Changes and stability of hand nicotine levels in children of smokers: Associations with urinary biomarkers, reported child tobacco smoke exposure, and home smoking bans.

BACKGROUND: Exposure to thirdhand smoke (THS) residue takes place through inhalation, ingestion, and dermal transfer. Hand nicotine levels have been proposed to measure THS pollution in the environment of children, but little is known about its variability and stability over time and correlates of change. OBJECTIVES: The goal was to determine the stability of hand nicotine in comparison to urinary biomarkers and to explore factors that influence changes in hand nicotine. METHODS: Data were collected from 0 to 11-year-old children (Mean age = 5.9) who lived with ≥1 tobacco smokers (N = 129). At a 6-week interval, we collected repeated measures of hand nicotine, four urinary biomarkers (cotinine, trans-3'-hydroxycotinine, nicotelline N-oxides, and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol), and parent-reported child tobacco smoke exposure (TSE). Dependent sample t-tests, correlations, and multivariable regression analyses were conducted to examine the changes in child TSE. RESULTS: Hand nicotine levels (r = 0.63, p < 0.001) showed similar correlations between repeated measures to urinary biomarkers (r = 0.58-0.71; p < 0.001). Different from urinary biomarkers, mean hand nicotine levels increased over time (t(113) = 3.37, p < 0.001) being significantly higher in children from homes without smoking bans at Time 2 (p = 0.016) compared to Time 1 (p = 0.003). Changes in hand nicotine correlated with changes in cotinine and trans-3'-hydroxycotinine (r = 0.30 and r = 0.19, respectively, p < 0.05). Children with home smoking bans at Time 1 and 2 showed significantly lower hand nicotine levels compared to children without home smoking bans. DISCUSSION: Findings indicate that hand nicotine levels provide additional insights into children's exposure to tobacco smoke pollutants than reported child TSE and urinary biomarkers. Changes in hand nicotine levels show that consistent home smoking bans in homes of children of smokers can lower THS exposure. Hand nicotine levels may be influenced by the environmental settings in which they are collected.

Hand nicotine as an independent marker of thirdhand smoke pollution in children's environments.

BACKGROUND: Hand nicotine (HN) levels measure children's exposure to tobacco smoke pollutants from thirdhand and secondhand smoke. HN is associated with urinary and salivary cotinine, but the associations of HN with other tobacco smoke exposure (TSE) markers remain unknown. OBJECTIVES: We compared levels of HN and four urinary TSE biomarkers: cotinine, trans-3'-hydroxycotinine (3HC), nicotelline N-oxides, and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), and children's sociodemographic and TSE patterns. We also examined if HN is a plausible pathway for children's exposure to active smoking. METHODS: Data were collected from 175 non-smoking patients (Mean (SD) age = 5.4 (3.4) years) who lived with ≥1 cigarette smoker(s). HN and TSE biomarker levels were determined using LC-MS/MS. Multivariate and multivariable regression analyses were conducted to examine associations between TSE markers and parent-reported measures, controlling for sociodemographics. RESULTS: Of the five markers of TSE, cotinine (R2 = 0.221; p = 0.003) and HN (R2 = 0.247; p = 0.001) showed the strongest overall associations. Of the five markers, only cotinine showed significantly higher levels among Black children (ß^=0.307,p<0.05) independent of age, reported exposure, and home smoking bans. Cotinine (ß^=0.010,p<0.05), NNAL (ß^=0.012,p<0.05), and HN (ß^=0.011,p<0.05) showed significant positive associations with reported exposure independent of race, age, and home smoking bans. NNAL (ß^=-0.285,p<0.05) and HN (ß^=-0.336,p<0.05), but not cotinine, 3HC, and N-oxides, showed significantly lower levels among children who lived in homes with smoking bans. Child age, hand surface area, home smoking ban, and reported exposure independently accounted for 21 % of the variance in HN levels (p = 0.002). HN accounted for 30 % of the variance in cotinine independent of child race and child age. DISCUSSION: HN levels were associated with modifiable tobacco-related behaviors and shows promise as a marker of sources of THS pollution in a child's environment not captured by measurement of urinary cotinine alone. HN levels provide additional information about TSE, complementing other biomarkers when assessing children's overall TSE.

Comparison of Liquid Chromatography Mass Spectrometry and Enzyme-Linked Immunosorbent Assay Methods to Measure Salivary Cotinine Levels in Ill Children.

Objective: Cotinine is the preferred biomarker to validate levels of tobacco smoke exposure (TSE) in children. Compared to enzyme-linked immunosorbent assay methods (ELISA) for quantifying cotinine in saliva, the use of liquid chromatography tandem mass spectrometry (LC-MS/MS) has higher sensitivity and specificity to measure very low levels of TSE. We sought to compare LC-MS/MS and ELISA measures of cotinine in saliva samples from children overall and the associations of these measures with demographics and TSE patterns. Method: Participants were nonsmoking children (N = 218; age mean (SD) = 6.1 (5.1) years) presenting to a pediatric emergency department. Saliva samples were analyzed for cotinine using both LC-MS/MS and ELISA. Limit of quantitation (LOQ) for LC-MS/MS and ELISA was 0.1 ng/ml and 0.15 ng/ml, respectively. Results: Intraclass correlations (ICC) across methods = 0.884 and was consistent in sex and age subgroups. The geometric mean (GeoM) of LC-MS/MS = 4.1 (range: < LOQ - 382 ng/mL; 3% < LOQ) which was lower (p < 0.0001) than the ELISA GeoM = 5.7 (range: < LOQ - 364 ng/mL; 5% < LOQ). Similar associations of cotinine concentrations with age ( < -0.10, p < 0.0001), demographic characteristics (e.g., income), and number of cigarettes smoked by caregiver ( > 0.07, p < 0.0001) were found regardless of cotinine detection method; however, cotinine associations with sex and race/ethnicity were only found to be significant in models using LC-MS/MS-derived cotinine. Conclusions: Utilizing LC-MS/MS-based cotinine, associations of cotinine with sex and race/ethnicity of child were revealed that were not detectable using ELISA-based cotinine, demonstrating the benefits of utilizing the more sensitive LC-MS/MS assay for cotinine measurement when detecting low levels of TSE in children.

Contribution of thirdhand smoke to overall tobacco smoke exposure in pediatric patients: study protocol.

BACKGROUND: Thirdhand smoke (THS) is the persistent residue resulting from secondhand smoke (SHS) that accumulates in dust, objects, and on surfaces in homes where tobacco has been used, and is reemitted into air. Very little is known about the extent to which THS contributes to children's overall tobacco smoke exposure (OTS) levels, defined as their combined THS and SHS exposure. Even less is known about the effect of OTS and THS on children's health. This project will examine how different home smoking behaviors contribute to THS and OTS and if levels of THS are associated with respiratory illnesses in nonsmoking children. METHODS: This project leverages the experimental design from an ongoing pediatric emergency department-based tobacco cessation trial of caregivers who smoke and their children (NIHR01HD083354). At baseline and follow-up, we will collect urine and handwipe samples from children and samples of dust and air from the homes of smokers who smoke indoors, have smoking bans or who have quit smoking. These samples will be analyzed to examine to what extent THS pollution at home contributes to OTS exposure over and above SHS and to what extent THS continues to persist and contribute to OTS in homes of smokers who have quit or have smoking bans. Targeted and nontargeted chemical analyses of home dust samples will explore which types of THS pollutants are present in homes. Electronic medical record review will examine if THS and OTS levels are associated with child respiratory illness. Additionally, a repository of child and environmental samples will be created. DISCUSSION: The results of this study will be crucial to help close gaps in our understanding of the types, quantity, and clinical effects of OTS, THS exposure, and THS pollutants in a unique sample of tobacco smoke-exposed ill children and their homes. The potential impact of these findings is substantial, as currently the level of risk in OTS attributable to THS is unknown. This research has the potential to change how we protect children from OTS, by recognizing that SHS and THS exposure needs to be addressed separately and jointly as sources of pollution and exposure. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT02531594 . Date of registration: August 24, 2015.