Associations of ambient air pollutant exposure with seminal plasma MDA, sperm mtDNA copy number, and mtDNA integrity

Current available evidence regarding the detrimental effects of low-level ambient air pollution on conventional semen parameters is inconclusive. In nonreproductive systems, air pollutant exposure has been demonstrated to induce oxidative stress (OS), which is a crucial mechanism that mediates sperm damage and male infertility. Thus, it may be essential to investigate the effects of air pollution on sperm quality in terms of the perspectives of OS and relative molecular damage.We assessed the associations of major air pollutant exposure to oxidative stress-mediated alterations in semen, including seminal plasma malondialdehyde (MDA), sperm mtDNA copy number, and integrity.The present study used data gathered from 516 young men participating in the Male Reproductive Health in Chongqing College student (MARCHS) cohort study during the follow-up stage in 2014 (n = 427 on the old campus, which is located in an urban area and has worse air quality, and n = 89 on the new campus, which is not urban and has better air quality). Data regarding major air pollutant exposure during 0–90, 0–9, 10–14 and 70–90 days before each semen examination (corresponding to the entire and three key periods of sperm development, respectively) were collected. The Mann-Whitney U nonparametric test was employed to compare distributions of major air pollutants and to explore differences in MDA, mtDNA copy number, and mtDNA integrity between the two campuses. A linear regression model was used as multivariable analysis to investigate associations of major air pollutant exposure with these biomarkers of oxidative damage to sperm and to adjust for potential confounders.During all four key periods of sperm development, compared with college students on the new campus, college students on the old campus were exposed to higher levels of PM10, PM2.5, NO₂, and CO, and had higher air quality index (AQI) values, indicating that these participants suffered from worse air quality. The levels of seminal plasma MDA in college students on the old campus were higher than those for the new campus (2.0 nmol/ml; 0.7, 3.6 vs. 1.6 nmol/ml; 0.4, 3.4, p < 0.001) (medians with 5th and 95th percentiles). There were no significant differences in sperm mtDNA copy number and mtDNA integrity between the two campuses. Furthermore, daily average PM10 exposure during 0–90 days before semen ejaculation was found to be significantly and positively associated with seminal plasma MDA level (10.4; 95% CI, 4.4, 16.4) (percentage change per 10-unit increase in air pollutant concentration; same meanings for the results below); daily average SO₂ exposure for 70–90 days and NO₂ exposure for 0–9 days prior to sampling were also positively associated with MDA level (74.7; 95% CI, 32.1, 119 and 11.9; 95% CI, 4.8, 19.0, respectively). AQI for 0–90 days and 70–90 days prior to sampling positively correlated with seminal plasma MDA concentrations (11.4; 95% CI, 4.7, 18.1 and 12.2; 95% CI, 5.3, 19.1, respectively). Additionally, daily average SO₂ exposures for 10–14 and 0–9 days prior to sampling were negatively associated with sperm mtDNA copy number and mtDNA integrity, respectively (−9.0; 95% CI, −16.4, −1.6 and −38.3; 95% CI, −64.1, −11.8, respectively). However, only the correlations between SO₂ exposure and AQI value for 70–90 days prior to sampling and MDA levels remained significant after multiplicity adjustment.The results indicate that bad air quality, especially SO₂ exposure during certain periods of sperm development, might be correlated with oxidative damage to sperm. These findings can deepen the understanding of the potential impacts of air pollution on sperm quality.