Smoking behaviour and compensation: A review of the literature with meta-analysis

A challenge in investigating the effect of public health policies on cigarette consumption and exposure arises from variation in a smoker's exposure from cigarette to cigarette and the considerable differences between smokers. In addition, limited data are available on the effects of spontaneous product switching on a smoker's cigarette consumption and exposure to smoke constituents. Over 1000 adult smokers of the same commercial 10mg International Organization for Standardization (ISO) tar yield cigarette were recruited into the non-residential, longitudinal study across 10 cities in Germany. Cigarette consumption, mouth level exposure to tar and nicotine and biomarkers of exposure to nicotine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone were measured every 6months over a 3 and a half year period. Cigarette consumption remained stable through the study period and did not vary significantly when smokers spontaneously switched products. Mouth level exposure decreased for smokers (n=111) who switched to cigarettes of 7mg ISO tar yield or lower. In addition, downward trends in mouth level exposure estimates were observed for smokers who did not switch cigarettes. Data from this study illustrate some of the challenges in measuring smokers' long-term exposure to smoke constituents in their everyday environment.

Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

A longitudinal study of smokers’ exposure to cigarette smoke and the effects of spontaneous product switching

Cunningham

Sommarström

Camacho

et al. 2015

“…Compensatory smoking has previously been shown (Hatsukami et al, 2006b) to limit the harm reduction value of decreased smoking of cigarettes, but the biological significance of the small changes reported here is questionable. An update on the literature relating to compensatory smoking is available (Scherer and Lee, 2014).…”

Section: Tablementioning

confidence: 99%

“…Critically, there do not appear to be any published reports on likely biomarker patterns in different types of dual use. It is probable that in most cases of dual use the number of CPD will be less than the CPD under the cigarettes-only condition (Benowitz et al, 1998;Lund and McNeill, 2013;Scherer and Lee, 2014), following the ''nicotine titration '' hypothesis (McMorrow and Foxx, 1983). Under such circumstances, the contribution of combusted tobacco product to effects, as measured by individual biomarkers, should be clearly understood.…”

Section: Introductionmentioning

confidence: 99%

Magnitudes of biomarker reductions in response to controlled reductions in cigarettes smoked per day: A one-week clinical confinement study

Theophilus¹,

Coggins²,

Chen³

et al. 2015

a b s t r a c tTobacco toxicant-related exposure reduction is an important tool in harm reduction. Cigarette per day reduction (CPDR) occurs as smokers migrate from smoking cigarettes to using alternative tobacco/nicotine products, or quit smoking. Few reports characterize the dose-response relationships between CPDR and effects on exposure biomarkers, especially at the low end of CPD exposure (e.g., 5 CPD). We present data on CPDR by characterizing magnitudes of biomarker reductions. We present data from a wellcontrolled, one-week clinical confinement study in healthy smokers who were switched from smoking 19-25 CPD to smoking 20, 10, 5 or 0 CPD. Biomarkers were measured in blood, plasma, urine, and breath, and included smoke-related toxicants, urine mutagenicity, smoked cigarette filter analyses (mouth level exposure), and vital signs. Many of the biomarkers (e.g., plasma nicotine) showed strong CPDR doseresponse reductions, while others (e.g., plasma thiocyanate) showed weaker dose-response reductions. Factors that lead to lower biomarker reductions include non-CPD related contributors to the measured response (e.g., other exposure sources from environment, life style, occupation; inter-individual variability). This study confirms CPDR dose-responsive biomarkers and suggests that a one-week design is appropriate for characterizing exposure reductions when smokers switch from cigarettes to new tobacco products.

“…Second, extensive, recently reviewed (Scherer and Lee, 2014), evidence from 19 brand-switching studies (9 in the USA) and 26 cross-sectional studies (11 in the USA) where a ''compensation index'' can be estimated, clearly indicates that switching to lower yield cigarettes decreases the effective dose to the smoker and so seems likely to decrease the risk of lung cancer. While compensation is substantial, it is not complete.…”

Section: Discussionmentioning

confidence: 99%

Is the shape of the decline in risk following quitting smoking similar for squamous cell carcinoma and adenocarcinoma of the lung? A quantitative review using the negative exponential model

Fry

Forey

et al. 2015

Self Cite

One possible contributor to the reported rise in the ratio of adenocarcinoma to squamous cell carcinoma of the lung may be differences in the pattern of decline in risk following quitting for the two lung cancer types. Earlier, using data from 85 studies comparing overall lung cancer risks in current smokers, quitters (by time quit) and never smokers, we fitted the negative exponential model, deriving an estimate of 9.93years for the half-life - the time when the excess risk for quitters compared to never smokers becomes half that for continuing smokers. Here we applied the same techniques to data from 16 studies providing RRs specific for lung cancer type. From the 13 studies where the half-life was estimable for each type, we derived estimates of 11.68 (95% CI 10.22-13.34) for squamous cell carcinoma and 14.45 (11.92-17.52) for adenocarcinoma. The ratio of the half-lives was estimated as 1.32 (95% CI 1.20-1.46, p<0.001). The slower decline in quitters for adenocarcinoma, evident in subgroups by sex, age and other factors, may be one of the factors contributing to the reported rise in the ratio of adenocarcinoma to squamous cell carcinoma. Others include changes in the diagnosis and classification of lung cancer.