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Health Effects of Criteria Air Pollutants from Power Plants 2002

Author: Jefferson H. Dickey MD

Executive Summary

The recent medical literature concerning air pollution is more convincing than ever, indicating that ozone and particulate air pollutants cause serious health effects to the general public. Air pollution causes increased chest symptoms, days lost from school and work due to chest illness, asthma attacks, increases in emergency room and hospital admissions, and increased mortality rates. The association between ozone and many adverse health effects is certainly causal, and the association with excess mortality is certainly robust and may well be causal. The causal nature of the association between particulate air pollution and adverse health effects and higher mortality rates appears to be firmly established according to the National Institutes of Health. The effect of particulate on mortality does not seem to have a safe threshold. The value of the health benefits nationally of lower particulate air pollution levels is estimated at $32 billion, and the benefit to public health of reduced power plant emissions seems well worth the cost.

This report reviews the recent medical literature concerning emissions of criteria pollutants (NOx, SO2, PM, and O3) derived from power plants which burn oil and coal. The structure of this report reflects a de facto evolution in scientific thinking which coincided with the legislatively mandated periodic review of the National Ambient Air Quality Standards (NAAQS) for ozone and particulate which occurred in 1996-7. At that time the medical literature reflected a remarkably robust set of data implicating ozone and particulate in clinically significant and serious health effects. This new report summarizes the medical literature accumulated between 1996 and early 2000, categorized according to study type.

Nitrogen oxides (NO2 and NO constitute "NOx" ) and sulfur dioxide (SO2) are primary pollutants, derived from combustion of sulfur and nitrogen containing fossil fuels, and are directly emitted by power plants. In a complex series of atmospheric reactions, nitrogen oxides are converted to nitric (HNO3) and nitrous (HNO2) acids and acid aerosols (a form of particulate matter (PM), or soot), and SO2 is converted to sulfuric acid, which is another constituent of acid aerosols. Acid aerosols are sometimes referred to as a component of "acid fog". Nitrogen oxides are also converted in another series of complex reactions in the presence of sunlight to ozone (O3).

The results of the recent health effects research are overwhelming. The new data describe a coherent picture of serious adverse health effects due to air pollution.

Ozone causes symptoms of chest tightness, shortness of breath, cough, wheeze, pulmonary inflammation, declines in lung function, increases in bronchial hyperreactivity, exacerbations of allergen induced asthma, and is associated in epidemiologic studies with de novo development of asthma as well as increased emergency room visits, increased hospitalizations, and increased mortality rates.

Particulate matter of the size which results from fossil fuel combustion penetrates efficiently into the gas exchange portions of the lung and is associated in epidemiologic studies with chest symptoms, small declines in lung function, increased asthma attacks, increased asthma medication use, increased days lost from school and work due to chest illness, increased emergency room use, increased hospitalizations, and increased mortality.

Data increasingly suggest that these pollutants are also associated with lung cancer.

The recent research is divided into 16 sections according to study type.

The new data on ozone effects on lung function are consistent with previous data. The recent advance in this area is the combining of many previous studies to develop a model which describes the impairment of lung function. The important determinants of lung function decline include: ozone concentration, duration of exposure, ventilatory rate (exercise level) during exposure, age, and smoking status. The presence of chronic obstructive lung disease (COPD) was identified as a factor which, when combined with exercise, produced greater than expected declines in lung function. Hence, COPD patients may be added to the list of groups unusually susceptible to adverse health effects from ozone: children who play outdoors, adults who work or exercise outdoor, and asthmatics.

Data continue to be generated indicating that ozone causes inflammation in the distal airways, with increases in white blood cells, proteins, cytokines, interleukins, and other inflammatory mediators leaving the blood stream and accumulating in the lung. These studies use the bronchoalveolar lavage technique (BAL), which measures abnormal exudative contents of the distal airways and alveoli. Some reports continue to find that allergic asthmatics may be more vulnerable to these effects. In addition, new data indicate that declines in spirometric lung function measurements do not correlate strongly with bronchial hyperreactivity or markers of inflammation. Hence, understanding exactly how lung function declines, increases in inflammation, and increases in bronchial hyperreactivity function independently continues to be an area of active research.

One of the most innovative new studies looked at BAL results of recreational joggers in New York City, and found that ozone air pollution correlated well with BAL markers of inflammation in these subjects.

The data on ozone exacerbations of allergen induced spirometric declines continues to evolve. While some previous observations found relatively low levels of ozone to aggravate allergen induced bronchial obstruction, more recent studies find that in most people, ozone induced exacerbation of allergen induced spirometric impairment occurs only at higher levels. The caveat remains that these studies are performed only on persons with mild allergic asthma, and not on persons with severe, persistent asthma. Hence, extrapolation to the broader population of persons with varying asthma severity is precluded.

Time series studies examining the relationship between community air pollution levels with asthmatic peak expiratory flow rates (PEFR) and medication use continue to find that air pollution is associated with declines in PEFRs and increases in asthma medication use. Two new studies performed combined analysis of previous time series PEFR studies in children. One examined the relationship with particulate air pollution and the other with ozone. Both found impairment in lung function as measured by PEFR in children to be associated with air pollution.

Several new studies examined cross sectionally the relationship between spirometric lung function and air pollution levels. All found air pollution to be associated with lower lung function levels, most robustly with particulates and acid aerosols. One innovative new study looked at lung function growth in children and found that lung growth was lower in children living in high ozone air pollution areas. This study is not conclusive and needs to be replicated before any conclusions can be drawn, but is consistent with pathophysiologic observations and a previously performed autopsy study which implicates pulmonary inflammation and scarring.

An interesting new study looked at de novo development of asthma over 15 years in a non-smoking prospective cohort and found that ozone air pollution was associated with new onset asthma in men, but not women. Because analysis was not adjusted for amount of time working outdoors, and replicating the study will be quite expensive and time consuming, firm conclusions cannot be drawn.

One of the areas of most active research looks to understand the cardiac effects of particulate air pollution. This research is compelled by observations in many other studies which find that particulate air pollution is not only associated with death from pulmonary causes, but also with cardiac etiologies. The new research looks at cardiac function as measured by 24 hour EKG (Holter), and finds, among other things, decreased heart rate variability when subjects are exposed to higher particulate levels. Decreased heart rate variability has been identified as a risk factor for cardiac disease.

Time series studies looking the relationship between air pollution levels and emergency room visits for asthma and other respiratory disease continue to overwhelmingly find significant and robust associations with particulate and ozone.

A couple new prospective cohort studies of asthmatics find that higher air pollution levels are associated with increased emergency room visits. One model which combined weather variables with air pollution variables accounted for 69% of the variability in asthmatic emergency room use.

The flow of studies of hospitalization rates as a function of air pollution levels continues unabated, with overwhelming evidence of elevated hospitalization rates due to air pollution.

Nineteen new studies examined the association between particulates and hospitalization rates. Only one of these studies failed to find an association between combustion derived air pollution and increased hospitalization rates. Two of the studies found the association with SO2 instead, and one found the association with particulate only when NOx was also in the model. Hence, in 18 of 19 studies, the association with particulate air pollution or its chemical antecedents was observed.

Fifteen new studies examined the association between ozone air pollution and hospitalization rates. Twelve studies found a significant association, one study found the association with NO2 instead. Two studies failed to find the association. In all, 13 of 15 studies found the association with ozone or its chemical antecedents.

The cascade of studies finding associations between air pollution and excess mortality rates continues unabated.

Eighteen new studies examined the association between particulate air pollution and excess mortality. Seventeen of these studies found the association.

Twelve new studies examined the association between ozone air pollution and excess mortality. Ten found the association and one found the association with NO2 instead. One study found ozone to be only marginally significant. No study completely failed to find an association between ozone or its chemical antecedent, NO2, and excess mortality rates.

One new meta-analysis of particulate time series mortality studies appeared in the literature. The results are entirely consistent with previous meta-analyses. The additional feature of this study was to reinforce the notion that when the contribution of fine fraction (smaller) particulate is higher (which occurs when the particulate is from fossil fuel combustion sources), the association between particulate and excess mortality rates is even stronger.

One new prospective cohort was recently reported. Not surprisingly, it found that particulate air pollution was associated with premature mortality, with the mortality rates among the more exposed groups being about 18% higher. In addition, as with all the previously reported prospective cohorts, air pollution was associated with increased lung cancer rates.

In sum, the data describing the health effects of ozone and particulate is robust and convincing. Air pollution causes increased chest symptoms, chest illness, asthma attacks, increases in emergency room and hospital admissions, and increased mortality rates. The association between ozone and many adverse health effects is certainly causal, and the association with excess mortality is certainly robust and may well be causal. The causal nature of the association between particulate air pollution and adverse health effects and higher mortality rates appears to be firmly established.

The National Institutes of Health has published in its scientific publication, Environmental Health Perspectives, an article which observes that the data associating particulate air pollution with adverse health outcomes is conclusive. While many researchers had previously taken that position, dissenting views were also published. With the panoply of data now before us, however, avoiding public responsibility to reduce air pollution levels is not tenable. With a major contribution to particulate and ozone air pollution coming from very outdated power plants, and with newer, much less polluting power plants increasingly satisfying power generating needs, the justification for maintaining outdated technology has faded. The time has come to clean up outdated, highly polluting power plants.

More . . . Introduction

Page Updated July 30, 2009