Evaluating the Impact of Chronic Care Model on Smoking Cessation: An Interventional Study.

BACKGROUND: This study aims to assess the effectiveness of the chronic care model (CCM) in helping primary healthcare workers quit smoking. The intervention involves implementing the CCM, which includes six key elements: the healthcare system, clinical care planning, clinical management information, self-management guidance, community resources, and decision-making. MATERIAL AND METHODS: The study is based on a population of 60 primary healthcare workers who smoke. The main outcome measure is smoking cessation, determined by cotinine levels in urine at the baseline, and at 6 and 12 months after the intervention. Other potential results include alterations in smoking-related behaviors and attitudes. Data analysis involves using descriptive statistics and inferential tests to determine the intervention's effectiveness in smoking cessation among primary healthcare workers. RESULTS:  The CCM is expected to have contributed to a substantial decrease in the smoking rate among primary healthcare workers. It is also seen that there is a great reduction in urine cotinine levels during the 12-month intervention period. Moreover, a positive shift in the smoking-related behaviors and attitudes of the participants is expected. CONCLUSION:  This study provides key data about the effectiveness of the CCM in helping primary healthcare workers stop smoking. This statement emphasizes the importance of considering socioeconomic factors in the design and implementation of smoking cessation interventions. This ensures that people of different incomes and social statuses have equal access to quitting smoking and achieve similar results.

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

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

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

Background: 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. Methods: 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. Results: 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: ß = -0.14, 95% CI: -0.20, -0.07; High: ß = -0.31, 95% CI: -0.39, -0.22). Moreover, both prebiotic and probiotic use exhibited an inverse relationship with serum cotinine levels (Prebiotic: ß = -0.19, 95% CI: -0.37, -0.01; Probiotic: ß = -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. Conclusion: Our findings suggest a negative correlation between dietary live microbe intake, as well as non-dietary prebiotic/probiotic consumption, and serum cotinine levels.

Predicting Time to Return to Cannabis Use After a Cessation Attempt: Impact of Cumulated Exposure to Nicotine-Containing Products.

Objective: Cannabis is frequently co-used with tobacco/nicotine products, especially among young adults. Little is known about the effects of this co-use on cannabis cessation outcomes. Within a sample of young adults using cannabis frequently (current use of ≥5 days/week in the past 3 months), this study aimed to (a) document sources of exposure to tobacco/nicotine products, whether used simultaneously with cannabis or on different occasions, (b) examine if the level of cumulated exposure to tobacco/nicotine (self-reported or from biochemical testing) could predict time to cannabis lapse during a cannabis abstinence period, and (c) explore the relationship between nicotine/tobacco exposure and time to cannabis lapse according to tobacco cigarette smoking status. Method: Urine cotinine measures and self-reported data on use of different tobacco/nicotine products, collected from 32 participants (aged 19 to 23), were analyzed to predict time to lapse during a 2-week period of attempted abstinence from cannabis, controlling for cannabis dependence and sex. Results: Half of participants (56.3%) used at least one tobacco/nicotine product. Higher urine cotinine, representing higher cumulated tobacco/nicotine exposure, was related to a higher risk of lapsing (Hazard Ratio [HR] = 1.64; 95%CI [1.04, 2.58]). The risk of lapsing was even higher ([HR] = 3.46; 95%CI [1.17, 10.25]) among heavily tobacco/nicotine exposed (>600 ng/mL, urine cotinine) participants than among unexposed (<50 ng/mL) or lightly/moderately exposed (50-600 ng/mL) participants. Among those smoking cigarettes (solely or in combination with other products), there was no relation between cotinine level and time to lapse, likely due to a reduced variability in abstinence probability and a high likelihood of lapse observed for higher cotinine levels, mainly achieved by cigarette use. Conclusions: With a rapidly changing landscape of tobacco/nicotine use, our results underscore the need to consider all sources of tobacco/nicotine exposure to fully understand the specific and cumulative contributions of tobacco/nicotine to cannabis cessation outcomes.

Analysis of patient health questionnaire-9 (PHQ-9) based depression prevalence according to a discordance between quantitative urinary cotinine levels and self-report of second-hand smoke exposure among adults: A cross-sectional study.

Background: Second-hand smoke (SHS) exposure appears to be more common among individuals with depression. However, self-report of SHS exposure is an inaccurate classification compared to confirming SHS exposure using urinary cotinine (UC). Additionally, the dose-response relationship between depression and UC is controversial. Methods: The severe stress rate and depression prevalence was estimated among 14530 Korean participants aged ≥19 years using data patient health questionnaire-9 (PHQ-9) and on UC from the Korean National Health and Nutrition Examination Survey. Measured UCs were divided into four categories: UC- (≤0.3 µg/L), UC± (0.4 µg/L-0.9 µg/L), UC+ (1.0 µg/L-11.9 µg/L), and UC++ (≥12.0 µg/L). Results: About 55.0 % participants were female and participants' mean age was 51.1 years. Non-smokers were 80.3 %. Among non-smokers, non-SHS exposure participants (SR-) and SHS exposure participants (SR+) were 83.0 % and 17.0 %, respectively. When UC- was used as the reference subgroup, the UC++ subgroup showed a higher depression prevalence, whereas the UC ± subgroup showed a lower prevalence. In the same UC categories, the depression prevalence and severe stress rate were higher among females than among males. Furthermore, the SR + subgroup had a higher severe stress rate than the SR- subgroup. Conclusions: Our study showed a paradoxical reduction in the depression prevalence and severe stress rate in the UC ± subgroup compared to the UC- subgroup. Additionally, the dose-response relationship between the SHS exposure biomarker and the depression prevalence was not linear. Our study indicates that an emotional stress-based model may be more appropriate for explaining the relationship between depression and SHS exposure.

Characterization of cotinine degradation in a newly isolated Gram-negative strain Pseudomonas sp. JH-2.

Cotinine, the primary metabolite of nicotine in the human body, is an emerging pollutant in aquatic environments. It causes environmental problems and is harmful to the health of humans and other mammals; however, the mechanisms of its biodegradation have been elucidated incompletely. In this study, a novel Gram-negative strain that could degrade and utilize cotinine as a sole carbon source was isolated from municipal wastewater samples, and its cotinine degradation characteristics and kinetics were determined. Pseudomonas sp. JH-2 was able to degrade 100 mg/L (0.56 mM) of cotinine with high efficiency within 5 days at 30 ℃, pH 7.0, and 1% NaCl. Two intermediates, 6-hydroxycotinine and 6-hydroxy-3-succinoylpyridine (HSP), were identified by high-performance liquid chromatography and liquid chromatograph mass spectrometer. The draft whole genome sequence of strain JH-2 was obtained and analyzed to determine genomic structure and function. No homologs of proteins predicted in Nocardioides sp. JQ2195 and reported in nicotine degradation Pyrrolidine pathway were found in strain JH-2, suggesting new enzymes that responsible for cotinine catabolism. These findings provide meaningful insights into the biodegradation of cotinine by Gram-negative bacteria.

Intensive Intervention on Smoking Cessation in Patients Undergoing Elective Surgery: The Role of Family Physicians.

Background and Objectives: The aim of this study was to determine the role of physicians in the intensive intervention and education regarding the smoking cessation of patients undergoing elective surgery under general anaesthesia. Materials and Methods: A randomised prospective study was conducted in family physicians' clinics in which smokers of both sexes, aged 21-65 years, without cognitive impairments, and who were not addicted to psychoactive substances voluntarily participated. Four weeks preoperatively, 120 smokers were randomised into two equal groups; the intervention group (IG) underwent an intervention for the purpose of smoking cessation and the control group (CG) underwent no intervention. Biochemical tests were performed in order to determine the smoking status of the participants in the phase of randomisation, one week preoperatively, as well as 40, 120, and 180 days and 12 months postoperatively. The examinees of the IG talked to the physician five times and received 140 telephone messages, leaflets, and motivational letters along with the pharmacotherapy, while the participants in the CG received little or no advice on smoking cessation. Results: The results of this study confirmed a significant influence of the intervention and education on the smoking abstinence in the IG compared to the CG (p < 0.001). The smokers in the IG had 7.31 (95% CI: 2.32-23.04) times greater odds of abstinence upon the 12-month follow-up than the smokers in the CG. The smokers in the IG who did not stop smoking had a lower degree of dependence and smoked fewer cigarettes (p < 0.0001) compared to those in the CG, as well as a multiple times higher prevalence of short- and long-term abstinence. Conclusions: It can be concluded that the intensive intervention and education can motivate patients preparing for elective surgery to stop smoking in the short- and long term.

Self-reported smoking, urine cotinine, and risk of type 2 diabetes: Findings from the PREVEND prospective cohort study.

BACKGROUND: Smoking is a major risk factor for type 2 diabetes (T2D), but the evidence has mostly relied on self-reports. We aimed to compare the associations of smoking exposure as assessed by self-reports and urine cotinine with T2D. METHODS: Using the PREVEND prospective study, smoking status was assessed at baseline by self-reports and urine cotinine in 4708 participants (mean age, 53 years) without a history of diabetes. Participants were classified as never, former, light current and heavy current smokers according to self-reports and analogous cut-offs for urine cotinine. Hazard ratios (HRs) with 95% CIs were estimated for T2D. RESULTS: During a median follow-up of 7.3 years, 259 participants developed T2D. Compared with self-reported never smokers, the multivariable adjusted HRs (95% CI) of T2D for former, light current, and heavy current smokers were 1.02 (0.75-1.4), 1.41 (0.89-2.22), and 1.30 (0.88-1.93), respectively. The corresponding adjusted HRs (95% CI) were 0.84 (0.43-1.67), 1.61 (1.12-2.31), and 1.58 (1.08-2.32), respectively, as assessed by urine cotinine. Urine cotinine-assessed but not self-reported smoking status improved T2D risk prediction beyond established risk factors. CONCLUSION: Urine cotinine assessed smoking status may be a stronger risk indicator and predictor of T2D compared to self-reported smoking status.

The longitudinal analysis for the association between smoking and the risk of depressive symptoms.

BACKGROUND: Despite high smoking rate in people with depressive symptoms, there is ongoing debate about relationship between smoking and depressive symptoms. METHODS: Study participants were 57,441 Korean men. We collected their baseline data between 2011 and 2012, and conducted follow-up from 2013 to 2019. They were categorized by smoking status (never: < 100 cigarettes smoking in life time, former: currently quitting smoking, and current smoker: currently smoking), smoking amount (pack/day and pack-year) and urine cotinine excretion. The development of depressive symptoms was determined in CES-D score ≥ 16. Cox proportional hazards model was used to analyze the multivariable-adjusted hazard ratio (HR) and 95% confidence intervals (CI) for depressive symptoms in relation to smoking status, smoking amount, and urine cotinine excretion. RESULTS: During 6.7 years of median follow-up, the risk of depressive symptoms increased in order of never (reference), former (HR = 1.08, 95% CI: 1.01-1.15) and current smoker (HR = 1.24, 95% CI: 1.16-1.32). Among current smoker, the risk of depressive symptoms increased proportionally to daily smoking amount (< 1 pack; HR = 1.21, 95% CI: 1.13-1.29, and ≥ 1 pack; HR = 1.34, 95% CI: 1.23 - 1.45). This pattern of relationship was consistently observed for pack-year in former smoker and current smoker. Additionally, urine cotinine excretion was proportionally associated with the risk of depressive symptoms. CONCLUSION: Exposure to smoking was associated with the increased risk of depressive symptoms. Dose dependent relationship was observed between smoking amount and the risk of depressive symptoms.

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

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

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 > 2.99 ng/ml [ß = 0.41 (0.07, 0.76), p = 0.018] and 0.05-2.99 ng/ml [ß = 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 ≤ 0.05 ng/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.

Active smoking in urban households: An association between urinary cotinine metabolite level and serum eGFR concentration.

INTRODUCTION: Smoking stands as a primary contributor to preventable deaths globally and is linked to an increased risk of developing kidney failure and other diseases. A few studies have focused on the negative correlation between serum cotinine and estimated glomerular filtration rate (eGFR), indicating decreased kidney function. This study investigated the associations between urinary cotinine metabolite concentration and serum eGFR among active smokers in urban households. METHODS: This was a cross-sectional study of active smokers in urban households' community Bangkok, Thailand from January to April 2023. The study involved 85 participants aged ≥18 years who were active smokers. Both urinary cotinine and serum eGFR concentrations were used as biomarkers. Independent sample t-tests were used to compare the urinary cotinine metabolite based on differences in the characteristic variable. We used multiple linear regression to test the association between cotinine metabolite and characteristics variables. Spearman's analysis was used to test the correlation between cotinine metabolite and eGFR concentration. RESULTS: The association between urinary cotinine metabolite and serum eGFR concentration decreased with increasing cotinine concentrations (r= -0.223, p=0.041), suggesting a decline in kidney function. However, this study found no significant difference between urinary cotinine metabolite and characteristic variables (p>0.05). Additionally, those who smoked for ≥10 years (117.40 ± 89.80 ng/mL), smoked ≥10 cigarettes per day (117.40 ± 89.80 ng/mL) and used conventional cigarettes (124.53 ± 115.10 ng/mL). The results of the multiple linear regression models analysis indicated that those who were smokers for ≥10 years (ß=0.076; 95% CI: -31.575-59.715) and those who were smoked ≥10 cigarettes/day (ß=0.126; 95% CI: -65.636-18.150) were not associated with urinary cotinine metabolite level. CONCLUSIONS: This study shows that the urinary cotinine metabolite level is associated with serum eGFR concentration among active smokers in urban households. The current study suggests that clinical identification and a prospective cohort study are needed before robust conclusions about how tobacco affects kidney efficiency.

A randomised controlled trial to evaluate the effectiveness of a culture and disease-specific, patient-centric multi-component tobacco cessation intervention package for the patients attending non-communicable disease clinics in Punjab, India.

BACKGROUND: Developing an infrastructure to support tobacco cessation through existing systems and resources is crucial for ensuring the greatest possible access to cessation services. The present study aims to evaluate the effectiveness of a newly developed multi-component cessation among tobacco users in Non- Communicable Disease (NCD) clinics, functioning under the National Programme for Prevention & Control of Cancer, Diabetes, Cardiovascular Diseases, & Stroke (NPCDCS) of the Government of India. METHODS: The intervention package consisting of culture- and disease-specific four face-to-face counselling sessions, pamphlets, and short text messages (bilingual) with follow-ups at 3rd, 6th, and 9th months with an endline assessment at 12th months was delivered to the intervention arm of the two-arm- parallel group randomised controlled trial at two selected NCD clinics. Self-reported seven-day abstinence, frequency of use, expenditure in seven days at each follow-up, FTND score, stage of change and plasma cotinine values were assessed at baseline, follow-ups, and endline (using Liquid Chromatography -Mass Spectrometry), as applicable. RESULTS: The intervention arm reported a significantly more reduction in self-reported frequency of tobacco use at 6 months (mean: 13.6, 95% CI (7.8-19.4)), 9 months (mean: 20.3, 95% CI (12.2-28.4)) and 12 months (mean: 18.7, 95% CI (8.7-28.7)). The plasma cotinine concentration at endline in the intervention arm was statistically significantly lower than the baseline concentration. CONCLUSION: Strengthening existing health systems is crucial for offering cessation support in the resource-restraint setting of LMICs to assist in quitting sustainably.

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

OBJECTIVE: To 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. METHODS: This 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). RESULTS: 5,397 (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. CONCLUSION: Leisure 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.

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

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

Immunological Signatures in Blood and Urine in 80 Individuals Hospitalized during the Initial Phase of COVID-19 Pandemic with Quantified Nicotine Exposure.

This research analyzes immunological response patterns to SARS-CoV-2 infection in blood and urine in individuals with serum cotinine-confirmed exposure to nicotine. Samples of blood and urine were obtained from a total of 80 patients admitted to hospital within 24 h of admission (tadm), 48 h later (t48h), and 7 days later (t7d) if patients remained hospitalized or at discharge. Serum cotinine above 3.75 ng/mL was deemed as biologically significant exposure to nicotine. Viral load was measured with serum SARS-CoV-2 S-spike protein. Titer of IgG, IgA, and IgM against S- and N-protein assessed specific antiviral responses. Cellular destruction was measured by high mobility group box protein-1 (HMGB-1) serum levels and heat shock protein 60 (Hsp-60). Serum interleukin 6 (IL-6), and ferritin gauged non-specific inflammation. The immunological profile was assessed with O-link. Serum titers of IgA were lower at tadm in smokers vs. nonsmokers (p = 0.0397). IgM at t48h was lower in cotinine-positive individuals (p = 0.0188). IgG did not differ between cotinine-positive and negative individuals. HMGB-1 at admission was elevated in cotinine positive individuals. Patients with positive cotinine did not exhibit increased markers of non-specific inflammation and tissue destruction. The blood immunological profile had distinctive differences at admission (MIC A/B↓), 48 h (CCL19↓, MCP-3↓, CD28↑, CD8↓, IFNγ↓, IL-12↓, GZNB↓, MIC A/B↓) or 7 days (CD28↓) in the cotinine-positive group. The urine immunological profile showed a profile with minimal overlap with blood as the following markers being affected at tadm (CCL20↑, CXCL5↑, CD8↑, IL-12↑, MIC A/B↑, GZNH↑, TNFRS14↑), t48h (CCL20↓, TRAIL↓) and t7d (EGF↑, ADA↑) in patients with a cotinine-positive test. Here, we showed a distinctive immunological profile in hospitalized COVID-19 patients with confirmed exposure to nicotine.

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

INTRODUCTION: 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. METHODS: 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. RESULTS: 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). CONCLUSIONS: Cross-sectional analyses of NHANES data showed gender differences in the association between serum cotinine and the development of CKD.

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

BACKGROUND: This 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. METHODS: Participants 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. RESULTS: Significant 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. CONCLUSION: Smoking, 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.

Role of parental smoking and environmental tobacco smoke exposure in childhood cancer: A study using hair cotinine analysis and questionnaires.

OBJECTIVES: In the etiology of childhood cancers, many genetic and environmental factors play a role. One of these factors could be cigarette smoking, and the main source of tobacco smoke exposure of children is parental smoking. However, establishing a causal relationship between parental smoking and childhood cancers has proven challenging due to difficulties in accurately detecting tobacco smoke exposure METHODS: To address this issue, we used hair cotinine analysis and a questionnaire to get information about tobacco smoke exposures of pediatric cancer patients and healthy children. A total of 104 pediatric cancer patients and 99 healthy children participated in our study. Parental smoking behaviors (pre-conceptional, during pregnancy, and current smoking) and environmental tobacco smoke (ETS) exposures of children are compared. RESULTS: We have found no differences between two groups by means of maternal smoking behaviors. However, the rates of paternal pre-conceptional smoking and smoking during pregnancy were significantly low in cancer patients (p < .05). These data suggest that social desirability bias among fathers of cancer patients may have contributed to this discrepancy. According to questionnaire, cancer patients had significantly lower ETS exposures than healthy children (p < .05). However, ETS exposure assessment through cotinine analysis demonstrated that cancer patients had higher exposure to ETS compared to healthy children (p < .001). CONCLUSION: Our findings provide evidence supporting the potential role of smoking as a risk factor for childhood cancers. This study also revealed that questionnaires could cause biases. We suggest that cotinine analysis along with validated questionnaires can be used to prevent biases in studies of tobacco smoke in the etiology of childhood cancers.

Low levels of nicotine and cotinine but not benzo[a]pyrene induce human trophoblast cell proliferation.

E-cigarettes use constitutes a source of thirdhand nicotine exposure. The increasing use of electronic cigarettes in homes and public places increases the risk of exposure of pregnant women to thirdhand nicotine. The effects of exposure of pregnant women to very low levels of nicotine have not been studied in humans but detrimental in experimental animals. The objective of this study is to investigate the effect of nanomolar concentrations of nicotine and its metabolite cotinine on the proliferation of JEG-3, a human trophoblast cell line. We also studied the proliferative effect of nanomolar concentrations of benzo[a]pyrene (B[a]P), a polycyclic hydrocarbon in tobacco smoke, for comparison. We treated JEG-3 cells in culture with nanomolar concentrations of nicotine, cotinine, and B[a]P. Their effect on cell proliferation was determined, relative to untreated cells, by MTT assay. Western blotting was used to assess the mitogenic signaling pathways affected by nicotine and cotinine. In contrast to the inhibitory effects reported with higher concentrations, we showed that nanomolar concentrations of nicotine and cotinine resulted in significant JEG-3 cell proliferation and a rapid but transient increase in levels of phosphorylated ERK and AKT, but not STAT3. Biphasic, non-monotonic effect on cell growth is characteristic of endocrine disruptive chemicals like nicotine. The mitogenic effects of nicotine and cotinine potentially contribute to increased villous epithelial thickness, seen in placentas of some smoking mothers. This increases the diffusion distance for oxygen and nutrients between mother and fetus, contributing to intrauterine growth restriction in infants of smoking mothers.