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This shocking piece was sent this morning by Red Flags Daily, the free
newsletter found at http://www.redflagsdaily.com
with a link to the Environmental Working Group memo found at:
http://www.ewg.org/policymemo/20021113/20030328.php
According the EPA data these chemicals do NOT break down, and will be
in our bodies and in the environment "indefinitely." Most of the
public is still not aware that synthetic chemicals are still not
required to be properly tested for human health effects and
persistence prior to marketing. It often takes decades for scientific
information to become available. Those who are informed feel we are
guinea pigs for the chemical/pharmaceutical industry. A. Hotz
___________________________________________________
EPA Issues Powerful Indictment Of Chemical in Teflon

Government Scientists Find Blood of U.S. Population Is Contaminated At
Levels That Could Cause Harm
EWG Concludes That Health Risks Are Even Higher Than Agency Believes

Summary

A draft risk assessment from the U.S. EPA has concluded that PFOA, a
critical component of Teflon production, and a chemical found in
scores of consumer products from clothes to stain repellents, food
packaging and cosmetics, presents unacceptably high developmental and
reproductive risks to humans. Based on powerful results from animal
reproduction studies, and a comparison of blood levels in the affected
animals with blood levels in people, EPA scientists conclude that
children with the highest measured blood levels of PFOA have less than
one tenth the protection, or less than one tenth the margin of safety,
than the level the agency considers to be safe. In EPA parlance, the
"margin of exposure" for these children is just 7, when it should
normally be 100 (EPA pg 51).

EWG's preliminary review of the EPA risk assessment and other studies
conducted by industry indicates that some children already have blood
levels of PFOA at or above the levels that cause serious toxicity in
laboratory studies.

Both EPA's and EWG's analyses conclude that current PFOA exposures in
children are well above safe levels.

The EPA risk assessment is the result of an internal priority review
of PFOA prompted by "unexpected toxicological and bioaccumulation
discoveries"(EPA pg 5) with respect to the entire family of
perfluorinated chemicals, particularly PFOS (perfluorooctane
sulfonates), the active ingredient in Scotchgard, which was forced off
the market by EPA in 2000. PFOS has many similar chemical and toxic
properties to PFOA. Neither compound breaks down in the environment,
both kill young rats at doses that have no effects on the others
(dams), and both cause a variety of cancers and other toxic effects.

According to EPA scientists, PFOA causes "significant increases in
treatment related deaths" (EPA pg 35) in offspring at doses that did
not affect the mothers, and a range of serious changes in the weight
of various organs, including the brain (decrease), prostate
(decrease), liver (increase), thymus (decrease), and kidneys (increase
in lower dose groups, decrease in high dose group) (EPA pg 36). The
deaths of a significant number of rat pups within 2 to 4 days after
weaning in experiments in which the mother was exposed is highly
unusual, and raises grave concerns about the toxicity of PFOA to
people.

There is also evidence of birth defects in humans from PFOA-exposed
workers. Although the draft risk assessment says that "reproductive
outcomes have not been examined" in people, in 1981 DuPont monitored
the pregnancies of seven women employed at its Teflon plant in
Parkersburg, West Virginia. According to an internal DuPont document
made public through litigation, two of these seven women gave birth to
babies with birth defects - one an "unconfirmed" eye and tear duct
defect, and one a nostril and eye defect. That same year, DuPont
reassigned 50 women at the plant to reduce PFOA exposure.

PFOA also causes tumors in at least 4 different organs in animal
tests, and has been associated with statistically significant
increases in prostate cancer death and seeking medical care for
prostate cancer in PFOA plant workers in two separate studies (EPA pg
17-23). Animal data strongly support the evidence that PFOA causes
prostate damage, but the EPA has yet to evaluate those risks.

Concerns about the hazards of PFOA are heightened by the widespread
exposure and near-universal contamination of the human population with
the chemical at levels similar to those that cause organ weight
changes and other indicators of toxicity in laboratory animals. PFOA
is present in the blood of more than 90 percent of the population of
the United States, and levels in some people in the general population
are as high as levels found in some PFOA factory workers. According to
the EPA document, DuPont and other manufacturers do not know the
primary sources of these exposures, or why some exposures in the
general population are so high. The EPA concludes: "It is not known
what the environmental concentrations of APFO (PFOA) are or the
pathways of human exposure to the general population."

Two factors, however, help to explain the situation. First, PFOA is
infinitely persistent in the environment. It never breaks down, as
opposed to other long- lived pollutants like PCBs and DDT, which have
half lives measured in decades. In addition, other major classes of
chemicals, in particular a group known as the telomer alchohols, break
down into PFOA. This means that if PFOA itself were banned today, the
levels in the global environment, wildlife and people could
substantially increase, probably for decades. The total amount of PFOA
generated by DuPont and other companies will remain in the
environment, and will circulate through the biosphere and through the
blood of the human race, indefinitely.

This brewing crisis represents a stunning breakdown of the regulatory
system for toxic chemicals. PFOA and related chemicals have been
widely used in consumer products for a half century, but it was not
until the past several years that scientists at the EPA had any data
that indicated these levels of risk. Why? Because industry is not
required to conduct health and safety tests on industrial chemicals
like PFOA and PFOS as a condition of their sale and use, no matter how
widely those chemicals are utilized in industrial or consumer
products. This absence of real regulatory authority over the chemical
industry means that EPA's authority is largely limited to requests for
data from chemical manufacturers after contamination presents a
crisis, as is the case with PFOA.

Specifics
Reproductive toxicity

EWG concurs with the EPA that PFOA causes serious reproductive effects
at doses that raise significant concerns about human risks, given
known blood levels of PFOA in the human population. In several places
in the draft document, however, we disagree with the EPA's assumptions
that appear to disregard significant animal test results and data.
Based on our review of EPA's hazard and risk assessments on PFOA, we
conclude that the compound is toxic at lower levels than EPA has
found, and thus poses a greater risk to humans than the agency has
estimated.

EPA proposes a "no effects" level at a dose where statistically
significant damage in test animals was reported. The risk assessment
calls a PFOA dose of 10 milligrams per kilogram of body weight per day
(10 mg/kg/d) a "no effects" level, termed the NOAEL (No Observed
Adverse Effects Level). Yet at lower doses, scientists have found
increases in death among the newborn pups of treated dams (female
rats): "The numbers of [rat] pups found dead or presumed cannibalized
were significantly increased in the 3 and 10 mg/kg/day [dose levels]
on day 1 of lactation" (EPA 2002). EPA chose not to consider the 3
mg/kg results an adverse effect because a clear dose-related trend was
not observed in the data. But given the severity of the effect and the
consistency of the effect with other studies (of PFOA and related
PFCs) that found deaths in young animals, we believe a more
conservative interpretation of this finding is both warranted and
consistent with past agency practice.

Organ weights and body weights were also significantly altered at
levels below the dose that the EPA concludes causes "no effects." PFOA
damaged the pituitary at all doses in female offspring, beginning at 3
mg/kg/d (the EPA "no effect" dose is 10 mg/kg/d): "the absolute weight
of the pituitary and the ratios of the pituitary weight to the
terminal body weight and to the brain weight were significantly (p
less than or equal to 0.05 or 0.01) decreased in the 3 mg/kg/d and
higher dosage groups, as compared to the control group values" (EPA
2002).

Commonly referred to as the master gland of the body, the pituitary
secretes hormones that regulate growth, reproduction, and many
metabolic processes. Change in pituitary size is a gross measure of
toxicity. In the study cited by the agency, 3M did not measure
pituitary function, such as levels of hormones released from the
pituitary. EPA did not consider weight changes in the pituitary an
adverse effect because, again, a clear dose-related trend in the data
was not found. Given the importance of the pituitary in sustaining
growth and life, EPA's interpretation of this finding could
significantly underestimate PFOA's toxicity and undermine public
health.

PFOA also impaired overall growth in test animals at one tenth the
supposed "no effect" dose: "Body weight gains in the 1 mg/kg/day
dosage group were significantly reduced on precohabitation days 1 to 8
and 8 to 15 and in the 10 mg/kg/day dosage group were significantly
reduced on DPs 8 to 15. Body weights in the 1 mg/kg/day dosage group
were also significantly reduced on DPs 8, 15, 22, 29." Reduction in
body weight gain is often considered an adverse effect by
toxicologists, because it is a measure of toxicity linked to many
other long-term outcomes.

Cancer

In the draft risk assessment, EPA reasons that human cancer risk from
PFOA exposures cannot be assessed due to scientific uncertainty about
the relevance of the rodent data to humans. EPA argues that "the
relevance of this mode of action [called peroxisome proliferation] for
humans is currently under scientific debate, and the Agency is engaged
in activities to resolve this issue. The risk assessment of PFOA and
its salts will be extended to include the cancer data once there is
resolution of this issue. Therefore, at this time, OPPT has narrowly
restricted the analysis to examine only the potential risks of
developmental toxicity." However, EWG believes that EPA's concern is
irrelevant to the majority of tumors found in PFOA-exposed animals in
laboratory studies.

Three of the four kinds of tumors linked to PFOA are not associated
with peroxisome proliferation and the debate surrounding it: mammary
gland, testes, and pancreas (Biegel et al. 2001; Sibinski 1987; U.S.
EPA 2002, p.6). Of the tumors scientists have found in animal studies,
only liver tumors are linked to peroxisome proliferation. Even DuPont
concedes that for testicular and pancreatic tumors, "the mechanism of
tumorigenesis is not completely understood, and therefore the
relevance to humans can not be completely ruled out" (DuPont 1997,
p.25). In an earlier assessment, EPA did not find that peroxisome
proliferation is responsible for all the tumor types induced by PFOA
(U.S. EPA 2002, p. 75-78).

More importantly, there is evidence of similar cancers among
PFOA-exposed workers. 3M and DuPont have reported increased rates of
death from, or medical care for, testicular, prostate, and pancreatic
cancers (Gilliland and Mandel 1998; Alexander 2001; Olson et al.
2001). These studies have involved so few people, however, that a
single incidence of cancer can change study results from a finding of
"no increase" to "statistically significant increase." Notably, the
increases found in these studies were not based on a single case, but
on 6 cases in a population where one case represents a significant
increase. Other design flaws in these studies, for example, estimating
exposures based on job history instead of PFOA blood levels, diminish
the chance of finding relationships between PFOA and cancer. Still,
cancer relationships are found, and the consistency of cancers among
workers and in laboratory studies is striking. We believe EPA's final
risk assessment for PFOA should reflect the apparent risk of all
cancers found in laboratory studies, not just the liver tumors related
to peroxisome proliferation.



References
Alexander, B (2001). Mortality study of workers employed at the 3M
Cottage Grove facility. Final Report. Division of Environmental and
Occupational Health, School of Public Health, University of Minnesota,
April 26, 2001, Reviewed in U.S. EPA Administrative Record AR226-1137
(page 143-146; PDF page 40-43).
Biegel, L. B., M. E. Hurtt, S. R. Frame, J. C. O'Connor, and J. C.
Cook. 2001. Mechanisms of extrahepatic tumor induction by peroxisome
proliferators in male CD rats. Toxicol Sci 60 (1):44-55.
DuPont. 1997. Hazard characterization for human health C8 exposure CAS
registry no. 3825-26-1, Prepared by L.B. Biegel, Senior Research
Toxicologist.
Gilliland, FD and Mandel, JS. 1993. Mortality among employees of a
perfluorooctanoic acid production plant. J Occup Med 35(9): 950-4.
Olsen, GW., Burlew, MM., Hocking, BB., Skratt, JC., Burris, JM and
Mandel, JH. 2001. An epidemiologic analysis of episodes of care of 3M
Decatur chemical and film plant employees, 1993-1998. Reviewed in US
Environmental Protection Agency Administrative Record AR226-1137
(pages 156-159; PDF page 53-56).
Sibinski, L. J. 1987. Two-Year oral (diet) toxicity/carcinogenicity
study of fluorochemical FC-143 in rats. Report prepared for 3M, St.
Paul, Minnesota by Riker Laboratories Inc. Study No. 0281CR0012.
Reviewed by the US EPA in "Draft Hazard Assessment of
Perfluorooctanoic Acid (PFOA) and its Salts" (AR226-1079; p. 52-53).
Also reviewed in "A Hazard Narrative for Perfluorooctanoate (PFOA)"
prepared by Environ International Corporation January, 2002 (p. 8-9).
US Environmental Protection Agency (US EPA). 2002. Revised draft
hazard assessment of PFOA and its salts. AR226-1136.
York, RG (2002). Oral (gavage) two-generation (one litter per
generation) reproduction study of ammonium perfluorooctanoate (APFO)
in rats. Report prepared for 3M, St. Paul, MN by Argus Research
(Horsham, PA). Sponsor's Study No. T-6889.6. Reviewed in US EPA
AR226-1092.

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