Community Health Risk Assessment of Primary Aluminum Smelter Emissions

Martin, Stephen Claude MD, MSc(A), ABPM(OM), FCBOM; Larivière, Claude BSc, CIH, ROH

Journal of Occupational & Environmental Medicine: May 2014 - Volume 56 - Issue - p S33–S39
doi: 10.1097/JOM.0000000000000135
Original Articles

Objective: Primary aluminum production is an industrial process with high potential health risk for workers. We consider in this article how to assess community health risks associated with primary aluminum smelter emissions.

Methods: We reviewed the literature on health effects, community exposure data, and dose–response relationships of the principal hazardous agents emitted.

Results: On the basis of representative measured community exposure levels, we were able to make rough estimates on health risks associated with specific agents and categorize these as none, low, medium, or high.

Conclusions: It is possible to undertake a rough-estimate community Health Risk Assessment for individual smelters on the basis of information available in the epidemiological literature and local community exposure data.

From the Department of Epidemiology, Biostatistics and Occupational Health (Dr Martin), McGill University, Montreal; and Expertise Industrial Hygiene Inc (Mr Larivière), Otterburn Park, Quebec, Canada.

Address correspondence to: Stephen Claude Martin, MD, MSc(A), ABPM(OM), FCBOM, Department of Epidemiology, Biostatistics and Occupational Health, McGill University, 1020 Pine Ave W, Montreal, QC H3A 1A2, Canada (; and/or Claude Larivière, BSc, CIH, ROH, Expertise Industrial Hygiene Inc, 503 du Verger-Tetreault, Otterburn Park (Quebec), Canada J3H 6L1.

Both authors are former employees of Rio Tinto Alcan (formerly Alcan Aluminium Ltd) and have received at times consultant fees since their departure for other types of service to the company (S.C.M. last fee more than 2 years ago; C.L. less than 2 years ago) but have not received remuneration in any way related to the preparation of this article from Rio Tinto Alcan or from any other source whatsoever.

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License, where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially.

Article Outline

The production of primary aluminum metal is a well-established and vital industrial process. Aluminum metal has innumerable applications in modern society, which has become very dependent on its availability. Unfortunately, the (Hall-Héroult) smelting process is fraught with many well-documented risks to the health of the workers who run it. Over the century since its inception, questions have also been raised regarding the process emissions' potential impacts on the health of residents of adjacent neighborhoods. This article reviews the known toxic exposures that emanate from smelters and considers some of the factors that could render certain of those exposures a concern for community health. It concerns itself solely with smelters using the Hall-Héroult electrolytic process. It does not consider downstream manufacture of aluminum products or the secondary production of aluminum through recycling processes. Also not covered in this article are alumina refineries, which extract and calcine anhydrous, smelter-grade aluminum oxide (alumina) from the raw ore (bauxite) using the Bayer process.

There are two basic types of aluminum smelters:

1. Søderberg smelters: In the Søderberg process (Fig. 1), the anodes in the electrolysis vessels (“pots”) are composed of a paste of petroleum coke and coal tar pitch. The process takes place at temperatures exceeding 900°C, generating copious coal tar pitch volatiles. These fumes are rich in carcinogenic polycyclic aromatic hydrocarbons (PAHs), which are released directly into the workplace during certain pot-tending tasks.

2. Prebake smelters: In this process (Fig. 2), anodes are “prebaked” (usually in a separate plant in ventilated anode-baking furnaces). The coal tar pitch volatiles have thus been driven off before the anode is introduced into the electrolytic “pot.” Some PAH exposure still occurs in certain operations (pot start-ups, cathode-relining operations), but generally at much lower concentration than in Søderberg smelters.

Beyond the major differences in anode composition and worker exposures to PAH, the other components of the processes are similar, involving passage of high electrical current through a molten electrolytic bath of cryolite (Na3AlF6) and aluminum fluoride (AlF3) into which alumina is dissolved. The principal occupational exposures are discussed hereafter.

Back to Top | Article Outline


The goals of this article were to consider the emissions of primary aluminum smelters that may have potential for harm to the health of neighbors of aluminum smelters and, on the basis of the results of epidemiological studies and community exposure data, to describe a Health Risk Assessment (HRA) method to identify those exposures that may need higher priority for control.

Back to Top | Article Outline


We collected 298 studies published in peer-reviewed journals by using keywords “aluminum smelter; Hall-Héroult process; fluoride; sulfur dioxide; PM; PM10; PM2.5; PAH; benzo[α]pyrene; occupational cancer; bladder cancer; lung cancer; health risk assessment; community health; noise” and others. We reviewed the following data:

* Epidemiological study results for health effects of aluminum production

* Known and suspected health hazards of aluminum smelters

* Studies of the health outcomes in communities with primary aluminum smelters

* Studies of health outcomes in communities (not specifically smelter towns) with exposure to the principal hazards identified earlier

* Smelter community exposure level data for the hazardous agents of interest

We then carried out an HRA using comparisons between actual or estimated community exposure levels and those associated with adverse outcomes in the smelter studies, nonsmelter communities, or both to assess risk in aluminum smelter communities. The final step was to assign each hazard to one of four risk categories: none, low, medium, or high (Table 1).

Back to Top | Article Outline

Identification of Potential Health Hazards in Smelters

Occupational exposures in primary aluminum smelters are well identified by Jelinic et al1 and the International Agency for Research on Cancer.2 These are presented in Table 2, with their respective health effect(s) and an indication regarding presence or absence of evidence for adverse health outcomes in smelter workers.

Back to Top | Article Outline

Typical Workplace Exposure Levels

Occupational exposure levels have been reported in numerous publications.1–3 Benke et al3 reviewed reported time-weighted average exposure concentrations to the principal contaminants measured in primary aluminum smelters from the 1950s to 1996 in several countries, for both prebake and Søderberg processes. Table 3 summarizes their data, which can serve as a basis for comparison to the much lower-exposure levels found in neighboring communities.

Back to Top | Article Outline

Review of Epidemiological Studies That Examine Health Outcomes in Relation to Exposures to Those Hazards in the Workplace

Occupational Cancers

The earliest reports of suspected increased cancer rates in primary aluminum smelter workers were from Russia.4 Both lung and stomach cancers appeared in higher than expected numbers, but smoking histories were unavailable. Subsequent studies in Canadian and Norwegian smelters confirmed increased incidence rates of lung cancer5–7 and bladder cancer.7–10 Dose–response relationships were clearly demonstrated between these effects and cumulative exposure dose to benzene-soluble matter and benzo[α]pyrene (BaP) after controlling for smoking. These studies and others11,12 have also found frustratingly inconsistent evidence for increased incidence rates for lymphomas as well as stomach and pancreatic cancers.

Back to Top | Article Outline

Occupational Lung Diseases

Back to Top | Article Outline


Data for an association between the Hall-Héroult process and asthma have been suspected for over 70 years. Scandinavian13 and Australian studies tend to conclude in its existence and call the disease “pot-room asthma,” even though North American studies have usually failed to confirm an excess incidence. Putative candidate causal agents include fluorides (HF and particulate), sulfur dioxide, and smelter dust (inhalable, total, respirable, ultrafine, or nanoparticulates). One US study did document an excess asthma incidence14 and found an association with gaseous fluoride. On the contrary, a recent Australian study15 found a stronger association with sulfur dioxide exposure. By far, the largest study ever undertaken of pulmonary health in the primary aluminum industry (personal communication; Richard Martin; Quebec smelter studies of 1982 and 1995–1998) involved more than 5000 Quebec smelter workers. Posthire asthma incidence rates were similar in exposed and nonexposed employees. Unfortunately, this study has not yet been submitted to a peer-reviewed journal.

Back to Top | Article Outline

Chronic Obstructive Pulmonary Disease

There is good consistency from morbidity–mortality studies for increased prevalence and mortality rates for this disease among electrolysis workers in aluminum production.16 The above-mentioned unpublished Quebec study showed a significant association between work with exposure to the electrolytic process and reduced forced expiratory volume in the first second of expiration (FEV-1) values. This was true for both types of smelter: Søderberg and Prebake, suggesting that PAHs are not a major influence in the generation of obstructive lung disease.

Back to Top | Article Outline

Lung Cancer

See Occupational Cancers section.

Back to Top | Article Outline

Beryllium Sensitization

Although there is significant exposure to beryllium-containing dust in certain smelters, beryllium sensitization in aluminum smelter workers appears to be rare in two studies performed in North America and Norway (prevalence of 0.47% and 0.28%, respectively).17,18

Back to Top | Article Outline

Noise-Induced Health Effects

Noise-induced hearing loss is well-documented in aluminum smelters where exposures in certain similar exposure groups or jobs can exceed 85 dBA for 8-hour shifts or 82 dBA for 12-hour shifts. The contribution of aluminum production operations to community sound pressure levels remains well below these levels and hence noise-induced hearing loss from smelter noise would not be expected in smelter towns.

Back to Top | Article Outline

Asbestosis, Mesothelioma, and Silicosis

These are diseases that have been identified in aluminum production facilities, but because their causal agents are not significant components of smelter emissions into the environment, they will not be discussed here. Electromagnetic fields will not be considered either, because the exposures within the smelters do not represent an “emission” to which residents can be significantly exposed. Even though electrical transmission lines do run through smelter communities, fields generated by them do not represent smelter-originating exposures and are hence beyond the scope of our topic.

Back to Top | Article Outline

Studies of Community Health Effects of Hazards Relevant to Primary Aluminum Smelter Emissions


Extrapolating from the dose–response relationships seen in the smelter employees, Gibbs19 estimates a risk of an additional 4.4 cases of lung cancer per 100,000 persons exposed for 50 years to 1 ηg/m3 BaP. Armstrong and Gibbs20 later revisited the dose–response relationship for smelter workers and found that a linear relationship model predicted a relative risk of 1.35 per 100 μg/m3-yrs cumulative BaP exposure and a multiplicative power curve model (the best fitting) predicted a RR of 2.68. Vyskocil et al21 looked at lifetime lung cancer risks in smelter and nonsmelter towns on the basis of available BaP exposure data. When performing quantitative risk assessment by using epidemiological data based on BaP exposures, they found (upper bound) lifetime excess lung cancer risks between 0.02 and 89 cancers per 100,000 residents in smelter towns. Occupational exposures in the smelter towns studied are almost exclusively in males, which would tend to confound the relationship between community exposure levels and cancer risk in men in those communities. Nevertheless, there was a linear relationship between community BaP exposure and lung cancer rates in women with a correlation coefficient (R) near 0.8. In addition, a study of lung cancer rates and regional BaP exposure in the same geographic region (Saguenay-Lac Saint Jean region of the Province of Quebec) did reveal an excess of lung cancer in women in the most highly exposed district of one smelter town.22

Back to Top | Article Outline


Neighborhood levels of airborne beryllium were 100- to 300-fold lower than EPA–recommended exposure limit of 0.01 μg/m3 at air quality–sampling stations near a smelter using beryllium-containing alumina (personal communication; Rio Tinto Alcan). Workers exposed to beryllium at or above an arbitrary action level below the American Conference of Governmental Industrial Hygienists new Threshold Limit Value were tested and found not to be sensitized to beryllium (Beryllium Lymphocyte Proliferation Test). Hence, it is reasonable to assume that community exposures are not causing beryllium-related sensitization or disease in residents living near that smelter.

Back to Top | Article Outline

Particulate Matter

There is now an impressive body of scientific literature concerning the health effects of community exposures to airborne particulates. The studies are shared between evaluation of the health effects of finer particulates with an aerodynamic diameter less than 2.5 μm (PM2.5) and evaluation of the effects of particles with less than 10-μm diameter (PM10).

Back to Top | Article Outline

Particulate Matter With Diameter Less Than 10 μm (PM10)

Studies abound on the potential health effects of exposure to particulate matter aerosols. Exposure to PM10 has been linked to respiratory symptoms of cough and wheeze, onset and exacerbation of asthma in adults and children, hospitalizations for respiratory and cardiovascular diseases, death rates in vulnerable groups (in the elderly and in late neonates), and low birth weight. A study of Swedish children showed a significant association between PM10 exposure in the first year of life and the onset of asthma before the age of 12 years.23 A meta-analysis of 36 European studies of PM10 levels (24-hour mean PM10 concentrations ranging from 10 to 167 μg/m3) and asthma symptoms in children showed a significant association.24 In a review of five European studies, an association between long-term PM10 and mortality rates (total deaths and cardiovascular and respiratory deaths) was confirmed, with statistically significant dose–response relationships.25 In a prospective cohort study26 of women in Germany, PM10 exposure was significantly associated with increased all-cause cardiopulmonary and lung cancer mortality rates.

Back to Top | Article Outline

Particulate Matter With Diameter Less Than 2.5 μm (PM2.5)

Similar results have been found for exposures to these finer particles; yet some studies have found the latter to be more strongly associated with adverse cardiovascular outcomes. In the elderly in Madrid,27 both PM10 and PM2.5 were associated with increased mortality from respiratory causes, while cardiovascular deaths were associated significantly only with PM2.5 exposure. In New York City28 over a 5-year period, out-of-hospital cardiac arrests were associated significantly with PM2.5 (RR more than 1.06 per increase in PM2.5 exposure of 10 μg/m3) during warm seasons but not with CO, ozone, SO2, or NO2. A similar investigation in Melbourne29 yielded almost identical results. A prospective cohort study of 125,000 female California teachers and former teachers followed over 10 years30 showed an association between PM10, PM2.5, and nitrogen oxides exposures and ischemic heart disease mortality and stroke incidence that was stronger for the PM2.5 exposure. That these effects are predominantly important in the more elderly is suggested by the failure to detect an association between PM2.5 and PM10 exposures and any adverse cardiopulmonary health effects in a cohort of 2800 young (mean age 32 years) US military personnel over an 18-month period in Southwest Asia.31 A recent study of asthmatic children living within a 7.5-km radius of a Søderberg smelter in the province of Quebec32 showed a significant association with time exposed downwind from the smelter emission source and hospitalizations for asthma and bronchiolitis. The PM2.5 and SO2 peak concentrations were 967 μg/m3 and 434 ppb, respectively.

Back to Top | Article Outline

Sulfur Dioxide

Sulfur dioxide is a well-known respiratory irritant and has been shown to reliably produce bronchoconstriction in persons with asthma in a dose-related manner, beginning at about 200 ppb in persons with mild to moderate asthma.33 A Montreal study34 of children living in proximity to a petroleum refinery revealed a dose-related association between increasing SO2 exposure and active asthma, which became statistically significant for poor asthma control. Another investigation35 in the same city found that short-term increases in SO2 were significantly associated with increased numbers of asthma episodes, emergency department visits, and hospitalizations for asthma (also in children). Although the emissions composition of oil refineries is quite different from aluminum smelters, these findings lend plausibility to a role for SO2 in exacerbation of asthma in community residents. Sulfur dioxide exposure was found in Shanghai to have independent linear association with total mortality even after controlling for PM10 exposure.36 The previously cited Quebec study32 of asthmatic children living near a Søderberg smelter revealed mean daily SO2 concentrations downwind of the smelter ranging up to 168 ppb and mean hourly concentrations up to 434 ppb.

Back to Top | Article Outline


Primary aluminum smelters emit fluorides in gaseous and particulate forms. The role of fluorides in community health has been less studied than PMs, SO2, and NOx. In aluminum smelter towns, their role is difficult to sort out, because they are invariably accompanied by significant amounts of particulate matter and SO2. A study of children in the Norwegian smelter town of Årdal37 did show a significant association between bronchial hyperresponsiveness and recent exposure to peak levels of both SO2 and fluorides. In aboriginal children living near an aluminum smelter in upstate New York, respiratory obstruction was associated with increased urinary fluoride.38 The previously mentioned study by Abramson et al15 on pot-room asthma may shed some light on the relative importance of fluoride versus SO2 on respiratory impact in the communities neighboring smelters. Median fluoride levels in the Årdal region over a 30-day period were 1.6 μg/m3 with a 10th percentile of 0.08 μg/m3 and 90th percentile of 2.8 μg/m3.

Back to Top | Article Outline


As mentioned under the “Review of Epidemiological Studies That Examine Health Outcomes in Relation to Exposures to Those Hazards in the Workplace” section earlier, the contribution of aluminum production operations to community levels does not reach the high levels required to cause hearing loss, and hence noise-induced hearing loss from smelter noise would not be expected in smelter towns. Nevertheless, smelter contribution to community noise can result in environmental levels close to 50 dBA (personal communication; Rio Tinto Alcan's Laterrière Works in Quebec). Background noise levels in the smelter community ranged from 35 to 38 dBA in the absence of smelter operations, and 44 to 48 dBA during operations (24 hours per day). The latter levels were well below those that have been associated with an increased risk of myocardial infarction in one study,39 but did fall in the range of “noisy area” (Leq more than 45 dBA) for which another study40 found a significant adjusted odds ratio of 1.58 in males for hypertension. Road traffic noise was also associated with hypertension in a Swedish town41 in both males and females. Another Swedish study42 showed a significant odds ratio of 1.27 for hypertension in 40- to 59-year-old subjects exposed to 60 to 64 dBA. Each 5-dB increase in Leq24 beyond 45 dBA was accompanied by an increased odds ratio of 1.38 for hypertension. The Laterrière smelter reduced community noise levels in 1999 by installing a muffling system into the emission stacks, resulting in exposures in the range of 33 to 40 dBA, hardly more than the preconstruction background ambient noise.

Back to Top | Article Outline


The HRA for aluminum smelter emissions is a daunting task that requires specific knowledge of industrial processes and their by-products, results of research into potential occupational and community health effects, regional exposure measurement results, the relative contributions of the smelter to those results, the demographic characteristics of the community, and the local community health outcomes data.

We encountered much uncertainty at several levels. One of the most difficult tasks is estimating the contribution of a given smelter to the concentration of airborne contaminants in the surrounding community. The more urban the setting and the more densely inhabited and industrialized, the more difficult that task will be. Some, like Boullemant,43 have been able to use novel approaches using isotope tracing to calculate the proportion of community PM2.5 that originated from the anodes of the local smelter, but such technical aids are the exception.

Much of the information available on community health impacts involves relative risks with increasing concentrations but is not as helpful in providing information about exposure thresholds below which harm is improbable. Care must be taken in extrapolating dose–response relationships from studies on workers to community residents, whose characteristics differ (eg, the latter include vulnerable groups like children, the elderly, pregnant women, higher numbers of persons with respiratory disorders, and other chronic illnesses and disabilities).

In estimating risk, we took a worst-case scenario approach and used highest measured community exposures, highest risk estimates from other sources,19–21 and considered studies that showed plausible community health impacts from the agents under consideration.

The useful life of modern primary aluminum smelters is usually 50 years or more. The design criteria for these industrial settings are determined to ensure their long-term compliance with local and international regulations on health, safety, and environment. Nevertheless, a serious threat is emerging; given the significant and sustained growth in global aluminum demand, the industry is facing a shortage of raw materials with low sulfur content, such as petroleum coke. Several sites are currently considering the use of petroleum coke at higher sulfur content, which could result in a significant increase in sulfur dioxide emissions and, in turn, the concentration of this pollutant in urban air of communities located in their vicinity, thus representing an increased risk to the health of general public.

Back to Top | Article Outline


We conclude that a community HRA can be carried out for an aluminum smelter by comparing representative community exposure levels to known health hazards present in emissions from primary aluminum production with the exposure levels that have been established as harmful in community health studies or in other health effect studies. Where community health data are lacking, the occupational health literature may provide insights into dose–response relationships, which could be used in risk assessment. It is important in such assessments to consider historical exposure levels because some of the health effects of interest involve long latency periods. The authors consider, depending on technology, proximity, and other factors, that risk is not zero for adverse community health effects from BaP (from Søderberg smelters only), fluoride, noise, particulate matter, and sulfur dioxide. Continuous improvement in emissions controls hence remains a high priority for all primary aluminum producers.

Back to Top | Article Outline


The authors thank (1) Mme Jany McKinnon of the Québec Ministère du Développement durable, de l'Environnement, de la Faune et des Parcs, for her indispensable assistance in providing air quality data from sampling stations in Québec smelter municipalities and (2) Elizabeth Czanyo, Canadian Medical Association librarian, for her help in finding relevant articles.

Back to Top | Article Outline


1. Jelinic JD, Nola IA, Udovicic R, Ostojić D, Zuskin E. Exposure to chemical agents in aluminium potrooms. Med Lav. 2007;98:407–414.
2. Occupational Exposures During Aluminium Production. IARC_Monographs 100F-22_2012.
3. Benke G, Abramson M, Sim M. Exposures in the alumina and primary aluminium industry: an historical review. Ann Occup Hyg. 1998;42:173–189.
4. Konstantinov VG, Kuzminykh AI. Tarry substances and 3:4 benzpyrene in the air of electrolytic shops of aluminum works and their carcinogenic significance. Gig Sanit. 1971;36:368–371.
5. Gibbs GW, Horowitz I. Lung cancer mortality in aluminum reduction plant workers. J Occup Med. 1979;21:347–353.
6. Gibbs GW. Mortality of aluminum reduction plant workers 1950 through 1977. J Occup Med. 1985;27:761–770.
7. Gibbs GW, Sévigny M. Mortality and cancer experience of Quebec aluminum reduction plant workers. Part 3: monitoring the mortality of workers first employed after January 1st, 1950. J Occup Environ Med. 2007;49:1269–1287.
8. Thériault G, Tremblay C, Cordier S, Gingras S. Bladder cancer in the aluminum industry. Lancet. 1984;323:947–950.
9. Spinelli JJ, Demers PA, Le ND, et al. Cancer risk in aluminum reduction plant workers (Canada). Cancer Causes Control. 2006;17:939–948.
10. Rønneberg A, Haldorsen T, Romunstad P, Andersen A. Occupational exposure and cancer incidence among workers from an aluminum smelter in western Norway. Scand J Work Environ Health. 1999;25:207–214.
11. Sim MR, Del Monaco A, Hoving JL, et al. Mortality and cancer incidence in workers in two Australian prebake aluminum smelters. Occup Environ Med. 2009;66:464–470.
12. Carta P, Aru G, Cadeddu C, et al. Mortality for pancreatic cancer among aluminum smelter workers in Sardinia, Italy. G Ital Med Lav Ergon. 2004;26:83–89.
13. Kongerud J, Boe J, Søyseth V, Naalsund A, Magnus P. Aluminium potroom asthma: the Norwegian experience. Eur Respir J. 1994;7:165–172.
14. Taiwo OA, Sircar KD, Slade MD, et al. Incidence of asthma among aluminum workers. J Occup Environ Med. 2006;48:275–282.
15. Abramson MJ, Benke GP, Cui J, et al. Is potroom asthma due more to sulphur dioxide than fluoride? An inception cohort study in the Australian aluminum industry. Occup Environ Med. 2010;67:679–685.
16. Gibbs GW, Armstrong B, Sévigny M. Mortality and cancer experience of Quebec aluminum reduction plant workers. Part 2. Mortality of three cohorts hired on or before January 1, 1951. J Occup Environ Med. 2007;49:1105–1123.
17. Taiwo OA, Slade MD, Cantley LF, Kirsche SR, Wesdock JC, Cullen MR Prevalence of beryllium sensitization among aluminium smelter workers. Occup Med (Lond). 2010;60:569–571.
18. Nilsen AM, Vik R, Behrens C, Drabløs PA, Espevik T. Beryllium sensitivity among workers at a Norwegian aluminum smelter. Am J Ind Med. 2010;53:724–732.
19. Gibbs GW. Estimating residential polycyclic aromatic hydrocarbon (PAH) related lung cancer risks using occupational data. Ann Occup Hyg. 1997;41(suppl 1):49–53.
20. Armstrong BG, Gibbs G. Exposure–response relationship between lung cancer and polycyclic aromatic hydrocarbons (PAHs). Occup Environ Med. 2009;66:740–746.
21. Vyskocil A, Viau C, Camus M. Risk assessment of lung cancer related to environmental PAH pollution sources. Hum Exp Toxicol. 2004;23:115–127.
22. Bouchard C. Space–time distribution of lung cancers in the Saguenay-Lac-Saint-Jean region [French]. Chicoutimi, Québec, Saguenay-Lac-Saint-Jean Regional Health and Social Services Administration. 2000;(condensed version):48.
23. Gruzieva O, Bergstrom A, Hulchiy O, et al. Exposure to air pollution from traffic and childhood asthma until 12 years of age. Epidemiology. 2013;24:54–61.
24. Weinmayr G, Romeo E, De Sario M, Weiland SK, Forastiere F. Short-term effects of PM10 and NO2 on respiratory health among children with asthma or asthma-like symptoms: a systematic review and meta-analysis. Environ Health Perspect. 2010;118:449–457.
25. Pelucchi C, Negri E, Gallus S, Boffetta P, Tramacere I, La Vecchia C. Long-term particulate matter exposure and mortality: a review of European epidemiological studies. BMC Public Health. 2009;9:453–461.
26. Heinrich J, Thiering E, Rzehak P, et al. Long-term exposure to NO2 and PM10 and all-cause and cause-specific mortality in a prospective cohort of women. Occup Environ Med. 2013;70:179–186.
27. Jimenez E, Linares C, Martinez D, Díaz J. Particulate air pollution and short-term mortality due to specific causes among the elderly in Madrid (Spain): seasonal differences. Int J Environ Health Res. 2011;21:372–390.
28. 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;172:917–923.
29. Dennekamp M, Akram M, Abramson MJ, et al. Outdoor air pollution as a trigger for out-of-hospital cardiac arrests. Epidemiology. 2010;21:494–500.
30. Lipsett MJ, Ostro BD, Reynolds P, et al. Long-term exposure to air pollution and cardiorespiratory disease in the California teachers study cohort. Am J Respir Crit Care Med. 2011;184:828–835.
31. Abraham JH, Baird CP. A case-crossover study of ambient particulate matter and cardiovascular and respiratory medical encounters among US military personnel deployed to southwest Asia. J Occup Environ Med. 2012;54:733–739.
32. Lewin A, Buteau S, Brand A, Kosatsky T, Smargiassi A. Short-term risk of hospitalization for asthma or bronchiolitis in children living near an aluminum smelter. J Expo Sci Environ Epidemiol. 2013;23:474–480.
33. Johns DO, Svendsgaard D, Linn WS. Analysis of the concentration–respiratory response among asthmatics following controlled short-term exposures to sulfur dioxide. Inhal Toxicol. 2010;22:1184–1193.
34. Deger L, Plante C, Jacques L, et al. Active and uncontrolled asthma among children exposed to air stack emissions of sulphur dioxide from petroleum refineries in Montreal, Quebec: a cross-sectional study. Can Respir J. 2012;19:97–102.
35. Smargiassi A, Kosatsky T, Hicks J, et al. Risk of asthmatic episodes in children exposed to sulfur dioxide stack emissions from a refinery point source in Montreal, Canada. Environ Health Perspect. 2009;117:653–659.
36. Chen G, Song G, Jiang L, et al. Short-term effects of ambient gaseous pollutants and particulate matter on daily mortality in Shanghai, China. J Occup Health. 2008;50:41–47.
37. Søyseth V, Kongerud J, Broen P, Lilleng P, Boe J. Bronchial responsiveness, eosinophilia, and short term exposure to air pollution. Arch Dis Child. 1995;73:418–422.
38. Ernst P, Thomas D, Becklake MR. Respiratory survey of North American Indian children living in proximity to an aluminum smelter. Am Rev Respir Dis. 1986;133:307–312.
39. Babisch W. Road traffic noise and cardiovascular risk. Noise Health. 2008;38:27–33.
40. Belojevic GA, Jakovljevic BD, Stojanov VJ, Slepcević VZ, Paunović KZ. Nighttime road-traffic noise and arterial hypertension in an urban population. Hypertens Res. 2008;31:775–781.
41. Bluhm GL, Berglind N, Nordling E, Rosenlund M. Road traffic noise and hypertension. Occup Environ Med. 2007;64:122–126.
42. Bodin T, Albin M, Ardö J, Stroh E, Ostergren PO, Björk J. Road traffic noise and hypertension: results from a cross-sectional public health survey in southern Sweden. Environ Health. 2009;8:38–48.
43. Boullemant A. PM2.5 emissions from aluminum smelters: coefficients and environmental impact. J Air Waste Manage Assoc. 2011;61:311–318.
Copyright © 2014 by the American College of Occupational and Environmental Medicine