Perinatal exposure to hazardous air pollutants and autism spectrum disorders at age 8
Open accessAbstract
BACKGROUND: Hazardous air pollutants are plausible candidate exposures for autism spectrum disorders. They have been explored in recent studies for their role in the development of these disorders. METHODS: We used a prevalent case-control design to screen perinatal exposure to 35 hazardous air pollutants for further investigation in autism etiology. We included 383 children with autism spectrum disorders and, as controls, 2,829 children with speech and language impairment. All participants were identified from the records-based surveillance of 8-year-old children conducted by the Autism and Developmental Disabilities Monitoring Network in North Carolina (for children born in 1994 and 1996) and West Virginia (born in 1992 and 1994). Exposures to ambient concentrations of metal, particulate, and volatile organic air pollutants in the census tract of the child's birth residence were assigned from the 1996 National Air Toxics Assessment annual-average model. We estimated odds ratios (ORs) for autism spectrum disorders and corresponding 95% confidence intervals (CIs), comparing across the 20th and 80th percentiles of log-transformed hazardous air pollutant concentration among the selected controls, using semi-Bayes logistic models and adjusting for sampling variables (surveillance year and state), a priori demographic confounders from the birth certificate and census, and covarying air pollutants. RESULTS: We estimated many near-null ORs, including those for metals, established human neurodevelopmental toxicants, and several pollutants that were elevated in a similar study in California. Hazardous air pollutants with more precise and elevated OR estimates included methylene chloride, 1.4 (95% CI = 0.7-2.5), quinoline, 1.4 (1.0-2.2), and styrene, 1.8 (1.0-3.1). CONCLUSIONS: Our screening design was limited by exposure misclassification of air pollutants and the use of an alternate developmental disorder as the control group, both of which may have biased results toward the null. Despite these limitations, methylene chloride, quinoline, and styrene emerged (based on this analysis and prior epidemiologic evidence) as candidates that warrant further investigation for a possible role in autism etiology.
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Epidemiological studies reported associations between autism and air pollution at the birth and early life residences.
“Epidemiological studies (86, 87) reported associations between autism and air pollution at the birth and early life residences.”
From Gene × Environment Interactions in Autism Spectrum Disorders: Role of Epigenetic Mechanisms (2014) · cites this paper as [87]
The elevated metal associations are notable because measurement error in the emissions-based model would be expected to attenuate observed odds ratios.
“The pattern of elevated associations was especially striking given the measurement error inherent in the emissions-based air pollutant model used in three of these studies, which would be expected to attenuate observed ORs.”
From Environmental Chemical Exposures and Autism Spectrum Disorders: A Review of the Epidemiological Evidence (2014) · cites this paper as [16]
In one study, lead and manganese appeared inversely related to autism risk, possibly due to a stronger association in the speech and language impairment comparison group.
“In one study, lead, and, to a lesser extent, manganese, appeared inversely related to autism risk, which could have been caused by a stronger association with the comparison group in this design: children with speech and language impairment”
From Environmental Chemical Exposures and Autism Spectrum Disorders: A Review of the Epidemiological Evidence (2014) · cites this paper as [16]
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- Authors
- Kalkbrenner, A. E., Daniels, J. L., Chen, J.-C., Poole, C., Emch, M., & Morrissey, J.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- University of Southern California (US)
- Corresponding author
- Kalkbrenner, Amy E.
- ORCID
- Venue
- Epidemiology
- Published
- 2010-09
- Volume
- 21
- Issue
- 5
- Pages
- 631-641
- ISSN
- 1044-3983 (ISSN-L)
- PMC
- PMC2989602
- OpenAlex
- W2130557242
- Cited by
- 184
- References
- 41
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 7 · 2023: 5 · 2022: 8 · 2021: 11 · 2020: 7 · 2019: 16 · 2018: 15 · 2017: 17 · 2016: 16 · 2015: 24 · 2014: 17 · 2013: 11 · 2012: 17
- FWCI
- 6.58
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Epidemiology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (2r24hd050924-06)
- National Institute of Environmental Health Sciences (P30ES10126), P30ES010126, T32ES007018)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R24 HD-050924)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Heavy Metal Exposure and Toxicity
- Keywords
- autism spectrum disorder, hazardous air pollutants, dichloromethane, quinoline, styrene, metals, particulate matter, volatile organic compounds, autism etiology, developmental neurotoxicity, exposure misclassification, developmental disabilities
- MeSH terms
- Air Pollutants, Bayes Theorem, Child, Child Development Disorders, Pervasive, Environmental Exposure, Female, Humans, Male, North Carolina, Pregnancy, Prenatal Exposure Delayed Effects, West Virginia, Confidence Intervals, Logistic Models, Odds Ratio, Case-Control Studies
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