Jeanine M Genkinger1, Laura Stigter2, Wieslaw Jedrychowski3, Tzu-Jung Huang4, Shuang Wang4, Emily L Roen2, Renata Majewska3, Agnieszka Kieltyka3, Elzbieta Mroz3, Frederica P Perera5. 1. Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA; Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, NY, USA; Columbia Center for Children's Environmental Health, Mailman School of Public Health, Columbia University, New York, NY, USA. Electronic address: jg3081@columbia.edu. 2. Columbia Center for Children's Environmental Health, Mailman School of Public Health, Columbia University, New York, NY, USA. 3. Department of Epidemiology and Preventive Medicine, Jagiellonian University College of Medicine, Krakow, Poland. 4. Department of Biostatistics, Mailman School of Public Health, Columbia University, New York, NY, USA. 5. Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, NY, USA; Columbia Center for Children's Environmental Health, Mailman School of Public Health, Columbia University, New York, NY, USA; Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, New York, NY, USA.
Abstract
PURPOSE: Prenatal polycyclic aromatic hydrocarbon (PAH) exposure has been shown to increase DNA adduct levels and to affect neurodevelopment. Micronutrients may modify the adverse effect of PAH on neurodevelopment. Thus, we examined if micronutrient concentrations modified the association between PAH exposure and neurodevelopmental outcomes. METHODS: 151 children from a birth cohort who had micronutrient concentrations measured in cord blood and completed the Child Behavioral Checklist (CBCL), between the ages of 6 and 9 years, were evaluated. Prenatal airborne PAH exposure was measured by personal air monitoring. The betas and 95% CI for the associations of antioxidant concentrations and PAH exposure with each of the outcomes of CBCL raw score and dichotomized standardized T-score (based on clinical cutpoints) were estimated, respectively, by multivariable poisson and logistic models. RESULTS: Children below the median for alpha-tocopherol and gamma-tocopherol concentrations, compared to those above, were more likely to have thought problems, aggressive behavior and externalizing problems (p<0.05). Lower carotenoid concentration was associated with more thought problems (MVβ=0.60, p<0.001) and externalizing problems (MVβ=0.13, p<0.05) for the same contrast. No statistically significant associations were observed between retinol concentrations and neurodevelopmental symptoms. Overall, no consistent patterns were observed when we examined the interaction between antioxidants (e.g., alpha-tocopherol) and PAH in relation to CBCL symptoms (e.g., internalizing and externalizing problems, p<0.05). CONCLUSIONS: Lower alpha-tocopherol, gamma-tocopherol and carotenoid levels may adversely affect healthy neurodevelopment, even after accounting for PAH exposure. Future research to confirm these findings are warranted given the importance of identifying modifiable factors for reducing harmful PAH effects.
PURPOSE: Prenatal polycyclic aromatic hydrocarbon (PAH) exposure has been shown to increase DNA adduct levels and to affect neurodevelopment. Micronutrients may modify the adverse effect of PAH on neurodevelopment. Thus, we examined if micronutrient concentrations modified the association between PAH exposure and neurodevelopmental outcomes. METHODS: 151 children from a birth cohort who had micronutrient concentrations measured in cord blood and completed the Child Behavioral Checklist (CBCL), between the ages of 6 and 9 years, were evaluated. Prenatal airborne PAH exposure was measured by personal air monitoring. The betas and 95% CI for the associations of antioxidant concentrations and PAH exposure with each of the outcomes of CBCL raw score and dichotomized standardized T-score (based on clinical cutpoints) were estimated, respectively, by multivariable poisson and logistic models. RESULTS:Children below the median for alpha-tocopherol and gamma-tocopherol concentrations, compared to those above, were more likely to have thought problems, aggressive behavior and externalizing problems (p<0.05). Lower carotenoid concentration was associated with more thought problems (MVβ=0.60, p<0.001) and externalizing problems (MVβ=0.13, p<0.05) for the same contrast. No statistically significant associations were observed between retinol concentrations and neurodevelopmental symptoms. Overall, no consistent patterns were observed when we examined the interaction between antioxidants (e.g., alpha-tocopherol) and PAH in relation to CBCL symptoms (e.g., internalizing and externalizing problems, p<0.05). CONCLUSIONS: Lower alpha-tocopherol, gamma-tocopherol and carotenoid levels may adversely affect healthy neurodevelopment, even after accounting for PAH exposure. Future research to confirm these findings are warranted given the importance of identifying modifiable factors for reducing harmful PAH effects.
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