Background: Cigarette smoking is a risk factor for several diseases, including cardiovascular disease, chronic obstructive pulmonary disease, and lung cancer, but the role of specific smoke constituents in these diseases has not been clearly established.Methods: The relationships between biomarkers of potential harm (BOPH), associated with inflammation [white blood cell (WBC), high sensitivity C-reactive protein (hs-CRP), fibrinogen, and von Willebrand factor (vWF)], oxidative stress [8-epi-prostaglandin F 2a (8-epiPGF 2a )] and platelet activation [11-dehydro-thromboxin B 2 (11-dehTxB 2 )], and machine-measured tar yields (grouped into four categories), biomarkers of exposure (BOE) to cigarette smoke: nicotine and its five metabolites (nicotine equivalents), 4-methylnitrosamino-1-(3-pyridyl)-1-butanol (total NNAL), carboxyhemoglobin, 1-hydroxypyrene, 3-hydroxypropylmercapturic acid, and monohydroxybutenyl-mercapturic acid, were investigated in 3,585 adult smokers and 1,077 nonsmokers.Results: Overall, adult smokers had higher levels of BOPHs than nonsmokers. Body mass index (BMI), smoking duration, tar category, and some of the BOEs were significant factors in the multiple regression models. Based on the F value, BMI was the highest ranking factor in the models for WBC, hs-CRP, fibrinogen, and 8-epiPGF 2a , respectively, and gender and smoking duration for 11-dehTxB 2 and vWF, respectively.Conclusions: Although several demographic factors and some BOEs were statistically significant in the model, the R 2 values indicate that only up to 22% of the variability can be explained by these factors, reflecting

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This article presents a comprehensive review of the menthol cigarette dependence-related literature and results from an original analysis of the Total Exposure Study (TES), which included 1,100 menthol and 2,400 nonmenthol adult smokers. The substantial scientific evidence available related to age of first cigarette, age of regular use, single-item dependence indicators (smoking frequency, cigarettes per day, time to first cigarette, night waking to smoke), smoking duration, numerous validated and widely accepted measures of nicotine/cigarette dependence, and our analysis of the TES do not support that menthol smokers are more dependent than nonmenthol smokers or that menthol increases dependence.

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We review approaches used to estimate the population health impact of introducing a Modified Risk Tobacco Product (MRTP). Thirteen models are described, some focussing on e-cigarettes, others more general. Most models are cohort-based, comparing results with or without MRTP introduction. They typically start with a population with known smoking habits and then use transition probabilities either to update smoking habits in the “null scenario” or to update joint smoking and MRTP habits in the “alternative scenario”. The models vary in the tobacco groups and transition probabilities considered. Based on aspects of the tobacco history developed, the models compare mortality risks, and sometimes life-years lost and health costs, between the scenarios. Estimating the effects on population health depends on frequency of use of the MRTP and smoking, and on the extent to which the products expose users to harmful constituents. Strengths and weaknesses of the approaches are summarized. Despite methodological differences, most modellers have assumed that the increase in risk of mortality from MRTP use, relative to that from cigarette smoking, is very low and have concluded that MRTP introduction is likely to have a beneficial impact. Further model development, supplemented by preliminary results from well-designed epidemiological studies, should enable more precise prediction of the anticipated effects of MRTP introduction.

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