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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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NOx consists of nitric oxide (NO) and nitrogen dioxide (NO2). Combustion processes are the main sources of NOx; about 90% of the NOx is released in the form of NO which is converted to NO2. Major sources are power stations (particularly coal fired power stations), vehicles (particularly if not fitted with catalytic converters) and certain industrial processes - mainly nitric acid manufacture. NO2 is a suffocating, brownish gas; nitrogen dioxide is a strong oxidizing agent that reacts in the air to form corrosive nitric acid, as well as toxic organic nitrates. It also plays a major role in the atmospheric reactions that produce ground-level ozone (or smog) and fine particulate matter (PM2.5) in the form of nitrates.
Nitrogen dioxide can irritate the lungs and lower resistance to respiratory infections such as influenza. The effects of short-term exposure are still unclear, but continued or frequent exposure to concentrations that are typically much higher than those normally found in the ambient air may cause increased incidence of acute respiratory illness in children. EPA's health-based national air quality standard for NO2 is 0.053 ppm (measured as an annual arithmetic mean concentration). Nitrogen oxides contribute to ozone formation and can have adverse effects on both terrestrial and aquatic ecosystems. Nitrogen oxides in the air can significantly contribute to a number of environmental effects such as acid rain and eutrophication in coastal waters like the Chesapeake Bay (USA). Eutrophication occurs when a body of water suffers an increase in nutrients that leads to a reduction in the amount of oxygen in the water, producing an environment that is destructive to fish and other animal life.
Short-term exposure effects:
Available data from animal toxicology experiments indicate that acute exposure to NO2 concentrations of less than 1880 µg/m3 (1 ppm) rarely produce observable effects. Normal healthy humans, exposed at rest or with light exercise for less than two hours to concentrations above 4700 µg/m3 (2.5 ppm), experience pronounced decreases in pulmonary function; generally, normal subjects are not affected by concentrations less than 1880 µg/m3 (1.0 ppm).
One study showed that the lung function of subjects with chronic obstructive pulmonary disease is slightly affected by a 3.75-hour exposure to 560 µg/m3 (0.3 ppm). A wide range of findings in asthmatics has been reported. Asthmatics are likely to be the most sensitive subjects, although uncertainties exist in the health database. The lowest concentration causing effects on pulmonary function was reported from two laboratories that exposed mild asthmatics for 30-110 minutes to 565 µg/m3 (0.3 ppm) NO2 during intermittent exercise. However, neither of these laboratories was able to replicate these responses with a larger group of asthmatic subjects. One of these studies indicated that NO2 can increase airway reactivity to cold air in asthmatic subjects. At lower concentrations, the pulmonary function of asthmatics was not changed significantly.
NO2 increases bronchial reactivity, as measured by the response of normal and asthmatic subjects following exposure to pharmacological bronchoconstrictor agents, even at levels that do not affect pulmonary function directly in the absence of a bronchoconstrictor. Some, but not all, studies show increased responsiveness to bronchoconstrictors at NO2 levels as low as 376-565 µg/m3 (0.2 to 0.3 ppm); in other studies, higher levels had no such effect. Because the actual mechanisms of effect are not fully defined and NO2 studies with allergen challenges showed no effects at the lowest concentration tested (188 µg/m3; 0.1 ppm), full evaluation of the health consequences of the increased responsiveness to bronchoconstrictors is not yet possible. Recent studies have shown an increased reactivity to natural allergens in the same concentration range. The results of repetitive exposures of such individuals, or the impact of single exposures on more severe asthmatics, are not known.
