Our Stolen Futurea book by Theo Colborn, Dianne Dumanoski, and John Peterson Myers



background on bisphenol A

Sakaue, M, S Ohsako, R Ishimura, S Kurosawa, M Kurohmaru, Y Hayashi, Y Aoki, J Yonemoto and C Tohyama. 2001. Bisphenol-A Affects Spermatogenesis in the Adult Rat Even at a Low Dose. Journal of Occupational Health 43:185 -190.


Sakaue et al. find that bisphenol A at affects characteristics of the adult rat testes at levels as low as 20 µg/kg (parts per billion), including a reduction in sperm count. The most surprising aspect of this finding is that the effects were seen in rats exposed to BPA after puberty. Because adult processes are thought to be less sensitive than developmental process, this is of concern not just because of the direct effect on the testis, but also because it implies that more sensitive lifestages will be sensitive to even lower levels. Impacts of in utero low-level exposure to BPA have been noted for other endpoints (e.g., prostate characteristics) as well as sperm count.

What did they do? Sakaue et al. exposed 13-week old rats for six days to different concentrations of BPA, delivered by gavage. They compared the impacts of exposure to control animals, measuring a series of parameters that reflect the condition of the testis, including weight of testis, daily sperm production, and protein action. The experiments were conducted in several rounds: first at 200 mg/kg of BPA, and then because of the positive results at this level, at a much lower ranges (down to 2 µg/kg).

They also performed an analysis of protein expression in the testes of males exposed to a single dose of BPA at 20 µg/kg. The analysis was done using two-dimensional polyacrylamide gel electrophoreisis.

What did they find? In their experiments examining sperm count, testicular weight and testicular structure, Sakaue et al. found significant affects of BPA exposure at levels as low as 20 µg/kg with hints (not significant) in the data at effects even down to 0.2 µg/kg (see figure, below).

An important background finding necessary to interpret their results is that in the control animals, the testis continue to develop from day 13 to day 18. Hence while these rats are post-pubertal, their testes are still developing.



Their measurements of daily sperm production (right) revealed that significant differences could be observed at 20 µg/kg. In this experiment, BPA dose ranged from 2 nanograms per kg (parts per trillion) to 2 milligrams/kg (parts per million). A dose-response relationship is suggested even at 200 ng/kg.

Significant differences from controls are indicated by the red dots (one dot, p <0.05; 2 dots, p < 0.005). Two control groups were used, one with no treatment, the other exposed to the mixture of ethanol and corn oil that was used to deliver the BPA, but without BPA.

Their analysis of details of the impacts of BPA led them to conclude that the effect of the contaminant was to BPA "suppressed the increase in germ cells per Sertolli cell" that normally takes place as the testis matures from week 14 to week 18.

The protein analysis using gel electrophoresis revealed changes in the expression patterns of three proteins. "These changes were repeatedly observed in different rats, indicating that administration of 20 µg/kg could affect protein expression in the adult testis."

What does this mean? According to the authors, "we show here for the first time that environmental endocrine disrupters such as BPA alter spermatogenesis in a linear manner in a dose range which is perhaps relevant to the daily level of exposure in man."

These findings add to the accumulating evidence indicating that regulatory agencies should immediately reassess acceptable exposure levels for people. Acceptable daily intake in the United States and Japan is now set at 50 µg/kg, more than twice the level observed here to cause adverse effects.

Industry maintains (Bisphenol A website, 23 December 2001) that human exposure to BPA is far lower than anything that is likely to cause adverse effects. They continue to contest accumulating evidence that BPA at very low levels does have biological impacts in animals, giving credence to negative studies from their own laboratories and dismissing positive studies from independent laboratories. This same pattern prevailed for years in public health debates about tobacco smoke and about lead.

Industry also claims that long experience with BPA has proven its safety. This is simply not true. The epidemiological studies that would test for the adverse effects observed in animals have not been done in people. What the absence of data on this proves is ignorance, not safety.





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