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Joe Schwarcz: When it comes to bisphenol A there is smoke, but is there fire?

During the 1930s, Swiss chemist Pierre Castan was researching materials for denture repair and American Sylvan Greenlee was working on novel paints.

From: http://www.montrealgazette.com/Date: 2014-03-18 08:43:37Views: 299

During the 1930s, Swiss chemist Pierre Castan was researching materials for denture repair and American Sylvan Greenlee was working on novel paints. Independently, the two hit upon epoxy resins, one of the most useful classes of chemicals ever developed. These resins find a wide array of uses in particular for abrasives industry, which usually serve as the bonding agent. Moreover, epoxy glues help hold together our cars, airplanes, furniture, boats, skis and electronic equipment. Without them, our world would literally become unglued. 

But there is a sticky point with epoxies, namely that they are formulated with that infamous chemical, bisphenol A (BPA). This has prompted a search for a replacement, particularly in canned foods where epoxy resin is used as a coating to separate the metal from the contents. Such a barrier is crucial because dissolved metal can catalyze decomposition and impart an undesirable taste to food. Furthermore, as the metal dissolves, pinholes can form in the can, opening an entry point for bacteria and undermining the whole canning process. Epoxy resins are ideal for the protective layer because they form an airtight seal, stand up to the heat and pressure of sterilization, do not chip even if the can is dinged, and do not alter the taste or smell of food.

Epoxy resins are polymers, meaning they are composed of long chains of individual molecules, or monomers, joined in a chainlike fashion. One of these monomers is bisphenol A, notorious because of its estrogen-like properties. Depending on whom one listens to, bisphenol A is either responsible for a stunning array of conditions ranging from cancer and heart disease to obesity, or is an innocent bystander, falsely accused. Because of the publicity that BPA has received, numerous experts have weighed in with their opinions, joined by a plethora of bloggers — many of whom are ignorant of the difference between hazard and risk, and have not the slightest familiarity with the basic principles of chemistry, biology and toxicology. As usual, the public is left stressed and confused.

Besides epoxy resins, bisphenol A is used to make thermal paper for cash-register receipts, as well as polycarbonate plastics for sporting equipment, cookware, automobile parts and water coolers. We touch cash receipts, eat canned foods and are exposed to dust that contains BPA as a result of abrasive contact with epoxy-based flooring, glues, paints and electronic equipment. Look for it and you will find it almost anywhere, except in blood, where it would matter the most. A recent Swedish study confirms earlier ones that found no detectable levels in the bloodstream of people — and proposes that previous studies that did detect the chemical used contaminated samples. Indeed, BPA and its breakdown products are known to be quickly eliminated in urine.

We are then l eft with the notion that levels in the urine are reflective of exposure, but not of biological activity, since that would require presence in the blood. Mennonite women who shun consumer products, don’t eat canned foods and don’t travel in cars do indeed have lower levels of BPA in their urine. However, they don’t have a longer life expectancy, and they do not have a different disease pattern from the general population. Even if they did, it could not be ascribed to BPA because of genetic differences and totally different lifestyles. Nevertheless, many studies are based on measurement of BPA in the urine, and given that the average North American has detectable levels, and that there is no shortage of disease, a little data dredging can link BPA to almost any condition one selects. Such associations can never prove cause and effect, but they can create worry.

There are also animal and laboratory studies galore about BPA. But what do we make of them? You can take mice, implant human prostate cells, feed them BPA, treat them with estrogen to mimic the natural rise in aging men, and you can show an increase in prostate cancer. Whether the doses used reflect human exposure is questionable, as is the reliability of implanted cells in young mice being a model for what happens in an adult male.

Another rodent BPA experiment led to headlines such as “Is there a link between migraines and plastic?” accompanied by pictures of plastic water bottles that are made of polyester and have nothing to do with BPA.

In this study, a tube was surgically implanted into the brains of female rats, apparently a procedure that creates migraine symptoms. I don’t doubt it. When these animals were subsequently injected with BPA, they showed less movement, avoided loud noises and strong light, exhibited signs of tenderness to the head and were more easily frightened. I suspect anyone with a tube implanted in their head would probably show signs of tenderness and fear. Such research gets you published and a few headlines. But it does little to advance our knowledge of bisphenol A.

There’s no doubt that when it comes to BPA there is smoke, but the big question is whether there is fire. The definitive experiment, of course, cannot be done, because we can’t use humans as guinea pigs and feed them chemicals of interest. So it comes down to relying on rodents, laboratory experiments and human epidemiological data to arrive at a hopefully reliable educated guess. This is exactly what the European Food Safety Authority (EFSA) has just done.

After examining a wealth of studies, the EFSA established a tolerable daily intake (TDI) of five micrograms/kg body weight/day, 10 times less than the previous TDI. A newer more reliable method of estimating risk was used based on actual amounts of BPA known to affect the kidneys, liver or mammary glands of animals. The highest estimate for combined oral and non-oral exposure to BPA in people was found to be 30 per cent to 50 per cent less than the new, lower TDI. The EFSA therefore concluded that exposure to BPA is too low to be of concern, the same conclusion arrived at by Health Canada and the U.S. Food and Drug Administration.

Still, it would be desirable to replace epoxy resins in canned foods with substances that don’t have the Damocles Sword of “endocrine disruptor” hanging over their head. Some other plastics and vegetable resins are available for foods of low acidity like beans, but so far none can match the efficacy and versatility of epoxy resins. But some ingenious chemist will undoubtedly solve the problem.

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