Environmental PAH exposure and male idiopathic infertility: a review on early life exposures and adult diagnosis

Abstract

<jats:title>Abstract</jats:title> <jats:p>The male reproductive system is acutely and uniquely sensitive to a variety of toxicities, including those induced by environmental pollutants throughout the lifespan. Early life hormonal and morphological development results in several especially sensitive critical windows of toxicity risk associated with lifelong decreased reproductive health and fitness. Male factor infertility can account for over 40% of infertility in couples seeking treatment, and 44% of infertile men are diagnosed with idiopathic male infertility. Human environmental exposures are poorly understood due to limited available data. The latency between maternal and in utero exposure and a diagnosis in adulthood complicates the correlation between environmental exposures and infertility. The results from this review include recommendations for more and region specific monitoring of polycyclic aromatic hydrocarbon (PAH) exposure, longitudinal and clinical cohort considerations of exposure normalization, gene-environment interactions, in utero exposure studies, and controlled mechanistic animal experiments. Additionally, it is recommended that detailed semen analysis and male fertility data be included as endpoints in environmental exposure cohort studies due to the sensitivity of the male reproductive system to environmental pollutants, including PAHs.</jats:p>

Sperm DNA Methylation Epimutation Biomarkers for Male Infertility and FSH Therapeutic Responsiveness

“…Male infertility over the past century has been observed to have dramatically declined 1,2 , with recent analysis of data for the past 50 years noting a 50% reduction in male sperm counts 2 . The primary causal factors suggested are environmental exposures influencing testis biology and sperm production 2–9 . In rodent models a number of defined toxicants and other exposures promote testis effects associated with a reduction in sperm number 5–7 .…”

“…Animal models have demonstrated the direct actions of a number of environmental toxicants to reduce sperm numbers and promote testis disease and male infertility 5–7 . Various human male exposures also have been shown to associate with poor sperm parameters and male infertility 8,9 . The primary molecular actions considered involve environmental epigenetics.…”

Variability in urinary biomarkers of human exposure to polycyclic aromatic hydrocarbons and its association with oxidative stress

“…PAHs are endocrine disrupters, reproductive toxicants, neurotoxicants and carcinogens ( Madeen and Williams 2017 ; Yin et al 2017 ). Long-term exposure to PAHs has been linked to lung, skin and bladder cancers and diabetes ( Uppstad et al 2011 ; Ramesh et al, 2011 ).…”

BaP exposure causes oocyte meiotic arrest and fertilization failure to weaken female fertility

“…Human activities such as industrial production, transportation, coal combustion, and sulfur dioxide emissions release various poisonous and harmful substances (2,3), which are atmospherically transported and deposited in urbanized areas where people live and work (4)(5)(6)(7). Among the large amounts of pollutants present in the cities, polycyclic aromatic hydrocarbons (PAHs) have attracted a great deal of attention because of their toxicity and persistence, which threaten human health and cause adverse disease effects (8)(9)(10), including reproductive defects (11)(12)(13). In the air, PAHs emitted from solid fuel combustion, like other volatile and semivolatile pollutants, adsorb on the suspended particulate matter (PM), a complex mixture of extremely small particles and liquid droplets made up of a carbonaceous fraction and inorganic constituents (14), to form the main elements threatening human health in smog, especially the health of susceptible populations, such as pregnant women and children (8).…”