Particulate Matter: Stronger Protection Is Necessary
August 20, 2012
In response to: Particulate Matter: Widespread and Deadly
Fine particulate matter, consisting of airborne particles with a diameter of 2.5 microns (PM2.5) contributes to the four leading causes of death in the United States: heart disease, cancer, chronic lower respiratory diseases, and stroke or cerebrovascular disease (1). Major epidemiological studies including the Harvard Six-Cities Study (2), its 2006 update (3), The American Cancer Study (4), the Women’s Health Initiative Study (5), and a 2009 study of longevity and particulate matter in 51 metropolitan areas (6) all link PM2.5 pollution with substantial mortality.
These studies establish the threats to health and to life from exposure to PM2.5. However, they examine the full cross-section of the population; they do not identify risks to vulnerable populations such as children, adults with chronic diseases, and the elderly. When impacts on vulnerable populations are considered, severe health effects emerge, even at low levels of exposure. For example, studies of children indicate that PM2.5 exposure during critical periods of lung development poses a significant and important health threat. In a 2000 study of children living in 12 cities in Southern California, Gauderman and his colleagues found that PM2.5 exposures in the most versus the least polluted city showed “significant negative effects on lung function growth in children at current ambient concentrations of particles [including PM2.5].”(7) In a subsequent prospective followup study, 1,759 children, average age 10 years, were followed for eight years. Deficits were found in the expected increases in their forced expiratory volume, a measurement of effective lung capacity. These deficits were attributed to PM2.5 exposure after researchers corrected for potential confounders.
These impacts suggest more stringent reductions in airborne PM levels are needed. But do proposed EPA standards provide adequate protection? How much protection is enough?
The Environmental Protection Agency (EPA) sets National Ambient Air Quality Standards or NAAQS for six principal pollutants, including PM. It proposes that the health-related NAAQS for particulate matter, averaged over 24 hours, be retained at the current concentration of 35 micrograms per cubic meter of air (µg/m3). PSR believes that this standard fails to provide sufficient protection for health, particularly for vulnerable populations. We would consider lowering the standard to 25 µg/m3 to be a step in the right direction, but even 25 µg/m3 fails to be optimally protective. We cite the following to support our position.
An early study linking peaks in PM concentration with cardiovascular disease was published by Peters and her associates in 2000. (8) In their review of medical records of patients discharged from a hospital due to an implanted pacemaker defibrillator, they found that among patients who had ten or more discharges – presumptive evidence for more severe disease – there was a significant association between the discharges and fine particle concentrations. In a subsequent refinement of that study, Peters and her associates (9) found a 48% increase in the risk of a myocardial infarct for an increase in the PM concentration of 25 µg/m3. Similarly, a very recent study examined records of 8,216 out-of-hospital cardiac arrests and PM2.5 concentration. (10) The study found a significant risk for cardiac arrest with an increase of 10 µg/m3 in the PM2.5 concentration. Of note, the 95% PM2.5 concentration during this time was 30 µg/m3, well below the proposed 24-hour standard.
Wellenius and his colleagues reported the results of PM in a study of stroke in nine US cities (11). This was a study confined to the Medicare population and points out the susceptibility of the growing number of individuals in this age group. They evaluated 155,503 ischemic strokes and 19,314 hemorrhagic strokes and found a significant association between stroke admissions and the same-day PM10 concentration. In an update, Wellenius et al examined the medical records of 1,205 patients with ischemic strokes confirmed by a neurologist (12). In this study, they were able to determine the time-of-onset of the stroke and link that to data from a central PM2.5 monitoring site. They reported a steadily increasing odds ratio for stroke as PM2.5 concentrations increased over five 5 µg/m3 intervals, beginning with concentrations of less than 5 µg/m3 and ending with concentrations greater or equal to 20 µg/m3. They reported the odds ratio for stroke during a period of “moderate” pollution (PM 2.5 in the range of 15 - 40µg/m3) was 1.34 when compared to a period when air quality was “good” (PM2.5 at less than 15 µg/m3). From their data, one can reasonably conclude that transient exposure to PM2.5 at the proposed concentration of 35 µg/m3 carries with it a significantly increased risk for ischemic stroke.
Not only have adverse health effects have been documented at or near the proposed standards for PM2.5; just as importantly, there does not appear to be any no observable effect level (NOEL). That is, health-damaging effects from PM2.5 are observed at low levels, and there is no threshold below which exposure seems to be safe. Because there is no NOEL for PM2.5 and increasing evidence that transient concentration peaks pose significant health threats, PSR does not believe that the current 24-hour standard of 35 µg/m3 fulfills the mission of EPA to protect human health. Similarly, the proposed reduction in the annual standard from the current level of 15 µg/m3 to between 12 - 13 µg/m3 is welcome but overdue and insufficient to protect health adequately.
On this basis, we contend that the EPA’s proposed standards fall short of providing adequate protection for Americans, particularly children, the elderly, and those with pre-existing health conditions. We urge the Agency to embrace a more precautionary approach to the provision of adequate health protection, especially for vulnerable populations, and to adopt lower concentration limits for both the annual and 24-hour standards.
(View the full text of PSR’s comments to the EPA on PM2.5 here.)
- Miniño AM, Xu J, Kochanek KD. Deaths: Preliminary Data for 2008. Centers for Disease Control, 2010.
- Dockery DW, Pope CA, III, Xu X et al. An association between air pollution and mortality in six U.S. cities. N Engl J Med 1993;329(24):1753-1759.
- Laden F, Schwartz J, Speizer FE, Dockery DW. Reduction in fine particulate air pollution and mortality: Extended follow-up of the Harvard Six Cities study. Am J Respir Crit Care Med 2006;173(6):667-672.
- Pope CA, III, Burnett RT, Thun MJ et al. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. JAMA 2002;287(9):1132-1141.
- Miller KA, Siscovick DS, Sheppard L et al. Long-term exposure to air pollution and incidence of cardiovascular events in women. N Engl J Med 2007;356(5):447-458.
- Pope CA, III, Ezzati M, Dockery DW. Fine-particulate air pollution and life expectancy in the United States. N Engl J Med 2009;360(4):376-386.
- Gauderman WJ, McConnell R, Gilliland F et al. Association between air pollution and lung function growth in southern California children. Am J Respir Crit Care Med 2000;162(4 Pt 1):1383-1390.
- Peters A, Liu E, Verrier RL et al. Air pollution and incidence of cardiac arrhythmia. Epidemiology 2000;11(1):11-17.
- Peters A, Dockery DW, Muller JE, Mittleman MA. Increased particulate air pollution and the triggering of myocardial infarction. Circulation 2001; 103(23):2810-2815.
- Silverman RA, Ito K, Freese J et al. Association of ambient fine particles with out-of-hospital cardiac arrests in New York City. Am J Epidemiol 2010;172(8):917-923.
- Wellenius GA, Schwartz J, Mittleman MA. Air pollution and hospital admissions for ischemic and hemorrhagic stroke among medicare beneficiaries. Stroke 2005;36(12):2549-2553.
- Wellenius GA, Burger MR, Coull BA et al. Ambient air pollution and the risk of acute ischemic stroke. Arch Intern Med 2012;172(3):229-234.
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