The public health consequences of large-scale natural gas extraction by hydrofracturing are all but unstudied. Regulation and permitting has been left to the states because Congress has exempted the process from regulation under the Clean Air and Clean Water Acts. States have all but ignored public health consequences in permitting decisions. And given the protection of formulae for fracking fluids as confidential business information, gauging present and potential health effects is extremely challenging.

Nevertheless, two scientists, Michelle Bamberger and Robert E. Oswald, have issued a preliminary study of what scientists might learn if they could conduct thorough analyses of the health impact of fracking. Their study, Impacts of Gas Drilling on Human and Animal Health, was published in New Solutions, Vol. 22(1) 51-77, 2012 and may be accessed on the Cumulative Impacts Project website.

Here are some excerpts:

“The large-scale use of chemicals with significant toxicity has given rise to a great deal of public concern, and an important aspect of the debate concerns the level of proof required to associate an environmental change with activities associated with gas drilling. Environmental groups typically invoke the precautionary principle. That is, if an action is suspected of causing harm to the environment, then in the absence of a scientific consensus, the burden of proof falls on the individual or organization taking the action.. . .

“Clear health risks are present in gas drilling operations. These cannot be eliminated but can be decreased by commonsense reforms. . . . Our study illustrates not only several possible links between gas drilling and negative health effects, but also the difficulties associated with conducting careful studies of such a link. Simple commonsense policy reforms could facilitate the collection of data that would lead to a careful assessment of the health consequences of gas drilling on both humans and animals.”

“The oil and gas industry has typically . . . approached the issue in a manner similar to the tobacco industry that for many years rejected the link between smoking and cancer. That is, if one cannot prove beyond a shadow of doubt that an environmental impact is due to drilling, then a link is rejected. This approach by the tobacco companies had a devastating and long-lasting effect on public health from which we have still not recovered, and we believe that a similar approach to the impacts of gas drilling may have equally negative consequences.”

“Animals, especially livestock, are sensitive to the contaminants released into the environment by drilling and by its cumulative impacts. Documentation of cases in six states strongly implicates exposure to gas drilling operations in serious health effects on humans, companion animals, livestock, horses, and wildlife. Although the lack of complete testing of water, air, soil and animal tissues hampers thorough analysis of the connection between gas drilling and health, policy changes could assist in the collection of more complete data sets and also partially mitigate the risk to humans and animals. Without complete studies, given the many apparent adverse impacts on human and animal health, a ban on shale gas drilling is essential for the protection of public health. In states that nevertheless allow this process, the use of commonsense measures to reduce the impact on human and animals must be required in addition to full disclosure and testing of air, water, soil, animals, and humans.”

In this extremely interesting article, Andrew Weil—America’s foremost integrative medicine physician—takes on the complex issue of hormesis. For those who follow CHE science dialogue closely, hormesis is controversial within the CHE community. Leading experts on EDCs are frequently suspicious of hormesis and point to industry funding for hormesis research. Weil takes a different tack, acknowledging that hormesis science may be valid but warning vigorously against its abuse. His last three paragraphs tell the story (emphasis added). Read the full article.

“In a larger sense, hormesis may help explain why people who lead strenuous lives with plenty of moderate physical challenges may be healthier and live longer than those in more comfortable circumstances. A 2008 paper titled “Hormesis in Aging” by researchers from the Laboratory of Cellular Aging, Department of Molecular Biology, University of Aarhus in Denmark concluded that “single or multiple exposure to low doses of otherwise harmful agents, such as irradiation, food limitation, heat stress, hypergravity, reactive oxygen species and other free radicals have a variety of anti-aging and longevity-extending hormetic effects.”

“All of which suggests that one of the best routes to health is to make yourself a little uncomfortable now and then. The most profitable discomforts are likely those with which human beings have a long evolutionary history such as physical exertion, getting hungry, regularly tipping back a modest measure of alcohol, short-term exposure to cold or heat, and so on. Conversely, novel stressors—such as the stew of noxious synthetic chemicals in the modern environment with which we have no evolutionary history—are best regarded as guilty until proven innocent.

Which brings up a word of caution: Throughout history, irresponsible politicians and commentators have cited the hormetic effect to justify reducing restrictions on pollution—claiming that a little poison or radiation in the water, air or food supply is good for us. This is dangerous nonsense. Hormesis appears to be of value only when dosages are very carefully controlled, which does not describe releasing random mixtures of toxins, especially synthetic ones, into general circulation. There’s still a great deal we don’t understand about hormesis. Until we do, the smartest policy for governments and industry is to keep the public’s exposure to environmental toxins as low as possible.

CHE’s January 19th call was on the interactions between gut microbiota and environmental chemicals in diabetes and obesity, a new area of research. Separately, gut microbiota and environmental chemicals may both contribute to the development of diabetes and obesity; what about the effects in combination?

The presenters reviewed research that shows that gut microorganisms can affect the absorption, distribution, metabolism, and elimination of environmental chemicals. For example, gut microbiota can cause a leaky gut, increasing absorption of chemicals. Gut microbes can modify polyaromatic hydrocarbons (PAHs) to turn them into estrogenic compounds. Microbiota can also affect detoxification processes in the liver.

An individual’s gut microbes may affect the rate at which they clear chemicals from their body. Seventy five percent of diabetogenic and obesogenic chemicals can be metabolized by gut microbes.

The interactions between gut microbiota and environmental chemicals may be significant not only for diabetes and obesity, but also for other diseases as well. It is a topic sure to see more research in the future.

To access slides and papers, visit the call page.

One fast decade ago, in early 2002, an invited group of about forty leaders from diverse disciplines met at the San Francisco Medical Society to talk about what might be done to improve research, education, practice and more in the broad field of environmental health. Some were longtime friends and colleagues and some were meeting one another for the first time. Various plans were made, but the most important result of that gathering was the organization and network we all know as CHE—the Collaborative on Health and the Environment.

I was honored to co-chair that first meeting and to serve as CHE’s Chairman since then. CHE was a somewhat amorphous concept, a vehicle for fostering closer links between scientists, clinicians, patients, advocates, and others concerned with—and impacted by—environmental factors including but not limited to chemicals in our environment and bodies. A small core group of committed people took on the varied tasks of building this concept into something more tangible, hopefully with varied positive impacts.

A “consensus statement” of concern and purpose went through fifteen drafts and became our unifying credo; a larger public conference at the University of California drew hundreds from around the nation and served as our public “launch.” We began regular conference calls on topics of important and timely interest. A landmark authoritative database of knowledge about toxics was developed and made available to all. Working groups on specific issues were developed to foster all manner of activities. Further conferences on crucial issues were presented, and smaller, targeted initiatives mounted to educate and influence science and policy.

I think it is a striking, and in my experience unusual, mark of our success that with very few exceptions, most of the people “present at the conception” are still active with CHE today. CHE’s unofficial motto of “science and civility” seems to have served us well, as even though we work in a heated realm, serious conflict has been rare. CHE’s “membership” of partners is over 4,000, a very diverse cohort in terms of background, training, discipline, location, and yes, perspective. The profile of those who have joined us in our work in various ways speaks to our credibility and, we hope, judgment.

In this coming year you will hear from a number of our core CHE group about how they see CHE at this point, but I wanted to begin with a message of my pride in being involved with CHE, my gratitude to all CHE partners for joining us, and my encouragement that we all continue on in this important work in CHE’s second decade. My best to you all.

Vitamin D plays an essential role in a number of biologic processes throughout the body. In addition to its long-recognized importance for bone health, vitamin D deficiency is increasingly acknowledged to be associated with a number of other diseases and disorders, including various kinds of cancer. A recently published study adds considerable support to yet another health impact—earlier age of menarche in otherwise healthy girls. If this finding holds up in future studies, the implications are profound.

If sunlight exposure is sufficient, adequate amounts of vitamin D are synthesized in the body. But many people, particularly those living in higher latitudes, are not exposed to enough sunlight to generate adequate stores. And, even in sunny places, skin cancer concerns limit sun exposure. Some foods are fortified with modest amounts of vitamin D in an attempt to address the deficiency. Nonetheless, vitamin D insufficiency remains extremely common in the general population. A recent report from the Institute of Medicine addresses this.

Previous studies reported earlier menarche in girls who live increasing distances from the equator, up to about 45-50 degrees latitude.[1] [2] Since vitamin D status is significantly sunshine dependent, vitamin D insufficiency has been proposed as one explanation. But these ecologic, observational studies are inherently limited and best suited to hypothesis generation. However, the more recent study measured vitamin D levels in a group of girls living in a single city before they experienced menarche and followed them for more than two years. It adds important new data.

This study was published in the October 2011 issue of The American Journal of Clinical Nutrition.[3] It was a prospective, longitudinal study of 242 girls in Bogota, Columbia, whose average age at baseline was 8.8 years when plasma vitamin D (25(OH)D) was measured. They were followed for an average of 30 months and periodically asked about the occurrence and date of menarche.

Fifty-seven percent of the girls who were vitamin D deficient (<50 nmol/L) reached menarche during the follow-up period compared to just 23% of those who had sufficient levels of vitamin D (>75 nmol/L). The average age of menarche in these two groups was 11.8 yrs and 12.6 yrs, respectively. These findings held up after adjustment for age and BMI, so that the results could not be explained by overweight or obesity. The authors concluded that inadequate levels of vitamin D were highly significantly associated with earlier menarche in this group of girls. The biologic mechanisms that might explain this remain speculative.

These findings are likely to have extremely important public health and research implications—particularly if they are replicable in studies of larger populations.

1) If there is a causal relationship between inadequate vitamin D status and earlier age of menarche, it’s yet another reason to do more about widespread vitamin D deficiency in the general population. In this study, just 11.6% of girls were vitamin D–deficient. For comparison, other studies show that 52% of Hispanic and African-American teens in Boston are vitamin D deficient, and a small sample of white pre-teen girls in Maine showed a 48% deficiency with at least one level of 25(OH)D below 50 nmol/L over a three-year period.[4]

2) Among the various kinds of cancer linked to low vitamin D levels, the evidence for increased risk of colorectal cancer is probably the strongest and most consistent. However, a link to breast cancer is sometimes although not always observed. A number of laboratory studies show that vitamin D can inhibit cellular proliferation and promote programmed cell death (apoptosis) and cellular differentiation in breast tissue.[5] [6] Laboratory rodents fed low levels of vitamin D develop more mammary tumors when exposed to a carcinogen than animals fed adequate amounts.[7] The effect is most marked in animals that are also fed a high-fat diet. It appears that vitamin D can inhibit both early and later events in mammary tumor development.

In addition, adequate amounts of vitamin D are necessary for normal mammary gland development. For example, in mammary gland organ culture studies, vitamin D–like compounds inhibit estrogen-induced ductal proliferation and branching.[8] This suggests that vitamin D status in pre-pubertal and pubertal girls could influence breast development and, thereby, breast cancer risk.

Epidemiologic studies virtually always look for associations between adult vitamin D status and breast cancer risk. None has attempted to study the influence of childhood vitamin D status on later breast cancer risk. This would of course be difficult to do and would require decades of data collection.

Thus, although laboratory and epidemiologic data confirm the plausibility of a causal connection between inadequate vitamin D and increased breast cancer risk, considerable uncertainty remains.

3) Collectively, these observations raise an additional question—one having to do with research study design and statistical analyses. Epidemiologic studies examining the relationship between vitamin D status and breast cancer risk usually “control for” age of menarche, since earlier menarche is itself associated with increased breast cancer risk. But this recent study suggests that controlling for age at menarche may not always be appropriate. If childhood vitamin D status influences age of menarche, it could thereby influence breast cancer risk. In general, variables within a causal pathway of an exposure-outcome of interest should not be controlled. In the recent IOM report Breast Cancer and the Environment: A Life Course Approach the committee said:

Moreover, confounders need to be understood as operating, not one-by-one, but rather in a complex network of causal relationships. Graphical tools, such as directed acyclic graphs (DAGs), are sometimes used to identify the appropriate confounders for control, and to identify which factors should not be controlled (Greenland et al., 1999; Hernan et al., 2002). This latter group consists of two categories of variables: (1) factors that are downstream of the exposure, and (2) factors that block a pathway between exposure and disease (e.g., they have antecedents, one that is associated with exposure and the other with disease). Some factors that are downstream of exposure may be intermediates on a causal pathway, but whether they are or not, control for them can introduce bias, except in very specific circumstances (Petersen et al., 2006). In most instances, factors that block an exposure–disease pathway should also not be controlled, in order to obtain unbiased measures of the association of interest.

Thus, in future studies of vitamin D and breast cancer risk, consideration will need to be given to a) childhood as well as adult levels of vitamin D and b) whether or not to control for age at menarche when that variable may be influenced by the exposure of interest (vitamin D status).

In summary, we can add earlier age of menarche to the list of potential health impacts that may be caused by inadequate levels of vitamin D—a common condition in the general population. This finding should be verified in a larger prospective study. The public health implications should not be underestimated.

======

Nothing in the above should be construed as medical advice for individuals. Excessive amounts of vitamin D may also have adverse effects. Vitamin D supplementation decisions can be most accurately guided by measurements of serum 25(OH)D levels. Most experts believe that vitamin D3 is the form that should be used as a supplement.

For those who are interested, the Institute of Medicine report finds the evidence for many of the vitamin D–health endpoints, including breast cancer, insufficient to use for determining a recommended daily intake. But for bone health, where there is consistent, strong evidence here is their conclusion:

Vitamin D: Recommended daily allowance (RDA) 600 IU daily, except 800 IU daily for men and women > 70 yrs of age; Tolerable upper limit (UL): 1000-1500 IU infants; 2500-3000 IU children; 4000 IU adolescents and adults

The IOM report estimates that the average vitamin D intake for males in the US is 300-400 IU daily; for females 200-400 IU daily (varies with age; does not account for vitamin D from sun exposure). Thus, on average, vitamin D intake in the US is well below the RDA of 600 IU daily and the estimated tolerable upper limit.

Conversion: 50 nmol vit D/L = 20 ng vit D/ml

The other day I was talking with a young friend who is “un-schooling,” meaning she is learning through a variety of life experiences, rather than from a traditional school curriculum. The “un-school” philosophy encourages children to initiate projects, while facilitated by adults, to maximize their education.

This got me thinking what it might mean to write an “un-appeal” letter—ideally not an unappealing letter, but one that would speak from the perspective of those who experience our work and use it as a touchstone to educate others. Since learning takes place across the lifespan, it occurred to me that instead of listing all our accomplishments to underscore how worthy CHE is of your investment, I could simply share a few unsolicited notes we recently received from those who are apparently benefitting from our services—so much so they wanted us to know how CHE is enriching their professional, and even personal, lives:   

“I’ve been a member of CHE for a few years now. I’m also a faculty member at Boston College, and teach an upper division course ‘Environmental Disruptors of Development’ that uses the primary literature in endocrine disruption as our main material. As part of the requirements for the course, students edit and significantly expand a Wikipedia page on a term related to the endocrine disruptor field.  My students have posted the complete versions of their pages on Wikipedia…I would REALLY appreciate getting input on these pages from members of the CHE community! There are many experts affiliated with CHE that could give my students some useful advice–with the added benefit of improving the information on endocrine disruptors and related areas that my class is putting into the public domain.”
- Laura Hake, PhD

“I am so very aligned with your thinking and have been trying to incorporate that perspective [see the CHE October newsletter introduction by Elise Miller, MEd, CHE Director] into the work that I have been doing for the last several years….This evolving science integration lends so much support to the general concepts of mind body medicine and ecologic medicine…I think that CHE could help to expand the universe of who thinks ‘environment’ is a part of their cause as well as offer support for our colleagues that will value our support from the environmental science world. We need to integrate across these worlds in which we work daily as well.”
- Mark Miller MD, MPH

“I just wanted to take a minute to thank you for the research digest that you send me. Increasingly I find myself looking through it, studying it, and even looking forward to it. Simply it contains the studies that I need to know about. Mostly they are studies that are not coming in through Medscape and my other physician resources.  Thank you so much for your efforts.”
- Kristen Allott, ND, LAc

“I continue to find CHE postings insightful and informative. They allow me to understand implications and impacts that as a non-scientist I would otherwise not be aware of. Your management of the lists [CHE working group listservs] is exceptional and I see very clearly that the quality of material circulated is exceptional and based in facts. Thank you! There’s a lot of junk “science” out there. As much as some of the truth is hard, it is comforting to know that I have a trustworthy source of information.”
- Sharon Peralta

“The fact sheet [Baby Care Products] is GREAT! There is so much information out there that it is hard to figure out what to read and even harder to determine from what one reads what is actually important. The fact sheet is simple and concise without a lot of the hype that I’ve seen on various websites.”
- Maren Whitson

“Thank you! It’s so wonderful that you’re organizing these calls [archived CHE Partnership calls] with such important figures in the environmental community!”
- Giovanna Joyce Imbesi

“My health has improved dramatically over this past year and I do have to give CHE a big part of the credit for this. I have spent much time trying to pass along what I have learned [from CHE] in my own words to my friends, family and even my government representatives when relevant issues came up.”
- Toni Lineberry

“I love your extensive, easy to use database. When I need to do research or refer others to your site, your site is abundant in information. Knowledge is power.”
- Christina Cicack

If you feel CHE’s work has given you the knowledge you have needed to enhance your own work or life in some way, please consider sending us a note. If this “un-appeal” letter has resonated with you, please also consider making a tax-deductable gift to CHE today.

Finally, I would like to extend my deepest gratitude for all of you who have taught us through your presentations on partnership calls, your insightful responses regarding emerging science, and your expertise and creativity that have shaped our priorities. I very much look forward to continuing to learn and work together in the New Year. 

Wishing you health and peace in 2012,  
Elise

An article from Stone Hearth News is titled “Traits can be inherited, with no DNA: Columbia University Medical Center research.”

This article struck me because of its possible implications for new areas of environmental health research beyond epigenetics. The study focused on “viral-silencing agents” that can be passed down to progeny circumventing the DNA process of inheriting traits that has long dominated the science of hereditary genetics. These agents, known as viRNAs, are able to turn off a virus’ capacity to take over a cell and thereby boost the immune systems of subsequent generations. If these agents can also be influenced by exposures to environmental contaminants, such as endocrine disrupting chemicals, then this could explain why some traits, apparently not associated with the genome, could be inherited. This may mean that the important research being undertaken on gene-environment interactions may now need to include studies that focus on RNA-environment interactions.

The smallest car in the world is one billionth of a metre. 60,000 times smaller than the thickness of a hair. And is self-propelled. Instead of carrying people or freight, it could transport molecules and atoms and be used to reconstruct damaged cells.

Nanoparticles can perform tasks that were previously never thought possible.

In recent years, nanomaterials have been increasingly used in consumer products, from sunscreens to food containers, heralded for making disinfectants that bit more effective or helping to disinfect your socks and underwear. They have even been used to clean up water contaminated with heavy metals.

But the shrinking of particles to a nanoscale can change their properties. As with many emerging technologies, we still have little understanding of the impacts these tiny particles have on our health and the environment. More and more studies are warning of the potential hazardous properties of nanoparticles. For example, nanosilver is known to wash through the sewage system into the water course and kill beneficial bacteria, which in turn disrupts ecosystems. Günter Oberdörster, a prominent expert on nanomaterials and author of the Environmental Health Perspectives (EHP) paper of the year in 2008, recently advised against any use of products containing nanomaterials in sprays, for cleaning surfaces or in self-cleaning materials.

Only this year did the European Union finally agree on a definition of nanomaterials. Although far from perfect, the definition sets the scene for future regulatory assessments on the health and environmental hazards of nanomaterials.

Under the European chemicals legislation, REACH (the regulation on the Registration, Evaluation and Authorisation of Chemicals), only three substances have been registered that are clearly specified as nanomaterials. Due to the small number of nanomaterial registrations under REACH, the registration dossiers do not clearly identify the specific hazards and risks of these substances.

There have been a few attempts in Europeto create a register of the nanomaterials on the market and in consumer products, but all have been voluntary and lacked teeth. Belgium andFrance however, while waiting for the European Commission to propose regulatory actions on nanomaterials, have created a mandatory register to collect information about all nanomaterials on the market, even those used in small quantities.

The technology is still in its infancy. To fully understand the hazards and risks of nanomaterials, it would be necessary to perform animal studies. Under REACH, which aims to minimise testing on animals and requires approval by the European Chemicals Agency, only one proposal for an animal study on a nanomaterial has been submitted. Without an understanding of the potential hazardous impacts of nanoparticles in consumer products, nano-producing companies could be putting our health and the environment at risk.  

ClientEarth, alongside other European environment and health NGOs and consumer organisations, is calling for the responsible use of nanomaterials. We need to see prompt measures to ensure that the nanomaterials placed on the market are safe, and that the safe use of these substances is documented. This can be done through a thorough implementation of the REACH regulation and the adaptation of the information requirements under REACH to address the knowledge gaps on nano.

As the use of nanomaterials continues to expand, to ensure safe use it will be necessary to take account of all fields of chemical use that are not fully addressed under REACH. This would include pesticides, biocides, cosmetics, food and food-contact materials legislation, as well as nanomaterials used in consumer products and their impact on production workers. To add to this, monitoring programs for soil and water need to be implemented in order to ensure that measures to control the risk of nanomaterials are established. To ensure the safe use of nanomaterials, we need a holistic approach to their regulation. The benefits of nanotechnologies must be weighed against the need to prevent any harmful impacts to our health and the environment.

Vito Buonsante is the Health and Environment Lawyer at ClientEarth, a European environmental nonprofit organization. He leads the work on toxics and in particular on the implementation of REACH. Find out more about ClientEarth’s work on toxic chemicals.

In a recent review, published in the leading diabetes journal Diabetologia, Hectors et al. (2011) describe how numerous environmental chemicals affect the insulin-producing beta cells of the pancreas. These effects, the authors argue, may be significant in the development of type 2 diabetes. Chemicals like bisphenol A, PCBs, dioxin, organophosphorous pesticides, arsenic, heavy metals, and others, can all affect how the beta cells function, and can interfere with their capacity to secrete insulin.

In type 2 diabetes, both insulin resistance—the body’s inability to respond correctly to insulin—and beta cell malfunction contribute to the disease. The inability of the beta cells to produce enough insulin leads to high blood glucose levels, and eventually diabetes (in many people with type 2, insulin production is higher than normal, to compensate for the insulin resistance—but it is still inadequate to bring blood glucose under control).   

But beta cell malfunction is not only significant for type 2 diabetes. Gestational diabetes, diabetes that appears temporarily during pregnancy, is also a disease of inadequate beta cell function. A pregnant woman’s body becomes more and more insulin resistant during the course of the pregnancy, and requires more and more insulin to keep her (and her fetus’s) blood sugar controlled. As in type 2 diabetes, if the beta cells can’t keep up with demand, due to some malfunction, gestational diabetes results, with dangers for both mother and child.

Type 1 diabetes is somewhat different, since it is an autoimmune disease. In type 1, the immune system attacks and destroys the beta cells entirely, leading to no insulin production, resulting in high blood sugar levels, diabetes, and lifelong dependence on pharmaceutical insulin. Researchers are trying to figure out why the beta cells are targeted in type 1 diabetes—why are the beta cells, and only the beta cells, attacked? Some researchers think that various environmental factors that affect beta cells, that can stress them, could make them more sensitive to an autoimmune attack, contributing to type 1 diabetes.

In the 1970s, a rat poison called Vacor was removed from the market after it was found to cause insulin-dependent diabetes in people who were poisoned with it. Vacor acts by destroying the beta cells. Yet some people with Vacor-induced diabetes also developed the same signs of autoimmunity as are seen in type 1 diabetes, the same autoantibodies. In this case, a beta cell toxin seems to have led to beta cell autoimmunity. Can other environmental chemicals, that target beta cells, do the same thing? We don’t know yet, but it is a question that needs to be asked.

Chemicals that affect beta cells should be analyzed as possible contributors to not only type 2 diabetes, but also type 1 and gestational diabetes. Growing research suggests that chemicals may indeed contribute to type 2, but so far, there is very little research on whether chemicals contribute to type 1 or gestational diabetes.

All three of these types of diabetes are increasing in incidence. Type 1 has been increasing in industrialized countries since World War 2, the time that these chemicals came into widespread use. Alarmingly, type 1 is increasing fastest in the youngest children, who, like my son, were diagnosed before they turned 5 years old. No one knows why. I think it is time to consider chemicals as potential contributors to this awful disease. I am not alone.

Three scientists and I wrote a letter to Diabetologia that was published this week, in response to Hectors et al’s review of beta cell disrupting chemicals. In it, we argued that these chemicals—that are in the bodies of children and pregnant women—should be considered in research of type 1 and gestational diabetes.

In the past couple of months, three new analyses have asked the question: Is exposure to the widespread environmental chemical bisphenol A (BPA) associated with type 2 diabetes in humans? These three add to two previous studies on the same topic, for a grand total of five. It is a good question to ask, since laboratory evidence shows that exposure to BPA can cause insulin resistance in animals, as well as disrupt the functioning of the insulin-producing beta cells in the pancreas, essentially a recipe for type 2 diabetes (Alonso-Magdalena et al).

As we might expect, the new evidence does not provide a clear-cut answer to that question.

Four of the five human studies on BPA and diabetes used the same dataset, the National Health and Examination Survey (NHANES), which is the Center for Disease Control and Prevention’s biennial biomonitoring survey of a large sample of US residents. Using NHANES data from 2003/04, Lang et al found that higher BPA concentrations in urine were associated with diabetes and cardiovascular diagnoses, but not with other common diseases. Melzer et al then analyzed NHANES data from a subsequent survey, from 2005/06, and found that in those years, BPA levels were lower than they had been in 2003/04. The association between heart disease and BPA remained significant in 2005/06. The associaton between BPA and diabetes was significant in pooled data (2003-06), but did not reach significance in 2005/06 alone.

That brings us to the three more recent analyses. Shankar et al also analyzed NHANES data, and found that pooled data from 2003-08 show a positive association between BPA and diabetes. Silver et al took a slightly different view of the 2003-08 NHANES data, defining diabetes by whether or not participants took a diabetes medication, or had high long-term blood glucose levels (instead of using self-reported diabetes, as in the previous analyses). These authors also found an overall positive association between BPA and diabetes in 2003-08 pooled data, although breaking down by year, the association was only significant in 2003/04, not 2005/06 or 2007/08. Curiously, average BPA levels in 2007/08 were up again slightly, after falling between 2003/04 and 2005/06.

The fifth study on BPA and diabetes analyzed a group of Chinese adults, whose average urinary BPA level was lower than in the US. Dividing participants into quartiles of BPA exposure, the data shows that risk of diabetes was higher in people in the second and fourth quartiles of exposure, but not the third. The overall trend was not significant (Ning et al).

As a whole, the human studies sometimes find significant associations between BPA and diabetes, especially in NHANES data from 2003/04, but not always, not in other years or in other surveys. All of these studies have the same main weakness: a cross-sectional design that only considers one snapshot in time, and does not include multiple exposure measurements or disease development over time. No human studies have yet looked to see whether developmental exposures to BPA increase the later risk of diabetes, despite animal evidence that in utero exposures can cause insulin resistance and reduce glucose tolerance in male mice, predisposing them to diabetes later in life. Considering that there is widespread exposure to BPA, including in pregnant women, aminiotic fluid, and umbilical cord blood, such studies are urgently needed.

References

Alonso-Magdalena P, Quesada I, Nadal A. 2011. Endocrine disruptors in the etiology of type 2 diabetes mellitus. Nat.Rev.Endocrinol. 7(6):346-353. http://www.ncbi.nlm.nih.gov/pubmed/21467970

Lang IA, Galloway TS, Scarlett A, Henley WE, Depledge M, Wallace RB, Melzer D. 2008. Association of urinary bisphenol A concentration with medical disorders and laboratory abnormalities in adults. JAMA 300(11):1303-1310. http://www.ncbi.nlm.nih.gov/pubmed/18799442.

Melzer D, Rice NE, Lewis C, Henley WE, Galloway TS. 2010. Association of urinary bisphenol a concentration with heart disease: evidence from NHANES 2003/06. PLoS.One. 5(1):e8673. http://www.ncbi.nlm.nih.gov/pubmed/20084273.

Ning G, Bi Y, Wang T, Xu M, Xu Y, Huang Y, Li M, Li X, Wang W, Chen Y, et al. 2011. Relationship of Urinary Bisphenol A Concentration to Risk for Prevalent Type 2 Diabetes in Chinese Adults: A Cross-sectional Analysis. Ann.Intern.Med. 155(6):368-374. http://www.ncbi.nlm.nih.gov/pubmed/21930854

Shankar A, Teppala S. 2011. Relationship between Urinary Bisphenol A Levels and Diabetes Mellitus. J.Clin.Endocrinol.Metab  http://www.ncbi.nlm.nih.gov/pubmed/21956417

Silver MK, O’Neill MS, Sowers MR, Park SK. 2011. Urinary Bisphenol A and Type-2 Diabetes in U.S.Adults: Data from NHANES 2003-2008. PLoS.One. 6(10):e26868. http://www.ncbi.nlm.nih.gov/pubmed/22046388