Dr. Tashkin is Emeritus Professor of Medicine in the Division of Pulmonary and Critical Care Medicine at the David Geffen School of Medicine at the University of California, Los Angeles (UCLA). He previously served as Director of the Clinical Pulmonary Function Laboratory at the UCLA Medical Center for approximately 30 years.
Dr. Tashkin’s research interests include the pulmonary effects of abuse of smoked substances (including marijuana, crack cocaine and tobacco) and community air pollution, the pathophysiology, prevention and treatment of COPD, the pathophysiology and clinical pharmacology of asthma and the evaluation and treatment of scleroderma-related interstitial lung disease (SSc-ILD). Dr. Tashkin has authored over 550 peer-reviewed journal articles as well as numerous book chapters, abstracts, editorials, and multimedia educational materials on various topics, including the health effects of marijuana and ‘crack’ cocaine, asthma, chronic obstructive pulmonary disease, airway disease management and the treatment of scleroderma-associated interstitial lung disease. Dr. Tashkin has presented numerous times in various settings, including annual association and society meetings, national and international conferences and symposia, and pulmonary grand rounds. Among his many professional activities, he is a member of the Editorial Board of Chest, Respiratory Research, Respiratory Medicine and the Journal of the COPD Foundation and Guest Editor for numerous leading scholarly medical journals. He has contributed to position papers on the effects of marijuana on lung health for the American Thoracic Society and the American Lung Association, as well as the most recent reports on the health effects of marijuana by the World Health Organization and the National Academies of Sciences, Engineering and Medicine. He is Chair of the External Advisory Committee for the American Lung Association Airways Clinical Research Centers. He has also served as a member or Chair of several Data and Safety Monitoring Boards (including several American Lung Association Airways Clinical Research Centers clinical trials) and several committees at UCLA.
Dr. Tashkin is the recipient of the 1999 American Lung Association Trudeau Award for many years of outstanding and dedicated service promoting pulmonary medicine, the American Lung Association of California’s 2003 California Medal for meritorious service in the campaign against lung disease and the 2010-2011 Dickson UCLA Emeritus Professorship Award.
Habitual marijuana smoking has been shown to impair the lung’s defense against infection (Tashkin Ann ATS 2015), implying that it might increase pneumonia risk. A few older epidemiologic studies support this possibility, but conflicting findings have been reported. HIV seropositive individuals are at particularly high risk of developing opportunistic infections, including pneumonia. We therefore examined whether marijuana increases the risk for pneumonia in participants in the Multicenter AIDS Cohort Study (MACS), an ongoing prospective study of men who have sex with men (MSM) regarding the natural history of HIV infection.
We examined data from the MACS, initiated in 1983. Participants could be HIV- (n=3,412) or HIV+ (n=3,675) at baseline, but an AIDS-defining illness was exclusionary. Participants were censored upon the date of pneumonia diagnosis, first AIDS-defining illness, death, loss-to-follow-up or study end date (12/31/13), whichever occurred first. The available study population comprised 6,111 (after excluding 706 seroconverters). We separately analyzed the 3278 and 2833 who were persistently HIV- and HIV+, respectively. Occurrence of any pneumonia, including community-acquired pneumonia and pneumocystis carinii pneumonia (PCP), was captured at semi-annual visits per protocol and confirmed by chest X-ray. Marijuana use and other covariates were measured biannually (twice-yearly) by in-person questionnaire. Frequency of marijuana use over the previous 6 months was categorized as daily, at least one/week or one/month, <one/month or never. We defined time of pneumonia from the date of current visit and assessed marijuana use and all other relevant exposures from information at the prior visit. We examined the following potential covariates: age, race/ethnicity, study site, PCP prophylaxis, pneumonia vaccination, tobacco smoking, use of other illicit substances, injection drug use, education, use of antiretroviral therapy, alcohol use, viral load, CD4 cell count, and hepatitis C infection. We used a cox proportional hazards model to estimate the hazard ratio for pneumonias (non-PCP and PCP separately) by marijuana use, adjusting for important covariates identified in prior bivariate analyses; further dose-response analyses were performed.
In multi-variate analysis, point estimates (95% CI) for marijuana smoking as an independent risk factor for non-PCP were 0.77 (0.057,1.04) and 0.964 (0.759,1.27) among persistently HIV- and HIV+ participants, respectively, and for PCP was 1.07 (0.89,1.30) among HIV+ participants. In further analyses, no evidence of a dose-response effect of marijuana on pneumonia risk was found.
These findings do not support an increase in risk of pneumonia among either HIV- or HIV+ men for any level of marijuana use.