Environmental tobacco smoke (ETS) and hyperlipidemia modified by perceived work stress.
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ABSTRACT:
SUBMITTER: Lin PY
PROVIDER: S-EPMC6964979 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Introduction: Numerous studies conducted in Europe and worldwide have indicated that employees of hospitality venues are the most exposed professional group to environmental tobacco smoke (ETS) in the workplace. The purpose of this study was to assess the exposure of employees of hospitality venues to ETS in the light of changes in anti-tobacco legislation in Poland. Materials and methods: The study consisted of two stages. The first stage was conducted in 2010, while the second in 2015. The study was conducted among employees of 300 randomly selected hospitality venues in the city of ?ód? (Poland). In total, 2607 questionnaires were analysed. The study used two survey questionnaires created and recommended by the Institute for Global Tobacco Control to study exposure to ETS. Statistical analysis was made with Statistica 13.1 PL (StatSoft, Poland). Results: In the group of all nonsmoking employees, individuals exposed to ETS at work in 2010 accounted for 72.6%; while in 2015 it was 51.8%. Factors affecting exposure to ETS in the workplace included, among others: age, marital status, education, position held, presence of a smoking room on the premises, and noncompliance with the provisions of the anti-tobacco laws. Conclusions: The prevalence of tobacco smoking among employees of hospitality venues decreased in 2010-2015, however, it remained high. More than half of nonsmoking employees were exposed to ETS at work.
| S-EPMC7277566 | biostudies-literature
Project description:BackgroundThere is a dearth of standardized studies examining exposure to environmental tobacco smoke (ETS) and its relationship to respiratory health among adults in developing countries.MethodsIn 2004, the Syrian Center for Tobacco Studies (SCTS) conducted a population-based survey using stratified cluster sampling to look at issues related to environmental health of adults aged 18-65 years in Aleppo (2,500,000 inhabitants). Exposure to ETS was assessed from multiple self-reported indices combined into a composite score (maximum 22), while outcomes included both self-report (symptoms/diagnosis of asthma, bronchitis, and hay fever), and objective indices (spirometric assessment of FEV1 and FVC). Logistic and linear regression analyses were conducted to study the relation between ETS score and studied outcomes, whereby categorical (tertiles) and continuous scores were used respectively, to evaluate the association between ETS exposure and respiratory health, and explore the dose-response relationship of the association.ResultsOf 2038 participants, 1118 were current non-smokers with breath CO levels < or = 10 ppm (27.1% men, mean age 34.7 years) and were included in the current analysis. The vast majority of study participants were exposed to ETS, whereby only 3.6% had ETS score levels < or = 2. In general, there was a significant dose-response pattern in the relationship of ETS score with symptoms of asthma, hay fever, and bronchitis, but not with diagnoses of these outcomes. The magnitude of the effect was in the range of twofold increases in the frequency of symptoms reported in the high exposure group compared to the low exposure group. Severity of specific respiratory problems, as indicated by frequency of symptoms and health care utilization for respiratory problems, was not associated with ETS exposure. Exposure to ETS was associated with impaired lung function, indicative of airflow limitation, among women only.ConclusionsThis study provides evidence for the alarming extent of exposure to ETS among adult non-smokers in Syria, and its dose-response relationship with respiratory symptoms of infectious and non-infectious nature. It calls for concerted efforts to increase awareness of this public health problem and to enforce regulations aimed at protecting non-smokers.
| S-EPMC549073 | biostudies-literature
Project description:ObjectiveMany children experience tobacco smoke exposure (TSE) and parents may take preventive measures to reduce TSE. The study goal is to assess if these strategies are associated with lower cotinine values, an objective biological measure of TSE.MethodsFamilies admitted to Children's Hospital Colorado from 2014 to 2018 who screened positive for TSE were invited to participate in a tobacco smoking cessation/reduction program. Caregivers were consented and asked about demographics, beliefs around smoking, and strategies to reduce TSE. Child urine samples were collected, tested for cotinine levels, and analyzed using geometric means. Bivariable comparisons and multivariable linear regression were completed using SAS v9.4 (SAS Institute, Cary, NC).ResultsTwo hundred thirteen children (81.4%) are included in this analysis. The median ages of children and parents were 4 and 32 years respectively. Fifty-seven percent of children were male, 36% were Hispanic, and 55% were white. Fifty-six percent of parents had at least some college education and 69% had an annual income less than $50K. The median daily cigarettes smoked per day were 10. Eighty-eight percent reported using at least 1 type of protective measure to prevent TSE and 90% believed they protect other household members from TSE. None of the strategies had a significant relationship with lower cotinine levels on bivariable or multivariable analyses.ConclusionsParental strategies to decrease TSE did not result in lower cotinine levels. Many measures are not evidence-based and do not protect children. Parent's clothing and homes may create a reservoir for nicotine. Education should focus on exposure elimination and cessation rather than protective measures.
| S-EPMC7442659 | biostudies-literature
Project description:BACKGROUND: Acute respiratory illness (ARI) is the most common cause of acute presentations and hospitalisations of young Indigenous children in Australia and New Zealand (NZ). Environmental tobacco smoke (ETS) from household smoking is a significant and preventable contributor to childhood ARI. This paper describes the protocol for a study which aims to test the efficacy of a family-centred tobacco control program about ETS to improve the respiratory health of Indigenous infants in Australia and New Zealand. For the purpose of this paper 'Indigenous' refers to Australia's Aboriginal and Torres Strait Islander peoples when referring to Australian Indigenous populations. In New Zealand, the term 'Indigenous' refers to M?ori. METHODS/DESIGN: This study will be a parallel, randomized, controlled trial. Participants will be Indigenous women and their infants, half of whom will be randomly allocated to an 'intervention' group, who will receive the tobacco control program over three home visits in the first three months of the infant's life and half to a control group receiving 'usual care' (i.e. they will not receive the tobacco control program). Indigenous health workers will deliver the intervention, the goal of which is to reduce or eliminate infant exposure to ETS. Data collection will occur at baseline (shortly after birth) and when the infant is four months and one year of age. The primary outcome is a doctor-diagnosed, documented case of respiratory illness in participating infants. DISCUSSION: Interventions aimed at reducing exposure of Indigenous children to ETS have the potential for significant benefits for Indigenous communities. There is currently a dearth of evidence for the effect of tobacco control interventions to reduce children's exposure to ETS among Indigenous populations. This study will provide high-quality evidence of the efficacy of a family-centred tobacco control program on ETS to reduce respiratory illness. Outcomes of our study will be important and significant for Indigenous tobacco control in Australia and New Zealand and prevention of respiratory illness in children.
| S-EPMC2846866 | biostudies-other
Project description:Human exposure to environmental tobacco smoke (ETS) is associated with an increased incidence of pulmonary and cardiovascular disease and possibly lung cancer. Metabolomics can reveal changes in metabolic networks in organisms under different physio-pathological conditions. Our objective was to identify spatial and temporal metabolic alterations with acute and repeated subchronic ETS exposure to understand mechanisms by which ETS exposure may cause adverse physiological and structural changes in the pulmonary and cardiovascular systems. Established and validated metabolomics assays of the lungs, hearts. and blood of young adult male rats following 1, 3, 8, and 21 days of exposure to ETS along with day-matched sham control rats (n = 8) were performed using gas chromatography time-of-flight mass spectrometry, BinBase database processing, multivariate statistical modeling, and MetaMapp biochemical mapping. A total of 489 metabolites were measured in the lung, heart, and blood, of which 142 metabolites were identified using a standardized metabolite annotation pipeline. Acute and repeated subchronic exposure to ETS was associated with significant metabolic changes in the lung related to energy metabolism, defense against reactive oxygen species, substrate uptake and transport, nucleotide metabolism, and substrates for structural components of collagen and membrane lipids. Metabolic changes were least prevalent in heart tissues but abundant in blood under repeated subchronic ETS exposure. Our analyses revealed that ETS causes alterations in metabolic networks, especially those associated with lung structure and function and found as systemic signals in the blood. The metabolic changes suggest that ETS exposure may adversely affects the mitochondrial respiratory chain, lung elasticity, membrane integrity, redox states, cell cycle, and normal metabolic and physiological functions of the lungs, even after subchronic ETS exposure.
| S-EPMC6707370 | biostudies-literature
Project description:The developing fetus is especially vulnerable to environmental toxicants, including tobacco constituents. The aim of this study was to assess the impact of environmental tobacco smoke (ETS) exposure during pregnancy on child neurodevelopment within the first two years of life. The study population consisted of 461 non-smoking pregnant women (saliva cotinine level <10 ng/mL). Maternal passive smoking was assessed based on the cotinine level in saliva analyzed by the use of high-performance liquid chromatography coupled with tandem mass spectrometry (HPLC-ESI + MS/MS) and by questionnaire data. The cotinine cut-off value for passive smoking was established at 1.5 ng/mL (sensitivity 63%, specificity 71%). Psychomotor development was assessed in children at the age of one- and two-years using the Bayley Scales of Infant and Toddler Development. Approximately 30% of the women were exposed to ETS during pregnancy. The multivariate linear regression model indicated that ETS exposure in the 1st and the 2nd trimesters of pregnancy were associated with decreasing child language functions at the age of one (? = -3.0, p = 0.03, and ? = -4.1, p = 0.008, respectively), and two years (? = -3.8, p = 0.05, and ? = -6.3, p = 0.005, respectively). A negative association was found for cotinine level ?1.5 ng/mL in the 2nd trimester of pregnancy and child cognition at the age of 2 (? = -4.6, p = 0.05), as well as cotinine levels ?1.5 ng/mL in all trimesters of pregnancy and child motor abilities at two years of age (? = -3.9, p = 0.06, ? = -5.3, p = 0.02, and ? = -4.2, p = 0.05, for the 1st, the 2nd, and the 3rd trimester of pregnancy, respectively; for the 1st trimester the effect was of borderline statistical significance). This study confirmed that ETS exposure during pregnancy can have a negative impact on child psychomotor development within the first two years of life and underscore the importance of public health interventions aiming at reducing this exposure.
| S-EPMC5551234 | biostudies-literature
Project description:BackgroundActive smoking has been linked to type 2 diabetes mellitus (T2DM) but only few recent studies have shown environmental tobacco smoke (ETS) to be associated with DM in never-smokers. We assessed the association between long term ETS exposure and DM, and explored effect modifications of this association in our sample.MethodsWe analysed 6392 participants of the Swiss study on air pollution and lung and heart diseases in adults (SAPALDIA). We used mixed logistic regression models to assess the cross-sectional association between ETS and DM. Selected variables were tested for effect modification and several sensitivity analyses were performed, mostly treating participants' study area as a random effect.ResultsThe prevalence of DM and ETS in the sample was 5.5% and 47% respectively. There were 2779 never-smokers with 4% diabetes prevalence. Exposure to ETS increased risk of DM in never-smokers by 50% [95% confidence interval (CI): 1.00, 2.26], and we observed a positive dose-response relationship between ETS exposure level and DM in never-smokers. Associations were strengthened (more than three-folds) by older age and chronic obstructive pulmonary disease, and were stronger in post-menopausal, obese, hypertriglyceridaemic and physically inactive participants. Estimates of association were robust across all sensitivity analyses (including inverse probability weighting for participation bias and fixed-effect analysis for study area). ETS had no substantial associations in current and ex-smokers in our study.ConclusionsWe found a positive association between ETS exposure and DM in never smokers. Additional longitudinal studies involving biomarkers are needed to further explore underlying mechanisms and susceptibilities.
| S-EPMC4192739 | biostudies-literature
Project description:Passive smoke intake by pregnant women may have detrimental effects such as spontaneous abortion, lower birth weight, stillbirth, and reduced infant lung function. To extend our knowledge on molecular effects of tobacco smoke exposure in pregnancy, we analyzed transcriptome alterations in passive smokers (PS) and compared them to those in active smokers (AS). Using Illumina Expression Beadchip with 24,526 transcript probes, gene expression patterns were assayed in placentas from PS (N=25) exposed to environmental tobacco smoke (ETS) throughout pregnancy and non-exposed (NS) counterparts (N=35), and in cord blood cells from their newborns. The ETS exposure was evaluated by questionnaire disclosure and cotinine measurement in maternal and cord bloods. A total of 196 genes were significantly deregulated in placentas of PS compared to NS. These genes were primary associated with extracellular matrix, apoptosis, blood clotting, response to stress, embryonic morphogenesis, and lipid metabolism. Cord blood of newborns of PS displayed differential expression of 116 genes encoding mainly neuronal factors, regulators of immunologic response, and protooncogenes. Gene ontology analyses highlighted some important biological processes that might be associated with placental insufficiency and fetal growth restriction in PS, such as fatty acid catabolism, coagulation, regulation of growth, and response to steroid hormone stimulus. The study demonstrates that even low dose exposure to ETS during pregnancy leads to the significant deregulation of transcriptional regulation in placental and fetal cells. The data suggest the effect of ETS on the fetus is primary indirect, mediated via deregulation of placental functions. Comparison of PS and AS indicated that ETS exposure and active smoking in pregnancy partly employ the same molecular mechanisms.
2011-07-20 | GSE30032 | GEO
Project description:OBJECTIVE: To measure the relation between environmental tobacco smoke, as estimated by smoking in spouses, and long term mortality from tobacco related disease. DESIGN: Prospective cohort study covering 39 years. SETTING: Adult population of California, United States. PARTICIPANTS: 118 094 adults enrolled in late 1959 in the American Cancer Society cancer prevention study (CPS I), who were followed until 1998. Particular focus is on the 35 561 never smokers who had a spouse in the study with known smoking habits. MAIN OUTCOME MEASURES: Relative risks and 95% confidence intervals for deaths from coronary heart disease, lung cancer, and chronic obstructive pulmonary disease related to smoking in spouses and active cigarette smoking. RESULTS: For participants followed from 1960 until 1998 the age adjusted relative risk (95% confidence interval) for never smokers married to ever smokers compared with never smokers married to never smokers was 0.94 (0.85 to 1.05) for coronary heart disease, 0.75 (0.42 to 1.35) for lung cancer, and 1.27 (0.78 to 2.08) for chronic obstructive pulmonary disease among 9619 men, and 1.01 (0.94 to 1.08), 0.99 (0.72 to 1.37), and 1.13 (0.80 to 1.58), respectively, among 25 942 women. No significant associations were found for current or former exposure to environmental tobacco smoke before or after adjusting for seven confounders and before or after excluding participants with pre-existing disease. No significant associations were found during the shorter follow up periods of 1960-5, 1966-72, 1973-85, and 1973-98. CONCLUSIONS: The results do not support a causal relation between environmental tobacco smoke and tobacco related mortality, although they do not rule out a small effect. The association between exposure to environmental tobacco smoke and coronary heart disease and lung cancer may be considerably weaker than generally believed.
| S-EPMC155687 | 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