Male infertility and environmental exposure to lead and cadmium

Humans are exposed occupationally and environmentally to metal aerosols inc luding lead (Pb2+) and cadmium (Cd2+). These toxicants accumulate in male r eproductive organs. Epidemiological studies have been equivocal about effec ts of Pb2+ and Cd2+ on hormone concentrations, male fertility and sperm par ameters. Comparison of Pb2+ and Cd2+ concentrations in fertile add infertil e men are problematic. Problem areas include failure to control confounding variables, but genetic polymorphisms as in somatic diseases may modulate P b2+ and Cd2+ damage. Multiple calcium (Ca2+) and potassium (K+) channel iso forms have been identified in human testes and spermatozoa. These Ca2+ and K+ channels are involved in early events of acrosome reactions. Ca2+ channe l are susceptible to Cd2+ poisoning and K+ channels to Pb2+. These channels offer entry paths for metallic toxicants into mature spermatozoa. Ion chan nel polymorphisms may cause differential sensitivities to Cd2+ and Pb2+, ex plaining in part prospective blinded studies showing high Cd2+ in varicocel e-related human infertility and high Pb2+ in unexplained infertility. In bo th forms of male infertility the ability to undergo an acrosome reaction de creases. Reverse transcriptase-polymerase chain reaction assays for Ca2+ an d K+ channel isoforms may identify susceptibility subgroups with lower resi stance to environmental exposures.