Cigarette Smoke Toxicology

The inhalation toxicity of tobacco smoke has become one of the major public health problems of the 20th century. The chemical complexity of tobacco smoke confounds the task of identifying its toxic constituents. Tobacco smoke is comprised of thousands of chemical components arising primarily from volatilization and pyrolysis of the tobacco leaf (Stedman 1968; Green 1977). The chemical gamut runs from traces of elemental metals, such as cadmium, to nonvolatile whole tobacco leaf components that have escaped degradation during the burning process (USDHHS 1981). Approximately 90 percent of the individual constitutents are organic compounds associated with both the particulate phase and the gas phase (Guerin 1980). It is not surprising that chronic inhalational exposure to this diverse mixture of potentially bioactive compounds can evoke a wide variety of toxicologic responses. Over the years, scientific and public concern has centered primarily on the carcinogenic and atherogenic effects of tobacco smoke. In contrast, relatively little is known about the involvement of tobacco smoke constituents in the pathogenesis of chronic obstructive lung disease (COLD) (USDHHS 1981). For the most part, smoke constituent toxicity studies, both epidemiologic (Dean et al. 1977; Higenbottam et al. 1980) and toxicologic (Walker et al. 1978; Lewis et al. 1979; Coggins et al. 19801, have been confined to a comparison of the varying amounts of particulate matter or tar delivered by smoke. In studies of this nature, attempts have been made to distinguish between the relative toxicities of the vapor phase and the particulate phase of tobacco smoke. The general conclusion reached is that gas phase components that penetrate to the small airways and alveoli may play a significant role in the production of peripheral airway and parenchyma1 diseases such as emphysema, whereas particulate phase components that deposit in larger airways may play a role in the development of disorders of the more proximal airways such as chronic bronchitis (USDHHS 1981). This generalization may not always hold, however. For example, in a review of the effects of smoking on mucociliary clearance, Newhouse (1977) noted considerable disagreement among investigators with regard to whether the vapor phase or the particulate phase was the major factor in smokeinduced dysfunction of the mucociliary transport system. Also, Coggins and associates (1980) observed an increase in both peripheral and central airway goblet cell number in rats after exposure to tobacco smoke from which most of the vapor phase had been removed. Cohen and James (1982) found that the level of oxidants in tobacco smoke (oxidants have been implicated in the pathogenesis of