Case study descriptions of acute onset of respiratory, neurologic, dermal, vascular, abdominal, and gastrointestinal sequelae near natural gas facilities contrast with a subset of emissions research, which suggests that there is limited risk posed by unconventional natural gas development (UNGD). An inspection of the pathophysiological effects of acute toxic actions reveals that current environmental monitoring protocols are incompatible with the goal of protecting the health of those living and working near UNGD activities. The intensity, frequency, and duration of exposures to toxic materials in air and water determine the health risks to individuals within a population. Currently, human health risks near UNGD sites are derived from average population risks without adequate attention to the processes of toxicity to the body. The objective of this paper is to illustrate that current methods of collecting emissions data, as well as the analyses of these data, are not sufficient for accurately assessing risks to individuals or protecting the health of those near UNGD sites. Focusing on air pollution impacts, we examined data from public sources and from the published literature. We compared the methods commonly used to evaluate health safety near UNGD sites with the information that would be reasonably needed to determine plausible outcomes of actual exposures. Such outcomes must be based on the pathophysiological effects of the agents present and the susceptibility of residents near these sites. Our study has several findings. First, current protocols used for assessing compliance with ambient air standards do not adequately determine the intensity, frequency or durations of the actual human exposures to the mixtures of toxic materials released regularly at UNGD sites. Second, the typically used periodic 24-h average measures can underestimate actual exposures by an order of magnitude. Third, reference standards are set in a form that inaccurately determines health risk because they do not fully consider the potential synergistic combinations of toxic air emissions. Finally, air dispersion modeling shows that local weather conditions are strong determinates of individual exposures. Appropriate estimation of safety requires nested protocols that measure real time exposures. New protocols are needed to provide 1) continuous measures of a surrogate compound to show periods of extreme exposure; 2) a continuous screening model based on local weather conditions to warn of periodic high exposures; and 3) comprehensive detection of chemical mixtures using canisters or other devices that capture the major components of the mixtures.
In the last decade hydraulic fracturing for natural gas has exploded on the Barnett Shale in Texas. The region is now home to the most intensive hydraulic fracking and gas production activities ever undertaken in densely urbanized areas. Faced with minimal state and federal regulation, Texas cities are on the front line in the effort to figure out how best to balance industry, land use, and environmental concerns. Local governments in Texas, however, do not currently have the regulatory authority, capacity, or the information required to close the regulatory gap. Using the community experience on the Barnett Shale as a case study, this article focuses on the legal and regulatory framework governing air emissions and proposes changes to the current regulatory structure.
Under both the state and federal programs, the regulation of hazardous air emissions from gas operations is based largely on questions of cost and available technology. There is no comprehensive cumulative risk assessment to consider the potential impact to public health in urban areas. Drilling operations are being conducted in residential areas. Residents living in close proximity to gas operations on the Barnett Shale have voiced serious concerns for their health, which have yet to be comprehensively evaluated. Given the complexity of the science, and the dearth of clear, transparent, and enforceable standards, inadequate studies and limited statistical analysis have been allowed to provide potentially false assurances. The politically expedient bottom line dominates with little attention paid to the quality of the science or the adequacy of the standards.
Determining and applying comprehensive health-based standards for hazardous air pollutants has been largely abandoned at the federal level given uncertainties in the science, difficulties of determining and measuring “safe” levels of toxic pollutants, and the potential for economic disruption. Neither the state nor the federal government has set enforceable ambient standards for hazardous air pollutants. Identifying cumulative air pollution problems that may occur in urban areas, the State of California has called upon local governments to identify “hot spots” and to consider air quality issues in their planning and zoning actions. In Texas, however, preemption discussions dominate the analysis. Any local government regulation that might provide protection from toxic air emissions otherwise regulated by the State must be justified by some other public purpose.
Texas should consider authorizing and encouraging local level air quality planning for industrial activities, similar to what California has done. Care should be taken to separate these facilities from sensitive receptors and “hot spots” that may already be burdened with excessive hazardous air emissions. Given the difficulty of the task, there is also an important role for the state and federal governments in working to establish ambient standards for hazardous air pollutants, as well as standards for health based assessment and public communication. The uncertainty inherent in any of these standards should be made clear and accessible to local governments so that it may be considered in making appropriate and protective land use decisions. Texas should consider allowing local governments to have the power to establish ambient air quality standards, emissions limitations, monitoring, reporting, and offsets for hazardous air pollutants, following the model applied to conventional air pollutants pursuant to the federal program.
Oil and natural gas production in the Western United States has grown rapidly in recent years, and with this industrial expansion, growing environmental concerns have arisen regarding impacts on water supplies and air quality. Recent studies have revealed highly enhanced atmospheric levels of volatile organic compounds (VOC) from primary emissions in regions of heavy oil and gas development and associated rapid photochemical production of ozone during winter. Here, we present surface and vertical profile observations of VOC from the Uintah Basin Winter Ozone Studies conducted in January – February of 2012 and 2013. These measurements identify highly elevated levels of atmospheric alkane hydrocarbons with enhancement rates of C2 – C6 non-methane hydrocarbon (NMHC) mean mole fractions during temperature inversion events in 2013at 200-300 times above the regional and seasonal background. Elevated atmospheric NMHC mole fractions coincided with build-up of ambient 1-hour ozone to levels exceeding 150 ppbv (parts per billion by volume). The total annual mass flux of C2-C7 VOC was estimated at 194 ± 56 x 106 kg yr-1, equivalent to the annual VOC emissions of a fleet of ~100 million automobiles. Total annual fugitive emission of the aromatic compounds benzene and toluene, considered air toxics, were estimated at 1.6 ± 0.4 x 106 and 2.0 ± 0.5 x 106 kg yr-1, respectively. These observations reveal a strong causal link between oil and gas emissions, accumulation of air toxics, and significant surface production in the atmospheric surface layer.
The “Industrial Heartland” of Alberta is Canada’s largest hydrocarbon processing center, with more than 40 major chemical, petrochemical, and oil and gas facilities. Emissions from these industries affect local signair quality and human health. This paper characterizes ambient levels of 77 volatile organic compounds sign(VOCs) in the region using high-precision measurements collected in summer 2010. Remarkably strong enhancements of 43 VOCs were detected, and concentrations in the industrial plumes were often similar to or even higher than levels measured in some of the world’s largest cities and industrial regions. For example maximum levels of propene and i-pentane exceeded 100 ppbv, and 1,3-butadiene, a known carcinogen, reached 27 ppbv. Major VOC sources included propene fractionation, diluent separation and bitumen processing. Emissions of the measured VOCs increased the hydroxyl radical reactivity (kOH), a measure of the potential to form downwind ozone, from 3.4 s–1 in background air to 62 s–1 in the most concentrated plumes. The plume value was comparable to polluted megacity values, and acetaldehyde, propene and 1,3-butadiene contributed over half of the plume kOH. Based on a 13-year record (1994 e2006) at the county level, the incidence of male hematopoietic cancers (leukemia and non-Hodgkin lymphoma) was higher in communities closest to the Industrial Heartland compared to neighboring counties. While a causal association between these cancers and exposure to industrial emissions cannot be confirmed, this pattern and the elevated VOC levels warrant actions to reduce emissions of known carcinogens, including benzene and 1,3-butadiene.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.