How work-place conditions, environmental toxicants and lifestyle affect male reproductive function.

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Major temporal and geographical shifts in male reproductive function is presently an issue worldwide. The hormonal disruption hypothesis has achieved considerable attention but epidemiological evidence in support of the theory is lacking. Several occupational hazards to male reproductive function are known but exposure prevalences are hardly sufficient to play a role for reduced sperm count in the general male population. Sedentary work may be an exception. Perhaps prolonged time in the sedentary position exhausts the testicular heat regulation. But so far studies addressing implications of the heat hypothesis in the general population are few. Neither change of sexual behaviour nor reduced period of sexual continence seems to be a likely explanation. Tobacco smoking and consumption of caffeine and alcoholic beverages in adulthood have a rather marginal impact on spermatogenesis and can hardly explain major shifts or regional differences in male reproductive health. However, prenatal effects following smoking during pregnancy might play a role because we have witnessed a smoking epidemic among fertile women in some countries during the second half of the twentieth century. Moreover, if genetic factors play more than a marginal role for testicular function and sperm count, pregnancy planning resulting in reduced family size during the past 100 years could possibly explain a decline in semen quality because the most fertile part of the population reproduce less while the subfertile probably continue to get a limited number of children.