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Comparison of Levels of Three Tobacco Smoke Exposure Biomarkers in Children of Smokers.

ABSTRACT: Objectives: Cotinine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), and N-oxides are biomarkers of tobacco smoke exposure (TSE) used to assess short- and longer-term TSE. The objective of this study was to assess the associations between these TSE biomarkers, sociodemographics, parental smoking, and child TSE patterns among 0-17-year-olds. Methods: A convenience sample of 179 pediatric patients (mean (SD) age = 7.9 (4.3) years) who lived with ≥1 smoker and who had parental assessments completed and urine samples analyzed for the three TSE biomarkers of interest were included. Biomarker levels were log-transformed, univariate regression models were built and Pearson correlations were assessed. Results: In total, 100% of children had detectable levels of cotinine and >96% had detectable NNAL and N-oxide levels. The geometric means of cotinine, NNAL, and N-oxide levels were 10.1 ng/mL, 25.3 pg/mL, and 22.9 pg/mL, respectively. The mean (SD) number of daily cigarettes smoked by parents was 10.6 (6.0) cigarettes. Child age negatively correlated with urinary cotinine (r = -0.202, p = 0.007) and log NNAL levels (r = -0.275, p < 0.001). The highest log-cotinine levels were in children who were younger, of African American race, and whose parents had a lower education, an annual income ≤USD15,000, and no smoking bans. The highest log-NNAL and N-oxide levels were in children whose parents had a lower education, had no smoking bans, and were around higher numbers of cigarettes. Conclusion: Children of smokers who were younger, African American, and had no smoking bans had the highest TSE biomarker levels. Targeted interventions are needed to reduce TSE levels among high-risk children.

SUBMITTER: Mahabee-Gittens EM

PROVIDER: S-EPMC8622785 | biostudies-literature |

REPOSITORIES: biostudies-literature

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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.

Project description:ObjectivesCotinine is the gold standard to estimate prevalence of secondhand tobacco smoke (SHS) exposure, and assay limit of detection (LOD) cut-points are typically used regardless of age. Our aim was to compare the concordance between mother-reported SHS exposure and serum cotinine categorising children as exposed with the assay LOD or age-specific cut-points.DesignData from the Health Outcomes and Measures of the Environment (HOME) Study, a prospective pregnancy and birth cohort.SettingHospital or participants' homes.Participants389 pregnant women aged 18 years and older, between 13 and 19 weeks of gestation, living in a five-county region of the Cincinnati, Ohio metropolitan area, and with follow-up on their children at birth and ages 12, 24, 36 and 48 months.Primary and secondary outcome measuresChildren's serum cotinine, mother-reported active smoking and SHS exposure were available at birth and during follow-up visits. We used Cohen's kappa index to assess concordance between maternal self-report and child's serum cotinine concentrations. We estimated optimal age-specific cut-points, their sensitivity-specificity and positive-negative predictive values with receiver operating characteristic curves.ResultsSelf-reported exposure and cotinine data were available for 280 women who gave birth to singleton child. When applying the assay LOD (0.015 ng/mL), concordance between maternal report and serum cotinine, without accounting for age, was below 0.23 at all times. When using age-specific cut-points (12 months: 0.11 ng/mL; 24 months: 0.08 ng/mL; 36 months: 0.05 ng/mL and 48 months: 0.04 ng/mL), concordance improved, being low at 12 months (0.39), moderate at 24 and 36 months (0.47 and 0.43) and high at 48 months (0.62).ConclusionsConcordance between mother-reported SHS exposure among children under 5 years and serum cotinine improved considerably after applying the cohort-specific and age-specific cut-points. Future studies are necessary to verify these results.

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).

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Comparison of Levels of Three Tobacco Smoke Exposure Biomarkers in Children of Smokers.

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