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Passive smoking assessed by salivary cotinine and self-report in relation to cause-specific mortality: 17-year follow-up of study participants in the UK Health and Lifestyle Survey
  1. G David Batty1,2,
  2. Catharine R Gale2,3,
  3. Barbara Jefferis4,
  4. Elisabeth Kvaavik5
  1. 1Department of Epidemiology and Public Health, University College London, London, UK
  2. 2Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, Edinburgh, UK
  3. 3MRC Lifecourse Epidemiology Unit, University of Southampton, Southampton, UK
  4. 4Department of Primary Care and Population Health, University College London, London, UK
  5. 5Norwegian Institute for Alcohol and Drug Research, Oslo, Norway
  1. Correspondence to Dr David Batty, Department of Epidemiology and Public Health, University College London, 1-19 Torrington Place, London WC1E 6BT, UK; david.batty{at}ucl.ac.uk

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.

  • Epidemiology
  • Smoking
  • Cardiovascular Disease
  • Cancer Epidemiology

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