Dataset Information

Association of secondhand tobacco smoke exposure during childhood on adult cardiovascular disease risk among never-smokers.

ABSTRACT:

Purpose

Adult secondhand tobacco smoke (SHS) exposure is related to stroke and coronary heart disease (CHD) risk, but long-term effects are less clear. We evaluated whether childhood SHS exposure affects subsequent stroke or CHD risk among adult black and white never-smokers followed for stroke and CHD.

Methods

In this prospective cohort study, inverse probability weights were calculated to correct for bias due to attrition and survey nonresponse. Cox proportional hazards models were used to assess hazard ratios and 95% confidence intervals for stroke or CHD, separately, by number of childhood household smokers.

Results

Of 13,142 eligible participants, 6136 had childhood SHS exposure assessed. Baseline mean (SD) age was 63.5 (9.0), 65% were female, 30% black, 46% reported 0 childhood household smokers, 36% reported 1, and 18% reported 2+. In 60,649 person-years, 174 strokes were observed (2.9% of participants), and in 45,195 person-years, 114 CHD events were observed (2.1% of participants). The weighted and adjusted hazard ratios (95% confidence intervals) of stroke for 2+ versus 0 childhood household smokers was 1.66 (1.29-2.13) and was 1.15 (0.82-1.59) for CHD.

Conclusions

We observed a significant association between childhood SHS exposure and stroke, but not CHD, after age 45 years and adjusting for missing information.

SUBMITTER: Pistilli M

PROVIDER: S-EPMC6441374 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature

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Publications

Association of secondhand tobacco smoke exposure during childhood on adult cardiovascular disease risk among never-smokers.

Pistilli Maxwell M Howard Virginia J VJ Safford Monika M MM Lee Brian K BK Lovasi Gina S GS Cushman Mary M Malek Angela M AM McClure Leslie A LA

Annals of epidemiology 20190205

<h4>Purpose</h4>Adult secondhand tobacco smoke (SHS) exposure is related to stroke and coronary heart disease (CHD) risk, but long-term effects are less clear. We evaluated whether childhood SHS exposure affects subsequent stroke or CHD risk among adult black and white never-smokers followed for stroke and CHD.<h4>Methods</h4>In this prospective cohort study, inverse probability weights were calculated to correct for bias due to attrition and survey nonresponse. Cox proportional hazards models w ...[more]

PMID: 30799203

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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).

Project description:IntroductionAcrolein is a highly ciliatoxic agent, a toxic respiratory irritant, a cardiotoxicant, and a possible carcinogen present in tobacco smoke including hookah tobacco.Methods105 hookah smokers and 103 non-smokers attended exclusively hookah smoking social events at either a hookah lounge or private home, and provided urine samples the morning of and the morning after the event. Samples were analyzed for 3-hydroxypropylmercapturic acid (3-HPMA), a metabolite of acrolein.ResultsGeometric mean (GM) urinary 3-HPMA levels in hookah smokers and non-smokers exposed to secondhand smoke (SHS) increased significantly, 1.41 times, 95% CI = 1.15 to 1.74 and 1.39 times, 95% CI = 1.16 to 1.67, respectively, following a hookah social event. The highest increase (1.68 times, 95% CI = 1.15 to 2.45; p = 0.007) in 3-HPMA post a hookah social event was among daily hookah smokers (GM, from 1991 pmol/mg to 3348 pmol/mg). Pre-to-post event change in urinary 3-HPMA was significantly positively correlated with pre-to-post event change in urinary cotinine among hookah smokers at either location of hookah event, (ρ = 0.359, p = 0.001), and among non-smokers in hookah lounges (ρ = 0.369, p = 0.012).ConclusionsHookah tobacco smoke is a source of acrolein exposure. Findings support regulating hookah tobacco products including reducing humectants and sugar additives, which are precursors of acrolein under certain pyrolysis conditions. We suggest posting health warning signs for indoor smoking in hookah lounges, and encouraging voluntary bans of smoking hookah tobacco in private homes.ImplicationsOur study is the first to quantify the increase in acrolein exposure in hookah smokers and non-smokers exposed to exclusively hookah tobacco SHS at hookah social events in homes or hookah lounges. Our findings provide additional support for regulating hookah tobacco product content, protecting non-smokers' health by posting health warning signs for indoor smoking in hookah lounges, and encouraging home bans on hookah tobacco smoking to safeguard vulnerable residents.

Dataset Information

Association of secondhand tobacco smoke exposure during childhood on adult cardiovascular disease risk among never-smokers.

Purpose

Methods

Results

Conclusions

Publications

Association of secondhand tobacco smoke exposure during childhood on adult cardiovascular disease risk among never-smokers.

Similar Datasets

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