Formation, Impacts and Regional Transport

Tropospheric Ozone:

Formation, Impacts and Regional Transport

Introduction

Ozone is an oxidant present in both the stratospheric level and the tropospheric level of the earth=s atmosphere. It is produced by a photochemical reaction, meaning that the role of solar radiation is essential in driving the chemistry of its formation. Ozone in the stratosphere occurs naturally and is necessary for the protection of the earth from harmful ultraviolet solar radiation. However, the excessive amounts of ozone in the troposphere result primarily from pollution, mostly from anthropogenic sources, and can have harmful effects on human health and the environment and vegetation.

Tropospheric or ground-level air pollution, also known as smog, has been a problem for centuries with the burning of wood and, in the industrial era, coal. It originally was associated with high concentrations of sulfur dioxide and soot particles and was dubbed ALondon Smog@ because of a severe episode there in 1952. In the 1940=s a different kind of smog B photochemical smog B was discovered in the Los Angeles area. Tropospheric ozone is the primary component of photochemical smog. (Finlayson-Pitts and Pitts, 1997).

Ozone has historically been regarded as the principal urban and regional air quality problem in the United States (Meng, et. al., 1997), and studies to determine the extent of its harmful effects on both humans and on the environment have been ongoing for decades. Because of the health concerns, ozone has been regulated by the U.S. Environmental Protection Agency under the Clean Air Act since 1971. (CAA, Section 7511). However, ozone is not an emitted pollutant and is instead formed in the atmosphere from other pollutants. Therefore, its regulation has focused on controlling the emissions of its precursors that contribute to its synthesis.

Major sources of ozone precursors are coal-fired utilities, many of which are located in the Midwestern United States. Recently, disputes between regions over emerging evidence of the long-distance transport of ozone across states has prompted the EPA and state regulatory agencies to begin addressing the transport problem through cooperative efforts.

Formation of Ozone

The process by which ozone (O3) is created involves a series of complex photochemically initiated reactions in the atmosphere involving nitrogen oxides (NOx), reactive hydrocarbons, and oxygen (O2). Solar radiation wavelengths of at least 290 nm are required for inducing photochemical reactions. (Finlayson-Pitts, 1997). A simplified version of this process is described as follows:

First, a photochemical reaction occurs by which NO2 is disassociated to produce NO and atomic oxygen:

NO2 + hv (l + 420 nm)  NO + O

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The atomic oxygen reacts with atmospheric oxygen and with M, an energy-absorbing third body, to produce ozone:

O2 + O + M  O3 + M

Finally, NO reacts with O3 to regenerate NO2 and, in the process, ozone is consumed.

O3 + NO  NO2 + O2

Under normal conditions and in the absence of competing reactants in the atmosphere, this cycle would have no net effect. The ambient NO and NO2 concentrations would not change and O3 and NO would be formed and destroyed in equal quantities. However, this cycle is disrupted when hydrocarbons are present because they are highly reactive with the oxygen or ozone atoms produced. Hydrocarbons that react with O2 produce hydrocarbon free radicals (RO2), which can further react with NO2, O2, O3 and other hydrocarbons to form more photochemical pollutants. (Stoker and Seager, 1975).

The free radicals that affect ozone are those that react very rapidly with NO to produce NO2.

NO + RO2  NO2 + RO

When this occurs, the cycle becomes unbalanced because NO is converted into NO2 faster than NO2 is disassociated into NO and O. The major consequence of this reaction is that, with NO removed from the cycle, the normal mechanism for O3 removal has been eliminated and the concentration of O3 in the air increases. (Stoker and Seager, 1975).

Sources of Ozone Precursors

Examining the process of ozone formation demonstrates that the two major precursors of ozone are nitrogen oxides and hydrocarbons. Although NOx and hydrocarbons are emitted into the atmosphere from natural sources, the amounts causing air quality deterioration are produced by anthropogenic sources. NOx are emitted from stationary sources through the combustion of fossil fuels. Power plants account for most of those emissions, followed by other industries, and commercial and home heating sources. Hydrocarbon emissions, on the other hand, result primarily from industrial processing and the evaporation of solvents, such as those in paints, varnishes, lacquers, coatings and similar products. Nevertheless, the major anthropogenic source of both of these pollutants is the internal combustion engine used in automobiles and trucks. The EPA estimates that motor vehicles are responsible for 37% of the anthropogenic emissions of hydrocarbons and 49% of nitrogen oxides. (EPA,1997). Given these major sources of ozone precursors, it is not surprising that high ozone levels are most frequently experienced in urban and more populous areas where most industry and automobile traffic are located.

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Another component essential to the formation of ozone is heat energy from the sun. Because of this need, there are significant variations in ozone concentrations during the course of a day depending on the amount of sunlight. Ozone levels are generally lowest in the morning hours, accumulating through midday, and decreasing rapidly after sunset and the time of day. (Christiani, 1993). Below is a graph of a typical day in an urban area (in this case Los Angeles) showing more specifically the pattern of emissions of NOx and hydrocarbons and the formation of ozone related to the time of day and the presence of sunlight.

1. Before daylight, NO, NO2 and hydrocarbon levels remain fairly stable. As human activity increases, NO peaks at around 6:00 to7:00 a.m., largely due to the early morning rush hour automobile traffic.

1. Hydrocarbons follow a similar pattern as they are also emitted from the automobiles, but peak at a later time.
2. As the sun rises, NO2 levels increase as NO reacts with O3.
3. NO begins to decrease at around 7:00 a.m. as it reacts with free radicals produced by increasing hydrocarbons, producing more NO2.
4. NO2 photochemically disassociates, producing more O, and the O combines with O2 to create more O3.
5. As the NO decreases and consumes less O3, levels of O3 increase, peaking between 12:00 and 3:00 p.m.
6. As the solar intensity decreases, and automobile traffic increases at about 5:00 to 8:00 p.m. with the evening rush hour, the concentration of NO goes up, and begins to consume the O3 that has built up during the day.

This cycle then begins again the next day and repeats daily in a typical urban area. In many other areas of the country, this ozone pattern is also dependent on the seasons. In those areas, higher concentrations of ozone are most often observed in the summertime when the sunlight is most intense and temperatures are highest. (NESCAUM, 1997).

Impacts of Ozone on Public Health and the EPA Standards

Ozone is a lung irritant that affects the respiratory tract and can be especially harmful to sensitive populations, such as children and individuals with asthma. (Weisel, et. al., 1995). Scientific studies of the impacts on humans have revealed a causal relationship between ozone exposure and irritation of the airways leading to inflammation, increased permeability in lung tissue and the destruction of pulmonary cells, and decreased lung function. (Spengler, 1993). There has also been a relationship established between ozone levels and emergency room visits in the Northeast due to respiratory-related problems. (Weisel, et. al.,1995). Exercising individuals typically experience airway inflammation and hyperreactivity, decreased athletic performance, increased cough, altered tracheobronchial clearance and increased permeability of the lung lining, especially during extended exposures. (Leikauf, 1995). Evidence is emerging that ozone possibly impacts the immune system defenses, making people more susceptible to respiratory illnesses, including bronchitis and pneumonia. (Jakab, et. al., 1995).

The severity of the impacts seems to vary with the concentrations of ozone and the length of exposure, i.e. intermittent or continuous. Intermittent acute exposures to ambient ozone result in reversible changes in lung function and respiratory symptoms. Elevated levels of daily ozone (peak hour) are associated with restricted activity, asthma symptoms and respiratory admissions to hospitals. (Spengler, 1993).

There has recently been more concern about long-term exposures to ozone of a chronic low-level nature, which may result in permanent loss of lung function and an increase in associated disease. (Last, et. al. 1994). Also, mixtures of ozone and other pollutants, such as NO2, have caused pulmonary fibrosis and death in chronically exposed laboratory rats, demonstrating a response greater than that to either ozone or NO2 alone. (Last, et. al. 1994). Two time-series studies have associated changes in daily mortality with ozone and other pollutants in Los Angeles and New York City. (Spengler, 1993).

The Clean Air Act regulates certain harmful pollutants by requiring the EPA to impose National Ambient Air Quality Standards (or NAAQS) for those pollutants. Under the EPA must promulgate two sets of standards: a primary standard sufficient to protect human health with an adequate margin of safety, and a secondary standard to protect the environment, including plants, animals, ecosystems, and visibility.

Ozone is one of the six criteria pollutants regulated under the Clean Air Act. Until recently, both the primary and secondary ambient air quality standard for ozone was set at 0.12 parts per million (ppm) for one hour, not to be exceeded more than once per year. To determine whether the standard is being met, ground-level ozone concentrations are measured continuously by monitoring devices and hourly averages are calculated. Any areas in which average hourly ozone levels exceeded 0.12 ppm more that once per year are classified as Aozone nonattainment areas.@ In 1992, an estimated 140 million people lived in ozone nonattainment areas. (Koenig, 1995)

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Other countries have set various 1-hour ozone air quality standards or guidelines as well, many of which are below 0.12 ppm. Canada has set a standard of 0.082 ppm, Japan, 0.06 ppm, and the World Health Organization (WHO) for Europe, 0.075 - 0.10 ppm. (Weisel, et. al., 1995) Last year, on September 16, 1997, after a lengthy scientific review process, the EPA lowered the standard for ozone to 0.08 ppm and is replacing the 1-hour averages with a new 8-hour average to protect against longer exposure periods. The EPA also replaced the previous secondary standard with an identical standard to the primary standard.

Many environmentalists and public health advocates were pleased when the EPA lowered the standard for ozone last year. Nevertheless, others question whether the 0.08 ppm standard averaged over 8 hours is sufficient to protect the public health, especially that of children, asthmatics and individuals that exercise frequently outdoors. In determining the effectiveness of the EPA standards in protecting the public health, it is interesting to examine some of the studies conducted on the health impacts of ozone relative to the EPA standards. Many of these studies were performed before the EPA changed the standard and thus reference the 0.12 levels. However, because in many urban areas ozone levels continue to exceed even the 0.12 ppm, these impacts are still very significant.

Research on the Impacts of Ozone on Human Health

There is a complex set of variables involved in the research of ozone=s adverse health effects and different studies use different combinations of these variables. For example, adverse human health effects, such as pulmonary function, can be measured by forced vital capacity (FVC), the forced expiratory volume in the first second (FEV1), and/or peak expiratory flow rate (PEFR). Other testing methods can reveal more localized effects, such as tests on lavage fluid, a saline solution used to rinse the lungs and airways of subjects after exposure, or biopsies of tissue samples. Researchers can conduct epidemiological studies, in which symptoms are recorded in diaries and through follow-up examinations while subjects perform functions in the natural environment, or controlled studies conducted in laboratories. Lastly, different studies use alternative concentrations of ozone (estimated peak daily ozone levels, average 24-hour levels, or levels averaged over a shorter time period) and for varying lengths of exposure.

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Several clinical and epidemiological studies have documented significant decrements in pulmonary airflow in individuals exposed levels of ozone at or below the level of 0.12 ppm ozone. (Leikauf, et. al., 1995). For example, earlier this year, a two-year study was published by researchers at Brigham and Women=s Hospital and the Harvard School of Public Health which showed that ozone levels common to non-urban parts of the U.S. were associated with decreases in lung function in adult hikers in New Hampshire. The study evaluated the effects of ozone and other air pollutants on the lung function of 530 nonsmokers hiking on New Hampshire=s Mount Washington over the course of two summers. The hikers ranged from age 18 to 64 and hiked an average of eight hours a day. During this time they were exposed to ozone levels of 0.021 to 0.074 ppm per hour. The overall average exposure was 0.04 ppm. The researchers measured the hikers FEV and FVC before and after their hikes. They found that a 0.05 ppm increase in ozone concentration was associated with decreased lung function over the course of the hike: an average 2.6% decline in FEV and a 2.2% decline in FVC. More significantly, the researchers found that hikers with a history of asthma or wheezing had an even greater decline: their ozone related changes were approximately four times greater that the other subjects. (Korrick, et. al., 1998).

In general, ozone-associated changes in pulmonary function are greater in natural rather than in controlled exposure settings. Although it is hypothesized that synergism or interaction with other with other uncontrolled environmental factors play a role in this finding, the explanation for this discrepancy continues to be unknown. (Korrick, et. al., 1998). However, the significance of the findings of the New Hampshire study is the potential of negative health impacts of relatively low levels of air pollutants, not only among residents of urban and industrial regions, but also among individuals engaged in outdoor recreation in wilderness areas.

As demonstrated by the New Hampshire study, asthmatics have been shown to be more sensitive to ozone levels than Ahealthy@ individuals. Dr. Jane Koenig reviewed recent research of ozone exposure in asthmatics compared to non-asthmatics. (Koenig, 1995). In one study, conducted by Dr. Koenig herself, ten asthmatic and eight nonasthmatic subjects participated. All were exposed to clean air, air containing 0.12 ppm, and air containing 0.24 ppm ozone through a head dome exposure system for 90 minutes during intermittent or moderate exercise. After exposure, bronchial lavage tests revealed increased white blood cells from subjects with asthma immediately after exposure to 0.24 ppm ozone and then again 24 hours after the exposure, indicating an inflammatory response to ambient levels of ozone inhalation. There was also an increase in the epithelial cells in the lining of the lungs and airways immediately after the exposure. No similar changes were seen in the nonasthmatic subjects. The researchers concluded that asthmatic individuals are more susceptible to acute inflammatory effects produced by low levels of ozone than the nonasthmatic individuals. (Koenig, et. al, 1995).