TESTIMONY
TO THE UNITED STATES SENATE
COMMITTEE
ON ENVIRONMENT AND PUBLIC WORKS
On
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 PM2.5
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 PM2.5 includes all particles below the
2.5 micron diameter cut-point and PM10 does include the PM2.5
size fraction. Consequently, studies of
PM10 can inform understanding of the health effects of PM2.5.
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 PM2.5 as a national monitoring network for PM2.5
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:
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
PM2.5 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 PM2.5
mass in many locations in the U.S.
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.
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 PM2.5. 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, NOx, 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, Vmax) |
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 (2nd
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 2nd and 5th 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, NOx, 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 |
5th grade cohorts of 1980, 1983, 1986, & 1989 attending school within 9 km2 radius of large CPP |
SO2, NOx, 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 |
3rd, 4th, 5th 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. |
|
|||||||
1. Cohen AA, Bromberg S, Buechley RW, Heiderscheit LT, Shy CM. Asthma and air pollution from a coal-fueled power plant. Am J Public Health 1972;62(9):1181-8.
2. Schenker MB, Speizer FE, Samet JM, Gruhl J, Batterman S. Health effects of air pollution due to coal combustion in the Chestnut Ridge Region of Pennsylvannia: results of cross-sectional analysis in adults. Arch Environ Health 1983;38(6):325-30.
3. Schenker MB, Vedal S, Batterman S, Samet JM, Speizer FE. Health effects of air pollution due to coal combustion in the Chestnut Ridge Region of Pennsylvannia: cross-section survey of children. Arch Environ Health 1986;41(2):104-8.
4. Vedal S, Schenker MB, Munoz A, Samet JM, Batterman S, Speizer FE. Daily air pollution effects on children’s respiratory symptoms and peak expiratory flow. Am J Public Health 1987;77(6):694-8.
5. Pershagen G, Hammar N, Vartianen E. Respiratory symptoms and annoyance in the vicinity of coal-fired plants. Environ Health Perspect 1986; 70:239-45.
6. Pershagen G, Hrubec Z, Lorich U, Ronnqvist P. Acute respiratory symptoms in patients with chronic obstructive pulmonary disease and in other subjects living near a coal-fired plant. Arch Environ Health 1984;39(1):27-33.
7. Henry RL, Abramson R, Adler JA, Wlodarcyzk J, Hensley MJ, Asthma in the vicinity of power stations: I. A prevalence study. Pediatr Pulmonol 1991;11(2):127-33.
8. Henry RL, Bridgman HA, Wlodarcyzk J, Abramson R, Adler JA, Hensley MJ, Asthma in the vicinity of power stations: II. Outdoor air quality and symptoms. Pediatr Pulmonol 1991;11(2):134-40.
9. Halliday JA, Henry RL, Hankin RG, Hensley MJ. Increased wheeze but not bronchial hyperreactivity near power stations. Journal of Epidemiology & Community Health 1993;47(4):282-6.
10.
Toeplitz R, Goren A, Goldsmith JR, Donagi A.
Epidemiological monitoring in the vicinity of a coal-fired power plant. Sci Total Environ 1984 Jan
27;32(3):233-46.
11. Goren AI, Helman S, Goldsmith JR. Longitudinal study of respiratory conditions among schoolchildren in Israel: Interim report of an epidemiological monitoring program in the vicinity of a new coal-fired power plant. Arch Environ Health 1988;43(2):190-4.
12. Goren AI, Goldsmith JR, Hellmann S, Brenner S. Follow-up of schoolchildren in the vicinity of a coal-fired power plant in Israel. Environ Health Perspect 1991;94:101-5.
13. Goren AI, Hellmann S, Glazer ED. Use of outpatient clinics as a health indicator for communities around a coal-fired power plant. Environ Health Perspect 1995;103:1110-5.
14. Goren AI, Hellman S. Has the prevalence of asthma increased in children? Evidence from a long term study. J Epi Comm Health 1997 Jun;51(3):227-32.
15. Charpin D, Kleisbauer JP, Fondarai J, Graland B, Viala A, Gouezo F. Respiratory symptoms and air pollution changes in children: the Gardanne coal-basin study. Arch. Environ. Health 1988;43:22-27.
16. Spix C, Heinrich J, Dockery D, Schwartz J, Volksch G, Schwinkowski K, Collen C, Wichmann HE. Air pollution and daily mortality in Erfurt, East Germany, 1980 – 1989. Environ. Health Perspect. 1993;101(6):518-526.