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Ambient ozone and fine particulate matter exposures and autism spectrum disorder in metropolitan Cincinnati, Ohio.

ABSTRACT: BACKGROUND:Epidemiological studies report fairly consistent associations between various air pollution metrics and autism spectrum disorder (ASD), with some elevated risks reported for different prenatal and postnatal periods. OBJECTIVES:To examine associations between ASD and ambient fine particulate matter (PM2.5) and ozone concentrations during the prenatal period through the second year of life in a case-control study. METHODS:ASD cases (n?=?428) diagnosed at Cincinnati Children's Hospital Medical Center were frequency matched (15:1) to 6420 controls from Ohio birth records. We assigned daily PM2.5 and ozone estimates for 2005-2012 from US EPA's Fused Air Quality Surface Using Downscaling model to each participant for each day based on the mother's census tract of residence at birth. We calculated adjusted odds ratios (aORs) using logistic regression across continuous and categorical exposure window averages (trimesters, first and second postnatal years, and cumulative measure), adjusting for maternal- and birth-related confounders, both air pollutants, and multiple temporal exposure windows. RESULTS:We detected elevated aORs for PM2.5 during the 2nd trimester, 1st year of life, and a cumulative period from pregnancy through the 2nd year (aOR ranges across categories: 1.41-1.44, 1.54-1.84, and 1.41-1.52 respectively), and for ozone in the 2nd year of life (aOR range across categories: 1.29-1.42). Per each change in IQR, we observed elevated aORs for ozone in the 3rd trimester, 1st and 2nd years of life, and the cumulative period (aOR range: 1.19-1.27) and for PM2.5 in the 2nd trimester, 1st year of life, and the cumulative period (aOR range: 1.11-1.17). DISCUSSION:We saw limited evidence of linear exposure-response relationships for ASD with increasing air pollution, but the elevated aORs detected for PM2.5 in upper exposure categories and per IQR unit increases were similar in magnitude to those reported in previous studies, especially for postnatal exposures.

SUBMITTER: Kaufman JA

PROVIDER: S-EPMC7232936 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature

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Ambient ozone and fine particulate matter exposures and autism spectrum disorder in metropolitan Cincinnati, Ohio.

Kaufman John A JA Wright J Michael JM Rice Glenn G Connolly Natalia N Bowers Katherine K Anixt Julia J

Environmental research 20190110

<h4>Background</h4>Epidemiological studies report fairly consistent associations between various air pollution metrics and autism spectrum disorder (ASD), with some elevated risks reported for different prenatal and postnatal periods.<h4>Objectives</h4>To examine associations between ASD and ambient fine particulate matter (PM<sub>2.5</sub>) and ozone concentrations during the prenatal period through the second year of life in a case-control study.<h4>Methods</h4>ASD cases (n = 428) diagnosed at ...[more]

PMID: 30684889

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Project description:BackgroundAmbient fine particulate matter [PM ≤2.5μm in aerodynamic diameter (PM2.5)] is a major health risk for children, particularly in South Asia, which currently experiences the highest PM2.5 levels globally. Nevertheless, there is comparatively little epidemiological evidence from this region to quantify the effects of PM2.5 on child survival.ObjectivesWe estimated the association between PM2.5 exposure and child survival in India.MethodsWe constructed a large, retrospective, and nationally representative cohort of children <5 years of age, born between 2009-2016, from the publicly available, cross-sectional 2015-2016 Demographic Health Surveys in India. In utero and post-delivery lifetime average ambient PM2.5 exposures were estimated with data from satellite remote sensing, meteorology, and land use information (model R2= 0.82). We used Cox proportional hazards regression to estimate the association between both average in utero and post-delivery lifetime PM2.5 and all-cause child mortality, controlling for individual- and household-level covariates, seasonality, location, and meteorology.ResultsOver 7,447,724 child-months of follow-up, there were 11,559 deaths at <5 years of age reported by the children's mothers. The mean concentrations of 9-month in utero and post-delivery lifetime average ambient PM2.5 exposure were 71.1 μg/m3 (range: 20.9-153.5 μg/m3) and 73.7 μg/m3 (range: 14.0-247.3 μg/m3), respectively. Estimated child mortality adjusted hazard ratios were 1.023 [95% confidence interval (CI): 1.008, 1.038] and 1.013 (95% CI: 1.001, 1.026) per 10-μg/m3 increase of in utero and post-delivery lifetime PM2.5, with both exposures in the model.DiscussionThis study adds to the growing body of evidence about the adverse health effects of PM2.5 by demonstrating the association between exposure, both in utero and post-delivery, on child survival at the national level in India. Strategies to reduce ambient air pollution levels, including steps to minimize in utero and early life exposures, are urgently needed in India and other countries where exposures are above recommended guideline values. https://doi.org/10.1289/EHP8910.

Project description:The contribution of precursor emissions from 17 mobile source sectors to ambient ozone and fine particulate matter levels across the U.S. were evaluated, using the CAMx photochemical model, to identify which mobile source sectors are projected to have the largest impacts on air pollution in 2025. Both onroad and nonroad sectors contribute considerably to projected air pollution across much of the country. Summer ozone season ozone contributions between 2 and 5 ppb, which are among the highest levels presented on the maps of mobile source sectors, are largely found in the southeast United States from the onroad sectors, most notably light-duty and heavy-duty vehicles, and along the coastline from the Category 3 (C3) marine sector. Annual average PM2.5 contributions between 0.5 to 0.9 ?g/m3, which are among the highest levels presented on the maps of mobile source sectors, are found throughout the Midwest and along portions of the east and west coast from onroad sectors as well as nonroad diesel and rail sectors. Additionally, contributions of precursor emissions to ambient ozone and PM2.5 levels were evaluated to understand the range of impacts from precursors in the various mobile source sectors. For most mobile source sectors, in most locations, NOX emissions contributed more to ozone than VOC emissions, and secondary PM2.5 contributed more to ambient PM2.5 than primary PM2.5. The largest ozone levels on the maps showing contributions from mobile source NOX emissions tended to be between 2 and 5 ppb, while the largest ozone levels on the maps showing contributions from mobile source VOC emissions tended to be between 0.9 and 2 ppb, except for southern California where ozone contributions from VOC emissions from onroad light duty vehicles were between 2 and 5 ppb. The largest contributions to ambient PM2.5 on the maps showing primary and secondary contributions from mobile source sectors tended to be between 0.1 and 0.5 ?g/m3. The contribution from primary PM2.5 extended over localized areas (urban-scale) and the contribution from secondary PM2.5 extended over more regional (multi-state) areas.

Project description:Exposures to ambient particulate matter (PM) are associated with increased morbidity and mortality. PM2.5 (<2.5 μm) and ozone exposures have been shown to associate with carotid intima media thickness in humans. Animal studies support a causal relationship between air pollution and atherosclerosis and identified adverse PM effects on HDL functionality. We aimed to determine whether brief exposures to PM2.5 and/or ozone could induce effects on HDL anti-oxidant and anti-inflammatory capacity in humans.Subjects were exposed to fine concentrated ambient fine particles (CAP) with PM2.5 targeted at 150 μg/m(3), ozone targeted at 240 μg/m(3) (120 ppb), PM2.5 plus ozone targeted at similar concentrations, and filtered air (FA) for 2 h, on 4 different occasions, at least two weeks apart, in a randomized, crossover study. Blood was obtained before exposures (baseline), 1 h after and 20 h after exposures. Plasma HDL anti-oxidant/anti-inflammatory capacity and paraoxonase activity were determined. HDL anti-oxidant/anti-inflammatory capacity was assessed by a cell-free fluorescent assay and expressed in units of a HDL oxidant index (HOI). Changes in HOI (ΔHOI) were calculated as the difference in HOI from baseline to 1 h after or 20 h after exposures.There was a trend towards bigger ΔHOI between PM2.5 and FA 1 h after exposures (p = 0.18) but not 20 h after. This trend became significant (p <0.05) when baseline HOI was lower (<1.5 or <2.0), indicating decreased HDL anti-oxidant/anti-inflammatory capacity shortly after the exposures. There were no significant effects of ozone alone or in combination with PM2.5 on the change in HOI at both time points. The change in HOI due to PM2.5 showed a positive trend with particle mass concentration (p = 0.078) and significantly associated with the slope of systolic blood pressure during exposures (p = 0.005).Brief exposures to concentrated PM2.5 elicited swift effects on HDL anti-oxidant/anti-inflammatory functionality, which could indicate a potential mechanism for how particulate air pollution induces harmful cardiovascular effects.

Project description:BACKGROUND: Studies have shown a relationship between air pollution and increased risk of cardiovascular morbidity and mortality. Due to the complexity of ambient air pollution composition, recent studies have examined the effects of co-exposure, particularly particulate matter (PM) and gas, to determine whether pollutant interactions alter (e.g. synergistically, antagonistically) the health response. This study examines the independent effects of fine (FCAPs) and ultrafine (UFCAPs) concentrated ambient particles on cardiac function, and determine the impact of ozone (O?) co-exposure on the response. We hypothesized that UFCAPs would cause greater decrement in mechanical function and electrical dysfunction than FCAPs, and that O? co-exposure would enhance the effects of both particle-types. METHODS: Conscious/unrestrained radiotelemetered mice were exposed once whole-body to either 190 ?g/m³ FCAPs or 140 ?g/m³ UFCAPs with/without 0.3 ppm O?; separate groups were exposed to either filtered air (FA) or O? alone. Heart rate (HR) and electrocardiogram (ECG) were recorded continuously before, during and after exposure, and cardiac mechanical function was assessed using a Langendorff perfusion preparation 24 hrs post-exposure. RESULTS: FCAPs alone caused a significant decrease in baseline left ventricular developed pressure (LVDP) and contractility, whereas UFCAPs did not; neither FCAPs nor UFCAPs alone caused any ECG changes. O? co-exposure with FCAPs caused a significant decrease in heart rate variability when compared to FA but also blocked the decrement in cardiac function. On the other hand, O? co-exposure with UFCAPs significantly increased QRS-interval, QTc and non-conducted P-wave arrhythmias, and decreased LVDP, rate of contractility and relaxation when compared to controls. CONCLUSIONS: These data suggest that particle size and gaseous interactions may play a role in cardiac function decrements one day after exposure. Although FCAPs?+?O? only altered autonomic balance, UFCAPs?+?O? appeared to be more serious by increasing cardiac arrhythmias and causing mechanical decrements. As such, O? appears to interact differently with FCAPs and UFCAPs, resulting in varied cardiac changes, which suggests that the cardiovascular effects of particle-gas co-exposures are not simply additive or even generalizable. Additionally, the mode of toxicity underlying this effect may be subtle given none of the exposures described here impaired post-ischemia recovery.

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Ambient ozone and fine particulate matter exposures and autism spectrum disorder in metropolitan Cincinnati, Ohio.

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Ambient ozone and fine particulate matter exposures and autism spectrum disorder in metropolitan Cincinnati, Ohio.

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