Seulbi Lee1, Sung Kyun Park2, Hyesook Park3, Woojoo Lee4, Ji Hyen Lee5, Yun-Chul Hong6, Mina Ha7, Yangho Kim8, Bo-Eun Lee9, Eunhee Ha10. 1. Department of Occupational and Environmental Medicine, College of Medicine, Ewha Womans University, Seoul, Republic of Korea; Department of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, MI, United States. 2. Department of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, MI, United States; Department of Environmental Health Sciences, School of Public Health, University of Michigan, Ann Arbor, MI, United States. 3. Department of Preventive Medicine, College of Medicine, Ewha Womans University, Seoul, Republic of Korea; Graduate Program in System Health Science and Engineering, Ewha Womans University, Seoul, Republic of Korea. 4. Department of Public Health Sciences, Graduate School of Public Health, Seoul National University, Seoul, Republic of Korea. 5. Department of Pediatrics, Ewha Womans University College of Medicine, Seoul, Republic of Korea. 6. Department of Preventive Medicine, College of Medicine, Seoul National University, Seoul, Republic of Korea. 7. Department of Preventive Medicine, College of Medicine, Dankook University, Cheonan, Republic of Korea. 8. Department of Occupational and Environmental Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Republic of Korea. 9. Environmental Health Research Division, National Institute of Environmental Research, Incheon, Republic of Korea. 10. Department of Occupational and Environmental Medicine, College of Medicine, Ewha Womans University, Seoul, Republic of Korea; Graduate Program in System Health Science and Engineering, Ewha Womans University, Seoul, Republic of Korea; Ewha Medical Research Institute, College of Medicine, Ewha Womans University, Seoul, Republic of Korea. Electronic address: Eunheeha@ewha.ac.kr.
Abstract
BACKGROUND: Prenatal exposure to bisphenol A (BPA) and phthalates could trigger immune response. Few studies have investigated the association between prenatal BPA and phthalate exposure and atopic dermatitis (AD) in infants. OBJECTIVE: We aimed to clarify the joint association of prenatal exposure to BPA and phthalate metabolites with AD incidence in 6-month-old infants. METHODS: We included 413 mother-child pairs from the Mothers and Children's Environmental Health (MOCEH) in a prospective birth cohort study. Maternal urinary BPA, mono-2-ethyl-5-hydroxyhexyl phthalate (MEHHP), mono-2-ethyl-5-oxohexyl phthalate (MEOHP), and mono-n-butyl phthalate (MnBP) concentrations were measured during early and late pregnancy. We applied the Bayesian kernel machine regression (BKMR) with probit regression to estimate the association of BPA and phthalate metabolites with AD incidence after adjusting for potential confounders. Individual association was estimated by differences in predicted probabilities comparing each individual chemical concentration at 75th versus 25th percentiles, while other chemicals were set at their median. Overall joint effect was estimated by differences in predicted probabilities comparing all chemical concentrations at 75th versus 25th percentiles. RESULTS: Individual effect of MEHHP in late pregnancy was strongly associated with incident AD [Difference: 0.244 (95% credible interval: -0.066, 0.554)] in the model including both early and late exposures. Furthermore, we confirmed overall joint association of urinary BPA and phthalate metabolites during pregnancy with a higher risk of AD [0.347 (0.168, 0.526) for late pregnancy exposure, and 0.307 (0.094, 0.521) for both early and late pregnancy]. Additionally, the joint association was more prominent among girls than that in boys. CONCLUSIONS: The joint association of prenatal exposure to BPA and phthalates could be associated with the incident AD in 6-month-old infants. Further studies are needed to confirm the synergistic effect of BPA and phthalate exposures on AD in children.
BACKGROUND: Prenatal exposure to bisphenol A (BPA) and phthalates could trigger immune response. Few studies have investigated the association between prenatal BPA and phthalate exposure and atopic dermatitis (AD) in infants. OBJECTIVE: We aimed to clarify the joint association of prenatal exposure to BPA and phthalate metabolites with AD incidence in 6-month-old infants. METHODS: We included 413 mother-child pairs from the Mothers and Children's Environmental Health (MOCEH) in a prospective birth cohort study. Maternal urinary BPA, mono-2-ethyl-5-hydroxyhexyl phthalate (MEHHP), mono-2-ethyl-5-oxohexyl phthalate (MEOHP), and mono-n-butyl phthalate (MnBP) concentrations were measured during early and late pregnancy. We applied the Bayesian kernel machine regression (BKMR) with probit regression to estimate the association of BPA and phthalate metabolites with AD incidence after adjusting for potential confounders. Individual association was estimated by differences in predicted probabilities comparing each individual chemical concentration at 75th versus 25th percentiles, while other chemicals were set at their median. Overall joint effect was estimated by differences in predicted probabilities comparing all chemical concentrations at 75th versus 25th percentiles. RESULTS: Individual effect of MEHHP in late pregnancy was strongly associated with incident AD [Difference: 0.244 (95% credible interval: -0.066, 0.554)] in the model including both early and late exposures. Furthermore, we confirmed overall joint association of urinary BPA and phthalate metabolites during pregnancy with a higher risk of AD [0.347 (0.168, 0.526) for late pregnancy exposure, and 0.307 (0.094, 0.521) for both early and late pregnancy]. Additionally, the joint association was more prominent among girls than that in boys. CONCLUSIONS: The joint association of prenatal exposure to BPA and phthalates could be associated with the incident AD in 6-month-old infants. Further studies are needed to confirm the synergistic effect of BPA and phthalate exposures on AD in children.