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Effects of `Crack' Cocaine on Pulmonary Alveolar Permeability

Donald P. Tashkin; Eric C. Kleerup; Carl K. Hoh; Kwang-Jin Kim; Milo M. Webber; Enrique Gil
Author and Funding Information

Affiliations: From the Department of Medicine, University of Southern California School of Medicine, Los Angeles,  From the Department of Radiology, UCLA School of Medicine, University of Southern California School of Medicine, Los Angeles,  From the Departments of Medicine, Physiology, and Biophysics and the Will Rogers Institute Pulmonary Research Center, University of Southern California School of Medicine, Los Angeles

Affiliations: From the Department of Medicine, University of Southern California School of Medicine, Los Angeles,  From the Department of Radiology, UCLA School of Medicine, University of Southern California School of Medicine, Los Angeles,  From the Departments of Medicine, Physiology, and Biophysics and the Will Rogers Institute Pulmonary Research Center, University of Southern California School of Medicine, Los Angeles

Affiliations: From the Department of Medicine, University of Southern California School of Medicine, Los Angeles,  From the Department of Radiology, UCLA School of Medicine, University of Southern California School of Medicine, Los Angeles,  From the Departments of Medicine, Physiology, and Biophysics and the Will Rogers Institute Pulmonary Research Center, University of Southern California School of Medicine, Los Angeles


1997 by the American College of Chest Physicians


Chest. 1997;112(2):327-335. doi:10.1378/chest.112.2.327
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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 (T½) were computed from time-activity curves for each lung.

Results: T½ 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 T½ were noted among tobacco, cocaine, and/or marijuana. No acute effect of experimental cocaine smoking on T½ 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.


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