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Depression is associated with both environmental tobacco smoke (ETS) and inflammation. However, whether systemic inflammation mediates the ETS-depression relationship is unclear. We analyzed 19,612 participants from the 2009–2018 National Health and Nutrition Examination Survey (representing approximately 206,284,711 USA individuals), utilizing data of depressive symptoms (assessed by Patient Health Questionnaire-9), blood cotinine level (an ETS biomarker), dietary inflammatory index (DII, assessed by 24-h dietary recall) and inflammation, represented by immune-inflammation index (SII) and systemic inflammation response index (SIRI). Weighted multivariable logistic regression showed that a higher blood cotinine level is significantly associated with a higher depressive symptoms risk (OR = 1.79, 1.35–2.38). After adjusting for covariates, the effect in smokers (OR = 1.220, 95 % CI: 1.140–1.309) is larger than that in non-smokers (OR = 1.150, 95 % CI: 1.009–1.318). Compared to the lowest level, depressive symptoms risks in participants with the highest level of SII, SIRI and DII are 19 % (OR = 1.19, 1.05–1.35), 15 % (OR = 1.15, 1.01–1.31) and 88 % (OR = 1.88, 1.48–2.39) higher, respectively. Weighted linear regression demonstrated positive correlations of SII (β = 0.004, 0.001–0.006), SIRI (β = 0.009, 0.005–0.012) and DII (β = 0.213, 0.187–0.240) with blood cotinine level. Restricted cubic splines model showed a linear dose-response relationship between blood cotinine and depressive symptoms (P non-linear = 0.410), with decreasing risk for lower DII. And SII and SIRI respectively mediate 0.21 % and 0.1 % of the association between blood cotinine and depressive symptoms. Cross-sectional design, and lack of medication data for depression. Positive association of ETS (blood cotinine) with depressive symptoms risk is partly mediated by systemic inflammation, and anti-inflammatory diet could be beneficial. [Display omitted] • Environmental tobacco smoke increases risk of depressive symptoms and inflammation. • SII and SIRI partly mediate the effect of blood cotinine on depressive symptoms. • Low DII mitigates the association of blood cotinine with depressive symptoms. [ABSTRACT FROM AUTHOR]

Exposure to environmental pollutants during pregnancy may cause adverse birth outcomes in newborns. This study examined links between exposure to various residential environmental characteristics during pregnancy and newborn birth weight/head circumference, using the Taiwan Birth Cohort Study (TBCS) database with 14,829 subjects. We conducted simple and multiple linear regression analyses to find out the associations between residential environmental characteristics (molds, environmental tobacco smoke [ETS], household insecticide use, and home renovation or painting) and birth outcomes (birthweight, head circumference), and adjusting for demographics and environmental variables. The standardized beta coefficients were calculated. We also analyzed whether the associations varied by newborn sex and maternal body mass index (BMI). The regression analysis indicated that molds on multiple walls at the residence were significantly associated with lower birthweight (standardized β = −0.025, p = 0.003) and with smaller head circumference (standardized β = −0.023, p = 0.008) than no mold on walls after adjustment. Exposure to ETS did not result in significance for birthweight reduction but a significant reduction in head circumference (standardized β = −0.018, p = 0.047). The birthweight reductions associated with molds were −0.024 SD (standard deviation) for boys and −0.028 SD for girls, whereas the head circumference reduction with molds was sex-specific, being only significant for girls (standardized β = −0.029, p = 0.021). The analysis on BMI-separated data indicated that all significance occurred to mothers having normal BMI. Mold presence correlated significantly with reduced birth weight and head circumference, while ETS exposure only reduced head circumference. Girls and mothers with normal BMI were more affected by these reductions than boys or under/overweight mothers. [Display omitted] • We explored the associations between residential environmental characteristics and birth outcomes. • Molds on walls relate to lower birthweight and smaller head circumference. • Environmental tobacco smoke is linked to reduced head circumference. • The birth outcome reductions appeared to be attributed more to girls than boys. • The birth outcome reductions came mostly from mothers with normal BMI. [ABSTRACT FROM AUTHOR]

The goal of this study was to describe environmental tobacco smoke (ETS) exposure using urinary biomarkers and its correlation with parent report, among children presenting to emergency room. This is a case control study among children aged 3 to 12 years at a tertiary pediatric emergency department in Israel. Children with respiratory (case) or gastrointestinal (control) symptoms were recruited and their accompanying parent completed a short survey. Urine samples were obtained and analyzed for nicotine, cotinine trans-3'-hydroxycotine. Clinical data were extracted from medical records. We compared tobacco exposure using urinary biomarkers, parent report, and Pearson's product-moment correlation, including 95% confidence intervals, between cases and controls. Forty-nine cases with respiratory symptoms and 96 controls with gastrointestinal symptoms were enrolled in the study. Parent-reported ETS exposure in the previous month was higher in the cases compared to control (71.4% vs 57.3%), although the difference was not statistically significant. The mean values of detectable biomarkers did not differ by between cases and controls. However, there was a correlation between urinary biomarkers and reported ETS exposure (0.278–0.460 for various biomarkers) only among cases. The majority of children in this study had detectable nicotine urinary biomarkers, regardless of their symptoms. However, correlation between parental report and urinary biomarkers was only found among children with symptoms potentially related to ETS. These findings imply that parents of children without respiratory symptoms may underestimate exposure. Efforts to educate parents and caregivers on the risks associated with exposure to ETS should be intensified, regardless of illness. [ABSTRACT FROM AUTHOR]

This study investigated the prevalence and correlates of current mental health and neurodevelopmental conditions among U.S. school-age children with tobacco smoke exposure (TSE). Data from the 2016–17 National Survey of Children's Health were analyzed. Multivariable logistic regression analyses among 6–11-year-olds (n = 21,539) and among subsamples aged 6–8 years (n = 10,100) and 9–11 years (n = 11,439) were conducted. Among 6–11-year-olds who lived with a smoker with no home TSE, the top mental health/neurodevelopmental conditions were other mental health conditions (22.1%), behavioral/conduct problems (21.7%), attention deficit disorder or attention deficit hyperactivity disorder (20.5%), depression (21.7%), and learning disability (19.3%). Children who lived with a smoker, with or without home TSE, were at increased odds of having anxiety problems, depression, attention deficit disorder or attention deficit hyperactivity disorder, behavioral/conduct problems, other mental health conditions, or learning disabilities. Many associations were more notable in younger children with home TSE. TSE is associated with mental health and neurodevelopmental conditions. Interventions to decrease TSE are needed to protect children. [ABSTRACT FROM AUTHOR]

Canine urothelial carcinoma (UC) initially responds favorably to treatment, but is ultimately lethal in most cases. Research to identify modifiable risk factors to prevent the cancer is essential. The high breed-associated risk for UC, e.g. 20-fold higher in Scottish terriers, can facilitate this research. The objective was to identify environmental and host factors associated with UC in a cohort of Scottish terriers. Information was obtained through dog owner questionnaires for 120 Scottish terriers ≥ 6 years old participating in a bladder cancer screening study, with comparisons made between dogs that did or did not develop UC during the 3 years of screening. Univariable models were constructed, and variables with P < 0.20 were included when building the multivariable model, and then removed using a backward stepwise procedure. P < 0.05 was considered statistically significant. Urine cotinine concentrations were measured by liquid chromatography-mass spectrometry to further investigate potential cigarette smoke exposure. Biopsy-confirmed UC which was found in 32 of 120 dogs, was significantly associated with the dogs living in a household with cigarette smokers (odds ratio [OR], 6.34; 95 % confidence intervals [CI], 1.16–34.69; P = 0.033), living within a mile of a marsh or wetland (OR, 21.23; 95 % CI, 3.64–123.69; P = 0.001), and history of previous bladder infections (OR, 3.87; 95 % CI, 1.0–14.98; P = 0.050). UC was diagnosed in 18 of 51 dogs (35.3 %) with quantifiable cotinine concentrations, and six of 40 dogs (15.0 %) without quantifiable cotinine concentrations in their urine (P = 0.0165). In conclusion, the main modifiable risk factor for UC in this cohort of dogs was exposure to second-hand tobacco smoke. [Display omitted] • Cigarette smoke exposure was associated with bladder cancer in Scottish terriers. • Dog owners are encouraged to avoid smoking to protect their dog's health. • Living near a marsh was also associated with bladder cancer. • Dogs could help identify gene-environment interactions leading to bladder cancer. [ABSTRACT FROM AUTHOR]

Background: Environmental tobacco smoke (ETS) exposure during pregnancy can cause preterm delivery and childhood cancer. The aim of this study was to measure ETS exposure in pregnant women and in newborn infants in Israel using urinary cotinine measurements, to assess predictors of ETS exposure in these vulnerable groups, and to assess associations with birth effects (birth weight, birth length, head circumference) in newborn infants.Methods: We analyzed urinary cotinine and creatinine in 265 non-smoking pregnant women and 97 newborns, and analyzed associations with self-reported exposure to ETS, paternal smoking, sociodemographic variables and with birth outcomes (birth weight, birth length, head circumference).Results: 37.7% of pregnant women and 29.0% of infants had urinary cotinine concentrations above the level of quantification (LOQ) of 1 μg/L, whereas 63.8% and 50.5%, respectively, had urinary cotinine concentrations above the level of detection (LOD) of 0.5 μg/L. Median unadjusted and creatinine adjusted urinary concentrations of cotinine in pregnant women were 0.7 μg/L, and 0.9 μg/g creatinine, respectively, and in newborn infants were 0.5 μg/L, and 1.3 μg/g creatinine, respectively. We did not find an association between maternal and infant urinary cotinine level. Maternal (but not infant) urinary cotinine was significantly associated with paternal smoking (p < 0.05). Infant (but not maternal) cotinine above the LOQ was negatively associated with birth weight (p < 0.05).Conclusions: In this high socioeconomic cohort, almost a third of newborn infants born to non-smoking mothers had quantifiable levels of urinary cotinine. This is the first study showing that newborns with quantifiable urinary cotinine levels have lower birth weight. [ABSTRACT FROM AUTHOR]

Urinary 3-hydroxybenzo[ a ]pyrene (3-OH-BaP) is a known biomarker for human exposure to carcinogenic polycyclic aromatic hydrocarbons (PAH). In this work, a new method for the ultra-sensitive quantification of this biomarker has been developed using the hyphenation of gas chromatography and atmospheric pressure laser ionization-mass spectrometry (GC-APLI-MS). In combination with an advanced sample preparation, a limit of detection (LOD) of 0.6 pg/L was achieved which is an improvement by a factor of at least 28 compared with existing methods. The limit of quantification (LOQ) is 1.8 pg/L. With this set-up 3-OH-BaP could be analyzed in urine samples of 7 smokers and 7 non-smokers. Concentrations ranged from 37 to 270 pg/L for non-smokers and from 374 to 1171 pg/L for smokers. For the first time, 3-OH-BaP was quantifiable in all non-smoker samples as no value was below the LOQ. Correlation of the urinary 3-OH-BaP values with the number of daily smoked cigarettes and with urinary cotinine values shows a clear relationship between 3-OH-BaP content and smoking habits. This innovative analytical method enables monitoring of low levels of the biomarker 3-OH-BaP in urine of non-occupationally exposed individuals including smokers, the general population with background PAH exposure and cohorts of low exposition such as newborns and children. • GC-APLI-MS was applied to the biomarker 3-hydroxybenzo[ a ]pyrene for the first time. • Limit of detection of 0.6 pg/L (urine) was achieved. • Samples of seven smoker and seven non-smoker urine samples were analyzed. • 3-Hydroxybenzo[ a ]pyrene was detected in all urine samples. • Significant difference between urinary 3-OH-BaP values of both groups was recognized. [ABSTRACT FROM AUTHOR]

Abstract The impact of pollution on children's health has been increasingly pointed out in numerous studies which emphasized their increased vulnerability compared to adults. This pilot study investigated the relevance of hair analysis for the assessment of children exposure to pollution and to environmental tobacco smoke (ETS). The methodology based on GC–MS/MS and LC-MS/MS, is the first one to investigate simultaneously parent PAH (n = 15), PAH metabolites (n = 56), nicotine and cotinine in a biological matrix. The method was applied to hair samples collected from 25 children, aged from 2 to 11 years, living in Paris, France, selected as densely populated area with urban pollution including vehicle exhausts, and Yeu Island, a French island in the Atlantic ocean, selected as control area with low population density and no fuel powered vehicles. Nicotine and cotinine were detected in all the samples at concentrations up to 2275 pg/mg and 110 pg/mg respectively, suggesting exposure to ETS in the two areas. 10 parent PAH and 10 metabolites were detected in 100% and in >90% of the samples respectively. Eight of these biomarkers presented a significantly higher concentration in children from Paris than from Yeu Island. The results suggest association between PAH exposure and estimated time of exposure to vehicle exhaust as well as higher exposure to both PAH and ETS in the youngest children. Although these findings need to be confirmed on wider populations, the results obtained in this pilot study strongly support the relevance of hair analysis for the biomonitoring of children exposure to urban pollution and ETS. Graphical abstract Unlabelled Image Highlights • Assessment of children exposure to pollution with hair analysis • Nicotine in 100% of the children indicates exposure to environmental tobacco smoke. • First method to analyse PAH parent (15) and metabolites (56) in a biological matrix • 10 parent PAH detected in 100% and 10 metabolites detected in >90% of subjects • Significant differences in exposure depending on children living area [ABSTRACT FROM AUTHOR]

Purpose: To examine if secondhand smoke (SHS) is associated with elevated risk of type II diabetes among California teachers. We also aim to determine if overall and central obesity are mediators or effect modifiers of this association.Methods: Using data from the California Teachers Study, conducted in 1995-2013 in California public schools, we obtained information on SHS exposure among 39,887 lifetime nonsmokers. The association between SHS and incident diabetes after 17 years of follow-up was assessed using Cox regression models. The mediation and modification effects of BMI and waist circumference on this association were tested.Results: At baseline, 70.2% of the nonsmokers reported exposure to SHS. Higher intensity, duration, and intensity-years of exposure to SHS were associated with higher multivariate adjusted risk of incident diabetes in a dose-response manner (hazard ratio = 1.28; 95% confidence interval, 1.11-1.48 for highest quartile vs. lowest quartile of exposure; P = .001 for trend). Participant's waist circumference (measured 2 years after baseline) could explain greater than 50% of the association between SHS and diabetes.Conclusions: SHS exposure is associated with increased risk of type II diabetes among nonsmokers of California teachers with obesity being a potentially important mediator but not an effect modifier for this association. [ABSTRACT FROM AUTHOR]

Abstract Background Environmental tobacco smoke (ETS) exposure in infants and children causes more frequent and severe asthma attacks, respiratory infections, ear infections, and sudden infant death syndrome. The aim of this study was to measure ETS exposure in children in Israel (ages 4–11 years) using urinary cotinine measurements, in order to compare exposure levels to other international populations, and to assess predictors of ETS exposure in children in Israel. Methods A subset of children who participated in the National Health and Nutrition Survey (RAV- MABAT) in 2015–2016 were invited to participate in the Second Israel Biomonitoring Survey. We analyzed urinary cotinine and creatinine concentrations in 103 children. Parents of study participants were interviewed in person on children's exposure to ETS at home and in other environments and on sociodemographic variables. We calculated creatinine-adjusted and unadjusted urinary cotinine geometric means in children and analyzed associations in univariable and multivariable analyses, between sociodemographic variables and parental – reported exposure, and urinary cotinine concentrations. Results Based on urinary creatinine measurement, over 60% of children are exposed to ETS (compared to <40% based on parental report). Linear regression showed a positive association between urinary cotinine concentration and reported ETS exposure (p = 0.001). Mean cotinine concentration among children whose parents reported that they are exposed to ETS at home (5.1 μg/l) was significantly higher than the concentration among children whose parents reported they are not exposed to ETS at home (1.6 μg/l, p < 0.001). There was an inverse relationship between total family income and urinary cotinine concentration (p < 0.05). In a multivariable model adjusted for ethnicity and other factors, family income was a significant predictor of urinary cotinine level (p = 0.04, slope = −0.49). Geometric mean creatinine adjusted concentrations in children in the current study were higher than in children in Canada and selected European countries. Conclusions We found evidence of widespread exposure to ETS in children in the study. There is an urgent need to protect children in Israel from exposure to ETS. Highlights • We measured urinary cotinine in 103 children to assess ETS exposure in Israel. • Over 60% of children were exposed to ETS compared to <40% based on parental report. • Lower family income was found to predict higher cotinine concentrations in children. • We found evidence of widespread exposure to ETS in children in the study. [ABSTRACT FROM AUTHOR]

Abstract Objective To determine if low-cost air-quality monitors providing personalised feedback of household second-hand smoke (SHS) concentrations plus standard health service advice on SHS were more effective than standard advice in helping parents protect their child from SHS. Design A randomised controlled trial of a personalised intervention delivered to disadvantaged mothers who were exposed to SHS at home. Changes in household concentrations of fine Particulate Matter (PM 2.5) were the primary outcome. Methods Air-quality monitors measured household PM 2.5 concentrations over approximately 6 days at baseline and at one-month and six-months post-intervention. Data on smoking and smoking-rules were gathered. Participants were randomised to either Group A (standard health service advice on SHS) or Group B (standard advice plus personalised air-quality feedback). Group B participants received personalised air-quality feedback after the baseline measurement and at 1-month. Both groups received air-quality feedback at 6-months. Results 120 mothers were recruited of whom 117 were randomised. Follow up was completed after 1-month in 102 and at 6-months in 78 participants. There was no statistically significant reduction in PM 2.5 concentrations by either intervention type at 1-month or 6-months, nor significant differences between the two groups at 1-month (p = 0.76) and 6-month follow-up (p = 0.16). Conclusions Neither standard advice nor standard advice plus personalised air-quality feedback were effective in reducing PM 2.5 concentrations in deprived households where smoking occurred. Finding ways of identifying homes where air-quality feedback can be a useful tool to change household smoking behaviour is important to ensure resources are targeted successfully. Highlights • Health professionals can successfully deliver personalised air quality information in home settings. • We found no evidence that air-quality feedback helps create a smoke-free home. • Finding parents for whom this intervention may work requires a targeted approach. [ABSTRACT FROM AUTHOR]

Background Exposure to indoor air pollutants at home was found to be associated with respiratory diseases. As lifestyle changes with rapid economic growth in Romania, the aim of our study is to describe the characteristics of Romanian homes and their impact on children's respiratory health. Methods Self-reported information on respiratory symptoms was collected from 280 Romanian elementary school students in 2011, and the symptoms were categorized into allergy, asthma-like, and flu-like symptoms. Home characteristics and demographic information were collected from questionnaires answered by parents. The association between home characteristics and respiratory health was assessed through multivariate logistic regression controlling for school indoor exposure. Results As compared to U.S. households, Romanian homes have a higher percentage of smokers, limited use of indoor climate control, and higher use of iron stoves. Exposure to environmental tobacco smoke was associated with both asthma and allergy symptoms. Additional risk factors identified for allergy symptoms include living in apartments, near pesticide sprayed areas, and the use of incense sticks. The significantly higher risk of flu-like symptoms was associated with mold and dampness issues, the use of air conditioner, gas heater/iron stove in children's bedroom. Conclusion Our findings suggest that an increase in respiratory symptoms among Romanian school-age children can be partly related to their environmental exposure at home. Since most of the identified risk factors are preventable, our results provide critical information and evidence for policymakers, to develop target intervention and education strategies. [ABSTRACT FROM AUTHOR]

Several studies have reported that certain aspects of the household environments are associated with adverse birth outcomes, but associations have been inconsistent. Few of these studies have been conducted in China. During 2011–2012, we conducted a retrospective cross-sectional study and collected 13,335 parents-reported questionnaires for 4–6-year-olds children in Shanghai, China. We investigated associations of household environmental factors (environmental tobacco smoke (ETS), cooking fuel, dampness, pet-keeping, and home renovation) during gestation with preterm birth (PTB, gestational age < 37 weeks), low birth weight (LBW, birth weight < 2500 g), term low birth weight (T-LBW, LBW when the gestational age was ≥ 37 weeks), and small for gestational age (SGA, birth weight < 10th percentile of birth weight for gestational age). A total of 4.1% children were premature; 2.9% had LBW and 1.6% had T-LBW; 8.1% were SGA. In the multiple logistic regression analyses, home renovation during gestation was associated with PTB (adjusted odds ratio (OR), 95% confidence intervals (CI): 1.68, 1.11–2.54) and LBW (1.64, 0.99–2.72). Paternal smoking was associated with PTB (1.18, 0.98–1.43). No significant associations were found for SGA. Neither household dampness nor cooking fuel were significantly associated with birth outcomes. For boys, paternal smoking was associated with PTB (1.31, 1.02–1.69); home renovation during gestation was associated with PTB (2.14, 1.27–3.61) and LBW (2.19, 1.09–4.43). Among children whose mothers were ≥ 34-year-olds during gestation, paternal smoking (1.73, 1.04–2.76) and home renovation during gestation (1.80, 1.18–2.76) was associated with PTB. Our findings demonstrate that home renovation and ETS during gestation may be risk factors for adverse birth outcomes. Associations of these factors with adverse birth outcomes appear to be stronger in boys and among mothers older than 34 years during gestation. Home renovation and ETS exposure should be avoided during gestation, especially for pregnancies with male fetuses and older pregnant women. [ABSTRACT FROM AUTHOR]

Numerous studies have explored the associations between environmental pollutants and pediatric health. Recent studies have investigated the issue in Asia, but no systematic review has been published to date. This study aims to elucidate the issue by summarizing relevant epidemiologic evidence for cohorts in Asia, using information from the Birth Cohort Consortium of Asia (BiCCA). Environmental pollutants include mercury, environmental tobacco smoke (ETS), polychlorinated biphenyls (PCB), perfluoroalkyl substances (PFAS) and phthalates. This study sought to classify the effects of such compounds on fetal growth and pregnancy outcomes, neurodevelopment and behavioral problems, allergic disease and immune function and the endocrine system and puberty. These evidences showed ETS has been associated with infant birth weight, children's neurodevelopment and allergy disease; mercury and PCB have been shown to affect children's neurodevelopment; phthalate has effects on endocrine function; PFAS alters children's neurodevelopment, the endocrine system, and the allergic response. However, more consistent and coordinated research is necessary to understand the whole picture of single environmental and/or co-exposure and children's health. Therefore, harmonization and international collaboration are also needed in Asia. [ABSTRACT FROM AUTHOR]

Environmental tobacco smoke (ETS) exposure is a main risk factor of lung cancer in never smokers. Epidermal Growth Factor Receptor (EGFR) mutations and ALK translocations are more frequent in never smokers' lung cancer than in ever-smokers. We performed a multicenter case-control study to assess if ETS exposure is associated with the presence of EGFR mutations and its types and if ALK translocations were related with ETS exposure. All patients were never smokers and had confirmed lung cancer diagnosis. ETS exposure during childhood showed a negative association on the probability of EGRF mutation though not significant. Exposure during adulthood, at home or at workplace, did not show any association with EGFR mutation. The mutation type L858R seemed the most associated with a lower probability of EGFR alterations for ETS exposure at home in adult life. There is no apparent association between ETS exposure and ALK translocation. These results might suggest that ETS exposure during childhood or at home in adult life could influence the EGFR mutations profile in lung cancer in never smokers, reducing the probability of presenting EFGR mutation. [ABSTRACT FROM AUTHOR]

PM 2.5 samples were collected at six indoor public places that contained dedicated smoking lounges. Samples were taken in the smoking lounges, at two indoor locations outside of the lounges, and in outdoor air near the venues. Organic carbon (OC), elemental carbon (EC), and non-polar organic compounds including polycyclic aromatic hydrocarbons (PAHs), n -alkanes ( n -C 16 to n -C 40 ), iso/anteiso-alkanes (C 29 to C 33 ), hopanes and phthalate esters (PAEs) were quantified. Average PM 2.5 levels of 170.2 ± 85.9 μg/m 3 in the lounges exceeded limits of 25 μg/m 3 set by World Health Organization (WHO); these levels were 5.4 and 3.9 times higher than those indoors and outdoors, respectively. High ratios of OC to PM 2.5 , OC to EC, and PAHs diagnostic ratios in the lounges indicated contributions from environmental tobacco smoke (ETS). The maximum carbon number (C max ) and carbon preference indices (CPI) for n -alkanes showed ETS transport from the enclosed lounges to nearby indoor non-smoking areas. Iso/anteiso-alkanes in the lounges were 876.5 ng/m 3 , ∼80 times higher than outdoor levels. 17α(H)-21β(H),30-norhopane and 17α(H)-21β(H),(22R)-homohopane were much higher in the lounges than outdoor air, but they cannot be directly attributed to ETS. Estimated carcinogenic risks of PAHs in the lounges exceeded the acceptable level of 10 − 6 . [ABSTRACT FROM AUTHOR]

Background and aims Despite worldwide reductions in active smoking, non-smokers continue to be exposed to environmental tobacco smoke, especially at home or workplace. There is a well-recognised association between active smoking and peripheral arterial disease, however, a relationship to environmental tobacco smoke exposure is less substantiated. The aims of this paper are to review the literature regarding the association between environmental tobacco smoke and peripheral arterial disease and identify the public health implications of the findings. Methods Selected electronic databases (Medline, EMBASE, CINAHL, PsychINFO and Scopus) were searched for studies published up to August 2017. Key words and inclusion/exclusion criteria applied. A manual search of reference lists of studies selected for review was also performed. Results Of the initial 150 studies identified, 12 met inclusion criteria for review. Three studies showed a positive association between environmental tobacco smoke exposure and definitive diagnosis of peripheral arterial disease, 6 studies demonstrated a positive association with features of vascular injury, and 3 studies found no significant positive or negative association. Conclusions An association between exposure to environmental tobacco smoke and development of peripheral arterial disease or clinically significant arterial injury in non-smokers is supported by moderate quality evidence in the literature. Larger, longitudinal observational studies addressing current limitations, including sources of bias, inconsistency and imprecision, are needed to provide more robust and consistent evidence. Regardless, evidence of potential detrimental impacts supports ongoing restrictions on freedom to smoke in public areas, including the workplace, and has implications for those exposed in the home environment. [ABSTRACT FROM AUTHOR]

Background and aims Evidence on the association between passive smoking and risk of aortic dissection or aneurysm is limited. This study aimed to investigate whether passive smoking increases risk of mortality from aortic dissection or aneurysm. Methods The Japan Collaborative Cohort (JACC) Study is a prospective community-based cohort study begun in 1988–90 and followed up to the end of 2009. We examined 48,677 individuals (mean age, 56 years; women, 46%) without history of stroke, coronary heart disease, or cancer, who provided valid responses to a lifestyle questionnaire including questions on active and passive smoking. We used 3 categories (passive smoking out of home, passive smoking at home, and passive smoking out of or at home combined) to divide never-smokers into 3 exposure groups: low, intermediate, and high exposures, respectively. The endpoint was underlying cause of death from aortic dissection or aneurysm. Results During the median 19-year follow-up of 48,677 study participants, 66 died of aortic dissection, and 75 of aortic aneurysm. Multivariable hazard ratios (95% confidence intervals) for the high passive-smoking group as compared with the low passive-smoking group were 2.45 (1.02–5.88) out of home, 1.82 (0.84–3.96) at home, and 2.35 (1.09–5.09) out of or at home combined. The corresponding hazard ratios for current smokers as compared with the low passive-smoking group were 3.97 (2.14–7.39), 3.41 (1.84–6.32) and 4.09 (1.99–8.39), respectively. Conclusions Out-of-home passive smoking and out-of- or at-home combined passive smoking were associated with increased mortality from aortic dissection or aneurysm. [ABSTRACT FROM AUTHOR]

Background This study aimed to investigate the association between cord blood cotinine levels and birth outcome, and to determine whether fetal metabolic gene polymorphisms of glutathione-S-transferase (GST) modulate the effect of environmental tobacco smoke exposure during pregnancy. Methods This study included 328 maternal and neonatal pairs. Maternal and cord blood cotinine levels were measured using high performance liquid chromatography. The GST T1 ( GSTT1 ) and GST M1 ( GSTM1 ) polymorphisms were examined using the polymerase chain reaction method. The birth outcomes included birth weight, length, and head circumference, and the risks of having low birth weight and being small for gestational age (SGA). Results Cord cotinine level had a dose-dependent impact on the reduction of birth weight, length, and head circumference in newborns. Elevation of cord blood cotinine concentration increased the rate of SGA and low birth weight. The neonates who had GSTT1 or GSTM1 polymorphism were associated with an increased risk of being SGA. A combination of the GSTT1 and GSTM1 null genotype exacerbated the effect of maternal environmental tobacco smoke exposure on SGA more than the presence of either genotype alone (odds ratio = 8.90, 95% confidence interval = 1.00–79.5). Conclusion Cord blood cotinine adversely affects birth outcomes. GSTT1 and GSTM1 null genotype may modify the effect of cord blood cotinine on birth outcomes. [ABSTRACT FROM AUTHOR]

Objective: To investigate secondhand smoke exposure (SHS) of children at home and the prevalence of parental smoking after implementation of the new tobacco control law in Macao. This study explored whether the smoking ban in public places in Macao has decreased the prevalence of smoking or led to increased SHS exposure of children at home. As smokers cannot smoke in public places any more, they may smoke at home more frequently; a displacement effect of smoke-free legislation. Study design: Cross-sectional survey. Methods: This study surveyed 337 fathers and 538 mothers. Questions from a subset of key questions from the Global Adult Tobacco Survey (2nd edition) were applied to assess the SHS exposure of children and the prevalence of parental smoking since the smoking ban. A classification tree analysis was used to analyse the factors increasing SHS exposure of children. Results: The prevalence of SHS exposure in children at home was 41.3%. The prevalence rates of paternal and maternal smoking were 43.7% and 3.8%, respectively. Compared with data reported by the Health Bureau of Macao SAR in 2011, the prevalence of parental smoking and the prevalence of SHS exposure of children at home have not decreased since the smoking ban. Analysis of the factors increasing the prevalence of SHS exposure of children indicated that fathers with an education level below high school were more likely to contribute to this increase, compared with fathers with a high school education or more (48.2% vs 32.4%, respectively). In addition, fathers represented the majority of smokers at home, accounting for 92.0% of 415 smoking parents. The prevalence of paternal smoking (82.0%) in the group of children with SHS exposure was much higher than that in the unexposed group (16.7%, Chi-squared test = 367.199, P = 0.000). The SHS exposure of children increased consistently with the decrease in paternal education level. This was consistent with the increasing prevalence of paternal smoking as paternal education level decreased. SHS exposure was most common among children whose fathers had an education level below high school and whose mothers were aged ≤29 years (75.0%). Conclusions: This study did not find any decline in the prevalence of parental smoking after the smoking ban. These parents were more likely to smoke at home after the ban, leading to more frequent SHS exposure for their children. [ABSTRACT FROM AUTHOR]

Low-cost interventions to decrease environmental tobacco smoke (ETS) exposure of pregnant women and their newborns are needed to lower health risks of exposed fetuses and infants. Baby's Breath is a tailored video intervention developed and tested in a randomized controlled trial. The study aimed to test the efficacy of tailored video versus usual care approaches to reduce the ETS exposure of fetuses of low-income women during and after pregnancy; and to assess this intervention separately among non-smoking and smoking women. Participating women, recruited early in pregnancy, who spoke English, were at least 18 years old, smoke exposed (current smokers, quit smoking on their own, or were exposed to smoke of others), pregnant with only one baby, and had access to a telephone and video player, were randomized to experimental or control conditions. Intervention participants received newsletters containing content aimed at smoking cessation and avoidance (5 during and 3 after pregnancy), in addition to videos (3 during and 2 after pregnancy) individually tailored on behavioral theory-based survey questions. Comparison participants received newsletters and videos on healthy pregnancy topics. Outcomes included salivary cotinine of both mother and baby (32 weeks gestation and 6 months postpartum) as well as self-reported ETS exposure and avoidance behaviors. This study may demonstrate the efficacy of a low-cost intervention to decrease ETS exposure, and will fill an important gap in describing the utility of this innovative intervention technology, as well as demonstration of potential benefits to this type of intervention. [ABSTRACT FROM AUTHOR]

Objectives: The study aimed to review the epidemiological evidence relating environmental tobacco smoke exposure to stroke in never smokers.Methods: The study is similar to our review in 2006, with searches extended to March 2016.Results: Twelve further studies were identified. A total of 28 studies varied considerably in design, exposure indices used, and disease definition. Based on 39 sex-specific estimates and the exposure index current spousal exposure (or nearest equivalent), the meta-analysis gave an overall fixed-effect relative risk estimate of 1.23 (95% confidence interval: 1.16-1.31), with significant (P < .05) heterogeneity. There was no significant heterogeneity by sex, continent, fatality, disease end point, or degree of adjustment for potential confounding factors. Relative risks were less elevated in prospective studies (1.15, 1.06-1.24) than in case-control studies (1.44, 1.22-1.60) or cross-sectional studies (1.40, 1.21-1.61). They also varied by publication year, but with no trend. A significant increase was not seen in studies that excluded smokers of any tobacco (1.07, .97-1.17), but was seen for studies that included pipe- or cigar-only smokers, occasional smokers, or long-term former smokers. No elevation was seen for hemorrhagic stroke. Relative risk estimates were similar using ever rather than current exposure, or total rather than spousal exposure. Eleven studies provided dose-response estimates, the combined relative risk for the highest exposure level being 1.56 (1.37-1.79). Many studies have evident weaknesses, recall bias, and particularly publication bias being major concerns.Conclusions: Although other reviewers inferred a causal relationship, we consider the evidence does not conclusively demonstrate this. We repeat our call for publication of data from existing large prospective studies. [ABSTRACT FROM AUTHOR]

Human exposure to polycyclic aromatic hydrocarbons (PAHs) in indoor environments can be particularly relevant because people spend most of their time inside buildings, especially in homes. This study aimed to investigate the most important particle-bound PAH sources and exposure determinants in PM 2.5 samples collected in 19 homes located in northern Italy. Complementary information about ion content in PM 10 was also collected in 12 of these homes. Three methods were used for the identification of PAH sources and determinants: diagnostic ratios with principal component and hierarchical cluster analyses (PCA and HCA), chemical mass balance (CMB) and linear mixed models (LMMs). This combined and tiered approach allowed the infiltration of outdoor PAHs into indoor environments to be identified as the most important source in winter, with a relevant role played by biomass burning and traffic exhausts to be identified as a general source of PAHs in both seasons. Tobacco smoke exhibited an important impact on PAH levels in smokers' homes, whereas in the whole sample, cooking food and natural gas sources played a minor or negligible role. Nitrate, sulfate and ammonium were the main inorganic constituents of indoor PM 10 owing to the secondary formation of ammonium sulfates and nitrates. [ABSTRACT FROM AUTHOR]

Objective: To assess the longitudinal relationship of environmental tobacco smoke (ETS) exposure during midlife, and its interaction with active smoking, with the risk of late-diagnosis incident uterine fibroids during the menopausal transition.Design: Thirteen-year prospective cohort study.Setting: Not applicable.Patient(s): Community-based, multiracial/ethnic cohort of 2,575 women aged 42 to 52 years at baseline, undergoing the menopausal transition.Intervention(s): Questionnaire and blood draws.Main Outcome Measure(s): Discrete-time proportional odds models were used to estimate the conditional odds ratio (OR) and 95% confidence interval (CI) of incident fibroids, adjusted for menopausal status, race/ethnicity, study site, age, education, estradiol levels, sex hormone use, body mass index, timing of blood draw, age at menarche, alcohol use, and smoking status and pack-years.Result(s): As part of SWAN, at each near-annual study visit, ETS exposure, smoking, and fibroid occurrence were self-reported via questionnaire, and blood draws were collected. Women who were exposed to ETS (≥1 person-hour/week) had 1.28 (95% CI, 1.03, 1.60) times the adjusted odds of incident fibroids in the ensuing year compared the unexposed. The odds were elevated in never smokers (adjusted OR 1.34; 95% CI, 1.06, 1.70) and former smokers (adjusted OR 2.57; 95% CI, 1.05, 7.23).Conclusion(s): In midlife, ETS exposure was associated with an increased risk of late-diagnosis incident fibroids in women undergoing the menopausal transition. [ABSTRACT FROM AUTHOR]

Studies in environmentally controlled rooms have been used over the years to assess the impact of environmental tobacco smoke on indoor air quality. As new tobacco products are developed, it is important to determine their impact on air quality when used indoors. Before such an assessment can take place it is essential that the analytical methods used to assess indoor air quality are validated and shown to be fit for their intended purpose. Consequently, for this assessment, an environmentally controlled room was built and seven analytical methods, representing eighteen analytes, were validated. The validations were carried out with smoking machines using a matrix-based approach applying the accuracy profile procedure. The performances of the methods were compared for all three matrices under investigation: background air samples, the environmental aerosol of Tobacco Heating System THS 2.2, a heat-not-burn tobacco product developed by Philip Morris International, and the environmental tobacco smoke of a cigarette. The environmental aerosol generated by the THS 2.2 device did not have any appreciable impact on the performances of the methods. The comparison between the background and THS 2.2 environmental aerosol samples generated by smoking machines showed that only five compounds were higher when THS 2.2 was used in the environmentally controlled room. Regarding environmental tobacco smoke from cigarettes, the yields of all analytes were clearly above those obtained with the other two air sample types. Graphical abstractfx1Highlights· Selected indoor air quality methods were validated using accuracy profiles. · The impact of a novel Tobacco Heating System on these methods was assessed. · Environmental tobacco smoke and background air samples were also validated. · The methods were apt for the detection and quantification of 18 constituents in air. · Methods were applied for evaluating the impact of tobacco products on indoor air. Abbreviations [ABSTRACT FROM AUTHOR]

Objective: To evaluate exposure to tobacco, marijuana, and indoor heating/cooking sources in relation to antimüllerian hormone (AMH) levels.Design: Cross-sectional analysis in a sample of premenopausal women (n = 913) enrolled in the Sister Study cohort (n = 50,884).Setting: Not applicable.Patient(s): Women, ages 35-54 years at time of enrollment, with an archived serum sample and at least one intact ovary and classified as premenopausal.Intervention(s): Not applicable.Main Outcome Measure(s): Serum AMH (ng/mL) levels ascertained by ultrasensitive ELISA assay.Result(s): Lower AMH levels were associated with sources of indoor heating, including burning wood (-36.0%; 95% confidence interval [CI], -55.7%, -7.8%) or artificial fire logs (-45.8%; 95% CI, -67.2%, -10.4%) at least 10 times/year in a residential indoor stove/fireplace. Lower AMH levels were also observed in women who were current smokers of ≥20 cigarettes/day relative to nonsmokers (-56.2%; 95% CI, -80.3%, -2.8%) and in women with 10+ years of adult environmental tobacco smoke (ETS) exposure (-31.3%; 95% CI, -51.3%, -3.1%), but no associations were observed for marijuana use.Conclusion(s): We confirmed previously reported findings of lower AMH levels in current heavy smokers and also found associations for long-term ETS exposure and indoor burning of wood or artificial fire logs. These findings suggest that combustion by-products from common exposures can have toxic effects on the human ovary. [ABSTRACT FROM AUTHOR]

The aims of the present study was to investigate the role of Environmental Tobacco Smoke (ETS) exposure in domestic environment, the smoking policies adopted at home on urinary excretion of 23 trace elements present in tobacco and/or tobacco smoke (Li, Be, B, Ti, V, Cr, Mn, Co, Ni, Cu, Zn, Ga, Rb, Sr, Cd, Sn, Sb, Te, Cs, Tl, Pb, Bi, U) among a sample of healthy Italian school-aged children. The levels of monitored trace elements in urine samples from 110 children (5–11 years) living in a rural area and recruited in a cross-sectional study were measured via inductively coupled plasma mass spectrometry, while information regarding demographic characteristics and ETS exposure of the participants were obtained from questionnaires. Univariate elaborations evidenced that Co and Mn levels increased in children exposed to ETS in domestic environment, but multiple linear regression analyses revealed the independent effect of the habit of cohabitant(s) smoker(s) of smoking at home when children is present on urinary concentrations of Li, Ti, V, Co, Ga and Sr. Besides, we found significant gender- and age-dependency of some monitored elements: females presented higher Cu and Pb levels, but lower Rb levels respect to males, while age displayed a significant negative independent effect on the Cr, Co, Rb, and Sn concentrations, but positive on Ga levels. Finally, u-creatinine was a significant predictor for almost all the analytes, but not for Mn, Cd, Sb, Ga. [ABSTRACT FROM AUTHOR]

Data from National Health and Nutrition Examination Survey for 2005–2012 were used to study the trends and variability in the levels of urinary thiocyanate (u-SCN), perchlorate (u-P8), and nitrate (u-NO3) by gender, race/ethnicity, active smoking, and exposure to environmental tobacco smoke (ETS) at home for those aged 12–19 and ≥ 20 years old. For those aged ≥ 20 years, adjusted levels of u-SCN, u-P8, and u-NO3 (i) were lower for males than females (p < 0.01), and (ii) were higher for non-Hispanic white (NHW) than non-Hispanic black (NHB) (p < 0.01). Also, for those aged ≥ 20 years NHB had higher adjusted levels than Mexican American (MA) for u-SCN (p < 0.01) but NHB had lower adjusted levels than MA for u-P8 (p < 0.01) and u-NO3 (p < 0.01). For those aged 12–19 years, adjusted levels of u-SCN, u-P8, and u-NO3 did not vary by gender (p > 0.05), and adjusted levels of u-P8 and u-NO3 for NHB were lower than for NHW (p < 0.01) as well as higher for NHB than MA for u-SCN (p < 0.01) and lower for NHB than MA (p < 0.01) for u-P8 and u-NO3. Among those aged ≥ 20 years, active smoking was associated with higher adjusted levels of u-SCN (p < 0.01) in a dose-response manner and active smoking was associated with lower adjusted levels of u-P8 (p < 0.01) in a dose-response manner. Exposure to ETS was associated with higher adjusted levels of u-SCN (p = 0.02) and lower adjusted levels of u-P8 (p < 0.01) among ≥ 20 years old. Adjusted levels of u-P8 decreased over 2005–2012 among both 12–19 (p < 0.01) and ≥ 20 years old (p = 0.04). There was borderline increase in the adjusted levels of u-NO3 for those aged ≥ 20 years (p = 0.05) over 2005–2012. [ABSTRACT FROM AUTHOR]

Background Despite studies having consistently linked exposure to single-source polycyclic aromatic hydrocarbons (PAHs) to breast cancer, it is unclear whether single sources or specific groups of PAH sources should be targeted for breast cancer risk reduction. Objectives This study considers the impact on breast cancer incidence from multiple PAH exposure sources in a single model, which better reflects exposure to these complex mixtures. Methods In a population-based case-control study conducted on Long Island, New York ( N = 1508 breast cancer cases/1556 controls), a Bayesian hierarchical regression approach was used to estimate adjusted posterior means and credible intervals (CrI) for the adjusted odds ratios (ORs) for PAH exposure sources, considered singly and as groups: active smoking; residential environmental tobacco smoke (ETS); indoor and outdoor air pollution; and grilled/smoked meat intake. Results Most women were exposed to PAHs from multiple sources, and the most common included active/passive smoking and grilled/smoked food intake. In multiple-PAH source models, breast cancer incidence was associated with residential ETS from a spouse (OR = 1.20, 95%CrI = 1.03, 1.40) and synthetic firelog burning (OR = 1.29, 95%CrI = 1.06, 1.57); these estimates are similar, but slightly attenuated, to those from single-source models. Additionally when we considered PAH exposure groups, the most pronounced significant associations included total indoor sources (active smoking, ETS from spouse, grilled/smoked meat intake, stove/fireplace use, OR = 1.45, 95%CrI = 1.02, 2.04). Conclusions Groups of PAH sources, particularly indoor sources, were associated with a 30–50% increase in breast cancer incidence. PAH exposure is ubiquitous and a potentially modifiable breast cancer risk factor. [ABSTRACT FROM AUTHOR]

Objective The aim of the current study is to examine the association of environmental tobacco smoke (ETS) exposure evident by serum cotinine level, and diabetes mellitus in never smokers. Previous studies suggest that active tobacco cigarette smoking is associated with diabetes mellitus risk. However it is not clear if the low-level “background” ETS exposure is associated with diabetes among never smokers. Methods We present evidence from five independent replications based on the US nationally representative National Health and Nutrition Examination Surveys (NHANES) conducted 2003–12. Our exposure of interest is ETS exposure among never smokers, measured by serum cotinine levels (ng/mL), and our main outcome is diabetes mellitus assessed via self-reported physician-diagnosis, current use of insulin and/or oral hypoglycemic medications, plasma fasting glucose levels ≥ 126 mg/dL or glycohemoglobin levels ≥ 6.5%. The conceptual model encompassed age, sex, ethnic self-identification, education, poverty-income ratio, alcohol drinking, total cholesterol and body mass index. Results In never smokers, higher serum cotinine levels were positively associated with diabetes mellitus (the meta-analytic summary estimate is 1.2, 95% CI = 1.1, 1.2). This association was not evident among never smokers with cotinine levels below 3 ng/mL. Conclusions These replications help sustain evidence of ETS–diabetes mellitus association, which might be explained by shared psychosocial characteristics. Prospective studies with appropriate biomarkers are needed to further investigate this association. [ABSTRACT FROM AUTHOR]

Introduction: A growing number of jurisdictions have implemented smoke-free vehicles when children are present due to the substantial health effects of secondhand smoke (SHS). Prior studies on the prevalence of SHS exposure in vehicles have mainly focused on adolescents. This study examined the prevalence and socio-demographic correlates of SHS exposure in vehicles among Canadian adults.Methods: A repeated cross-sectional data on youth and adult data were drawn from the 2009-2012 Canadian Tobacco Use Monitoring Survey (n=58, 195). Multivariable logistic regression analysis was used to examine the socio-demographic correlates of exposure to SHS in vehicles.Results: Overall, 19% in 2009 and 18% in 2012 of adults reported SHS exposure in vehicles in the past month. Disparities in the SHS exposure prevalence were observed, with a higher SHS exposure among current smokers, former smokers, males, younger adults, living in a household with smoking-related exposure, and those with less education. The multivariable analyses showed significant associations between socio-demographic characteristics and SHS exposure. Higher odds SHS exposure was found for those younger (aged 20-24, OR=16.27, CI=11.09-23.88; 25-44, OR=6.12, CI=4.14-9.06; 45-64, OR=2.79, CI=1.95-4.02) compared to those aged 65 and over. Likewise, those with less education had greater odds of SHS exposure.Conclusions: Findings suggest that adults SHS exposure is high, especially for young adults and those with less education. Adult passengers may need protection from SHS given that no level of SHS exposure is safe. [ABSTRACT FROM AUTHOR]

Attention deficit hyperactivity disorder (ADHD) is caused by the interaction of genetic and environmental factors. The objective of this study was to examine the effects of prenatal exposure to alcohol and environmental tobacco smoke (ETS). Among the 30,552 parents who responded to a survey, the answers of 19,940 who replied to questions on prenatal exposure to ETS, alcohol consumption, and completed the DuPaul Rating Scale were analyzed. Results revealed that risk of ADHD significantly increased as a result of exposure to alcohol by 1.55 times (95% CI 1.33–1.82), maternal smoking during pregnancy by 2.64 times (95% CI 1.45–4.80), and paternal smoking during pregnancy by 1.17 times (95% CI 1.98–1.39). When the subjects whose mothers did not smoke during pregnancy were divided into 4 groups, the prevalence was 1.16 times higher (95% CI 1.02–1.33) in the group exposed to ETS but not alcohol, 1.19 times higher (95% CI 0.91–1.57) in the group exposed to alcohol but not ETS, and 1.58 times higher (95% CI 1.31–1.91) in the group exposed to ETS and alcohol. The differences between the groups were statistically significantly ( P <0.0001). This result shows that simultaneous exposure to ETS and alcohol during pregnancy increases the risk of ADHD. [ABSTRACT FROM AUTHOR]

The detection of nicotine, an organic tracer for Environmental Tobacco Smoke (ETS), in the collected PM 10 samples from Delhi region's ambient environment, in a appropriately designed investigation was initiated over four years (2006–2009) to: (1) Comprehend seasonal and inter-annual variations in the nicotine present in PM 10 ; (2) Extract regression based linear trend profile manifested by nicotine in PM 10 ; (3) Determine the non-linear trend timeline from the nicotine data, and compare it with the obtained linear trend; (4) Suggest the possible use of the designed experiment and analysis to have a qualitative appraisal of Tobacco Smoking activity in the sampling region. The PM 10 samples were collected in a monthly time-series sequence at a known receptor site. Quantitative estimates of nicotine (ng m −3 ) were made by using a Thermal Desorption Gas Chromatography Mass Spectrometry (TD-GC/MS). The annual average concentrations of nicotine (ng m −3 ) were 516 ± 302 (2008) > 494 ± 301 (2009) > 438 ± 250 (2007) > 325 ± 149 (2006). The estimated linear trend of 5.4 ng m −3 month −1 corresponded to 16.3% per annum increase in the PM 10 associated nicotine. The industrial production of India's tobacco index normalized to Delhi region's consumption, pegged an increase at 10.5% per annum over this period. [ABSTRACT FROM AUTHOR]

Introduction Environmental Tobacco Smoke (ETS) has been linked to numerous health problems. While research has demonstrated high prevalence of tobacco use among individuals receiving treatment for substance use disorders (SUDs), no studies have examined ETS among individuals receiving treatment for SUDs, paying specific attention to non-smokers who may be at risk for high exposure to ETS. Methods Participants (N = 261) enrolled in outpatient substance abuse treatment completed a survey, in which 14 items were used to quantify ETS exposure and smoking policies across several environments. Results Among smokers, 85% reported that their significant others also smoked as compared to 15% among non-smokers (χ 2 = 6.624, p < .05). A logistic regression examined the characteristics that predicted smoking in the home. The overall model was significant, (χ 2 = 36.046, p < .0005) with variables that independently predicted smoking in the home included having less than a high school diploma, being female, and living with a smoker. Income, age, and living with children were not found to be significant. Overall, 42% white collar workers 26% of service workers and 30% of blue collar workers reported no exposure to ETS. Sixty-seven percent of smokers strongly agreed or agreed that the hazards of secondhand smoke have been clearly demonstrated versus 58% of non-smokers. Conclusions Smokers and non-smokers enrolled in outpatient substance abuse treatment are frequently exposed to ETS at home, work, and in social settings. The dangers of ETS should be addressed among this population through education, smoke-free policies, and cessation resources, with help from their treatment facility. [ABSTRACT FROM AUTHOR]

Passive exposure to tobacco smoke is a global public health problem, while there are few data on public place monitoring and general population exposure assessment in central China. This study aimed to examine the levels of airborne nicotine (n = 256) in ten kinds of different public places in Wuhan, central China, and assess short-term and long-term smoke exposure in 340 non-smokers aged 18-67 who worked in these public places using tobacco biomarkers [i.e., cotinine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), respectively]. The highest median concentration of airborne nicotine (17.0 μg/m3) was observed in internet cafes, approximately 304-fold of the lowest value found in nurseries (55.9 ng/m3). Among the other studied public places, restaurants had the highest median concentrations (ng/m3) of airborne nicotine (3,120), followed by subway stations (810), hotels (624), government officess (286), middle schools (269), health institutions (268), public institutions (190), and primary schools (140). Urinary cotinine and NNAL were found in almost all the participants, and the highest concentrations were found in non-smokers from the internet cafes [specific gravity (SG)-corrected urinary median concentrations: 23.1 ng/mL, geometric mean (GM): 24.1 ng/mL, range: 0.62-1679 ng/mL] for cotinine and 104 pg/mL (GM: 97.6 pg/mL, range: 32.3-236 pg/mL) for NNAL, respectively]. Urinary cotinine concentrations in male non-smokers (median: 2.02 ng/mL) were significantly higher than those in female non-smokers (1.44) (P < 0.01). Participants aged 18-27 were detected with the highest urinary cotinine and NNAL concentrations. Urinary cotinine and NNAL concentrations were significantly correlated with daily and monthly working hours, respectively. Besides, a positive correlation was observed between log-transformed urinary concentrations of cotinine and NNAL (r = 0.32, P < 0.001). This is the first time to report matched data on airborne nicotine and urinary cotinine/NNAL among employees in different public places. This study demonstrated ubiquitous exposure to environmental tobacco smoke in the studied public places. [ABSTRACT FROM AUTHOR]

Atopic dermatitis (AD) is a chronic relapsing inflammatory skin disease and a growing health concern, especially in children, because of its high prevalence and associated low quality of life. Genetic predisposition, environmental triggers, or interactions between them contribute to the pathophysiology of AD. Therefore, it is very important to identify and control risk factors from the environment in susceptible subjects for successful treatment and prevention. Both indoor and outdoor air pollution, which are of increasing concern with urbanization, are well-known environmental risk factors for asthma, whereas there is relatively little evidence in AD. This review highlights epidemiologic and experimental data on the role of air pollution in patients with AD. Recent evidence suggests that a variety of air pollutants, such as environmental tobacco smoke, volatile organic compounds, formaldehyde, toluene, nitrogen dioxide, and particulate matter, act as risk factors for the development or aggravation of AD. These air pollutants probably induce oxidative stress in the skin, leading to skin barrier dysfunction or immune dysregulation. However, these results are still controversial because of the low number of studies, limitations in study design, inaccurate assessment of exposure and absorption, and many other issues. Further research about the adverse effects of air pollution on AD will help to expand our understanding and to establish a better strategy for the prevention and management of AD. [ABSTRACT FROM AUTHOR]

The use of biomarkers permits the detection of smoking having taken place in an environment. However, no single biomarker is able to differentiate clearly between different types of environments. Multivariate classification models have helped us to differentiate between outdoors, non-smoking indoors, well ventilated smoking indoors, and smoking environments without good air exchange. We found that the variables that enabled us to classify environments most accurately were indoor temperature, 2,5-dimethylfuran and ethyltoluene. A successful prediction rate of 86.5% was obtained by applying both direct fitting and cross validation discriminant (leave-one-out) analyses. Our results show that although a good air exchange ratio decreases the levels of volatile organic compounds in indoor air due to tobacco smoke, significant contamination still remains. [ABSTRACT FROM AUTHOR]

Environmental tobacco smoke, inhaled by active firsthand smokers and their entourage, is associated with morbidity and mortality. Many children are passively exposed to secondhand smoke worldwide. Infants and young children account for the largest global disease burden associated with prenatal and postnatal secondhand smoke, probably due to underdeveloped neurological, immune, and respiro-circulatory systems. There is an increasingly robust association between tobacco smoke exposure, before and after birth, and executive function problems in children, adding to current and future disease burden estimates in public health. This review summarizes research advancements which address the link between environmental tobacco smoke and the development of attention deficits and hyperactive behavior, both as symptoms and as part of a mental health disorder in childhood. The multiple effects of tobacco smoke inhalation are best understood in terms of disruptions in normative processes involving cellular communication, structural development, and epigenetic influences which have the potential to become intergenerational. It is concluded that public health efforts be directed toward increasing parental awareness and compliance with existing guidelines that recommend no safe level of exposure. [ABSTRACT FROM AUTHOR]

Abstract: Objectives: Smoking plays major role in development of vascular and respiratory serious diseases. It has been reported that negative smoker children are prone for conductive hearing impairment due to repeated attacks of Eustachian tube dysfunction and middle ear effusion. This study aims to identify negative smoking as potential risk factor for development of sensorineural hearing loss. Study: This study was done between January 2010 and November 2012. 411 children aged 5-11 years (8.2±1.5) participated in this study; they were children attending the Ear, Nose, and Throat clinic of a tertiary care hospital and their siblings. The inclusion criteria were: (i) normal speech and language, (ii) absence of any disease or condition that may cause sensorineural hearing loss, and (iii) normal middle ear function on the day of hearing assessment. They were divided into three groups according to the exposure to second-hand smoke at home; group of “no exposure” whereas no smoker in the family (131 children), group of ‘mild exposure” whereas the father was the only smoking parent and smoking was prohibited at home (155 children), and group of “heavy exposure”, whereas the mother was smoking, or the father was freely smoking at home and in the presence of his children (125 children). Audiological evaluation in the form of pure tone and speech audiometry and immitancemetry was done for the study group. Results: Audiological evaluation revealed that the prevalence of hearing loss was 3.8%, 4.5% and 12% in the “no exposure”, “mild exposure”, and “heavy exposure” groups, respectively. Significant difference was only detected between the high exposure group and the other two groups. All children had minimal sensorineural hearing loss, i.e. threshold of frequencies showing hearing loss was 20 or 25dB HL. The risk ratios (95% confidence interval) for hearing loss in the study subgroups were 1.18 (0.38, 3.64) for mild exposure group (p >0.05), 3.14 (1.18, 8.3) for heavy exposure group (p <0.05). Conclusions: Passive smoking in childhood correlates with sensorineural hearing loss, and it is an important risk factor for development of minimal hearing loss. Strict prevention of children exposure to second-hand smoke should be encouraged by every mean. [Copyright &y& Elsevier]

Background/Purpose: Cigarette smoking, exposure to secondhand smoke, and arsenic exposure are well known risk factors for developing urothelial carcinoma (UC). We investigated the combined effects of cigarette smoking, exposure to secondhand smoke, and the presence of urinary total arsenic on the risk of developing UC. Methods: We conducted a hospital-based, case–control study involving 261 UC patients and 672 cancer-free control individuals between September 2002 and May 2009. Results: Individuals who had smoked <100 cigarettes in their lifetime (never smokers) and had a high urinary total arsenic level (≥15.40 μg/g creatinine), and those who had smoked >100 cigarettes in their lifetime (ever smokers) and had a high urinary total arsenic level, had increased risks of developing UC (3.20-fold and 6.45-fold greater), respectively, compared to individuals who were never smokers and had a low urinary total arsenic level. Individuals who had high urinary total arsenic levels and had been exposed to secondhand smoke, and individuals with high urinary arsenic levels who had not been exposed to secondhand smoke, had increased chances (2.71-fold and 5.00-fold greater, respectively) of developing UC, compared to individuals who were not exposed to secondhand smoke and had low urinary total arsenic levels. Ever smokers who had been exposed to secondhand smoke and had a high urinary total arsenic level had the greatest increased risk for developing UC (10.82-fold greater). Conclusion: Individuals in a Taiwanese population who smoked cigarettes, were exposed to secondhand smoke, and a high urinary total arsenic level, had a significant risk for developing UC. [Copyright &y& Elsevier]

Abstract: Background: Over one-third of all children live with at least one parent who smokes cigarettes, which is associated with compromised child health. The impact of secondhand smoke exposure (SHSe) in medically fragile infants born prematurely is likely to be much higher. The Baby's Breath II study tests whether a hospital-initiated, motivational-enhancement program will result in less SHSe relative to conventional care in high-risk, low birthweight (LBW) infants discharged from a neonatal intensive care unit (NICU). The design and protocol for the ongoing BBII trial is described. Methods/design: Eligible participants are: (1) primary caregivers (typically mothers) of NICU infants who were born at LBW (<2500g) or ventilated for more than 12h; and (2) who smoke or live with at least one smoker. This randomized controlled trial has two conditions: Motivational interviewing plus incentives (MI+) and conventional care (CC). MI+ participants receive two hospital-based and two home-based counseling sessions, as well as incentives (i.e., prize-based draws) for (a) intervention attendance and (b) biochemical validation (i.e., urine cotinine dipstick) indicative of low or no infant SHSe. Participants in the control group receive conventional education-based care. Assessments are completed at baseline, mid-point, and 1- and 4-months post-intervention. Discussion: This study is the first to determine the efficacy of a brief intervention for reducing SHSe among high-risk, LBW infants discharged from a NICU, with the potential for saving lives and healthcare costs. Strengths, limitations and challenges to the conduct of this trial are discussed. [Copyright &y& Elsevier]

There is uncertainty in the risk of pancreatic cancer with particular aspects of smoking, such as a dose–response relationship and cumulative amount, in Japanese men and women. Very few studies have addressed the role of passive smoking in pancreatic cancer among Japanese women. We examined the association between active or passive smoking and the risk of death from pancreatic cancer using data from the Japan Collaborative Cohort Study. The cohort participants (46,395 men and 64,190 women) were followedup for mortality from baseline (1988–1990) through December 31, 2009. Cox proportional hazards regression models were used to estimate relative risks (RR) and 95% confidence intervals (CI). During follow-up, we recorded 611 pancreatic cancer deaths. After adjustment for potential confounding factors, current smokers had a significantly increased risk of death from pancreatic cancer compared with non-smokers, with an RR of 1.70 (95% CI: 1.33–2.19). The risk of death from pancreatic cancer significantly increased with increasing numbers of cigarettes smoked per day. Exposure to environmental tobacco smoke (ETS) in public spaces was not associated with risk of death from pancreatic cancer. The RR for women who reported ETS exposure was 1.20 (95% CI: 0.87–1.67). Women exposed to ETS during childhood or adolescence had 1.21-fold increased risk, but the association was statistically insignificant. Cigarette smoking is associated with an approximately 70% increase in the risk of death from pancreatic cancer. Further studies with improved exposure assessment are needed to better quantify the association between passive smoking and pancreatic cancer. [ABSTRACT FROM AUTHOR]

Summary: Objectives: To examine the relationship between cigarette smoking and incidence and mortality rates of pulmonary tuberculosis (TB) and treatment outcomes. Materials: From 1995 to 2010, we analyzed data from 1062 patients with TB and from 2001 to 2004, 2951 contacts in Southern Mexico. Patients with acid-fast bacilli or Mycobacterium tuberculosis in sputum samples underwent epidemiological, clinical and mycobacteriological evaluation and received treatment by the local DOTS program. Results: Consumers of 1–10 (LS) or 11 or more (HS) cigarettes per day incidence (1.75 and 11.79) and mortality (HS, 17.74) smoker–non-smoker rate ratios were significantly higher for smokers. Smoker population was more likely to experience unfavorable treatment outcomes (HS, adjusted OR 2.36) and retreatment (LS and HS, adjusted hazard ratio (HR) 2.14 and 2.37). Contacts that smoked had a higher probability of developing active TB (HR 2.38) during follow up. Conclusions: Results indicate the need of incorporating smoking prevention and cessation, especially among men, into international TB control strategies. [ABSTRACT FROM AUTHOR]

Abstract: A method with atmospheric pressure chemical ionization tandem mass spectrometry (APCI-MS/MS) was developed and applied to direct analysis of Environmental Tobacco Smoke (ETS), using 3-ethenylpyridine (3-EP) as a vapour-phase marker. In this study, the ion source of APCI-MS/MS was modified and direct analysis of gas sample was achieved by the modified instrument. ETS samples were directly introduced, via an atmospheric pressure inlet, into the APCI source. Ionization was carried out in positive-ion APCI mode and 3-EP was identified by both full scan mode and daughter scan mode. Quantification of 3-EP was performed by multiple reaction monitoring (MRM) mode. The calibration curve was obtained in the range of 1–250 ng L−1 with a satisfactory regression coefficient of 0.999. The limit of detection (LOD) and the limit of quantification (LOQ) were 0.5 ng L−1 and 1.6 ng L−1, respectively. The precision of the method, calculated as relative standard deviation (RSD), was characterized by repeatability (RSD 3.92%) and reproducibility (RSD 4.81%), respectively. In real-world ETS samples analysis, compared with the conventional GC–MS method, the direct APCI-MS/MS has shown better reliability and practicability in the determination of 3-EP at trace level. The developed method is simple, fast, sensitive and repeatable; furthermore, it could provide an alternative way for the determination of other volatile pollutants in ambient air at low levels. [Copyright &y& Elsevier]

Background: Exposure to tobacco smoke is a well-known risk factor for childhood asthma and reduced lung function, but the effect on airway inflammation in preschool-aged children is unclear. Objective: To examine the effect of parental smoking on lung function and fractional concentration of exhaled nitric oxide (Feno) in relation to both parental reports and children''s urine cotinine concentrations in preschool-aged children with multiple-trigger wheeze. Methods: A total of 105 3- to 7-year-old children with multiple-trigger wheeze and lung function abnormalities were recruited. Lung function was assessed by impulse oscillometry, and Feno measurements were performed. Exposure to tobacco smoke was determined by parental reports and measurement of children''s urinary cotinine concentrations. Results: Forty-three percent of the children were exposed to environmental tobacco smoke according to parental reports. The Feno level was significantly higher in children with a smoking mother (n = 27) than in children with a nonsmoking mother (23.4 vs 12.5 ppb, P = .006). The Feno level expressed as z score and the cotinine level correlated significantly (P = .03). Respiratory resistance at 5 Hz was higher in children exposed to maternal smoking than in others (0.99 vs 0.88 kPas/L, P = .005). Urinary cotinine concentrations reflected well parental reports on their daily smoking and increased relative to the number of cigarettes smoked in the family (P < .01). Atopy was found in 75% of the children, but it was not associated with the Feno value (P = .65). Conclusion: Maternal smoking was associated with increased Feno value and poorer lung function in steroid-naive preschool children with multiple-trigger wheeze. Larger controlled trials are needed to generalize the results. [Copyright &y& Elsevier]

Abstract: Given the widespread incidence of smoking as well as its deleterious health effects, it is crucial to examine practical and cost effective prognostic markers assessing its health impact. Heart rate variability (HRV) is a straightforward and cost effective technique to foresee health problems of cardiovascular nature and may be used to predict in advance smoking-induced health effects. In this review we evaluate the existing biological evidence regarding the effects of smoking on HRV and their associated cardiovascular consequences. In addition, we summarize fundamental information on the various HRV indicators and their diagnostic significance in relation to heart failure. An in depth analysis of the various HRV indices characterizing changes in the activation of the autonomic nervous system is provided together with a critical evaluation of all evidence published to date on the influence of chronic and acute active and passive smoking on HRV. Overall, the vast majority of published evidence suggests that acute and chronic active and passive smoking generate marked disruptions in the normal autonomic nervous system functioning characterized by increased sympathetic drive and reduced HRV and parasympathetic modulation. The proposed mechanisms that may generate this smoke-induced HRV reduction as well as its clinical implications are thoroughly evaluated. [Copyright &y& Elsevier]

Abstract: Fine particulate matter samples were collected in an urban ambient fixed site and, outside and inside residencies in Athens greater area, Greece. n-Alkanes, iso/anteiso-alkanes and polycyclic aromatic hydrocarbons (PAHs) were identified by gas chromatography and mass spectrometry. The values of concentration diagnostic ratios indicated a mixture of vehicular emissions, fuel evaporation, oil residues and environmental tobacco smoke (ETS) in outdoor and indoor samples. Particulate iso/anteiso-alkanes, specific tracers of ETS, were detected in both non-smoking and smoking households. The indoor-to-outdoor ratios of particulate iso/anteiso-alkanes and unresolved complex mixture (a tracer of outdoor air pollution) in non-smoking households were comparable to the measured air exchange rate. This suggested that penetration of outdoor air was solely responsible for the detection of tobacco smoke particulate tracers in indoor non-smoking environments. Overall, residential outdoor concentrations accounted for a large fraction (from 25 up to 79%) of indoor aliphatic and polyaromatic hydrocarbons. Open windows/doors and the operation of an air condition unit yielded also in higher indoor concentrations than those measured outdoors. [Copyright &y& Elsevier]

Abstract: Prolactin (PRL) and thyroid stimulating hormone (TSH) serve important roles in the reproductive and other systems. Active smoking is associated with changes in PRL and TSH secretion, but the relationship between secondhand tobacco smoke (STS) exposure and these hormones is unclear. We measured PRL and TSH in serum as well as cotinine in follicular fluid (to estimate STS exposure) among 314 nonsmoking women undergoing in vitro fertilization treatment. We observed a significant increase in PRL concentrations (p =0.03) among STS-exposed nonsmokers compared to unexposed nonsmokers. There was no significant difference in TSH concentration (p >0.4) among those exposed to STS compared to those who were unexposed. STS exposure is associated with an increase in circulating PRL but not TSH levels. Future studies are needed to confirm our results, identify biological mechanisms involved, and better understand the potential clinical and public health implications. [Copyright &y& Elsevier]

Abstract: The World Health Organisation called for research assessing the safety of electronic cigarette (e-cigarette). We evaluated the acute effect of active and passive e-cigarette and tobacco cigarette smoking on complete blood count (CBC) markers in 15 smokers and 15 never-smokers, respectively. Smokers underwent a control session, an active tobacco cigarette smoking session, and an active e-cigarette smoking session. Never-smokers underwent a control session, a passive tobacco cigarette smoking session, and a passive e-cigarette smoking session.The results demonstrated that CBC indices remained unchanged during the control sessionand the active and passive e-cigarette smoking sessions (P >0.05). Active and passive tobacco cigarette smoking increased white blood cell, lymphocyte, and granulocyte counts for at least one hour in smokers and never smokers (P <0.05).It is concluded that acute active and passive smoking using the e-cigarettes tested in the current study does not influence CBC indices in smokers and never smokers, respectively. In contrast, acute active and passive tobacco cigarette smoking increase the secondary proteins of acute inflammatory load for at least one hour. More research is needed to evaluate chemical safety issues and other areas of consumer product safety of e-cigarettes, because the nicotine content in the liquids used may vary considerably. [Copyright &y& Elsevier]

Abstract: Environmental tobacco smoke (ETS) is an air pollutant with a relevant impact on public health. In addition, ETS is a significant stimulus that may elicit different responses depending on previous experience and current status regarding smoking. Exposure to cigarette cues has been shown to be a reliable method for inducing subjective and physiological responses. However, the role of ETS as a stimulus has not received, to date, enough attention in the research literature. This study aimed to analyse both the autonomic and subjective responses of smokers and non-smokers to exposure to ETS. To that end, 41 non-smokers and 57 smokers were exposed to ETS, in a controlled laboratory setting. We measured the subjective perception of smoke, unpleasantness, heart rate and skin conductance to compare the reactions of smokers and non-smokers to ETS. Additionally, subjective tobacco craving after exposure was assessed for current smokers. We found different psychophysiological responses to ETS exposure for smokers and non-smokers. Smokers showed a generalised increase in autonomic activity, significantly greater than that of non-smokers. In addition, heart rate increase during exposure to ETS was positively correlated with subjective craving. Our data suggested that ETS was an important stimulus and acted as a relevant cue for smokers; it induced both psychophysiological reactions and subjective craving. Hence, this kind of stimulus within the cue-reactivity research paradigm may be useful for studying the effect of ETS on smokers'' reactions, craving, quitting attempts, or relapse probabilities. [Copyright &y& Elsevier]