Collecting Hand Wipe Samples to Assess Thirdhand Smoke Exposure

Abstract Background As smoking prevalence has decreased in Canada, particularly during pregnancy and around children, and technological improvements have lowered detection limits, the use of traditional tobacco smoke biomarkers in infant populations requires re-evaluation. Objective We evaluated concentrations of urinary nicotine biomarkers, cotinine and trans-3’-hydroxycotinine (3HC), and questionnaire responses. We used machine learning and prediction modeling to understand sources of tobacco smoke exposure for infants from the CHILD Cohort Study. Methods Multivariable linear regression models, chosen through a combination of conceptual and data-driven strategies including random forest regression, assessed the ability of questionnaires to predict variation in urinary cotinine and 3HC concentrations of 2017 3-month-old infants. Results Although only 2% of mothers reported smoking prior to and throughout their pregnancy, cotinine and 3HC were detected in 76 and 89% of the infants’ urine (n = 2017). Questionnaire-based models explained 31 and 41% of the variance in cotinine and 3HC levels, respectively. Observed concentrations suggest 0.25 and 0.50 ng/mL as cut-points in cotinine and 3HC to characterize SHS exposure. This cut-point suggests that 23.5% of infants had moderate or regular smoke exposure. Significance Though most people make efforts to reduce exposure to their infants, parents do not appear to consider the pervasiveness and persistence of secondhand and thirdhand smoke. More than half of the variation in urinary cotinine and 3HC in infants could not be predicted with modeling. The pervasiveness of thirdhand smoke, the potential for dermal and oral routes of nicotine exposure, along with changes in public perceptions of smoking exposure and risk warrant further exploration.

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Thirdhand smoke exposure: Differences in smoke exposure indices and cultural norms between hotels and motels in South Korea

Indoor and Built Environment ◽

10.1177/1420326x211012431 ◽

2021 ◽

pp. 1420326X2110124

Author(s):

Myung-Bae Park ◽

Tae Sic Lee ◽

Jee Eun Oh ◽

Do Hoon Lee

Keyword(s):

South Korea ◽

Smoke Exposure ◽

Cultural Norms ◽

Cultural Environment ◽

Legal Regulations ◽

Thirdhand Smoke ◽

Urinary Cotinine ◽

Before And After ◽

Study Participants ◽

Cotinine Concentration

The legal regulations and cultural environment for smoking bans in hotels and motels in South Korea differ depending on the type of accommodation. The aim of this study was to assess the thirdhand smoke exposure for hotel and motel guests staying at accommodations who are expected to be relatively vulnerable to thirdhand smoke. Biomarkers for 28 participants were assessed before and after lodging at a hotel or motel for approximately 14 h. Hotel participants had statistically decreased urinary cotinine concentrations after their stay, whereas motel participants experienced increased concentrations. The concentration of nicotine-derived nitrosamine ketone in dust in hotels was lower than that in motels, and the higher dust nicotine-derived nitrosamine ketone concentration in motels had more effect on an increase in urinary cotinine concentration. Both hotels and motels legally allowed smoking in guest rooms. However, the study participants in hotels were less exposed to thirdhand smoke than those in motels.

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The association of respiratory symptoms with secondhand and thirdhand smoke exposure in Hong Kong primary school students

10.5353/th_b5662589 ◽

2015 ◽

Author(s):

Haibo Hu

Keyword(s):

Hong Kong ◽

Primary School ◽

Respiratory Symptoms ◽

Smoke Exposure ◽

Primary School Students ◽

School Students ◽

Thirdhand Smoke

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Thirdhand smoke: a new dimension to the effects of cigarette smoke on the developing lung

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00393.2010 ◽

2011 ◽

Vol 301 (1) ◽

pp. L1-L8 ◽

Cited By ~ 37

Author(s):

Virender K. Rehan ◽

Reiko Sakurai ◽

John S. Torday

Keyword(s):

Protein Synthesis ◽

Nicotinic Acetylcholine Receptors ◽

Acetylcholine Receptors ◽

In Utero ◽

Smoke Exposure ◽

Peroxisome Proliferator ◽

Differentiation Markers ◽

Peroxisome Proliferator Activated Receptor ◽

Thirdhand Smoke ◽

Ppar Γ

The underlying mechanisms and effector molecules involved in mediating in utero smoke exposure-induced effects on the developing lung are only beginning to be understood. However, the effects of a newly discovered category of smoke, i.e., thirdhand smoke (THS), on the developing lung are completely unknown. We hypothesized that, in addition to nicotine, other components of THS would also affect lung development adversely. Fetal rat lung explants were exposed to nicotine, 1-( N-methyl- N-nitrosamino)-1-(3-pyridinyl)-4-butanal (NNA), or 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), the two main tobacco-specific N-nitrosamine constituents of THS, for 24 h. We then determined key markers for alveolar paracrine signaling [epithelial differentiation markers surfactant phospholipid and protein synthesis; mesenchymal differentiation markers peroxisome proliferator-activated receptor γ (PPAR-γ), fibronectin and calponin], the BCL-2-to-Bax ratio (BCL-2/Bax), a marker of apoptosis and the involvement of nicotinic acetylcholine receptors (nAChR)-α3 and -α7 in mediating NNA's and NNK's effects on the developing lung. Similar to the effects of nicotine, exposure of the developing lung to either NNK or NNA resulted in disrupted homeostatic signaling, indicated by the downregulation of PPAR-γ, upregulation of fibronectin and calponin protein levels, decreased BCL-2/Bax, and the accompanying compensatory stimulation of surfactant phospholipid and protein synthesis. Furthermore, nAChR-α3 and -α7 had differential complex roles in mediating these effects. NNK and NNA exposure resulted in breakdown of alveolar epithelial-mesenchymal cross-talk, reflecting lipofibroblast-to-myofibroblast transdifferentiation, suggesting THS constituents as possible novel contributors to in utero smoke exposure-induced pulmonary damage. These data are particularly relevant for designing specific therapeutic strategies, and for formulating public health policies to minimize THS exposure.

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