|
| Block 8: Environmental Issues and Public Health - Air Pollution Chapter 3: The Main Air Pollutants; Their Health Impacts; Exposure - Response Relationships |
 |
 |
 |
 |
 |
The classical (or common) air pollutants are SO2, NO2, CO, ozone and PM. The adverse health effects of these ambient air pollutants on exposed communities, demonstrated through many epidemiological studies (WHOa, 2002) include:
|
|
The expected health effects depend on the pollutant, the level (pollutant concentration) and duration of exposure, and the personal susceptibility of an individual.
Summaries of the sources and the health and environmental effects of the common air pollutants are as follows . (More detailed descriptions of the health impacts of these pollutants are to be found in references 1 and 2 - WHOa and WHOb.) In each case, a more detailed excerpt from reference 1 (WHOa, Chapter 3) follows the summary.
Sulphur dioxide belongs to the family of gases called sulphur oxides (SOx ). These gases are formed when fuel containing sulphur (mainly coal and oil) is burned, and during metal smelting and other industrial processes. Vehicle fuels (petrol and diesel) contain significant levels of sulphur and hence contribute to the emission of SO2 and sulphate particulates. SO2 in the atmosphere is converted to sulphuric acid (H2SO4) and other sulphate particulates. Large scale emissions of SO 2from power stations contribute to acid rain.
The major health concerns associated with exposure to high concentrations of SO2 include effects on breathing (decreased lung function), respiratory illness, alterations in pulmonary defences, and aggravation of existing cardiovascular disease. Children, the elderly, and people with asthma, cardiovascular disease or chronic lung disease (such as bronchitis or emphysema), are most susceptible to adverse health effects associated with exposure to SO2.
Short-period exposures (less than 24 hours):
Most information on the acute effects of SO2 comes from controlled chamber experiments on volunteers exposed to SO2 for periods ranging from a few minutes up to one hour (WHO 1999a). Acute responses occur within the first few minutes after commencement of inhalation. Further exposure does not increase effects. Effects include reductions in the mean forced expiratory volume over one second (FEV1), increases in specific airway resistance (sRAW), and symptoms such as wheezing or shortness of breath. These effects are enhanced by exercise that increases the volume of air inspired, as it allows SO2 to penetrate further into the respiratory tract.
A wide range of sensitivity has been demonstrated, both among normal subjects and among those with asthma. People with asthma are the most sensitive group in the community. Continuous exposure-response relationships, without any clearly defined threshold, are evident. To develop a guideline value, the minimum concentrations associated with adverse effects in asthmatic patients exercising in chambers have been considered. An example of an exposure-response relationship for asthmatic patients is shown in Figure 3.1, expressed in terms of change in FEV1 after a 15-minute exposure.
 |
| Figure 3.1 Dose-response relationship of reduction of mean FEV1 with increasing concentrations of sulphur dioxide with exercise (after subtracting the effect of exercise alone) in patients with moderate and severe asthma (Source: Linn et al 1987/WHO 1994) |
Exposure over a 24-hour period:
Information on the effects of exposure averaged over a 24-hour period is derived mainly from epidemiological studies in which the effects of SO2, SPM and other associated pollutants are considered. Exacerbation of symptoms among panels of selected sensitive patients seems to arise in a consistent manner when the concentration of SO2 exceeds 250 µg/m3 in the presence of SPM. Several more recent studies in Europe have involved mixed industrial and vehicular emissions now common in ambient air. At low levels of exposure (mean annual levels below 50 µg/m3; daily levels usually not exceeding 125 µg/m3) effects on mortality (total, cardiovascular and respiratory) and on hospital emergency admissions for total respiratory causes and chronic obstructive pulmonary disease (COPD), have been consistently demonstrated. These results have been shown, in some instances, to persist when black smoke and SPM levels were controlled for, while in others no attempts have been made to separate the pollutant effects. In these studies no obvious threshold levels for SO2 [emphasis added] has been identified.
Long-term exposure:
Earlier assessments examined findings on the prevalence of respiratory symptoms, respiratory illness frequencies, or differences in lung function values in localities with contrasting concentrations of SO2 and SPM, using data from the coal-burning era in Europe. The lowest-observed-adverse-effect level of SO2 was judged to be at an annual average of 100 µg/m3 , when present with SPM. More recent studies related to industrial sources of SO2, or to the changed urban mixture of air pollutants, have shown adverse effects below this level. But a major difficulty in interpretation is that long-term effects are liable to be affected not only by current conditions, but also by the qualitatively and quantitatively different pollution of earlier years. However, cohort studies on differences in mortality between areas with contrasting pollution levels indicate that mortality is more closely associated with SPM, than with SO2.
