Residential Proximity to Freeways and Autism in the CHARGE Study

Department of Preventive Medicine, Zilkha Neurogenetic Institute, Keck School of Medicine, Children's Hospital Los Angeles, University of Southern California, Los Angeles, California 90033, USA.
Environmental Health Perspectives (Impact Factor: 7.98). 12/2010; 119(6):873-7. DOI: 10.1289/ehp.1002835
Source: PubMed


Little is known about environmental causes and contributing factors for autism. Basic science and epidemiologic research suggest that oxidative stress and inflammation may play a role in disease development. Traffic-related air pollution, a common exposure with established effects on these pathways, contains substances found to have adverse prenatal effects.
We examined the association between autism and proximity of residence to freeways and major roadways during pregnancy and near the time of delivery, as a surrogate for air pollution exposure.
Data were from 304 autism cases and 259 typically developing controls enrolled in the Childhood Autism Risks from Genetics and the Environment (CHARGE) study. The mother's address recorded on the birth certificate and trimester-specific addresses derived from a residential history obtained by questionnaire were geocoded, and measures of distance to freeways and major roads were calculated using ArcGIS software. Logistic regression models compared residential proximity to freeways and major roads for autism cases and typically developing controls.
Adjusting for sociodemographic factors and maternal smoking, maternal residence at the time of delivery was more likely be near a freeway (≤ 309 m) for cases than for controls [odds ratio (OR)=1.86; 95% confidence interval (CI), 1.04-3.45]. Autism was also associated with residential proximity to a freeway during the third trimester (OR=2.22; CI, 1.16-4.42). After adjustment for socioeconomic and sociodemographic characteristics, these associations were unchanged. Living near other major roads at birth was not associated with autism.
Living near a freeway was associated with autism. Examination of associations with measured air pollutants is needed.

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    • "In this review, we focus on environmental chemicals. Environmental chemicals that have been implicated as risk factors for ASD include polychlorinated biphenyls (PCBs), lead, bisphenol A (BPA), mercury, and pesticides (Tables 1–2)5253545556575859606162. However, mechanisms by which these environmental factors interact with genetic susceptibilities to confer individual risk for ASD remain largely speculative. "
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    ABSTRACT: There is now compelling evidence that gene by environment interactions are important in the etiology of autism spectrum disorders (ASDs). However, the mechanisms by which environmental factors interact with genetic susceptibilities to confer individual risk for ASD remain a significant knowledge gap in the field. The epigenome, and in particular DNA methylation, is a critical gene expression regulatory mechanism in normal and pathogenic brain development. DNA methylation can be influenced by environmental factors such as diet, hormones, stress, drugs, or exposure to environmental chemicals, suggesting that environmental factors may contribute to adverse neurodevelopmental outcomes of relevance to ASD via effects on DNA methylation in the developing brain. In this review, we describe epidemiological and experimental evidence implicating altered DNA methylation as a potential mechanism by which environmental chemicals confer risk for ASD, using polychlorinated biphenyls (PCBs), lead, and bisphenol A (BPA) as examples. Understanding how environmental chemical exposures influence DNA methylation and how these epigenetic changes modulate the risk and/or severity of ASD will not only provide mechanistic insight regarding gene-environment interactions of relevance to ASD but may also suggest potential intervention strategies for these and potentially other neurodevelopmental disorders.
    Full-text · Article · Jan 2016
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    • "Recently , several investigations have focused on ASD risk and ambient criteria air pollutants (traffic related and/or from industry)1213141516.Volk et al. (2011Volk et al. ( , 2013) examined the relationship between traffic-related air pollution and autism in California in two population based case– control studies from the Childhood Autism Risks from Genetics and the Environment (CHARGE) study. The first reported increased risk among those living within 1,000 feet of a major freeway[12], and the second found that increased autism risk was associated with exposure to model-based indicators of traffic-related air pollutant (TRP) mixture as well as regional measures of NO 2 , PM 2.5 , and PM 10[13][21]. Given these few epidemiological investigations and the heavy industrial background of southwestern Pennsylvania, the objective of the current study was to conduct an exploratory case–control study in this area to assess if neurotoxic air pollutants, as modeled by NATA, were associated with the risk of ASD. "
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    ABSTRACT: Background: Autism spectrum disorders (ASD) constitute a major public health problem affecting one in 68 children. There is little understanding of the causes of ASD despite its serious social impact. Air pollution contains many toxicants known to have adverse effects on the fetus. We conducted a population based case-control study in southwestern Pennsylvania to estimate the association between ASD and 2005 US EPA modeled NATA (National Air Toxics Assessment) levels for 30 neurotoxicants. Methods: A total of 217 ASD cases born between 2005 and 2009 were recruited from local ASD diagnostic and treatment centers. There were two different control groups: 1) interviewed controls (N = 224) frequency matched by child's year of birth, sex and race with complete residential histories from prior to pregnancy through the child's second birthday, and 2) 5,007 controls generated from a random sample of birth certificates (BC controls) using residence at birth. We used logistic regression analysis comparing higher to first quartile of exposure to estimate odds ratios (ORs) and 95 % confidence intervals (CI), adjusting for mother's age, education, race, smoking status, child's year of birth and sex. Results: Comparing fourth to first quartile exposures for all births, the adjusted OR for styrene was 2.04 (95 % CI = 1.17-3.58, p = 0.013) for the interviewed case-control analysis and 1.61 (95 % CI = 1.08-2.40, p = 0.018) for the BC analysis. In the BC comparison, chromium also exhibited an elevated OR of 1.60 (95 % CI = 1.08-2.38, p = 0.020), which was similarly elevated in the interviewed analysis (OR = 1.52, 95 % CI = 0.87-2.66). There were borderline significant ORs for the BC comparison for methylene chloride (OR = 1.41, 95 % CI = 0.96-2.07, p = 0.082) and PAHs (OR = 1.44, 95 % CI = 0.98-2.11, p = 0.064). Conclusions: Living in areas with higher levels of styrene and chromium during pregnancy was associated with increased risk of ASD, with borderline effects for PAHs and methylene chloride. These results are consistent with other studies. It is unclear, however, whether these chemicals are risk factors themselves or if they reflect the effect of a mixture of pollutants. Future work should include improved spatiotemporal estimates of exposure to air toxics, taking into account the dynamic movement of individuals during daily life.
    Full-text · Article · Oct 2015 · Environmental Health
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    No preview · Article · Sep 2015 · Journal of neuroimmunology
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