ABSTRACT
Any scientist involved in the study of spermatogenesis is struck both by the beautiful complexity of this highly organized process and by its seeming fragility. In contrast, viewed from the perspective of fertility or sperm counts, spermatogenesis appears anything but fragile-robust even-and this would probably be the view of many pathologists in the pharmaceutical industry. The truth, as usual, is probably somewhere in between these two extreme perceptions, but the contrast has an important message to give us, namely, that the perceived susceptibility of spermatogenesis to disruption depends really on how it is being assessed. In humans, there are only isolated instances in which industrial chemicals have been shown to exert adverse effects on spermatogenesis, notably the case of the nematocide dibromochloropropane (DBCP), which causes catastrophic impairment of spermatogenesis (Whorton et al., 1979). Back in 1992, l wrote an article (Sharpe, 1992) that argued that people should not be misled into complacency by the lack of evidence that other industrial and environmental chemicals apparently had little impact on human male fertility or sperm production. My reasoning was that this absence of data was more a reflection of the absence of sensitive endpoints than anything else. The endpoints most commonly used for assessment of adverse reproductive effects of industrial chemical in humans (i.e., sperm counts, fertility) were only capable of detecting catastrophes; anything less would go undetected (Sharpe, 1992, 1993a). Almost on cue, the saga of "falling sperm counts" in the human male broke to emphasize my message (Carlsen et al., 1992). It is very much the same message that I hope to put over in this short chapter, though it is now modified by the "wisdom" of our new (and probably imperfect) perceptions about "new" pathways via which environmental chemicals may affect male reproductive function.
