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Rationale: Lung cancer surgical morbidity has been decreasing, increasing attention to quality-of-life measures. A chronic sequela of lung cancer surgery is the use of postoperative oxygen at home after discharge. Prospective studies are needed to identify risk predictors for home oxygen (HO 2 ) use after curative lung cancer surgery. Objectives: To prospectively assess risk factors for postoperative oxygen use and postsurgical morbidity in patients undergoing curative lung cancer surgery. We hypothesized that obesity, poor preoperative pulmonary function, and smoking status would contribute to the risk of postoperative oxygen use. Methods: This study included patients undergoing surgery for a first primary non-small cell lung cancer at Mount Sinai from 2016 to 2020. Univariate, multivariable logistic regression analyses and adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were assessed. Results: Of the 433 patients with diagnosed pathologic stage I non-small cell lung cancer, 63 (14.5%) were discharged with HO 2 . By using multivariable analyses, we found that the body mass index (BMI) (OR for a BMI of 25-30 kg/m 2 , 4.0; 95% CI, 1.6-11.2; OR for a BMI ⩾30 kg/m 2 , 6.1; 95% CI, 2.4-17.5) and the preoperative diffusing capacity of the lung for carbon monoxide (Dl CO ) (OR for a Dl CO of <40%, 24.9; 95% CI, 3.6-234.1; OR for a Dl CO of 40-59%,  3.1; 95% CI, 1.3-7.2) were significant independent risk factors associated with the risk of HO 2 use after adjusting for other covariates. Although current smoking significantly increased the risk in the univariate analysis, it was no longer significant in the multivariable model. Conclusions: Obesity and the Dl CO were significant as risk factors for oxygen use at home after discharge. These findings allow for identification of patients at risk of being discharged with HO 2 after lung resection surgery.

Objectives: Lung cancer screening (LCS) with low-dose computed tomography (LDCT) has been a reimbursable preventive service covered by Medicare since 2015. Geographic disparities in the access to LDCT providers may contribute to the low uptake of LCS. We evaluated LDCT service availability for older adults in the United States (US) based on Medicare claims data and explored its ecological correlation with smoking prevalence. Materials and Methods: We identified providers who provided at least 11 LDCT services in 2016 using the Medicare Provider Utilization and Payment Data: Physician and Other Supplier Public Use File. We constructed a 30-mile Euclidian distance buffer around each provider's location to estimate individual LDCT coverage areas. We then mapped the county-level density of LDCT providers and the county-level prevalence of current daily cigarette smoking in a bivariate choropleth map. Results: Approximately 1/5 of census tracts had no LDCT providers within 30 miles and 46% of counties had no LDCT services. At the county level, the median LDCT density was 0.5 (interquartile range (IQR): 0-5.3) providers per 1000 Medicare fee-for-service beneficiaries, and cigarette smoking prevalence was 17.5% (IQR: 15.2-19.8%). High LDCT service availability was most concentrated in the northeast US, revealing a misalignment with areas of high current smoking prevalence, which tended to be in the central and southern US. Conclusions: Our maps highlight areas in need for enhanced workforce and capacity building aimed at reducing disparities in the access and utilization of LDCT services among older adults in the US.

The term myelodysplastic syndromes (MDS) include a diverse group of diseases in which the bone marrow production of blood cells is disrupted. In spite of the wealth of information on therapeutic options, little is known about the epidemiology of MDS, including population variations and risk factors. A narrative review of published literature and meta-analyses were conducted, identifying and summarizing key reports that describe the association between smoking, alcohol and MDS. There were 10 case-control studies that looked at the association between smoking and MDS, for a total of 1839 cases and 2831 controls. The meta-estimate for the association between ever smoking and MDS was 1.45 (95% CI: 1.21-1.74), with heterogeneity among studies (p=0.05), but no evidence of publication bias. The relationship between alcohol consumption and MDS has been examined in five studies, including 745 cases and 1642 controls. The overall association was 1.31 (95% CI: 0.79-2.18), with significant heterogeneity (p=0.003) and no evidence of publication bias. This re-analysis of published data strongly suggests that smoking is significantly associated with MDS, while alcohol does not seem to play a major role in MDS etiology. Large epidemiological studies incorporating biomarkers of exposure, along with pooled analysis are needed to better address the contribution of lifestyle factors to the development of MDS., (2009 Elsevier Ltd. All rights reserved.)

This review summarizes the carcinogenic effects of tobacco smoke and the basis for interaction between tobacco smoke and genetic factors. Examples of published papers on gene-tobacco interaction and cancer risk are presented. The assessment of gene-environment interaction in tobacco-related cancers has been more complex than originally expected for several reasons, including the multiplicity of genes involved in tobacco metabolism, the numerous substrates metabolized by the relevant genes and the interaction of smoking with other metabolic pathways. Future studies on gene-environment interaction and cancer risk should include biomarkers of smoking dose, along with markers of quantitative historical exposure to tobacco. Epigenetic studies should be added to classic genetic analyses, in order to better understand gene-environmental interaction and individual susceptibility. Other metabolic pathways in competition with tobacco genetic metabolism/repair should be incorporated in epidemiological studies to generate a more complete picture of individual cancer risk associated with environmental exposure to carcinogens.

To evaluate the roles of CYP1A1 polymorphisms [Ile 462Val and T 6235C (MspI)] and deletion of GSTM1 and GSTT1 in lung cancer development in Asian populations, a pooled analysis was conducted on 13 existing studies included in Genetic Susceptibility to Environmental Carcinogenesis database. This pooled analysis included 1,971 cases and 2,130 controls. Lung cancer risk was estimated as odds ratios (OR) and 95% confidence intervals (95% CI) using unconditional logistic regression model adjusting for age, sex, and pack-year. The CYP1A1 6235C variant was associated with squamous cell lung cancer (TC versus TT: OR, 1.42; 95% CI, 0.96-2.09; CC versus TT: OR, 1.97; 95% CI, 1.26-3.07; P trend = 0.003). In haplotype analysis, 462Val-6235T and Ile-C haplotypes were associated with lung cancer risk with reference to the Ile-T haplotype (OR, 3.41; 95% CI, 1.78-6.53 and OR, 1.39; 95% CI, 1.12-1.71, respectively). The GSTM1-null genotype increased squamous cell lung cancer risk (OR, 1.36; 95% CI, 1.05-1.77). When the interaction was evaluated with smoking, increasing trend of lung cancer risk as pack-year increased was stronger among those with the CYP1A1 6235 TC/CC genotype compared with those with TT genotype (P interaction = 0.001) and with the GSTM1-null genotype compared with the present type (Pinteraction = 0.08, when no genotype effect with no exposure was assumed). These results suggest that genetic polymorphisms in CYP1A1 and GSTM1 are associated with lung cancer risk in Asian populations. However, further investigation is warranted considering the relatively small sample size when subgroup analyses were done and the lack of environmental exposure data other than smoking.

Tobacco smoking is a major risk factor for lung cancer causing, among other effects, oxidative stress and lipid peroxidation. Malondialdehyde (MDA)-DNA adducts can be induced by direct DNA oxidation and by lipid peroxidation. We measured the relationship between bronchial MDA-DNA adducts and tobacco smoking, cancer status, and selected polymorphisms in 43 subjects undergoing a bronchoscopic examination for diagnostic purposes. MDA-DNA adducts were higher in current smokers than in never smokers (frequency ratio (FR) = 1.51, 95% confidence interval (CI) 1.01-2.26). MDA-DNA adducts were also increased in lung cancer cases with respect to controls, but only in smokers (FR = 1.70, 95% CI 1.16-2.51). Subjects with GA and AA cyclin D1 (CCND1) genotypes showed higher levels of MDA-DNA adducts than those with the wild-type genotype (FR = 1.51 (1.04-2.20) and 1.45 (1.02-2.07)). Lung cancer cases with levels of MDA-DNA adducts over the median showed a worse, but not statistically significant, survival, after adjusting for age, gender, and packyears (hazard ratio = 2.48, 95% CI 0.65-9.44). Our findings reinforce the role of smoking in lung carcinogenesis through oxidative stress. Subjects who carry at least one variant allele of the CCND1 gene could accumulate DNA damage for altered cell-cycle control and reduced DNA repair proficiency.

The recent introduction of biomarkers in population studies of lung cancer has improved the traditional epidemiological approach, especially in the detection of high risk groups. Many inhalable carcinogens form DNA adducts, an initial event in lung carcinogenesis, and therefore the identification of easily accessible sources of DNA for population studies is considered a leading priority in the field. In this study we compared the frequency of DNA adducts in samples from nasal brushing, bronchial biopsy and peripheral blood lymphocytes (PBL) in a group of 55 subjects, both smokers and non-smokers, undergoing bronchoscopy for diagnostic purposes. Polymorphisms in the CYP1A1, GSTM1 and GSTT1 genes were also evaluated. The level of DNA adducts measured by (32)P-labelling assay in nasal mucosa (10(8) relative adduct level, mean +/- SD 1.10 +/- 0.66) was higher than in bronchial mucosa (0.82 +/- 0.36) and in PBL (0.54 +/- 0.39, P < 0.01). DNA adducts measured in nasal mucosa and in PBL were correlated with those in bronchial mucosa (P < 0.01 and P < 0.05, respectively). DNA adducts in smokers were significantly increased in both nasal mucosa and PBL, with a significant dose-response linear trend (P < 0.05). No significant effect on DNA adduction of the genetic polymorphisms investigated was found. Nasal mucosa brushing proved to be a suitable procedure for the (32)P-labelling assay and its use in population studies should be further explored.

This article aims at evaluating the impact of cigarette smoking and alcohol consumption on different semen parameters (volume, concentration, motility, morphology, total sperm count and viability), by reviewing all the published literature on smoking, alcohol and sperm morphology. The studies on smoking and sperm abnormalities show a limited effect of smoking on conventional sperm parameters. The data on alcohol are more sparse, and show an apparent protective effect of moderate alcohol drinking on sperm parameters, probably due to the antioxidant effect of some alcoholic beverages. Unfortunately, none of the studies that considered both alcohol and smoking habits conducted the analysis of the joint effect of the two exposure factors. More standardized laboratory assays and increased sample size studies involving subjects with various level of exposure to alcohol and smoking are needed to better establish the role of these factors in male infertility.

Polymorphisms in genes that encode for metabolic enzymes have been associated with variations in enzyme activity between individuals. Such variations could be associated with differences in individual exposure to carcinogens that are metabolized by these genes. In this study, we examine the association between polymorphisms in several metabolic genes and the consumption of tobacco in a large sample of healthy individuals. The database of the International Collaborative Study on Genetic Susceptibility to Environmental Carcinogens was used. All the individuals who were controls from the case-control studies included in the data set with information on smoking habits and on genetic polymorphisms were selected (n = 20938). Sufficient information was available on the following genes that are involved in the metabolism of tobacco smoke constituents: CYP1A1, GSTM1, GSTT1, NAT2 and GSTP1. None of the tested genes was clearly associated with smoking behavior. Information on smoking dose, available for a subset of subjects, showed no effect of metabolic gene polymorphisms on the amount of smoking. No association between polymorphisms in the genes studied and tobacco consumption was observed; therefore, no effect of these genes on smoking behavior should be expected., (Copyright 2004 Wiley-Liss, Inc.)

Polymorphisms for genes encoding the metabolic enzymes cytochrome P450 1A1 (CYP1A1) and glutathione S-transferase M1 (GSTM1) might contribute to the variability in individual susceptibility to lung cancer. The role of CYP1A1 and GSTM1 in lung carcinogenesis might be more important at low levels of exposure to carcinogens. Non-smokers represent a population at low exposure, however, they are often overlooked because of the small number of cases. We therefore conducted a pooled analysis of 14 case-control studies on lung cancer in Caucasian non-smokers with comparable information on genetic polymorphisms included in the International Collaborative Study on Genetic Susceptibility to Environmental Carcinogens. We pooled the raw data from a total of 302 cases and 1631 controls with random effects models. We also evaluated the possibility of inclusion bias and conducted influence analyses. The odds ratio (OR) of lung cancer for the variant CYP1A1 Ile(462)Val polymorphism (Ile/Val, Val/Val) was 2.99 [95% confidence interval (95%CI) 1.51-5.91]; this effect was stronger on lung adenocarcinoma (OR 4.85, 95%CI 2.03-11.6). After excluding outlying or imprecise studies, we did not observe a significant effect of the CYP1A1 MspI (T(3801)C) polymorphism or GSTM1 null genotype (OR 1.20, 95%CI 0.89-1.63). Furthermore, our analyses suggested a combined effect of the CYP1A1 Ile(462)Val polymorphism and GSTM1 null genotype. The OR for the combination of the CYP1A1 Ile(462)Val variant and GSTM1 null genotype was 4.67 (95%CI 2.00-10.9) compared with the concurrent presence of the CYP1A1 wild-type and GSTM1 non-null genotype. We did not observe a modification of the effect of the GSTM1 null genotype according to exposure to environmental tobacco smoke and urban/rural residence. Our study therefore suggests that the CYP1A1 Ile(462)Val variant allele might play a role in lung carcinogenesis among non-smokers, possibly in combination with the GSTM1 null genotype.

Susceptibility to lung cancer may in part be attributable to inter-individual variability in metabolic activation or detoxification of tobacco carcinogens. The glutathione S-transferase M1 (GSTM1) genetic polymorphism has been extensively studied in this context; two recent meta-analyses of case-control studies suggested an association between GSTM1 deletion and lung cancer. At least 15 studies have been published after these overviews. We undertook a new meta-analysis to summarize the results of 43 published case-control studies including >18 000 individuals. A slight excess of risk of lung cancer for individuals with the GSTM1 null genotype was found (odds ratio (OR) = 1.17, 95% confidence interval (CI) 1.07-1.27). No evidence of publication bias was found (P = 0.4), however, it is not easy to estimate the extent of such bias and we cannot rule out some degree of publication bias in our results. A pooled analysis of the original data of about 9500 subjects involved in 21 case-control studies from the International Collaborative Study on Genetic Susceptibility to Environmental Carcinogens (GSEC) data set was performed to assess the role of GSTM1 genotype as a modifier of the effect of smoking on lung cancer risk with adequate power. Analyses revealed no evidence of increased risk of lung cancer among carriers of the GSTM1 null genotype (age-, gender- and center-adjusted OR = 1.08, 95% CI 0.98-1.18) and no evidence of interaction between GSTM1 genotype and either smoking status or cumulative tobacco consumption.

Smoking is a known risk factor for bladder cancer. The product of the GSTM1 gene, glutathione S-transferase M1 (GSTM1), is involved in the detoxification of polycyclic aromatic hydrocarbons found in tobacco smoke; a homozygous deletion of this gene in approximately 50% of Caucasians and Asians results in a lack of GSTM1 enzyme activity. Most studies examining the relation between bladder cancer and GSTM1 have reported an increased risk associated with a lack of GSTM1 activity. The authors performed meta- and pooled analyses of published and unpublished, case-control, genotype-based studies that examined this association (17 studies, 2,149 cases, 3,646 controls) and excluded studies conducted in populations with a high prevalence of exposure to known bladder cancer risk factors other than tobacco smoke. Using random effects models in the meta-analysis, the authors obtained a summary odds ratio of 1.44 (95% confidence interval (CI): 1.23, 1.68) for GSTM1 null status with all studies included. Results from studies with at least 100 cases and 100 controls produced a summary odds ratio of 1.42 (95% CI: 1.26, 1.60). Pooled analyses using original data sets from 10 studies (1,496 cases and 1,444 controls) and adjusting for age, sex, and race produced similar results. There was no evidence of multiplicative interaction between the GSTM1 null genotype and ever smoking in relation to bladder cancer, although there was a suggestion of additive interaction (additive interaction = 0.45, 95% CI: -0.03, 0.93). These results indicate that, among populations studied to date, GSTM1 null status is associated with a modest increase in the risk of bladder cancer.

Objectives: To develop and validate a clinical frailty index to characterize aging among responders to the 9/11 World Trade Center (WTC) attacks. Methods: This study was conducted on health monitoring data on a sample of 6197 responders. A clinical frailty index, WTC FI-Clinical, was developed according to the cumulative deficit model of frailty. The validity of the resulting index was assessed using all-cause mortality as an endpoint. Its association with various cohort characteristics was evaluated. Results: The sample's median age was 51 years. Thirty items were selected for inclusion in the index. It showed a strong correlation with age, as well as significant adjusted associations with mortality, 9/11 exposure severity, sex, race, pre-9/11 occupation, education, and smoking status. Discussion: The WTC FI-Clinical highlights effects of certain risk factors on aging within the 9/11 responder cohort. It will serve as a useful instrument for monitoring and tracking frailty within this cohort. [ABSTRACT FROM AUTHOR]

Background: It has been difficult to determine the individual impact of prenatal and postnatal tobacco smoke exposure (TSE) on childhood lung function, as children are often exposed to both.Objective: The goal of this study was to determine the association between current TSE and airflow obstruction while adjusting for self-reported prenatal TSE.Methods: Children aged 6 to 11 years who participated in the National Health and Nutrition Examination Survey (2007-2012) who had serum cotinine levels measured and spirometry performed were included. Logistic regression was used to determine the association between log-transformed serum cotinine level and airflow obstruction while adjusting for confounders; the analysis was then stratified according to asthma status. The final model included both log-transformed serum cotinine level and prenatal exposure as covariates.Results: The sample consisted of 2,070 children; 9.6% had airflow obstruction. The association between cotinine levels and airflow obstruction was significant in an unadjusted analysis (OR, 1.12 [95% CI, 1.02-1.23]). In the multivariate analysis with both exposures included as covariates, serum cotinine level was not significantly associated with airflow obstruction (ORadj, 1.07 [95% CI, 0.94-1.21]), and no association was seen in children with asthma and nonasthmatic children. Prenatal smoking was associated with airflow obstruction in children with asthma (ORadj, 2.51 [95% CI, 1.08-5.79]) but not in nonasthmatic children (ORadj, 1.08 [95% CI, 0.53-2.18]).Conclusions: Current TSE was not independently associated with airflow obstruction in school-aged children. Prenatal TSE was associated with airflow obstruction in children with asthma. Repeated studies into potential mediators and confounders of this relationship are needed. [ABSTRACT FROM AUTHOR]

This study was performed to quantify the association between mortality and known and unknown secondhand smoke (SHS) exposure as measured by cotinine levels in non-smokers. Data collected from 1999 to 2010 in the National Health and Nutrition Examination Survey (NHANES) were linked to the National Death Index. Self-reported non-smokers aged ≥20 years (N = 20 175) were studied. Serum cotinine was measured at recruitment; non-smokers were those with cotinine below the reported race-specific cut-off points (5.92, 4.85 and 0.84 ng/ml for non-Hispanic blacks, non-Hispanic whites and Mexican Americans, and 3.08 ng/ml for all other groups). Serum cotinine levels were significantly associated with overall survival (HRadj 1.17, 95% CI: 1.13-1.22 per natural-log unit change in cotinine), death for all medical causes, lung cancer, all cancers and heart diseases, after adjustment for gender, race/ethnicity, body mass index, smoking history and education. Similar results were observed when non-smokers reporting no SHS exposure at home or work were analyzed. There was a statistically significant trend in years of life lost (YLL), adjusted for confounders, across cotinine categories both in nonsmokers (YLLadj: 5.6, 6.4, 6.8, 7.5; P for trend < 0.0001) and non-smokers reporting no SHS exposure (YLLadj: 5.5, 6.1, 6.3, 6.7; P for trend = 0.002). Serum cotinine levels identify SHS-attributable mortality in subjects who would have otherwise been overlooked by questionnaire data, providing further evidence that the economic toll of SHS may be substantially higher than what was reported based on questionnaires. [ABSTRACT FROM AUTHOR]

Prostate cancer disparities have been reported in men of African descent who show the highest incidence, mortality, compared with other ethnic groups. Few studies have explored the genetic and environmental factors for prostate cancer in men of African ancestry. The glutathione-S-transferases family conjugates carcinogens before their excretion and is expressed in prostate tissue. This study addressed the role of GSTM1 and GSTT1 deletions on prostate cancer risk in populations of African descent. This multi-institutional case–control study gathered data from the Genetic Susceptibility to Environmental Carcinogens (GSEC) database, the African-Caribbean Cancer Consortium (AC3) and Men of African Descent and Carcinoma of the Prostate Consortium (MADCaP). The analysis included 10 studies (1715 cases and 2363 controls), five in African-Americans, three in African-Caribbean and two in African men. Both the GSTM1 and the GSTT1 deletions showed significant inverse associations with prostate cancer [odds ratio (OR): 0.90, 95% confidence interval (CI) 0.83–0.97 and OR 0.88, 95% CI: 0.82–0.96, respectively]. The association was restricted to Caribbean and African populations. A significant positive association was observed between GSTM1 deletion and prostate cancer in smokers in African-American studies (OR: 1.28, 95% CI: 1.01–1.56), whereas a reduced risk was observed in never-smokers (OR: 0.66, 95% CI: 0.46–0.95). The risk of prostate cancer increased across quartiles of pack-years among subjects carrying the deletion of GSTM1 but not among subjects carrying a functional GSTM1. Gene–environment interaction between smoking and GSTM1 may be involved in the etiology of prostate cancer in populations of African descent. [ABSTRACT FROM AUTHOR]

To investigate the role of microsomal epoxide hydrolase (mEH) polymorphisms in the aetiology of lung cancer and to assess the interaction between mEH polymorphisms and smoking, we performed a meta-analysis of seven published studies, which included 2078 cases and 3081 controls, and a pooled analysis of eight studies (four published and four unpublished at that time) with a total of 986 cases and 1633 controls. The combined metaanalysis odds ratios (ORs) were 0.98 (95% confidence interval [CI] = 0.72-1.35) for polymorphism at amino acid 113 in exon 3 (His/His versus Tyr/Tyr genotype) and 1.00 (95% CI= 0.71-1.41) for polymorphism at amino acid 139 in exon 4 (Arg/Arg versus His/ His genotype). In the pooled analysis, we observed a significant decrease in lung cancer risk (OR = 0.70, 95% CI = 0.51-0.96) for exon 3 His/His genotype after adjustment for age, sex, smoking and centre. The protective effect of exon 3 polymorphism seems stronger for adenocarcinoma of the lung than for other histological types. The OR for high predicted mEH activity, compared with low activity, was 1.54 (95% CI = 0.77-3.07) in the meta analysis and 1.18 (95% CI = 0.92-1.52) in the pooled analysis. We did not find a consistent modification of the carcinogenic effect of smoking according to mEH polymorphism, although the risk of lung cancer decreased among never smokers with high mEH activity and among heavy smokers with the exon 3 His/His genotype. In conclusion, this study suggests a possible effect of mEH polymorphisms at exon 3 in modulating lung cancer. If present, this effect may vary among different populations, possibly because of interaction with genetic or environmental factors. [ABSTRACT FROM AUTHOR]

Perfluoroalkyl acids (PFAS) are known endocrine disrupting chemicals, potentially affecting thyroid function. Smoking has been associated with PFAS levels as well as with thyroid function. The impact of smoking on the association between PFAS and thyroid function remains to be elucidated, so the objective was to assess the effect of PFAS exposure on thyroid function in the general population, stratified by smoking status, using the National Health and Nutrition Examination Survey (NHANES). NHANES adult participants who were part of the 2011–2012 laboratory subsample and had PFAS and thyroid function measured were included (n = 1325). Adjusted linear regression models and stratified analyses were performed. There was a significant positive association between perfluorooctanesulfonic acid (PFOS) (p = 0.003), perfluorononanoic acid (PFNA) (p = 0.014), total PFAS (p = 0.004) concentrations and free T4 (FT4). No significant associations were found between perfluorooctanoic acid (PFOA), PFOS, perfluorohexane sulfonate (PFHxS), PFNA, total PFAS and total T4 (TT4) or thyroid stimulating hormone (TSH). In non-smokers, a significant positive association was found between PFOS (p = 0.003), PFHxS (p = 0.034), PFNA (p = 0.012), total PFAS (p = 0.003) and FT4 while no significant associations were found in smokers. The present study showed that increased PFAS exposure was associated with increased FT4 in non-smokers, while no association was found in smokers. These results confirm that smoking modifies the association between PFAS exposure and thyroid function. [ABSTRACT FROM AUTHOR]

• We compared self-reported and cotinine-based smoking status in non-trial settings. • We focused on a nationally representative sample of adults eligible for lung cancer screening. • The sensitivity, specificity, and Kappa coefficient were 86.4%, 99.7%, and 83.1%, respectively. • Self-reported smoking status is reliable among adults at high risk for developing lung cancer. Self-reported smoking behavior is widely used in identifying the eligibility for lung cancer screening (LCS). In clinical trials, self-reported smoking status was shown to be a reliable measure, while its effectiveness outside of trial settings remains to be clarified. We aimed to verify self-reported smoking status with serum cotinine levels among LCS-eligible adults from the National Health and Nutrition Examination Survey (NHANES). From the combined 1999-2018 NHANES data, we selected adults (aged ≥18 years) with complete data on serum cotinine and smoking behavior, and determined their LCS eligibility according to the United States Preventive Services Task Force recommendation. Using established race/ethnicity specific cotinine cutpoints as the gold standard, we verified self-reported current smoking status with five measures: sensitivity (Se), specificity (Sp), positive predictive value (PPV), negative predictive value (NPV), and reliability Kappa. We also compared these performance measures in subgroups stratified by sex, race/ethnicity, education, family income to poverty ratio, health insurance, and secondhand smoking exposure (SHS) at home. All analyses took into account the complex survey design. Approximately 9.3% (n = 2335, equivalent to 8.82 million weighted population) of all adults who currently smoke or formerly smoked were eligible for LCS. The prevalence of current smoking was 52.6% and 60.8% based on self-report and cotinine, respectively. The Se and Sp were 86.4% (95%CI: 83.9%-88.9%) and 99.7% (95%CI: 99.4%-100%), respectively; PPV and NPV were 99.8% (95%CI: 99.6%-100%) and 82.6% (95%CI: 79.4%-85.7%), respectively; and Kappa was 0.83 (95%CI: 0.80-0.86). The reliability Kappa was higher among females than males (0.87 (95%CI: 0.82-0.93)) vs 0.80 (95%CI: 0.77-0.84), the lowest among non-Hispanic white (0.82 (95%CI: 0.78-0.86)), and higher among those with SHS (0.72 (95%CI: 0.63-0.80) vs (0.68 (95%CI: 0.61-0.76)). Self-reported smoking status is reasonably reliable among adults with high risk for developing lung cancer in the general population. [ABSTRACT FROM AUTHOR]