期刊
JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY
卷 61, 期 11, 页码 1253-1265出版社
WILEY
DOI: 10.1111/jcpp.13189
关键词
Attention deficit hyperactivity disorder; adversity; child behavior checklist; child development; toxicants
资金
- National Institute for Environmental Health Sciences (NIEHS)
- U.S. Environmental Protection Agency (US EPA) [NIEHS/EPA P01ES09600/RD82702701, NIEHS/EPA P01ES09600/RD832141, NIEHS/EPA P01ES09600/RD834509, NIEHS/EPA P50ES09600/RD83615401, NIEHS K23ES026239, NIEHS R01ES014393, NIEHS RC2ES018784, NIEHS R01ES13163, NIEHS R01ES08977, NIEHS 5P50ES009600]
- New York Community Trust
- Trustees of the Blanchette Hooker Rockefeller Fund
- John and Wendy Neu Foundation
Background Risk for childhood psychopathology is complex and multifactorial, implicating direct and interacting effects of familial and environmental factors. The role of environmental neurotoxicants in psychiatric risk is of growing concern, including polycyclic aromatic hydrocarbons (PAH), common in air pollution. Prenatal PAH exposure is linked to adverse physical, behavioral, and cognitive outcomes as well as increasing psychiatric risk. It is unclear whether environmental exposures, like PAH, magnify the effects of exposure to early life stress (ELS), a critical risk factor for psychopathology. The current work aimed to test potential interactions between prenatal PAH exposure and psychosocial/socioeconomic stress on psychiatric symptoms in school-age children. Methods Data were from the Columbia Center for Children's Environmental Health Mothers and Newborns longitudinal birth cohort study. Prenatal PAH exposure was ascertained though air monitoring during pregnancy and maternal PAH-DNA adducts at delivery. Mothers reported on ELS (child age 5) and on child psychiatric symptoms across childhood (child age 5, 7, 9, and 11) using the Child Behavior Checklist (CBCL). Results Significant prenatal airborne PAH x ELS interactions (FDR-corrected) predicted CBCL Attention (beta = 0.22, t(307) = 3.47, p < .001, p(fdr )= .003) and Thought Problems T-scores (beta = 0.21, t(307) = 3.29, p = .001, p(fdr )= .004) at age 11 (n = 319). Relative to those with lower exposure, children with higher prenatal PAH exposure exhibited stronger positive associations between ELS and CBCL Attention and Thought Problem T-scores. This interaction was also significant examining convergent ADHD measures (Conners, DuPaul) and examining maternal PAH-DNA adducts (beta = 0.29, t(261) = 2.48, p = .01; n = 273). A three-way interaction with assessment wave indicated that the PAH x ELS interaction on Attention Problems was stronger later in development (beta = 0.03, t(1,601) = 2.19, p = .03; n = 477). Conclusions Prenatal exposure to PAH, a common neurotoxicant in air pollution, may magnify or sustain the effects of early life psychosocial/socioeconomic stress on psychiatric outcomes later in child development. This work highlights the critical role of air pollution exposure on child mental health.
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