On National Public Radio September 30, anti-smoking crusader Stanton Glantz, PhD, a UCSF faculty member, repeatedly and emphatically equated Cannabis and tobacco smoke. Steve Robinson, MD, remembered reading something on the subject in a CME course produced by NETce .com for California physicians. He forwards the following text and citations.


Contaminants in the Cannabis Plant
Cannabis may be contaminated by a variety of organisms, such as  Aspergillus fungus and bacteria, that can result in fulminant pneumonia, especially in immunocompromised persons. Nonbiologic contaminants can include heavy metals such as aluminum and cadmium from the soil, with cadmium readily absorbed into the plant at high concentrations. Organophosphate pesticides are found less often in cannabis grown outdoors versus indoor cultivation [112]. Concerns over inorganic and biologic contaminant ingestion prompted Health Canada and the OMC to carefully control all aspects of cultivation, test the product for the presence of mold spores and 28 different metals including heavy metals, and pre-emptively irradiate all cannabis products before distribution to medical or research users [26; 71]. This is not currently done to most cannabis available in the United States.

Pulmonary Function
Physician and patient concerns over pulmonary harm from cannabis smoking have been based on the known hazards from smoking tobacco, findings of carcinogenic compounds in cannabis smoke, and earlier epidemiological studies associating long-term cannabis use with respiratory dysfunction [113]. This has contributed to reluctance over medical smoked cannabis use, but more recent scientific data challenge these assumptions. Although many carcinogens and tumor promoters are common to tobacco and cannabis smoke, differences in the active constituents result in different biological outcomes. Molecules in tobacco smoke enhance carcinogenic pathways through several mechanisms, including circumvention of normal cellular checkpoint protective mechanisms; activation of respiratory epithelial cell nicotine receptors; promotion of tumor angiogenesis; stimulation of enzymes that convert polycyclic aromatic hydrocarbons found in smoke into carcinogens; and prevention of apoptotic cascades (cell death) in cells accumulating sufficient genetic damage. In contrast, molecules in cannabis smoke inhibit carcinogenic pathways through down-regulation of immunologically-generated free radical production (the innate response to inhaled smoke and particulate); THC blockade of enzymatic conversion of smoke constituents into carcinogens; the absence of cannabinoid receptors in respiratory epithelial cells (which maintains DNA damage checkpoint mechanism integrity with prolonged cannabis smoke exposure); and the anti-angiogenic, tumor-retardant, and anti-inflammatory activity of many cannabinoid smoke constituents [114; 115; 116].

These factors appear in the results of a 20-year longitudinal study of pulmonary health in 5,115 participants who smoked cannabis [117]. The authors stated that pulmonary risks from cannabis smoking had been overstated and found that, unlike tobacco smoking, cannabis smoking had no effect on measures of pulmonary function. Medicinal use of smoked cannabis was also found to be very unlikely to produce adverse effects on pulmonary function [117]. In 878 Canadians 40 years of age and older, history of tobacco smoking or tobacco and marijuana smoking, but not marijuana-only smoking, significantly elevated the risk of respiratory problems or chronic obstructive pulmonary disease (COPD) relative to non-smokers [118].

Vaporizing systems have been developed to further minimize pulmonary risks from smoked cannabis. These involve heating the plant material short of combustion and then inhaling the mist (instead of smoke). Vaporization may produce smaller quantities of the toxic smoking byproducts carbon monoxide, polycyclic aromatic hydrocarbons and tar, and compared with smoked cannabis, vaporization was found to significantly reduce carbon monoxide levels [95; 96].

cme-cover113. Taylor DR, Poulton R, Moffitt TE, Ramankutty P, Sears MR. The respiratory effects of cannabis dependence in young adults. Addiction. 2000;95(11):1669-1677.

114. Melamede R. Cannabis and tobacco smoke are not equally carcinogenic. Harm Reduction Journal. 2005;2:21.

115. Heeschen C, Jang JJ, Weis M, et al. Nicotine stimulates angiogenesis and promotes tumor growth and
atherosclerosis. Nat Med. 2001;7(7):833-839.

116. Roth MD, Marques-Magallanes JA, Yuan M, et al. Induction and regulation of the carcinogen-metabolizing
enzyme CYP1A1 by marijuana smoke and delta (9)-tetrahydrocannabinol. Am J Respir Cell Mol Biol.

117. Pletcher MJ, Vittinghoff E, Kalhan R, et al. Association between marijuana exposure and pulmonary
function over 20 years. JAMA. 2012;307(2):173-181.

118. Tan WC, Lo C, Jong A, et al. Marijuana and chronic obstructive lung disease: a population-based study.

MEMO: The effects of cannabis and tobacco on the lungs was the subject of a talk by the eminent UCLA pulmonologist Donald Tashkin,  covered by O’Shaughnessy’s.