Impact of Environmental Toxin Exposure on Male Fertility Potential

Sarah C. Krzastek; Jack Farhi; Marisa Gray; Ryan P. Smith


Transl Androl Urol. 2020;9(6):2797-2813. 

In This Article

Prevention and Treatment of Damage Induced by Environmental Toxins

The most effective means of minimizing the negative effects of environmental toxins is exposure avoidance or reduction. Given the broad number of potential environmental toxins, it would be extremely difficult for an individual to eliminate all possible exposures. Interestingly, proprietary silicone wristbands have been shown to detect a number of harmful compounds including polycyclic aromatic hydrocarbons and may provide consumers with previously unavailable data on personalized exposure profiles.[137,138] A cross-sectional study conducted in 2018 showed that while in utero exposure to maternal tobacco use was associated with decreased semen quality, decreases in maternal tobacco use over time did not correspond to improvements in semen quality. This suggests additional etiologies for persistent impairments in semen quality over time.[139]

Some studies suggest that impairments in spermatogenesis may be reversible with removal of exposure to the offending agent, for example as with weight loss, alcohol, tobacco or use of certain medications.[4,100,135] The ability to reverse the damage may depend on the timing and type of exposure. While eliminating an environmental toxin may help improve semen parameters in men presenting with subfertility, improving semen parameters in men who were exposed to toxic agents in utero may prove more difficult. Small studies suggest that smoking cessation may improve semen parameters.[140] Similarly, certain chemotherapeutic agents are more gonadotoxic than others, and adverse impacts on spermatogenesis may be mitigated by using alternative agents or lower doses as able.[135] Animal models have also suggested that the addition of GnRH analogues during chemotherapy may preserve the potential of spermatogonia to differentiate following treatment.[135] This has not borne out in human studies.

As it is difficult to remove men from toxins ubiquitous throughout our environment, much interest has been placed on identifying treatment options to protect men from, or reverse, the negative effects of these agents. As discussed above, scrotal hyperthermia may be an underlying mechanism for the negative fertility outcomes from certain environmental exposures. Scrotal cooling has been investigated as a way to improve semen parameters in the setting of hyperthermia induced by varicoceles and has been shown to improve semen parameters including sperm concentration, motility and morphology.[141,142] More recently, a systematic review by Nikolopoulos and colleagues in 2013 reviewed the evidence associating scrotal cooling with changes in semen parameters.[143] The authors noted that most studies on the topic were small observational studies with no randomized controlled trials, so no firm conclusions could be drawn, but all studies included did show a trend towards improvement in sperm count, as well as six of eight studies showing improvements in sperm motility and/or morphology.

ROS may be another etiology of reason for impaired semen parameters following environmental exposures. Therefore, it is logical to hypothesize that administration of antioxidants may protect against or blunt the effects of these toxins. Antioxidants including Zinc, Vitamins E and C, Selenium, Coenzyme Q10, Ferulic acid, and even melatonin have been shown to have protective effects on spermatogenesis in animal models and reduce semen ROS and DNA fragmentation in human studies.[144–146] There is no definitive evidence to support the use of antioxidant supplementation in subfertile men to improve pregnancy and live birth rates due to a lack of high quality studies.[147] However, given their low cost and few side effects, antioxidants and multivitamins are frequently recommended to men presenting with subfertility.[148,149]

The literature is fraught with limited high-quality evidence to support any one therapy for treatment of impaired fertility linked to environmental exposures. Due to the diversity of exposures to environmental toxins which may have a negative impact on fertility, the need for change on a global scale becomes more apparent. It may prove futile to try to limit exposures until a paradigm shift takes place to reduce the release of these toxins and subsequent human exposures. Until a stronger link can be defined, men presenting with fertility concerns should be counseled to minimize environmental exposures and may consider regular consumption of dietary antioxidants or use of a daily multivitamin.