Tobacco Smoke Exposure and Urinary Cadmium in Women from Northern Mexico.
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ABSTRACT:
SUBMITTER: Merida-Ortega A
PROVIDER: S-EPMC8656637 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Furan, a possible human carcinogen, is found in heat treated foods and tobacco smoke. Previous studies have shown that humans are capable of converting furan to its reactive metabolite, cis-2-butene-1,4-dial (BDA), and therefore may be susceptible to furan toxicity. Human risk assessment of furan exposure has been stymied because of the lack of mechanism-based exposure biomarkers. Therefore, a sensitive LC-MS/MS assay for six furan metabolites was applied to measure their levels in urine from furan-exposed rodents as well as in human urine from smokers and nonsmokers. The metabolites that result from direct reaction of BDA with lysine (BDA-N(?)-acetyllysine) and from cysteine-BDA-lysine cross-links (N-acetylcysteine-BDA-lysine, N-acetylcysteine-BDA-N(?)-acetyllysine, and their sulfoxides) were targeted in this study. Five of the six metabolites were identified in urine from rodents treated with furan by gavage. BDA-N(?)-acetyllysine, N-acetylcysteine-BDA-lysine, and its sulfoxide were detected in most human urine samples from three different groups. The levels of N-acetylcysteine-BDA-lysine sulfoxide were more than 10 times higher than that of the corresponding sulfide in many samples. The amount of this metabolite was higher in smokers relative to that in nonsmokers and was significantly reduced following smoking cessation. Our results indicate a strong relationship between BDA-derived metabolites and smoking. Future studies will determine if levels of these biomarkers are associated with adverse health effects in humans.
| S-EPMC5473163 | biostudies-literature
Project description:BackgroundAirports may represent significant sources of secondhand smoke (SHS) exposure for both travelers and employees. While previously common smoking rooms have largely disappeared from US airports, smoking continues to occur outdoors at terminal entrances. SHS may be especially high at arrival areas, since they oftentimes are partially enclosed by overhead departures, creating stagnant microenvironments. This study assessed particulate matter <2.5 microns in diameter (PM2.5), a common surrogate for SHS, at airport terminal locations to evaluate both outdoor exposure risk and possible indoor drift of SHS from outdoor sources.MethodsA convenience sample of nine airport terminal arrival areas in the US state of Florida was surveyed between February and July 2018. PM2.5 levels were assessed outdoors and indoors at terminal entrances and at control areas far into terminal interiors. We also examined the impact of smoking location on SHS exposure by correlating cigarette and passing vehicle counts with PM2.5 levels at terminals with contrasting proximity of designated smoking locations to terminal entrances.ResultsAlthough outdoor PM2.5 levels (mean 17.9, SD 6.1 µg/m3) were significantly higher than indoors (p < 0.001), there was no difference between indoor areas directly inside terminal entrances and areas much further interior (mean 8.8, SD 2.6 vs mean 8.5, SD 3.0 µg/m3, p=0.49). However, when smoking areas were in close proximity to terminal entrances, the number of lit cigarettes and vehicular traffic per minute predicted 70% of the variance of PM2.5 levels (p < 0.001), which was attributable mostly to the cigarette number (β = 0.83; 95% CI (0.55 to 1.11); p < 0.001). This effect was not observed at smoking areas further away.ConclusionPM2.5 data did not suggest indoor drift from outside smoking. Nevertheless, absolute exposure outdoors was high and correlated with the location of designated smoking areas. Further studies are needed to examine the effect of microclimate formation on exposure risk.
| S-EPMC6377972 | 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:BackgroundIt is known that environmental tobacco smoke (ETS) has adverse effects on pregnancy and birth outcomes. We aimed to assess the impact of ETS in pregnant women with and without asthma.MethodsA cohort study was conducted from August 2014 to June 2015 enrolling 1603 pregnant women during their 2nd trimester. Data on tobacco exposure were collected at first visit and women were followed through pregnancy till postpartum.ResultsOf the 1603 women, 231 reported passive smoking, 223 non-asthmatics and 8 asthmatics. Women exposed to ETS during pregnancy were more likely to have an infant admitted to the pediatric ward (10.8% vs. 6.5%, p = 0.026) and to have low one- and five-minute Apgar scores (1 min: 6.1% vs. 2.6%, p = 0.011; 5 min: 2.2% vs. 0.7%, p = 0.039). Complications of pregnancy were also elevated in women exposed to ETS (53.7% vs. 42.3%, p = 0.002). Asthma had no additional effect beyond the impact of ETS except for cesarean sections that were more frequent in women with asthma exposed to ETS.ConclusionsDue to the small number of women with asthma exposed to ETS, combined effects of asthma and ETS were only found for cesarean sections. Still counseling of pregnant women about adverse effects of ETS should consider women's asthma as an additional reason to avoid ETS.
| S-EPMC7240917 | 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:Seafood provides essential polyunsaturated fatty acids (PUFA) and other nutrients to pregnant women and their fetus(es) while a diet rich in finfish can be a major pathway of monomethyl mercury (MeHg+) exposure. We measured total mercury concentration ([THg]) in hair samples provided by 75 women in Baja California Sur (BCS) to assess its relationship with age, parity, tobacco smoke exposure, and diet based on survey methodologies. Generalized linear models (GLM) were used to explain the possible association of the different variables with [THg] in hair. Median [THg] in hair was 1.52 µgg-1, ranging from 0.12 to 24.19 µgg-1 and varied significantly by segment. Approximately 72% (54/75) of those evaluated exceed 1 µgg-1 [THg] and 8% (6/75) exceed 5 µgg-1 [THg] in hair. Although frequency of fish consumption contributed significantly to explaining hair [THg], fish consumption only explained 43% of [THg] in a GLM incorporating tobacco exposure and body mass index. This study establishes possible relationships among multiple potential sources of exposure and other factors related to [THg] in hair of women in the prenatal period. A more detailed examination of other sources of exposure and factors contributing to [THg] is warranted.
| S-EPMC5304913 | biostudies-literature
Project description:Tobacco exposure has been linked with sinonasal pathology and may be associated with allergic sensitization. This study evaluates the association between exposure to active smoking or secondhand smoke (SHS) and the prevalence of rhinitis and allergic sensitization in the US adult population.Cross-sectional study in 4,339 adults aged 20-85 in the National Health and Nutrition Examination Survey, 2005-2006. Never smoking was defined as reported lifetime smoking less than 100 cigarettes and serum cotinine levels <10ng/ml, while active smoking was defined as self-reported smoking or serum cotinine concentrations > 10 ng/mL. Self-reported rhinitis was based on symptoms during the past 12 months, and allergen sensitization was defined as a positive response to any of the 19 specific IgE antigens tested.Almost half of the population (43%) had detectable levels of IgE specific to at least one inhaled allergen and 32% reported a history of rhinitis. After multivariate adjustment, there was a statistically significant association between the highest serum cotinine tertile and rhinitis in active smokers (OR 1.42; 95%CI 1.00-2.00). The association between active smoking and rhinitis was stronger in individuals without allergic sensitization (OR 2.47; 95%CI 1.44-4.23). There was a statistically significant association between increasing cotinine tertiles and decreased odds of inhaled allergen sensitization (p-trend <.01).Tobacco smoke exposure was associated with increased prevalence of rhinitis symptoms, but not with allergic sensitization. The results indicate that the relationship between tobacco smoke exposure and sinonasal pathology in adults may be independent of allergic sensitization.
| S-EPMC4501790 | biostudies-other
Project description:BackgroundThirdhand smoke (THS) is the persistent residue resulting from secondhand smoke (SHS) that accumulates in dust, objects, and on surfaces in homes where tobacco has been used, and is reemitted into air. Very little is known about the extent to which THS contributes to children's overall tobacco smoke exposure (OTS) levels, defined as their combined THS and SHS exposure. Even less is known about the effect of OTS and THS on children's health. This project will examine how different home smoking behaviors contribute to THS and OTS and if levels of THS are associated with respiratory illnesses in nonsmoking children.MethodsThis project leverages the experimental design from an ongoing pediatric emergency department-based tobacco cessation trial of caregivers who smoke and their children (NIHR01HD083354). At baseline and follow-up, we will collect urine and handwipe samples from children and samples of dust and air from the homes of smokers who smoke indoors, have smoking bans or who have quit smoking. These samples will be analyzed to examine to what extent THS pollution at home contributes to OTS exposure over and above SHS and to what extent THS continues to persist and contribute to OTS in homes of smokers who have quit or have smoking bans. Targeted and nontargeted chemical analyses of home dust samples will explore which types of THS pollutants are present in homes. Electronic medical record review will examine if THS and OTS levels are associated with child respiratory illness. Additionally, a repository of child and environmental samples will be created.DiscussionThe results of this study will be crucial to help close gaps in our understanding of the types, quantity, and clinical effects of OTS, THS exposure, and THS pollutants in a unique sample of tobacco smoke-exposed ill children and their homes. The potential impact of these findings is substantial, as currently the level of risk in OTS attributable to THS is unknown. This research has the potential to change how we protect children from OTS, by recognizing that SHS and THS exposure needs to be addressed separately and jointly as sources of pollution and exposure.Trial registrationClinicalTrials.gov Identifier: NCT02531594 . Date of registration: August 24, 2015.
| S-EPMC6498613 | biostudies-literature
Project description:ContextIn 2006, we reviewed the evidence on environmental tobacco smoke (ETS) and breast cancer in nonsmoking women. Since then various studies and reviews have been published but opinion remains divided.ObjectiveTo provide an updated review.MethodsWe extracted study details, derived relative risk (RR) estimates with confidence intervals (CIs) for various ETS exposure indices, and conducted meta-analyses.ResultsThe update increased the number of studies from 22 to 47. Using an index for each study most closely equivalent to "spouse ever smoked", a weak but significant association was seen (random-effects RR = 1.15, 95% CI = 1.07-1.23). However, the estimates were heterogeneous: higher for Asian studies than for North American or European studies, higher for studies adjusting for fewer potential confounding variables, and close to 1.0 for prospective studies, regardless of whether or not they asked detailed questions on ETS exposure. The RR for eight prospective studies asking detailed questions was 1.003, 95% CI = 0.96-1.05. Risk was increased in premenopausal women (RR = 1.36, 95% CI = 1.15-1.60), but not postmenopausal women. Dose-response findings were similarly heterogeneous. No significant increase was seen for childhood or workplace exposure, but an increase was seen for total exposure (RR = 1.22, 95% CI = 1.09-1.37).ConclusionsIncreases mainly derived from case-control studies are prone to recall bias. Study weaknesses and possible publication bias limit interpretation. Considering also the weak association of smoking with breast cancer, and the much lower exposures from ETS than from smoking, our analyses do not clearly demonstrate that ETS exposure increases risk of breast cancer in nonsmokers. More research is needed.
| S-EPMC5020324 | biostudies-literature
Project description:Arsenic, cadmium and lead levels in tobacco filler and cigarette smoke were determined in a 568-sample worldwide survey. Median tobacco levels for arsenic, cadmium and lead were 237, 769 and 397 ng/g respectively, comparable to those previously reported albeit somewhat lower for lead and cadmium. Median mainstream smoke yields for arsenic, cadmium and lead were <3.75, 18.2, and <12.8 ng/cig. under ISO, and <8.71, 75.1 and <45.7 ng/cig. under Health Canada Intense (HCI) smoking regime respectively. In the case of cigarettes with activated carbon, a selective retention of cadmium but not lead or arsenic was observed. This effect was more pronounced under ISO than under HCI smoking regimes. Cadmium selective retention by activated carbon was confirmed by testing specially designed prototype cigarettes and the causes for this selective filtration were investigated. The differences between cadmium, arsenic and lead in terms of their speciation in tobaccos and in cigarette smoke could be related to their distribution in the ash, butt, mainstream (in gas-phase and particulate-phase) and sidestream smoke of a smoked cigarette. The possible formation of organometallic cadmium derivatives in the smoke gas-phase is discussed, the presence of which could adequately explain the observed cadmium selective filtration.
| S-EPMC5598168 | biostudies-literature