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,146 O AMERICAN JOURNAL OF RESPIRATORY Arvp CRITICAL CARE MEDICINE
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<br />figure 4. Declines In FEV, (in liters) with age (in years) by continuity
<br />of tobacco smoking (never, intermittent and continuing), estimated
<br />from random effects modal In men. Slope coefficients for annual de-
<br />cline in FEVs (in milliliters) for never, Intermittent and continuing
<br />tobacco smokers are &hewn at the bottom of the figura.
<br />The reason for she discrepancy between the results of these
<br />two longitudinal studies is unclear. One possible reason might
<br />be due to population sampling differences, since the randomly
<br />selected Tucson sample was more likely to be representative of
<br />the marijuana smoking population as a whole than was the Los
<br />Angeles convenience sample, which may have selectively under.
<br />recruited "sicker" smokers. Other possible reasons for these
<br />discrepant results include differences in environmental or oc.
<br />cupational exposures, concomitant substanceabuse (aside from
<br />tobacco, such as crack cocaine, phencyclidine, or heroin), inLen-
<br />sity and continuity of marijuana smoking, and other host char.
<br />acteristics, such as allergy and concomitant illness. With regard
<br />to possible confounding by differences in intensity and/or con-
<br />tinuity of marijuana use, It is noteworthy that the marijuana
<br />smokers in the present study were particularly heavy current users
<br />(mean of over 3 joints/d) and reported heavy lifetime use (mean
<br />of 43 to 56 joint -yr, defined as the number of joints per day limes
<br />the number of years smoked), and most (82% or MTS and 73%a
<br />of MS) continued to smoke marijuana during the entire follow-
<br />up period. In contrast, the marijuana smokers in the Tucson co-
<br />hort were much lighter smokers (< I joint/d, on average), and
<br />reported a much lower lifetime intensity of use (mean of 9.3
<br />marijuana joint -yr, when calculated as the number ofjoints per
<br />day times she number of years smoked) (19). Although the authors
<br />do nes specify the continuity of marijuana use in their cohort
<br />of ever marijuana users, continuing or quitting marijuana smok-
<br />ing did not influence the decrements in Jung function estimated
<br />from thew model. Thus. differences in current and lifetime amount
<br />of marijuana use, or in continuity of use during the course of
<br />follow-up, do not appear to account for the discrepant results
<br />of the two studies, since one would not expect the more intense
<br />and prolonged use among the Lot Angeles marijuana smokers
<br />to have rtsulled In the much lower rate of decline in FEV, rela-
<br />tive to nonsmoking (and even tobacco smoking) than that which
<br />was observed in the Tucson study.
<br />Specifically excluded from the present study were individuals
<br />with preexisting chronic chest disease, Including asthma or a his-
<br />tory of intravenous drug abuse or of smoking substances other
<br />than tobacco and/or marijuana. Moreover, only a small minority
<br />of the follow-up sample from this cohort (12.6%s) initiated cock
<br />P..06
<br />VOL 155 1997
<br />cocaine smoking during the follow-up period, and none initi-
<br />ated intravenous drug abuse. Asthma or other chest Ulness was
<br />not listed as an exclusionary criterion for participation in the
<br />Tucson study (16, 19). It is unlikely, however, that the presence
<br />of these Illnesses would have accounted for the difrerentially
<br />grater rate of loss of lung function in the marijuana smokers
<br />compared with the nonsmoking or tobacco smoking participants
<br />in the Tucson study (19). Although a higher rate of Initiation of
<br />smoking or other illicit substances (e.g., crack cocaine, which
<br />would be included as a nontobacco substance) by the nontobaceo
<br />smokers in tbeTucson follow-up sample might have contributed
<br />to the observed excessive rates of decline among these smokers,
<br />it is of interest that habitual crack smoking has generally not
<br />been associated with impairment in spirometric indices, at least
<br />in cross-secdonel studies (26, 27).
<br />Although a "healthy smoker" effect might have accounted for
<br />the absence of an abnormally rapid decline in lung function in
<br />the marijuana smoking volunteers for the Los Angeles study, this
<br />possibility seems unlikely, since tobacco -smoking participants
<br />in the some study did exhibit accelerated declines in FEV 1, and
<br />one would not expect that a "healthy smoker" effect would be
<br />confined only to the marijuana smokers. Additional evidence
<br />against a "hcallhy smoker" effect in the Los Angeles marijuana
<br />smokers Is their relatively high prevalence of symptoms of chronic
<br />and acute bronchitis at Visit 1, which was comparable with the
<br />prevalence of these same symptoms in the tobacco smokers in
<br />the same study (I5), as well as in the nonlobacco (marijuana)
<br />smokers in the Tucson study (16).
<br />A weakness of the present study is the relatively low follow-
<br />up rate (65%a), raising the possibility of a difrerential loss to
<br />Follow-up of the sicker participants, who might have exhibited
<br />grater rates of decline in lung Function over time. Although the
<br />latter possibility cannot be excluded, the fact (hat nearly all
<br />participants who could be contacted and did not move out of
<br />the area returned for retesting, that follow-up rates were com-
<br />parable across smoking categories, and that baseline lung
<br />function was similar in those who did and those who did not
<br />undergo follow-up rating diminishes the likelihood or this ex-
<br />planation for the lack of a demonstrable impact of continuing
<br />marijuana smokingoo lung -function decline, particularly since
<br />an accelerated decline in FEV, was detected in the tobacco.
<br />smoking participants.
<br />Other potential confounding influences (hat might have af-
<br />fected the results of this longitudinal study of lung function
<br />change include systematic differences in technician or equipment
<br />performance. However, the same equipment was used through-
<br />out the entire study, and all tests were performed by two highly
<br />experienced technicians who adhered to a rigorous daily calibra-
<br />tion and quality control protocol (28), and were cross -trained
<br />in spirometry using the Same Instrument. hforeover, any instru-
<br />ment drift or intertechnician variability in test performance would
<br />not be expected to differentially influence the results only in the
<br />marijuana smokers, since subjects in all smoking categories were
<br />tested at similar times throughout the follow-up period.
<br />Our failure to rind evidence or progressive lung dysfunction
<br />in the continuing marijuana smokers who we followed contrasts
<br />with our own observations that the proportion of these smokers
<br />who reported symptoms of chronic bronchitis was comparable
<br />with that of the tobacco smokers in The same cohort (15), and
<br />that many of the continuing marijuana smokers have shown
<br />as extensive histopathologic altcmijons on bronchial mucosal
<br />biopsies as the tobacco -only smokers (17, I8). However, these
<br />similarities between the effects of habitual smoking of mariju-
<br />ana and tobacco on chronic respiratory symptoms and proximal
<br />bronchial histopathology do not necessarily imply similar con-
<br />sequences with respect to bronchiolar and alveolar injury that
<br />might lead to smoking-related obstructive small airways disease
<br />
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