PM2.5-dominant disruption of male reproductive hormone homeostasis: Prospective cohort evidence on differential effects from fine versus coarse particulate matter.

Current evidence regarding the associations between particulate matter (PM) exposure and male reproductive hormone homeostasis remains limited and inconsistent, and the distinct effects of different PM size fractions require further investigation. We therefore investigated the associations of PM2.5, PM2.5-10, and PM10 exposure with male reproductive hormone homeostasis. A total of 3284 male partners from couples seeking assisted reproductive treatment were included from the Anhui prospective assisted reproductive cohort. Individual-level PM concentrations over the 0-90, 0-180, 181-360, and 0-360 days exposure windows were assessed. Linear regression and cubic spline analysis were used to explore the associations of PM exposure with serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone (T), prolactin (PRL), estradiol (E2), and T/LH, and T/E2 ratios. Subgroup analysis was conducted to assess potential effect modification by age, body mass index, residential greenness, and apparent temperature. PM10 exposure was associated with decreased T and T/LH levels. PM2.5 exposure was associated with increased FSH levels and decreased T and E2 levels. In the 0-360 day exposure window, each 10 μg/m3 increase in PM2.5 was associated with a 0.0675 increase in log-transformed FSH (95% CI: 0.0231, 0.1120) and a 0.1136 decrease in log-transformed T (95% CI: -0.1604, -0.0667). The association between PM2.5 and PRL was modified by age; among men younger than 30 years, PM2.5 exposure was associated with increased PRL levels in the 0-360 day window (β = 0.0881, 95% CI: 0.0315, 0.1447). In addition, PM2.5 exposure was associated with decreased T/LH and T/E2 ratios, suggesting disruption of hormonal homeostasis at multiple levels rather than uniform changes in individual endocrine endpoints. In contrast, PM2.5-10 exposure did not show consistent associations with reproductive hormone homeostasis in the overall liner models. Overall, in this clinical population of men from couples seeking assisted reproductive treatment, PM2.5, but not PM2.5-10, exposure may disrupt male hormonal homeostasis, and younger men may represent a more susceptible subgroup. Our findings underscore the need for public health interventions to reduce PM2.5 pollution and thereby help protect male reproductive endocrine health, while further validation in general male populations is warranted.