Fat's Hidden Trigger -- Phthalates, Bisphenol A - various

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July/August 2007 (#121) " src= " http://www.thegreenguide.com/images/arrow.gif "

width=14 align=absMiddle border=0> Fat's Hidden Trigger

 

Fat's Hidden Trigger

by Emily Main

 

Filed under: Green diet, Phthalates, Obesity and Overweight, Bisphenol A

 

 

If you've ever suspected that there's a reason you can't burn off those last

five pounds, you may be on to something. Recent studies on certain

hormone-disrupting and environmentally persistent compounds are leading

researchers to believe there's a plausible link between these ubiquitous

chemicals and our ever-expanding waistlines.

 

The World Health Organization estimates that 1 billion of the world's nearly 7

billion citizens are overweight, 300 million of whom are defined as clinically

obese. " People want to blame 40-ounce Cokes--and that's important--but there's

reason to believe there are other things in play, " says Richard Stahlhut, M.D.,

M.P.H., preventive medicine resident at the University of Rochester Medical

Center.

 

Stahlhut and his colleagues wondered if a group of hormone-disrupting

chemicals called phthalates (pronounced " thay-lates " ), found in a wide array of

everyday products, might be adding to this epidemic. Analyzing data from the

Centers for Disease Control and Prevention's most recent National Health and

Nutrition Examination Survey, Stahlhut and his colleagues compared six phthalate

metabolites (phthalates processed by the body) found in men's urine samples to

their corresponding waist circumferences. Two of the phthalates targeted were

DEHP, used in synthetic fragrances and polyvinyl chloride (PVC) products (i.e.

floor tiles, shower curtains and hospital IV bags), as well as DBP, used in nail

polishes, floor finishes and paints.

 

The results, published online last March in Environmental Health Perspectives

(EHP), revealed that American men with abdominal obesity or insulin resistance

(a precursor to diabetes) were more likely to have high levels of the

metabolites in their urine than men without those problems. Stahlhut is quick to

point out that there's no definitive link proving that excessive phthalate

exposure causes obesity, but the study does suggest a possible connection.

" [These results are] what you would expect if phthalates are lowering

testosterone levels, " Stahlhut says, and " low testosterone in adult men, from

whatever cause, is known to cause abdominal obesity and insulin resistance. "

Past research has demonstrated the effects of phthalates on testosterone; a 2006

Danish study of infant boys found that those exposed to phthalates via breast

milk had lower testosterone levels and abnormal reproductive development.

 

Fredrick vom Saal, Ph.D., a developmental biologist at the University of

Missouri, is currently studying the obesity-inducing effects on pregnant mice of

BPA, a hormone-disrupting chemical found in #7 polycarbonate bottles, dental

sealants and can linings. Presenting preliminary results at the American

Association for the Advancement of Science's annual meeting last February, he

discovered that these mice, which had been fed very low doses of BPA, had

offspring that exhibited abnormal growth later in life. While it's not clear

that BPA is linked to obesity, says vom Saal, " we do know that it makes animals

bigger. It doesn't categorize them as obese, but obesity is a very particular

aspect of growth. "

 

In yet another study in press online at Environmental Science & Technology,

researchers from the Johns Hopkins Bloomberg School of Public Health tested cord

blood taken from newborns for ten environmentally persistent perfluorochemicals

(PFCs), including perfluorooctanoic acid (PFOA), used in the manufacture of

non-stick pans and in microwave popcorn bags, and the now-banned

perfluorooctanoic sulfonate (PFOS). High levels of both were associated with low

birth weight, itself a risk factor for obesity later in life. " We do know, in

the case of animals, that some of these chemicals have effects later in life, "

says Lynn Goldman, M.D., one of the study's lead authors.

 

While all these links are preliminary, the studies point to " where folks need

to focus effort, " says Stahlhut. " There's some exposure or combination of

exposures that everybody thinks is okay but isn't. "

 

Fortunately, awareness is being raised. In California, a ban on phthalates in

children's toys reached the senate floor before defeat and Maine's legislature

is considering a bill that would bar the sale of any children's product

containing BPA or phthalates. Until such legislation reaches your state, " People

have to protect themselves, " says Stahlhut. Vom Saal's research points out that

BPA is harmful even before children are born, so such laws may not offer the

highest level of protection. " This is a very, very complex problem, and it will

take many years to get to the bottom of it, " Stahlhut adds. " The organic

approach--avoiding complex chemicals you don't really need, and otherwise being

'zen' about it--may be a reasonable strategy. "

 

What You Can Do

 

* Exercise regularly.

 

* Eat less fat. PFOA and PFOS don't build up in fat, says Goldman, but many

PFCs do. " As a general precaution, eating less fat and less animal fat is a good

idea, " she advises.

 

* Purchase cookware without non-stick features, and avoid microwave popcorn:

PFOA released from bags accounts for over 20 percent of the chemical measured in

Americans' blood.

 

* Choose phthalate-free products: See Moisturizers and Flooring product

reports (www.thegreenguide.com/reports) and www.greenerpenny.com. When pregnant,

ask ahead about your hospital's policy on PVC in medical devices.

 

* See the Baby Bottle and Plastic Containers product reports for

non-polycarbonate bottles at www.thegreenguide.com/reports.

 

* Avoid canned products that may be packaged in cans lined with BPA. See " The

Bisphenol-A Debate: A Suspect Chemical in Plastic Bottles and Cans, " and " A

Survey of Bisphenol-A in U.S. Canned Foods " .

 

http://www.thegreenguide.com/doc/121/fat

 

--

 

Environ Health Perspect. 2007 June; 115(6): A312.

 

 

Copyright This is an Open Access article: verbatim copying and redistribution

of this article are permitted in all media for any purpose

 

Enviornews

Science Selections

 

Phthalates and Metabolism: Exposure Correlates with Obesity and Diabetes in

Men

Melissa Lee Phillips

 

The prevalence of obesity, insulin resistance, and diabetes has increased

considerably in the past few decades. Many plausible contributing factors have

been identified for this increase, among them low testosterone levels in men.

Research has found that exposure to certain synthetic chemicals adversely

affects testicular function in animals and possibly in humans. A new analysis

looked for—and found—that exposure to one class of these chemicals, phthalates,

correlated with two metabolic abnormalities in men: abdominal obesity and

insulin resistance [EHP 115:876–882; Stahlhut et al.].

 

Phthalates are commonly used in products such as cosmetics, soaps, pesticides,

lubricants, plastics, and paints. They are widespread; indeed, more than 75% of

the U.S. population carries detectable levels of several phthalate metabolites.

Studies have also found associations between some phthalate metabolites and

antiandrogenic effects in humans, including both infant and adult males.

 

The authors used 1999–2002 data from the CDC National Health and Nutrition

Examination Survey (NHANES) to look for a connection between phthalate exposure

and metabolic disease in adult men. They compared urine concentrations of six

phthalate metabolites to the participants’ waist circumference and measures of

insulin resistance. The analysis controlled for a variety of potential

confounders, including age, ethnicity, fat and calorie consumption, physical

activity, and smoking status.

 

Four phthalate metabolites were significantly associated with greater waist

circumference and three with increased insulin resistance. When the authors

further controlled their models for measures of participants’ kidney and liver

function, the associations decreased somewhat but remained significant for all

but one metabolite.

 

The authors caution that this first look at phthalates, obesity, and insulin

resistance is limited by the study’s cross-sectional design and the single

measurement of urine phthalate metabolites (an imperfect measure of long-term

exposure). In addition, although the study was based on the hypothesis that

phthalates cause metabolic abnormalities by decreasing androgen levels or

function, the authors couldn’t examine this mechanism, because the NHANES data

do not contain measures of sex hormones in men. They note that other mechanisms

could also be involved in a relationship between phthalates and metabolic

disease.

 

If phthalates are eventually shown conclusively to contribute to obesity or

diabetes in men, it’s still not clear how these chemicals would affect the

opposite sex, since low testosterone has been associated with a lower (not

higher) prevalence of metabolic disease in women. If further longitudinal

studies confirm that phthalate exposure contributes to obesity, diabetes, and

related disorders, actions to reduce phthalate exposure could effectively lessen

the chemicals’ contribution to metabolic disorders, because phthalates are

quickly metabolized and excreted by the body.

 

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1892143

 

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Are Common Chemicals Feeding Obesity Epidemic? Study suggests exposure to

phthalates linked to abdominal fat, insulin resistance in men.

 

By Amanda Gardner

HealthDay Reporter

 

(SOURCES: Richard Stahlhut, M.D., preventive medicine resident, University of

Rochester School of Medicine & Dentistry, New York; Ted Schettler, M.D., science

director, Science and Environmental Health Network, Ames, Iowa; Environmental

Health Perspectives)

 

THURSDAY, March 15 (HealthDay News) -- Exposure to a class of chemicals

commonly found in soap and plastics could be fueling the obesity epidemic by

contributing to abdominal obesity and insulin resistance in men, a new study

suggests.

 

The chemicals, known as phthalates, have already been implicated in male

reproductive problems including low sperm counts and low testosterone levels.

However, it's too soon to know whether they are actually causing these health

problems, cautioned the researchers and others.

 

" It's premature for folks to be alarmed, " said study author Dr. Richard

Stahlhut, a resident in preventive medicine at the University of Rochester

School of Medicine & Dentistry in New York.. " What is more alarming is the

reason we are doing studies like this. Another study showed that testosterone

levels had dropped about 22 percent in men, and that sperm counts had dropped to

levels that are considered subfertile or infertile. "

 

" It's an important observation that chemical exposures could be contributing

to obesity and diabetes in the general population, " added Dr. Ted Schettler,

science director for the Science and Environmental Health Network. " This is one

more example of a family of chemicals that may be contributing to this problem,

but this study has obvious limits that the authors acknowledge in great detail. "

 

The study was published in the March 14 online edition of Environmental Health

Perspectives.

 

Phthalates have been widely used for more than half a century in everything

from paint to time-released medicines, but only recently have they become a

topic of concern. Animal studies show that phthalates decrease testosterone

levels while human studies have found that phthalates are associated with poor

sperm quality in men.

 

This study follows up on other studies that correlated abnormal sperm counts

and low testosterone levels with phthalates. Men with low testosterone levels

develop abdominal obesity and insulin resistance, so these authors speculated

that phthalates might be behind the depressed testosterone levels.

 

" That's the missing link, testosterone as a [possible] link between phthalates

and obesity, " Stahlhut said.

 

Stahlhut and his team analyzed urine, blood samples and other data collected

for the National Health and Nutritional Examination Survey (NHANES), a large

government survey, from 1999 to 2002.

 

Of the adult men available, 1,451 had data on phthalate exposures, obesity and

waist circumference. Of these, 651 also had data on fasting glucose and insulin

levels needed to calculate insulin resistance.

 

According to the analysis, more than 75 percent of the U.S. population has

measurable levels of several phthalates detectable in their urine.

 

Men with the highest levels of phthalates in their urine had more belly fat

and insulin resistance, even after adjusting for other factors.

 

One drawback of the data, and therefore of the study, is that no information

on hormone levels was available, nor was there any long-term data.

 

In any event, phthalates are unlikely to be the whole story. The chemicals

have been shown, in animal studies, to have an effect on thyroid hormone, which

could also be a pathway to increased obesity.

 

" This is just part of the search for answers, " Stahlhut said. " The thing we're

certain of is not that phthalates are doing this, but that phthalates require

very careful scrutiny. I'm certain that the declines in testosterone and sperm

production require urgent investigation, and I'm certain that phthalates are on

the list of chemicals that could be part of the issue. "

 

" It's a complex, multi-factorial problem, " Schettler added. " What the authors

are suggesting is that a chemical exposure may be one among many factors. The

study is certainly hypothesis-generating. It clearly makes a case that this

potential link ought to be studied in more detail in more systematic ways. "

 

More information

 

Visit the American Diabetes Association for more on type 2 diabetes.

 

 

2007 ScoutNews, LLC. All rights reserved.

 

HealthDayNews articles are derived from various sources and do not reflect

federal policy. healthfinder.gov does not endorse opinions, products, or

services that may appear in news stories. For more information on health topics

in the news, visit the healthfinder.gov health library.

http://www.healthfinder.gov/news/newsstory.asp?docID=602778

 

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Chemicals May Play Role in Rise in Obesity

 

By Elizabeth Grossman

Special to The Washington Post

Monday, March 12, 2007; A06

 

Too many calories and too little exercise are undeniably the major factors

contributing to the obesity epidemic, but several recent animal studies suggest

that environmental exposure to widely used chemicals may also help make people

fat.

 

The evidence is preliminary, but a number of researchers are pursuing

indications that the chemicals, which have been shown to cause abnormal changes

in animals' sexual development, can also trigger fat-cell activity -- a process

scientists call adipogenesis.

The chemicals under scrutiny are used in products from marine paints and

pesticides to food and beverage containers. A study by the Centers for Disease

Control and Prevention found one chemical, bisphenol A, in 95 percent of the

people tested, at levels at or above those that affected development in animals.

 

These findings were presented at last month's annual meeting of the American

Association for the Advancement of Science. A spokesman for the chemical

industry later dismissed the concerns, but Jerry Heindel, a top official of the

National Institute of Environmental Health Sciences (NIEHS), who chaired the

AAAS session, said the suspected link between obesity and exposure to " endocrine

disrupters, " as the chemicals are called because of their hormone-like effects,

is " plausible and possible. "

 

Bruce Blumberg, a developmental and cell biologist at the University of

California at Irvine, one of those presenting research at the meeting, called

them " obesogens " -- chemicals that promote obesity.

 

Obesity has become a major health concern as people in the United States and

around the world have become increasingly overweight, raising their risk of

cardiovascular diseases, diabetes, stroke and certain cancers. The World Health

Organization estimates that more than a billion adults worldwide are overweight

and 300 million are obese. Scientists have begun examining a wide range of

possible causes beyond eating too much and exercising too little -- including

possible chemical exposures.

 

Blumberg began to suspect a link while trying to pinpoint how one endocrine

disrupter, tributyltin, affects genetic mechanisms in the reproductive system.

Tributyltin is used as a marine and agricultural fungicide, an antimicrobial

agent in industrial water systems, and in plastics; it can cause serious sexual

abnormalities in marine animals.

 

" What we discovered, " Blumberg said, is that tributyltin disrupted genetic

interactions that regulate fat-cell activity in animals. " Exposure to

tributyltin is increasing the number of fat cells, so the individual will get

fatter faster as these cells produce more of the hormones that say 'feed me,' "

Blumberg said. The exposed animals, he added, remain predisposed to obesity for

life.

 

Retha R. Newbold, a developmental biologist at the NIEHS, has seen similar

lifetime effects in her work with diethylstilbestrol (DES), a potent synthetic

estrogen she has studied for 30 years.

 

Newbold's research has shown that mice exposed to DES during early development

produced more fat cells, larger fat cells, and more abdominal fat than those not

exposed. Exposed mice became obese adults and remained obese even on reduced

calorie and increased exercise regimes. Like tributyltin, DES appeared to

permanently disrupt the hormonal mechanisms regulating body weight.

 

" Once these genetic changes happen in utero, they are irreversible and with

the individual for life, " Newbold said.

 

DES was widely prescribed for women during pregnancy from the 1940s until

1971, when it was withdrawn after being linked to cancer. Taken by perhaps 8

million women, DES has caused reproductive abnormalities in children and

grandchildren of women who took it. Whether its effects include promoting

obesity has yet to be determined, but its effects on animal metabolism -- it is

also used to fatten livestock -- are similar to those caused by bisphenol A, a

chemical most people now encounter daily.

 

" Exposure to bisphenol A is continuous, " said Frederick vom Saal, professor of

biological sciences at the University of Missouri at Columbia. Bisphenol A is an

ingredient in polycarbonate plastics used in many products, including refillable

water containers and baby bottles, and in epoxy resins that line the inside of

food cans and are used as dental sealants. In 2003, U.S. industry consumed about

2 billion pounds of bisphenol A.

 

Researchers have studied bisphenol A's effects on estrogen function for more

than a decade. Vom Saal's research indicates that developmental exposure to low

doses of bisphenol A activates genetic mechanisms that promote fat-cell

activity. " These in-utero effects are lifetime effects, and they occur at

phenomenally small levels " of exposure, vom Saal said.

 

Steven Hentges of the American Chemistry Council said his organization's

review of the scientific literature found that a preponderance of the bisphenol

A studies have shown no adverse effects, including no increased body weight.

" Our conclusion is that there is no risk to human health, " said Hentges.

 

But many scientists disagree, including vom Saal, who called the ACC's

statements a " blatant lie. "

 

Research into the impact of endocrine-disrupting chemicals on obesity has been

done only in laboratory animals, but the genetic receptors that control fat cell

activity are functionally identical across species. " They work virtually the

same way in fish as they do in rodents and humans, " Blumberg said. " Fat cells

are an endocrine organ. "

 

Ongoing studies are monitoring human levels of bisphenol A, but none have been

done of tributyltin, which has been used since the 1960s and is persistent in

the marine food web. " Tributyltin is the only endocrine disrupting chemical that

has been shown without substantial argument to have an effect at levels at which

it's found in the environment, " Blumberg said.

 

Concern over tributyltin's reproductive effects on marine animals has resulted

in an international agreement discontinuing its use in anti-fouling paints used

on ships. The EPA has said it plans next year to assess its other applications,

including as an antimicrobial agent in livestock operations, fish hatcheries and

hospitals.

 

Bisphenol A is approved by the Food and Drug Administration for use in

consumer products, and the agency says the amount of bisphenol A or tributyltin

that might leach from products is too low to be of concern. But the National

Toxicology Program, part of the National Institutes of Health, is reviewing

bisphenol A, and concerns about its estrogenic effects prompted California

legislators to propose banning it from certain products sold in-state, a move

industry has fought vigorously.

 

Researchers said the next step is to learn if these apparent animal

" obesogens " are affecting people.

 

" Our job is to follow the science, and based on these animal studies, this is

worth taking a look at, " said Heindel of the NIEHS.

 

http://www.washingtonpost.com/wp-dyn/content/article/2007/03/11/AR2007031100918_\

pf.html

 

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Does plastic make us fat? A ubiquitous chemical in common plastic may play a

role in the obesity epidemic. The chemical industry is unamused.

 

Andrew Leonard

 

The basic story line of " The Toxic Origins of Disease, " a superb exposé in the

June issue of PLoS Biology by science writer Liza Gross, fulfills a classic

archetype. Publicly funded scientists determine that a commonly used substance

may be harmful to human health. The industry that produces said substance

responds in an all-out assault to undermine their data. Cue a lobbying firm that

cut its teeth representing tobacco companies and the cast of characters is

perfect.

 

In this case, the chemical at issue is bisphenol A, a basic building block of

polycarbonate plastic, and, according to Gross, " one of the highest-volume

chemicals in commercial production. " A bevy of publicly funded researchers have

found evidence that low doses of bisphenol A interfere with embryonic

development in animals by exposing them to higher levels of hormones, such as

estrogen, than normal. The chemical industry has fought back by commissioning

scores of studies that find exactly the opposite. This leads to some lovely

statistical info-nuggets: A survey conducted in 2005 found that of " 115

published studies concerning effects of low doses of bisphenol A in experimental

animals, 94 percent of publicly funded studies found evidence of harm while 100

percent of chemical industry studies found no evidence of harm. "

 

Gross' treatment of the struggle over bisphenol A is a case study in how to do

hard-science muckracking. She is sensitive to the nuances involved in exploring

complex biological interactions that involve numerous variables, rigorous in her

presentation of the chemical industry's push-back, and through it all,

thoroughly compelling. I've been a fan of the Public Library of Science's

efforts to break the stranglehold that closed-access journals have over the

publication of scientific research since its inception, but aggressive

journalism like this raises the ante several notches higher.

 

The efforts of the chemical industry to combat findings that a ubiquitous

synthetic chemical (traces of which can be found in the urine of just about

every living human being in the United States ) might cause developmental and

reproductive defects in humans, even when ingested in low doses, are not

surprising. But there is one aspect to this story that is quite eye-opening.

 

There appears to be evidence that the damage done by bisphenol A during

embryonic development may be scrambling the signals that fat cells normally

receive during prenatal and neonatal development. After the initial distortion,

the affected fat cells never work properly again. Affected animals are unable to

properly metabolize their normal diets, leading to obesity. And guess what? The

introduction of bisphenol A into the human environment in significant quantities

tracks pretty closely, in timing, to the advent of the so-called obesity

epidemic in the United States.

 

The equation that connects bisphenol A to obesity is complex. It's not a

simple matter of 1 plus 1 equaling 2. Gross concludes " The Toxic Origins of

Disease " by quoting Fred vom Saal, one of the first scientists to discover the

possible harm caused by exposure to low doses of bisphenol A.

" We think that environmental chemicals like bisphenol A are likely to target

subpopulations of individuals that are rendered very sensitive to these

chemicals by virtue of their genes, genetic background, maternal -- fetal

interactions .... and the amount of hormones they're exposed to. "

 

The connection between fetal growth restriction, environmental estrogens, and

obesity risk may be especially relevant for infertile couples, who are

increasingly opting for in vitro fertilization [iVF]. For various reasons, many

IVF babies are born premature and growth-restricted. Vom Saal worries that

exposing this " highly sensitive subgroup " of babies to environmental chemicals

that lead to accelerated postnatal growth will permanently alter their capacity

to metabolize even normal diets and predispose them, like the mice in his

experiments, to a lifetime of obesity.

 

Vom Saal acknowledges that trying to unravel all the " phenomenally complex "

interactions and components that contribute to obesity is " like chipping away at

the pyramid, " but he has no doubt that animal studies on bisphenol A's effects

have relevance to humans. " This chemical is harming snails, insects, lobsters,

fish, frogs, reptiles, birds, and rats, " vom Saal says, " and the chemical

industry is telling people that because you're human, unless there's human data,

you can feel completely safe. "

http://www.salon.com/tech/htww/2007/07/16/obesity/

 

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April 16,

2007

 

 

 

Volume 85, Number 16

p. 38 Insights Bisphenol A On Trial Only an unbiased panel with

appropriate expertise can resolve apparently conflicting results of health

studies Bette Hileman In industrialized countries, nearly everyone is exposed

to bisphenol A (BPA), a weak synthetic estrogen. Most of the 2 billion to 3

billion lb produced in the U.S. each year is used to make polycarbonate food

containers, baby bottles, refillable water containers, compact discs, and resins

that line metal food and beverage cans. The Centers for Disease Control &

Prevention has found measurable levels—0.4 to 8.0 parts per billion—of BPA in

95% of U.S. urine samples.

 

Although BPA is only one of thousands of synthetic chemicals the U.S.

population encounters, it may be the most important for the developing fetus and

perhaps young children. Every time children consume food or drink from a can,

they are exposed to a small amount of BPA. Every time babies drink from clear

polycarbonate plastic bottles, they ingest the chemical.

 

Because of this widespread exposure, researchers have conducted many studies

of the health effects of low doses of BPA. Among government-funded experiments

on lab animals and tissues, 153 found adverse effects and 14 did not.

Contrarily, all 13 studies of BPA funded by chemical corporations reported no

harm. The studies indicating harm report a variety of deleterious effects in

rodent offspring exposed in the womb: abnormal weight gain, insulin resistance,

prostate cancer, and excessive mammary gland development.

 

What can explain the vast discrepancies in the findings of government-funded

and industry experiments? In a commentary in Environmental Health Perspectives,

University of Missouri biologist Frederick S. vom Saal points to several reasons

low-dose studies failed to find adverse effects. One is the strain of rodent

used. For example, two large industry-funded studies used the Sprague-Dawley

rat, a strain known to be insensitive even to strong, well-characterized

estrogens, such as diethylstilbestrol. So it is not surprising that these rats

show no response to the weaker estrogen BPA. Many other rodent strains are far

more sensitive, vom Saal wrote.

 

Another reason is that different batches of the feed used in several industry

studies had highly variable estrogenic activities. Phytoestrogens, such as

genistein in soy, as well as other estrogenic components, can be present in

variable amounts in different batches, vom Saal reports. In some studies,

estrogenic substances in the feed may have masked the effects of BPA, he says.

 

In light of the potential health effects of BPA exposure and the inconsistent

study outcomes, it is especially important that an unbiased panel with no

conflicts of interest and with a detailed knowledge of the field evaluate the

literature on BPA, consider the weight of evidence in regard to adverse effects,

and choose valid studies to include in its report.

 

Bias is the reason for the recent outcry from environmental groups and

lawmakers when they became aware that outside contractor Sciences International

(SI) was deeply involved in the National Toxicology Program's assessment of BPA

(C & EN, March 12, page 13). SI helped select the scientific panel, reviewed the

literature, and wrote the original draft report—essentially a literature

review—on BPA for NTP's Center for the Evaluation of Risks to Human

Reproduction. SI has worked for two BPA manufacturers, Dow Chemical and BASF.

NTP is housed at the National Institute of Environmental Health Sciences

(NIEHS).

 

It would seem that a scientific literature review would be an objective,

cut-and-dried exercise where conflicts of interest could have little influence.

But reality is almost the opposite. For example, researchers in the field know

that the biologically active fraction of total circulating BPA is the part that

is not bound to plasma proteins, because protein-bound BPA cannot diffuse

through cell membranes. So it is the levels of unbound BPA that must be compared

when evaluating study results. But some sections of the original draft report on

BPA compared results of studies that were measuring total BPA to others that

were measuring only the unbound fraction. Another source of bias is omission of

critical information from a review.

 

Because BPA causes adverse effects in rodents that are almost identical to

some of the health problems that have recently increased in human populations,

many researchers believe BPA may be partially responsible. The incidence of

human prostate cancer rose 85% from 1975 to 2002, and insulin resistance, which

leads to type 2 diabetes, became a much more prevalent health problem. The

incidence of childhood obesity has more than quadrupled over the past 40 years.

 

When newborn rats are exposed to low doses of BPA, they develop early-stage

prostate cancer as adults. Low doses of BPA also cause insulin resistance in lab

animals. Several of the most alarming studies released recently link obesity

with BPA. After vom Saal and other researchers exposed pregnant rodents to low

levels of BPA, their pups gained weight rapidly and stayed overweight for the

rest of their lives, while the control animals grew normally.

 

A similar phenomenon has been observed recently in humans, says Jerry Heindel

of the NIEHS. Some full-term infants gain weight abnormally fast and stay obese

throughout childhood. He believes that in utero exposure to BPA, or to a mixture

of environmental chemicals, may be playing some role in childhood obesity.

High-calorie diets and lack of exercise are certainly important but may not be

the only factors leading to excessive weight gain in children.

 

It seems urgent to investigate whether exposure to certain chemicals in the

womb is one possible cause of prostate cancer, insulin resistance, and childhood

obesity.

 

http://pubs.acs.org/cen/government/85/8516gov2.html

 

 

 

 

 

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