[beachguy_inthongs]

Authors
Sherman MP, Roth MD, Gong H Jr, Tashkin DP
Title
Marijuana smoking, pulmonary function, and lung macrophage oxidant release.
Source
Pharmacology, Biochemistry & Behavior
Date
1991 Nov
Issue
40(3)
Pages
663-9
Abstract
Pulmonary alveolar macrophages lavaged from tobacco smokers release increased levels of oxidants and have been implicated in the pathophysiology of emphysema. It is unknown whether lung macrophages recovered from marijuana smokers also liberate excessive levels of oxidants. To evaluate this possibility, pulmonary alveolar macrophages were obtained by bronchoalveolar lavage from nonsmokers, smokers of marijuana only, smokers of tobacco only, and smokers of tobacco plus marijuana. Spontaneous and stimulated superoxide anion release was measured by the superoxide dismutase-inhibitable reduction of ferricytochrome c. These findings were correlated with recent lung function tests. Superoxide anion production by macrophages, studies of small airway integrity (closing volume, closing capacity, and the slope of Phase III of the single-breath nitrogen washout curve), and evaluation of alveolar gas exchange (diffusing capacity of carbon monoxide) were similar in both nonsmokers and marijuana smokers. However, tobacco smoking was associated with both significantly higher levels of superoxide anion release by pulmonary alveolar macrophages and significant abnormalities of small airway function and alveolar diffusing capacity. Based on the results of this study, pulmonary alveolar macrophages of marijuana-only smokers do not produce increased amounts of oxidants when compared to macrophages of non-smoking subjects. This observation may account for the absence of abnormalities in small airway function and alveolar diffusing capacity in marijuana-only smokers, in contrast to the presence of such findings in smokers of tobacco, regardless of marijuana use.

Id Code
92391787
Authors
Wu HD, Wright RS, Sassoon CS, Tashkin DP
Title
Effects of smoked marijuana of varying potency on ventilatory drive and metabolic rate.
Source
American Review of Respiratory Disease
Date
1992 Sep
Issue
146(3)
Pages
716-21
Abstract
Ventilatory responses to hypercapnia in experienced marijuana smokers have previously been shown to decrease, increase, or not change acutely after marijuana. In one study, minute ventilation (VE) and O2 consumption (VO2) increased but hypoxic ventilatory response did not change after smoking marijuana. We further investigated the effects of marijuana of increasing potency (0, 13, and 20 mg THC) on ventilatory and mouth occlusion pressure (P0.1) responses to hypercapnia and hypoxia in 11 young, healthy men who smoked marijuana regularly but refrained from any smoked substance, alcohol, caffeine, or other drugs for greater than or equal to 12 h before study. Ventilatory and P0.1 responses to hypoxia and hypercapnia were measured on 3 separate days before and 5 and 35 min (hypoxia) and 15 and 45 min (hypercapnia) after smoking. In a companion 3-day study, 12 young male habitual marijuana smokers underwent measurements of VE, VO2, and CO2 production (VCO2) before and 5 to 135 min after smoking marijuana containing 0, 15, or 27 mg THC. None of the active marijuana preparations caused significant changes in ventilatory or P0.1 responses to either hypercapnia or hypoxia or in resting VE, VO2 or VCO2. We conclude that smoking marijuana (13 to 27 mg THC) has no acute effect on central or peripheral ventilatory drive or metabolic rate in habitual marijuana smokers. These conclusions cannot be applied to infrequent users of marijuana without further study.

Authors
- Tashkin DP, Kleerup EC, Hoh CK, Kim KJ, Webber MM, Gil E
Title
- Effects of 'crack' cocaine on pulmonary alveolar permeability.
Language
- Eng
Date
- 1997 Aug
Issue
- 0012-3692
Source
- Chest
Pages
- 327-35
Country
- UNITED STATES
Abstract
- BACKGROUND: Lung clearance of 99mTc-labeled diethylenetriamine pentaacetate (DTPA) is a sensitive test of altered alveolar epithelial permeability that has been found to be increased in smokers of tobacco, as well as a small number of healthy smokers of crack cocaine, suggesting the possibility of subclinical crack-related lung injury. STUDY OBJECTIVE: To evaluate further whether habitual smoking of cocaine alone alters alveolar permeability, whether crack smoking adds to or potentiates the effects of tobacco and/or marijuana, and whether experimental cocaine smoking acutely alters DTPA lung clearance. DESIGN: Observational cohort study (habitual cocaine smoking) and single-blind crossover study (experimental cocaine administration). SUBJECTS: Fourteen habitual smokers of cocaine alone (CS), 19 smokers of cocaine and tobacco (CTS), 3 smokers of cocaine and marijuana, 12 smokers of cocaine, tobacco, and marijuana (CMTS), and 5 smokers of marijuana plus tobacco (MTS). Results obtained in the crack-smoking subjects were compared with data previously obtained in 10 nonsmokers (NS), 9 smokers of tobacco alone (TS), 10 smokers of marijuana alone (MS), and 4 additional MTS. METHODS: Subjects underwent measurements of DTPA radioaerosol lung clearance after refraining from marijuana and/or cocaine for > 12 h and from tobacco for >2 h. Ten of the 48 crack users were tested on two days 1 to 2 weeks apart within 2 h of experimental smoking of three physiologically active or inactive doses (total 98.8+/- 15.5 or 8.5+/-2.5 mg, respectively) of cocaine base. Lung clearance half-times (T1/2) were computed from time-activity curves for each lung. RESULTS: T1/2 values for each lung in CS and MS were comparable to those of NS, while TS, MTS, CTS, and CMTS had significantly shorter clearance rates than NS (p<0.01; three-way analysis of variance). No additive or interactive effects on T1/2 were noted among tobacco, cocaine, and/or marijuana. No acute effect of experimental cocaine smoking on T1/2 was noted. CONCLUSION: Whereas regular smoking of tobacco alone or with other substances increases alveolar epithelial permeability, habitual smoking of cocaine and/or marijuana has no measurable effect on alveolar permeability in the absence of tobacco nor any additive effect to that of tobacco alone.
Research Institute
- Department of Medicine, UCLA School of Medicine, Los Angeles, CA 90095- 1690, USA.
Source
- Chest 1997 Aug;112(2):327-35

Authors
- Tashkin DP, Simmons MS, Sherrill DL, Coulson AH
Title
- Heavy habitual marijuana smoking does not cause an accelerated decline in FEV1 with age.
Language
- Eng
Date
- 1997 Jan
Issue
- 1073-449X
Source
- Am J Respir Crit Care Med
Pages
- 141-8
Country
- UNITED STATES
Abstract
- 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 FEV1) in comparison with the effect of nonsmoking and regular tobacco smoking. A convenience sample of 394 healthy young Caucasian adults (68% men; age: 33 +/- 6 yr; mean +/- 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. FEV1 was measured in all 394 participants at study entry and in 255 subjects (65 %) on up to six additional occasions at intervals of > or = 1 yr (1.7 +/- 1.1 yr) over a period of 8 yr. Random-effects models were used to estimate mean rates of decline in FEV1 and to compare these rates between smoking groups. Although men showed a significant effect of tobacco on FEV1 decline (p < 0.05), in neither men nor women was marijuana smoking associated with greater declines in FEV1 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 FEV1. 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.
Research Institute
- Department of Medicine, UCLA Schools of Medicine and Public Health, Los Angeles, CA 90095-1690, USA.
Source
- Am J Respir Crit Care Med 1997 Jan;155(1):141-8