It was with great interest that we read the article entitled ‘Cigarette smoking and the risk of venous thromboembolism: The Tromso Study’ by Enga et al. . Smoking is one of the risk factors in the development of thromboembolic disease affecting coronary, peripheral and cerebral arteries in individuals . Studies have shown that the risk of developing a disease due to cigarette smoking not only depends on the number of cigarettes smoked by an individual per day but also on several other variables such as the brand of the cigarette smoked, the method of smoke inhalation (superficial inhalation or deep inhalation of smoke) and the duration of smoking [3,4]. A burning cigarette is a complex system consisting of many chemical and physical processes. There are two main regions in the burning section of the cigarette (i.e. a combustion zone and a pyrolysis/distillation zone). Each mechanism and its interaction have a great effect on the levels of chemical constituents of the smoke inhaled by the smoker, which ultimately have different effects on them. In the combustion zone oxygen reacts with carbonized tobacco, producing gaseous products, and in the pyrolysis zone the smoke cools down and forms the aerosols .
Thus when a smoker inhales a bolus of smoke, it mainly contains two fractions: (i) particulate matter containing nicotine produced when the smoke cools down in the cooler pyrolysis zone, which reaches the lungs, and (ii) a gaseous phase containing carbon monoxide and other gases produced when oxygen reacts with carbonized tobacco in the combustion zone .
A burning cigarette produces three kinds of smoke: (i) mainstream smoke, which is inhaled by the smoker and then exhaled, (ii) sidestream smoke, which is produced from the burning end of the cigarette, and (iii) smoke exhaled to the general atmosphere by smokers. Thus the environmental factors also influence the effect of smoking on smokers . LPS and ergosterol present in tobacco smoke contribute to inflammation and airway diseases. It has been found in recent studies that the levels of ergosterol present in the cigarette smoke were significantly higher in rooms with ongoing smoking than in rooms without smoking . Thus the smoker is not only at the risk of disease due to his own smoking but the risk is constantly aggravated when he is constantly exposed to smoke exhaled from other smokers in the vicinity.
Tobacco smoke produces over 6000 different chemicals and chemical compounds, which have different adverse effects on the body. The contents of the cigarette and their quantity also vary between different brands of cigarettes and so will their affects on the individual using them. Studies conducted in the US and in India have shown that the contents of tobacco and the additives or the flavoring agents, which determined the addiction of the smokers to a particular brand of cigarette, varied between different brands of cigarettes . Some people, especially in India, have the habit of chewing tobacco and smoking as well, which doubles the risk of developing a disease. Moreover, ‘bidis’ are crude forms of cigarettes that do not have a filter and smokers generally prefer deep inhalations, which contribute to an increased risk of development of disease .
Thus, there are a number of factors that have to be taken into consideration while studying the effect of smoking on the individual.
In a study conducted at our Institute on young Indians with myocardial infarction we found that a large number of them were smokers . Another study was conducted to find out whether smoking directly affects platelets, important cells in the initiation of the thrombotic process in the arteries. The study was conducted in two groups of smokers (i.e. acute and chronic smokers) with an age-matched control group. The acute and immediate effects of smoking on platelets were seen in individuals immediately after smoking one cigarette. There was an increase in the total WBC counts and increased platelet activation, with the chronic smokers showing activated platelets in their circulation even after they had not smoked for 4–6 h . We also found in our study that there was a difference in the platelet aggregation and platelet activation between the different brands of cigarettes depending upon their nicotine content and other additives and the way the smoke was inhaled by the smoker [unpublished data].
The authors have mentioned in their study that due to the change in smoking habits over the time between smokers and non-smokers there are chances of misclassification during the follow-up studies, which can affect the final results of the study. The conflicting data that exist with respect to smoking may be attributed to the different variables discussed above. Consideration of these variables when analyzing data while carrying out studies related to the effect of smoking may be helpful in coming to fruitful conclusions.