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Introduction: The Angiotensin-Converting Enzyme 2 (ACE2) is the main receptor of the SARS-CoV-2. There is contradictory evidence on how the exposure to nicotine may module the concentration of soluble ACE2 (sACE2). The aim of this study was to assess the association between nicotine and sACE2 concentrations in saliva samples., Methods: Pooled analysis performed with data retrieved from two studies (n = 634 and n = 302). Geometric mean (GM) concentrations of sACE2, both total and relative to the total amount of protein in the sample, were compared according to sociodemographic variables and variables associated to nicotine. Multivariable linear regression models were fitted to explore the associations of sACE2 with nicotine adjusting for sex, age and body mass index. Spearman's rank-correlation coefficients were estimated between the concentrations of nicotine and cotinine, and pack-years, the concentration of relative sACE2 and the isoforms of sACE2., Results: We observed a significant increase of 0.108‰ and 0.087 ng/μl in the relative and absolute salivary sACE2 GM concentrations, respectively, between the lowest and highest nicotine levels. Similar results were observed for cotinine. These associations did not change in the multivariable linear models. There was a low correlation of nicotine and cotinine concentration with the concentration of relative salivary sACE2 (r s  = 0.153 and r s  = 0.132, respectively), pack-years (r s  = 0.222 and r s  = 0.235, respectively) and with the concentration of isoform 40 KDa (r s  = 0.193 and r s  = 0.140, respectively)., Conclusion: Salivary nicotine concentration seems to be limitedly associated with the concentration of sACE2., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Inc. All rights reserved.)

A straightforward, high-throughput method was developed and fully validated for the simultaneous determination of the specific tobacco biomarkers nicotine and its main metabolite cotinine in a wide dynamic range and supporting the most common human biological matrices (urine, oral fluid and hair). Sample preparation was performed inside the very HPLC injection vials by pipetting 0.5 mL of the liquid samples, deuterated internal standards in alkaline solution and dichloromethane as extraction solvent. Solid samples (i.e. around 10 mg hair) were first submitted to alkaline digestion in the HPLC vials and processed accordingly. The organic phase (reached through the upper aqueous layer) was directly injected without further treatment. Instrumental analysis was performed using hydrophilic interaction (HILIC) ultra-high performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS). Total chromatographic time was 2 min. The method covers a wide dynamic range making it fit-for-purpose for the analysis of samples covering entire populations, irrespective of the level of exposure or tobacco use. Calibration curves (r (2) > 0.995) covered the range 1-2000 ng/mL (or 0.05-100 ng/mg hair) for nicotine and 0.1-2000 ng/mL (or 0.005-100 ng/mg hair) for cotinine. Within-run and between-run precision and accuracy were typically below 10 %, and always below 20 % at the lower limit of quantification. The method was successfully applied to the analysis of samples from different projects involving multiple matrices.

Background: Tobacco smoke pollution (TSP) has major negative effects on infant health. Our objectives were to determine the effectiveness of a brief primary care intervention directed at parents who smoke in reducing babies' TSP exposure, and to establish variables related to greater exposure., Method: A multicentre, open, cluster-randomised clinical trial in Catalonia. The 83 participating primary health paediatric teams of the Catalan Health Service recruited 1101 babies whose parents were smokers. The intervention group (IG) received a brief TSP intervention; the control group (CG) received the usual care. Outcomes were measured by parents' reported strategies to avoid TSP exposure. Baseline clinical data and characteristics of each baby's TSP exposure were collected, along with infant hair samples and parents' tobacco use and related attitudes/behaviours. At 3-month and 6-month follow-up, behavioural changes to avoid TSP exposure were recorded; the association between reported parental behaviours and nicotine concentration in infant hair samples was tested in a random sample of 253 babies at baseline and 6 months., Results: During follow-up, TSP-avoidance strategies improved more in the IG than in the CG: 35.4% and 26.9% ( p=0.006) at home, and 62.2% and 53.1% in cars (p=0.008). Logistic regression showed adjusted ORs for appropriate measures in the IG versus CG of 1.59 (95% CI 1.21 to 2.09) at home and 1.30 (95% CI 0.97 to 1.75) in cars. Hair samples showed that 78.7% of the babies tested were exposed. Reduced nicotine concentration was associated with improved implementation of effective strategies reported by parents at home (p=0.029) and in cars (p=0.014)., Conclusions: The intervention produced behavioural changes to avoid TSP exposure in babies. The proportion of babies with nicotine (>=1ng/mg) in hair samples at baseline is a concern., Trial Registration Number: Clinical Trials.gov Identifier: NCT00788996., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.)

Objective: We assessed and characterized the relationship among biomarkers of secondhand smoke (SHS) exposure in non-smokers according to their exposure at home as measured by airborne markers., Methods: We conducted an observational study on exposure to SHS at home using airborne markers (nicotine and benzene) and biomarkers from the non-smokers living in these homes. We selected 49 non-smoking volunteers from different homes: 25 non-smokers living with at least one smoker and 24 non-smokers living in smoke-free homes. We installed two passive devices to measure nicotine and benzene concentrations in the main room of the house (i.e., the living room). One week later, the researcher returned to the volunteer's home to collect the two devices, obtain saliva and urine samples, and administer a SHS questionnaire., Results: Salivary and urinary cotinine concentrations highly correlated with air nicotine concentrations measured at the volunteers'homes (rsp=0.738 and rsp=0.679, respectively). The concentrations of airborne markers of SHS and biomarkers in non-smokers increased with increasing self-reported intensity and duration of SHS exposure at home during the previous week (p<0.05). The multivariable regression model showed a significant association with nicotine in air at home (β=0.126, p=0.002 for saliva and β=0.115, p=0.010 for urine)., Conclusions: Our findings suggest that, even in countries with comprehensive smoke-free legislation, exposure to SHS at home continues to be the main source of exposure for non-smokers who live in non-smoke-free homes. Therefore, public health policies should promote smoke-free homes., (Copyright © 2014 Elsevier Inc. All rights reserved.)