Marker Of Tobacco Smoke Exposure Research Articles

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.

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.

Hand nicotine as an independent marker of thirdhand smoke pollution in children's environments

BackgroundHand nicotine (HN) levels measure children's exposure to tobacco smoke pollutants from thirdhand and secondhand smoke. HN is associated with urinary and salivary cotinine, but the associations of HN with other tobacco smoke exposure (TSE) markers remain unknown. ObjectivesWe compared levels of HN and four urinary TSE biomarkers: cotinine, trans-3′-hydroxycotinine (3HC), nicotelline N-oxides, and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), and children's sociodemographic and TSE patterns. We also examined if HN is a plausible pathway for children's exposure to active smoking. MethodsData were collected from 175 non-smoking patients (Mean (SD) age = 5.4 (3.4) years) who lived with ≥1 cigarette smoker(s). HN and TSE biomarker levels were determined using LC-MS/MS. Multivariate and multivariable regression analyses were conducted to examine associations between TSE markers and parent-reported measures, controlling for sociodemographics. ResultsOf the five markers of TSE, cotinine (R2 = 0.221; p = 0.003) and HN (R2 = 0.247; p = 0.001) showed the strongest overall associations. Of the five markers, only cotinine showed significantly higher levels among Black children (β^=0.307,p<0.05) independent of age, reported exposure, and home smoking bans. Cotinine (β^=0.010,p<0.05), NNAL (β^=0.012,p<0.05), and HN (β^=0.011,p<0.05) showed significant positive associations with reported exposure independent of race, age, and home smoking bans. NNAL (β^=−0.285,p<0.05) and HN (β^=−0.336,p<0.05), but not cotinine, 3HC, and N-oxides, showed significantly lower levels among children who lived in homes with smoking bans. Child age, hand surface area, home smoking ban, and reported exposure independently accounted for 21 % of the variance in HN levels (p = 0.002). HN accounted for 30 % of the variance in cotinine independent of child race and child age. DiscussionHN levels were associated with modifiable tobacco-related behaviors and shows promise as a marker of sources of THS pollution in a child's environment not captured by measurement of urinary cotinine alone. HN levels provide additional information about TSE, complementing other biomarkers when assessing children's overall TSE.

Association between serum cotinine and α-Klotho levels among adults: Findings from the National Health and Nutrition Examination Survey 2007-2016.

INTRODUCTIONSerum 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.METHODSThis 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.RESULTSThe serum cotinine level was negatively associated with the α-Klotho level (β= -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 (β= -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 (β=0.085, 95% CI: 0.000 to 0.170).CONCLUSIONSBased on our study results, serum cotinine level was associated with the serum α-Klotho level.

Smoking intensity and urinary nicotine metabolites by socioeconomic status in the Heinz Nixdorf Recall study

BackgroundSmoking intensity, which is generally based on self-reported average cigarettes per day (CPD), is a major behavioural risk factor and strongly related to socioeconomic status (SES). To assess the validity of the CPD measure, correlations with objective markers of tobacco smoke exposure – such as urinary nicotine metabolites – were examined. Yet, it remains unclear, whether this correlation is affected by SES, which may indicate imprecise or biased self-reports of smoking intensity.MethodsWe investigated the role of SES in the association between CPD and nicotine metabolites in current smokers among the participants of the population-based, prospective Heinz Nixdorf Recall Study. We determined urinary cotinine and additionally trans-3′-hydroxy-cotinine. SES was assessed by the International Socio-Economic Index of occupational status, and education. We calculated correlations (Pearson’s r) between logarithmised CPD and cotinine in subgroups of SES and analysed SES and further predictors of cotinine in multiple linear regression models separately by gender.ResultsMedian reported smoking intensity was 20 CPD in male and 19 CPD in female smokers. Men showed higher cotinine concentrations (median 3652 μg/L, interquartile range (IQR) 2279–5422 μg/L) than women (3127 μg/L, IQR 1692–4920 μg/L). Logarithmised CPD correlated moderately with cotinine in both, men and women (Pearson’s r 0.4), but correlations were weaker in smokers with lower SES: Pearson’s r for low, intermediate, and high occupational SES was 0.35, 0.39, and 0.48 in men, and 0.28, 0.43, and 0.47 in women, respectively. Logarithmised CPD and urinary creatinine were main predictors of cotinine in multiple regression models, whereas SES showed a weak negative association in women. Results were similar for trans-3′-hydroxy-cotinine.ConclusionsDecreasing precision of self-reported CPD was indicated for low SES in men and women. We found no strong evidence for biased self-reports of smoking intensity by SES.

Tobacco smoke exposure and sleep: estimating the association of urinary cotinine with sleep quality.

A majority of studies on tobacco smoke exposure and sleep quality have relied on self-reported smoking, resulting in potential exposure misclassification and biases related to self-report. The objective of this study was to investigate associations between urinary cotinine, a biological marker of tobacco smoke exposure, and sleep quality measures, including sleep duration, sleep continuity or efficiency, sleep satisfaction and alertness during normal waking hours. Using data on a national sample of 10 806 adults (aged 18-79 years) from the Canadian Health Measures Survey (2007-2013), we performed binary logistic regression analyses to estimate associations between urinary cotinine concentrations and sleep quality measures, while controlling for potential confounders. Additionally, we performed ordinal logistic regression to assess the association between urinary cotinine concentrations and increased number of sleep problems. Overall, 28.7% of adult Canadian survey respondents had urinary cotinine concentrations above the limit of detection (LOD), nd the prevalence of each sleep problem ranged from 5.5% to 35.6%. Elevated urinary cotinine concentrations (quartile 4 vs. <LOD) were associated with significantly higher odds of short or long sleep duration (OR = 1.41; 95% CI: 1.02-1.95; p-trend = .021), trouble falling or staying asleep (OR = 1.71; 95% CI: 1.28-2.27; p-trend = .003), sleep dissatisfaction (OR = 1.87; 95% CI: 1.21-2.89; p-trend = .011), and increased number of sleep problems (OR = 1.64; 95% CI: 1.19-2.26; p-trend = .001). Stronger associations were observed among females compared to males. Using a biological marker of tobacco smoke exposure, our study contributes to the body of literature of toxic environmental exposures on sleep quality by supporting an association between tobacco smoke exposure and poorer sleep quality. To address the limitations of a cross-sectional study design and to better assess the temporality of tobacco smoke exposure and sleep quality, longitudinal studies are recommended.

Urinary Cotinine Concentration and Self-Reported Smoking Status in 1075 Subjects Living in Central Italy.

Background: Urinary cotinine, a metabolite of nicotine, is a marker of tobacco smoke exposure. A cutoff value for cotinine concentration can be set to distinguish smokers from non-smokers, independently from self-declared status. Method: Cotinine was determined by isotopic dilution High Performance Liquid Chromatography coupled to tandem mass spectrometry (HPLC-MS/MS) between 2013 and 2014 on urine samples of a population of 1075 subjects. Results: 296 subjects have a cotinine level higher than 100 μg/g of creatinine (cutoff), with a median cotinine concentration of 1504.70 μg/g of creatinine. The mean is 27.5% of smokers and 60.5% in this group are females. The median value for non-smokers is 5.6 μg/g of creatinine. Two hundred and seventy-five subjects declared to be smokers in the questionnaire, but 6 (2.2%) present urinary cotinine levels lower than cutoff; 800 subjects declared to be non-smokers, but 26 of them presented urinary cotinine levels that were higher than the cutoff (3.3%). Conclusion: Using the cutoff of 100 μg/g, the misclassification of smokers resulted to be 2.2%, indicating that the selected value is suitable for studying the human exposures to environmental and occupational pollutants, including those produced by smoking.

Chairside quantitative immunochromatographic evaluation of salivary cotinine and its correlation with chronic periodontitis.

Background:Cigarette smoking is an established and modifiable risk factor for periodontitis. Periodontitis appears to be dose-dependent on smoking. The purpose of this study was to assess a reliable marker of tobacco smoke exposure (salivary cotinine) chairside and to confirm the quantitative association between smoking and chronic periodontitis.Materials and Methods:Saliva samples from 80 males, aged 30–60 years, with chronic periodontitis, were evaluated chairside using NicAlert™ cotinine test strips (NCTS). Patients were divided into two groups: A (cotinine negative) and B (cotinine positive). Plaque index (PI), Gingival index (GI), gingival bleeding index (GBI), probing pocket depth (PPD), clinical attachment level (CAL), and gingival recession (GR) were compared between the two groups and among the subjects of group B.Results:Comparison showed that the severity of PPD (P<0.001), CAL (P<0.001), and GR (P<0.001) was more in group B than in group A. Severity of all periodontal parameters increased with increased salivary cotinine among the subjects in group B.Conclusion:Quantitative direct association can be established between salivary cotinine and the severity of periodontitis. Immunochromatography-based cotinine test strips are a relatively easy method for quantification of salivary cotinine chairside. Immediate and personalized feedback from a chairside test can improve compliance, quit rates, and ease reinforcing smoking cessation.

Credibility of a smoking questionnaire based on urine cotinine level for patients with bladder cancer – a preliminary report

An analysis of the reliability of a questionnaire on smoking in 96 patients with transitional cell carcinoma (TCC) of the bladder. The credibility of the questionnaire was evaluated based on the detection of cotinine, an objective marker of tobacco smoke exposure, in urine. It was confirmed that approximately 18% of smokers did not admit to smoking, did not comply with recommendations to stop smoking, and about 4% of non-smokers were exposed to tobacco smoke unknowingly.

Biomarkers of exposure to tobacco smoke and environmental pollutants in mothers and their transplacental transfer to the foetus. Part II. Oxidative damage

Oxidative damage to macromolecules may have numerous negative health consequences. We measured oxidative damage to DNA, proteins and lipids in 80 newborns and 79 mothers, analyzed the effect of mother's tobacco smoke exposure on oxidative stress, and assessed correlations between oxidative stress markers and bulky and PAH (polycyclic aromatic hydrocarbons)-specific DNA adducts. Mean levels (±S.D.) of 8-oxodeoxyguanosine (8-oxodG) per 10 5 dG in the placenta were 2.85 ± 0.78; we did not see a difference between 8-oxodG levels in newborns born to mothers exposed and unexposed to tobacco smoke. Protein carbonyl levels, a marker of protein oxidation, were comparable in the umbilical cord and in maternal venous blood plasma (17.4 ± 3.2 and 17.6 ± 4.2 nmol/ml plasma in newborns and mothers, respectively, p = 0.66). Lipid peroxidation measured as levels of 15-F 2t-isoprostane (15-F 2t-IsoP) in plasma was significantly higher in newborns than in mothers (362 ± 129 and 252 ± 130 pg/ml in newborns and mothers, respectively, p < 0.001). We did not find any effect of tobacco smoke exposure on either biomarker in any group. Levels of both protein carbonyls and 15-F 2t-IsoP in cord blood significantly correlated with those in maternal plasma ( p < 0.001). 8-oxodG levels positively correlated with plasma carbonyls in cord plasma, as well as with cotinine levels (marker of tobacco smoke exposure) in maternal plasma. 8-oxodG levels also correlated with bulky DNA adducts in lymphocyte DNA of newborns and mothers and with PAH-DNA adducts in the placenta. Our results showed higher lipid peroxidation in newborns than in mothers, close correlation of analyzed oxidative stress markers between newborns and mothers, and a relationship between oxidative stress and induction of DNA adducts.

Biomarkers of Induced Active and Passive Smoking Damage

In addition to the well-known link between smoking and lung cancer, large epidemiological studies have shown a relationship between smoking and cancers of the nose, oral cavity, oropharynx, larynx, esophagus, pancreas, bladder, kidney, stomach, liver, colon and cervix, as well as myeloid leukemia. Epidemiological evidence has reported a direct link between exposure of non-smokers to environmental tobacco smoke and disease, most notably, lung cancer. Much evidence demonstrates that carcinogenic-DNA adducts are useful markers of tobacco smoke exposure, providing an integrated measurement of carcinogen intake, metabolic activation, and delivery to the DNA in target tissues. Monitoring accessible surrogate tissues, such as white blood cells or bronchoalveolar lavage (BAL) cells, also provides a means of investigating passive and active tobacco exposure in healthy individuals and cancer patients. Levels of DNA adducts measured in many tissues of smokers are significantly higher than in non-smokers. While some studies have demonstrated an association between carcinogenic DNA adducts and cancer in current smokers, no association has been observed in ex or never smokers. The role of genetic susceptibility in the development of smoking related-cancer is essential. In order to establish whether smoking-related DNA adducts are biomarkers of tobacco smoke exposure and/or its carcinogenic activity we summarized all data that associated tobacco smoke exposure and smoking-related DNA adducts both in controls and/or in cancer cases and studies where the effect of genetic polymorphisms involved in the activation and deactivation of carcinogens were also evaluated. In the future we hope we will be able to screen for lung cancer susceptibility by using specific biomarkers and that subjects of compared groups can be stratified for multiple potential modulators of biomarkers, taking into account various confounding factors.

Levels of hemoglobin and lipid peroxidation metabolites in blood, catalase activity in erythrocytes and peak expiratory flow rate in subjects with passive exposure to tobacco smoke

Exposure to tobacco smoke is an extremely important risk factor determining the development of respiratory diseases, cardiovascular diseases and cancer. Passive exposure is common and often not realized by the exposed subjects. Markers of tobacco smoke exposure are nicotine metabolites, i.e. cotinine and trans-3'-hydroxycotinine. The objective of the study was to assess the level of passive exposure to tobacco smoke among students and the exposure impact on the blood hemoglobin level, peak expiratory flow (PEF), lipid peroxidation level and antioxidant enzyme activity. A total of 104 subjects were enrolled in the study. The subjects were categorized in 3 subgroups depending on nicotine metabolite levels in blood (subgroup I with metabolite level > 100 ng/ml (high exposure); subgroup II with the metabolite level of 10-100 ng/ml; subgroup III with metabolite level <10 ng/ml). The blood hemoglobin level, PEF, levels of lipid peroxidation metabolites--malondialdehyde and 4-hydroxynonenal (MDA + 4-HNE) and catalase (CAT) activity were determined in all the subjects. The study showed statistically significant differences in levels of lipid peroxidation metabolites and CAT activity. Levels of MDA + 4-HNE were higher in subgroup I than in subgroup II or III (I: 3.84 +/- 1.64 mmol/l; II: 2.25 +/- 0.94 mmol/l; III: 1.90 +/- 0.82 mmol/l; pI-II < 0.01; pI-III <0.001). CAT activity was statistically significantly lower in subgroup I than in subgroup III (I: 0.38 +/- 0.01 x 10(6) IU/g hemoglobin [Hb]; II: 0.38 +/- 0.03 x 10(6) IU/g Hb; III: 0.41 +/- 0.04 x 10(6) IU/g Hb; pI-III <0.05). Passive exposure to tobacco smoke in the study population of students is common. The observed effects of passive exposure to tobacco smoke are similar to those of active smoking. It is postulated to undertake actions aiming at limiting passive exposure to tobacco smoke.

Les marqueurs d’exposition au tabagisme passif

Tobacco smoke is one of the most common air pollutants found in the indoor environment. Passive smoking is defined as the involuntary inhalation of tobacco smoke present in the air. This article examines the advantages and limitations of the methods that are available to measure environmental tobacco smoke exposure. Passive smoking can be assessed either by measuring tobacco smoke pollutants found in the air directly or by using biomarker assays, an indirect measure of exposure. As far as the direct measurement of air pollutants is concerned, nicotine and 3-Ethenylpyridine levels seem most suitable because of their specificity. Four specific biological markers of tobacco smoke exposure are available: nicotine, cotinine, thiocyanates, and protein or DNA adducts. Only urinary cotinine assay can be retained as a reliable marker of exposure to tobacco smoke. It has been used as a reference in most epidemiological studies but only reflects tobacco exposure over the preceding 48 hours. The measurement of nicotine and cotinine levels in the appendages of the skin (hair and nails) reflects exposure to tobacco over the previous three months and could become a better reference marker in epidemiological and toxicological studies.

Diesel exhaust exposure among adolescents in Harlem: a community-driven study.

This study sought individual-level data on diesel exhaust exposure and lung function among adolescents in Harlem as part of a community-driven research agenda. High school students administered in-person surveys to seventh grade students to ascertain information on demographics, asthma history, and self-reported and maternal smoking. Urine samples were assayed for 1-hydroxypyrene (1-HP), a marker of diesel exhaust exposure, and cotinine, a marker of tobacco smoke exposure. Computer-assisted spirometry was used to measure lung function. Three quarters (76%) of the participating students had detectable levels of 1-HP. Three students (13%) had an FEF25-75 of less than or equal to 80% of their predicted measurements, and 4 students (17%) had results between 80% and 90% of the predicted value, all of which are suggestive of possible lung impairment. These data suggest that most adolescents in Harlem are exposed to detectable levels of diesel exhaust, a known exacerbator and possible cause of chronic lung disorders such as asthma. Community-driven research initiatives are important for empowering communities to make needed changes to improve their environments and health.

The Elimination Half-Life of Urinary Cotinine in Children of Tobacco-Smoking Mothers

Exposure to environmental tobacco smoke (ETS) is strongly associated with childhood morbidity. Cotinine, the major metabolite of nicotine, is a useful marker of tobacco smoke exposure. Cotinine levels in infants are higher than in older children or adults exposed to the same reported quantity of ETS. One hypothesis to explain this difference is that the urinary elimination half-life of cotinine is different between infants and older children. Urine was collected at admission, 12, 24 and 48 h, cotinine levels were subsequently measured and then standardized by correcting for creatinine excretion. Urinary elimination half-life of cotinine was calculated in 31 infants and 23 older children. The median half-life was 28.3 h (range 6.3–258.5 h) in infants, and 27.14 h (range 9.7–99.42 h) in older children. A Mann–Whitney U test showed no significant difference in the median half-life of cotinine between the two age groups (P=0.18). Multivariate linear regression analysis demonstrated no significant relationship between half-life of cotinine and corrected cotinine level (P=0.24). Our results support the hypothesis that higher cotinine levels in infants is due to greater exposure, rather than slower metabolism of cotinine.

A review of the use of saliva cotinine as a marker of tobacco smoke exposure

Cotinine, the major metabolite of nicotine, is a useful marker of exposure to tobacco smoke. It can be measured in plasma, urine, or saliva. However, distinguishing between active and passive smoking on the basis of a cotinine measurement may be difficult. In order to evaluate the relationship between saliva cotinine concentration and self-reported tobacco smoke exposure in both active and passive smokers, an English-language literature search using MEDLINE was conducted (1973–1989), and the bibliographies of identified articles were reviewed. Of 43 originally identified articles, only 22 met the criteria for inclusion. Specific information regarding population studied, reported tobacco smoke exposure, method of measurement, and cotinine concentrations was assessed. Passive smokers usually have cotinine concentrations in saliva below 5 ng/ml, but heavy passive exposure can result in levels ⩾10 ng/ml. Levels between 10 and 100 ng/ml may result from infrequent active smoking or regular active smoking with low nicotine intake. Levels >100 ng/ml are probably the result of regular active smoking. Four categorizations of tobacco smoke exposure are suggested on the basis of saliva cotinine concentrations.

Discrepancies between self-reported and validated cigarette smoking in a community survey of New Mexico Hispanics.

In a population-based survey of respiratory disease in New Mexico Hispanics, we validated self-reports of cigarette use by 1,317 subjects against salivary cotinine level and end-tidal carbon monoxide concentration. For identifying likely deceivers about cigarette smoking among self-reported never smokers and former smokers, we used cutoff values of 20 ng/ml and 8 parts per million (ppm) for salivary cotinine and carbon monoxide, respectively. Among males and females, age-standardized prevalences of current smokers based upon questionnaire reports were 30.9 and 27.1%, respectively. After adjustment for cotinine alone, these percentages were 36.2 for males and 31.1 for females, and after adjustment for cotinine and carbon monoxide level, the corresponding percentages were 39.1 for males and 33.2 for females. We conclude that self-reports about smoking habits may lead to underestimation of the prevalence of current smokers and that questionnaire responses should be validated with biologic markers of tobacco smoke exposure.