Dataset Information

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

ABSTRACT:

Background/Aims

There is no study assessing the effect of changes of secondhand smoke (SHS) exposure and new-onset hypertension. We investigated the effect of a change of SHS exposure status on new-onset hypertension in self-reported and cotinine-verified never smokers.

Methods

Out of individuals enrolled in the Kangbuk Samsung Health Study between 2011 and 2016, 87,486 self-reported and cotinine-verified never smokers without hypertension at baseline visit were included with a median follow-up of 36 months. Individuals were divided into four groups on the basis of their SHS exposure status at baseline and at follow-up: no, new, former, and sustained SHS exposure groups.

Results

The incidence rates per 10,000 person-year of new-onset hypertension in no, new, former, and sustained SHS exposure groups were 84.7, 113.3, 102.0, and 123.7, respectively (p < 0.001). A multivariable Cox-hazard analyses showed that new and sustained SHS exposure groups increased their hazard ratio (HR) for new-onset hypertension compared to no SHS exposure group (HR, 1.31; 95% confidence interval [CI], 1.08 to 1.60 for new SHS exposure group; and HR, 1.24; 95% CI, 1.06 to 1.45 for sustained SHS exposure group). However, being part of the former SHS exposure group did not increase the risk of new-onset hypertension (HR, 0.91; 95% CI, 0.81 to 1.03).

Conclusions

This study showed that either new, or sustained SHS exposure, but not former SHS exposure, increased the risk for new-onset hypertension in self-reported never smokers verified as nonsmokers by urinary cotinine. These findings show the possibility that changing exposure to SHS even for a relatively short period can modify the risk of new-onset hypertension in self-reported and cotinine-verified never smokers.

SUBMITTER: Kim B

PROVIDER: S-EPMC8588976 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundProlonged past exposure to secondhand tobacco smoke (SHS) in never-smokers is associated with abnormal lung function and reduced diffusing capacity suggestive of an associated lung tissue injury and damage. The mechanisms by which past SHS exposure may contribute to lung tissue damage are unknown. Elastin is a major constituent of extracellular matrix in lung parenchyma.ObjectiveTo determine whether past exposure to SHS is associated with ongoing lung tissue damage as indicated by elevated elastin degradation products that are linked to lung function.MethodsWe measured the plasma levels of elastin degradation markers (EDM) from 193 never-smoking flight attendants with a history of remote SHS exposure in aircraft cabins and 103 nonsmoking flight attendants or sea-level control participants without such history of cabin SHS exposure and examined those levels versus their lung function with adjustment for covariates. The cabin SHS exposure was estimated based on airline employment history and years of the smoking ban enactment.ResultsThe median [interquartile range] plasma EDM level for all participants was 0.30 [0.24-0.36] ng/mL with a total range of 0.16-0.65 ng/mL. Plasma EDM levels were elevated in those with a history of exposure to cabin SHS compared to those not exposed (0.33±0.08 versus 0.26±0.06 ng/mL; age- and sex-adjusted P<0.001). In those with a history of cabin SHS exposure, higher EDM levels were associated with a lower diffusing capacity (parameter estimate [PE] 95% [confidence interval(CI)]=4.2 [0.4-8.0] %predicted decrease per 0.1 ng/mL increase in EDM; P=0.030). Furthermore, EDM levels were inversely associated with forced expiratory volume in 1 second (FEV1), FEV1 to forced vital capacity (FVC) ratio , and forced expiratory flow rate between 25% and 75% ( FEF25%-75%) (PE [95%CI]=5.8 [2.1-9.4], 4.0 [2.2-5.7], and 12.5 [5.8-19.2] %predicted decrease per 0.1 ng/mL increase in EDM, respectively; P<0.001). Plasma EDM mediated a substantial fraction of the association of SHS with FEV1, FVC, and FEF25%-75% (P<0.05).ConclusionsLong after past exposure to SHS, there is ongoing elastin degradation beyond what is expected from the aging process, which likely contributes to lower lung function and a reduced pulmonary capillary bed as seen in chronic obstructive pulmonary disease (COPD).