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Researchers in the U.S. have linked exposures to trace amounts of bisphenol A, a widely used chemical that leaks from many plastics products, to prostate cancer in animal experiments.

The discovery is considered the first direct scientific evidence connecting prostate cancer to bisphenol A, or BPA, a chemical used to make the polycarbonate for hard plastic water bottles and baby bottles, and the dental sealants used on children's teeth, among its many consumer uses.

The dose causing the adverse effect, given to newborn rats, was set by the researchers to be similar to the amounts commonly found in the blood of people in Western countries exposed to polycarbonate plastic and other BPA-containing consumer items. This dose was 60 per cent below levels Health Canada considers safe, and suggests that current regulatory standards may be too lax.

Dr. Shuk-Mei Ho, one of the researchers who conducted the experiment, said applying the results of any animal experiment to humans should be done "with caution," although she added that the discovery sheds light on a possible cause for prostate cancer.

"This is the first study that shows a clear connection, at least in a rodent," between the cancer and the chemical exposures, said Dr. Ho, chair of the department of environmental health at the University of Cincinnati.

The finding was outlined in the journal Cancer Research.

Dr. Ho said it might be prudent for pregnant women and young boys to try to reduce their exposure to BPA because the period around birth was found to be a vulnerable point for the prostates of the animals subjected to the chemical.

Prostate cancer, which typically afflicts men over 50, is the most commonly diagnosed cancer in Canadian males, with about 20,700 cases expected this year and approximately 4,200 deaths.

The incident rate of prostate cancer has soared in recent decades, and is more than twice as prevalent as it was in the late 1960s. This has led some researchers to speculate that the spike in rates is due to exposures to chemicals that have come into widespread use in recent years, although this view is questioned.

Dr. Laurence Klotz, professor in the department of surgery at the University of Toronto and a leading Canadian prostate expert, says improved testing may be causing the rise in the incidence rate. Changing diets, including more fatty food, could also be an factor, he said. But the new research shouldn't be dismissed: "It's an important paper that further raises concerns about the potential role of these contaminants."

The investigation into possible environmental links to prostate cancer has zeroed in on chemicals, such as bisphenol A, that have a shape that allows them to mimic hormones when absorbed by living things.

In the 1930s, BPA was found to be a synthetic version of the female hormone estrogen. Despite its potential to have a biological effect, in the 1950s chemical companies began to use it as the basic building block for polycarbonate plastic and epoxy resins.

Although estrogen is considered a female hormone, it can also influence the male prostate. The gland, located near the bladder, produces seminal fluid, which transports sperm.

In the experiment, a team of researchers from the University of Cincinnati and the University of Illinois gave newborn male rats trace doses of BPA, equivalent to 10 parts per billion, at a period when their prostates were growing rapidly. When these animals were exposed to estrogen as adults, they were found to be more likely than unexposed rats to develop precancerous prostate lesions.

The experimental procedure has some applicability to human males, whose estrogen levels typically rise with age, in part because they tend to become fatter and fat leads to an increase in the amount of testosterone a male converts into estrogen.

Dr. Ho said the effect on the animal's prostate wasn't caused by a genetic mutation, but by the alteration in the function of one of the rats' genes, a relatively new field of research known as epigenetics.

BPA exposure is believed to have caused the continued operation of a gene that helps regulate an enzyme important for cell growth. The gene is supposed to gradually stop operating as an animal ages, because the cell growth isn't needed. In this case, the gene remains turned on, spurring abnormal growth.