PART THREE

Mary OBrien HWN #337

Land managers and users need to focus on cumulative effects and the interdependence of
various elements of the ecosystem. Cumulative effects are often impossible to quantify, and risk
assessors get nervous when they can't reduce decisions to numbers. Yet, effects are cumulative.

Business and government presently rely on the "prove harm" method of pollution control to justify
practices that damage ecosystems, wildlife and people. Using this approach, harmful practices
are allowed to continue until a cause-and-effect relationship has been demonstrated to a
scientific certainty, which may take 50 years or longer. Three key assumptions
underlie this old approach:

Assumption #1: Humans can "manage" the environment by deciding how much damage the Earth
(or any portion of the Earth) can safely absorb without harm. Scientists call this the Earth's
"assimilative capacity." According to the approach, scientists can reliably decide how much of any
harmful practice the Earth, or any portion of the Earth (such as the Mississippi River, or
Chesapeake Bay, or an eagle, or a human), can safely assimilate or absorb without causing
harm. (This is what every risk assessment claims to do.)

Assumption #2: Once a system's "assimilative capacity" has been decided, then we can and will
see to it that no greater damage is permitted. We will set limits, river by river, factory by factory,
technology by technology, chemical by chemical, everywhere on the planet, so that the total,
cumulative damage does not exceed the 'assimilative capacity" of the Earth.

Assumption #3: We already know which practices (and which substances) are harmful and which
are not; or, in the case of practices 9and substances) that we never suspected are harmful, we
will be warned of their possible dangers by traumatic, but sub-lethal shocks that alert us to the
danger before it is too late.

Recent history shows us that all three assumptions are dead wrong. To cite but one example:
scientists hired by the Ethyl Corporation and by Dupont and General Motors argued for several
decades that there is a "safe" amount of lead, an amount that humans could "assimilate". We
know now--50 years too late--those scientists were wrong. As a result, nearly all Americans,
especially children, have had their intellectual capacity diminished by low-level lead poisoning,
and we are faced with a mammoth, phenomenally expensive job cleaning lead out of our homes,
and out of many surface soils of the U.S.

As a result of the 'prove harm' approach, ecosystems are being damaged everywhere on Earth,
in ways we only dimly understand. For example, measuring "productivity" by fish harvesters, the
Chesapeake Bay has lost 90% of its productivity during the last 100 years. The causes are
poorly understood, but the devastation is unmistakable. Harm to humans is also increasing: for
example, in the U.S. we are seeing steady increases in many cancers, asthma, infertility,
attention-deficit disorder, ectopic (tubal) pregnancies, gross birth defects, and so on.

Government and polluters can use risk assessment to dump quantities of toxic chemicals on

Risk assessments permit legalized killing and maiming

Instead of reducing actual pollution, mathematical models and other tricks of the risk assessors
are being used to "prove" that we are decreasing risks even as we are increasing
harmful practices.

The precautionary principle should be applied. Whenever it is acknowledged that a practice (or
substance) could cause harm, even without conclusive scientific proof that it has caused harm or
does harm, the practice (or substance) should be prevented or eliminated. Americans should be
willing, they say to trade a few thousand lives so that they can sell biosolids

The Delaney Clause is the only zero carcinogen standard in the U.S.  pressure to replace
Delaney with a  1 in a million risk standard.

Risk assessments are only as good as the knowledge that goes into them, and scientific
knowledge of the effects of pesticides in our food will always be incomplete. A risk assessment
based policy plays Russian roulette with many human lives. Each year we learn that last year's
knowledge was flawed. Pesticides that seemed "safe" last year are recognized as unsafe this
year. Delaney is based on the sensible maxim, "Better safe than sorry."

Rather than get rid of the Delaney clause, we should consider adding new clauses that prohibit
not only carcinogens in our food, but also chemicals that interfere with the immune, reproductive,
endocrine, and nervous system, extending the reach of Delaney's "zero carcinogens" policy.

Americans have been led to believe that pesticide residues on food are the exception rather than
the rule. The truth is quite different: if you eat in this country, you eat pesticides. Of special
concern is the diet of infants and children. infants and children are routinely exposed to
combinations of 2 or 3  (in rare cases as many as 8) pesticides on each food they consume.

A report in June of 1993 from the Environmental Working Group (EWG) in Washington, D.C.
analyzed pesticides in the diets of children, based on pesticide data from two different sources:
14, 595 samples taken by the U.S FDA, plus 4,500 samples taken by a private testing laboratory
hired by supermarkets.

Analyses of 4,500 samples of fruits and vegetables taken from supermarket warehouses from
1990 through 1992 found 2 or more pesticides on 62 % of orange samples, 444 % of apple
samples, and from one-quarter to one-third of cherry, peach, strawberries, celery, pear and
grape samples.

Analyses of 14, 595 samples of the same crops from the FDA for the period of 199001992
confirmed the findings of multiple pesticides on typical foods. In addition, the FDA data revealed
108 different pesticides on 22 fruits and vegetables: 42 different pesticides were detected on
tomatoes, 38 different pesticides were detected on strawberries, and 34 different pesticides were
detected on apples. (p. 1)

HWN #356 1993

The plain truth is that American children are continuously exposed to a complex, low-level mixture
of pesticides in food. The health effects of these exposures are known and are
not being investigated.

The Environmental Working Group's report in June revealed that, when cancer risks from just 8
pestices on 20 fruits and vegetables are added together, the average child exceeds the EPA
lifetime one-in-a-million risk standard by his or her first birthday.

In addition to pesticides in food, millions of American children are also exposed to pesticides in
their drinking water. By the time the average midwestern child is old enough to walk he or she
may surpass EPA's lifetime acceptable cancer risk (one in a million) from pesticides in drinking
water if the water is drawn from a surface water source. By age 6 these same children may have
accumulated more than 10 times the EPA's lifetime "acceptable" cancer risk, which is
one-in-a-million. (pp. 49-50)

Risk assessors assume that infants, children and adults all respond identically to identical
chemical exposures. No consideration is given to special sensitivities of infants or

We know that children may be more sensitive than adults to pesticide exposures because
scientific studies have shown that children are more sensitive than adults to many chemical
compounds, such as aspirin; hexachlorobenzene; hexachlorophene; lead; mercury; nitrate;
phenobarbital; tetracycline; and tobacco smoke (p. 7) Children are known to be more sensitive
than adults to radiation. It is only reasonable to assume that children will be more sensitive
than adults to some pesticides.

Furthermore, no consideration is given to the fact that diseases that develop slowly, such as
cancers, will have longer to develop in exposed children than in exposed adults.

Children ages one through 5 eat 3 to 4 times more food per unit of body weight than the average
American. For example, the average American eats 15 grams (about half an ounce) of food for
each kilogram (2.2 pounds) of body weight each day; but a one-year old eats 45 grams of food
per  kilogram of body weight  each day (p11).

In addition, children eat foods that are different from the food eaten by average Americans.
One-year-olds eat 69 foods at greater than twice the national average (per unit of body weight)
and consume 24 foods at greater than 5 times the national average (p. 13)

For example, infants less than one year old eat coconut oil at 39 times the national average;
apple juice at 15 times the national average; fresh pears at 12 times the national average; fresh
peaches at almost 9 times the national average; carrots at 8 times the national average; rice at 7
times the national average; milk at nearly 7 times the national average; fresh apples at 6 times
the national average (p.13)

These are average consumption rates. Naturally, some children will eat above-average amounts,
and thus will accumulate pesticide risks at above-average rates 9p 14)

The FDA under reports pesticide residues in the food supply: from 80 to 100 percent of residue
analyses at 5 of 12 FDA regional laboratories were not capable of finding 80% of pesticides used
in agriculture today (p 2)

The "inert" ingredients in pesticides may be toxic themselves, but in risk assessment they are
ignored. In 1991 EPA released a list of 1820 different chemicals used as "inert" ingredients.
Some popular  "inert" ingredients are xylene, toluene, vinyl chloride, ethly benezene, and
methylene chloride (p, 10) For 1450 of the 1820 chemicals listed (80 percent) EPA had no
toxicity information.

In sum, the present techniques for estimating the risk of pesticides--especially the risks to
children--are based on false assumptions and false or missing data. Risk assessment is a
technique that can be manipulated to reach any conclusion the risk assessor wishes to reach.

The Delaney clause is an existing law that forbids known cancer-causing chemicals in processed
foods, such as ketchup and soup. Under Mr. Clinton's new proposal, the zero carcinogen rule
would be replaced by a one-in-a-million' risk standard. In other words, under the administration's
proposal, cancer-causing pesticides would be allowed in processed foods (as well as raw foods)
and the amount that's allowed would be decided by using risk assessment.

According to the American Academy of Pediatrics, somewhere between 2 and 4 million American
children have sufficient lead in their blood to diminish their IQ, reduce their physical stature,
damage their hearing, decrease their hand-eye coordination and impair their ability to pay
attention in school. This damage is thought to be permanent. Lead is a soft, gray toxic metal that
has been mined from the earth and formed into useful items for 5000 years. Its toxicity to miners
and workers was well established among ancient Greeks and Romans long before the birth of

The Academy said flatly in 1993, "Childhood lead poisoning is preventable." Then why hasn't it
been prevented? It's a fair question.

For the last 30 years, instead of asking how to prevent lead poisoning, the medical community
has taken a risk assessment approach, asking, "How much lead is safe for industry to put into
children?" In 1960, the medical community answered the question by saying it was safe for a child
to have 60 micrograms of lead in each deciliter (10th of a liter) of blood (or 60 mcg/dL). That
answer turned out to be wrong, and in 1975 the medical community answered the question by
saying 30 mcg/dL was safe. That, too, turned out to be wrong, and in 1985 they set 25 mcg/dL as
the safe level. That, too, turned out to be wrong, and in 1991 the medical community said 10
mcg/dL was safe. And as we shall see, the National Research Council now believes that even this
"safe' level may not be safe.

But first let's review what happens to children with more than 10 mcg/dL lead in their blood. The
American Academy of Pediatrics recently reviewed 18 scientific studies showing that lead
diminishes a child's mental abilities. "The relationship between lead levels and IQ deficits was
found to be remarkably consistent," the Academy said. "A number of studies have found that for
every 10 mcg/dL increase in blood lead levels, there was a lowering of mean (average) IQ in
children by 4 to 7 points. This may not sound like a major loss, but an average IQ loss of 5 points
puts 50% more children into the IQ 80 category, which is borderline for normal intelligence. It also
reduces the number of high IQs; for example, one small group that should have contained 5
children with IQs of 125 contained none.

The American Academy of Pediatrics says such losses are permanent and they translate into
reduced educational attainment, diminished job prospects, and reduced earning power. Two
groups of children in first and second grade--one with 25 mcg/dL and the other with 35
mcg/dL--were studied into adulthood. The high-lead group was seven times as likely not to
graduate from high school and six times as likely to have reading scores two grades below
expected, after adjusting for a number of factors, including socioeconomic status and parental IQ.
The high-lead children also had higher absenteeism in their final year of school, lower class rank,
poorer vocabulary and grammatical reasoning scores, longer reaction times, and poorer
hand-eye coordination.

In addition to paint, house dust also contains lead tracked into homes from soil outside. Between
1920 and 1980, the oil and automobile companies aggressively defended and protected their
right to spew toxic lead into every neighborhood in America; they left a legacy of 30 million tons of
lead in soils before the nation came to its senses and put a muzzle on these industries.

But the damage was already done, and the poisoning now continues everywhere. A study in the
early 1980s showed that, among white children, 7 % in higher socioeconomic status areas and
25 % in poorer communities had blood lead levels greater than  15 mcg/dL. Among black children
in poor communities, this prevalence was 55%.

The lead problem was inevitable, given the decision to allow lead in paint, gasoline, and other
products. The National Research Council in its 1993 book on the lead problem, summarized the
situation starkly: "Once lead is mined and introduced into the environment, it persists. Over time,
lead in various forms becomes available to the body as small particles. Most of the 300 million
metric tons of lead ever produced remains in the environment largely in soil and dust. That
explains, in part, why background concentrations of lead in modern North Americans are higher
by a factor of 100 to 1000 than they were in pre-Columbia Americans. Today's production
evolves into tomorrow's background exposure, and despite reductions in the use of lead for
gasoline, overall lead production continues to grow and federal agencies have not addressed the
impact of future increases of lead in the environment.

In sum, if you mine lead out of the ground, it will eventually spread into the environment. It will get
into soil, then into food and water. Eventually it will get into humans (not to mention wildlife),
where it will take its toll on health. This is inevitable. The only way to avoid this outcome, is to stop
mining lead out of the deep earth. Zero discharge.

The National Research Council says modern humans are estimated to have total body burdens
of lead approximately 300-500 times those of our prehistoric ancestors..According to careful
measurements of human bones, pre-Columbian inhabitants of North America had average blood
lead levels of 0.016 mcg/dL some 625 times lower than the 10 mcg/dL now established as "safe"
for our children. On the face of it, it seems unlikely that levels of a potent nerve poison 625 times
natural background can be "safe" in children.

The National Research Council admits as much: There is growing evidence that even very small
exposures to lead can produce subtle effects in humans. Therefore, there is the possibility that
future guidelines may drop below 10 mcg/dL as the mechanisms of lead toxicity become better

Despite 80 years of research, the toxicity of lead in children is still not fully understood. According
to the Council, "Childhood lead poisoning involves injury in at least 3 organ systems: the central
nervous system (specifically, the brain), the kidney, and the blood-forming organs. Other systems
are also affected, but the nature of their toxic injury has not been as well characterized." p.32 In
other words, we know additional damage (beyond the 3 organ systems) is occurring, but we don't
understand it.

Furthermore, the Council says, "Once lead is absorbed from a specific source, it is added to a
body burden that contributes to various health effects. Therefore, exposures small enough to
have been viewed as of little importance are now taken more seriously. In other words, we must
consider the aggregate impact of multiple small lead sources in assessing health risk."p.99

At any step of a risk analysis, many assumptions are introduced by the analyst, and it must be
recognized that the numerical results are strongly dependent on these assumptions."

Dioxin is the most toxic chemical ever discovered and it is produced as a byproduct of several
different industrial processes. The Federal Agency for Toxic Substances and Disease Registry
(ATSDR) says 2,3,7,8-TCDD is highly toxic to all laboratory animals tested (p. 11). There have
been severe chronic effects on experimental animals from low dosages.

Cloracne is a systemic disease that is more disfiguring than teenage acne and its effects last for
years (in some cases decades) after exposure (pp. 3,39)

There is  "suggestive evidence" that 2,3,7,8,-TCDD causes liver damage in humans (pp. 3,
52-3). It definitely causes severe liver damage in animals.

In animals, 2,3,7,8,-TCDD is toxic to the immune system; such effects have not been proven in
humans (pp. 3, 40, 54-56)

In animals, 2,3,7,8-TCDD causes reproductive disorders, including spontaneous abortions.
Monkeys are particularly sensitive to reproductive effects from exposure of 2,3,7,8-TCDD. Such
effects have not been proven in humans (pp. 3, 27, 58-9). In animals, dioxin causes genetic
damage (pp. 60-1)

Scientists within EPA have asked that the dioxin question he reviewed again because some of the
key studies of dioxin and cancer were fraudulent and EPA had relied on these fraudulent
studies to set current standards. (HWN # 173, May 21, 1990)

Seveso, Italy

On July 10, 1976, an industrial disaster occurred at a chemical plant operated by the
pharmaceutical giant, Hoffman-La Roche, in the town of Meda, Italy . A visible chemical cloud
containing dioxin (2,3,7,8-TCDD and other dioxins) spread over several square miles of
populated countryside; most heavly hit was the community of Seveso. More than 200,000 people
aged 20 to 74 lived in towns near the accident. Nearly 31,000 people aged 20 to 74 lived in
zones contaminated to some degree by the accident and about 200 individuals had such high
exposures that they developed chloracne; an acute condition known to be caused by exposure
to dioxin.

A team of Italian physicians and researchers has been studying health conditions, including
death certificates, of 30,703 people aged 20 to 74 living in areas termed "exposed", comparing
peoples' experience there against a larger population of 167,391 individuals aged 20 to 74 living
nearby in non-exposed areas. A report in the American Journal of Epidemiology reveals several
elevated disease rates among the exposed group.

The report covers the decade 1976 to 1986, which is a short period in which to find caner
occurrences. All cancers exhibit a "latency period" ( a delay period) between the a time a
cancer-causing exposure occurs and a cancer actually develops; the latency period varies from  
7 to 40 or 50 years. Thus, a study of cancers occurring 10 years after an exposure to
cancer-causing chemicals could only reveal the earliest evidence of cancers and should be
understood to be preliminary in nature.

Zones A,B, and R Zone A is closest to the accident site. In Zone A, women had elevated cancers
of the gall bladder and biliary tract. They also had elevated occurrences of circulatory diseases
and of chronic rheumatic heart disease. Men in Zone A had elevated occurrences of
cerebrovascular disease (such as stroke).

Zone R extends several miles distant and Zone B is between the two.

Zone B. In Zone B, men had elevated melanomas (serious skin cancer) and cancers of the lining
of the chest cavity (pleura); women in Zone B had elevated incidence of soft tissue sarcomas.

Zone R. Men had elevated incidence of cancer of the lining of the chest cavity (pleura), and they
had increased incidence of all blood diseases, and of cererovascular disease; women had
increased incidence of cancer of the uterus, as well as hypertensive vascular disease.

During the second half of the decade, in Zone A there were no elevated cancer levels. In Zone B,
men showed elevated incidence of cancers of the lung, cancers of the lining of the chest cavity
(pleura), serious skin cancers (melanomas), Hodgkins disease. In Zone B, women showed
increased incidence of soft tissue sarcomas and of the thyroid gland. In Zone R, men showed
elevated incidence of leukemia, and women showed elevated incidence of cancer of the brain. It
is perhaps relevant to note that two previous studies have implicated brain cancer with exposure
to dioxins in weed killers.

A. Blair et al "Lung cancers and other causes of death among licensed pesticide applicators",
Journal of the National Cancer Institute, Vol. 71 (1983) pp. 31-7.

D. Coggon et al "Mortality of workers exposed to 2-methyl-4-chlorophenohyacetic acid"
Scandinavian Journal of Work, Environment and Health Vol. 12 (1986) pp. 448-454. Increased
incidence of soft tissue sarcomas (rare cancers of the connective tissues).

Seveso study confirmed that it is definitely misleading and untrue when anyone says there is "no
evidence" of cancer or other serious diseases among humans exposed to dioxins. HWN #
175, Apr. 4, 1990.

HWN Sept 2, 1993

A study in Epidemiology reveals that people exposed to dioxin during the Seveso explosion have
begun to exhibit excessive numbers of cancers. Pier Alberto Bertazzie et al "Cancer incidences in
a population accidentally exposed to 2,3,7,8,-TCDD (dioxin) Epidemiology , Vol. 4 Sept., 1993,
pp.  398-406.

The small A Zone was most heavily contaminated, but its 724 residents were evacuated, (Heavy
contamination means that each square yard of land contained 13 to 49 micrograms of dioxin; a
microgram is a millionth of a gram and there are 28 grams in an ounce). The B Zone was less
heavily contaminated but its 4824 residents were not evacuated; Zone B contained 43
micrograms of dioxin per square yard of soil, or less. The R Zone was even less contaminated (
average contamination being 4.3 microgams per square yard), so its 31, 647 residents were
probably exposed to low levels. Another 181, 579 people living beyond Zone R served as a
control group living in "uncontaminated" areas.

The greatest cancer increases has occurred in Zone B. In Zone A the numbers are small and no
significant cancer increases have occurred. In Zone R one kind of cancer has increased: soft
tissue sarcoma. Previous studies have linked dioxin exposure to soft tissue sarcoma in humans.

In Zone B, among women there has been an observable increase in cancers of the gall bladder
and biliary tract (the system that delivers bile from the liver to the small intestines) and in cancer
related to the blood-forming systems (multiple myeloma and myeloid leukemia.

Among men in Zone B, there were observable increases in cancers of the blood-forming system,
and in one kind of non-Hodgkins lymphoma (a cancer of the lymph system)

The EPA's draft document concludes that four separate studies of workers exposed to dioxin
have revealed an "overall increased mortality from all malignancies combined."

HWN #171 Mar. 7 1990

For years, industry scientists have been claiming there's no evidence that dioxins cause cancer
in humans. Now there is mounting evidence that such claims rely heavily on studies that are
fraudulent. Two companies recently accused of producing fraudulent dioxin-and-health data are
Monsanto and BASF.

A scientist with USEPA, says Monsanto falsified data in important studies that Monsanto used to
support the claim that dioxin does not cause cancer in humans. Dr. Cate Jenkins, a chemist in
EPA's Office of Solid Waste and Emergency Response, says EPA itself relied upon Monsanto's
fraudulent data in setting health standards for dioxin, and Jenkins has asked the EPA's Science
Advisory Board to reopen the matter of EPA's dioxin standards, to take a fresh look at
available data. Two important sources of dioxin in the environment are old chemical dumps and
the incineration of municipal solid wastes, which is why EPA is concerned about allowable levels
of human exposures to dioxin.

The British technical journal, New Scientist, says, "A new analysis by a West German
epidemiologist may have established the first clearcut evidence of a direct link between exposure
to dioxins and cancer in humans." Friedemann Rohleder, an independent specialist, has
produced a report detailing an unexpectedly high incidence of cancer among workers exposed to
dioxins during an industrial accident at a chemical plant in 1953.

"The plant, operated by the West German company BASF, made trichlorophenol. Rohleder claim
the company presented the data in a way that disguised the cancers", says New Scientist.

Each of these claims of fraud relates to an industrial accident in which workers were exposed to
dioxins; follow-up medical studies funded by the responsible companies have been published in
mainstream scientific journals, claiming to show that no excess cancers have occurred in the
dioxin-exposed workers. In fact, excess cancers have occurred, but it appears that the data have
been manipulated to hide the facts.

The Monsanto Case

In 1949, an explosion occurred at a Monsasnto chemical factory in Nitro, West Virginia; as a
result, many workers in the plant were exposed to the herbicide 2,4, 5-/t, which was contaminated
with dioxin. (This herbicide was later the principal component of Agent Orange, the chemical
defoliant used by the U.S. in Vietnam.) In subsequent years, two Monsanto scientists, J. A. Zack
and R. W. Gaffey, studied the exposed workers, comparing their health against the health of a
similar group of workers who were not exposed to dioxin or 2,4, 5-T.

According to court documents attached to the EPA memo, :"Zack and Gaffey deliberately and
knowingly omitted 5 deaths from the exposed group and took four workers who had been
exposed and put these workers in the unexposed group, serving, of course, to decrease the
death rate in the exposed group and increase the death rate in the unexposed group."
Other studies of this same accident were also fraudulent, according to the same court
documents, including a study by R.R. Suskind published in the Journal of the American Medical
Association. "This published study of the workers exposed in the 1949 accident reported only 14
cancers in the exposed group and 6 in the unexposed group (a smaller cohort). However, the
medical records produced {by Monsanto} to the Plaintiffs conclusively prove gross
miscalculations and omissions..there were 28 cancers in the group that had been exposed to
only 2 cancers in the unexposed group." Mr. Suskind published two other reports on the same
accident, using his same data, to reach the conclusion that dioxin does not cause cancer.

The BASF Case

On the night of November 17, 1953, a runaway chemical reaction spewed dioxin-contaminated
chemicals over workers and community residents of two small German cities, Mannheim and
Ludwigshafen. Subsequently, an epidemiology study was used to deny workers any
compensation for ailments they claimed they suffered as a result of exposure. In keeping with
German law, the workers retained their own expert to review the data. Their expert, Friedemann
Rohleder, received the data from the BASF company itself. He analyzed the data and found that
some workers suffering from chloracne, which is universally acknowledged to be evidence of high
exposure to dioxin, had been placed in the low-exposure  or non-exposed group. He found
evidence of "diluting" the exposed group with 20 plant supervisory staff, who Rohleder believes,
were not exposed. When Rohleder omitted the 20 supervisory staff, his analysis revealed
statistically significant increases in two groups of cancers: cancers of the respiratory organs
(lungs, trachea, etc.), and cancers of the digestive tract. "This analysis adds further evidence to
an association between dioxin exposure and human malignancy," Rohleder told New Scientist.

A new study of Vietnam veterans, conducted by Air Force physicians, links dioxin exposure to
increases in cancer, birth defects, psychological damage, liver damage, cardiovascular
deterioration, and degeneration of the endocrine system. The new work stops short of saying
dioxin exposures caused the observable health damage among dioxin-exposed vets, but it
explicitly reverses the conclusions of a 1984 Air Force study which said dioxin exposures had
been shown to be harmless.

The study is continuing, and will begin using sensitive new blood tests to determine past
exposures to dioxin; future study may be able to pin down, or rule out, direct causal effects. In the
meantime, advocates of mass burn incinerators and other dioxin-producing facilities can no
longer claim lack of evidence that dioxin harms humans.

The new work is part of the Air Force's ongoing study of Vietman veterans who participated in
Operation Ranch Hand, which was a military program spraying herbicides on the jungles of
Vietnam from 1961 to 1972, to defoliate and thus eradicate Viet Cong hiding places. In
manufacture, the herbicides (Agent Orange, Pink, Green and Purple) were contaminated with
dioxin (33 ppm to 66 ppm {parts per million}.

The study compares two groups of Vietnam veterans--one group of 1045 Ranch Hands who
definitely had dioxin exposures and another group of 773 veterans not known to have been
exposed to dioxin. In addition, 2708 wives and former wives of veterans in the two groups
participated in the study.

The study team first reviewed more than 400 published articles on the effects of dioxin on
animals and humans; from this they derived a profile of 190 different health effects that might be
expected to be related to dioxin exposure. They examined the 1818 study participants for these
190 health effects.


The study found that  4.59% of the Ranch Hands have some kind of cancer, compared to 2.33 %
of the unexposed group. Thus, the overall risk of cancer among the dioxin-exposed group is
doubled (risk increased by a factor of 1.97). The greatest risk increase is for skin cancers (where
the risk is increased by a factor of 2.6), whereas the risk of "systemic cancers" (non-skin
cancers) is increased by a factor of 1.2; in other words, the dioxin-exposed group has a 20%
greater chance of getting a non-skin cancer.

Birth Defects

Analyzing for birth defects, the study looked at children born before the Vietnam experience and
children born after Vietnam. Prior to Vietnam, the dioxin-exposed group had born 85% as many
children with birth defects as the non-exposed group; after Vietnam, the exposed group bore
139% as many children with birth defects. The earlier Air Force study had said birth defects
among dioxin-exposed families were limited to "minor skin lesions" but the new study reverses
that conclusion; 32 children with severe defects were born to families in the exposed group, vs.
18 in the non-exposed group. The total number of birth defects in the two groups was: 80 with
defects out of 917 total births in the exposed group vs. 48 with defects out of 744 total births in
the non- exposed group.

Psychological Damage Psychological testing revealed significant increases in fatigue, anger,
anxiety, and isolation among the dioxin-exposed group compared to the non-exposed group.

Liver Functions The new study looked at nine chemical measures of liver function and in three
categories the dioxin-exposed group showed reduced liver functions, compared to the
non-exposed group. In addition, among the exposed group, 16 showed enlarged livers, vs. six
among the nonexposed group. Furthermore, 13 among the exposed group had a verifiable
medical history of liver disorder other than hepatitis, jaundice, or cirrhosis, vs. only two with such
histories among the nonexposed group.

Cardiovascular System

Heart disease rates and heart attack rates did not differ among the two groups. However, during
physical examination, 10 different heart pulse measurements were taken in the extremities (e.g.,
the ankle), and statistically significant abnormalities were found in one or more pulses in the
extremities are evidence of blood circulation problems.

Endocrine System

The endocrine system is a body control system composed of a group of glands that maintain a
stable internal environment by producing chemical regulatory substances called hormones.
Glands that participate in the endocrine system include the pituitary, thyroid, parathyroid and
adrenal glands, as well as the pancreas, ovaries and testicles. The new study looked at five
chemical measures of endocrine system functions. In three of the five measures, the
dioxin-exposed group showed abnormal functioning of the endocrine system, conpared to the
non-exposed group. Functioning of the endocrine system reduces with age, but the new study
showed that, among the dioxin-exposed group, functioning of the endocrine system is
being reduced much faster than among the non-exposed group.

Thus the study shows that, in six out of 11 areas of suspected dioxin effects, exposed Vietnam
veterans have health problems in greater proportion than the comparison group.

Lets compare it to one single aspirin tablet. One aspirin tablet weighs 5 grains (or 325 miligrams,
or 325 trillion femtograms), so to express one "safe" lifetime dose of 2,3,7,8,-TCDD, you would
take a single aspirin tablet and divide it into 32 million (actually 32,172,218) minuscule pieces.
Then one of those tiny pieces would represent one "safe" lifetime dose of 2,3,7,8,-TCDD.

One other way to understand the toxicity of dioxin is to compare the dioxin "reference dose" they
have set for other common toxic materials. The "reference dose" is the highest amount they
believe you could regularly eat without incurring any disease (not considering cancer).

The reference dose for dioxin is 0.000,000,001 milligrams per kilogram of body weight per day.
mg/kg/day; the reference dose for the toxic metal cadmium is 0.001 mg/kg/day and the
"reference dose" for the toxic metal arsenic is the same as for cadmium/ Thus we can see that
EPA considers dioxin in food 1,000,000 times (one million times) more toxic than cadmium or
arsenic, not counting the cancer hazard from biota. HWN Mar. 21, 1990.

HWN #212 Dec. 19, 1990

For more than a decade Vietnam veterans have sought compensation for illnesses they believe
were caused by their wartime exposure to herbicides, which were used heavily during the war to
defoliate the jungle, to reduce available cover for enemy troops. U.S. soldiers and airmen who
prepared, handled or sprayed the herbicides, and ground troops who were doused, have been
routinely denied compensation by the federal Department of Veterans Affairs (VA) because the
VA has taken the position that there is not enough scientific evidence linking herbicide exposure
to disease.

Now an independent scientific review sponsored by the American Legion, the Vietnam Veterans
of America, and the National Veterans Legal Services Project has concluded that there is a
"significant statistical association "between exposure to chemical herbicides and several serious
illnesses. According to the April, 1990, report of the Agent Orange Scientific Task Force, there is
"a significant statistical association" between exposure to the herbicide Agent Orange and
various cancers (non-Hodgkins lymphoma and soft tissue sarcomas), serious skin disorders
(chloracne), and liver disorders. The Task Force said, "The aggregate interpretation of several
sound studies showing a statistically significant association for each of these
conditions makes this conclusion inescapable."

The VA does not allow consideration of animal studies, so only human data were evaluated for
the 1990 report. The 1990 report is based on a review of 285 different published
reports of human exposure to an herbicides and /or dioxins.

Since the 1990 report, the VA has reversed itself and declared that soft tissue sarcomas and
nonHodgkins lymphomas in Vietnam vets is compensable.

Science has known since the mid-1960s that dioxin is an extremely powerful promoter of cancer
in laboratory animals, but industry researchers have recently been claiming that humans
somehow are exempt from the dioxin danger, The question of dioxin's hazard to humans took on
real urgency inthe early '80s when 15,000 veterans sued Dow chemical and other producers of
Agent Orange (a dioxin-contaminated herbicide widely used to defoliate the jungle in Vietnam
from 1962-1971); the vets sought money damages for health effects (cancer, defective offspring,
etc) they said they were experiencing. Lawyers for the Vietnam vets offered documentary
evidence that Dow chemists convened a private meeting of their competitors in 1965 to share
new information that impurities {dioxins} in the herbicide 2,4,5,-T (principal component of Agent
Orange) caused severe liver damage in rabbits. According to court records, a chemist at
Hercules Powder Company who attended the private Dow meeting in 1965, received a phone call
from a Doe executive who "warned him to keep the findings away from the federal government"
according to a reporter for Nature, the British science journal. If this is true, it would not be the
first time, nor the last, that money has influenced the outcomes, and the uses of scientific data.
Peter David, "Dioxin--When was the danger known?" Nature Vol. 303 May 12, 1983. p.104

Hormone disrupters

Gradually during recent years a new body of knowledge has developed showing that some
chemicals in food and water can mimic hormones and disrupt the development of living things like
fish, birds, and mammals, including their sexual development.

In some cases the effects on the wildlife have been dramatic. For example, male herring gulls on
Lake Ontario, exposed to DDT and other organochlorine compounds, developed female sex
organs. Female-female pairing has been observed in herring gulls on Lake Michigan and on
Santa Barbara Island, California. Because humans share the same basic mechanisms of growth
and development as wildlife, an increasing number of scientists has become concerned that
humans may already be affected without recognizing.

In July of this year an international group of 21 scientists met at Wingspread in Racine, Wisconsin
 to asess what is known about these matters. They have now released a "consensus statement"
containing information and opinions about the nature and possible causes of these problems.
The five-page statement is called "Chemically Induced Alterations in Sexual Development: The
Wildlife/Human Connection."

Hormones are produced by the endocrine system--a bodily system consisting of the specialized
cells, tissues, and organs that create and secrete (usually into the blood) organic chemicals
called hormones, which then regulate other kinds of cells in the body. Particular hormones only
affect particular cells that contain "receptors" for those hormones. A small amount of a hormone
attaches to a "receptor site" and the hormone-receptor pair then initiates a cascade of chemical
changes, often with major and far-reaching consequences.

The endocrine system shares with the nervous system the job of adjusting the body's response
to a changing external environment. The nervous system copes with environmental changes on
an immediate basis, whereas the endocrine system copes with environmental changes on a
sustaining basis... In a developing fetus, it is the endocrine system that regulates cell division and
organ differentiation. The endocrine system regulates patterns and timing of bird migration and
of hibernation in mammals. Examples of endocrine glands in humans include the adrenal gland,
pancreas, thyroid, pituitary, ovaries and testes.

The scientists gathered at Wingspread last July focused on the sex hormones--the androgens
that make males look and act like males and the estrogen that make females look and act like
females. The Wingspread Statement begins "Many compounds introduced into the environment
by human activity are capable of disrupting the endocrine system of animals, including fish,
wildlife, and humans. The consequences of such disruption can be profound because of the
crucial role hormones play in controlling development".

The following consensus was reached by participants at the workshop.

We are certain of the following:

1. A large number of man-made chemicals that have been released into the environment, as well
as a few natural ones, have the potential to disrupt the endocrine system of animals, including
humans. Among these are the persistent, bioaccumulative, organohalogen compounds that
includes some pesticides (fungicides, herbicides, and insecticides) and industrial chemicals,
other synthetic products, and some metals.

"Many wildlife populations are already affected by these compounds. The impacts include thyroid
dysfunction {impaired} or abnormal functioning} in birds and fish; decreased fertility in birds, fish,
shellfish, and mammals; decreased hatching success in birds, fish and turtles; gross birth
deformities in birds, fish and turtles; metabolic abnormalities {impaired or abnormal use of
energy, manufacture of tissue, or handling of resulting wastes} in birds, fish, and mammals'
behavioral abnormalities in birds; demasculinization and feminization in male fish, birds, and
mammals ; defeminization and masculinization of female fish and birds; and compromised
{impaired} immune systems in birds and mammals.

The patterns of effects vary among species and among compounds. Four general points can
nonetheless be made: (1) the chemicals of concern may have entirely different effects on the
embryo, fetus, or perinatal {meaning near the time of birth from the 28th week of pregnancy
through the first week of life, in humans} organism than on the adult; (2) the effects are most
often manifested in offspring, not in the exposed parent; (3) the timing of exposure in the
developing organism is crucial in determining its character and future potential; and (4) although
critical exposure occurs during embryonic development {from conception through the end of the
second month of pregnancy}, obvious manifestations {effects} may not occur until maturity.

Laboratory studies corroborate the abnormal sexual development observed in the field and
provide biological mechanisms to explain the observations in wildlife.

"Humans have been affected by compounds of this nature, too. The effects of DES
(diethylstilbesterol), a synthetic therapeutic agent, like many of the compounds mentioned {in
footnote} are estrogenic {meaning they act like estrogen, a family of female sex hormones}.
Daughters born to mothers who took DES now suffer increased rates of clear cell
adenocarcinoma (cancer), various genital tract abnormalities, abnormal pregnancies, and some
changes in immune responses. Both sons and daughters exposed in utero {while in the uterus}
experience congenital anomalies of their reproductive system and reduced fertility. The effects
seen in utero DES-exposed humans parallel those found in contaminated wildlife and laboratory
animals, suggesting that humans may be at risk to those same environmental hazards as wildlife."

2. We estimate with confidence that: "Some of the developmental impairments reported in
humans today are seen in adult offspring of parents exposed to synthetic hormone disruptors
(agonists and antagonists) released in the environment. The concentrations of a number of
synthetic hormone agonists and antagonists measured in the U.S. human population today are
well within the range and dosages at which effects are seen in wildlife populations. {An agonist is
a chemical that is not a hormone but mimics a natural hormone; ab antagonist interferes with a
natural hormone}. In fact, experimental results {in animals} are being seen at the low end of
current environmental concentrations {in humans}.

Unless the environmental load of synthetic hormone disruptors is abated and controlled, large
scale dysfunction at the population level is possible. The scope and potential hazard to wildlife
and humans are great because of the probability of repeated and/or constant exposure to
numerous synthetic chemicals that are known to be endocrine disruptors."

Both exogenous {external source} and endogenous (internal source) androgens (male
hormones) and estrogens (female hormones) can alter the development of brain function.

"Any perturbation {disturbance} of the endocrine system of a developing organism may alter the
development of that organism: typically these effects are irreversible. For example, many
sex-related characteristics are determined hormonally during a window of time in the early stages
of development, and can be influenced by small changes in hormone balance. Evidence
suggests that sex-related characteristics once imprinted may be irreversible."

A footnote on page 1 of the Wingspread Statement says, "Chemicals known to disrupt the
endocrine system include: DDT and its degradation products, DEHP di(2-ethylhexyl)phthalate),
dicofol, HCB (hexachlorobenzene), kelthane, kepone, lindane, and other hexachlorocyclohexane
congeners, mexthoxychlor, octachlorostyrene, synthetic pyrethroids, triazine herbicides, EBDC
fungicides, certain PCB congeners, 2,3,7,8-TCDD and other dioxins 2,3,7,8-TCDF and other
furans, cadmium, lead, mercury tributyltin, and other organo-tin compounds, alkyl phenols
(non-biodegradable detergents and anti-oxidants present in modified polystyrene and PVCs),
styrene dimers and trimers, soy products, and laboratory animal and pet food products." HWN
#263 DEC 11, 1991 .

HWN # 290 June 17 1992

Three new studies by researchers at University of Wisconsin reveal that very low doses of dioxin
alter the sexual development of young male rats, causing demasculinization and feminization.

Thomas A. Mably et al "In utero and lactational exposure of male rats to
2,3,7,8-Tetrachlorodibenzo-p-dioxin 1. Effects on androgenic status, Toxicology and Applied
Pharmacology, Vol. 114 May 1992 pp. 97-107

Thomas A. Mably et al "In utero and lactational exposure of male rats to
2,3,7,8-Tetrachlorodibenzo-p-dioxin 2. Effects on sexual behavior and the regulation of luteinizing
hormone secretion in adulthood. Toxicology and Applied Pharmacology ,
Vol. 114 May 1992 pp. 108-117

Thomas A. Mably et al "In utero and lactational exposure of male rats to
2,3,7,8-Tetrachlorodibenzo-p-dioxin. 3. Effects on spermagogeneses and reproductive capability
Toxicology and Applied Pharmacology, Vol. 114 May 1992 pp.118-126

Dr. Linda S. Birnbaum, a scientist with USEPA calls the new studies "highly significant". Birnbaum
is one of the chief scientists conducting the EPA's formal reassessment of the toxicity of dioxin.
As we reported earlier, many scientists including Birnbaum, now consider dioxin an "environmental
hormone". The new Wisconsin studies support that view.

The Wisconsin researchers, led by Dr. Richard E. Peterson, showed that dioxin interferes with
the sexual development of male rats exposed to dioxin before, and shortly after, birth.
Pregnant female rats were given a single oral dose of dioxin on the 15th day of pregnancy; their
male offspring showed reduced levels of male hormones in their blood and a variety of sexual
aberrations that stayed with them as they matured. The young males are demasculinized and
feminized by doses of dioxin too low to cause any measurable toxicity in the mother rat. The
sexual changes in the young males are both physiological and behavioral, and last into

Dioxin passes through the placenta and enters the fetus, so the rat fetuses received part of the
mother's dose immediately. After birth, the baby rats continued to receive a small dose of dioxin
through their mother's milk. Peterson says the baby rats received the bulk of their dose through
milk. In rats and humans both, females rid their bodies of dioxin chiefly by excreting it in their milk.
Dioxin is soluble in fats and oils, and milk is high in fat.

Peterson and co-workers point out that male rats typically inseminate a female rat with up to 10
times as many sperm as are typically needed to ensure impregnation. Humans, by contrast,
typically release only about as many sperm as would be required for fertilization. "As a result,"
Peterson and his co-workers write, human reductions in sperm production "similar in magnitude
to that in rats would be expected to reduce fertility in man." In other words, rats can continue to
reproduce despite a reduction in sperm count because they produce an excess of sperm, but
humans do not produce excess sperm so a reduction in human sperm count would likely reduce
humans' ability to reproduce."

Are environmental chemicals causing men to lose their masculine characteristics?

A recent study in the British Medical Journal concludes that men in western countries today have
sperm counts less than half as high as their grandfathers had at the same age. In addition, the
occurrence of cancer of the testicles has increased 3-fold to 4-fold during the past period,
including undescended testicles (a condition called cryptorchidism) and a birth defect called
hypospadias in which the male urinary canal is open for a variable distance on the underside of
the penis.

An article published last month in The Lancet, another prestigious British medical journal, asks
whether these phenomena can all be traced to the same cause, namely exposure of males very
early in life to female sex hormones (estrogens) or to environmental chemicals that act like