Exposure to Marijuana Smoke Does Not Effect Lungs

Exposure to cannabis smoke, even over the long-term, is not associated with adverse effects on pulmonary function. That’s the conclusion of a major clinical trial published today in the prestigious Journal of the American Medical Association (JAMA).

Investigators at the University of California, San Francisco analyzed the association between marijuana exposure and pulmonary function over a 20 year period in a cohort of 5,115 men and women in four US cities.

Predictably, researchers “confirmed the expected reductions in FEV1 (forced expiratory volume in the first second of expiration) and FVC (forced vital capacity)” in tobacco smokers. By contrast, “Marijuana use was associated with higher FEV1 and FVC at the low levels of exposure typical for most marijuana users. With up to 7 joint-years of lifetime exposure (eg, 1 joint/d for 7 years or 1 joint/wk for 49 years), we found no evidence that increasing exposure to marijuana adversely affects pulmonary function.”

The study concludes, “Our findings suggest that occasional use of marijuana … may not be associated with adverse consequences on pulmonary function.”

To those familiar with the science of cannabis, JAMA’s findings should come as no great surprise. They are consistent with previous findings reporting no significant decrease in pulmonary function associated with moderate cannabis smoke exposure. For instance, according to a 2007 literature review conducted by researchers at the Yale University School of Medicine and published in the Archives of Internal Medicine (and summarized by NORML here), cannabis smoke exposure is not associated airflow obstruction (emphysema), as measured by airway hyperreactivity, forced expiratory volume, or other measures.

Further, in 2006, the results of the largest case-controlled study ever to investigate the respiratory effects of marijuana smoking reported that cannabis use was not associated with lung-related cancers, even among subjects who reported smoking more than 22,000 joints over their lifetime. (Read NORML’s summary of this study here.)

“We hypothesized that there would be a positive association between marijuana use and lung cancer, and that the association would be more positive with heavier use,” the study’s lead researcher, Dr. Donald Tashkin of the University of California at Los Angeles stated. “What we found instead was no association at all, and even a suggestion of some protective effect” among marijuana smokers who had lower incidences of cancer compared to non-users.

A previous 1997 retrospective cohort study consisting of 64,855 examinees in the Kaiser Permanente multiphasic health checkup in San Francisco and Oakland also reported, “[E]ver- and current use of marijuana were not associated with increased risk of cancer … of the following sites: colorectal, lung, melanoma, prostate, breast, cervix.”

Separate studies of cannabis smoke and pulmonary function have indicated that chronic exposure may be associated with an increased risk of certain respiratory complications, including cough, bronchitis, phlegm. However, the ingestion of cannabis via alternative methods such as edibles, liquid tinctures, or via vaporization — a process whereby the plant’s cannabinoids are heated to the point of vaporization but below the point of combustion –- virtually eliminates consumers’ exposure to such unwanted risk factors and has been determined to be a ‘safe and effective’ method of ingestion in clinical trial settings.

 
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The following text is taken directly from the US government's National Cancer Institute website: http://www.cancer.gov/cancertopics/pdq/cam/cannabis/healthprofessional/page4

* ANTI-TUMOR EFFECTS

One study in mice and rats suggested that cannabinoids may have a protective effect against the development of certain types of tumors. During this 2-year study, groups of mice and rats were given various doses of THC by gavage. A dose-related decrease in the incidence of hepatic adenoma tumors and hepatocellular carcinoma was observed in the mice. Decreased incidences of benign tumors (polyps and adenomas) in other organs (mammary gland, uterus, pituitary, testis, and pancreas) were also noted in the rats. In another study, delta-9-THC, delta-8-THC, and cannabinol were found to inhibit the growth of Lewis lung adenocarcinoma cells in vitro and in vivo. In addition, other tumors have been shown to be sensitive to cannabinoid-induced growth inhibition.

Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis and metastasis. Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death. These compounds have been shown to induce apoptosis in glioma cells in culture and induce regression of glioma tumors in mice and rats. Cannabinoids protect normal glial cells of astroglial and oligodendroglial lineages from apoptosis mediated by the CB1 receptor.

In an in vivo model using severe combined immunodeficient mice, subcutaneous tumors were generated by inoculating the animals with cells from human non-small cell lung carcinoma cell lines. Tumor growth was inhibited by 60% in THC-treated mice compared with vehicle-treated control mice. Tumor specimens revealed that THC had antiangiogenic and antiproliferative effects.

* ANTI-INFLAMMATORY EFFECTS

In addition, both plant-derived and endogenous cannabinoids have been studied for anti- inflammatory effects. A mouse study demonstrated that endogenous cannabinoid system signaling is likely to provide intrinsic protection against colonic inflammation. As a result, a hypothesis that phytocannabinoids and endocannabinoids may be useful in the prevention and treatment of colorectal cancer has been developed.

* ANTIVIRAL PROPERTIES

Another study has shown delta-9-THC is a potent and selective antiviral agent against Kaposi sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8. The researchers concluded that additional studies on cannabinoids and herpesviruses are warranted, as they may lead to the development of drugs that inhibit the reactivation of these oncogenic viruses. Subsequently, another group of investigators reported increased efficiency of KSHV infection of human dermal microvascular epithelial cells in the presence of low doses of delta-9-THC.

* APPETITE STIMULATOR

Many animal studies have previously demonstrated that delta-9-THC and other cannabinoids have a stimulatory effect on appetite and increase food intake. It is believed that the endogenous cannabinoid system may serve as a regulator of feeding behavior. The endogenous cannabinoid anandamide potently enhances appetite in mice. Moreover, CB1 receptors in the hypothalamus may be involved in the motivational or reward aspects of eating.

* AS A PAIN KILLER

Understanding the mechanism of cannabinoid-induced analgesia has been increased through the study of cannabinoid receptors, endocannabinoids, and synthetic agonists and antagonists. The CB1 receptor is found in both the central nervous system (CNS) and in peripheral nerve terminals. Similar to opioid receptors, increased levels of the CB1 receptor are found in sections of the brain that regulate nociceptive processing. CB2 receptors, located predominantly in peripheral tissue, exist at very low levels in the CNS. With the development of receptor-specific antagonists, additional information about the roles of the receptors and endogenous cannabinoids in the modulation of pain has been obtained.

Cannabinoids may also contribute to pain modulation through an anti-inflammatory mechanism; a CB2 effect with cannabinoids acting on mast cell receptors to attenuate the release of inflammatory agents, such as histamine and serotonin, and on keratinocytes to enhance the release of analgesic opioids has been described.

The American Public Health Association, American Nurses Association, Leukemia and Lymphoma Society, National Academy of HIV Medicine, two former U.S. surgeon generals, and hundreds of other medical professional groups all say that marijuana should be available to patients whose doctors recommend it.

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