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No previous review has formally modelled the decline in IHD risk following quitting smoking. From PubMed searches and other sources we identified 15 prospective and eight case-control studies that compared IHD risk in current smokers, never smokers, and quitters by time period of quit, some studies providing separate blocks of results by sex, age or amount smoked. For each of 41 independent blocks, we estimated, using the negative exponential model, the time, H, when the excess risk reduced to half that caused by smoking. Goodness-of-fit to the model was adequate for 35 blocks, others showing a non-monotonic pattern of decline following quitting, with a variable pattern of misfit. After omitting one block with a current smoker RR 1.0, the combined H estimate was 4.40 (95% CI 3.26–5.95) years. There was considerable heterogeneity, H being 10years for 12. H increased (p

Epidemiological studies relating a particular exposure to a specified disease may present their results in a variety of ways. Often, results are presented as estimated odds ratios (or relative risks) and confidence intervals (CIs) for a number of categories of exposure, for example, by duration or level of exposure, compared with a single reference category, often the unexposed. For systematic literature review, and particularly meta-analysis, estimates for an alternative comparison of the categories, such as any exposure versus none, may be required. Obtaining these alternative comparisons is not straightforward, as the initial set of estimates is correlated. This paper describes a method for estimating these alternative comparisons based on the ideas originally put forward by Greenland and Longnecker, and provides implementations of the method, developed using Microsoft Excel and SAS. Examples of the method based on studies of smoking and cancer are given. The method also deals with results given by categories of disease (such as histological types of a cancer). The method allows the use of a more consistent comparison when summarizing published evidence, thus potentially improving the reliability of a meta-analysis.

Recent authoritative reviews consider smoking has no effect on breast cancer risk, but some studies report an increase from environmental tobacco smoke (ETS). We reviewed the overall evidence on ETS and breast cancer in nonsmoking women. We extracted details of available studies, derived relative risk (RR) estimates with confidence intervals (CIs) for various ETS exposure indices and conducted meta-analyses. Using an index for each study most closely equivalent to "spouse ever smoked," a weak, but significant, association was seen (random-effects RR = 1.12, 95% CI = 1.02-1.24, n = 22). However, the estimates were heterogeneous: close to 1.0 for prospective, North American and larger studies, and those adjusting for many potential confounders, but significantly (p.05) elevated in case-control, European, and smaller studies, and those accounting for fewer potential confounders. Risk was increased in premenopausal women (RR = 1.54, 95% CI = 1.16-2.05, n = 10), but not postmenopausal women. Dose-response findings were similarly heterogeneous. No significant increase was seen for ETS in childhood or the workplace or from the spouse specifically, but an increase was seen for total exposure (RR = 1.54, 95% CI = 1.17-2.04, n = 6). Increases mainly derive from case-control studies asking detailed ETS histories, where RRs depend heavily on who is classified in the totally unexposed reference group, and may be prone to recall bias. Results from prospective studies using similar histories are needed. Study weaknesses and possible publication bias also limit interpretation. Because of the inherent implausibility that ETS exposure might cause breast cancer, given the similar risks of smokers and nonsmokers, one cannot confidently conclude ETS exposure increases risk in nonsmokers.

Background Interest is rising in smokeless tobacco as a safer alternative to smoking, but published reviews on smokeless tobacco and cancer are limited. We review North American and European studies and compare effects of smokeless tobacco and smoking. Methods We obtained papers from MEDLINE searches, published reviews and secondary references describing epidemiological cohort and case-control studies relating any form of cancer to smokeless tobacco use. For each study, details were abstracted on design, smokeless tobacco exposure, cancers studied, analysis methods and adjustment for smoking and other factors. For each cancer, relative risks or odds ratios with 95% confidence intervals were tabulated. Overall, and also for USA and Scandinavia separately, meta-analyses were conducted using all available estimates, smoking-adjusted estimates, or estimates for never smokers. For seven cancers, smoking-attributable deaths in US men in 2005 were compared with deaths attributable to introducing smokeless tobacco into a population of never-smoking men. Results Eighty-nine studies were identified; 62 US and 18 Scandinavian. Forty-six (52%) controlled for smoking. Random-effects meta-analysis estimates for most sites showed little association. Smoking-adjusted estimates were only significant for oropharyngeal cancer (1.36, CI 1.04–1.77, n = 19) and prostate cancer (1.29, 1.07–1.55, n = 4). The oropharyngeal association disappeared for estimates published since 1990 (1.00, 0.83–1.20, n = 14), for Scandinavia (0.97, 0.68–1.37, n = 7), and for alcohol-adjusted estimates (1.07, 0.84–1.37, n = 10). Any effect of current US products or Scandinavian snuff seems very limited. The prostate cancer data are inadequate for a clear conclusion. Some meta-analyses suggest a possible effect for oesophagus, pancreas, larynx and kidney cancer, but other cancers show no effect of smokeless tobacco. Any possible effects are not evident in Scandinavia. Of 142,205 smoking-related male US cancer deaths in 2005, 104,737 are smoking-attributable. Smokeless tobacco-attributable deaths would be 1,102 (1.1%) if as many used smokeless tobacco as had smoked, and 2,081 (2.0%) if everyone used smokeless tobacco. Conclusion An increased risk of oropharyngeal cancer is evident most clearly for past smokeless tobacco use in the USA, but not for Scandinavian snuff. Effects of smokeless tobacco use on other cancers are not clearly demonstrated. Risk from modern products is much less than for smoking.