x-p: Regular Cannabis Smoking not associated with lung cancer [View all]

[RainDog]

Last edited Fri Jun 27, 2014, 06:58 PM - Edit history (1)

More than 2000 controls and nearly 3000 subjects were included in the study from 4 different English-speaking nations.

Their findings are similar to those of a 2013 review published in the journal Annals of the American Thoracic Society, which concluded: "...Habitual use of marijuana alone does not appear to lead to significant abnormalities in lung function. ... Overall, the risks of pulmonary complications of regular use of marijuana appear to be relatively small and far lower than those of tobacco smoking."

An accompanying commentary appearing in the same journal affirmed, "...Cannabis smoking does not seem to increase risk of chronic obstructive pulmonary disease (COPD) or airway cancers. In fact, there is even a suggestion that at low doses cannabis may be protective for both conditions."

Preclinical studies have documented that cannabinoids possess potent anti-cancer properties, including the inhibition of lung cancer cell growth. To date, however, scientists have yet to conduct controlled clinical trials replicating these results in human subjects.
http://norml.org/news/2014/06/26/study-habitual-marijuana-smoking-not-associated-with-increased-risk-of-lung-cancer

http://onlinelibrary.wiley.com/doi/10.1002/ijc.29036/abstract

Abstract

To investigate the association between cannabis smoking and lung cancer risk, data on 2159 lung cancer cases and 2985 controls were pooled from 6 case-control studies in the US, Canada, UK and New Zealand within the International Lung Cancer Consortium. Study-specific associations between cannabis smoking and lung cancer were estimated using unconditional logistic regression adjusting for sociodemographic factors, tobacco smoking status and pack-years; odds-ratio estimates were pooled using random effects models. Sub-group analyses were done for sex, histology, and tobacco smoking status. The shapes of dose-response associations were examined using restricted cubic spline regression. The overall pooled OR for habitual vs. non-habitual or never users was 0.96 (95% CI: 0.66-1.38). Compared to non-habitual or never users, the summary OR was 0.88 (95%CI: 0.63-1.24) for individuals who smoked 1 or more joint-equivalents of cannabis per day and 0.94 (95%CI: 0.67-1.32) for those consumed at least 10 joint-years. For adenocarcinoma cases the ORs were 1.73 (95%CI: 0.75-4.00) and 1.74 (95%CI: 0.85-3.55), respectively. However, no association was found for the squamous cell carcinoma based on small numbers. Weak associations between cannabis smoking and lung cancer were observed in never tobacco smokers. Spline modeling indicated a weak positive monotonic association between cumulative cannabis use and lung cancer, but precision was low at high exposure levels. Results from our pooled analyses provide little evidence for an increased risk of lung cancer among habitual or long-term cannabis smokers, although the possibility of potential adverse effect for heavy consumption cannot be excluded.

A 2008 study concluded: Δ9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo

http://www.nature.com/onc/journal/v27/n3/abs/1210641a.html

Abstract

Δ9-Tetrahydrocannabinol (THC) is the primary cannabinoid of marijuana and has been shown to either potentiate or inhibit tumor growth, depending on the type of cancer and its pathogenesis. Little is known about the activity of cannabinoids like THC on epidermal growth factor receptor-overexpressing lung cancers, which are often highly aggressive and resistant to chemotherapy. In this study, we characterized the effects of THC on the EGF-induced growth and metastasis of human non-small cell lung cancer using the cell lines A549 and SW-1573 as in vitro models. We found that these cells express the cannabinoid receptors CB1 and CB2, known targets for THC action, and that THC inhibited EGF-induced growth, chemotaxis and chemoinvasion. Moreover, signaling studies indicated that THC may act by inhibiting the EGF-induced phosphorylation of ERK1/2, JNK1/2 and AKT. THC also induced the phosphorylation of focal adhesion kinase at tyrosine 397. Additionally, in in vivo studies in severe combined immunodeficient mice, there was significant inhibition of the subcutaneous tumor growth and lung metastasis of A549 cells in THC-treated animals as compared to vehicle-treated controls. Tumor samples from THC-treated animals revealed antiproliferative and antiangiogenic effects of THC. Our study suggests that cannabinoids like THC should be explored as novel therapeutic molecules in controlling the growth and metastasis of certain lung cancers.