ABSTRACT
The earliest report linking environmental exposure to adverse human male reproductive effects dates back to 1775 when an English physician, Percival Pott, reported a high incidence of scrotal cancer in chimney sweeps. This observation led to safety regulations in the form of bathing requirements for these workers [1]. Brenneke, Hertwig, Muller, and Snell were among the first to formally study effects of exposures on offspring in mice, demonstrating that irradiated males sired smaller litters and linking chromosomal abnormalities in fertilized eggs to sperm irradiation [2]. Similarly, Auerbach and Robson, and Bock and Jackson later used mice to show that chemically exposed males had reduced fertility with induction of chromosomal abnormalities and other male germline mutations [2-5]. That male-mediated reproductive harm may occur in humans as a result of toxicant exposures became firmly established only relatively recently when Lancranjan et al. studied lead-exposed workers in Romania in 1975 [6], and later in 1977, when Whorton et al. examined the effects of dibromochloropropane (DBCP) on male workers in California [7]. Since these discoveries, additional human reproductive toxicants have been identified through the convergence of laboratory and observational findings. It has also been increasingly recognized that men’s nonchemical exposures, both exogenous (e.g., physical exposures such as genital hyperthermia, pressure, and radiation therapy) and endogenous (e.g., constitutional factors such as age and genetic variation), may affect men’s reproductive health and capacity [8-14]. The purpose of this chapter is to provide an overview of methods used to study the effects of exposures on male reproduction and their reproductive health, with a primary emphasis on the implementation and interpretation of human studies.
