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Is Ambient PM2.5 Sulfate Harmful?

[do action=”authors”]Thomas Grahame1 and Richard Schlesinger2[/do]

[do action=”affiliations”]1U.S. Department of Energy, Washington, DC, E-mail:, 2Pace University, New York, New York[/do]

[do action=”citations”]Environ Health Perspect 120:a454–a454 (2012). [Online 1 December 2012]

[do action=”notes”]The authors declare they have no actual or potential competing financial interests.[/do]

Lepeule et al. (2012) associated reduced PM2.5 (particulate matter ≤ 2.5 μm in aerodynamic diameter) with decreased mortality over almost four decades. Because the sulfate/PM2.5 ratio dropped among six localities but the PM2.5 mortality coefficient did not “substantially” increase, the authors concluded that sulfate must be “about as toxic” as average PM2.5. In a two-pollutant world, perhaps.

When a single source emits several PM2.5 species, and a specific species is emitted from several sources, chemical-specific associations might not reflect inherent toxicity but rather status as a marker of harmful coemissions (Grahame and Hidy 2007; Mostofsky et al. 2012). Furthermore, because total PM2.5 is often associated with adverse health outcomes, association of a constituent representing a large portion of total mass (e.g., sulfate) may occur unrelated to any inherent toxicity (Mostofsky et al. 2012).

Toxicological studies have not indicated adverse health effects from sulfate per se (Schlesinger and Cassee 2003). However, reducing a unit of black carbon (BC) increased life expectancy 4–9 times more than reducing a unit of PM2.5 (Janssen et al. 2011). Evidence from both toxicological and human panel studies with accurate subject exposure consistently has linked BC with adverse cardiovascular health outcomes (Grahame and Schlesinger 2010). Metals and other emissions from older steel plants are particularly toxic (Dye et al. 2001).

Substantial reductions in BC and polycyclic aromatic hydrocarbons from diesel engines and coke ovens, various metals from steel plants, and nickel and vanadium from residual oil have occurred over the time frame examined by Lepeule et al. (2012). Sulfur was coemitted by all of these sources. Because less abundant but more toxic PM2.5 species were also substantially reduced over this period, changes in the sulfate/PM2.5 ratio as applied to mortality might reflect toxicity of coemissions, not of sulfate. Is sulfate inherently toxic or merely a coemission of harmful PM species?

Researchers must use models that include many relevant PM2.5 species to successfully parse adverse health effects of each (Grahame and Hidy 2007). BC (and to a lesser extent nickel) remains consistently associated with adverse health outcomes when increasingly sophisticated models—all including 18 PM2.5 species—are used; however, sulfate associations become negative and insignificant (Mostofsky et al. 2012).

Further, subject exposure measures must be reasonably accurate; associations found with accurate exposure may not be found when central monitor concentrations are proxies for exposure across a metropolitan area (Suh and Zanobetti 2010).

Human panel studies can examine effects of PM2.5 species with more accurate subject exposure. Schwartz et al. (2005) found consistent associations for measures of heart rate variability with BC, but fewer associations for PM2.5. In that study, the authors used an algorithm separating BC from PM2.5 and found no associations with the PM2.5 remainder (termed “secondary PM2.5” by the authors), which would include both secondary sulfate and its reaction products.

Any conclusions regarding sulfate toxicity are premature until consistent results from advanced models (Mostofsky et al. 2012), which are able to examine many chemical species and incorporate good exposure measures, are available and are congruent with toxicology.

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Dye JA, Lehmann JR, McGee JK, Winsett DW, Ledbetter AD, Everitt JI, et al. 2001. Acute pulmonary toxicity of particulate matter filter extracts in rats: coherence with epidemiological studies in Utah Valley residents. Environ Health Perspect 109(suppl 3):395–403.

Grahame T, Hidy GM. 2007. Pinnacles and pitfalls for source apportionment of potential health effects from airborne particle exposure. Inhal Toxicol 19:727–744.

Grahame TJ, Schlesinger RB. 2010. Cardiovascular health and particulate vehicular emissions: a critical evaluation of the evidence. Air Qual Atmos Health 3:3–27.

Janssen, NAH, Hoek G, Simic-Lawson M, Fischer P, van Bree L, ten Brink H, et al. 2011. Black carbon as an additional indicator of the adverse health effects of airborne particles compared with PM10 and PM2.5. Environ Health Perspect 119:1691–1699.

Lepeule J, Laden F, Dockery D, Schwartz J. 2012. Chronic exposure to fine particles and mortality: an extended follow-up of the Harvard Six Cities Study from 1974 to 2009. Environ Health Perspect 120:965–970.

Mostofsky E, Schwartz J, Coull BA, Koutrakis P, Wellenius GA, Suh HH, et al. 2012. Modeling the association between particle constituents of air pollution and health outcomes. Am J Epidemiol 176(4):317–326.

Schlesinger RB, Cassee F. 2003. Atmospheric secondary inorganic particulate matter: the toxicological perspective as a basis for health effects risk assessment. Inhal Toxicol 15:197–235.

Schwartz J, Litonjua A, Suh H, Verrier M, Zanobetti A, Syring M, et al. 2005. Traffic related pollution and heart rate variability in a panel of elderly subjects. Thorax 60:455–461.

Suh HH, Zanobetti A. 2010. Exposure error masks the relationship between traffic-related air pollution and heart rate variability. J Occup Env Med 52 (7):685–692.

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