Environmental Public Health Dimensions of Shale and Tight Gas Development

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Abstract

Background: The United States has experienced a boom in natural gas production due to recent technological innovations that have enabled this resource to be produced from shale formations.

Objectives: We reviewed the body of evidence related to exposure pathways in order to evaluate the potential environmental public health impacts of shale gas development. We highlight what is currently known and identify data gaps and research limitations by addressing matters of toxicity, exposure pathways, air quality, and water quality.

Discussion: There is evidence of potential environmental public health risks associated with shale gas development. Several studies suggest that shale gas development contributes to ambient air concentrations of pollutants known to be associated with increased risk of morbidity and mortality. Similarly, an increasing body of studies suggest that water contamination risks exist through a variety of environmental pathways, most notably during wastewater transport and disposal, and via poor zonal isolation of gases and fluids due to structural integrity impairment of cement in gas wells.

Conclusion: Despite a growing body of evidence, data gaps persist. Most important, there is a need for more epidemiological studies to assess associations between risk factors, such as air and water pollution, and health outcomes among populations living in close proximity to shale gas operations.

Citation: Shonkoff SB, Hays J, Finkel ML. 2014. Environmental public health dimensions of shale and tight gas development. Environ Health Perspect 122:787–795; http://dx.doi.org/10.1289/ehp.1307866

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Most cited references 93

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Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease.

C. Pope, Richard Burnett, George Thurston … (2004)

Epidemiologic studies have linked long-term exposure to fine particulate matter air pollution (PM) to broad cause-of-death mortality. Associations with specific cardiopulmonary diseases might be useful in exploring potential mechanistic pathways linking exposure and mortality. General pathophysiological pathways linking long-term PM exposure with mortality and expected patterns of PM mortality with specific causes of death were proposed a priori. Vital status, risk factor, and cause-of-death data, collected by the American Cancer Society as part of the Cancer Prevention II study, were linked with air pollution data from United States metropolitan areas. Cox Proportional Hazard regression models were used to estimate PM-mortality associations with specific causes of death. Long-term PM exposures were most strongly associated with mortality attributable to ischemic heart disease, dysrhythmias, heart failure, and cardiac arrest. For these cardiovascular causes of death, a 10-microg/m3 elevation in fine PM was associated with 8% to 18% increases in mortality risk, with comparable or larger risks being observed for smokers relative to nonsmokers. Mortality attributable to respiratory disease had relatively weak associations. Fine particulate air pollution is a risk factor for cause-specific cardiovascular disease mortality via mechanisms that likely include pulmonary and systemic inflammation, accelerated atherosclerosis, and altered cardiac autonomic function. Although smoking is a much larger risk factor for cardiovascular disease mortality, exposure to fine PM imposes additional effects that seem to be at least additive to if not synergistic with smoking.

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Long-term ozone exposure and mortality.

Michael Jerrett, Richard Burnett, C. Pope … (2009)

Although many studies have linked elevations in tropospheric ozone to adverse health outcomes, the effect of long-term exposure to ozone on air pollution-related mortality remains uncertain. We examined the potential contribution of exposure to ozone to the risk of death from cardiopulmonary causes and specifically to death from respiratory causes. Data from the study cohort of the American Cancer Society Cancer Prevention Study II were correlated with air-pollution data from 96 metropolitan statistical areas in the United States. Data were analyzed from 448,850 subjects, with 118,777 deaths in an 18-year follow-up period. Data on daily maximum ozone concentrations were obtained from April 1 to September 30 for the years 1977 through 2000. Data on concentrations of fine particulate matter (particles that are < or = 2.5 microm in aerodynamic diameter [PM(2.5)]) were obtained for the years 1999 and 2000. Associations between ozone concentrations and the risk of death were evaluated with the use of standard and multilevel Cox regression models. In single-pollutant models, increased concentrations of either PM(2.5) or ozone were significantly associated with an increased risk of death from cardiopulmonary causes. In two-pollutant models, PM(2.5) was associated with the risk of death from cardiovascular causes, whereas ozone was associated with the risk of death from respiratory causes. The estimated relative risk of death from respiratory causes that was associated with an increment in ozone concentration of 10 ppb was 1.040 (95% confidence interval, 1.010 to 1.067). The association of ozone with the risk of death from respiratory causes was insensitive to adjustment for confounders and to the type of statistical model used. In this large study, we were not able to detect an effect of ozone on the risk of death from cardiovascular causes when the concentration of PM(2.5) was taken into account. We did, however, demonstrate a significant increase in the risk of death from respiratory causes in association with an increase in ozone concentration. 2009 Massachusetts Medical Society

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Methane contamination of drinking water accompanying gas-well drilling and hydraulic fracturing.

Stephen Osborn, Avner Vengosh, Nathaniel R. Warner … (2011)

Directional drilling and hydraulic-fracturing technologies are dramatically increasing natural-gas extraction. In aquifers overlying the Marcellus and Utica shale formations of northeastern Pennsylvania and upstate New York, we document systematic evidence for methane contamination of drinking water associated with shale-gas extraction. In active gas-extraction areas (one or more gas wells within 1 km), average and maximum methane concentrations in drinking-water wells increased with proximity to the nearest gas well and were 19.2 and 64 mg CH(4) L(-1) (n = 26), a potential explosion hazard; in contrast, dissolved methane samples in neighboring nonextraction sites (no gas wells within 1 km) within similar geologic formations and hydrogeologic regimes averaged only 1.1 mg L(-1) (P < 0.05; n = 34). Average δ(13)C-CH(4) values of dissolved methane in shallow groundwater were significantly less negative for active than for nonactive sites (-37 ± 7‰ and -54 ± 11‰, respectively; P < 0.0001). These δ(13)C-CH(4) data, coupled with the ratios of methane-to-higher-chain hydrocarbons, and δ(2)H-CH(4) values, are consistent with deeper thermogenic methane sources such as the Marcellus and Utica shales at the active sites and matched gas geochemistry from gas wells nearby. In contrast, lower-concentration samples from shallow groundwater at nonactive sites had isotopic signatures reflecting a more biogenic or mixed biogenic/thermogenic methane source. We found no evidence for contamination of drinking-water samples with deep saline brines or fracturing fluids. We conclude that greater stewardship, data, and-possibly-regulation are needed to ensure the sustainable future of shale-gas extraction and to improve public confidence in its use.

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Author and article information

Journal

Journal ID (nlm-ta): Environ Health Perspect

Journal ID (iso-abbrev): Environ. Health Perspect

Journal ID (publisher-id): EHP

Title: Environmental Health Perspectives

Publisher: NLM-Export

ISSN (Print): 0091-6765

ISSN (Electronic): 1552-9924

Publication date (Electronic): 16 April 2014

Publication date (Print): August 2014

Volume: 122

Issue: 8

Pages: 787-795

Affiliations

[1 ]Physicians Scientists and Engineers for Healthy Energy, Oakland, California, USA

[2 ]Department of Environmental Science, Policy, and Management, University of California, Berkeley, Berkeley, California, USA

[3 ]Physicians Scientists and Engineers for Healthy Energy, New York, New York, USA

[4 ]Department of Public Health, Weill Cornell Medical College, New York, New York, USA

Author notes

Address correspondence to S.B. Shonkoff, 436 14th St., Suite 808, Oakland, CA 94612 USA. Telephone: (510) 899-9706. E-mail: sshonkoff@ 123456psehealthyenergy.org

Article

Publisher ID: ehp.1307866

DOI: 10.1289/ehp.1307866

PMC ID: 4123033

PubMed ID: 24736097

SO-VID: 95f4fb2d-b3ae-490f-a84c-873be2219bf2

License:

Publication of EHP lies in the public domain and is therefore without copyright. All text from EHP may be reprinted freely. Use of materials published in EHP should be acknowledged (for example, “Reproduced with permission from Environmental Health Perspectives”); pertinent reference information should be provided for the article from which the material was reproduced. Articles from EHP, especially the News section, may contain photographs or illustrations copyrighted by other commercial organizations or individuals that may not be used without obtaining prior approval from the holder of the copyright.

History

Date received : 09 November 2013

Date accepted : 02 April 2014

Date: 16 April 2014

Date: 01 August 2014

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Most cited references 93

Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease.

Long-term ozone exposure and mortality.

Methane contamination of drinking water accompanying gas-well drilling and hydraulic fracturing.

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Cited by 32

Most referenced authors 941