher exposures than the
population at large are also identified. For most of the organochlorines, these
individuals include nursing infants, occupationally exposed individuals, and people
who have a high fish or sea mammal consumption such as Inuit and other Arctic
indigenous people.
Occupational Exposure
Tissue levels of organochlorines in occupationally exposed individuals are briefly
discussed in this report. In comparison with studies on tissue levels in the general
population, research on tissue levels in occupationally exposed individuals is limited.
It is also of concern is that adverse health effects have been associated with
occupational exposures to some organochlorines, and these chemicals are still
produced or used in many areas of the world.
Nursing Infants
With regard to nursing infants, persistent chemicals whiph have accumulated in a
woman’s body during her lifetime pass into her breast milk and hence to her infant.
Indeed, lactation is one way that a mother can significantly reduce her own body
burden of organochlorines, but this is at the expense of her nursing infant (Schecter
1996c). The fully breast-fed infant is nourished solely by human milk usually for a
period of up to 6 months. Such exclusive consumption, which differs markedly from
that of the general population as a whole, potentially exposes the infant to
contaminants in breast milk at a time when intake of contaminants per body mass is at
its highest. As breast milk is at the top of the food chain, it contains higher
9
concentrations of organochlorines than most other diets, thus placing breast-fed
infants at special risk for potential toxic effects (see Quinsey et al. 1996).
Despite potential disadvantages of breast feeding to infants, because of chemical
contaminants in milk, it is important to recognise that breast feeding conveys many
advantages. Breast feeding has both nutritional and immunological benefits and
promotes good health generally. In many countries, breast feeding confers measurable
benefits such as decreased rates of infectious disease and increased rates of growth
and development (Sonawane 1995). The advantages of breast feeding have therefore
led to its encouragement and recommendation by health experts, even though there is
concern over chemical contaminants in human milk (eg. WHO 1996, MAFF 1997).
Exposure of the foetus in the womb to organochlorines via placental transfer, and
exposure of the infant via breast milk are of great concern to health, because these
chemicals may interfere with processes of growth and development. Immature
physiological functions of the foetus and infant theoretically make these age groups
more vulnerable to chemical exposure (Ostergaard and Knudsen 1998). The World
Health Organisation (WHO 1986) concluded that infants may be more vulnerable
than older children to chemicals for several reasons, including their larger body
surface area compared to weight, higher metabolic rate and oxygen consumption, and
different body composition. In addition, infants may be more susceptible to
organochlorines because of their immature liver and kidneys, and the central nervous
system is not fully protected in infancy. Also, several components of the immune
system are not fully developed at birth and it is possible for chemicals to interfere
with the development of this system (Ostergaard and Knudsen 1998). In sum, both the
foetus and infant are potentially the most vulnerable lifestages to toxic insult from
chemical exposure. It is important to note that effects caused during development may
not just affect the health of the foetus or infant, but may cause permanent irreversible
damage. Some effects may not even become apparent until later in life (Colbom et
aL\993).
For persistent organochlorines listed by UNEP, there is experimental evidence that
some adversely affect developmental processes (eg. ASTDR 1997). In addition, those
which are endocrine-disrupters could potentially be detrimental to development.
Subtle effects on development have been associated with exposure to PCBs and /or
dioxins in more highly exposed members of the general population (Allsopp et
al. 1995, Allsopp et al. 1997). In the Netherlands, studies on healthy women and their
children from the general population revealed that subtle effects on the nervous
system were associated with in utero and lactational exposure to PCBs and dioxins
(Koopman-Esseboom et alA995, Ilsen et al. 1996).
L3.2 Acceptable Daily Intakes of Organochlorines
In an attempt to protect public health, regulatory agencies perform risk assessments to
set levels of chemical contaminants in the food supply which deemed to be ‘safe’ and
therefore permissible. Depending on the regulatory body concerned, permissible
levels set for consumption of chemical contaminants in food are known by as
Acceptable or Admissible Daily Intakes (ADIs), and Tolerable Daily Intakes (TDIs).
The ADI of a chemical has been defined as the daily intake of a chemical that, during
a lifetime, appears to be without appreciable risk on the basis of all the facts known at
10
that time (see Stevens et al. 1993). The concept of the ADI is based on the assumption
that a threshold exists below which a chemical does not cause toxicity. They are
usually based on experiments on the toxicity of the chemical concerned in laboratory
animals, from which a lowest observable effect level (LOAEL) or no observed
adverse effect level are obtained. In general, the lowest dose value is used to
determine a ‘safe’ level in humans. This result is then divided by a safety factor,
usually the arbitrary number of 100, to account for differences in response of
laboratory animals and humans, and differences in sensitivity among humans
(Ostergaard and Knudsen 1996).
ADIs have been set by the World Health Organisation (WHO) for a number of
organochlorine pesticides including total DDT compounds, HCB, (aldrin + dieldrin),
heptachlor, heptachlor epoxide, total chlordane and lindane (WHO 1997), see table
11. ADIs have not been established for oxychlordane, aldrin, /rany-nonochlor, p,p'DDE, p,p’-DDT, isomers of PCBs, and a and B-HCH (Quinsey et al. 1996). ADIs for
dioxins have been set by a number different regulatory bodies such as US EPA and
WHO (US EPA 1994b, WHO 1992). WHO have very recently reassessed the TDI
they previously set for dioxins. ADIs/TDIs for dioxins are further discussed in section
2.5.1).
The food consumption patterns of infants and children are different from those of
adults, but no separate ADIs have been yet been established for infants or children. In
the present system, ADIs set for dioxins and organochlorine pesticides are designed to
prevent adverse health effects over a whole lifetime exposure in a 70kg adult, where a
mixed diet has a dilution effect on the consumption of contaminants (Quinsey et
al. 1996). The application of ADIs to intake of organochlorines over the short-time
period of breastfeeding is unclear (Sonaware 1995). Nevertheless, it is of great
concern that current levels of some organochlorines in human milk mean that the ADI
is exceeded when applied to infant intake. Since infants may be more susceptible to
the toxic effects of chemicals than adults, because for example, they are undergoing
rapid tissue growth and development, then it is most likely that current ADIs are
higher than appropriate for infants (Quinsey et al. 1996). It is noted by these authors
that infancy is a critical period in development and guidelines for the intake of
organochlorines should not be exceeded.
In this report, an attempt is made to estimate whether ADIs would be exceeded for a
breast-fed infant, based on levels of organochlorines in breast milk reported for
different countries. This is possible by calculating the “Estimated Dietary Intake”
(EDI), which is the amount of a contaminant taken in through diet. For a breast-fed
infant, the EDI for a particular organochlorine is the intake of that chemical it would
have through breast milk. The EDI can be compared to the ADI to find out whether it
is exceeded (Dogheim et alAWV).
Several studies on levels of organochlorines in breast milk have calculated EDIs to
determine whether an infant’s intake of various organochlorines exceeds the ADI. To
calculate the EDI, estimations of the volume of milk consumed by the infant and the
fat content of the milk are made. Typically, values used are 0.75 litres of milk per day
for a baby weighing 5 kg in the first 2 to 3 months of life, and a milk fat content of
3.5% (WHO personal communication, Quinsey et al. 1996). However, in reality the
actual volume of milk intake varies widely from one individual to another, and the fat
content of breast milk is also variable. The use of estimated values to calculate the
1]
EDI therefore only gives an approximation of the actual intake of contaminants in the
milk. A more accurate way to calculate intake of organochlorines by an infant is to
measure the concentration of an organochlorine in breast milk from each mother, and
the volume of milk her baby consumeTeach day. Whether an individual baby's intake
of an organochlorine exceeds the ADI is then known. However, very few studies have
measured the daily volume of milk taken in by each individual baby. One recent study
did measure actual intakes of milk by individual babies and subsequently calculated
whether or not the ADI was exceeded for various organochlorines. It reported that
actual intakes of organochlorines by infants determined in this way was different to
results calculated using estimated milk intakes. The study therefore concluded that
using inferred estimated milk intakes were not reliable indicators of actual intakes.
Despite this finding, it is nevertheless deemed scientifically acceptable to estimate
milk intakes (Quinsey et al. 1996).
In this report, the concept of the EDI is used to provide an approximate guide to the
extent to which ADIs are exceeded in different countries, based on average levels in
breast milk. Figures for volume of milk intake and milk fat content used in
calculations are as those given above.
2.
POLYCHLORINATED DIBENZO-p-DIOXINS (PCDDs),
POLYCHLORINATED DIBENZOFURANS (PCDFs) and
POLYCHLORINATED BIPHENYLS (PCBs)
2.1
Introduction
The term “dioxins” is a common term, but not proper chemical nomenclature, for a
class of chemicals known as polychlorinated dibenzo-p-dioxins (PCDDs) and
polychlorinated dibenzofurans (PCDFs). The number of chlorine atoms in these
compounds varies between 1 and 8, resulting in a possible 75 different PCDDs and
135 PCDFs. The most toxic congener (member of the group) of these chemicals is
2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Another group of chemicals, the PCBs,
constitute a group of 209 congeners. Certain PCBs have been found to exert similar
toxicity to TCDD, and are known as dioxin-like PCBs. Other related groups of
chemicals which have dioxin-like toxicity include the brominated and
chloro/brominated dioxins (see section 2.7). A recent analytical study reported the
presence of more than 100 phenolic organohalogenated substances in human blood,
that is chlorinated, brominated and mixed chloro-brominated phenols, hydroxylated
and dihydroxylated PCB metabolites (Wehler et alAMI). There is evidence that
chemicals which cause dioxin-like toxicity exert their toxic effects by binding to a
receptor in cells known as the Aryl Hydrocarbon (Ah) receptor.
Analytical techniques developed during the past few decades have made it possible to
measure PCDD/Fs and PCBs down to parts per trillion, and on occasion, parts per
quadrillion levels in human tissues (Schecter et al.WM). Studies have focused on the
levels of 17 PCDD/F congeners in adult human tissues. These 17 toxic congeners are
the 2,3,7,8-substituted PCDD/Fs (Schecter 1994). The techniques for measuring
PCDD/Fs and PCBs improved greatly in accuracy in the early 1990s (WHO 1996).
PCBs have been measured by a variety of methods. Levels have been reported as an
approximation of total PCB content expressed in terms of a commercial PCB mixture
12
such as Aroclor 1242 or 1260, or as individual PCB congeners. It is only in the past
few years that techniques have been developed to measure levels of the dioxin-like
congeners. These include non-ortho, mono-ortho and di-ortho PCB congeners. These
PCBs are especially toxic, since they act like dioxins in the body. They have recently
been found to be present in significant concentrations in human tissues.
The concentration of PCDD/Fs and dioxin-like PCBs in environmental or biological
samples, are often converted and expressed in terms of toxic equivalents (TEQ). This
system is a means of expressing the combined toxicity of mixtures of PCDD/Fs and
PCBs, rather than indicating just the concentration. The system most commonly
adopted is the International TEQ (Schecter 1994).
In the International TEQ system, the most toxic congener, TCDD, is assigned a dioxin
toxic equivalency factor (TEF) of 1.0. Other congeners are given a TEF value ranked
in relation to this. For example, one of the least toxic congeners included ii^the TEQ
system is OCDD which is designated the lowest TEF value of 0.001. To determine the
TEQ value of a congener, the concentration of the congener is multiplied by its TEF
value. The total toxicity (total TEQ) for a mixture of PCDD/Fs and PCB, can then be
established by summing values for the individual congeners together (NATO/CCMS
1988, Ahlborg et al. 1994). Note that throughout this section and in the
corresponding tables, the levels of PCDD/Fs and PCBs are expressed as International
TEQ, specifically parts per trillion TEQ, calculated on an extractable fat basis, unless
other units are specified. There are other TEQ systems in use, for example Nordic
TEQs, in which the TEF values vary slightly from the International TEQ system, so
that they are not directly comparable. In this report, there are a few figures that are
presented as Nordic rather than International TEQs, and this is clearly denoted in the
text.
With regard to PCBs, the TEQ system only considers those congeners which are
thought to exert their effects through the Ah receptor, that is, dioxin-like PCBs.
However, there are PCBs which act via mechanisms other than the Ah receptor. These
PCBs are not considered by the TEQ system but they are not necessarily harmless
(see Fisher et al. 1998).
2.2
Studies on Tissue Levels of PCDD/Fs in the General Population of
Different Countries
Many studies published in the 1980s and 90s have reported on the levels of PCDD/Fs
in human milk, blood and adipose tissue. In this review of the data, emphasis is placed
on breast milk levels for which most literature was found to be available.
Studies have shown that levels of dioxins differ somewhat between different human
tissue types. Blood lipid generally contains the highest dioxin and furan levels,
secondly adipose tissue lipid, and finally milk lipid (Schecter 1998).
A general observation of human tissue levels of PCDD/Fs on a world-wide basis is
that the highest levels are evident in industrialised countries. This is due to the release
of these chemicals as by-products of many industrial processes, notably those
involving production, use or disposal of organochlorines. In addition, dietary habits
may also play a role in the levels of PCDD/Fs in human tissues. The highest levels of
PCDD/Fs are present in meat, fish and dairy products (MAFF 1992). It is therefore
13
probable that diets in counties involving consumption of high levels these foodstuffs
could result in increased levels of PCSD/Fs in human tissue.
Several studies were carried out in the 1980s that investigated levels of PCDD/Fs in
human tissues from a number of countries (reviewed by Schecter 1994). These studies
showed that levels of PCDD/Fs in human milk, blood and adipose tissue varied
widely between different countries (see tables la, 1c, Id). Levels were considerably
lower in less industrial countries, such as Thailand, China, Pakistan, Africa, northern
Vietnam and Russia. Higher levels were characteristic of more industrial countries,
such as the USA and some European countries, reflecting higher chemical use and
contamination in these regions. Within each country itself, there was usually little
geographic variation in levels of PCDD/Fs. An exception to this is Vietnam, where
levels are much higher in South Vietnam than in North Vietnam. This is because of
the use of Agent Orange in South Vietnam the war, a herbicide which was
contaminated by dioxins, and also as a result of more industrial contamination. When
the individual dioxin congeners are considered, characteristic patterns emerge for
some countries. For example, European tissue samples have higher levels of a
congener (2,3,4,7,8-PnCDF) than US and Canadian samples, which may be due to the
use of more leaded petrol in Europe (Schecter 1994).
Blood
Table la shows results of studies on blood levels which spanned 1980 to 1991. In
these studies, samples from individuals were taken and then pooled together before
analysis. Results showed that similar total TEQ levels were found in Europe and in
the US. For example, levels of 41 ppt TEQ were recorded in the US and levels of 42
ppt TEQ in Germany. Studies conducted in the 1990s show that levels in these
countries are now lower. For example, a value of 26 ppt TEQ was recently recorded
for the US (table lb). For the most toxic dioxin congener, TCDD, an average of 3 to 6
ppt TEQ is reported for the US (US EPA 1994).
More recently levels of dioxins in humans have been characterised for the first time in
three Middle Eastern countries (table lb), (Schecter et alA991). Blood samples were
collected in 1995 and 1996 from the Palestinian West Bank, Gaza and Israel. Samples
taken in the Binghamton, New York, in 1996 are also given. It appears that levels in
Israel (26.6 ppt TEQ) are similar to those now present in the US (26.8 ppt TEQ).
Levels are somewhat lower in the West Bank (16.9 ppt TEQ) and Gaza (8.4 ppt
TEQ), reflecting levels in less industrialised countries (Schecter et al. 1997). Recent
analysis of blood samples in Germany showed levels (16.5 ppt TEQ) were lower than
those recently measured in the US (Papke and Ball 1997). Sources of dioxins in the
Middle East are believed to be food imported from Europe and elsewhere, use of
herbicides such as 2,4-D phenoxyherbicides, incineration of plastics and toxic
chemicals and other incineration. Incineration of waste is common and dioxin
standards for emissions have not yet been established. Large municipal waste
incinerators are planned in Israel (Schecter et al. 1991).
Adipose Tissue
Table 1c shows adipose tissue levels of PCDD/Fs (TEQ) which were reported for
various countries. There was more variation in adipose tissue levels between countries
than reported for blood levels. However, research on adipose tissue involved fewer
samples compared to work on blood levels, which reduces confidence in the accuracy
14
of the mean TEQs reported (Ryan et alAWh Schecter 1994, US EPA 1994). The
levels found in Japan, Europe, North America and South Vietnam were similar. In
comparison, levels in China and North Vietnam are lower than in the more
industrialised countries (Ryan et al. 1987).
Recently, a study reported adipose tissue levels of PCDD/Fs in Korea, an
industrialised Asian country (Kang et al. 1997). The mean level of PCDD/Fs in 32
individuals was 18 ppt TEQ. This value is in the same order of magnitude as levels
reported for China and South Vietnam in the 1980s, but lower than levels in other
industrialised countries. A recent study in two different regions in Japan, 1992,
recorded levels of 50.4 and 43.8 ppt TEQ in adipose tissue. Lower levels were found
in the same two regions in 1993 were reported, respectively 17.4 and 25.6 ppt
(Sawamoto et al. 1994). This study was based on very limited sample numbers
although levels are not dissimilar to those reported in the 1980s, 38 ppt TEQ (see
table 1c).
J
Breast Milk
Table Id shows levels of PCDD/Fs found in breast milk in the 1980s for various
countries reported by Schecter (1994). Again these studies showed that higher levels
were evident in industrialised countries while lower levels were found in less
industrialised countries. For instance, levels were similar (20-27 ppt TEQ) in USA,
Canada, Japan, Germany and highest in South Vietnam. Lower levels (9-13 ppt TEQ)
were found in Russia, Pakistan and North Vietnam. The lowest levels (3 ppt TEQ)
were found in Thailand and Cambodia.
The most comprehensive set of studies to date on the levels of PCDD/Fs and PCBs in
human tissue from many countries was performed by the World Health Organisation
(WHO) on breast milk samples in the late 1980s and early 1990s (WHO 1996). This
research was undertaken to assess the exposure to PCDD/Fs and PCBs that infants
would be subjected to by breast-feeding and the possible health risks of such
exposure. Other, more detailed studies on breast milk levels within countries during
this period have also been carried out in The Netherlands and in Germany (see Liem
and Theelen 1997, Furst et al. 1994). In addition, several studies undertaken in recent
years have been published on breast milk levels in western countries. These include
studies in Sweden (Noren 1993), Norway, Sweden and Denmark (Clechaas et
al. 1992), Germany (Beck et al. 1994), Netherlands (Koopman-Esseboom et al.\994),
UK (Weame et al.\9%), France and Spain (Gonzalez et alAW\ Jimenez et alAWb),
Japan (Hashimoto et alA995), New Zealand (Bates et al. 1994) and USA (Schecter et
alA996).
The WHO study collected breast milk samples initially in 1987-88 and in a second
round of studies in 1992-93. In the second round, samples of breast milk from
women in 17 countries were taken from 39 different areas with different pollution
levels. With the exception of two countries, The Netherlands and Denmark, samples
for each country were pooled, (i.e. mixed together), and subsequently analysed for
PCDD/Fs and PCBs.
Results of the 1992-3 study are given in table 2a. The highest PCDD/F levels (20 to
30 pg TEQ/g fat or ppt) were found in Belgium, Canada (Gaspe and Hudson Bay
regions), Finland (Helsinki), Spain (Gipuzkoa) and The Netherlands. In the majority
15
of milk samples, levels were in the range of 10 to 20 ppt TEQ. The lowest levels (410 ppt TEQ) were measured for Albania, Hungary, Pakistan and the less industrialised
regions in Croatia, Norway and the Russian Federation (WHO 1996). The results
were thus complementary with research conducted the 1980s by Schecter et al.(YWl)
discussed above on breast milk since they also demonstrated that levels of PCDD/Fs
were lower in less industrialised countries.
Several studies have reported on levels of PCDD/Fs in human milk from countries
that were not assessed in the WHO study (see table 2b). A study on levels in France
(Gonzalez et al. 1993) reported a level of 20.1 ppt TEQ. This is similar to levels in
some other European countries. This study also recorded a level of 13.3 ppt TEQ for
Spain which is somewhat lower than the level of 19.4 ppt TEQ reported by WHO. A
study on breast milk samples taken 1986-91 in Estonia, Finland, Norway and Sweden
showed that similar levels of PCDD/Fs in breast milk were apparent in these countries
(Mussalo-Rauhamaa and Lindstrom 1995). Data for these countries are presented in
table 2b since the WHO study (WHO 1996) did not report figures for Estonia or
publish figures for Sweden. A study in New Zealand reported a mean TEQ of 16.5 ppt
for urban women and 18.1 ppt for rural women (Bates et al. 1994). A recent study in
Japan reported levels of PCDD/Fs in human milk (Hashimoto et al.X^S). Figures for
this study were presented on a whole milk basis rather than on a lipid basis and so are
not directly comparable with figures from studies presented here. However, the
authors documented that levels found in breast milk samples taken from several
places in Japan were similar to other industrialised countries in Europe. This concurs
with results for Japan in the 1980s (table Id), which showed that Japanese levels were
similar to European, Canadian and North American levels (Schecter et al. 1994).
Slight regional differences in levels of PCDD/Fs have been found to occur within
some countries. For instance, slightly but not statistically significantly elevated levels
were reported for urban or industrial areas compared to rural areas in Austria,
Belgium, Canada, Norway and Sweden in 1988 by WHO. A study in the Netherlands
found that human milk contained levels of a number of PCDD/Fs and dioxin-like
PCBs which were significantly higher in the western industrialised areas of the
Netherlands compared to the more rural north (Koopman-Esseboom et al. 1994).
To summarise on concentrations of PCDD/Fs in human tissues, it is evident that
levels are generally higher in more industrialised countries and lower in less
industrialised countries. On the same theme, regional differences within countries
have also been found. Importantly, information on tissue levels of dioxins has been
generated largely by researchers in the West, and the most wide-reaching study has
been co-ordinated by WHO (WHO 1996). Analysis of PCDD/Fs is relatively
expensive and WHO has certified fewer than 50 laboratories world-wide for the
analysis of PCDD/Fs (Schecter 1998). The majority of studies have been performed in
in
western countries, and most information published for European countries. Data is
also documented for several Asian countries in the 1980s, discounting India, and one
study in the 1990s investigated levels in three Middle Eastern countries. Only very
limited data was available for Africa (1980s) and no studies were found for South
American countries.
16
2.3
Studies on Tissue Levels of PCBs in the General Population of Different
Countries in the 1980/90s
In addition to PCDD/Fs, some studies have also measured levels of PCBs in human
tissues. Recent studies which have monitored PCDD/Fs and dioxin-like PCBs, have
found that PCBs contribute substantially to the total dioxin TEQ.
Comparisons of levels of PCBs in human tissues is difficult, because in some studies
PCB mixtures have been measured while in others specific PCB congeners have been
measured. In addition, the congeners which have been assessed vary from study to
study. Finally, the techniques used to measure PCBs have vastly improved in the past
few years. Due to such differences in published studies, this report only discusses data
from different countries for which comparisons can be made.
Breast milk
The WHO 1992-3 study measured dioxin-like PCBs (non-ortho and mono-ortho
PCBs) and several indicator PCBs. The specific congeners which were measured
were: non-ortho PCBs with IUPAC numbers 77,126 and 169; mono-ortho PCBs nos.
105 and 118; marker PCBs nos. 28, 52, 101, 138, 153, 180. The study showed that
levels of these compounds did not correspond to the ranking of high to low levels of
PCDD/Fs which had been found for the different countries. Thus, countries which had
displayed high levels PCDD/Fs in human breast milk did not necessarily also have
comparably high levels of PCBs. In fact, most countries and regions were found to
have similar levels of PCBs, and only a few had significantly higher or lower levels.
The majority of samples had levels of dioxin-like PCBs below 15 ppt TEQ. High
levels of dioxin-like PCBs (20-30 ppt TEQ) were found in Lithuania and in two
samples from Canada ( in Basse Cote-Nord, Hudson Bay), whilst levels of marker
PCBs were higher in the Czech Republic (Uherske Hradiste), Slovak Republic
(Michalovce) and Canada (Hudson Bay). Notably lower levels of all PCBs were
found in Albania, Pakistan and Hungary. Results of the WHO study and other studies
on areas in the former Soviet Union, show that while levels are PCDD/Fs are similar
to many European countries, levels of PCBs are notably higher (Traag and Yuft
1997).
In The Netherlands, a recent study on 78 individual breast milk samples also
measured dioxin-like PCBs. The specific non-ortho congeners which were measured
(nos.77, 126 and 169) were the same as those in the WHO study, but in addition to the
mono-ortho congeners measured by the WHO study (nos 105 and 118), this study also
measured other mono and di-ortho congeners (nos. 156,157,167, 180 and 189). The
study concluded that dioxin-like PCBs contributed to about half the total TEQ and
PCDD/Fs the other half. For example, the average total TEQ value in the study was
43 ppt TEQ, for which PCDD/Fs contributed 23.5 ppt and PCBs the remainder.
Examining data in table 2a from the WHO study reveals that the contribution that
PCBs make to the total dioxin TEQ varies considerably between different countries.
For example, in Belgium PCBs are very low in comparison with PCDD/Fs, whereas
in Tromso, Norway the TEQ for PCBs is twice that of the PCDD/Fs. The WHO study
also reported that the contribution that mono-ortho and non-ortho PCBs made to the
PCB TEQ varied from one region or country to another (WHO 1996).
17
Blood
Studies on blood concur with research on breast milk in that they also show that PCBs
may also contribute significantly to the total TEQ. In a recent study, blood samples of
5 individuals of the general population in Kansas City, Missouri were analysed. The
study found that the total PCDD/Fs plus dioxin-like PCBs in these US samples
averaged 69.2 TEQ. (All measurable non-ortho PCBs, 77, 126 and 169, and mono and
di-ortho PCBs were analysed). Of the total TEQ, PCDDs contributed 26%, PCDFs
7% and PCBs 68% (non-ortho 9% mono-ortho 56%, diortho 2%). These results imply
that PCBs may contribute substantially to total dioxin TEQ in blood in US adults.
Similarly, a study in Wales, UK, found that PCBs made an important contribution to
the total dioxin TEQ. This research indicated that PCBs contributed at least twice as
much to the total TEQ than PCDD/Fs (Duarte-Davidson 1993).
2.4
Time Trends
Methods for analysing PCDD/Fs and PCBs in breast milk have improved remarkably
during the 1990s. Results of the second (1992-3) round of the WHO study were
consequently more accurate than those of the first round due to this fact, and because
of improved study design, for example, less laboratories used to analyse samples. In
the first round, when results from different countries were compared, only a tendency
could be reported on human milk levels because of inaccuracies in the data which
may have arisen from sample analysis. Despite such possible inaccuracies, data on the
levels of PCDD/Fs and marker PCBs in the first and second round of studies have
been compared in an attempt to identify any trends in the levels of these chemicals
that may be occurring with time.
PCDD/Fs
For the 11 countries studied in the first and second round, which included some
Scandinavian and European countries and Canada, it was concluded that levels of
PCDD/Fs were not increasing with time. In fact, the levels in some countries in
1992/3 had decreased compared to 1987/8. Some countries showed a dramatic
decrease of up to 50%. The overall annual decrease in PCDD/F levels in Europe and
Canada was estimated to be 7.2% per year (standard deviation 0.8%). Table 2a shows
levels of PCDD/Fs found in the 1987/8 and 1992/3 studies. Trends cannot be
established for countries outside of Eof&pe and Canada in the WHO study because
data from these countries was not gathered in the first round of studies.
A study in Sweden showed that there was a decrease in the levels if PCDD/Fs in
breast milk between 1980 and 1985, but not between 1985 and 1989 (Noren 1993).
Detailed studies in the Netherlands (reviewed by Liem and Theelen 1996) and in
Germany (Furst et al.VFM) have also shown that breast milk levels of PCDD/Fs have
declined in recent years. Studies in these countries constitute the most extensive
dataset based on individual analysis of breast milk samples, although again some
uncertainties in results due to the study designs cannot be ruled out. In the
Netherlands, a survey in 1993 found a mean level in breast milk of 23.5 ppt TEQ.
This was 32% lower than the mean level of 34.2 ppt TEQ which was found in 1988.
Similarly, a recent analysis of data based on individual breast milk samples and
pooled breast milk samples in Germany, found that levels had decreased by 30% from
23 ppt TEQ in 1991 to 16 ppt TEQ in 1995. At the same time, blood levels were also
18
reported to decline from a level of 42 ppt TEQ in 1989 to 19 ppt TEQ in 1994 (Furst
et al. 1994) and to 16.5 ppt TEQ in 1996 (Papke and Ball 1997). In the UK, breast
milk levels were reported to fail by 35% between 1987/88 and 1993/94 (Weame et
alA996).
Taken together, these European studies suggest that measures taken in the past few
years to reduce dioxin emissions and subsequent contamination of the environment
and food chain, may have already resulted in the reduction of human body burdens in
these countries. Results from diet studies in the Netherlands and Germany and the UK
also indicate that dietary intake levels have decreased ( Liem and Theelen 1997, see
Schecter et al. 1996, Weame et al. 1996). It has been suggested that declining levels in
food and human milk and blood may reflect environmental regulations for
incinerators and a decrease in the use of leaded petrol. Nevertheless, it has been noted
that it is difficult to explain in biological terms the extent of the decline in human
levels of dioxins over a short time period, because the half -lives of elimination of
dioxins (7 to 11 years) would predict a slower decrease with time (Schecter et
alA997).
Although the above studies suggest that PCDD/F TEQ levels have decreased in the
last few years in several European countries and Canada, levels in some countries
such as Denmark and Finland do not show a decline. In addition, recent research in
the US does not clearly show a decrease in body burden. When 4 individual blood
samples were considered from 1995 (8.7 ppt TEQ), levels appeared to have decreased
since the 1980s and 1992 (26 and 23 ppt TEQ respectively). Similarly, breast milk
data for 5 individual samples from 1995/6 showed a decline from 20 to 8.1 ppt TEQ.
However, when pooled US blood samples, (n=100), taken in 1996, Binghamton, New
York, were considered, there was no declining trend in recent years, with levels in
1996 being 27.6 ppt TEQ (Schecter et alA996). The authors noted that both the
above mentioned German (Furst et al. 1994) and US studies represented samples from
among the largest collections of blood and milk in these countries. However, these
results may not be completely representative of levels in the general population since
the samples were not collected in a systematic fashion (Schecter et alAWlb).
In summary, available research on time trends of PCDD/F levels in human milk
shows that levels are not increasing in Canada, USA, and several European countries.
The research indicates that levels in some of these countries has declined over the past
decade but in others has remained stable. There are still uncertainties in assessing time
trends of PCDD/F levels within and between studies because of possible differences
in sampling strategies and analytical techniques. No data on time trends was located
for developing countries.
PCBs
The situation regarding PCBs is somewhat different to PCDD/Fs. The few studies
available show PCB levels have remained more steady and less of a decline is
apparent. A study in Sweden analysed blood samples which had been stored frozen
for several years. It found PCBs declined between 1972 and 1980, but did not decline
between 1985 and 1989 (Noren 1993). A study on-breast milk in Germany reported
that for PCB congeners 138, 153 and 180, levels appeared to remain constant from
1984 to 1989, although in the following two years results indicated a slight decline
(Furst et al. 1994). Studies in 1988 and 1993 in the Netherlands reported no change in
19
indicator PCB levels in breast milk (Liem and Theelen 1997). However, a diet survey
has revealed reductions in the dietary exposure to these PCBs between 1978 and
1993. It has been suggested that this discrepancy between human tissue levels and
levels in dietary foodstuffs may occur because PCBs have longer elimination half
lives (take longer to be eliminated from the body) than PCDD/Fs. The WHO study
was inconclusive regarding trends in PCBs because different, and sometimes less
reliable, analytical methods were used by some laboratories in the first round of the
study (WHO 1996).
2.5
Highly Exposed Populations
2.5.1
Nursing Infants
Nursing infants are exposed to chemical contaminants from their mother’s breast
milk. Studies that have examined levels of PCDD/Fs and PCBs in breast milk,
compared with the amount of these compounds excreted by the infants, have shown
that they are highly absorbed by the infants. For instance, it was found for most
PCDD/F and PCB congeners that the absorption from mother’s milk of the ingested
compounds was over 95% (Dahl et al. 1995).
s
The quantities of PCDD/Fs and PCBs that are absorbed by the infant via breast
feeding have prompted concern. Studies have shown that while the mother’s body
burden of these chemicals decreases during lactation, at the same time the infant’s
body burden increases. For example, the decreasing maternal body burden was shown
in a study of Swedish women. It was found that the level of PCDD/Fs and PCBs in
breast milk decreased by at least 12% per month during the first 3 months of breast
feeding (Lindstrom et al.WM, Dahl et al.\995). Another study on a woman who
nursed twins for two years reported the levels of PCDD/Fs in breast milk decreased
from 16.9 to 3.1 ppt TEQ during this period, and levels in blood fell from 14 9 to 4 9
(SChuCter et aL 1996b and 1996c)- 7116 decrease in a mother’s body burden of
k
j Wlth a concomitant increase in the body burden of the child was illustrated
by a study on a German woman and her first and second child. Both infants were
reast fed for 6-7 months. Following breast-feeding, the level of PCDD/Fs in blood
from the first child was 37.5 ppt TEQ and in the second child was 16.0 ppt TEQ.
These levels significantly exceeded those of the mother. When each child was 1 year
old the level of PCDD/Fs m the first child’s blood was 3.6 times higher than the
mother and the level in the second child’s blood was 2.9 times higher (Abraham et
• I y
kz J •
ADIs have been set for PCDD/Fs, but these are highly variable depending on the
regulatory body in question. For example, the Tolerable Daily Intake set by WHO is
10 picogram TEQ per kg body weight per day (pg TEQ/kg/d), (WHO 1992) This TDI
was updated very recently to 1-4 pg TEQ/kg/d. The ADI set by US EPA in their draft
reassessment of dioxins 1S 0.006 pg TEQ /kg/d (US EPA 1994b). This is 100 to 666
times lower than the TDI set by WHCt^
Regulatory agencies can assess foodstuffs to make sure that levels of chemicals in the
food do not exceed the established limits that are set for the protection of public
=• r I COmmercial foods’ breast milk cannot be regulated (Rogan and Ragan
1994). It is however possible to estimate the intake of chemicals by an infant via
breast milk and compare the intake with the ADI. For example, the US EPA
20
calculated the average daily dose of PCDD/Fs to which an infant would be exposed
after one year of breast feeding assuming the mothers milk contained 20 ppt TEQ
(US EPA 1994). The figure of 20 ppt TEQ in milk is synonymous with levels in
breast milk found in many industrialised countries. The calculation predicted that the
average daily dose would be 60 pg TEQ/kg body weight/day. This figure exceeds the
ADI of 0.006 pg/kg/day set by the US EPA by 1000-fold, and exceeds the TDI of 1 -4
pg/kg/day set by WHO. A study by Schecter et al\\996b) also showed that breast
feeding caused the ADI to be exceeded. The study estimated the intake of PCDD/Fs
by twins who had been breast-fed for two years. The average daily TEQ intake for
each twin was estimated to be 66 ppt TEQ/kg/day during the first year, and thus
exceeded the ADI. It is also of note that the US EPA estimated that the range of
background exposure for the general population is 1-3 pg TEQ/kg/day. 1 his figure is
similar to the WHO TDI of 1-4 pg/kg/day and greatly exceeds the ADI of 0.006
pg/kg/day proposed by the US EPA.
2.5.2 Arctic Regions
People residing in Arctic regions who consume a diet rich in seafood can be exposed
to relatively high levels of some organochlorine contaminants. To date,
organochlorine contaminants have been documented in blood from mothers living in
ten different Arctic regions as part of the Arctic Monitoring and Assessment
Programme (AMAP) circumpolar study (AMAP 1997). Participating countries
included Canada, Norway, Russia and Sweden. It was reported that average levels of
PCDD/Fs in breast milk were similar to non-Arctic regions (10-20 ppt TEQ on an
extractable fat basis). However, PCBs were elevated in some regions compared to
non-Arctic regions. The highest PCB levels were found in Northwest Greenland and
Nunavik, Northern Quebec.
A separate study was recently undertaken on PCDD/F and PCB blood levels in 499
Inuit adults from the Hudson Bay and Ungava Bay regions in Nunavik, Arctic Quebec
(Ayotte et al. 1997). Inuit people residing in the region are exposed to higher than
average levels of organochlorines through their traditional diet which includes large
quantities of sea mammal fat. In this study, individual blood samples were pooled
together into 20 samples categorised into the same age group, sex and region of
residence. These samples were compared to control samples taken from residents of
Southern Quebec. For PCBs, the study measured non-ortho PCB congeners (nos.
77,126 and 169), and mono and di-ortho congeners (nos. 105, 118, 156, 157, 170 and
180). Results showed striking differences in PCB levels between the two populations.
For Inuit men and women aged 18-39 residing in Nunavik, the total PCB
concentration was 2.0 mg/kg lipids. This is 15-fold greater than residents of Southern
Quebec where the total PCB concentration was 0.13 mg/kg. PCDD/Fs levels were
also higher in Inuit residing in Nunavik. The mean concentration was 89 ppt TEQ
which was 3.4-fold greater than residents of Southern Quebec (26 ppt TEQ).
PCBs were found to contribute very substantially (78%) to the total TEQ. Mono and
di-ortho PCBs represented 64% of the total TEQ concentration, non-ortho congeners
represented 14% while PCDD/Fs represented only 20%. This is in contrast to samples
from Southern Quebec where PCDD/Fs contributed 56%, mono and di-ortho PCB
congeners 24%, and non-ortho PCBs 20%.
21
y
A higher PCB contribution to the total TEQ appears to be typical for individuals who
consume large amounts of species from the marine food web since such species are a
high source of these chemical contaminants. For instance, a study in the Faroe islands
reported the highest PCB levels were found in the breast milk of women who
frequently ate whale meat/blubber. The levels of PCBs were 7 to 12 times higher than
in breast milk from other European women, whereas levels of PCDD/Fs were not
elevated (Grandjean et al. 1995). Another study in Sweden reported that fish from the
Baltic Sea were a major source of PCBs in people’s diets. For example, a higher fish
intake was associated with higher PCB levels in blood. The PCB contribution to the
total dioxin TEQ was nearly 80% among high consumers of fish (Asplund et
al. 1994).
In 1997, the AMAP circumpolar study reported that current exposure to PCDD/Fs is
at, or just below, tolerable daily intakes in most circumpolar nations. However, when
dioxin-like PCBs are added to the PCDD/Fs, this pushes the total dioxin TEQ
exposure well above tolerable daily intakes set by regulatory authorities (AMAP
1997). The study on Inuit women from Nunavik (Ayotte et alA997) concluded that
body burdens of PCBs and dioxin-like compounds are close to those which induced
adverse health effects in laboratory animals. However, the study speculated that
dietary benefits from the sea-food based diet still outweigh the hypothetical risks for
health.
2.5.3
Residence in Contaminated Environments
A study on tissue levels and health of a Native American community who reside
along the St. Lawrence River in New York, US, and in Ontario and Quebec, Canada,
has been continuing over the past few years. Environmental sampling has revealed
high PCB contamination in regions close to the inhabitants. The source of the PCB
contamination is most likely from leaks and discharges of nearby industries that
occurred in the past. This is of great concern since the Mohawk community rely on
local game and fish for food. The study found that Mohawk women who gave birth in
1986-89 had twice the level of total PCBs in their breast milk compared to a control
group from the general population. However, Mohawk women who gave birth in
1990 did not have higher levels in their breast milk. This was most likely due to a
significantly lower intake of fish by the mothers over time, probably as a result of
health advice. Unfortunately, in one region, Cornwall Island, levels in breast milk
remained high in mothers who have resided in the area for over 6 years. The high
levels were not related to fish consumption, but only to the time of residence in the
region. It was suggested that the PCB contamination in the area could be coming from
several sources, and the high levels in breast milk reflected multiple exposures to the
women (Fitzgerald et al. 1994).
Another study on a fishing populatiorrthat inhabits small coastal communities along
the Lower North Shore of the St. Lawrence River, Quebec, found that residents had
elevated blood PCB levels which were similar to those reported previously for Inuit in
the Canadian Arctic. The total TEQ for PCDD/Fs and PCBs in the fishing population
Was 5 -fold greater than the TEQ in urban residents in the region. The study found
that the high levels appeared to be due to largely to the consumption of seabird’s eggs
rather than fish in this area. Consumption of a single seabird egg would result in an
individual exceeding the TDI set by Health Canada for both PCDD/Fs and PCBs
(Ryan et al. 1997b).
22
In some areas of rural China, residents have been exposed to elevated levels of
dioxins because of the spraying of a dioxin-contaminated pesticide, sodium
pentachlorophenol (Na-PCP), to control the spread of snail-bome schistosomiasis.
Residents of sprayed areas had higher blood levels of total PCDD/Fs (9 to 16.3 ppt
TEQ) compared to residents living in areas which were not sprayed (4.8 to 6.4 ppt
TEQ). In addition, levels in breast milk of mothers from the sprayed regions (5.4 ppt
TEQ) were about twice those of unexposed mothers (2.6 ppt TEQ). The authors
suggested that although tissue levels of the general population in China are low
compared with levels in more industrialised countries, the higher levels in persons
exposed to Na-PCP are cause for concern (Schecter et al. 1994b).
2.5.4 Occupational Exposure
PCBs were in widespread use from the 1930s until the 70s. Their use declined
steadily thereafter as many countries throughout the world banned or severely limited
their production. Only recently however, it was revealed in unconfirmed press reports
that PCBs are still being manufectured in Russia (Washington Post 1998).
Main uses of PCBs included dielectrics in transformers and capacitors and as cooling
fluids in hydraulic systems. Studies on health impacts of PCBs on workers at
capacitor plants have been reported in the past (reviewed by Silberhom et al.\99O). In
1987, workers who had been employed for 4 to 37 years at a power plant in Zagreb, in
former Yugoslavia were found to have blood levels 2 to 4 times those of the general
population due to their handling of PCB containing materials (Krauthacker 1990).
Although PCBs are no longer deliberately manufactured, it is possible that
occupational exposure may still occur in some instances because, for example, they
are present in many old electrical appliances that will eventually have to be disposed
of. Also, PCBs have been detected in air emissions from incinerators. One theory is
that they are emitted from incinerators when PCBs are present in refuse fed to the
incinerator (US EPA 1994). A recent study at a hazardous waste incinerator in
Sweden found that the pattern of some PCB congeners present in workers blood was
similar to the pattern found in air samples at the plant. This indicated some influence
of occupational exposure in the workers although the total level of PCBs in workers
was not significantly different from blood samples taken from the general population
(Selden et al. 1997).
PCDD/Fs are produced as by-products from a wide variety of industrial processes
including the production of some chlorinated chemicals, for example, chlorophenols
and various pesticides, incineration of municipal and hazardous waste, various
metallurgical processes, certain processes in the pulp and paper industry and the
production of PVC. Consequently, there are numerous occupations where individuals
could be potentially exposed to dioxins. Indeed many studies have documented
elevated blood levels of dioxins in workers from several occupations, examples of
which are given below. In addition, there have also been accidents which have
resulted in populations being highly exposed to dioxins, such as Seveso, Italy in 1976.
Past and present production ofchlorophenols and phenoxyherbicides
Several studies have shown that occupational exposure to dioxins occurred in workers
in the 1960s, 70s and 80s at factories that produced trichlorophenol (TCP), or various
phenoxyherbicides such as 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) and 2,4-D.
23
High levels of TCDD are characteristic of occupational exposure to these
trichlorophenol-containing chemicals. For example, in Ufa Russia, two decades after
production at a plant ceased, former workers were found to have blood levels of
TCDD which were up to 10 times those of background levels in the region. Levels of
other PCDD/Fs were two to three times as high as background levels (Schecter et
aI-1992, Kruglov et al. 1995). A more recent analysis of blood samples taken in 1992
from some of these Russian workers showed that the levels of TCDD were about
twice those of in the initial reports. In addition, even administrative workers at the
plant had notably greater blood levels of PCDD/Fs than normal (Ryan et al.\99'la).
Another study on female workers from the plant was undertaken to investigate
whether their children, who are now adults, had raised blood levels as a result of
exposure transplacentally and via breast feeding. Twenty years on after initial
exposure from their mothers, the children were found to have TCDD levels which
were 150 to 2000 times higher than the general population. In most cases, levels were
™gher in the children than their mother’s, indicating that relatively large amounts of
TCDD were transfened from mothers to the children (Schecter et al. 1994c).
A study of former workers from a phenoxyherbicide plant in Sweden showed that
then^blood contained elevated levels of TCDD and PCDD/Fs, 16-21 years after they
had fimshed their employment with the plant. Mean levels of TCDD were 8 times
higher than non-exposed persons and the total PCDD/F TEQ was over 2-fold higher
(Rappe et al. 1994). At a herbicide plant in Germany which closed in 1984, the
average TEQ for total PCDD/Fs in workers blood measured in 1988-91 was 249 5
which was 6 times higher than background levels in the general population at that ’
time of 40.8 ppt TEQ (Papke et al. 1992).
Elevated dioxin levels in workers have been demonstrated to be present up to 34 years
after substantial exposure. This shows the extreme persistence of dioxin in human
ssues (Schecter 1998). The half-life of these chemicals in the body in workers who
have been highly exposed to dioxins has been estimated. The half-life is the time
taken for the level in the body to reach half its former level. For TCDD, varying halfhves have been reported ranging from 6.9 to 11.3 years. Less is known about hdfhves of the other 2,3,7,8-substituted dioxins and furans. A recent study noted that
alf-hves for most PCDDs were in the same order of magnitude as TCDD, and halflives were for most PCDFs were slightly shorter (Flesch-Janys et al. 1994).
0"aJ.^xp°sure l° dioxins from production of pentachlorophenol has been
Unllk®1116 Production of trichlorophenol products where high levels of
LnaFnXcT
Pentachlorophenol typically results in different dioxin
congeners being elevated. Studies at factones that produced pentachlorophenol in
Germany (Papke et al. 1992), and more recently in China (Olie et al. 1997), have
s own increased levels of dioxins in workers. In Germany, the mean level’recorded in
XeraTe T^ WaS
TEQ
3 timeS greater 01311 016 national
average. The maximum and minimum levels recorded were respectively 946.5 and
• ♦»,
EQ’ At thC chemical Plant in China the same production process of PCP as
m the Germany plant was reported to be used. However, levels of PCDD/Fs in the
blood of workers are outstandingly high. In six of the workers who were tested levels
TOO l^lwfen 1168 “d 7480 ppt TEQ and in one worker the level was 22,308 ppt
In
^background level in Chinese general population has been reported to be
ZU.9 ppt TEQ.
24
Metal Industries
A study of metal reclamation workers in Germany found that certain PCDD/Fs were
elevated in their blood. The mean value for the total PCDD/Fs was 90.2 ppt TEQ
which is over twice the national average of 40.8 ppt TEQ (Papke et al. 1992). Another
study found elevated levels of dioxins in the blood of men whose occupation involved
metal burning (Menzel et al. 1996). A recent study in Germany found that levels of
repair welders were somewhat elevated and should be further investigated. However,
the greatest concern was for workers performing thermal oxygen cutting at scrap
metal reclamation and demolition sites. The median blood level in these workers was
44.4 ppt TEQ, which is elevated in comparison to a value of 17.3 for the general
population of Germany. Levels in the workers blood increased with time of
employment, confirming there was a causal link between occupation and blood levels.
The source of dioxin in this occupation was found to be due to PVC in anticorrosive
paints on the metal. The authors concluded that it is necessary to exclude such
exposure to workers in the future by banning PVC as a component of anticorrosive
paint (Menzel et al. 1998).
Incineration
Municipal waste incinerators, which are commonly used to dispose of domestic
waste, are known to emit dioxins. Workers may be exposed to contaminated soot and
flue ash at such facilities. Studies at older types of incinerators in New York and in
Germany found elevated levels of some PCDD/Fs congeners in the blood of workers
(Schecter 1994). A more recent study at a municipal waste incinerator in Germany
also found levels of some congeners were statistically significantly elevated (Hazel
and Frankort 1996). However, another study at a modem state of the art incinerator in
Germany did not find elevated levels in workers blood (Schecter et al. 1994).
Research on workers at 3 chemical waste incinerators in Germany did not find
elevated levels of dioxins in workers (Papke et al.WM). A study in Finland has been
conducted on workers who were involved in hazardous waste disposal. Levels of
dioxins in the blood of most workers was not elevated, but certain PCDD/Fs were
elevated about two-fold in some workers. Differences in blood levels between
workers was not unexpected because they had jobs in different parts of the plant
which could lead to varying levels of exposure (Luotamo et al. 1993).
Production of Chlorine and PVC
Workers involved in the production of chlorine in the chloralkali industry and in the
production of vinyl chloride (VCM), a precursor of PVC, could be potentially
exposed to PCDD/Fs. A recently published Swedish study found that overall levels of
PCDD/Fs were not different from those of referent individuals not working in the
industry. However, the distribution pattern of congeners in the workers blood was
notably different to referents. Specifically, two PCDF congeners were related to work
in the VCM and chloralkali industries (Hansson et al. 1997).
Pulp and Paper Industry
PCDD/Fs are produced as unwanted by-products when pulp and paper is bleached
with chlorine-based chemicals. Studies which investigated occupational exposure to
PCDD/Fs at pulp and paper mills in Finland and the US, found that levels of the
compounds in workers blood were not statistically significantly elevated. (Rosenberg
et al. 1994, Tepper et al. 1995).
25
f
Summary
From the above information, it appears that occupational exposure to dioxins that
resulted in extremely elevated levels in workers, such as production of TCP and
phenoxy-herbicides, may no longer occur because of increased safety standards and
the closure of some chlorophenol and herbicide plants. Nevertheless, it is also
apparent that there are occupations that continue to expose workers to dioxins and
may result in increased body burdens. Given this fact, and given the high number of
occupations involving potential exposure to dioxins, it could be considered that there
is currently a paucity of data concerning occupational exposure to dioxins. For
example, there is little information in published scientific literature for the handling of
hazardous wastes, production of PVC, spraying phenoxy or chlorophenol based
pesticides, and more studies are required to investigate certain processes in the metal
industry. Of further and perhaps greater concern, is the very limited data available for
developing countries where industrial standards may be lower than currently
employed m western nations. For instance, the case of production of PCP at a plant in
dioXs UStrateS 11121 W°rkerS at this faCtOry 316 exP°sed t0 exceedingly high levels of
2.6
Relevance to Human Health
Infants
It is of great concern that ADIs set for PCDD/Fs are exceeded by breast-fed infants in
developed countries. As previously mentioned (section 1.3.2), infancy is a critical
fOr,he
The relevance for health of infants exceeding ADIs is however not known
ofPcSsdSnTTi? eStimatC riskS t0 infant health duet0 intal<e
ot PCDD/Fs during breast feeding, byrijetter characterising their exposure to the
c emicals^ Mathematical models are used to estimate the body burden of the infant
Irimbakdy b'5d,en^an,then be compared to estimated body burdens in laboratory
animals, or body burdens m humans at which a particular health effect is known to
occur (eg. Rogan and Ragan 1994, Aydtte et al. 1994). Such comparisons between
health effe
data are deemed reasonable since many studies have noted that
health effects induced by TCDD occur at similar doses in most animal species
might beeexnecdedeto°b
3 particular effect in experimental animals
(DeVito\TaL1995)
"
Same effect in humans
^?>natydy hasesdmatcd health risks to Inuit infants since Inuit breast milk has been
ound to contain high levels of PCBs (Ayotte et al. 1994). Based on levels in Inuit
breast milk, the maximum estimated body burden an infant would be likely to attain
NO^UrecordeTf^ 264
adip°Se tiSSUe’ This flgure does not exceed
tn I -t • r
d d/ cancer and reproductive effects in rats. However, this exposure
abormo!?rtS ‘"I Tt0 “PT6 3t Which Other adverse health effects occurred in
laboratoty animals. For example, the exposure is 4.6 times lower than adverse
productive effects which occurred on male rats exposed to TCDD in utero and
DmvWe
T’ Using,SU? methods t0 estimate health risks to infants can thus
provide an indication that for some infants there is only a small margin of safety
26
between their exposure and exposure which is known to cause effects in laboratory
animals. This itself is obviously of great concern, and becomes more so when it is
considered that human sensitivity to a particular effect may vary between individuals.
Direct investigations of the potential health impacts to infants resulting from in utero
and lactational exposure to PCDD/Fs and PCBs, rather than estimating health risks,
has come from epidemiology studies. Several studies of highly exposed infants, and
infants exposed to current background levels of PCDD/Fs have shown associations
between PCDD/F and/or PCB exposure and various subtle effects on nervous system
function and changes in immune system cells (see Allsopp et al. 1997)
Adults
A recent study estimated body burdens in experimental animals that produced effects
on health, and body burdens in humans which have been associated with health
effects. The stud^ compared these results to body burdens of the general population
(DeVito et al. 1995). Cancer in animals was found to occur at body burdens of 944137 000 ng TCDD/kg body weight and non-cancer effects at 10-12,500 ng/kg. The
average human body burden in the general US population was estimated to be 13 ng
TEQ/kg body weight, and in highly exposed persons ranging from 96-7000 ng
TEQ/kg body weight. For several health effects, body burdens in the general
population were found to be similar to, or within an order of magnitude of the body
burdens in experimental animals. For instance, experiments in which animals have
been exposed to TCDD show that one of the most sensitive targets for TCDD toxicity
is the immune system. Immune alterations, including altered lymphocyte subsets in
marmosets and enhanced viral susceptibility in mice, have been reported at body
burdens equivalent to human background exposures, although the clinical significance
of such parameters is not known. Presently, it is still unknown whether levels of
dioxins in the general adult population are causing effects on human health (DeVito et
al. 1995), but the fact that tissue levels in the general population are close to those
known to cause health effects in animals is of great concern.
2.7
Polychlorinated diphenyl ethers (PCDEs) and polybrominated dibenzo-pdioxins and dibenzofurans (PBDD/Fs)
Aside from PCDD/Fs and PCBs, there are other dioxin-like compounds found in
human tissues. Over 100 phenolic organohalogenated substances were detected in a
recent analysis of human blood, including chlorinated, brominated and mixed
chlorobrominated phenols, hydroxylated and dihydroxylated PCB metabolites
(Wehlere/a/. 1997).
Polybrominated dibenzo-p-dioxins (PBDDs) and dibenzo furans (PBDFs) as well as
mixed brominated and chlorinated phenols, are structurally similar to PCDD/Fs. They
are formed as by-products of combustion processes such as incineration, but
PBDD/Fs are also used as flame retardants. They have been identified as potential
environmental pollutants. Like PCDD/Fs, these chemicals are thought to exert
biological effects through the Ah receptor. They have similar, if not identical,
biological effects to PCDD/Fs. It has been proposed that the TEQ system could also
be applied to the PBDD/Fs. There are however only limited data on the presence of
these compounds in biological tissues (Mennear and Lee 1994). In addition to
PBDD/Fs, there are many other environmental contaminants, mostly organohalogens.
27
which have the potential to cause adverse effects through the Ah receptor mechanism.
These chemicals may contribute in addition to the dioxin-like toxicity of chemical
mixtures in biological tissues. However, their toxicity is not represented by the TEQ
system (Giesy et al. 1994).
One study reported that PBDD/Fs were either not detectable, or were present at low
concentrations (less than 20 ppt on a lipid basis), in human breast milk samples from
Swedish women (Wiberg et al.\99T). The authors suggested that these compounds are
of minor concern for human health, whereas PCDD/Fs, present at higher
concentrations, are a more serious environmental problem. Nevertheless, it is of
concern that PBDD/Fs add to the body burden of dioxin-like compounds in humans,
and that less is known about their toxicity than other PCDD/Fs. In addition, exposure
to PBDD/Fs may be an occupational problem. For example, workers could be
exposed in plastic and textile industries which produce or manufacture goods that are
treated with brominated flame retardants. One study on resin production, which
involved extrusion blending of polybutyleneterephthalate with
decabromodiphenylether, found this process lead to the formation of PBDD/Fs.
Research on workers employed in this process reported that blood levels of PBDD/Fs
in these individuals correlated well with the amount of time they had been employed
and therefore exposed (Zober et al. 1991).
Polychlorinated diphenyl ethers (PCDEs) are chemicals that are generated from
combustion sources and from chlorophenol preparations. A recent study has
monitored the levels of PCDEs in Finnish human adipose tissue and in fish tissue
from various species. The study found four PCDE congeners in human adipose tissue
(estimated TEQ < 3 ppt, on an extractable fat basis). Similar levels were detected in
Canadian and US human tissue samples in separate studies. The researchers
concluded that the most likely sources of these compounds in the Finnish environment
is from wood preservative, and in human tissue is from consuming fish (Koistinen et
al. 1995). PCDEs have also been detected in human milk in Germany and recently in
human blood in Sweden. Although levels of these chemicals are two orders of
magnitude lower than PCB levels, the study suggested that the relevance of the PCDE
levels is unknown, since too few toxicological studies have been performed to date on
these chemicals (Wehler et alAWI).
3.
DICHLORODIPHENYL TRICHLOROETHANE (DDT) and
DICHLORODIPHENYL DICHLOROETHANE (DDE)
3.1
Introduction
Since the 1940s DDT has been widely used throughout the world to combat
agricultural pests, indoor insects, and in sanitation campaigns against malaria. Its use
has been totally banned in developed countries, due to its persistent, bioaccumulative
properties, adverse impacts on wildlife and suspected effects on humans. However,
DDT remains in use in some developing countries. The WHO currently recommends
the use of DDT for malarial outbreaks, although public health experts do not
uniformly endorse its use. DDT targets adult insects and cannot kill larvae. Resistance
of insects to DDT has occurred world-wide (Lopez-Carillo et al.\996, RiveroRodriguez et al. 1997).
28
DDT and its metabolites DDE and DDD are commonly found in human tissue
samples, and have been reported as being the most widespread contaminant in human
milk (Jensen and Slorach 1991). In many countries, despite being banned several
years ago, DDT compounds continue to be found in human tissues, demonstrating the
remarkable biological persistence of this chemical (Sonawane 1995). The isomers
p,p’DDT and p,p’-DDE can be detected in breast milk. Levels of the o.p'-DDT and
p,p’-DDD isomers are much lower, such that p,p’-DDT and p,p'-DDE are the major
contributors to the total sum of DDT compounds (DDT + DDE + DDD). In humans,
levels of DDT and DDE in blood serum have been found to increase with increasing
age (ASTDR 1997).
J
Countries where very high levels of DDT and DDE are found in human tissue are
those where DDT is still used in agriculture or to control vector-borne diseases such
as malaria. Despite the undesirable properties of DDT, it is used in developing
countries primarily due to cost-benefit efficacy and broad spectrum toxicity (Nair et
al. 1996). In India, it is used both in agriculture and in vector control programmes. As
a result, the environment suffers high contamination with DDT and there are elevated
levels in human tissues (Kashyap et al.V)94).
3.2
Levels in Breast Milk
Tables 3a and 3b list the concentration of DDT compounds found in human milk in
various countries and tables 3c and 3d show p,p-DDE levels. DDT is generally
reported as p,p’-DDT and sometimes as total DDT.
The studies showed that DDE is a very widespread contaminant of human milk. It
was present in virtually all samples of breast milk that were tested from many
different countries. For instance, most studies reported DDE contamination in 100%
samples, and 3 reported it in 96, 97 and 99% of samples. DDT was also found to be
present in breast milk from all countries, although the proportion of samples
containing p,p’-DDT was less than for p,p-DDE. The number of samples which
contained p,p’-DDT ranged from 21.5% in Spain to over 95% in several countries.
Jensen and Slorach (1991) reported large differences in human tissue levels of DDT
and DDE between different countries. Elevated levels were found in south-eastern
US, southern and eastern Europe, and in developing countries. Studies presented in
tables 3a-d in the present report, also showed that by far the highest DDT and DDE
levels were evident in developing countries. These included some countries in South
America, Asia and Africa. The studies also showed that relatively high levels were
apparent in eastern Europe and in a few western European countries. The lowest
levels were evident in some western and north-western European countries and the
US.
The highest DDT and DDE levels were present in India (DDT 13.1 ppm and DDE
12.5 ppm) and Zimbabwe (DDT 9.07 and DDE 13.6 ppm). High levels of DDT, over
1 ppm, were also apparent in Kenya (3.73 ppm), Mexico (1.27 ppm), Nigeria (2.27
ppm) Turkey (2.35 ppm). South Vietnam (4.7 ppm) and Egypt. High levels of DDE
were also reported for some of these countries. Those with DDE levels around and
over 2.5 ppm included Brazil (2.53 ppm), Kenya (2.95 ppm), Mexico (5.01 ppm),
Thailand (3.61 ppm), Turkey, (2.4 ppm), and South Vietnam (6.7 ppm). Note that
29
levels reported for Thailand and South Vietnam are based on a limited number of
samples, but nevertheless reflect the fact that DDT was used in sanitation campaigns
at the time of study (Schecter el alA^^
Several countries were reported to have p,p’DDE levels around 1 to 2ppm, including
Australia (0.96 ppm), Faroe Islands (2.01 ppm), France (2.18 ppm), former East
Germany (1.13 ppm), Italy (2.2 ppm), Jordan (2.04 ppm), Kazakstan (1.96 ppm),
Nigeria (1.33 ppm), Russia (1.26 ppm) Slovak Republic (1.66 ppm). Concentrations
lower than 1 ppm were evident in the USA and some European countries,
Netherlands, Norway, Spain, Sweden, UK.
Considering the contribution that different DDT compounds make to the total sum of
DDT in breast milk (i.e. DDT + DDE + DDD), it is apparent that DDE is the greatest
contributor in western countries. Thus DDE levels are much higher than DDT levels
in breast milk in such countries, which is clearly evident in tables 3a-d. However, in
developing countries where DDT is still in use, DDE has been found to contribute less
to the total, around 50%, whilst DDT compounds contribute more (Kalra et al. 1994).
Detection of p,p -DDT in human tissue and human milk samples indicates recent
exposure to the parent compound, whereas p,p’-DDE represents chronic exposure
(Quinsey et al. 1995, Rivero-Rodriguez et alAWT). Thus higher levels of p,p’-DDT in
breast milk samples from developing countries is most likely caused by the continued
use of DDT and therefore continued exposure to the compound in these regions
(Kalra et al. 1994).
Marked regional differences in levels of DDT and DDE in human milk are apparent in
coimtries where DDT is still in use. For instance a study in India found that women
residing in areas Fairdkot, where DDT is used in cotton-growing, had higher breast
milk levels of DDT and DDE than women living in the urban community of Ludhiana
where use of pesticides is less (Kalra et al. 1994).
Regional differences relating to DDT usage are also evident in other countries. For
mstance, aerial spraying of DDT is carried out in the Kariba area of Zimbabwe in tse
tse fly vector control programmes. As shown in the tables 3a-d breast milk levels of
DDT and DDE are considerably higher Kariba (9.07 and 13.60 ppm) than the national
average breast milk levels (1.33 and 4.49 ppm), (Chikuni et alA997). Similarly, in a
tropical region of Mexico, higher DDT and DDE levels were found in human milk in
suburban areas of Veracruz than in urban areas. This was reported to be due to the
spraying of DDT in suburban areas for malarial control which resulted in inhalation of
DDT vapours by mothers, causing extensive exposure and eventual elimination in
breast milk. Levels of DDT and DDE in breast milk respectively were 0.422 and
2.709 ppm in urban Veracruz versus 2.460 and 8.253 ppm in the suburban area
(Waliszewski et al. 1996). In non-agricultural and non-tropical areas of Mexico, such
as Mexico city, DDT is still found to accumulate in human tissues but to a lesser
degree. For example, in Mexico city, mean breast milk levels of p,p’-DDE were
reported to be 0.594 ppm (Lopez-Carillo et al. 1996). This is 10-fold lower than
human breast milk in the tropical area of Veracruz, mean 5.017 ppm.
In Kazakstan, average DDE levels were 1.96 ppm, but in rural areas the figure was
higher, 3.3 ppm. This was possibly because of its persistence in the food chain, since
its use on cotton crops was curtailed in the 1970s. In a region by the Aral Sea, the
ratio of DDT to DDE was elevated which suggested recent exposure to the parent
30
compound, possibly from pesticide-laden dust blowing from the dry lake bed (Hooper
et al. 1997). A recent study conducted on the health of children who are living in
areas close to the Aral Sea, found they had high blood levels of DDT compounds. The
levels were 20 times higher than children living in Stockholm, Sweden (Jensen et
alAMT).
The AMAP study of maternal blood levels of POPs in Arctic countries found
particularly high levels of DDT and DDE in north-western Russia. Levels of DDT
were about 3 to 20 times higher than levels in other countries (Gilman et al. 1997). It
was suggested that these very high levels could be either due to significant uses of the
pesticide in this region or to significant amounts in the food supply. The study found
somewhat elevated levels in Greenland and Canada. It was noted that levels of certain
POPs in Arctic regions were consistent with the relative amounts consumed in
traditional foods, especially where marine mammals were a large part of the diet.
1
3.3
Time Trends
In countries where DDT has been banned, the body burden of this pesticide and its
metabolites have declined with time in recent years. Studies on breast milk have
reported a downward trend in levels of DDT compounds in Canada, USA, Australia,
several European countries including Spain, UK, Norway and Sweden, and Turkey
(respectively, Mes 1994, Sonawane 1995, Stevens et alA993y Hernandez et al. 1993,,
Dwarka et al. 1995, Johnasen et al. 1994, Atuma et al. 1998, Cok et al. 1997).
For a few countries, including Australia, USA, Canada and Norway, data is available
from the 1970s, and shows a general decrease in breast milk levels of DDT from this
time until the 1990s. Recent studies have presented figures which also illustrate the
decline in DDT levels. For example, in the UK, a p,p’-DDE level of 1.6 ppm was
recorded in 1979/80, and in 1989/91 the level was 4 times lower, 0.4 ppm. This
represents a 75% drop in levels. It reflects the withdrawal of DDT from agricultural
use in the UK and prohibition of the compound in the European Community (Dwarka
et al. 1995). In Norway, total DDT levels are estimated to have fallen by 75% between
1982 and 1991 (Johansen et al. 1994). In Sweden levels also fell between 1986 and
1990, but DDE levels increased slightly between 1990 and 1994. The authors did not
offer an explanation of this increase (Atuma et al. 1998). Studies carried out in Canada
indicate a decline in breast milk levels of DDT compounds from 1967 to 1986 (Mes
1994). Total DDT was estimated to decline by 64% between 1986 and 1992 in
Canada (Newsome et al. 1995). Similarly, studies in the province of Quebec, Canada,
show that levels in 1988/90 were 61% lower than levels reported 10 years previously
(Dewailly et al. 1996). In Australia, studies showed a progressive decrease in total
DDT levels between 1974 and 1991. Levels fell by about 33% between 1980 and
1991 (Stevens et al. 1993).
In non-westem or developing countries little information was available in recent
literature to determine whether levels of DDT had fallen at all in the past few years. In
Iran, a survey of adipose tissue levels in 1991/2, noted that levels had fallen from
those recorded 1974-6 and were now equivalent to levels found in most western
countries (Burgaz et al. 1995). One report of blood levels of DDT in Gujarat state,
India, reported that lower levels than had been found previously, indicating a lowered
usage of DDT in this region (Kashyap et al. 1994). In Mexico, studies on adipose,..,.
ISO
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31
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AI
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tissue levels of DDT do not appear to indicate a decline in levels (Lopez-Carillo et
alAMG).
3.4
Highly Exposed Populations
3.4.1
Nursing Infants
A recent study showed that maternal DDE levels were significantly reduced as a
result of lactation. The study monitored a woman’s blood and breast milk levels of
DDE during a 2.5 year period while she nursed twins. Levels in breast milk decreased
considerably over time from 0.246 to 0.0459 ppm milk fat (Schecter et alAWfc).
An ADI of 20 ug/kg/day was set in 1994 for any combination of DDT, DDD plus
DDE (WHO 1997). Table 11 shows the estimated concentrations of DDT, DDD plus
DDE in breast milk fat and whole milk which should not be exceeded if an infants
intake is not to exceed the ADI. Table 3e shows the total sum of DDT compounds for
different countries. Comparison of the estimated levels which should not be exceeded
(table 11), with mean levels of DDT compounds in breast milk reported for different
countries (table 3e), reveals that estimated infant intakes are close to the ADI in
several countries. Estimated intakes exceed the ADI in Kenya, Mexico, Nigeria and
Thailand. The highest exceedances are for India and Zimbabwe, where in some
regions, estimated infant intakes are over 6-fold higher than the ADI.
3.4.2
Occupational Exposure
Occupational exposure to DDT can result in very high tissue levels of DDT and DDE
compounds. A study in Veracruz, Mexico, investigated adipose tissue levels of DDT
compounds in a group of workers whose occupation involved spraying houses with
DDT and other pesticides to control malaria vectors (Rivero-Rodriguez et alA99T).
Comparisons were made with the general population of Veracruz state for whom
adipose tissue levels may reflect direct exposure to the sanitation campaigns and
exposure through diet, (mean p,p’-DDT concentration of 1.34 ppm, p,p’-DDE, 14.1
ppm and total DDT 15.65 ppm fat), (Waliszewski et al. 1995). Adipose tissue levels of
total DDT in the workers who sprayed DDT were found to be 6-fold higher than
levels the general population (mean p,p’-DDT 31.0 ppm fat, p,p’-DDE 60.98 ppm fat,
and total DDT 104.48 ppm fat), (Rivero-Rodriguez et alAWT)
3.5
Relevance to Human Health
Numerous animal studies have been carried out on DDT, but human data is more
limited. The central nervous system is a major target organ in humans and animals.
Studies in humans have reported symptoms of hypersensitivity to contact, tremors,
and convulsions following occupational exposure or ingestion at high doses. Such
effects have also been observed in laboratory animals following oral administration of
DDT (ASTDR 1997).
Animal studies have shown that the liver and reproductive system could be potential
target organs in humans. Several adverse effects on the liver have been demonstrated
in animals. In humans, alteration of liver enzymes in occupationally exposed humans
has been associated with DDT exposure, although there is no evidence whether the
liver damage this reflects is irreversible. No human studies have indicated
32
reproductive toxicity associated with DDT exposure. Animal studies however, show
that long-term, low level exposure to DDT results in decreased fertility, stillbirths,
and increased foetal mortality (ASTDR 1997). DDT and DDE have also been
identified as endocrine-disrupting chemicals (see Allsopp et al. 1997). For instance.
DDT was shown to cause estrogenic effects in laboratory animals (eg. Bustos et al.
1988). DDE was shown to be anti-androgenic in laboratory studies and caused effects
in laboratory animals consistent with this mechanism (Kelce et al 1995). It has been
suggested that the endocrine-disrupting properties of DDT. and possibly other
chemicals, may be responsible for adverse effects on the reproductive systems of wild
alligators in Lake Apopka, Florida (Guillette et al. 1994).
Studies on animals have reported immunotoxic effects of DDT. It has been suggested
that immune responses observed in animals may be indicative of effects in humans
subjected to long-term, low level exposure (ASTDR 1997).
Exposure to DDT in utero or in ne^vboms has been shown to cause developmental
neurotoxicity in animals such as effects on behaviour. The levels of DDT that cause
behavioural changes in mice are comparable to levels to which human infants have
been exposed. It is not certain whether effects from DDT exposure could occur from
exposure via breast milk in human infants (ASTDR 1997).
Studies on animals have demonstrated that long-term DDT exposure can cause cancer
including lymphomas, and liver and adrenal tumours. It has been suggested that
studies conducted on occupational exposure to DDT in humans are not conclusive of
an association between exposure and the development of cancer because of
inadequacies in the studies (ASTDR). One study on occupational exposure has
however suggested a link between exposure and pancreatic cancer (Garabrant et
al. 1992, see Allsopp et al. 1995).
Recent studies on women in the US and Mexico found that women with higher levels
of DDT in their breast milk lactated for shorter time periods than women with lower
levels. It was suggested that DDE, and possibly other estrogenic chemicals could be
contributing to declines in the duration of lactation that are evident throughout the
world (Gladen and Rogan 1995).
4.
HEXACHLORBENZENE (HCB)
4.1
Introduction
HCB has a variety of sources including its previous use as a fungicide for seed grain.
It is produced as an unwanted by-product or impurity in the manufacture of
chlorinated solvents, other chlorinated compounds, such as vinyl chloride, and several
pesticides. It is also produced as a by-product in waste streams of chlor-alkali plants
and wood preserving plants, and in fly ash and flue gas effluents from municipal
waste incineration. Its main source in the environment today is from the manufacture
of pesticides (Foster 1995, ATSDR 1997).
33
4.2
Levels in Breast Milk
Levels of HCB in breast milk from different countries reported on a lipid and on a
whole milk basis are shown in tables 4a and 4b respectively. The tables indicate that
HCB is a widespread contaminant of human milk. In all except three countries, Spain,
Brazil and Egypt, HCB was found in greater than 90% of the samples tested. HCB is
found in human milk in countries such as India, where it was never used as a
fungicide, and where the highest levels are detected in industrialised regions (see
Thomas and Colbom 1992).
A previous review of data on levels of HCB in breast milk observed that the average
world-wide background concentration was about 0.1 ppm (Jensen and Slorach, 1991).
Studies presented in table 4a show that the majority of countries have levels around
0.04 to 0.2 ppm. Falling into this category are Australia, Kazakstan, Turkey, Mexico
and European countries France, Germany, Netherlands, Italy, Norway and Sweden.
Among these countries, northern European countries Norway and Sweden, and
Mexico have levels at the lower end of the range. Another South American country,
Brazil, also had relatively low levels, 0.02 ppm. Other countries with comparatively
low levels of around 0.02 ppm or less, were Canada, Spain, UK, and in Asia, South
Vietnam and Thailand. The highest levels of HCB were reported for Jordan (0.29
ppm, median), Perth in Australia (0.411 ppm), and eastern European countries, the
Czech Republic (0.639 ppm), and Slovakia (0.829 ppm). Researchers suggested that
particularly high HCB levels in human milk in Slovakia may be caused by its use in
and its formation during the manufacture of chlorinated solvents (Kocan et
The AMAP study of maternal blood levels of POPs in Arctic countries reported that
HCB levels were significantly elevated in some Arctic regions, in particular,
Greenland. It was noted that the patterns of certain POPs in maternal tissue were
consistent with the relative amounts of traditional food consumed, especially where
marine mammals formed a large amount of the diet (Gilman et al. 1997).
4.3
Time Trends
A few studies in developed countries have reported a decline in levels of HCB in
blood and milk in recent years. A study in Denmark observed that levels in breast
milk m 1993 had fallen to less than half the value measured in 1986 (Hilbert et
al. 1996). Similarly, in Norway levels decreased by about 50% between 1986 and
1991 (Johansen et al. 1994). Statistically significant declines in breast milk were also
reported to occur m Sweden between 1981 (mean 0.096), 1986 (0.057), and 1990
(0.037) (Vaz et al. 1993). A study of the general population in Barcelona, Spain,
revealed that blood levels in 1993 (range 0.7 to 19.7, mean 4.13 ng/ml) were
significantly lower than levels found in the same population in 1986 (range 1.6 to
94.2, mean 11.09 ng/ml), (To-Figueras et al. 1995).
Studies which have reported informal on trends of HCB levels, appear to be those
where HCB levels are now relatively low, that is northern Europe and Spain No
specific data on trends in countries where HCB levels are comparatively high were
found in the recent literature.
34
4.4
Highly Exposed Populations
4.4.1 Nursing Infants
HCB is transferred from mother to foetus through the placenta, and can readily pass to
the nursing infant through breast milk. One study measured a significant drop in
breast milk HCB concentrations throughout 98 days of lactation (see Thomas and
Colbom 1992). A study on a woman in Sweden observed that maternal HCB levels
were significantly reduced by lactation. Levels of HCB during her first pregnancy
(0.12 ppm) were higher than in her second pregnancy (0.06 ppm) and third pregnancy
(0.04 ppm). This was due to excretion of the compound from her body during
lactation and transfer to the foetus during her pregnancies (Vaz et alA 993).
Experiments in laboratory rats have also shown that HCB is passed to young through
milk. Lactation resulted in the maternal body burden being reduced by 15-20% (see
ATSDR 1997).
A temporary ADI value of 0.6 ug/kg/day was set for HCB in 1976 but withdrawn in
1978. In pesticide evaluations published by WHO (1997), a tentative ADI of 0.6
ug/kg/day is given, and this is considered below any dosage rate known to be harmful.
Table 11 shows the ADI for HCB and the estimated concentrations of HCB in breast
milk fat and whole milk which should not be exceeded if an infants intake is not to
exceed the ADI. Comparison of the estimated levels which should not be exceeded
with mean levels of HCB in breast milk reported for different countries (tables 4a and
b), indicates that the mean breast milk levels exceed the ADI in several countries.
These include Australia, Czech Republic, Egypt, France, Eastern and Western
Germany, Italy, Russia and the Slovak Republic. The highest exceedances of the ADI
are for the Czech Republic and Slovak Republic for which the mean values exceed the
ADI by around 6 and 8 fold.
A recent study in Australia provided information on actual rather than estimated
infant intakes of HCB from breast milk. It found that about a quarter of infants in the
study received daily intakes of HCB from breast milk which exceeded the ADI. Some
intakes were 48 times in excess of the ADI. In a few cases, the intakes approached the
NOAELs in animals that are used as a basis for ADIs (Quinsey et al. 1995 and 1996).
4.4.2
Occupational Exposure
There are several occupations which could result in exposure to HCB, although there
appear to be few recent studies in the literature which document tissue levels in
workers. Several studies in the 1970s found elevated levels of HCB in blood of
persons occupationally exposed to this compound. Workers at a carbon tetrachloride
and perchloroethylene production facility had plasma levels of 0.223 ppm. Workers
involved in the manufacture of chlorinated solvents had blood levels ranging from
0.0055 to 1.121 ppm (mean 0.310 ppm) in 1974, and 0.022 to 0.467 ppm (0.170
mean) in 1977. Pesticide sprayers applying HCB contaminated
dimethyltetrachloroterephthalate (DCPA) had mean plasma levels of 0.040 ppb (see
ASTDR 1997).
More recently, two studies on occupational exposure to HCB have been conducted in
Sweden. HCB is released by the use of hexachloroethane for hydrogen removal
(degassing) in molten aluminium. A study on tissue levels in workers in Swedish
aluminium foundries noted that this process was banned a few years ago due to the
35
release of HCB. The study found that the mean level of HCB in workers blood. 2 to 4
years on after the process had been banned, was elevated to a level 4 times higher
than in workers who were not exposed to the process (0.313 vs 0.066 ppm), (Selden et
al. 1994).
In another study, workers at hazardous waste incineration plants were investigated
since they are exposed to many chemicals including organochlorines. Levels of HCB
in blood samples from workers were significantly elevated, by almost two-fold (0.063
vs 0.035 ppm) (Selden et al.\991).
4.5
Relevance to Human Health
A wide range of toxic effects due to HCB exposure have been reported in
experimental animals, including porphyria and other liver effects, skin lesions,
neurological effects, altered enzyme levels and several types of cancer. Adverse
effects on reproduction and development and on the immune system have also been
reported. In humans, much of the information on adverse effects of HCB is derived
from an incident which occuned in Turkey in the late 1950s, when people ate breads
made from HCB-treated wheat. About 500 people were fatally poisoned during the
incident and about 4000 became sick. Infants died who were breast fed by HCB
exposed mothers. Exposure to HCB was not quantified in follow up research of the
incident, but analysis of human milk reported a level of 0.51 ppm in exposed and 0.07
ppm in unexposed women. (This level is in the same order of magnitude as levels in
human milk found in eastern European countries today). Elevated levels of HCB in
human milk were still found in the region 20 to 30 years after the accident. Adverse
health effects to adults from the contamination included skin lesions due to altered
porphyrin metabolism. Many developmental effects were evident in children who
survived the incident such as skin, neurologic and orthopedic abnormalities
(Sonawane 1995, ATSDR 1997).
Liver toxicity appears to be the most sensitive effect caused by chronic HCB exposure
in adult animals and humans. In humans, chronic exposure to HCB at the incident in
Turkey caused hepatic porphyria. More recently, several studies in north-east Spain
have reported high levels in human adipose in populations residing in areas polluted
by organochlorines. A link between HCB contamination and the high and variable
incidence of porphyria cutanea tarda has been hypothesised (Enriquez de Salamanca
et al. 1990).
Another health effect of HCB is immunotoxicity. A review of animal data noted that
immune dysfunction occurs at lower doses than those associated with most other toxic
effects. It was suggested that this may be an area of concern for human exposure to
HCB (ASTDR 1997). The chemical also causes various reproductive toxicities in
adult female animals, including ovarian and menstrual cycle effects, reduced
gestational viability and fertility. Alteration of levels of hormones has been reported
including reproductive hormones progesterone and oestradiol, as well as thyroid
hormones. Studies in animals found effects on the ovary at levels only two orders of
magnitude higher than HCB levels imhe general human population. Considering
evidence available from animal studies, it has been suggested that HCB represents a
concern to ovarian function in humans. It may also have the potential of advancing
ovarian failure and menopause onset (Foster 1995).
36
HCB is known to cross the placenta and be transferred via breast milk to young and
causes various developmental effects in animals. In humans, there are no specific
studies on the impacts of HCB on development in utero. although a number of
developmental abnormalities were reported in children before they reached puberty,
following their accidental exposure to HCB at the poisoning incident in Turkey
(ATSDR1997).
HCB is known to cause multiple tumour types in laboratory animals when given
orally, including cancers of the liver, parathyroid, thyroid and bile duct. Animal
studies suggest that HCB has the potential to cause cancer in humans and it is
considered a probable human carcinogen. No malignant tumours have been reported
in humans following HCB exposure, although liver cancers, in association with
porphyria, have been reported in several human studies (ASTDR 1997). A recent
study has reported an excess of soft tissue sarcoma and thyroid cancer in a small
population with elevated serum HCB levels living near an organochlorine
manufacturing factory (Grimalt et al. 1994). The serum levels were 5 to 6-fold higher
than baseline levels which have been reported for the general population of Barcelona
Spain (To-Figueras et al. 1995). It was suggested that since these baseline levels refer
to a very large human population, the toxic risk to the general population does not
seem negligible. The study noted that the range of serum levels reported for the
general population of Barcelona cannot be considered safe with the relation to the
possible long term effects of HCB, and further efforts to reduce exposure and intake
through the food chain should be encouraged.
5.
HEXACHLOROCYCLOHEXANES
5.1
Introduction
Technical grade hexachlorocyclohexane (HCH) is an insecticide, which is comprised
of a mixture of different isomeric forms of HCH. The approximate isomer content is
alpha-HCH (53-70%), beta-HCH (3-14%), gamma-HCH (11-18%), delta-HCH (610%), others (3-10%). The insecticide lindane is the common name for the gamma
isomer. It is produced by purification of the technical HCH mixture (see Thomas and
Colbom 1992).
Although lindane and technical grade HCH have been banned or severely restricted in
many countries they are still widespread use. In India, DDT and HCH together
contribute to more than 70% of the total pesticide consumption (Nair et al. 1996).
Most of the HCH used in India is for agricultural purposes and around 10% is
consumed in vector control programs (Kashyap et al.Y)94). Lindane is also used in
many western countries in medications including shampoo for head lice.
Quantitatively, the most important isomers are alpha-, beta-, and gamma-HCH.
Bioaccumulation of these chemicals in tissues of some animals has been recorded,
although the alpha and gamma isomers do not concentrate highly through the
foodchain. The beta-isomer is however more persistent (Johnston 1989). Human
intake of HCH compounds is largely through food consumption (Toppari et al. 1995).
Alpha, beta and gamma-HCH isomers have been recorded in human breast-milk with
the beta-isomer being the most ubiquitous. The generally less widespread nature of
the alpha and gamma isomers in comparison to beta-HCH is due to the more rapid
37
clearance of these isomers from the body (National Research Council 1993). Like
many persistent organochlorines, HCH levels in the body have been found to increase
with age (ASTDR 1997).
5.2
Levels in Breast Milk
Levels of alpha-, beta- and gamma-HCH in breast milk from different countries
reported on a lipid and on a whole milk basis are shown in tables 5a and 5b
respectively. All three isomers are detectable in breast milk from different countries in
these studies. Beta-HCH is very persistent and this is reflected in the widespread
occurrence of the isomer. It was found in 90 to 100% of samples tested where data
was available. The percentage of alpha and gamma isomers in samples was more
variable between different countries. For instance gamma-HCH was detected in 17%
of samples in Canada, but in 80 to 100% of samples in France, Turkey and India. The
differences probably reflect where lindane was still in use.
In general, beta-HCH is not only more widespread in breast milk than alpha and
gamma-HCH, but it is also present in higher concentrations. This is again a result of
the persistent nature of beta-HCH and the more rapid clearance from the body of
alpha and gamma-HCH. The levels of both beta and gamma-HCH vary widely
between different countries, by more than two orders of magnitude.
Exceptionally high levels of beta-HCH in breast milk were evident in India (4.37-8.83
ppm). In a previous review, Jensen and Slorach (1991) noted that the average
concentration of HCH was 6 ppm in India and in China. In the present review, very
high levels of beta-HCH were also evident in Kazakstan (2.21 ppm) and Russia (1.58
ppm). High levels of beta-HCH, ranging from 0.5 to 1.0 ppm, were observed in two
South American countries, Brazil (0.9 ppm) and Mexico (0.56 ppm), and in Turkey
(0.52). Below this, levels ranging from 0.1 to 0.5 ppm were found in France,
Australia, Jordan, and two Asian countries, South Vietnam and Thailand. The lowest
levels, below 0.1 ppm, were recorded in US, Canada, Spain, Germany, UK and the
Czech Republic. For gamma-HCH, the highest levels were also apparent in India and
Kazakstan.
Regional differences in breast milk levels within a country were reported for India.
Levels of alpha-, beta- and gamma-HCH were found to be around twice as high in an
agricultural area compared to an urban area in Punjab (Kalra et al.YWl).
Information on levels of HCH compounds was located in the literature for several but
not all western European countries, US, Canada, and a few Asian and Latin American
countries. With the exception of Jordan, data on Middle eastern regions was lacking
and no studies were found on Africa.
The AMAP study on maternal blood levels of POPs in Arctic countries recently
reported very high levels of beta-HCH in north-western Russia. Levels of 0.225 ppm
were recorded which are around 25 times greater than blood levels in Norway and
Sweden. It was suggested that the high levels were either a result of significant uses of
HCH in the region, or significant amounts in the food supply (Gilman et al.\99T).
38
5.3
Time Trends
A gradual decrease in the levels of beta-HCH were reported to occur in breast milk
samples from Sweden between the mid 1970s and 1985 (Noren 1993), and between
1981, 1986 and 1990 (Vaz et al. 1993). In Canada, a small decrease was documented
between 1986 (0.69 ppb whole milk) and 1992 (0.55 ppb whole milk) (Newsome et
al. 1995). Some reduction in levels was also evident in the US between 1970 and 1983
(see ASTDR 1997).
5.4
Highly Exposed Populations
5.4.1
Nursing Infants
Maternal levels of HCH are reduced during lactation. For example, levels of betaHCB were shown to decrease during three pregnancies of a Swedish woman due to
transplacental transfer and excretion tlirough lactation. The levels in breast milk in
during the first pregnancy were 0.088 ppm, the second 0.058 ppm and the third 0.038
ppm (Vaz e/ al. 1993).
No ADI has been set for beta-HCH, but a temporary ADI of 1 ug/kg/day was set for
gamma-HCH (lindane) in 1997 (WHO 1997). Table 11 shows estimated
concentrations of lindane in breast milk fat and whole milk that should not be
exceeded if an infant’s intake is not to exceed the ADI. Comparison of the estimated
levels which should not be exceeded with mean levels of lindane in breast milk
reported for different countries (table 5a and b), indicates that the mean breast milk
levels exceed the ADI in two countries, namely India and Jordan. By far the greatest
exceedance of the ADI is for India. An infants estimated intake of lindane from breast
milk in India, based on mean levels in breast milk fat, exceeds the ADI by up to 12
times.
5.4.2
Occupational Exposure
Workers may be exposed to HCH compounds at manufacturing plants and during
agricultural usage. Alpha-, beta- and gamma-HCH have been detected in the blood
and adipose tissue of individuals occupationally exposed to HCH in pesticide
formulation (ASTDR 1997)
5.5
Relevance to Human Health
In studies on laboratory animals, many health effects following exposure to HCH
have been documented (ASTDR 1997), and beta and gamma-HCH were found to
have oestrogen-like effects (see Toppari et al.\995, Thomas and Colbom 1992). A
review of toxicological information suggested that the possible human health effects
associated with exposure to HCH are adverse hematological effects, liver and kidney
effects, immunological, neurological and reproductive effects and cancer (ASTDR
1997).
A number of health effects in humans have been recorded following occupational
exposure. These studies were conducted during of prior to the 1980s. Health effects
include blood disorders in individuals exposed to gamma-HCH at work or in homes,
where HCH vaporisers were operated; increased liver enzymes in workers exposed to
39
technical grade HCH principally by inhalation in a pesticide formulating plant;
several neurological effects including abnormal EEG, vertigo, headaches, seizures and
convulsions in individuals occupationally exposed to gamma-HCH. and in individuals
exposed accidentally or intentionally tolarge amounts of gamma-HCH by ingestion;
and, alterations of reproductive hormones in men occupationally exposed to HCH and
gamma-HCH. Alpha-, beta-, gamma- and technical grade HCH are carcinogenic in
laboratory animals. It has been proposed that animal data suggests that liver cancer
may be of potential concern to human individuals exposed to HCH isomers for
prolonged periods of time (ASTDR 1997).
The relevance of current background levels of HCH compounds to the health of the
general population is difficult to assess from cunent toxicological data.
6.
DIELDRIN, ALDRIN AND ENDRIN
Chlorinated cyclodienes are noted to be both environmentally persistent and among
the more toxic pesticides. Despite restriction of their production in recent years in
some countries, residues of these pesticides continue to be reported as being present in
human tissues. The chlorinated cyclodiene pesticides include aldrin, dieldrin,
chlordane, oxychlordane, heptachlor and heptachlor epoxide,.
6.1
Introduction
Dieldrin, aldrin and endrin are very persistent insecticides that have been banned in
m
many countries but remain in use in some developing countries. Dieldrin is a
metabolite of aldrin that persists in adipose tissue (Sonawane et al. 1995). Several
studies have detected dieldrin in human milk. Aldrin and endrin have also been found
in human milk, although the data are very limited.
6.2
Levels in Human Milk
Levels of dieldrin in breast milk from different countries reported on a lipid basis are
shown in tables 7a. The available data showed that the occurrence of detectable
concentrations of dieldrin in human milk was variable ranging from 5% in Jordan to
100% in Australia.
A previous review reported that the average level of dieldrin in human milk was 0.05
ppm on a lipid basis (Jensen and Slorach 1991). Similar levels were noted in the
present report, which showed that levels in the majority of countries were between
0.01 and 0.1 ppm. Higher levels were reported for Victoria in Australia (0.159 ppm),
France (0.19 ppm), USA (0.541), Iraq (1 ppm) and Uruguay (1 ppm). The lowest
levels, below 0.01 ppm, were present in Canada, Russia, Spain, and South Vietnam.
Levels of dieldrin in human milk world-wide are thus highly variable between
countries ranging by more than two orders of magnitude from 1.0 to less than 0 01
ppm.
Very few studies were found on levels of aldrin and endrin in human milk. Endrin
levels were reported for France (table 7b), and aldrin levels for Australia, France and
Turkey (table 7c). Aldrin was found to be present in 75% of samples in France, 88%
in Turkey, but only 5% in Australia. Levels were similar, 0.02 to 0.047 ppm, in all
40
three countries. A study in Mexico reported that aldrin was not detected in human
The AMAP study of maternal blood levels of POPs in
milk (Waliszewski et
Arctic countries did not report elevated levels of aldrin in Canada, Greenland,
Sweden, Norway, Iceland or Russia (Gilman et al. 1997).
6.3
Time Trends
In recent years, levels of dieldrin in human milk have decreased according to reports
from some countries. A study in Sweden reported a gradual decline in levels between
1972, shortly after most uses were banned and 1985 (Noren 1993). A study in
Denmark reported a steady decline between 1982 and 1993 (Hilbert et al. 1996).
Research in Canada noted a decline in levels between 1986 and 1992 (Newsome et
aZ.1995).
6.4
Highly Exposed Populations
6.4.1 Nursing Infants
An ADI of 0.2 ug/kg/day has been set for endrin and a value of 0.1 ug/kg/day has
been set for dieldrin combined with aldrin (WHO 1997). Estimated concentrations of
dieldrin, aldrin and endrin in breast milk fat and whole milk which should not be
exceeded if an infants intake is not to exceed the ADI are given in table 11. Levels of
endrin in breast milk were only located in the scientific literature for France. The
mean breast milk level in this study is slightly greater than the ADI for endrin.
Since there are very few studies which provided breast milk levels of both dieldrin
and aldrin, data on dieldrin only (table 7a) and aldrin only (table 7c) are considered
separately. Comparison of the estimated levels which should not be exceeded with
mean levels of dieldrin in breast milk reported for different countries (table 11),
indicate that the mean breast milk levels exceed the ADI in several countries. These
include Australia, Brazil, Eastern Germany, Jordan, Thailand, UK, USA and
Uruguay. The highest exceedances of the ADI are for Iraq, Uruguay and one study in
Brazil, which all exceed the ADI by greater than 50 times. When data on aldrin alone
is considered, the ADI for dieldrin + aldrin is exceeded 1-2 fold for countries where
studies were available, that is Australia, France and Turkey.
A study in Australia provided specific information on actual rather than estimated
infant intakes of dieldrin from breast milk. It found that dieldrin was detected in 43%
of samples tested. Of these, 88% would have resulted in doses exceeding the ADI
(Quinsey et alA^S).
7.
HEPTACHLOR AND HEPTACHLOR EPOXIDE
7.1
Introduction
Heptachlor is a constituent of technical-grade chlordane, approximately 10% by
weight. Heptachlor epoxide (HE) is an oxidation product of heptachlor and of
chlordane. Technical-grade heptachlor usually consists of 72% heptachlor and 28%
impurities such as trans-chlordane, cis-chlordane, and nonachlor. Heptachlor has been
used for the control of termites, ants and soil insects in cultivated and uncultivated
41
soils, and for the control of household insects. The general population is primarily
exposed to heptachlor and heptachlor epoxide through diet (ASTDR 1997).
7.2
Levels in Breast Milk
Levels of heptachlor and heptachlor epoxide in breast milk from different countries
reported on a lipid and on a whole milk basis are shown in tables 6a, 6b and 6c.6d
respectively. The occurrence of heptachlor and HE in human milk varied from
country to country. For example, the percentage of samples positive for heptachlor
varied between 33% in Spain to 89% in Australia. The percentage positive for HE
varied from 17% in Brazil to 92% and 95% in Spain and France respectively. Studies
prior to 1990 in the US showed that between 25% and 100% of human milk samples
contained heptachlor and HE (see Sonawane 1995).
A previous review of levels of heptachlor and heptachlor epoxide in breast milk,
reported that average levels world-wide were 0.05 ppm. High levels were recorded for
Spain (2.5 ppm) and Italy (0.48 ppm). Heptachlor epoxide was also elevated in
Belgium, Israel and Guatemala (Jensen and Slorach 1991). In the US, levels were
reported to range from 0.035 to 0.13 ppm (see Sonawane 1995). In the present
review, similar high levels were not reported for HE . Levels in most countries,
including Spain, were below 0.05 ppm. Exceptions were Australia (0.061 ppm) and
France (0.097 ppm). For heptachlor, however, a very high level was reported in
Jordan (0.7 ppm). All other countries had levels below 0.05 ppm.
It should be noted that data on levels of heptachlor and heptachlor epoxide in human
milk in different countries were quite limited. Published studies were only found for
ten countries. This included a few European countries, Turkey, Egypt, Canada, Russia
and Brazil. No studies were located for Asian countries.
7.3
Time Trends
Little data was published on time trends of heptachlor. One study in Canada however
reported a decline of about 70% in human milk levels of heptachlor epoxide between
1986 and 1992 (Newsome et al. 1995).
7.4
Highly Exposed Populations
7.4.1
Nursing Infants
An ADI of 0.1 ug/kg/day was set for heptachlor and heptachlor epoxide in 1994
(WHO 1997). Table 11 shows the estimated concentrations of heptachlor and HE in
breast milk fat and whole milk which should not be exceeded if an infant’s intake is
not to exceed the ADI. Comparison of the estimated levels which should not be
exceeded with mean levels of heptachlor and HE in breast milk reported for different
countries (table 6a-d), indicate that the mean breast milk levels exceed the ADI in
several countries. These include Australia, France, Germany, and Jordan.
A study in Spain which estimated intakes of dieldrin from breast milk reported that
the mean levels of heptachlor and HE did not exceed the ADI. However, 11.7% of
samples that contained the chemicals exceeded the ADI (Hernandez et al.V)93).
42
A study in Australia provided specific information on actual rather than estimated
infant intakes of heptachlor from breast milk. It found that heptachlor was present in
less than one third of samples which were tested, but levels in all these samples
exceeded the ADI (Quinsey et al. 1995).
7.4.2
Occupational Exposure
Workers involved in the manufacture of heptachlor, and in its application are at risk
of exposure to heptachlor (ASTDR 1997). However, the available data on exposure of
workers to heptachlor appears to be very limited.
7.5
Relevance to Human Health
Animal studies have identified heptachlor as being a toxic to the central nervous
system. It is likely that the nervous system is also a target system in humans. Signs of
neurotoxicity have been reported in humans following exposure to technical-grade
chlordane, which contains between 6 and 30% heptachlor. However, these effects
cannot be solely attributed to heptachlor. Animal studies also show that heptachlor
causes toxicity to the liver, and indicate that the liver would be a target organ in
humans. Studies show that heptachlor may affect the male and female reproductive
systems in animals. Only limited human data are available on reproductive and
developmental toxicity in humans and these are inconclusive (ASTDR 1997).
8.
CHLORDANE
8.1
Introduction
Technical grade chlordane is a mixture of alpha and gamma-chlordane and transnonachlor (Quinsey et al. 1995). Its uses were mainly as a field crop insecticide and in
the control of termites. It is extremely persistent in the environment. It has been
reported to persist in some soils for over 20 years, and is known to bioconcentrate in
the food web (ASTDR 1997).
Chlordane is metabolised in humans and in most other organisms to two persistent
epoxides: heptachlor epoxide and oxychlordane. Food is the most significant source
of exposure to chlordane and these metabolites. Indoor air can also be an important
source of exposure to technical chlordane where it has been used as a pesticide in
homes (Dearth and Hites 1991). Chlordane vaporises gradually in treated homes for
over ten years (ASTDR 1997). It was used widely for termite control in homes the US
for between 1960 and 1988. Its use in the US has now stopped, but exposure
continues since it has a half-life in the environment of 5 and possibly 15 years (Dearth
and Hites 1991). The US ERA estimated that, up to 1988, 1.3 to 1.8 million people per
year in the US were exposed to cyclodiene termiticides, as occupants of newly treated
buildings. They also estimated that about 30 million buildings in the US had been
treated for termites with these chemicals, resulting in the exposure of over 80 million
people (ASTDR 1997).
43
8.2
Levels in Human Milk
Jensen and Slorach (1991) reported that chlordane was found more frequently in
human milk in the US than elsewhere. The average level in breast milk world-wide
was 0.08 ppm although the highest levels (> 2ppm) were found in Mexico and Iraq.
In this report, data for different countries are shown in table 8. Comparisons between
different countries are difficult, because of the varying ways in which levels were
reported, for example, as alpha-chlordane, gamma-chlordane or oxy chlordane. With
the exception of an oxychlordane value of 0.13 ppm for Victoria, Australia, levels of
chlordane and oxychlordane were all below the previous reported average value of
0.08 ppm. This included studies in Canada, France, Japan, Russia, Thailand, USA and
South Vietnam.
The AMAP study on maternal blood levels of POPs in Arctic countries reported that
levels of chlordane metabolites were significantly elevated in Greenland and Canada
where communities relied on a seafood diet which included sea mammals (Gilman et
al.\99T). For example, levels of oxychlordane were 0.0608 and 0.0278 ppm in blood
lipid in Greenland and Canada respectively. These levels were much greater than
levels in other countries, for instance 0.0019 and 0.0037 in Sweden and Norway
respectively.
8.3
Time Trends
A review of data on chlordane in 1991 concluded that the levels of chlordane
compounds in people are not declining. For instance, mean adipose tissue levels
found in a US study in 1986-88 were Q.048, 0.088 and 0.12 ppm for heptachlor
epoxide, oxychlordane, and trans-nonachlor respectively. These results showed no
apparent decline from a previous study, the National Human Adipose Tissue
monitoring program from 1974-1982 where the levels of the compounds were 0.070.09, 0.09-0.12, and 0.06-0.14 ppm. Thus, with the exception of heptachlor epoxide
which may also be coming from other sources, following ten years of regulation in the
US, there had been no measurable decline in levels of chlordane compounds at this
time (Dearth and Hites 1991).
8.4
Highly Exposed Populations
8.4.1
Nursing Infants
An ADI of 0.5 ug/kg/day was established for chlordane in 1994 (WHO 1997). Table
11 shows the estimated concentrations of chlordane in breast milk fat and whole milk
that should not be exceeded if an infants intake is not to exceed the ADI. While some
studies on levels of chlordane in breast milk have recorded levels of oxychlordane,
others have reported on the alpha and gamma isomers (see table 8). Data is only
available for a few countries, but none of these exceeded the ADI.
8.4.2
Exposure in Treated Buildings/Occupational Exposure
A study in Japan showed that the concentration of chlordane and oxychlordane in the
milk fat of women living in chlordane treated houses (0.0138 ppm and 0.0336 ppm
respectively), was much higher than in breast milk of women who were not exposed
in this way (0.0036 and 0.0193 ppm). Several occupations may lead to chlordane
44
exposure including its manufacture, formulation, shipping, storage, application, and
disposal (see ASTDR 1997).
9.
TOXAPHENE
9.1
Introduction
Toxaphene is a trade name for an insecticide which consists of a mixture of at least
177 separate components, the major constituents being chlorobomanes. More than
half a million metric tons of toxaphene has been produced since the mid-1940s. These
production figures are almost comparable to those of PCBs. It is estimated that 8090% of all toxaphene produced has been used in cotton growing. In addition, fisheries
managers in Canada and the US have applied toxaphene as a fish poison to nd lakes
of undesirable fish. As a result of the large scale production of toxaphene, its
bioaccumulative properties and its high toxicity to fish, this pesticide may be
considered a threat to the aquatic ecosystem to the same extent as PCBs (de Boer and
Wester 1993).
Toxaphene is a global pollutant distributed by long-range transport on air currents. It
is bioconcentrated by marine organisms to high levels, and appears to biomagnify
through aquatic food chains (ASTDR 1997). Toxaphene has hardly been used in
western Europe. Nevertheless, exposure through the foodchain is possible in countries
where toxaphene has not been used. For example, concentrations of toxaphene m
cod hake and haddock from the North Sea were found to exceed the German
tolerance standard for levels in food by 2-8 fold. High concentrations are also evident
in Baltic fish due to the use of toxaphene in eastern Europe. The highest
concentrations have been detected in fish from Canadian and Arctic waters, in which
levels are at least a factor of 10 higher than in North Sea fish (de Boer and Wester
1993).
9.2
Levels in Breast Milk
Few studies have monitored the level of toxaphene constituents in human tissues,
blood or milk (see table 9). Comparisons between different studies are difficult
because of differences in analytical methods. One study on 16 human breast milk
samples from Nicaragua, Central America, found that levels were high (2.0 mg/kg
lipid weight) in comparison with levels in Finnish breast milk (0.005-0.5 mg/kg) and
Swedish breast milk 0.1 mg/kg (de Boer and Wester 1993). This is probably a
reflection of the continued use of toxaphene in Nicaragua.
93
Highly Exposed Populations
9.3.1 Nursing Infants
Nursing infants can be exposed to toxaphene via breast milk. However, estimates of
risks to nursing infants is complicated because the identified congeners were usually
partially metabolised and there is little information on the toxicity of such congeners
(ATSDR 1997). No ADI has been proposed for toxaphene.
45
9.3.2
Other Groups
Occupational exposure to toxaphene is possible during the manufacture or application
of the pesticide. Other groups with potentially high exposure to toxaphene include
arctic indigenous people who rely on a seafood diet and consume aquatic mammals.
In some countries, individuals residing near to hazardous waste disposal sites
contaminated with toxaphene may be more highly exposed. In addition, infants and
young children who are given vitamin supplements from cod liver oil could have a
higher exposure to toxaphene (ASTDR 1997).
9.4
Relevance to Health
Animal studies have shown that short-arid long-term exposure toxaphene is toxic to
the liver and kidney. It has been suggested that individuals exposed to toxaphene may
be at risk for compromised liver and kidney function and liver injury. Long term
exposure to toxaphene can also result in neurotoxic effects in humans and animals.
Laboratory rats which were exposed in utero and via lactation to toxaphene had slight
changes in motor function and behaviour. Toxaphene can also cause cancer in animals
and this evidence suggests that it may also be carcinogenic in humans (ATSDR 1997).
10.
MIREX
10.1
Introduction
About 75% of mirex that was produced was used as a fire retardant additive, while
25% was used as a pesticide. It was used as a fire retardant additive in various
coatings, plastics, rubber, paint, paper and electrical goods. Uses of mirex as an
insecticide included fire ant control in USA, leaf cutter ants in South America,
harvester termites in South Africa, mealybugs in pinapples in Hawaii, and
yellowjacket wasps in the USA. Although mirex was banned in the USA in 1976, its
release into the environment continues from waste disposal sites. Mirex is very
persistent in the environment and bioaccumulates and biomagnifies in aquatic and
terrestrial food chains (ASTDR 1997).
10.2
Levels in Breast Milk
Research on levels of mirex in human tissues appears to be very limited. A few
studies found traces of mirex in human milk from North America (see Sonawane
1995). The AMAP study on maternal blood levels of POPs in Arctic countries found
that levels were highly elevated in Greenland (0.0091 ppm blood lipid), and
somewhat in Canada (0.0045 ppm), in comparison with other countries in the study.
For example, levels in Sweden, Norway, Iceland and Russia were between 0.001 and
0.002 ppm. It was noted that patterns of certain POPs found in maternal blood
samples are consistent with relative amounts consumed in traditional foods,
particularly where marine mammals form a large part of the diet (Gilman et alAWT).
46
TABLES
Tables 1 and 2 show levels of PCDD/Fs and PCBs in human blood/milk/adipose tissue.
Tables 3 to 9 show levels of organochlorine pesticides in human milk.
For tables on organochlorine pesticides, the data are presented in separate tables showing
levels in human milk measured on a lipid basis, and levels in human milk measured on a
whole milk basis. For data presented on a whole milk basis, figures reported in studies as
per kg or g weight of milk are shown as ppm, and figures reported as per litre are left
unchanged. These figures approximate to ppm.
In tables 1 to 10, n represents the number of samples taken. For tables 3 to 9 on
organochlorine pesticides, the date that samples were taken in each study are given where
this information was available. In tables 1 to 10, values denoted * are the median rather
than the mean.
Table la
Mean Blood Levels of PCDD/Fs, 1980-91
PCDD/F
TEQ
USA
n=100
Germany
n=85
North
Vietnam
(Hanoi)
n=32
South
Vietnam
(Dong
Nai)
n=33
Guam
n=10
Soviet
Union (St.
Petersburg)
n=50
Soviet
Union
(Baikal
City)
n=8
41
42
10
49
32
17
18
Table la shows mean blood levels of PCDD/Fs (total TEQ, ppt, lipid) for general
populations in various countries, 1980-91.
Source: Schecter (1994)
Table lb
Mean Blood Levels of PCDD/Fs, 1996
PCDD/Fs TEQ
Gaza
n=39
Palestinian West
Bank
n=20
Israel
(Jerusalem)
n=50
USA (New York)
n=100
8.44
16.91
26.64
26.84
Table lb shows mean blood levels of PCDD/Fs (total TEQ, ppt, lipid) for general
populations in various countries in 1996
Source: Schecter (1994)
47
Table 1c
Mean Adipose Tissue Levels of PCDD/Fs, 1980s
PCCD/F
TEQ
USA
n=15
Germany
n=4
China
n=7
Japan
n=6
Canada
n=46
North
Vietnam
n=26
South
Vietnam
n=41
24
69
18
38
36
4
30
Table 1c shows mean adipose tissue levels of PCDD/Fs (total TEQ, ppt, lipid) for general
populations in various countries (1980s)
Source: Schecter (1994)
Table Id
Mean Breast Milk Levels of PCDD/Fs, 1980s
PCCD/Fs
TEQ
PCDD/Fs
TEQ
USA
n=43
Germany
n=185
Japan
n=6
Canada
n=200
n=7
20
27
27
26
13
North
Vietnam
(Hanoi)
n=30
South
Vietnam (Da
Nang)
n=l 1
Thailand
n=10
Cambodia
n=8
Russia
n=23
9
34
3
3
12
Pakistan
Table Id shows mean breast milk levels (pooled) of PCDD/Fs (total TEQ, ppt, lipid) for
general populations of various countries (1980s).
Source: Schecter et al. (1997)
48
Table 2a
Mean Levels of PCDD/Fs and Dioxin-like PCBs, 1987/88 and 1992/3
COUNTRY
AREA
Albania
Tirana
Librazhd
Vienna
(urban)
Tulin (rural)
Brixlegg
(industrial)
Brabant
Wallou
Liege_____
Brussels
Maritimes
Quebec
Ontario
Prairies
British
Columbia
Canada (all
provinces)
Gaspe
Basse CoteNord
Ungave Bay
Hudson Bay
Krk
Zagreb
Kladno
Austria
Belgium
Canada
Croatia
Czech
Republic
ppt TEQ
(PCDD/F|
1987/88
ppt TEQ
IPCDD/Fj
1992/3
ppt TEQ
[dioxin-like
PCBs|
1992/93
54
10
10
13
17.1
4.8
3.8
10.7
2.3
I. 7
II. 7
51
21
18.6
10.9
14.0
12.4
19.0
8
33.7
20.8
7.4
20
6
20
20
20
20
20
40.2
38.8
15.6
18.1
17.6
19.4
23.0
27.1
26.6
10.8
15.7
4.7
7.8
4.1
6.8
7.7
3.2
3.5
100
14.5
5.3
12
4
23.2
14.6
12.7
25.4
4
14.3
20.9
8.4
13.5
12.1
14.1
21.3
6.1
8.0
6.0
18.4
9.8
No. SAMPLES IN
POOL (n) in
1987/88 1992/3
13
19
34
76
31
23
14
41
To
13
11
12.0
11.8
11
13.4
18.1
14.6
42
48
17.8
15.2
4.5
38
31
40
10
24
10
18.0
Germany
Uherske
Hradiste
7 different
cities
Helsinki
Kuopio
Berlin
32.0
21.5
12.0
16.5
4.6
2.4
11.7
Hungary
Budapest
100
20
9.1
8.5
1.7
Denmark
Finland
15.5
49
Lithuania
Netherlands
Norway
Pakistan
Russian
Federation
Slovak
Republic
Spain
Ukraine
United
Kingdom
7.8
16.6
1.4
20.4
12
13.3
20.5
12
14.4
20.7
34.2
22.4
11.3
10
18.9
10.1
19.5
10
10
15.0
19.4
9.3
12.5
10.4
9.5
1
3.9
15.2
2.3
8.6
Karhopol
Michalovce
1
10
5.9
15.1
4.9
13.3
Bizkaia
Gipuzkoa
Kiev nr. 1
Kiev nr.2
Birmingham
19
10
5
5
20
37.0
19.4
25.5
11.0
13.3
17.9
10.6
8.2
15.0
11.5
4.3
Glasgow
23
29.1
15.2
4.0
10
12
Scentes
Palanga
(coastal)
Vilnius city
(urban)
Anykshchiai
(rural)
50
mean of 17
individual
samples_____
Tromso
(coastal)
Ham ar (rural)
Skien/Porsgru
nn (industrial)
Lahore
Arkhankeisk
10
17
11
10
10
11.3
Table 2a shows the mean levels of PCDD/Fs and dioxin-like PCBs (total TEQ, ppt, lipid)
in pooled breast milk samples from different countries studied by WHO in 1987/88 and
1992/3.
Footnote: Sum TEQ of dioxin-like PCBs presented in the table equates to the sum of non
ortho PCBs TEQ (nos 77, 126, 169) plus the sum of mono-ortho PCBs (nos 105 and
118). Units of ppt TEQ fat are equivalent to pg TEQ/g fat.
Source: WHO (1996)
50
Table 2b
Mean Levels of PCDD/Fs in Breast Milk, 1990s
1
Country/ Year
Samples Taken
Number of
Samples
ppt TEQ
|PCDD/Fs)
Reference
Estonia
Tarto & Tallinin
1991_________
France
Faroe Islands
12
17.5 (Nordic)
Mussalo-Rauhamaa
and Lindstrom 1995
15______________ 20.1
4 individual samples 6.7
9.5________
9 pooled samples
16.9 (Nordic)
69
Gonzalez et al. 1993
Abraham et al. 1995
Finland
Helsinki & Kuopio
1986-88_________
Israel
Jerusalem 1996
New Zealand
urban
rural
Norway
Hamar, Skien &
Tromso 1987
Palestinian West
Bank
near Bethlehem
1996____________
Spain
Sweden
Sundsvall, Umea,
Goteborg, Borlange
1987____________
Russia
Murmansk, northern
Russia, 1993
USA
New York, 1996
1
10.19
Mussalo-Rauhamaa
and Lindstrom 1995
Schecter et al. 1997
Bates et al. 1994
38
30
16.5
18.1 _______
17.1 (Nordic)
5
6.46
Schecter et al. 1997
13
40
13.31
22.4 (Nordic)
Gonzalez et al. 1993
Mussalo-Rauhamaa
and Lindstrom 1995
30
15.8
Polder et al. 1996
5 individual samples 8.13
100 pooled samples 27.6
Mussalo-Rauhamaa
and Lindstrom 1995
Schecter et al. 1997
Schecter et al. 1996
Table 2b shows mean levels of PCDD/Fs (total TEQ, ppt, lipid) in pooled breast milk
samples from different countries in studies published in the 1990s.
Footnote: (Nordic) denotes that the Nordic TEQ system was used and not the
International TEQ system.
0 7103
T able 3a
Mean Levels of DDT in Breast Milk on a lipid basis
Ccuntrj/Year of
Study
Number of
samples
%
samples
Positive
DBJ
Mean Concentration
of DDT Compound
(ug/g fat or ppm)
Reference
Compound
Measured
Australia
Perth, 1991
Victoria
128
100%
DDT
0.8 (median)
60
97%
p.p’DDT
0.225
0.672
Stevens et al.
1993
Quinsey et al.
1995________
Barkatina et al.
1998
0.862
Matuo et al.
1992
Belarus
6 different
regions
Brazil
Ribeirao Preto
Region, Sao
Paulo 1983/4
30
100%
sum DDT
(p,p-DDE
+
p,p’DDT)
total DDT
(p,p’DDT
+
p,p’DDE)
Porto Alegre,
(capital of the
state of Rio
Grande do Sul
-an
agricultural
region)______
Canada 1992
Samples from
several regions
across the
country______
Czech
Republic
Prague
30
73%
p,p’-DDT
0.12
Beretta and
Dick 1994
497
99%
p,p’-DDT
0.0221
Newsome el al.
1995
0.998
Schoula et al.
1996
Faroe Islands
4 indi
vidual
9 pooled
20
100%
Total DDT
(p,p’-DDE
+
p,p’DDT)
p,p’-DDT
0.159
Abraham et al.
1995
85%
DDT
0.064
0.044
France
1990
52
17
Bordet et al.
1993
I
Germany
Eastern
Germany
(former GDR)
1990-91
497
p,p'-DDT
0.134
West Germany
1990-91
>1000
p,p’-DDT
0.061
Alder et al.
1994
Lower Saxony, 156
1992/3
India
Punjab:
Ludhiana
40
(urban)
99%
Total DDT
0.38 (median)
Schlaud et al.
1995
100%
p,p’-DDT
7.18
Kalra et al.
1994
58
100%
p,p’-DDT
13.81
DDT
0.15
Larsen et al.
1994
Fairidkot
(agricultural
region with
high pesticide
use for cotton)
Italy
Rome, Milan,
Florence and
Pavia.
Jordan
Amman
1989/90
Kazakstan
Southern
Kazakstan
1994________
Kenya 1994
Mexico
Veracruz, a
tropical region,
1994/5
59
100%
p,p’-DDT
0.45 (median)
Alawi et al.
1992
75
99%
p,p’-DDT
0.3
Hooper et al.
1997
p,p’DDT
3.73
Heyce 1994
sum DDT
(p,p-DDE
+
p.p’DDT)
p,p’-DDT
6.99
43
100%
1.271
Waliszewski et
al. 1996
53
Nigeria 1986
p,p’DDT
2.27
3.83
Norway
Oslo, 1991
28
Russia
Kola
Peninsula,
northern
Russia, 1993
30
sum DDT
(p,p-DDE
+
p,p’DDT)
sum DDT
(sum of all
DDT, DDE
and DDD
isomers)
p,p’-DDT
5 different
regions,
1988/89
Slovak
Republic
1993/4_______
Spain
Madrid 1991
Sweden
Uppsala 1990
Thailand
Bangkok 198587__________
Turkey
Manisa in west
and Van in east
Turkey 1995/6
24
50
Kayseri region
1988 (an
agricultural
area with
previous heavy
use of
organochlorine
pesticides)
51
54
Atuma and Vaz
1986
0.338
Johansen et al.
1994
0.178
Polder et al.
1996
p,p’-DDT
0.387
Schecter et al.
1990
p,p’-DDT
0.126
Kocan et al.
1995
p,p’-DDT
0.012
Hernandez et al.
13
p,p’-DDT
0.03
Vaz et al. 1993
3
p,p-DDT
0.731
Schecter et al.
1989
p,p’-DDT
0.10
Cok etal. 1997
sum DDT
(1.115 x
p,p’DDE+
p,p’DDT)
2.357
p,p’-DDT
0.410
51
104
21.5%
1993_________
44%
96%
Ustunbas et al.
1994
UK
Samples from
England,
Ireland,
Scotland and
Wales 1989-91
193
p,p’-DDT
<0.02
Dwarka et al.
1995
USA
New York
1985-87
South
Vietnam
Ho Chi Minh
City 1985-87
Zimbabwe
7
p,p-DDT
0.023
Schecter et al.
1989
7
p,p-DDT
4.70
Schecter et al.
1989
p,p’DDT
1.33
sum DDT
(p,p-DDE
+
p,p’DDT)
6.50
p,p’DDT
9.07
sum DDT
25.26
1994
Kariba area
1994 (where
DDT is in use)
39
Chikuni et al.
1997
Table 3a shows the mean levels of DDT in breast milk on a lipid basis (ppm) for various
countries.
55
Table 3b
Mean Levels of DDT in Breast Milk on a Whole Milk Basis
Country/Year of
Study
Number
of
samples
%
samples
Positive
DDT
Compound
Measured
Concentration of DDT
Compound (ppm)
Reference
0.0226 mg/1
Barkatina et al.
1998
30
100%
sum DDT
(p,p-DDE
+
p,p’DDT)
p,p’-DDT
0.006
Matuo et al.
1992
497
99%
p,p’-DDT
0.00064
Newsome et al.
1995
31
80.6%
p,p’-DDT
0.0175
Dogheim et al.
1991
20 different
regions 1993
60
49%
p,p’-DDT
0.00293
Saleh et al.
1996
Cairo, 1994
11
71%
p,p’-DDT
0.00933
India
Dehli
Punjab:
Ludhiana
(urban)
25
92%
p,p’-DDT
0.158 mg/1
Dogheim et al.
1996
Nairet al. 1996
47
100%
p,p’-DDT
0.141
82
100%
p,p’-DDT
0.313
Belarus
6 different
regions
Brazil
~
Ribeirao Preto
Region, Sao
Paulo 1983/4
Canada 1992
Samples from
several regions
across the
country
Egypt
Cairo, 1987
Fairidkot
(agricultural
region with
high pesticide
use for cotton)
56
Kalra et al.
1994
Poland
different
regions,
DDT
industri
al area
158
5.5 ug/1
Czaja et al.
1997
2.8 ug/1
less in
dustrial
areas
199
Samples from
different
regions olf the
country
253
Spain
Madrid 1991
UK
Samples from
England,
Ireland,
Scotland and
Wales 1989-91
51
21.5%
p’p-DDT
0.00285 mg/1
Czaja et al.
1997b
p,p’-DDT
0.0004
Hernandez et al.
<0.0001
Dwarka et al.
1993_________
p,p’-DDT
193
1995
Table 3b shows the mean levels of DDT in breast milk on a whole milk basis (ppm) for
various countries.
Table 3c
Mean Levels of DDE in Breast Milk on a Lipid Basis
Country/Year of
Study
Number of
samples
%
samples
Positive
DDE
Compound
Measured
Concentration of DDE
Compound (ppm)
Reference
Australia
Victoria
Brazil
60
100%
p,p’-DDE
0.96
Quinsey et al.
Porto Alegre,
(capital of the
state of Rio
Grande do Sul
- an
agricultural
region)
1995_______
30
100%
p,p’-DDE
2.53
Beretta and
Dick 1994
57
Canada 1992
Samples from
several
regions across
the country
497
Quebec 1988- 536
90__________
Faroe Islands 4 indi
vidual
9 pooled
France
20
1990_______
Germany
Eastern
497
Germany
(former GDR)
1990-91
100%
p,p’-DDE
0.222
Newsome et al.
1995
100%
p,p’-DDE
0.34
100%
p,p’-DDE
2.010
Dewailly et al.
1996________
Abraham et al.
1995
100%
DDE
0.981
2.183
p,p’-DDE
1.130
p,p’-DDE
0.589
p,p’-DDE
10.0
West
Germany
1990-91
India
Punjab:
Ludhiana
(urban)
>1000
40
100%
Fairidkot
(agricultural
region with
high pesticide
use for cotton)
Italy
Rome, Milan,
Florence and
Pavia_______
Jordan
Amman
1989/90
Kazakstan
southern
58
100%
58
Alder et al.
1994
Kalra et al.
1994
12.85
DDE
2.2
Larsen et al.
1994
59
100%
p,p’-DDE
2.04 (median)
Alawi et al.
1992
76
100%
p,p’-DDE
1.960
Hooper et al.
1997
100%
p,p’DDE
p,p’-DDE
2.95
5.017
Heyce 1994
Waliszewski et
Kazakstan
1994_______
Kenya 1994
Mexico
Bordet et al.
1993
43
al. 1996
Veracruz, a
tropical
region, 1994/5
The
Netherlands
Nigeria 1986
10
p,p’-DDE
0.705
p,p-DDE
1.33
Dagnelie et al.
1992________
Atuma and Vaz
1986________
Russia
Kola
Peninsula,
northern
Russia, 1993
I 5 different
regions,
1988/89
Slovak
Republic
1993/4
Spain
Madrid 1991
Sweden
Uppsala 1990
Thailand
Bangkok
1985-87
Turkey
Manisa in
vVest and Van
in east Turkey
1995/6
p,p’-DDE
30
1.269
Polder et al.
1996
24
p,p'-DDE
1.408
Schecter et al.
1990
50
p,p’-DDE
1.667
Kocan et al.
1995
p,p’-DDE
0.6041
Hernandez et al.
13
p,p’-DDE
0.35
Vaz et al. 1993
3
p,p-DDE
3.610
Schecter et al.
51
100%
1993_________
1989
104
100%
p,p’DDE
2.013
Cok etal. 1997
Kayseri region | 51
1988 (an
agricultural
area with
previous
heavy use of
organochlorin
e pesticides)
"UK
193
Samples from
England,
Ireland,
Scotland and
Wales 198991
100%
p,p’-DDE
2.389
Ustunbas et al.
1994
99%
p,p’-DDE
0.40
Dwarka et al.
1995
59
USA
New York
1985-87
South
Vietnam
Ho Chi Minh
City, 1985-87
Zimbabwe
1994
mean national
level
7
p,p-DDE
0.541
Schecter el al.
1989
7
p,p-DDE
6.70
Schecter et al.
1989
p,p’-DDE
4.49
Chikuni et al.
1997
Kariba area
1994 (only
area in
Zimbabwe
where DDT is
still in use)
39
p,p’DDE
13.60
Table 3c shows the mean levels of DDE in breast milk on a lipid basis (ppm) for various
countries.
Table 3d
Mean Levels of DDE in Breast Milk on a Whole Milk Basis
Country/Year of
Study
Number
of
samples
%
samples
Positive
DDE
Compound
Measured
Concentration of DDE
Compound
Brazil
Ribeirao Preto
Region, Sao
Paulo 1983/4
Canada 1992
Samples from
several regions
across the
country
Egypt
Cairo, 1987
30
100%
p,p’-DDE
0.019
Matuo et al.
1992
497
100%
p,p’-DDE
0.00678
Newsome et al.
1995
31
97%
p,p’DDE
0.03886
Dogheim et al.
1991
20 different
regions, 1993
60
100%
p,p’-DDE
0.02137
Saleh et al.
1996
Cairo, 1994
11
100%
p,p’-DDE
0.1
Dogheim et al.
1996
60
Reference
______ £
India
Dehli
Punjab:
Ludhiana
(urban)
Fairidkot
(agricultural
region with
high pesticide
use for cotton)
Poland
different
regions,
47
96%
p,p'-DDE
0.672 mg/1
Nair et al. 1996
100%
p,p'-DDE
0.196 mg/1
Kalra et al.
1994
82
0.277 mg/1
100%
p,p’-DDE
industri
al area
158
d.0254 mg/1
Czaja et al.
1997
0.0275 mg/1
less in
dustrial
areas
199
Samples from
different
regions of the
country
Spain
Madrid 1991
UK
Samples from
England,
Ireland,
Scotland and
Wales 1989-91
p,p’-DDE
0.0252 mg/I
Czaja et al.
1997b
100%
p,p’-DDE
0.0187
Hernandez et al.
99%
p,p’-DDE
0.009
Dwarka et al.
253
51
1993_________
193
1995
Table 3d shows mean levels of DDE in breast milk on a whole milk basis (ppm) for
various countries
61
Table 3e
Levels of Total DDT in Breast Milk
Country
Australia Victoria
Belarus
Brazil
Canada_________
Czech Republic
Faroe Islands
France
Eastern Germany
West Germany
India Ludhiana ~~
Fairidkot_________
Italy__________ _
Jordan
~~
Kazakstan
~~~
Kenya
Mexico_______
Nigeria______
Norway
Russia
—
Slovak Republic
Spain______ —
Sweden_____
Thailand
Turkey
UK
'
USA
South Vietnam
Zimbabwe National
average
Kariba region
Sum DDT Compounds
Reference
“0.225+0.96 = 0.321
Quinsey et al. 1995
0.672
Barkatina et al. 1998
0.12+2.53 = 2.65
Beretta and Dick 1994
0.0221+0.222 = 0.244
Newsome et al. 1995
0.998
Schoula et al. 1996
0.064+0.981 = 1.045
Abraham et al. 1995
0.044+2.183 = 2.227
Bordet et al. 1993
0.134+ 1.130= 1.264
Alder et al. 1994
0.061+0.589 = 0.65
Schlaud et al. 1995
7.18+10.0= 17.18
Kalra et al. 1994
13.81 + 12.85 = 26.66
0.15+2.2 = 2.35________
Larsen et al. 1994
0.45+2.04 = 2.49 (median) Alawi et al. 1992_____
0.3+1.96 = 2.26
Hooper et al. 1997
"6^9
--------- Heyce 1994
~
1.271+5.017 = 6.288
Waliszewski et al. 1996
T83
"
Autuma and Vaz 1986
0.338
Johansen et al. 1994
0.178+1.269= 1.447
Polder et al. 1996
0.126+1.667= 1.793
Kocan et al. 1995
”0.012+0.604 = 0.616
Hernandez et al. 1993
0.03+0.35 = 0.38
Vazetal. 1993
0.731+3.61 =4.341
Schecter et al. 1989
2357
Coketal. 1997_______
0.02+0.4 = 0.42
Dwarka et al. 1995
0.023+0.541 =0.564
Schecter et al. 1989
4?7
- Schecter et al. 1989
630
Chikuni et al. 1997
25.26
e sum of p,p -DDT plus p,p -DDE. The data was compiled from tables 3a and 3c.
62
Table 4a
Mean Levels of HCB in Breast Milk on a Lipid Basis
CountryA'ear of
Study
Number of
samples
%
samples
Positive
Mean Concentration
ofHCB
(mg/kg fat, or ppm)
Reference
Australia
Perth, 1991
128
100%
0.10 (median)
Stevens et al.
1993
Victoria 1993
60
98%
0.411
63%
0.02
Quinsey et al.
1995_______
Berreta and
kick 1994
100%
0.0145
Newsome et al.
1995
0.639
Schoula et al.
1996
<0.1
Abraham et al.
1995
0.147
Bordet et al.
1993
Alder et al.
1994
Brazil
30
Porto Alegre,
(capital of the
state of Rio
Grande do Sul
- an
agricultural
region)
Canada 1992 497
Samples from
several
regions across
the country
Czech
17
Republic
Prague
Faroe Islands 4 indi
vidual
9 pooled
France
1990_______
Germany
Eastern
Germany
(former GDR)
1990-91
79
497
0.167
West
Germany
1990-91
>1000
0.218
Lower
Saxony,
1992/3
156
100%
99%
0.223 (median)
Schlaud et al.
1995
63
Italy
Rome, Milan,
Florence and
Pavia
Jordan
Amman
1989/90
Kazakstan
southern
Kazakstan
1994_______
Mexico
Veracruz, a
tropical
region, 1994/5
The
Netherlands
Norway
Oslo, 1991
Russia
Kola
Peninsula,
northern
Russia, 1993
5 different
regions,
1988/89
Spain
Madrid 1991
Slovak
’
Republic
1993/94
Sweden
Uppsala 1990
Thailand
Bangkok
1985-87
64
0.18
Larsen et al.
1994
59
93%
0.29 (median)
Alawi et al.
1992
76
100%
0.091
Hooper et al.
1997
43
100%
0.047
Waliszewski et
al. 1996
10
0.083
28
0.041
30
0.129
Dagnelie et al.
1992_______
Johansen et al.
1994________
Polder et al.
1996
24
0.245
Schecter et al.
1990
0.0008
51
67.8%
50
0.829
Hernandez et al.
1993_________
Kocan et al.
1995
13
0.037
Vazetal. 1993
3
0.007
Schecter et al.
1989
104
96%
0.050
Cok et al. 1997
Kayseri region 51
1988 (an
agricultural
area with
previous
heavy use of
organochlorine
pesticides)
“UK
193
Samples from
England,
Ireland,
Scotland and
Wales
7
USA
New York
1985-87
South
7
Vietnam
Ho Chi Minh
City 1985-87
96%
0.084
Ustunbas et al.
1994
0.02
Dwarka et al.
1995
0.022
Schecter et al.
Turkey
Manisa in
west and Van
in east Turkey
1995/6
1989
0.003
Schecter et al.
1989
Table 4a shows the mean levels of HCB in breast milk on a lipid basis (ppm) for various
countries
65
Table 4b
Mean Levels of HCB in Breast Milk on a Whole Milk Basis
Country/Year of
Study
Number
of samples
%
samples
Positive
Mean Concentration
ofHCB
(mg/kg whole milk or
ppm)
Reference
Canada 1992
Samples from
several regions
across the
country______
Egypt
Cairo, 1987
Poland
various regions
497
100%
0.00044
Newsome et al.
1995
31
10%
0.01167
Dogheim et al.
1993_________
Czaja et al. 1997
Samples from
different
regions of the
country
UK
Samples from
England,
Ireland,
Scotland and
Wales
industrial
area
158
less in
dustrial
areas
199
0.0016 mg/1
0.0022 mg/1
253
0.002 mg/1
Czaja et al.
1997b
193
<0.001
Dwarka et al.
1995
Table 4b shows the mean levels of HCBJ^ breast milk on a whole milk basis (ppm) for
various countries
66
Table 5a
Mean Levels of HCH Compounds in Breast Milk on a Lipid Basis
Compound
Measured
Concentration of
HCH Compound
(mg/kg fat, or ppm)
Reference
128
a-HCH
0.071
Quinsey et al.
1995
60
B-HCH
0.345
g-HCH
sum aHCH + BHCH
0.108
0.417
30.7%
gammaHCH
0.0344
Matuo et al.
1992
80%
a-HCH
0.04
Beretta and Dick
1994
100%
B-HCH
0.9
50%
g-HCH
0.02
93%
B-HCH
0.0226
17%
g-HCH
0.00103
14%
a-HCH
B-HCH
0.00031
0.071
Schoula et al.
1996
B-HCH
<0.04
Abraham et al.
1995
Country/Year of
Study
Number of
samples
Australia
%
samples
Positive
Victoria 1993
Belarus
Samples from
6 different
regions
Brazil
Ribeirao Preto
Region, Sao
Paulo 1983/4
30
Porto Alegre,
30
capital of the
state of Rio
25
Grande do Sul
- an
30
agricultural
region where
pesticides are
extensively
used
Canada 1992 497
Samples from
several
regions across
the country
Czech
Republic
7
Barkatina et al.
1998
Newsome et al.
1995
frague
"aroe Islands
4 indi
vidual
9 pooled
67
France
1990
20
Germany
Eastern
Germany
(former GDR)
1990-91
497
West
Germany
1990-91
>1000
Lower
Saxony,
1992/3
India
Dehli
Punjab:
Ludhiana
(urban)
Fairidkot
(agricultural
region with
high pesticide
use for cotton)
68
156
61
40
58
85%
100%
100%
a-HCH
B-HCH
g-HCH
a-HCH
0.052
0.287
0.037
0.0008
B-HCH
0.083
g-HCH
0.0098
a-HCH
<0.01
B-HCH
0.075
g-HCH
0.016
97%
B-HCH
0.045
10%
g-HCH
0.016
51%
a-HCH
1.83
95%
B-HCH
8.83
90%
g-HCH
2.31
98%
a-HCH
0.65
100%
B-HCH
4.37
80%
g-HCH
0.21
100%
a-HCH
1.76
100%
B-HCH
8.20
91%
g-HCH
0.41
Bordet et al.
1993
Schlaud et al.
1995
Banerjee et al.
1997
Kalra et al. 1994
Jordan
Amman
59
a-HCH
0.12 (median)
100%
B-HCH
0.40
74
76
37.3%
98%
100%
g-HCH
a-HCH
B-HCH
0.078
2.210
Hooper et al.
1997
43
40%
a-HCH
0.018
Waliszewski et
al. 1996
100%
B-HCH
0.561
52%
g-HCH
sum a + B
+ gamma
HCH. (BHCH
accounted
for 93% of
the sum)
sum HCH
(of which
99% is BHCH)
0.022
0.036
1989/90
Kazakstan
southern
Kazakstan
1994_______
Mexico
Veracruz, a
tropical j
region, 1994/5
Norway
28
Oslo, 1991
Russia
Kola
Peninsula,
northern
Russia, 1993
5 different
regions,
1988/89
Spain
Madrid 1991
Sweden
Uppsala 1990
Thailand
Bangkok
1985-87
Alawi et al. 1992
55.9%
30
24
51
68.6%
a-HCH
B-HCH
g-HCH
a-HCH
0.23
Johansen et al.
1994
0.858
Polder et al.
1996
0.129
1.589
0.0094
0.0342
Schecter et al.
1990
Hernandez et al.
1993
3
-
85.7%
B-HCH
0.235
64.7%
g-HCH
B-HCH
0.0105
0.02
a-HCH
0.001
B-HCH
0.119
g-HCh
0.003
Vazetal. 1993
Schecter et al.
1989
69
Turkey
Manisa in west
and Van in east
Turkey 1995/6
Kayseri region
1988 (an
agricultural area
with previous
heavy use of
organochlorine
pesticides)
UK
Samples from
England,
Ireland,
Scotland and
Wales
USA
New York
1985-87
South Vietnam
Ho Chi Minh
City 1985-87
Cok et al. 1997
104
51
75%
a*HCH
0.096
19
100%
B-HCH
0.522
51
97%
g-HCH
0.156
B-HCH
0.08
g-HCH
<0.02
a-HCH
0.001
B-HCH
0.020
g-HCH
a-HCH
0.002
0.003
B-HCH
0.221
g-HCH
0.023
193
7
7
Ustunbas et al.
1994
Dwarka et al
1995
Schecter et al.
1989
Schecter et al.
1989
Table 5a shows the mean levels of HCH compounds in breast Milk on a lipid basis (ppm)
for various countries.
70
Table 5b
Mean Levels of HCH Compounds in Breast Milk on a Whole Milk Basis
Country/Year of
Study
Number
of
samples
Belarus
Samples from 6
different regions
Canada 1992
497
Samples from
several regions
across the
country
Egypt
31
Cairo, 1987
%
samples
Positive
Compound
Measured
Concentration of HCH
Compound (mg/kg
whole milk, or ppm)
Reference
0.0142
Barkatina et al.
1998
93%
sum aHCH + BHCH
B-HCH
0.00071 (0.71 ppb)
Newsome et al.
1995
17%
g-HCH
0.00004 (0.04 ppb)
14%
51.6%
a-HCH
a-HCH
B-HCH
g-HCH
0.00001 (0.01 ppb)
0.00279
0.01337
0.00072
Dogheim et al.
1991
20 different
regions, 1993
60
95%
g-HCH
0.00842
Salehet al. 1996
Cairo, 1994
11
156
a-HCH
B-HCH
g-HCH
Total HCH
B-HCH
0.00314
0.1912
<0.0010
0.19344
0.045
Dogheim 1996
Germany
_>ower Saxony,
992/3______
ndia
Dehli
64%
82%
0
82
97%
10%
g-HCH
0.016
100%
a-HCH
0.045mg/l
28%
B-HCH
0.198 mg/1
100%
g-HCH
0.084 mg/1
51%
a-HCH
0.08
95%
B-HCH
0.24
90%
g-HCH
0.06
98%
a-HCH
0.015
100%
B-HCH
0.09
Dehli
Punjab:
Ludhiana
(urban)
25
61
47
Schlaud et al.
1995
Nair et al. 1996
Banerjee et al.
1997
Kalraetal. 1994
71
Fairidkot
(agricultural
region with high
pesticide use for
cotton)
Poland
industrialised
and less
industrialised
areas, 1995/6??
82
Samples from
different regions
of the country
253
Spain
Madrid 1991
80%
g-HCH
0.004
100%
a-HCH
0.031
100%
91%
B-HCH
g-HCH
0.188
0.011
a-HCH
0.00055 mg/1
B-HCH
0.003 mg/1
g-HCH
0.00045 mg/1
a-HCH
mean 0.0006 mg/1
B-HCH
0.00365 mg/1
g-HCH
357
51
68.6%
a-HCH
0.00045 mg/1
MOI
85.7%
B^HCH
0.0072
64.7%
g-HCH
0.0003
Czaja et al. 1997
Czaja et al.
1997b
Hernandez et al.
1993
Table 5b shows the mean levels of HCH compounds in breast milk on a whole milk basis
(ppm) for various countries
Table 6a
Mean Levels of Heptachlor in Breast Milk on a Lipid Basis
Country[\ear of
Study
Number
of samples
%
samples
Positive
Mean Concentration of
Heptachlor (mg/kg fat, or
PPm)
Reference
Australia
Perth, 1991
Germany
Lower Saxony,
1992/3
128
89%
0.02 (median)
Stevens et al. 1993
156
74%
0.022 (median)
Schlaud et al. 1995
72
Jordan
Amman
1989/90
Spain
Madrid 1991
Turkey
Kayseri region
1988 (an
agricultural
area with
previous heavy
use of
organochlorine
pesticides)
59
68%
0.70 (median)
Alawi et al. 1992
51
33.3%
0.0044
Hernandez et al. 1993
32
38%
0.198
Ustunbas et al. 1994
Table 6a shows the mean levels of heptachlor in breast milk on a lipid basis (ppm) for
various countries
Table 6b
Mean Levels of Heptachlor in Breast Milk on a Whole Milk Basis
Country/Year of
Study
Number
of samples
%
samples
Positive
Mean Concentration of
Heptachlor (mg/kg whole
milk or ppm)
Reference
Australia
Perth, 1991
Egypt
Cairo, 1987
128
89%
0.02 (median)
Stevens et al. 1993
Dogheim et al. 1991
33.3%
mean 1.0 ppb whole
milk, range 1.0-1.0 ie.
the compound was
detectable
0.1 ng/g
Spain
Madrid 1991
31
51
Hernandez et al. 1993
Table 6b shows the mean levels of heptachlor in breast milk on a whole milk basis (ppm)
for Various Countries.
73
Table 6c
Mean Levels of Heptachlor Epoxide in Breast Milk on a Lipid Basis
Country/Year of
Study
Number
of samples
Australia
Victoria
Brazil
Porto Alegre,
capital of the
state of Rio
Grande do Sul an agricultural
region where
pesticides are
extensively
used
Canada 1992
Samples from
several regions
across the
country
France
1990
Germany
Eastern
Germany
(former GDR)
1990-91
West Germany
1990-91
Russia
5 different
regions,
1988/89
Spain
Madrid 1991
74
Concentration of
Heptachlor Epoxide
(mg/kg fat, or ppm)
Reference
60
%
samples
Positive
’30%
0.061
Quinsey et al. 1995
30
17%
0.02
Beretta and Dick
1994
497
68%
0.00377
Newsome et al. 1995
20
95%
0.097
Bordet et al. 1993
497
0.008
Alder et al. 1994
>1000
0.014
24
0.0118
Schecter et al. 1990
0.0311
Hernandez et al. 1993
51
92.1%
Turkey
Kayseri region
1988 (an
agricultural
area with
previous heavy
use of
organochlorine
pesticides)
32
16%
0.011
Ustunbas et al. 1994
Van in east and
Manisa in west
Turkey 1995/6
104
96%
0.072
Cok et al. 1997
I
Table 6c shows the mean levels of heptachlor epoxide in breast milk on a lipid basis
(ppm) for various countries.
Table 6d
Mean Levels of Heptachlor Epoxide in Breast Milk on a Whole Milk Basis
Country/Year of
Study
Number
of samples
%
samples
Positive
Concentration of
Heptachlor Epoxide
(mg/kg whole milk, or
PPm)
Reference
Canada 1992
Samples from
several regions
across the
country
France
1990________
Spain
Madrid 1991
497
68%
0.00011
Newsome et al. 1995
20
95%
0.097
Bordet et al. 1993
51
92.1%
0.0009
Hernandez et al. 1993
Table 6d shows the mean levels of heptachlor epoxide in breast milk on a whole milk
basis (ppm) for various countries.
75
Table 7a
Mean Levels of Dieldrin in Breast Milk on a Lipid Basis
Country/Year of
Study
Number
of samples
%
samples
Positive
Mean Concentration of
dieldrin (mg/kg, or ppm)
Reference
Australia
Perth, 1991
128
100%
0.05 (median)
Stevens et al. 1993
Victoria_____
Brazil
Ribeirao Preto
Region, Sao
Paulo 1983/4
60
30
43%
3%
0.159
1.31
Quinsey et al. 1995
Matuo et al. 1992
Porto Alegre,
capital of the
state of Rio
Grande do Sul an agricultural
region where
pesticides are
extensively
used_________
Canada 1992
Samples from
several regions
across the
country______
France
”
1990
Germany
Eastern
Germany
(former GDR)
1990-91
30
83%
0.07
Beretta and Dick
1994
497
94%
0.00978
Newsome et al. 1995
20
55%
0.19
Bordet et al. 1993
497
0.042
Alder et al. 1994
West Germany
1990-91
>1000
0.009
Lower Saxony,
1992/3
Iraq
156
76
66%
0.014 (median)
Schlaud et al. 1995
1.00
Jensen and Slorach
1991
Jordan
Amman
1989/90
The
Netherlands
Russia
5 different
regions,
1988/89
Spain
Madrid 1991
Thailand
Bangkok 198587__________
Turkey
Kayseri region
1988 (an
agricultural
area with
previous heavy
use of
organochlorine
pesticides)
"UK
Samples from
England,
Ireland,
Scotland and
Wales 1989-91
USA
New York
1985-87
Urugary
0.05
Alawi et al. 1992
10
0.013
Dagnelie et al. 1992
24
<0.002-0.003
Schecter el al. 1990
0.0039
Hernandez et al. 1993
0.069
Schecter et al. 1989
0.0067
Ustunbas et al. 1994
193
0.03
Dwarka et al. 1995
7
0.541
Schecter et al. 198587
1.00
Jensen and Slorach
0.004
Schecter et al. 1989
59
51
5%
11.7%
3
32
19%
1991___________
South Vietnam
Ho Chi Minh
City
7
Table 7a shows the mean levels of dieldrin in breast milk on a lipid basis (ppm) for
various countries
77
Table 7b
Mean Levels of Endrin in Breast Milk on a Lipid Basis
Country/Year of
Study
Number
of samples
France
1990
20
%
samples
Positive
40%
Concentration of Endrin
(mg/kg fat, or ppm)
Reference
0.058
Bordet et al. 1993
Table 7b shows the mean levels of endrin in breast milk on a lipid basis (ppm) for France.
Table 7c
Mean Levels of Aldrin in Breast Milk on a Lipid Basis (ppm)
Country/Year of
Study
Number
of samples
Australia
Victoria 1993
France ~~
1990________
Turkey
Kayseri region
1988 (an
agricultural
area with
previous heavy
use of
organochlorine
pesticides)
60
%
Concentration of Aldrin
samples (mg/kg fat, or ppm)
Positive
5%
mean 0.02
Quinsey et al. 1995
20
75%
0.024
Bordet et al. 1993
32
88%
mean 0.047
Ustunbas et al. 1994
Reference
Table 7c shows the mean levels of aldrin in breast milk on
a lipid basis (ppm) for various
countries.
Table 8.
Mean Levels of Chlordane in Breast Milk on a Lipid Basis
Country/Year of
Study
Number
of samples
Australia
Perth, 1991
128
Victoria
60
78
%
Concentration of
samples Chlordane (CL)
Positive Tompound (mg/kg fat,
or ppm)
17%
~median <0.01 mg/kg
fat,
80%
oxychlordane 0.13
Reference
Stevens et al. 1993
Quinsey et al. 1995
Canada
National survey
1987
Indigenous
people
Canada 1992
Samples from
several regions
across the
country
France
1990
497
see Dearth and Hites
1991
g-CL 0.003
aCL 0.012
g-CL 0.00016
Newsome et al. 1995
a-CL 0.00021
11%
20
Japan
1986
Russia
Kola Peninsula,
northern
Russia, 1993
5 different
regions,
1988/89
Thailand
Bangkok 198587
USA
New York
1985-87
South
Vietnam
Ho Chi Minh
City 1985-87
2%
g-CL 0.008
a-CL 0.019
90%
a-CL 0.078
40%
g-CL 0.006
a-CL 0.0031
Bordet et al. 1993
Dearth and Hites
1991
30
g-CL 0.0012
sum CL 0.059
Polder et al. 1993
24
oxychordane 0.0056
Schecter et al. 1990
3
oxychlordane 0.005
Schecter et al. 1989
7
oxychlordane 0.006
Schecter et al. 1989
7
oxychlordane 0.003
Schecter et al. 1989
Table 8 shows the mean levels of chlordane in breast milk on a lipid basis (ppm) for
various countries.
79
Table 9
Mean Levels of Toxaphene in Breast Milk on a Lipid Basis (ppm)
Country /Year of
Study
Number of
samples
Honduras
1
%
samples
Positive
Concentration of
toxaphene mg/kg fat, or
ppm
Reference
1.4
Boer and Webster
1993______________
Pyysalo and Antervo
1985______________
Boer and Webster
1993______________
Boer and Webster
1993______________
Vaz and Blomkvist
1985
0.05-0.5
Finland
Netherlands
1
Nicaragua
1993
Sweden
16
0.65
100%
2:0
0.1
Table 9 shows the mean levels of toxaphene in breast milk on a lipid basis (ppm) for
various countries.
Table 10
Summary of Mean Levels of Organochlorine Pesticides in Breast Milk on a Lipid
Basis (ppm)
Country
Australia
Victoria
Belarus
Brazil
Sao Paulo
Porto-Algre
Canada
Czech
Republic
Faroe
Islands
France
Germany
India
Dehli
Ludhiana
Fairidkot
Italy
80
p,p’DDT
p,p’DDE
Dieldrin
HCB
HE
B-HCH
g-HCH
0.225
0.672
(sum)
0.96
0.159
0.411
0.061
0.345
0.108
0.12
0.0221
0.998
(sum)
0.064
2.53
0.222
0.07
0.00978
0.02
0.0145
0.639
0.02
0.00377
0.9
0.0226
0.0344
0.02
0.001
0.044
0.38 *
2.183
7.18
13.81
0.15
10.0
1.31
0.981
0.071
<0.1
0.19
0.14*
0.147
0.223*
12.85
0.18
<0.04
0.097
0.014
0.287
0.045
0.037
8.83
4.37
8.20
2.31
0.21
0.41
0.016
Jordan
Kazakstan
Kenya
Mexico
The
Netherlands
Nigeria
Norway
Russia
Kola
Peninsula
5 different
regions
Slovak
Republic
Spain
Sweden
Thailand
Turkey
Mania, Van
Kayseri
UK
USA
South
Vietnam
Zimbabwe
national av.
Kariba
0.45*
0.3
3.73
1.271
2.04*
1.96
2.95
5.017
0.705
nd
0.29*
0.091
0.013
0.047
0.083
0.05*
2.27
0.338
(sum)
07178"
1.269
0.387
1.408
0.126
T667
0.012
0.03
0.731
0.6041
0.0039
0.35
3.610
0.069
0.0008
0.037
0.007
0.1
0.41
<0.02
0.023
4.70
2.01
2.389
0.40
0.541
6.70
0.0067
0.03
0.026
0.004
0.05
0.084
0.02
0.022
0.003
1.33
4.49
9.07
13.60
0.40
2.210
0.23
0.561
0.022
0.0118
1.589
0.0094
0.0311
0.235
0.02
0.119
0.0105
0.522
0.08
0.020
0.221
0.156
<0.02
0.002
0.023
nd
1.33
0.041
0.129
<0.0023.0
0.245
0.829
0.011
0.003
Table 10 shows a summary of information compiled in this report on the mean levels of
several organochlorine pesticides in human breast milk from various countries.
Foonote: For DDT, (sum) denotes the total of DDT compounds measured including
DDE.
Source: see tables 3a, 3c, 4a, 5a, and 6c.
*
81
Table 11.
ADIs set by WHO (1997) and estimated approximate level of organochlorines in
breast milk which should not be exceeded if the ADI is not exceeded.
Pesticide
SDDT
HCB___________
Lindane (y HCH)
Dieldrin + aldrin
combined
Endrin_______
Heptachlor
Heptachlor epoxide
Chlordane
ADI (WHO)
mg/kg body
weight
Level in milk which should not be
exceeded if the ADI is not to be
exceeded
mg/kg whole milk
mg/kg fat
0.02
0.0006
0.001
0.0001
0.133
3.80
0.0002
0.0001
0.0001
0.0005
0.004
w
0.0066
0.00066
0.19
0.0013
0.00066
0.00066
0.0033
0.038
019
0.019
0.019
0.095
*
82
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