I REFER to Dr Alan R. King's letter (South China Morning Post, January 16) in which he raises the issue of the classification of Environmental Tobacco Smoke (ETS) as a ''Class A'' carcinogen by the United States Environmental Protection Agency.
The public should also be informed that the American Heart Association Council on Cardiopulmonary and Critical Care concluded in 1992, ''that environmental tobacco smoke is a major preventable cause of cardiovascular disease and death''. This position paper was published in Circulation, one of the most prestigious journals in the field of cardiovascular disease. The reasons for the above statements are as follows.
Burning cigarettes emit two types of smoke: mainstream smoke which is directly inhaled into the smoker's lungs and side-stream smoke which is emitted into the surrounding air from the burning cigarettes between puffs. ETS is about 85 per cent sidestream and 15 per cent exhaled mainstream smoke. Several thousand chemicals, including no fewer than 40 carcinogens are contained in ETS.
Those physically close to someone actively smoking are exposed to ETS not only while the cigarette is lit but continue to breathe in air contaminated with ETS long after the cigarette has been extinguished. Non-smokers exposed to ETS at home suffer a 30 per cent increase in both the likelihood of developing lung cancer and the risk of suffering from cardiovascular disease. These statistics may be worse for those who are similarly exposed to ETS in the workplace. Extensive analysis of medical literature has led to the estimation that 15,000 to 19,000 coronary deaths in the US may occur annually in non-smoking spouses exposed to ETS, and as many as 40,000 cases of cardiovascular disease per annum in the US may be related to ETS.
ETS produces acute effects on cardiovascular functions in human beings. Nicotine speeds up heart rate and elevates blood pressure, effects that may be detrimental to patients with coronary heart disease. Cigarette smoking increases platelet stickiness (which enhances clotting in arteries), and damages the inner lining of the arterial wall. Polycyclic aromatic hydrocarbons present in ETS may accelerate hardening of arteries.
ETS increases carbon monoxide levels in the blood, resulting in a lower threshold for angina and an increased risk of irregular heart rhythms in exercising non-smokers with coronary artery disease. ETS also impairs exercise performance in healthy people. More importantly, studies have shown an increase in the incidence of non-fatal heart disease, including angina and heart attacks, among non-smokers exposed to ETS.