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tobacco use

Monday 31 May 2004

Use of tobacco products, including cigarettes, cigars, pipes, and snuff, is associated with more mortality and morbidity than any other personal, environmental, or occupational exposure.

Cigarette smoking contributes to 440,000 premature deaths per year in the United States, resulting in an annual economic loss of $157 billion from health-related costs. Lung cancer, cardiovascular disease, and chronic respiratory disease account for most of the deaths related to smoking.

Beginning in World War I, annual cigarette consumption increased in men, followed by women, reaching a peak of 4336 cigarettes per capita in 1963.

After the Surgeon General’s Advisory Committee report, released in 1964, concluded that cigarette smoking is one of the most important risk factors for lung cancer, per capita consumption of cigarettes declined to less than 3000 in 1995.

Among children and adolescents, smoking continues to be a major public health problem; early exposure to carcinogens in tobacco smoke may increase the risk of developing lung cancer.
Smoking also interacts with other environmental and occupational exposures in an additive or synergistic fashion. The most important example of such synergism is the increase in risk of lung cancer in cigarette smokers exposed to asbestos.

Mainstream cigarette smoke inhaled by the smoker is composed of a particulate phase and a gas phase; tar is the total particulate phase without water or nicotine.

There are 0.3 to 3.3 billion particles per milliliter of mainstream smoke and more than 4000 constituents, including 43 known carcinogens.

In addition to these chemical carcinogens, cigarette smoke contains carcinogenic metals such as arsenic, nickel, cadmium, and chromium; potential promoters such as acetaldehyde and phenol; irritants such as nitrogen dioxide and formaldehyde; cilia toxins such as hydrogen cyanide; and carbon monoxide.

Carbon monoxide is a colorless, odorless gas produced during incomplete combustion of fossil fuels or tobacco. It has 200 times higher affinity for hemoglobin than oxygen does and it impairs release of oxygen from hemoglobin. Thus, carbon monoxide exposure decreases the delivery of oxygen to peripheral tissues. Carbon monoxide also binds to other heme-containing proteins such as myoglobin and cytochrome oxidase.

Nicotine is an important constituent of cigarette smoke. It is an alkaloid that readily crosses the blood-brain barrier and stimulates nicotine receptors in the brain. It is also responsible for the acute pharmacologic effects associated with tobacco use that are most likely mediated by catecholamines: increased heart rate and blood pressure, increased coronary artery blood flow, increased contractility and cardiac output, and mobilization of free fatty acids. Nicotine is responsible for tobacco addiction.

The inhaled agents in cigarette smoke may act directly on the mucous membranes, may be swallowed in saliva, or may be absorbed into the bloodstream from the abundant alveolar capillary bed.

By various routes of delivery, the constituents of cigarette smoke act on distant target organs and cause a variety of systemic diseases.

The greatest numbers of deaths attributable to cigarette smoking are due to lung cancer, ischemic heart disease, and chronic obstructive lung disease. Lung cancer is caused by multiple carcinogens and promoters in cigarette smoke.

Specific preneoplastic changes are found in the tracheobronchial lining of cigarette smokers. These cellular changes are dose related, and the incidence of lung cancer is directly related to the number of cigarettes smoked.

Cessation of smoking reduces but does not completely eliminate the risks of lung cancer and coronary artery disease. It is estimated that 30% of all cancer deaths and up to 90% of all lung cancer deaths are attributable to cigarette smoking.

Cigarette smoking is a multiplicative risk factor with hypertension and hypercholesterolemia for development of coronary artery disease and arteriosclerosis. It is also a multiplicative risk factor for acute myocardial infarction and stroke in women who take oral contraceptives.

Smoking may contribute to cardiac arrest by increasing platelet adhesion and aggregation, triggering arrhythmia, and by causing an imbalance between the demand for oxygen and supply to the myocardium. Smokers also suffer from increased morbidity due to acute respiratory tract infections, including influenza, and acute and chronic sinusitis.

Ciliatoxins in cigarette smoke impair tracheobronchial clearance, and many of the gas phase constituents of smoke are direct irritants of the respiratory epithelium.

The fetus is especially vulnerable to the consequences of maternal smoking. Even 10 cigarettes per day can cause fetal hypoxia; fetal carboxyhemoglobin levels are higher than maternal levels. The consequences of fetal hypoxia are low birth weight, prematurity, and increased incidence of spontaneous abortion; serious complications at the time of delivery include premature rupture of the membranes, placenta previa, and abruptio placentae.

Cigarette smoking is especially hazardous in the workplace. Smokers have higher rates of accidental injuries, and cigarette smoke may act as a vector to transport other hazardous agents into the lungs, such as radon gas in miners. Similar to asbestos exposure, cigarette smoke is synergistic with radon decay products in causing lung cancer. Cigarette smoke exacerbates bronchitis, asthma, and pneumoconiosis associated with exposure to silica, coal dust, grain dust, cotton dust, and welding fumes.

Tobacco use also increases the prevalence of peptic ulcers; smoking impairs healing of ulcers and increases the likelihood of recurrence. Smoking may also increase pyloric reflux and decrease bicarbonate secretion from the pancreas.

In addition to the health hazards of mainstream tobacco smoke, there are risks associated with exposure to sidestream smoke, also called passive smoking or environmental tobacco smoke (ETS). In 1986, two reports issued by the National Research Council and the Surgeon General concluded that ETS increases the risk of lung cancer, ischemic heart disease, and acute myocardial infarction.

The Environmental Protection Agency classified ETS as a known human carcinogen in 1992. ETS is especially hazardous for infants and young children. Maternal smoking increases the incidence of sudden infant death syndrome. Young children in households of cigarette smokers suffer from an increased incidence of respiratory and ear infections and exacerbation of asthma.

References

- Hecht SS. Tobacco carcinogens, their biomarkers and tobacco-induced cancer.Nat Rev Cancer. 2003 Oct;3(10):733-44. PMID: #14570033#