Smoked marijuana as a cause of lung injury

Division of Pulmonaiy & Critical Care Medicine, Department of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095-1690, USA.
Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace / Fondazione clinica del lavoro, IRCCS [and] Istituto di clinica tisiologica e malattie apparato respiratorio, Università di Napoli, Secondo ateneo 07/2005; 63(2):93-100.
Source: PubMed


In many societies, marijuana is the second most commonly smoked substance after tobacco. While delta9-tetrahydrocannabinol (THC) is unique to marijuana and nicotine to tobacco, the smoke of marijuana, like that of tobacco, consists of a toxic mixture of gases and particulates, many of which are known to be harmful to the lung. Although far fewer marijuana than tobacco cigarettes are generally smoked on a daily basis, the pulmonary consequences of marijuana smoking may be magnified by the greater deposition of smoke particulates in the lung due to the differing manner in which marijuana is smoked. Whereas THC causes modest short-term bronchodilation, regular marijuana smoking produces a number of long-term pulmonary consequences, including chronic cough and sputum, histopathologic evidence of widespread airway inflammation and injury and immunohistochemical evidence of dysregulated growth of respiratory epithelial cells, that may be precursors to lung cancer. The THC in marijuana could contribute to some of these injurious changes through its ability to augment oxidative stress, cause mitochondrial dysfunction, and inhibit apoptosis. On the other hand, physiologic, clinical or epidemiologic evidence that marijuana smoking may lead to chronic obstructive pulmonary disease or respiratory cancer is limited and inconsistent. Habitual use of marijuana is also associated with abnormalities in the structure and function of alveolar macrophages, including impairment in microbial phagocytosis and killing that is associated with defective production of immunostimulatory cytokines and nitric oxide, thereby potentially predisposing to pulmonary infection. In view of the growing interest in medicinal marijuana, further epidemiologic studies are needed to clarify the true risks of regular marijuana smoking on respiratory health.

    • "More than one third of marijuana users in that study endorsed at least one CUD symptom (Nocon et al., 2006). CUD is associated with elevated risk for use and misuse of other illicit substances (Hall & Lynskey, 2005; Macleod et al., 2004) in addition to physical health problems such as bronchitis and lung damage (Tashkin, 2005; Taylor et al., 2000). Adolescent and young adult female marijuana users face other risks as well, including increased likelihood of experiencing physical or sexual assault (Kilpatrick et al., 1997; Martino et al., 2004; Testa et al., 2003). "
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    ABSTRACT: Childhood sexual abuse (CSA) is associated with elevated risk of early marijuana use and cannabis use disorder (CUD). Both the prevalence of CSA and the course of marijuana use differ between African Americans and European Americans. The current study aimed to determine whether these differences manifest in racial/ ethnic distinctions in the association of CSA with early and problem use of marijuana. Data were derived from female participants in a female twin study and a high-risk family study of substance use (n = 4,193, 21% African-American). Cox proportional hazard regression analyses using CSA to predict initiation of marijuana use and progression to CUD symptom(s) were conducted separately by race/ethnicity. Sibling status on the marijuana outcome was used to adjust for familial influences. CSA was associated with both stages of marijuana use in African-American and European-American women. The association was consistent over the risk period (hazard ratio [HR] = 1.57, 95% confidence interval [CI] [1.37, 1.79] for initiation; HR = 1.51, 95% CI [1.21, 1.88] for CUD symptom onset) in European-American women. In African-American women, the HRs for initiation were 2.52 (95% CI [1.52, 4.18]) before age 15, 1.82 (95% CI [1.36, 2.44]) at ages 15-17, and nonsignificant after age 17. In the CUD symptom model, CSA predicted onset only at age 21 and older (HR = 2.17, 95% CI [1.31, 3.59]). The association of CSA with initiation of marijuana use and progression to problem use is stable over time in European-Ameri-can women, but in African-American women, it varies by developmental period. Findings suggest the importance of considering race/ethnicity in prevention efforts with this high-risk population.
    No preview · Article · Jul 2015 · Journal of studies on alcohol and drugs
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    • "Les liens entre le tabac et le cancer bronchique sont clairement établis depuis les travaux de Doll et Peto [2] [3], en revanche ceux qui existent avec le cannabis sont moins bien connus 4—7. Des effets carcinogènes de la fumée de cannabis indépendants de ceux du tabac sont identifiés [8]. Le cannabis est la substance psychoactive (SPA) illicite la plus consommée dans le monde [9]. "
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    ABSTRACT: Cannabis is the most commonly smoked illicit substance in the world. It can be smoked alone in plant form (marijuana) but it is mainly smoked mixed with tobacco. The combined smoking of cannabis and tobacco is a common-place phenomenon in our society. However, its use is responsible for severe pulmonary consequences. The specific impact of smoking cannabis is difficult to assess precisely and to distinguish from the effect of tobacco. Marijuana smoke contains polycyclic aromatic hydrocarbons and carcinogens at higher concentration than tobacco smoke. Cellular, tissue, animal and human studies, and also epidemiological studies, show that marijuana smoke is a risk factor for lung cancer. Cannabis exposure doubles the risk of developing lung cancer. This should encourage clinicians to identify cannabis use and to offer patients support in quitting.
    Full-text · Article · Jun 2014 · Revue des Maladies Respiratoires
    • "longitudinal study of 1037 New Zealand youths followed until the age of 26[20]found impaired respiratory function in dependent cannabis users but this finding was not replicated in a longer-term follow-up of US users.[19]Chronic cannabis smoking has not been found to increase the risk of emphysema in 8–20-year follow-ups in cannabis smokers in the USA[21,22]and New Zealand.[23]Respiratory cancers Cannabis smoke contains many of the same carcinogens as tobacco smoke, some at higher levels[24]and it is mutagenic and carcinogenic in the mouse skin test. "
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    ABSTRACT: This paper summarizes the most probable of the adverse health effects of regular cannabis use sustained over years, as indicated by epidemiological studies that have established an association between cannabis use and adverse outcomes; ruled out reverse causation; and controlled for plausible alternative explanations. We have also focused on adverse outcomes for which there is good evidence of biological plausibility. The focus is on those adverse health effects of greatest potential public health significance - those that are most likely to occur and to affect a substantial proportion of regular cannabis users. These most probable adverse effects of regular use include a dependence syndrome, impaired respiratory function, cardiovascular disease, adverse effects on adolescent psychosocial development and mental health, and residual cognitive impairment. Copyright © 2013 John Wiley & Sons, Ltd.
    No preview · Article · Jan 2014 · Drug Testing and Analysis
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