BPA in canned foods

We found alarming levels of BPA in a range of canned foods – including baby foods.
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01 .Introduction


In brief

  • We tested 38 canned foods, covering major brands of baby food, baked beans, coconut milk, corn kernels, evaporated milk, ham, olive oil, pineapple, sardines, spaghetti, tomato soup, tomatoes and tuna.
  • Five samples contained more than 200 parts per billion (ppb) of Bisphenol A (BPA), a chemical many experts now believe can cause serious health problems. A further 17 samples contained BPA at levels within the 10ppb-200ppb range.
  • We found higher levels of BPA than reported in similar tests overseas.
  • Of even greater concern, we found relatively high levels of BPA in some canned baby and infant foods.

You can take action by emailing Australia’s Parliamentary Secretary for Health and Ageing and tell him that you want all foods made for babies and toddlers to be BFA-free.

What we found

While none of the foods we tested contained BPA in excess of the European Union’s limit of 600ppm (there is no limit set in Australia), 33 of the 38 samples contained some BPA.

Just one serving of 29 of them would give a 70kg adult more BPA than some experts now believe to be a safe daily level of exposure (0.0024 micrograms per kilogram of body weight per day). Those with the highest amounts of BPA (more than 200ppb) were samples of Edgell Corn Kernels, John West Tuna Olive Oil Blend and, particularly concerning, three canned baby or infant foods – all from Heinz.

We haven’t given actual BPA levels because:

  • Levels in the same product bought at a different time or from a different store could differ from our test results.
  • Our test only represents a snapshot of the market and doesn’t provide enough information to draw general conclusions about levels of BPA in any particular brand or type of product.
  • Our findings are of concern because they indicate the extent of potential exposure.

Genuine health concerns

Our national regulator, Food Standards Australia New Zealand (FSANZ), maintains that the very low levels of BPA in food pose no significant health risks. 

For adults, our dietary intake appears to be well below the daily upper limit of safe exposure set by the US Food and Drug Administration and European Food Safety Authority (50 micrograms per kilogram of body weight).

Infants and small children are at greater risk because of their small body weight and rapid growth. One serving of several of the infant foods we tested delivers about 50 micrograms of BPA in one hit, so a 10kg infant would get 10% of the safe exposure limit from this one source alone.

Worse, new scientific evidence is suggesting that the limit of safe exposure should be set much lower.


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Brands are in alphabetical order within groups; country of origin listed.



(A) Baby food (“all ages from 6 months”)
(B) We tested a second batch and found BPA between 199ppb and 100ppb
(C) Toddler food; 1-3 years
(D) Baby food (“4-6 months”)
(E) Made in Australia from local and imported ingredients
(F) Made in New Zealand from local and imported ingredients

cans-table-2 cans-table-1


Table notes
(A) Made from local and imported ingredients.
(B) Made in New Zealand from local and imported ingredients.

Simplot (manufacturer of Edgell and John West) told CHOICE they are sensitive to consumer concerns and have cans with BPA-free linings under test.

In response to CHOICE’s test results, Heinz has announced it will move to BPA-free packaging for baby food products. A company spokesman said, “While we believe there is no risk to consumers, we are keen to allay any concern and so have opted to remove BPA from all baby food packaging.”

In the UK, Heinz has also committed to moving to alternatives – and for its beans, pasta and many soups, protective coating is only applied to the can ends.

In Japan, most manufacturers voluntarily changed their can linings in 1998 to reduce or eliminate the use of BPA.

In the US, however, the canning industry is claiming that viable substitutes are not yet available. Sixteen products on test contained less than 10ppb of BPA, and eight of these contained no detectable BPA at all.

So it’s clearly possible for manufacturers to produce canned food with little or no BPA contamination.

CHOICE verdict

We would like to see the food industry take more urgent action to phase out food packaging materials that release toxic chemicals into food. This includes plasticisers such as phthalates, used in some food containers and PVC cling wrap, as well as BPA-based polycarbonate bottles and epoxyresins for lining cans.

While FSANZ is currently surveying the BPA content of a range of Australian processed foods (and expects to report on the findings next month), we would also urge the regulator to be more proactive in protecting Australian consumers.

Safety laws recently put into place by the EU shift the burden of proof to industry, requiring manufacturers to prove their products don’t harm human health or the environment. We believe similar rules should also operate here. As a matter of urgency, CHOICE wants the government to phase out the use of BPA-containing packaging for all baby foods and foods designed for toddlers and young children.

In the meantime, you can reduce (although not necessarily eliminate) exposure to BPA and other risky chemicals by taking the following steps:

  • Choose fresh food whenever possible
  • Consider alternatives to canned food, beverages and juices
  • Use glass or ceramic containers when heating food in microwave ovens.

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.

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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