Environmental effects on male fertility

  The U.S. Environmental Protection Agency has studied sperm concentrations over the past several decades, with a 50% decline in sperm concentration from 1940 to 1990, and not only the same studies around the world since 1995, with six studies showing a 16%-32% decline in sperm concentration over time and three studies finding no significant decrease in sperm. Although a gradual decline in semen quality was found in men, there was little effect on fertility potential. Reduced semen quality has now been found to be most commonly associated with environmental chemicals, most commonly endocrine disruption.  The two substances that are clearly causing reduced male fertility are the heavy metals lead and cadmium and dibromochloropropane from pesticides. Heavy metals cause weak spermatozoa because it can act directly on testicular support cells, causing a decrease in androgen secretion by the testes. Pesticide-induced sperm count reduction is associated with continued exposure, causes reduced pregnancy rates in mates, and is associated with sperm acrosome hypoplasia, but the mechanism of occurrence is still unknown.  Plasticizers (food packaging, medical catheters) and phthalates in cosmetics have been correlated with semen quality. Although high doses induce spermatogenic tubule spermatogenic cell death to produce azoospermia, studies have found no alteration in sperm quality or fertility for in utero insemination.  Tobacco, alcohol, alpha and beta blockers, statins, and antidepressants may affect testicular function and cause a decrease in sperm quality, but effects from cumulative adult exposure are not currently being considered. Individuals who are already at the threshold of male infertility can be particularly sensitive to environmental damage, and heavy exposure to alcohol or statin drugs can affect spermatogenesis and maturation.  In animal models, exposure of male fetuses to high levels of endocrine disruptors (phthalates) during gestation can alter their reproductive development, leading to an increased incidence of cryptorchidism, hypospadias, and epididymal dysplasia. Environmental exposure alone, on the other hand, is unlikely to disrupt male reproductive development. Dibromoacetic acid, a byproduct of drinking water disinfectants, reduces the fertility of spermatozoa in the caudal epididymis of rats and also causes sperm acrosome hypoplasia in rabbits.  Relative to model animals, human testes produce less sperm and lower quality sperm in ejaculate than other animals, so a toxic substance that is not harmful to model animals may severely impair testicular or epididymal function and thus render a fertile male infertile.