Publications by authors named "John S Fry"

Background: For smokers not intending to quit, switching to a reduced-risk nicotine product should be healthier than continuing smoking. We estimate the health impact, over the period 2000-2050, had the nicotine pouch ZYN hypothetically been introduced into the US in 2000. ZYN's toxicant profile and method of use is like that for Swedish snus, a product with known health effects much less than smoking.

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Background: Recent estimates indicated substantially replacing cigarettes by e-cigarettes would, during 2016-2100, reduce US deaths and life-years lost (millions) by 6.6 and 86.7 (Optimistic Scenario) and 1.

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The evidence on harms and benefits of e-cigarettes partly concerns whether their use encourages smokers to quit.  We addressed this using data from the nationally representative PATH study, with detailed accounting for potential confounding variables. We considered adults aged 25+.

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Interest exists in whether youth e-cigarette use ("vaping") increases risk of initiating cigarette smoking. Using Waves 1 and 2 of the US PATH study we previously reported adjustment for vaping propensity using Wave 1 variables explained about 80% of the unadjusted relationship. Here data from Waves 1 to 3 are used to avoid over-adjustment if Wave 1 vaping affected variables recorded then.

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In our latest update of the evidence on smoking bans and heart disease we summarize 59 studies. We take account of the underlying trends in incidence rates as far as possible by using control data in eight studies, and by adjustment based on observed trends in cases pre- and post-ban in 40 studies, being unable to make an adjustment in the remaining 11 studies. Overall, based on 62 independent estimates from the 59 studies, we estimate that bans reduce incidence by 5.

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We present analyses relating cigarette type to lung cancer based on a case-control study in five European countries. The analyses involved 3561 cases and 2301 controls with diseases not associated with smoking. Subjects completed a detailed questionnaire, including a lifetime smoking history.

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We use Population Health Impact Modelling to assess effects on tobacco prevalence and mortality of introducing a Reduced Risk Tobacco Product (RRP). Simulated samples start in 1990 with a US-representative smoking prevalence. Individual tobacco histories are updated annually until 2010 using estimated probabilities of switching between never/current/former smoking where the RRP is not introduced, with current users subdivided into cigarette/RRP/dual users where it is.

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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.

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We update an earlier review of smoking bans and heart disease, restricting attention to admissions for acute myocardial infarction. Forty-five studies are considered. New features of our update include consideration of non-linear trends in the underlying rate, a modified trend adjustment method where there are multiple time periods post-ban, comparison of estimates based on changes in rates and numbers of cases, and comparison of effect estimates according to post-ban changes in smoking restrictiveness.

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We quantified the decline in COPD risk following quitting using the negative exponential model, as previously carried out for other smoking-related diseases. We identified 14 blocks of RRs (from 11 studies) comparing current smokers, former smokers (by time quit) and never smokers, some studies providing sex-specific blocks. Corresponding pseudo-numbers of cases and controls/at risk formed the data for model-fitting.

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We attempted to quantify the decline in stroke risk following quitting using the negative exponential model, with methodology previously employed for IHD. We identified 22 blocks of RRs (from 13 studies) comparing current smokers, former smokers (by time quit) and never smokers. Corresponding pseudo-numbers of cases and controls/at risk formed the data for model-fitting.

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A higher concentration of high density lipoprotein cholesterol (HDL-C) in ex-smokers than smokers has consistently been observed. Better evidence of quitting effects comes from within-subject changes. We extend an earlier meta-analysis to quantify the reduction, and investigate variation by time quit and other factors.

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The excess lung cancer risk from smoking declines with time quit, but the shape of the decline has never been precisely modelled, or meta-analyzed. From a database of studies of at least 100 cases, we extracted 106 blocks of RRs (from 85 studies) comparing current smokers, former smokers (by time quit) and never smokers. Corresponding pseudo-numbers of cases and controls (or at-risk) formed the data for fitting the negative exponential model.

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Background: Reduced FEV1 is known to predict increased lung cancer risk, but previous reviews are limited. To quantify this relationship more precisely, and study heterogeneity, we derived estimates of β for the relationship RR(diff) = exp(βdiff), where diff is the reduction in FEV1 expressed as a percentage of predicted (FEV1%P) and RR(diff) the associated relative risk. We used results reported directly as β, and as grouped levels of RR in terms of FEV1%P and of associated measures (e.

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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.

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Recent studies have compared rates of acute myocardial infarction before and after introducing smoking bans. Some meta-analyses report post-ban reductions up to 19%, implausibly large considering likely changes in smoking habits and passive smoke exposure. Our literature reassessment demonstrates major weaknesses in many studies and meta-analyses, including failure to consider data from control areas or existing trends in acute myocardial infarction rates, incorrect estimation of variability, and use in some meta-analyses of results for population subsets or estimates apparently unrelated to the data reported.

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Background: The rate of forced expiratory volume in 1 second (FEV1) decline ("beta") is a marker of chronic obstructive pulmonary disease risk. The reduction in beta after quitting smoking is an upper limit for the reduction achievable from switching to novel nicotine delivery products. We review available evidence to estimate this reduction and quantify the relationship of smoking to beta.

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We compared risk of lung cancer and chronic obstructive pulmonary disease (COPD) associated with flue-cured and blended cigarettes. Mortality and smoking data were collected for 1971-2000 by sex, age, and period for three countries with a mainly flue-cured market and four with a blended market. Epidemiological relative risk estimates for current and ex smoking were summarized.

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Overexpression of Bcl-x(L) in multiple cancers correlates with resistance to chemotherapy and radiation therapy, and provides a rationale for development of small-molecule Bcl-x(L) inhibitors. Based on knockout studies, nonneoplastic cells also require Bcl-x(L) survival functions, particularly when challenged with cytotoxic agents. We analyze the selective cytotoxicity of one Bcl-x(L) inhibitor, 2-methoxy antimycin A, toward cells with excess exogenous Bcl-x(L) in isogenic cell line pairs.

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