Cotinine-assessed secondhand smoke exposure and risk of cardiovascular disease in older adults
Authors: B Jefferis, D Lawlor, S Ebrahim, S Wannamethee, et al
Reference: Heart 2010; 96:854-859 (open access)
http://heart.bmj.com/content/96/11/854.abstract
Reviewer: Joaquin Barnoya, MD, MPH, Contributing Editor, ProCor; Research Assistant, Professor of Surgery, Washington University in St. Louis, Missouri, USA; Director, Research and Education, Unidad de Cirugia Cardiovascular de Guatemala, Guatemala
Reviewer comments: This study shows how a decrease in secondhand smoke (SHS) exposure can also lead to a decrease in risk of coronary heart disease (CHD) in older men and women. This is the first cohort study assessing the relationship between low levels of SHS exposure and CHD risk in older adults. As age becomes a more important risk factor (compared to young adults) and SHS levels decrease as a results of smoke-free environments the contribution of passive smoking to CHD risk will decrease. Regardless, the study supports the need for the early implementation of smoke-free environments as they will lead to a decrease in risk of CHD.
Purpose of study: To determine the association between cotinine levels and coronary CHD in older British men and women exposed to SHS at lower levels than those experienced 20 years ago.
Location of study: UK
Study design: Between 1998 and 2000, 4252 men (who were already part of a cohort study) attended a follow up visit at age 60-79 years. Between 1999 and 2001, 4286 women attended the same follow up visit. Participants completed questionnaires regarding smoking history and CHD risk factors. Information on partner smoking status and employment status was also gathered. Serum samples were assayed for cotinine in 2007 and 2008. The limit of detection was 0.05 ng/ml. Consistent with other literature, 99% (7085) of non-smokers (at least 5 years) had cotinine levels less than or equal to 15 ng/ml. The outcome measure was first fatal or non-fatal myocardial infarction occurring after the follow up visit up to June 2008 (men) and September 2007 (women). Cox proportional hazards regression models were used to estimate the associations between serum cotinine and risk of CHD.
Results: This analysis includes 5374 non-smokers (52% were never-smokers) and as comparison group 306 light smokers (1-9 cigarettes/day). Geometric mean cotinine levels ere 104.5 ng/m (Interquartile range, IQR, 66-227) in active smokers and 0.15 ng/ml (IQR, 0.05-0.3). Of the 5374 non-smokers, 42% had undetectable cotinine levels. A doubling cotinine level and CHD risk among non-smokers (adjusted for age, gender and region of residence) was not statistically significant (HR 1.02, 95% CI 0.95-1.11). Increasing cotinine categories showed no association with CHD risk when compared with participants with undetectable levels of cotinine. Active smokers when compared with the same reference group had an adjusted 2.14 (95% CI 1.39-3.52) risk of MI.
