Heavy Habitual Marijuana Smoking Does Not Cause an Accelerated Decline in FEV, With Age

DONALD P. TASHKIN, MICHAEL S. SIMMONS, DUANE L. SHERRILL, and ANNE H. COULSON

Departments of Medicine and Epidemiology, UCLA Schools of Medicine and Public Health, Los Angeles; and Division of Respiratory Sciences, University of Arizona College of Medicine, Tucson, Arizona

To assess the possible role of daily smoking of marijuana in the development of chronic obstructive pulmonary disease (COPD), we evaluated the effect of habitual use of marijuana with or without tobacco on the age-related change in lung function (measured as FEVI) in comparison with the effect of nonsmoking and regular tobacco smoking. A convenience sample of 394 healthy young Caucasian adults (68% men; age: 33 t 6 yr; mean t SD) including, at study entry, 131 heavy, habitual smokers of marijuana alone, 112 smokers of marijuana plus tobacco, 65 regular smokers of tobacco alone, and 86 nonsmokers of either substance were recruited from the greater Los Angeles community. FEVI was measured in all 394 participants at study entry and in 2SS subjects (6S %) on up to six additional occasions at intervals of ;~: 1 yr (1.7 t 1.1 yr) over a period of 8 yr. Random-effects models were used to estimate mean rates of decline in FEVI and to compare these rates between smoking groups. Although men showed a significant effect of tobacco on FEVI decline (p < 0.05), in neither men nor women was marijuana smoking associated with greater declines in FEVI than was nonsmoking, nor was an additive effect of marijuana and tobacco noted, or a significant relationship found between the number of marijuana cigarettes smoked per day and the rate of decline in FEVI. We conclude that regular tobacco, but not marijuana, smoking is associated with greater annual rates of decline in lung function than is nonsmoking. These findings do not support an association between regular marijuana smoking and chronic COPD but do not exclude the possibility of other adverse respiratory effects. Tashkin DP, Simmons MS, Sherrill DL, Coulson AN. Heavy habitual marijuana smoking does not cause an accelerated decline in FEVI with age.    AM I RESPIR crlrr rARE Mea 1497:ISS:141-144.

Marijuana remains the most commonly smoked illicit substance in American society (1, 2). After more than a decade of declining prevalence of marijuana use in the United States, an upswing in its use has recently been demonstrated, especially among young individuals (1, 2). Because the constituents of marijuana smoke are similar in many respects to those of tobacco (3, 4), it is possible that habitual smoking of marijuana may lead to some of the same respiratory effects that derive from regular tobacco use. This possibility is supported by several animal and cellular studies, which have shown that chronic exposure to marijuana smoke can injure respiratory tissue (5-9). Although earlier studies in humans yielded conflicting data about the association between heavy marijuana smoking and clinical evidence of respiratory illness (10-14), more recent clinical studies have demonstrated a relationship between habitual marijuana use and symptoms of chronic bronchitis (15, 16). Moreover, histopathologic studies have revealed epithelial alterations in biopsies from proximal bronchi

(Received in original form April 3, 1996 and in revised form June 28, 1996)

Supported by Grant No. Rí71 DA03013 from the National Institutes of Health/National institute on Drug Abuse.

Correspondence and requests for reprints should be addressed to Donald P. Tashkin, M.D., Department of Medicine, UCLA School of Medicine, Los Angeles, CA 90095-1690.

Am I Respir Crit Care Med    Vol 155. pp 141-1411, 1997

of marijuana smokers (goblet-cell metaplasia, reserve-cell hyperplasia, squamous metaplasia) (17, 18) that are consistent with symptoms of mucus hypersecretion.

In contrast to the concordance of findings in recent studies with respect to the impact of regular marijuana smoking on chronic respiratory symptoms, cross-sectional studies of marijuana users in Los Angeles (15) and of smokers of nontobacco (presumably and hereafter referred to as marijuana) in "Iltcson (16) have revealed conflicting effects on lung function. The Los Angeles study (15) failed to demonstrate any relationship between marijuana use and impairment in tests of lung function, including sensitive indices of small airways dysfunction, whereas the 'Meson study (16) demonstrated obstructive ventilatory defects additive to those attributable to regular tobacco use. Recent analysis of longitudinal data from the Tucson study (19) estimated significant decrements in FEV, in continuing male (but not female) marijuana smokers ;i ; 1 yr after marijuana smoking was first reported. Moreover, these decrements were twice as large as the estimated decrements in continuing tobacco smokers, and the effects of both habits were additive. The latter data suggest that marijuana smoking might be a significant risk factor for progressive airflow obstruction.

To further evaluate the possibility that continuing marijuana smoking might lead to progressive declines in lung function not consistently apparent in cross-sectional studies, we invited nonsmokers and smokers of marijuana and/or tobacco who were participants in a cohort study of the pulmonary effects of habitual

Reprinted with permission of American Journal of Respiratory and Critical Care Medicine. Copyright 0 1997 American Lung Association.