Early BPA exposure linked to prostate cancer risk

June 24, 2013

Early exposure to bisphenol A (BPA) leads to an increased cancer risk in an animal model of human prostate cancer, according to new research findings from the University of Illinois at Chicago.

Early exposure to bisphenol A (BPA) leads to an increased cancer risk in an animal model of human prostate cancer, according to new research findings from the University of Illinois at Chicago.

The study, presented at the Endocrine Society’s annual meeting in San Francisco, was one of several papers from the meeting demonstrating the hormone-disrupting effects of BPA, an additive commonly found in plastic water bottles and soup can liners. A second study linked BPA exposure with cryptorchidism.

The University of Illinois study provides “the first direct evidence that exposure to BPA during development, at the levels we see in our day-to-day environment, increases the risk for prostate cancer in human prostate tissue,” said lead author Gail S. Prins, PhD.

The increased risk can be traced to prostate stem and progenitor cells, which become sensitized to estrogen early in development through exposure to BPA, which mimics estrogen in the body. Environmental exposure to compounds like BPA that mimic hormones has become common, according to Dr. Prins.

Prostate stem cells pass on the increased estrogen sensitivity to the prostate tissues they produce throughout life. Because prostate cancer is fueled in part by naturally rising estrogen levels in aging men, the prostate tissue's increased sensitivity to estrogen makes the development of cancer much more likely, Dr. Prins said.

Previous animal studies by Dr. Prins and colleagues showed that exposure to elevated estrogen or BPA during embryonic development increased the rate of prostate cancer later in life. In the current study, she took human prostate stem cells from deceased young adult male organ donors and implanted the cells into mice, where they formed human prostate tissue.

To mimic exposure to BPA during early prostate development, Dr. Prins fed the mice BPA for the first 2 weeks after the transplant, at doses in line with those seen in pregnant American women. The tissue was then allowed to mature for a month into a human prostate-like tissue.

Next, Dr. Prins exposed the mice to elevated estrogen levels for 2 to 4 months, to mimic the normal rise in estrogen seen in aging men.

Signs of cancer developed in the human prostate tissue in one-third of the mice fed BPA, as compared to 12% of mice that had not been fed BPA. If the stem cells were exposed to BPA before implantation and again during development, 45% showed signs of cancer.

The study linking BPA exposure and cryptorchidism alone “cannot be considered as definitive evidence for an environmental cause of undescended testis,” said lead author Patrick Fenichel, MD, PhD, of the University Hospital of Nice in France. “But it suggests, for the first time in humans, a link that could contribute to one co-factor of idiopathic undescended testis, the most frequent congenital malformation in male newborns.”

 

 

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