Introduction: Exposure to polycyclic aromatic hydrocarbons (PAHs), particularly those emitted from traffic sources, poses significant risks to fetal development and endocrine regulation. Despite increasing concern about urban air pollution, evidence on prenatal traffic-related PAH exposure and neonatal
thyroid function is still limited-particularly in the Middle East. This study aimed to assess the association between
prenatal exposure to traffic-related PAHs and thyroid-stimulating hormone (TSH) levels in neonates bom in an urban setting in Iran. Methodology: In this cross-sectional study, ۱۹۵ pregnant women in their third trimester (۷th month and end of ۹th month) were randomly recruited from healthcare centers across Shiraz, Iran. Maternal blood samples were used to estimate fetal PAH exposure, based on placental transfer. Eight PAHs were quantified via GC-MS, including Benzo(a)pyrene, Benzo(b)fluoranthene, and Chrysene. Maternal interviews and questionnaires captured demographic and exposure data. Residential locations were geocoded, and traffic exposure was estimated using ۵۰۰-meter buffer traffic density. Neonatal TSH was measured via heel-prick sampling during routine screening within ۳-۵ days of birth. Multivariable linear regression (R v۴.۰.۲) assessed the association between maternal PAHs and neonatal TSH, adjusting for key confounders. The study received ethics approval from the local IRB (IR.QUMS.REC. ۱۳۹۷.۳۴۵). Results: Phenanthrene and Fluoranthene were the most abundant PAHs in maternal serum, with mean concentrations of ۳۱.۵ and ۲۸.۷ ng/mL, respectively. Total PAH levels ranged from ۲۸.۴ to ۱۸۴.۷ ng/m³, with an average of ۹۶.۲ ng/m³. Traffic density within a ۵۰۰-meter radius of maternal homes was strongly correlated with serum PAH levels (r = ۰.۶۱, p ۰.۰۰۱), confirming traffic as the main exposure source. Newborns of mothers in the highest PAH exposure textile had significantly elevated TSH levels (۵.۸۲ ± ۱.۲۱ mIU/L) compared to those in the lowest tertile (۴.۹۳ ± ۱.۰۹ mIU/L, p ۰.۰۱). Regression analysis showed that every ۱۰ ng/m³ increase in total PAH exposure was associated with a ۰.۱۸ mIU/L rise in
neonatal TSH (۹۵% CI: ۰.۰۷-۰.۲۹, p = ۰.۰۰۲). The association remained significant after adjusting for key confounders. No meaningful differences were observed in birth weight, length, or head circumference across exposure groups. Conclusion: This study provides evidence that
prenatal exposure to traffic-derived PAHs may disrupt neonatal thyroid function. Findings highlight fetal endocrine vulnerability to urban pollution and support targeted air quality policies in high-traffic areas.
