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Sulfur Oxides: Sources, Exposures and Health Effects
Sulfur Oxides: Sources, Exposures and Health Effects X Pan, Peking University School of Public Health, Beijing, China & 2011 Elsevier B.V. All rights reserved.
Introduction Sulfur oxides are a group of air pollutants, which consist of both gaseous and particulate chemical species. There are generally four gas-phase compounds, namely, sulfur monoxide, sulfur dioxide, sulfur trioxide, and disulfur monoxide; but only sulfur dioxide (SO2) occurs at sufficient concentrations in ambient atmospheres to be of public health concern. The particulate phase sulfur oxides consist of acidic sulfates, including sulfuric acid (H2SO4) and its products of neutralization with atmospheric ammonia: letovicite [(NH4)3H(SO4)2], ammonium bisulfate (NH4HSO4), and ammonium sulfate [(NH4)2SO4]. Although most of the toxicological database for acidic sulfates focuses on sulfuric acid, which is the most acidic of the particulate sulfates, this species rarely occurs alone in ambient air, which generally contains some combination of the various sulfates. This chapter reviews the sources, health effects, and criteria of sulfur dioxide and sulfuric acid in ambient/outdoor air. SO2 is a colorless gas with a specific gravity 1.4337. It can be detected by taste by most people at concentrations in the range 1000–3000 mg m3 and has a pungent, irritating odor at higher concentrations, above 10 000 mg m3. It dissolves easily in water to form sulfurous acid (H2SO3), and then can be slowly oxidized to sulfuric acid by the oxygen from the air. In the presence of catalyzing impurities, such as manganese or iron salts, it is more rapidly converted. Sulfur dioxide can also react either catalytically or photochemically in the gas phase with other air pollutants to form sulfur trioxide, sulfuric acid, and sulfates, while these compounds comprise main parts of acid rain. However, as an important air pollutant, sulfur dioxide has always been a key parameter for the evaluation of the air quality all over the world. Sulfuric acid can be formed by rapidly hydrated sulfur trioxide (SO3), which is generally a highly reactive gas in the presence of moisture in ambient air. Therefore, it is sulfuric acid in the form of an aerosol that is found in the air rather than sulfur trioxide; and in general, it is associated with other pollutants in droplets or solid particles extending over a wide range of sizes. It can be emitted into the atmosphere directly, or may result from the various reactions with other compounds mentioned earlier and form the secondary pollutant in ambient air, which often is more irritating and hygroscopic than sulfur dioxide. Sulfuric acid may also be formed from the oxidation of hydrogen sulfide in ambient air. The acid is
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strongly hygroscopic, and droplets containing it readily take up further moisture from the air until they are in equilibrium with their surroundings. The sulfuric acid may react further with compounds in the air to produce other sulfates. Some sulfate enters the air directly from the combustion sources or industrial emissions. However, magnesium sulfate is present in the aerosol generated from ocean spray nearby oceans. A wide range of sulfur compounds is represented in the complex mixture of urban air pollutants; however, considering from a practical point of view, only the gas sulfur dioxide, sulfuric acid and sulfates as main components of sulfur oxides need to be considered and also absorbed on the suspended particulate matter (PM). In many developed countries, air pollution by SO2 has been controlled to relatively lower levels; however, there is an increasing trend of SO2 emission into the ambient air in the developing countries, along with the fast development of the local economy.
Sources of Sulfur Oxides Sulfur is very prevalent in all raw materials, including crude oil, coal, and ore that contains common metals such as aluminum, copper, zinc, lead, and iron. Compounds of sulfur are found in small quantities in ambient air, even in the areas far from sources of air pollution. In the gas phase, they are present as hydrogen sulfide or sulfur dioxide, and in particulate form they may be present as sulfate. Sulfur dioxide and hydrogen sulfide may also be emitted directly by volcanoes or sea spray; however, most emissions of sulfur into the air are in the form of sulfur dioxide resulting from the combustion of fossil fuel for heating and energy production. Various industrial activities such as petroleum processing, smelter operations, and wood pulping also produce significant emissions of sulfur dioxide and other sulfur compounds. Sulfur oxides gases are formed when fuel-containing sulfur, such as coal and oil, is burned, and when gasoline is extracted from oil or metals are extracted from ore. SO2 dissolves in water vapor to form acid, and interacts with other gases and particles in the air to form sulfates and other products that can be harmful to people and their environment. US Environmental Protection Agency (USEPA) reports that more than 65% of SO2 released into the air, or more than 13 million tons per year, comes from electric utilities, especially those that burn coal. Other sources of
Sulfur Oxides: Sources, Exposures and Health Effects
SO2 are industrial facilities that derive their products from raw materials such as metallic ore, coal, and crude oil, or that burn coal or oil to produce process heat. Examples are petroleum refineries, cement manufacturing, and metal-processing facilities. Also, locomotives, large ships, and some nonroad diesel equipment currently burn high sulfur fuel and release SO2 into the air in large quantities. In urban areas, most of the sulfur dioxide in the air comes from the combustion of fuels, but many factors, including the type of fuel (the content of sulfur), the combustion efficiency, and the flue velocity, influence the quantity and quality of emissions. In cold and temperate parts of the world, the burning of coal for domestic heating purposes has been a major contributor to the concentration of sulfur dioxide in urban air. This is particularly true of China in a situation where approximately 70% of the energy demands have to come from coal at present and near future. Such sources are liable to have a disproportionate effect on concentrations in the immediate vicinity, because of the low levels of the chimneys and the low emission velocity. Even in warmer climates, domestic sources may be of importance, particularly if coal is used for cooking purposes. The emission of sulfur dioxide into the air from motor vehicles is generally much smaller compared with those from domestic and industrial pollution sources; however, it is close to the ground and within the breathing zone and hence may have more health impacts on the exposed population, which often depend on the proximity to the traffic. Source strength may vary with time of day, day of week, and season of the year. The relevant meteorological conditions are important factors in determining the
ultimate ambient concentrations of sulfur dioxide arising from sources. Where heating is required during the winter season, emissions of sulfur dioxide is usually much higher than that in the summer. For the source control of sulfur oxides, the more effective means of reducing emissions is to change to fuels with lower sulfur content. The level of sulfur oxides in ambient air depends very much on the ability of wind and turbulence to disperse the pollutants rapidly. When these processes fail, the results can be disastrous, as they were in London in 1952. However, there are some factors affecting the dispersion of sulfur dioxide as it is emitted from combustion sources, for example, temperature and efflux velocity of the gases, stack height, topography and the proximity to other buildings, and local meteorological factors. It has been estimated that about one-fourth of the sulfur dioxide emitted into the air is kept on various surfaces, including soil, water, grass, and vegetation in general. The remainder is transformed into sulfuric acid or sulfates by various processes in the presence of moisture, and is then mainly produced as acid rain. The ‘acid rain’ is considered to be a secondary ambient pollutant, which is more harmful to human health. It is a relatively popular environmental problem in developing world, for example, in China (Figure 1). Some reports think emissions are primarily in the form of sulfur dioxide in cities close to sources, whereas in rural areas, concentrations of sulfates may be similar to those of sulfur dioxide in the ambient environment. The overall conversion of sulfur dioxide to sulfate is an extremely complex process with many interrelated variables, which include the absorption rate of sulfur
Ratio to national Acid rain occurrence land area <5%
67.4%
5%−10%
6.8% 10.4%
10−25% 25−50% 50−75% >75%
8.2% 5.4% 1.8%
No data
Figure 1
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Nationwide distribution of acid rain incidence in China 2006 (acid rain means the rain with pH value less than 5.6).
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dioxide, the sizes of the particles or droplets involved, their chemical composition, the rate of diffusion of reactants within the aerosol, and the relative humidity. Generally, the half-life of sulfur dioxide in ambient air is estimated to be 3–5 h, if it has not been transformed into sulfuric acid or sulfates.
Occurrence in Ambient/Outdoor Air As a result of changes in sources and emission control on vehicle, power plants, and industry, annual mean levels of sulfur dioxide in the major cities of Europe, the United States, and also in some developing countries have fallen in the past two decades and are now generally less than 100 mg m3. Daily mean concentrations have also fallen and are now generally less than 100 mg m3 in developed countries. Peak concentrations over shorter averaging periods may still be high, both in cities with a high use of coal for domestic heating and when plumes of effluent from power station chimneys fall to the ground. Transient peak concentrations could reach at several thousand micrograms per cubic meters. Concentrations of sulfur dioxide in recent years in Asia vary from approximately 200 mg m3 in some Chinese cities to less than 20 mg m3 in others, such as Taipei and Hong Kong. It varies greatly among different developing countries. These data of sulfur oxides are generally based on international and local monitoring network, which are largely concentrated in the urban areas, especially in developing countries, where there is no ambient monitoring network in most of the rural areas. There is no good enough information to date for the situations of ambient sulfur oxides pollution in large part of rural areas of the developing countries. In fact, the concentrations of sulfur oxides in ambient air depend not only on emission from the sources, but also on the local meteorological and other related factors.
Routes of Exposure and Conversion Factors Inhalation is the only route of exposure to sulfur dioxide that is of interest with regard to its effects on health. 1 ppm ð201 C; 1013 hPaÞ ¼ 2660 mg m 3
1 mg m 3 ¼ 0:375 9 ppm
Health Effects of Sulfur Oxides Toxicology Sulfur dioxide is a respiratory irritant that is highly soluble in the aqueous surfaces of the respiratory airways. Because of this high solubility, most of the sulfur dioxide is absorbed in the nose and upper airways and very little reaches the lungs directly. Inhalation of high ambient concentrations of sulfur dioxide can cause stimulation of the nerves in the air passages, resulting in a reflex cough, irritation, and chest tightness. Absorption of sulfur dioxide is concentration-dependent, with 85% absorption in the nose at 4–6 mg m3. With the common ambient concentrations of sulfur dioxide, absorption in the upper airways may be inefficient. Increased flow rates reduce the percentage of inspired sulfur dioxide absorbed in the nose and upper airways, and thus exercise promotes delivery to the smaller airways. At extremely high concentrations, the death or pathological changes including laryngotracheal and pulmonary edema can be induced in the respiratory tract of experimental animals. The gas is quite corrosive and can also cause damage to buildings and other materials. Exposure–effect curves have been developed for experimental animals in the 1970s. The study showed that the increases in pulmonary flow resistance in guinea pigs were positively associated with the exposure to sulfur dioxide concentrations ranging from 20 to 660 mg m3 for a 15–20 min period. Studies with guinea pigs at lower concentrations have shown that a sodium chloride aerosol administered concomitantly enhances the effects of sulfur dioxide on the lungs in the form of bronchoconstriction and increased airway resistance. It was known that the sodium chloride could deliver the absorbed sulfur dioxide deep into the lungs as a carrier, and the increased humidity in the respiratory tract could react with the sulfur dioxide to form sulfurous acid, especially if catalysts were present. Sulfuric acid mist and some of the sulfate salts are more powerful respiratory irritants than sulfur dioxide, and this effect is also related to particle size (smaller particles tending to be more irritating). Sulfuric acid mist with a mass median diameter (MMD) of 2 mm was more toxic to animals. Some of the nonreactive compounds, such as manganese salts or oxides, can catalyze the reaction of sulfur dioxide to sulfuric acid. In short-term exposure studies, concentration seemed to be more important than duration and death was related to laryngospasm and bronchospasm. Sulfuric acid mist also caused lung damage that seemed to be related to the total dose. The animal studies showed that long-term exposure of sulfur dioxide to rats could cause interstitial pneumonia, bronchitis, tracheitis, and peribronchitis and increased activity of serum cholinesterase. Some studies in China recently reported that SO2 exposure can reduce the levels of glutathione (GSH) and
Sulfur Oxides: Sources, Exposures and Health Effects
the activities of Cu, Zn-superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) in the body of experimental animals, which suggest that SO2 exposure can cause oxidative damage to lungs, heart, brain, liver, as well as testicles of the body; and this effect of SO2 shows a gender difference in oxidative stress and antioxidation status. A lot of toxicology evidences indicate that SO2 and its derivatives may cause toxicological damage to multiple organs of animals, and some of them are even more severe than damages in lungs. Therefore, SO2 is a systemic toxin. Peroxidation stress, which was caused by a lot of free radicals produced during the period of the sulfite and bisulfite oxidation, may be the main toxicological mechanism of it. However, many studies reported that SO2 pollution even at lower concentrations also had a potential risk to the genetic material deoxyribonucleic acid (DNA) of the cells in mammalian animals. SO2 exposure could also change the expression of apoptosis-related genes, and induce apoptosis in liver of rat and may have relations with some apoptosis-related diseases. The inhalation of SO2 could increase the gene expressions of messenger ribonucleic acid (mRNA) on the transcription and translation levels in human bronchial epithelial (BEP2D) cells, and result in mucus overproduction and inflammation responses, and decrease the activities and mRNA levels of P-450 in livers and lungs of rats. SO2 exposure maybe a risk factor in human genetic toxicology. Sulfur oxides also have cooperated effects on the health with other ambient pollutants, e.g., ozone, nitrogen oxides, and especially for particulate matter. Many studies showed that SO2 could be absorbed on the surface of air particles and be inhaled to lower respiratory tract together with the particles damaging the body. It is not clear for the mechanism of combined exposure to sulfur dioxide and PM or other gaseous pollutants.
Epidemiology A lot of epidemiological studies have proved that sulfur oxides can have significant effects on the human respiratory system. In addition, sulfur dioxide can also cause narrowing of the air passages, particularly in people suffering from asthma and chronic lung disease. These people frequently have narrowed airways, and any further restriction will have a disproportionately large effect, compared to people with uncompromised respiratory systems. The main focus of the air pollution epidemiological studies in the past decade has been on the health effects of PM. However, a lot of studies have also examined sulfur dioxide and other gaseous pollutants as potential confounders of the effects of PM. Thus, during the past decade a large number of risk estimates for sulfur dioxide
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have accumulated, providing a more comprehensive assessment of relative importance of the classical air pollutants. Although these researches have neither resolved the issue of confounding between sulfur dioxide and PM or other pollutants, nor have they systematically examined the synergistic effects, the accumulating risk estimates are still useful in assessing the potential adverse health impacts of sulfur dioxide. Effects of Short-Term Exposures The most clear effects on population mortality due to exposure to sulfur oxides have been the sudden increases of daily death count during episodes of high ambient pollution. The most notable example occurred in London in 1952. The ‘London Smog’ episode lasted for 5 days and it was estimated that the number of extra deaths during and immediately after this period was approximately 4000 more than expected under normal circumstances. The high-risk subpopulation was mainly the people suffering from heart or lung disease or both, and the elderly. The daily deaths were about three times more than expected at that time of the year. Concentrations of sulfur dioxide as high as 3.7 mg m3 (1.3 ppm) were recorded in the center of the urban area. Concentrations of PM were too great to be measured properly. Early studies, mostly in European countries and the United States, in the 1970s suggested that daily mortality was positively associated with the ambient concentration of sulfur dioxide. When sulfur dioxide concentration increased by 70–700 mg m3, there was likely to be a significant increase in total population mortality. However, these results were often interfered by other confounding factors, for example, PM, nitrogen dioxide, and meteorological factors (temperature and humidity). Maybe the effects of sulfur dioxide were overestimated. An earlier study reported that after controlled for season, day of week, and temperature, there was a marked reduction in the average level of sulfur dioxide from 510 to 170 mg m3 but virtually no change in smoke shade. Their observations indicated that, despite this reduction in sulfur dioxide, there had been no reduction in the adverse health effects. Analysis indicated that the adverse health effects were associated principally (80%) with the PM and only to a small extent (20%) with sulfur dioxide. The authors also pointed out that, the effects attributable to sulfur dioxide increased threefold when they estimated mortality on temperature and sulfur dioxide alone by regression analysis. In recent years, many studies reported that excess risk of cause-specific mortality of ischemic heart disease and respiratory diseases related to increased level of ambient SO2. Increase in ambient SO2 was closely associated with increased mortality, notably after adjustment for the concentration of PM10 and CO. A Chinese study of
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61 000 deaths found that higher air levels of PM10, SO2, and NO2 corresponded to significantly higher death rates. However, one study with time series analysis in Beijing reported that the reduction of daily ambient SO2 level will accompany with the decreased cause-specific daily mortality of cardiovascular and respiratory diseases of the exposed population in urban area of Beijing. During the past 30 years many epidemiological evidences showed that the level of daily ambient SO2 was positively associated with an increased risk of hospital admissions, emergency room visits, and hospital outpatient visits for respiratory diseases, ischemic heart disease or myocardial infarction, and other diseases of the exposed population. The results indicated that irritative symptoms increased significantly when sulfur dioxide levels exceeded 310 mg m3. Symptoms such as nose and throat irritation, followed by bronchoconstriction and dyspnea, especially in asthmatic individuals, are usually experienced after exposure to increased levels of sulfur dioxide. The studies demonstrated a significant risk that particularly affected children and patients aged 65 and more. Peak levels of SO2 in the air can cause temporary breathing difficulty for people with asthma who are active outdoors. Recent studies on daily mortality rates and hospital admissions for cardiac disease in Hong Kong, Canada, and London suggested that health effects of the exposed population were significantly associated with 24-h SO2 concentrations down to only 5 mg m3 (the highest mean SO2 level was less than 10 mg m3). The increased level of ambient SO2 could affect significantly the lung functions of the exposed schoolchildren. The studies showed that the schoolchildren living in higher level of ambient SO2 had lower level of the forced vital capacity (FVC), FEV1.0, and peak expiratory flow rate (PEFR) than that of the control area and it suggested that development of pulmonary functions of these children were depressed by ambient SO2. Asthmatic subject is a sensitive subgroup for SO2 exposure; generally, the high level and acute changes of SO2 could significantly reduce the PEFR level and increase the number of asthma attacks in them. Earlier study showed that when sulfur dioxide concentrations exceeded 200 mg m3 or the temperature was lower than 0 1C, there was a significant increase in the frequency of asthmatic attacks. Levels of sulfates exceeding 20 mg m3 and nitrate levels exceeding 2 mg m3 did not result in such an effect. It was reported that higher daily levels of SO2 have been linked to significantly increased influenza admissions. SO2 reacts with other chemicals in the air to form tiny sulfate particles. When these are breathed, they gather in the lungs and are associated with increased respiratory symptoms and disease, difficulty in breathing, and premature death.
Effects of Long-Term Exposures Earlier studies on the chronic effects of air pollutants relied on cross-sectional comparisons that could be subject to ecological confounding. Recent studies often involve investigations of large cohorts for which detailed individual-level information is collected to adjust for confounding. Generally, long-term exposures to high levels of SO2 gas cause respiratory illness and aggravate existing heart disease. In the past 30 years, ambient levels of sulfur oxides are declining in many US and western European cities; thanks to emission controls on vehicles, heating, power generation, and industry. However, the health problems caused by long-term exposure to sulfur oxides still exist in the developed world. With the fast development of domestic economy and large demand of energy consumption, outdoor sulfur oxides pollution problems remain in developing world, especially in some large cities such as Beijing, Shanghai, Bombay, Karachi, Cairo, Sao Paulo, and Mexico City. Most studies of the health effects of ambient/outdoor SO2 pollution have dealt with respiratory health issues. Many of the studies have involved children and most of these studies have reported higher rates of asthma and other respiratory problems. SO2 can worsen childhood asthma at relatively modest concentrations, which are well below USEPA standards and WHO guideline. Both a French study and a Chinese study found that increasing levels of outdoor SO2 were associated with significantly higher rates of childhood asthma and allergic rhinitis. Low to moderate levels of outdoor SO2 can greatly increase respiratory problems in the elderly. Some studies showed that higher outdoor level of SO2 was associated with significantly higher rates of hospital admissions for chronic obstructive pulmonary disease (COPD). An Australian study found that higher airborne levels of SO2 were associated with significantly higher rates of childhood hospital admissions for pneumonia and acute bronchitis. Higher outdoor SO2 levels were associated with significantly higher childhood emergency room visits for pneumonia and respiratory illness in China. Lung function changes have generally been assessed using measurements of ventilatory capacity such as FEV0.75, FEV1, FVC, and peak expiratory flow (PEF). Lower levels of FEV1.0 and PEFR among the exposed population were also observed in the areas of higher SO2 residents, but it is difficult to separate the independent effects of sulfur dioxide. It was recently found that higher outdoor air levels of SO2 were also associated with significantly higher rates of preterm birth, low birth weight, and ventral septal defects of the baby. The possibility that ambient is a causal factor in cancer of the lung has given rise to considerable concern for a long time, but until now there is not enough
Sulfur Oxides: Sources, Exposures and Health Effects
epidemiological evidence that SO2 is a direct risk factor of cancer, even if some in vitro tests in the laboratory showed some positive results about it. Few studies recently reported that it seems the ambient SO2 pollution was associated with the mortality of lung cancer; however, most reports thought SO2 to be a cancer-promoting factor, rather than cancer-inducing. This issue should be of continuous concern to a researcher.
Other Impacts of Sulfur Oxides Reduction of Ambient Visibility SO2 and its derivatives could decrease the visibility of outdoor air. SO2 and sulfuric acid mist can form haze, which occurs when light is scattered or absorbed by particles and gases in the air. Sulfate particles are the major cause of reduced visibility in many parts of the world. Acid Rain SO2 and nitrogen oxides react with other substances in the air to form acids, which fall on earth as rain, fog, snow, or dry particles. The rain with pH value less than 5.6 is called ‘acid rain,’ and is generally caused by relatively higher levels of nitrogen oxides and their acidic derivatives in the air. Acid rain is formed near areas that have high SO2 air pollution, and sometimes may be carried by the wind for hundreds of miles. Acid rain accelerates the decay of building materials and paints, including irreplaceable monuments, statues, and sculptures, which constitute important part of the world’s cultural heritage. Plant and Soil Damage Acid rain reduces the pH value of soil and changes chemical component of soil, damages forests, and decreases the output of crops. Acid rain makes lakes and
Table 1
streams acidic and unsuitable for fish. Long and continued exposure changes the natural variety of plants and animals in an ecosystem. Air Quality Standard (Guideline) of Sulfur Oxides in Ambient Air Clean air is considered to be a basic requirement of human health and well-being. However, air pollution continues to pose a significant threat to health worldwide. WHO estimates the burden of disease due to air pollution; more than 2 million premature deaths every year can be attributed to the effects of urban outdoor and indoor air pollution (caused by the burning of solid fuels). More than half of this disease burden is borne by the populations of developing countries, where sulfur oxides are still one of the important ambient air pollutants. For offering guidance in reducing the health impacts of air pollution, WHO air quality guideline (AQG) was created in 1987 and updated in 1997; these guidelines are based on expert evaluation of current scientific evidence. To inform policymakers and to provide appropriate targets for a broad range of policy options for air quality management in different parts of the world, WHO has undertaken to review the accumulated new scientific evidence and to consider its implications for its AQGs, especially including important new research from lowand middle-income countries where air pollution levels are at their highest; WHO updated a new one in the form of revised guideline values for selected air pollutants (including SO2), which is applicable across all WHO regions in 2005 (Table 1). We can see in Table 1 that the interim targets are given for the 24-h SO2 guideline values in WHO AQG. These are proposed as incremental steps in a progressive reduction of air pollution and are intended for use in areas where pollution is high. These targets aim to promote a shift from high air pollutant concentrations, which have acute and serious health consequences, to lower air pollutant
WHO Air Quality Guideline (2005): WHO air quality guidelines and interim targets for SO2 (24-h and 10-min concentrations)
Interim target-1 (IT-1)a Interim target-2 (IT-2)
Air quality guideline (AQG) a
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24-h average (mg m3)
10-min average (mg m3)
125 50
– –
20
Formerly the WHO Air Quality Guideline (WHO, 2000).
500
Basis for selected level
Intermediate goal based on controlling either motor vehicle emissions, industrial emissions, or emissions from power production. This would be a reasonable and feasible goal for some developing countries (it could be achieved within a few years), which would lead to significant health improvements that, in turn, would justify further improvements (such as, aiming for the AQG value)
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concentrations. If these targets were to be achieved, one could expect significant reductions in risks for chronic health effects arising from ambient SO2 pollution. Some controlled studies for exercising asthmatics show that a proportion experience changes in pulmonary function and respiratory symptoms after periods of exposure to SO2 as short as 10 min. Thus, WHO recommends that a SO2 concentration of 500 mg m3 should not be exceeded over averaging periods of minute duration for short-term exposure. But attention must be paid to the 10 min time to measure in AQG, while the relevant criteria/guideline are for 30 or 60 min time to measure in some countries, where the value is just for reference. However, because short-term SO2 exposure depends very much on the nature of local sources and the prevailing meteorological conditions, it is not possible to apply a simple factor to this value to estimate corresponding guideline values over longer time periods, such as 1 h. The latest evidence to emerge includes a study conducted in Hong Kong, the United States, and Canada, where they found that the reduction in the sulfur content of fuels could be achieved over a very short period of time, and if there was a threshold for health effects of ambient SO2, it would have to be very low. There is still considerable uncertainty as to whether SO2 is the pollutant responsible for the observed adverse effects or whether it is a surrogate for ultrafine particles or some other correlated substance. Since the revised 24-h guideline may be quite difficult for some countries to achieve in the short term, a stepped approach using interim goals is recommended. For instance, a country could move toward compliance with the guideline by controlling emissions from one major source at a time, selecting from among motor vehicle sources, industrial sources, and power sources (which would achieve the greatest effect on SO2 levels for the lowest cost), and follow this up with monitoring of public health and SO2 levels for health effect gains. Demonstrating health benefits should provide an
incentive to mandate controls for the next major source category.
Further Reading Akimoto H (2003) Global air quality and pollution. Science 302: 1716--1719. Barnett AG, Williams GM, Schwartz J, et al. (2005) Air pollution and child respiratory health: A case-crossover study in Australia and New Zealand. American Journal of Respiratory and Critical Care Medicine 171: 1272--1278. Burnett RT, Stieb D, Brook JR, et al. (2004) Associations between short-term changes in nitrogen dioxide and mortality in Canadian cities. Archives of Environmental Health 59: 228--236. Chen Y, Yang Q, Krewski D, et al. (2004) Influence of relatively low level particulate air pollution and hospitalization for COPD in elderly people. Inhalation Toxicology 16: 21--25. Curtis L, Re W, Smith-Willis P, Fenyves E, and Pan Y (2006) Adverse health effects of outdoor air pollutants. Environment International 32: 815--830. Dockery DW, Pope CA 3rd, Xu X, et al. (1993) An association between air pollution and mortality in six US cities. New England Journal of Medicine 329: 1753--1759. Gilboa SM, Mendola P, Olshan AP, et al. (2005) Relation between ambient air quality and selected birth defects, Seven County Study, Texas, 1997–2000. American Journal of Epidemiology 162: 236--252. Kampa M and Castanas E (2008) Human health effects of air pollution. Environmental Pollution 151: 362--367. Lee JT, Kim H, Song H, et al. (2002) Air pollution and asthma among children in Seoul, South Korea. Epidemiology 13: 481--484. Li R, Meng Z, and Xie J (2007) Effects of sulfur dioxide derivatives on four asthma-related gene expressions in human bronchial epithelial cells. Toxicology Letters 175: 71--81. Pan X, Yue W, He K, and Tong S (2007) Health benefit evaluation of the energy use scenarios in Beijing, China. Science of the Total Environment 374: 242--251. Pope CA 3rd, Burnett RT, Thurston GD, et al. (2004) Cardiovascular mortality and long-term exposure to particulate air pollution: Epidemiological evidence of general pathophysiological pathways of disease. Circulation 109: 71--77. Qin G and Meng Z (2005) Effect of sulfur dioxide inhalation on CYP1A1 and CYP1A2 in rat liver and lung. Toxicology Letters 160: 34--42. US Environmental Protection Agency (EPA) (2000) America’s Children and the Environment. Publication EPA 240-R-00-006. Washington, DC: USEPA. Wong CM, Wong CM, Lam TH, et al. (1998) Comparison between two districts of the effects of an air pollution intervention on bronchial responsiveness in primary school children in Hong Kong. Journal of Epidemiology and Community Health 52: 571--578.
Introduction Sulfur oxides are a group of air pollutants, which consist of both gaseous and particulate chemical species. There are generally four gas-phase compounds, namely, sulfur monoxide, sulfur dioxide, sulfur trioxide, and disulfur monoxide; but only sulfur dioxide (SO2) occurs at sufficient concentrations in ambient atmospheres to be of public health concern. The particulate phase sulfur oxides consist of acidic sulfates, including sulfuric acid (H2SO4) and its products of neutralization with atmospheric ammonia: letovicite [(NH4)3H(SO4)2], ammonium bisulfate (NH4HSO4), and ammonium sulfate [(NH4)2SO4]. Although most of the toxicological database for acidic sulfates focuses on sulfuric acid, which is the most acidic of the particulate sulfates, this species rarely occurs alone in ambient air, which generally contains some combination of the various sulfates. This chapter reviews the sources, health effects, and criteria of sulfur dioxide and sulfuric acid in ambient/outdoor air. SO2 is a colorless gas with a specific gravity 1.4337. It can be detected by taste by most people at concentrations in the range 1000–3000 mg m3 and has a pungent, irritating odor at higher concentrations, above 10 000 mg m3. It dissolves easily in water to form sulfurous acid (H2SO3), and then can be slowly oxidized to sulfuric acid by the oxygen from the air. In the presence of catalyzing impurities, such as manganese or iron salts, it is more rapidly converted. Sulfur dioxide can also react either catalytically or photochemically in the gas phase with other air pollutants to form sulfur trioxide, sulfuric acid, and sulfates, while these compounds comprise main parts of acid rain. However, as an important air pollutant, sulfur dioxide has always been a key parameter for the evaluation of the air quality all over the world. Sulfuric acid can be formed by rapidly hydrated sulfur trioxide (SO3), which is generally a highly reactive gas in the presence of moisture in ambient air. Therefore, it is sulfuric acid in the form of an aerosol that is found in the air rather than sulfur trioxide; and in general, it is associated with other pollutants in droplets or solid particles extending over a wide range of sizes. It can be emitted into the atmosphere directly, or may result from the various reactions with other compounds mentioned earlier and form the secondary pollutant in ambient air, which often is more irritating and hygroscopic than sulfur dioxide. Sulfuric acid may also be formed from the oxidation of hydrogen sulfide in ambient air. The acid is
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strongly hygroscopic, and droplets containing it readily take up further moisture from the air until they are in equilibrium with their surroundings. The sulfuric acid may react further with compounds in the air to produce other sulfates. Some sulfate enters the air directly from the combustion sources or industrial emissions. However, magnesium sulfate is present in the aerosol generated from ocean spray nearby oceans. A wide range of sulfur compounds is represented in the complex mixture of urban air pollutants; however, considering from a practical point of view, only the gas sulfur dioxide, sulfuric acid and sulfates as main components of sulfur oxides need to be considered and also absorbed on the suspended particulate matter (PM). In many developed countries, air pollution by SO2 has been controlled to relatively lower levels; however, there is an increasing trend of SO2 emission into the ambient air in the developing countries, along with the fast development of the local economy.
Sources of Sulfur Oxides Sulfur is very prevalent in all raw materials, including crude oil, coal, and ore that contains common metals such as aluminum, copper, zinc, lead, and iron. Compounds of sulfur are found in small quantities in ambient air, even in the areas far from sources of air pollution. In the gas phase, they are present as hydrogen sulfide or sulfur dioxide, and in particulate form they may be present as sulfate. Sulfur dioxide and hydrogen sulfide may also be emitted directly by volcanoes or sea spray; however, most emissions of sulfur into the air are in the form of sulfur dioxide resulting from the combustion of fossil fuel for heating and energy production. Various industrial activities such as petroleum processing, smelter operations, and wood pulping also produce significant emissions of sulfur dioxide and other sulfur compounds. Sulfur oxides gases are formed when fuel-containing sulfur, such as coal and oil, is burned, and when gasoline is extracted from oil or metals are extracted from ore. SO2 dissolves in water vapor to form acid, and interacts with other gases and particles in the air to form sulfates and other products that can be harmful to people and their environment. US Environmental Protection Agency (USEPA) reports that more than 65% of SO2 released into the air, or more than 13 million tons per year, comes from electric utilities, especially those that burn coal. Other sources of
Sulfur Oxides: Sources, Exposures and Health Effects
SO2 are industrial facilities that derive their products from raw materials such as metallic ore, coal, and crude oil, or that burn coal or oil to produce process heat. Examples are petroleum refineries, cement manufacturing, and metal-processing facilities. Also, locomotives, large ships, and some nonroad diesel equipment currently burn high sulfur fuel and release SO2 into the air in large quantities. In urban areas, most of the sulfur dioxide in the air comes from the combustion of fuels, but many factors, including the type of fuel (the content of sulfur), the combustion efficiency, and the flue velocity, influence the quantity and quality of emissions. In cold and temperate parts of the world, the burning of coal for domestic heating purposes has been a major contributor to the concentration of sulfur dioxide in urban air. This is particularly true of China in a situation where approximately 70% of the energy demands have to come from coal at present and near future. Such sources are liable to have a disproportionate effect on concentrations in the immediate vicinity, because of the low levels of the chimneys and the low emission velocity. Even in warmer climates, domestic sources may be of importance, particularly if coal is used for cooking purposes. The emission of sulfur dioxide into the air from motor vehicles is generally much smaller compared with those from domestic and industrial pollution sources; however, it is close to the ground and within the breathing zone and hence may have more health impacts on the exposed population, which often depend on the proximity to the traffic. Source strength may vary with time of day, day of week, and season of the year. The relevant meteorological conditions are important factors in determining the
ultimate ambient concentrations of sulfur dioxide arising from sources. Where heating is required during the winter season, emissions of sulfur dioxide is usually much higher than that in the summer. For the source control of sulfur oxides, the more effective means of reducing emissions is to change to fuels with lower sulfur content. The level of sulfur oxides in ambient air depends very much on the ability of wind and turbulence to disperse the pollutants rapidly. When these processes fail, the results can be disastrous, as they were in London in 1952. However, there are some factors affecting the dispersion of sulfur dioxide as it is emitted from combustion sources, for example, temperature and efflux velocity of the gases, stack height, topography and the proximity to other buildings, and local meteorological factors. It has been estimated that about one-fourth of the sulfur dioxide emitted into the air is kept on various surfaces, including soil, water, grass, and vegetation in general. The remainder is transformed into sulfuric acid or sulfates by various processes in the presence of moisture, and is then mainly produced as acid rain. The ‘acid rain’ is considered to be a secondary ambient pollutant, which is more harmful to human health. It is a relatively popular environmental problem in developing world, for example, in China (Figure 1). Some reports think emissions are primarily in the form of sulfur dioxide in cities close to sources, whereas in rural areas, concentrations of sulfates may be similar to those of sulfur dioxide in the ambient environment. The overall conversion of sulfur dioxide to sulfate is an extremely complex process with many interrelated variables, which include the absorption rate of sulfur
Ratio to national Acid rain occurrence land area <5%
67.4%
5%−10%
6.8% 10.4%
10−25% 25−50% 50−75% >75%
8.2% 5.4% 1.8%
No data
Figure 1
291
Nationwide distribution of acid rain incidence in China 2006 (acid rain means the rain with pH value less than 5.6).
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dioxide, the sizes of the particles or droplets involved, their chemical composition, the rate of diffusion of reactants within the aerosol, and the relative humidity. Generally, the half-life of sulfur dioxide in ambient air is estimated to be 3–5 h, if it has not been transformed into sulfuric acid or sulfates.
Occurrence in Ambient/Outdoor Air As a result of changes in sources and emission control on vehicle, power plants, and industry, annual mean levels of sulfur dioxide in the major cities of Europe, the United States, and also in some developing countries have fallen in the past two decades and are now generally less than 100 mg m3. Daily mean concentrations have also fallen and are now generally less than 100 mg m3 in developed countries. Peak concentrations over shorter averaging periods may still be high, both in cities with a high use of coal for domestic heating and when plumes of effluent from power station chimneys fall to the ground. Transient peak concentrations could reach at several thousand micrograms per cubic meters. Concentrations of sulfur dioxide in recent years in Asia vary from approximately 200 mg m3 in some Chinese cities to less than 20 mg m3 in others, such as Taipei and Hong Kong. It varies greatly among different developing countries. These data of sulfur oxides are generally based on international and local monitoring network, which are largely concentrated in the urban areas, especially in developing countries, where there is no ambient monitoring network in most of the rural areas. There is no good enough information to date for the situations of ambient sulfur oxides pollution in large part of rural areas of the developing countries. In fact, the concentrations of sulfur oxides in ambient air depend not only on emission from the sources, but also on the local meteorological and other related factors.
Routes of Exposure and Conversion Factors Inhalation is the only route of exposure to sulfur dioxide that is of interest with regard to its effects on health. 1 ppm ð201 C; 1013 hPaÞ ¼ 2660 mg m 3
1 mg m 3 ¼ 0:375 9 ppm
Health Effects of Sulfur Oxides Toxicology Sulfur dioxide is a respiratory irritant that is highly soluble in the aqueous surfaces of the respiratory airways. Because of this high solubility, most of the sulfur dioxide is absorbed in the nose and upper airways and very little reaches the lungs directly. Inhalation of high ambient concentrations of sulfur dioxide can cause stimulation of the nerves in the air passages, resulting in a reflex cough, irritation, and chest tightness. Absorption of sulfur dioxide is concentration-dependent, with 85% absorption in the nose at 4–6 mg m3. With the common ambient concentrations of sulfur dioxide, absorption in the upper airways may be inefficient. Increased flow rates reduce the percentage of inspired sulfur dioxide absorbed in the nose and upper airways, and thus exercise promotes delivery to the smaller airways. At extremely high concentrations, the death or pathological changes including laryngotracheal and pulmonary edema can be induced in the respiratory tract of experimental animals. The gas is quite corrosive and can also cause damage to buildings and other materials. Exposure–effect curves have been developed for experimental animals in the 1970s. The study showed that the increases in pulmonary flow resistance in guinea pigs were positively associated with the exposure to sulfur dioxide concentrations ranging from 20 to 660 mg m3 for a 15–20 min period. Studies with guinea pigs at lower concentrations have shown that a sodium chloride aerosol administered concomitantly enhances the effects of sulfur dioxide on the lungs in the form of bronchoconstriction and increased airway resistance. It was known that the sodium chloride could deliver the absorbed sulfur dioxide deep into the lungs as a carrier, and the increased humidity in the respiratory tract could react with the sulfur dioxide to form sulfurous acid, especially if catalysts were present. Sulfuric acid mist and some of the sulfate salts are more powerful respiratory irritants than sulfur dioxide, and this effect is also related to particle size (smaller particles tending to be more irritating). Sulfuric acid mist with a mass median diameter (MMD) of 2 mm was more toxic to animals. Some of the nonreactive compounds, such as manganese salts or oxides, can catalyze the reaction of sulfur dioxide to sulfuric acid. In short-term exposure studies, concentration seemed to be more important than duration and death was related to laryngospasm and bronchospasm. Sulfuric acid mist also caused lung damage that seemed to be related to the total dose. The animal studies showed that long-term exposure of sulfur dioxide to rats could cause interstitial pneumonia, bronchitis, tracheitis, and peribronchitis and increased activity of serum cholinesterase. Some studies in China recently reported that SO2 exposure can reduce the levels of glutathione (GSH) and
Sulfur Oxides: Sources, Exposures and Health Effects
the activities of Cu, Zn-superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) in the body of experimental animals, which suggest that SO2 exposure can cause oxidative damage to lungs, heart, brain, liver, as well as testicles of the body; and this effect of SO2 shows a gender difference in oxidative stress and antioxidation status. A lot of toxicology evidences indicate that SO2 and its derivatives may cause toxicological damage to multiple organs of animals, and some of them are even more severe than damages in lungs. Therefore, SO2 is a systemic toxin. Peroxidation stress, which was caused by a lot of free radicals produced during the period of the sulfite and bisulfite oxidation, may be the main toxicological mechanism of it. However, many studies reported that SO2 pollution even at lower concentrations also had a potential risk to the genetic material deoxyribonucleic acid (DNA) of the cells in mammalian animals. SO2 exposure could also change the expression of apoptosis-related genes, and induce apoptosis in liver of rat and may have relations with some apoptosis-related diseases. The inhalation of SO2 could increase the gene expressions of messenger ribonucleic acid (mRNA) on the transcription and translation levels in human bronchial epithelial (BEP2D) cells, and result in mucus overproduction and inflammation responses, and decrease the activities and mRNA levels of P-450 in livers and lungs of rats. SO2 exposure maybe a risk factor in human genetic toxicology. Sulfur oxides also have cooperated effects on the health with other ambient pollutants, e.g., ozone, nitrogen oxides, and especially for particulate matter. Many studies showed that SO2 could be absorbed on the surface of air particles and be inhaled to lower respiratory tract together with the particles damaging the body. It is not clear for the mechanism of combined exposure to sulfur dioxide and PM or other gaseous pollutants.
Epidemiology A lot of epidemiological studies have proved that sulfur oxides can have significant effects on the human respiratory system. In addition, sulfur dioxide can also cause narrowing of the air passages, particularly in people suffering from asthma and chronic lung disease. These people frequently have narrowed airways, and any further restriction will have a disproportionately large effect, compared to people with uncompromised respiratory systems. The main focus of the air pollution epidemiological studies in the past decade has been on the health effects of PM. However, a lot of studies have also examined sulfur dioxide and other gaseous pollutants as potential confounders of the effects of PM. Thus, during the past decade a large number of risk estimates for sulfur dioxide
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have accumulated, providing a more comprehensive assessment of relative importance of the classical air pollutants. Although these researches have neither resolved the issue of confounding between sulfur dioxide and PM or other pollutants, nor have they systematically examined the synergistic effects, the accumulating risk estimates are still useful in assessing the potential adverse health impacts of sulfur dioxide. Effects of Short-Term Exposures The most clear effects on population mortality due to exposure to sulfur oxides have been the sudden increases of daily death count during episodes of high ambient pollution. The most notable example occurred in London in 1952. The ‘London Smog’ episode lasted for 5 days and it was estimated that the number of extra deaths during and immediately after this period was approximately 4000 more than expected under normal circumstances. The high-risk subpopulation was mainly the people suffering from heart or lung disease or both, and the elderly. The daily deaths were about three times more than expected at that time of the year. Concentrations of sulfur dioxide as high as 3.7 mg m3 (1.3 ppm) were recorded in the center of the urban area. Concentrations of PM were too great to be measured properly. Early studies, mostly in European countries and the United States, in the 1970s suggested that daily mortality was positively associated with the ambient concentration of sulfur dioxide. When sulfur dioxide concentration increased by 70–700 mg m3, there was likely to be a significant increase in total population mortality. However, these results were often interfered by other confounding factors, for example, PM, nitrogen dioxide, and meteorological factors (temperature and humidity). Maybe the effects of sulfur dioxide were overestimated. An earlier study reported that after controlled for season, day of week, and temperature, there was a marked reduction in the average level of sulfur dioxide from 510 to 170 mg m3 but virtually no change in smoke shade. Their observations indicated that, despite this reduction in sulfur dioxide, there had been no reduction in the adverse health effects. Analysis indicated that the adverse health effects were associated principally (80%) with the PM and only to a small extent (20%) with sulfur dioxide. The authors also pointed out that, the effects attributable to sulfur dioxide increased threefold when they estimated mortality on temperature and sulfur dioxide alone by regression analysis. In recent years, many studies reported that excess risk of cause-specific mortality of ischemic heart disease and respiratory diseases related to increased level of ambient SO2. Increase in ambient SO2 was closely associated with increased mortality, notably after adjustment for the concentration of PM10 and CO. A Chinese study of
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61 000 deaths found that higher air levels of PM10, SO2, and NO2 corresponded to significantly higher death rates. However, one study with time series analysis in Beijing reported that the reduction of daily ambient SO2 level will accompany with the decreased cause-specific daily mortality of cardiovascular and respiratory diseases of the exposed population in urban area of Beijing. During the past 30 years many epidemiological evidences showed that the level of daily ambient SO2 was positively associated with an increased risk of hospital admissions, emergency room visits, and hospital outpatient visits for respiratory diseases, ischemic heart disease or myocardial infarction, and other diseases of the exposed population. The results indicated that irritative symptoms increased significantly when sulfur dioxide levels exceeded 310 mg m3. Symptoms such as nose and throat irritation, followed by bronchoconstriction and dyspnea, especially in asthmatic individuals, are usually experienced after exposure to increased levels of sulfur dioxide. The studies demonstrated a significant risk that particularly affected children and patients aged 65 and more. Peak levels of SO2 in the air can cause temporary breathing difficulty for people with asthma who are active outdoors. Recent studies on daily mortality rates and hospital admissions for cardiac disease in Hong Kong, Canada, and London suggested that health effects of the exposed population were significantly associated with 24-h SO2 concentrations down to only 5 mg m3 (the highest mean SO2 level was less than 10 mg m3). The increased level of ambient SO2 could affect significantly the lung functions of the exposed schoolchildren. The studies showed that the schoolchildren living in higher level of ambient SO2 had lower level of the forced vital capacity (FVC), FEV1.0, and peak expiratory flow rate (PEFR) than that of the control area and it suggested that development of pulmonary functions of these children were depressed by ambient SO2. Asthmatic subject is a sensitive subgroup for SO2 exposure; generally, the high level and acute changes of SO2 could significantly reduce the PEFR level and increase the number of asthma attacks in them. Earlier study showed that when sulfur dioxide concentrations exceeded 200 mg m3 or the temperature was lower than 0 1C, there was a significant increase in the frequency of asthmatic attacks. Levels of sulfates exceeding 20 mg m3 and nitrate levels exceeding 2 mg m3 did not result in such an effect. It was reported that higher daily levels of SO2 have been linked to significantly increased influenza admissions. SO2 reacts with other chemicals in the air to form tiny sulfate particles. When these are breathed, they gather in the lungs and are associated with increased respiratory symptoms and disease, difficulty in breathing, and premature death.
Effects of Long-Term Exposures Earlier studies on the chronic effects of air pollutants relied on cross-sectional comparisons that could be subject to ecological confounding. Recent studies often involve investigations of large cohorts for which detailed individual-level information is collected to adjust for confounding. Generally, long-term exposures to high levels of SO2 gas cause respiratory illness and aggravate existing heart disease. In the past 30 years, ambient levels of sulfur oxides are declining in many US and western European cities; thanks to emission controls on vehicles, heating, power generation, and industry. However, the health problems caused by long-term exposure to sulfur oxides still exist in the developed world. With the fast development of domestic economy and large demand of energy consumption, outdoor sulfur oxides pollution problems remain in developing world, especially in some large cities such as Beijing, Shanghai, Bombay, Karachi, Cairo, Sao Paulo, and Mexico City. Most studies of the health effects of ambient/outdoor SO2 pollution have dealt with respiratory health issues. Many of the studies have involved children and most of these studies have reported higher rates of asthma and other respiratory problems. SO2 can worsen childhood asthma at relatively modest concentrations, which are well below USEPA standards and WHO guideline. Both a French study and a Chinese study found that increasing levels of outdoor SO2 were associated with significantly higher rates of childhood asthma and allergic rhinitis. Low to moderate levels of outdoor SO2 can greatly increase respiratory problems in the elderly. Some studies showed that higher outdoor level of SO2 was associated with significantly higher rates of hospital admissions for chronic obstructive pulmonary disease (COPD). An Australian study found that higher airborne levels of SO2 were associated with significantly higher rates of childhood hospital admissions for pneumonia and acute bronchitis. Higher outdoor SO2 levels were associated with significantly higher childhood emergency room visits for pneumonia and respiratory illness in China. Lung function changes have generally been assessed using measurements of ventilatory capacity such as FEV0.75, FEV1, FVC, and peak expiratory flow (PEF). Lower levels of FEV1.0 and PEFR among the exposed population were also observed in the areas of higher SO2 residents, but it is difficult to separate the independent effects of sulfur dioxide. It was recently found that higher outdoor air levels of SO2 were also associated with significantly higher rates of preterm birth, low birth weight, and ventral septal defects of the baby. The possibility that ambient is a causal factor in cancer of the lung has given rise to considerable concern for a long time, but until now there is not enough
Sulfur Oxides: Sources, Exposures and Health Effects
epidemiological evidence that SO2 is a direct risk factor of cancer, even if some in vitro tests in the laboratory showed some positive results about it. Few studies recently reported that it seems the ambient SO2 pollution was associated with the mortality of lung cancer; however, most reports thought SO2 to be a cancer-promoting factor, rather than cancer-inducing. This issue should be of continuous concern to a researcher.
Other Impacts of Sulfur Oxides Reduction of Ambient Visibility SO2 and its derivatives could decrease the visibility of outdoor air. SO2 and sulfuric acid mist can form haze, which occurs when light is scattered or absorbed by particles and gases in the air. Sulfate particles are the major cause of reduced visibility in many parts of the world. Acid Rain SO2 and nitrogen oxides react with other substances in the air to form acids, which fall on earth as rain, fog, snow, or dry particles. The rain with pH value less than 5.6 is called ‘acid rain,’ and is generally caused by relatively higher levels of nitrogen oxides and their acidic derivatives in the air. Acid rain is formed near areas that have high SO2 air pollution, and sometimes may be carried by the wind for hundreds of miles. Acid rain accelerates the decay of building materials and paints, including irreplaceable monuments, statues, and sculptures, which constitute important part of the world’s cultural heritage. Plant and Soil Damage Acid rain reduces the pH value of soil and changes chemical component of soil, damages forests, and decreases the output of crops. Acid rain makes lakes and
Table 1
streams acidic and unsuitable for fish. Long and continued exposure changes the natural variety of plants and animals in an ecosystem. Air Quality Standard (Guideline) of Sulfur Oxides in Ambient Air Clean air is considered to be a basic requirement of human health and well-being. However, air pollution continues to pose a significant threat to health worldwide. WHO estimates the burden of disease due to air pollution; more than 2 million premature deaths every year can be attributed to the effects of urban outdoor and indoor air pollution (caused by the burning of solid fuels). More than half of this disease burden is borne by the populations of developing countries, where sulfur oxides are still one of the important ambient air pollutants. For offering guidance in reducing the health impacts of air pollution, WHO air quality guideline (AQG) was created in 1987 and updated in 1997; these guidelines are based on expert evaluation of current scientific evidence. To inform policymakers and to provide appropriate targets for a broad range of policy options for air quality management in different parts of the world, WHO has undertaken to review the accumulated new scientific evidence and to consider its implications for its AQGs, especially including important new research from lowand middle-income countries where air pollution levels are at their highest; WHO updated a new one in the form of revised guideline values for selected air pollutants (including SO2), which is applicable across all WHO regions in 2005 (Table 1). We can see in Table 1 that the interim targets are given for the 24-h SO2 guideline values in WHO AQG. These are proposed as incremental steps in a progressive reduction of air pollution and are intended for use in areas where pollution is high. These targets aim to promote a shift from high air pollutant concentrations, which have acute and serious health consequences, to lower air pollutant
WHO Air Quality Guideline (2005): WHO air quality guidelines and interim targets for SO2 (24-h and 10-min concentrations)
Interim target-1 (IT-1)a Interim target-2 (IT-2)
Air quality guideline (AQG) a
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24-h average (mg m3)
10-min average (mg m3)
125 50
– –
20
Formerly the WHO Air Quality Guideline (WHO, 2000).
500
Basis for selected level
Intermediate goal based on controlling either motor vehicle emissions, industrial emissions, or emissions from power production. This would be a reasonable and feasible goal for some developing countries (it could be achieved within a few years), which would lead to significant health improvements that, in turn, would justify further improvements (such as, aiming for the AQG value)
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Sulfur Oxides: Sources, Exposures and Health Effects
concentrations. If these targets were to be achieved, one could expect significant reductions in risks for chronic health effects arising from ambient SO2 pollution. Some controlled studies for exercising asthmatics show that a proportion experience changes in pulmonary function and respiratory symptoms after periods of exposure to SO2 as short as 10 min. Thus, WHO recommends that a SO2 concentration of 500 mg m3 should not be exceeded over averaging periods of minute duration for short-term exposure. But attention must be paid to the 10 min time to measure in AQG, while the relevant criteria/guideline are for 30 or 60 min time to measure in some countries, where the value is just for reference. However, because short-term SO2 exposure depends very much on the nature of local sources and the prevailing meteorological conditions, it is not possible to apply a simple factor to this value to estimate corresponding guideline values over longer time periods, such as 1 h. The latest evidence to emerge includes a study conducted in Hong Kong, the United States, and Canada, where they found that the reduction in the sulfur content of fuels could be achieved over a very short period of time, and if there was a threshold for health effects of ambient SO2, it would have to be very low. There is still considerable uncertainty as to whether SO2 is the pollutant responsible for the observed adverse effects or whether it is a surrogate for ultrafine particles or some other correlated substance. Since the revised 24-h guideline may be quite difficult for some countries to achieve in the short term, a stepped approach using interim goals is recommended. For instance, a country could move toward compliance with the guideline by controlling emissions from one major source at a time, selecting from among motor vehicle sources, industrial sources, and power sources (which would achieve the greatest effect on SO2 levels for the lowest cost), and follow this up with monitoring of public health and SO2 levels for health effect gains. Demonstrating health benefits should provide an
incentive to mandate controls for the next major source category.
Further Reading Akimoto H (2003) Global air quality and pollution. Science 302: 1716--1719. Barnett AG, Williams GM, Schwartz J, et al. (2005) Air pollution and child respiratory health: A case-crossover study in Australia and New Zealand. American Journal of Respiratory and Critical Care Medicine 171: 1272--1278. Burnett RT, Stieb D, Brook JR, et al. (2004) Associations between short-term changes in nitrogen dioxide and mortality in Canadian cities. Archives of Environmental Health 59: 228--236. Chen Y, Yang Q, Krewski D, et al. (2004) Influence of relatively low level particulate air pollution and hospitalization for COPD in elderly people. Inhalation Toxicology 16: 21--25. Curtis L, Re W, Smith-Willis P, Fenyves E, and Pan Y (2006) Adverse health effects of outdoor air pollutants. Environment International 32: 815--830. Dockery DW, Pope CA 3rd, Xu X, et al. (1993) An association between air pollution and mortality in six US cities. New England Journal of Medicine 329: 1753--1759. Gilboa SM, Mendola P, Olshan AP, et al. (2005) Relation between ambient air quality and selected birth defects, Seven County Study, Texas, 1997–2000. American Journal of Epidemiology 162: 236--252. Kampa M and Castanas E (2008) Human health effects of air pollution. Environmental Pollution 151: 362--367. Lee JT, Kim H, Song H, et al. (2002) Air pollution and asthma among children in Seoul, South Korea. Epidemiology 13: 481--484. Li R, Meng Z, and Xie J (2007) Effects of sulfur dioxide derivatives on four asthma-related gene expressions in human bronchial epithelial cells. Toxicology Letters 175: 71--81. Pan X, Yue W, He K, and Tong S (2007) Health benefit evaluation of the energy use scenarios in Beijing, China. Science of the Total Environment 374: 242--251. Pope CA 3rd, Burnett RT, Thurston GD, et al. (2004) Cardiovascular mortality and long-term exposure to particulate air pollution: Epidemiological evidence of general pathophysiological pathways of disease. Circulation 109: 71--77. Qin G and Meng Z (2005) Effect of sulfur dioxide inhalation on CYP1A1 and CYP1A2 in rat liver and lung. Toxicology Letters 160: 34--42. US Environmental Protection Agency (EPA) (2000) America’s Children and the Environment. Publication EPA 240-R-00-006. Washington, DC: USEPA. Wong CM, Wong CM, Lam TH, et al. (1998) Comparison between two districts of the effects of an air pollution intervention on bronchial responsiveness in primary school children in Hong Kong. Journal of Epidemiology and Community Health 52: 571--578.