Table 8.3 presents only a partial list and includes the type of injury produced by these agents. Nicotine, an alkaloid present in tobacco leaves, is not a direct cause of tobacco-related diseases, but it is highly addictive. Nicotine binds to receptors in the brain and, through the
Table 8.3 Effects of Selected Tobacco Smoke Constituents
NicotineGanglionicstimulationanddepression,tumorpromotion http://ebooksmedicine.net
Table 8.4 Organ-Specific Carcinogens in Tobacco Smoke
Lung,larynxPolycyclicaromatichydrocarbons4-(Methylnitrosoamino)-1-(3-pyridyl)1-butanone(NNK)210Polonium
PancreasNNK(?)
Bladder4-Aminobiphenyl,2-naphthylamine
Oralcavity:smokingPolycyclicaromatichydrocarbons,NNK,NNN
Oralcavity:snuffNNK,NNN,210polonium
DatafromSzczesnyLB,HolbrookJH:Cigarettesmoking.InRomWH,editor:Environmental and occupational medicine, ed2,Boston,1992,Little,Brown,pp1211.
release of catecholamines, is responsible for the acute effects of smoking, such as increased heart rate and blood pressure, and increased cardiac contractility and output.
The most common diseases caused by cigarette smoking involve the lung and include emphysema, chronic bronchitis, and lung cancer, all discussed in Chapter 13. The mechanisms responsible for some tobacco-induced diseases include the following:
Direct irritant effect on the tracheobronchial mucosa, producing inflammation and increased mucus production (bronchitis). Cigarette smoke also causes the recruitment of leukocytes to the lung, increasing local elastase production and subsequent injury to lung tissue that leads to emphysema.
Carcinogensis. Components of cigarette smoke, particularly polycyclic hydrocarbons and nitrosamines ( 8.4 ), are potent carcinogens in animals and probably are involved in the causation of lung carcinomas in humans (see Chapter 13). The risk of developing lung cancer is related to the intensity of exposure, frequently expressed in terms of “pack years” (e.g., one pack daily for 20 years equals 20 pack years) or in cigarettes smoked per day (
Fig. 8.8 ). In addition to lung cancers, tobacco smoke contributes to the development of cancers of the oral cavity, esophagus, pancreas, and bladder.
Table 8.4 lists organ-specific carcinogens contained in tobacco smoke. Moreover, smoking multiplies the risk of disease associated with other carcinogens; well-recognized examples are the 10-fold increased incidence of lung carcinomas in asbestos workers and uranium miners who smoke than in those who do not. The combination of tobacco (chewed or smoked) and alcohol consumption has multiplicative effects on the risks of oral, laryngeal, and esophageal cancers. An example of the carcinogenic interaction of these all-too-common vices is shown for laryngeal cancer (
Fig. 8.9
Atherosclerosis and its major complication, myocardial infarction, are strongly linked to cigarette smoking. The causal mechanisms probably relate to several factors, including increased platelet aggregation, decreased myocardial oxygen supply (because of lung disease coupled with hypoxia related to CO in cigarette smoke) accompanied by increased oxygen demand, and a decreased threshold for ventricular fibrillation. Almost one-third of all heart attacks are associated with cigarette smoking. Smoking has a multiplicative effect on risk when combined with hypertension and hypercholesterolemia.