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| Block 8: Environmental Issues and Public Health - Air Pollution Chapter 3: The Main Air Pollutants; Their Health Impacts; Exposure - Response Relationships (Continued) |
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Ground-level ozone (the primary constituent of smog) is the most complex, difficult to control, and pervasive of the six principal air pollutants. Unlike other pollutants, ozone is not emitted directly into the air by specific sources. Ozone is created by sunlight acting on NOx and VOC in the air. There are thousands of types of sources of these gases. Some of the common sources include gasoline vapors, chemical solvents, combustion products of fuels, and consumer products. Emissions of NOx and VOC from motor vehicles and stationary sources can be carried hundreds of miles from their origins, and result in high ozone concentrations over very large regions.
Scientific evidence indicates that ground-level ozone not only affects people with impaired respiratory systems (such as asthmatics), but healthy adults and children as well. Exposure to ozone for 6 to 7 hours, even at relatively low concentrations, significantly reduces lung function and induces respiratory inflammation in normal, healthy people during periods of moderate exercise. It can be accompanied by symptoms such as chest pain, coughing, nausea, and pulmonary congestion. Recent studies provide evidence of an association between elevated ozone levels and increases in hospital admissions for respiratory problems in several U.S. cities. Results from animal studies indicate that repeated exposure to high levels of ozone for several months or more can produce permanent structural damage in the lungs. Ozone damages crops and forest ecosystems.
O3 toxicity occurs in a continuum in which higher concentrations, longer exposure duration, and greater activity levels during exposure cause greater effects. Short-term acute effects include pulmonary function changes, increased airway responsiveness and airway inflammation, and other symptoms. These health effects are statistically significant at 160 µg/m3 (0.08 ppm) for 6.6 hour exposures in a group of healthy exercising adults, with the most sensitive subjects experiencing a more than 10% functional decrease within 4-5 hours. Controlled exposure of heavily exercising adults, or children to an O3 concentration of 240 µg/m3 (0.l2 ppm) for 2 hours, also produced decreases in pulmonary function. There is no question that substantial acute adverse effects occur during exercise with one hour exposure to concentrations of 500 µg/m3 or higher, particularly in susceptible individuals or subgroups. Field studies in children, adolescents, and young adults have indicated that pulmonary function decrease can occur as a result of short term exposure to O3 concentrations in the range 120-240 µg/m3 and higher. Mobile laboratory studies have observed changes in pulmonary function in children or asthmatics exposed to O3 concentrations of 280-340 µg/m3 (0.14-0.17 ppm) for several hours. Respiratory symptoms, especially coughing, have been associated with O3 concentrations as low as 300 µg/m3 (0.15 ppm). O3 exposure has also been reported to be associated with increased respiratory hospital admissions and exacerbation of asthma. The effects are observed with exposures to ambient O3 (and co-pollutants) and with controlled exposures to O3 alone. This demonstrates that the functional and symptomatic responses can be attributed primarily to O3. A number of studies evaluating animals (rats and monkeys) exposed to O3 for a few hours or days have shown alterations in the respiratory tract, in which the lowest-observed-effect levels were in the range of 160-400 µg/m3 (0.08-0.2 ppm). These included the potentiation of bacterial lung infections, inflammation, morphological alterations in the lung, increases in the function of lung enzymes active in oxidant defenses, and increases in collagen content. Long-term exposure to O3 in the range of 240-500 µg/m3 (0.12 to 0.25 ppm) causes morphological changes in the epithelium and interstitium of the centri-acinar region of the lung, including fibrotic changes.
Figures 3.2 to 3.5 summarize the O3 levels at which two representative adverse health outcomes, based on controlled exposure experiments, may be expected. The dose-response relationships in these figures represent expert judgment based on the collective evidence from numerous studies and linear extrapolation in a few cases where data were limited.
Interestingly, these dose-response relationships appear to be non linear.
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| Figure 3.2: Change in FEV1 as a function of O3 concentration in the most sensitive 10% of active young adults and children. |
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| Figure 3.3: Inflammatory change (neutrophil influx in lungs of healthy young adults exercising outdoors at more than 40 l/min expiratory volume in the lung) as a function of O3 concentration. |
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| Figure 3.4: Figure 3.4: Increase in hospital admissions for respiratory conditions as a function of O3 concentration. |
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| Figure 3.5: Change in symptom exacerbation among adults and asthmatics as a function of O3 concentration. |
