Biomarkers of Exposure to Secondhand and Thirdhand Tobacco Smoke: Recent Advances and Future Perspectives

Torres, Sonia Felipe; Merino, Carla; Paton, Beatrix; Correig, X.; Ramírez, Noelia

doi:10.3390/ijerph15122693

Cited by 101 publications

(98 citation statements)

References 109 publications

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“…First, the true condition of smoking status was determined based solely on urinary cotinine levels. Nicotine and cotinine have relatively short biological half-lives: 11 h and 17 h to 4 days, respectively [37,38]. Because the samples we collected were spot urine samples, we may have missed appropriate times in participants who smoked infrequently.…”

Section: Limitationsmentioning

confidence: 99%

Determination of Urinary Cotinine Cut-Off Concentrations for Pregnant Women in the Japan Environment and Children’s Study (JECS)

Nishihama

Nakayama

Tabuchi

et al. 2020

IJERPH

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Few studies have assessed the accuracy of self-reported questionnaires to determine smoking habits relative to urinary biomarkers. This study investigated urinary cotinine cut-off concentrations distinguishing active, passive and non-smokers among pregnant women who participated in the Japan Environment and Children’s Study, a nationwide birth cohort study. Pregnant participants with measured urinary cotinine concentrations (UCCs) and who completed self-reported questionnaires on smoking status were included (n = 89,895). The cut-off values (COVs) for active and passive smokers were calculated by fitting mixed normal distribution functions to UCCs. The sensitivity and specificity of the questionnaires were subsequently evaluated. The median (interquartile range) UCC was 0.24 (0.083–0.96) µg/g-creatinine, with the detection rate of 89%. The COV for distinguishing active smokers from passive and non-smokers was 36.8 µg/g-creatinine. When this COV was considered to represent the true condition, the questionnaire had a sensitivity of 0.523, a specificity of 0.998, a positive predictive value (PPV) of 0.967 and a negative predictive value (NPV) of 0.957. The COV for distinguishing passive smokers from non-smokers was 0.31 µg/g-creatinine, with the questionnaire having a sensitivity of 0.222, a specificity of 0.977, a PPV of 0.868 and an NPV of 0.644. As many as 78% of passive smokers might be misclassified as non-smokers.

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Section: Limitationsmentioning

confidence: 99%

Determination of Urinary Cotinine Cut-Off Concentrations for Pregnant Women in the Japan Environment and Children’s Study (JECS)

Nishihama

Nakayama

Tabuchi

et al. 2020

IJERPH

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“…Biochemical verification is the gold standard used to validate levels of tobacco smoke exposure (TSE) in children and the tobacco use status of smokers in clinical trials [1][2][3][4][5][6]. Since pediatric TSE…”

Section: Introductionmentioning

confidence: 99%

“…Thus, cotinine is the most commonly reported measure to indicate children's recent exposure to tobacco smoke. Since the concentration of cotinine in blood and saliva are highly correlated, saliva is often used to assess TSE in children since the collection is non-invasive, relatively simple, and well-tolerated [1,2].The analytic methods most commonly used to assess cotinine are enzyme-linked immunosorbent assay (ELISA), liquid chromatography with triple quadruple tandem mass spectrometry (LC-MS/MS), and gas chromatography with mass spectrometry (GC-MS) [1]. Compared to ELISA, LC-MS/MS and GC-MS are considered to be state-of-the-art methods that are highly reliable and have excellent sensitivity and specificity to detect very low levels of TSE [1,13].…”

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confidence: 99%

“…These differences are particularly pronounced in young children due to their increased exposure to tobacco smoke from active SHS or aged SHS (i.e., THS) due to close contact with caregivers who smoke, increased time spent indoors, increased contact with surfaces (e.g., floor, furniture), and high levels of hand-to-mouth behavior. This variability leads to differences in cotinine levels in children exposed to similar concentrations of nicotine (e.g., number of cigarettes smoked by their primary caregiver) from SHS or THS [2,8,[27][28][29][30]. It is not known if these differences are observed and/or how they compare when measuring cotinine with LC-MS/MS and ELISA.Thus, the primary objectives of this study were: to assess the cotinine levels of children who were exposed to varying levels of tobacco smoke in broad SHS and THS environments, and to compare the cotinine levels obtained using LC-MS/MS and ELISA.…”

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confidence: 99%

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confidence: 99%

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

Mahabee‐Gittens

Mazzella

Doucette

et al. 2020

IJERPH

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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 to 382 ng/mL; 3% < LOQ) which was lower (p < 0.0001) than the ELISA GeoM = 5.7 (range: < LOQ to 364 ng/mL; 5% < LOQ). Similar associations of cotinine concentrations with age (β < −0.10, p < 0.0001), demographic characteristics (e.g., income), and number of cigarettes smoked by caregiver (β > 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.includes exposure from both secondhand smoke (SHS) and thirdhand smoke (THS), measurement needs to be reliable, highly sensitive and specific so that even low levels of THS exposure can be detected [1,7]. Nicotine is predominantly derived from combustible and noncombustible tobacco/nicotine products. Over 70% of nicotine is metabolized to cotinine by the liver enzyme CYP2A6 [8]. Cotinine is nicotine's major proximate metabolite with a mean half-life of 16 h; some studies have reported higher median half-life levels of up to 28.3 h in infants and older children [1,[9][10][11]. In combination with cotinine, the other nicotine metabolites are nicotine, trans-3'-hydroxy cotinine (3HC), cotinine glucuronide, nicotine glucuronide, and 3HC glucuronide, which in combination, estimates the approximate daily intake of nicotine [1,12]. Cotinine concentrations are relatively stable and can be detected in the blood, saliva, urine, hair, and nails of children who are exposed to SHS and THS [1]. Thus, cotinine is the most commonly reported measure to indicate children's recent exposure to tobacco smoke. Since the concentration of cotinine in blood and saliva are highly correlated, saliva is often used to assess TSE in children since the collect...

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A biomarker‐based study of prenatal smoking exposure and autism in a Finnish national birth cohort

et al. 2021

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Maternal exposure to tobacco smoke during pregnancy is a common and persistent exposure linked to adverse neurodevelopmental outcomes in the offspring. However, previous studies provide mixed evidence regarding the relationship between prenatal smoking and offspring autism. This study used cotinine level, a biomarker for nicotine, to investigate the relationship between prenatal smoking and autism. The authors conducted a population-based case-control study nested in a national cohort of all births in Finland from 1987 to 2005. Cases diagnosed with childhood autism (ICD-10/9 code F84.0/299.0) through 2007 were identified using data from linked national registers. Each case was matched with a control on date of birth (AE30 days), sex, and place of birth (N = 962 pairs). Maternal serum cotinine levels were prospectively measured in first-to early secondtrimester serum samples archived in a national biobank using a quantitative immunoassay. Data were analyzed using conditional logistic regression. Prenatal maternal levels of serum cotinine were not associated with the odds of autism, whether cotinine was classified continuously, by deciles, or using previously defined categories corresponding to probable maternal smoking status. After adjusting for maternal age, paternal age, previous births, and any history of parental psychiatric disorder, the odds ratio for categorical high versus low cotinine, using a 3-level exposure variable, was 0.98 (95% CI = 0.76, 1.26; p = 0.88). In conclusion, this national birth cohort-based study does not provide evidence for an association between maternal cotinine, a biomarker of maternal smoking, and risk of autism.

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Biomarkers of Exposure to Secondhand and Thirdhand Tobacco Smoke: Recent Advances and Future Perspectives

Cited by 101 publications

References 109 publications

Determination of Urinary Cotinine Cut-Off Concentrations for Pregnant Women in the Japan Environment and Children’s Study (JECS)

Determination of Urinary Cotinine Cut-Off Concentrations for Pregnant Women in the Japan Environment and Children’s Study (JECS)

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

A biomarker‐based study of prenatal smoking exposure and autism in a Finnish national birth cohort

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