G David Batty1, Catharine R Gale2, Barbara Jefferis3, Elisabeth Kvaavik4. 1. Department of Epidemiology and Public Health, University College London, London, UK Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, Edinburgh, UK. 2. Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, Edinburgh, UK MRC Lifecourse Epidemiology Unit, University of Southampton, Southampton, UK. 3. Department of Primary Care and Population Health, University College London, London, UK. 4. Norwegian Institute for Alcohol and Drug Research, Oslo, Norway.
Abstract
BACKGROUND: Evidence that passive smoking is a risk factor for cardiovascular disease and selected cancers is largely derived from studies in which this exposure is self-reported. Objective assessment using biochemical techniques may yield a more accurate estimate of risk, although each approach has its strengths and weaknesses. We examined the association of salivary cotinine, a widely utilised biomarker for passive smoking, and self-reported passive smoking in the home, with mortality from all causes, cardiovascular disease and all cancers combined. METHODS: In 1992, investigators on the UK Health and Lifestyle Survey collected data on salivary cotinine, self-reported smoking (direct and passive) and a range of covariates in 3731 men and women aged 25 years and over. Mortality was ascertained using linkage to national death records. RESULTS: Analyses were based on 2523 individuals (1433 [57%] women) who classified themselves as non-smokers (never and former). Seventeen years of follow-up gave rise to 588 deaths (253 from cardiovascular disease and 146 from cancer). In men, adjusted hazard ratios (HR) for the association between cotinine levels (1.3-15.0 [high] vs ≤0.3 [low] ng/mL) and the various mortality outcomes were weak for total mortality (HR; 95% CI: 1.22; 0.91 to 1.64) and cardiovascular disease (1.25; 0.78 to 1.99) and absent for all cancers combined (1.10; 0.61 to 2.00). Corresponding associations were generally stronger when self-reported passive smoking (some vs none) was the exposure of interest: 1.53 (1.12 to 2.08), 1.88 (1.20 to 2.96) and 1.58 (0.85 to 2.93). The pattern of association for women in both sets of analyses was less consistent. CONCLUSIONS: In men in the present study, compared with our biochemical marker of passive smoking, cotinine, mortality was generally more consistently associated with self-reported passive smoking. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
BACKGROUND: Evidence that passive smoking is a risk factor for cardiovascular disease and selected cancers is largely derived from studies in which this exposure is self-reported. Objective assessment using biochemical techniques may yield a more accurate estimate of risk, although each approach has its strengths and weaknesses. We examined the association of salivary cotinine, a widely utilised biomarker for passive smoking, and self-reported passive smoking in the home, with mortality from all causes, cardiovascular disease and all cancers combined. METHODS: In 1992, investigators on the UK Health and Lifestyle Survey collected data on salivary cotinine, self-reported smoking (direct and passive) and a range of covariates in 3731 men and women aged 25 years and over. Mortality was ascertained using linkage to national death records. RESULTS: Analyses were based on 2523 individuals (1433 [57%] women) who classified themselves as non-smokers (never and former). Seventeen years of follow-up gave rise to 588 deaths (253 from cardiovascular disease and 146 from cancer). In men, adjusted hazard ratios (HR) for the association between cotinine levels (1.3-15.0 [high] vs ≤0.3 [low] ng/mL) and the various mortality outcomes were weak for total mortality (HR; 95% CI: 1.22; 0.91 to 1.64) and cardiovascular disease (1.25; 0.78 to 1.99) and absent for all cancers combined (1.10; 0.61 to 2.00). Corresponding associations were generally stronger when self-reported passive smoking (some vs none) was the exposure of interest: 1.53 (1.12 to 2.08), 1.88 (1.20 to 2.96) and 1.58 (0.85 to 2.93). The pattern of association for women in both sets of analyses was less consistent. CONCLUSIONS: In men in the present study, compared with our biochemical marker of passive smoking, cotinine, mortality was generally more consistently associated with self-reported passive smoking. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
Entities:
Keywords:
Cancer Epidemiology; Cardiovascular Disease; Epidemiology; Smoking