Higher nicotine and carbon monoxide levels in menthol cigarette smokers with and without schizophrenia
UMDNJ-Robert Wood Johnson Medical School and UMDNJ-School of Public Health Tobacco Dependence Program, New Brunswick, NJ 08901, USA. Nicotine & Tobacco Research
(Impact Factor: 3.3).
08/2007; 9(8):873-81. DOI: 10.1080/14622200701484995
This study examined whether smoking menthol cigarettes was associated with increased biochemical measures of smoke intake. Expired carbon monoxide (CO) and serum nicotine and cotinine were measured in 89 smokers with schizophrenia and 53 control smokers immediately after smoking an afternoon cigarette. Serum nicotine levels (27 vs. 22 ng/ml, p = .010), serum cotinine levels (294 vs. 240 ng/ml, p = .041), and expired CO (25 vs. 21 ppm, p = .029) were higher in smokers of menthol compared with nonmenthol cigarettes, with no differences in 3-hydroxycotinine/cotinine ratios between groups when controlling for race. Backward stepwise linear regression models showed that, in addition to having a diagnosis of schizophrenia, smoking menthol cigarettes was a significant predictor of nicotine and cotinine levels. Individuals with schizophrenia or schizoaffective disorder smoked more generic or discount value brands (Basic, Doral, Monarch, USA, Wave, others) compared with control smokers (28% vs. 6%, p = .002) but did not smoke more brands with high nicotine delivery as estimated by the U.S. Federal Trade Commission method. Although rates of mentholated cigarette smoking were not higher in smokers with schizophrenia overall, they were significantly higher in non-Hispanic White people with schizophrenia compared with controls of the same ethnic/racial subgroup (51% vs. 28%, p<.0001). The higher exhaled CO in menthol smokers suggests that the higher nicotine levels are at least partly related to increased intake of smoke from menthol cigarettes, although menthol-mediated inhibition of nicotine metabolism also may be a factor. Menthol is an important cigarette additive that may help explain why some groups have lower quit rates and more smoking-caused disease.
Available from: Darlene H Brunzell
- "Individuals with schizophrenia have a high risk for tobacco dependence. Epidemiological studies estimate that as many as 80% of individuals diagnosed with schizophrenia smoke cigarettes and clinical reports indicate that those with schizophrenia are particularly heavy smokers (Hughes et al, 1986; Glassman, 1993; Olincy et al, 1997; Kalman et al, 2005; Tidey et al, 2005; Williams et al, 2005, 2007; McKee et al, 2009). In support of a self-medication hypothesis, some studies have shown that smoking enhances cognition, improves sensory-gating deficits, and relieves side effects of neuroleptic therapeutics (Leonard et al, 1998, 2007; Sacco et al, 2005; Levin and Rezvani, 2007; D'Souza and Markou, 2011). "
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ABSTRACT: Individuals diagnosed with schizophrenia have an exceptionally high risk for tobacco dependence. Postmortem studies show that these individuals have significant reductions in α7 nicotinic acetylcholine receptors (nAChRs) in several brain areas. Decreased α7-mediated function might not only be linked to schizophrenia but also to increased tobacco consumption. The purpose of this study was to determine whether pharmacological blockade of α7 nAChRs would increase motivation of rats to intravenously self-administer nicotine (NIC) during a progressive ratio schedule of reinforcement (PR). Before PR, rats received local infusions of 0, 10, or 20 pmol of a selective α7 nAChR antagonist, α-conotoxin ArIB [V11L,V16D] (ArIB) into the nucleus accumbens (NAc) shell or the anterior cingulate cortex, brain areas that contribute to motivation for drug reward. We additionally sought to determine whether local infusion of 0, 10, or 40 nmol of a selective α7 nAChR agonist, PNU 282987, into these brain areas would decrease motivation for NIC use. Infusion of ArIB into the NAc shell and anterior cingulate cortex resulted in a significant increase in active lever pressing, breakpoints, and NIC intake, suggesting that a decrease in α7 nAChR function increases motivation to work for NIC. In contrast, PNU 282987 infusion resulted in reductions in these measures when administered into the NAc shell, but had no effect after administration into the anterior cingulate cortex. These data identify reduction of α7 nAChR function as a potential mechanism for elevated tobacco use in schizophrenia and also identify activation of α7 nAChRs as a potential strategy for tobacco cessation therapy.
Available from: PubMed Central
- "A study by Williams and colleagues  compared cotinine levels of menthol- and non-menthol-smoking patients with and without schizophrenia. The laboratory study of 142 people assessed blood cotinine levels during a typical smoking day, two minutes after smoking a usual-brand cigarette. "
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ABSTRACT: Since the 1920s, menthol has been added to cigarettes and used as a characterizing flavor. The health effects of cigarette smoking are well documented, however the health effects of menthol cigarettes as compared to non-menthol cigarettes is less well studied. This review discusses menthol's effects on 1) biomarkers of tobacco smoke exposure, 2) toxicity and cellular effects, 3) lung function and respiration, 4) pulmonary and/or vascular function, 5) allergic reactions and inflammation, and 6) tobacco-related diseases. It is concluded that menthol is a biologically active compound that has effects by itself and in conjunction with nicotine, however much of the data on the other areas of interest are inconclusive and firm conclusions cannot be drawn.
Available from: Peter N Lee
- "Of six studies on puff volume, two studies [26,27] found no effect, three [29-31] a significant decrease when smoking mentholated cigarettes, and one  a significant increase. While three studies [26,33,34] found an increase in CO level associated with mentholation (and one  claimed an increase not apparent from the analyses presented), many studies [25,28,29,31,35-39] found no effect of mentholation, and one  reported reduced CO in mentholated cigarette smokers. Three studies [32-34] reported a significant increase in cotinine level associated with mentholation, but nine studies [27,37-44] did not, one of these being based on more subjects (3,341) than all the other studies combined. "
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ABSTRACT: US mentholated cigarette sales have increased considerably over 50 years. Preference for mentholated cigarettes is markedly higher in Black people. While menthol itself is not genotoxic or carcinogenic, its acute respiratory effects might affect inhalation of cigarette smoke. This possibility seems consistent with the higher lung cancer risk in Black men, despite Black people smoking less and starting smoking later than White people. Despite experimental data suggesting similar carcinogenicity of mentholated and non-mentholated cigarettes, the lack of convincing evidence that mentholation increases puffing, inhalation or smoke uptake, and the similarity of lung cancer rates in Black and White females, a review of cigarette mentholation and lung cancer is timely given current regulatory interest in the topic.
Epidemiological studies comparing lung cancer risk in mentholated and non-mentholated cigarette smokers were identified from MedLine and other sources. Study details were extracted and strengths and weaknesses assessed. Relative risk estimates were extracted, or derived, for ever mentholated use and for long-term use, overall and by gender, race, and current/ever smoking, and meta-analyses conducted.
Eight generally good quality studies were identified, with valid cases and controls, and appropriate adjustment for age, gender, race and smoking. The studies afforded good power to detect possible effects. However, only one study presented results by histological type, none adjusted for occupation or diet, and some provided no results by length of mentholated cigarette use.The data do not suggest any effect of mentholation on lung cancer risk. Adjusted relative risk estimates for ever use vary from 0.81 to 1.12, giving a combined estimate of 0.93 (95% confidence interval 0.84-1.02, n = 8), with no increase in males (1.01, 0.84-1.22, n = 5), females (0.80, 0.67-0.95, n = 5), White people (0.87, 0.75-1.03, n = 4) or Black people (0.90, 0.73-1.10, n = 4). Estimates for current and ever smokers are similar. The combined estimate for long-term use (0.95, 0.80-1.13, n = 4) again suggests no effect of mentholation.
Higher lung cancer rates in Black males cannot be due to their greater preference for mentholated cigarettes. While some study weaknesses exist, the epidemiological evidence is consistent with mentholation having no effect on the lung carcinogenicity of cigarettes.
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