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Secondhand smoke exposure assessed using serum cotinine: associations with myocardial infarction, stroke and cardiovascular risk factors in adult men and women
  1. B. J. Jefferis1,
  2. G. D. O. Lowe2,
  3. P. Welsh2,
  4. D. A. Lawlor3,
  5. S. Ebrahim4,
  6. S. G. Wannamethee1,
  7. D. G. Cook5,
  8. P. H. Whincup5
  1. 1
    British Regional Heart Study, Department of Primary Care and Population Health, UCL Medical School, London, UK
  2. 2
    Division of Cardiovascular and Medical Sciences, University of Glasgow, Royal Infirmary, 10 Alexandra Parade, Glasgow, UK
  3. 3
    MRC CAiTE Centre, University of Bristol, Oakfield House, Oakfield Grove, Bristol, UK
  4. 4
    Non-Communicable Diseases Epidemiology Unit, Department of Epidemiology and Population Health, London School of Hygiene and Tropical Medicine, Keppel Street, London, UK
  5. 5
    Division of Community Health Sciences, St George’s, University of London, Cranmer Terrace, London, UK

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    Second-hand smoke (SHS) exposure is associated with elevated CVD risks. Previous studies have implicated altered platelet activity or endothelial dysfunction and changes in circulating levels of HDL, homocysteine and inflammatory markers. However most studies have imprecise exposure measurements and the mechanism remains uncertain. Therefore we examine associations between cotinine, a circulating biochemical marker of SHS exposure, and CVD risk factors, incident CHD and stroke in non-smoking men and women.


    4252 men and 4286 women aged 60–79 years in parallel prospective population-based studies assessed in Primary Care centres in 25 British towns in 1998–2000, with median 7.7 year follow-up for fatal and non-fatal MI (n = 445) and stroke (n = 386). Medical history, health behaviours and demographic data were reported in questionnaires and nurses recorded an ECG, made anthropometric measurements and took fasting blood samples which were analysed for serum cotinine and CVD risk markers. Cross-sectional associations between log cotinine and CVD risk markers were investigated using linear regression; prospective associations between log cotinine and incident CVD were analysed using Cox regression.


    Results were similar for men and women and are reported for genders combined. Among 4749 persistent non-smokers without pre-existing CVD or diabetes, geometric mean cotinine was 0.15 ng/mL (IQR 0.05 to 0.30). Active smokers had lower blood pressure, HDL, BMI and waist circumference, higher triglycerides and consistently elevated inflammatory and haemostatic markers than non-smokers with undetectable cotinine (⩽0.05 ng/mL). In non-smokers, higher cotinine levels were associated with higher CRP, fibrinogen, vWF and t-PA and lower albumin levels which persisted on adjustment for health behaviours, demographic factors and BMI, although not with blood pressure or lipids. A doubling in cotinine level was associated with 0.03 mg/L (95% CI 0.01 to 0.05) increase in log CRP level. However cotinine was not associated with MI: in non-smokers the HR was 1.02 (95% CI 0.94 to 1.11) per doubling in cotinine level, adjusted for socio-demographic behavioural and CVD risk factors. The adjusted HR of MI for smokers (1–9 cigarettes/day) compared to undetectable cotinine was 2.14 (95% CI 1.39 to 3.52). The adjusted HR for stroke in non-smokers was 0.91 (95% CI 0.82 to 1.00) per doubling in cotinine level and for smokers (1–9 cigarettes/day) compared to undetectable cotinine the adjusted HR of stroke was 1.03 (95% CI 0.52 to 2.04).


    In this elderly cohort with very low SHS exposure, cotinine was positively associated with levels of endothelial, inflammatory and haemostatic factors but had little effect on risks of CHD or stroke. Findings emphasise the continued importance of reducing SHS exposure, even at very low levels.