TESTIMONY TO THE UNITED STATES SENATE

COMMITTEE ON ENVIRONMENT AND PUBLIC WORKS

HEALTH EFFECTS OF PARTICULATE MATTER

October 2, 2002

BY:

Jonathan M. Samet, M.D., M.S.

Professor and Chairman, Department of Epidemiology

Bloomberg School of Public Health

Johns Hopkins University

6i5 N. Wolfe St., Suite 6041

Baltimore, M.D. 21205

Introduction

Senator Jeffords and members of the Senate Committee on Environment and Public Works, thank you for the opportunity to speak with you today concerning the health effects of particulate matter and particularly fine particulate matter arising from power plant emissions. This topic has been a focus of my research for several decades. As background, my training includes medicine with specialization in internal medicine and subspecialization in pulmonary diseases. I also have a Masters degree in epidemiology from the Harvard School of Public Health and my career has been spent in the settings of academic medicine, largely at the University of New Mexico School of Medicine, and of academic public health, now at the Johns Hopkins Bloomberg School of Public Health where I am Professor and Chair of the Department of Epidemiology.

Over 20 years ago, I first carried out research directed at the health effects of particulate matter. These studies were carried out in Steubenville, Ohio, where we assessed how air pollution affected the numbers of persons needing care for respiratory and other diseases in the emergency room of the community hospital, and in western Pennsylvania, where we carried out a series of studies to assess the effects of large, coal-fired power plants on the respiratory health of women and children in the surrounding communities. With colleagues at Harvard and Marshall University, I participated in an extensive study of the respiratory health of children in Kanawha County, West Virginia, following the Bhopal episode. Since 1994, with colleagues at Johns Hopkins, my research has focused on the effect of airborne particles and other pollutants on mortality. Our most recent work, the National Morbidity, Mortality, and Air Pollution Study (NMMAPS) uses publicly available data from the 90 largest cities in the U.S. to provide a national picture of the effect of particles on mortality, both total and from cardiac and respiratory causes of death. I have also conducted large studies directed at indoor air pollutants, such as tobacco smoke and nitrogen dioxide.

Because of my research interest in particulate air pollution, I have served as a consultant member of the Clean Air Scientific Advisory Committee (CASAC) of the Environmental Protection Agency’s Science Advisory Board for the mid-1990s review of the Particulate Matter (PM) National Ambient Air Quality Standard (NAAQS) and again for the review now in progress. I also chair the National Research Council’s Committee on Research Priorities for Airborne Particulate Matter, which set out a national plan for research on particulate matter in its first report in 1998. The Committee is now evaluating progress since 1998 in reducing scientific uncertainties concerning particulate matter.

What is particulate matter and how are we exposed to it?

The air that we breathe contains myriad particles that come from numerous sources that are both natural, e.g., the abrasive action of wind, and are generated by human activity, e.g., the burning of coal in a power plant. There are both outdoor and indoor sources, such as cigarette smoking and cooking. The particles in air are a complex mixture reflecting the diversity of these sources; they vary in chemical composition, shape, and size. The particles include sand, pollen and other biological materials, carbonaceous material from combustion, and particles formed secondarily from chemical and physical transformations of gaseous emissions from combustion and other sources.

Particles are often described by their size, which is a key determinant of how long they remain suspended in the air and also of whether they will reach the lung when inhaled and where they will deposit in the lung. The size of particles is described by their aerodynamic diameter in microns, a measure that is based on equivalence to a particle having a standard size and mass. Typically, in urban air, the distribution of particles by size is trimodal. The largest size mode, generally above about 5 microns in aerodynamic diameter, primarily contains dust and other particles that have been resuspended by wind and mechanical action, e.g., motor vehicles, and also some large biological particles, such as pollens. The intermediate size mode, centered below one micron contains primarily products formed by combustion including primary particles emitted directly by the sources, such as diesel soot, and particles formed secondarily. There may be a third size mode of very tiny particles that are the immediate consequence of combustion.

These size characteristics are quite relevant to health considerations since larger particles tend to be filtered out by defense mechanisms in the nose and upper airway, and only the smaller particles, less than approximately 3.5 microns reach the lung. The sites of deposition within the lung also depend on size; the smaller particles tend to penetrate more deeply, reaching the smallest airways and the lung’s alveoli or air sacs. Thus, injury to the lungs and other organ systems from particulate air pollution is thought to result primarily from the smaller particles. There is also concern, however, that persons with asthma may be adversely affected by responses to the larger particles that reach the upper airway.

The Environmental Protection Agency has set NAAQS for progressively smaller size fractions of particles, reflecting evolving understanding of how particles affect health and also measurement capability. The first particle standard was for Total Suspended Particles (TSP), which encompassed nearly all airborne particles. That standard was replaced in 1987 by a standard for PM₁₀ and the new standard for PM_2.5 was added with the 1997 NAAQS revisions. The shift towards measuring and regulating smaller size fractions is well justified by scientific knowledge of the behavior of particles in the respiratory system. The size fractions for PM are inclusive: that is PM_2.5 includes all particles below the 2.5 micron diameter cut-point and PM₁₀ does include the PM_2.5 size fraction. Consequently, studies of PM₁₀ can inform understanding of the health effects of PM_2.5.

We are exposed to particles in all places where we spend time, both indoors and outdoors. While we spend relatively little time outdoors, particles in outdoor air, particularly the finer particles, do penetrate indoors. Consequently, the doses of particles from outdoor sources like power plants are received not only while we are outdoors, but also while we are indoors.

How do particles affect health?

We inhale about 10,000 liters of air per day containing countless particles. Fortunately, the lung does have mechanisms for removing particles and for detoxifying them but these mechanisms may not be sufficient if the particles are too numerous or have high toxicity. The general mechanisms of particle toxicity appear to reflect the inflammatory responses that they evoke in the lung following deposition. There may be more specific mechanisms at play as well, reflecting immune responses to antigens or the actions of carcinogens in particles. While scientific understanding of these mechanisms is still evolving, we have evidence that particles stimulate the lung’s inflammatory cells, leading to the release of various mediators that continue the inflammatory process. Particles are thought to possibly affect the heart by release of mediators into the circulation. The severity of the response to particles and perhaps the nature of the response itself are likely to vary with key characteristics of the particles, such as metal content, acidity, or the various organics that are adsorbed on the surfaces of particles. Better understanding of the toxicity-determining characteristics of particles is one of the research priorities set by the National Research Council’s Committee.

What do we know about the health effects of particulate matter?

The health effects of air pollution have been investigated for about half-century, following the extraordinary air pollution disasters in Donora, Pennsylvania in 1948 and in London in 1952. These and other episodes of evident excess mortality and morbidity showed that high levels of air pollution could quickly damage the public’s health. Over the 50 years that the health effects of air pollution have been investigated, we have carried out many studies in communities using epidemiological approaches to assess the health effects of air pollution, including particulate matter. One challenge faced by researchers in investigating the health effects of air pollution is to attempt to separate the effects of one pollutant from the others that co-exist in the pollutant mixture that is present in the air that we breathe. Nonetheless, substantial evidence has now accumulated, much of it summarized in the references that I have cited in the bibliography for this testimony.

I will focus on summarizing the more recent literature, as the earlier studies were generally carried out at levels of air pollution that are higher than measured today and the characteristics of the air pollution mixture have changed over time, as sources have changed both in their numbers and characteristics. Because researchers often use the monitoring data collected for regulatory purposes, most of the recent evidence on PM draws on measures of PM₁₀, rather than PM_2.5 as a national monitoring network for PM_2.5 has only recently been implemented.

A 1996 review by the American Thoracic Society offered a summary of literature to that time, synthesizing the information concerning major pollutants and listing health effects among the populations at greatest risk (Table 1). The more recent scientific literature includes thousands of papers on particles, so that I can only offer a general summary of the findings. The following general conclusions can be offered based on the now available evidence:

Daily Mortality: Beginning in the early 1990s, many studies carried out in the United States and other countries have linked daily mortality counts to levels of air pollutants, and specifically to particles, on the same or recent days. More recently, several multi-city studies, including our NMMAPS project, have confirmed the association of particulate air pollution with mortality from all causes and from cardiovascular and respiratory causes. As anticipated based on the concept that persons with chronic cardiovascular and respiratory diseases are vulnerable to air pollution, the effect of particles is stronger for cardiac and respiratory causes than for total mortality. In the multi-city approach, we are able to take better control for other pollutants in assessing effects of particles than with the single city approach. In NMMAPS, we estimate that the effect of PM₁₀ on mortality is an increment of about 0.2% for each 10 microgram per cubic meter increase in concentration. Chicago, for example, has about 100 deaths daily; with a 20 microgram increment in concentration, about 0.5 additional deaths are projected on average. While we and others have recently needed to update our findings because of a previously unidentified statistical issue, the findings are proving robust in showing increased daily mortality associated with air pollution.
Long-Term Mortality: The daily time-series studies indicate an effect of particles on mortality rates, but the data do not provide an indication of longer-term consequences. Longer-term follow-up or cohort studies provide information relevant to the question of the extent of life-shortening resulting from particulate air pollution. The strongest evidence on this question comes from two studies: the Harvard Six Cities Study and the American Cancer Society’s Cancer Prevention Study II (CPS II). Both studies show that persons living in more polluted communities tend to have higher mortality rates over the approximately two decades that the participants in these studies have been observed. These analyses take into account factors that might artificially introduce an apparent association with air pollution, such as smoking and socioeconomic status. The initial findings from the two studies were replicated with a re-analysis organized by the Environmental Protection Agency. The general pattern of findings suggests that the increased mortality observed in these studies is most strongly associated with particulate air pollution. Several other studies have now been reported and others are in progress. Gaining a better understanding of the long-term effects of particulate air pollution is another of the research priorities of the National Research Council’s committee.
Hospitalization and Emergency Care: Using the time-series approach, a number of investigators have addressed associations of air pollution with daily counts of hospitalizations or emergency room visits. The files of the Medicare system have been used frequently for this purpose, as they provide nearly complete coverage of persons over 65 years of age in most communities. For example, Drs. Joel Schwartz and Antonella Zanobetti at the Harvard School of Public Health and members of the NMMAPS team, analyzed Medicare data from 14 U.S. cities. They have found associations of PM₁₀ with hospitalization for cardiovascular diseases and chronic obstructive pulmonary diseases. There have been similar findings from other investigators in the United States, Europe, and other countries.
Cardiovascular Disease: Persons with chronic cardiovascular diseases, particularly coronary heart disease, have been considered as susceptible to air pollution exposure, including to particulate air pollution. A series of recent studies indicate possible adverse cardiac effects of particulate air pollution, although the evidence is still somewhat mixed and preliminary. Studies show that air pollution may adversely affect the heart’s rhythm and even trigger potentially fatal rhythm disturbances in high-risk persons with implanted defibrillation devices. There are supporting experimental studies.
Asthma: Persons with asthma are made susceptible to air pollution by the responsiveness of their lungs to environmental triggers. Studies that monitor the health status of persons with asthma on a day-to-day basis indicate that particulate air pollution can have adverse effects.

In summary, there is now substantial epidemiological evidence linking particulate air pollution to adverse health effects, ranging from increased mortality and life-shortening to medical morbidity in people who are susceptible because they have a chronic heart or lung disease. While few of these studies have incorporated PM_2.5 as the primary exposure indicator, our understanding of particle dosimetry in the lungs implies that particles in the respirable size range are responsible for these effects. Emissions associated with power plants contribute to the PM_2.5 mass in many locations in the U.S.

Studies of the impact of power plants

Studies have been carried out that directly address the health effects of coal-fired power plants on surrounding communities. In a recent review, a graduate student in the Department of Epidemiology of the Bloomberg School of Public health identified 16 publications (Table 2) describing the findings of such studies. These source-directed studies considered the effects of multiple pollutants, including particulate matter. In general, their findings indicate adverse effects of coal-fired power plants on the public health in surrounding communities.

Summary and Conclusions

The health effects of air pollution have been a focus of research for nearly a half century, giving clear evidence that the high levels of the past had obvious adverse effects on health and providing a warning that air pollution continues to adversely affect public health, even at the lower levels of outdoor air pollution today. While air pollution constitutes a complex mixture with many potentially toxic components, the evidence consistently indicates that airborne particles in urban environments have adverse effects on health, causing premature mortality and excess morbidity. Based on our knowledge of how particles penetrate into the lung, these effects likely reflect the deposition of smaller particles in the size range encompassed by PM_2.5. These particles have many man-made sources, including vehicles, industry, and electric power generation by coal-fired power plants. Epidemiological studies of communities located adjacent to such plants show that the health of community residents can be harmed, although links to specific products of combustion cannot be made. Risk assessment approaches can be used for the purpose of estimating the burden of disease and ill health associated with power generation in coal-fired power plants.

BIBLIOGRAPHY

(1) Air Pollution and Health. Holgate ST, Samet JM, Koren HS, Maynard RL (eds). San Diego: Academic Press, 1999.

(2) American Thoracic Society, Committee of the Environmental and Occupational Health Assembly. Health effects of outdoor air pollution. Part 1. Am J Resp Crit Care Med 1996; 153:3-50.

(3) American Thoracic Society, Committee of the Environmental and Occupational Health Assembly, Bascom R, Bromberg PA, Costa DA, Devlin R et al. Health effects of outdoor air pollution. Part 2. Am J Resp Crit Care Med 1996; 153:477-498.

(4) Samet JM, Zeger S, Dominici F, Curriero F, Coursac I, Dockery D et al. The National Morbidity, Mortality, and Air Pollution Study (NMMAPS). Part 2. Morbidity and mortality from air pollution in the United States. 2000. Cambridge, MA: Health Effects Institute.

(5) Samet JM, Zeger S, Dominici F, Dockery D, Schwartz J. The National Morbidity, Mortality, and Air Pollution Study (NMMAPS). Part I. Methods and methodological issues. 2000. Cambridge, MA: Health Effects Institute.

(6) Anderson HR, Spix C, Medina S, Schouten J, Castellsague J, Rossi G et al. Air pollution and daily admissions for chronic obstructive pulmonary disease in 6 European cities: results from the APHEA project. Eur Respir J 1997; 10:1064-1071.

(7) Katsouyanni K, Schwartz J, Spix C, Touloumi G, Zmirou D, Zanobetti A et al. Short term effects of air pollution on health: A European approach using epidemiologic time series data: The APHEA protocol. J Epidemiol Community Health 1995; 50(Suppl 1):S12-S18.

(8) Katsouyanni K, Touloumi G, Spix C, Schwartz J, Balducci F, Medina S et al. Short-term effects of ambient sulphur dioxide and particulate matter on mortality in 12 European cities: results from the APHEA project. Br Med J 1997; 314:1658-1663.

(9) Katsouyanni K, Touloumi G, Samoli E, Gryparis A, Le Tertre A, Monopolis Y et al. Confounding and effect modification in the short-term effects of ambient particles on total mortality: results from 29 European cities within the APHEA2 project. Epidemiol 2001; 12:521-531.

(10) Spix C, Anderson R, Schwartz J, Vigotti M, Le Tertre A, Vonk JM et al. Short-term effects of air pollution on hospital admissions of respiratory diseases in Europe. A quantitative summary of the APHEA study results. Arch Environ Health 1997; 53:54-64.

(11) Sunyer J, Spix C, Quenel P, Ponce de Leon A, Ponka A, Barumamdzadeh T et al. Urban air pollution and emergency admissions for asthma in four European cities: The APHEA project. Thorax 1997; 52:760-765.

(12) Touloumi G, Samoli E, Katsouyanni K. Daily mortality and "winter type" air pollution in Athens, Greece -- a time series analysis within the APHEA project. J Epidemiol Community Health 1996; 50(Suppl 1):S47-S51.

(13) Touloumi G, Katsouyanni K, Zmirou D, Schwartz J, Spix C, Ponce de Leon A et al. Short-term effects of ambient oxidant exposure on mortality: a combined analysis within the APHEA project. Am J Epidemiol 1997; 146:177-185.

(14) Zmirou D, Schwartz J, Saez M, Zanobetti A, Wojtyniak B, Touloumi G et al. Time-series analysis of air pollution and cause-specific mortality. Epidemiol 1998; 9(5):495-503.

Table 2. Attributes of Epidemiological Studies of Coal-Fired Power Plant (CPP) Emissions

Study, Location, Year Published	Design	Population(s)	Pollutants and Exposure Metrics	Health Endpoints and Metric	Confounders Addressed *	General Findings	Ref.

New Cumberland West Virginia 1972	Panel 7-month	Asthmatics residing ½ mile from local CPP; Caucasian 80% adult n=20	SO₂, TSP, nitrates, sulfates, soiling index Three monitoring locations; daily means, peaks, lags	Daily asthma or wheezing attack Diary survey with some physician diagnosis	Age, sex, smoking history, allergic history, duration of asthma, temperature, humidity, wind speed, barometric pressure	Temperature and air pollution (esp. suspended sulfates) significantly associated with attack rate	1
Chestnut Ridge (I) Western Pennsylvania 1983	Cross-sectional	Adult women residing within 20 km² study area containing 4 large CPP n=5,557	SO₂, TSP, NO_x, O₃, haze 17 monitoring sites; 3-hr, 24-hr, 1-yr, and 4-yr means by 36 districts; three pollution level strata: low, medium, high	Chronic cough, chronic phlegm, dyspnea grade 3, wheeze most days or nights Telephone survey using ATS-DLD-78 adult questionnaire	Age, SES, ex-cigarette smoking, cigarettes per day, years smoked, cigarette tar content, cigarette smoke inhalation, spouse smoking, length of residence in area	Small increased risk of wheeze in nonsmokers independently associated with SO₂. OR of 1.26 (all current residents) and 1.40 (residents ≥ 5 yrs) No associations identified for smokers or other covariates.	2
Chestnut Ridge (II) Western Pennsylvania 1986	Cross-sectional	Children (16-11 yrs) from public school districts within 20 km² study area containing 4 large CPP n=4,071	SO₂, TSP See above; exposure classified as low, medium, or high based on 3-hr, 24-hr, and 1-yr SO₂ data	Chronic cough or phlegm, persistent wheeze, chest illness within previous year preventing usual activity for ≥ 3 days, serious chest illness before age 2, pulmonary function measures (FVC, FEV, V_max)	Age, sex, SES, maternal smoking, gas stove use, parental history of allergy or respiratory disease, person completing questionnaire	Risk of serious chest illness before age 2 associated with SO₂ strata (OR range 1.13 – 2.10, p < 0.05). Other endpoints not associated. Absence of chronic symptoms.	3
Chestnut Ridge (III) Western Pennsylvania 1987	Panel 8-month	Sample of children from the Chestnut Ridge (II) study, from areas with consistently high pollutant levels; 3 groups evaluated (1) persistent wheeze, (2) without persistent wheeze but with cough/ phlegm for ≥ 3 months, (3) no symptoms n=128 (diaries) n=144 (PEFRs) n=122 (2^nd questionnaire)	SO₂, NO₂, O₃, CoH, and Temperature Maximum hourly levels for each 24-hr period at 17 monitoring stations; minimum hourly temperature from central monitor station	Incidence rates of URI, LRI, wheeze episodes. Change in daily peak expiratory flow rate (PEFR).	Standardized for SO₂ and temperature strata, symptom occurrence on previous day, informal matching for age, sex, and geographic distribution	Air concentrations lower than expected during study period, based on previous years. No important associations relative to air pollution. Cooler temperature was associated with URI and LRI. Low participation rates.	4
Finland 6 Areas Study Helsinki region of Finland 1986	Cross-sectional	Residents (15-64 yrs) living at least 3 years in one of six “affected” communities with at least one CPP & six “unaffected” communities. n=11,310 Residents near 1 CPP followed up with medical exam (n=171).	Specific pollutants not considered. Exposure based on proximity to CPP.	Hawking, cough with and without phlegm, cough with phlegm for at least 3 months, acute dyspnea	Age, sex, smoking status.	Several relationships were identified by investigators before adjusting for smoking status. An association between prevalence of cough without phlegm and proximity to CPP for nonsmokers. No associations for smokers. Medical exam follow up produced no verification of associations other than for smoking status.	5
Espoo, Finland Espoo, Finland 1984	Panel 4-month	Hospital COPD patients (n₁=43) and respiratory sensitive residents (n₂=155) living near CPP Grouped into three categories: COPD, cough, or irritative symptoms	Ambient SO₂, NO₂, suspended particles, soot; concentrations of particulates measured at 3 stations, and the others at 9 stations, recording daily, 24-hr means CPP emitted SO₂ and particulate indices based on continuous flue gas monitoring and daily coal consumption.	Daily “attacks” of cough, eye, or throat irritation Daily dairies of subjects	Temperature, geographic location relative to CPP	No association between CPP emissions and ambient air data. Temperature negatively associated with “attacks” for hospital COPD patients. After controlling for temperature, increase in risk of attacks between low vs. high days for SO2 emissions index and subjects sensitive to eye/throat irritation and for ambient soot and COPD patients (both p<0.01).	6
Lake Munmorah New South Wales, Australia 1993	Cross-sectional	Children (kinder-garten to year 6) from “impacted” town and reference town n₁=447 n₂=404	Measures of air pollution not evaluated.	Asthma, wheeze, bronchial hyper-reactivity, past bronchitis, asthma attacks, asthma attack severity, medication use, various allergies, dry cough at night, chest colds, eczema, episodes of abdominal pain, lung function metrics Questionnaire, skin tests, lung function tests	Age, sex, atopy, father’s occupation, home smoking	Children of the impacted town were more likely to have asthma (OR= 1.97) but not more severe asthma. They were also more likely to have current wheeze (OR: 2.16) and bronchial hyper-reactivity (OR: 1.96 for both).	9
Hadera (I & II) Hadera, Israel 1984	Repeated Cross-sectional	Children in grades 2, 5, and 8 in 1980 and 1983 attending school within 9 km² radius of large CPP n₁₉₈₀=2655 n₁₉₈₃=1788 Large portion of two 1980 cohorts re-examined	No specific measures provided. Three population areas designated for exposure assessment of low, moderate, high “expected” pollution	Cough, sputum, cough and sputum, pneumonia, measles, other respiratory symptoms (general), FVC, FEV₁, PFR Modified ATS-questionnaires sent home; lung function tests	School-grade, gender, SES, maternal smoking, history of family respiratory disease, respiratory disease in sibs or parents	The 1980 2^nd and 5^th grade cohorts were specifically examined. Higher prevalence of respiratory symptoms found in younger cohort. Mixed results among three population areas. Results suffer from exposure misclassification and a lack of exposure data.	10, 11
Hadera (III) Hadera, Israel 1984	Repeated Cross-sectional	Children in grades 2, 5, and 8 in 1980, 1983, & 1986 attending school within 9 km² radius of large CPP	SO₂, NO_x, O₃, CO, TSP, total hydrocarbons Twelve monitoring stations (automatic), daily concentrations Three population areas, as above.	Same as above	Same as above	Respiratory symptoms more prevalent in younger generations, with statistical significant increases for cough and sputum, and asthma for one community. Mixed results for lung function measures. Reported air quality indicated that planned gradient of pollutant levels not obtained. Associations reported to be not caused by CPP.	12
Hadera (IV) Hadera, Israel 1984	Weekly surveys for 9 years	Populations served by 8 local health clinics	Meteorological and pollutant data collected as described above. Three population areas designated for exposure assessment of low, moderate, high “expected” pollution	Daily health service use in clinics, total daily visits, and number of visits for respiratory tract complaints.	Seasonal trends in services, influenza epidemics	No time trends or associations observed. Possible loss of patients to other clinics and turnover of patients served make results difficult to interpret.	13
Hadera (V) Hadera, Israel 1984	Repeated cross-sectional	5^th grade cohorts of 1980, 1983, 1986, & 1989 attending school within 9 km² radius of large CPP	SO₂, NO_x, O₃, CO, TSP, total hydrocarbons Twelve monitoring stations (automatic), daily concentrations Three population areas, as above.	Same as Hadera I, II, and III	Same as Hadera I, II, and III	Statistically significant increases in asthma and wheezing with shortness of breath. Small, clear dose-response shown over time. Bronchitis and cough with sputum showed no important change. Ambient pollutant levels were very low during study period - increased prevalent symptoms explained by other (unmeasured) causes, according to authors.	14
Gardanne Coal-Basin near Marseille, France 1988	Panel 4-month	3^rd, 4^th, 5^th grade school children living in various communities in a coal mining & emitting region n=450	SO₂ and respirable particulates 27 monitoring stations, 15-minute automatic	Morning cough, eye irritation, runny nose, sneezing, wheezing in chest, fever Daily diaries submitted weekly	Temperature, effect lags, copollutant	Statistically significant association detected for SO₂ and morning cough and wheezing in the chest at high pollution communities. Other positive associations reported for single communities. No lag effects found. Suffers from lack of controlling for known confounders (e.g., home smoking).	15
Erfurt Erfurt, East Germany 1993	Time Series	Population of Erfurt (approx. 200,000 total), heavy coal pollution number of daily events ranged from 0 to 20	SO2 (1980-1989) and suspended particulates (1988-1989, only) One centrally located continuous monitor, daily mean and maximum 30-min concentrations	Daily mortality counts Hand counting of death certificates from local health departments	Temperature, humidity, meteorology, various lag times, short-term (2 week) harvesting, copollutant, influenza outbreaks, season	Dose response coefficients identified for SO2 and suspended particulates. SO2: 5-95% quartile increase => 10% mortality increase SP: 5-95% quartile increase => 22% mortality increase	16

* The degree to which each confounding variable was addressed varies significantly both within and among the studies. In some cases, a variable is listed that was measured and qualitatively addressed, but may not have been specifically controlled for during analysis.

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