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    Studies target BPA, plasticizers in prostate cancer, fecundity

    Levels of bisphenol A (BPA) in men’s urine could be a marker of prostate cancer, and male exposure to other environmental chemicals used in the manufacture of plastics appear to negatively impact time to pregnancy, two separate studies have found.

    The first study, published online in PLOS ONE (March 3, 2014), provides the first evidence that urinary BPA levels may help predict prostate cancer and that disruption of a cell duplication cycle through exposure to low-dose BPA may cause cancer development in the prostate, according to researchers from the University of Cincinnati.

    BPA, an environmental pollutant with estrogen activity, is commonly used to make hard, clear plastic and is common in many food product containers. It has been linked to neurologic defects, diabetes, and a number of cancers, including prostate and breast cancer.

    Lead investigator Shuk-mei Ho, PhD, of the Cincinnati Cancer Center and UC College of Medicine, says that while animal studies have shown that BPA contributes to the development of prostate cancer, human data are scarce.

    "The adverse health effects of BPA are extensive, and studies in animals have proven this,” Dr. Ho said. "However, human studies linking BPA exposure to heightened cancer risk are limited. Our study examined the association between urinary BPA levels and prostate cancer and assessed the effects of BPA on the initiation of centrosome abnormalities as an underlying mechanism promoting prostate cancer formation.”

    A centrosome is an organelle required for proper cell division, and centrosome abnormalities are frequently observed in cancers.

    In the study, Dr. Ho and colleagues assessed the PSA of 60 urology patients using urine samples. Higher levels of BPA were found in prostate cancer patients than in non-prostate cancer patients (5.74 µg/g creatine vs. 1.43 µg/g creatine), and the difference was even more significant in patients less than 65 years of age.

    Additionally, researchers examined prostate cells—normal and cancerous—using immunofluorescence, allowing them to visualize the distribution of the target molecule and look specifically at centrosomal abnormalities and growth patterns.

    "Exposure to low doses of BPA increased the percentage of cells with centrosome amplification two- to eightfold,” Dr. Ho said. "BPA is not a recognized carcinogen, and questions surrounding the mechanism behind the positive correlation of BPA exposure with prostate cancer have arisen.”

    In a statement, the American Chemistry Council said “this very small study fundamentally misinterprets well-understood facts about how BPA is processed in the body, and inappropriately interprets a statistical association to suggest that recent BPA exposure is a key predictor of prostate cancer.”

    “The fundamental flaw in this report is the authors’ complete misunderstanding of important analysis from the U. S. Centers for Disease Control and Prevention (CDC) on interpretation of BPA exposure measurements from single urinary spot samples,” the Chemistry Council added. “Because BPA is processed quickly in the body and eliminated, measuring BPA levels at one point in time provides essentially no information about BPA levels at an earlier time period. In direct contrast, the authors suggest that a single urine sample collected from study participants when prostate cancer is diagnosed could represent their exposures when prostate cancer initiated and developed, which likely would have been many decades earlier. This suggestion is absolutely contrary to the analysis from CDC and, accordingly, this study has no capability to establish a cause-and-effect relationships from the reported statistical associations.”

    Continue to next page for coverage of the second study.


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