Megan Powers

Writer’s comment: While taking ECI 149, an introduction to air pollution, I discovered my particular sensitivity to the idea that air pollution could cause asthma. My sister suffers from asthma, and it worries me that a good joke can cause her to laugh hard enough to start an asthma attack, but it worries me more that the air pollution thresholds mandated by the Environmental Protection Agency may not be adequate to protect those already diagnosed with the condition or even to prevent healthy people from becoming afflicted. My ENL 104E (Scientific Writing) instructor gave me the perfect opportunity to gain a better understanding of the problem by researching the topic and writing this literature review.
- Megan Powers

Instructor’s comment: Megan’s review paper, written for English 104E: Scientific Writing, synthesizes the results of a well-selected group of articles that explore relationships between asthma and air pollution. That laboratory science is at base a social enterprise is nicely exemplified by the focus of the studies she reviews, just as Megan’s personal interest in the topic is traceable to her concern for her sister’s struggles with asthma symptoms. In drawing from the articles she reviews and in organizing her paper, Megan maintains a good balance between discussing air-borne pollutants themselves and their physical effects, between analysis and implication. The result is a readable and interesting explanation of current work on this increasingly important subject.
- Sondra Reid, English Department



Introduction

While air pollution is currently controlled nationwide under the Clean Air Act and mandated by the Environmental Protection Agency (EPA), air pollution levels that do not exceed those set by the EPA have been shown to be associated with an increased incidence of respiratory diseases, such as asthma. One indication that air pollution has affected acute asthma is the increase in hospital admissions above the normal annual trend that occurred in 1991 and 1994, an increase that coincided with increased air pollution and heavy haze due to forest fires and volcano eruptions near the study’s location (Chew et al., 1999). Further analysis conducted by Chew et al. (1999) suggests that these air pollutants also have influenced acute asthma beyond the episodes of increased air pollution. This finding has important implications for the growing number of asthma sufferers who are continually being exposed to rising concentrations of air pollutants.
     Because most of the population is exposed to air pollution and because there are ways to reduce pollutant levels, the role of air pollution in the history of asthma has become a great concern for public health (Baldi et al., 1999). In order to reset EPA air-quality standards and to determine which therapeutic actions can be applied to patients to prevent deterioration of their asthma conditions (Neukirch et al., 1998), researchers have found it increasingly necessary to discover the relationships between asthma symptoms and episodes of air pollution and to identify the pollutants that are responsible for the rise in the number of people seeking respiratory medical treatment.

Pollutants of Concern

     Epidemiologic studies have determined that the following are the major air pollutants contributing to respiratory diseases: sulfur dioxide (SO2), nitrogen dioxide (NO2), ozone (O3), and particulate matter (PM) less than 10 mm and less than 2. 5 mm in diameter (PM10 and PM2.5, respectively) (Baldi et al., 1999; Chew et al., 1999; McConnell et al., 1999; McDonnell et al., 1999; Neukirch et al., 1998; Ostro et al., 1998; Sheppard et al., 1999; Taggart et al., 1996). Particulate matter is the product of solid and liquid particles being directly emitted into the air from such things as diesel engine soot, road and agricultural dust, and manufacturing processes, while SO2, NO2, and O3, are predominately byproducts of fuel combustion.
     In controlled studies of the inhalation of either SO2 or O3, subjects with asthma have been shown to be especially sensitive to these pollutants, with decrements in pulmonary function, increases in asthmatic bronchial hyperresponsiveness, and increases in symptoms of respiratory distress (Taggart et al., 1996; Sheppard et al., 1999). Exposure to SO2 produces a transient reflex bronchoconstriction, and exposure to O3 induces airway inflammation (in itself capable of producing bronchoconstriction), causing the stimulation of pain receptors and a decrease in lung volume (Taggart et al., 1996). Another significant correlation between SO2 and respiratory health has been found between the daily levels of SO2 and the number of visits per day to emergency rooms by children with asthma (Chew et al., 1999). The finding that asthmatic children are affected by SO2 is consistent with the results of adults (asthmatic and nonasthmatic) who have been exposed to SO2 in the laboratory. However, asthmatics have been found to be more sensitive to SO2 exposure than nonasthmatics (Baldi et al., 1999).
     The precise effects of NO2 on health remain controversial, although their presence has been demonstrated in experimental studies of respiratory infections of asthmatics. Short-term effects of NO2 have been studied mainly for indoor exposure; indoor levels of exposure often exceeded those encountered outdoors (Neukirch et al., 1998).
     Conventional wisdom holds that ozone only exacerbates asthma. However, the study of McDonnell et al. (1998) suggests that long-term ozone exposure plays a role in the development of asthma in both humans and laboratory animals. McDonnell et al. (1998) chose to use gender-specific models in their ozone study because of the observed differences in time spent by men or women in ozone-rich areas. It was found that men were exposed to more ozone on average during time spent either at work or play when compared with women. For adult males, the risk of developing asthma increased approximately two-fold for a 27 ppb (parts per billion) increment increase of ozone. This association was not seen in women, whose average time either at work or play was not spent in ozone-rich areas.
     Research by Ostro et al. (1998) on PM10 has shown consistently strong associations between the occurrence of adverse health effects and the exposure to ambient concentrations of PM10, concentrations that are below the levels set by the EPA. Among children with asthma, increased particulate air pollution was associated with a significantly increased prevalence of chronic phlegm and bronchitis (McConnell et al., 1999). The adverse health effects of particulate matter are further related to asthmatics as shown by an increase in the rate of asthma hospital admissions when PM levels increased (Sheppard et al., 1999).

Temporal and Regional Differences

     Although panel studies have found relationships between peaks in air pollutants and the frequency of asthmatic symptoms collected daily, only a few studies have focused on investigating the long-term effects of continuous levels of air pollution on asthmatics (Baldi et al., 1999). For the first time in a panel of asthmatic adults, Neukirch et al. (1998) have shown that the effects of pollution last several days after exposure occurs. Moreover, in studies of pollution episodes, the maximal effect on lung function was observed in children two weeks after the episode occurred. These long-term effects suggest that doctors can give asthma patients the option to modify their treatment for a short time after an air pollution episode has occurred to better manage their asthma (Neukirch et al., 1998).
     Urban and industrial areas can contain greater amounts of air pollution than less-industrialized areas, making studies in those areas ideal for evaluating health effects. In Southern California, an area infamous for its high levels of air pollution, ambient particulate matter is relatively low in sulfates. However, the air pollution in the eastern U.S. is relatively high in sulfates. Studies in the eastern U.S. have shown that children with or without asthma suffer the same risk of developing lower respiratory symptoms from exposure to particulate matter. However, McConnell et al. (1999) focus on the regional difference between Southern California and the eastern U.S. to suggest that there is an increased risk among asthmatic children associated with exposures to particulate matter that does not depend on the presence of SO2-derived particulate sulfates.

Proposed Standards

     Detrimental effects of air pollutants on asthma, even at concentrations deemed safe or below proposed air-quality standards, have been observed in epidemiological studies. One such case, in which the daily PM10 concentrations never exceeded 70% of the current EPA ambient air-quality standards, showed a significant association between daily counts of emergency room visits for the treatment of asthma and PM10 exposure on the previous day (Chew et al. 1999). This correlation suggests that exposure to increased levels of certain air pollutants, even within the acceptable range, may still help to trigger acute asthma. The results of Chew et al. (1999) support the premise that asthmatics are more susceptible to air pollutants deemed safe than the general population and that children are more susceptible than adolescents or adults.

Conclusion

     Since the studies of asthmatics were conducted during levels of air pollution considered to be well within current standards, more stringent emissions controls may be necessary to reach a safe pollutant level. The new standards will need to include factors for asthmatics, as they are more sensitive to air pollutants than the majority of the population. While it is currently accepted that air pollutants exacerbate asthma symptoms, studies suggest that air pollutants, ozone in particular, also play a role in the development of adult-onset asthma (McDonnell et al., 1999). Assuming that air pollution is implicated in adult-onset asthma, standards for air pollution levels should ensure that the asthma-afflicted population does not continue to grow. Further study will be necessary to determine safer thresholds for each pollutant.


Literature Cited

Baldi, I., Tessier, J.F., Kauffmann, F., Jacqmin-Gadda, H., Nejjari, C., Salamon, R. (1999). Prevalence of asthma and mean levels of air pollution: Results from the French PAARC survey. European Respiratory Journal 14(1), 132–138.

Chew, F.T., Goh, D.Y.T., Ooi, B.C., Saharom, R., Hui, J.K.S., Lee, B.W. (1999). Association of ambient air-pollution levels with acute asthma exacerbation among children in Singapore. Allergy 54(4), 320–329.

McConnell, R., Berhane, K., Gilliland, F., London, S.J., Vora, H., Avol, E., Gauderman, W.J., Margolis, H.G., Lurmann, F., Thomas, D.C., Peters, J.M. (1999). Air pollution and bronchitic symptoms in Southern California children with asthma. Environmental Health Perspectives 107(9), 757–760.

McDonnell, W.F., Abbey, D.E., Nishino, N., Lebowitz, M.D. (1999). Long-term ambient ozone concentration and the incidence of asthma in nonsmoking adults: The ahsmog study. Environmental Research 80, 110–121.

Neukirch, F., Segala, C., Moullec, Y.L., Korobaeff, M., Aubier, M. (1998). Short-term effects of low-level winter pollution on respiratory health of asthmatic adults. Archives of Environmental Health 53(5), 320–328.

Ostro, B., Chestnut, L. (1998). Assessing the health benefits of reducing particulate matter air pollution in the United States. Environmental Research 76, 94–106.

Sheppard, L., Levy, D., Norris, G., Larson, T.V., Koenig, J.Q. (1999). Effects of ambient air pollution on nonelderly asthma hospital admissions in Seattle, Washington, 1987–1994. Epidemiology 10(1), 23–30.

Taggart, S.C.O., Custovic, A., Francis, H.C., Faragher, E.B., Yates, C.J., Higgins, B.G., Woodcock, A. (1996). Asthmatic bronchial hyperresponsiveness varies with ambient levels of summertime air pollution. European Respiratory Journal 9(6), 1146–1154.