Serum Cotinine Levels Research Articles

Unraveling the link: environmental tobacco smoke exposure and its impact on infertility among American women (18-50 years).

The detrimental effects of environmental tobacco smoke (ETS) on women's reproductive health have been widely recognized. However, the detailed association between exposure to environmental tobacco smoke and the incidence of infertility remains under-explored. This investigation focuses on exploring this potential connection. For this analysis, we extracted data from the US National Health and Nutrition Examination Survey (NHANES) database, covering the years 2013 to 2018, focusing on individuals with recorded serum cotinine levels and infertility information. ETS exposure and fertility status were analyzed as independent and dependent variables, respectively. We applied weighted multivariate logistic regression method to evaluate the impact of ETS on infertility, including subgroup analyses for more detailed insights. The study encompassed 3,343 participants. Logistic regression analysis revealed a notable positive correlation between ETS exposure and infertility, with an odds ratio (OR) of 1.64 (95% Confidence Interval [CI]: 1.14-2.36). We observed a non-linear relationship between ETS exposure and infertility risk. Notably, infertility risk increased by 64% in serum cotinine levels above 0.136 compared to that in serum cotinine levels below 0.011. Further, subgroup analysis and interaction tests showed consistent results across different segments, underscoring the robustness of the ETS-infertility link. Our findings suggest that environmental tobacco smoke exposure may be a contributing factor to infertility. These results reinforce the recommendation for women in their reproductive years to avoid ETS exposure, especially when planning for pregnancy.

Association of secondhand smoke exposure with all-cause mortality and cardiovascular death in patients with hypertension: Insights from NHANES

Background and aimThe impact of environmental chemical exposure on blood pressure (BP) is well-established. However, the relationship between secondhand smoke exposure (SHSE) and mortality in hypertensive patients in the general population remains unclear. Methods and resultsThis cohort study included US adults in the National Health and Nutrition Examination Survey from 2007 to 2018. All-cause mortality and cause-specific mortality outcomes were determined by associating them with the National Death Index records. Cox proportional risk models were used to estimate hazard ratios (HRs) for all-cause mortality and cardiovascular disease (CVD) mortality, and 95% confidence intervals (CIs) for SHSE. The cohort included 10,760 adult participants. The mean serum cotinine level was 0.024 ng/mL. During a mean follow-up period of 76.9 months, there were 1729 deaths, including 469 cardiovascular disease deaths recorded. After adjusting for lifestyle factors, BMI, hypertension duration, medication use, and chronic disease presence, the highest SHSE was significantly associated with higher all-cause and CVD mortality. ConclusionsThis study demonstrates that higher SHSE is significantly associated with higher all-cause mortality and CVD mortality. Further research is necessary to elucidate the underlying mechanisms.

Correlation analysis between smoke exposure and serum neurofilament light chain in adults: a cross-sectional study

BackgroundSmoke exposure is a prevalent and well-documented risk factor for various diseases across different organ systems. Serum neurofilament light chain (sNfL) has emerged as a promising biomarker for a multitude of nervous system disorders. However, there is a notable paucity of research exploring the associations between smoke exposure and sNfL levels.MethodsWe conducted a comprehensive analysis of the National Health and Nutrition Examination Survey (NHANES) cross-sectional data spanning the years 2013 to 2014. Serum cotinine levels were classified into the following three groups: < 0.05, 0.05–2.99, and ≥ 3 ng/ml. Multiple linear regression models were employed to assess the relationships between serum cotinine levels and sNfL levels. Additionally, we utilized restricted cubic spline analyses to elucidate the potential nonlinear relationship between serum cotinine and sNfL levels.ResultsA total of 2053 participants were included in our present research. Among these individuals, the mean age was 47.04 ± 15.32 years, and males accounted for 48.2% of the total study population. After adjusting the full model, serum cotinine was positively correlated with sNfl in the second group (β = 0.08, 95%CI 0.01–0.15) and in the highest concentration of serum cotinine (β = 0.10, 95%CI 0.01–0.19) compared to the group with the lowest serum cotinine concentrations. Current smokers, in comparison to non-smokers, exhibited a trend toward elevated sNfL levels (β = 0.07, 95%CI 0.01–0.13). Furthermore, subgroup analyses revealed interactions between serum cotinine levels and different age groups (P for interaction = 0.001) and gender stratification (P for interaction = 0.015) on sNfL levels.ConclusionThe study suggested that serum cotinine was significantly and positively associated with sNfl levels in adult participants. Furthermore, current smokers tend to exhibit elevated sNfL levels. This research sheds light on the potential implications of smoke exposure on neurological function impairment and underscores the importance of further exploration in this area.

Association Between the Serum Copper Levels and Environmental Tobacco Exposure on the Risk of Overweight and Obesity in Children: a Study Based on the National Health and Nutrition Examination Survey.

This study was to assess the individual effects of serum copper levels and environmental tobacco exposure and their joint effects on the risk of overweight and obesity among children and adolescents of 6 to 19year olds. We analyzed cross-sectional data from 1849 children and adolescents participating in the National Health and Nutrition Examination Survey (NHANES) collected between 2011 and 2016. Environmental tobacco exposure was determined by cotinine levels. The serum copper level was divided into < median group and ≥ median groups according to the median of 109.81µg/dL. The outcome was overweight/obese in children and adolescents. Weighted multinomial multivariate logistic regression models were used to assess the association of serum copper and cotinine levels, with the risk of overweight/obesity, and the joint effects on the risk of overweight and obesity among children and adolescents. The subgroup analyses based on age, gender, and household smoking status were conducted. Among 1849 children and adolescents, 332 children and adolescents had overweight BMI, and 450 children and adolescents had obese BMI. Higher serum copper levels were associated with the risk of obesity in children and adolescents (odds ratio (OR) 2.96, 95% confidence interval (CI) 1.39-6.31, P = 0.006). A positive association between increasing levels of cotinine levels and the risk of overweight (OR 1.83, 95% CI 1.16-2.87, P = 0.010) and obesity (OR 2.56, 95% CI 1.03-6.40, P = 0.044) in children and adolescents was observed. A remarkable association was found between higher serum copper in combination with higher cotinine levels and the risk of overweight (OR 3.23, 95% CI 1.19-8.83, P = 0.023) and obesity (OR 8.76, 95% CI 2.14-35.87, P = 0.003) in children and adolescents. The subgroup analyses revealed positive associations between high serum copper levels in combination with high cotinine levels and overweight and obesity in children and adolescents aged ≥ 12years, of female sex, and without smoking family members. There may exist a joint effect of serum copper levels and environmental tobacco exposure on overweight/obesity among children and adolescents. These findings offer an insight that early weight control and reduction of tobacco exposure and the detection of serum copper levels may be important in reducing the risk of obesity in children.

Association Between Secondhand Smoke Exposure and Nonalcoholic Fatty Liver Disease in the General U.S. Adult Nonsmoker Population.

Smoking is a cause of nonalcoholic fatty liver disease (NAFLD), but the dose-response relationship between secondhand smoke exposure (SHS) and NAFLD is unclear. This study sought to determine the relationship between SHS and NAFLD risk among adult nonsmokers in the United States. Data from 7412 adult nonsmokers aged ≥20 years who participated in the National Health and Nutrition Examination Survey (NHANES) between 2007 and 2016 were used in this study. SHS was defined as a nonsmoker with a serum cotinine concentration of 0.05-10.00 ng/mL. NAFLD was identified using the U.S. fatty liver index (USFLI), hepatic steatosis index (HSI), and fatty liver index (FLI). Weighted multivariable logistic regression and restricted cubic spline models were applied to evaluate the relationship between SHS and NAFLD risk. The participants had a weighted mean age of 49.2 years, and 55.5% were female. SHS was associated with NAFLD (odds ratio [OR] 1.22; 95% confidence interval CI: 1.05 to 1.42), showing a linear dose-response relationship (natural log of cotinine level: OR 1.10, 95% CI: 1.05 to 1.17). Sensitivity analyses using different NAFLD definitions (HSI: OR 1.21, 95% CI: 1.01 to 1.46; FLI: OR 1.26, 95% CI: 1.06 to 1.49), excluding participants taking hepatotoxic drugs, and propensity score-adjusted analysis yielded similar results. The association between SHS and NAFLD was consistent in analyses stratified by age, sex, and race/ethnicity. Among this nationally representative sample of U.S. adults, SHS had a linear dose-response relationship with the risk of NAFLD, suggesting that measures to lower SHS might lower NAFLD risk. This study assessed the association between secondhand smoke exposure and the risk of nonalcoholic fatty liver disease (NAFLD) using data from 7412 adult nonsmokers aged 20 years or older who participated in the United States NHANES between 2007 and 2016. Secondhand smoke exposure was measured using serum cotinine levels. Three different noninvasive indexes were used to measure NAFLD. Secondhand smoke exposure was associated with an increased risk of NAFLD, with a linear dose-response relationship. The results of sensitivity analyses and subgroup analyses were consistent.

The roles of serum vitamin D and tobacco smoke exposure in insomnia: a cross-sectional study of adults in the United States.

Tobacco smoke exposure and vitamin D (VD) status were both associated with insomnia. However, the combined effect of smoking and VD on insomnia has not been discussed. This study aimed to explore the role of VD in the association between tobacco smoke exposure and insomnia. Data on adults were extracted from the National Health and Nutrition Examination Surveys (NHANES) database in 2005-2008 for this cross-sectional study. Weighted univariate and multivariate logistic regression analyses were used to explore the associations between serum cotinine, serum VD, and insomnia. A surface diagram was drawn to reflect the effect of VD on the association between serum cotinine and insomnia. In addition, the potential regulating effect of VD in subgroups of smoking status was also performed. The evaluation index was odds ratios (ORs) with 95% confidence intervals (CIs). Among the eligible participants, 1,766 had insomnia. After adjusting for covariates, we found that elevated serum cotinine levels were associated with higher odds of insomnia [OR = 1.55, 95% CI: (1.22, 1.97)]. However, the relationship between serum VD level and insomnia was not significant (P = 0.553). Higher serum cotinine levels were also associated with higher odds of insomnia [OR = 1.52, 95% CI: (1.17, 1.98)] when serum VD level was <75 nmol/L; however, this relationship became non-significant when serum VD concentration was elevated (P = 0.088). Additionally, the potential regulating effect of VD was also found in adults who were not smoking. VD may play a potential regulative role in the association between tobacco smoke exposure and insomnia. Further studies are needed to clarify the causal relationships between VD, tobacco smoke exposure, and insomnia.

Smoking and multiple sclerosis risk in black people: A nested case-control study

BackgroundSmoking is a well-established risk factor for MS; however, it is not known whether its effect on disease risk varies by race/ethnicity. MethodsWe conducted a nested case-control study among US military personnel who have serum samples stored at the Department of Defense Serum Repository. We measured serum cotinine levels, a marker of tobacco smoke exposure, in 157 Black and 23 White individuals who developed MS during follow-up. Controls were randomly selected and matched to each case by age, sex, race/ethnicity, dates of sample collection, and branch of military service. ResultsSmoking was not associated with an increased risk of MS in Black people (RR: 1.08, 95 % CI: 0.63–1.85). The results remained similar in analyses restricted to smoking status at baseline, to samples collected 5 years before symptom onset, and using different cut-off levels in cotinine to define smoking status. Smoking was not statistically significantly associated with MS risk in White people, but the point estimate was similar to what has previously been reported in other studies (RR: 1.85, 95 % CI: 0.56–6.16). ConclusionsSmoking was not associated with MS risk in Black people. Given the consistent association between smoking and MS risk in predominantly White populations, this may suggest that the association between smoking and MS varies by race/ethnicity.

Differential Impact of Smoking on Methylome and Transcriptome in Crohn's Disease and Ulcerative Colitis.

Smoking is an environmental factor that differentially impacts Crohn's disease (CD) and ulcerative colitis (UC). The mechanism of impact of smoking on disease risk and clinical outcomes remains to be established. This study used a prospective cohort of patients with CD or UC. Self-reported smoking status was validated using serum cotinine measurement. We profiled methylation changes in peripheral blood using the Illumina Methylation BeadChip. Transcriptomic profiling was performed on ileal and colonic tissue using an Illumina TruSeq platform. We compared the methylation and transcriptional changes in current, former, and never smokers stratified by disease type. Our cohort included 200 patients with CD or UC with methylation profiles and 160 with transcriptomic data. The mean serum cotinine level was higher in current compared with former or never smokers. Epigenetic changes common to both CD and UC included hypomethylation at AHRR. Smoking-associated MGAT3 hypomethylation was associated with severe disease course only in UC, while IER3 hypomethylation was associated with worse course only in CD. Smoking downregulated several inflammatory pathways in UC. Current smoking in CD but not in UC was associated with upregulation of several genes mediating Paneth cell function. Genes with opposite direction of effects in CD and UC include HSD3B2 and GSTA1. Our findings suggest both common and differential effects of cigarette smoking on CD and UC. Paneth cell dysfunction may mediate adverse impact of smoking on CD. Bile acid and oxidative stress pathways may be relevant for the differential effect of smoking on CD and UC.

Association of environmental tobacco smoke exposure with chronic constipation: a nationwide survey (NHANES 2005-2010).

Environmental tobacco smoke (ETS) exposure has been proven to induce digestive diseases such as hepatic steatosis, cirrhosis, and gastrointestinal cancer, yet little is known about the link between ETS exposure and constipation. This study aimed to investigate the impact of ETS exposure on the risk of chronic constipation in adults aged 20years or older. This is a cross-sectional study based on population. A total number of 7705 participants from the National Health and Nutrition Examination Survey (NHANES) 2005-2010 were included. Cotinine, an alkaloid found in tobacco, serves as a reliable and precise biomarker for measuring exposure to ETS. Hence, the categorization of exposure to ETS was conducted based on serum cotinine levels, resulting in four distinct categories. The association between ETS exposure and the risk of constipation was assessed using multivariable restricted cubic spline and logistic regression with odds ratio (OR) and 95% confidence interval (CI). The weighted prevalence of constipation in this study was estimated to be 7.51% based on stool consistency, or 3.11% based on stool frequency. The fully adjusted models indicated a positive correlation between exposure to ETS and constipation as measured by stool frequency, among adults with poor dietary quality (OR (95% CI): moderate exposure: 2.49 (1.05, 5.94); high exposure: 2.36(1.13, 4.95), P for trend = 0.03), while no significant difference was observed in the subgroup with a higher healthy eating index. Furthermore, the log10-transformed serum cotinine level exhibited a non-linear inverted U-shaped association with constipation in individuals with poor dietary quality (P overall = 0.0207, P non-linear = 0.0427). Conversely, a J-shaped non-linear relationship was observed in the subgroup with a higher healthy eating index (P overall = 0.0028, P non-linear = 0.0036). Our results show that ETS exposure appears to be positively associated with stool frequency-related chronic constipation in adults with poor dietary quality.

Factors Affecting the Serum Cotinine Level of Male Smokers in Malang, Indonesia

Background: In tobacco, nicotine is the primary toxic agent that causes health problems. As a primary metabolite of nicotine, cotinine is frequently used as an accurate measure of exposure to tobacco smoke. This study aims to find the factors affecting the serum cotinine level of male smokers in Malang, Indonesia. Methods: This cross-sectional study was conducted on 183 men who smoke regularly in Malang, Indonesia. They were selected by a purposive sampling method. Nicotine dependency and cotinine level were measured using the Fagerstrom test for nicotine dependence and the human cotinine ELISA Kit, respectively. Multiple linear regression analysis was performed to determine the effect of age, smoking duration, cigarette type, and the nicotine dependence on the continue level. ANOVA and independent t-test were also used for testing the study hypothesis. The significance level was set at 0.05. Results: Based on the ANOVA results, the factors of age, smoking duration, type of cigarette, and nicotine dependence together had a significant effect on the cotinine level (P&lt;0.001). Based on the independent t-test results, only the age factor had a significant effect on the cotinine level (P&lt;0.001). Conclusion: Older male smokers may have higher cotinine level. Other factors including duration of smoking, type of cigarette, and nicotine dependence have no significant effect on cotinine level of male smokers.

Association of Dietary Flavonoid Intake with Serum Cotinine Levels in the General Adult Population.

Cotinine, the primary metabolite of nicotine, can be utilized as a marker for active smoking and as an indicator of exposure to secondhand smoke. However, the direct relationship between dietary flavonoid intake and serum cotinine levels remains a subject of ongoing investigation. In this study, we utilized data from the National Health and Nutrition Examination Survey (NHANES) 2007-2010 and 2017-2018 to assess the association between dietary flavonoid intake and serum cotinine levels in adults through multiple linear regression analysis. A weighted quantile sum (WQS) regression model was used to assess the association of the mixture of six dietary flavonoids with serum cotinine levels in adults, which could represent the overall effect of the mixture of six dietary flavonoids. We also conducted stratified analyses by smoke status to explore multiple linear regression associations between different flavonoid intake and serum cotinine levels. A total of 14,962 adults were included in the study. Compared to the group with the lowest dietary flavonoid intake, total flavonoid intake in the second (β = -0.29 [-0.44, -0.14]), third (β = -0.41 [-0.58, -0.24]), and highest groups (β = -0.32 [-0.49, -0.16]) was inversely related to the levels of serum cotinine after adjusting the full model. An RCS model showed that when the total dietary flavonoid intake was less than 99.61 mg/day, there was a negative linear association between dietary flavonoid intake and the serum cotinine. The WQS regression model also showed that the intake of a mixture of six dietary flavonoids was significantly negatively correlated with serum cotinine levels (β = -0.54 [-0.61, -0.46], p <0.01), with anthocyanins having the greatest effect (weights = 32.30%). Our findings imply a significant correlation between dietary flavonoid intake and serum cotinine levels among adults. The consumption of a combination of six dietary flavonoids was consistently linked to lower serum cotinine levels, with anthocyanins displaying the most pronounced impact.

Factors predicting willingness to quit snus and cigarette use among young males

The health hazards of smoking are well recognised and recently knowledge about the harmful effects of nicotine and snus is accumulating. We investigated the factors increasing the willingness of young Finnish males to quit snus and cigarette smoking. We conducted a questionnaire study conducted in 3 out of 16 Finnish Defence Forces units which included 6508 male conscripts, of whom 4706 responded (response rate 72%, mean age 19.4 years). Factors related to the willingness to quit use were analysed by ordinal regression models. Backward selection following the Akaike information criterion (AIC) was used for the model. The prevalence figures of daily snus use and smoking were 17% and 25%, respectively. 16% of the daily snus users were also daily smokers and 29% were occasional smokers. Multivariate analysis showed that the willingness to quit snus use was associated with the perception of health hazards (OR 3.09, 95% CI 1.94–4.93) and with ≥ 2 quit attempts (OR 3.63, 95% CI 2.44–5.40). The willingness to quit smoking was associated with ≥ 2 quit attempts (OR 3.22, 95% CI 2.32–4.49), and with advice to quit smoking (OR 1.65, 95% CI 1.17–2.32). We created a brief two-question assessment model for snus dependence. With this model, nicotine dependence of daily snus users was congruent with that of nicotine dependence of smokers. A direct comparison with serum cotinine levels is necessary before our assessment model can be used as a proxy for dependence. Regular snus use predisposes to nicotine addiction and accumulated health hazards. Our findings underscore the importance of health promotion efforts in early adolescence and of active support for quitting snus use. Easily applicable tools to estimate nicotine addiction are needed for everyday clinical use.

Prevalence of Underreported Nicotine Exposure Among US Nonsmoking Adults: A Comparison of Self-Reported Exposure and Serum Cotinine Levels From NHANES 2013-2020.

Secondhand smoke (SHS) poses a significant health risk. However, individuals who do not smoke may be unaware of their exposure, thereby failing to take protective actions promptly. We assessed the prevalence of underreported nicotine exposure in a nationally representative sample of US nonsmoking adults using data from the US National Health and Examination Survey. Individuals with underreported nicotine exposure were defined as those who reported no exposure to all tobacco products (traditional tobacco, nicotine replacements, and e-cigarettes) or SHS, yet had detectable levels of serum cotinine (>0.015 ng/mL). We fitted logistic regression models to determine sociodemographic and chronic condition factors associated with underreported nicotine exposure. Our analysis included 13 503 adults aged 18 years and older. Between 2013 and 2020, the prevalence of self-reported SHS exposure, serum cotinine-assessed nicotine exposure, and underreported nicotine exposure among US nonsmokers were 22.0%, 51.2%, and 34.6%, respectively. Remarkably, 67.6% with detectable serum cotinine reported no SHS exposure. Males, non-Hispanic blacks, individuals of other races (including Asian Americans, Native Americans, and Pacific Islanders), and those without cardiovascular diseases were more likely to underreport nicotine exposure than their counterparts. The median serum cotinine value was higher in respondents who reported SHS exposure (0.107 ng/mL) than in those who reported no exposure (0.035 ng/mL). We estimate that approximately 56 million US residents had underreported nicotine exposure. Over a third of US nonsmokers underreport their nicotine exposure, underlining the urgent need for comprehensive public awareness campaigns and interventions. Further research into sociodemographic determinants influencing this underreporting is needed. Understanding the extent of underreported nicotine exposure is crucial for developing effective public health strategies and interventions. It is imperative to bolster public consciousness about the risks associated with SHS. Additionally, surveillance tools should also incorporate measures of exposure to outdoor SHS and e-cigarette vapor to enhance the quality of data monitoring. Findings from this study can guide tobacco control initiatives and inform smoke-free air legislation.

Interaction between Serum Cotinine and Magnesium Intake with Childhood Asthma: A Cross-Sectional Study

Introduction: Serum cotinine and magnesium intake are often associated with childhood asthma. This study evaluated the interaction between serum cotinine and magnesium intake and childhood asthma. Methods: This cross-sectional study included 14,159 subjects from the National Health and Nutrition Examination Survey 2005–2018. Serum cotinine levels were classified according to the lower quartile: ≤0.2089 ng/mL as low level and >0.2089 ng/mL as high level. Magnesium intake was categorized as high (>98 mg/1,000 kcal) or low level (≤98 mg/1,000 kcal) based on the upper quartile. Weighted logistic regression analyses were adopted to analyze the association between cotinine, magnesium intake, and childhood asthma. Additionally, the combined effect of cotinine and magnesium intake on childhood asthma risk was examined. The stratified analyses were based on gender, body mass index, and family history of asthma to further examine the relationship between cotinine, magnesium intake, and childhood asthma. Results: The prevalence of asthma was approximately 17.56%. Compared to low-level cotinine, high-level cotinine was associated with asthma (odds ratio [OR] = 1.25, 95% confidence interval (CI): 1.04–1.50). Low-level magnesium intake was related to asthma compared with high-level magnesium intake (OR = 1.21, 95% CI: 1.04–1.40). Using interaction analysis, we also found that the combined effect of cotinine and magnesium intake was associated with childhood asthma risk, and the interaction between high-level cotinine and low-level magnesium intake was associated with the highest risk of childhood asthma (OR = 1.35, 95% CI: 1.04–1.74). Additionally, this interaction was also found in males, overweight/non-overweight, and those with family history of asthma. Conclusion: There was an interaction between serum cotinine and magnesium intake on childhood asthma. The results suggested that implementing smoking bans in certain settings (e.g., communities, schools) and promoting the consumption of magnesium-rich foods may be effective strategies for preventing childhood asthma.

Associations between smoke exposure and kidney stones: results from the NHANES (2007-2018) and Mendelian randomization analysis.

It is currently controversial whether smoke exposure is associated with the risk of kidney stones. Herein, publicly available databases were combined to explore relationships with the risk of nephrolithiasis in terms of smoking status and serum cotinine concentrations. First, we conducted an observational study using data from 2007 to 2018, based on the National Health and Nutrition Examination Survey (NHANES) database. Univariate analysis, multivariate logistic regression, trend testing, restricted cubic spline (RCS), and multiple imputation (MI) were the main analytical methods of our study. Then, A Mendelian randomization (MR) analysis was performed to explore the causal relationship between serum cotinine and nephrolithiasis. Genetic instruments for serum cotinine and pooled data for kidney stones were derived from publicly available large-scale genome-wide association studies (GWAS). Inverse-variance weighting (IVW) was the primary method for our MR analysis. A total of 34,657 and 31,352 participants were included in the observational study based on smoking status and serum cotinine concentrations, respectively. Under full adjustment of covariates, current smokers had an increased risk of kidney stones compared to non-smokers [OR = 1.17 (1.04-1.31), P = 0.009, P for trend = 0.010]. Compared with serum cotinine of <0.05 ng/ml, serum cotinine levels of 0.05-2.99 ng/ml [OR = 1.15 (1.03-1.29), P = 0.013] and ≥3.00 ng/ml [OR = 1.22 (1.10-1.37), P < 0.001] were observed to have a higher risk of nephrolithiasis (P for trend < 0.001). In addition, a non-linear relationship between log2-transformed serum cotinine and the risk of nephrolithiasis was found (P for non-linearity = 0.028). Similar results were found when serum cotinine (log2 transformation) was used as a continuous variable [OR = 1.02 (1.01-1.03), P < 0.001] or complete data was used to analyze after MI. In the MR analysis, genetically predicted high serum cotinine was causally related to the high risk of nephrolithiasis [IVW: OR = 1.09 (1.00-1.19), P = 0.044]. Current smoking and high serum cotinine concentrations may be associated with an increased risk of kidney stones. Further research is needed to validate this relationship and explore its underlying mechanisms.

Joint effect of overweight/obesity and tobacco exposure on hypertension in children aged 6-17 years: a cross-sectional study.

To assess the individual effects of overweight/obesity and tobacco exposure, and their combined effects on hypertension in children. This cross-sectional study included 6,339 children aged 6-17 years from National Health and Nutrition Examination Surveys 1999-2018. Participants' height, weight and blood pressure (BP) were measured by trained technicians. Hypertension was defined as: mean systolic BP (SBP) and/or diastolic BP (DBP) ≥ 90th percentile for sex, age, and height (for children aged 1-13 years), and SBP ≥120 mmHg and/or a DBP ≥80 mmHg (for adolescents aged 13-17 years); or self-reported having been diagnosed with hypertension or taking antihypertensive medication. Gender- and age-specific body mass index (BMI) cut-points were used to define overweight/obesity: "overweight" was defined as a BMI > 1 standard deviation (SD); "obesity" was defined as BMI > 2SD; and "thinness" was defined as BMI < -2SD. Tobacco exposure was defined as having serum cotinine levels >0.05 µg/L or reporting the presence of at least one smoker in the household. Weighted univariate and multivariate logistic regression models were used to assess overweight/obesity and tobacco exposure with the odds of hypertension, and the combined effects of overweight/ obesity and tobacco exposure on hypertension, followed by strata-specific analyses. Odds ratios (OR) with 95% confidence intervals (CI) were calculated. The prevalence of overweight/obesity and tobacco exposure was significantly higher in the hypertension group than in the non-hypertension group. Overweight/obesity (OR = 1.67, 95%CI: 1.26-2.21/ OR = 2.38, 95%CI: 1.67-3.39) and tobacco exposure (OR = 1.58, 95%CI: 1.16-2.14) were associated with a higher odd of hypertension in children, respectively. Additionally, we also observed the combined effect between overweight (OR = 3.05, 95%CI: 1.96-4.75)/obesity (OR = 3.68, 95%CI: 2.24-6.03) and tobacco exposure were related to hypertension odds in children, with a significant effect in different populations. There may exist joint effect of overweight/obesity and tobacco exposure on the odds of hypertension in American children. These findings offer an insight that early weight control and reduction of tobacco exposure may be important to reduce odds of hypertension in children.

Relationships between Serum Biomarkers of Oxidative Stress and Tobacco Smoke Exposure in Patients with Mental Disorders.

The role of cigarette smoking as an aggravating factor of systemic oxidative stress in patients with mental disorders has not been extensively investigated, although significantly higher rates of smoking are recorded in these subjects in comparison with the general population. In the present study, we tested the hypothesis that smoking might be an exacerbator of systemic oxidative stress, being directly correlated with the degree of exposure to tobacco smoke. We analyzed, in 76 adult subjects from a public health care unit, the relationships between serum cotinine levels as a marker of tobacco smoke exposure, and three biomarkers of oxidative stress: the serum glutathione (GSH), the advanced oxidation protein products (AOPPs), and the total serum antioxidant status (FRAP). The results indicate that the degree of tobacco smoke exposure was inversely associated with GSH levels in both passive and active smokers, suggesting that smoke particulate components' toxicity is associated with a systemic GSH depletion. Paradoxically, the lowest AOPP levels which were positively associated with GSH, were recorded in active smoking patients whereas in passive smokers individual values of AOPPs decreased along with the increase in GSH levels. Our data suggest that an enhanced inhalation of particulate constituents of cigarette smoke could induce critical changes in systemic redox homeostasis and GSH can no longer exert its antioxidant role.

The contribution of secondhand tobacco smoke to blood lead levels in US children and adolescents: a cross-sectional analysis of NHANES 2015–2018

BackgroundLead is a major developmental neurotoxicant in children, and tobacco smoke has been suggested as a source of lead exposure in vulnerable populations. This study evaluates the contribution of secondhand tobacco smoke (SHS) to blood lead levels (BLLs) in children and adolescents.MethodsWe analyze data from 2,815 participants aged 6–19 years who participated in the National Health and Nutrition Examination Survey (2015–2018) to investigate the association between serum cotinine levels and BLLs. A multivariate linear regression was conducted to estimate geometric means (GMs) and the ratios of GMs after adjusting for all covariates.ResultsThe geometric means of BLLs in study participants aged 6 − 19 years were 0.46 µg/dl (95% CI 0.44, 0.49). After adjusting for relevant participant characteristics, the geometric means of BLLs were 18% (BLL 0.48 µg/dl, 95% CI 0.45, 0.51) and 29% (BLL 0.52 µg/dl, 95% CI 0.46, 0.59) higher in participants who had intermediate serum cotinine levels (0.03 − 3 ng/mL) and those who had high serum cotinine levels (> 3 ng/mL) respectively, compared to participants who had low serum cotinine levels (BLL 0.41 µg/dl, 95% CI 0.38, 0.43).ConclusionsSHS exposure may be a source of BLLs in US children and adolescents. Efforts to reduce lead exposure in children and adolescents should include strategies to reduce SHS exposure.

COVID-19 and smoking: Considerations after two years

COVID-19 and smoking: Considerations after two years

Evaluation of serum cotinine, total protein, thiocyanate, neuron specific enolase and uric acid levels of cigarette smokers in calabar metropolis, nigeria: a cross sectional study

Cigarette smoke contains harmful chemicals with deleterious health effects leading to oxidative stress and neuronal damage. This study investigated the levels of serum cotinine (COT), thiocyanate (thioc), uric acid (UA), neuron specific enolase (NSE), and the association between these variables in cigarette smokers. This cross sectional study enrolled 60 cigarette smokers and 45 non-smokers as participants. Serum thiocyanate and UA were estimated by colorimetric methods. Serum cotinine and NSE were determined by ELISA methods. Height and weight were measured and BMI computed. Data were analyzed using Student’s t-test, ANOVA, and Pearson’s correlation at P&lt;0.05. Serum cotinine, thioc and NSE concentrations were significantly higher while BMI and UA levels were significantly lower (P&lt;0.05) in smokers than in the controls. Age was not significantly different between the two groups (P&gt;0.05). Age, COT, UA, thioc and NSE vary significantly (P&lt;0.05) between the light, moderate and heavy cigarette smokers. From the least significant difference post hoc analyses, the mean age and UA level of light smoker were significantly higher (P&lt;0.05) compared with the moderate smokers, while COT level of moderate smokers was significantly higher (P&lt;0.05) compared with light smokers. Neuron specific enolase level of moderate cigarette smokers was higher (P&gt;0.05) compared with the light smokers. The mean age of light smokers was significantly higher (P&lt;0.05) compared with the heavy smokers, while the COT, thioc and NSE levels of light smokers were significantly lower (P&lt;0.05) compared with the heavy smokers. Serum UA, thioc and NSE levels of moderate smokers were significantly lower (P&lt;0.05), than those of the heavy smokers. Significant negative correlations were observed between age and COT (r = -0.554, P&lt;0.001), age and thioc (r = -0.421, P= 0.001), age and NSE (r = -0.346, P=0.001), age against smoking pack years (r = -0.623, P&lt;0.001) respectively. Significant positive correlations were observed between serum thioc and NSE (r = 0.324, P=0.012), COT against smoking pack years (r = 0.399, P=0.002), and NSE against smoking pack years (r = 0.311, P=0.015), correspondingly. This study has shown that high levels of cotinine and thiocyanate are associated with increased levels of neuron specific enolase, smoking pack years and decreased uric acid in smokers.