Association between secondhand smoke exposure and new-onset hypertension in 65169 self-reported never smokers verified by cotinine

Abstract

Abstract Background No study has reported the relationship between secondhand smoke (SHS) exposure and new-onset hypertension (NOHT) in self-reported never-smokers verified by cotinine. Purpose This longitudinal study was conducted to evaluate whether the change of SHS exposure status at baseline and at follow-up affects NOHT in self-reported and cotinine-verified never-smokers. Methods Out of individuals enrolled in the Kangbuk Samsung Cohort study (KSCS) between 2012 and 2016, 65,169 self-reported and cotinine-verified never-smokers without hypertension at baseline visit (20,046 men; age 36±5.7 years) were included. The mean follow-up period in this study was 32 months (6–58 months). SHS exposure was defined as having experienced passive smoking indoors at home or the workplace. Individuals were divided into 4 groups on the basis of their SHS exposure status at baseline and at follow-up: no SHS exposure group (Group I) as individuals without SHS exposure both at baseline and at follow-up; new SHS exposure group (Group II) as those without SHS exposure at baseline and with SHS exposure at follow-up; ex-SHS exposure group (Group III) as those with SHS exposure at baseline and without SHS exposure at follow-up; continuous SHS exposure group (Group IV) as those with SHS exposure both at baseline and at follow-up. New-onset hypertension was defined as systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg, or current use of antihypertensive medication(s) at follow-up. Results The incidence of NOHT in the overall population was 2.5%; the incidence in group I, II, III, and IV was 2.3%, 3.2%, 2.9%, and 3.1%, respectively (p<0.001). The results in a multivariate Cox-hazard model adjusted for the baseline variables including age, sex, body mass index, waist circumference, vigorous exercise, alcohol consumption and presence of diabetes showed that Group II and IV increased relative risks (RRs) for NOHT compared to Group I (RR[95% CI], 1.44 [1.17, 1.77] for Group II and 1.21 [1.01, 1.45] for Group IV) However, Group III did not increase the risk of NOHT (0.95 [0.83, 1.08]). In another model adjusted for the variables in the above model and creatinine, uric acid, total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides and high-sensitivity C reactive protein showed that only Group II increased the risk for NOHT (1.43 [1.16, 1.77] in Group II, 0.94 [0.82, 1.07] in Group III, 1.18 [0.98, 1.41] in Group IV). Conclusions This study showed that the new and continuous SHS exposure, but not ex-SHS exposure, increased the risk for NOHT in self-reported never-smokers verified as nonsmokers by urinary cotinine. In particular, the relationship to increased risk for NOHT was more obvious in individuals with new SHS exposure than in those with continuous SHS exposure. These findings suggest that it is important to continuously minimize SHS exposure and prohibit smoking at home and at workplace to reduce the risk of developing hypertension. Funding Acknowledgement Type of funding source: None