Persistent Questions about Particulate Matter
August 22, 2012
In response to: Particulate Matter: Widespread and Deadly
Researchers from EPA have estimated that over 100,000 people die prematurely each year in the US due to particulate matter (PM) exposure (1), and reductions in PM pollution during the 1980s and 1990s have been associated with as much as 15% of the increase in life expectancy in the US during that period (2). With these large public health impacts comes a significant amount of regulatory attention, and many recent air pollution regulations have been motivated or informed by the health effects of PM.
Although there are many important questions being addressed by a large and growing literature on PM (over 10,000 publications in PubMed use the keyword “particulate matter,” more than half of which have been published since 2007), two questions are persistent and significant from a public policy perspective:
1) Are some constituents of PM more toxic than others?
2) Are health effects observed at lower levels of PM, including below the current National Ambient Air Quality Standard (NAAQS)?
The importance of both of these questions is self-evident – if we are investing resources to control benign constituents of PM, then we are spending money without any public health gains. Similarly, if we are making policy decisions for a more toxic constituent of PM by assuming that it is an “average” particle, then we are not adequately protecting public health. And, the aforementioned analysis by EPA researchers (1) found that more than 80% of the public health burden of PM occurs in locations with annual average PM2.5 concentrations less than 10 µg/m3, well below the current NAAQS. If health effects were not present at these lower levels of pollution, then the public health burden of PM would be far lower.
While there remains uncertainty and controversy about both questions, recent research has provided some useful insight. For example, we recently published a study (3) in which we surveyed the literature on the effects of major particle constituents (elemental carbon, organic carbon, sulfate, and nitrate), and then conducted a new time-series analysis of daily hospital admissions and exposure to these particle constituents for 12 million Medicare enrollees across the US. In our literature review, we determined that the published literature was inadequate to answer the questions needed for health risk assessment studies like those done by EPA – in particular, the methods used in the literature did not allow us to determine the probability that a particle constituent was more or less toxic than another constituent.
In our new time-series analysis, we used methods that would let us determine the probability that particle constituents were more or less toxic than one another, as well as the probability that particle constituents were more or less toxic than the total mixture of PM2.5. We found a high probability that elemental carbon and nitrate were more toxic than PM2.5 for cardiovascular hospital admissions, a low probability that organic carbon had greater toxicity than PM2.5, and approximately equal probabilities that sulfate had greater or lesser toxicity than PM2.5. For respiratory hospital admissions, comparisons were more equivocal, with the highest probability that organic carbon had greater toxicity than PM2.5. There were a number of caveats in these comparisons, including the fact that they cannot be directly applied for outcomes like mortality due to long-term exposures, but they provided a sense of how differences in toxicity could be better understood. However, no specific constituent was either responsible for all observed effects or clearly exonerated. This is broadly consistent with the overall epidemiological literature, in which health effects of PM have been seen in many different cities and countries with very different pollution profiles, which would not have occurred if some of the major contributors to PM mass were not associated with adverse health outcomes.
Regarding the question of whether there is a threshold of effect for PM2.5, investigators have increasingly conducted health studies in places with sufficiently low levels of air pollution to be able to detect a threshold if it were to exist, applying statistical methods that can address this question. For example, a recent study in Canada (4) used satellite data to estimate PM2.5 concentrations in areas with limited monitoring, and looked at the shape of the association between PM2.5 and mortality. The investigators found significant and near-linear associations for all non-accidental mortality and cardiovascular disease, down to approximately 2 µg/m3, with evidence that the association was stronger at low PM2.5 levels for ischemic heart disease. Another recent study, a follow-up of the long-running Harvard Six Cities Study (5), found a significant linear association down to 8 µg/m3, the lowest level of air pollution observed in the study. The investigators also found little change in the association over a period that involved a significant reduction in the proportion of sulfate particles, supporting a conclusion that sulfate particles have similar toxicity as PM2.5 as a whole.
Some have questioned the plausibility of PM-related health effects without any evident threshold of effect, as this runs counter to the standard assumption for chemicals that there is a level below which the body is able to repair any damage. However, researchers have increasingly emphasized the role of cumulative exposures and stressors in influencing health outcomes, and a recent National Academy of Sciences committee (6) concluded that thresholds may not be present when there are significant background exposures and disease processes. For common diseases like cardiovascular disease, there are a number of risk factors, like diet, smoking, and lack of exercise. If PM influences a similar health outcome as these factors, any incremental exposure may contribute to health effects.
In summary, there is compelling evidence that the public health burden from PM in the US is large, with health effects continuing to be exhibited. Particle constituents from multiple sources, including traffic and power plants, have been associated with adverse health outcomes. Continued research is needed in multiple areas, but policy measures that reduce PM concentrations in a cost-effective manner should be adopted to protect public health.
1. Fann, N.; Lamson, A. D.; Anenberg, S. C.; Wesson, K.; Risley, D.; Hubbell, B. J., Estimating the national public health burden associated with exposure to ambient PM2.5 and ozone. Risk Anal 2012, 32, (1), 81-95.
2. Pope, C. A., 3rd; Ezzati, M.; Dockery, D. W., Fine-particulate air pollution and life expectancy in the United States. N Engl J Med 2009, 360, (4), 376-386.
3. Levy, J. I.; Diez, D.; Dou, Y.; Barr, C. D.; Dominici, F., A meta-analysis and multisite time-series analysis of the differential toxicity of major fine particulate matter constituents. Am J Epidemiol 2012, 175, (11), 1091-1099.
4. Crouse, D. L.; Peters, P. A.; van Donkelaar, A.; Goldberg, M. S.; Villeneuve, P. J.; Brion, O.; Khan, S.; Atari, D. O.; Jerrett, M.; Pope, C. A.; Brauer, M.; Brook, J. R.; Martin, R. V.; Stieb, D.; Burnett, R. T., Risk of nonaccidental and cardiovascular mortality in relation to long-term exposure to low concentrations of fine particulate matter: a Canadian national-level cohort study. Environ Health Perspect 2012, 120, (5), 708-714.
5. Lepeule, J.; Laden, F.; Dockery, D.; Schwartz, J., Chronic exposure to fine particles and mortality: An extended follow-up of the Harvard Six Cities Study from 1974 to 2009. Environ Health Perspect 2012, 120, (7), 965-970.
6. Committee on Improving Risk Analysis Approaches Used by the U.S. EPA. Science and Decisions: Advancing Risk Assessment; National Academy of Sciences: Washington, DC, 2008.
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