The research of Dr. Donald Tashkin

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Dr. Donald Tashkin, the medical director of UCLA’s Pulmonary Function Laboratory, has conducted research on the effects of marijuana on the lungs for over thirty years. Though his work was funded by the National Institute on Drug Abuse who were hoping to link marijuana use with lung disease, Dr. Tashkin has found that in some ways the opposite is true. With over 5,000 subjects throughout the world, his research found no decrease in pulmonary function. Among moderate users he even noted an increase in lung capacity. Though he initially was a skeptic, he has recently come out as a proponent of legalizing marijuana.

“Early on, when our research appeared as if there would be a negative impact on lung health, I was opposed to legalization because I thought it would lead to increased use and that would lead to increased health effects,” Tashkin says. “But at this point, I’d be in favor of legalization. I wouldn’t encourage anybody to smoke any substances. But I don’t think it should be stigmatized as an illegal substance. Tobacco smoking causes far more harm. And in terms of an intoxicant, alcohol causes far more harm.” *

In all his studies, Dr. Tashkin has found no link between marijuana use and an increase in lower respiratory tract infections, or any significant abnormalities in lung function. Additionally, he has found no compelling research to suggest that marijuana use can lead to an increased risk in either lung or upper airway cancer.

below please find some interesting videos and publications concerning the work of Dr. Tashkin

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Tracheobronchial Histopathology in Habitual Smokers of Cocaine, Marijuana, andor Tobacco

Histopathologic and Molecular Alterations in Bronchial Epithelium in Habitual Smokers of Marijuana, Cocaine, andor Tobacco

Airway Inflammation in Young Marijuana and Tobacco Smokers

Does Cannabis Use Predispose to Chronic Airflow Obstruction?

Effects of Smoked Substance Abuse on Nonspecific Airway Hyperresponsiveness

Heavy habitual marijuana smoking does not cause an accelerated decline in FEV1 with age