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


  Emerging science on mechanisms affecting sperm quantity and quality  


Kuriyama, SN, CE Talsness, K Grote and I Chahoud. 2004. Developmental exposure to low dose PBDE 99: 1- effects on male fertility and neurobehavior in rat offspring. Environmental Health Perspectives, in press.

Kuriyama et al. report that rats exposed in the womb to a single low dose of a widespread brominated flame retardant become hyperactive and have decreased sperm counts. The effects are observed at an exposure level within the range that has been found in samples of breast milk from US mothers.

Gray, LE, J Ostby, E Monosson and WR Kelce. 1999. Environmental antiandrogens: low doses of the fungicide vinclozolin alter sexual differentiation of the male rat. Toxicology and Industrial Health 15: 48-64.

Gray et al. found that ejaculated sperm counts in adult mice were reduced by about 90% for males that had been in the womb when their mothers were exposed, via feeding, to 50 mg/kg/day of vinclozilin, a powerful anti-androgen used as a fungicide. More...


  Sharpe, RM, JS Fisher, MM Millar, S Jobling and JP Sumpter. 1995.Gestational and lactational exposure of rats to xenoestrogens results in reduced testicular size and sperm production Environmental Health Perspectives 103(12):1136-1143.

In this experiment, Sharpe et al. tested a key hypothesis on the mechanism by which exposures to endocrine disruptors in utero might affect adult sperm count. This hypothesis, advanced by Sharpe and Skakkebaek in 1993, proposes that the reported decline in sperm count is part of a syndrome of disorders of the male reproductive tract that may have arisen because of increased exposure of the developing fetus to estrogens, including xenoestrogens. By this hypothesis, altering the fetal hormone experience reduces the capacity of the adult male to produce sperm because it results in inadequate growth of specialized cells (Sertoli cells) necessary to support sperm production.

Sharpe et al. gave pregnant rats water containing the synthetic estrogen DES and two common estrogenic chemicals found in the environment (octylphenol, a detergent breakdown product, and butyl benzyl phthalate, a plasticizer that is among the most ubiquitous of all environmental contaminants). Exploring possible relevance to humans, the researchers administered low doses--doses they said were roughly comparable to estimated human intake--to the rats throughout their pregnancy and for the 21 days they were nursing their pups. Octylphenol and butyl benzyl phthalate produced effects similar to DES: males exposed to these estrogenic chemicals in early life had smaller testicles and sperm production reduced by as much as 21 percent when they reached adulthood.

  Hess, RA and PS Cooke. 1996.Neonatal thyroid status as one determinant of adult testis size. pp 11-14 in Chapin, RE, JT Stevens, CL Hughes, WR Kelce, RA Hess and GP Daston. Symposium Overview. Endocrine modulation of reproduction. Fundamental and Applied Toxicology 29: 1-17.
Hess and Cooke summarize work showing that neonatal thyroid status in rats is an important determinant of adult testis size and thus of adult sperm count. "Hypothyroidism" in utero produces overgrowth of testes while "hyperthyroidism" can lead to dramatically smaller testes. According to Hess and Cooke, in the normal animal, thyroid (T3) concentrations increase during the neonatal period and inhibit Sertoli cell differentiation. In other words, thyroid is an important signal shutting off testicular growth. Hypothyroidism causes a reduction in T3 and therefore Sertoli cell growth is not inhibited appropriately, leading to enlarged testes (hypergonadism).

This is relevant to the toxicology of endocrine disruption because some PCBs (e.g., Aroclor 1242 and 1254) are known to induce hyperthyroidism and thus cause enlarged testes and greater numbers of Sertoli cells. Individuals thus affected can have higher sperm counts than normal. Also see Cooke et al. 1994.





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