Smoking as a Cause of COPD

The most common cause of COPD is a history of active or passive smoking. In fact, it has been estimated that smoking accounts for 80% to 90% of the risk of developing COPD and is responsible for 82% of all deaths due to COPD. Chronic bronchitis symptoms, for example, are at least 4 times more common in smokers than in nonsmokers. Cigarette smokers have a greater annual average rate of decline in forced expiratory volume in 1 second, and the differences between smokers and nonsmokers accelerate as cigarette consumption increases.

The tobacco-associated risk for developing COPD is measured in “pack years” of smoked cigarettes. A patient’s pack years are calculated by multiplying the duration of smoking (in years) by the average number of cigarettes smoked per day, then divided by 20 to convert the total to packs. Twenty pack years or more of smoking have been identified as a predictor of COPD.

Determining Pack Years

# of years smoked  X  # cigarettes smoked/day =  # of pack years

It is important to recognize that exposure to any form of inhaled tobacco—cigarettes, cigars, or pipe tobacco— substan­tially increases the likelihood of COPD as well as other tobacco-associated disease including lung cancer, coronary disease, etc. While pipe and cigar smokers have a lower morbidity and mortality rate for COPD than cigarette smokers, the rate is higher than for nonsmokers. In addition, recent studies have suggested that the emerging popular habit of cigar smoking is likely to result in an increase of mouth and throat cancer in the coming years. Cigar smoking has also been clearly linked to COPD.

As age increases, loss of pulmonary function accelerates quickly with continued smoking. As with many smoking-related illnesses, cessation is the single most important factor affecting outcome in patients at all stages of COPD. While the relative risks for COPD decline more slowly than for heart disease or cancer, stopping smoking has been shown to have a beneficial effect on pulmonary function. The rate of decline can return to that of nonsmokers, particularly among younger people. Evidence shows that stopping prior to age 35 is of greater benefit than ceasing at a later age.

It is presently unclear whether passive (“sidestream” or “secondhand”) tobacco exposure increases the risk of COPD, but children of smoking parents have a higher prevalence of respiratory symptoms and disease. There is limited evidence that children exposed to passive smoking have a small but significant loss in lung function, according to tests of pulmonary function. Passive smoking is also clearly associated with an increased incidence of lung cancer in the nonsmoking spouses of active smokers, making tobacco-associated diseases a type of acquired familial disease.

While smoking accounts for the vast majority of cases of COPD, 15% to 20% of all heavy smokers develop the disease. It is unknown why only some people are susceptible, but hypotheses include genetically acquired abnormalities of pulmonary function, or a deficiency of pulmonary enzymes that protect against the harmful effects of smoking.