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Health Effects of Ozone in Patients with Asthma

Review Key Points

Introduction

People with asthma are the only segment of the population that has been identified to be the most acutely responsive to ozone exposure. Although younger adults (teens to thirties) experience larger lung function changes than do older adults (fifties to eighties), the limited data available do not suggest that children have larger responses than young adults for a given exposure. Children are generally at risk of higher exposure, however, and therefore at risk of larger acute responses because they tend to be more active and spend more time playing outdoors than most adults.

In particular, following respiratory exposure to ozone, people with asthma experience:

  • Increased frequency of asthma attacks
  • Increased use of health care services

Furthermore, based upon non-human primate data, very young children may be at special risk of effects upon respiratory system development, the long-term effects of which are not known. Also, those exposed early in life have the potential for the greatest lifetime exposures. Individuals with chronic lung diseases characterized by impaired lung function may theoretically be at higher risk since even small additional decrements in lung function could result in disproportionate effects. The extent to which this is true is not known.

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What is asthma?

Clinically, asthma is a chronic inflammatory disease of the airways in which many cell types play a role, in particular mast cells, eosinophils, and T lymphocytes. In susceptible individuals, the inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night and/or early morning. These symptoms are usually associated with widespread but variable airflow obstruction that is at least partly reversible, either spontaneously or with treatment. The inflammation also causes an associated increase in airway responsiveness to a variety of stimuli. The basic physiologic alterations of asthma are bronchospasm, measured by reduction in obstructive (airflow-related) lung function, edema, and hypersecretion.

Evidence of bronchial inflammation is obtained from:

  • Measuring nonspecific bronchial hyperresponsiveness
  • Bronchoalveolar lavage (BAL)
  • Bronchial biopsies
  • Induced sputum

The majority of asthma is associated with allergic responses to common airborne allergens such as household dust mites (HDM), pollens, animal dander, and molds. The disease has a definite genetic component. In genetically predisposed individuals, exposure to allergens can lead to immunologic sensitization.

Sensitization involves the production of antibodies that belong to the immunoglobulin E (IgE) class. Upon re-exposure to allergens, immediate and delayed (late-phase) responses may occur in a subpopulation of sensitized individuals. These responses include airway inflammation (characterized by the presence of inflammatory cells such as eosinophils and activated T-helper lymphocytes) and airway obstruction that is reversible either spontaneously or with appropriate medication.

 

Schematic diagram depicting factors involved in induction and exacerbation of asthma. Figure 8: Factors involved in induction and exacerbation of asthma. Induction of asthma may occur in genetically susceptible people upon exposure to common allergens or certain chemicals. Nonspecific irritants and promoters may facilitate induction through injury and increased uptake of allergens or by modulating immune responses (dashed arrow). Both allergens and irritants may exacerbate existing asthma.

Inflammation and airway obstruction in asthma are reversible. Consequently, severity of the disease is variable (double-headed arrows), depending on environmental influences as well as susceptibility factors as indicated here.

Induction of asthma refers both to the acquisition of immunologic sensitivity to allergens and the progression to a clinically detectable disease that is indicated by reversible airway obstruction. Exacerbation of asthma may occur with subsequent re-exposure to allergens or by exposure to a number of nonspecific triggers of lung inflammation and airway obstruction, such as respiratory viruses, tobacco smoke, or certain air pollutants like ozone.

It also has been suggested that some of these triggers facilitate the induction of asthma by increasing sensitization to allergens. This may occur via modulation of immune responses or injury to airway epithelium, effects that allow allergens to penetrate the immune system barrier and to be taken up by antigen-processing cells.

Susceptibility factors that are indicative of the potential for exposure to allergens and nonallergic triggers include, in addition to the genetic component:

  • Overall health status
  • Lifestyle
  • Socioeconomic status
  • Residential location
  • Overall exposure history

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Why should we be concerned about the potential effects of ozone on those with asthma?

The prevalence of asthma in the United States has doubled in the last 20 years. More than 20 million people now report having the disease. Asthma has increased most rapidly in children younger than 17 years old, who also account for the highest overall rates of asthma among the population at large. Higher rates of asthma are also reported among minorities and inner-city poor populations. Although asthma-related deaths are infrequent (< 6000 in 1997), mortality rates have increased 66% since 1980.

Illness associated with asthma accounts for an estimated 10 million patient visits and more than 470,000 hospital admissions annually; this translates to an estimated loss of 3 million work days and 90 million days of restricted activity for people with asthma each year. The costs related to this disease are enormous, with an estimated cost in the United States in 1996 of $14 billion.

Trends toward increased prevalence, deaths, and costs of the disease have also been observed in many other countries. The increase in asthma incidence cannot be reconciled simply by changes in diagnostic categorization, and it has been too rapid to be explained by alterations in the gene pool. For these reasons, there has been a growing interest in the association between the environment and asthma.

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How does ozone affect people with asthma?

There are two major mechanisms by which people with asthma might be more severely affected by ozone than those without asthma. The first is that those with asthma might be more responsive or sensitive to ozone and therefore experience the lung function changes and respiratory symptoms common to all, but either at lower concentrations or with greater magnitude. There is evidence that this may be true, but it is likely to play a small role in the response of people with asthma. By far, the greater concern is that the injury, inflammation, and increased airway reactivity induced by ozone exposure may result in a worsening of a person's underlying asthma status, increasing the probability of an asthma attack or requiring more treatment.

Epidemiologic studies indicate that there is a relationship between ambient ozone concentration and medication use among children with asthma, and ER visits and hospital admissions for asthma. In a camp for children with asthma in New York, it was observed that on days when ozone concentrations were high, children in camp used their asthma inhalers more frequently than on days when ozone levels were low. Presumably this was due to a perception that their asthma was worse on those days. Measures of peak expiratory flow in these children were lower on days when ozone levels were high, supporting this hypothesis.

Graph showing asthma inhalers were used more frequently during days when ozone concentrations were high. Figure 9: Unscheduled daily asthma medication use by children with asthma is associated with summertime haze air pollution. Use of inhaled beta-adrenergic agonist medication to alleviate asthma aggravation is plotted against ozone concentrations during summer asthma camps conducted for children 7 to 13 years old, during the last week of June, 1991 through 1993, in the Connecticut River Valley, downwind of New York City. Each child's normal physician-prescribed medications were maintained throughout each week. An increase in the 1-hour daily maximal ozone concentration from 84 to 160 ppb was significantly associated with increased unscheduled medications administered per day. Source: Thurston et al., 1997

 

In Atlanta, GA, in Buffalo and New York City, NY, and in many other places throughout the United States, visits to the hospital emergency room for asthma were more frequent on days when ozone concentrations were high (generally above 110 ppb as a 1-hour average or 60 ppb as a 7-hour average) compared to low ozone days. Similarly, in a number of places, hospital admissions for asthma or for all respiratory conditions combined were higher following days when ozone levels were elevated.

 

Bar chart showing the mean number of visits for asthma or reactive airway disease on days grouped by the maximum 1-hour ozone level. Figure 10: Childhood asthma and reactive airway disease appears to be exacerbated after periods of high ozone pollution. No dose-response relationship was observed between the number of clinic visits and 1-hour maximum ozone levels under 0.11 ppm; however, when ozone levels equaled or exceeded 0.11 ppm, the number of visits to hospital clinics for childhood asthma or reactive airway disease on the following day was about one-third higher than at other times. Source: White et al., 1994

 

The validity of these epidemiologic observations has been supported by the results of controlled experimental ozone exposures in human volunteers in which markers of asthma status were measured after ozone and after clean air exposures. In these studies, ozone has been demonstrated to worsen airway inflammation, to increase the airway response to inhaled allergen, and to increase nonspecific airway responsiveness, each of which is likely to indicate worsening asthma.

In one study, people with asthma exposed to 0.16 ppm ozone were observed to have larger changes in PMNs and BAL protein than individuals without asthma, suggesting a more intense inflammatory response. Exposure to 0.20 ppm ozone increased the numbers of eosinophils found in the BAL fluid of people with asthma. In contrast, eosinophils are not found in the BAL of individuals without asthma as a result of ozone exposure.

In another study, house dust mite (HDM) sensitive individuals underwent airway challenge with HDM antigen after ozone exposure and after air exposure. As seen in Figure 11, after ozone exposure, the concentration of HDM needed to cause a 20% fall in FEV1 was reduced compared to the air exposure, suggesting that people with asthma would have a greater response to environmental levels of HDM following ozone exposure.

Many studies have demonstrated that nonspecific airway responsiveness is greater following ozone exposure. These findings are consistent with ozone causing an increase in asthma severity and, taken together, provide a plausible biological mechanism for the epidemiological observations that ambient ozone exposure results in a higher probability of experiencing an asthma attack and other manifestations of worsening asthma.

 

Graph showing that ozone exposure increases the responsiveness of allergic people with asthma to inhaled house dust mite antigen. Figure 11: Ozone exposure increases the responsiveness of people with allergic asthma to inhaled house dust mite antigen. The graph shows the airway responsiveness of people with mild allergic asthma to inhaled house dust mite allergen after 7.6-hour exposures to both ozone (0.16 ppm) and filtered air. The point on the far left side of the graph indicates the average concentration of inhaled house dust mite antigen required to produce a 20% decrease in FEV1 following air exposure. The point on the far right indicates the average concentration required to produce a 20% FEV1 decrease following the ozone exposure. On average, after an ozone exposure less antigen is required to produce the FEV1 decrease compared to an air exposure. The points in the center of the graph are the data for the individual participants after both air and ozone exposure. Seven out of nine participants required a lower dose of antigen to produce a 20% FEV1 decrement following the ozone exposure compared to the air exposure. Source: Kehrl et al., 1999

 

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