POPULATION AND AUSTRALIA

CHD at an earlier age than non-smokers. W.omen who smoke cigarettes have a greater risk of sudden death from CHD than do non-smoking women. Experimental studies demonstrate that (i) the elevated levels of carboxyhaemoglobin seen in smokers may result in significantly decreased cardiac work performance and precipitation of ischaemic ECG changes and arrhythmias where clinical and subclinical CHD exists; (U) nicotine acts Indirectly to cause elevation of plasma free fatty acids; (Ill) there are strong associations between cigarette smoking and development of peripheral vascular disease and atherosclerotic brain infarction. Cigarette smoking has been identified as the major cause of lung cancer, which Is the most common site of cancer in males in the 35 to 74 years age group, and cancer is the second leading cause of death in this age group in the United States. There Is a dose-response relationship between cigarette consumption and the risk of development of lung cancer, the risk for smokers in general ranging from 7·61 to 14'20 times that for non-smokers, while male heavy smokers may have up to 23·9 times the risk. While the incidence of lung cancer in women is lower, there is similarly an association between cigarette smoking and lung cancer mortality in females. The most common types of cancer seen are oat-cell and epidermoid carcinomas, but there is some evidence that adenocarcinomas may also be associated with cigarette smoking. Certainly, autopsy studies have shown that changes in the bronchial mucosa which precede bronchogenic carcinoma are more common in smokers than in non-smokers. Cell and tissue culture studies have demonstrated that constituents of tobacco and cigarette smoke condensate may produce malignant transformation, and numerous complete carcinogens and cooarcinogens (tumour promoters) have been isolated from and identified in cigarette smoke condensate. There is also an increased risk of development of lung cancer in ,pipe and cigar smokers compared to non-smokers, with a dose-response relationship, but the risk is less than that of cigarette smokers. This lesser risk is consistent with dUlerences in inhalation patterns of these two groups of smokers. Recent epidemiological data suggest that the incidence of lung cancer in women continues to rise in correlation with the trend towards an increase in smoking among women. Data from experimental studies in animals suggest that chronic respiratory infections may enhance the carcinogenicity of components of cigarette smoke, as may alterations in the immune system. Cigarette smoke components induce aryl hydrocarbon hydroxylase activity in pulmonary alveolar macrophages, but the role of this in tumorigenesis or as a host defence mechanism is presently clear.