Early pregnancy exposure to organophosphate esters and risk of infant atopic dermatitis: Sex-Specific association analyses in a community-based birth cohort.
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BACKGROUND: Atopic dermatitis (AD) is a common chronic inflammatory skin disorder. The association between early pregnancy exposure to organophosphate esters (OPEs) and the risk of infant AD, as well as the underlying mechanisms, remains unclear. METHODS: Based on the Maternal Key Nutritional Factors and Offspring's Atopic Dermatitis (MKNFOAD) birth cohort, we assessed associations between first-trimester exposure to eight OPEs and offspring AD risk during the first year of life. A pregnant C57BL/6 mouse model exposed to OPEs was established; AD-like skin lesions were induced in the offspring using MC903. We investigated the effects of reactive oxygen species-mediated oxidative stress on skin lesions in pups and OPE-treated HaCaT cells. Transcriptomic analysis of OPE-treated HaCaT cells was performed to identify potential molecular pathways. RESULTS: Early gestational exposure to Tris-2,3-dibromo propyl-phosphate (TDBPP) was associated with increased infant AD risk (adjusted odds ratio [OR] = 3.77, 95% confidence interval [CI]: 1.56-9.13, p < 0.01). Exploratory analyses suggested sex-specific associations between gestational OPE exposure and AD risk (TDBPP in boys: adjusted OR = 2.68, 95% CI: 0.99-7.27, p = 0.05; girls: adjusted OR = 10.88, 95% CI: 1.67-70.95, p = 0.01). Pups born to OPE-exposed dams exhibited greater ear thickness and more severe inflammatory infiltration than controls (p < 0.05). Transcriptomic analysis showed enrichment of tumor necrosis factor and MAPK signaling pathways in OPE-treated HaCaT cells. CONCLUSIONS: This study provides evidence that early gestational exposure to TDBPP is associated with increased infant AD risk. Exploratory analyses suggest sex-specific effects. We also established an animal model and identified mechanistic pathways for future research.