Cigarette Smokers Versus Cousers of Cannabis and Cigarettes: Exposure to Toxicants

Abstract

Introduction Cannabis and tobacco couse is common and could expose users to higher levels of toxicants. No studies have examined biomarkers of toxicant exposure in cousers of cannabis and cigarettes, compared with cigarette smokers (CS). Aims and Methods Adult daily CS were recruited from 10 US sites for a study of reduced nicotine cigarettes. In this analysis of baseline data, participants were categorized as either cousers of cannabis and tobacco (cousers; N = 167; urine positive for 11-nor-9-carboxy-Δ 9-tetrahydrocannnabinol and self-reported cannabis use ≥1×/week), or CS (N = 911; negative urine and no self-reported cannabis use). Participants who did not meet either definition (N = 172) were excluded. Self-reported tobacco and cannabis use and tobacco and/or combustion-related biomarkers of exposure were compared between groups. Results Compared to CS, cousers were younger (couser Mage = 38.96, SD = 13.01; CS Mage = 47.22, SD = 12.72; p < .001) and more likely to be male (cousers = 67.7%, CS = 51.9%, p < .001). There were no group differences in self-reported cigarettes/day, total nicotine equivalents, or breath carbon monoxide, but cousers had greater use of non-cigarette tobacco products. Compared to CS, cousers had higher concentrations of 3-hydroxypropylmercapturic acid, 2-cyanoethylmercapturic acid, S-phenylmercapturic acid, 3-hydroxy-1-methylpropylmercapturic acid (ps < .05), and phenanthrene tetraol (p < .001). No biomarkers were affected by number of cannabis use days/week or days since last cannabis use during baseline (ps > .05). Conclusions Cousers had higher concentrations of biomarkers of exposure than CS, but similar number of cigarettes per day and nicotine exposure. Additional studies are needed to determine whether cannabis and/or alternative tobacco products are driving the increased toxicant exposure. Implications Cousers of cannabis and tobacco appear to be exposed to greater levels of harmful chemicals (ie, volatile organic compounds and polycyclic aromatic hydrocarbons), but similar levels of nicotine as CS. It is unclear if the higher levels of toxicant exposure in cousers are due to cannabis use or the increased use of alternative tobacco products compared with CS. It is important for studies examining biomarkers of exposure among CS to account for cannabis use as it may have a significant impact on outcomes. Additionally, further research is needed examining exposure to harmful chemicals among cannabis users.

Acrolein and other toxicant exposures in relation to cardiovascular disease among marijuana and tobacco smokers in a longitudinal cohort of HIV-positive and negative adults

“…Among plasma metabolites associated with tobacco smoking, elevated acrolein metabolite 3HPMA was associated with increased CVD diagnoses in logistic regression models adjusted for tobacco smoking and traditional risk factors, while metabolites showing strongest associations with marijuana smoking in mixed-effects models (methylnaphthyl sulfate (2) and o-cresol sulfate) were not associated with increased CVD diagnoses in adjusted analyses. Taken together, these findings indicate marijuana smoke-exposure biomarkers reported in previous studies [ 5 , 6 ] are present at lower concentrations in exclusive marijuana smokers compared with tobacco smokers, and also show that acrolein exposure from tobacco smoke is associated with CVD.…”

“…While plasma and urinary biomarkers of smoke exposure have been well-characterized in tobacco smokers [ 9 , 10 , 13 , 40 , 41 , [51] , [52] , [53] ], only a few studies limited to analyses of urine samples have been reported in marijuana smokers [ 5 , 6 , 54 ]. Consistent with a previous study [5] , the urine acrylonitrile metabolite CYMA (N-acetyl-S-(2-cyanoethyl)-L-cysteine) and acrylamide metabolites AAMA (N-acetyl-S-(2-carbamoylethyl)-L-cysteine) and GAMA (N-acetyl-S-(2-carbamoyl-2-hydroxyethyl)- l -cysteine) were significantly elevated in marijuana smokers in both cross-sectional comparisons and mixed-effects models adjusted for tobacco smoking and other confounders.…”

“…Marijuana smoke contains some of the same toxic combustion products present in tobacco smoke [ 4 , 5 ], raising the possibility that exposure to some smoke-related toxicants could have adverse effects on health in heavy users. However, few studies have measured smoke exposure biomarkers in exclusive marijuana smokers or dual marijuana-tobacco smokers compared with exclusive tobacco smokers and non-smokers [ 6 , 7 ].…”

An Examination of Risk Factors for Tobacco and Cannabis Smoke Exposure in Adolescents Using an Epigenetic Biomarker

“…Our results also provide evidence that co-users of tobacco and cannabis on average have greater cumulative exposure to smoke and its toxic components ( 44 ), including PAHs ( 71 ). By 12th grade, those positive for both cotinine and THC showed a significantly lower average methylation at cg05575921 than those positive for THC alone ( p < 0.001), cotinine alone ( p < 0.001), or negative for both ( p < 0.001).…”

“…Importantly, while demethylation of cg05575921 appears to be driven by exposure to polyaromatic hydrocarbons (PAHs) and other compounds of tobacco smoke, this mechanism does not appear to be specific to combusted tobacco alone ( 38 – 42 ). Both tobacco ( 43 ) and cannabis ( 44 ) smoke contain high levels of PAHs, which when inhaled increase expression of the Aryl Hydrocarbon Receptor ( AHR) , and subsequently CYP1A1 ( 45 ), facilitating detoxification of these compounds. Lastly, expression of AHRR increases as a regulatory response to increased AHR expression ( 40 ), which if unregulated may result in carcinogenesis ( 39 ).…”