Serum Cotinine Levels Research Articles

Exploring the associations of tobacco smoking and serum cotinine levels with selected inflammatory markers in adults with HIV in South Africa

This study examined the associations between tobacco smoking and serum cotinine levels, an objective biochemical measure of tobacco smoke exposure, with markers of inflammation, i.e., interferon-gamma (IFN-γ), interleukin 10 (IL-10), interleukin 2 (IL-2) and tumour necrosis factor-alpha (TNF-α) in people living with HIV (PLWH).These specific markers were selected because of their hypothesised associations with smoking, PLWH and their outcomes. In a random sample of ≥ 18-year-old PLWH receiving care at 17 public healthcare facilities across the Western Cape Province in South Africa, data collection included self-reported smoking history, and serum levels of cotinine and selected inflammatory markers. The inflammatory marker data were log transformed because of the skewedness of their distribution. Linear regression models (1) adjusted for age and gender, and (2) fully adjusted for age, gender, current alcohol use, body mass index and CD4 counts were used to examine the associations between smoking tobacco or serum cotinine and inflammatory markers. Level of significance was p < 0.05. Among 749 PLWH who were mainly women (79%), the mean age was 38.5 (8.9) years and similar when stratified by smoking status. Serum cotinine levels exhibited a striking discrepancy, with a median of 154 ng/mL among current smokers, in stark contrast to the consistent median values of 10 ng/mL observed among past and never smokers. In regression models adjusted for age and gender, current smoking and frequent smoking were associated with lower IL-2 but higher TNF-α. Log-cotinine exhibited associations with IFN-γ, IL-10, and TNF-α, while cotinine levels ≥ 10 ng/mL compared to < 10 ng/mL were associated with higher IFN-γ and TNF-α. In fully adjusted models, log-cotinine and cotinine levels ≥ 10 ng/mL displayed significant associations with higher IFN-γ and lower IL-2. This study underscores the importance of investigating the interplay between smoking tobacco or serum cotinine levels with pro-inflammatory cytokines in PLWH. It signals the need for comprehensive research to unravel the potential synergistic impacts of smoking tobacco and HIV infection on chronic inflammation and immune dysregulation, shedding light on critical avenues for intervention and management strategies.

Association between acute tobacco exposure and fractional exhaled nitric oxide in patients with chronic obstructive pulmonary disease: National health and Nutrition Examination Survey (NHANES) 2007–2012

BackgroundFractional exhaled nitric oxide (FeNO) is a marker of type 2 airway inflammation. Tobacco exposure can lower FeNO levels. However, the effect of acute tobacco exposure on FeNO in patients with chronic obstructive pulmonary disease (COPD) is unclear. This study aimed to investigate the relationship of acute tobacco exposure with FeNO and eosinophils in COPD patients. MethodsThis retrospective cohort study included 445 patients with COPD based on the 2007–2012 National Health and Nutrition Examination Survey. Serum cotinine levels were examined to assess environmental tobacco smoke exposure. The patients were divided into five groups based on cotinine levels: Q1 (first quintile), Q2 (second quintile), Q3 (third quintile), Q4 (fourth quintile) and Q5 (fifth quintile). Logistic regression models and linear logistic regression models were used to evaluate the relationship between serum cotinine and FeNO and EOS levels. ResultsApproximately 16.5 % (75/445) of the participants had elevated FeNO (>25 bbp). In the unadjusted model, COPD patients with the lowest quintile of serum cotinine levels (0.011–0.0185 ng/mL) had higher FeNO levels compared to those with the highest quintile (≥309 ng/mL) (odds ratios (OR), 5.86 [2.11–16.20]). These findings remained consistent even after adjusting for covariates of demographics, lifestyle, diabetes, coronary heart disease, tumours, hypertension, using oral or inhaled steroids within 2 days, asthma and respiratory symptoms within 7 days. Furthermore, a standard deviation increase of ln-transformed cotinine levels was associated with decreased FeNO levels (OR, 0.45 [0.33, 0.60]). No significant correlation was observed betweenserum cotinine and blood eosinophils. After high extents of tobacco exposure, no correlation was found between FeNO and eosinophils.Our findings indicate that high cotinine levels are associated with decreased FeNO in COPD patients but not with blood eosinophils. This reveals that smoking may affect FeNO levels in patients with COPD, whereas it does not appear to influence blood eosinophil levels.

Association between serum cotinine and total testosterone in adult males based on NHANES 2011–2016

The relationship between smoking and testosterone levels in adult males remains a topic of ongoing debate. Serum cotinine is considered a reliable marker of both smoking intensity and exposure to tobacco smoke. Therefore, we aim to examine the association between serum cotinine levels and total testosterone concentrations in adult males using data from the U.S. National Health and Nutrition Examination Survey (NHANES) database. Our study assessed the relationship between serum cotinine and total testosterone using weighted linear regression models and subgroup analysis. A fully adjusted model with smooth curve fitting was employed to investigate the potential nonlinear association between serum cotinine and total testosterone. Threshold effects were analyzed to identify the inflection point between serum cotinine and total testosterone. Indeed, a total of 7797 participants were included in our study. After adjusting for potential confounding variables, the findings indicate a positive association between serum cotinine levels and total testosterone levels (β: 0.05, 95%CI: 0.02, 0.09). Furthermore, applying smoothed curve fitting analysis and threshold effects, an inflection point was detected at a serum cotinine level of 487 ng/ml. Above this threshold, total testosterone levels declined with increasing serum cotinine levels. In conclusion, the findings of our study suggest a positive association between elevated serum cotinine levels and total testosterone levels in adult men. However, it is essential to note that this association may be reversed at excessively high serum cotinine concentrations.

Joint effect of docosahexaenoic acid intake and tobacco smoke exposure on learning disability in children and adolescents: a cross-sectional study from the NHANES database

BackgroundDocosahexaenoic acid (DHA) has been reported to be associated with the children’s neurodevelopment, who may be exposed to tobacco smoke simultaneously. The evidence about joint effect of DHA intake and tobacco smoke exposure on children and adolescents’ learning disabilities (LD) was limited. The objective of this study was to assess the joint effect of DHA intake and tobacco smoke exposure on children and adolescents’ LD.MethodsA cross-sectional analysis of the NHANES 1999–2004 was performed. Children and adolescents aged 6–15 years old were included. The outcome was diagnosed by parental report of ever health professionals or school representative-identified LD. Dietary DHA intake data were obtained by food frequency questionnaire and tobacco smoke exposure levels were evaluated by serum cotinine levels. Weighted univariable and multivariate logistic regression analyses were conducted to determine the joint effect of DHA intake and tobacco smoke exposure on LD in children and adolescents, with odds ratios (ORs) and 95% confidence intervals (CIs). This joint association was further assessed after stratification by age, gender, body mass index, the history of attention deficit disorder and seen mental health professional.ResultsWe identified 5,247 children and adolescents in present study, of whom 593 (11.30%) had LD. After adjusting covariates, we observed children and adolescents with DHA intake (OR = 0.76, 95%CI: 0.61–0.96) was related to lower incidence of LD; children who exposure to tobacco smoke was related to higher incidence of LD (OR = 1.54, 95%CI: 1.07–2.23); children and adolescents who exposure to tobacco smoke and without DHA intake were related to highest odds of LD (OR = 2.08, 95%CI: 1.37–3.17, P for trend = 0.042), that was, DHA and tobacco smoke exposure may have a joint effect on the odds of LD in children and adolescents. Subgroup analyses suggested this joint effect was robust especially among children and adolescents with normal & underweight BMI and without the history of attention deficit disorder and seen mental health professional.ConclusionIncreasing the DHA intake and reducing tobacco smoke exposure may have a potential role in the prevention of LD in children and adolescents. This joint effect warrants further investigation by large-scale prospective study.

Serum cotinine levels and adolescents’ sleep health outcomes from NHANES 2005 to 2018

The association between tobacco smoke exposure and sleep has been widely discussed, but the correlation between serum cotinine levels and sleep health outcomes in adolescents has not been well described. This study aimed to further evaluate the association between serum cotinine levels and sleep health outcomes in adolescents using data from the National Health and Nutrition Examination Survey (NHANES) from 2005 to 2018. This cross-sectional study included participants aged 16–19 years from the NHANES 2005–2018. A weighted multivariate logistic regression model was used for the primary analysis. A restricted cubic spline (RCS) model was employed to investigate the non-linear association between serum cotinine levels and trouble sleeping. Subgroup analyses based on population characteristics were also conducted. In total, 2630 participants were included, which are representative of the 11.5 million US adolescents. Higher serum cotinine levels (≥ 3 ng/ml) were significantly associated with trouble sleeping in the fully adjusted model (odds ratio [OR] 1.817). The RCS model revealed a non-linear relationship between serum cotinine levels and trouble sleeping. Subgroup analyses indicated that this relationship was consistent and stable across various population characteristics. Serum cotinine levels are associated with sleep health outcomes in adolescents, with high serum cotinine levels being linked to increased trouble sleeping and longer or shorter sleep duration.

The link between serum cotinine levels and gallstones prevalence in adults: a cross-sectional analysis using NHANES data (2017-2020).

Gallstones represent a prevalent health issue globally, resulting in significant annual healthcare costs. While tobacco exposure is recognized for its association with numerous diseases, its correlation with gallstones remains contentious. Serum cotinine, a metabolite of nicotine, serves as a widely utilized indicator for assessing tobacco exposure. Crucially, no research has yet examined the association between serum cotinine levels and the gallstones. This study is designed as a cross-sectional analysis, utilizing data from the NHANES public database. The relationship between serum cotinine levels and gallstones was analyzed using multinomial logistic regression models and smooth curve fitting. Subgroup analyses and interaction tests were performed to examine the potential contributions of different populations and covariates to the findings. A total of 5,856 participants were included in this study. After adjusting for relevant covariates, the multiple logistic regression model results indicated that for each unit increase in serum cotinine concentration above 0.29 ng/mL, there was a 29% increase in the prevalence of gallstones. Furthermore, smooth curve fitting analysis revealed a positive correlation between these variables. These findings underscore the impact of tobacco exposure on gallstone prevalence. This study demonstrates a positive correlation between tobacco exposure, as measured by serum cotinine levels, and the prevalence of gallstones, thus adding to the body of existing research on this relationship.

Association between serum cotinine levels and urinary incontinence in adults in the United States: a population-based cross-sectional analysis

Environmental tobacco smoke (ETS) exposure has been shown to be associated with a variety of diseases, but evidence regarding the association between it and urinary incontinence (UI) is limited. Cotinine, a metabolite of nicotine in the human body, can more accurately quantify the level of human exposure to tobacco smoke. The study utilized data from seven survey cycles (2007-March 2020 Pre-pandemic) of the National Health and Nutrition Examination Survey (NHANES) program. Weighted multivariable logistic regression analysis, subgroup analysis, interaction tests, smooth curve fitting, and threshold effect models were used to analyze the relationship between serum cotinine and UI. Additionally, a 1:1 nearest neighbor propensity score matching (PSM) method was employed to minimize the impact of confounding factors. Before and after PSM, serum cotinine levels were higher in individuals with UI than those without (P < 0.05). Both before and after PSM, UI was positively correlated with serum cotinine levels, with a significantly increased risk of urinary incontinence when serum cotinine levels were in the Q3 range (before PSM: OR = 1.89, 95% CI = 1.59–2.24; after PSM: OR = 1.60, 95% CI = 1.28-2.00). Smooth curve fitting before and after PSM showed an approximate J-shaped non-linear dose-response relationship between log-transformed serum cotinine levels and UI. This study indicates that among American adults, there is a positive relationship between serum cotinine levels and UI, which is also significant in self-reported non-smoking populations. Therefore, reducing exposure to environmental tobacco smoke (e.g., avoiding second-hand smoke) in work and daily life may help alleviate the occurrence of UI, and serum cotinine levels have the potential to be a tool for predicting the degree of risk of developing UI.

Association between serum cotinine and muscle mass: results from NHANES 2011–2018

PurposeRecently, the detrimental effect of cigarette smoking on muscle metabolism has attracted much attention, but the relationship between cigarette smoking and muscle mass is poorly understood. Thus, this study investigated the association between exposure to cigarette smoke, defined based on serum cotinine, and muscle mass in the US population.MethodsWe utilized National Health and Nutrition Examination Survey (NHANES) data between 2011 and 2018 for analysis. Data on serum cotinine, muscle mass (quantified by appendicular skeletal muscle mass index, ASMI), and covariates were extracted and analyzed. Weighted multivariate linear regression analyses and smooth curve fittings were performed to investigate the association between serum cotinine and ASMI. Subgroup analyses were stratified by gender, race and smoking status. When nonlinearity was detected, the threshold effects were analyzed using a two-piecewise linear regression model.ResultsIn total, 8004 participants were included for analysis. The serum level of cotinine was negatively associated with ASMI in the fully adjusted model. Furthermore, comparing participants in the highest vs. the lowest tertile of serum cotinine, we found that ASMI decreased by 0.135 Kg/m2. In subgroup analysis stratified by gender and race, the association between serum cotinine and ASMI remained significant in all genders and races. In addition, the association remained significant among current and former smokers, but not among those who never smoked. Smooth curve fittings showed nonlinear relationships between serum cotinine and ASMI, with the inflection points identified at 356 ng/mL.ConclusionsOur study revealed that serum cotinine was negatively related to muscle mass. This finding improves our understanding of the deleterious effects of cigarette smoking on muscle mass and highlights the importance of smoking cessation for muscle health.

Association of electronic-cigarette, number of cigarettes, and marijuana use with high-risk Human Papillomavirus (HPV) among men and women: A cross-sectional analysis of a nationally representative sample

BackgroundSmoking is associated with an increased risk of HPV infection. However, the use of e-cigarettes and marijuana, number of cigarettes, and serum cotinine concentrations in relation with HPV (6, 11, 16, 18) and high-risk HPV (16 or 18) infections in underserved and understudied populations remain poorly understood. MethodsData included 687 males and 664 females among whom 489 were White, 375 were Black and 342 were Hispanics from the NHANES 2013–2016 with HPV and high-risk HPV infections. Smoking history included current and past smokers, number of cigarettes, use of e-cigarettes, marijuana, and serum cotinine levels. Weighted multivariable-adjusted logistic regression models were conducted. ResultsHigh-risk HPV infection was associated with current smoking history plus ≥ 20 cigarettes/day (OR=1.92, 95 % CI=1.09, 3.37) in the overall population. E-cigarettes use (5 days) was positively associated with high-risk HPV infection (OR=2.43, 95 % CI=1.13, 5.22) in the overall population, with similar findings with e-cigarette (past 30 days) among women and Whites. ConclusionHigh number of cigarettes, e-cigarette usage and marijuana were associated with HPV and high-risk HPV infections in the overall population. Most of these associations remained significant when stratified by gender and race/ethnicity. Increasing use of e-cigarettes and marijuana in these population warrants further investigation for the prevention of HPV infection and related cancers.

E-Cigarette Use, Cigarette Smoking, and Sex are Associated with Nasal Microbiome Dysbiosis.

Previous research suggests that e-cigarettes can alter immune function, including in the nasal mucosa, in unique ways. The respiratory microbiome plays a key role in respiratory host defense, but the effects of e-cigarettes on the respiratory or nasal microbiome, are not well understood. Using 16S rRNA gene sequencing on nasal samples from adult e-cigarette users, smokers, and nonsmokers, we determined that e-cigarette use and cigarette smoking are associated with differential respiratory microbiome dysbiosis and substantial sex-dependent differences in the nasal microbiome, particularly in e-cigarette users. Staphylococcus aureus, a common respiratory pathogen, was more abundant in both e-cigarette users and smokers in comparison with nonsmokers, while Lactobacillus iners, often consider a protective species, was more abundant in smokers but less abundant in e-cigarette users in comparison with nonsmokers. In addition, we identified significant dysbiosis of the nasal microbiome between e-cigarette users and smokers with high versus low serum cotinine levels, an indicator of tobacco product use and toxicant exposure. We also analyzed nasal lavage fluid for immune mediators associated with host-microbiota interactions. Our analysis identified disruption of immune mediators in the nose of e-cigarette users and smokers, which is indicative of disrupted respiratory mucosal immune responses. Taken together, our data identified unique, sex-dependent host immune dysfunction associated with e-cigarette use in the nasal mucosa. More broadly, our data highlight the need for continued inclusion and careful consideration of sex as an important variable in the context of toxicant exposures. This is the first study investigating the effects of e-cigarette use and sex on the nasal microbiome, which is considered an important gatekeeper for protecting the lower respiratory tract from pathogens. We found significant sex, exposure group, and serum cotinine level associated differences in the composition of the nasal microbiome, demonstrating the importance of considering sex in future nasal microbiome studies and warranting further investigation of the mechanisms by which e-cigarette use dysregulates nasal immune homeostasis.

Association between tobacco smoke exposure and serum parathyroid hormone levels among US adults (NHANES 2003–2006)

Tobacco smoke exposure has been demonstrated to impede bone remodeling and diminish bone density, yet research regarding its correlation with parathyroid hormone (PTH) remains limited. This study aims to investigate the relationship between tobacco smoke exposure and serum PTH levels in adults aged 20 years and older. This study included 7,641 participants from two cycles of the National Health and Nutrition Examination Survey (NHANES, United States, 2003- 2006). Reflect tobacco smoke exposure through serum cotinine levels, and use an adjusted weighted multivariate linear regression model to test the independent linear relationship between serum cotinine and PTH. Stratified analysis was conducted to validate the sensitivity of the conclusions. Smooth curve fitting and threshold effect analysis were performed to assess the non-linear relationship. After comprehensive adjustment using weighted multivariate regression analysis, a negative correlation was found between serum cotinine and PTH levels. The interaction p-values in subgroup analyses were all greater than 0.05. Moreover, smooth curve fitting indicated a non-linear relationship between serum cotinine and PTH, with a turning point observed. Our research indicates that tobacco smoke exposure is negatively correlated and independent of serum parathyroid hormone levels, indicating that long-term tobacco smoke exposure may lead to parathyroid dysfunction in adults.

Secondhand Nicotine Absorption From E-Cigarette Vapor vs Tobacco Smoke in Children

ImportanceWith the prevalence of e-cigarette use (vaping) increasing worldwide, there are concerns about children’s exposure to secondhand vapor.ObjectiveTo compare nicotine absorption among children who are (1) exposed to secondhand tobacco smoke only or (2) exposed to secondhand vapor only with (3) those exposed to neither.Design, Setting, and ParticipantsThe US Continuous National Health and Nutrition Examination Survey (NHANES) is a repeat cross-sectional survey. Participants are interviewed in their homes and, several days after, visit a mobile examination center to provide biological specimens. This study uses data from a nationally representative sample of US households from 2017 to 2020. Participants were children aged 3 to 11 years with serum cotinine levels incompatible with current firsthand nicotine use (ie, <15 μg/L). The final analysis was conducted on January 9, 2024.ExposuresReported exposure to secondhand smoke or vapor indoors in the past 7 days (only secondhand smoke, only secondhand vapor, or neither). Covariates included age, sex, ethnicity, family income, body weight, and height.Main Outcomes and MeasuresThe primary outcome was serum cotinine concentration, an objective biomarker of nicotine absorption. Geometric mean cotinine levels and 95% CIs were calculated using log-normal tobit regression, accounting for the complex survey design and weights.ResultsThe mean (SD) age of the 1777 children surveyed was 7.4 (2.6) years, 882 (49.6%) were female, and 531 (29.9%) had family incomes below the poverty level. Nicotine absorption, as indexed by serum cotinine level, was highest among children only exposed to secondhand smoke (0.494 μg/L μg/L; 95% CI, 0.386-0.633 μg/L), followed by those exposed only to secondhand vapor (0.081 μg/L; 95% CI, 0.048-0.137 μg/L), equating to 83.6% (95% CI, 71.5%-90.5%; P < .001) lower nicotine absorption. Among children with no reported secondhand exposure, the geometric mean cotinine level was 0.016 μg/L (95% CI, 0.013-0.021 μg/L), or 96.7% (95% CI, 95.6%-97.6%; P < .001) lower than for those with exposure to secondhand smoke. Results were similar after covariate adjustment.Conclusions and RelevanceIn this cross-sectional study of US children, nicotine absorption was much lower in children who were exposed to secondhand vapor vs secondhand smoke, but higher than in those exposed to neither. These findings suggest that switching from smoking to vaping indoors may substantially reduce, but not eliminate, children’s secondhand exposure to nicotine and other noxious substances.

Exploratory analysis on the association of dietary live microbe and non-dietary prebiotic/probiotic intake with serum cotinine levels in the general adult population.

Previous research has indicated the potential involvement of the microbiota in smoking-related processes. The present study seeks to examine the relationship between dietary live microbes, as well as probiotic or prebiotic consumption, and serum cotinine levels. This study used data from the National Health and Nutrition Examination Survey 1999-2018. Dietary intake information and probiotic/prebiotic intake data was collected through self-reported questionnaires. Participants were stratified into low, medium, and high intake groups according to their consumption of foods with varying microbial content. Multiple linear models were applied to explore the relationships of dietary live microbes, probiotic or prebiotic use with the serum cotinine level. A total of 42,000 eligible participants were included in the final analysis. The weighted median serum cotinine level was 0.05 (0.01, 10.90) ng/ml. Participants with low, medium, and high dietary microbe intake represented 35.4, 43.6, and 21.0% of the cohort, respectively. Furthermore, participants were stratified into three groups based on their overall consumption of foods with variable microbe contents. The association between dietary live microbe intake and serum cotinine levels remained robust across all models, with medium intake as the reference (Model 2: β = -0.14, 95% CI: -0.20, -0.07; High: β = -0.31, 95% CI: -0.39, -0.22). Moreover, both prebiotic and probiotic use exhibited an inverse relationship with serum cotinine levels (Prebiotic: β = -0.19, 95% CI: -0.37, -0.01; Probiotic: β = -0.47, 95% CI: -0.64, -0.30). Subgroup analyses revealed no discernible interactions between dietary live microbe, prebiotic, probiotic use, and serum cotinine levels. Our findings suggest a negative correlation between dietary live microbe intake, as well as non-dietary prebiotic/probiotic consumption, and serum cotinine levels.

Association between serum cotinine and hepatic steatosis and liver fibrosis in adolescent: a population-based study in the United States.

Tobacco exposure is known to be associated with a higher prevalence and incidence of liver diseases. Cotinine, a metabolite of nicotine, is a typical indicator of tobacco exposure. However, the relationship of serum cotinine levels with hepatic steatosis and liver fibrosis remains controversial and these relationships need more research to explored in American teenagers. Cross-sectional data included 1433 participants aged 12-19 from the National Health and Nutrition Examination Survey (NHANES) from 2017 to 2020 were thoroughly used for this study. The linear relationships between serum cotinine levels and the Liver Stiffness Measurement (LSM) and Controlled Attenuation Parameter (CAP) were examined using multiple linear regression models. Subgroup analysis, interaction tests, and nonlinear interactions were also carried out. Serum cotinine levels > 2.99ng/ml [β = 0.41 (0.07, 0.76), p = 0.018] and 0.05-2.99ng/ml [β = 0.24 (0.00, 0.49), p = 0.048] showed a significant positive connection with LSM in multivariate linear regression analysis when compared to serum cotinine levels ≤ 0.05ng/ml (p for trend = 0.006). Moreover, we discovered an inverted U-shaped association of log2-transformed cotinine with LSM with an inflection point of 4.53 using a two-stage linear regression model. However, according to multiple regression analysis, serum cotinine and CAP did not significantly correlate (p = 0.512). In conclusion, this study demonstrated that smoking cessation and keep away from secondhand smoking may beneficial for liver health in American teenagers.

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.

Sex disparities in the association between serum cotinine and chronic kidney disease.

Despite the existence of numerous studies highlighting the adverse effects of smoking on kidney function, the investigation of the correlation between serum cotinine and chronic kidney disease (CKD) remains inconclusive due to insufficient evidence. Consequently, the primary objective of this study was to ascertain the association between serum cotinine levels and CKD. This study analyzed data from 10900 Americans participating in the National Health and Nutrition Examination Survey between 2005 and 2016. The independent variable under investigation was log serum cotinine, while the dependent variable was the presence of CKD. To investigate the potential linear and non-linear correlations between serum cotinine and CKD, logistic regression models and generalized additive models (GAM) were employed. Furthermore, stratified analyses and interaction tests were conducted to evaluate potential disparities in the relationship between serum cotinine and CKD, based on sex. The median age in the study participants was 49.28 ± 17.96 years, and the median log serum cotinine (ng/mL) was -0.54 ± 1.68. The prevalence of CKD was found to be 17.04%. Multifactorial regression analysis did not show a statistically significant association between log serum cotinine and CKD (OR=1.02; 95% CI: 0.98-1.06, p=0.4387). A statistically significant non-linear association between log serum cotinine and CKD was also not observed in the GAM analysis (p non-linear value=0.091). Subgroup analyses revealed sex differences in the association between log serum cotinine and CKD. Briefly, males had a positive association between log serum cotinine and incident CKD (OR=1.08; 95% CI: 1.02-1.15, p=0.0049). In females, there was a U-shaped association between log serum cotinine and CKD, with an optimal inflection point for log serum cotinine of -0.30 (serum cotinine=0.5 ng/mL). Cross-sectional analyses of NHANES data showed gender differences in the association between serum cotinine and the development of CKD.

NHANES-based analysis of the correlation between leisure-time physical activity, serum cotinine levels and periodontitis risk

ObjectiveTo investigate the association of leisure-time physical activity and serum cotinine levels with the risk of periodontitis in the general population and to further analyze the interaction between leisure-time physical activity and serum cotinine levels on the risk of periodontitis.MethodsThis was a cross-sectional study, extracting data from 9605 (56.19%) participants in the National Health and Nutrition Examination Survey (NHANES) database from 2009 to 2014, and analyzing the relationship and interaction effects of serum cotinine level, leisure time physical activity, and risk of periodontitis by weighted univariate logistic modeling; Effect sizes were determined using ratio of ratios (OR), 95% confidence intervals (95% CI).Results5,397 (56.19%) of 9,605 participants had periodontitis; an increased risk of periodontitis was found in those in the leisure time physical activity intensity < 750 MET × min/week group (OR = 1.44, 95% CI: 1.17–1.78). Serum cotinine levels ≥ 0.05 ng/ml were associated with an increased risk of periodontitis (OR = 1.99, 95% CI: 1.69–2.33). The group with low leisure physical activity and serum cotinine levels ≥ 0.05 ng/ml had an increased risk of periodontitis compared to the group with high leisure physical activity and serum cotinine levels < 0.05 ng/ml (OR = 2.48, 95% CI: 1.88–3.27). Interaction metrics RERI = 0.90 (95% CI: 0.44–1.36) and API = 0.36 (95% CI: 0.18–0.55); CI for SI = 2.55 (95% CI: 1.03–6.28). for API 0.36.ConclusionLeisure time physical activity intensity interacted with smoking exposure on periodontitis risk and may provide the general population with the opportunity to Increasing leisure-time physical activity and smoking cessation may provide recommendations for the general population.

Prolidase could be considered a sign of inflammation associated with cigarette smoking.

Smoking causes inflammation, thickening, and narrowing of the airways. This inflammatory process is a reaction to free radicals and oxidants. Smoking affects collagen metabolism and tissue remodeling. Prolidase enzyme hydrolyzes iminodipeptides with hydroxyproline and C terminal proline. It plays a crucial role in the metabolism of collagen and the remodeling of the matrix. The present study aims to reveal the association of prolidase with inflammation caused by smoking and to compare serum prolidase levels with oxidative-antioxidative status in healthy individuals. A total of 76 participants (38 smokers and 38 nonsmokers) were involved in the present study. Serum cotinine levels were measured to show the exposure to nicotine in tobacco smoke by using the competitive inhibition enzyme immunoassay method. Serum prolidase, total oxidant status (TOS), and total antioxidant status (TAS) were determined by the enzyme-linked immunosorbent (ELISA) method, respectively. The correlation between smoking, serum prolidase levels, TOS, and TAS was investigated. TAS and serum prolidase levels of smokers were considerably lower than those in non-smokers (p < 0.001, p = 0.012 respectively). However, no differences were observed in TOS between the two groups. There was no statistically significant correlation between serum prolidase levels, TAS, and TOS. Moreover, no relationship was observed between respiratory function parameters and serum prolidase levels. To the best of our knowledge, the present study is the first study to demonstrate the role of prolidase in smoking-related inflammation. The results achieved in the present study suggest that smoking creates an imbalance in the oxidant-antioxidant activity. Smoking decreases prolidase levels, leading to decreased collagen turnover. Chronic pulmonary disease might be related to this decrease in collagen turnover.

Investigating the interplay of smoking, cardiovascular risk factors, and overall cardiovascular disease risk: NHANES analysis 2011–2018

BackgroundThis study explores the intricate relationship between smoking, cardiovascular disease (CVD) risk factors and their combined impact on overall CVD risk, utilizing data from NHANES 2011–2018.MethodsParticipants were categorized based on the presence of CVD, and we compared their demographic, social, and clinical characteristics. We utilized logistic regression models, receiver operating characteristics (ROC) analysis, and the chi-squared test to examine the associations between variables and CVD risk.ResultsSignificant differences in characteristics were observed between those with and without CVD. Serum cotinine levels exhibited a dose-dependent association with CVD risk. The highest quartile of cotinine levels corresponded to a 2.33-fold increase in risk. Smoking, especially in conjunction with lower HDL-c, significantly increases CVD risk. Combinations of smoking with hypertension, central obesity, diabetes, and elevated triglycerides also contributed to increased CVD risk. Waist-to-Height Ratio, Visceral Adiposity Index, A Body Shape Index, Conicity Index, Triglyceride-Glucose Index, Neutrophil, Mean platelet volume and Neutrophil to Lymphocyte ratio demonstrated significant associations with CVD risk, with varying levels of significance post-adjustment. When assessing the combined effect of smoking with multiple risk factors, a combination of smoking, central obesity, higher triglycerides, lower HDL-c, and hypertension presented the highest CVD risk, with an adjusted odds ratio of 14.18.ConclusionSmoking, when combined with central obesity, higher triglycerides, lower HDL-c, and hypertension, presented the highest CVD risk, with an adjusted odds ratio of 14.18.

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...