Air pollutants which have the greatest effect on the respiratory system are sulphur dioxide, nitrogen dioxide, ozone, polycyclic aromatic hydrocarbons, and suspended particulates. Although sulphur dioxide is not a major problem in Australian cities because of the widespread use of low-sulphur fuels, motor vehicle emissions nonetheless contribute significant amounts of nitric oxide and reactive hydrocarbons. Suspended particulates include small solid and liquid substances including acid droplets, dust, smoke, fog, fumes, pollens and lead.(132)
Although development and aggravation of respiratory symptoms has been associated with these pollutants, there is no conclusive evidence that lung cancer is caused by ambient air pollution. There is biological plausibility for a link between exposure to ambient polycyclic aromatic hydrocarbons, but this has not been directly investigated.(132) Studies of lung cancer and exposure to pollution are complicated by difficulties in excluding the confounding effects of tobacco smoke and occupational, dietary and other exposures to carcinogens and problems in obtaining precise measurements of exposure to ambient pollution on an individual (rather than population) level over time.(133,134) A Victorian review of the health effects of air pollution has commented that 'the effects of factors such as tobacco and alcohol would far outweigh the small background of environmentally induced cancers that may occur.'(134)
Epidemiological investigations have not shown strong effects of air pollution on lung cancer.(1) In 1981 Doll and Peto estimated that combustion by-products in the atmosphere were unlikely to account for more than 1% of all lung cancer cases, and that pollution in all its forms probably accounted for something like 2% of all cancers.(135)
Although some studies have shown a higher rate of lung cancer in urban areas compared to rural areas, this is not clearly attributable to air pollution levels. These findings are confounded by occupational exposures, and different patterns of smoking behaviour between city and country populations.(133)
It is possible that some air pollutants interact with cigarette smoke to increase cancer incidence over and above that which would be expected to result from tobacco use alone.(135)
It should be noted that on a worldwide scale, Australian cities are comparatively free of smog (see Table 3.2).
People in Western society spend more than 80% of their time indoors.(132) There are a number of causes of indoor air pollution. The major source is tobacco smoke.(134,137,138) According to Streeton,(134) 'The most prevalent and damaging indoor pollutant ... is tobacco smoke. Exposure to tobacco smoke, inhaled either actively or passively, is a major threat to health in our society'. Other sources of indoor pollution include fumes from heating or cooking,(134) building materials, furnishings and office equipment, or infiltration from an outdoor polluting source.(137,138)
'Sick building syndrome' is an umbrella term generally used to apply to the development of a number of symptoms thought to be caused by exposure to the indoor environment. These symptoms include eye, nose and throat irritation, mucosal dryness, erythema, mental fatigue and headaches, upper respiratory infections, hoarseness, wheezing and cough, itching, nausea and dizziness.(139) They may be related to a distinct viral or other agent, or appear sporadically among affected workers.
Three general steps have been recommended for dealing with building related illness:(137)
The most important of these is the prohibition of cigarette smoking in indoor environments. It is also important in the construction or refurbishing of buildings that the materials used release minimal amounts of volatile compounds. Ventilation systems also need to be well designed and maintained.
See Chapter 6, Section 10 and Chapter 14, Section 20 for discussion about the tobacco industry's exploitation of 'sick building syndrome'. The health effects of inhalation of environmental tobacco smoke (passive smoking) are discussed in Chapter 4.