BPA in canned foods

We found alarming levels of BPA in a range of canned foods – including baby foods.
 
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04.The BPA debate

No one disputes that BPA is toxic at high levels of exposure. Experts are divided over whether BPA at the low levels found in foods poses significant risks to human health.

FSANZ, in line with the US Food and Drug Administration (FDA), The UK Food Standards Agency, and other national food regulators, maintains that the safe level of the chemical to ingest is 50 micrograms per kilogram of body weight per day.

None of the foods we tested delivers more than 10% of this amount per serving. But a number of independent scientists recently expressed concern that this limit is based on experiments done in the 1980s, rather than on the hundreds of recent animal and laboratory studies that suggest we could be at risk from much lower doses.

The case for a high safe limit

  • The currently accepted safe limit, based on extensive animal studies, was originally set by the US Environmental Protection Agency in 1988 and subsequently adopted by the FDA.
  • The European Food Safety Authority reviewed the evidence in 2006 and concurred with the FDA’s safe limit. The Authority’s experts pointed to inconsistent findings in studies of low-dose effects, and questioned the scientific rigour of many of them.
  • Two recent industry funded overviews also concluded there’s no consistent evidence for harmful effects from low doses of BPA, and a big study (also industry funded) published earlier this year found no effects from BPA on brain development in rats.

The case for a low safe limit

There’s growing evidence to suggest exposure to low levels of BPA may be linked to an alarmingly diverse list of illnesses such as infertility, obesity, breast and prostate cancer, diabetes, cardiovascular disease, thyroid malfunction and attention deficit disorder.

  • In 2007, an international panel of 38 experts concluded that “the wide range of adverse effects of low doses of BPA in laboratory animals … is a great cause for concern with regard to the potential for similar adverse effects in humans”.
  • In 2008, an FDA special scientific advisory panel reported that the agency’s basis for setting safety standards to protect consumers was inadequate and should be re-evaluated. A major US study has since identified a direct link between exposure to low levels of BPA and increased risk of diabetes and heart disease.
  • In 2009, the International Endocrine Society declared endocrine disruptors were a significant concern for public health and called for regulation to reduce human exposure.

Some critics of the current high safety limit also challenge a core assumption made by food regulators that experiments with high doses will necessarily reveal potential hazards from low doses. This assumption originates from the work of the 16th century toxicologist Paracelus, whose dictum “the dose makes the poison” (implying that even toxic substances can be safe as long as the dose remains below a certain threshold) is still a bedrock principle for toxicologists.

Decades of research in endocrinology has consistently shown that hormonally active compounds can cause effects at low doses opposite to those at high doses. So with endocrine disruptors such as BPA, a low dose can be worse than a higher size dose. While the evidence for lowdose effects from BPA is far from conclusive, there’s now far too much of it to be ignored.

 

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The sources we used in preparing this article included:

Biello, D, Plastic (not) fantastic: food containers leach a potentially harmful chemical, Scientific American, February 19, 2008.
Brotons, J.A. et al. (1995). Xenoestrogens released from lacquer coating in food cans, Environmental Health Perspectives, 103, 608-612.
Bucher, J.R. (2009). Bisphenol A: where now?, Environmental Health Perspectives, 117, A96-A97.
Consumer Reports (US), December 2009.
European Food Safety Authority, Opinion of the scientific panel on food additives, flavourings, processing aids and materials in contact with food on a request from the commission related to 2,2-bis(4-hydroxyphenylpropane) (Bisphenol A), Question number EFSA-Q-2005-100, November 2006.
Food Standards Australia New Zealand, Bisphenol A and food packaging, 19 January 2010.
Kang, J.H. et al. (2006). Human exposure to bisphenol A, Toxicology, 226, 79-89.
Lang, I.A. et al. (2008). Association of urinary bisphenol A concentration with medical disorders and laboratory abnormalities in adults, Journal of the American Medical Association, 300, 1303-1310;
Myers, J.P., et al. (2009). A clash of old and new scientific concepts in toxicity, with important implications for public health, Environ Health Perspect., 117, 1652-1655.
Richter, C.A. et al. (2007). In vivo effects of bisphenol A in laboratory rodent studies, Reproductive Toxicology, 24, 199-224.
Stump, D.G. et al. (2010). Developmental neurotoxicity study of dietary bisphenol A in Sprague-Dawley rats, Toxicological Sciences, 115, 167-182.
Vogel, S.A. (2009). The politics of plastics: The making and unmaking of bisphenol A “safety”, American Journal of Public Health, 99, S559-S562.
vom Saal, F.S. and Myers, J.P. (2008). Bisphenol A and risk of metabolic disorders, Journal of the American Medical Association, 300, 1353-1355;
vom Saal, F.S. et al. (2007). Chapel Hill bisphenol A expert panel consensus statement: integration of mechanisms, effects in animals and potential to impact human health at current levels of exposure, Reproductive Toxicology, 24, 131-138.
von Goetz, N. et al. (2010). Bisphenol A: How the most relevant exposure sources contribute to total consumer exposure, Risk Analysis, Jan 29.
Wade, V. et al. (2006). Large effects from small exposures. III Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure, Endocrinology, 147, S56-S69.

 
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