Cross-sectional study of urinary biomarkers of environmental tobacco and e-cigarette exposure and asthma morbidity.
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ABSTRACT:
SUBMITTER: Ruran HB
PROVIDER: S-EPMC9814889 | biostudies-literature | 2022 Sep
REPOSITORIES: biostudies-literature
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Cross-sectional study of urinary biomarkers of environmental tobacco and e-cigarette exposure and asthma morbidity.
Ruran Hana B HB Maciag Michelle C MC Murphy Sharon E SE Phipatanakul Wanda W Hauptman Marissa M
Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology 20220607 3
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Project description:BackgroundEnvironmental tobacco smoke (ETS) exposure is associated with poor asthma outcomes in children. However, little is known about natural changes in ETS exposure over time in children with asthma and how these changes may affect health-care utilization. This article documents the relationship between changes in ETS exposure and childhood asthma morbidity among children enrolled in a clinical trial of supervised asthma therapy.MethodsData for this analysis come from a large randomized clinical trial of supervised asthma therapy in which 290 children with persistent asthma were randomized to receive either usual care or supervised asthma therapy. No smoking cessation counseling or ETS exposure education was provided to caregivers; however, children were given 20 min of asthma education, which incorporated discussion of the avoidance of asthma triggers, including ETS. Asthma morbidity and ETS exposure data were collected from caregivers via telephone interviews at baseline and at the 1-year follow-up.ResultsAt baseline, 28% of caregivers reported ETS exposure in the home and 19% reported exposure outside of the primary household only. Among children whose ETS exposure decreased from baseline, fewer hospitalizations (p = 0.034) and emergency department (ED) visits (p < or = 0.001) were reported in the 12 months prior to the second interview compared to the 12 months prior to the first interview. Additionally, these children were 48% less likely (p = 0.042) to experience an episode of poor asthma control (EPAC).ConclusionsThis is the first study to demonstrate an association between ETS exposure reduction and fewer EPACs, respiratory-related ED visits, and hospitalizations. These findings emphasize the importance of ETS exposure reduction as a mechanism to improve asthma control and morbidity. Potential policy implications include supporting ETS reductions and smoking cessation interventions for parents and caregivers of children with asthma. Research to identify the most cost-effective strategy is warranted.
| S-EPMC2763557 | biostudies-literature
Project description:BACKGROUND:How carcinogen exposure varies across users of different, particularly noncigarette, tobacco products remains poorly understood. METHODS:We randomly selected 165 participants of the Golestan Cohort Study from northeastern Iran: 60 never users of any tobacco, 35 exclusive cigarette, 40 exclusive (78% daily) waterpipe, and 30 exclusive smokeless tobacco (nass) users. We measured concentrations of 39 biomarkers of exposure in 4 chemical classes in baseline urine samples: tobacco alkaloids, tobacco-specific nitrosamines (TSNA), polycyclic aromatic hydrocarbons (PAH), and volatile organic compounds (VOC). We also quantified the same biomarkers in a second urine sample, obtained 5 years later, among continuing cigarette smokers and never tobacco users. RESULTS:Nass users had the highest concentrations of tobacco alkaloids. All tobacco users had elevated TSNA concentrations, which correlated with nicotine dose. In both cigarette and waterpipe smokers, PAH and VOC biomarkers were higher than never tobacco users and nass users, and highly correlated with nicotine dose. PAH biomarkers of phenanthrene and pyrene and two VOC metabolites (phenylmercapturic acid and phenylglyoxylic acid) were higher in waterpipe smokers than in all other groups. PAH biomarkers among Golestan never tobacco users were comparable to those in U.S. cigarette smokers. All biomarkers had moderate to good correlations over 5 years, particularly in continuing cigarette smokers. CONCLUSIONS:We observed two patterns of exposure biomarkers that differentiated the use of the combustible products (cigarettes and waterpipe) from the smokeless product. Environmental exposure from nontobacco sources appeared to contribute to the presence of high levels of PAH metabolites in the Golestan Cohort. IMPACT:Most of these biomarkers would be useful for exposure assessment in a longitudinal study.
| S-EPMC6935158 | biostudies-literature
Project description:BackgroundPreviously, we reported that prenatal exposures to polycyclic aromatic hydrocarbons (PAH) and postnatal environmental tobacco smoke (ETS) in combination were associated with respiratory symptoms at ages 1 and 2 years. Here, we hypothesized that children exposed to both prenatal PAH and ETS may be at greater risk of asthma and seroatopy at ages 5-6 years, after controlling for current pollution exposure.MethodsPrenatal PAH exposure was measured by personal air monitoring over 48 h. ETS exposure, respiratory symptoms and asthma at ages 5-6 years were assessed through questionnaire. Immunoglobulin (Ig) E was measured by Immunocap.ResultsA significant interaction between prenatal PAH and prenatal (but not postnatal) ETS exposure on asthma (p < 0.05), but not IgE, was detected. Among children exposed to prenatal ETS, a positive nonsignificant association was found between prenatal PAH exposure and asthma (OR 1.96, 95% CI [0.95-4.05]). Among children without exposure to prenatal ETS, a negative nonsignificant association was found between prenatal PAH exposure and asthma (OR 0.65, 95% CI [0.41-1.01]). Prenatal PAH exposure was not associated with asthma or IgE at age 5-6 years.ConclusionsCombined prenatal exposure to PAH and ETS appears to be associated with asthma but not seroatopy at age 5-6. Exposure to PAH alone does not appear associated with either asthma or seroatopy at age 5-6 years. Discerning the differential effects between ETS exposed and ETS nonexposed children requires further study.
| S-EPMC3081952 | biostudies-literature
Project description:BackgroundAdverse psychosocial working conditions-in particular poor job decision latitude and poor social support at work-may impair the effective implementation of asthma self-management behaviour at work and may be associated with increased asthma morbidity. In this study, we investigate for the first time the association of job decision latitude and social support at work with (1) four asthma-specific self-management behaviours at work (i.e., physical activity, trigger avoidance, acute symptom management, and communication) and with (2) asthma morbidity.MethodsA total of 221 employees with asthma recruited through three rehabilitation clinics completed questionnaires (response rate = 29.3%). Job decision latitude and social support were measured using items from the Copenhagen Psychosocial Questionnaire. The four asthma self-management behaviours were mainly assessed by self-developed items. We used the Asthma Control Test and the Marks Asthma Quality of Life Questionnaire to measure asthma morbidity. We dichotomized all variables and conducted logistic regression analyses to calculate odds ratios with 95% CIs.ResultsLow job decision latitude and low social support were significantly associated with poorer trigger avoidance (odds ratios ≥ 2.09) and poorer acute symptom management (odds ratios ≥ 2.29); low social support was further related to significantly less communication (odds ratio = 2.82). Low job decision latitude and low social support were also associated with significantly poorer asthma control (odds ratios ≥ 1.95) and poorer asthma-specific quality of life (odds ratios ≥ 2.05). The relationships with asthma morbidity were attenuated after adjustment for the four asthma self-management behaviours (odds ratios ranging from 1.1 to 1.9).ConclusionsAdverse psychosocial working conditions are associated with poorer asthma self-management behaviour at work and with increased asthma morbidity. The latter association may be mediated by asthma self-management behaviour.Trial registration German Clinical Trials Register, registration number: DRK S00011309, date of registration: 22.12.2016.
| S-EPMC6509772 | biostudies-literature
Project description:IntroductionFew studies have comprehensively characterized toxic chemicals related to waterpipe use and secondhand waterpipe exposure. This cross-sectional study investigated biomarkers of toxicants associated with waterpipe use and passive waterpipe exposure among employees at waterpipe venues.MethodWe collected urine specimens from employees in waterpipe venues from Istanbul, Turkey and Moscow, Russia, and identified waterpipe and cigarette smoking status based on self-report. The final sample included 110 employees. Biomarkers of exposure to sixty chemicals (metals, volatile organic compounds (VOCs), polycyclic aromatic hydrocarbons (PAHs), nicotine, and heterocyclic aromatic amines (HCAAs)) were quantified in the participants' urine.ResultsParticipants who reported using waterpipe had higher urinary manganese (geometric mean ratio (GMR): 2.42, 95% confidence interval (CI): 1.16, 5.07) than never/former waterpipe or cigarette smokers. Being exposed to more hours of secondhand smoke from waterpipes was associated with higher concentrations of cobalt (GMR: 1.38, 95% CI: 1.10, 1.75). Participants involved in lighting waterpipes had higher urinary cobalt (GMR: 1.43, 95% CI: 1.10, 1.86), cesium (GMR: 1.21, 95% CI: 1.00, 1.48), molybdenum (GMR: 1.45, 95% CI: 1.08, 1.93), 1-hydroxypyrene (GMR: 1.36, 95% CI: 1.03, 1.80), and several VOC metabolites.ConclusionWaterpipe tobacco users and nonsmoking employees of waterpipe venues had higher urinary concentrations of several toxic metals including manganese and cobalt as well as of VOCs, in a distinct signature compared to cigarette smoke. Employees involved in lighting waterpipes may have higher exposure to multiple toxic chemicals compared to other employees.
| S-EPMC6513716 | biostudies-literature
Project description:To examine the relationship between tobacco cigarette brand recognition, and e-cigarette use in adolescents.Cross-sectional observational study.High schools in Scotland.Questionnaires were administered to pupils in Secondary 2 (S2 mean age: 14.0 years) and Secondary 4 (S4 mean age: 15.9 years) across 4 communities in Scotland. An 86% response rate with a total sample of 1404 pupils was achieved.Self-reported previous use of e-cigarettes and self-reported intention to try e-cigarettes in the next 6 months.75% (1029/1377) of respondents had heard of e-cigarettes (69.5% S2, 81.1% S4), and of these, 17.3% (10.6% S2, 24.3% S4 n=1020) had ever tried an e-cigarette. 6.8% (3.7% S2, 10.0% S4 n=1019) reported that they intended to try an e-cigarette in the next 6 months. Recognition of more cigarette brands was associated with greater probability of previous e-cigarette use (OR 1.20, 99% CI 1.05 to 1.38) as was having a best friend who smoked (OR 3.17, 99% CI 1.42 to 7.09). Intention to try e-cigarettes was related to higher cigarette brand recognition (OR 1.41, 99% CI 1.07 to 1.87), hanging around in the street or park more than once a week (OR 3.78, 99% CI 1.93 to 7.39) and living in areas of high tobacco retail density (OR 1.20, 99% CI 1.08 to 1.34). Never having smoked was a protective factor for both future intention to try, and past e-cigarette use (OR 0.07, 99% CI 0.02 to 0.25; and OR 0.10, 99% CI 0.07 to 0.16, respectively).Higher cigarette brand recognition was associated with increased probability of previous use and of intention to use e-cigarettes. The impact of tobacco control measures such as restricting point-of-sale displays on the uptake of e-cigarettes in young people should be evaluated.
| S-EPMC4769402 | biostudies-other
Project description:IntroductionThe aerosol composition of electronic cigarettes (ECs) suggests that exposure to toxicants during use is greatly reduced compared to exposure from combustible cigarettes (CCs).MethodsThis randomized, parallel-group, clinical study enrolled smokers to switch to Vuse Solo (VS) Digital Vapor Cigarettes (Original or Menthol) or Nicorette 4 mg nicotine gum (NG) in a controlled setting. Subjects who smoked CCs ad libitum for 2 days during a baseline period were then randomized to ad libitum use of either VS or NG for 5 days. Biomarkers of 23 toxicants were measured in 24-hour urine samples and blood collected at baseline and following product switch.ResultsA total of 153 subjects completed the study. Total nicotine equivalents decreased in all groups, but higher levels were observed in the VS groups compared to the NG groups, with decreases of 38% and 60%-67%, respectively. All other biomarkers were significantly decreased in subjects switched to VS, and the magnitude of biomarker decreases was similar to subjects switched to NG. Decreases ranged from 30% to greater than 85% for constituents such as benzene and acrylonitrile.ConclusionsThese results indicate that exposure to toxicants when using VS is significantly reduced compared to CC smoking, and these reductions are similar to those observed with use of NG. Although statistically significantly decreased, nicotine exposure is maintained closer to CC smoking with VS use compared to NG use. This research suggests that use of VS exposes consumers to fewer and lower levels of smoke toxicants than CCs while still providing nicotine to the consumer.ImplicationsThis is the first study to report changes in nicotine delivery and biomarkers of tobacco exposure following a short-term product switch from CCs to either an EC or NG in a controlled environment. The study shows that nicotine exposure decreased in both groups but was maintained closer to CC smoking with the EC groups. Biomarkers of tobacco combustion decreased to similar levels in both EC and gum groups.
| S-EPMC6698949 | biostudies-literature
Project description:ObjectivesTobacco exposure is an established risk factor for pancreatic cancer and chronic pancreatitis; however, its role in pancreatic insufficiency is not clear.MethodsThis controlled, cross-sectional study examined smokers and nonsmokers with no history of pancreatic disease. Histories and validated inventories of alcohol and tobacco use were obtained, and pancreatic insufficiency was assessed using the fecal elastase-1 assay.ResultsOf 7854 patients approached, 226 were interviewed and 200 enrolled. The rates of pancreatic insufficiency [18% (18/100)] and severe pancreatic insufficiency [10% (10/100)] were significantly higher in smokers than in controls [6% (6/100), P = 0.009 and 1% (1/100), P = 0.010, respectively]. On multivariate logistic regression, the risk of pancreatic insufficiency in smokers was significantly increased [odds ratio, 4.34 (1.37-13.75); P = 0.012], controlling for alcohol use and relevant covariates. Tobacco exposure was associated with the highest odds ratio for pancreatic insufficiency. Alcohol consumption was strongly associated with tobacco exposure (P < 0.001), but not with pancreatic insufficiency by multivariate analysis (P = 0.792).ConclusionsThis study suggests that tobacco exposure is independently associated with pancreatic exocrine insufficiency in patients without a prior diagnosis of pancreatic disease. Tobacco exposure seems to have greater detrimental effects on pancreatic function than alcohol in this population.
| S-EPMC6355146 | biostudies-literature
Project description:BackgroundWhile smokeless tobacco (ST) causes oral cancer and is associated with cardiovascular diseases, less is known about how its effects differ from other tobacco use. Biomarkers of potential harm (BOPH) can measure short-term health effects such as inflammation and oxidative stress.MethodsWe compared BOPH concentrations [IL6, high-sensitivity C-reactive protein, fibrinogen, soluble intercellular adhesion molecule-1 (sICAM-1), and F2-isoprostane] across 3,460 adults in wave 1 of the Population Assessment of Tobacco and Health study (2013-2014) by tobacco use groups: primary ST users (current exclusive ST use among never smokers), secondary ST users (current exclusive ST use among former smokers), exclusive cigarette smokers, dual users of ST and cigarettes, former smokers, and never tobacco users. We estimated geometric mean ratios using never tobacco users, cigarette smokers, and former smokers as referents, adjusting for demographic and health conditions, creatinine (for F2-isoprostane), and pack-years in smoker referent models.ResultsBOPH levels among primary ST users were similar to both never tobacco users and former smokers. Most BOPH levels were lower among ST users compared with current smokers. Compared with never tobacco users, dual users had significantly higher sICAM-1, IL6, and F2-isoprostane. However, compared with smokers, dual users had similar biomarker levels. Former smokers and secondary ST users had similar levels of all five biomarkers.ConclusionsST users have lower levels of inflammatory and oxidative stress biomarkers than smokers.ImpactST use alone and in combination with smoking may result in different levels of inflammatory and oxidative stress levels.
| S-EPMC8254764 | biostudies-literature
Project description:The urinary metabolites cyanoethyl mercapturic acid (CEMA) and 3-hydroxypropyl mercapturic acid (3-HPMA) have been widely used as biomarkers of exposure to acrylonitrile and acrolein, respectively, but there are no published data on their consistency over time in the urine of cigarette smokers. We provided, free of charge over a 20 week period, Spectrum NRC600/601 research cigarettes to cigarette smokers in the control arm of a randomized clinical trial of the reduced nicotine cigarette. Urine samples were collected at weeks 4, 8, 12, 16, and 20 and analyzed for CEMA and 3-HPMA, and total nicotine equivalents (TNE) using validated methods. Creatinine-corrected intra-class correlation coefficients for CEMA, 3-HPMA, and TNE were 0.67, 0.46, and 0.68, respectively, indicating good longitudinal consistency for CEMA, while that of 3-HPMA was fair. A strong correlation between CEMA and TNE values was observed. These data support the use of CEMA as a reliable biomarker of tobacco smoke exposure. This is the first report of the longitudinal stability of the biomarkers of acrylonitrile and acrolein exposure in smokers. The data indicate that CEMA, the biomarker of acrylonitrile exposure, is consistent over time in cigarette smokers, supporting its use. While 3-HPMA levels were less stable over time, this biomarker is nevertheless a useful monitor of human acrolein exposure because of its specificity to this toxicant.
| S-EPMC6319718 | biostudies-literature