A potential mechanism by which air pollutants may affect reproductive health is by endocrine disruption. Air pollutants are made up of mixtures of particulate matter that may include endocrine disruptors, such as polycyclic aromatic hydrocarbons (PAHs) and heavy metals.
Air pollution is known to contribute to respiratory and cardiovascular diseases, including lung cancer, stroke, heart disease, and chronic respiratory conditions. Mounting research suggests that polluted air may also negatively impact reproductive health.
Exposure to endocrine disruptors during critical developmental periods may have permanent negative effects on the reproductive system. In males, these periods are during the male programming window and mini puberty. The male programming window occurs between gestational weeks 8 and 14, and mini puberty occurs approximately during the first six months of life. Testosterone levels rise and peak at around age 1 to 3 months, resulting in penile and testicular growth.
Recently, anogenital distance has been used as a marker of endocrine disruption and a potential predictor of future reproductive health. Some cross-sectional studies have linked shorter anogenital distance in males to reduced fertility, lower sperm quality, and lower sex steroid hormone concentrations.
In a study published in the November 2023 issue of Environmental Health Perspectives, Emily Barrett, Ph.D., associate professor at the Rutgers University School of Public Health, and her colleagues used data from The Infant Development and Environment Study (TIDES) to investigate the relationship between early exposure to air pollutants and endocrine disruptions, as evidenced by anogenital distance alterations.
TIDES is an ongoing longitudinal study that recruited pregnant individuals from 2010 and 2012 who used prenatal clinics from medical centers at the University of California-San Francisco, University of Minnesota, University of Rochester, or University of Washington in Seattle. As part of the study, anogenital distance was measured at birth in all children born of the participants and at one year in male children. Penis width was also measured.
Barrett and her team compared this data with the estimated levels of fine particulate matter (PM2.5) and nitrogen dioxide (NO2), both of which are pollutants released during the burning of diesel, oil, gasoline, and wood, within the residential areas of the TIDES participants during pregnancy.
The researchers found that exposure to PM2.5 during the male programming window was associated with shorter and less masculinized anogenital distance at birth in males. Exposure to PM2.5 during minipuberty was associated with shorter anogenital distance at one year of age.
NO2 exposure had little effect on anogenital distance. However, exposures during the male programming window as well as mini puberty were both associated with smaller penis width at one year of age.
Barrett and her colleagues conclude that exposure to pollutants, such as PM2.5 and NO2, during critical developmental periods may disrupt reproductive development.
They wrote, “Our results indicate that in addition to the many cardiovascular and pulmonary sequelae of exposure to air pollutants, there may be impacts on the developing human reproductive system that may occur through disruption of typical hormone activity during gestation and infancy.”
The researchers added, “Moving forward, longitudinal studies are needed to examine the long-term sexually dimorphic reproductive sequelae of early life alterations in [anogenital distance] related to air pollution or other endocrine-disrupting exposures.”