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In this study, we assessed trends of serum cotinine levels over time among US children ages 3-11 years and compared the risk of asthma in groups exposed to passive tobacco smoke. We utilized National Health and Nutrition Examination Survey (NHANES) data collected from 2003 to 2014 (n = 8064). Serum cotinine level, household smoker status, asthma status, and sociodemographic information were extracted for multiple regression analyses. The adjusted biannual change in log (cotinine) in comparison to earlier NHANES survey cycles was - 0.196 (p 0.001) overall, - 0.055 (p = 0.089) among children with household smoker(s), and - 0.129 (p 0.001) among children without. The proportion of children living with household smokers decreased from 24.9% in the 2003-2004 cycle to 11.4% in the 2013-2014 cycle. The adjusted odds ratios (ORs) for asthma were 1.34 (95% confidence interval (CI): 1.00-1.80; 2nd tertile vs 1st tertile) and 1.69 (95%CI: 1.25-2.29; 3rd tertile vs1st tertile), respectively. Highly exposed asthmatic children, in the 3rd cotinine tertile (0.13 ng/mL), were primarily Non-Hispanic Black (61.0%) and whose family incomes were below poverty guidelines. Overall results reveal passive smoke exposure level among children ages 3-11 in the US decreased over the study period. Nevertheless, higher exposure to passive smoke is still associated with higher odds of childhood asthma. Targeted smoking cessation interventions in clinical practices are needed to reduce tobacco smoke exposure and related asthma risk in children, particularly in low-income and minority groups.

Chronic Bronchitis is a common condition which is characterized by persistent cough, with expectoration for at least three months of the year for t wo consecutive years. It is more prevalent these days because of the exposure to both active and passive smoke, air pollution, occupational hazards etc; Prevalence is directly related to that of tobacco chewing, smoking and excess usage of biomass fuels es pecially in low and middle income countries. Current estimate suggest that 80 million people worldwide suffer from moderate to severe chronic obstructive bronchitis. In India this is the second most common disorder after pulmonary tuberculosis. Kaphaja Kas a, a Vata Kapha pradhana pranavaha srotovikara, bears a greater resemblance with Chronic Bronchitis. In the present situation as there is a need to come up with a more comprehensive, economical and safe medication, a clinical observational study was conduc ted to evaluate the combined effect of Pippalyadi Qwatha, Shatyadi leha and Vasa Swarasa in the management of chronic bronchitis. Total 50 patients were incidentally selected and assigned into single group. All patients were administered with Pippalyadi qw atha, Shatyadi leha and Vasa Swarasa for 48 days. Data was collected on 0 day, 15 th day, 30 th day and 48 th day of study period. Results were statistically analyzed before and after the treatment. Combined effect of drugs showed statistically highly signifi cant results with 'P' value 0.000. Overall assessment showed marked relief in 22 patients followed by 26 patients with Moderate relief and 2 patients with no relief.

PurposeThis paper aims to explore the beliefs and attitudes of young mothers in relation to smokefree homes and passive smoke in Guernsey, and to encourage them to contribute to the designing of a smokefree home leaflet and pack aimed at young mothers.Design/methodology/approachSemi‐structured interviews were conducted with 11 participants (aged 17‐23 years).FindingsMost participants were smokers, however, they all knew what passive smoke was and asserted that their homes were smokefree. Even if they were unable to list specific impacts of second hand smoke on children, they all agreed that children should be protected. A few of them described the difficulties in telling people not to smoke around their children in other people's homes and in cars. Moreover, some young mothers said that they found it hard to persuade their partners not to smoke around the children.Originality/valueThis paper presents the respondents ideas for promoting and supporting smokefree homes for young mothers and informing a smokefree home leaflet and home pack: providing information about passive smoking during parenting sessions, preferably after the baby has been born; giving parents a pack with giveaways linked to smokefree homes; encouraging parents to be assertive to friends and family who try to smoke around children; and getting both partners involved.

Although active smoking is known to enhance platelet thromboxane production, no data on passive smoking are available yet. In an 18 m3 room, the influence of single and repeated exposure to passive smoke for 60 minutes was assessed in nonsmokers and smokers. Smokers and nonsmokers were matched for sex and age. All the evaluated parameters (plasma TXB2, serum TXB2, malondialdehyde, 11-dehydro-TXB2, conversion of exogenous arachidonic acid to hydroxy-5,8,10-heptadecatrienoic acid, and TXB2) were higher in smokers than nonsmokers at baseline conditions, immediately and 6 hours after passive exposure to cigarette smoke. Repeated exposure of nonsmokers rendered their platelets more activated, so they became closer to the behavior of smokers. Contributing to the development of hemostatic imbalance, these results indicate that passive smoking may enhance thromboxane A2 release from the platelets.

Summary We document the main risk factors that determine children’s exposure to passive smoke, and we use econometric techniques to provide a new economic quantification of the effect of this exposure on child health. One of our main contributions is the use of a large nationally representative sample of children drawn from the Health Survey for England, for whom we match parental and household smoking and demographic characteristics. We use an objective measure of children’s exposure, namely the level of cotinine in their saliva. We find that both parental and child carer smoking behaviour are major risk factors in determining children’s exposure to passive smoke. For a child who is exposed to a high number of passive smoking risk factors, the income equivalence of such exposure is £16000 per year. Finally, comprehensively controlling for child passive smoking does not explain the observed gradient between household income and parental-reported child health in England.

Purpose The aim of the study was to investigate the effect of cigarette smoke on the auditory tube and middle ear mucosa after long-term exposure (4 and 6 months). Materials and methods Fifteen rats were divided into 3 groups. The experimental groups were exposed to cigarette in a smoking chamber for 4 and 6 months (n = 5 each). A control group (n = 5) was placed in the same chamber without exposure to cigarette smoke. Histologic changes of the auditory tube mucosa were observed through light and electron microscopes. Histologic changes of the middle ear mucosa were also observed through light microscopes. Results The histologic changes consisted of a proliferation of goblet cells and an increase of mucus secretion in auditory tube. Squamous metaplasia was paradoxically decreased according to the duration of exposure in auditory tube. The number of goblet cell was gradually increased according to the duration of exposure in the auditory tube and middle ear. Conclusions Long-term passive smoke directly affects the auditory tube and middle ear mucosa. Histologic changes of auditory tube mucosa consisted of goblet cell proliferation and excessive mucus secretion.

Introduction Active smoking and exposure to passive smoke are responsible for numerous adverse pregnancy outcomes for women and their infants. The aim of this study was to explore the perceptions, attitudes, patterns of personal tobacco use and exposure to environmental smoke among a sample of pregnant women in Greece. Material and Methods A cross sectional survey was undertaken of 300 women identified from the perinatal care records of the Maternity Departments of two hospitals in Athens between February 2013 and May 2013. Data on active and passive maternal smoking status in the first, second, and third trimesters of pregnancy, fetal and neonatal tobacco related complications, exposure to environmental tobacco smoke during pregnancy, quit attempts, behaviors towards avoiding passive smoking and beliefs towards smoking cessation during pregnancy were collected using self-administered questionnaires on the 3rd postnatal day. Women also completed the Edinburgh Postnatal Depression Scale (EPDS). Results Of 300 women recruited to the study 48 % reported tobacco use during the first trimester of pregnancy. Amongst participants who were tobacco users, 83.3 % reported making an attempt to quit but less than half (45.1 %) were successful. Among women who continued to smoke during pregnancy the majority (55.8 %) reported that they felt unable to quit, and 9.3 % reported that they considered smoking cessation was not an important health issue for them. Participants who continued to smoke during pregnancy were more likely to report fetal (χ2 = 11.41; df = 5; p

PURPOSE A colorectal adenoma (CRA) is a well-defined precursor to colorectal cancer (CRC). Additionally, smoking is a potent risk factor for developing a CRA, as well as CRC. However, the association between exposure to environmental tobacco smoke (ETS) and the risk for developing a CRA has not yet been fully evaluated in epidemiologic studies. We performed a cross-sectional analysis on the association between exposure to ETS at the workplace and the risk for developing a CRA. METHODS The study was conducted on subjects who had undergone a colonoscopy at a health promotion center from January 2012 to December 2012. After descriptive analyses, overall and subgroup analyses by smoking status were performed by using a multivariate logistic regression. RESULTS Among the 1,129 participants, 300 (26.6%) were diagnosed as having CRAs. Exposure to ETS was found to be associated with CRAs in all subjects (fully adjusted odds ratio [OR], 1.95; 95% confidence interval [CI], 1.08-2.44; P = 0.001). In the subgroup analysis, exposure to ETS in former smokers increased the risk for developing a CRA (fully adjusted OR, 4.44; 95% CI, 2.07-9.51; P < 0.001). CONCLUSION Exposure to occupational ETS at the workplace, independent of the other factors, was associated with increased risk for developing a CRA in all subjects and in former smokers. Further retrospective studies with large sample sizes may be necessary to clarify the causal effect of this relationship.

SummaryFew studies have demonstrated the pathologic reactions yielded by smoke inhalation on the airway in rats. Aim: The aim of this study was to analyze the possible histopathological effects produced by chronic cigarette smoke inhalation on the vocal folds of rats. Study design: Experimental. Material and Method: 36 male rats (Rattus norvergicus Wistar strain), aged 60 days, were kept in cages and exposed to inhalation of the smoke produced by 10 cigarettes lit 3 times a day, 7 days a week, for periods of 25, 50 and 75 days, and their respective controls. Thereafter the animals were killed and their larynxes were dissected and submitted to histological processing for achievement of histological sections, which were stained with Hematoxylin and Eosin and analyzed by light microscopy. Results: The rats exposed to smoke displayed smaller (p< 0,05) body mass than the control group. There was hyperplasia and squamous metaplasia in the free edge of the vocal fold and squamous hyperplasia on the middle portion of the vocal fold in all 3 study periods. Moreover, the 50-day group revealed keratinizing metaplasia in this area. Morphological alterations in other areas of the larynx and inflammatory reaction of the lamina propria were also not observed. Conclusion: It was concluded that the passive inhalation of cigarette smoke yields important morphological changes in the vocal fold epithelium, which may progress to neoplasia.

It is unknown if teenagers and caregivers give similar responses when interviewed about the teen's asthma. We analyzed data for 63 urban African-American teen-caregiver pairs. Caregivers underestimated teen smoking by 30%, gave lower estimates for teen exposure to passive smoke, and disagreed with teens on controller medication usage. Teen-caregiver responses were not significantly different for estimates of symptom-days, activity limitations, or nights awakened; nor were they significantly different for report of emergency department visits or hospitalizations. Agreement was weak for perceived asthma control and severity. Teen-caregiver agreement on asthma depends on the type of information being sought.

Background: Guidelines advocate the use of spirometry to assess lung function in asthmatic. Inhaled corticosteroid(ICS) therapy is a mainstay of treatment for asthma, but the clinical response is variable. Aim: To assess the time variation of FEV1% in treated children with Persistent Asthma (PA). Methods: 110 children with PA, with two visits between September 2011 and December 2014 at the IBIM pediatric clinic were studied. Spirometry was performed using Pony FX, Cosmed, Italy; values were expressed as %pred using GLI-2012equation. The time trend of FEV1% for each subject was estimated through separate regressions. A linear regression model for the individual slopes (FEV1% average month variations) with respect to the intercepts (initial FEV1% values) was estimated. For the 71 children which had a FEV1%

Nitric oxide (NO) is produced and detected in the exhalate from the respiratory tract where it plays important regulatory functions. Exhaled nitric oxide (eNO) concentrations are reduced in active cigarette smokers between cigarettes and in nonsmoking subjects during short-term exposure to environmental tobacco smoke. In this study, the authors evaluated eNO before and after an acute exposure to environmental tobacco smoke in healthy, nonsmoking subjects (n = 12). Baseline eNO levels were measured by chemiluminescence at baseline (1 hr before exposure), shortly after the end of exposure, and 10 and 30 min after the end of exposure. Mean room air NO concentration increased from 3 ppb to 4 ppm (range, 560 ppb-8.5 ppm) during the exposure period. Carboxyhemoglobin levels were assessed before and after the exposure with spectrophotometry. All subjects had decreased eNO with exposure to environmental tobacco smoke (mean +/- standard error of the mean: 16.65 +/- 1.35 ppb to 13.86 +/- 1.33 ppb; p.001). These concentrations remained significantly decreased at 10 min and recovered within 30 min. No modifications in airway resistance or increase in carboxyhemoglobin levels were observed. Exposure to environmental tobacco smoke transiently--but consistently--decreased eNO concentration in healthy, nonsmoking subjects, suggesting that second-hand smoke can directly affect NO in the airway environment.

The first generation of studies evaluating the association between exposure to tobacco smoke and breast cancer merely compared active to nonactive smokers, with varying degrees of detail in the definition of active smoking. With rare exceptions, studies of this kind failed to show an effect of smoking on breast cancer risk. However, such analysis is probably insufficient. The most recent reports on the smoking-breast cancer connection have two characteristics. Some have separated women exposed to passive smoking from those nonexposed to either active or passive smoke. Other reports have focused on factors that modify the effect of smoking on breast cancer incidence, such as genetic markers or hormone receptors. A minority of reports combines these two characteristics. This review addresses the epidemiologic evidence for a link between smoking and breast cancer and discusses the implications of this evidence for future studies.

The present study was performed to investigate the effect of oltipraz on passive smoke-induced alteration in renal glyoxalase system of rats. Adult Sprague-Dawley rats were exposed daily to passive cigarette smoke in a whole-body exposure chamber 6 h per day for 2, 4 and 12 weeks. The animals being sacrificed after 2 and 12 weeks were maintained on control diet, powdered 4% Teklad rat chow (Harlan Teklad, Madison, WI, USA). The 4 weeks group was divided into three subgroups, one receiving control diet, other two receiving control diet supplemented with two doses of oltipraz (either 167 or 500 ppm), starting 1 week prior to initiation of smoke exposure until the end of the experiment. The activity of glyoxalase I was higher in animals exposed for 4 and 12 weeks of passive smoke than those exposed for 2 weeks. There was no significant difference between 4 and 12 weeks. Glyoxalase II activity was lower in animals exposed to passive smoke for 4 weeks than those exposed for 2 weeks. However, the activity approached the basal level after 12 weeks of exposure. Furthermore, oltipraz treatment maintained the activity of both glyoxalase closer to the basal levels.

Asthma is a common chronic multifactorial disease that affects >300 million people worldwide. Outdoor and indoor pollution exposure has been associated with respiratory health effects in adults and children. Smoking still represents a huge public health problem and millions of children suffer the detrimental effects of passive smoke exposure. This study was designed to review the current evidences on exposure to passive smoke as a risk factor for asthma onset in childhood. A review of the most recent studies on this topic was undertaken to provide evidence about the magnitude of the effect of passive smoking on the risk of incidence of asthma in children. The effects of passive smoking are different depending on individual and environmental factors. Environmental tobacco smoke (ETS) is one of the most important indoor air pollutants and can interact with other air pollutants in eliciting respiratory outcomes during childhood. The increased risk of respiratory outcomes in children exposed to prenatal and early postnatal passive smoke might be caused by an adverse effect on both the immune system and the structural and functional development of the lung; this may explain the subsequent increased risk of incident asthma. The magnitude of the exposure is quite difficult to precisely quantify because it is significantly influenced by the child's daily activities. Because exposure to ETS is a likely cause for asthma onset in childhood, there is a strong need to prevent infants and children from breathing air contaminated with tobacco smoke.

5 million people in the world die of active smoking and more than 600 000 nonsmokers die from exposure to passive smoke annually [1]. Smoking is recognised as one of the major preventable causes of death. It significantly increases the chances of developing a respiratory disorder and over half of respiratory disease-related deaths are due to smoking [2],[3]. One of the key points in the fight against the tobacco epidemic is to encourage as many smokers as possible to quit [4]. The emergence of electronic nicotine delivery systems (ENDS), or electronic (e)-cigarettes, presents complex considerations in this context. E-cigarettes have been subject to regulatory, legal and evidentiary gaps, and they have been met with contrasting reaction from public health experts, clinicians, scientists and governments [5]–[10]. Some focus strongly on the benefits of these products based on the available evidence while others highlight the risks, also based on the evidence. In certain assessments, they are the beginning of the end for tobacco use, while in others, they herald a new public health threat [11]–[14]. It is argued that e-cigarettes and other novel nicotine devices could provide an effective alternative to conventional cigarettes. The case for the potential benefit is that e-cigarettes could lead to a significant decrease in the prevalence of smoking, prevent many deaths and episodes of serious illness, and help to reduce health inequalities that tobacco smoking currently exacerbates [15]. Moreover, e-cigarettes do not involve the combustion of tobacco, and …

Objective: The effects of passive smoking on the voice and laryngeal structures of 20 female passive smokers and 20 age-matched nonsmokers were examined. Methods: The voice evaluation consisted of acoustic, aerodynamic, and videostroboscopic analyses. Results: Three passive smokers displayed mild edema or erythema. Passive smokers had higher mean flow rates and shorter mean maximum phonation times during sustained vowels at comfortable, low-, and high-pitch levels. However, means were only outside normal limits and significantly different from nonsmokers at high pitch. Variables such as the number of years and hours per day subjects were exposed to environmental tobacco smoke were considered. Conclusion: The majority of the variables indicated that vocal fold structure and function were not adversely altered by exposure to passive smoke. Differences between these results and clinical observations are highlighted.

Secondhand smoke (formerly referred to as passive smoke) is the involuntary breathing of other people's tobacco smoke. Many of the 5,000 chemicals in cigarette smoke are poisonous and around 50 are known to cause cancer in some people. Despite there being a reduction in the number of smokers in the UK overall, over 40 per cent of British children live in a household where at least one person smokes (Office for National Statistics 2001). Children's nurses are ideally placed to raise this sensitive issue with parents, but this is not easy. Knowing where to refer parents for support in stopping smoking is as important as asking about smoking during routine assessment.

To the Editor: We read with interest the well-written article by Alshaarawy et al1 that investigated the association of hypertension with secondhand smoke in 2889 never smokers from the National Health and Nutrition Examination Survey. Authors demonstrated that serum cotinine was positively associated with both systolic blood pressure (BP) and prevalence of hypertension. Although the determinant as depicted by serum cotinine levels—at first sight—seems appropriate to evaluate the exposure of participants to passive smoke, there are some obscured points that need to be clarified. It is not reported whether cotinine assessment was performed on the same day of BP measurements. We should …

Fundação de Amparo a Pesquisa no Estado do Rio Grande do Sul Smoking is the second major reason of death worldwide, amounting 5 millions of deaths annually. The adverse effects of cigarette smoking are not limited to active smokers, but also to passive smokers, which comprise one third of worldwide adult population. Cigarette smoking contain nicotine and other addiction related compounds, as well as components that can generate oxidative stress (OS), an unbalance between oxidants and antioxidants of the body, probably responsible for the pathogenesis of smoke-related disorders. The shells of pecan nut (Carya illinoensis) are an industrial byproduct of low cost and high antioxidant potential, whose tea is popularly used as treatment for drug and smoking intoxications, however without scientific validation. Therefore, the present study investigated the possible protection of pecan nut shells aqueous extract (AE) against abstinence behavioral parameters and OS biochemical parameters in animals exposed to passive cigarette smoke. Swiss mice received drinking water or AE (25g/L), ad libitum, in the place of water during one week before and during 3 weeks of cigarette smoke exposure (6, 10 and 14 cigarettes/day each week, respectively), which occurred in a modified incubator. The environmental concentration of carbon monoxide and total suspended particulate matter in the incubator were 130ppm and 188mg/m3, respectively. Fifteen hours after the last cigarette smoke exposure, the animals were evaluated in the open-field test and in the marble burning test. Twenty hours after the last cigarette smoke exposure, the animals were anesthetized and euthanized by exsanguination (cardiac puncture), with collection of blood and removal of brain for biochemical analysis. Data were analyzed by one or two-way ANOVA, followed by Duncan s test when necessary. The protocol of cigarette smoke exposure increased total concentration of carbon dioxide in blood and the hematocrit, which are indirect biochemical markers of cigarette smoke exposure, and reduced the body weight gain of animals without altering fluid intake. In the open-field test, animals exposed to passive smoke showed increase in locomotor and exploratory activities, self-cleaning time and fecal pellets number, as well as in the number of beads hidden in the marble burning test, than the controls. The animals that received AE did not develop these behavioral changes, which indicate anxiety, characteristic related to smoking abstinence. In this study, the involvement of smoking with oxidative damages described in the literature was confirmed by increasing cerebral and erythrocyte lipid peroxidation, increasing in erythrocyte catalase (CAT) activity and decreasing in plasma ascorbic acid. The pecan shells AE was able to protect the mice exposed to cigarette smoke of the lipid peroxidation and decrease of plasma ascorbic acid levels. CAT activity remained high in erythrocytes and increased in brain of animals exposed to cigarette smoke and that received AE, possible as a compensatory mechanism to eliminate excess of reactive oxygen species (ROS) induced by cigarette smoke. It is hypothesized that these biochemical results are in large part due the high antioxidant potential of AE, confirmed by in vitro assays of ABTS (2,2'-azino-bis(3-ethylbenzthiazoline-6-sulphonic acid)) and DPPH (2,2- diphenyl-1-picrylhydrazyl) and by measuring of total phenolic compounds and condensed tannins levels. By Pearson correlation, were observed positive correlations between behavioral parameters evaluated and erythrocyte lipid peroxidation, confirming the involvement of anxiety and OS. The results presented here show the protective effect of pecan nut shells AE on anxiety-like sings of cigarette withdrawal and on oxidative damages and altered antioxidant defenses induced by passive cigarette smoke in mice. Moreover, the popular use of pecan nut shell extract against cigarette smoke was confirmed. It is believed that this industrial byproduct can be considered in the treatment of smoking, increasing the poor therapeutic armamentarium currently employed for this end. Further studies elucidating the components present in this extract, as well as neural mechanisms related to these results are needed. O tabagismo representa a segunda maior causa de mortes no mundo, sendo responsável por 5 milhões de mortes anuais. Não apenas os fumantes ativos estão sujeitos aos efeitos danosos do cigarro, mas também os fumantes passivos, que compreendem um terço da população adulta mundial. A fumaça do cigarro contém nicotina e outros compostos relacionados à adição, bem como constituintes capazes de gerar estresse oxidativo (EO), um desequilíbrio entre os oxidantes e as defesas antioxidantes do organismo, possivelmente responsável pelos efeitos danosos do cigarro sobre o organismo. A casca da noz pecã (Carya illinoensis) é um subproduto industrial de baixo custo e elevado poder antioxidante, cujo chá é utilizado popularmente para tratar intoxicações medicamentosas e resultantes do tabagismo. Porém, até o momento, esse emprego não apresenta validação científica. Em vista disso, o presente estudo investigou a possível atividade protetora do extrato aquoso bruto (EAB) da casca da noz pecã sobre parâmetros comportamentais de abstinência e parâmetros bioquímicos de EO em animais expostos ao fumo passivo. Camundongos Swiss receberam água potável ou EAB (25g/L), ad libitum, no lugar da água de beber, uma semana antes e durante toda exposição à fumaça do cigarro, a qual teve duração de 3 semanas (6, 10 e 14 cigarros/dia em cada semana, respectivamente) e ocorreu em incubadora modificada. A concentração ambiental de monóxido de carbono e material particulado total na incubadora foram 130ppm e 188mg/m3, respectivamente. Quinze horas após a última exposição ao fumo passivo os animais foram avaliados no teste do campo aberto e no teste de esconder esferas. Vinte horas após a última exposição ao fumo passivo os animais foram anestesiados e eutanasiados por exsanguinação (punção cardíaca), com coleta de sangue e retirada do cérebro para as análises bioquímicas. Os dados foram analisados por ANOVA de uma ou duas vias, seguido pelo teste de Duncan quando necessário. O protocolo de exposição ao fumo passivo elevou a concentração total de dióxido de carbono sanguíneo e o hematócrito, os quais são marcadores indiretos de exposição à fumaça do cigarro, bem como reduziu o ganho de peso dos animais sem alterar o consumo de líquidos. No campo aberto, animais expostos ao fumo passivo apresentaram aumento da atividade locomotora e exploratória, do tempo de auto-limpeza e do número de bolos fecais, bem como mostraram aumento do número de esferas escondidas no teste de esconder esferas em relação aos controles. Os animais que receberam EAB não desenvolveram essas modificações comportamentais, as quais indicam ansiedade, característica essa relacionada à abstinência ao cigarro. Neste estudo, o envolvimento do tabagismo com os danos oxidativos já descritos na literatura foi confirmado através do aumento da peroxidação lipídica cerebral e eritrocitária, aumento da atividade da catalase (CAT) eritrocitária e redução das concentrações plasmáticas de ácido ascórbico. O EAB da casca de noz pecã protegeu os animais expostos ao fumo passivo da peroxidação lipídica e da redução dos níveis plasmáticos de ácido ascórbico. A atividade da CAT permaneceu aumentada nos eritrócitos e elevou-se no cérebro dos animais expostos ao fumo passivo e tratados com EAB em relação aos controles, possivelmente pela indução de mecanismos compensatórios que visam eliminar o excesso de espécies reativas de oxigênio (EROs) induzido pelo cigarro. Hipotetizou-se que esses resultados bioquímicos devem-se, em grande parte, ao elevado potencial antioxidante do EAB, confirmado através dos testes in vitro do ABTS (2,2´- azinobis(3-etilbenzotiazolina-6-ácido sulfônico) e do DPPH (2,2-difenil-1-picrilhidrazil) e pela dosagem de compostos fenólicos totais e taninos condensados. Através de correlação de Pearson, foram observadas correlações positivas entre os parâmetros comportamentais e a peroxidação lipídica eritrocitária, confirmando o envolvimento da ansiedade com o EO. Os resultados apresentados aqui evidenciam os efeitos protetores do EAB das cascas da noz pecã sobre os sinais de ansiedade durante abstinência e sobre danos oxidativos e defesas antioxidantes alterados pelo fumo passivo em camundongos. Ademais, confirma-se o uso popular do extrato das cascas de noz pecã frente danos induzidos pelo cigarro e entende-se que esse subproduto da indústria pode ser considerado no tratamento do tabagismo, o que aumentaria o carente arsenal terapêutico empregado atualmente no tratamento do tabagismo. Maiores estudos elucidando os componentes presentes nesse extrato, bem como os mecanismos neurais relacionados aos resultados encontrados são necessários.

Full protection is needed urgently On the 24 March, the tobacco advisory group of the Royal College of Physicians (RCP) in England published its report on passive smoking and children. The report details the effects of exposure to secondhand smoke in children and includes a chapter on associated costs, a consideration of ethical problems, and a review of potential strategies to tackle the problem.1 The report attests to the substantial expansion of research on the health effects of passive smoking and the measurement of harmful exposure.1 We now know that no level of exposure is safe; that exposure to passive smoke in childhood is strongly associated with a range of respiratory effects and serious diseases, including sudden infant death syndrome; and that exposure is a likely cause of brain tumours, leukaemia, and meningitis in children.1 2 3 However, the report excludes established late effects of in utero, childhood, and adolescent exposure including reductions in the fertility of female offspring,4 and breast cancer in premenopausal adult women.2 5 In fact, evidence is mounting that non-smokers exposed as children are at risk of a range of adult …

Background Very few studies have evaluated the adverse effect of passive smoking exposure among active smokers, probably due to the unproven assumption that the dose of toxic compounds that a smoker inhales by passive smoke is negligible compared to the dose inhaled by active smoke. Methods In a controlled situation of indoor active smoking, we compared daily benzo(a)pyrene (BaP) dose, estimated to be inhaled by smokers due to the mainstream (MS) of cigarettes they have smoked, to the measured environmental tobacco smoke (ETS) they inhaled in an indoor environment. For this aim, we re-examined our previous study on daily personal exposure to BaP of thirty newsagents, according to their smoking habits. Results Daily BaP dose due to indoor environmental contamination measured inside newsstands (traffic emission and ETS produced by smoker newsagents) was linearly correlated (p = 0.001 R2 = 0.62) with estimated BaP dose from MS of daily smoked cigarettes. In smoker subjects, the percentage of BaP daily dose due to ETS, in comparison to mainstream dose due to smoked cigarettes, was estimated with 95% confidence interval, between 14.6% and 23% for full flavour cigarettes and between 21% and 34% for full flavour light cigarettes. Conclusions During indoor smoking, ETS contribution to total BaP dose of the same smoker, may be not negligible. Therefore both active and passive smoking exposures should be considered in studies about health of active smokers.

This quantitative study was commissioned by the DHSSPS as part of their smoke-free monitoring and evaluation strategy after the introduction of smoke-free legislation in Northern Ireland in April 2007.The research was undertaken to determine the impact of smoke-free legislation on non-smoking adults who live with a smoker.Using research carried out both before and after the introduction of smoke-free legislation, this study details for the first time the attitudes and knowledge of non-smoking adults living with smokers in Northern Ireland, in relation to second-hand smoke.The study also reports non-smokers' exposure to second-hand smoke in a range of environments.

Background : Environmental tobacco smoke is a known human carcinogen and passive smoking has now emerged as a health threat. Home is the major source of exposure to tobacco smoke among children. Objective : To explore parents’ smoking behaviour and their perceptions towards passive smoking and its effects on their children. Method : A cross-sectional, household survey was conducted on 179 smoking parents in an Indian town using a semi-structured questionnaire which gathered information about demographic factors and 21 questions assessing their smoking behaviour and perceptions about passive smoking. Results : Thirty two percent reported that they did not know smoking caused cancer and only 25% strongly believed that if parents smoked, it had a harmful effect on children's health. Conclusion : Low education, unskilled jobs and a past experience of smoking related health problems have an influence on the way passive smoke and its harmful effects are perceived by smoking parents.

We report the first national data on smoking before, during, and after pregnancy. Estimates are based on the 1986 Linked Telephone Survey that reinterviewed 1,550 White women 20-44 years of age who were respondents to the 1985 National Health Interview Survey. An estimated 39 percent of White women who had smoked before pregnancy quit smoking while pregnant (27 percent when they found out they were pregnant and 12 percent later during pregnancy). Women with less than 12 years of education were five times as likely to smoke and one-fourth as likely to quit as those with 16 or more years of education. Women who smoked more than one pack of cigarettes per day before pregnancy were one-fifth as likely to quit as those smoking less. Of the women who quit, 70 percent resumed smoking within one year of delivery. Of those who relapsed, 67 percent resumed smoking within three months of delivery and 93 percent within six months. There is little evidence of educational differentials in relapse rates. The fact that relapse remains high suggests that while health of the fetus is a strong influence on women's smoking habits, women may be less aware of the effect of passive smoke on the infant.

A number of people in the USA who are still current smokers remain a staggering figure. Although this number continues to decrease, there is still a considerable amount of second-hand smoke. More importantly and for the purpose of this review, the detrimental effects of passive smoke in children is significant. We will not review the specific health effects of passive smoke, but for pediatricians, in particular, it is important to place in perspective programs that are available to influence the parents of children to stop smoking. Indeed, approximately 25% of all children aged 3–11 live in a household with at least one smoker. Despite the increasing number of communities in the states that have instituted restrictions or complete bans on smoking in the workplace and in many public areas, the principal site of smoking remains the home.

This paper examines the silencing of science, that is, efforts to prevent the making of specific scientific claims in any or all of the arenas in which these claims are typically reported or circulated. Those trying to mute the reporting or circulation of scientific claims are termed “partisans.” The paper examines silencing through a systematic examination of the “rapid responses” to a smoking study published in the British Medical Journal claiming that secondhand smoke is not as dangerous as conventionally believed. Media coverage of the smoking study is also examined, as is the question of whether there is self-silencing by the media regarding doubts about the negative effects of passive smoke. The results suggest that the public consensus about the negative effects of passive smoke is so strong that it has become part of a regime of truth that cannot be intelligibly questioned.

The American Academy of Otolaryngology--Head and Neck Surgery has been concerned about the effect of environment degradation on health. There is particular interest in the deleterious health effects of secondary smoke. This report reviews the recent literature regarding passive smoke and clinical disorders and discusses management strategies.

Tuberculosis (TB) and cigarette consumption are relatively high in Indonesia. Passive smoking may increase the risk of infection and disease in adults and children exposed to TB. An association between passive smoking and Mycobacterium tuberculosis infection in children has not been well documented. Objective To assess for an association between passive smoking and M. tuberculosis infection in children who had household contact with a TB patient. Methods This cross-sectional study was conducted in February and March 2011. Children aged 5 to 18 years who had household contact with a TB patient underwent tuberculin testing for M. tuberculosis infection. Subjects were divided into two groups: those exposed to passive smoke and those not exposed to passive smoke. Chi-square test was used to assess for an association between passive smoking and M. tuberculosis infection. Results There were 140 children enrolled in this study, with 70 exposed to passive smoke and 70 not exposed to passive smoke. Prevalence of M. tuberculosis infection was significantly higher in the passive smoking group than in those not exposed to passive smoke (81.4% and 52.9%, respectively, (P= 0.0001)). In the passive smoking group there were significant associations between nutritional state, paternal and maternal education, and M. tuberculosis infection. But no associations were found between M. tuberculosis infection and familial income or BCG vaccination. Conclusion Among children who had household contact with a TB patient, they who exposed to passive smoke are more likely to have M. tuberculosis infection compared to they who not exposed to passive smoke. (Paediatr Indones. 2015;55:29-34.).

▪ Abstract The release of previously secret internal tobacco industry documents has given the public health community unprecedented insight into the industry's motives, strategies, tactics, and data. The documents provide information that is not available from any other source and describe the history of industry activities over the past 50 years. The documents show that the tobacco industry has been engaged in deceiving policy makers and the public for decades. This paper begins with a brief history of the tobacco industry documents and describes the methodological challenges related to locating and analyzing an enormous number of poorly indexed documents. It provides an overview of selected important findings of document research conducted to date, including analyses of industry documents on nicotine and addiction, product design, marketing and promotion, passive smoke, and internal activities. The paper concludes with a discussion of the implications of tobacco document research for public health and the application of such research to fields other than tobacco control.

PURPOSE: To study the potentially adverse health effects of environmental tobacco smoke (ETS) exposure in young children, a short five-question survey was developed to identify routine exposure to ETS in a large epidemiological study. METHODS: The survey is administered to parents of a healthy cohort of children starting at age 3 months. To validate the survey, urinary cotinine levels were measured on 50 children from this cohort who were selected based on ETS exposure as reported in the survey: 24 with no exposure and 26 with exposure. Cotinine was adjusted for creatinine. RESULTS: Overall, children with some form of reported ETS exposure had urinary cotinine levels 7.5 times higher than those who were not exposed. Analysis of variance shows that mean levels of log transformed cotinine in children whose parent(s) smoke in the home, parent(s) who smoke but not in the home, and non-smoking parents are 137.13, 75.60, and 43.28 respectively ( p = 0.0009), indicating decreasing levels of cotinine as reported exposure decreases. Using a cut-point of 30ng/mg of cotinine to differentiate unexposed and exposed to ETS, we found 80% agreement with our survey. A Spearman's ranked correlation coefficient of 0.62 indicates a direct relationship between cotinine and an ETS exposure intensity score ( p CONCLUSIONS: These results suggest that the 5-question survey reflects the child's exposure to passive smoke and that the survey is sensitive to varying levels of exposure.

To the Editor. Passive smoke exposure is a highly prevalent respiratory irritant and its impact on children's health has been clearly documented, particularly increased asthma morbidity and acute infections (eg, otitis media and upper respiratory infections in young children). A significant number of children are exposed to passive smoke, ranging from 24% during pregnancy (maternal smoking) to 43% of young children (ages 2 months to 11 years) who live in a household with at least one smoker.1 ,2 Younger children experience the greatest risk from passive smoke exposure, as evidenced by major clinical and economic burdens. Increased rates of medical services and hospitalizations are seen in young children who are exposed to passive smoke, particularly children with asthma.3 ,4 Increased pediatric asthma morbidity has been particularly noted in young children (

There is little information on the long-term consequences for employees when no-smoking policies are established in the workplace. Our study was designed to assess changes in employee health and smoking behavior. Of the original 60 subjects, 40 employees (18 smokers, 22 nonsmokers) completed this study, which was conducted in a major medical institution. Nonsmokers were recruited as part of the study to determine whether they showed evidence of workplace carbon monoxide associated with passive smoke, potentially inhaled at the work site. Baseline measurements of smoking frequency, carbon monoxide, and weight were obtained during the month preceding the smoking restrictions and at 6 and 18 months afterward. Smokers made significant reductions in daily smoking during the first 6 months but gradually returned to prepolicy levels over the following year. Smokers, in particular, showed increases in weight. Smokers gained 4.93 lb after 18 months, whereas nonsmokers gained 2.25 lb in the same period. Nonsmoker employees showed no evidence of workplace carbon monoxide exposure associated with passive smoke. We discuss the implications of the findings for no-smoking policies in the workplace.

Background . Studies that have investigated the association between exposure to passive smoke and increased risk for disease have had inconclusive results and have raised questions about whether women exposed to passive smoke differ from those not exposed. Methods . The study population included 120 women non-smokers who reported that they had been exposed to passive smoke in the 24 hr prior to the interview and 213 women who reported no exposure. Women were queried about demographic, lifestyle, sexual, and reproductive factors. Results . Exposed women were younger, less educated, and slightly heavier than nonexposed women. They were more likely to be divorced or separated (OR = 3.3, 95% CI = 1.4-7.6, P = 0.005), to have had first intercourse at or before age 16 (OR = 1.4, 95% CI = 1.0-1.9, P = 0.04), and to have had three or more live births (OR = 2.9, 95% CI = 1.2-6.8, P = 0.02). Women exposed to passive smoke were more likely to have consumed two or more cups of coffee (OR = 2.0, 95% CI = 1.1-3.8, P = 0.03), two or more glasses of beer (OR = 3.7, 95% CI = 1.1-12.5, P = 0.03), or to have smoked marijuana in the past 24 hr (OR = 14.7, 95% CI = 1.8-122.3, P = 0.01) than women who were not exposed. There were no differences noted between exposed and nonexposed women in history of gynecologic diseases or number of cervical microorganisms. Conclusion . Women exposed to passive smoke differed from those not exposed on several factors that should be considered in future studies that seek to investigate smoking-related disease risk.

It is well-established that second-hand cigarette smoke affects the health of everyone who is exposed to it. However, second-hand smoke is particularly dangerous for children, increasing their risk of developing asthma, chest infections and triggering asthma attacks. In addition, previous research shows that smoking just one cigarette in a car, even with the window open, creates a greater concentration of second-hand smoke than a whole evening9s smoking in a pub. Hence, exposing children to second-hand smoke in a car is exceptionally hazardous. This study sought information regarding children9s experiences of, and attitudes towards, being exposed to second-hand cigarette smoke, including exposure in cars. 1001 children aged 8–15 (51% male, 49% female) were surveyed online via a self-completion questionnaire between 20 and 27 January 2011. 51% of respondents had been in a car when someone has been smoking at some time. Of the 512 respondents who had been in a car while someone was smoking, 31% said they would ask them to stop, 24% said they were too embarrassed to ask them to stop, 9% said they were too scared to say anything and 21% said they didn9t mind. All respondents were asked how they felt when an adult smokes near them. 58% said it made them smell of smoke, 49% said it made them feel sick, 44% said it made them cough and only 7% said it didn9t bother them. 86% of all respondents said they would like the Government to stop people from smoking when children are in the car, with only 4% saying they would not and 10% saying they did not know. This survey shows that an overwhelming majority of children would support legislation to protect children from passive smoke in the car. This work also suggests that when exposed to second-hand smoke while travelling in a car, many children do not feel able to ask the smoker to stop. More work is needed to empower children and give them a voice to help change legislation around smoking in private cars and to increase awareness of the dangers of second-hand smoke.

MPs have added their voices to a growing movement to ban adults smoking in cars with children in them. The Labour MP Alex Cunningham’s 10 minute rule bill urging ministers to implement a ban on smoking in cars won the backing of 77 other MPs and is due to be debated for a second time in November. Mr Cunningham’s Stockton North constituency is 15th in the British Lung Foundation’s ranking of areas where children are most likely to be exposed to cigarette smoke. Speaking in the House of Commons he said, “The science is clear. Experts say that children are particularly vulnerable to passive smoke, as they …

To the Editor. —I found the article by Joseph and O'Neil1to be an excellent account of how well hospital smoke-free policies may be implemented. However, I found the ethical implications of the article to be disturbing. Because hospitals' no-smoking policies are medically appropriate does not imply that they are ethically justifiable. The Department of Veterans Affairs (VA) certainly may prevent smoking patients from subjecting nonsmoking patients to the risks as well as the nuisance of passive smoke. However, it is much more difficult to justify preventing patients from smoking to promote their own health. Health promotion to attain the goal of personal longevity is, as I believe some authors have correctly argued,2,3the popular, personal ethic of today that is largely replacing older ethics, such as living life for the betterment of society or the attainment of an afterlife. To act contrary to the ethic of life