The composition of cigarette smoke: a retrospective, with emphasis on                 polycyclic components

Rodgman, Alan; Smith, Carr J.; Perfetti, Thomas A.

doi:10.1191/096032700701546514

Cited by 161 publications

(98 citation statements)

References 116 publications

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“…Comparing marijuana to tobacco, there were generally lower levels of phenolics in mainstream smoke of marijuana, although resorcinol was higher. These slight reductions may support combustion temperature differentials, although the use of pyrolysis studies on tobacco under controlled conditions for comparison to cigarette smoking has been put in question, given the complexity of the latter (8). Tables 9 and 10 present the data for PAHs and aza-arenes from marijuana and tobacco in mainstream and sidestream smoke, respectively.…”

Section: Resultsmentioning

confidence: 99%

A Comparison of Mainstream and Sidestream Marijuana and Tobacco Cigarette Smoke Produced under Two Machine Smoking Conditions

Moir

Rickert²,

Levasseur³

et al. 2007

Chem. Res. Toxicol.

392

313

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The chemical composition of tobacco smoke has been extensively examined, and the presence of known and suspected carcinogens in such smoke has contributed to the link between tobacco smoking and adverse health effects. The consumption of marijuana through smoking remains a reality and, among youth, seems to be increasing. There have been only limited examinations of marijuana smoke, including for cannabinoid content and for tar generation. There have not been extensive studies of the chemistry of marijuana smoke, especially in direct comparison to tobacco smoke. In this study, a systematic comparison of the smoke composition of both mainstream and sidestream smoke from marijuana and tobacco cigarettes prepared in the same way and consumed under two sets of smoking conditions, was undertaken. This study examined the suite of chemicals routinely analyzed in tobacco smoke. As expected, the results showed qualitative similarities with some quantitative differences. In this study, ammonia was found in mainstream marijuana smoke at levels up to 20-fold greater than that found in tobacco. Hydrogen cyanide, NO, NO x , and some aromatic amines were found in marijuana smoke at concentrations 3-5 times those found in tobacco smoke. Mainstream marijuana smoke contained selected polycyclic aromatic hydrocarbons (PAHs) at concentrations lower than those found in mainstream tobacco smoke, while the reverse was the case for sidestream smoke, with PAHs present at higher concentrations in marijuana smoke. The confirmation of the presence, in both mainstream and sidestream smoke of marijuana cigarettes, of known carcinogens and other chemicals implicated in respiratory diseases is important information for public health and communication of the risk related to exposure to such materials.

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Section: Resultsmentioning

confidence: 99%

A Comparison of Mainstream and Sidestream Marijuana and Tobacco Cigarette Smoke Produced under Two Machine Smoking Conditions

Moir

Rickert²,

Levasseur³

et al. 2007

Chem. Res. Toxicol.

392

313

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“…(Johnson et al 2009), contains such chemicals, whereas cigarette smoke extract generated by bubbling cigarette smoke through culture media corresponds to only water-soluble smoke chemicals (Muller and Gebel 1998). With respect to inhibition of OATP1B1 and OCT1, a major role for PAHs, that constitute major toxic components of cigarette smoke (Rodgman et al 2000), can likely be excluded owing to the fact that both benzo(a)pyrene and phenanthrene features that determine such a cis-stimulatory effect remain however very poorly characterized.…”

Section: Discussionmentioning

confidence: 99%

Alteration of human hepatic drug transporter activity and expression by cigarette smoke condensate

et al. 2016

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Smoking is well-known to impair pharmacokinetics, through inducing expression of drug metabolizing enzymes. In the present study, we demonstrated that cigarette smoke condensate (CSC) also alters activity and expression of hepatic drug transporters, which are now recognized as major actors of hepatobiliary elimination of drugs. CSC thus directly inhibited activities of sinusoidal transporters such as OATP1B1, OATP1B3, OCT1 and NTCP as well as those of canalicular transporters like P-glycoprotein, MRP2, BCRP and MATE1, in hepatic transporters-overexpressing cells. CSC similarly counteracted constitutive OATP, NTCP and OCT1 activities in human highly-differentiated hepatic HepaRG cells. In parallel, CSC induced expression of BCRP at both mRNA and protein level in HepaRG cells, whereas it concomitantly repressed mRNA expression of various transporters, including OATP1B1, OATP2B1, OAT2, NTCP, OCT1 and BSEP, and enhanced that of MRP4. Such changes in transporter gene expression were found to be highly correlated to those caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin, a reference activator of the aryl hydrocarbon receptor (AhR) pathway, and were counteracted, for some of them, by siRNA-mediated AhR silencing. This suggests that CSC alters hepatic drug transporter levels via activation of the AhR cascade. Importantly, drug transporter expression regulations as well as some transporter activity inhibitions occurred for a range of CSC concentrations similar to those required for inducing drug metabolizing enzymes and may therefore be hypothesized to be relevant for smokers. Taken together, these data established human hepatic transporters as targets of cigarette smoke, which could contribute to known alteration of pharmacokinetics and some liver adverse effects caused by smoking. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. SummarySmoking is well-known to impair pharmacokinetics, through inducing expression of drug metabolizing enzymes. In the present study, we demonstrated that cigarette smoke condensate (CSC) also alters activity and expression of hepatic drug transporters, which are now recognized as major actors of hepatobiliary elimination of drugs. CSC thus directly inhibited activities of sinusoidal transporters such as OATP1B1, OATP1B3, OCT1 and NTCP as well as those of canalicular transporters like P-glycoprotein, MRP2, BCRP and MATE1, in hepatic transporters-overexpressing cells. CSC similarly counteracted constitutive OATP, NTCP and OCT1 activities in human highly-differentiated hepatic HepaRG cells. In parallel, CSC induced expression of BCRP at both mRNA and protein level in HepaRG ce...

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“…This is due to the presence of compounds such as polycyclic aromatic hydrocarbons (PAH), N-nitrosamines particularly nicotine-derived nitrosamines, aromatic amines, benzene and heavy metals, which are independently established as carcinogens for humans, in the tobacco smoke (Rodgman et al, 2000;Hoffman et al, 2001;Pfeifer et al, 2002). This study found that almost all of the smoking variables studied (smoking status, type of tobacco and pack-years of exposure of tobacco) conferred an increased oral cancer risk of at least two-fold.…”

Section: Discussionmentioning

confidence: 99%

Tobacco (Kretek) Smoking, Betel Quid Chewing and Risk of Oral Cancer in a Selected Jakarta Population

Amtha

Razak²,

Basuki³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Purpose: This study aimed to determine the association between tobacco consumption (kretek) and betel quid chewing with oral cancer risk. Materials and Methods: A total of 81 cases of oral cancers were matched with 162 controls in this hospital-based study. Information on sociodemographic characteristics and details of risk habits (duration, frequency and type of tobacco consumption and betel quid chewing) were collected. Association between smoking and betel quid chewing with oral cancer were analysed using conditional logistic regression. Results: Slightly more than half of the cases (55.6%) were smokers where 88.9% of them smoked kretek. After adjusting for confounders, smokers have two fold increased risk, while the risk for kretek consumers and those smoking for more than 10 years was increased to almost three-fold. Prevalence of betel quid chewing among cases and controls was low (7.4% and 1.9% respectively). Chewing of at least one quid per day, and quid combination of betel leaf, areca nut, lime and tobacco conferred a 5-6 fold increased risk. Conclusions: Smoking is positively associated with oral cancer risk. A similar direct association was also seen among betel quid chewers.

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The composition of cigarette smoke: a retrospective, with emphasis on polycyclic components

Cited by 161 publications

References 116 publications

A Comparison of Mainstream and Sidestream Marijuana and Tobacco Cigarette Smoke Produced under Two Machine Smoking Conditions

A Comparison of Mainstream and Sidestream Marijuana and Tobacco Cigarette Smoke Produced under Two Machine Smoking Conditions

Alteration of human hepatic drug transporter activity and expression by cigarette smoke condensate

Tobacco (Kretek) Smoking, Betel Quid Chewing and Risk of Oral Cancer in a Selected Jakarta Population

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