Exposure to secondhand smoke not associated with CV risk factors in never smokers
Secondhand smoke exposure (SHSE) is likely to increase the risk of cardiovascular mortality and morbidity, but in this cross-sectional, population-based study, evidence suggests that there is no consistent relationship between SHSE measured subjectively by self-report questionnaires and objectively by urine cotinine levels and blood pressure (BP), lipid or fasting glucose levels.
Furthermore, results remain unchanged even after stratification according to sex and verification by total study population with adjustment of medication.
Researchers obtained data on healthy adults (n=7,376; mean age 45.4 years; 75.2 percent women) who had never smoked, for whom there were available urine cotinine levels, from the Korea National Health and Nutrition Examination Survey 2008 to 2011. The main outcomes were systolic (S)BP, diastolic (D)BP, serum lipid profiles and fasting glucose.
Except for a marginally positive association with DBP (p=0.060), self-reported SHSE had no significant relationship with the study outcomes. Based on unadjusted analysis, higher cotinine levels correlated with lower SBP, total cholesterol, low-density lipoprotein cholesterol and triglyceride. All associations lost statistical significance after multivariable adjustment. [J Hypertens 2017;35:1976–1982]
In addition, a positive association existed between fasting glucose and urine cotinine in quartiles but not logarithm-transformed cotinine.
“This study found no significant adverse relationship between any dependent variables and SHSE as assessed by self-report questionnaires,” researchers said. “Quantitative assessment of SHSE using urine cotinine levels did not alter this relationship.”
Several studies have shown strong and consistent evidence that SHSE is associated with elevated risk of morbidity and mortality, particularly cardiovascular mortality and ischaemic heart disease. Furthermore, SHSE may increase the risk of coronary heart disease (CHD) by 25 to 30 percent and influence morbidity and mortality associated with acute coronary syndrome. [N Engl J Med 1999;340:920–926; Cardiol Rev 2013;21:94–100; Heart 2007;93:309–312; Heart 2009;95:1415–1418; Tob Induc Dis 2015;13:38]
Some mechanisms that have been proposed include platelet and endothelial dysfunction, increased arterial stiffness, increased oxidative stress and inflammation, and reduced energy metabolism, according to researchers.
Acute effects have also been proposed, such as an increase in resting heart rate (HR), BP, blood level of carboxyhaemoglobin and carbon monoxide, and a significant decrease in microcirculatory flow and HR variability. [Circulation 2005;111:2684–2698; Microcirculation 2014;21:587–592; Blood Press Monit 2010;15:251–256]
“In this study, we failed to find any consistent and meaningful changes in BP, cholesterol and fasting glucose levels attributable to SHSE. One potential explanation is publication bias… Second is a difference in the study population… Finally, the source for measuring cotinine levels differed,” researchers said. [J Hypertens 2015;33:2210–2214; Am J Hypertens 2009;22:853–859; Eur J Vasc Endovasc Sur 2014;48:703–710; BMJ 2004;329:200–205]
“As there has been cumulated evidence that SHSE is associated with an increased risk of cardiovascular mortality and morbidity, this study's findings suggest further long-term prospective studies are needed to evaluate the effect of SHSE as a cardiovascular risk factor,” they added.