The occupational exposure that resulted in the greatest effect on sperm count and fertility was the workplace exposure to the nematocide dibromochloropropane (DBCP). This toxicant induced azoospermia or oligospermia in a high percentage of exposed workers, both those involved in its manufacture and those involved in its application on crops (28-30). In a substantial proportion of DBCP-exposed workers who became azoospermic, no recovery of sperm counts occurred after removal from exposure (28,29). This lone example is frequently cited as reassuring evidence of the rarity of such workplace effects on sperm counts and male fertility. In reality, this reassurance is a veil. The effects of DBCP were revealed, even though the affected workforces comprised fairly low numbers, because it had catastrophic effects on sperm counts/fertility. We can be reassured that similar catastrophes will also reveal themselves, but more modest effects of occupation on sperm counts/fertility will remain difficult or impossible to identify in all but large, well-controlled studies. The latter are hugely expensive and laborious, both of which act as strong deterrents to their application. In recognition of such obstacles, a multicenter European study (the Asclepios study) to investigate the effect of occupation on male reproductive health and fertility was initiated some years ago (31) and has been responsible for producing some of the most definitive data.
The DBCP example means that in nonscientific circles, the concept that pesticide exposure results in lowered sperm counts/infertility has become more or less accepted as dogma. In reality, there are relatively few studies that support this stance (32-35), and many of these are studies in developing countries, where exposure controls may be less vigorous than in developed countries. Furthermore, there are numerous studies in which occupational pesticide exposure is associated with no change in semen quality and/or fertility and no effect on testosterone levels (36-40); these include comparative studies of organic and nonorganic farmers. Although it is difficult to draw firm conclusions from these conflicting studies, it is reasonable to expect that occupational exposure to current, nonpersistent pesticides is unlikely to exert major adverse effects on semen quality and fertility in most men, but effects in individuals who might be exposed to unusually high pesticide levels should still be considered. Therefore, exposure of the general population to pesticides via contamination of food, etc. is likely to be considerably less than in men who are occupationally exposed and, consequently, risks of testicular dysfunction are extremely low. This may account for the lack of published evidence for any consistent relationship between subnormal semen quality and/or testosterone levels and pesticide exposure (37,41,42), although two small recent studies have provided limited evidence for a negative relationship between semen parameters and PCB and/or dichlorodiphenylethane (DDE) levels in blood (43,44).
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