RESUMEN
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.
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Cotinina , Encuestas Nutricionales , Contaminación por Humo de Tabaco , Incontinencia Urinaria , Humanos , Cotinina/sangre , Cotinina/orina , Estados Unidos/epidemiología , Femenino , Masculino , Estudios Transversales , Incontinencia Urinaria/epidemiología , Incontinencia Urinaria/sangre , Persona de Mediana Edad , Adulto , Contaminación por Humo de Tabaco/efectos adversos , Anciano , Adulto JovenRESUMEN
PURPOSE: Recently, 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. METHODS: We 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. RESULTS: In 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. CONCLUSIONS: Our 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.
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Cotinina , Músculo Esquelético , Encuestas Nutricionales , Humanos , Cotinina/sangre , Masculino , Femenino , Adulto , Persona de Mediana Edad , Estados Unidos/epidemiología , Estudios Transversales , Adulto Joven , Fumar Cigarrillos/sangre , Fumar Cigarrillos/epidemiología , AncianoRESUMEN
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.
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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.
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Biomarcadores , Cotinina , Hipertensión , Monoaminooxidasa , Contaminación por Humo de Tabaco , Adulto , Femenino , Humanos , Masculino , Persona de Mediana Edad , Presión Arterial , Biomarcadores/sangre , Enfermedades Cardiovasculares/diagnóstico , Enfermedades Cardiovasculares/sangre , Enfermedades Cardiovasculares/epidemiología , Cotinina/sangre , Hipertensión/diagnóstico , Hipertensión/sangre , Hipertensión/epidemiología , Hipertensión/fisiopatología , Monoaminooxidasa/sangre , Valor Predictivo de las Pruebas , Medición de Riesgo , Factores de Riesgo , Fumadores , Fumar/efectos adversos , Fumar/sangre , Fumar/epidemiología , Encuestas y Cuestionarios , Contaminación por Humo de Tabaco/efectos adversosRESUMEN
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.
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Cotinina , Hígado Graso , Cirrosis Hepática , Humanos , Cotinina/sangre , Adolescente , Masculino , Femenino , Cirrosis Hepática/sangre , Cirrosis Hepática/epidemiología , Cirrosis Hepática/patología , Estados Unidos/epidemiología , Estudios Transversales , Niño , Hígado Graso/sangre , Hígado Graso/epidemiología , Encuestas Nutricionales , Adulto Joven , Hígado/patología , Hígado/metabolismoRESUMEN
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.
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Enfermedades Cardiovasculares , Hipertensión , Humanos , Fumar/efectos adversos , Fumar/epidemiología , Enfermedades Cardiovasculares/diagnóstico , Enfermedades Cardiovasculares/epidemiología , Enfermedades Cardiovasculares/complicaciones , Factores de Riesgo , Obesidad Abdominal/diagnóstico , Obesidad Abdominal/epidemiología , Obesidad Abdominal/complicaciones , Encuestas Nutricionales , Cotinina , Hipertensión/complicaciones , Obesidad/complicaciones , Factores de Riesgo de Enfermedad Cardiaca , TriglicéridosRESUMEN
Purpose: 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. Methods: 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. Results: 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. Conclusion: 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.
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Infertilidad , Contaminación por Humo de Tabaco , Embarazo , Humanos , Femenino , Estados Unidos/epidemiología , Contaminación por Humo de Tabaco/efectos adversos , Contaminación por Humo de Tabaco/análisis , Encuestas Nutricionales , Cotinina/análisisRESUMEN
BACKGROUND: Smoke 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. METHODS: We 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. RESULTS: A 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 (ß = 0.08, 95%CI 0.01-0.15) and in the highest concentration of serum cotinine (ß = 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 (ß = 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. CONCLUSION: The 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.
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Contaminación por Humo de Tabaco , Adulto , Masculino , Humanos , Persona de Mediana Edad , Estudios Transversales , Encuestas Nutricionales , Cotinina/análisis , Filamentos Intermedios/química , BiomarcadoresRESUMEN
OBJECTIVE: The study aimed to examine the relationship between secondhand smoke (SHS) exposure and severe headaches or migraine in never-smoking adults verified by serum cotinine. BACKGROUND: Current evidence about the association between self-reported SHS exposure and headaches or migraine is limited and contradictory. An important issue lies in the lack of actual SHS exposure assessment through biomarkers. METHODS: We conducted a cross-sectional study on 4560 never-smoking adults from the National Health and Nutrition Examination Survey (NHANES), 1999-2004. The SHS exposure was evaluated by measuring serum cotinine concentrations. The information regarding severe headaches or migraine was based on self-reporting. RESULTS: The overall prevalence rate of severe headaches or migraine was 20% (919/4560). After adjusting for relevant covariates, we found that heavy SHS exposure (serum cotinine at 1 to 10 ng/mL) was positively associated with severe headaches or migraine (OR: 2.02, 95% CI [1.19, 3.43]); however, no significant association was found between low SHS exposure (serum cotinine at 0.05 to 0.99 ng/mL) and severe headaches or migraine (OR: 1.15, 95% CI [0.91, 1.47]). Restricted cubic spline analysis showed that the natural logarithm of serum cotinine had a linear relationship with severe headaches or migraine (p = 0.335 for nonlinearity). Stratified analysis indicated that individuals with a BMI of <25 (p < 0.001 for interaction) and sedentary activity (p = 0.016 for interaction) modified the relationship between SHS exposure and severe headaches and migraine. Even after altering the definition of SHS exposure, excluding drugs that might affect the metabolism of serum cotinine, and multiple imputation, our sensitivity analysis results remained stable. CONCLUSIONS: The study demonstrated that heavy SHS exposure (serum cotinine at 1 to 10 ng/mL) had a significant positive association with severe headaches or migraine in never-smoking adults. Prospective studies are necessary to verify this relationship in the future.
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Trastornos Migrañosos , Contaminación por Humo de Tabaco , Humanos , Adulto , Encuestas Nutricionales , Contaminación por Humo de Tabaco/efectos adversos , Cotinina/análisis , Estudios Transversales , Estudios Prospectivos , Trastornos Migrañosos/epidemiología , Cefalea/epidemiología , Cefalea/etiología , FumarRESUMEN
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 (ß = -0.29 [-0.44, -0.14]), third (ß = -0.41 [-0.58, -0.24]), and highest groups (ß = -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 (ß = -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.
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Cotinina , Flavonoides , Encuestas Nutricionales , Antocianinas , PolifenolesRESUMEN
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.
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Asma , Contaminación por Humo de Tabaco , Masculino , Humanos , Encuestas Nutricionales , Cotinina , Estudios Transversales , Magnesio , Asma/diagnósticoRESUMEN
Purpose: 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. Materials and methods: 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. Results: 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]. Conclusion: 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.
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BACKGROUND: Accumulating epidemiological studies have demonstrated that smoking caused damage to human health. However, these studies almost focused on the individual smoking pattern rather than the toxic ingredients of tobacco smoke. Despite the exact accuracy of cotinine as a smoking exposure biomarker, there were few studies investigating the association between serum cotinine and human health. This study aimed to provide novel evidence about the harmful effect of smoking on systemic health from the perspective of serum cotinine. METHODS: All used data was acquired from 9 survey cycles (2003-2020) of the National Health and Nutrition Examination Survey (NHANES) program. The mortality information of participants was derived from the National Death Index (NDI) website. The disease status of participants, including respiratory, cardiovascular, and musculoskeletal diseases, was obtained from questionnaire surveys. The metabolism-related index, including obesity, bone mineral density (BMD), and serum uric acid (SUA), was obtained from examination data. Multiple regression methods, smooth curve fitting, and threshold effect models were used for association analyses. RESULTS: With a total of 53,837 subjects included, we detected an L-shaped association between serum cotinine and obesity-related index, a negative association between serum cotinine and BMD, a positive association between serum cotinine and nephrolith and coronary heart disease (CHD), a threshold effect of serum cotinine on hyperuricemia (HUA), osteoarthritis (OA), chronic obstructive pulmonary disease (COPD), and stroke, as well as a positive saturate effect of serum cotinine on asthma, rheumatoid arthritis (RA), all-cause, cardiovascular disease (CVD)-cause, cancer-cause, and diabetes-cause mortality. CONCLUSIONS: In this study, we investigated the association between serum cotinine and multiple health outcomes, indicating the systematic toxicity of smoking exposure. These findings provided novel epidemiological evidence about how passive exposure to tobacco smoke affects the health condition of the general US population.
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Fumar , Contaminación por Humo de Tabaco , Humanos , Contaminación por Humo de Tabaco/efectos adversos , Encuestas Nutricionales , Cotinina , Ácido Úrico , ObesidadRESUMEN
Background: Tobacco exposure is considered to be a risk factor for reduced bone mineral density (BMD), which may result in osteopenia. Cotinine, a metabolite of nicotine, is commonly utilized as a marker of tobacco exposure. Nevertheless, there are limited clinical data on the associations between osteoporosis (OP) or osteopenia and smoking status or serum cotinine level. Methods: We thoroughly examined the NHANES cross-sectional data from 2005 to 2010, 2013 to 2014, and 2017 to 2018. Multivariate logistic regression models were applied to assess the associations among smoking status and serum cotinine levels as well as OP and osteopenia. The relationships between serum cotinine level and OP and osteopenia were also assessed using the restricted cubic spline (RCS) method. Results: A total of 10,564 participants were included in this cross-sectional study. The mean age of the study population was 64.85 ± 9.54 years, and the patients were predominantly male (51.9%). We found that the relationships between higher serum cotinine levels (≥3 ng/ml) and the prevalence of osteoporosis (Model 1: OR=2.27 [1.91-2.69]; Model 2: OR=2.03 [1.70-2.43]; Model 3: OR=2.04 [1.70-2.45]; all p for trend <0.001) remained significant after adjustment for covariates by applying the lowest serum cotinine levels (<0.05 ng/ml) as the reference. Similar results were observed for current smokers, who were more likely to develop OP compared with nonsmokers (Model 1: OR=2.30 [1.90-2.79]; Model 2: OR=2.16 [1.77-2.64]; Model 3: OR=2.16 [1.77-2.65]). Moreover, higher serum cotinine levels were found to be strongly and positively correlated with the prevalence of osteopenia (OR=1.60 [1.42-1.80]). A similar relationship was observed between current smokers and the prevalence of osteopenia compared with nonsmokers (OR=1.70 [1.49-1.94]). RCS regression also showed that serum cotinine levels were nonlinearly and positively correlated with OP and osteopenia, with inflection points of 5.82 ng/ml and 3.26 ng/ml, respectively. Conclusion: This study showed that being a smoker was associated with the prevalence of OP or osteopenia compared with being a nonsmoker and that there was a strong nonlinear positive dose-response relationship between serum cotinine levels and OP and osteopenia.
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Enfermedades Óseas Metabólicas , Osteoporosis , Contaminación por Humo de Tabaco , Humanos , Masculino , Anciano , Persona de Mediana Edad , Femenino , Fumar/epidemiología , Cotinina/análisis , Estudios Transversales , Contaminación por Humo de Tabaco/análisis , Encuestas NutricionalesRESUMEN
The joint effects between smoke exposure (SE) and physical activity (PA) on hypertension are still unclear, and the effect of SE is still debated. To explore associations and joint effects of SE and PA on hypertension, the data of 14,456 selected participants from the NHANES (2013-2018) were used for analyses. SE status was divided by serum cotinine concentrations. Moderate-to-vigorous intensity PA (MVPA) and insufficient or no PA (INPA) were divided by the Global Physical Activity Questionnaire. Hypertension was assessed by blood pressure and questionnaires. Survey logistic multivariable regression models were conducted for data analyses. In fully adjusted models, hypertension risk among SE participants increased (OR = 1.175, 95% CI: 1.036-1.332), especially those who were <40 years or female. However, the risk among MVPA participants decreased (OR = 0.747, 95% CI: 0.663-0.841), especially those who were ≥40 years. Additionally, the OR for MVPA participants without SE when compared with INPA ones without SE was 0.740 (95% CI: 0.654-0.837), especially those who were <60 years. However, the OR for MVPA participants with SE was 0.880 (95% CI: 0.747-1.037). For INPA participants, we did not observe significant ORs for SE compared with non-SE participants (p > 0.150). In conclusion, SE increased the risk of hypertension and MVPA reduced it, but SE could reduce such protective effect.
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Ejercicio Físico , Hipertensión , Humanos , Femenino , Encuestas Nutricionales , Actividad Motora/fisiología , Hipertensión/epidemiología , HumoRESUMEN
BACKGROUND: The purpose of this study was to explore the interaction between serum cotinine (a marker of environmental tobacco smoke exposure) and body mass index (BMI) on asthma in children. METHODS: This cross-sectional study relied on representative samples of American children included in the National Health and Nutrition Examination Survey in 1999-2018. Multivariate logistic regression analyses were to evaluate the association between serum cotinine level, BMI z-score and asthma. Serum cotinine was dichotomized at 0.0436 ng/mL. Interactions were examined by the estimated joint effect of BMI and serum cotinine levels. We also performed interaction analyses in age and ethnicity subgroups. RESULTS: Among the 11,504 children aged 3 to 12 years included in the analysis, 15.86% (n = 1852) had childhood asthma, 15.68% (n = 1837) were overweight, and 17.31% (n = 2258) were obese. Compared to low serum cotinine, high serum cotinine was significantly associated with asthma [odds ratio (OR) = 1.190, 95% confidence interval (CI): 1.004-1.410]. Overweight (OR = 1.275, 95%CI: 1.079-1.506) and obesity (OR = 1.636, 95%CI: 1.354-1.977) were significantly associated with asthma compared with normal weight. The adjusted attributable proportion of interaction = 0.206 (95%CI: 0.075-0.337) and the adjusted synergy index = 1.617 (95%CI: 1.126-2.098) indicated that there was a significant synergistic effect of serum cotinine levels and BMI on asthma. In males, females, non-Hispanic White and other Hispanic, there were synergistic interactions between serum cotinine levels and BMI on asthma. CONCLUSION: A synergistic interaction between serum cotinine and overweight/obesity on childhood asthma was found. For children with asthma, both intensive weight interventions in overweight or obese children and intensive passive smoking interventions in children exposed to the environment may be important.
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Asma , Obesidad Infantil , Contaminación por Humo de Tabaco , Asma/epidemiología , Asma/etiología , Índice de Masa Corporal , Niño , Cotinina , Estudios Transversales , Femenino , Humanos , Masculino , Encuestas Nutricionales , Sobrepeso , Obesidad Infantil/epidemiología , Contaminación por Humo de Tabaco/efectos adversos , Estados Unidos/epidemiologíaRESUMEN
INTRODUCTION: Serum cotinine is a sensitive and specific marker of tobacco smoke exposure. α-Klotho is an anti-ageing molecule, which plays an important role in several diseases. We aimed to examine the association between smoke exposure indicated by the serum cotinine and α-Klotho levels, as previous reports regarding the level of α-Klotho in smokers have been inconsistent. METHODS: This secondary dataset analysis included 9833 participants (aged 40-79 years; 47.0% females and 53.0% males) from the US National Health and Nutrition Examination Survey 2007-2016. Independent variables were serum cotinine level, age, sex, race, body mass index (BMI), and alcohol consumption. The outcome variable was serum α-Klotho level. Multiple linear regression analysis was used to examine the association between serum cotinine and α-Klotho levels. RESULTS: The serum cotinine level was negatively associated with the α-Klotho level (ß= -0.107, 95% CI: -0.155 to -0.059, p<0.0001) after adjusting for age, BMI, sex, race, and alcohol consumption. The α-Klotho level in participants with cotinine ≥3 ng/mL decreased by 44.514 pg/mL (p<0.0001) compared to that in participants with cotinine <3 ng/mL. There is a non-linear relationship between serum cotinine and α-Klotho levels. The piecewise linear models indicated a significant threshold effect between serum cotinine and α-Klotho levels. On the left of the inflection point (cotinine <130 ng/mL), the serum cotinine level increased with decreased α-Klotho level (ß= -0.519, 95% CI: -0.682 to -0.356). On the right of the inflection point (cotinine ≥130 ng/mL), the serum cotinine level increased with increased α-Klotho level (ß=0.085, 95% CI: 0.000 to 0.170). CONCLUSIONS: Based on our study results, serum cotinine level was associated with the serum α-Klotho level.
RESUMEN
The objective of this study was to examine long-term trends in serum cotinine (COT) concentrations, as a measure of secondhand smoke (SHS) exposure, in U.S. nonsmokers using data from the National Health and Nutrition Examination Surveys (NHANES) from 2003 to 2018. We analyzed NHANES serum COT results from 8 continuous NHANES 2 year cycles from 2003 to 2018 using a liquid chromatography−tandem mass spectrometry assay that has been maintained continuously at the Centers for Disease Control and Prevention (CDC) since 1992. Serum COT concentrations (based on the geometric means) among nonsmokers in the U.S. decreased by an average of 11.0% (95% confidence interval (CI) [8.8%, 13.1%]; p < 0.0001) every 2 year cycle. From 2003 to 2018, serum COT concentrations in U.S. nonsmokers declined by 55.0%, from 0.065 ng/mL in 2003−2004 to 0.029 ng/mL in 2017−2018 (p < 0.0001). Significant decreases in serum COT concentrations were observed in all demographic groups. While disparities between these groups seems to be shrinking over time, several previously observed disparities in SHS exposure remain in 2017−2018. Serum COT concentrations of the non-Hispanic Black population remained higher than those of non-Hispanic Whites and Mexican Americans (p < 0.0001). Additionally, serum COT concentrations were significantly higher for children aged 3−5 years than other age groups (p ≤ 0.0002), and men continued to have significantly higher serum COT concentrations than women (p = 0.0384). While there is no safe level of exposure to SHS, the decrease in serum COT concentrations in the U.S. population as well as across demographic groupings represents a positive public health outcome and supports the importance of comprehensive smoke-free laws and policies for workplaces, public places, homes, and vehicles to protect nonsmokers from SHS exposure.
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Cotinina , Contaminación por Humo de Tabaco , Niño , Exposición a Riesgos Ambientales , Femenino , Humanos , Masculino , No Fumadores , Encuestas NutricionalesRESUMEN
BACKGROUND: Allergic rhinitis (AR) is one of the most common allergic diseases affecting children. Objective assessment of nasal obstruction is possible through active anterior rhinomanometry (AAR). Several factors, such as passive smoke exposure (PSE), are triggers for worsening nasal obstruction and chronic inflammation. PSE affects bacterial eubiosis in the upper respiratory tract. This study evaluates the influence of PSE and cotinine levels on both nasal obstruction and local microbiome composition in children with AR. METHODS: Fifty patients (aged between 6 and 16 years) with AR monosensitized grass pollen were enrolled. They underwent skin prick tests, a nasal swab to evaluate the microbial composition of the anterior nostrils, a basal AAR, a post-decongestion AAR, and spirometry. Serum cotinine levels were assessed to evaluate PSE. RESULTS: A significantly lower percentage of mean nasal flow (mNF%) was observed before and after hydrazine administration in subjects exposed to passive smoke (Exp group) compared with the non-exposed group. In contrast, higher cotinine levels were observed in the Exp group than in the controls. PSE has been associated with a decrease in biodiversity and a change in the nasal microbiome composition; instead, although to a different extent, the abundance of specific taxa resulted in being correlated to cotinine levels and nasal flow. CONCLUSION: Children with AR exposed to passive smoke with positive serum cotinine could represent a risk factor for developing nasal obstruction and microbial dysbiosis, suggesting their possible role in pathophysiological processes.
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Microbiota , Rinitis Alérgica , Adolescente , Niño , Disbiosis , Humanos , Proyectos Piloto , FumarRESUMEN
CONTEXT: Periodontitis and chronic obstructive pulmonary disease (COPD) are chronic progressive inflammatory conditions. Smoking has been associated with both chronic periodontitis and COPD. Hence, the present study was designed to correlate serum levels of cotinine with the severity of periodontal disease with or without COPD. SETTINGS AND DESIGN: A total of eighty patients, twenty healthy individuals, twenty patients with chronic generalized periodontitis without smoking and without COPD, twenty patients who are smokers with chronic periodontitis without COPD and twenty patients who are smokers with chronic periodontitis and COPD in the age range of 43-65 years were selected for the study. SUBJECTS AND METHODS: Serum cotinine level assessment, smoking history, and periodontal examination were done in all the patients and the data obtained were statistically analyzed. RESULTS: The mean serum cotinine level was highest in smokers with chronic periodontitis and COPD (93.642 ± 14.727) and it differed significantly between the four groups (P < 0.001). There is a significant positive correlation between the number of cigarettes and serum cotinine levels in both groups involving smoking. There was no significant correlation between serum cotinine level and clinical attachment loss in chronic periodontitis smokers with or without COPD. CONCLUSIONS: The result of this study indicates that increased smoking with COPD causes a higher chance of progression of periodontal destruction but it is not statistically significant. Furthermore, this study indicates that the assessment of serum cotinine levels is a reliable method to evaluate smoking exposure.