Health Effects of Criteria Air Pollutants from Power Plants 2002

Author: Jefferson H. Dickey MD

• Executive Summary
• Introduction
• Health Effects/Review of Pre-1996 Data
• Health Effects/American Thoracic Society Summary
• Health Effects/New Data: 1996-2000
• Summary and Conclusions
• References

Health Effects: Review of Pre-1996 Data

Pre-1996 Data / Sulfur Dioxide (SO2) / Health Effects

The major health concerns associated with exposure to high concentrations of SO2 include effects on breathing, respiratory illness, alterations in pulmonary defenses, and aggravation of existing cardiovascular disease. Children, the elderly, and people with asthma, cardiovascular disease or chronic lung disease (such as bronchitis or emphysema), are most susceptible to adverse health effects associated with exposure to SO2. The odor threshold is about 0.5 ppm and 6-10 ppm causes irritation of the eyes, nose, and throat. SO2 may cause chronic obstructive lung disease after high dose exposure. SO2 causes asthma exacerbations in some exercising asthmatics at levels as low as 0.25 ppm, an adverse health effect which the US EPA has heretofore failed to regulate.

Sulfur dioxide reacts in the atmosphere to create H2SO4, which forms an acid aerosol. This may be the actual species responsible for many of the health effects observed in epidemiologic studies (see section on particulates). It is epidemiologically difficult to separate SO2 from particulate effects, hence SO2 is commonly associated with increases in hospitalization and mortality rates from cardiorespiratory disease. However, some studies find evidence of health effects of aerosols in virtual absence of sulfur, implying that SO2 may be an important but not necessary component of these acid aerosols.⁵

Pre-1996 Data / Nitrogen Dioxide / Health Effects

Nitrogen dioxide (NO2) is absorbed in both large and small airways. Very high concentrations (>200 ppm) are very dangerous, causing lung injury, fatal pulmonary edema, and bronchopneumonia. Lower concentrations cause impaired mucociliary clearance, particle transport, macrophage function, and local immunity. A recent report of railroad car accident resulted in a substantial but unmeasured community exposure. Headache and respiratory symptoms were reported, especially in those with underlying pulmonary disease. Animal studies find increased mortality with concomitant microbial pathogen exposure. In humans, high exposures (2 to 5 ppm) for 3 hours cause airway inflammation and higher levels of antigen-specific serum IgE, local IgA, IgG, and IgE antibody. Moderate exposure to NO2 to 260 ppb (0.260 ppm or 0.490 mg/m3) for 30 minutes causes increased nonspecific hyperreactivity, and in a 6.6% lower PEFR in the late phase of asthmatic reaction to antigen. Levels around 80 ppb have been associated with a significant increase in acute respiratory infections, sore throat, colds and absences from school.

Epidemiologically, commonly encountered exposures (>30 ppb) have been associated with airways hyper reactivity, and even lower exposures (15 ppb) with stuffy nose and cough. While ambient NO2 levels have been associated in epidemiologic meta-analyses with declines in spirometry and cardiorespiratory events, NO2 is less clearly implicated than particulate, sulfur dioxide, and ozone.

Pre-1996 Date / Ozone / Overview of Condition

Ambient tropospheric ozone pollution at sufficient levels can cause upper and lower respiratory irritative symptoms, restrictive and obstructive spirometric changes, and increased responsiveness to methacholine and allergen bronchoprovocation. In epidemiologic studies, ozone has been associated with increased de novo development of chronic respiratory illness and increased incidence of emergency department visits and hospitalizations for asthma and respiratory disease. Animal studies suggest increased susceptibility to bacterial infection. Some evidence supports an association between ambient ozone exposure and increased daily mortality rates. Ozone induced illness is probably very infrequently recognized as such, but may be suspected especially during formation and especially persistence of relatively stagnant hot ambient air masses. Since bright sunlight is present driving the chemical reactions, health effects from heat exposure may be concomitant.

Pre-1996 Data / Ozone / Pathophysiology

Ozone gas is a very strong oxidant, reacting with biomolecules (alkanes, alkenes, amines, sterols, sulfhydryls, lipids and others) to form ozonides, then free radicals. This triggers inflammation which includes prostaglandins (PGE2, PGF2, TXB2), neutrophils, fibronectin, interleukin-6, lactate dehydrogenase, cytokines, fibronectin, elastase, plasminogen activator, coagulation factors, and other proteins in association with increases in airway permeability. Macrophage function is impaired (possibly related to the increase in PGE2), and this has been associated with increased susceptibility to bacterial pulmonary infection in animal experiments. Pre-treatment with non-steroidal anti-inflammatory drugs (NSAIDs) reduces this effect. Some evidence indicates chronic lung scarring, especially at the bronchoalveolar junction.

Pre-1996 Data / Ozone / Symptoms

Ozone induced illness observed in the laboratory includes conjunctival irritation, upper respiratory irritation, cough, shortness of breath, wheezing, decreased tidal volume, nausea, malaise, and headache. Also associated with ozone pollution is a peculiar chest pain which is substernal, commonly tearing or burning in character, which gradually increases in intensity with inspiration and declines during expiration. Asthmatic children playing outdoors on high ozone air pollution days are roughly 20 to 40% more likely to suffer an asthmatic exacerbation.

Pre-1996 Data / Ozone / Pulmonary Function

Pulmonary function is variably impaired. DLCO (diffusion capacity - a measure of gas exchange) may drop. Declines in FEV1 and FVC show great interindividual variability. Laboratory exposures provide the following data but probably underestimate the effects of community exposures (due to interactive effects of other pollutants, allergens, and to other exposure dynamics). While spirometric changes tend to decrease after several sequential days exposure, tolerance does not seem to develop to bronchial hyper responsiveness. Although ozone has been shown to decrease athletic performance, it has not been shown to exacerbate exercise induced asthma.

Pre-1996 Data / Ozone / Pulmonary Function⁶

Pre-1996 Data / Ozone / Susceptible Populations

Great interindividual variability exists in ozone responsiveness, with a few individuals suffering clinically important reactions, most persons experiencing mild responses, with the remainder little affected. Persons at risk include persons with asthma or chronic lung disease, and those who are active outdoors for prolonged periods. Examples of this latter group are athletes, children at play, and outdoor workers such as laborers, policemen and firemen, farmers, linemen, loading dock workers, construction workers, and foresters. Ozone related spirometric compromise is more marked in individuals with chronic obstructive lung disease, than in otherwise healthy smokers. Increasing evidence suggests that asthmatics, after exposure to ozone, have increased bronchial reactivity to subsequent allergens. Some non-asthmatics show a similar pattern.

Pre-1996 Data / Particulate / Epidemiology / Weight of Evidence

The precise clinical syndrome resulting from particulate has not been well defined clinically, and the clinician will often be uncertain about the contribution of these pollutants in a given patient's exacerbation of lung or heart disease. Adverse health effects from PM are suggested by extensive epidemiologic observation, and by animal and human studies following laboratory exposures. Epidemiologic studies have difficulty describing the effects of individual pollutants in what are typically mixed exposures. Nonetheless the case that particulate pollution represents a substantial public health concern is bolstered by the remarkable consistency across different study techniques, geographies, weather conditions, particle sources, and investigators, as well as the coherence seen across a wide range of health effects and outcome measures.

Pre-1996 Data / Particulate Size, Chemistry, and Pathophysiology

Particulate airway distribution, and apparently health effects, are dependent on size of the particles, and on the structural and functional characteristics of the airways. Near universal pulmonary access is achieved by smaller particles (<PM3); nearly all particles larger than PM10 are trapped in the upper airways where they tend to be cleared by mucociliary mechanisms. A recent study has confirmed at autopsy the deposition distribution observed in the exposure chamber - the apical parenchyma of the lung retains particles smaller than 2.5 micron aerodynamic diameter.⁷ Persons with obstructive pulmonary disease (smokers, asthmatics, and patients with small airway disease or chronic obstructive pulmonary disease [COPD]) have greater distal airway deposition of particles, and this effect is inversely and well correlated with predicted FEV1.

A robust epidemiologic data set associates PM10 with adverse health effects.^{1, 8-12}

However, more recent epidemiologic studies have contributed to understanding the size specificity of health effects, and have increasingly implicated the gasses and smaller particles as the more relevant components of hazardous particulate exposure.^13-16

National Research Council has urged EPA to increase research into the toxicology of particulate chemical components and the relationship between monitored community exposures and personal exposure.¹⁷

Pre-1996 Data / Particulate / Clinical Syndrome

Acute symptoms and signs include restricted activity (including days lost from school and work due to respiratory illness), respiratory illnesses, and exacerbations of asthma and COPD. Clinical observations include declines in lung function, increased asthma medication use, increased emergency department visits, increased hospitalization, increased cardiac and respiratory mortality. Although asthmatics seem to increase bronchodilator use during acid aerosol air pollution episodes, they see relatively little improvement in their peak flow meter recordings. Groups at particular risk of acute illness include the elderly (>65 years), and persons with chronic heart and lung diseases.

Clinical associations with chronic particulate pollution observed in epidemiologic studies include bronchitis, chronic cough, respiratory illness, COPD and asthma exacerbations, decreased longevity, and lung cancer.

The most important data on life expectancy and lung cancer come from two prospective cohort studies in the United States. Both the Harvard six cities study¹³ and the American Cancer Society cohorts¹⁶ found higher community exposures to fine particulate air pollution to be associated with premature mortality and increased lung cancer incidence after adjusting for cigarette smoking and other risk factors. The premature mortality findings are consistent with studies using cross sectional, time series, and case control methodologies, and with the several meta-analyses of the time series studies.^{1, 11, 18} The lung cancer findings are not unexpected in light of the recent data which have elucidated a mechanism by which polycyclic aromatic hydrocarbons (commonly adsorbed on particulate air pollution) cause lung cancer.

Pre-1996 Data / Meta-Analysis of Particulate Health Effects (for a 10 mcg/m3 increase in PM10, a relatively small difference in exposure)^{3, 18}

Total mortality 1%

Cardiovascular mortality 1.4%

Respiratory mortality 3.4%

Respiratory hospitalizations 0.8%

Asthma hospitalizations 1.9%

Asthma ED visits 3.4%

Asthma exacerbations and increase in bronchodilator use 3%

Health effects may be observed for several days after peak exposures, and detectable for up to several weeks after substantial air pollution episodes. At relevant concentrations the mortality dose response relationship is essentially linear, with increases seen even with very low exposures. The annual attributable mortality in the USA is estimated to be in the tens of thousands, (http://www.nrdc.org/nrdcpro/bt/tableGu.html) and the World Health Organization estimates that about 460,000 excess deaths globally are due to suspended particulate matter.

Pre-1996 Data / Particulate / Review

Perhaps the most interesting observations of a "natural experiment" of human mortality due to particulate air pollution were performed by Dr. Arden Pope¹² at Brigham Young University in Utah. His summary of his observations follows:

"Utah Valley has provided an interesting and unique opportunity to evaluate the health effects of respirable particulate air pollution (PM10). Residents of this valley are predominantly nonsmoking members of the Church of Jesus Christ of Latter-day Saints (Mormons). The area has moderately high average PM10 levels with periods of highly elevated PM10 concentrations due to local emissions being trapped in a stagnant air mass near the valley floor during low-level temperature inversion episodes. Due to a labor dispute, there was intermittent operation of the single largest pollution source, an old integrated steel mill. Levels of other common pollutants including sulfur dioxide, ozone, and acidic aerosol are relatively low. Studies specific to Utah Valley have observed that elevated PM10 concentrations are associated with: (1) decreased lung function; (2) increased incidence of respiratory symptoms; (3) increased school absenteeism; (4) increased respiratory hospital admissions; and (5) increased mortality, especially respiratory and cardiovascular mortality."