Health Effects of Coal Plant Emissions

Health Effects of Coal Plant Emissions Map

Click on a Project Name for More Information

Three new projects  [PDF-22KB] will improve our current understanding of the link between power plant emissions, PM2.5, and human health.

The health effects component of NETL's Air Quality Research Program is designed to enhance the body of scientific evidence relating stack emissions from coal plants to adverse health effects resulting from human exposure to air pollution. Despite knowledge of the significant amounts of PM2.5 and mercury that coal plants emit to the atmosphere, the actual amount of health damage resulting from these emissions is uncertain. To devise cost-effective policies and strategies for reducing the health effects of these pollutants, a better understanding of the benefits to be derived from reducing coal plant emissions of PM2.5, its precursors, and mercury is needed.

Primary PM2.5
Because primary PM2.5 (fly ash) from coal plants accounts for less than 1 percent of the total ambient PM2.5 mass, additional reductions in fly ash emissions from coal plants will probably not help attainment of the National Ambient Air Quality Standards (NAAQS) for PM2.5. Although some transition metals typically found in fly ash from coal power plants (such as iron) have been linked to adverse health effects in some toxicology studies, these studies have typically used dosages of fly ash that were well in excess (~10,000x) of the dosages humans normally receive by breathing ambient air. Therefore, it is currently unclear whether current fly ash emissions from coal plants actually constitute a significant threat to human health when viewed in the context of typical ambient environments and realistic human exposures. 

Secondary PM2.5
Recent epidemiologic research has yielded somewhat contradictory results with regard to the human health effects of secondary inorganic components of PM2.5 (ammonium sulfates and nitrates), which are typically linked to coal plant emissions of SO2 and NOx. Several well-publicized epidemiology studies conducted over the past 10 years have suggested that sulfate particles were positively correlated with adverse health effects such as respiratory disease, cardiovascular disease, and lung cancer. However, in these studies, particulate sulfate concentrations were highly correlated with total PM2.5 mass concentrations; many other key components of PM2.5, notably carbon species, were not measured. If one or more of the unmeasured PM2.5 components were actually the problematic constituent(s) and were also closely correlated with total PM2.5 mass the statistical association between particulate sulfate and adverse health effects would exist even if sulfates were not a causative factor. Conversely, results from a recent set of well-controlled, short-term epidemiology studies in Atlanta, GA, in which a vast array of PM2.5 components were measured, suggested that adverse health effects were most closely associated with carbon monoxide and/or the carbonaceous fraction of PM2.5. These carbonaceous species are related primarily to emission sources other than power plants (e.g., motor vehicles, wood burning). Importantly, the sulfate and nitrate components of PM2.5 were never positively correlated with adverse health outcomes in the Atlanta studies.

Reduction of secondary inorganic PM2.5 (via reduction of SO2 and NOx emissions from power plants) is a major component of the Environmental Protection Agency's (EPA) current strategy for reducing ambient PM2.5 mass. However, evaluation of previous toxicological literature suggests that these secondary inorganic particles, on their own, have little biological potency in humans and animals at environmentally relevant levels. To understand and quantify the human health benefits of reducing SO2 and NOx emissions from coal power plants, it is important to develop a more complete understanding of the toxicological properties of secondary sulfate and nitrate particles as they occur in ambient environments and in human exposure. 

Mercury
Unlike other pollutants associated with power plant emissions (e.g., PM2.5 and ozone), concentrations of mercury in ambient air are generally far too low to constitute a health or environmental hazard. However, because mercury can convert to toxic methylmercury after it is deposited in terrestrial and aquatic environments, it can bioaccumulate in aquatic food chains and expose humans to potentially harmful doses of mercury via food (primarily fish) consumption. Although coal plants are the largest known anthropogenic source of atmospheric mercury in the United States, U.S. coal plant emissions constitute less than 1 percent of total global mercury emissions. Because mercury emissions are often transported around the globe before being deposited, the benefits (i.e., decreases in mercury deposition and human exposure in the United States) of unilaterally reducing mercury emissions from U.S. coal plants are uncertain.

Current Research
Initial efforts under this component of the NETL Air Quality Research Program include a project involving the exposure of laboratory animals to actual plant emissions that have been aged and converted to reaction products in a mobile reaction chamber that simulates the conditions and dilution levels experienced by coal power plant plumes en route to ambient receptor sites. The project thus simulates exposure to PM2.5 from coal-fired power plant emissions in a much more realistic manner than previous experiments that used fresh coal combustion products. NETL has also co-sponsored a workshop to help develop a plan for using a laboratory setting to generate meaningful, reproducible, repeated inhalation exposures of sufficient numbers of animals for a sufficient time to characterize health hazards of PM2.5 from coal combustion and to manipulate the exposure variables modifying those hazards. Three new projects [PDF-22KB] will improve our current understanding of the link between power plant emissions, PM2.5, and human health. NETL is also sponsoring a risk assessment to estimate the reduction in human health risk that may be achieved through reduction in coal plant emissions of mercury.