[Pharmwaste] How the World Works - Does plastic make us fat?

[James Bukowski]

How My World Works * if you eat too much and exercise too little, you
get fat.  Plastic has nothing to do with it.


http://ecb.jrc.it/DOCUMENTS/Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/bisphenolasum325.pdf


http://www.bfr.bund.de/cd/7300

http://www.hcra.harvard.edu/rip/risk_in_persp_August2004.pdf 

http://www.gradientcorp.com/coinfo/pdf/RiskBull1.pdf 

http://toxsci.oxfordjournals.org/cgi/content/full/68/1/1#NAGEL-ETAL-1997

James



James Bukowski, CIH HEM
Environmental Health Officer
Virginia Tech (1980)

>>> "DeBiasi,Deborah" <dldebiasi at deq.virginia.gov> 7/20/2007 9:55 AM
>>>
http://www.salon.com/tech/htww/2007/07/16/obesity/index.html 

How the World Works - Does plastic make us fat?

The basic story line of "The Toxic Origins of Disease
(http://biology.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pbio.0050193),"
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." 


-- Andrew Leonard

11:20 EST, July 16, 2007

Deborah L. DeBiasi
Email:   dldebiasi at deq.virginia.gov 
WEB site address:  www.deq.virginia.gov 
Virginia Department of Environmental Quality
Office of Water Permit Programs
Industrial Pretreatment/Toxics Management Program
Mail:          P.O. Box 1105, Richmond, VA  23218 (NEW!)
Location:  629 E. Main Street, Richmond, VA  23219
PH:         804-698-4028
FAX:      804-698-4032

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