Active smoking is a widely accepted risk factor for cardiovascular disease and is recognized as a major public health problem. Passive smoking, also known as secondhand smoke exposure (SHSE), is thought to have similar cardiovascular consequences and the risk has been postulated to be equivalent to that of active smoking. A major component of this risk involves the connection with chronic hypertension. There are several population-based observational studies investigating the relationship between SHSE and chronic hypertension, all of which demonstrate a positive association. Given that SHSE appears to be a risk factor for chronic hypertension, SHSE should also be a risk factor for hypertensive end-organ disease. Many studies have sought to investigate this relationship, but this has yet to be fully elucidated. In this review, we focus on the current evidence regarding the association between SHSE and hypertension as well as exploration of the links between SHSE and hypertensive end-organ damage.

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Introduction Serum cotinine is a sensitive and specific biomarker for tobacco exposure including second-hand smoke exposure (SHS). We sought to examine whether SHS is associated with heart failure (HF) among non-hospitalized adults. Methods This analysis included 11 219 non-smokers (age 48.4 ± 20.5 years, 55.9% women, 70.5% whites) from the United States Third National Health and Nutrition Examination (NHANES) years 1988–1994. SHS was defined as serum cotinine ≥1 ng/mL. To assess dose-response, cut-points of serum cotinine ≥3 ng/mL and ≥6 ng/mL were used. Multivariable logistic regression was used to examine the association between SHS and HF. The consistency of this association was tested among subgroups stratified by race, gender, and comorbidities. NHANES years 2003–2006 were examined for longitudinal comparison. Results 18.9% (n = 2125) of participants had SHS exposure while 3.7% (n = 416) had HF. After adjusting for covariates, SHS was associated with a 35% increased odds of HF with a dose-response relationship between levels of serum cotinine and HF. This association was stronger in males than females (interaction p-value = 0.03) and those with a history of CVD versus those without (interaction p-value < 0.001). This association persisted in the NHANES 2003–2006 analysis. Conclusion There is a dose-response relationship between SHS and HF with possible effect modification by gender and prior CVD. This is a novel finding that underscores the harmful effects of passive smoking on the cardiovascular system and highlights the needs for further prohibition of smoking in public areas and a personalized risk assessment among high-risk groups, especially in regions with less-stringent public health policies. Implications This study showed a novel association between secondhand smoke exposure and prevalent heart failure among non-smokers, adding to the list of harmful cardiovascular manifestations of secondhand smoke exposure. This was more apparent in men and those with a prior history of cardiovascular disease. Heart failure is a debilitating disease process, so this finding has important policy implications in low-income countries and poor communities with less-stringent health policies because they are known to have the highest levels of exposure. Smoke-free policies targeting these regions would thus yield substantial public health benefits.