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Chemical in Plastics Is Tied to Prostate Cancer

THE NATION

Bisphenol A, found in baby bottles and microwave cookware, permanently altered genes in newborn lab rats, a study finds.

June 01, 2006|Marla Cone | Times Staff Writer

Linking prostate cancer to a widespread industrial compound, scientists have found that exposure to a chemical that leaks from plastic causes genetic changes in animals' developing prostate glands that are precursors of the most common form of cancer in males.

The chemical, bisphenol A, or BPA, is used in the manufacture of hard, polycarbonate plastic for baby bottles, microwave cookware and other consumer goods, and it has been detected in nearly every human body tested.

For The Record
Los Angeles Times Friday June 02, 2006 Home Edition Main News Part A Page 2 National Desk 1 inches; 57 words Type of Material: Correction
Prostate cancer: An article in Thursday's Section A about a study that linked prostate cancer to a widespread industrial compound said that rats "were injected with doses 100 to 1,000 times higher than the most recent human testing done by federal officials in 2004." It should have said the testing was reported by federal officials in 2004.

Scientists and health experts have theorized for more than a decade that chemicals in the environment and in consumer products mimic estrogens and may be contributing to male and female reproductive diseases, particularly prostate cancer.

The new study of laboratory rats suggests that prostate cancer, which usually strikes men over 50, may develop when BPA and other estrogen-like, man-made chemicals pass through a pregnant woman's womb and alter the genes of a growing prostate in the fetus. One in every six men develops prostate cancer, a rate that has increased over the last 30 years.

Researchers at the University of Illinois at Chicago and the University of Cincinnati exposed newborn rats to low doses of BPA and found the structure of genes in their prostate cells was permanently altered, a process of reprogramming in early life that promotes cancer in adulthood. One key gene was switched on, producing too much of a cell-damaging enzyme that has been detected in cancerous prostate cells but not normal cells.

Also, as the rats aged, they were more likely than unexposed animals to develop precancerous lesions, or cellular damage, in the prostate that have been known for years to lead to prostate cancer in humans.

"The present findings provide the first evidence of a direct link between developmental low-dose bisphenol A ... and carcinogenesis of the prostate gland," according to the researchers. Results from the team, led by Gail S. Prins, associate professor of andrology at the University of Illinois at Chicago, and Shuk-mei Ho, chair of environmental health at the University of Cincinnati, are reported today in the journal Cancer Research.

Exposure to the chemical "may provide a fetal basis for this adult disease" in humans, the report said.

Dr. Rebecca Sokol, a USC medical school professor who specializes in male hormone research, called the study "cutting-edge." She said it added to a growing body of research, called epigenetics, that suggested environmental chemicals could alter how DNA sequences turned on and off in a fetus, permanently imprinting the genes of a child and sensitizing him or her to disease in adulthood.

Such findings could have major implications for human disease and could, in part, explain why the prostate cancer rate has surged. BPA, used for about half a century, is a key building block in the manufacture of polycarbonate plastic and ranks among the world's most widely used industrial chemicals.

Prins, Ho and other researchers cautioned that the study was conducted on rats, which sometimes reacted differently to chemicals than humans did. Replicating the work in humans is virtually impossible because 50 or more years usually pass from exposure in the womb to the onset of prostate cancer.

"You can't say from the results of this study that this is going to affect humans," Sokol said. But she said the results were in line with previous animal research that showed chemicals could induce genetic changes that altered sperm and other reproductive functions.

The prostate gland, which develops in human males when they are fetuses, is extremely sensitive to natural estrogen. As a result, scientists have long theorized that prostate cancer could be increasing in men because of their exposure to estrogen-like chemicals in the womb.

Unlike carcinogenic chemicals that can cause profound damage to DNA, BPA seems to inflict subtle changes that are passed from one generation to the next, Sokol said.

"The big focus today is whether or not environmental toxicants will induce heritable changes in gene function.... In other words, is there something that happens to alter genes without actually altering the genetic code?" asked Sokol, who studies the effects of chemicals on sperm. "This [new study] is cutting-edge research in this field and the role that environmental toxicants may play in altering the genetics of exposed offspring."

Steve Hentges, a representative of the American Plastics Council, called it "fascinating research, a good piece of research" that should be studied further. But he said the "real question is what does this mean for human health," because there are too many limitations in the study for it to apply to humans.

"No one has actually observed prostate cancer after any treatment with BPA," he said.

The study's authors said the animals developed the precancerous lesions and genetic changes when exposed to low concentrations of the chemical similar to the amounts found in human blood and fetuses.

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