Prenatal and early life exposures to combustion products, polycyclic aromatic hydrocarbons (PAHs), from smoking, pollution, and food contamination are indicated causes of infertility in men. The long latency period between early life PAH exposures and adult infertility diagnosis make establishing causation challenging.
In a review article from Reviews on Environmental Health on early life exposures and adult diagnosis, the authors make recommendations for research on human PAH exposure and on male idiopathic infertility, where the causes are unknown, to understand the mechanism, risk, and intervention strategies.
There is growing evidence that fetal and early life exposures to polycyclic aromatic hydrocarbons (PAHs) can lead to infertility in men. Male unexplained infertility is often diagnosed by the failure to conceive a child after one year of trying and by the identification of abnormal sperm development or low sperm count without an underlying medical cause.
Infertility diagnosis hard to study
In the United States the average age of first time fathers is 24 years old, meaning that most men will not be diagnosed as infertile until that time or later. The relationship of early life PAH exposures and male infertility is understudied, in part, because it is difficult to study. There is a long latency period from early life exposures to the diagnosis of infertility. A lifetime of other exposures and lifestyle choices create noise that makes isolating the singular variable of early life PAH exposures difficult.
Characterizing and recording environmental PAH exposures is necessary for longitudinal correlation to early life exposures and male infertility incidences. PAHs occur in a variety of mixtures and vary greatly by local environment, sources of food, and eating habits. The analysis of the composition of PAHs bound to air pollution particulate matter would increase knowledge of the toxicity from exposures. The same surveillance could be useful for foodstuffs as PAH food contamination varies by location from sources such as atmospheric PAH pollutant deposition to crops, drying methods, smoking methods, and crop management methods (weed burning). Additionally, it was recommended that male infertility be included in clinical cohort studies as a metric of overall health and environmental exposures.
Spermatogenesis (the development of sperm cells) is incredibly sensitive to environmental pollution, and because it is a low fidelity process, imperfect sperm cells are allowed to proceed to the easily accessible biofluid, semen.
Though infertility is a potentially devastating medical condition, it can be non-mortal evidence of environmental pollutant exposure, indicating that intervention is necessary to protect the health and safety of a population being exposed to pollutants.
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