"Why should care workers be any different from prison workers?" A qualitative study of second-hand smoke exposure during home-care visits and potential measures to eliminate exposure.

INTRODUCTION: Despite world-leading measures in place to protect employees from second-hand smoke exposure in workplaces in the United Kingdom, workers who deliver health and social care in private homes remain unprotected legally in this setting from second-hand smoke exposure (SHS). METHODS: Fourteen individuals took part in either an in-depth telephone interview (n = 11) or an online focus group discussion (n = 3), including home-care workers (n = 5) and managers (n = 5) based in Lanarkshire (Scotland) and local/national policy makers (n = 4). Participants were asked about the extent to which exposure to SHS is an issue during home visits and possible additional measures that could be put in place to eliminate exposure. RESULTS: Participants highlighted the difficulties in balancing the provision of care in a person's own home with the right of workers to be able to breathe clean air and be protected from SHS. Current strategies to reduce staff exposure to SHS during home visits were often reported as inadequate with SHS not a hazard considered by managers beyond protecting pregnant staff or those with pre-existing respiratory conditions such as asthma. Simple respiratory protective equipment (as used during the COVID-19 pandemic) was rightly identified as being ineffective. Methods such as nicotine replacement therapy and e-cigarettes were identified as potential ways to help people who smoke achieve temporary asbstinence prior to a home visit. CONCLUSION: Implementing appropriate and proportionate measures to protect home-care workers from the harms posed by SHS should be a priority to help protect the health of this often overlooked occupational group.

Altered levels of IFN-γ, IL-4, and IL-5 depend on the TLR4 rs4986790 genotype in COPD smokers but not those exposed to biomass-burning smoke.

Introduction: Chronic obstructive pulmonary disease (COPD) is associated with tobacco smoking and biomass-burning smoke exposure. Toll-like receptor 4 (TLR4) single-nucleotide polymorphisms (SNPs) may contribute to its pathogenesis. The study aimed to assess the association of rs4986790 and rs4986791 in the TLR4 gene in a Mexican mestizo population with COPD secondary to tobacco smoking (COPD-TS) and biomass-burning smoke (COPD-BBS) and to evaluate whether the genotypes of risk affect cytokine serum levels. Materials and methods: We enrolled 2,092 participants and divided them into two comparisons according to their environmental exposure. SNPs were genotyped using TaqMan probes. Serum cytokine levels (IL-4, IL-5, IL-6, IL-10, and INF-γ) were quantified by ELISA. Results: The rs4986790 AA genotype in COPD-TS was associated with a higher COPD risk (OR = 3.53). Haplotype analysis confirmed this association, identifying a block containing the rs4986790 allele (A-C, OR = 3.11). COPD-TS exhibited elevated IL-6, IL-4, and IL-5 levels compared with smokers without COPD (SWOC), whereas COPD-BBS displayed higher IFN-γ, IL-6, and IL-10 levels. The AA carriers in the COPD-TS group had elevated IL-4, IL-5, and IFN-γ compared with carriers of AG or GG. Conclusion: The rs4986790 common allele and the A-C haplotype (rs4986790-rs4986791) were associated with a higher COPD risk in smokers; COPD patients carrying the AA genotype showed increased pro-inflammatory cytokines.

Effect of dietary antioxidant quality score on tobacco smoke exposure and asthma in children and adolescents: a cross-sectional study from the NHANES database.

BACKGROUND: Asthma is a common non-communicable disease in children, and airway inflammation is the main pathological change of asthma. Tobacco smoke exposure (TSE) can cause systematic inflammation and oxidative stress, which may further aggravate the progression of asthma. Dietary antioxidants can relieve the inflammation and oxidative stress in human body. This study aims to assess the effect of overall antioxidant capacity of dietary intake, evaluating by dietary antioxidant quality score (DAQS), in the association between TSE and childhood asthma. METHODS: Data of this cross-sectional study were extracted from the National Health and Nutrition Examination Surveys (NHANES) 2007-2018. DAQS was calculated based on the daily dietary intake of selenium, zinc, magnesium, vitamin A, C and E. TSE was measured by serum cotinine concentration. The weighted univariate and multivariate logistic regression models were employed to evaluate the role of DAQS in the association between TSE and asthma among children and adolescents. Subgroup analysis was conducted to further evaluate the association based on gender. RESULTS: Totally 11,026 children and adolescents were included, of whom 1,244 (11.28%) had asthma. After adjusted all covariates, TSE was associated with the high odds of childhood asthma (OR = 1.26, 95%CI = 1.05-1.52). Among children exposed to tobacco smoke, those with higher DAQS level (OR = 1.15, 95%CI: 0.88-1.50) had a reduced risk of asthma compared with those children with lower DAQS level (OR = 1.43, 1.08-1.89), especially among girls (OR = 1.42, 95%CI: 0.93-2.17). CONCLUSION: High DAQS may have a moderating effect on asthma in children; that is, the higher DAQS, the lower the odds of asthma in children who exposed to tobacco smoke. Our study provides a reference for developing more targeted strategies for prevention and treatment of asthma in children.

Metformin ameliorates neuroinflammatory environment for neurons and astrocytes during in vitro and in vivo stroke and tobacco smoke chemical exposure: Role of Nrf2 activation.

Despite the protective nature of the blood-brain barrier (BBB) and brain-protecting tissues, some types of CNS injury or stress can cause cerebral cytokine production and profound alterations in brain function. Neuroinflammation, which can also be accompanied by increased cerebral cytokine production, has a remarkable impact on the pathogenesis of many neurological illnesses, including loss of BBB integrity and ischemic stroke, yet effective treatment choices for these diseases are currently lacking. Although little is known about the brain effects of Metformin (MF), a commonly prescribed first-line antidiabetic drug, prior research suggested that it may be useful in preventing BBB deterioration and the increased risk of stroke caused by tobacco smoking (TS). Therefore, reducing neuroinflammation by escalating anti-inflammatory cytokine production and declining pro-inflammatory cytokine production could prove an effective therapeutic strategy for ischemic stroke. Hence, the current investigation was planned to explore the potential role of MF against stroke and TS-induced neuroinflammation and reactive oxygen species (ROS) production. Our studies revealed that MF suppressed releasing pro-inflammatory mediators like tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß) by aiming at the nuclear factor kappa B (NF-κB) signaling pathway in primary neurons and astrocytes. MF also upregulated anti-inflammatory mediators, like interleukin-10 (IL-10), and interleukin-4 (IL-4), by upregulating the Nrf2-ARE signaling pathway. Adolescent mice receiving MF along with TS exposure also showed a notable decrease in NF-κB expression compared to the mice not treated with MF and significantly decreased the level of TNF-α, IL-1ß, MCP-1, and MIP-2 and increased the levels of IL-10 and IL-4 through the activation of Nrf2-ARE signaling pathway. These results suggest that MF has anti-neuroinflammatory effects via inhibiting NF-κB signaling by activating Nrf2-ARE. These studies support that MF could be a strong candidate drug for treating and or preventing TS-induced neuroinflammation and ischemic stroke.

Secondhand tobacco smoke exposure in homes and vehicles in youth: disparities among racial, and sexual and gender minorities.

Background: Secondhand smoke exposure (SHSe) among youth is a serious public health concern, leading to an increased risk of conditions such as asthma and respiratory infections. However, there is little research on SHSe among vulnerable populations, such as racial and sexual minorities. Understanding the factors associated with youth SHSe in homes and vehicles is crucial to developing better protective policies. Methods: This study utilized 2020 data from the National Youth Tobacco Survey, a representative sample of middle- and high-school students in the US. The primary outcomes were youth SHSe at home and while riding in a vehicle. Multinomial regression models were used to assess factors associated with SHSe. Results: The data included 9,912 students enrolled in grades 6 through 12 in the United States who reported never using any form of tobacco. Non-Hispanic Black students living with someone who does not use any form of tobacco products were significantly more likely to experience moderate [OR = 2.1 (1.1-3.9), p = 0.03] and severe [OR = 5.1 (2.2-11.7), p < 0.001] secondhand smoke exposure (SHSe) in homes compared to their non-Hispanic White counterparts. Heterosexual female students had lower odds of reporting moderate SHSe in the home compared to heterosexual males [OR = 0.7 (0.6-0.99), p = 0.02], whereas bisexual females had two-fold increased odds of severe SHSe in homes [OR = 2.0 (1.2-3.4), p = 0.01]. Conclusion: Significant efforts are needed to develop targeted interventions to reduce SHSe in homes and vehicles, particularly in these vulnerable populations.

Chronic obstructive pulmonary disease related to wood smoke and impact of the combined exposure to tobacco.

BACKGROUND: Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2023 highlights the need to explore aetiotypes of chronic obstructive pulmonary disease (COPD) beyond the tobacco-smoking COPD. Exposure to wood smoke (WS) is a risk factor for COPD in women, but the effect of the combined exposure to tobacco smoke (TS) in the general population and among COPD patients, and the characteristics of WS-COPD are unclear. METHOD: This was an analysis of data from PREPOCOL (Prevalence of COPD in Five Colombian Cities Situated at Low, Medium, and High Altitude), a random cross-sectional population-based study (n = 5,539) focusing on the effect of combined WS and TS exposure and WS-COPD characterisation. RESULTS: Prevalence of COPD was significantly higher in those exposed to both WS and TS (16.0%) than in those exposed to WS (6.7%) or TS (7.8%) only (P < 0.001). Exposure to WS was associated with COPD in men (OR 1.53, P = 0.017). WS-COPD individuals were more frequently female, older, shorter and had higher forced expiratory volume in 1 sec (FEV1) (all P < 0.05). Those exposed to both WS and TS had more symptoms and worse airflow limitation (P < 0.001). CONCLUSIONS: This was the first random population-based study showing that WS is an associated risk factor for COPD also in men, and that people exposed to both WS and TS have a significantly higher prevalence of COPD. Similarly, COPD subjects exposed to both types of smoke have more symptoms and greater airflow obstruction. This suggests an additive effect of WS and TS.

CONTEXTE: L'Initiative mondiale pour les maladies pulmonaires obstructives chroniques (Global Initiative for Chronic Obstructive Lung Disease, GOLD) 2023 met en évidence l'importance d'explorer les différents étiotypes de la maladie pulmonaire obstructive chronique (COPD, pour l'anglais « chronic obstructive pulmonary disease ¼) en dehors de la COPD liée au tabagisme. L'exposition à la fumée de bois (WS, pour l'anglais « wood smoke ¼) représente un facteur de risque de la COPD chez les femmes, cependant, l'impact de l'exposition simultanée à la fumée de tabac (TS, pour l'anglais « tobacco smoke ¼) chez la population générale et chez les patients atteints de COPD, ainsi que les caractéristiques spécifiques de la WS-COPD, demeurent peu clairs. MÉTHODES: Il s'agit d'une étude transversale aléatoire basée sur la population (n = 5 539) qui analyse les données de PREPOCOL (Prevalence of COPD in Five Colombian Cities Situated at Low, Medium, and High Altitude). L'étude se concentre sur l'effet de l'exposition combinée à la WS et à la TS ainsi que sur la caractérisation de la WS-COPD. RÉSULTATS: La prévalence de la COPD était significativement plus élevée chez les personnes exposées à la fois à la WS et à la TS (16,0%) que chez celles exposées uniquement à la WS (6,7%) ou à la TS (7,8%) (P < 0,001). L'exposition à la WS était associée à la COPD chez les hommes (OR 1,53 ; P = 0,017). Les personnes atteintes de WS-COPD étaient plus fréquemment des femmes, d'un âge plus avancé, de plus petite taille et présentaient un volume expiratoire maximal en 1 seconde (FEV1) plus élevé (tous P < 0,05). Les personnes exposées à la fois à la WS et à la TS ont montré plus de symptômes et une plus grande limitation du débit d'air (P < 0,001). CONCLUSION: Il s'agit de la première étude aléatoire basée sur la population qui démontre que la WS est un facteur de risque lié à la COPD, même chez les hommes, et que les individus exposés à la fois à la WS et à la TS présentent une prévalence significativement plus élevée de la COPD. De plus, les personnes souffrant de COPD qui sont exposés aux deux types de fumée manifestent davantage de symptômes et une obstruction pulmonaire plus sévère. Cela laisse supposer qu'il y a un effet cumulatif de la WS et de la TS.

[Assessment of exposure to seconhand smoke in health surveys in Spain]. / La valoración de la exposición al humo ambiental de tabaco en las encuestas de salud de España.

OBJECTIVE: To describe the questions used to assess exposure to secondhand smoke (SHS) in Spanish health surveys. METHOD: Extraction and analysis of the literals of the questions on SHS in the health surveys in Spain identified on the website of the Ministry of Health, the National Plan on Drugs and Health Departments of the autonomous communities. RESULTS: Three nationwide surveys assessed SHS exposure, with variability in questions, responses, and recall periods. Catalonia in 2022, and Galicia and the Basque Country in 2018, assessed exposure in detail. CONCLUSIONS: Questions assessing self-reported exposure to SHS are survey-dependent. There is a need for a set of questions to assess exposure in a homogeneous way in health surveys.

Fractional exhaled nitric oxide (FeNO) among school children in Java and Sumatra, Indonesia: associations with respiratory symptoms, house dust mite sensitization and the home environment.

OBJECTIVE: To study associations between fractional exhaled nitric oxide (FeNO) and asthma, airway symptoms, sensitization to common allergens, outdoor pollution and home environment among 380 students in eight junior high schools in two areas in Indonesia. METHODS: Data on health and home were collected by a face-to face interview before measuring FeNO and performing skin prick test against common allergens. Exploratory linear mixed and logistic regression models were employed. RESULTS: Geometric mean of FeNO was 17.8 ppb (GSD 2.09) and 139 students (36.6%) had elevated FeNO (>20 ppb). In total, 107 students (28.2%) were sensitized to house dust mite (HDM) (Der p1 or Der f1), 4 (1.1%) to cat and 3 (0.8%) to mold (Cladosporium or Alternaria). Moreover, 20 students (5.3%) had diagnosed asthma, 38 (10.0%) had current wheeze, and 107 (28.2%) had current rhinitis. HDM sensitization, diagnosed asthma, current wheeze, and current rhinitis were associated with FeNO. In total, 281 students (73.9%) had mold or dampness, 232 (61.1%) had environmental tobacco smoke (ETS) and 43 (11.3%) had other odor at home. Indoor mold or dampness and other odor at home were associated with FeNO. ETS was negatively associated with FeNO. CONCLUSION: HDM sensitization and elevated FeNO can be common among children in this part of Indonesia. The high prevalence of elevated FeNO indicate that undiagnosed childhood asthma is common. Dampness, mold and odor at home can be associated with increased FeNO while ETS can be associated with decreased FeNO.

Association between tobacco smoke exposure and depression: the NHANES 2005-2018 and Mendelian randomization study.

OBJECTIVE: The relationship between tobacco smoke exposure (TSE) and depression is controversial. This study combined observational research and Mendelian randomization (MR) to explore the relationship of depression with both smoking status and cotinine levels. METHOD: We collected relevant data from the National Health and Nutrition Examination Survey (NHANES) database from 2005 to 2018, and used weighted multifactorial logistic regression modelling to assess the correlation between TSE and depression, and assessed the causal relationship of depression with both smoking status and cotinine levels by MR. RESULT: Current smokers had the highest risk of depression (OR 1.94; P < 0.01); there was a positive trend for correlation between daily smoking and depression (OR 1.66; P for trend < 0.01). Serum ketamine levels above 3.00 ng/ml had a higher risk of depression (OR 2.13; P < 0.001). MR results showed that current smoking (OR = 4.66; P < 0.001) and previous smoking (OR 2.09; P < 0.01) were risk factors for the onset of depression, and that there was no causal association between cotinine levels and depression. CONCLUSION: Smoking is significantly associated with depression and plays a potential causal role in the development of depression. Cotinine was significantly associated with depression, however MR results showed no causal relationship between cotinine and depression.

Asbestos-Related lung Cancer: An underappreciated oncological issue.

Asbestos, a group of class I (WHO) carcinogenic fibers, is the main cause of mesothelioma. Asbestos inhalation also increases the risk to develop other solid tumours with lung cancer as the most prominent example [91]. The incidence of asbestos-related lung cancer (ARLC) is estimated to be to six times larger than the mesothelioma incidence thereby becoming an important health issue [86]. Although the pivotal role of asbestos in inducing lung cancer is well established, the precise causal relationships between exposures to asbestos, tobacco smoke, radon and 'particulate' (PM2.5) air pollution remain obscure and new knowledge is needed to establish appropriate preventive measures and to tailor existing screening practices[22,61,65]. We hypothesize that a part of the increasing numbers of lung cancer diagnoses in never-smokers can be explained by (historic and current) exposures to asbestos as well as combinations of different forms of air pollution (PM2.5, asbestos and silica).

PD-L2 mediates tobacco smoking-induced recruitment of regulatory T cells via the RGMB/NFκB/CCL20 cascade.

Programmed cell death ligand 2 (PD-L2), a ligand for the receptor programmed cell death 1 (PD-1), has an identity of 34% with its twin ligand PD-L1 and exhibits higher binding affinity with PD-1 than PD-L1. However, the role of PD-L2 in non-small cell lung cancer (NSCLC) progression, especially tobacco-induced cancer progression, has not been fully understood. Here, we found that PD-L2 promoted tumor growth in murine models with recruitment of regulatory T cells (Tregs). In patients with NSCLC, PD-L2 expression level in tumor samples was higher than in counterpart normal controls and was positively associated with patients' response to anti-PD-1 treatment. Mechanismly, PD-L2 bound its receptor Repulsive guidance molecule B (RGMB) on cancer cells and activated extracellular signal-regulated kinase (Erk) and nuclear factor κB (NFκB), leading to increased production of chemokine CCL20, which recruited Tregs and contributed to NSCLC progression. Consistently, knockdown of RGMB or NFκB p65 inhibited PD-L2-induced CCL20 production, and silencing of PD-L2 repressed Treg recruitment by NSCLC cells. Furthermore, cigarette smoke and carcinogen benzo(a)pyrene (BaP) upregulated PD-L2 in lung epithelial cells via aryl hydrocarbon receptor (AhR)-mediated transcription activation, whose deficiency markedly suppressed BaP-induced PD-L2 upregulation. These results suggest that PD-L2 mediates tobacco-induced recruitment of Tregs via the RGMB/NFκB/CCL20 cascade, and targeting this pathway might have therapeutic potentials in NSCLC.

Changes in prevalence and socioeconomic inequalities in secondhand smoke exposure in Spanish children, 2016-2019.

INTRODUCTION: Children are vulnerable to secondhand smoke (SHS) exposure, especially those with lower socioeconomic status. This study assesses the changes in prevalence and socioeconomic inequalities in SHS exposure in children younger than 12 years old in Spain between 2016 and 2019. METHODS: We conducted two cross-sectional studies among representative samples of households with children aged <12 years in Spain, in 2016 (n=2411) and 2019 (n=2412). Families were interviewed to assess children's SHS exposure in private settings and outdoor public venues and their adoption of home and car smoke-free rules. We used the education level of the home main earner as a proxy for socioeconomic position. Changes over time in the prevalence and socioeconomic inequalities of SHS exposure and smoke-free rules were estimated through adjusted Poisson regression models with robust variance according to sociodemographic covariates (adjusted prevalence ratios, APRs). RESULTS: In 2019, 70.5% of children were exposed to SHS in Spain. No changes between 2016 and 2019 were found for overall SHS exposure, exposure at home, and at school entrances. SHS exposure increased at public transport stations (APR=1.24; 95% CI: 1.03-1.49) and outdoor hospitality venues (APR=1.17; 95% CI: 1.07-1.29) while it decreased in cars (APR=0.74; 95% CI: 0.56-0.98) and parks (APR=0.87; 95% CI: 0.77-0.98). Households with lower education level had higher prevalence of SHS exposure at home in 2019 compared with those with university studies (primary: APR=1.30; 95% CI: 1.11-1.51; secondary: APR=1.12; 95% CI: 1.00-1.25) and were less likely to adopt home indoor smoke-free rules (primary: APR=0.88; 95% CI: 0.79-0.99; secondary: APR=0.95; 95% CI: 0.89-1.02). Socioeconomic inequalities in SHS exposure at home persisted between 2016 and 2019 (p>0.05), while decreased in smoke-free rules in cars (p=0.039). CONCLUSIONS: Reported SHS exposure among children in Spain remained high between 2016 and 2019. Inequalities persisted at home, highlighting the need for measures to reduce such exposure with an equity perspective.

Impairment of Gal-9 and Tim-3 crosstalk between Tregs and Th17 cells drives tobacco smoke-induced airway inflammation.

Overexpression of T-cell immunoglobulin and mucin-domain containing-3 (TIM-3) on T cells has been observed in smokers. However, whether and how galectin-9 (Gal-9)/TIM-3 signal between T-regulatory cells (Tregs) and type 17 helper (Th17) cells contributes to tobacco smoke-induced airway inflammation remains unclear. Here, we aimed to explore the role of the Gal-9/TIM-3 signal between Tregs and Th17 cells during chronic tobacco smoke exposure. Tregs phenotype and the expression of TIM-3 on CD4+ T cells were detected in a mouse model of experimental emphysema. The role of TIM-3 in CD4+ T cells was explored in a HAVCR2-/- mouse model and in mice that received recombinant anti-TIM3. The crosstalk between Gal-9 and Tim-3 was evaluated by coculture Tregs with effector CD4+ T cells. We also invested the expression of Gal-9 in Tregs in patients with COPD. Our study revealed that chronic tobacco smoke exposure significantly reduces the frequency of Tregs in the lungs of mice and remarkably shapes the heterogeneity of Tregs by downregulating the expression of Gal-9. We observed a pro-inflammatory but restrained phenotypic transition of CD4+ T cells after tobacco smoke exposure, which was maintained by TIM-3. The restrained phenotype of CD4+ T cells was perturbed when TIM-3 was deleted or neutralised. Tregs from the lungs of mice with emphysema displayed a blunt ability to inhibit the differentiation and proliferation of Th17 cells. The inhibitory function of Tregs was partially restored by using recombinant Gal-9. The interaction between Gal-9 and TIM-3 inhibits the differentiation of Th17 cells and promotes apoptosis of CD4+ T cells, possibly by interfering with the expression of retinoic acid receptor-related orphan receptor gamma t. The expression of Gal-9 in Tregs was reduced in patients with COPD, which was associated with Th17 response and lung function. These findings present a new paradigm that impairment of Gal-9/Tim-3 crosstalk between Tregs and Th17 cells during chronic tobacco smoke exposure promotes tobacco smoke-induced airway/lung inflammation.

Unburned Tobacco Smoke Affects Neuroinflammation-Related Pathways in the Rat Mesolimbic System.

Tobacco use disorder represents a significant public health challenge due to its association with various diseases. Despite awareness efforts, smoking rates remain high, partly due to ineffective cessation methods and the spread of new electronic devices. This study investigated the impact of prolonged nicotine exposure via a heat-not-burn (HnB) device on selected genes and signaling proteins involved in inflammatory processes in the rat ventral tegmental area (VTA) and nucleus accumbens (NAc), two brain regions associated with addiction to different drugs, including nicotine. The results showed a reduction in mRNA levels for PPARα and PPARγ, two nuclear receptors and anti-inflammatory transcription factors, along with the dysregulation of gene expression of the epigenetic modulator KDM6s, in both investigated brain areas. Moreover, decreased PTEN mRNA levels and higher AKT phosphorylation were detected in the VTA of HnB-exposed rats with respect to their control counterparts. Finally, significant alterations in ERK 1/2 phosphorylation were observed in both mesolimbic areas, with VTA decrease and NAc increase, respectively. Overall, the results suggest that HnB aerosol exposure disrupts intracellular pathways potentially involved in the development and maintenance of the neuroinflammatory state. Moreover, these data highlight that, similar to conventional cigarettes, HnB devices use affects specific signaling pathways shaping neuroinflammatory process in the VTA and NAc, thus triggering mechanisms that are currently considered as potentially relevant for the development of addictive behavior.

An intercontinental comparison of the influence of smoking on the occurrence of nonsyndromic cleft lip and palate: a meta-analysis and systematic review.

BACKGROUND: The influence of smoking on nonsyndromic clefts has been a topic of research for many years. However, few studies have investigated the effect of smoking on causing clefts in different gene pools. METHODS: A meta-analysis was conducted of case-control studies related to smoking. Keywords such as "clefts," "cleft lip," "cleft palate," "orofacial cleft," and "smoking" were used to search the MEDLINE, Embase, and Cochrane databases. RESULTS: In total, 51 articles were reviewed. The RevMan software was utilized for the analysis, and the Mantel-Haenszel method was employed to pool the odds ratios (ORs) and 95% confidence intervals. Although the overall OR, a measure of the association between exposure and outcome, was higher for smokers than for non-smokers, this association was significantly stronger in individuals from Asia and South America (1.73), and lowest in Europe (1.31). Among active and passive smokers in Asia, the OR was approximately 0.93, indicating an equivalent impact from both types of smoking. CONCLUSION: This analysis indirectly suggests that restriction measures targeting both active and passive smoking are crucial in Asia.

Cytisine for smoking cessation: A 40-day treatment with an induction period.

INTRODUCTION: Cytisine is a smoking cessation drug now used worldwide. Most of the data available in the literature predict a 25-day treatment, accepted on the basis of previous clinical experience in Eastern Europe. There are few studies on dosing, and only recently some researchers have tried a longer treatment period. METHODS: This real-world retrospective cross-sectional study analyzed data collected consecutively from 2015 to 2021, in seven smoking cessation centers in north-central Italy. The aim of this study is to evaluate the effectiveness and tolerability of a 40-day cytisine treatment with an induction phase and a slower reduction schedule. Data were collected from a group of 871 patients treated with cysteine, varenicline, and nicotine replacement therapy (NRT). The sample was not randomized. Behavioral support (4-6 sessions, each lasting 20-30 min, plus the evaluation session) was delivered to all patients. RESULTS: Subgroups taking cytisine (n=543 for 40 days), varenicline (n=281 for 12 weeks), and NRT (n=47 for eight weeks) showed biochemically confirmed smoking abstinence at 6 months of 50.5%, 55.9%, and 51.0%, respectively, with a statistically significant difference between cytisine versus varenicline (p<0.01) but not between cytisine versus NRT (p=0.5597). Adverse events were 4.4% with cytisine and 33.3% with varenicline. Behavioral support was an important factor in effectiveness. CONCLUSIONS: This study produced preliminary evidence that the 40-day regimen of cytisine, appears to have less effectiveness in comparison to varenicline but the magnitude of the effect is comparable. The results and tolerability seem to be better than in most other studies.

Relation Between Exposure to Tobacco Smoke Assessed by Serum Cotinine Concentration and Questionnaire Method, and Serum Renalase Concentration-the Importance of the Coexistence of Arterial Hypertension and Other Cardiovascular Diseases.

Exposure to tobacco smoke (ETS) is one of the main risk factors for cardiovascular disease (CVD). Renalase is a protein that may play a role in the pathogenesis of CVD. The aim of the study was to assess the relationship between ETS and serum renalase concentration. A group of 109 patients was recruited for this study (49.7 ± 14.7 years). In accordance with the questionnaire, patients were divided into the following subgroups: subgroup A- declaring themselves active smokers (n = 36), subgroup B- declaring themselves non-smokers and exposed to environmental tobacco smoke (n = 35), subgroup C- declaring themselves non-smokers and not exposed to environmental tobacco smoke (n = 38). The same patients were divided based on cotinine concentration into the following subgroups: subgroup D- active smokers (n = 42), subgroup E- non-smokers exposed to environmental tobacco smoke (n = 66), and subgroup F- non-smokers not exposed to environmental tobacco smoke (n = 1). Serum cotinine concentration and serum renalase concentration were measured using ELISA tests. Serum renalase concentration was statistically significantly higher in subgroup C than in subgroups A and B and in subgroup E and F than in D. There was a negative correlation between serum cotinine concentration and serum renalase concentration (r = -0.41, p < 0.05). Regression analysis showed that higher BMI, higher diastolic blood pressure, coronary artery disease and higher serum cotinine concentration are independent risk factors of lower serum renalase concentration. The questionnaire method of assessing exposure to tobacco smoke was characterized by high sensitivity, but only moderate specificity, especially in terms of assessing environmental exposure to tobacco smoke. In summary, the study showed an independent relationship between exposure to tobacco smoke and lower serum renalase concentration.

The impact of exposure to tobacco smoke and e-cigarettes on asthma-related outcomes: Systematic review informing the EAACI guidelines on environmental science for allergic diseases and asthma.

To inform the clinical practice guidelines' recommendations developed by the European Academy of Allergy and Clinical Immunology systematic reviews (SR) assessed using GRADE on the impact of environmental tobacco smoke (ETS) and active smoking on the risk of new-onset asthma/recurrent wheezing (RW)/low lung function (LF), and on asthma-related outcomes. Only longitudinal studies were included, almost all on combustion cigarettes, only one assessing e-cigarettes and LF. According to the first SR (67 studies), prenatal ETS increases the risk of RW (moderate certainty evidence) and may increase the risk of new-onset asthma and of low LF (low certainty evidence). Postnatal ETS increases the risk of new-onset asthma and of RW (moderate certainty evidence) and may impact LF (low certainty evidence). Combined in utero and postnatal ETS may increase the risk of new-onset asthma (low certainty evidence) and increases the risk of RW (moderate certainty evidence). According to the second SR (24 studies), ETS increases the risk of severe asthma exacerbations and impairs asthma control and LF (moderate certainty evidence). According to the third SR (25 studies), active smoking increases the risk of severe asthma exacerbations and of suboptimal asthma control (moderate certainty evidence) and may impact asthma-related quality-of-life and LF (low certainty evidence).

Early life exposure to secondhand tobacco smoke and eating behaviors at age 12 years.

BACKGROUND: Prenatal or early childhood secondhand tobacco smoke (SHS) exposure increases obesity risk. However, the potential mechanisms underlying this association are unclear, but obesogenic eating behaviors are one pathway that components of SHS could perturb. Our aim was to assess associations of prenatal and early childhood SHS exposure with adolescent eating behaviors. METHODS: Data came from a prospective pregnancy and birth cohort (N = 207, Cincinnati, OH). With multiple informant models, we estimated associations of prenatal (mean of 16 and 26 weeks of gestation maternal serum cotinine concentrations) and early childhood cotinine (average concentration across ages 12, 24, 36, and 48 months) with eating behaviors at age 12 years (Child Eating Behaviors Questionnaire). We tested whether associations differed by exposure periods and adolescent's sex. Models adjusted for maternal and child covariates. RESULTS: We found no statistically significant associations between cotinine measures and adolescent's eating behaviors. Yet, in females, prenatal cotinine was associated with greater food responsiveness (ß: 0.23; 95% CI: 0.08, 0.38) and lower satiety responsiveness (ß: -0.14; 95% CI: -0.26, -0.02); in males, prenatal and postnatal cotinine was related to lower food responsiveness (prenatal: ß: -0.25; 95% CI: -0.04, -0.06; postnatal: ß: -0.36; 95% CI: -0.06, -0.11). No significant effect modification by sex or exposure window was found for other eating behaviors. CONCLUSION: Prenatal and early childhood SHS exposures were not related to adolescent's eating behavior in this cohort; however, biological sex may modify these associations.

Prevalence of Wheezing and Its Association with Environmental Tobacco Smoke Exposure among Rural and Urban Preschool Children in Mpumalanga Province, South Africa.

BACKGROUND: This study aimed to investigate the prevalence of wheezing and its association with environmental tobacco smoke exposure among rural and urban preschool children in Mpumalanga province, South Africa, an area associated with poor air quality. METHODS: In this study, parents/caregivers of preschool children (n = 3145) completed a modified International Study of Asthma and Allergies in Childhood (ISAAC) questionnaire. Data were analysed using multiple logistic regression models. RESULTS: The overall prevalence of Wheeze Ever was 15.14%, with a higher prevalence in urban preschoolers than rural preschoolers (20.71% vs. 13.30%, p < 0.000). Moreover, the total prevalence of Asthma Ever was 2.34%. The prevalence was greater in urban preschoolers than in rural preschoolers (3.92% vs. 1.81%, p < 0.001). In the final adjusted model, both urban- and rural-area children who lived with one or more people who smoked in the same household (WE: OR 1.44, 95% CI 1.11-1.86) (CW: OR 2.09, 95% CI 1.38-3.16) and (AE: OR 2.49, 95% CI 1.12-5.54) were found to have an increased likelihood of having Wheeze Ever, Current Wheeze, and Asthma Ever as compared to those who lived with non-smokers. CONCLUSIONS: The implementation of smoking limits and prohibition is crucial in areas that are frequented or utilized by children. Hence, it is imperative for healthcare providers to actively champion the rights of those who do not smoke within the society, while also endorsing legislative measures aimed at curtailing the extent of tobacco smoke exposure.