BPA levels in urine and risk for prostate cancer — is the association “real”?

A small study published this week in the journal PLoS One this week has provided further evidence of the possibility that significant exposure to the toxic chemical bisphenol A may be associated with heightened risk for a diagnosis of prostate cancer.

The study by Tarapore et al. (and an associated media release from the University of Cincinnati Academic Health Center) inevitably resulted in a great deal of media coverage. (This article in Newsweek seems to be pretty typical.)

So what did Tarapore et al. really show?

The authors looked at data from 60 patients attending a urology clinic. Some had been diagnosed with prostate cancer; others had not. From a purely clinical perspective, they showed that:

  • Levels of BPA in the urine of the prostate cancer patients was significantly higher than in the non-prostate cancer patients (after adjustment for serum creatinine levels).
    • BPA levels in the urine of the prostate cancer patients averaged 5.74 µg/g.
    • BPA levels in the urine of the non-prostate cancer patients averaged 1.43 µg/g.
  • This difference in BPA levels in urine was even more apparent in the younger patients (< 65 years of age).
  • There was a trend toward a negative association between urinary BPA levels and serum PSA levels among the prostate cancer patients but not among the prostate cancer-free patients.

Scientifically, they were also able to show a number of effects of exposure to BPA on prostate cancer cell lines in vitro, including effects on centrosomal abnormalities, microtubule nucleation, and anchorage-independent growth.

Tarapore et al. conclude that their findings:

suggest that urinary BPA level is an independent prognostic marker in prostate cancer and that BPA exposure may lower serum PSA levels in prostate cancer patients. Moreover, disruption of the centrosome duplication cycle by low-dose BPA may contribute to neoplastic transformation of the prostate.

While we certainly wouldn’t want to discount these findings, we also would want to suggest some caution about over-interpretation of these data.

As the authors themselves observe in their abstract: “Human exposure to bisphenol A (BPA) is ubiquitous” today. That is unlikely to be a good thing. However, ubiquitous exposure of men to bisphenol A does not seem to have been associated with any massive increase in risk for clinically significant prostate cancer over the past 40 years, and so one does have to wonder whether any association between exposure to bisphenol A and risk for prostate cancer is of real clinical significance. There is absolutely no doubt that age is still the single greatest risk factor for a diagnosis of prostate cancer (whether clinically significant or not).

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