Summary: Children who experience elevated prenatal exposure to air pollution and exposure to early life stress have an increased risk of developing both attention problems and cognitive difficulties.
Source: Columbia University
Children with elevated exposure to early life stress in the home and elevated prenatal exposure to air pollution exhibited heightened symptoms of attention and thought problems, according to researchers at Columbia University Mailman School of Public Health and Columbia Psychiatry. Early life stress is common in youth from disadvantaged backgrounds who also often live in areas with greater exposure to air pollution.
Air pollution has negative effects on physical health, and recent work has begun to also show negative effects on mental health. Life stress, particularly early in life, is one of the best-known contributors to mental health problems. The new study is one of the first to examine the combined effects of air pollution and early life stress on school-age children. Results appear in the Journal of Child Psychology and Psychiatry.
“Prenatal exposure to polycyclic aromatic hydrocarbons, a neurotoxicant common in air pollution, seems to magnify or sustain the effects of early life social and economic stress on mental health in children,” says first author David Pagliaccio, PhD, assistant professor of clinical neurobiology in psychiatry at Columbia Psychiatry.
“Air pollutants are common in our environment, particularly in cities, and given socioeconomic inequities and environmental injustice, children growing up in disadvantaged circumstances are more likely to experience both life stress and exposure to neurotoxic chemicals,” says senior author Amy Margolis, PhD, assistant professor of medical psychology in psychiatry at Columbia Psychiatry.
“These exposures have a combined effect on poor mental health outcomes and point to the importance of public health programs that try to lessen exposure to these critical risk factors, to improve not only physical, but psychological health,” says Julie Herbstman, PhD, associate professor of environmental health science and director of the Columbia Center for Children’s Environmental Health at Columbia Mailman School of Public Health.
Data were from the CCCEH Mothers and Newborns longitudinal birth cohort study in Northern Manhattan and the Bronx, which includes many participants who self-identify as African American or Dominican. Mothers wore an air monitoring backpack during the third trimester of pregnancy to measure exposure to air pollutants in their daily lives. When their children were 5 years old, mothers reported on stress in their lives, including neighborhood quality, material hardship, intimate partner violence, perceived stress, lack of social support, and general distress levels. Mothers then reported on their child’s psychiatric symptoms at ages 5, 7, 9 and 11.
The combined effect of air pollution and early life stress was seen across several measures of thought and attention problems/ADHD at age 11. (Thought problems included obsessive thoughts and behaviors or thoughts that others find strange.) The effects were also linked to PAH-DNA adducts–a dose-sensitive marker of air pollution exposure.
The researchers say PAH and early life stress may serve as a “double hit” on shared biological pathways connected to attention and thought problems. Stress likely leads to wide-ranging changes in, for example, epigenetic expression, cortisol, inflammation, and brain structure and function. The mechanism underlying the effects of PAH is still being interrogated; however, alterations in brain structure and function represent possible shared mechanistic pathways.
Earlier studies making use of the same longitudinal cohort data found that prenatal exposure to air pollution combines with material hardship to significantly increase ADHD symptoms in children. A separate study found a combination of air pollution and poverty lowered child IQ.
Co-authors of the current study include Frederica Perera, Deliang Tang, Jeff Goldsmith, and Virginia Rauh of Columbia Mailman School; and Bradley Peterson of Keck School of Medicine, University of Southern California.
Funding: Funding was provided by the National Institute for Environmental Health Sciences (NIEHS) and the U.S. Environmental Protection Agency (P01ES09600/RD82702701, PES09600/RD832141, P01ES09600/RD834509, P50ES09600/RD83615401, K23ES026239, R01ES014393, RC2ES018784, R01ES13163, R01ES08977, P50ES009600), the New York Community Trust, Trustees of the Blanchette Hooker Rockefeller Fund, and the John and Wendy Neu Foundation. The authors have declared that they have no competing or potential conflicts of interest.
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Prenatal exposure to polycyclic aromatic hydrocarbons modifies the effects of early life stress on attention and Thought Problems in late childhood
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 × ELS interactions (FDR‐corrected) predicted CBCL Attention (β = 0.22, t(307) = 3.47, p < .001, pfdr = .003) and Thought Problems T‐scores (β = 0.21, t(307) = 3.29, p = .001, pfdr = .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 (β = 0.29, t(261) = 2.48, p = .01; n = 273). A three‐way interaction with assessment wave indicated that the PAH × ELS interaction on Attention Problems was stronger later in development (β = 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.