This review is based primarily on the recent epidemiological studies conducted in occupational settings in order to explore the relationship between exposures to chemical agents and the possible effects on male reproductive function. The paper examines evidence of the effects of metals, solvents, pesticides and dioxin. The effects considered are primarily the possible alterations of sperm quality and reduction of fertility. Many studies have identified small groups of workers with exposures to these agents, presenting some alteration in the spermatological or fertility profile, but the results are difficult to replicate in other settings with different individuals and different levels of exposure. From examination of the concentrations of environmental and occupational pollutants in the blood and in the seminal fluid of exposed individuals, it appears that, in general, the concentrations are much lower in the seminal fluid and in sperm cells, making this a less useful marker of exposure.

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A wide number of pesticides, including highly persistent organochlorinated compounds, such as lindane (LIN), may induce reproductive and developmental alterations by directly binding to the estrogen/androgen receptors or altering steroid hormone metabolism. In the present work, we have investigated whether LIN in utero exposure of CD1 mice affects the reproductive system in male offspring by causing an impairment of the CYP-dependent steroid hormone metabolism. Dam exposure to 25 mg kg(-1) b.w. LIN occurred during critical developmental periods, from gestational days 9 to 16. Effects on hepatic CYP-mediated testosterone (TST) hydroxylase, aromatase activities and testicular parameters were tested at postnatal days (PND 50, 65-69, 100) that are critical for sexual maturation in CD1 mice. In the adult F1 mice significant changes of male reproductive endpoints (testis weight, spermatid number) as well as dramatic effects on CYP-mediated TST metabolism were observed on PND 65-69, in the absence of any of systemic toxicity. The levels of TST 6beta- and 2alpha-hydroxylation and dehydrogenation showed the highest level of reduction, suggesting CYP 3A and 2C families as the major target of LIN induced effects. All changes were almost recovered on PND 100. No effects on aromatase activity were evidenced. Overall, these findings provide useful information for a better characterization of the LIN mode of action. They suggest that LIN-induced toxicity in males is linked to an impairment of steroid hormone homeostasis, due to CYP-mediated TST catabolism modulation and differs from LIN receptor-mediated mechanism previously reported in females.