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“This article has been removed: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been removed at the request of the author. This abstract was inadvertently published in the journal when the authors

had requested that it should not. “
“Marijuana smoke is a complex mixture composed of thousands of chemical compounds, APO866 clinical trial many of which are qualitatively similar to those found in tobacco smoke (Moir et al., 2008). Like tobacco smoke, marijuana smoke has been associated with numerous adverse pulmonary effects in humans including airway inflammation, chronic bronchitis, edema, mucus hypersecretion, and the impairment of large airway function and lung efficiency (Lee and Hancox, 2011 and Tashkin, 2005). Moreover, Aldington et al. showed that the impairment of large airway function and lung efficiency is 2.5–5 times greater in marijuana

smokers than tobacco smokers (Aldington et al., 2007). Like tobacco smoke, previous studies have also shown marijuana smoke to be genotoxic both in vitro and in vivo (see learn more Maertens et al., 2009 for a review). In addition, it is suspected that marijuana smoke may be carcinogenic. Indeed, some agencies such as the California Environmental Protection Agency have placed marijuana smoke on their list of chemicals known to cause cancer (Tomar et al., 2009). However, since there is a paucity of marijuana-only smoking populations to complete definitive studies, epidemiological studies conducted to date

are limited in scope, and often confounded by concurrent CYTH4 tobacco smoking (Aldington et al., 2008, Hashibe et al., 2006, Sasco et al., 2002, Sidney et al., 1997 and Voirin et al., 2006). Therefore, a clear and widely accepted empirical link between marijuana smoking and cancer does not exist. Information on the pharmacokinetics of marijuana smoke, and the mechanisms by which it may cause adverse effects, is also limited. Several mechanisms have been proposed including genotoxicity (Ammenheuser et al., 1998, Busch et al., 1979, Chiesara et al., 1983, Leuchtenberger et al., 1973, Sherman et al., 1995, Stenchever et al., 1974, Vassiliades et al., 1986 and Wehner et al., 1980), alterations in endocrine function (Lee et al., 2006 and Lee et al., 2005), alterations in cell signaling pathways (Hart et al., 2004), and immune suppression (Baldwin et al., 1997, Massi et al., 2006 and Rieder et al., 2010). However, many of these findings are based on the testing of individual cannabinoids (e.g., Δ9-tetrahydrocannabinol, cannabinol, cannabidiol) found in marijuana smoke, as opposed to the whole smoke or smoke condensate. Genome-wide expression profiling may provide information to permit a better understanding of the toxicological pathways perturbed by exposure to marijuana smoke. Currently, there are no published studies that have used a whole genome toxicogenomics approach to evaluate responses to marijuana smoke. However, Sarafian et al.