February 15, 2013
The Wall Street Journal

No Ill Effect Found in Human BPA Exposure

ROBERT LEE HOTZ

BOSTON—Human exposure to a controversial ingredient in many plastic bottles and food containers is too low to be worrisome, according to a closer look at 150 studies of an additive called bisphenol A, widely known as BPA.

A toxicologist at the federal Pacific Northwest National Laboratory reported Friday that he had re-examined studies covering blood levels of BPA, which in high enough doses can mimic the sex hormone estrogen, among 30,000 people in 19 countries, including women and infants.

He found the exposure levels generally much too low to affect the human body.

"It is thousands of times lower than the levels you see in animals that do cause effects," said Justin Teeguarden, a senior research scientist who conducted the analysis at the Department of Energy laboratory in Richland, Wash.

Mr. Teeguarden presented his research, which was funded by the Environmental Protection Agency, at the annual meeting here of the American Association for the Advancement of Science.

The findings are the latest in a broad-ranging scientific controversy that has continued for a decade or more over the safety of the world's food supply and the possible role that BPA may play in a variety of public-health problems.

Among other applications, BPA is used in bottles, soda cans, food containers and many other consumer goods, to harden the plastics from which they are made and to prevent the growth of germs.

Last summer, the Food and Drug Administration banned its use in baby bottles and infant cups but continued to stand behind its safety in other products.

The World Health Organization, the European Food Safety Authority and Japan's National Institute of Advanced Industrial Science and Technology have all discounted its risk to human health.

Write to Robert Lee Hotz at sciencejournal@wsj.com

A version of this article appeared February 16, 2013, on page A3 in the U.S. edition of The Wall Street Journal, with the headline: No Ill Effect Found in Human BPA Exposure.

BPA is Back -- New Science Proves Safety

HEALTH & WELLNESS on 02.18.13

By Christine Lepisto

BPA is not so bad after all. At least, there is not enough of it in our bodies to be causing obesity, diabetes, cancer, liver disease or heart attacks -- just a few of the modern diseases that have been correlated with the growing presence of this plastic additive in baby and drinking bottles as well as canned food linings.

The news stems from a session at last week's conference of the American Association for the Advancement of Science (AAAS) entitled: Can Exposure Science Quell the Furor over Environmental Endocrine Disruption?

The Furor Over BPA

Concerned parents have been inundated by studies finding toxic chemicals in the bodies of pregnant women and in our kids' favorite canned soups and pasta.

BPA belongs to a class of chemicals suspected to act as endocrine disruptors. What that means in non-scientific terms is that BPA can act like the chemical messengers our body uses naturally. If our body gets the wrong message at the wrong time, the result can be birth defects, neurological problems, even diseases that might be passed on to future generations.

No wonder advocates for childrens' health have suggested we look for alternatives to BPA.

Fueling the furor is an overwhelming sense of loss of control: these chemicals are in our environment, in our food, in everyday household items. Who is in charge of keeping us safe in the face of harmful chemicals?

Can Science Quell the Furor?

If this science came from an industry-funded source, it could be ignored pending independent confirmation. But work funded entirely by the United States Environmental Protection Agency (EPA) under the Science to Achieve Results (STAR) program certainly merits a bit of trust.

At the AAAS conference, six topics examined recent exposure science on BPA. Presenting a review of BPA concentrations in humans -- representing 30,000 people, including women and infants, in 19 countries -- the authors posed the question of whether BPA concentrations in humans are high enough to cause endocrine disruption. The answer is stated bluntly: "They are not."

Which raises the next question:

can this knowledge affect the public’s view of the risks posed by BPA?

Why Facts Don't Quell Fear

A scientists will keep an open mind and look for studies that can repeat the same conclusion, just to make sure we did not overlook some important factor or have a flaw in the design of our study. But the information presented in this seminar gives strong support to the idea that we do not need to fear BPA as current levels of exposure.

But a scientist saying so does not suffice. Especially not when fear makes better headlines. Which brings us to a real problem: this stuff is complex.

The 'exposure science' that was discussed amongst members of the American Association for the Advancement of Science has math, models, and medicine underlying it that make it virtually impossible for the average concerned parent to understand. Here is an overview, in much simpler language:

·        The amount of BPA found in a review of many studies was not as high as that found in some studies, suggesting that the studies that found high levels of BPA reflect contaminated samples or some other form of distortion.

·        The amount of BPA found in urine is not a good indicator of how much BPA the body has in the bloodstream, where it might confuse the body, leaning to disease. This simple statement is, in the scientific discussion, hidden behind a lot of techno-speak about intestines, livers, and chemical reactions required for the BPA to be harmful in the blood.

·        The body still prefers estrogen, the endocrine messenger our bodies are designed to understand, so it would take a lot more BPA "screaming" its message before our bodies would start listening.

So do you feel better about BPA based on the simple version of the facts?

But other scientists will continue to publish reports about BPA and other endocrine disruptors in which they continue to find mechanisms by which these chemicals could cause harm. Those studies are not lies: these chemicals can have harmful effects when studied under different conditions. Just not at the levels of actual human exposure, according to the facts above.

The Important Message for Parents

We always look for the take-away message that gives control back to those of us trying to do our best for our kids in a complicated world. Which brings us to the most important message that the sum of science on BPA delivers so far: a lifestyle rich in BPA does correlate with disease. BPA probably cannot be blamed, at least at the levels encountered. The scientists discussing BPA point to another insidious hazard:

Diet is the main source of BPA. So an obvious possibility is that poorer diets are associated with higher intake of BPA.

Poorer diets -- that means processed foods high in sugars and fats -- could be the real reason why studies show people with higher BPA levels suffer from obesity, diabetes, and cardiovascular disease. The parent hoping to give their child a better future will be thankful for the can linings that keep food safe to eat when offering their kids their favorite canned meals, accepting BPA's role in reducing food-borne illnesses, because there really is no BPA substitute. Then they will balance those convenient moments with many more meals of good, fresh home cooking. But that is not science; it's just plain common sense.

http://parentables.howstuffworks.com/health-wellness/bpa-back-new-science-proves-safety.html

Exposure to BPA May be Too Low to Cause Problems

Tue, 02/19/2013

Pacific Northwest National Laboratory

 

A controversial component of plastic bottles and canned food linings that have helped make the world’s food supply safer has recently come under attack: bisphenol A. Widely known as BPA, it has the potential to mimic the sex hormone estrogen if blood and tissue levels are high enough. Now, an analysis of almost 150 BPA exposure studies shows that in the general population, people's exposure may be many times too low for BPA to effectively mimic estrogen in the human body.

The analysis, presented at the American Association for the Advancement of Science's annual meeting by toxicologist Justin Teeguarden of the Department of Energy's Pacific Northwest National Laboratory, shows that BPA in the blood of the general population is many times lower than blood levels that consistently cause toxicity in animals. The result suggests that animal studies might not reflect the human BPA experience appropriately.

"Looking at all the studies together reveals a remarkably consistent picture of human exposure to BPA with implications for how the risk of human exposure is interpreted," says Teeguarden. "At these exposure levels, exposure to BPA can’t be compared to giving a baby the massive dose of estrogens found in a birth control pill, a comparison made by others.”

In addition to evaluating the likelihood of BPA mimicking estrogen in humans, Teeguarden also analyzed another set of BPA studies that looked at the chemical’s toxicity in animals and cells in the lab. These 130 studies are significant as a group because they refer to the exposures as "low dose," implying they are very relevant to human exposures.

According to his analysis, however, the "low doses" actually span an immense range of concentrations, a billion-fold. In addition, only a small fraction of the exposures in these self-described “low dose” studies are in the range of human exposures, from 0.8 percent to 7 percent depending on the study.

"The term low-dose cannot be understood to mean either relevant to human exposures or in the range of human exposures. However, this is in fact what it has come to mean to the public, as well as many in the media," says Teeguarden.

Analysis of 150 Exposure Studies

The first analysis covered 30,000 individuals, including women and infants, in 19 countries. Human blood concentrations were calculated multiple ways using many kinds of exposure data.

Teeguarden looked to see if BPA concentrations were sufficiently high to be a significant source of estrogen-like activity in the blood. Researchers have long known that BPA can bind to the same proteins that estrogen does – called estrogen receptors – when estrogen is doing its job in the body. However, in most cases, BPA does so much more weakly than estrogen. To trigger biological effects through receptors, BPA concentrations have to be high enough in the blood to overcome that weakness.

"Systematically testing the estrogenicity, or the bioactivity of BPA at the part per trillion concentrations we expect in human blood would seem the most scientific way to substantiate or refute this conclusion," says Teeguarden.

Teeguarden analyzed the data in these studies using multiple independent approaches applied systematically to the data from thousands of individuals. The results showed that human blood levels of BPA are expected to be too far below levels required for significant binding to four of the five key estrogen receptors to cause biological effects.

Teeguarden's analysis also confirmed the findings of many academic and government scientists that biologically active BPA is at such low concentrations in the blood that it is beneath toxicologists' current ability to detect it, raising questions about the role of sample contamination in studies reporting high levels of BPA.

Analysis of 130 Toxicity Studies

In this analysis, Teeguarden compiled all the BPA studies that included the term "low dose" as it referred to human exposure by using such terms as "low-concentration," "environmentally relevant," or "human exposure." From the 130 studies found, he and his PNNL biologist Sesha Hanson-Drury compiled all the doses that were actually used in the studies.

The results showed that a small fraction of the "low doses” used in these studies are within the range of human exposures, with the vast majority being at least 10 to thousands of times higher than what humans are exposed to daily. In addition, the range of concentrations spans from upwards of 10 grams per kilogram of weight per day down to 100 picograms per kilogram of weight per day (a picogram is one millionth of a gram).

"Unfortunately, the low dose moniker has been used by some to promote the importance of selected toxicity studies, for example, in arguments to ban BPA," says Teeguarden. "For BPA and all chemicals, we need more accurate language to present these findings so the public and scientists in other disciplines can understand how human exposures compare to exposures in laboratory studies reporting toxicity.”

What the Sex Lives of California Mice Can Tell You

 

By Alan Caruba

According to Cheryl Rosenfeld, an associate professor of biomedical sciences in the University of Missouri’s Bond Life Science Center, loading up a bunch of California mice with a mega-dose of bisphenol A (BPA) showed researchers that “What we have observed in those models is that BPA affects male rodents differently from females.”

The February 11 UM news release that announced this was titled “Bisphenol A affects sex-specific reproductive behaviors in a monogamous animal species” with a sub-headline that said “Animal findings suggest that gender may also influence chemical risks for humans.”

So, humans are expected to demand that BPA be banned based on the behavior of BPA-besotted California mice, but not the deer mice on which previous similar research was conducted. As noted in the release, “The two rodent species have contrasting mating behaviors.” That’s right, it depends on the sexual proclivities of the species of the mice involved and one has to make a mighty leap of faith that Ms. Rosenfeld’s research applies to humans.

Rosenfeld’s earlier work received notice in a January 2, 2013 Science Daily article which pointed out that, “Following a three-year study using more than 2,800 mice, a University of Missouri researcher was not able to replicate a series of previous studies by another research group investigating the controversial chemical BPA.”

A synopsis of the earlier study noted that “Rosenfeld’s group extended the studies to include animal numbers that surpassed the prior studies to verify their findings were not a fluke and to provide sufficient numbers of animals to ensure that significant differences would be detected if they existed. However, even these additional numbers of animals and extended experiments failed to reproduce the earlier findings.”

It’s worth noting that Ms. Rosenfeld’s later research involving monogamous California mice represented a dose that is a 1,000 times greater than a human would ingest. This research suggests that the anticipated outcome would demonstrate that BPA is harmful.

It reflects a global propaganda campaign to ban a chemical that has been safely in use for fifty years. This campaign is the subject of my six-part series on BPA that can be found at http://thebpafile.blogspot.com/, a blog I maintain that includes other articles on the subject.

As noted on The BPA File, “In 2011, ‘the German Society of Toxicology released a review of more than five thousand previous studies of PBA exposure that concluded that BPA exposure represents no noteworthy risk to the health of the human population, including newborns and babies. Researchers concluded that BPA is neither mutagenic nor likely to be a carcinogen.”

Five thousand studies! At what point does 50 years of safe use to coat the insides of aluminum food cans, protecting the contents against food pathogens such as botulism, put this campaign by environmental groups and others to rest? How many more studies do we need to demonstrate the safety of BPA in making shatterproof safety goggles, DVDs, and scores of other products we use every day?

In March 2012 an Associated Press health reporter, Matthew Perrone, reported that “The Food and Drug Administration has rejected a petition from environmentalists (the Natural Resources Defense Council) that would have banned the plastic-hardening chemical bisphenal-A from all food and drink packaging, including plastic bottles and canned food.” The petition was rejected because the “petitioners did not present compelling scientific evidence to justify new restrictions…”

How compelling is yet another study that involved feeding California mice 1,000 times more BPA than humans would ever ingest? And how would any rational person conclude that alleged changes in monogamous California mice—but not the polygamous deer mice—could be extrapolated to suggest that humans would be affected?

An August 8, 2011 editorial in The Wall Street Journal, “Postscript to a Panic”, noted a study, “financed by the EPA…involved feeding (human) subjects a BPA-rich diet for 24 hours. Researchers then monitored their blood and urine for traces of the chemical” only to find that “the result was BPA levels too low to detect.”

The sheer absurdity of the campaign to get BPA banned reflects a deeper, more sinister agenda by environmental organizations like the Natural Resources Defense Council. It is the belief that the Earth’s human population must be reduced to protect it. Banning BPA would put millions at risk of death from food-borne diseases like botulism.

Given the tenacity with which such groups prosecute their agendas, we can be assured that these obsessed anti-BPA “researchers” aren’t going to go away.

© Alan Caruba, 2013

Dumb and Dumber BPA "Science"

by Angela Logomasini on January 16, 2013

   

Rationalizations to support claims that the chemical bisphenol A (BPA) poses a real and serious health threat have gone from dumb to dumber! Even reputable researchers make their case by regularly citing one inconclusive study to suggest another inconclusive study is meaningful. But science doesn’t work that way.

Used to make hard, clear plastics and resins that line cans containing everything from soda to soup, BPA is a target of the greens who get plenty help from researchers who use creative rationalizations to spin their findings.

A recent example comes from one of the authors of yet another study on BPA using data from the National Health and Nutrition Examination Survey (NHANES). It suggests that BPA levels could contribute to heart and kidney disease. But reliance on NHANES data raises a host of questions about the study’s value, as explained in a prior post and in a peer reviewed paper detailing why it isn’t reasonable to draw conclusions from this data. Without even considering that serious defect, we can see from one of the researchers comments that the study isn’t particularly compelling anyway. One of the study’s authors, Dr. Leonardo Trasande, explains in Science Daily:

While our cross-sectional study cannot definitively confirm that BPA contributes to heart disease or kidney dysfunction in children, together with our previous study of BPA and obesity, this new data adds to already existing concerns about BPA as a contributor to cardiovascular risk in children and adolescents.

In other words, the value of this latest study rests at least in part on the value of the prior study for which Trasande is also an author. This prior study appeared in the Journal of the American Medical Association last year that suggested BPA contributes to obesity, but, as I noted then, the authors say the findings are inconclusive. Specifically, Trasande and coauthors state within the JAMA study:

BPA exposure is plausibly linked to childhood obesity, but evidence is lacking to date … This cross-sectional study, when considered in isolation, is at best hypothesis generating.

Why and how could a study with findings are “at best hypothesis generating” strengthen an “unconfirmed” finding of another study? Supposedly it can because the authors in the JAMA study maintain that it is more than “hypothesis generating” because of findings from yet another study. This one dates back to 2004, and it too is inconclusive, as I detailed in my post on the JAMA study.

Perhaps most telling of all are the studies that Trasnade and his colleagues don’t mention, including a recent rodent study that could not find an association between BPA and obesity. They also don’t mention an EPA-funded study that shows humans pass BPA quickly from the human body — making it unlikely to have any impacts. Nor do they mention, the study questioning the underlying NHANES data.

In sum, ignoring evidence to the contrary, Trasade suggests that his latest inconclusive study is meaningful because of finding of the inclusive JAMA study, which is only made more than “hypothesis generating” because of the existence of yet another inconclusive study.

This very fishy line of reasoning really isn’t about science. It’s about an agenda, as Trasnade explains in Science Daily:

It [his research] further supports the call to limit exposure of BPA in this country, especially in children … Removing it from aluminum cans is probably one of the best ways we can limit exposure. There are alternatives that manufacturers can use to line aluminum cans.

While he may mean well, this advice is the more dangerous proposition because BPA resins are used to prevent the development of pathogens like E. coli in our food. Without it, many people could suffer from real kidney disease, and some could die.

Source: OpenMarket.Org
http://www.openmarket.org/2013/01/16/dumb-and-dumber-bpa-science/?utm_source=feedburner&utm_medium=email&utm_campaign=Feed%3A+Openmarketorg+%28OpenMarket.org%29

NYU School of Medicine Tells Big Lies About BPA

The Dihydrogen Monoxide Award

January 9. 2013 ~ http://hansoffplastics.com

We spend a lot of time and effort ferreting through outrageous media coverage of science issues in determining our Dihydrogen Monoxide Award winners but this time, we’re doing something a little different.

This week’s award goes to the dutiful flacks at the NYU School of Medicine for their January 9, 2013 news release on the results of a study of the chemical bisphenol A (BPA) whose co-lead author is a university researcher. In fairness, we should state that a flack’s job is to get media coverage of whatever it is they’re pushing. However, we don’t think that should include shopping around false information in pursuit media coverage and the January 9 release is chock full of blatantly false information.

Let’s start with this whopper, which nicely sets the stage for whipping the media into a frenzy. It’s a close cousin of the old “banned substance” lie:

“The study adds to the growing concerns about BPA, which was recently banned by the U.S. Food and Drug Administration…”

FACT: The US Food and Drug Administration has done nothing of the sort – ever! As a matter of fact, the FDA has explicitly refused to ban BPA. Oh dear, did the good PR folks at NYU forget that the FDA gave a gigantic smack-down to the Natural Resources Defense Council when the agency rejected the NRDC’s petition to ban BPA? Not very professional, kids. As an antidote for this sort of problem, we recommend reading. It’s very helpful, especially for those interested in facts. Just think of the motto of Faber College – Knowledge is Good.

Apparently not content with promoting the exact opposite position of an American regulatory agency, NYU’s School of Medicine decided to look north and east for new positions to misrepresent:

“Its use has been banned in the European Union and Canada…”

Wow! These guys are just makin’ up stuff left and right! As recently as September 2012, Canada went out of its way to affirm the safety of BPA in food contact applications.

Not only that, but Health Canada also went so far as to note that their position affirming the safety of BPA was the same as policies in the European Union, the United States and Japan!

“… based on the overall weight of evidence, the findings of the previous assessment remain unchanged and Health Canada’s Food Directorate continues to conclude that current dietary exposure to BPA through food packaging uses is not expected to pose a health risk to the general population, including newborns and young children. This conclusion is consistent with those of other food regulatory agencies in other countries, including notably the United States, the European Union and Japan.” (Emphasis added)

As for the European Union, not only has the EU’s food safety body declared BPA safe for use in food contact, it went out of its way to explain why French efforts to ban the stuff are wrong headed.

Whoa, Nelly! How can a guy get so many fundamental facts wrong in ginning up a news release and not get banned from writing future news releases? It’s a mystery to us too.

There there’s the classic “banned from baby bottles,” line. It thrives on misinterpreting the facts:

“Its use has been banned… in the United States for use in baby bottles and sippy cups.”

This is a factual statement. But what makes it such a cheap shot is the fact that the only reason FDA took the action of banning BPA from baby bottles is because it was asked to ban it for that purpose – BY THE PEOPLE WHO MAKE BABY BOTTLES!

Check out this coverage by USA Today. First, we have the headline:

After baby bottle makers voluntarily ban BPA, FDA makes it official

Then there’s the third paragraph of the USA Today article, which we conveniently repeat hear for your review:

“Consumers can be confident these products do not contain BPA,” FDA spokeswoman Shelly Burgess said. She said the agency did not act because it believes BPA is unsafe but because the bottle industry wanted a formal ban for baby products. “We continue to support the safety of BPA for use in products that hold food.”

Let me repeat that: “She said the agency did not act because it believes BPA is unsafe but because the bottle industry wanted a formal ban for baby products.”

See what we mean? The people who make baby bottles stopped using the stuff years ago and asked the FDA to formally ban the stuff, which it did, and in the process the FDA reiterated “… the safety of BPA.”

One thing that was not factually flawed was how the news release tried to make the case for more money for more research. After all, that may be the point here – to use a bunch of false information to create a lot of bad reporting to raise more money so more researchers can increase their prestige and salaries by conducting more research. It’s kind of a vicious cycle, you know?

So congratulations to the cracker-jack flack squad at NYU’s School of Medicine for winning this week’s Dihydrogen Monoxide Award! We give this award four stars. After all, it manages to completely misrepresent the BPA policy positions affecting a score of nations and hundreds of millions of people. It takes a special kind of skill to pull a boner of this proportion.

BPA Studies Alleging Toxicity Unreproduceable

Previous Studies On Toxic Effects of BPA Couldn't Be Reproduced

Jan. 2, 2013 — Following a three-year study using more than 2,800 mice, a University of Missouri researcher was not able to replicate a series of previous studies by another research group investigating the controversial chemical BPA. The MU study is not claiming that BPA is safe, but that the previous series of studies are not reproducible. The MU study, published in the Proceedings of the National Academy of Sciences, also investigated an estrogenic compound found in plants, genistein, in the same three-year study.

"Our findings don't say anything about the positive or negative effects of BPA or genistein," said Cheryl Rosenfeld, associate professor of biomedical sciences in MU's Bond Life Science Center. "Rather, our series of experiments did not detect the same findings as reported by another group on the potential developmental effects of BPA and genistein when exposure of young occurs in the womb."
Creating reliable data on the effects of the chemicals on mice is important to human health since people are frequently exposed to BPA and genistein and humans share similar biological functions with mice. BPA is a chemical used in certain plastic bottles and may be found in the lining of some canned goods and receipt paper. Genistein occurs naturally in soy beans and is sold as a dietary supplement. Research by Fredrick VomSaal, professor of biological science at MU, and others suggests the chemicals may have other adverse effects on many animals, including humans.

Researcher who conducted the original series of experiments claimed that exposure to BPA and genestein resulted in yellow coat color, or agouti, offspring that were more susceptible to obesity and type 2 diabetes compared to their brown coat color, healthy siblings. However, Rosenfeld and her team did not obtain the same results when repeating the study over a three-year period.
After failing to repeat the original experiments findings with similar numbers of animals,

Rosenfeld's group extended the studies to include animal numbers that surpassed the prior studies to verify that their findings were not a fluke and to provide sufficient number of animals to ensure that significant differences would be detected if they existed. However, even these additional numbers of animals and extended experiments failed to reproduce the earlier findings. However, the current studies demonstrate that a maternal diet enriched in estrogenic compounds leads to a greater number of offspring that express an agouti gene compared to those that do not, even though equal ratios should have been born.

"This finding suggests that certain uterine environments may favor animals with a 'thrifty genotype' meaning that the agouti gene of mice may help them survive in unfavorable uterine environments over those mice devoid of this gene, Yet, the downside of this expression of the agouti during early development is that the animals may be at risk for later metabolic disorders, such as obesity and diabetes" Rosenfeld said. "In this aspect, humans also have an agouti gene that encodes for the agouti signaling protein (ASIP) that is expressed in fat tissue and pancreas, and there is some correlation that obese individuals exhibit greater expression of this gene compared to leaner individuals. Therefore, the agouti gene may have evolved to permit humans the ability to survive famine, but its enhanced expression may also potentiate metabolic diseases under bountiful food conditions."

While the research casts doubt on the previous study, Rosenfeld said that by understanding the genetic profile of the mice in the first series of studies, scientists could learn more about the correlation between certain genes and obesity. This could eventually influence prevention and treatment programs for patients with diabetes and other obesity-related diseases in humans.

Web address:
http://www.sciencedaily.com/releases/2013/01/
130102140526.htm