Environmental tobacco smoke at home and in public places prior to smoking ban enforcement: Assessment by hair analysis in a population of young adult students.

Despite inititatives to reduce tobacco consumption, smoking remains a primary cause of death for both smokers and nonsmokers exposed to environmental tobacco smoke (ETS). The characteristics of some specific groups can make them more exposed to ETS or limit the benefit of prevention measures. This study investigated determinants of ETS in a population of young adult students, considered at higher risk of exposure due to their specific lifestyle. This cross-sectional study involved 90 students aged 20 ± 1.7 years, from the University of Luxembourg, prior to the smoking ban enforcement in public places in the country. Participants reported their tobacco consumption and exposure to ETS at home and/or in public places, and provided a hair sample analyzed for nicotine and cotinine. Nicotine and cotinine were significantly higher in smokers than in nonsmokers' hair in general (median: 2.6 vs. 0.9 ng/mg and 87.1 vs. 22.5 pg/mg respectively). However, nonsmokers exposed to ETS at home and in public places had comparable concentrations to smokers (nic = 2.2 ng/mg; cot = 56.2 pg/mg), whereas unexposed nonsmokers presented significantly lower values (nic = 0.4 ng/mg, cot = 8.5 pg/mg). Nonsmokers exposed to ETS only at home presented higher values than nonsmokers only exposed in public places (nic: 1.3 vs. 0.8 ng/mg, cot: 70.4 vs. 15.0 pg/mg). The study shows the widespread exposure to ETS in this population, the importance of exposure assessment, and the relevance of hair analysis for this purpose. Results suggest that ETS can lead to equivalent exposure to active smoking and that exposure at home can highly contribute to ETS, which is not solved by smoking ban in public places.

Identification of beta-arrestin-1 as a diagnostic biomarker in lung cancer.

BACKGROUND: Distinguishing lung adenocarcinoma (ADC) from squamous cell carcinoma (SCC) has a tremendous therapeutic implication. Sometimes, the commonly used immunohistochemistry (IHC) markers fail to discriminate between them, urging for the identification of new diagnostic biomarkers. METHODS: We performed IHC on tissue microarrays from two cohorts of lung cancer patients to analyse the expression of beta-arrestin-1, beta-arrestin-2 and clinically used diagnostic markers in ADC and SCC samples. Logistic regression models were applied for tumour subtype prediction. Parallel reaction monitoring (PRM)-based mass spectrometry was used to quantify beta-arrestin-1 in plasma from cancer patients and healthy donors. RESULTS: Beta-arrestin-1 expression was significantly higher in ADC versus SCC samples. Beta-arrestin-1 displayed high sensitivity, specificity and negative predictive value. Its usefulness in an IHC panel was also shown. Plasma beta-arrestin-1 levels were considerably higher in lung cancer patients than in healthy donors and were higher in patients who later experienced a progressive disease than in patients showing complete/partial response following EGFR inhibitor therapy. CONCLUSIONS: Our data identify beta-arrestin-1 as a diagnostic marker to differentiate ADC from SCC and indicate its potential as a plasma biomarker for non-invasive diagnosis of lung cancer. Its utility to predict response to EGFR inhibitors is yet to be confirmed.