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July 2006 Issue

Shuk-Mei Ho, PhD, is an expert in hormonal carcinogenesis and proteomics.
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Chemical Found in Plastics Linked to Prostate Cancer

By Amanda Harper
Published July 2006

Baby and disposable water bottles. Plastic eating utensils. Compact discs. Even some food cans.

These everyday consumer products all have one thing in common: bisphenol A (BPA), a potentially dangerous chemical used in the manufacturing of plastics that current UC research suggests provides an important clue as to why some males are more likely to develop prostate cancer.


Shuk-mei Ho, PhD, chair of UC’s environmental health department, recently identified the first evidence of a direct link between BPA exposure while in the womb and prostate cancer development later in life.


In a laboratory study, Ho found that animals exposed to low doses of the natural human estrogen estradiol, or the environmental estrogen BPA, during fetal development were more likely to develop an early form of prostate cancer (prostatic intraepithelial neoplasia) than those that were not exposed. 


These findings imply that exposure to environmental and natural estrogens during fetal development could affect the way prostate genes behave, leading to higher rates of prostate disease during aging.

BPA, which can leach out of plastics when heated, is one of many man-made chemicals known as “endocrine disruptors,” which permanently alter the function of the endocrine system by mimicking the role of the body’s natural hormones.


“In this study, early BPA exposure made the prostate more susceptible to precancerous lesions, which are brought on by the adult animal’s exposure to elevated estradiol,” says Ho.

“This is an important discovery, because BPA has been found in human maternal and fetal circulation. If it has such a long-lasting effect—by reprogramming how adult tissues respond many years later—then potential exposure sources during pregnancy need to be scrutinized and minimized.”


Ho’s research team showed that early BPA exposure permanently changed methylation or “tagging” of specific stretches of DNA and the way certain genes are packaged within the nuclei of prostate cells. The gene expression changes, but the DNA sequences and content do not, says Ho.


They found that a specific altered gene—known as phosphodiesterase 4 (PDE4D4) —did not shut down through the natural aging process. Although the gene should normally phase out in adult life, when exposed to estradiol or BPA early in life the animals continued to produce it at high levels.


“We know now that PDE4D4 plays an important role in regulating cellular function, so when it doesn’t shut down as it should, it begins to promote prostate disease instead,” says Ho.


Any application of these findings, she says, to human prostate disease require further study.


“We need to understand the mechanism behind disease to inspire better lifestyle changes and smart manufacturing changes that will make a broader impact on human health,” says Ho. “If we can develop strong biomarkers, we can manage and prevent diseases much earlier.”


More than 1.6 million pounds of BPA, the molecular building block of polycarbonate plastics, are produced in the United States annually.


This research was done in conjunction with Gail Prins, PhD, of the University of Illinois and funded by National Institutes of Health and U.S. Department of Defense grants.

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