Mortality from Copper Smelter Emissions Circa 1967

Environ Health Perspect 115:A439-A443 (2007). doi:10.1289/ehp.10441 available via http://dx.doi.org [Online 15 August 2007]

Referencing: Mortality Effects of a Copper Smelter Strike and Reduced Ambient Sulfate Particulate Matter Air Pollution

Pope et al. (2007) found lowered monthly mortality rates during a 1967–1968 copper smelter strike, coincident with and attributed to widespread reduced airborne sulfate levels. The authors cited three "intervention" studies associating particulate emissions reductions with mortality reductions as supportive. Evidence below suggests that mortality reductions in the study by Pope et al. and "interventions" are likely linked to reductions in particulate matter (PM) types known to be harmful: high levels of biologically active metals and partially burned carbon.

The first "intervention" study (Pope et al. 1992), examined PM–mortality associations over 4 years, encompassing closure of a Utah steel mill (sulfate not measured; sulfur dioxide levels were "low"). Mortality rates were 40% greater than expected when the mill was operating, suggesting toxicity of mill emissions. Strongest associations were with respiratory disease, then cardiovascular disease. Filter extracts when the mill was operating contained high levels of lead, copper, and zinc and were more toxic (Frampton et al. 1999).

Mattson and Guidotti (1980) found women living in communities near copper smelters (1968–1975) in Arizona experienced highly elevated relative risks (RRs) for acute respiratory disease mortality: averaged RR for all six mining towns (40,000 combined population) was 5.61. Later, Small et al. (1981) found levels of arsenic, Cu, and Zn elevated by factors up to 100,000 in Arizona smelter plumes. Lead levels in plumes were comparable with those of other metals. Thus, Pb, Cu, and Zn levels were elevated when either the steel mill or copper smelters were operating, and acute mortality (especially respiratory) was elevated simultaneously.

Mortality associations with blood Pb have recently been found at low levels of Pb (Menke et al. 2006). Blood Pb has a half-life of about 1 month, reflecting current exposure; associations may indicate both chronic and acute effects (Schober et al. 2006)—relevant information for copper smelter emissions.

The second "intervention" study (Hedley et al. 2002) found mortality rate reductions following a mandated 1990 reduction of sulfur in residual oil and diesel fuels in Hong Kong. Later, Hedley et al. (2006) found that ambient vanadium and nickel were reduced up to 90%, concomitantly with reductions of sulfur in residual oil. Mortality or inflammatory associations with ambient residual oil emissions but not secondary sulfate were previously found (Grahame and Hidy 2004; Janssen et al. 2002; Maciejczyk and Chen 2005).

The third "intervention" (Clancy et al. 2002) found that mortality rates declined after uncontrolled domestic burning of coal was banned in Dublin, Ireland. Wintertime black smoke levels declined from 80 µg/m³ before the ban to 20 µg/m³ afterward; sulfate was not measured. Given the toxicology of partly burned hydrocarbons, mortality reduction would be expected.

The three "supporting" studies do not provide evidence that widespread secondary sulfate reductions were related to mortality reductions during the interventions. Rather, high levels of specific metals, or of black smoke, appear to have health relevance.

Toxicology suggests secondary sulfates per se are unlikely to be harmful at ambient levels (Schlesinger and Cassee 2003). Resolving this inconsistency requires researching mechanisms by which secondary sulfate or precursors are necessary to create a toxic mixture at ambient levels; for example, how much do which metals increase in solubility due to such processes, and how much harm occurs that would not otherwise occur? Either soluble or insoluble metals common to steel mills and copper smelter emissions can be harmful at high doses (Ghio et al. 1999). Research suggestions are available (Grahame and Schlesinger (2007).

The author declares he has no competing financial interests.

References

Clancy L, Goodman P, Sinclair H, Dockery DW. 2002. Effect of air-pollution control on death rates in Dublin, Ireland: an intervention study. Lancet 360: 1210–1214.

Frampton MW, Ghio AJ, Samet JM, Carson JL, Carter JD, Devlin RB. 1999. Effects of aqueous extracts of PM₁₀ filters from the Utah Valley on human airway epithelial cells. Am J Physiol 277(5 Pt 1):L960–L967.

Ghio AJ, Stonehuerner J, Dailey L, Carter JD. 1999. Metals associated with both the water-soluble and insoluble fractions of an ambient air pollution particle catalyze an oxidative stress. Inhal Toxicol 11:37–49.

Grahame T, Hidy G. 2004. Using factor analysis to attribute health impacts to particulate pollution sources. Inhal Toxicol 16(suppl 1):143–152.

Grahame TJ, Schlesinger RB. 2007. Health effects of airborne particulate matter: do we know enough to consider regulating specific particle pypes or sources? Inhal Toxicol 19:457–481.

Hedley AJ, McGhee SM, Wong CM, Barron B, Chau P, Chau J, et al. 2006. Air Pollution: Costs and Paths to a Solution. Hong Kong:Civic Exchange. Available: http://www.civic-exchange.org/publications/2006/VisibilityandHealthE.pdf [accessed 1 August 2007].

Janssen NAH, Schwartz J, Zanobetti A, Suh HH. 2002. Air conditioning and source-specific particles as modifiers of the effect of PM₁₀ on hospital admissions for heart and lung disease. Environ Health Perspect 110:43–49.

Maciejczyk P, Chen LC. 2005. Effects of subchronic exposures to concentrated ambient particles (CAPs) in mice: VIII. Source-related daily variations in in vitro responses to CAPs. Inhal Toxicol 17:243–253.

Mattson ME, Guidotti TL. 1980. Health risks associated with residence near a primary copper smelter: a preliminary report. Am J Ind Med 1:365–374.

Menke A, Muntner P, Batuman V, Silbergeld EK, Guallar E. 2006. Blood lead below 0.48 mmol/L (10 mg/dL) and mortality among U.S. adults. Circulation 114: 1388–1394.

Pope CA III, Rodermund DL, Gee MM. 2007. Mortality effects of a copper smelter strike and reduced ambient sulfate particulate matter pollution. Environ Health Perspect 115:679–683.

Pope CA III, Schwartz J, Ransom MR. 1992. Daily mortality and PM₁₀ pollution in the Utah Valley. Arch Environ Health 47:211–217.

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.

Schober SE, Mirel LB, Graubard BI, Brody DJ, Flegal KM. 2006. Blood lead levels and death from all causes, cardiovascular disease, and cancer: results from the NHANES III mortality study. Environ Health Perspect 114: 1538–1541

Small M, Germani MS, Small AM, Zoller WH. 1981. Airborne plume study of emissions from the processing of copper ores in southeastern Arizona. Environ Sci Technol 15(3): 293–299.

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Mortality from Copper Smelter Emissions: Pope Responds

Environ Health Perspect 115:A439-A443 (2007). doi:10.1289/ehp.10441R available via http://dx.doi.org [Online 15 August 2007]

Grahame's thoughtful and well-documented letter addresses one of the most important issues regarding our analysis of the mortality effects of a copper smelter strike in the U.S. Southwest (Pope et al. 2007). Grahame's basic contentions are that changes in exposure to secondary sulfate alone were not sufficient to explain the observed mortality effects, and that the mortality effects were more likely due to changes in exposure to co-pollutants, such as biologically active metals and black smoke.

My coauthors and I agree with Grahame regarding several points. As he argues in his letter and as we briefly discussed in our article, the copper smelter strike also resulted in changes in exposure to metals and other co-pollutants. There is certainly evidence that metals, black carbon, and other by-products of incomplete combustion and high temperature industrial processes contribute to the pollution's toxicity—as part of the complex mixture of fine particles.

We respectfully disagree in part with Grahame regarding the lack of evidence implicating secondary sulfate particles as contributing to adverse health effects. He asserts that the three "supporting" intervention studies "do not provide evidence that widespread secondary sulfate reductions were related to mortality reductions during the interventions." However, in addition to changes in metals, black smoke, and other co-pollutants, one thing that all three intervention studies had in common was substantive changes in exposure to sulfate particles. In Utah Valley (Pope et al. 1992), the steel mill (largely from its coke ovens) was responsible for over 75% of the valley's total sulfur oxide emissions. During wintertime temperature inversions, high concentrations of fine particulate matter with a relatively high proportion of sulfates occurred. The closure of the steel mill resulted in a disproportionately large drop in exposure to both metals, sulfates, and other mill-related pollutants.

Mortality reductions in Hong Kong were also associated with reductions in sulfur oxide exposure (Hedley et al. 2002). In Dublin, although sulfates were not measured, the banning of bituminous coal certainly resulted in an abrupt reduction in particulate pollution—including sulfate particles (Clancy et al. 2002).

In addition to the intervention studies discussed above, there is ample epidemiologic evidence that sulfate pollution, as part of complex mixtures, contributes to adverse health effects. For example, the Harvard Six-Cities Study (Dockery et al. 1993) and the American Cancer Society prospective cohort studies (Pope et al. 2002) of long-term air pollution exposure found both fine particulates and sulfate particles to be associated with mortality risk. A workshop of several research teams on source apportionment of particulate matter health effects found that the sulfate-related component of fine particles was most consistently associated with daily mortality (Thurston et al. 2005). The relative toxicity of sulfates per se and the additive or synergistic effects of related co-pollutants remains a matter of study and debate (Chen et al. 2006; Grahame and Schlesinger 2007). Nevertheless, epidemiologic studies of the adverse health effects of air pollution (Pope and Dockery 2006) have implicated fine particulate pollution from at least three general sources: coal combustion, high-temperature industrial processes, and traffic sources.

Overall, the literature suggests that sulfates—as part of mixtures of fine particles that include metals, black carbon, and other by-products of coal combustion, high-temperature industrial processes, and vehicle emissions—can contribute to adverse health effects. We reaffirm our conclusion that the results of our analysis of the mortality effects of the copper smelter strike "contribute to the growing body of evidence that ambient sulfate particulate matter and related air pollutants are adversely associated with human health."

The authors declare they have no competing financial interests.

References

Chen LC, Thurston GD, Schlesinger RB. 2007. Acid aerosols as a health hazard. In: Air Pollution and Health (Ayres J, Maynard R, Richards R, eds). London:Imperial College Press, 111–161.

Clancy L, Goodman P, Sinclair H, Dockery DW. 2002. Effect of air-pollution control on death rates in Dublin, Ireland: an intervention study. Lancet 360: 1210–1214.

Dockery DW, Pope CA, Xu X, Spengler JD, Ware JH, Fay ME, et al. 1993. An association between air pollution and mortality in six U.S. cities. N Engl J Med 329: 1753–1759.

Grahame TJ, Schlesinger RB. 2007. Health effects of airborne particulate matter: do we know enough to consider regulating specific particle types or sources? Inhal Toxicol 19:457–481.

Hedley AJ, Wong CM, Thach TQ, Ma S, Lam TH, Anderson HR. 2002. Cardiorespiratory and all-cause mortality after restrictions on sulphur content of fuel in Hong Kong: an intervention study. Lancet 360:1646–1652.

Pope CA III, Burnett RT, Thun MJ, Calle EE, Krewski D, Ito K, et al. 2002. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. JAMA 287:1132–1141.

Pope CA III, Dockery DW. 2006. Health effects of fine particulate air pollution: lines that connect. J Air Waste Manage Assoc 56:709–742.

Pope CA III, Rodermund DL, Gee MM. 2007. Mortality effects of a copper smelter strike and reduced ambient sulfate particulate matter air pollution. Environ Health Perspect 115:679–683.

Pope CA III, Schwartz J, Ransom MR. 1992. Daily mortality and PM₁₀ pollution in the Utah Valley. Arch Environ Health 47:211–217.

Thurston GD, Ito K, Mar T, Christensen WF, Eatough DJ, Henry RC, et al. 2005. Workgroup report: workshop on source apportionment of particulate matter health effects—intercomparison of results and implications. Environ Health Perspect 113:1768–1774.