چکیده مقاله
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, 195 pregnant women in their third trimester 7th month and end of 9th 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 500 meter buffer traffic density Neonatal TSH was measured via heel prick sampling during routine screening within 3 5 days of birth Multivariable linear regression R v4 0 2 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 1397 345 Results: Phenanthrene and Fluoranthene were the most abundant PAHs in maternal serum, with mean concentrations of 31 5 and 28 7 ng/mL, respectively Total PAH levels ranged from 28 4 to 184 7 ng/m³, with an average of 96 2 ng/m³ Traffic density within a 500 meter radius of maternal homes was strongly correlated with serum PAH levels r = 0 61, p 0 001 , confirming traffic as the main exposure source Newborns of mothers in the highest PAH exposure textile had significantly elevated TSH levels 5 82 ± 1 21 mIU/L compared to those in the lowest tertile 4 93 ± 1 09 mIU/L, p 0 01 Regression analysis showed that every 10 ng/m³ increase in total PAH exposure was associated with a 0 18 mIU/L rise in neonatal TSH 95% CI: 0 07 0 29, p = 0 002 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
کلیدواژهها
نویسندگان
Samaneh Dehghani
Department of Environmental Health, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
Hamed Soleimani
Department of Environmental Health, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
Kazem Naddafi
Student's Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran
Narges Velayati
Department of Environmental Health, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
شیوه ارجاع
Dehghani, Samaneh and Soleimani, Hamed and Naddafi, Kazem and Velayati, Narges,1404,Prenatal Exposure to Traffic-Related Polycyclic Aromatic Hydrocarbons and Neonatal Thyroid Function: A Cross-Sectional Study in Shiraz, Iran,37th International Congress on Pediatrics,Tehran
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مجموعه مقالات سی و هفتمین کنگره بیماری های کودکان17 مهر 1404 · تهران