Pipe and cigar smoking was associated with an obstructive pattern of spirometry characterized by decrements in the FEV1 and FEV1/FVC ratio and by an increased risk of airflow obstruction in this large, multiethnic study. These results, together with the extensive literature on the effects of tobacco smoke on the development of COPD and the increase in cotinine levels among current pipe and cigar smokers in this cohort, suggest that pipe and cigar smoking produce a measureable increase in the risk of COPD.
Tobacco smoke is the major cause of COPD (6
). However, it is not entirely clear whether pipe and cigar smoke may damage the lung via the same mechanism as cigarettes. Some people who smoke pipes and cigars claim to not inhale, or at least inhale less, than cigarette smokers. The elevated cotinine levels in the current study, however, belie this notion and provide a biological measure of nicotine exposure. Our results are also consistent with prior observations of elevated carboxyhemoglobin saturations in pipe and cigar smokers, particularly among former cigarette smokers who may be more likely to inhale than never cigarette smokers (20
). Cigar smoke particles have been shown to be deposited in the lung, regardless of report of inhalation (22
). These findings strongly suggest that tobacco smoke from cigars and particularly from pipes is absorbed systemically.
Cotinine levels among pipe and cigar smokers were lower than among people who smoke cigarettes; however, relative differences in cotinine levels reflect differences in nicotine absorption but not necessarily exposure to harmful products of tobacco smoke. Most cigarettes contain filters whereas pipes and cigars are unfiltered and may therefore yield a higher dose of tobacco smoke for the same dose of nicotine. Furthermore, pipe and cigar smoke exposes the smoker to more side-streamed smoke, which may be particularly harmful (23
). However, similar effects of pipe and cigar to cigarette smoking on CYP1A2 activity, the major pathway activating carcinogens from tobacco smoke, and DNA adduct levels have not been found, possibly due to differences in inhalation (25
Despite recent increases in pipe and cigar smoking, prior studies on pipe and cigar smoking and lung function are few. We conducted an English-language MEDLINE search through July, 2009 to identify studies that examined the association between pipe and/or cigar smoking and lung function. Consistent with our results, pipe and cigar smokers in the Copenhagen City Heart Study had an increased rate of decline in lung function compared to non-smokers (26
), as well as an increased risk of mucous hypersecretion (28
). The Copenhagen City Heart Study demonstrated this association in a relatively homogeneous European sample, whereas the current study extends these findings to a multiethnic sample in the US.
Other studies of pipe and cigar smoking and COPD have relied upon ICD-based measures. In addition to the findings in the two US cohorts (9
), pipe and cigar smoking were associated with an increased mortality rate from emphysema and chronic bronchitis in Sweden (29
), and British men who switched from cigarettes to pipes and cigars had an increased risk of dying from COPD, ischemic heart disease or lung cancer compared to those who quit smoking all together (20
). A prospective cohort study in the Netherlands recently showed that pipe and cigar smoking was associated with reduce life expectancy, although to a lesser extent than cigarette smoking (30
). Other studies investigating the effects of pipe and cigar smoking are limited to overall mortality, coronary artery disease, and risk of lung cancer (31
Major strengths of this study include the large, multi-ethnic, population-based sample with standardized measures of spirometry, cotinine and pipe and cigar smoking. The major limitations are the cross-sectional design, the retrospective ascertainment of cumulative pipe and cigar smoking, and the relatively small proportion of participants who smoked pipes or cigars but not cigarettes. Cross-sectional studies of lung function can yield different results from longitudinal studies and are potentially subject to selection bias. However, our cross-sectional findings are consistent with the longitudinal results from Copenhagen (26
). Confounding, particularly by cigarette smoking, may have contributed to the observed associations. However, we controlled for precise measures of the major potential confounders, in addition to performing analyses stratified by smoking history, restricting to participants who had never smoked cigarettes, and using up-weighting estimates of cigarette pack-years, all of which yielded consistent results.
Misclassification of smoking technique is unlikely to have accounted for the differences in urinary cotinine levels between cigar and pipe smokers who never smoked cigarettes. A small number of the 1,620 participants who reported never smoking had detectable levels of cotinine; almost all of these were likely due to environmental tobacco smoke exposure (i.e., levels <100 mg/dl) but only 7 were unequivocally consistent with active smoking. Given the generally healthy cohort and generally subclinical decrements in lung function, recall bias of smoking history is unlikely to have been substantial or differential with respect to the outcomes.
The proportion of participants who smoked pipes or cigars but not cigarettes was small. Effect estimates in this group were therefore relatively imprecise; however, results for pipe or cigar smokers as a group and pipe-years as a cumulative measure were highly consistent with those from the entire sample and statistically significant for airflow obstruction. The interaction term for cigar-years suggested a possible greater impact of cigar smoking among participants who had ever smoked cigarettes compared to those who never smoked cigarettes, which further research will have to refute or confirm.
In conclusion, pipe and cigar smoking was associated with decrements in lung function consistent with obstructive lung disease. These findings, together with increased cotinine levels in current pipe and cigar smokers, suggest that long-term pipe and cigar smoking may damage the lungs and contribute to the development of COPD. Practitioners should consider pipe and cigar smoking a risk factor for COPD and counsel cessation of pipe and cigar smoking regardless of smoking history.