Secondhand Smoke Exposure Research Articles

Secondhand smoke exposure in public outdoor spaces in the Netherlands: The stronger the smell, the more exposure to nicotine.

While secondhand smoke exposure in outdoor spaces has been investigated before, no data on outdoor secondhand smoke exposure have been collected in the Netherlands. Such data could help policymakers gain support for smoke-free outdoor public spaces. Between May and November 2021, we visited 25 outdoor locations across the Netherlands. At each location, we conducted four measurements with smokers and one measurement without smokers. During each measurement, we counted the number of smokers present and we rated tobacco smell intensity on a five-point scale. Airborne nicotine and 3-ethenylpyridine (3-EP) data were collected through active sampling on thermal desorption tubes. The contents of these tubes were later analyzed using gas chromatography-mass spectrometry. Using linear mixed models, we investigated the association between levels of nicotine and the presence of smokers, the number of smokers, and the intensity of tobacco smell. We also investigated these association with levels of 3-EP. Nicotine levels were higher when smokers were present (B=1.40; 95% CI: 0.69-2.11, p<0.001). For each additional smoker present, we measured higher levels of nicotine (B=0.23; 95% CI: 0.10-0.37, p=0.001). When the smell of tobacco smoke was noted to be stronger by the researchers, higher levels of nicotine were measured through sampling (B=0.85; 95% CI: 0.44-1.26, p<0.001). We found similar results for 3-EP levels. This study showed that both nicotine and 3-EP are useful in quantifying levels of secondhand smoke in various outdoor locations. The level of nicotine exposure outdoors was positively associated with the number of smokers nearby. The intensity of the tobacco smell was also related to nicotine exposure: the stronger the smell of tobacco smoke, the more nicotine was measured in the air.

Susceptibility to e-cigarette adoption among tobacco-naïve youths: a cross-sectional study in Shenzhen, China.

The rise in e-cigarette use among youth is a significant global public health issue. It is important to identify those at increased risk and implement effective strategies to reduce e-cigarette popularity among the youth. This study aims to identify predictors of e-cigarette uptake in youths with no prior tobacco use, considering individual, familial and the broader societal environmental factors. For this investigation, a group of 2,487 tobacco-free youths was selected from 15 high schools in Shenzhen, China. Susceptibility to e-cigarettes was determined by assessing the possibility of future use and the openness to trying e-cigarettes if presented by friends. Both chi-square tests and logistic regression were applied to identify factors linked to susceptibility to e-cigarette use. Among the respondents, 5.5% (n = 136) were found to be susceptible to e-cigarette use. The analysis revealed factors tied to this risk: perceptions of e-cigarettes, the impact of vaping peers, paternal parenting styles, the extent of social support, exposure to messages both for and against e-cigarettes use, and secondhand smoke (SHS) exposure. Youths who downplayed the addictive nature of e-cigarettes (aOR = 2.01; 95% CI: 1.14-3.55; p = 0.016), those with friends who engaged in vaping (aOR = 3.43-7.64; 95%CI: 2.36-20.42; p < 0.001), those experiencing over-protective or rejective maternal parenting (aOR = 1.68-3.01; 95%CI: 1.11-5.77; p = 0.001-0.014) or rejective paternal parenting (aOR = 3.63; 95%CI: 1.99-6.59; p < 0.001), those aware of e-cigarette advertisements (aOR = 1.82; 95%CI: 1.28-2.60; p = 0.001), and those exposed to SHS at home (aOR = 1.68; 95%CI: 1.17-2.41; p = 0.005) or at public places (aOR = 1.72-1.79; 95%CI: 1.21-2.57; p = 0.002-0.003) were more prone to e-cigarettes. In contrast, youths who believed using e-cigarettes reduces one's attractiveness (aOR = 0.34; 95%CI: 0.16-0.72; p = 0.005) or perceived that vaping made social interactions less enjoyable (aOR = 0.26; 95%CI: 0.12-0.58; p = 0.001), those who benefited from high social support (aOR = 0.30-0.60; 95%CI: 0.17-0.97; p < 0.001), and those who noticed message about e-cigarettes' adverse consequence (aOR = 0.54; 95%CI: 0.38-0.77; p = 0.001) were less likely to be inclined toward e-cigarette use. The propensity of the youth to e-cigarette usage is shaped by a multiple element. An all-encompassing strategy that addresses the individual, familial, and the broader societal aspects is imperative for the effective prevention of e-cigarette initiation among youth.

Health Risks Associated with Tobacco Consumption in Humans: An Overview

Tobacco use remains a significant public health concern globally, with over 8 million anticipated deaths annually by 2030, despite declining rates in some high-income nations. Smoking is prevalent worldwide, particularly in developing and middle-income countries, where over 80% of smokers reside. The inhalation of tobacco substances leads to various diseases, including cancer and respiratory ailments, resulting in more deaths than AIDS, tuberculosis, and other major causes combined. Secondhand smoke exposure also poses significant health risks. The economic burden of tobacco-related deaths and diseases is substantial, especially in low- and middle-income economies, where almost 80% of tobacco-related deaths occur. Lack of awareness, societal influence, and ineffective enforcement of anti-tobacco laws contribute to widespread tobacco use. Although anti-tobacco campaigns and policies have shown some success, challenges persist, particularly in rural areas where tobacco dependence is high. In India, despite declining tobacco use attributed to awareness campaigns and increased taxes on cigarettes, certain demographics, such as middle-aged individuals, illiterates, and rural residents, continue to have high tobacco consumption rates due to inadequate implementation of anti-tobacco norms and limited access to information. Quitting smoking can significantly extend life expectancy and reduce the risk of smoking-related diseases. However, nicotine addiction poses a challenge, with only a small percentage of users successfully quitting without assistance. Professional support and cessation drugs can double the likelihood of successful quitting, and nicotine replacement therapy has shown effectiveness. Overall, there is no safe level of cigarette use, emphasizing the importance of comprehensive tobacco control efforts to mitigate the global health and economic impacts of tobacco use. This review deals with the health risks associated with tobacco consumption in humans. Keywords: Tobacco, Nicotine, Carcinogens, Cancer, Cardiovascular diseases.

Association between secondhand smoke exposure and rheumatoid arthritis in US never-smoking adults: a cross-sectional study from NHANES

While smoking is widely acknowledged as a risk factor for rheumatoid arthritis (RA), the connection between secondhand smoke (SHS) exposure and RA in never-smoking adults remains limited and inconsistent. This study aims to explore and quantify this association using serum cotinine levels. We conducted a cross-sectional study with 14,940 adults who self-report as never smokers, using National Health and Nutrition Examination Survey data from 1999 to 2018. Based on previous literature, SHS exposure was categorized into four groups according to serum cotinine levels. Compared to individuals in the unexposed group (serum cotinine < 0.05 ng/mL), the adjusted odds ratio (OR) for RA was 1.37 (95% CI 1.14–1.64, p = 0.001) in the low exposure group (serum cotinine at 0.05 to 0.99 ng/mL) after adjusting for covariates. However, no significant association was found in the moderate exposure group (serum cotinine at 1 to 10 ng/mL) or the heavy exposure group (serum cotinine ≥ 10 ng/mL). Furthermore, we detected a non-linear, positively saturated correlation between the cotinine levels after log2 transformation and RA, with a turning point at approximately − 2.756 ng/mL (OR = 1.163, 95% CI 1.073–1.261, p = 0.0002). The stability of the results was confirmed by subgroup analysis.

DNA methylation signatures of youth-onset type 2 diabetes and exposure to maternal diabetes

ObjectiveYouth-onset type 2 diabetes (T2D) is physiologically distinct from adult-onset, but it is not clear how the two diseases differ at a molecular level. In utero exposure to maternal type 2 diabetes (T2D) is known to be a specific risk factor for youth-onset T2D. DNA methylation (DNAm) changes associated with T2D but which differ between youth- and adult-onset might delineate the impacts of T2D development at different ages and could also determine the contribution of exposure to in utero diabetes.MethodsWe performed an epigenome-wide analysis of DNAm on whole blood from 218 youth with T2D and 77 normoglycemic controls from the iCARE (improving renal Complications in Adolescents with type 2 diabetes through REsearch) cohort. Associations were tested using multiple linear regression models while adjusting for maternal diabetes, sex, age, BMI, smoking status, second-hand smoking exposure, cell-type proportions and genetic ancestry.ResultsWe identified 3830 differentially methylated sites associated with youth T2D onset, of which 3794 were moderately (adjusted p-value < 0.05 and effect size estimate > 0.01) associated and 36 were strongly (adjusted p-value < 0.05 and effect size estimate > 0.05) associated. A total of 3725 of these sites were not previously reported in the EWAS Atlas as associated with T2D, adult obesity or youth obesity. Moreover, three CpGs associated with youth-onset T2D in the PFKFB3 gene were also associated with maternal T2D exposure (FDR < 0.05 and effect size > 0.01). This is the first study to link PFKFB3 and T2D in youth.ConclusionOur findings support that T2D in youth has different impacts on DNAm than adult-onset, and suggests that changes in DNAm could provide an important link between in utero exposure to maternal diabetes and the onset of T2D.

Evaluating precision medicine tools in cystic fibrosis for racial and ethnic fairness.

Patients with cystic fibrosis (CF) experience frequent episodes of acute decline in lung function called pulmonary exacerbations (PEx). An existing clinical and place-based precision medicine algorithm that accurately predicts PEx could include racial and ethnic biases in clinical and geospatial training data, leading to unintentional exacerbation of health inequities. We estimated receiver operating characteristic curves based on predictions from a nonstationary Gaussian stochastic process model for PEx within 3, 6, and 12 months among 26,392 individuals aged 6 years and above (2003-2017) from the US CF Foundation Patient Registry. We screened predictors to identify reasons for discriminatory model performance. The precision medicine algorithm performed worse predicting a PEx among Black patients when compared with White patients or to patients of another race for all three prediction horizons. There was little to no difference in prediction accuracies among Hispanic and non-Hispanic patients for the same prediction horizons. Differences in F508del, smoking households, secondhand smoke exposure, primary and secondary road densities, distance and drive time to the CF center, and average number of clinical evaluations were key factors associated with race. Racial differences in prediction accuracies from our PEx precision medicine algorithm exist. Misclassification of future PEx was attributable to several underlying factors that correspond to race: CF mutation, location where the patient lives, and clinical awareness. Associations of our proxies with race for CF-related health outcomes can lead to systemic racism in data collection and in prediction accuracies from precision medicine algorithms constructed from it.

Bridging Differences in Cohort Analyses of the Relationship between Secondhand Smoke Exposure during Pregnancy and Birth Weight: The Transportability Framework in the ECHO Program.

Estimates for the effects of environmental exposures on health outcomes, including secondhand smoke (SHS) exposure, often present considerable variability across studies. Knowledge of the reasons behind these differences can aid our understanding of effects in specific populations as well as inform practices of combining data from multiple studies. This study aimed to assess the presence of effect modification by measured sociodemographic characteristics on the effect of SHS exposure during pregnancy on birth weights that may drive differences observed across cohorts. We also aimed to quantify the extent to which differences in the cohort mean effects observed across cohorts in the Environmental influences on Child Health Outcomes (ECHO) consortium are due to differing distributions of these characteristics. We assessed the presence of effect modification and transportability of effect estimates across five ECHO cohorts in a total of 6,771 mother-offspring dyads. We assessed the presence of effect modification via gradient boosting of regression trees based on the H-statistic. We estimated individual cohort effects using linear models and targeted maximum likelihood estimation (TMLE). We then estimated transported effects from one cohort to each of the remaining cohorts using a robust nonparametric estimation approach relying on TMLE estimators and compared them to the original effect estimates for these cohorts. Observed effect estimates varied across the five cohorts, ranging from significantly lower birth weight associated with exposure [; 95% confidence interval (CI): , ] to higher birth weight with wide CIs, including the null (; 95% CI: , 99.8). Transported effect estimates only minimally explained differences in the point estimates for two out of the four cohort pairs. Our findings of weak to moderate evidence of effect modification and transportability indicate that unmeasured individual-level and contextual factors and sources of bias may be responsible for differences in the effect estimates observed across ECHO cohorts. https://doi.org/10.1289/EHP13961.

Association between indoor air pollution and depression: a systematic review and meta-analysis of cohort studies

ObjectivesIncomplete combustion of solid fuel and exposure to secondhand smoke (SHS) are the primary causes of indoor air pollution (IAP), potentially leading to detrimental effects on individual mental health. However,...

Availability of receptors for advanced glycation end-products (RAGE) influences differential transcriptome expression in mice exposed to chronic secondhand smoke

The receptor for advanced glycation end-products (RAGE) has a central function in orchestrating inflammatory responses in multiple disease states. RAGE is a transmembrane pattern recognition receptor with particular interest in lung disease due to its naturally abundant pulmonary expression. Our previous research demonstrated an inflammatory role for RAGE following acute exposure to secondhand smoke (SHS). However, chronic inflammatory mechanisms associated with RAGE remain unclear. In this study, we assessed transcriptional outcomes in mice exposed to chronic smoke in the context of RAGE expression. RAGE knockout (RKO) and wild type (WT) mice were exposed to SHS five times weekly via a nose-only delivery system (Scireq Scientific, Montreal, Canada) for six months and compared to mice exposed to room air (RA) only. Total lung RNA was isolated using the Direct-zol RNA MiniPrep kit (Zymo Research, Irvine, CA) and mRNA was purified using poly-T oligo-attached magnetic beads. Synthesis of cDNA, library construction, and sequencing was performed using standard approaches. We specifically compared the phenotypic and environmental conditions from WT+RA, WT+SHS, and RKO+SHS mice. Preprocessing and analysis of RNA-sequencing gene expression data included read trimming, mapping and quantifying the reads to transcripts, and calculating significant differentially expressed genes. The results of these analyses were summarized and compared via Venn diagrams, volcano plots, and functional gene cluster enrichment analysis. Notable gene clusters were specific to cytoskeletal elements, inflammatory signaling, and ciliogenesis. Finally, gene ontologies (GO) demonstrated significant biological pathways that were differentially impacted by the presence of RAGE. These data collectively identify several opportunities to further dissect RAGE signaling in the context of SHS exposure and foreshadow possible therapeutic modalities. This work was supported by funding from the National Institutes of Health (NIH 1R15-HL152257). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Availability of Receptors for Advanced Glycation End-Products (RAGE) Influences Differential Transcriptome Expression in Lungs from Mice Exposed to Chronic Secondhand Smoke (SHS).

The receptor for advanced glycation end-products (RAGE) has a central function in orchestrating inflammatory responses in multiple disease states including chronic obstructive pulmonary disease (COPD). RAGE is a transmembrane pattern recognition receptor with particular interest in lung disease due to its naturally abundant pulmonary expression. Our previous research demonstrated an inflammatory role for RAGE following acute exposure to secondhand smoke (SHS). However, chronic inflammatory mechanisms associated with RAGE remain ambiguous. In this study, we assessed transcriptional outcomes in mice exposed to chronic SHS in the context of RAGE expression. RAGE knockout (RKO) and wild-type (WT) mice were delivered nose-only SHS via an exposure system for six months and compared to control mice exposed to room air (RA). We specifically compared WT + RA, WT + SHS, RKO + RA, and RKO + SHS. Analysis of gene expression data from WT + RA vs. WT + SHS showed FEZ1, Slpi, and Msln as significant at the three-month time point; while RKO + SHS vs. WT + SHS identified cytochrome p450 1a1 and Slc26a4 as significant at multiple time points; and the RKO + SHS vs. WT + RA revealed Tmem151A as significant at the three-month time point as well as Gprc5a and Dynlt1b as significant at the three- and six-month time points. Notable gene clusters were functionally analyzed and discovered to be specific to cytoskeletal elements, inflammatory signaling, lipogenesis, and ciliogenesis. We found gene ontologies (GO) demonstrated significant biological pathways differentially impacted by the presence of RAGE. We also observed evidence that the PI3K-Akt and NF-κB signaling pathways were significantly enriched in DEGs across multiple comparisons. These data collectively identify several opportunities to further dissect RAGE signaling in the context of SHS exposure and foreshadow possible therapeutic modalities.

Occupational second-hand smoke exposure: A comparative shotgun proteomics study on nasal epithelia from healthy restaurant workers

Non-smokers exposed to second-hand smoke (SHS) present risk of developing tobacco smoke-associated pathologies. To investigate the airway molecular response to SHS exposure that could be used in health risk assessment, comparative shotgun proteomics was performed on nasal epithelium from a group of healthy restaurant workers, non-smokers (never and former) exposed and not exposed to SHS in the workplace. HIF1α-glycolytic targets (GAPDH, TPI) and proteins related to xenobiotic metabolism, cell proliferation and differentiation leading to cancer (ADH1C, TUBB4B, EEF2) showed significant modulation in non-smokers exposed. In never smokers exposed, enrichment of glutathione metabolism pathway and EEF2-regulating protein synthesis in genotoxic response were increased, while in former smokers exposed, proteins (LYZ, ATP1A1, SERPINB3) associated with tissue damage/regeneration, apoptosis inhibition and inflammation that may lead to asthma, COPD or cancer, were upregulated. The identified proteins are potential response and susceptibility/risk biomarkers for SHS exposure.

The crossroads of work and home: linkages between smoke-free policies at work and household environments

BackgroundTobacco use causes over eight million global deaths annually, with seven million directly attributed to tobacco use and 1.2 million to second hand smoke (SHS). Smoke-free environments are crucial to counter SHS. Although India banned smoking in public places in 2008, SHS exposure remains high. Studies have noted that limiting smoking in workplaces, restaurants, etc., helps to reduce overall smoking and reduce SHS exposure. Under this background, the study explores the linkages between smoke-free workplaces and living in smoke-free homes in India.MethodsThe two rounds of the GATS India (2009-10 and 2016-17) have been used for the study. The study focuses on male tobacco smokers working indoors or outdoors or both indoors and outdoors. The sample for the study was 2,969 for GATS 1 and 2,801 for GATS 2. Dependent variables include living in a smoke-free home, while the independent variables were adherence to a smoke-free office policy and socio-demographic variables. The two rounds of the GATS data were pooled for analysis. Statistical analysis involves bivariate and multivariate analysis.ResultsFindings reveal that 41% of respondents worked in smoke-free workplaces in GATS 2. Nationally, smoke-free homes increased from 35% in 2009–2010 to 44% in 2016-17. Individuals with smoke-free workplaces were more likely to have smoke-free homes. The Southern region consistently exhibited the highest proportion of smoke-free homes. Urban areas and higher education correlated with increased smoke-free homes. Logistic regression analysis confirmed that workplace smoke-free status is a significant predictor of smoke-free homes. In GATS 2, respondents aged 30 years and above were less likely to have smoke-free homes, while education and Southern region residence positively influenced smoke-free homes.ConclusionsThe correlation between smoke-free workplaces and smoke-free homes is linked to stringent workplace no-smoking policies, potentially deterring individuals from smoking at home. Opportunities exist for the expansion and stringent implementation of the smoke-free policies among Indian working adults, leveraging the workplace as a key setting for evidence-based tobacco control. The study highlights positive trends in India’s smoke-free homes, crediting workplace policies. Effective policies, education, and regional strategies can advance smoke-free homes, stressing the pivotal role of workplace policies and advocating broader implementation.

Effectiveness of a computer-facilitated intervention on improving provider delivery of tobacco treatment in a thoracic surgery and oncology outpatient setting: A pilot study.

Effective tobacco treatments are available but are often not delivered to individuals with an actual or potential diagnosis of thoracic malignancy. The specific aims of this study were to identify the prevalence of tobacco use and examine the effectiveness of the Clinical and community Effort Against Smoking and secondhand smoke Exposure (CEASE), a system-level computer-facilitated intervention, to improve provider delivery of tobacco treatment in a thoracic surgery and oncology outpatient setting. A pre-post-test design was used to assess the effectiveness of CEASE. A 3-step approach was used to integrate tobacco treatment into routine care: ask about tobacco use, assist with cessation, and refer to a quitline. An end-of-visit survey was conducted to collect prevalence of tobacco use and delivery of tobacco treatment. Descriptive statistics and Fisher's exact test were used for analysis. A total of 218 individuals were enrolled; 105 participants were in usual care (UC) and 113 were in the CEASE group. Of those who enrolled, 27.6% were never smokers in UC and 27.7% in CEASE, 60% were former smokers in UC and 50% in CEASE, and 12.4% were current smokers in UC and 21.4% in CEASE. Significant differences were noted in delivery of tobacco treatment with 15.4% having received tobacco treatment in UC compared to 62.5% in CEASE (p<0.004). A computer-facilitated intervention increased provider delivery of tobacco treatment in a thoracic surgery and oncology outpatient setting. This intervention provided a low-resource approach that has the potential to be scaled and implemented more broadly.

Measuring air quality in smoking and nonsmoking areas of Nevada casinos (Reno/Sparks): Potential exposure of minors to secondhand smoke.

To understand the potential exposure to tobacco smoke in Washoe County (Reno/Sparks), Nevada casinos by measuring air quality in smoking areas relative to non-smoking/non-gaming areas in which minors may be present. To act as a pilot study in community-based health research and policy campaigns by evaluating low-cost air monitors to measure personal secondhand smoke (SHS) exposure. We used customized mobile apps, AtmoTube PRO Air Monitors, and hand clickers to measure the timing and minute-by-minute levels of PM2.5 (a tobacco smoke marker). The app was used to record the number of smokers, minors, and total patrons associated with ~10-minute sequential time periods in standardized casino locations, including outdoor areas, slots, tables, restaurants, bars/lounges, arcades, among others. Between April and May 2022, we successfully visited 14 casinos and 18 distinct types of indoor casino locations. We found high PM2.5 peaks in casino locations even with zero, or a low percentage of, observed active smokers, including in both gaming/non-gaming areas. Indoor areas, regardless of smoking/non-smoking areas, consistently had higher PM2.5 levels than outdoor background levels. Indoor locations had median PM2.5 levels up to 18 times higher than the lowest outdoor background levels. Minors were present throughout all casino locations, and thus were likely exposed to elevated PM2.5 levels. Potential PM2.5 exposures due to smoking can be high regardless of ventilation systems. Small proportions of smokers in a location can lead to high levels of exposure. Establishing comprehensive smoke-free casinos is the only way to protect against SHS harms.

A study on the dual use of e-cigarettes and cigarettes among adolescents in Shandong Province

Objective: To understand the current status and its associated factors of dual use of e-cigarettes and cigarettes among adolescents in Shandong Province and explore the reasons for dual use behavior. Methods: A self-administered survey was conducted among 7 999 middle school students who were selected by stratified multi-stage cluster sample method. Data were weighted and analyzed by the SPSS 25.0 complex program. Results: In Shandong Province, the prevalence rates of attempting and current dual use of e-cigarettes and cigarettes among adolescents appeared as 7.7% and 1.3%, respectively. Male, friends smoking, and secondhand smoke exposure in the past 7 days were risk factors for dual use. Compared with cigarette smokers, dual users have no differences in cognition and behavior in quitting smoking (P>0.05). The main reason for dual users to smoke e-cigarettes was curiosity. Conclusions: Dual use of e-cigarettes and cigarettes is common among adolescents in Shandong Province, and its influencing factors are similar to traditional cigarettes. Dual use is not a transitional stage for smoking cessation. Dual users are more likely to continue smoking in the future, which should be paid attention and concern.

Abstract LB231: The mutagenic forces shaping the genomic landscape of lung cancer in never smokers

Abstract While most lung cancers are associated with tobacco smoking, prior studies have indicated that 15-20% of cases are found in never smokers. Lung cancer in never smokers (LCINS) shows demographic variations, being more common in females and Asian populations. Epidemiological studies have also identified environmental risk factors for LCINS, including exposure to secondhand tobacco smoke and air pollution. As part of the Sherlock-Lung project (current data freeze of 1217 samples), we generated deep WGS data from a large international cohort of 871 treatment-naïve LCINS recruited from 28 locations across four continents. Our cohort allowed mapping the genomic landscape operative in lung cancer histologies commonly found in never smokers, including adenocarcinomas (n=737) and carcinoids (n=61), as well as other histologies rarely attributed to never smokers (n=73). Information on passive smoking was collected for 458 patients, with 250 being exposed to secondhand smoke. We identified driver alterations and performed mutational signature analyses for single base substitutions (SBS), indels, doublet base substitutions (DBS), copy number alterations, and structural variants. We detected eighteen SBS signatures, with eight not previously linked to LCINS, including SBS4, associated with smoking but also observed in lifelong non-smokers exposed to different environmental mutagens, such as indoor pollution. Several additional signatures were detected in other variant types, including a novel indel signature. Notably, secondhand smoke exposure corresponded to increased SBS burden, although it was not associated with specific signatures. In contrast, we observed a signature-specific association of air pollution (measured as PM2.5 exposure) with SBS, indel, and DBS burden. SBS4 and correlated signatures ID3 and DBS2 were positively associated with PM2.5 exposure. Similarly, clock-like signature SBS5 was highly correlated with PM2.5, potentially acting as a readout of a promotion mechanism where lung cells undergo more cell divisions in individuals living in highly polluted areas. We also observed variability across histologies and ancestries for signatures and driver mutations, including enrichment of signatures SBS17b and SBS40a as well as KRAS mutations in adenocarcinomas from Europeans; aristolochic-acid associated signature SBS22a, and EGFR and TP53 mutations in adenocarcinomas from East Asians; and signature SBS8 and ARID1A mutations in carcinoids from Europeans. The unprecedented size of our cohort allowed us to refine the prevalence and intensity of the driver mutations and mutational signatures involved in LCINS, as well as their variability across ancestries, geographical locations, and histologies. Our results indicate that air pollution may act as both initiator and promoter of neoplastic expansion of LCINS. Citation Format: Marcos Diaz-Gay, Tongwu Zhang, Azhar Khandekar, Burçak Otlu, Shuvro Nandi, Christopher D. Steele, Nathaniel Rothman, Stephen J. Chanock, Qing Lan, Ludmil B. Alexandrov, Maria Teresa Landi. The mutagenic forces shaping the genomic landscape of lung cancer in never smokers [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 2 (Late-Breaking, Clinical Trial, and Invited Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(7_Suppl):Abstract nr LB231.

Association between secondhand smoke exposure and serum sex hormone concentrations among US female adults: a cross-sectional analysis using data from the National Health and Nutrition Examination Survey, 2013–2016

ObjectiveTo estimate the association between secondhand smoke (SHS) exposure and serum sex hormone concentrations in female adults (never smokers and former smokers).DesignCross-sectional analysis.SettingUS National Health and Nutrition Examination Survey, 2013–2016.Outcome...

Mortality attributable to secondhand smoke exposure in the autonomous communities of Spain

Introduction and objectivesExposure to secondhand smoke (SHS) causes cardiovascular disease, respiratory disease, and cancer. The aim of this study was to estimate the mortality attributed to SHS in people aged ≥ 35 years in Spain and its autonomous communities (AC) by sex from 2016 to 2021. MethodsEstimates of SHS-attributable mortality were calculated by applying the prevalence-dependent method where SHS exposure was derived from the adjustment of small-area models and based on the calculation of population-attributed fractions. Sex, age group, AC, and cause of death (ischemic heart disease and lung cancer) were included. The estimates of attributed mortality are presented with their 95% confidence interval (95%CI). Crude and age-standardized rates were estimated for each sex and AC. ResultsFrom 2016 to 2021, SHS exposure caused 4,970 (95%CI, 4,787-5,387) deaths, representing 1.6% of total mortality for ischemic heart disease and lung cancer. The burden of attributed mortality differed widely among the AC, with Andalusia having the highest burden of attributed mortality (crude rate: 46.6 deaths per 100 000 population in men and 17.0/100 000 in women). In all the AC, the main cause of death in both sexes was ischemic heart disease. The highest burden of mortality was observed in nonsmokers. ConclusionsThe burden of SHS-attributable mortality was high and varied geographically. The results of this study should be considered to advance tobacco control legislation in Spain.

The effect of active smoking and secondhand smoke exposure on early outcomes of ambulatory surgery: A prospective observational study

PurposeSince the hospital stay of patients after ambulatory surgery is short, it is important to determine the factors that may cause problems in the early postoperative period. Among these factors, the effects of which are not fully known are active smoking and secondhand smoke exposure. This study aimed to elucidate how active smoking and secondhand smoke exposure effect early outcomes of ambulatory surgery. MethodsA prospective observational study was conducted with 124 patients (42 active smokers, 40 nonsmokers exposed to secondhand smoke and 42 nonsmokers) who underwent ambulatory general surgery. Patients were closely monitored for cardiac and respiratory complications, as well as pain, opioid use, and nausea and vomiting until discharge from the hospital. ResultsPostoperative complications were observed in 50.8 % of the patients. Hypotension was more common in active smokers compared with nonsmokers and nonsmokers exposed to secondhand smoke. Smokers were more likely to require postoperative supplemental oxygen therapy. Pain intensity at 1st and 4th hours after surgery was significantly higher in smokers (p < 0.005). In addition, nonsmokers exposed to secondhand smoke exhibited more severe pain than nonsmokers (p = 0.001). There were no statistically significant differences between the groups with regard to opioid consumption. ConclusionAlthough smoking and secondhand smoke exposure are not associated with serious complications after ambulatory surgery, patients' comfort and the success of ambulatory surgery may be negatively affected due to severe pain associated with smoking and secondhand smoke exposure.

Secondhand smoke increases the risk of developing chronic obstructive pulmonary disease

Smoking is the most important risk factor for chronic obstructive pulmonary disease (COPD), however evidence from large-scale studies on whether secondhand smoke (SHS) increases the risk of COPD is still lacking. We conducted this large longitudinal study to investigate the association between SHS and the development of COPD. This is a longitudinal study. Data on 6519 subjects who were never-smokers, had no history of COPD, and had complete lung function records were extracted from the Taiwan Biobank. They were divided into two groups according to SHS exposure: no exposure and exposure groups. Data were collected when participants enrolled in the study and during regular follow-up. Cox proportional hazards regression models were used to estimate the relative risk (RR) and 95% confidence interval (CI) for the association between SHS and the risk of developing COPD. At 48 months of follow-up, 260 (4%) participants in the no exposure group and 34 (7%) participants in the exposure group developed COPD. The RR of incident COPD development was significantly higher in the exposure group than that in the no exposure group after adjusting for confounders (RR = 1.49; 95% CI 1.04 to 2.14; P value = 0.031). There is a dose–response relationship between the duration of exposure to SHS and the risk of incident COPD, which demonstrates that an additional hour of exposure to SHS per week was associated with a 1.03-fold increased likelihood of developing COPD after adjusting for confounders (RR = 1.03; 95% CI 1.00 to 1.05; P value = 0.027). SHS exposure contributes to the development of COPD. This finding can help raise awareness of the harms of SHS and provide a reference for formulating anti-smoking policies.