Secondhand smoke exposure associated with HF risk

A prospective cohort study showed objectively measured—but not self-reported—exposure to secondhand smoke was associated with a 45% higher risk of incident HF in nonactive smokers compared with no exposure.

This summary is based on the publication of Lin GM, Lloyd-Jones DM, Colangelo LA, et al. - Association between secondhand smoke exposure and incident heart failure: The Multi-Ethnic Study of Atherosclerosis (MESA). Eur J Heart Fail. 2024 Jan 30 [Online ahead of print]. doi: 10.1002/ejhf.3155

Introduction and methods

Background

The association between exposure to secondhand tobacco smoke (SHS) and the prevalence of HF has been investigated in only 2 cross-sectional studies [1,2]. To date, no cohort studies have been conducted on the temporal association between SHS exposure and incident HF.

Aim of the study

The authors investigated the associations of self-reported and urinary cotinine–determined SHS exposure with incident HF among nonactive smoking adults.

Methods

The MESA study (Multi-Ethnic Study of Atherosclerosis) is a prospective, longitudinal, population-based study among 6814 participants aged 45–84 years who were free of known CVD and HF at baseline (July 2000 to July 2002) [3]. Data on self-reported SHS exposure were available for 5548 nonactive smoking individuals. SHS exposure was also objectively assessed by baseline urinary cotinine measurements in a cohort subset of 3376 nonactive smoking participants. Median follow-up duration was 17.7 years.

Outcome

The outcome of interest was a composite of definite or probable HF.

Main results

Self-reported SHS exposure

• In the group with self-reported SHS exposure, 353 total HF events were identified during follow-up (incidence rate: 4.30 per 1000 person-years).
• Multivariable Cox proportional hazards regression analysis adjusted for demographic variables, traditional CVD risk factors, physical activity, tobacco pack-years, and medication use showed that the highest tertile of the SHS exposure time (7–168 h/week; n=674) was not associated with the incidence of any HF event compared with no SHS exposure (0 h/week; n=3340) (HR: 0.70; 95%CI: 0.49–1.00; P=0.052).
• There were also no significant graded associations between increase in self-reported SHS exposure time and incident HFrEF, HFpEF, or HF of ischemic origin (all P>0.05).
• Only for incident HF of nonischemic origin, a significant (inverse) association was observed in the highest tertile of the SHS exposure time versus no SHS exposure (HR: 0.62; 95%CI: 0.41–0.94; P=0.02).

Objectively measured SHS exposure

• In the group with urinary cotinine measurements at baseline, 196 total HF events occurred (incidence rate: 3.61 per 1000 person-years).
• Participants with SHS exposure (i.e., urinary cotinine >7.07 ng/mL) had a higher risk of incident HF compared with those with undetectable urinary cotinine (≤7.07 ng/mL) (HR: 1.45; 95%CI: 1.03–2.06; P=0.034).
• Significant associations with SHS exposure were also found for incident HFrEF (HR: 1.93; 95%CI: 1.08–3.45; P=0.026) and incident HF of nonischemic origin (HR: 1.46; 95%CI: 1.01–2.12; P=0.046), but not for HFpEF events (HR: 1.30; 95%CI: 0.83–2.03; P=0.25) and HF of ischemic origin (HR: 1.45; 95%CI: 0.56–3.72; P=0.45).
• In exploratory subgroup analyses, there were no significant heterogeneities in HF risk by age (≥65 years vs. <65 years), sex, race/ethnicity, or past smoking status (former vs. never) (all P for moderation>0.05).

Conclusion

In the prospective, longitudinal, population-based MESA study, objectively measured SHS exposure (i.e., urinary cotinine >7.07 ng/mL) was associated with a 1.45-fold increased risk of any HF event in current nonactive smokers compared with no SHS exposure. Urinary cotinine–determined SHS exposure was also associated with incident HFrEF and HF of nonischemic origin. In contrast, self-reported SHS exposure did not appear to be an accurate measure for the evaluation of HF risk.

According to the authors, this latter (negative) finding may be attributed to “contamination by lifetime cumulative amounts of SHS exposure, unmeasurable environmental smoke, and recall bias from participants.” With regard to the objectively measured SHS exposure, they admit that, given the relatively short half-life of urinary cotinine (~20 h), their “study’s main limitation was the lack of multiple tests for urinary cotinine to evaluate long-term SHS exposure status.”

Find this article online at Eur J Heart Fail.

References

1. Loprinzi PD. The association of serum cotinine and congestive heart failure diagnosis among never smokers: Considerations by physical activity behavior. Int J Cardiol 2016;203:1042–1043. https://doi.org/10.1016/j.ijcard.2015.11.114

2. Skipina TM, Upadhya B, Soliman EZ. Secondhand smoke exposure is associated with prevalent heart failure: Longitudinal examination of the National Health and Nutrition Examination Survey. Nicotine Tob Res 2021;23:1512–1517. https://doi.org/10.1093/ntr/ntab047

3. Lin GM, Lloyd-Jones DM, Colangelo LA, Szklo M, Heckbert SR, Chen LY, et al. Secondhand tobacco smoke exposure, urine cotinine, and risk of incident atrial fibrillation: The Multi-Ethnic Study of Atherosclerosis. Prog Cardiovasc Dis 2022;74:38–44. https://doi.org/10.1016/j.pcad.2022.10.006