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BodyBurden The Pollution in People

Authors:
BodyBurden
The Pollution in People.
Jane Houlihan
with Richard Wiles
Kris Thayer
Sean Gray
the power of information
http://www.ewg.org
Acknowledgements
Thanks to Dr. Michael McCalley and Dr. Phillip Landrigan of the Mt. Sinai
School of Medicine for their invaluable help in the design and conduct of
this study. We are indebted to Kate Holcombe for her coordination and
follow-through with sampling logistics. Special thanks to Tim Greenleaf
for his excellent work on the design and layout of the report, and to Ken
Cook for his guidance throughout the entire project.
This report was made possible by grants from The Mitchell Kapor Foun-
dation, Lucy R. Waletzky, M.D., The Beldon Fund, The W. Alton Jones
Foundation, and The Turner Foundation. The opinions expressed in this
report are those of the authors and do not necessarily reect the views
of the supporters listed above. EWG is responsible for any errors of fact
or interpretation contained in this report.
Copyright © January 2003 by Environmental Working Group. All rights
reserved. Manufactured in the United States of America. Printed on
recycled paper.
EWG is a nonprot research organization with ofces in Washington,
DC and Oakland, CA. EWG uses the power of information to educate the
public and decision-makers about a wide range of environmental issues,
especially those affecting public health.
Kenneth A. Cook, President
Richard Wiles, Senior Vice President
Mike Casey, Vice President for Public Affairs
Jane Houlihan, Vice President for Research
Bill Walker, Vice President/West Coast
EWG — the power of information
http://www.ewg.org
EXECUTIVE SUMMARY
In a study led by Mount Sinai School of Medicine in New York,
in collaboration with the Environmental Working Group and
Commonweal, researchers at two major laboratories found 167
chemicals, pollutants, and pesticides in the blood and urine
of nine adult Americans. Study results appear in a recently-
published edition of the journal Public Health Reports (Thornton,
et al. 2002) – the rst publicly available, comprehensive look at
the chemical burden we carry in our bodies.
None of the nine volunteers works with chemicals on the job. All
lead healthy lives. Yet the subjects contained an average of 91
compounds each – most of which did not exist 75 years ago.
Scientists have not studied the health risks of exposures to
complex chemical mixtures, such as those found in this study. For
two-thirds of the chemicals found, many of which are banned,
researchers have partially studied the extent to which these
chemicals can harm human health. They have found that these
112 compounds can threaten nearly every organ in the body at
every stage of life (Table 1).
In total, the nine subjects carried:
ü 76 chemicals linked to cancer in humans or
animals (average of 53),
ü 94 chemicals that are toxic to the brain and
nervous system (average of 62),
ü 86 chemicals that interfere with the hormone
system (average of 58),
ü 79 chemicals associated with birth defects or
abnormal development (average of 55),
ü 77 chemicals toxic to the reproductive system
(average of 55), and
ü 77 chemicals toxic to the immune system (average
of 53).
The blood and urine from the nine volunteers were tested for
210 chemicals that can be divided into seven basic groups
(Table 2). Of the chemical groups tested, the most prevalent
were those contained in 24 classes of semivolatile and volatile
chemicals, with 77 detected. These classes include well-known
industrial solvents and gasoline ingredients, such as xylene and
ethyl benzene, that are used in a variety of common products
like paints, glues, and re retardants. The laboratory found 48
Scientists have not studied the
health risks of exposures to
complex chemical mixtures, such
as those found in this study.
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FOOTNOTES
[1] Chemicals listed as linked to cancer are those classied by the National
Toxicology Program as “known” human carcinogens, or “reasonably anticipated” to
be human carcinogens; or those classied by the Environmental Protection Agency
as “known” or “probable” human carcinogens.
[2] Cancer: 3 heavy metals, 1 phthalate, 9 organochlorine pesticides, 8 furans, 7
dioxins and 48 PCBs
[3] Birth defects / developmental delays: 4 heavy metals, 2 phthalates, 7
organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 3 other semivolatile or
volatile organic compounds
[4] Vision: 1 heavy metal, 1 phthalate, 2 organochlorine pesticides and 7 other
semivolatile or volatile organic compounds
[5] Hormone system: 4 heavy metals, 5 phthalates, 3 organophosphate pesticides
and metabolites, 9 organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 2
other semivolatile or volatile organic compounds
[6] Stomach or intestines: 3 heavy metals, 3 phthalates, 2 organophosphate
pesticides and metabolites, 9 organochlorine pesticides, 8 furans, 7 dioxins, 48
PCBs and 4 other semivolatile or volatile organic compounds
[7] Kidney: 4 heavy metals, 5 phthalates, 3 organochlorine pesticides, 8 furans, 7
dioxins, 48 PCBs and 5 other semivolatile or volatile organic compounds
[8] Brain, nervous system: 4 heavy metals, 4 phthalates, 7 organophosphate
pesticides and metabolites, 9 organochlorine pesticides, 8 furans, 7 dioxins, 48
PCBs and 7 other semivolatile or volatile organic compounds
[9] Reproductive system: 4 heavy metals, 2 phthalates, 8 organochlorine
pesticides, 8 furans, 7 dioxins and 48 PCBs
[10] Lungs/breathing: 4 heavy metals, 3 phthalates, 2 organophosphate pesticides
and metabolites, 5 organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 5
other semivolatile or volatile organic compounds
[11] Skin: 3 heavy metals, 5 phthalates, 2 organophosphate pesticides and
metabolites, 4 organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 7 other
semivolatile or volatile organic compounds
[12] Liver: 4 heavy metals, 6 phthalates, 3 organochlorine pesticides, 48 PCBs and
8 other semivolatile or volatile organic compounds
[13] Cardiovascular system or blood: 4 heavy metals, 2 phthalates, 2
organophosphate pesticides and metabolites, 7 organochlorine pesticides, 8
furans, 7 dioxins, 48 PCBs and 4 other semivolatile or volatile organic compounds
[14] Hearing: 1 heavy metal, 48 PCBs and 1 other semivolatile or volatile organic
compound
[15] Immune system: 4 heavy metals, 1 phthalate, 6 organochlorine pesticides, 8
furans, 7 dioxins, 48 PCBs and 3 other semivolatile or volatile organic compounds
[16] Male reproductive system: 4 heavy metals, 5 phthalates, 2 organochlorine
pesticides, 7 dioxins, 48 PCBs and 4 other semivolatile or volatile organic
compounds
[17] Female reproductive system: 2 heavy metals, 2 phthalates, 1 organochlorine
pesticide, 7 dioxins, 48 PCBs and 1 other semivolatile or volatile organic compound
Table 1: The chemicals we found are linked to serious health problems
* Some chemicals are associated with multiple health impacts, and appear in multiple categories in this table.
Source: Environmental Working Group compilation.
Average
number found
in 9 people
Health Effect or Body System Affected
Total found in
all 9 people
Range
(lowest and highest
number found in all 9
people)
cancer [1] 76 [2]
36 to 65
birth defects / developmental delays 79 [3]
37 to 68
vision 11 [4]
4 to 7
hormone system 86 [5]
40 to 71
stomach or intestines 84 [6]
41 to 72
kidney 80 [7]
37 to 67
brain, nervous system 94 [8]
46 to 73
reproductive system 77 [9]
37 to 68
lungs/breathing 82 [10]
38 to 67
skin 84 [11]
37 to 70
liver 69 [12]
26 to 54
cardiovascular system or blood 82 [13]
37 to 68
hearing 50 [14]
16 to 47
immune system 77 [15]
35 to 65
male reproductive system 70 [16]
28 to 60
female reproductive system 61 [17]
24 to 56
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PCBs in the nine people tested. PCBs were banned in the United
States in 1976 but are used in other countries and persist in the
environment for decades. Their most common use was as an
insulating uid in electrical capacitors and transformers, vacuum
pumps, and gas-transmission turbines. Lead was found in all 9
participants, and methylmercury was found in 8.
Health professionals are not trained to link health problems to an
individual’s chemical exposure, but it is increasingly evident that
background exposures to industrial chemicals and pesticides are
contributing to a portion of the steady increase in some health
problems in the population. A number of signicant health
effects potentially linked to chemical exposures are increasingly
prevalent:
Cancer. Between 1992 and 1999, cancer incidence increased for
many forms of the disease, including breast, thyroid, kidney,
liver, skin and some forms of leukemia. The incidence of
childhood cancer increased by 26 percent between 1975 and
1999, with the sharpest rise estimated for brain and other
nervous system cancers (50 percent increase) and acute
lymphocytic leukemia (62 percent increase). The incidence
of testicular cancer also rose between 1973 and 1999 (NCI
2002). The probability that a US resident will develop cancer
at some point in his or her lifetime is 1 in 2 for men and 1 in
3 for women (ACS 2001). Just 5 to 10 percent of all cancers
are linked to inherited, genetic factors (ACS 2001). For the
remainder, a broad array of environmental factors plays a
pivotal role.
We found 76 carcinogens in nine people. On average, each
study participant contained 53 chemical carcinogens.
Major nervous system disorders. Several recent studies have
determined that the reported incidence of autism may
be increasing, and is now almost 10 times higher than in
the mid-1980’s (Byrd 2002, Chakrabarti and Fombonne
2001, CDC 2000, Yeargin-Allsopp et al. 2003, Bertrand et
a. 2001). The number of children being diagnosed and
treated for attention decit disorder (ADD) and attention
decit hyperactivity disorder (ADHD) has also increased
dramatically in the past decade (Robison, et al. 1999,
Robison, et al. 2002, Zito, et al. 2000). The causes are
largely unexplained, but environmental factors, including
chemical exposures, are considered a potential cause
or contributor. Environmental factors have also been
It is increasingly evident that
background exposures to industrial
chemicals and pesticides are
contributing to a portion of the
steady increase in some health
problems in the population.
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increasingly linked with Parkinson’s disease (Checkoway
and Nelson 1999, Engel, et al. 2001).
We found 94 chemicals toxic to the nervous system in nine
people. On average, each study participant contained 62
nervous system toxicants.
Defects of the reproductive system. Studies show that
sperm counts in certain parts of the world are decreasing
(Swan, et al. 2000, Toppari, et al. 1996). Scientists have
measured signicant regional differences in sperm count
that cannot be explained by differences in genetic factors
(Swan, et al. in press). Girls may be reaching puberty
earlier, based on comparing current appearance of breast
development and pubic hair growth with historical data
(Herman-Giddens, et al. 1997). Incidence of hypospadias,
a birth defect of the penis, doubled in the United States
between 1970 and 1993, and is estimated to affect one
of every 125 male babies born (Paulozzi, et al. 1997).
The incidence of undescended testicles (cryptorchidism)
and testicular cancer also appear to be rising in certain
parts of the world (Bergstrom, et al. 1996, McKiernan,
et al. 1999, Toppari, et al. 1996). Testicular cancer is
now the most common cancer in men age 15 to 35 (NCI,
2000). Several studies have suggested links between
developmental exposure to environmental contaminants
and cryptorchidism or testicular cancer (Hardell, et al. in
press, Hosie, et al. 2000, Toppari, et al. 1996, Weidner,
et al. 1998).
We found 77 chemicals linked to reproductive damage in
nine people. On average the nine subjects contained 55
reproductive toxicants.
Toxic effects do not require high doses
Hundreds of studies in the peer-reviewed literature show that
adverse health effects from low dose exposures are occurring
in the population, caused by unavoidable contamination with
PCBs, DDT, dioxin, mercury, lead, toxic air pollutants, and other
chemicals. The health effects scientists have linked to chemical
exposures in the general population include premature death,
asthma, cancer, chronic bronchitis, permanent decrements in
IQ and declines in other measures of brain function, premature
birth, respiratory tract infection, heart disease, and permanent
decrements in lung capacity (EPA 1996, EPA 2000, Gauderman,
et al. 2002, Jacobson and Jacobson 2002, Jacobson, et al.
Hundreds of studies in the peer-
reviewed literature show that
adverse health effects from low
dose exposures are occurring in
the population.
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2002, Kopp, et al. 2000, Longnecker, et al. 2001, NAS 2000,
NTP 2002, Pope, et al. 2002, Salonen, et al. 1995, Sydbom, et
al. 2001).
A growing body of literature links low dose chemical exposures
in animal studies to a broad range of health effects previously
unexplored in high dose studies. In low dose testing, scientists
are using sophisticated techniques to measure subtle but
important changes in the functioning of apparently undamaged
organ systems, including alterations in immune function (such
as antibody response), enzyme activity, hormone levels, cellular
changes in tissues, neurobehavioral parameters, organ growth,
and hormone and neurotransmitter receptor levels. Importantly,
many low dose effects are detected following developmental
exposure. These tests focus on the effects of chemical exposures
comparable to those that occur in the general population, and
far below the levels that have traditionally been considered safe
based on the results of studies that feed lab animals high doses
Table 2: 167 compounds from seven chemical groups were
found in the nine people tested
Source: EWG compilation of blood and urine analysis from two major national laboratories
Number of
chemicals
tested for in
all 9 people
Total
number of
chemicals
found in
people
tested
Average
number of
chemicals
found in
people
tested
Range of chemical concentrations found
in people tested
PCBs 73
48 33 57,290 to 455,790 pg/g in blood lipid
Dioxins and furans 17
15 14 15.7 to 36.6 pg/g TEQ in blood lipid
Organophosphate
pesticide metabolites
9
7 3
Organochlorine
pesticides and
metabolites
23
10 4 615 to 3084 ug/L in urine
Phthalates 6
6 4 97.2 to 904.8* ug/g in blood lipid
Other semivolatile and
volatile chemicals (24
classes)
77
77 31 not quantified
Metals 5
4 2 varies by metal
Total 210 167 91
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of a given compound. Using these protocols, scientists are
nding that low doses of chemicals can be far more harmful than
previously believed (Figure 1).
Low dose studies often identify toxic effects at levels far below
those identied as the “no effect” level in high dose studies.
For instance, through low dose studies of bisphenol A (BPA), a
plasticizer chemical commonly used in dental sealants and plastic
water bottles, scientists have revealed health effects at levels
2,500 times lower than EPA’s “lowest observed effect” dose, with
adverse outcomes ranging from altered male reproductive organs
and aggressive behavior, to abnormal mammary gland growth,
early puberty, and reduced breast feeding (Figure 2).
In the face of a powerful and growing body of literature linking
low dose chemical exposures and health harms in the general
population, the chemical industry continues to claim that low
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Source: EWG compilation; footnotes at the end of the chapter.
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dose exposures to hundreds of chemicals simultaneously are
safe. These claims, however, are nearly always based on a lack of
scientic information on the toxicity of dose exposures, not on a
denitive, scientic proof of safety.
High dose animal studies provide the foundation for federal
exposure limits for contaminants in consumer products, drinking
water, food, and air. Indeed, the nation’s regulatory system for
chemical exposures is dependent on the notion that high dose
studies reveal all the toxic properties of a chemical being tested.
We now know that this is not true. A number of factors, each
of which can be as important as the exposure dose, determine a
compound’s toxicity:
Timing. The timing of a dose can often determine the
toxicity of the chemical. Low dose chemical exposures during
fetal development or infancy are known to produce more serious
toxic effects than similar exposures during adulthood for many
chemicals. Lead and mercury are the classic examples, where low
dose exposures in utero and during infancy cause permanent brain
and nerve damage, while the same doses cause no observable
effects in adults. Few high dose studies, with the exception
of those required for food use pesticides, target vulnerable
periods of development. Most high dose studies include only
adult animals. Low dose studies almost always involve in utero
exposures.
Genetic vulnerability. Some people are more susceptible to
environmental contaminants because of genetic factors. For
example, EPA-funded research has documented a 10,000-fold
variability in human respiratory response to airborne particles
(including allergens and pharmaceuticals) (Hattis, et al. 2001).
This variability explains, in part, why we all breathe the same air,
but not all of us have asthma attacks. Laboratory animal studies,
often conducted with genetically-uniform animals, cannot reveal
genetically-induced adverse effects that may occur in a small but
signicant percentage of a highly diverse human population.
Mechanisms. Chemicals produce a spectrum of health effects
that can both vary with dose, and affect the target organ in
different ways depending on dose. For instance, some chemicals
produce opposite effects at high and low doses – a phenomenon
call biphasic dose response. Some produce different effects at
high and low doses. Some produce adverse effects at low doses,
but not at higher doses. DES, a potent synthetic estrogen, has
been shown to stimulate prostate growth at 0.02, 0.2, and 2
μg/kg-day, but inhibit prostate growth at doses of 100 and 200
μg/kg-day (vom Saal, et al. 1997). Perchlorate, a component of
The nation’s regulatory system for
chemical exposures is dependent
on the notion that high dose
studies reveal all the toxic
properties of a chemical being
tested. We now know that this is
not true.
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rocket fuel that contaminates drinking water, causes changes
in the size of certain parts of the brain at 0.01 – 1 mg/kg-day,
but not at 30 mg/kg-day (Argus 1998). Current government
testing regimes do not require tests to dene different effects of
chemicals across a wide range of doses.
Another problem with the assertion that low dose exposures are
safe, or trivial, simply because they are small, is that the toxicity
of mixtures is almost never studied. Current high dose studies,
like those required for pesticides used on food, are conducted
with puried single chemicals. In the real world, people are
exposed to low dose mixtures of several hundred chemicals.
Scientists do not understand the toxicity of these mixtures, and
with few exceptions are not investigating them.
In the rare cases in which scientists have studied the effects of
mixtures, they have found adverse health effects. In two recent
studies scientists dosed laboratory animals with a mixture of 16
organochlorine chemicals, lead, and cadmium, each applied at
its individual regulatory “safe” dose, and found that the animals
developed impaired immune response and altered function of the
thyroid, a gland that is critical for brain development (Wade, et
al. 2002a, Wade, et al. 2002b).
Our body burden
Scientists refer to the chemical exposure documented here as an
individuals’ “body burden” – the consequence of lifelong exposure
to industrial chemicals that are used in thousands of consumer
products and linger as contaminants in air, water, food, and soil.
There are hundreds of chemicals in drinking water, household
air, dust, treated tap water and food. They come from household
products like detergent, insulation, fabric treatments, cosmetics,
paints, upholstery, computers and TVs, and they accumulate in
fat, blood and organs, or are passed through the body in breast
milk, urine, feces, sweat, semen, hair and nails. (Easton, et al.
2002, EPA 2002d, OECD 2002, Rudel, et al. 2001, Thornton, et al.
2002, USGS 2002).
We know that:
ü U.S. chemical companies hold licenses to make
75,000 chemicals for commercial use. The federal
government registers an average of 2,000 newly
synthesized chemicals each year.
ü The government has tallied 5,000 chemical
ingredients in cosmetics; more than 3,200
Scientists refer to the chemical
exposure documented here as
an individuals’ “body burden”
– the consequence of lifelong
exposure to industrial chemicals
that are used in thousands of
consumer products and linger as
contaminants in air, water, food,
and soil.
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chemicals added to food; 1,010 chemicals used in
11,700 consumer products; and 500 chemicals used
as active ingredients in pesticides (EPA 1997b,
EPA 2002b, EPA 2002c, FDA 2002a, FDA 2002b,
FDA 2002c).
ü In 1998 U.S. industries reported manufacturing 6.5
trillion pounds of 9,000 different chemicals (EPA
2001), and in 2000 major U.S. industries reported
dumping 7.1 billion pounds of 650 industrial
chemicals into our air and water (EPA 2002a).
At least 20 major peer-reviewed scientic journals are devoted
almost entirely to studies of health effects from chemical
exposures. But despite the ever-growing volume of data on the
nature and consequences of exposure to industrial chemicals,
scientists and doctors cannot answer the most basic questions:
0.001
0.01
0.1
1
10
100
0.02 mg/kg - early puberty in females (10)
and reduced sperm production (
8, 9)
0.05 mg/kg - safe dose for humans according
to US EPA (1)
50 mg/kg - testicular tumors and decreased body weight (1)
1.5 mg/kg - altered brain structure (4)
0.05 mg/kg - increased prostate size (5)
0.025 mg/kg - abnormal mammary gland
growth and prostate development (
6, 7)
0.01 mg/kg - altered maternal care (reduced
breast feeding and time spent with pups) (11
)
0.0024 mg/kg - early puberty in females (12)
0.002 mg/kg - altered male reproduction
organs (13
, 14) and aggressive behavior (14)
5 mg/kg - no effects in lab animals according
to a European government panel (2,3)
50 mg/kg - lowest dose that harms animals
according to US EPA (1)
Daily dose (milligrams of bisphenol A per kilogram of body weight)
Some effects observed in laboratory animals
Regulatory benchmarks
Figure 2: Many studies show harmful effects far below doses that regulators consider “safe”
Source: EWG compilation; footnotes at the end of the chapter.
12
13
What health effects can be linked to the mixtures of
industrial chemicals found in the human body?
Beyond a handful of chemicals, the answer is not known. The
reason: there is no legal requirement to test most chemicals for
health effects at any stage of production, marketing, and use.
Under the Toxic Substances Control Act (TSCA), chemical
companies can continue making chemicals and putting new
compounds on the market without conducting studies of their
effects on people or the environment. Some companies conduct
rudimentary screening studies prior to production, but fewer than
half of all applications to the EPA for new chemical production
include any toxicity data at all. The government approves 80
percent of these applications with no restrictions, usually in less
than three weeks. When data are provided, they are typically
cursory in nature, because the government lacks the authority to
request anything more than that. Eight of 10 new chemicals win
approval in less than three weeks, at an average rate of seven a
day. If there are no data, the government justies approval with
results of computer models that estimate if a chemical will harm
human health or the environment (EPA 1997a, GAO 1994).
For chemicals that are already on the market, the EPA can request
data only when it can substantiate that the chemical is causing
harm, which it generally cannot do without the toxicity data it
is seeking to request. In practice, this means that studies are
required only after independent scientists have accumulated a
body of evidence demonstrating potential harm, a process that
typically takes decades.
What mixtures of industrial chemicals are found in the bodies
of the general population in the U.S.?
Not known (even this study denes only a fraction of the
chemicals in the nine people tested). The reason: beyond
chemicals that are added to food or used as drugs, there is
no requirement for chemical manufacturers to: disclose how
their chemicals are used or the routes through which people
are exposed; understand the fate of their chemicals in the
environment; measure concentrations of their products in the
environment or in people; or develop and make public analytical
methods that would allow other scientists to gather information.
Companies sometimes develop methods to test for chemicals in
the blood or urine of their workers, but they do not routinely
disclose the methods or results to the government or the public.
There is no legal requirement to
test most chemicals for health
effects at any stage of production,
marketing, and use... In practice,
this means that studies are
required only after independent
scientists have accumulated a
body of evidence demonstrating
potential harm, a process that
typically takes decades.
12
13
The government has spearheaded most of the limited testing that
has been performed for the general population in studies funded
by taxpayers. The government’s studies have not kept pace with
the ever-expanding array of new toxic chemicals. The country’s
most comprehensive program for detecting industrial chemicals in
the human body is run by a government program that reported on
27 chemicals in 2001 (CDC 2001). The chemical industry provided
direct funding for none of this multi-million dollar effort, but
instead paid their trade association’s press ofce to educate the
national media on the safety of industrial chemicals in the days
following the government’s report release. In their upcoming
report on chemical exposures, CDC is expected to release
information on 116 chemicals, or about 70 percent of the number
identied in this study.
A few types of consumer products, such as cosmetics and home
pesticides, must carry partial ingredient labels so consumers can
make informed choices. Federal law, however, does not require
the chemical industry to disclose ingredients in most household
consumer products, including cleaners, paints and varnishes,
and chemical coatings on clothing and furniture, or the so-called
“inert” ingredients in pesticides, which are typically more than 95
percent of the retail product. The EPA has compiled a database
of more than 1,000 chemicals they believe might be present
in 11,700 consumer products, using data the Agency gathered
from chemical encyclopedias, air sampling studies in the open
scientic literature, and manufacturers. But the companies have
classied the chemical recipes for 9,300 of these products as
“condential business information.”
The EPA attempts to track local exposures to chemical pollutants
through two testing programs, one for tap water and another
for ambient air. But testing captures only a small fraction of the
chemicals a person is exposed to over the course of a day. By
contrast, some local and state air monitoring programs track only
ve chemical contaminants, most of them linked to automobile
exhaust. Water suppliers test tap water for 70 contaminants, but
the list excludes hundreds of chemicals known to contaminate
public water supplies [e.g., (USGS 2002)].
Can an individual participate in a testing program to learn
what industrial chemicals are in his or her body?
Not easily. In this study the laboratory costs alone were $4,900
per person. Scientists spent two years designing the study,
gaining approval of the study plan from Mount Sinai School of
Medicine’s Institutional Review Board, and recruiting subjects.
People can request body burden tests through their personal
In their upcoming report on
chemical exposures, CDC is
expected to release information on
116 chemicals, or about 70 percent
of the number identied in this
study.
14
15
physicians, but in general the methods used by available
commercial labs are not sensitive, the available tests are limited,
or both. The CDC lists “availability of analytical methods” as one
of two major constraining factors in its national biomonitoring
program (CDC 2002).
Conclusions and Recommendations
This study, combined with work from the Centers for Disease
Control and Prevention, and a thorough review of the scientic
literature reveals ubiquitous and insidious pollution of the
human population with hundreds of chemicals, pollutants, and
pesticides. In large measure this is the result of a regulatory
system that leaves the EPA with few tools to study the health
effects or the extent of human exposure to the thousands of
chemicals found in consumer products. The widespread use
of poorly studied chemicals in the absence of any meaningful
regulatory structure to control them has led to:
Pervasive contamination of the human population with
hundreds of chemicals at low dose mixtures that have not
been examined for potential health effects.
An industry that has no legal obligation to conduct safety
tests or monitor for the presence of its chemicals in the
environment or the human population – and a nancial
incentive not to do so.
A federal research establishment that is unequipped,
both technically and nancially, to monitor the human
population for commercial chemicals or to study their
health effects.
An ever-increasing load of chemical contamination in
the human population and global environment that is
comprised of poorly studied chemicals, nearly all of which
have never before been encountered in all of evolutionary
history.
The chemical industry tightly controls the testing and the
information ow on any issue related to their products. In
general, the more recently a chemical has been introduced into
commerce, the less scientists understand its toxicity, and the less
likely it is that scientists will know how to test for it in people
and the environment. The few chemicals or chemical families that
have been well-studied are those for which scientists uncovered,
often accidentally, environmental catastrophes that can include
The chemical industry tightly
controls the testing and the
information ow on any issue
related to their products.
14
15
widespread pollution of the environment or human population
(Figure 3).
Chemical companies are not required to disclose methods that
could be used to test for their chemicals in the environment
or the human body. Typically only after a compound has been
on the market for decades, and has contaminated a signicant
portion of the environment, do independent scientists learn how
to detect and quantify it. At that point, CDC may choose to
include the chemical in its national biomonitoring program. Even
then there is no guarantee that the manufacturer will provide CDC
with the methodology to detect it, or that the methods will be
reliable. For example, three years after 3M announced that it was
removing peruorinated chemicals in Scotchgard from the market,
chiey because 3M found that the human population is widely
contaminated with the chemicals, the CDC has yet to develop
69
178
2,419
5,328
5,791
5,794
7,062
7,422
11,134
0 2000 4000 6000 8000 10000 12000
Brominated Flame
Retardants (PBDEs)
Perfluorinated Chemicals
Bisphenol A
Dioxin
DDT
Ozone
PCBs
Triazine Herbicides
Benzene
1980s - contamination of drinking water supplies for millions of
people across the Midwest
1970s - global contamination, potent carcinogen (banned in 1976)
1980s - skyrocketing asthma rates and asthma-related deaths
among urban children
1970s - dramatic wildlife losses, iminent extinction of eagles and
other birds, global contamination (banned in 1976)
1970s - global contamination, one of the most potent carcinogens
ever known
1990s - major reproductive toxin (damages multiple organs) and
widespread human exposure from leaching plastics (bottles)
1999 - global contamination including the blood of all 699 US
children tested, low-dose deaths of newborn lab animals (3M 1999)
1999 - levels increasing exponentially in human breast milk
(Meironyte 1999), disruption of thyroid hormones (Zhou 2001) and
potential fetal brain damage
1960s - workers dying of leukemia, widespread use and exposure
among workers and the general population
Uncovered catastrophies that led (or may be leading) to
periods of intense scientific study
Number of studies in National Institutes of Health's
compr
ehensive medical and toxicological library (PubMed)
Figure 3: Chemicals are intensively studied only after they harm
human health or contaminate the biosphere
Source: EWG compilation
16
17
a method it considers reliable that would allow it to add the
chemicals to its national biomonitoring program.
This situation is unacceptable.
At a minimum, people have a right to know what chemicals are
in their bodies and what harm they might cause. The sole source
of this information is the chemical manufacturers themselves,
who historically have resisted all efforts to make basic health
information on their products available to the public, regulators
and independent scientists.
Without disclosure of information on the environmental fate,
human contamination, and health effects of these chemicals,
regulators cannot effectively prioritize efforts to reduce the
health risks from the current contaminant load in the human
population.
Regardless of whether or not Congress revises the nation’s laws or
policies:
The chemical industry must submit to EPA and make public
on individual company web sites, all internal studies on the
properties, environmental fate, potential human exposure
pathways and exposure levels, concentrations in workers and
the general population, levels in the environment, worker
and community health, measured effects in wildlife, toxicity,
mechanisms of action and any other information relevant to
human exposures and potential health effects for all chemicals
reasonably likely to be found in people, drinking water, or indoor
air.
Revisions to the nation’s laws and policies governing chemical
manufacture and use include the following provisions:
Industry must be required to prove the safety of a new
chemical before it is put on the market.
The EPA must have the unencumbered authority to request
any and all new data on a chemical that is already on the
market.
The EPA must have the clear authority to suspend a
chemical’s production and sale if the data requested are
not generated, or if they show that the chemical, as used,
is not safe for the most sensitive portion of the exposed
population.
At a minimum, people have a right
to know what chemicals are in
their bodies and what harm they
might cause.
16
17
Chemicals that persist in the environment or
bioaccumulate in the food chain must be banned.
Chemicals found in humans, in products to which children
might be exposed, in drinking water, food, or indoor air,
must be thoroughly tested for their health effects in low
dose, womb-to-tomb, multi-generational studies focused
on known target organs, that include sensitive endpoints
like organ function and cognitive development. Studies
to dene mechanisms of action (how a chemical harms
the body) must be conducted.
The chemical industry must develop and make public
analytical methods to detect their chemicals in the
human body, and conduct biomonitoring studies
to nd the levels of their chemicals in the general
population.
Chemical manufacturers must fully disclose the
ingredients of their products to the public.
* * *
FIGURE 1 REFERENCES:
1. IRIS (Integrated Risk Information System). 2003b. Bisphenol A (CASRN 80-
05-7): Reference dose for chronic oral exposure (RfD) - last revised in 1993.
Available online at http://www.epa.gov/iris/subst/0356.htm
2. EPA (Environmental Protection Agency). 2002. Atrazine revised risk
assessment. Available online athttp://www.epa.gov/oppsrrd1/reregistration/
atrazine/
3. Hayes TB, Collins A, Lee M, Mendoza M, Noriega N, Stuart AA, Vonk A. 2002.
Hermaphroditic, demasculinized frogs after exposure to the herbicide atrazine
at low ecologically relevant doses. Proc Natl Acad Sci U S A 99:5476-80.
4. IRIS (Integrated Risk Information System). 2003a. Methoxychlor: CASRN:
72-43-5. Available online at http://toxnet.nlm.nih.gov/
5. Welshons WV, Nagel SC, Thayer KA, Judy BM, Vom Saal FS. 1999. Low-dose
bioactivity of xenoestrogens in animals: fetal exposure to low doses of
methoxychlor and other xenoestrogens increases adult prostate size in mice.
Toxicol Ind Health 15:12-25.
6. Schonfelder G, Flick B, Mayr E, Talsness C, Paul M, Chahoud I. 2002. In utero
exposure to low doses of bisphenol A lead to long-term deleterious effects in
the vagina. Neoplasia 4:98-102.
7. Sakaue M, Ohsako S, Ishimura R, Kurosawa S, Kurohmaru M, Hayashi Y, Aoki
Y, Yonemoto J, Tohyama C. 2001. Bisphenol-A affects spermatogenesis in the
adult rat even at a low dose. J Occup Health 43:185-190
8. Ramos JG, Varayoud J, Sonnenschein C, Soto AM, Mu–oz de Toro M, Luque
EH. 2001. Prenatal exposure to low doses of bisphenol A alters the periductal
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19
stroma and glandular cell function in the rat ventral prostate. Biology of
Reproduction 65:1271-1277.
9. vom Saal FS, Cooke PS, Buchanan DL, Palanza P, Thayer KA, Nagel SC,
Parmigiani S, Welshons WV. 1998. A physiologically based approach to
the study of bisphenol A and other estrogenic chemicals on the size of
reproductive organs, daily sperm production, and behavior. Toxicology &
Industrial Health 14:239-60.
10. Nagel SC, vom Saal FS, Thayer KA, Dhar MG, Boechler M, Welshons WV. 1997.
Relative binding afnity-serum modied access (RBA-SMA) assay predicts the
relative in vivo bioactivity of the xenoestrogens bisphenol A and octylphenol.
Environmental Health Perspectives 105:70-76.
11. Howdeshell KL, Hotchkiss AK, Thayer KA, Vandenbergh JG, vom Saal FS. 1999.
Exposure to bisphenol A advances puberty. Nature 401:763-4.
FIGURE 2 REFERENCES
1 IRIS (Integrated Risk Information System). 2003. Bisphenol A (CASRN 80-
05-7): Reference dose for chronic oral exposure (RfD) - last revised in 1993.
Available online at http://www.epa.gov/iris/subst/0356.htm.
2 Tyl, RW, CB Myers, MC Marr, BF Thomas, AR Keimowitz, DR Brine, MM Veselica,
PA Fail, TY Chang, JC Seely, RL Joiner, JH Butala, SS Dimond, SZ Cagen, RN
Shiotsuka, GD Stropp and JM Waechter. 2002. Three-generation reproductive
toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. Toxicol Sci
68(1): 121-46.
3 SCF (Scientic Committee on Food). 2002. Opinion of the Scienc Committee
on Food on Bisphenol A. European Commission Health & Consumer Protection
Directorate – Scientic Committee on Food. May 3, 2002.
4 Kubo, K, O Arai, R Ogata, M Omura, T Hori and S Aou. 2001. Exposure
to bisphenol A during the fetal and suckling periods disrupts sexual
differentiation of the locus coeruleus and of behavior in the rat. Neurosci Lett
304(1-2): 73-6.
5 Gupta, C. 2000. Reproductive malformation of the male offspring following
maternal exposure to estrogenic chemicals. Proceedings of the Society of
Experimental Biology & Medicine 224(2): 61-68.
6 Ramos, JG, J Varayoud, C Sonnenschein, AM Soto, M Muñoz de Toro and
EH Luque. 2001. Prenatal exposure to low doses of bisphenol A alters the
periductal stroma and glandular cell function in the rat ventral prostate.
Biology of Reproduction 65: 1271-1277.
7 Markey, CM, EH Luque, M Munoz de Toro, C Sonnenschein and AM Soto.
2001. In utero exposure to bisphenol A alters the development and tissue
organization of the mouse mammary gland. Biology of Reproduction 65:
1215-1223.
8 Sakaue, M, S Ohsako, R Ishimura, S Kurosawa, M Kurohmaru, Y Hayashi, Y
Aoki, J Yonemoto and C Tohyama. 2001. Bisphenol-A affects spermatogenesis
in the adult rat even at a low dose. J Occup Health 43: 185-190.
9 vom Saal, FS, PS Cooke, DL Buchanan, P Palanza, KA Thayer, SC Nagel, S
Parmigiani and WV Welshons. 1998. A physiologically based approach to
the study of bisphenol A and other estrogenic chemicals on the size of
reproductive organs, daily sperm production, and behavior. Toxicology &
Industrial Health 14(1-2): 239-60.
10 Honma, S, A Suzuki, DL Buchanan, Y Katsu, H Watanabe and T Iguchi. 2002.
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19
Low dose effect of in utero exposure to bisphenol A and diethylstilbestrol on
female mouse reproduction. Reprod Toxicol 16(2): 117-22.
11 Palanza, PL, KL Howdeshell, S Parmigiani and FS vom Saal. 2002. Exposure
to a low dose of bisphenol A during fetal life or in adulthood alters maternal
behavior in mice. Environ Health Perspect 110 Suppl 3: 415-22.
12 Howdeshell, KL, AK Hotchkiss, KA Thayer, JG Vandenbergh and FS vom Saal.
1999. Exposure to bisphenol A advances puberty. Nature 401(6755): 763-4.
13 Nagel, SC, FS vom Saal, KA Thayer, MG Dhar, M Boechler and WV Welshons.
1997. Relative binding afnity-serum modied access (RBA-SMA) assay
predicts the relative in vivo bioactivity of the xenoestrogens bisphenol A and
octylphenol. Environmental Health Perspectives 105(1): 70-76.
14 Kawai, K, T Nozaki, H Nishikata, S Aou, M Takii and C Kubo. in press 2003.
Aggressive behavior and serum testosterone concentration during the
maturation process of male mice: the effects of fetal exposure to bisphenol A.
Environ Health Perspect.
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21
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21
CHAPTER 1: The Study and Methodology
In this study, led by scientists at Mount Sinai School of Medicine
in New York City, nine adults from six states volunteered to
submit blood and urine samples for a broad suite of chemical
analyses. The tests targeted 210 industrial chemicals, including
7 dioxins, 10 furans, 73 PCBs, 5 heavy metals, 9 organophosphate
pesticide metabolites, 23 organochlorine pesticides and
metabolites, 6 phthalates, and 77 other semivolatile and volatile
organic compounds from 24 chemical classes.
A total of 167 industrial chemicals, pollutants and pesticides
were found in the blood and urine of nine individuals. On
average, analysts found 91 chemicals per person, with a range of
from 77 to 106 pollutants and pesticides in the nine individuals
studied.
The investigation was a pilot study for a larger, planned
investigation of attitudinal responses to provide information
about one’s personal body burden inventory. The study design
was approved by Mount Sinai’s Institutional Review Board (Baltz
et al. 2000). Study results appear in a recently-published edition
of the journal Public Health Reports (Thornton et al. 2002).
Blood and urine samples were collected in Summer 2000. Five
questionnaires were administered to subjects immediately
following blood sample collection focusing on patient
demographics and exposure history, knowledge of body burden
issues, typical personal choices on environmentally-relevant
consumer decisions, awareness of prominent environmental
issues, and attitudes about environmental policies. These
questionnaires were developed by Mount Sinai for use in
future assessments of the relationship between an individual’s
knowledge of their personal body burden and their willingness to
act on issues of toxic pollution.
Scientists spent two years designing the study, gaining approval
of the study plan from Mount Sinai School of Medicine’s
Institutional Review Board, and recruiting subjects. The goal of
the study was to test a small group of people for a broad range
of industrial contaminants. Ideally, researchers would have liked
to identify all chemical contaminants in the blood and urine of
the participants. Reaching this goal was not possible for three
reasons. First, no one knows exactly what compounds to look
for in people among the thousands of chemicals in commerce
today. Second, methods are not publicly available to nd all the
22
23
chemicals that are believed to contaminate people. Third, the
cost of testing for the chemicals known to contaminate people
is prohibitive, well beyond the $4,900 per person costs of this
limited study.
Limitations of the study
Extent of contamination not known
The suite of chemicals to which a person is exposed over the
course of a day or a year is not measured or dened by any
scientic testing program. The federal government attempts to
track local exposures to chemical pollutants through two basic
testing programs, one for tap water and another for ambient air.
The government also requires a few types of consumer products
- cosmetics and home pesticides, for instance - to carry partial
ingredient labels so consumers can make more informed choices
at the store. The State of California requires companies to post
a warning on the label if a product contains a chemical linked
to cancer or birth defects. But testing, monitoring and labeling
requirements capture only a small fraction of the chemicals a
person is exposed to over the course of a day. Even if Mount
Sinai investigators had records on each subject’s use of consumer
products, and results from their public tap water testing and local
air pollution monitoring, the investigators would have few clues
to the specics of the suite of industrial chemicals present in
that person’s body.
Water suppliers test tap water for 70 contaminants, typically
every year or every few years. The list of 70 is largely not
coincident with the hundreds of chemicals now known to
contaminate public water supplies. And even for these 70
chemicals, the mandated test methods are often outdated and
insensitive. CDC’s methods for nding chlorinated volatile organic
chemicals in human blood – some of them common tap water
contaminants linked to cancer and birth defects - are about 1000
times more sensitive than the standard methods used by water
suppliers to nd the same chemicals in tap water.
Available air testing is even less complete. Some state or local
governments test city air for ve chemical pollutants, most
of them linked to gasoline combustion. Although a series of
population-wide studies have linked these chemical pollutants
to premature death, asthma, chronic bronchitis, respiratory
tract infection, heart disease and permanent decrements in lung
capacity (Gauderman, et al. 2002, Kagawa 2002, Kopp, et al.
22
23
2000, Sakaue, et al. 2001), the CDC includes only one of the ve
in its blood and urine testing program.
Federal law does not require the chemical industry to disclose
ingredients in most household consumer products, including
cleaners, paints and varnishes, and chemical coatings on
clothing and furniture. The EPA has compiled a database of 1,000
chemicals they believe might be present in 11,700 consumer
products, using data the Agency gathered in large part from air
sampling studies and product formulation information in the
open scientic literature (EPA 1997b). Any of these chemicals,
and countless combinations, could be present in the human body.
Methods for detection not available or too expensive
Testing for chemicals has more to do with available methods,
technologies, and cost than it does with foreknowledge of
chemicals that are known or expected to occur in a particular
person’s body.
For the vast majority of industrial chemicals in the human body,
scientists have yet to develop a test method for body uids or
tissues. Only three years ago Dr. John Brock of the Centers for
Disease Control and Prevention reported that he had developed
a method to detect chemical plasticizers called phthalates in the
human body (Blount, et al. 2000). Although manufacturers of
cosmetics and plastics have used phthalates widely for at least
fty years, the analysis of these chemicals in human uids had
eluded scientists until Brock’s innovation.
Because of their prevalence in consumer products, phthalates
are ubiquitous contaminants in the air and dust of cars, homes,
ofces, and even analytical laboratories testing samples of
human uids and tissues. Scientists struggle to distinguish
the difference between “background” contamination and the
phthalates present in human samples. Brock’s test instead
targets one of the body’s breakdown products of phthalate
chemicals, and ignores the background contaminants. The CDC
can now reliably test for phthalates in human urine.
Most commercial laboratories, however, do not offer tests for
phthalate breakdown products in human urine, presumably
because the demand is low. A person could contract with a
laboratory to analyze a urine sample, but would likely be faced
with method start-up costs that could run in the thousands of
dollars.
24
25
The same is true for a chemical solvent called m-xylene that
scientists nd in human blood (Ashley, et al. 1994) and that
manufacturers use in vinyl ooring and varnish removers. The
chemical is affordable - a liter bottle of m-xylene runs about $20
from chemical supply companies, and a quart of varnish remover
in the hardware store costs about half that. But consumers would
face a $1000 charge for chemical analysis to quantify levels of m-
xylene in their blood, assuming they manage to locate one of the
handful of laboratories in the country with the necessary testing
equipment willing to take on a project as small as a single blood
sample.
Scotchgard provides another example. Three years after 3M
withdrew its family of Scotchgard chemicals from the market
— following an accidental discovery that the chemicals have
contaminated the human population — the government still
has not developed a test method of sufcient reliability to
include the chemicals in its biomonitoring program. CDC names
the “availability of analytic methods to measure levels of the
chemical in people” as one of two major criteria used to select
chemicals for testing in their national biomonitoring program
(CDC 2002).
And even when methods are available, testing costs are high,
and well outside the reach of most individuals who might be
interested in knowing their own body burden. For instance,
the laboratory used by Mt. Sinai charged $1,250 for analysis
of 17 dioxins and furans in a single blood sample. Largely
because of budget constraints and limits in the availability of
test methods, Mount Sinai scientists chose not to test for major
classes of chemicals known to occur in humans, including the
tens or perhaps hundreds of chemicals found in carpet, clothing,
furniture, and food packaging from peruorinated chemical
families and the family of brominated ame retardants.
Study Participants
Andrea Martin, Sausalito, Calif.; Contaminants found: 95.
Andrea is a cancer survivor, and the founder and former
Executive Director of the Breast Cancer Fund in San Francisco.
Recognized as one of the nation’s leading advocates for cancer
survivors, Martin’s group pushes for a national action agenda
for environmental causes of breast cancer. Her ascent of Mount
Fuji two years ago with nearly 500 breast cancer survivors and
supporters epitomizes her group’s commitment to celebrate the
courage and faith of the 3 million women in the U.S. living with
24
25
this devastating disease. She has recently undergone surgery to
remove a brain tumor unrelated to breast cancer.
Bill Moyers, New Jersey; Contaminants found: 84. During
his 25 years in broadcasting, Bill Moyers has pursued a broad
spectrum of journalism. In presenting Moyers with one of his
two prestigious Gold Batons, the highest honor of the Alfred
I. DuPont Columbia University Awards, Columbia University
President Michael Sovern called Moyers “a unique voice, still
seeking new frontiers in television, daring to assume that viewing
audiences are willing to think and learn.” Moyers reported the
results of his body burden tests in his Emmy award-winning
expose of the chemical industry, “Trade Secrets: A Moyers
Reports,” which rst aired on PBS in March, 2001
Sharyle Patton, Bolinas, Calif.; Contaminants found: 105.
Sharyle Patton is co-director of the Collaborative on Health and
Environment, a group of individuals and organizations interested
in linkages between environment and health. She was previously
the northern co-chair of the International Persistent Organic
Pollutants (POPS) Elimination Network, a network of over 350
non-governmental organizations around the world which worked
successfully for the positive conclusion of the UN treaty on POPS,
signed in May 2001. She has been active in UN conferences on
women’s reproductive health and sexual rights issues.
Lucy R. Waletzky M.D., Pleasantville, NY; Contaminants found:
78. In addition to her work as a physician and practicing
psychiatrist, Dr. Waletzky is board member of the National
Audubon Society, and one of the group’s prominent experts on
the effects of pesticides and toxic chemicals on the environment.
She also serves on the Board of the Memorial Sloan Kettering
Cancer Society and is a member of the Westchester County Pest
Management Committee.
Davis Baltz, Berkeley, Calif.; Contaminants found: 106. Davis
moved to California with his family when he was four months
old, and grew up in Berkeley, California. His chemical body
burden is the product of his childhood and current exposures
in the U.S., as well as chemical exposures accumulated during
seven years of work and travel across Asia and Africa. Among
his diverse experiences, Davis has evaluated farmer training
26
27
programs to reduce pesticide use in Indonesia, supervised refugee
resettlement in Thailand’s refugee camps, observed elections
in Sri Lanka, edited news in Korea, and assisted community
organizing efforts with farmer groups in the Philippines. He
holds a Masters degree in International Community Economic
Development. He currently acts as a Senior Research Associate for
Commonweal in Bolinas, California, where he works to eliminate
the use of toxic chemicals in the healthcare industry.
Michael Lerner, Bolinas, Calif.; Contaminants found: 101.
Michael Lerner is president and founder of Commonweal, a health
and environmental research institute in Marin County, California.
He has worked for thirty years with at-risk children, people with
cancer, and environmental health initiatives. He is married to
Sharyle Patton, who was also a participant in the Body Burden
Study.
Lexi Rome, Mill Valley, Calif.; Contaminants found: 86. As
co-director of the Commonweal Sustainable Futures Project,
Rome led a collaborative learning program for leaders in the
environmental, philanthropic, and policy-making communities
in the San Francisco Bay Area, tackling such diverse problems
as population, consumption, and a sustainable future. Now
retired, she is pursuing volunteer opportunities, working on
local environmental issues, and developing sustainable, organic
ranching methods in Montana.
Monique Harden, New Orleans, La.; Contaminants found: 77.
Monique is an attorney who specializes in environmental justice
concerns in New Orleans, the city where she was raised. She
organizes communities who live on the fenceline with polluting
industries, using both litigation and advocacy to ght cases
driven by economic justice concerns. Among the victories she
can claim is a precedent-setting decision by the Environmental
Protection Agency to deny a Clean Air Act permit to a company
proposing a new facility in a neighborhood that was 80 percent
African American and already surrounded by 12 industrial
facilities responsible for 17 million pounds of air pollutants.
Charlotte Brody, Round Hill, Va.; Contaminants found: 85.
Charlotte Brody, RN, is a founder and an Executive Director of the
Health Care Without Harm Campaign — an international coalition
of 390 organizations in 44 countries working to make health care
more environmentally responsible and sustainable. A registered
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27
nurse and mother of two, Charlotte has served as the Organizing
Director for the Center for Health, Environment Justice in Falls
Church, Virginia, the Executive Director of a Planned Parenthood
afliate in North Carolina and the Coordinator of the Carolina
Brown Lung Association, an occupational safety and health
organization focused on cotton textile workers.
Sample collection
Blood sample collection. Qualied health care personnel drew 13
vials (Vacutainers™) of blood from each subject. Filled vials were
tted into custom foam containers, placed in prepared coolers
lled with ice packs, stored under refrigeration, and then shipped
overnight to Midwest Research Institute in Kansas City, Missouri.
Urine sample collection. Each participant collected a 24-hour
urine sample in a 3500 milliliter low density polyethylene urine
collection container manufactured by Hedwin. Container was
refrigerated or stored in a cooler between uses. Upon completing
the 24-hour collection cycle, including one rst morning void,
study participants thoroughly mixed the sample by shaking, then
poured the sample into four smaller plastic containers provided
by the laboratory. Containers were prewashed with acid as
necessary. Sample containers were shipped overnight to Pacic
Toxicology in Woodland Hills, California.
Analytic methods
Analysis of PCBs, dioxins, and furans. The technical approach
for analysis of blood samples for congener-specic PCBs,
polychlorinated dibenzodioxins (dioxins), and polychlorinated
dibenzofurans (furans) relies on techniques based on EPA
methods 1613 and 1668, rened by Midwest Research
Institute. Analysis was performed using high resolution gas
chromatography/high resolution mass spectrometry (HRGC/
HRMS).
13
C-labeled PCBs, dioxins and furans were added to each
sample for use as internal standards.
Extraction was accomplished using end-over-end tumbling with
a rugged rotary extractor. Extract was dried, concentrated,
and transferred to a pre-weighed 1 dram vial. The sample
lipid fraction was determined by a series of evaporation steps
conducted until successive measurements of sample weight
reached steady state.
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29
Samples were prepared for chromatography using a modied acid/
neutral silica gel chromatography solution, prepared according
to EPA Methods 1613 and SOP MRI 5201, Revision 2, with micro-
scale adaptation of the chromatography column. Sample extracts
were split into two samples of equal volume, one for PCB analysis,
one for dioxin and furan analysis. The dioxin and furan split was
processed through alumina and carbon column chromatography
cleanup procedures according to EPA Method 1613. The extract
was further concentrated.
The extract designated for dioxin and furan analysis was analyzed
according to a laboratory adaptation of EPA Methods 8290
and 1613 using an Autospec Ultima HRMS and an OpusQuan
Data system. The calibration range was extended by a factor
of 10 below the range specied in EPA methods. The extract
designated for PCB analysis was analyzed on a VG-70S HRMS and
an OpusQuan data system according to EPA Method 1668 with
modications to include calibration standards for each of the 75
target PCB congeners over the relevant concentration range.
Congener-specic PCBs were analyzed using a high resolution
mass spectrometer, operating at 10,000 mass resolving power
in the selected ion monitoring (SIM) mode, according to
EPA Method 1668 with target analyte list of 75 specic PCB
congeners.
Data reduction of PCBs, dioxins and furans was performed by
OpusQuan data systems to calculate the concentrations of analyte
responses against radiolabeled internal quantitation standards
and recovery standards.
Analysis of organochlorine pesticides, phthalates, and other VOCs
and SVOCs. The extraction method described for PCBs, dioxins,
and furans was also used for pesticides, phthalates, and SVOCs.
Co-extracted biological interferences were separated from the
pesticides and other VOCs and SVOCs using gel permeation
chromatography column cleanup according to EPA SW-846 Method
3640 followed by Florisil solid phase extraction (Method 3620).
Sample extracts were split into two samples of equal volume, one
for pesticide analysis, one for analysis of phthalates and other
VOCs and SVOCs.
Sample extracts for pesticides were analyzed by high-resolution
gas chromatography/electron capture detector (HRGC/ECD) based
on EPA Method 8081. A Hewlett-Packard 6890 HRGC/ECD system
was used for analysis and data were acquired and processed using
a Turbochrom data system.
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29
Sample extracts for phthalates and other VOCs and SVOCs
were analyzed by high-resolution gas chromatography/mass
spectrometry (HRGC/MS) based on EPA Method 8270C. A Fisons
MD-800 quadruple GC/MS system was used for analysis and
data were acquired and processed using LabBase data system.
Deuterated PAHs were used as internal standards.
The VOCs and SVOCs were tentatively identied based on a NIST
library search by the LabBase software. Spectral data of the
chromatographic peaks were matched to data in the NIST library
using a forward/reverse t. The mass spectra of the identied
compounds were manually veried against the identied library
spectra and found to meet the 70 percent to 100 percent
forward/reverse t project specic objective.
Analysis of lead and mercury. Whole blood samples were
analyzed for lead and methylmercury using Inductively Coupled
Plasma/Mass Spectroscopy (ICP/MS). Samples were prepared
by EPA Method 200.11. Lead analysis was performed according
to EPA Method 200.8. Mercury speciation was performed using
high performance liquid chromatograph (HPLC) to separate
methylmercury from inorganic mercury, as described in the
literature, prior to introduction into the ICP/MS.
Analysis of organophosphate pesticide metabolites. Urine
was analyzed for organophosphate pesticide metabolites
according to procedures described in CDC (CDC 2001), using gas
chromatograph/ame photometric detector (GC/FPD) methods.
Chlorpyrifos metabolite 3,5,6-trichloropyridinol was analyzed
using gas chromatograph/mass spectrometry (GC/MS) methods.
Malathion metabolites monocarboxylic acid and dicarboxylic acid
were analyzed using GC/FPD methods.
Analysis of urinary metals. Speciated arsenic in urine was
analyzed using gas chromatograph/atomic absorption
spectrophotometery (GC/AAS) methods. Cadmium was analyzed
using inductively coupled plasma/mass spectrometry (ICP/MS)
methods, and chromium was analyzed using graphic furnace/
atomic absorption spectrophotometery (GF/AAS) methods.
Results
Chemicals detected. The laboratory detected 167 chemicals
of 210 tested, including 48 PCBs, 15 dioxins and furans, 7
organophosphate pesticide metabolites, 10 organochlorine
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31
Table 3: Exposures found in this study are largely unavoidable.
Source: EWG compilation; * Analytical results for phthalates in blood can be affected by background contamination
of laboratory equipment, but data from CDC show that phthalates are ubiquitous pollutants in people.
Number of
chemicals
found in 9
people
Number of 9
people these
were found in
Concentration
range
(average)
Units Uses Primary Sources of exposure
PCBs
48 of 73 9 of 9
57,290 to 455,790
pg/g in
blood lipid
basis
Dioxin-like PCBs
5 of 12 9 of 9 1.5 to 10.9
pg/g TEQ
in blood
lipid basis
Dioxins and furans
15 of 17 9 of 9 15.7 to 36.6
pg/g TEQ
in blood
lipid basis
There are no industrial uses of
dioxins or furans. Dioxins and furans
are pollution from waste incineration
and fuel combustion (e.g. wood,
coal, or oil) and pollution formed
during chlorine bleaching, chemical
manufacturing, drinking water
chlorination, and industrial
processes.
Contamination in seafood, meat and
dairy products.
Organophosphate
pesticide metabolites
7 of 9 9 of 9 4.0 to 70.4
ug/L in
urine
Organophosphate pesticides are used
as fungicides, herbicides, insecticides
and termiticides.
Contamination in fruits, vegetables,
dairy, and meat products; Direct
exposure from home use
Organochlorine
pesticides and
metabolites
10 of 23 9 of 9 615 to 3084
pg/g in
blood lipid
basis
Organochlorine pesticides are used
as fungicides, insecticides and
termiticides.
Contamination in fruits, vegetables,
dairy, and meat products; Direct
exposure from mosquito control spraying
prior to the 1970s
Phthalates
6 of 6 9 of 9
97.2 to 904.8
[only Bis(2-
ethylhexyl)phthal
ate was
quantified]
ug/g in
blood lipid
basis
Phthalates are used as plasticizers,
solvents, desensitizing agents, dye
carriers, perfume fixatives, and
defoaming agents, as well as in nail
polishes and explosives.
Exposure occurs upon contact or
consumption of plastics, cosmetics,
contaminated food, carpet, explosives,
sealants, varnishes, paints, and primers
Other semivolatile
and volatile
chemicals (24
classes)
77 9 of 9 not quantified
The SVOCs and VOCs found in these
9 people are used in products from
aviation fuel to food flavorings.
Daily life: exposures may occur from
contaminated food, paints, furniture, or
any number of other common consumer
products
Metals
4 of 5 (see below)
9 of 9 1.01 to 3.23
ug/dL in
whole
blood
Lead is released as pollution from
burning fossil fuels, mining and
manufacturing. Lead is used in
ammunition, aviation fuel, batteries,
cables, x-ray shields, and ceramics.
Lead has also been historically used
in paint, crystal tableware, gasoline,
and drinking water pipes.
Chipping paint in older homes and water
from lead pipes or lead solder in homes
built before 1986
7 of 9 0.63 to 25.9
ug/L in
whole
blood
Methylmercury is created in the
environment by bacteria converting
mercury pollution, especially
mercury from coal-fired power
plants.
Canned tuna and other seafood that
accumulates methylmercury from the
environment
1 of 9 21
ug/L in
urine
Arsenic is used in pressure-treated
lumber, alloying constituents, certain
types of glass, doping agents in
germanium and silicon solid state
products, dipoles and other
electronic devices, copper and lead
alloys, and even medicines.
Contact with outdoor lumber decks and
playsets treated with Chromated Copper
Arsenate (CCA); Contaminated drinking
water
3 of 9 0.5 to 0.7
ug/L in
urine
Cadmium is released as pollution
from mining and industrial
operations and coal or waste
combustion. Cadmium is used in
baking enamels, batteries (Ni-Cd),
electronics, fire protection systems,
industrial machinery, lithography,
machinery enamel, marine
equipment, optics, pigments, nuclear
reactor control rods, electroplating
for automotive, aircraft & electronic
parts, and to manufacture
fungicides.
Foods contaminated with cadmium
(shellfish, and some organ meats);
Contaminated air near coal or waste
combustion plants
Arsenic, inorganic
Cadmium
Contamination in seafood, meat and
dairy products.
Lead
Methylmercury
PCBs, banned in 1976, were used in
adhesives, carbonless reproducing
paper, cutting oils, dedusting agents,
electrical capacitors, electrical
transformers, vacuum pumps, gas-
transmission turbines, fire
retardants, hydraulic fluid, ink,
lubricants, pesticide extenders,
plasticizer, heat transfer systems,
wax extenders
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31
pesticides and metabolites, 6 phthalates, 77 semivolatile and
volatile chemicals, and 4 metals (Tables 2 and 3).
Of the chemical groups tested, the most prevalent were those
contained in 24 classes of semivolatile and volatile chemicals,
with 77 detected. These classes include well-known industrial
solvents and gasoline ingredients, including xylene and ethyl
benzene, and are used in a variety of common products like
paints, glues, and re retardants. The laboratory found 48 PCBs
in the nine people tested. PCBs were banned in the United
States in 1976 but .are used in other countries and persist in
the environment for decades. Their most common use was as an
insulating uid in electrical capacitors and transformers, vacuum
pumps, and gas-transmission turbines. Lead was found in all 9
participants, and mercury was found in 8.
Assessment of health effects linked to each chemical detected in
blood or urine. We compiled available information on adverse
effects associated with each chemical detected in study
participants’ blood and urine. Information was drawn from 81
studies found in the peer-reviewed literature (indexed on the
National Institutes of Health’s PubMed database) and various
government health effects assessments (such as those published
by the Agency for Toxic Substances and Disease Registry and the
Environmental Protection Agency).
Potential manufacturers, products, and uses of each chemical.
We compiled data on potential manufacturers and uses of each
chemical through a literature search that included review of nine
standard industry, government, and academic references (Ash and
Ash 2000, Burdock 1994, CDC 2001, CTFA 2002, EPA 1997b,
Farm Chemicals Handbook 2001, Heinrich 2000, NIH 2002a,
NIH 2002b).
Data we have compiled on consumer product uses of particular
chemicals draws from a database compiled by EPA that contains
product ingredient lists encompassing 1,000 chemicals in 11,700
consumer products. The Agency compiled the data from chemical
encyclopedias, air sampling studies in the open scientic
literature, and manufacturers. But the companies have classied
the chemical recipes for 9,300 of these products as “condential
business information,” so our nal product analysis included only
a fraction of the data submitted to EPA by the manufacturers.
These nine information sources show that the chemicals found in
this group of nine people are associated with:
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33
183 types of consumer products, including brake uid,
paint, pesticides, ame retardants (Table 4);
164 past or current manufacturers, including Shell, Union
Carbide, Exxon, Dow, and Monsanto; and
64 chemical functions, including plasticizers, froth
otation agents, and defoaming agents.
Interpretation of Results for Semivolatile and Volatile Organic
Chemical Scan
The tests that identied semivolatile and volatile organic
chemicals in participants’ blood were different from other tests
run in this study, and require a different interpretation. These
tests did not target and then verify specic industrial chemicals
in the samples. Rather, lab technicians worked backwards,
rst scanning the blood extract for all semivolatile and volatile
components, identifying the chemical “ngerprint” of the sample,
and then tentatively identifying the blood components by
matching the weights of molecules in the blood, identied with
an instrument called a mass spectrometer, to molecular weights
in an electronic library of thousands of chemicals.
Our search of standard government and industry references and
Internet databases turned up information on 22 of 77 chemicals
identied, including data on potential health effects from
exposure, chemical manufacturers and commercial uses. Among
the chemicals identied are some clearly linked to industrial uses,
such as xylene and ethylbenzene, both components of gasoline
and both used in a wide range of other consumer products.
Other industrial chemicals found in study participants’ blood are
obscure – for example, health effect or use information is not
available in standard references for 3-bromodecane or 3-bromo,
3-methyl pentane.
Some of the chemicals found may be natural components of
human tissues, and may have industrial uses in addition to being
present naturally. This is the case for palmitic acid, identied in
all nine study participants. Palmitic acid is a natural component
of human fat and the primary fat in meat and dairy products,
but is also produced in high volume by the pine tree pulping
industry, and added to pharmaceuticals, shampoo, soaps, shaving
creams, soaps, and processed or baked foods. In a 1998 survey
of high production volume chemicals, EPA found that basic health
and safety studies have not been conducted for palmitic acid.
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33
Table 4: Hundreds of consumer products contain the chemicals found in
the nine participants in this study.
Source: EWG compilation from 10 government and industry sources on the 167 compounds found in
the nine study participants.
acrylic sprays
dental impression
materials
lacquers solder wire driers
adhesives detergent latex paint solvents
aerosol adhesives detergents light switches in cars spot cleaners
aerosol greases drugs liniment spot removers
aerosol undercoatings dyes liquid nails spray abrasives
aerosol undercoats electronic equipment liquid plastics spray acrylics
airplane parts enamel sprays liquid soap spray adhesives
ammunition enamels lotion spray epoxys
anti-infective lotion epoxy enamels lozenges spray films
anti-lock brakes epoxy finishes lubricants spray lacquers
automobile undercoatings epoxy sprays medication spray laquers
aviation fuel erasable ink mosquito repellent spray lubricants
avicides (kills birds) explosives nail polishes spray paints
bakeware fireproofings
nematicides (kills nematode
worms)
spray primers
banned insecticide floor cleaners oil finishes spray varnishes
batteries flooring ointment stain/lacquers
battery cleaners fluorescent lamps outdoor lumber (pesticide) stain/sealers
battery protectors foam insulations paint stain/varnishes
belt dressings food (additive) paint brush cleaners stains
bleach food (flavoring) paint removers starting fluids
brake fluid food (pollutant) paint thinners steam cleaners
cables food (synthetic flavoring) paper texture coatings
car parts food packaging particleboards thermometers
car waxes fungicides perfume thermoset overprints
carb cleaners furniture pesticides thermostats
carbon cleaners furniture refinishers pigments tire cleaners
carpet gasket removers plastic tire shiners
caulking compounds gasoline plumbing cleaners toothpaste
ceramics general purpose cleaners polishing compounds Turkey red oil
chemotherapy drugs germicides polyshadess vaccinations
child-proof wall finishes glass primers vaginal pharmaceuticals
chipping paint in older
homes
grease removers rawhides varnish
cleaners gum cutters rocket propellants varnish remover
cleaning fluids hair conditioners rubber VCR head cleaners
cold cream hair spray rubber moldings VCR head lubricants
colognes hair sprays rubbing alcohol vinyl floorings
computers hand cleaners rug shampoos
water from lead-soldered pipes in older
homes
conditioners hand cream rust guards wax strippers
contact cements
heat-sealable overprint
(CAP)s
seafood weapons and ammunition
contact lens cleaning
solution
industrial and lubricating
oils
sealant tapes window cleaners
copper & brass polishes inks sealants windshield cleaners
cosmetics insect repellant shampoo wood finishes
cough syrup insecticide shaving cream wood lighteners
crystal tableware
insecticide (banned in
U.S.)
silicone sprays wood preservatives
decorative ink lacquer silicones x-ray shields
dental amalgams (fillings) lacquer thinners soap
34
35
The Agency requested additional data from the manufacturers,
noting that palmitic acid is used commercially in a complex
mixture, and that industry has yet to identify all the components
of the mixture. While scientists know that ingestion of palmitic
acid can raise levels of serum cholesterol, increasing risks of
cardiovascular disease, scientists have not yet studied other basic
health endpoints, particularly those that may be associated with
the commercial mixture.
The laboratory did not quantify the levels of the chemicals
identied in the scan, so these tests do not allow us to
distinguish between components that may be both naturally
occurring, and present in excess from exposures to the chemical
as a contaminant in air, water, food, or as an ingredient in
consumer products. For instance, hippuric acid is typically
found in human urine, but is also formed when the body breaks
down the common, carcinogenic industrial solvent called
trichloroethylene (TCE), and is used as a marker to human
exposures to TCE.
Broad scans such as the semivolatile and volatile chemical scans
run in this study can provide valuable preliminary information
to scientists that guide the design of more detailed, specic
studies. For example, Dr. John Brock, formerly of the Centers for
Disease Control and Prevention, developed new methods to test for
phthalates in people after noticing the presence of phthalates in
routine blood scans, and questioning the common explanation that
phthalates appear in scans as an artifact of background laboratory
contamination. His research found surprisingly high levels of
phthalates in human urine, spurring four cosmetics companies
to announce phthalate-free cosmetic lines because of concerns
about the chemicals’ ability to induce birth defects in laboratory
animals.
34
35
36
37
36
37
CHAPTER 2: Chemical Exposure
Industrial chemicals are widespread
Chemicals end up in people from pollution in air, water and food;
from pesticides and additives in food; through thousands of
consumer products from stain repellants to paints and plastics;
and from a wide array of new building materials. For infants and
children, exposures can also come from their parents’ workplaces,
or from contamination in mother’s milk.
Industries release millions of tons of industrial chemicals to the
environment every year. An emissions tracking system in the
US called the Toxics Release Inventory shows that companies
discharged 7.1 billion pounds of 650 industrial chemicals to air
and water in the year 2000 alone (EPA 2002a). This program
monitors only a subset of US industries.
The federal government’s National Toxicology Program considers
228 chemicals as either known human carcinogens, or “reasonably
anticipated” to cause cancer in humans (NTP 2002). The State of
California considers 475 chemicals to be carcinogenic, and 266
chemicals to be linked to birth defects (OEHHA 2002). No one is
systematically tracking human exposure to any of these chemicals
in spite of their known human health hazards.
In a 1992-2000 survey of 139 rivers and streams in 30 states,
many of which are used as drinking water supplies, the U.S.
Geological Survey identied 95 components of treated human
sewage, including steroids, DEET insect repellant, antibiotics,
and persistent breakdown products of cigarettes and detergents.
Drinking water treatment facilities are not designed to remove
these chemicals, and 85 percent of them are unregulated in
drinking water and thus allowed to occur in any amount in
treated tap water. USGS found 82 chemicals in one of the water
bodies tested, and at least 10 chemicals in 35 percent of the
streams and rivers tested (USGS 2002).
In recent tests of air and dust samples from homes, scientists
in Massachusetts found a broad range of chemicals in each
air sample, including phthalate plasticizers used in cosmetics,
paints, and other consumer products, and brominated ame
retardants used in upholstery, computers, and televisions (Rudel,
et al. 2001). In its national water sampling programs, USGS
routinely detects a broad range of pesticides in rivers and streams
used for drinking water, including a neurotoxic insecticide called
diazinon, found in nearly a third of the water bodies tested. 3M
CASE STUDY: DDT
In 1939 a Swiss chemist named Dr. Paul
Hermann Muller discovered something
new about a chemical called dichlorodiph
enyltrichloroethane: it was effective as a
contact poison for the common housey,
the mosquito, and louse. His chemical,
called DDT, would become the world’s most
popular insecticide, and a life-saving tool
in countries plagued by malaria-carrying
mosquitoes and typhoid-spreading lice.
The World Health Organization estimates
that during its peak decades of use DDT
saved 25 million lives, and Dr. Muller
was awarded the 1948 Nobel Laureate in
Medicine for his discovery.
Despite its clear public health benets,
the U.S. Environmental Protection Agency
banned the use of DDT in 1973 when
thirty years of scientic evidence on the
unexpected, harmful consequences of
DDT use overwhelmed the benets of its
continued application (EPA 1972). In a
series of scientic studies, DDT was found
not only to be linked to reproductive
damage responsible for plummeting
populations of bald eagles and alligators,
but also to persist in human fat tissue
and to contaminate human breast milk
(ATSDR 2002a, IPCS 1989). Although DDT
has been banned for three decades now,
mothers in the U.S. – and across much of
the world – continue to pass the persistent
insecticide and its breakdown products on
to their babies each time they nurse (ATSDR
2002a).
The National Toxicology Program considers
DDT to be “reasonably anticipated to be a
human carcinogen” (NTP 2002). DDT is also
believed to disrupt the human hormone
system in ways that can, for example, shut
down human milk production sooner than
normal, depriving newborns of their only
source of natural nutrition (Gladen and
Rogan 1995). In a recent study linking
preterm birth to levels of a DDT metabolite
in maternal blood, the authors estimate
that DDT may have been responsible for as
many as 15 percent of infant deaths in the
US during the 1960s (Longnecker, et al.
2001).
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39
recently released a study in which they report nding persistent
Scotchgard chemicals in tap water from two of six cities tested
(Columbus, Georgia and Pensacola, Florida) (3M 2001).
Companies win government approval to manufacture seven new
chemicals every day, adding to the roster of more than 75,000
chemicals currently registered for commercial use in the U.S.
These companies produce 15,000 chemicals in quantities of more
than 10,000 pounds per year; 2,800 at a rate of more than a
million pounds per year; and the top 50 chemicals at a combined
rate of nearly one trillion pounds per year (Kirschner 1996).
Hundreds if not thousands of these chemicals pass through or
are stored in the human body after exposures to ingredients
in consumer products or contaminants in air, water, food, and
soil. The chemicals are lodged in human fat, blood, and organs,
or excreted in breast milk, urine, semen, sweat, feces, hair, and
nails.
Scientists know of many individual chemicals that are harmful
to humans – certain chlorinated solvents and insecticides, lead,
PCBs and methylmercury, to name only a few – but have generally
not studied the health effects of complex mixtures of industrial
chemicals in the human body. And scientists have yet to dene
the composition of these mixtures in individual humans.
The only program for detecting industrial chemicals in the human
body is spearheaded not by the industries responsible for the
exposures, but by the federal government’s Centers for Disease
Control and Prevention (CDC) in Atlanta, Georgia. Each year the
CDC’s national biomonitoring program analyzes stored human
blood, serum, urine, and hair samples for a range of industrial
chemicals and pollutants.
Last March, in their rst national report to dene chemical
exposures in the general population, CDC reported on 27
chemicals (CDC 2001). The study represented the culmination
of millions of dollars of taxpayer-funded research. The chemical
industry provided direct funding for none of this effort, but
instead paid their trade association’s press ofce to educate
the national media on the safety of these exposures in the days
following CDC’s report release.
CDC found two of the 27 chemicals in their study, or seven
percent, at levels of potential concern. They found both of
these chemicals - mercury (from contaminated seafood) and a
plasticizer known as DBP (from cosmetics and other consumer
products) - in women of childbearing age at levels that provide
little to no margin of safety from levels associated with health
CASE STUDY: Peruorinated organic
chemicals. In 1976 Donald Taves, a
dentist with the University of Rochester’s
School of Medicine and Dentistry, made
an unexpected discovery when analyzing
a sample of his own blood in his research
on uoride in drinking water. Instead
of the simple uoride chemicals used
in tap water, he found complex organic
uoride chemicals in his blood, completely
unrelated to uoridated tap water. Dr.
Taves and his collaborators identied
one of the compounds as belonging to a
broad chemical family called peruorinated
organics, manufactured by 3M and DuPont
for Scotchgard and Teon products. In
further work, Dr. Taves found peruorinated
chemicals in all but two of 141 human
blood samples – evidence of what he called
“widespread contamination of human
tissues” (Guy, et al. 1976). A total of nine
studies published between 1972 and 1989
veried his ndings in the U.S., Argentina,
China, and Japan, and during that time 3M
and DuPont ran testing programs tracking
chemical levels in their workers.
Despite this evidence, 21 years later,
in the summer of 1997, 3M’s medical
director expressed “complete surprise”
when company-sponsored tests showed
peruorinated chemicals not only in
workers’ blood, but also in blood bank
samples that were to be used as background
controls in the tests (3M 2000). In a series
of follow-up studies conducted over the
past ve years, 3M has found that their
chemicals have universally contaminated
humans and wildlife, including 100
percent of the children tested in the
U.S., Arctic polar bears, and Great Lakes
bald eagles (Giesy and Kannan 2001,
Olsen, et al. 2002). Under pressure from
EPA, 3M withdrew a small fraction of its
peruorinated chemicals from the market
in May 2000 when 3M animal tests showed
surprising death rates among newborn rats
exposed to low levels of these chemicals,
coincident with their studies proving global
human and environmental contamination
(Auer 2000). Three years after the
phaseout, the government still lacks a
reliable method that would allow the
chemicals’ inclusion in the CDC’s national
biomonitoring program.
CASE STUDY: Brominated ame
retardants. Fifty years ago the plastics
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39
effects in exposed human populations and laboratory animals.
Both chemicals are linked to birth defects. Of the plasticizer
DBP, CDC scientists noted that “from a public health perspective,
these data provide evidence that…exposure is both higher and
more common than previously suspected” (Blount, et al. 2000).
DBP has been in wide commercial use in consumer products,
particularly cosmetics, for 50 years.
Biomonitoring data from the CDC have been pivotal in efforts to
focus regulatory agencies on the hazards of DBP and mercury in
the U.S. population. Unlike industry biomonitoring data, CDC
data are publicly available. EWG and other organizations have
used these data to document DBP- and mercury-related health
risks in the population that had previously been ignored or not
well understood. In response to EWG analyses, the Food and Drug
Administration (FDA) has agreed to reevaluate its health advisory
for methylmercury. The FDA has taken no action on DBP, in spite
of CDC data showing that a small but signicant portion of the
population is exposed to levels above federal safety limits. But
several major cosmetics manufacturers have removed DBP from
their products, a step that likely would not have occurred in the
absence of biomonitoring data from the CDC.
industry began experimenting with
chemical coatings that would allow their
otherwise highly ammable plastics to meet
re and smoke regulations for consumer
products. This work paid off, opening up
nearly every niche of ofce and household
goods to the world of polymer plastics,
and resulting in a massive industry that
produces a third of a trillion dollars of
products each year in the U.S. alone. The
current ame retardant market is dominated
by brominated organic chemicals, many
of which are now known to be persistent,
toxic and to accumulate up the food chain
and in humans.
These chemicals are still largely unknown
to the public, but the products that contain
them are quite familiar, ranging from
computers and televisions to coffee makers,
vacuum cleaners and sofa pillows. The
most widely used compounds are PBDEs, or
polybrominated diphenyl ethers.
Scientists are increasingly concerned about
the PBDEs because they are similar to PCBs.
They are persistent organic pollutants
(POPs) that may cause cancer, birth
defects, nerve damage, thyroid dysfunction
and immune system suppression (Darnerud,
et al. 2001, Hooper and McDonald 2000).
They not only bioaccumulate but also
biomagnify, with increasing concentrations
found at higher levels in the food chain.
Some types of PBDEs will be banned in
the European Union beginning in 2003,
but they remain unregulated in the United
States and Canada (Darnerud, et al. 2001,
Renner 2001).
PBDEs were rst detected in human breast
milk in 1972, and a recent Swedish study
found that breast milk concentrations are
doubling every ve years (Meironyte, et al.
1999). The latest research indicates that
the San Francisco Bay Area is a PBDE hot
spot: A study by the California Department
of Toxic Substances Control found that
concentrations of PBDEs in breast tissue
samples from Bay Area women were the
highest detected worldwide – three to
25 times greater than European samples
(She, et al. 2002). Recent samples from
San Francisco Bay harbor seals found PBDE
levels among the highest reported for that
species, with concentrations rising almost
100-fold between 1989 and 1998 (She, et
al. 2002).
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41
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41
CHAPTER 3: Low Doses Can Hurt You
Many of the exposures reported here are below the levels thought
to be toxic in standard high dose toxicology studies relied
upon by industry and regulators. The government’s historic
dependence on high dose studies has created an institutional and
scientic bias that encourages regulators and industry to assert,
with little supporting data, that low doses like those reported
here cause no adverse effects.
In this context, the standard response by industry representatives
to stories involving chemical contamination is that these “trace”
doses are too tiny to cause adverse effects (ACSH 1999). The
science, however, leads to the opposite conclusion. Adverse
health effects from low dose exposures are occurring in the
population, caused by unavoidable environmental contamination
with PCBs, DDT, dioxin, mercury and lead.
Although the chemical industry will assert that low dose
exposures to hundreds of chemicals simultaneously is safe, the
safety claims are based on a lack of scientic information on the
toxicity of low-dose exposures, not on denitive scientic proof
of safety.
Roots of the myth of low dose safety
Chemical toxicology today falls into two camps: Regulatory
toxicology, where scientists, generally in the pay of chemical
companies, conduct high dose animal studies under prescribed
protocols for the purpose of meeting government requirements;
and research toxicology, primarily conducted at independent
university and government research centers, where scientists
focus on low dose exposures to chemicals that lead to harmful
effects on the body.
Regulatory toxicology targets relatively crude measures of toxicity
such as cancer, birth defects, and obvious signs of organ damage.
Research toxicology goes beyond this to look at how chemicals
can alter the functioning of organ systems that otherwise appear
intact.
Many adverse effects are caused by low dose exposures that occur
during critical periods of fetal development or infancy but do not
manifest until later in life. Often these effects arise from insults
that trigger a cascade of effects that alter the proper functioning
of organ systems, sexual development, behavior or reproduction.
Some examples include alterations of nervous system
INDUSTRIAL CHEMICALS AND
HUMAN DISEASE
The onset or progression of most
health problems can be inuenced
by environmental contaminants.
The following diseases are
prevalent and have shown an
increased incidence not explained
by better detection or longer
lifespans. Evidence from many
low dose toxicity studies indicates
that trace exposures can target
organs and cause effects that can
contribute to the occurrence of
these diseases in people.
Breast cancer. Among girls
born today, one in eight is
expected to get breast cancer
and one in 30 is expected to
die from it. Invasive female
breast cancer increased an
average of 1.5 percent per
year between 1973 and 1996,
for a total increase of 25.3
percent. Among those 65
and younger, breast cancer
incidence rose 1.2 percent
per year, corresponding
to a doubling every two
generations (58 years).
If trends continue, the
granddaughters of today’s
young women could face a one
in four chance of developing
breast cancer (NCI 1996, NCI
1997).
42
43
development that play out as behavioral problems or IQ decits;
or disruption of normal hormonal signaling that results in fertility
problems, birth defects of reproductive organs, early puberty, or
cancers of the reproductive organs. Alteration of immune system
function can also occur, leading to increased susceptibility to
illness and disease. Scientists are nding that many chemicals in
widespread use today cause these types of effects at doses well
below those thought to cause “no effect” in high dose regulatory
studies.
The following is a guide through some of the highlights and
basic concepts of low dose chemical toxicity. The discussion
is presented in greater detail below, but can be summarized as
follows:
In many cases low doses are toxic. Science has evolved
considerably since the 16
th
century when Paracelsus coined
the adage, “The dose makes the poison.” We now know
that many other factors, particularly the timing of the
dose, genetic variability, and health status of the exposed
individual, are equally, if not more important. Low
doses of lead, mercury or PCBs at specic days of fetal
development or infancy can cause permanent problems
that are not manifest during exposure, but only later
during childhood, adolescence and beyond (ATSDR 2000,
Jacobson and Jacobson 1996, NAS 2000). The same dose
in the adult may have little or no effect. Among people
breathing the same polluted urban air, only some will
develop asthma. A recent study evaluating differences
in human response to airborne particles found that the
most sensitive members of a population respond to doses
150 to 450-fold lower than median (50
th
percentile)
responders (Hattis, et al. 2001). Factors that contribute
to these differences include variations in breathing rates,
deposition and elimination of air particles from the
respiratory tract, and differences in lung response to the
chemicals found in the air.
Susceptibility to disease results from a complex interplay
between biological factors, such as specic genetic traits,
and the environment, which would include exposure
to other chemicals (environmental, recreational or
therapeutic) and lifestyle factors such as stress levels,
nutrition, tness, and smoking status. Genetic variation
contributes to the incidence of diseases induced by
industrial contaminants. For example, inherited mutations
of the BRCA1 and BRCA2 genes account for ve to ten
percent of all breast cancers (Tripathy and Benz 1997).
Testicular cancer. At its
current pace, the incidence of
testicular cancer is doubling
about every one and a half
generations (39 years). In the
U.S. the incidence of testicular
cancer rose 41.5 percent
between 1973 and 1996, an
average of 1.8 percent per
year (NCI 1996, NCI 1997).
While rates of testicular cancer
continue to drop among older
men (65 and up), testicular
cancer remains the most
common cancer among young
men, with the highest rate of
diagnosis among men between
the ages of 30 and 34.
Prostate cancer. Prostate
cancer rates rose 4.4 percent
a year between 1973 and
1992, or more than a doubling
of risk in a generation. Since
1992, the incidence has
declined, but it is still 2.5
times its 1973 rate. Part of
this increase can be explained
by better detection, but
increased incidence has also
been accompanied by an
increase in mortality - which
better detection cannot
explain. Prostate cancer is
now the most common cancer
among U.S. men, and the
second most lethal, killing an
estimated 31,900 men in the
year 2000 alone (NCI 1996,
NCI 1997).
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43
For most chemicals science provides little or no basis for
assertions that low dose exposures are safe, particularly
those that start in utero and continue to old age, as is the
case with most of the chemicals identied in this study.
This knowledge gap is due to study designs, dictated by
food and drug regulations, that in general do not require
testing of low doses, and in no cases expose animals to
chemicals from conception through old age – a so-called
womb to tomb study that most accurately comports with
real world human exposures.
Most safety claims for trace exposures are based on
ndings from high dose studies. Such extrapolations do
not ensure safety. Low dose safety is not well predicted by
the high dose studies required for chemicals used in foods
and drugs. High dose studies tend to look for readily
observable, overt toxic effects like cancer, malformations
visible at birth, and organ damage, such as liver toxicity.
High dose studies usually involve only adult animals. Low
dose studies typically look for less obvious effects that
involve impaired function of organ systems in animals
exposed during development. Examples include decreased
sperm counts, altered hormone levels, impaired immune
function, altered growth and development of reproductive
organs and behavioral and intelligence decits. Low dose
studies almost always involve exposures in utero or early
life.
Many chemicals produce different or even opposite effects
at high and low doses – a phenomenon called biphasic
dose response. For example, DES, a potent synthetic
estrogen, has been shown to simulate prostate growth at
0.02, 0.2, and 2 μg/kg-day, but inhibit prostate growth at
doses of 100 and 200 μg/kg-day (vom Saal, et al. 1997).
Perchlorate, a component of rocket fuel and drinking
water contaminant, causes changes in the size of certain
parts of the brain at 0.01 – 1 mg/kg-day, but not at 30
mg/kg-day (Argus 1998).
Current regulatory high dose studies are conducted with
puried single chemicals. In the real world, people are
exposed to exotic low dose mixtures of several hundred
different chemicals. The toxicity of these mixtures is
not known, and is not being investigated. In two recent
studies scientists dosed laboratory animals with a mixture
of 16 organochlorine pesticides, lead, and cadmium, each
applied at its individual regulatory “safe” dose, and found
Declining sperm count. An
analysis of 101 studies (1934-
1996) by Dr. Shanna Swan
of the University of Missouri
conrms results of previous
studies: average sperm counts in
industrialized countries appear to
be declining at a rate of about one
percent each year (Swan, et al.
2000).
Hypospadias. Data from the
Centers for Disease Control and
Prevention (CDC) show that rates
of hypospadias in the U.S. began
climbing in about 1970, and
continued this increase through the
1980s. This condition is a physical
deformity of the penis in which the
opening of the urethra occurs on
the bottom of the penis instead of
the tip. Currently the occurrence
of hypospadias appears to be
stable, at about 1 in 125 births
(Paulozzi, et al. 1997).
Undescended testicles. This
birth defect, where testicles fail
to completely descend into the
scrotum during pregnancy, occurs
in two to ve percent of full-term
boys in Western countries. Rates
of the defect increased greatly in
the U.S. in the 1970s and 1980s.
Men born with this defect are at
higher risk for testicular cancer and
breast cancer (Paulozzi 1999).
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45
that the animals developed impaired immune response
and altered function of the thyroid, a gland that is critical
for correct brain development (Wade, et al. 2002a, Wade,
et al. 2002b).
Some people are more sensitive to low dose exposures
than others. EPA-funded research has documented a
10,000 fold variability in human response to certain
airborne particles (Hattis, et al. 2001). This genetic
variability in response explains, in part, why we all
breathe the same air, but not all of us have asthma
attacks.
Documented low dose effects in people
The scientic evidence for human harm from industrial chemicals
and pesticides extends far beyond occupational exposures.
Countless studies in the peer-reviewed literature show that
adverse health effects from low dose exposures are occurring in
the population, caused by unavoidable contamination with PCBs,
DDT, dioxin, mercury, lead, and other chemicals. Among the
many health effects scientists have linked to chemical exposures
in the general population, are premature death, asthma, cancer,
chronic bronchitis, permanent decrements in IQ and declines in
other measures of brain function, premature birth, respiratory
tract infection, heart disease, and permanent decrements in
lung capacity (EPA 1996, EPA 2000, Gauderman, et al. 2002,
Jacobson and Jacobson 2002, Jacobson, et al. 2002, Kopp, et
al. 2000, Longnecker, et al. 2001, NAS 2000, NTP 2002, Pope,
et al. 2002, Salonen, et al. 1995, Sydbom, et al. 2001).
PCBs at 9.7 ng/ml (parts per billion or ppb) in maternal serum
during fetal development can cause adverse brain development,
and attention and IQ decits that appear to be permanent
(Jacobson and Jacobson 1996). Notably, it was the maternal PCB
levels and not the PCB levels in children at 4 and 11 years of age
(by which time child PCB levels had decreased substantially) that
was associated with IQ decit – underscoring the limitations of
studies that try to correlate current body burdens with adverse
health outcome in the absence of measuring in utero exposures.
Dioxin at 80 parts per trillion in paternal – but not maternal
– serum causes a signicant change in the sex ratio of children
(Mocarelli, et al. 1996, Mocarelli, et al. 2000). At this tiny dose,
men father nearly twice as many girls as boys. Eighty parts per
trillion is equivalent to one drop of dioxin in a seven mile long
string of bathtubs (7,400 bathtubs).
44
45
Lead above 100 parts per billion in the blood of a two year old
can cause learning decits, behavioral problems and a signicant
decrease in IQ in adolescence and adulthood (CDC 1997). The
same dose has no effect on adults. One hundred ppb is the
equivalent of 1 drop of water in 6 bathtubs. A 5/1,000ths ounce
chip of lead paint can put a child in the emergency room with
lead poisoning [Calculated based on (CDC 1997, EPA 1998a)].
Methylmercury causes measurable delays in brain function in
children exposed to levels corresponding to 58 parts per billion in
maternal blood (NAS 2000).
DDE above 15 ppb in maternal blood is associated with preterm
birth, and low birth weight, with weight corrected for gestational
age (Longnecker, et al. 2001). DDE is a metabolite of DDT. Using
the associations derived from tests of archived samples from a
pool of 42,000 women, researchers estimated that DDT exposures
could have accounted for up to 15 percent of infant deaths
during the 1960s. Low birth weight like that linked to DDE is
increasingly recognized as a risk factor for insulin resistance
or Type II diabetes, high blood pressure, and cardiovascular
disease later in life (Godfrey and Barker 2001, Hales and Barker
2001). Even if these lower birth weight babies “catch up” later,
the damage may have already been done. A substantial number
of studies have found that low birth weight followed by an
accelerated growth rate during childhood is a signicant risk
factor for high blood pressure, stroke, insulin resistance and
glucose intolerance (Eriksson, et al. 2000a, Eriksson, et al. 2002,
Eriksson, et al. 2000b, Eriksson, et al. 1999, Eriksson and Forsen
2002, Forsen, et al. 2000, Ong and Dunger 2002, Stettler, et al.
2002).
Chlorpyrifos (dursban) above 8 pg/g (parts per trillion) in the
blood of non-smoking women was strongly associated with
decreased birth weight and body length in babies of African
American women in New York City (Perera, et al. 2003). In the
same study, increased air exposure to PAHs was correlated with
decreased birth weight – an effect that was independent from
the chlorpyrifos nding – and decreased head circumference. The
babies of women exposed to the highest PAH levels had a 10%
reduction in body weight (Perera, et al. 2003).
Byproducts of tap water chlorination were linked to statistically
signicant increases in birth defects in New Jersey at 40 parts
per billion in water, and miscarriages in California at 75 parts per
billion (Bove, et al. 1995, Waller, et al. 1998).
Perchlorate in drinking water at levels as low as one to two ppb,
46
47
(0.2 to 0.4 ug/kg/day) is associated with altered thyroid hormone
levels in infants (Schwartz 2001). Perchlorate is a component of
rocket fuel that also was used in the 1960s as a drug to regulate
thyroid hormone activity. Adequate levels of thyroid hormone
are critical for normal brain development (Gruters, et al. 2002,
Zoeller, et al. 2002).
Low dose effects in animals
As researchers continue to study the effects of exposure to low
levels of contaminants, more effects are observed – especially in
developmentally exposed organisms. In the natural environment,
low dose effects are often observed in aquatic species, such as
sh and frogs. This nding has prompted chemical industry
representatives to belittle these results as irrelevant to human
exposures. The truth, however, is not that simple. Even though
the specic effects may differ between humans and wildlife,
the general toxicity is often quite similar. For example, if
a contaminant causes reproductive effects in sh - such as
production of a hormone that humans don’t possess or other
effect not caused in humans - the chemical is also likely to affect
reproduction in mammals. DES (a potent estrogen) increases
levels of vitellogenin – a protein that humans do not produce
– in sh. Vitellogenin is an indicator of estrogenic activity
(Folmar, et al. 2002). In mammals, DES causes increased growth
of uterine cells, again an indicator of estrogenic activity (EPA
1998c). In either case, DES causes adverse reproductive effects
in sh, mammals and humans, although the specic endpoint
may differ.
The dangers of nearly every chemical banned or restricted in the
US were rst identied in laboratory animals or wildlife. Animals
are strong predictors of hazards to human health – a premise that
applies to “all of experimental biology and medicine” (Klassen
1996). For instance, the vast majority of known and reasonably
anticipated human carcinogens cause cancer in laboratory
animals (NTP 2002).
Bisphenol A. A number of low dose studies have focused on
effects of bisphenol A, a building block of polycarbonate plastics
that is used in dental sealants and to line virtually all aluminum
and steel cans, among many other uses. The seminal study, by
Nagel et al (1997), found increased prostate weight in male
mice exposed as fetuses to 2 μg/kg/d. In subsequent studies,
scientists have now linked low dose bisphenol A exposures to
altered development of the mammary gland (25 μg/kg/d and 100
μg/kg) (Colerangle and Roy 1997, Markey, et al. 2001), vagina
(100 μg/kg/d) (Schonfelder, et al. 2002a) and prostate
46
47
(2 - 50 μg/kg/d) (Gupta 2000, Nagel, et al. 1997, Ramos, et al.
2001); earlier onset of puberty in female mice (2.4 and 20 μg/
kg/d) (Honma, et al. 2002, Howdeshell, et al. 1999); effects on
behavior (2 to 40 μg/kg/d) (Adriani, et al. in press 2003, Dessi-
Fulgheri, et al. 2002, Facciolo, et al. 2002, Farabollini, et al.
1999, Kawai, et al. in press, Palanza, et al. 2002) and decreased
sperm production (20 μg/kg/d) (Sakaue, et al. 2001, vom Saal,
et al. 1998). Scientists found increased rates of embryonic
development at 1 nM (0.23 ppb) ((Takai, et al. 2000a, Takai, et
al. 2000b).
Infants ingest bisphenol A in formula at an estimated daily rate
of 1.6 μg/kg-day (SCF 2002), giving little safety margin from
the doses that cause effects in animal studies (doses as low as 2
ug/kg/d).
Human fetal plasma BPA levels were recently reported at between
0.2 to 9.2 ng/ml (ppb) (Schonfelder, et al. 2002b). The median
BPA level in this study (2.3 ng/ml (ppb)) is consistent with a
median of 2.2 ng/ml (ppb) reported in a recent Japanese study
(Ikezuki, et al. 2002). Notably, some of the effects cause by
BPA in animal studies appear to be increasingly common in
some segments of the human population, including early onset
of puberty (Herman-Giddens, et al. 1997) and decreased sperm
production (Swan, et al. 2000, Toppari, et al. 1996).
Atrazine. Five studies published in the past year have found that
exposure to 100 parts per trillion of atrazine in water causes
deformities in frogs, including hermaphroditism (individuals
with both male and female sex organs), underdeveloped testes,
and a decrease in the number of germ cells (sperm and eggs)
(Hayes, et al. 2002a, Hayes, et al. 2002b, Hayes, et al. in press,
Tavera-Mendoza, et al. 2002a, Tavera-Mendoza, et al. 2002b).
Hermaphroditism is extremely rare and was not detected in any
unexposed frogs (Hayes, et al. 2002b). Atrazine is the most
commonly used weed killer in U.S. agriculture, and is found in the
tap water of 10 million people in corn belt states. The level that
causes these effects, 100 parts per trillion, is commonly found in
corn belt tap water and is 30 times less than the legal maximum
contamination limit for atrazine of 3 parts per billion.
Aldicarb. Numerous studies have found that low doses of aldicarb
impair immune function at low doses (Dean, et al. 1990a, Dean,
et al. 1990b, Hajoui, et al. 1992, Olson, et al. 1987, Selvan,
et al. 1989, Shirazi, et al. 1990). Immunologic effects were
observed at concentrations as low as 0.1 to 1 ppb (Dean, et al.
1990b, Olson, et al. 1987, Selvan, et al. 1989).
48
49
Nonylphenol. An ingredient of certain plastics and a surfactant
used in detergents and pesticides produces low dose effects in
aquatic organisms (i.e. sh and frogs). Nonylphenol at less than
1 ppb in water produced female specic proteins in male sh
(Tabata, et al. 2001), altered reproductive hormone levels (Giesy,
et al. 2000, Harris, et al. 2001) and decreased sword length in
swordtail sh (Kwak, et al. 2001). Slightly higher concentrations
(~ 22 ppb) cause an increase in the number of female-appearing
frogs (Kloas, et al. 1999). In frogs, low concentrations of NP
(100 nM; ~ 22 ppb) decreased the number and differentiation of
neural crest-derived melanocytes (pigment producing cells); and
this effect was specic to estrogenic compounds tested (Bevan,
et al. 2002). Nonylphenol is one of the most frequently detected
contaminants of streams in the U.S. (Kolpin, et al. 2002). It was
found in 50% of 139 streams in 30 states (median 0.8; max 40
μg/L or ppb).
DDT at 18 ng/ml (ppb) in the blood of mice caused signicant
increases in the height and thickness of uterine and vaginal
epithelial cells respectively. These changes are considered to be
indicators of estrogenic response. Changes in uterine epithelial
cell height were also observed at β-HCH of 42 ng/ml (ppb)
(Ulrich, et al. 2000).
Trenbolone, a synthetic androgen (male hormone) used in beef
production, impaired reproduction of sh at 50 parts per trillion
(decreased number of eggs spawned) (Ankley and Touart 2002),
and caused the “masculinization” of female sh at doses as low
as 5 μg/L (5 ppb) – the female minnows grew characteristic male
spikes on the tops of their heads.
Regulatory requirements don’t include low dose studies.
For most chemicals scientists have not studied the effects of low
dose exposures, particularly in utero. Most available toxicity data
comes from high dose studies on adult animals. The dearth of
low dose data does not stop industry representatives from issuing
blanket assurances about the safety of low dose exposures. When
“experts” assert that low doses cause no effects in animals, it is
almost always because they haven’t looked.
Most experiments designed to identify low dose toxicity differ
substantially from those used in standard high dose studies
required for food additives and drugs. These low dose studies
are sometimes referred to as non-guideline studies, because they
involve investigations that extend beyond the narrow limits of
agency study guidelines or protocols.
48
49
Research scientists (primarily academic and government
researchers) have more exibility to develop innovative study
designs and investigate more sophisticated and subtle indices
of toxicity. In contrast, industry scientists typically conduct
“guideline” studies that fulll minimal regulatory requirements,
which are often based on decades old science and relatively crude
endpoints.
High dose regulatory studies do not look for the outcomes that
are most likely to arise from low dose exposures. For example,
high dose study designs look for overt easily observable effects,
like cancer, gross birth defects, acute poisoning, or overt organ
damage. Low dose research studies typically examine functional
decits, where apparently healthy organs or systems, do not
function properly. Outcomes are measured as altered growth
and development of reproductive organs, behavioral changes,
abnormal immune function, and changes in hormone levels.
The vast majority of “low dose” studies involve follow-up of
developmentally-exposed animals (or humans) in ways not
addressed by regulatory toxicology studies. For example, there
is no regulatory study that follows animals exposed in utero to
an age corresponding to old age – referred to as a “womb to
tomb” study. Instead, animals exposed in utero are followed, at
a maximum, until they are young adults (~ 4 to 5 months). This
makes it impossible to address questions such as whether in-utero
or early life exposure to industrial chemicals or pesticides can
predispose an individual to cancer, degenerative nervous system
disorders, diabetes, or other diseases more prevalent at the end
of life for the vast majority of chemicals. In general, research
studies follow developmentally exposed animals for longer periods
of time and study endpoints in greater detail.
Low doses studies often reveal toxic effects at levels high
dose studies consider safe.
High dose animal studies cannot accurately predict either the
safety or hazard of low dose exposures. This is particularly true
when high dose studies on adult animals are applied to low dose
in-utero or infant exposures. Lead, mercury and PCBs are classic
examples, where high dose animal studies on mature animals
failed to identify the hazards of low dose fetal and childhood
exposure.
In many other cases low dose research found adverse health
effects at levels well below the supposed “no effect” level
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51
determined in standard high dose regulatory guideline studies
(Figure 1).
Atrazine was presumed by pesticide manufacturers and the
EPA to cause no effects below 3 ppb (EPA 2002). Subsequent
work by Tyrone Hayes shows that atrazine produces frogs with
both male and female sex organs at levels 30 times lower than
this (Hayes, et al. 2002b).
Methoxychlor, an insecticide and chemical relative of DDT,
was presumed to cause no effects to the fetus at doses below
5 mg/kg/d (IRIS 2003b). Subsequent low dose research found
that methoxychlor causes signicant changes in prostate size at
a dose 250 times lower in animals exposed in utero (Welshons, et
al. 1999).
Bisphenol A is assumed to cause no harmful effects below
a dose of 5 mg/kg/d, according to a recent risk assessment
conducted by European Commission Scientic Committee on Food
(SCF 2002). Yet signicant effects on reproductive organ size and
development have been found repeatedly at levels up to 1000
times lower (Colerangle and Roy 1997, Gupta 2000, Howdeshell,
et al. 1999, Markey, et al. 2001, Nagel, et al. 1997, Ramos, et
al. 2001, Sakaue, et al. 2001, Schonfelder, et al. 2002a, vom
Saal, et al. 1998).
Methylmercury is assumed to cause no harmful effects
below a concentration of 11 mg/kg in hair, according to the
Environmental Protection Agency (NAS 2000). Yet researchers in
the Netherlands found a doubling in the risk of heart attacks and
death from coronary heart disease at methylmercury levels of 2
mg/kg in hair, or about one fth of assumed safe levels (Salonen,
et al. 1995). Increased diastolic and systolic blood pressure
and decreased heart rate variability in developmentally exposed
children have also been observed at doses below the EPA no
effect level (NAS 2000, Sorensen, et al. 1999).
Dibutyl phthalate (DBP) was presumed by the EPA to cause
no harmful effects in animals below 125 mg/kg/d based on a
1953 study (IRIS 2003a). More recent studies have shown that
DBP causes male reproductive toxicity at 100 mg/kg/d, including
delayed puberty, cellular changes in the testis and retained
nipples (CERHR 2000, Mylchreest, et al. 1999, Mylchreest, et al.
2000). Decreased numbers of live pups have been observed at an
even lower dose of 52 mg/kg/d (CERHR 2000, Wine, et al. 1997).
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Many chemicals produce different or even opposite effects
at high and low doses – a phenomenon called biphasic dose
response.
Chemicals that produce a biphasic dose response are relatively
common, and these responses are observed for a variety of
effects. The prevalence of these types of effects underscores
how wrong one could be by assuming that high dose studies
accurately predict low dose toxicity.
Perchlorate, a component of rocket fuel and drinking
water contaminant, causes changes in the size of certain
parts of the brain at 0.01 – 1 mg/kg-day, but not at 30
mg/kg-d (Argus 1998). We know that perchlorate causes
these effects at lower doses because it is a relatively well-
studied chemical by virtue of its use as a pharmaceutical.
In contrast, most environmental contaminants would
not be assessed for effects on thyroid hormone or brain
structure at all.
Bisphenol A (BPA), an estrogenic endocrine disruptor
commonly found in plastics used in dental sealants and
as liners in most aluminum and steel cans, can produce
opposite effects at low and high doses. BPA increases
the developmental rate of embryonic cells at 1 nM (0.229
ppb), while concentrations 100,000 fold higher (100 μM
or 22829 ppb) will decrease developmental rate (Takai, et
al. 2000a, Takai, et al. 2000b). In prostate cancer cells,
BPA will increase cell proliferation at concentrations 100
times less than the levels that inhibit cell growth (1 vs
100 nM or 0.229 vs 22.9 ppb)(Wetherill, et al. 2002).
Atrazine produced more pronounced hermaphroditism
and testicular toxicity in frogs at 0.1 ppb than at 25 ppb
(Hayes, et al. in press).
Pyrethroid insecticides induce hyperactivity in rats at
doses up to 0.7 mg/kg but no hyperactivity at a dose 60
times higher (42 mg/kg) (Eriksson, et al. 1991).
DES, a potent synthetic estrogen, has been shown to
cause stimulatory low dose effects on the weights of the
prostate (0.02, 0.2, and 2 μg/kg-day) and uterus (0.1 μg/
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kg-day), but inhibit growth at higher doses, 200 μg/kg-
day and 100 μg/kg-day, respectively (Alworth, et al. 2002,
vom Saal, et al. 1997).
Hormesis
While most industry representatives dismiss low dose adverse
effects, some embrace a concept called hormesis – a low dose
biphasic dose response where low dose effects are benecial
and high doses are toxic. The concept of hormesis is easily
conceptualized with vitamins; low doses of many vitamins are
benecial, while high doses can cause adverse effects including
kidney toxicity (vitamin D), gastrointestinal upset (vitamins
A and D), headaches (vitamin A), increased susceptibility to
hemorrhage (vitamin E) and general sense of fatigue (vitamins A
and E) (Merck & Co. Inc. 2002).
Although there is considerable scientic support for hormesis
with respect to vitamins and minerals, some in the chemical
industry are distorting the concept to argue that the low doses
of environmental contaminants may also be “benecial.” A
recent report on hormesis by the Texas Institute for Advancement
of Chemical Technology (TIACT), a “non-prot, charitable
organization… dedicated to the advancement of chemical
technology through an informed public,” contains the most
distorted arguments put forth to date. The authors propose
hormesis as a rationale for bringing back into commerce long-
banned chlorinated chemicals such as PCBs and DDT.
“The scientic acceptance of hormesis with its possible
benets at low-level exposure could come at no better
time than the present when environmentalists and
others are calling for bans on more and more chemicals,
such as chlorinated hydrocarbons (emphasis added)
to prevent low-level exposures. Furthermore, the low-
exposure paradigm (emphasis in original) would make
it possible for society to enjoy, safely, the benets of
many chemicals that have been banned in the past or
could be banned in the future” (rst page of the executive
summary) (TIACT 1998). TIACT is supported by donations
from Dow, BASF, Bayer, Shell Chemical Company, and
Syngenta.
This extreme view of hormesis is not generally accepted.
However, hormesis does help explain low dose effects seen in
toxicology studies. Scientists have found that while low doses
can stimulate a process in the body, high doses can inhibit the
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same process. For example, low doses of estrogens will stimulate
breast cancer cells to grow (proliferate). High doses of the
estrogen can inhibit cell growth – presumably because the high
doses can damage the cell to the point of dysfunction or death
(Lippman, et al. 1976). Similarly, low doses of pharmacological
estrogens stimulate uterine growth in rodents, while high doses
– well above therapeutic doses – will cause uterine weight to
decrease (Alworth, et al. 2002, Shelby, et al. 1996).
Some people are more sensitive to low dose exposures than
others.
People differ in response to the same amount of chemical
exposure as a function of their age, differences in metabolic
and detoxication pathways, nutritional state, body weight,
genetic variability, gender, preexisting conditions, and lifestyle
(such as smoking and drinking status). In regulatory toxicology,
the default factor used to take these differences into account,
referred to as an intraspecies factor, is 10-fold – meaning that
the response from one person to another is expected to be no
greater than 10 times different.
Chemical response
The assumption of 10-fold variability is not likely realistic when
one considers the range of responses in the most sensitive
populations of people, rather than simple average differences.
For example, recent EPA-funded research found that some people
are 10,000 times more sensitive than the average (median)
person to certain forms of airborne particles (Hattis, et al. 2001).
Age
In general, fetuses, infants and children are more sensitive
to chemical exposure than adults. One reason is age-related
differences in metabolism. A comparison of the half-lives (a
measure of how fast a chemical leaves the body) for 45 different
pharmaceuticals in neonates and adults found that on average
it takes neonates 3 to 9 times longer to eliminate 1/2 of the
administered dose depending on the primary elimination pathway
for that chemical (such as CYP or P450, glucuronidation, renal,
other non-CYP elimination pathways) (Ginsberg, et al. 2002a).
But averages can mask signicant differences. Approximately
seven percent (6/85) of 1-week (< 7 days) to 2-month old babies
had an elimination half-life more than 10 times longer than the
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55
adult average level (Hattis, et al. in press). Only one percent
(1/85) of the 1-week to 2-month old infants had a faster half-life
than the adult average value (Hattis, et al. in press).
The enzyme paraoxonase (PON) is essential to metabolize toxic
breakdown products of organophosphate (OP) compounds,
including OP insecticides. People with high PON levels
metabolize insecticides faster than people with lower PON levels
(Hulla, et al. 1999). Human infants do not begin to produce
adult-type levels of PON until they are around 2 years of age
(Ecobichon and Stephens 1973), making them potentially more
vulnerable to OP exposure.
Similarly, the elderly are also more sensitive to chemical effects,
which is why the recommended dosage for many drugs is 25 to
50% of that given to younger adults.
Hexachlorobenzene (HCB), an organochlorine pesticide, is more
toxic to the young than to adults. In Turkey during the mid to
late-1950s, a fungicide containing ten percent HCB was used
to make bread, resulting in an extremely high rate of infant
mortality (95%) in breast-fed babies born to mothers who ate the
bread. There was no detectable change in mortality for exposed
adults (ATSDR 2002b). The infants who died had skin lesions,
cardio- respiratory failure, weakness and convulsions. HCB also
causes neurotoxicity in adulthood following developmental
exposure. Symptoms include a jerkiness of movement like that
seen in Parkinson’s disease (ATSDR 2002b). Other effects observed
in adults exposed as children include osteoporosis of hand bones,
small hands, swelling and spindling of ngers (ATSDR 2002b).
While HCB exposure has not been denitively linked to impaired
immune function in humans, exposure to several organochlorines
(including HCB) has been associated with increased risk of
otitis media (inammation of the middle ear) in the rst year
of life (Dewailly, et al. 2000). A German study found that HCB
levels were higher in a group of boys undergoing surgery for
undescended testicles compared to boys with no testicular
abnormalities (Hosie, et al. 2000). More recently, mothers of men
with testicular cancer were found to have higher levels of HCB
compared to mothers of men without this disease (Hardell, et al.
in press).
Genetic differences
Levels of polycyclic aromatic hydrocarbon (PAH)-DNA adducts,
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55
a biological marker of PAH exposure, vary up to 24-fold in a
population of normal adults, reecting signicant differences in
PAH exposure and response (Dickey, et al. 1997). However, in
people who lack an important detoxication enzyme, glutathione
S-transferase M1 (GSTM1), PAH-DNA adducts vary by 52-fold.
Activity of an enzyme used to metabolize alcohol (as well
as the industrial chemicals toluene, vinyl chloride and 2-
methoxyethanol), aldehyde dehydrogenase-2 (ALDH2), vary up to
26 fold between susceptible people in Asian populations and the
US median. Similarly, activity of another enzyme important in OP
detoxication, malaoxonase, varies 7-fold within humans – and
this number does not begin to include differences between adults
and children (Sams and Mason 1999). These numbers exceed the
default factor of 3.2 fold used to account for pharmacokinetic
variability in risk assessment (Ginsberg, et al. 2002b).
Progress in government’s efforts to gather low dose study
data.
In 1996 EPA convened an expert committee to develop animal
testing protocols for low dose studies, to be conducted for a
broad range of industrial chemicals that are suspects for low
dose effects. Although the original committee and its successor
have met regularly for six years now, they have yet to nalize a
single testing protocol. One particular protocol still in draft form
is a standard uterine growth test used since the 1930s to ag
chemicals that could impair reproduction and development.
The committee’s drafts leave out some critical indicators, like
tests for brain function in studies of chemicals that suppress
thyroid hormones key to brain growth and development. One of
the industrial chemicals known to disrupt thyroid function and
potentially impair fetal and infant brain development is a rocket
fuel ingredient called perchlorate that contaminates an estimated
ten percent of the public water supplies in California and that
scientists believe crosses the placenta and passes from mother to
infant in breast milk (EWG 2000).
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CHAPTER 4: TSCA and Reform
Imagine a regulatory system designed in theory to protect
hundreds of millions of people from the potential harm of tens of
thousands of chemicals in products they use every day. Imagine
that this system did not require any health or safety studies
prior to the marketing and sale of a chemical; did not require
any monitoring of chemicals once they were in use; allowed
producers to claim virtually all information related to a chemical
as condential business information and thus forever shield
it from public view; and did not allow the public any right to
sue or otherwise force testing or monitoring when independent
scientists conrmed that signicant contamination or hazards
may exist.
You have just imagined the Toxic Substances Control Act, the
nation’s chief regulatory statute for commercial chemicals. TSCA,
as it is known, is famous for the lack of authority it provides
the Environmental Protection Agency. Under TSCA a chemical
company is under no legal obligation to understand how its
products might harm human health. And in fact, only after
scientists have amassed a body of evidence linking the chemical
to human harm can the federal government ban it or leverage a
phase out. A string of Congressional hearings and reports from
the General Accounting Ofce have thoroughly documented this
fact. With no statutory power to request data on a chemical prior
to proving harm, which it typically cannot prove without the
data it is seeking, the EPA has essentially given up trying to use
TSCA to better understand the potential hazards of the tens of
thousands of chemicals in use today.
More than 63,000 chemicals were granted blanket approval
for use in consumer and industrial products with the passage
of TSCA in 1976. The federal government reviews the safety
of chemicals invented since that time through an application
process that does not require health and safety test data and that
discourages voluntary testing. Companies submit basic toxicity
data with fewer than half of all applications to manufacture new
chemicals; the government approves 80 percent of these with no
restrictions and no requests for tests. Eight of 10 new chemicals
win approval in less than three weeks, at an average rate of seven
a day.
Companies can volunteer any studies they may have performed
to les and dockets maintained by the Environmental Protection
Agency, but in the absence of any voluntary submissions, EPA
is forced to rely on computer models to estimate if an industrial
THE REGULATORY PRECEDENT
OF PESTICIDES
Industrial chemicals are governed by
the nearly nonexistent health and safety
standards of the Toxic Substances Control
Act (TSCA). Pesticides, in contrast,
comply with rigorous mandatory testing
requirements, proof that the chemical
industry can conduct health and safety
studies on its products with minimal
economic impact.
Pesticides in food are regulated under
section 408 of the Food Drug and Cosmetic
Act, which requires chemical companies to
show that there is a “reasonable certainty
of no harm” from exposure to a pesticide,
for all exposed individuals, including
explicit consideration of the fetus, infant
and small child. This standard, which is
well dened in case law and regulations,
applies to all uses and all routes of
exposure to a pesticide (food, air, and
water considered together). “Reasonable
certainty of no harm” is protective of the
public health, particularly where the nding
is contingent on fetal and infant exposure,
but is not so protective that it cannot be
met, or that companies can argue that it is
onerous.
Section 408 also requires that pesticides
with common mechanisms of toxicity
be added together when assessing
compliance with the reasonable certainty
of no harm standard. This means that
groups of pesticides, for example, all
organophosphates, are added together
when measuring compliance. In contrast,
TSCA does not require that regulators
assess the additive risks. Many major
chemical classes commonly used in
consumer products are characterized
by common mechanisms of toxicity
- phthalates, peruorinated chemicals,
and polybrominated diphenyl ethers,
for example - and none are assessed in
aggregate by EPA.
When data are not available, legal
exposures for infants and children are
required to be 10 times lower than for
adults, and economic benets are not
allowed as an escape valve, or a means to
permit higher risk.
To ensure that these tough standards
can be met, the other governing statute,
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chemical might be toxic to humans.
In 1998 EPA found that chemical manufacturers had failed to
volunteer even the most basic information on chemical properties
or toxicity for an estimated 43 percent of the 2800 chemicals
produced in the highest quantities in the U.S. (EPA 1998b). A
voluntary testing program grew out of this nding. Under this
program, called the High Production Volume chemical testing
program, or HPV program, participating companies submit their
interpretation (but not the data) of eighteen basic screening
tests, only one-third of which are directly relevant to human
health and none of which include even a standard two-year
cancer study, or tests for birth defects linked to low doses.
The group that leads the federal government’s efforts to assess
testing needs on the health effects of industrial chemicals,
the Interagency Testing Committee, or ITC, recently identied
through the use of computer models 392 industrial chemicals
expected to build up in the human body for which EPA lacks basic
data from the manufacturers on chemical properties, uses, and
toxicity. Among these are chemicals used in fragrances, dyes and
pigments, polyurethane foam, and pesticides. There is no plan to
study the presence of these chemicals in humans.
In effect, the nation has no regulatory system for chemicals that
are not directly added to food (pesticides and food additives).
Instead we have a shell of a program that by law has weak
authority to study, much less restrict, the use of chemicals in
commerce.
This statutory void has produced:
Widespread, pervasive contamination of the human
population with hundreds of chemicals at low dose
mixtures that have never been examined for any of their
potential health effects.
An industry that has no legal obligation to conduct safety
tests or monitor for the presence of its chemicals in the
environment or the human population – and a signicant
nancial incentive not to do so.
A federal research establishment that is completely
unequipped, both technically and nancially, to monitor
the human population for commercial chemicals or to
study their health effects.
FIFRA (the Federal Insecticide Fungicide
and Rodenticide Act), grants the EPA
administrator broad (virtually unlimited)
authority to request data, and to suspend
the sale of the product when data are not
generated (section 3, particular 3(c)2(B),
and section 6). This is the key reform.
The legislative history of FIFRA is
instructive. Beginning in the early 1980’s
a series of congressional committee
investigations and GAO reports documented
that basic health studies had not been
conducted for most pesticides on the
market at that time. In response, Congress
amended FIFRA in 1988 to require that all
pesticides be “reregistered,” which meant
that they had to be tested by contemporary
standards and re-evaluated for their health
risks.
This forced the EPA to deal with the
same problem that they face today when
considering a comprehensive testing
program for toxic chemicals: what to do
with all the chemicals already on the
market?
EPA’s response, which largely was
successful, albeit slow, was to impose strict
timelines for testing and reevaluation while
granting EPA clear authority to require any
test for any pesticide, and the authority
to suspend the sale of a pesticide if the
manufacturer refuses to do the test or
fails to submit it on time. Compare this
with TSCA where EPA must go through a
rulemaking just to get one test on one
chemical.
As a result of these amendments, EPA
now requires about 120 tests for pesticide
registration. These tests range from acute
and chronic toxicity, to metabolism,
environmental fate and residue chemistry.
These tests include toxicity tests that
will support regulatory decision making,
not the supercial screening tests being
conducted under the HPV testing program.
EPA has re-evaluated nearly all pesticides
of any signicance, starting in the early
1990’s with more than 100 pesticide active
ingredients in about 20,000 different
products applied to food crops. There is no
reason that these same test requirements
could not be applied in a tiered fashion
to commercial chemicals regulated under
TSCA.
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An ever increasing load of chemical contamination in
the human population and global environment that is
comprised almost entirely of poorly studied chemicals that
have never before been encountered in all of evolutionary
history.
In this study, a total of 167 chemicals, pollutants and pesticides
were found in the blood and urine of nine individuals in a series
of comprehensive tests. On average, analysts found 91 chemicals
per person, with a range of from 77 to 106 pollutants and
pesticides in the nine individuals studied.
The chemical industry and its supporters argue that 50 or more
carcinogens in an individual’s bloodstream is safe and accounts
for negligible increased cancer risk. The doses, they say, are too
low to cause harm.
But there is no science to support this assertion.
The truth is that nobody knows the effects of the low dose
mixtures of chemicals identied in this study, and the hundreds
of other chemicals that are certain to be present in the body, but
for which we could not test. Federal law imposes few health and
safety testing requirements on the chemical industry, and sets
few public health goals for chemical exposure or use.
Instead, industry decides what tests are done, when they are
done, what the results mean, and who gets to see them. Overall,
this system has left a void of scientic knowledge on the health
and environmental hazards of nearly all chemicals found in
consumer products and in people.
Safety margins erode further - new chemicals are invented
daily.
The chemical industry gains permission to put more than 2000
new chemicals into the biosphere each year, with no knowledge
of the health impact on the exposed human population. People
are given no warning of this exposure nor do they have the
option not to be exposed.
The predictable outcome of this arrangement is that the dangers
of chemicals are discovered only after widespread exposure
and harm has occurred. The more recently a chemical has been
introduced into commerce, the less scientists understand its
toxicity, and the less likely it is that scientists will know how
to test for it in people and the environment. New chemicals
TESTING REQUIREMENTS ALONE CAN
REMOVE DANGEROUS PRODUCTS FROM THE
ENVIRONMENT
By themselves, testing requirements
have driven many hazardous compounds
off the market. One good example is
methoxychlor, a DDT relative, which
was banned with little fanfare in 1999
when the manufacturer simply refused
to conduct required health studies.
Another good example is pesticides used
in aircraft cabins. In 1995 EPA asked all
manufacturers of pesticides applied inside
commercial airplanes to do the exposure
studies needed to show the use was safe.
Not a single manufacturer of more than
200 products was willing to do the tests
(because they knew that the use was not
safe), and all uses of pesticides inside
aircraft were unceremoniously banned in
the United States in 1998.
Another great example of the power of
FIFRA’s data generation authority involves
the toxic byproducts of chlorinating tap
water. The Safe Drinking Water Act does not
give the EPA authority to require toxicity
tests for drinking water contaminants. As
a result, the agency is forced to negotiate
test programs with polluters or the affected
industry, or to pay for the testing from
their own research funds. But because
chlorine is a pesticide (it kills microbes in
water), EPA was able to use the data call-in
authority of FIFRA to require the chlorine
industry to do a broad range of toxicity
tests on chlorination byproducts that they
otherwise had not planned to do.
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61
enter the marketplace with no, or only a handful of, toxicity
studies. The few chemicals or chemical families that have been
well-studied are those for which scientists uncovered, often
accidentally, catastrophes or widespread contamination (Figure
2). For instance, the earnest study of DDT toxicity did not start
until the discovery that the chemical was driving into extinction
a number of bird species, including bald eagles. Intense research
on the toxicity of peruorinated chemicals is beginning only now,
after 3M discovered that these Scotchgard ingredients, in use for
50 years, have broadly contaminated humans and are more toxic
than previously believed.
And even for the best-studied chemicals, scientists have yet to
gain a full understanding of health effects. When setting safety
standards for electrical insulators called PCBs, banned in the
U.S. since the 1970s, the World Health Organization reviewed
1,200 studies on PCB’s harmful effects and properties, but
found only 60 that were relevant. In a similar review of PCBs
the U.S. government enumerated 14 categories of uncertainty
encompassing every step from human exposure to manifestation
of health effects (EPA 1996). PCBs are among the best-studied
chemicals in the world.
Chemical companies are not required to develop or divulge
methods to test for the presence of their chemicals in the
environment or the human body. Typically, only after a
compound has been on the market for decades and contaminated
a signicant portion of the environment do independent
scientists learn how to detect and quantify it. At that point,
the Centers for Disease Control and Prevention (CDC) may
choose to test for it in the general population, but even then
there is no guarantee that the manufacturer will provide CDC
with the methodology to detect it, or that the methods will
be reliable. For instance, three years after 3M announced that
it was removing the principle peruorinated compound, PFOS
(Scotchgard), from the market, chiey because it contaminated
the blood stream of the entire human race, the CDC still does not
have a test method that it considers reliable to nd the chemical
in human blood.
Ignorance by Design
Detailed analyses by the U.S. EPA (EPA 1998b) and Environmental
Defense (ED 1998) make clear how few health effects studies are
available even for chemicals produced in the highest volumes. In
a review of all publicly available toxicity and environmental fate
studies, they found no information – not a single test - for 43
percent of the 2600 chemicals produced in the highest volumes in
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61
the US, with yearly production volumes of more than 1,000,000
pounds. Our study offers stark conrmation: for 55 compounds
found in the nine individuals tested (one third of the chemicals
identied), there is no information available - on chemical uses
or health effects - in any of the eight standard industry and
government references used for this analysis.
The work by the EPA and ED was important in establishing a
baseline measure of data availability. But the tallies in the EPA
and ED reports are only as meaningful as the studies they are
counting. Both analyses focus on a limited universe of toxicity
screens that themselves are not detailed enough to support
regulation, and are not targeted toward the most meaningful
and relevant health effects. But far worse than the numbers is
the policy outcome that these analyses produced: a voluntary
program for industry to conduct hundreds more of these same
toxicity screens.
Launched with much fanfare in 1999, the so-called high
production volume chemical screening, or HPV program, has not
yielded data for EPA to review. Instead chemical manufacturers
are submitting summaries of the screening studies, leaving EPA
and the public at the mercy of industry’s interpretations of the
data, which are not subject to independent peer review. The
program is voluntary, and the EPA is powerless to demand any
additional information. At the same time the HPV program
provides invaluable public relations cover for the chemical
manufacturers in the form of thousands of “studies” being
conducted “voluntarily” at “great expense.”
And even if the actual screening study data were submitted,
much of it would be of limited use. Consider the so-called cancer
screens. In reality, what industry calls a cancer screen for public
relations purposes under the HPV program, is nothing but a
mutagenicity assay in a lab dish that both industry and regulators
routinely dismiss as inconclusive in the absence of two-year
animal studies conrming a carcinogenic effect.
Scientists often study the wrong thing
The nature of our ignorance of chemical exposure is more
complicated than tallies of study numbers can convey. There
are fundamental problems with even the best regulatory study
methodologies when they are applied to the body burden of
chemicals identied in this study. The vast majority of toxicity
tests required by government regulators have limited relevance to
the exposures that are occurring in the human population.
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63
In a typical animal study required by the EPA, scientists test a
single chemical in adult animals at high doses. The outcomes
analyzed can include increases in the occurrence of tumors,
changes in organ weight, or visible birth defects. Scientist
don’t typically look for functional changes in response, such as
brain development, following developmental exposure. Required
developmental toxicity studies do not evaluate development
after birth and tend to be less sensitive than studies that do
assess postnatal function. A 1998 EPA draft report titled “A
Retrospective Analysis of Twelve Developmental Neurotoxicity
Studies Submitted to the USEPA Ofce of Prevention, Pesticides
and Toxic Substances (OPPTS)” found that the developmental
neurotoxicity study resulted in a lower “no observed effect level”
for 10 of 12 chemicals compared to the required developmental
rat studies that did not look at brain development (Makris, et
al. 1998). The developmental neurotoxicity test is not a required
test. EPA has requested it for only a small number of chemicals.
In contrast to high dose regulatory studies, people are exposed
to multiple chemicals, from conception to death, at relatively low
doses. The effects that occur can be subtle, detected across the
general population as slight drops in IQ or fertility, or increases
in specic types of cancer.
Some scientists, particularly those employed by the chemical
industry, argue that “the mere presence” of small amounts
of hundreds of chemicals in your bloodstream is biologically
insignicant. High dose animal studies are typically offered as
proof of this assertion. The truth, however, is that high dose
animal studies cannot prove or disprove the safety of chemical
exposures at lower doses, particularly when these studies are
conducted primarily on adult animals, do not look for health
endpoints relevant to low dose exposures, and do not account for
interactions with other chemicals to which people are routinely
exposed.
Industry’s dogmatic allegiance to the high dose theory of
toxicology can be traced to the 16th century philosopher
Paracelsus, whose philosophy is summarized in the well-known
adage “The dose makes the poison.” The scientic and regulatory
infrastructure in the US is based on studies that feed animals
high doses of chemicals in the belief that a high dose will elicit
any and all toxic effects that a compound can produce. In
practice, if a high dose doesn’t elicit a readily measured toxic
effect, then industry argues and regulators assume that the
substance is not toxic. We now know that this is not true.
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Science has advanced in the past 500 years, and outside of
regulatory toxicology it is generally accepted that other factors
besides dose, most notably the timing of the dose, are equally as
important factors in determining the toxic effect.
The most obvious example is fetal exposure, where exposure
in utero can produce long lasting adverse effects at amounts
that produce no observable effects in adults. This outcome is
documented in the scientic literature for lead, mercury and
PCBs, where exposures in the parts per billion range in the womb
or during infancy can lower IQ’s or alter behavior, while the
same dose produces no observable effects in an adult. Dioxin is
another case in point. Men with 80 parts per trillion of dioxin in
their blood father nearly twice as many girls as boys. This effect
would not have been predicted based on studies of adults.
Many of the compounds detected in this study have been studied
and found to cause adverse human effects at low doses. Other
chemicals detected in this study have not been tested at all.
Policy Recommendations
TSCA reform
Seven chemicals or chemical classes have been regulated or
banned under the Toxic Substances Control Act (TSCA). When
compared to the 75,000 chemicals registered for commercial
use, the impact of TSCA is nearly imperceptible in the overall
context of human chemical exposure. It is little wonder that the
chemical industry considers TSCA the only truly workable federal
environmental law.
Under TSCA, chemicals are assumed safe until they are proven
hazardous. At the same time, the law does not require that
manufacturers conduct health and safety studies, nor does it
impose a duty on manufacturers to monitor how their products
are used or where they end up in the environment.
As a starting point for a major environmental statute, this is
problematic.
TSCA puts the burden of proving a chemical’s hazards squarely
on the shoulders of the EPA (section 4 (1)(A)). The statute then
prohibits the EPA from requiring safety tests unless the agency
can prove that the chemical presents an unreasonable risk
– which it can almost never prove because it cannot require the
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65
studies needed to make that nding. If the agency assembles
enough data to require industry to conduct safety studies, it must
go through the lengthy process of promulgating a test rule, very
similar to a regulatory rule making, to mandate even one test for
one chemical. When the data are generated, industry can claim
the tests as condential business information or trade secrets,
and thus shield the tests from independent peer review or public
scrutiny.
This law is so fundamentally broken that the statute needs to be
rewritten. Revisions to the nation’s toxic substance laws must
include the following provisions:
For chemicals currently manufactured and used
commercially, the chemical industry must submit to EPA
all internal studies on the properties, environmental fate,
potential human exposure pathways and exposure levels,
concentrations in workers and the general population,
levels in the environment, worker and community health,
measured effects in wildlife, toxicity, mechanisms of
action and any other information relevant to human
exposures and potential health effects. These studies
must be made available to the public.
Industry must be required to prove the safety of a new
chemical before it is put on the market.
The EPA must have the unencumbered authority to request
any and all new data on a chemical that is already on the
market.
The EPA must have the clear authority to suspend a
chemical’s production and sale if the data requested are
not generated, or if they show that the chemical, as used,
is not safe for the most sensitive portion of the exposed
population.
Chemicals that persist in the environment or
bioaccumulate in the food chain must be banned.
Currently EPA cannot demand the data needed to make
this determination, and industry is not volunteering it.
Chemicals found in humans, in products to which children
might be exposed, in drinking water, food, or indoor air,
must be thoroughly tested for their health effects in low
dose, womb-to-tomb, multi-generational studies focused
on known target organs, that include sensitive endpoints
like organ function and cognitive development. Studies
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to dene mechanisms of action (how a chemical harms
the body) must be conducted.
The chemical industry must develop and make public
analytical methods to detect their chemicals in the
human body, and conduct biomonitoring studies
to nd the levels of their chemicals in the general
population.
Chemical manufacturers must fully disclose the
ingredients of their products to the public.
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... This report neglected a vast range of other chemicals which are known to contaminate humans, and about which evidence of harm is building. The Environmental Working Group (EWG), an independent group in the USA, found 167 chemicals in the blood and urine of nine adult Americans (Houlihan et al., 2003). None of these volunteers worked with chemicals as part of their jobs, and yet each of them contained an average of 91 of the The following sections review these POPs and their potential health effects. ...
... About 17% of children in the USA suffer from one of these disabilities. The number of children being treated for attention deficit disorder (ADD) and attention deficit hyperactivity disorder (ADHD) has increased dramatically in the last ten years (Houlihan et al., 2003; Shettler et al., 2000). The re p o rted incidence of autism is also increasing (Houlihan et al., 2003). ...
... The number of children being treated for attention deficit disorder (ADD) and attention deficit hyperactivity disorder (ADHD) has increased dramatically in the last ten years (Houlihan et al., 2003; Shettler et al., 2000). The re p o rted incidence of autism is also increasing (Houlihan et al., 2003). The causes are not known but chemical e x p o s u res are considered a potential contributor (Wo o d w a rd, 2001). ...
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In early 2003, Greenpeace exposed the presence of persistent, bioaccumulative chemical pollutants in samples of house dust taken from homes across the UK. Research published by Greenpeace in October 2003 reveals that these same chemicals can be found in many consumer products readily available on every high street.This report completes the loop of chemical exposure by illustrating two disturbing developments. Firstly, that many of the same chemicals used routinely in consumer products and present in house dust, are also present in the human body, including in prenatal and newborn children. Secondly, that these chemicals are likely to be having a detrimental effect on the health of children and the human population at large. Significantly, the report also draws together the available evidence that illustrates how and why prenatal and newly born children are particularly at risk from chemical pollutants. Preface: Dr Vyvyan Howard, Developmental Toxico-Pathologist, University of Liverpool
... The Environmental Working Group (EWG), an independent group in the USA, found 167 chemicals in the blood and urine of nine adult Americans (Houlihan et al., 2003). None of these volunteers worked with chemicals as part of their jobs, and yet each of them contained an average of 91 of the 210 chemicals tested for. ...
... About 17% of children in the USA suffer from one of these disabilities. The number of children being treated for attention deficit disorder (ADD) and attention deficit hyperactivity disorder (ADHD) has increased dramatically in the last ten years (Houlihan et al., 2003;Shettler et al., 2000). The re p o rted incidence of autism is also increasing (Houlihan et al., 2003 • S p e rm counts in many parts of the world a re decreasing by about 1% per year in industrialised countries. ...
... The number of children being treated for attention deficit disorder (ADD) and attention deficit hyperactivity disorder (ADHD) has increased dramatically in the last ten years (Houlihan et al., 2003;Shettler et al., 2000). The re p o rted incidence of autism is also increasing (Houlihan et al., 2003 • S p e rm counts in many parts of the world a re decreasing by about 1% per year in industrialised countries. There are significant regional diff e rences in sperm counts that cannot be explained by genetic factors (Swan et al., 2000). ...
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En 2003 Greenpeace demostró la presencia de contaminantes químicos persistentes y bioacumulativos en muestras de polvo recogidas en hogares europeos. Otras investigaciones de Greenpeace revelaron que se pueden encontrar estas mismas sustancias en muchos productos de consumo cotidiano. Este informe cierra el ciclo presentando dos realidades inquietantes. La primera que muchas de las sustancias químicas encontradas en productos de consumo y en el polvo doméstico también están en el cuerpo humano, incluyendo a los nonatos y a los recién nacidos. La segunda que es probable que estos productos químicos tengan un efecto perjudicial en la salud humana, particularmente en la infantil. El informe Legado Químico, de la Dra Catherine N Dorey, aúna las pruebas que ilustran cómo y por qué la infancia corre un especial riesgo ante los contaminantes químicos. Las pruebas presentadas por académicos, gobiernos e instituciones internacionales, no son fáciles de desestimar, ya que todas hacen una contribución específica al creciente banco de investigación internacional que refuerza la conclusi ón de este informe: la actual legislación no protege a la infancia del «ataque» químico que comienza desde el mismo momento de la concepci ón. El estudio se centra en siete productos químicos clave: los alquilfenoles, el bisfenol A, los pirorretardantes bromados, los compuestos organoestánnicos, los ftalatos, las parafinas cloradas y los almizcles sintéticos; y demuestra la presencia de estas sustancias en los niños y niñas, el incremento de exposición de este grupo y el consecuente aumento de los posibles impactos en la salud, qué enfermedades están relacionadas con la exposición química y los impactos especí- ficos sobre la salud de los siete productos analizados.
... The growing medical and personal needs of the human population have escalated the release of pharmaceutical and personal care products (PPCPs) into the natural environment. [1][2][3] This has raised major concerns related to the environment and human health. Limited research has been conducted to determine the occurrence and direct health risks of primary PPCP compounds, yet, environmental degradation, transformation, and the fate of PPCPs are poorly understood. ...
... 6 A comparison of ibuprofen and clofibric acid decays, under various experimental conditions, is shown in Figure 1. Here, the degradation Fate, Transformation, and Toxicological Impacts of Pharmaceutical and Personal Care Products in Surface Waters 2 Environmental Health Insights was monitored using high-performance liquid chromatography analysis of the remaining primary compound. Under dark conditions, the decay of either ibuprofen or clofibric acid was minimal, with only ~10% loss of the initial concentration after 250 hours. ...
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With the growth of the human population, a greater quantity of pharmaceutical and personal care products (PPCPs) have been released into the environment. Although research has addressed the levels and the impact of PPCPs in the environment, the fate of these compounds in surface waters is neither well known nor characterized. In the environment, PPCPs can undergo various transformations that are critically dependent on environmental factors such as solar radiation and the presence of soil particles. Given that the degradation products of PPCPs are poorly characterized, these “secondary residues” can be a significant environmental health hazard due to their drastically different toxicologic effects when compared with the parent compounds. To better understand the fate of PPCPs, we studied the degradation of selected PPCPs, including ibuprofen and clofibric acid, in aqueous solutions that contained kaolinite clay and were irradiated with a solar simulator. The most abundant degradation products were identified and assessed for their toxicologic impact on selected microorganisms. The degraded mixtures showed lower toxicity than the starting compounds; however, as these degradation products are capable of further transformation and interaction with other PPCPs in natural waters, our work highlights the importance of additionally characterizing the PPCP degradation products.
... Sinai School of Medicine, and Commonweal [18]) researchers discovered 167 pollutants (out of the 211 tested) in the blood and urine of nine volunteers, with an average of 56 carcinogens in each person. Aggregate study results appeared in Public Health Reports [19], but study participants voluntarily placed their individual data on the internet, with photos and personal biographies to accompany the contaminant data [18]. Voluntary though it was, the website would not have sat well with most IRBs, who would perceive that as a violation of confidentiality. ...
... For example, in the "Body Burden" study (a joint project of Environmental Working Group, Mt. Sinai School of Medicine, and Commonweal [18]) researchers discovered 167 pollutants (out of the 211 tested) in the blood and urine of nine volunteers, with an average of 56 carcinogens in each person. Aggregate study results appeared in Public Health Reports [19], but study participants voluntarily placed their individual data on the internet, with photos and personal biographies to accompany the contaminant data [18]. ...
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We report on the challenges of obtaining Institutional Review Board (IRB) coverage for a community-based participatory research (CBPR) environmental justice project, which involved reporting biomonitoring and household exposure results to participants, and included lay participation in research. We draw on our experiences guiding a multi-partner CBPR project through university and state Institutional Review Board reviews, and other CBPR colleagues' written accounts and conference presentations and discussions. We also interviewed academics involved in CBPR to learn of their challenges with Institutional Review Boards. We found that Institutional Review Boards are generally unfamiliar with CBPR, reluctant to oversee community partners, and resistant to ongoing researcher-participant interaction. Institutional Review Boards sometimes unintentionally violate the very principles of beneficence and justice which they are supposed to uphold. For example, some Institutional Review Boards refuse to allow report-back of individual data to participants, which contradicts the CBPR principles that guide a growing number of projects. This causes significant delays and may divert research and dissemination efforts. Our extensive education of our university Institutional Review Board convinced them to provide human subjects protection coverage for two community-based organizations in our partnership. IRBs and funders should develop clear, routine review guidelines that respect the unique qualities of CBPR, while researchers and community partners can educate IRB staff and board members about the objectives, ethical frameworks, and research methods of CBPR. These strategies can better protect research participants from the harm of unnecessary delays and exclusion from the research process, while facilitating the ethical communication of study results to participants and communities.
... In addition to citizen science projects, advocacy biomonitoring involves measuring people's exposures with the purpose of developing knowledge to be used for activism and public outreach (Morello-Frosch et al. 2009). Pioneered by the Environmental Working Group's "Body Burden" study of 10 individuals (Houlihan et al. 2003), advocacy biomonitoring involves laypeople, working through activist organizations to produce important environmental health science. These projects are often initiated by non-scientists, who contract outside laboratories to conduct the chemical analyses. ...
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This book examines the relationship between environmental justice and citizen science, focusing on enduring issues and new challenges in a post-truth age. Debates over science, facts, and values have always been pivotal within environmental justice struggles. For decades, environmental justice activists have campaigned against the misuses of science, while at the same time engaging in community-led citizen science. However, post-truth politics has threatened science itself. This book makes the case for the importance of science, knowledge, and data that are produced by and for ordinary people living with environmental risks and hazards. The international, interdisciplinary contributions range from grassroots environmental justice struggles in American hog country and contaminated indigenous communities, to local environmental controversies in Spain and China, to questions about “knowledge justice,” citizenship, participation, and data in citizen science surrounding toxicity. The book features inspiring studies of community-based participatory environmental health and justice research; different ways of sensing, witnessing, and interpreting environmental injustice; political strategies for seeking environmental justice; and ways of expanding the concepts and forms of engagement of citizen science around the world. While the book will be of critical interest to specialists in social and environmental sciences, it will also be accessible to graduate and postgraduate audiences. More broadly, the book will appeal to members of the public interested in social justice issues, as well as community members who are thinking about participating in citizen science and activism. Toxic Truths includes distinguished contributing authors in the field of environmental justice, alongside cutting-edge research from emerging scholars and community activists.
... We see Commoner speaking about the endocrine-disrupting effects of substances like dioxin, but it never becomes clear just what role he had in the mobilization to document and publicize these effects and force the hand of government agencies inclined to study rather than regulate them (see Krimsky, 2000). We see Commoner focusing on industrial pollutants' infiltration into the human body (a theme he had pursued since the days of atmospheric nuclear testing), but whatever role he might have had in the blossoming of movement concern about "body burden" in the 1990s and early 2000s (e.g., Houlihan et al. 2003) remains fuzzy. We see Commoner arguing extensively that the poor and racial minorities are disproportionately exposed to industrial contamination (a theme for him since the 1960s), and applauding the emergence of the environmental justice movement, but his relationship with that movement in the 1980s and 1990s is never sharply defined. ...
... Scientific findings and recent events have escalated public concern over pesticide residues on food, and food contamination generally. These include (1) findings that low doses of hormone-mimicking chemicals can have negative chronic impacts on the body's endocrine, immune, and neurological systems (Colborn, 1995;Porter et al., 1984;Porter et al., 1999;vom Saal et al., 1997), (2) reports on people's "body burden" of synthetic chemicals that demonstrate the importance of dietary exposure in causing widespread bodily pesticide contamination (Duncan, 2006;Houlihan et al., 2003;Schafer et al., 2004), and (3) food scares, including recent reports about the death of U.S. pets caused by melaminecontaminated pet food ingredients imported from China (Snyder, 2007;The Lancet, 2007) and consumer methamidophos poisonings in Japan blamed on Chinese dumplings (Channel News Asia, 2008). i A recent study of consumer confidence in food systems showed that while 85 and 88 percent of U.S. consumers perceived local and regional produce as somewhat or very safe, respectively, only 12 percent consider the global food system safe (Pirog and Larson, 2007, 3 p. ...
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