Tobacco and Public Health - TCSC Indonesia

JONATHAN M. SAMET 291
a thousand degrees centigrade in the burning coal of the cigarette (US Department of
Health Education and Welfare 1964). The resulting smoke, comprising numerous gases
and also particles, includes myriad toxic components that can cause injury through
inflammation and irritation, asphyxiation, carcinogenesis, and other mechanisms.
Some examples are carbon monoxide, cyanide, radioactive polonium, benzo-(a)pyrene,
oxides of nitrogen, acrolein, benzene, and particles. Active smokers inhale
mainstream smoke (MS), the smoke drawn directly through the end of the cigarette.
Passive smokers inhale smoke that is often referred to as secondhand smoke or ETS,
comprising a mixture of mostly sidestream smoke (SS) given off by the smoldering
cigarette and some exhaled MS. Sidestream smoke is generated at lower temperatures
than MS, and consequently concentrations of many toxic compounds are greater in SS
than MS. However, SS is rapidly diluted following its generation as it disperses into the
air. Concentrations of tobacco smoke components in secondhand smoke
are far below the levels of MS inhaled by the active smoker, but there are qualitative
similarities between secondhand smoke and MS (US Department of Health and
Human Services 1986; IARC 2002).
Both active and passive smokers absorb tobacco smoke components through the
lung’s airways and alveoli and many of these components, such as the gas carbon
monoxide, then enter into the circulation and are distributed systemically. There is also
uptake of such components as benzo-(a)-pyrene directly into the cells that line the
upper airway and the lung’s airways. Some of the carcinogens undergo metabolic
transformation into their active forms and evidence now indicates that metabolismdetermining
genes may affect susceptibility to tobacco smoke (Nelkin et al. 1998). The
genitourinary system is exposed to toxins in tobacco smoke through the excretion of
compounds in the urine, including carcinogens. The gastrointestinal tract is exposed
through direct deposition of smoke in the upper airway and the clearance of smokecontaining
mucus from the trachea through the glottis into the esophagus. Not
surprisingly, tobacco smoking has proved to be a multisystem cause of disease.
There is a substantial scientific literature on the mechanisms by which tobacco
smoking causes disease. This body of research includes characterization of many components
in smoke, some having well-established toxicity, such as nicotine, hydrogen
cyanide, benzo-(a)-pyrene, carbon monoxide, and nitrogen oxides. The toxicity of
smoke has been studied by exposing animals to tobacco smoke and smoke condensate,
in cellular and other laboratory systems for evaluating toxicity, and by assessing smokers
for evidence of injury by tobacco smoke, using biomarkers such as tissue changes and
levels of damaging enzymes and cytokines. The data from these studies amply document
the powerful toxicity of tobacco smoke. The mechanisms of disease causation
by tobacco smoke include changes in the genetic material of cells that leads to malignancy;
inflammatory injury to the cells lining the surfaces, such as the lung’s airways
where smoke deposits, and to more distant sites, such as the blood vessels, that are
affected by circulating tobacco smoke components; impairment of the body’s defense