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June 1989, Volume 39, Issue 6



Huma Oureshi  ( PMRC Research Centre, Jinnah Postgraduate Medical Centre, Karachi. )

In USA since 1964 the Surgeon General has identified smoking as the single most important cause of preventable mortality, but it is only rece­ntly that attention has been focussed on the adverse effects of involuntary passive smoking on human health1,2. Involuntary smoking occurs when non smok­ers are exposed to tobacco smoke of smokers in enclosed environments3. There are two main sour­ces of environmental tobacco smoke, namely the main stream (exhaled smoke of the smoker) and the side stream (smoke emitted from the lit end of the cigarette). Qualitatively, the two types of smokes have similar components but midstream smoke has a higher PH, smaller particles and higher con­centration of carbon monoxide1,2. Approximately 85% of the smoke generated during cigarette smoking consists of side stream smoke but the ad­verse effect of involuntary smoking depends upon various factors like filtered or non filtered cigarette, low or high tar/nicotine, smoking rate, room size, ventilation and duration of exposure . Markers which measure tobacco smoke exposure in, non smokers include carbon monoxide thiocyanate, nicotine and cotinine, and urinary mutagenes4. Of these nicotine5-11 and cotinine12-19 have received maximum attention, with cotinine as the most ac­cepted short term marker in epidemiological studies because of its long half life, lack of fluctua­tions during smoke exposure and its non invasive determination in urine and saliva. Strong correla­tion exists between urinary cotinine levels and ex­posure to tobacco smoke14-16. On the basis of biochemical markers, the level of exposure to en­vironmeiflal tobacco smoke is approximately equal to smoking 0.1 - 1 cigarette/day in UK11,14 and upto 2/day in Japan17. In areas which are heavily polluted with sidestream smoke (CO 20 um/L) tobacco smoke inhalation by involuntary smokers is equal to half to one cigarette/day20. The health effect of environmental tobacco smoke in non smokers married to smokers is 1.41 to 1.87 which drops to 1.09 to 1.45 in non smokers married to non smokers2 showing a 7.421. 6.8%22-26 death rate due to lung cancer in non smokers/­100,000 person years. Three prospective studies also showed a slightly higher risk of lung cancer in non­smokers married to smokers22,27,28 , while 10 of 15 case controlled studies also showed an increased risk of lung cancer in non smokers, married to smokers as compared to those married to non smokers29-47 while others reported no increased risk31,33,36,42,43. Six of these studies showed a dose response relation between passive smoking and lung cancer29,30,37-40. Several studies show a strong association of environmental tobacco smoke to squamous cell and small cell carcinoma than with other cell types affected by lung cancer32,34,35,37,39,41.­ No increased risk of lung cancer was repo­rted from USA33,43, Hong Kong31,42 and UK36 in non smoker females married to smokers, however in view of misclassification of exposure31,33,36,42,43. interviewer and observer bias33,36 and improper matching of case/controls31,42, the results of these studies should be regarded with caution. Most studies though are not comparable in terms of study design, population size, tobacco type, manner of consumption, extent and duration of tobacco smoke in the working place but almost all showed a posi­tive association of lung cancer in passive smokers. The effect of passive smoking on chronic respiratory symptoms has also been studied. Of 9 studies48-56, S showed a significant association49,53 while 4 did not48,54-56. In one of the studies extend­ing over 20 years49, the effect of passive smoke exposure at the work place showed a significant reduction in forced and expiratory flow and FEVi in non smokers exposed to smoke than in non smokers not exposed to environmental smokp. Similarly a French study50 showed a dose response relation between reduction in pulmonary function and increase in number of cigarettes smoked daily by the spouse, moreover percent reduction in forced expiratory flow was observed only in non smoking females over the age of 40 years. Significant association of exacerbation of asthma with tobacco smoke exposure has been reported in two studies57,59 while the third showed no association58. Variations in results are probably due to variations in patient’s characteristics especially their hyper responsiveness59. Cardiovascular diseases are also strongly as­sociated with various risk factors, including smok­ing60. Four of five studies showed association of tobacco smoke exposure in non smokers to the oc­currence of heart disease52,61-63. In one study, with a 12 years follow up of non smokers aged 25 or over, a significant higher mortality rates from arteriosclerotic heart disease was observed in both sexes when they lived with smokers, but a sig­nificant dose response trend was observed in feniales only63. The possible effects of exposure to parental tobacco smoke on the frequency and severity of acute respiratory illness in children has been studied in 4 prospective and 9 case controlled studies. Almost all of them showed an increas fre­quency of both upper and lower respiratory problems in children of smokers than non smokers64-72, moreover mother’s smoking had a stronger influence68,69. A positive dose response reduction has been found in the children’s lung function and the number of smokers within the house. Younger children are more strongly af­fected than the older ones. Similarly an association of exposure of parental smoke has been found with increased frequency of chronic middle ear ef­fusions and infections in children aged 4 years or below73-77. The long term effects of smoke associated problems and reduction in pulmonary function in children has not been studied but the higher in­cidence of lung cancer in adults exposed to en­vironmental smoke as a public health problem78. Further studies should be undertaken to accurately measure the exposure to tobacco smoke in environ­ment.


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