Abstract

Context: Autism is a heterogeneous disorder with genetic and environmental factors likely contributing to its origins. Examination of hazardous pollutants has suggested the importance of air toxics in the etiology of autism, yet little research has examined its association with local levels of air pollution using residence-specific exposure assignments.

Objective: To examine the relationship between traffic-related air pollution, air quality, and autism.

Design: This population-based case-control study includes data obtained from children with autism and control children with typical development who were enrolled in the Childhood Autism Risks from Genetics and the Environment study in California. The mother’s address from the birth certificate and addresses reported from a residential history questionnaire were used to estimate exposure for each trimester of pregnancy and first year of life. Traffic-related air pollution was assigned to each location using a line-source air-quality dispersion model. Regional air pollutant measures were based on the Environmental Protection Agency’s Air Quality System data. Logistic regression models compared estimated and measured pollutant levels for children with autism and for control children with typical development.

Setting: Case-control study from California.

Participants: A total of 279 children with autism and a total of 245 control children with typical development.

Main Outcome Measures: Crude and multivariable adjusted odds ratios (AORs) for autism.

Results: Children with autism were more likely to live at residences that had the highest quartile of exposure to traffic-related air pollution, during gestation (AOR, 1.98 [95% CI, 1.20-3.31]) and during the first year of life (AOR, 3.10 [95% CI, 1.76-5.57]), compared with control children. Regional exposure measures of nitrogen dioxide and particulate matter less than 2.5 and 10 μm in diameter (PM2.5 and PM10) were also associated with autism during gestation (exposure to nitrogen dioxide: AOR, 1.81 [95% CI, 1.37-3.09]; exposure to PM2.5: AOR, 2.08 [95% CI, 1.93-2.25]; exposure to PM10: AOR, 2.17 [95% CI, 1.49-3.16) and during the first year of life (exposure to nitrogen dioxide: AOR, 2.06 [95% CI, 1.37-3.09]; exposure to PM2.5: AOR, 2.12 [95% CI, 1.45-3.10]; exposure to PM10: AOR, 2.14 [95% CI, 1.46-3.12]). All regional pollutant estimates were scaled to twice the standard deviation of the distribution for all pregnancy estimates.

Conclusions: Exposure to traffic-related air pollution, nitrogen dioxide, PM2.5, and PM10 during pregnancy and during the first year of life was associated with autism. Further epidemiological and toxicological examinations of likely biological pathways will help determine whether these associations are causal.

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Abstract

This exploratory study was designed to assess air quality in a rural western Colorado area where residences and gas wells co-exist. Sampling was conducted before, during, and after drilling and hydraulic fracturing of a new natural gas well pad. Weekly air sampling for 1 year revealed that the number of non-methane hydrocarbons (NMHCs) and their concentrations were highest during the initial drilling phase and did not increase during hydraulic fracturing in this closed-loop system. Methylene chloride, a toxic solvent not reported in products used in drilling or hydraulic fracturing, was detected 73% of the time; several times in high concentrations. A literature search of the health effects of the NMHCs revealed that many had multiple health effects, including 30 that affect the endocrine system, which is susceptible to chemical impacts at very low concentrations, far less than government safety standards. Selected polycyclic aromatic hydrocarbons (PAHs) were at concentrations greater than those at which prenatally exposed children in urban studies had lower developmental and IQ scores. The human and environmental health impacts of the NMHCs, which are ozone precursors, should be examined further given that the natural gas industry is now operating in close proximity to human residences and public lands.

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Abstract

Increased drilling in urban areas overlying shale formations and its potential impact on human health through decreased air quality make it important to estimate the contribution of oil and gas activities to photochemical smog. Flares and compressor engines used in natural gas operations, for example, are large sources not only of NOx but also offormaldehyde, a hazardous air pollutant and powerful ozone precursor We used a neighborhood scale (200 m horizontal resolution) three-dimensional (3D) air dispersion model with an appropriate chemical mechanism to simulate ozone formation in the vicinity ofa hypothetical natural gas processing facility, based on accepted estimates of both regular and nonroutine emissions. The model predicts that, under average midday conditions in June, regular emissions mostly associated with compressor engines may increase ambient ozone in the Barnett Shale by more than 3 ppb beginning at about 2 km downwind of the facility, assuming there are no other major sources of ozone precursors. Flare volumes of 100,000 cubic meters per hour ofnatural gas over a period of 2 hr can also add over 3 ppb to peak 1-hr ozone somewhatfurther (>8 km) downwind, once dilution overcomes ozone titration and inhibition by large flare emissions of NOx. The additional peak ozone from the hypothetical flare can briefly exceed 10 ppb about 16 km downwind. The enhancements of ambient ozone predicted by the model are significant, given that ozone control strategy widths are of the order of a few parts per billion. Degrading the horizontal resolution of the model to 1 km spuriously enhances the simulated ozone increases by reducing the effectiveness of ozone inhibition and titration due to artificial plume dilution.

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Abstract

BACKGROUND: Technological advances (e.g. directional drilling, hydraulic fracturing), have led to increases in unconventional natural gas development (NGD), raising questions about health impacts.

OBJECTIVES: We estimated health risks for exposures to air emissions from a NGD project in Garfield County, Colorado with the objective of supporting risk prevention recommendations in a health impact assessment (HIA).

METHODS: We used EPA guidance to estimate chronic and subchronic non-cancer hazard indices and cancer risks from exposure to hydrocarbons for two populations: (1) residents living >½ mile from wells and (2) residents living ≤ ½ mile from wells.

RESULTS: Residents living ≤ ½ mile from wells are at greater risk for health effects from NGD than are residents living >½ mile from wells. Subchronic exposures to air pollutants during well completion activities present the greatest potential for health effects. The subchronic non-cancer hazard index (HI) of 5 for residents ≤ ½ mile from wells was driven primarily by exposure to trimethylbenzenes, xylenes, and aliphatic hydrocarbons. Chronic HIs were 1 and 0.4. for residents ≤ ½ mile from wells and >½ mile from wells, respectively. Cumulative cancer risks were 10 in a million and 6 in a million for residents living ≤ ½ mile and >½ mile from wells, respectively, with benzene as the major contributor to the risk.

CONCLUSIONS: Risk assessment can be used in HIAs to direct health risk prevention strategies. Risk management approaches should focus on reducing exposures to emissions during well completions. These preliminary results indicate that health effects resulting from air emissions during unconventional NGD warrant further study. Prospective studies should focus on health effects associated with air pollution.

Copyright © 2012 Elsevier B.V. All rights reserved.

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Abstract

The multispecies analysis of daily air samples collected at the NOAA Boulder Atmospheric Observatory (BAO) in Weld County in northeastern Colorado since 2007 shows highly correlated alkane enhancements caused by a regionally distributed mix of sources in the Denver-Julesburg Basin. To further characterize the emissions of methane and non-methane hydrocarbons (propane, n-butane, i-pentane, n-pentane and benzene) around BAO, a pilot study involving automobile-based surveys was carried out during the summer of 2008. A mix of venting emissions (leaks) of raw natural gas and flashing emissions from condensate storage tanks can explain the alkane ratios we observe in air masses impacted by oil and gas operations in northeastern Colorado. Using the WRAP Phase III inventory of total volatile organic compound (VOC) emissions from oil and gas exploration, production and processing, together with flashing and venting emission speciation profiles provided by State agencies or the oil and gas industry, we derive a range of bottom-up speciated emissions for Weld County in 2008. We use the observed ambient molar ratios and flashing and venting emissions data to calculate top-down scenarios for the amount of natural gas leaked to the atmosphere and the associated methane and non-methane emissions. Our analysis suggests that the emissions of the species we measured are most likely underestimated in current inventories and that the uncertainties attached to these estimates can be as high as a factor of two.

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Abstract

BACKGROUND: Air pollution exposure during pregnancy might have trimester-specific effects on fetal growth.

OBJECTIVE: We prospectively evaluated the associations of maternal air pollution exposure with fetal growth characteristics and adverse birth outcomes in 7,772 subjects in the Netherlands.

METHODS: Particulate matter with an aerodynamic diameter < 10 μm (PM10) and nitrogen dioxide (NO2) levels were estimated using dispersion modeling at the home address. Fetal head circumference, length, and weight were estimated in each trimester by ultrasound. Information on birth outcomes was obtained from medical records.

RESULTS: In cross-sectional analyses, NO2 levels were inversely associated with fetal femur length in the second and third trimester, and PM10 and NO2 levels both were associated with smaller fetal head circumference in the third trimester [-0.18 mm, 95% confidence interval (CI): -0.24, -0.12 mm; and -0.12 mm, 95% CI: -0.17, -0.06 mm per 1-μg/m3 increase in PM10 and NO2, respectively]. Average PM10 and NO2 levels during pregnancy were not associated with head circumference and length at birth or neonatally, but were inversely associated with birth weight (-3.6 g, 95% CI: -6.7, -0.4 g; and -3.4 g, 95% CI: -6.2, -0.6 g, respectively). Longitudinal analyses showed similar patterns for head circumference and weight, but no associations with length. The third and fourth quartiles of PM10 exposure were associated with preterm birth [odds ratio (OR) = 1.40, 95% CI: 1.03, 1.89; and OR = 1.32; 95% CI: 0.96, 1.79, relative to the first quartile]. The third quartile of PM10 exposure, but not the fourth, was associated with small size for gestational age at birth (SGA) (OR = 1.38; 95% CI: 1.00, 1.90). No consistent associations were observed for NO2 levels and adverse birth outcomes.

CONCLUSIONS: Results suggest that maternal air pollution exposure is inversely associated with fetal growth during the second and third trimester and with weight at birth. PM10 exposure was positively associated with preterm birth and SGA.

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Abstract

Exposure to air pollution during pregnancy has been suggested to be a risk factor for preterm birth; however, epidemiologic evidence remains mixed and limited. The authors examined the association between ambient levels of particulate matter <2.5 μm in aerodynamic diameter (PM(2.5)) and the risk of preterm birth in North Carolina during the period 2001-2005. They estimated the risks of cumulative and lagged average exposures to PM(2.5) during pregnancy via a 2-stage discrete-time survival model. The authors also considered exposure metrics derived from 1) ambient concentrations measured by the Air Quality System (AQS) monitoring network and 2) concentrations predicted by statistically fusing AQS data with process-based numerical model output (the Statistically Fused Air and Deposition Surfaces (FSD) database). Using the AQS measurements, an interquartile-range (1.73 μg/m(3)) increase in cumulative PM(2.5) exposure was associated with a 6.8% (95% posterior interval: 0.5, 13.6) increase in the risk of preterm birth. Using the FSD-predicted levels and accounting for prediction error, the authors also found significant adverse associations between trimester 1, trimester 2, and cumulative PM(2.5) exposure and preterm birth. These findings suggest that exposure to ambient PM(2.5) during pregnancy is associated with increased risk of preterm birth, even in a region characterized by relatively good air quality.

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Abstract

BACKGROUND: Studies have identified relationships between air pollution and birth weight, but have been inconsistent in identifying individual pollutants inversely associated with birth weight or elucidating susceptibility of the fetus by trimester of exposure. We examined effects of prenatal ambient pollution exposure on average birth weight and risk of low birth weight in full-term births.

METHODS: We estimated average ambient air pollutant concentrations throughout pregnancy in the neighborhoods of women who delivered term singleton live births between 1996 and 2006 in California. We adjusted effect estimates of air pollutants on birth weight for infant characteristics, maternal characteristics, neighborhood socioeconomic factors, and year and season of birth.

RESULTS: 3,545,177 singleton births had monitoring for at least one air pollutant within a 10 km radius of the tract or ZIP Code of the mother’s residence. In multivariate models, pollutants were associated with decreased birth weight; -5.4 grams (95% confidence interval -6.8 g, -4.1 g) per ppm carbon monoxide, -9.0 g (-9.6 g, -8.4 g) per pphm nitrogen dioxide, -5.7 g (-6.6 g, -4.9 g) per pphm ozone, -7.7 g (-7.9 g, -6.6 g) per 10 microg/m3 particulate matter under 10 microm, -12.8 g (-14.3 g, -11.3 g) per 10 microg/m3 particulate matter under 2.5 microm, and -9.3 g (-10.7 g, -7.9 g) per 10 microg/m3 of coarse particulate matter. With the exception of carbon monoxide, estimates were largely unchanged after controlling for co-pollutants. Effect estimates for the third trimester largely reflect the results seen from full pregnancy exposure estimates; greater variation in results is seen in effect estimates specific to the first and second trimesters.

CONCLUSIONS: This study indicates that maternal exposure to ambient air pollution results in modestly lower infant birth weight. A small decline in birth weight is unlikely to have clinical relevance for individual infants, and there is debate about whether a small shift in the population distribution of birth weight has broader health implications. However, the ubiquity of air pollution exposures, the responsiveness of pollutant levels to regulation, and the fact that the highest pollution levels in California are lower than those regularly experienced in other countries suggest that precautionary efforts to reduce pollutants may be beneficial for infant health from a population perspective.

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Abstract

Exposing children to environmental pollutants during important times of physiological development can lead to long-lasting health problems, dysfunction, and disease. The location of children’s schools can increase their exposure. We examined the extent of air pollution from industrial sources around public schools in Michigan to find out whether air pollution jeopardizes children’s health and academic success. We found that schools located in areas with the highest air pollution levels had the lowest attendance rates-a potential indicator of poor health-and the highest proportions of students who failed to meet state educational testing standards. Michigan and many other states currently do not require officials considering a site for a new school to analyze its environmental quality. Our results show that such requirements are needed. For schools already in existence, we recommend that their environmental quality should be investigated and improved if necessary.

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Abstract

BACKGROUND:
Previous studies have reported positive associations between maternal exposure to air pollutants and several adverse birth outcomes. However, there have been no studies assessing the association between environmental levels of hazardous air pollutants, such as benzene, and neural tube defects (NTDs), a common and serious group of congenital malformations.

OBJECTIVE: Our goal was to conduct a case-control study assessing the association between ambient air levels of benzene, toluene, ethylbenzene, and xylene (BTEX) and the prevalence of NTDs among offspring.

METHODS: The Texas Birth Defects Registry provided data on NTD cases (spina bifida and anencephaly) delivered between 1999 and 2004. The control group was a random sample of unaffected live births, frequency matched to cases on year of birth. Census tract-level estimates of annual BTEX levels were obtained from the U.S. Environmental Protection Agency 1999 Assessment System for Population Exposure Nationwide. Restricted cubic splines were used in mixed-effects logistic regression models to determine associations between each pollutant and NTD phenotype.

RESULTS: Mothers living in census tracts with the highest benzene levels were more likely to have offspring with spina bifida than were women living in census tracts with the lowest levels (odds ratio = 2.30; 95% confidence interval, 1.22-4.33). No significant associations were observed between anencephaly and benzene or between any of the NTD phenotypes and toluene, ethylbenzene, or xylene.

CONCLUSION: In the first study to assess the relationship between environmental levels of BTEX and NTDs, we found an association between benzene and spina bifida. Our results contribute to the growing body of evidence regarding air pollutant exposure and adverse birth outcomes.

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Abstract

OBJECTIVE: There is growing interest in disentangling the health effects of spatially clustered social and physical environmental exposures and in exploring potential synergies among them, with particular attention directed to the combined effects of psychosocial stress and air pollution. Both exposures may be elevated in lower-income urban communities, and it has been hypothesized that stress, which can influence immune function and susceptibility, may potentiate the effects of air pollution in respiratory disease onset and exacerbation. In this paper, we attempt to synthesize the relevant research from social and environmental epidemiology, toxicology, immunology, and exposure assessment to provide a useful framework for environmental health researchers aiming to investigate the health effects of environmental pollution in combination with social or psychological factors.

DATA SYNTHESIS: We review the existing epidemiologic and toxicologic evidence on synergistic effects of stress and pollution, and then describe the physiologic effects of stress and key issues related to measuring and evaluating stress as it relates to physical environmental exposures and susceptibility. Finally, we identify some of the major methodologic challenges ahead as we work toward disentangling the health effects of clustered social and physical exposures and accurately describing the interplay among these exposures.

CONCLUSIONS: There is still tremendous work to be done toward understanding the combined and potentially synergistic health effects of stress and pollution. As this research proceeds, we recommend careful attention to the relative temporalities of stress and pollution exposures, to nonlinearities in their independent and combined effects, to physiologic pathways not elucidated by epidemiologic methods, and to the relative spatial distributions of social and physical exposures at multiple geographic scales.

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