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Smoke Exposure (smoke + exposure)
Kinds of Smoke Exposure Selected AbstractsSmoke Exposure and Ethanol Ingestion Modulate Intrapulmonary Polymorphonuclear Leukocyte Killing, but Not Recruitment or PhagocytosisALCOHOLISM, Issue 9 2006Elizabeth A. Vander Top Background: People who smoke and abuse alcohol are uniquely susceptible to pulmonary infections caused by Streptococcus pneumoniae, the pneumococcus. The primary cellular defense against pneumococci within the lungs is the polymorphonuclear leukocyte (PMN). Cigarette smoke and ethanol (EtOH) are known to alter certain PMN functions, but little is known about their concurrent effects. Methods: Male Sprague,Dawley rats were exposed twice daily for 8 weeks to cigarette smoke (smoke-exposed) or room air (sham-exposed). During the final week of exposure, the rats were pair-fed a liquid diet containing either 36 or 0% EtOH calories. Polymorphonuclear leukocytes were prerecruited into the rats' lungs by transtracheal injection of lipopolysaccharide. Five hours later, the rats were infected transtracheally with S. pneumoniae, and PMN recruitment, phagocytosis, and bactericidal activity were quantified within their lungs. Chemokine levels were also measured in bronchoalveolar lavage fluids, lung homogenates, and sera. Results: Neither PMN recruitment nor phagocytic uptake of pneumococci was altered by EtOH ingestion or smoke exposure. Killing of the organisms, however, was significantly decreased in sham-exposed, but not smoke-exposed, rats ingesting EtOH. Parallel results were determined for serum cytokine-induced neutrophil chemoattractant-1 (CINC-1), with EtOH ingestion significantly decreasing the levels in sham-exposed, but not smoke-exposed, rats. Pulmonary levels of macrophage inflammatory protein-2 (MIP-2) and CINC-1 were highly elevated by the combination of EtOH and smoke. Conclusions: One week of EtOH ingestion by rats impaired the ability of their PMNs to kill S. pneumoniae within their lungs. This was not due to decreased recruitment of the PMNs to the lungs or to diminished phagocytosis of intrapulmonary pneumococci. The addition of twice-daily cigarette smoke exposure to this short-term EtOH ingestion model restored PMN bactericidal ability to levels observed in the absence of either treatment. These EtOH-induced and smoke-induced alterations in PMN killing may be related to alterations in both pulmonary and systemic inflammatory chemokine levels. [source] Smoke Exposure Exacerbates an Ethanol-Induced Defect in Mucociliary Clearance of Streptococcus pneumoniaeALCOHOLISM, Issue 5 2005Elizabeth A. Vander Top Background: Alcoholics and smokers are particularly susceptible to pulmonary infections caused by Streptococcus pneumoniae, the pneumococcus. Infection begins when pneumococci colonizing the nasopharynx are aspirated into the lower respiratory tract. The major host defense against this movement is the mucociliary clearance apparatus. Both cigarette smoke and ethanol (EtOH) exposure alter ciliary beating and protein kinase activity in the respiratory mucosa in vitro, but their effects on bacterial clearance in the intact animal have not been determined. Methods: Male Sprague Dawley rats were exposed twice daily for 12 weeks to either the smoke generated from 30 cigarettes (smoke,exposed) or room air (sham,exposed). For the last five weeks of smoke exposure, the rats were fed Lieber-DeCarli liquid diets containing 0%, 16%, 26%, or 36% EtOH calories. The rats then were infected intranasally with S. pneumoniae, and movement of the organisms into the lower respiratory tract was quantified by plate counts of the tracheas and lungs 4 hr later. Ciliary beat frequency (CBF) analysis was performed on tracheal ring explants from each animal before and after stimulation with the ,-agonist isoproterenol, and tracheal epithelial cell protein kinase C (PKC) activity was measured. Results: Ingestion of any of the EtOH-containing diets resulted in a dose-dependent increase in movement of S. pneumoniae into the rats' lungs. This EtOH-induced defect was augmented further by concurrent smoke exposure, although smoke exposure alone had little effect on S. pneumoniae movement. Smoke, but not EtOH exposure, activated tracheal epithelial cell PKC. Increased movement of organisms into lungs correlated with a decrease in CBF and loss of the ciliary response to isoproterenol. Conclusion: EtOH ingestion in our model facilitated movement of S. pneumoniae into rats' lungs, a phenomenon exacerbated by concurrent smoke exposure. Furthermore, the organism's movement into the lungs correlated with a blunting of the rats' ciliary response to an established stimulus. Defects in mucociliary clearance thus may be one cause of the increased risk of pneumococcal infections in people who abuse alcohol, particularly if they also smoke. [source] Smoke exposure interacts with ADAM33 polymorphisms in the development of lung function and hyperresponsivenessALLERGY, Issue 6 2009N. E. Reijmerink Introduction:,ADAM33 is the first identified asthma gene by positional cloning, especially asthma combined with bronchial hyperresponsiveness (BHR). Moreover, ADAM33 is associated with early-life lung function and decline of forced expiratory volume in 1 s (FEV1) in the general population. In utero and postnatal cigarette smoke exposure (CSE) are associated with reduced lung function, and development of BHR and asthma. We hypothesized that this may occur via interaction with ADAM33. Aim:, To replicate the role of ADAM33 in childhood lung function and development of BHR and asthma. Furthermore, we investigated gene,environment interaction of ADAM33 with in utero and postnatal CSE in the Dutch PIAMA cohort. Methods:, Six ADAM33 single-nucleotide polymorphisms (SNPs) were genotyped. Rint was measured at age 4 and 8 years, FEV1 and BHR at age 8 years; asthma was based on questionnaire data at age 8. Results:, In the total cohort, the rs511898 A, rs528557 C, and rs2280090 A alleles increased the risk to develop asthma (+BHR). There existed interaction between in utero but not postnatal CSE and the rs528557 and rs3918396 SNPs with respect to development of BHR, the rs3918396 SNP with Rint at age 8 and the rs528557 SNP with FEV1% predicted. Conclusions:, We confirm associations between ADAM33 and the development of asthma (+BHR). This is the first study suggesting that interaction of in utero CSE with ADAM33 results in reduced lung function and the development of BHR, which needs further confirmation. [source] Trends in and predictors of second-hand smoke exposure indexed by cotinine in children in England from 1996 to 2006ADDICTION, Issue 3 2010Michelle Sims ABSTRACT Aims To explore trends in and predictors of second-hand smoke (SHS) exposure in children. To identify whether inequalities in SHS exposure are changing over time. Design Repeated cross-sectional study with data from eight annual surveys conducted over an 11-year period from 1996 to 2006. Setting England. Participants Nationally representative samples of children aged 4,15 years living in private households. Measurements Saliva cotinine (4,15-year-olds), current smoking status (8,15-year-olds), smoking status of parents and carers, smoking in the home, socio-demographic variables. Findings The most important predictors of SHS exposure were modifiable factors,whether people smoke in the house on most days, whether the parents smoke and whether the children are looked after by carers who smoke. Children from more deprived households were more exposed and this remained the case even after parental smoking status has been controlled for. Exposure over time has fallen markedly among children (59% decline over 11 years in geometric mean cotinine), with the most marked decline observed in the period immediately preceding smoke-free legislation. Declines in exposure have generally been greater in children most exposed at the outset. For example, in children whose parents both smoke, median cotinine declined annually by 0.115 ng/ml compared with 0.019 ng/ml where neither parent smokes (P < 0.05). Conclusions In the 11 years leading up to smoke-free legislation in England, the overall level of SHS exposure in children as well as absolute inequalities in exposure have been declining. Further efforts to encourage parents and carers to quit and to avoid smoking in the home would benefit child health. [source] The feasibility of smoking reduction: an updateADDICTION, Issue 8 2005John R. Hughes ABSTRACT Aim To update conclusions of a previous review of smoking reduction on the extent to which (1) smokers spontaneously reduce their smoking, (2) smokers who try to quit and fail return to smoking less, (3) smokers can substantially reduce and maintain reductions via pharmacological and behavioral treatments and (4) smokers compensate when they reduce. Method Qualitative systematic review. Data sources Systematic computer searches and other methods. Study selection Published and unpublished studies of smokers not trying to stop smoking. We located 13,26 studies for each of the four aims. Data extraction The first author entered data with confirmation by second author. Data synthesis Due to the heterogeneity of methods and necessity of extensive recalculation, a meta-analysis was not feasible. Results Few daily smokers spontaneously reduce. Among those who try to stop smoking and relapse, some return to reduced smoking but whether they maintain this reduction is unclear. Nicotine replacement (and perhaps behavior therapies) can induce smokers not interested in quitting to make significant reductions in their smoking and maintain these over time. Some compensatory smoking occurs with reduction but significant declines in smoke exposure still occur. Conclusions These results indicate that reduction is feasible when aided by treatment. Whether reduction should be promoted will depend on the effect of reduction on health outcomes and future cessation. [source] Physiological costs of the hearing due to noise exposure, additional physical stress, and combined exposure to alcohol and cigarette smokeHUMAN FACTORS AND ERGONOMICS IN MANUFACTURING & SERVICE INDUSTRIES, Issue 3 2002H. Strasser In 2 studies, each with 5 test series, physiological costs of the hearing due to legally tolerable noise exposures of 94 dB (A) for 1 hr have been measured audiometrically. The temporary threshold shifts (TTS) and their restitution time, as well as cardiovascular responses in work-related heart rate increases, of 10 and 8 subjects (Ss), respectively, could be shown to be modulated by additional physical stress and combined exposure to alcohol (Study 1) and cigarette smoke (Study 2). Moderate dynamic muscle work (50 W) administered via a bicycle ergometer either immediately after noise, or simultaneous to the noise exposure, significantly reduced restitution time as well as the integrated restitution temporary threshold shift (IRTTS). A physical stress to 100 W,which exceeded the endurance level when demanded simultaneously to the noise exposure,did not show any favorable effects. However, if the same physical stress succeeded the noise exposure, and when it was interrupted several times for the audiometric measurements, it also brought about significant accelerations of the restitution processes. Some reductions in physiological costs of the hearing were found due to an intervening alcohol consumption (blood alcohol concentration , 0.08%) prior to the noise exposure and a simultaneous physical load of 50 W. Smoking 10 cigarettes instead of the consumption of alcohol was associated with a reduced TTS, but a prolonged restitution time. IRTTS as total physiological costs of the most unfavorable combination of noise, simultaneous high physical workload, and preceding smoke exposure was increased. The results of the test series with cigarette smoke,probably due to the small group of just 8 Ss and the counteracting effects of the agents carbon monoxide (CO) and nicotine,were not statistically significant, but these exposures were associated with a substantial activation of the cardiovascular system. Significant heart rate increases are evidence that CO and nicotine must not be neglected as influential factors in the context of physiological costs that the organism, and especially the hearing, has to pay for noise exposures. © 2002 Wiley Periodicals, Inc. [source] The effect of environmental tobacco smoke exposure on allergic sensitization and allergic rhinitis in adultsINDOOR AIR, Issue 4 2005R. Topp First page of article [source] Exposure to the carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in smokers from 3 populations with different risks of lung cancerINTERNATIONAL JOURNAL OF CANCER, Issue 10 2009Kiersten S. Derby Abstract Native Hawaiian smokers are at higher risk and Japanese-American smokers at lower risk of lung cancer (LC), compared with white smokers, even after accounting for smoking history. Because variation in carcinogen exposure/metabolism may occur separately of smoking amount, we compared urinary biomarkers of uptake and detoxification of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK),a potent lung carcinogen,among 578 smokers in these ethnic/racial groups in Hawaii. We measured the NNK metabolite 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and its glucuronide (NNAL-Gluc) and examined total NNAL (NNAL + NNAL-Gluc) and the NNAL detoxification ratio (NNAL-Gluc:NNAL). Native Hawaiians and Japanese,Americans had lower age- and sex-adjusted mean total NNAL, compared with whites. When further adjusting for urinary nicotine equivalents (the sum of nicotine, cotinine, trans -3,-hydroxycotinine and their respective glucuronides), only the difference between Japanese,Americans and whites was eliminated. Therefore, consistent with their lower LC risk, a lower cigarette smoke exposure explains the lower NNK dose of Japanese,Americans, but it does not explain that of Native Hawaiians. The mean detoxification ratio was also lower in Native Hawaiians and Japanese,Americans, compared with whites, even after adjusting for nicotine equivalents (p < 0.0001). Lower NNAL glucuronidation in Native Hawaiians might contribute to their increased LC risk; however, this is inconsistent with the low glucuronidation ratio similarly observed in the low-risk Japanese-American group and because Native Hawaiians had lower total NNAL levels. Thus, exposure and detoxification of NNK are unlikely to explain, by themselves, the differences in LC risk among the 3 populations studied. © 2009 UICC [source] Correlates of smoking among adolescents with asthmaJOURNAL OF CLINICAL NURSING, Issue 5-6 2010Su-Er Guo Aims and objective., This study examined the correlates of smoking among asthmatic adolescents to gain a better understanding of who is at particular risk. Background., Smoking is especially harmful to individuals with asthma. However, smoking is surprisingly prevalent among asthmatic individuals, with prevalence rates similar to or higher than those of the general adult or adolescent populations. Despite this notable finding, there has been little research about factors (i.e. biophysical, psychosocial and behavioural) influencing asthmatic adolescents' tobacco use patterns. Design., A Canadian provincial cross-sectional survey. Method., The study about adolescents' tobacco use and health status was conducted in secondary schools in 2004, 608 asthmatic adolescents participated. Demographic factors, biophysical (body mass index and physical health), psychosocial factors (parents' and peers' smoking, environmental tobacco smoke exposure and depression) and behavioural factors (marijuana use, alcohol use and exercise frequency) were explored. Multinomial logistic regression analyses were conducted to identify risk factors associated with tobacco use. Results and conclusions., Of the 608 asthmatic adolescents, 17·4% currently smoked and 12·0% formerly smoked. Girls, compared with boys, were more likely to smoke (OR: 3·34, 95% CI: 1·62,6·96) after adjusting for differences in the other demographic, biophysical, psychosocial and behavioural factors. Asthmatic girls who had relatively higher body mass index, were in the higher school grades, used marijuana or alcohol, had minor to severe depressive symptoms, had environmental tobacco smoke exposure in their homes and had friends who smoked or were currently more likely to smoke. The former smokers had similar risk factors including higher body mass index, environmental tobacco smoke exposure at home, friends who smoked and marijuana use. Relevance to clinical practice., Despite their health condition, asthmatic adolescents continue currently or formerly to smoke. Gender appropriate prevention and cessation interventions for asthmatic adolescents may need to address important psychosocial and environmental factors that increase the risk of these adolescents initiating and maintaining tobacco use. [source] Tobacco smoke exposure in hospitalised Aboriginal children in Central AustraliaJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 4 2009Lee Hudson Aim: Child exposure to tobacco smoke is detrimental to health. Australian Aboriginal people have a higher rate of cigarette smoking compared with the national average. Thus, we aim to measure the proportion of children admitted to Alice Springs Hospital who are exposed to tobacco smoke at home, to correlate this with prevalence of regular cough and gauge smokers' interest in quitting. Method: A questionnaire was administered verbally to carers of children admitted to Alice Springs Hospital, November 2006 to January 2007. Main outcome measures were presence of a smoker at home and presence of a regular cough. We measured the interest of carers and speculated interest of other smokers in quitting. Eighty-two questionnaires were completed (60% of children admitted during the study period). Eighty-nine per cent of children were Aboriginal. Results: As so few non-Aboriginal children were included in the study, their results were not included in analysis. Sixty-four per cent of children lived with at least one smoker. Seventy per cent of children exposed to smoke at home lived with more than one smoker. Point prevalence of reported regular cough was 33%. Forty-three per cent of children who lived with at least one smoker had regular cough compared with 13% in those who did not (P= 0.035). The rate ratio for regular cough when living with a smoker versus when not living with a smoker was 2.77 (95% confidence interval: 1.06,7.23). Forty-two per cent of the smokers expressed interest in quitting. Conclusion: It is concerning that the majority of hospitalised children were exposed to tobacco smoke at home, while fewer than half of smokers were interested in quitting. [source] Smoke Exposure and Ethanol Ingestion Modulate Intrapulmonary Polymorphonuclear Leukocyte Killing, but Not Recruitment or PhagocytosisALCOHOLISM, Issue 9 2006Elizabeth A. Vander Top Background: People who smoke and abuse alcohol are uniquely susceptible to pulmonary infections caused by Streptococcus pneumoniae, the pneumococcus. The primary cellular defense against pneumococci within the lungs is the polymorphonuclear leukocyte (PMN). Cigarette smoke and ethanol (EtOH) are known to alter certain PMN functions, but little is known about their concurrent effects. Methods: Male Sprague,Dawley rats were exposed twice daily for 8 weeks to cigarette smoke (smoke-exposed) or room air (sham-exposed). During the final week of exposure, the rats were pair-fed a liquid diet containing either 36 or 0% EtOH calories. Polymorphonuclear leukocytes were prerecruited into the rats' lungs by transtracheal injection of lipopolysaccharide. Five hours later, the rats were infected transtracheally with S. pneumoniae, and PMN recruitment, phagocytosis, and bactericidal activity were quantified within their lungs. Chemokine levels were also measured in bronchoalveolar lavage fluids, lung homogenates, and sera. Results: Neither PMN recruitment nor phagocytic uptake of pneumococci was altered by EtOH ingestion or smoke exposure. Killing of the organisms, however, was significantly decreased in sham-exposed, but not smoke-exposed, rats ingesting EtOH. Parallel results were determined for serum cytokine-induced neutrophil chemoattractant-1 (CINC-1), with EtOH ingestion significantly decreasing the levels in sham-exposed, but not smoke-exposed, rats. Pulmonary levels of macrophage inflammatory protein-2 (MIP-2) and CINC-1 were highly elevated by the combination of EtOH and smoke. Conclusions: One week of EtOH ingestion by rats impaired the ability of their PMNs to kill S. pneumoniae within their lungs. This was not due to decreased recruitment of the PMNs to the lungs or to diminished phagocytosis of intrapulmonary pneumococci. The addition of twice-daily cigarette smoke exposure to this short-term EtOH ingestion model restored PMN bactericidal ability to levels observed in the absence of either treatment. These EtOH-induced and smoke-induced alterations in PMN killing may be related to alterations in both pulmonary and systemic inflammatory chemokine levels. [source] Cotinine as a biomarker of tobacco exposure: Development of a HPLC method and comparison of matricesJOURNAL OF SEPARATION SCIENCE, JSS, Issue 4-5 2010Guilherme Oliveira Petersen Abstract Tobacco dependence reaches one-third of the world population, and is the second leading cause of death around the world. Cotinine, a major metabolite of nicotine, is the most appropriate parameter to evaluate tobacco exposure and smoking status due to its higher stability and half-life when compared to nicotine. The procedure involves liquid,liquid extraction, separation on a RP column (Zorbax® XDB C8), isocratic pump (0.5,mL/min of water,methanol,sodium acetate (0.1,M),ACN (50:15:25:10, v/v/v/v), 1.0,mL of citric acid (0.034,M) and 5.0,mL of triethylamine for each liter) and HPLC-UV detection (261,nm). The analytical procedure proved to be sensitive, selective, precise, accurate and linear (r>0.99) in the range of 5,500.0,ng/mL for cotinine. 2-Phenylimidazole was used as the internal standard. The LOD was 0.18,ng/mL and the LOQ was 5.0,ng/mL. All samples from smoking volunteers were collected simultaneously to establish a comparison between serum, plasma, and urine. The urinary cotinine levels were normalized by the creatinine and urine density. A significant correlation was found (p<0.01) between all matrices. Results indicate that the urine normalization by creatinine or density is unnecessary. This method is considered reliable for determining cotinine in serum and plasma of smokers and in environmental tobacco smoke exposure. [source] Smoke Exposure Exacerbates an Ethanol-Induced Defect in Mucociliary Clearance of Streptococcus pneumoniaeALCOHOLISM, Issue 5 2005Elizabeth A. Vander Top Background: Alcoholics and smokers are particularly susceptible to pulmonary infections caused by Streptococcus pneumoniae, the pneumococcus. Infection begins when pneumococci colonizing the nasopharynx are aspirated into the lower respiratory tract. The major host defense against this movement is the mucociliary clearance apparatus. Both cigarette smoke and ethanol (EtOH) exposure alter ciliary beating and protein kinase activity in the respiratory mucosa in vitro, but their effects on bacterial clearance in the intact animal have not been determined. Methods: Male Sprague Dawley rats were exposed twice daily for 12 weeks to either the smoke generated from 30 cigarettes (smoke,exposed) or room air (sham,exposed). For the last five weeks of smoke exposure, the rats were fed Lieber-DeCarli liquid diets containing 0%, 16%, 26%, or 36% EtOH calories. The rats then were infected intranasally with S. pneumoniae, and movement of the organisms into the lower respiratory tract was quantified by plate counts of the tracheas and lungs 4 hr later. Ciliary beat frequency (CBF) analysis was performed on tracheal ring explants from each animal before and after stimulation with the ,-agonist isoproterenol, and tracheal epithelial cell protein kinase C (PKC) activity was measured. Results: Ingestion of any of the EtOH-containing diets resulted in a dose-dependent increase in movement of S. pneumoniae into the rats' lungs. This EtOH-induced defect was augmented further by concurrent smoke exposure, although smoke exposure alone had little effect on S. pneumoniae movement. Smoke, but not EtOH exposure, activated tracheal epithelial cell PKC. Increased movement of organisms into lungs correlated with a decrease in CBF and loss of the ciliary response to isoproterenol. Conclusion: EtOH ingestion in our model facilitated movement of S. pneumoniae into rats' lungs, a phenomenon exacerbated by concurrent smoke exposure. Furthermore, the organism's movement into the lungs correlated with a blunting of the rats' ciliary response to an established stimulus. Defects in mucociliary clearance thus may be one cause of the increased risk of pneumococcal infections in people who abuse alcohol, particularly if they also smoke. [source] Cigarette smoke facilitates allergen penetration across respiratory epitheliumALLERGY, Issue 3 2009K. Gangl Background:, The association between cigarette smoke exposure and allergic airway disease is a matter for debate. We sought to investigate in an in vitro system whether active smoking reduces the integrity and barrier function of the respiratory epithelium and thus facilitates allergen penetration. Methods:, We cultured the human bronchial epithelial cell line 16HBE14o, in a transwell culture system as a surrogate for the intact respiratory epithelium. The cell monolayer was exposed to standardized cigarette smoke extract (CSE). The extent and effects of trans-epithelial allergen penetration were measured using 125I-labelled purified major respiratory allergens (rBet v 1, rPhl p 5 and rDer p 2) and histamine release experiments. Results:, Exposure of cells to concentrations of CSE similar to those found in smokers induced the development of para-cellular gaps and a decrease in trans-epithelial resistance. CSE exposure induced a more than threefold increase in allergen penetration. Increased subepithelial allergen concentrations provoked a substantial augmentation of histamine release from sensitized basophils. Conclusions:, Our results indicate that cigarette smoke is a potent factor capable of reducing the barrier function of the respiratory epithelium for allergens and may contribute to increased allergic inflammation, exacerbation of allergic disease and boosting of IgE memory. [source] Influence of physical inactivity on the prevalence of hay feverALLERGY, Issue 11 2006Y. Kohlhammer Background:, Atopic diseases constitute a major public health problem, increasing constantly in frequency and severity. While treatments are improving, the main cause for an increasing trend of hay fever and its definite triggers remain unclear. The aim of our study was to assess whether physical inactivity could be a risk factor for hay fever. Methods:, We analysed data of a cohort of children aged 5,14 years at baseline (1992,1993) who were followed up until 2003,2005. Parental-reported information on physical activity (being active, doing sports) was obtained for 2429 children participating at the baseline survey (active: n = 1923; semi-active: n = 364; inactive: n = 142). A total of 1703 children (70.1%) were reapproached at least once during follow-up. Logistic regression models were applied to study associations between hay fever, allergic sensitization and physical activity, adjusted for potentially relevant confounders such as age, gender, study site, parental education, breastfeeding, crowding, daycare, dampness or visible moulds, contact to cats, current or prior environmental tobacco smoke exposure and parental atopy. Results:, Significantly higher rates of hay fever were seen for inactive children [aOR 2.39 (95% CI 1.31,4.36) for baseline survey 1992,1993 and aOR 1.76 (95% CI 1.14,2.71) for the follow-up-period until 2005]. In addition, the relative risk of incident cases of hay fever increased depending on inactivity [aRR 1.50 (95% CI 1.05,2.13)]. No association was found between physical inactivity and allergic sensitization assessed by radioallergosorbent test determinations. Conclusions:, Although the underlying biological mechanisms could not be clarified, increasing physical activity in childhood is suggested to prevent hay fever. [source] Lower levels of plasmacytoid dendritic cells in peripheral blood are associated with a diagnosis of asthma 6 yr after severe respiratory syncytial virus bronchiolitisPEDIATRIC ALLERGY AND IMMUNOLOGY, Issue 5 2009Eli Silver Plasmacytoid dendritic cells (pDC) play a crucial role in antiviral immunity and promoting Th1 polarization, possibly protecting against development of allergic disease. Examination of the relationship between peripheral blood plasmacytoid DC levels and manifestations of asthma and atopy early in life. We have isolated peripheral blood mononuclear cells (PBMC) from 73 children (mean age ± SD: 6.6 ± 0.5 yr old) participating in the RSV Bronchiolitis in Early Life (RBEL) study. Flow cytometry was performed on PBMC detecting DC surface-markers: Blood Dendritic Cell Antigens (BDCA) 1, 3, and 2 which identify myeloid type 1, type 2, and plasmacytoid cells, respectively. Total serum IgE, peripheral eosinophil count, and allergy skin tests were documented. About 45% (n = 33) of study participants had physician-diagnosed asthma by 6 yr of age. These children had significantly lower quantities (mean ± SD) of plasmacytoid DC than their non-asthmatic counterparts (1020 ± 921 vs. 1952 ± 1170 cells per 106 PBMC, p = 0.003). We found significantly lower numbers of myeloid dendritic cells in children with asthma (3836 ± 2472 cells per 106 PBMC) compared with those without asthma (4768 ± 2224 cells per 106 PBMC, p = 0.02); however, this divergence was not significant after adjusting for covariates of age, gender, race, skin test reactivity, smoke exposure, and daycare attendance. We did not identify any direct association between DC levels and markers of atopy: skin test reactivity, peripheral eosinophilia, and IgE level. Children who are diagnosed with asthma after severe RSV bronchiolitis appear to have a relative deficiency of plasmacytoid DC in peripheral blood. [source] Soluble CD14 at 2 yr of age: Gender-related effects of tobacco smoke exposure, recurrent infections and atopic diseasesPEDIATRIC ALLERGY AND IMMUNOLOGY, Issue 4 2006K. C. Lødrup Carlsen The endotoxin receptor soluble CD14 (sCD14) has been implicated in the ,hygiene hypothesis' suggesting reduced allergic sensitization with bacterial stimulation. However, the relationship between early life sCD14 and allergic diseases is conflicting. We aimed to investigate whether possible risk factors for allergic diseases were associated with sCD14 levels at 2 yr of age. In the nested case,control study of the birth cohort studies ,Environment and Childhood Asthma study in Oslo' 411 children selected with recurrent bronchial obstruction (rBO) (n = 241) and no bronchial obstruction (n = 170) by 2 yr were investigated with skin prick test and structured parental interview at age 2 yr. Exposure to tobacco smoke, pets and infections was recorded semi-annually by questionnaires (0,2 yr). The sCD14 was analysed from frozen, stored serum by ELISA technique. Regression analyses were performed in all subjects with complete data (n = 406, 180 girls), and in girls and in boys separately. Mean sCD14 (ng/ml) was significantly higher among girls 2035 (1973,2096) vs. 1947 (1890,2004) (boys). The sCD14 was significantly reduced among girls exposed to antenatal maternal smoking and with parental asthma, after adjusting for age, parental rhino-conjunctivitis, pet keeping and childhood infections. Recurrent otitis media (OM) increased and common colds significantly decreased sCD14 levels in girls. Boys with atopic dermatitis and rBO had reduced sCD14. Pet exposure was not significantly associated with sCD14. We report novel gender-related effects of sCD14 in early life and suggest that gender, tobacco smoke exposure, age and middle ear disease in particular should be accounted for when assessing the role of sCD14 in childhood allergic diseases. [source] Bimodal skin reactivity to histamine in atopic children in Singapore: influence of specific sensitizationsPEDIATRIC ALLERGY AND IMMUNOLOGY, Issue 6 2004Mona Iancovici Kidon Histamine skin prick test (SPT) is used as the ,golden standard' for positive control in in vivo immediate type hypersensitivity testing. The skin reactivity to histamine can, however, be modulated by a bevy of extraneous factors. We aimed to define whether histamine skin reactivity in atopic children in Singapore is influenced by age, ethnic origin, gender, environmental exposure or specific sensitization patterns. A retrospective analysis of children, with specific aeroallergen sensitization (as measured by at least one allergen-specific SPT with a wheal size >3 mm compared with the negative control) from the outpatient speciality clinic of the KK Children's Hospital, during 06/2002,06/2003. A total of 315 patients were included, 235 (75%) were males, 252 (80%) were Chinese, age mean was 7.7 yr (range: 2,15). Patients were referred to the SPT with a diagnosis of one or more of: allergic rhinitis 287 (91%), asthma 112 (36%) or atopic dermatitis 60 (19%). The mean histamine response showed a bimodal distribution, independent of age, ethnic origin, gender or phenotypical expression of allergic disease. Histamine skin reactivity was higher in atopic patients with polysensitization (mean 5.0 mm vs. 2.9 mm in monosensitized patients, p < 0.001), and in patients with mould sensitization (mean 5.1 mm vs. 3.3 mm in patient not sensitized to moulds, p < 0.001). The presence of passive smoking increased the likelihood of a diminished histamine skin response. Histamine skin response data strongly suggested the presence of two heterogeneous subpopulations. Children with polysensitization and mould sensitization were more likely to show a large significant histamine response, whereas children with passive smoke exposure, showed a diminished skin reactivity to histamine. [source] The effects of exposure to environmental tobacco smoke on pulmonary function in children undergoing anesthesia for minor surgeryPEDIATRIC ANESTHESIA, Issue 5 2006JAMES M. O'ROURKE FFARCSI Summary Background:, The objectives of this study were to assess whether children exposed to environmental tobacco smoke (ETS) present for surgery with poorer pulmonary function, and experience a more pronounced deterioration in pulmonary function following anesthesia and surgery, than non-ETS-exposed children. Methods:, Fifty-four children aged 5,15 years with a history of ETS exposure from one or both parents and 54 children with no such ETS history were included in the study. All participants were presenting for ambulatory surgery and were judged to conform to American Society of Anesthesiology class I or II. Spirometry was performed preoperatively, postoperatively in the recovery ward when the child met criteria for discharge (Aldrete score 8), and before discharge from the day ward. Results:, The ETS-exposed group had a significantly lower mean preoperative peak expiratory flow rate (PEFR) (9.5 points lower percent predicted, 95% confidence interval ,18.1 to ,1.0, P = 0.03). Although not statistically significant, they also had lower percent predicted baseline mean values of the other spirometric variables that were measured (forced expiratory volume in 1 s ,4.5%, P = 0.07; forced vital capacity ,4.1%, P = 0.10; forced expiratory flow between 25% and 75%,3.6%, P = 0.44). Pulmonary function tests (PFTs) performed in recovery were between 8% and 14% worse than preoperative values, but the results were similar in the two groups of children. PFTs performed before hospital discharge demonstrated an near-complete recovery to baseline values. Again the pattern was similar in exposed and nonexposed children. Conclusions:, Environmental tobacco smoke exposure is associated with lower preoperative PEFR values, but does not impact on recovery from anesthesia for healthy children undergoing ambulatory anesthesia. [source] Food allergy and asthma morbidity in childrenPEDIATRIC PULMONOLOGY, Issue 6 2007Alyson B. Simpson MD Abstract Background Coexisting food allergy and asthma is a significant problem in the pediatric population. Studies have looked at the association between food sensitization and asthma severity. It is unknown whether specific food allergies are associated with increased asthma morbidity. Objective We studied the independent effect that allergy to egg, milk, fish, and peanut has on the number of hospitalizations and courses of systemic steroids in children with asthma. Methods We performed a medical record review to evaluate the effect food allergy to egg, fish, peanut, and milk has on asthma morbidity. We reviewed the records of 201 children aged 3 months to 14 years with the diagnosis of asthma (ICD-9 codes 493.90, 493.91, and 493.92), of which 88 had coexistent food allergy. All children in the food allergy group had food-specific IgE concentrations greater than the 95% positive predictive value. We compared the rate of hospitalizations and use of systemic steroids between children with asthma and food allergies and those without coexisting food allergy using direct-entry, multiple regression analysis. Patients were adjusted for the severity of their asthma based on symptoms documented at their first visit to the allergist according to the National Asthma Education and Prevention Program guidelines and presence of environmental allergy, eczema, smoke exposure, and gastroesophageal reflux. Results Peanut and milk allergies were both associated with increased number of hospitalizations (P,=,0.009, 0.016), and milk allergy was associated with increased use of systemic steroids (P,=,0.001). Conclusion Peanut and milk allergies were associated with increased hospitalization and steroid use and may serve as early markers for increased asthma morbidity. Pediatr Pulmonol. 2007; 42:489,495. © 2007 Wiley-Liss, Inc. [source] Aspiration during swallowing in typically developing children of the first nations and inuit in CanadaPEDIATRIC PULMONOLOGY, Issue 10 2006Gina R. Rempel MD Abstract Children of the First Nations and Inuit in Canada have a high propensity for lower respiratory tract infections. Overcrowding, poor housing, passive smoke exposure, and lack of breast feeding (Martens P, Bond R, Jebamani L, Burchill C, et al. http://www.umanitoba.ca/centres/mchp/reports/pdfs/rfn_pdfs/rfn_report.pdf.; MacMillan H, Walsh C, Jamieson E, Crawford A, Boyle M. http://www.hcsc.gc.ca/fnihbdgspni/fnihb/aboriginalhealth/reports_summaries/regional_survey_ch1.pdf.; Wardman AE, Khan NA. Int J Circumpolar Health 2004;63:81,92) have been cited as important contributing factors in the occurrence of lower respiratory tract infections. However, aspiration during swallowing has thus far not been considered as a co-factor in the occurrence of lower respiratory tract infections in these children. We present a retrospective case series of seven typically developing children of the Canadian First Nations and Inuit, in whom aspiration during swallowing was detected in the course of investigating associations with recurrent lower respiratory tract infections. None of the children had any of the known risk factors for aspiration during swallowing such as developmental variation, prematurity, neuromotor problems, or anatomic abnormalities of the upper aerodigestive tract. We speculate that aspiration during swallowing in typically developing children may be an important, previously unrecognized co-factor in the occurrence of lower respiratory tract infections, particularly in the communities of the Canadian First Nations and Inuit. Further prospective studies will be needed to determine whether aspiration during swallowing represents an independent risk factor for the occurrence of lower respiratory tract infections in these children. Pediatr Pulmonol. 2006, 41:912,915. © 2006 Wiley-Liss, Inc. [source] Association of tobacco smoke exposure and respiratory syncitial virus infection with airways reactivity in early childhoodPEDIATRIC PULMONOLOGY, Issue 6 2001Alan Adler MD Abstract Exposure to infectious agents and environmental tobacco smoke are thought to induce bronchial hyperresponsiveness (BHR). This study was undertaken to determine the effects of passive exposure to tobacco smoke and respiratory syncitial virus (RSV) lower respiratory infection (LRI) during infancy on the occurrence of BHR in the first 2 years of life. Eighty-six cases of documented RSV (mean age, 188 days) and 78 controls (mean age, 162 days) were enrolled from the clinic and in-patient service of a single hospital. None had a history of prior LRI. Subjects were studied at 6-month intervals up to 19 months of age with a standardized respiratory illness and parental smoking questionnaire, partial expiratory flow-volume curves by the "hug" (rapid thoracic compression) technique, and methacholine challenge. Exposure to maternal and paternal cigarette smoking, maternal history of asthma, and mold exposure were associated with decreased levels of length-corrected maximal flow at functional residual capacity (V,maxFRC). RSV-LRI was not related to V,maxFRC. After adjustment of V,maxFRC for these factors, V,maxFRC was a significantly and positively correlated with a methacholine concentration provoking a 40% fall in V,maxFRC (PC40) and negatively correlated with dose-response slope. After adjustment for V,maxFRC, there were no independent effects of tobacco smoke exposure or RSV-LRI on methacholine responses. These data do not support a role for RSV as a risk factor for airways reactivity in childhood and indicate that exposure to tobacco smoke affects airways reactivity through its effects on airways. Pediatr Pulmonol. 2001; 32:418,427. © 2001 Wiley-Liss, Inc. [source] Effect of protective filters on fire fighter respiratory health: field validation during prescribed burnsAMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 1 2009Annemarie J.B.M. De Vos MPH, ICCert Abstract Background Bushfire smoke contains a range of air toxics. To prevent inhalation of these toxics, fire fighters use respiratory equipment. Yet, little is known about the effectiveness of the equipment on the fire ground. Experimental trials in a smoke chamber demonstrated that, the particulate/organic vapor/formaldehyde (POVF) filter performed best under simulated conditions. This article reports on the field validation trials during prescribed burns in Western Australia. Methods Sixty-seven career fire fighters from the Fire and Emergency Services Authority of Western Australia were allocated one of the three types of filters. Spirometry, oximetry, self-reported symptom, and personal air sampling data were collected before, during and after exposure to bushfire smoke from prescribed burns. Results Declines in FEV1 and SaO2 were demonstrated after 60 and 120 min exposure. A significant higher number of participants in the P filter group reported increases in respiratory symptoms after the exposure. Air sampling inside the respirators demonstrated formaldehyde levels significantly higher in the P filter group compared to the POV and the POVF filter group. Conclusions The field validation trials during prescribed burns supported the findings from the controlled exposure trials in the smoke chamber. Testing the effectiveness of three types of different filters under bushfire smoke conditions in the field for up to 2 hr demonstrated that the P filter is ineffective in filtering out respiratory irritants. The performance of the POV and the POVF filter appears to be equally effective after 2 hr bushfire smoke exposure in the field. Am. J. Ind. Med. 52:76,87, 2009. © 2008 Wiley-Liss, Inc. [source] Effect of protective filters on fire fighter respiratory health during simulated bushfire smoke exposureAMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 9 2006Annemarie J.B.M. De Vos RN Abstract Background Bushfire fighters are potentially subject to risks from bushfire smoke. Although many different protective masks and filters are available, it is not clear which is the most effective from a health and safety perspective. The effect of protective filters on the respiratory health of Western Australian urban career fire fighters under controlled simulated conditions is investigated. Methods Sixty-four healthy Fire and Emergency Services Authority of Western Australia (FESA) urban career fire fighters were subjected to controlled simulated bushfire smoke in an open smoke chamber for 15 min. The fire fighters were allocated one of the three types of protective filters: particulate only (P), particulate/organic vapor (POV), and a particulate/organic vapor/formaldehyde (POVF) filter using a double-blind randomized procedure. Personal air sampling inside the fire fighters' masks, spirometry, oximetry, and self-reported symptom data were collected at baseline and at two time intervals after the smoke exposure. Results A significant decline in oxygen saturation was seen immediately after exposure, however, the decline was small and no significant relationships could be established between this and the type of filter used. A significantly higher number of participants in the P and POV filter groups self-reported an increase in coughing, wheezing, and shortness of breath compared to the POVF group. Air sampling demonstrated a significantly higher level of formaldehyde and acrolein inside the masks fitted with P filters compared to POV and POVF filters. Conclusions Testing the effectiveness of P, POV, and POVF filters under controlled conditions has demonstrated that the POVF filter provides statistically significant better protection for the fire fighters' airways in a simulated bushfire exposure chamber. Am. J. Ind. Med. © 2006 Wiley-Liss, Inc. [source] Altered expression of antimicrobial molecules in cigarette smoke-exposed emphysematous mice lungsRESPIROLOGY, Issue 7 2008Yoko SHIBATA Background and objective: The natural history of COPD, a disease usually caused by cigarette smoking, is associated with frequent respiratory infections. Consistent with human COPD, bacterial clearance in the lungs has been reported to be impaired in mice exposed to cigarette smoke. In the airways, several antimicrobial molecules such as surfactant proteins (SP), beta-defensins (BD), secretory leucocyte protease inhibitor (SLPI) and lysozyme play important roles in the defence against invading pathogens. This study evaluated the expression of antimicrobial molecules in mice lungs with cigarette smoke-induced emphysematous changes. Methods: Six B6C3F1 mice were exposed to cigarette smoke (2 cigarettes/day/mouse for 6 months) or room air. Gene expression within the lungs of mice in both groups was assessed by RT-PCR. Results: The expression of SP-A, BD2, BD3 and SLPI was significantly elevated in the lungs of cigarette smoke-exposed mice compared with air-exposed mice. BD1 expression decreased in the smoke-exposed mice and lysozyme expression was unchanged. Conclusions: Chronic cigarette smoke exposure did not suppress the expression of antimicrobial molecules in the lung. Altered expression of antimicrobial molecules in this mouse model does not explain the impaired host defence against respiratory microbes seen in patients with COPD. [source] Increased surfactant protein-D and foamy macrophages in smoking-induced mouse emphysemaRESPIROLOGY, Issue 2 2007Noriyuki HIRAMA Background and objective: The molecular mechanisms underlying COPD remain undetermined. The lungs of surfactant protein-D (SP-D) deficient mice show emphysema and an excessive number of foamy macrophages. This study aims to elucidate roles of SP-D and foamy macrophages in smoking-induced mouse emphysema. Methods: Twenty B6C3F1 mice were exposed to cigarette smoke (2 cigarettes/day/mouse for 6 months). The mice were killed, and formalin-fixed, paraffin-embedded lung sections were carried out on seven mice, BAL was carried out on six mice, and seven mice were used to make lung homogenates. In in vitro studies, A549 cells were transduced with the SP-D expression plasmid and treated with cigarette smoke extract to evaluate cell viability. Results: Emphysema was induced in the mice by chronic cigarette smoke exposure. Increased expression of matrix metalloproteinase-9 and -12 was observed, and foamy alveolar macrophages accumulated in the smoke-exposed lungs. Immunostaining of BAL cells revealed the major source of matrix metalloproteinase-12 to be foamy alveolar macrophages. Furthermore, SP-D was elevated in emphysema lungs. Expression of transcription factors, Fra-1, junB and C/EBP, (which induce SP-D) were significantly elevated in emphysema lungs. The in vitro expression of SP-D gene in A549 cells prolonged cell survival following exposure to cigarette smoke condensate. Conclusions: The accumulation of foamy alveolar macrophages may play a key role in the development of smoking-induced emphysema. Increased SP-D may play a protective role in the development of smoking-induced emphysema, in part by preventing alveolar cell death. [source] Pathology of the Olfactory Epithelium: Smoking and Ethanol Exposure,THE LARYNGOSCOPE, Issue 8 2004J Vent MD Abstract Objective: To investigate the effects of tobacco smoke on the olfactory epithelium. Cigarette smoking has been associated with hyposmia; however, the pathophysiology is poorly understood. The sense of smell is mediated by olfactory sensory neurons (OSNs) exposed to the nasal airway, rendering them vulnerable to environmental injury and death. As a consequence, a baseline level of apoptotic OSN death has been demonstrated even in the absence of obvious disease. Dead OSNs are replaced by the mitosis and maturation of progenitors to maintain sufficient numbers of neurons into adult life. Disruption of this balance has been suggested as a common cause for clinical smell loss. This current study will evaluate the effects of tobacco smoke on the olfactory mucosa, with emphasis on changes in the degree of OSN apoptosis. Study Design: A rat model was used to assess the olfactory epithelium after exposure to tobacco smoke. Methods: Rats were exposed to tobacco smoke alone (for 12 weeks), smoke plus dietary ethanol (for the final 5 weeks), or to neither (control). Immunohistochemical analysis of the olfactory epithelium was performed using an antibody to the active form of caspase-3. Positive staining for this form of the caspase-3 enzyme indicates a cell undergoing apoptotic proteolysis. Results: Control rats demonstrated a low baseline level of caspase-3 activity in the olfactory epithelium. In contrast, tobacco smoke exposure triggered a dramatic increase in the degree of OSN apoptosis that affected all stages of the neuronal lineage. Conclusions: These results support the following hypothesis: smell loss in smokers is triggered by increased OSN death, which eventually overwhelms the regenerative capacity of the epithelium. [source] Effects of paternal cigarette smoking on testicular function, sperm fertilizing capacity, embryonic development, and blastocyst capacity for implantation in ratsANDROLOGIA, Issue 2 2004A. Kapawa Summary. We evaluated the effects of paternal smoking on testicular function, sperm fertilizing capacity, embryonic development, and blastocyst capacity for implantation. Rats of group A were exposed to cigarette smoke for 10 weeks. Rats of group B were exposed to the smoke of incense sticks for 10 weeks. Rats of group C served as a control group. Rats of group D were exposed to cigarette smoke for 7 weeks only. Experimental period was 10 weeks in all groups. At the end of the experimental period serum testosterone responses to human chorionic gonadotropin stimulation, andro-gen-binding protein activity in testicular cytosols, epididymal sperm motility, and oocyte fertilization rate, oocyte cleavage rate, and blastocyst development rate after in vitro fertilization (IVF) trials were significantly smaller in group A compared with groups B and C. In contrast, fertilization rate, cleavage rate, and blastocyst development rate after intracytoplasmic sperm injection (ICSI) procedures were not significantly different among groups A, B, C, and D. Both after IVF trials and ICSI techniques, the proportion of the alive offspring to the number of transferred oocytes was significantly smaller in group A than in groups B and C. Cigarette smoke-exposure results in a secretory deficiency of Leydig and Sertoli cells leading to an impaired epididymal sperm maturation process and diminished capacity of spermatozoa to penetrate oocytes. In addition paternal cigarette smoke exposure affects the embryonic ability for implantation. [source] Craniosynostosis and maternal smoking,BIRTH DEFECTS RESEARCH, Issue 2 2008Suzan L. Carmichael Abstract BACKGROUND: Several previous studies suggested increased risk of craniosynostosis among infants born to women who smoked. METHODS: This study used data from the National Birth Defects Prevention Study, a multi-state, population-based case-control study of infants delivered from 1997,2003. Nonmalformed, liveborn controls were selected randomly from birth certificates or birth hospitals. Data from maternal telephone interviews were available for 531 cases and 5008 controls. RESULTS: Smoking during the first month of pregnancy was not associated with craniosynostosis. Smoking later in pregnancy was associated with increased risk, but only among mothers who smoked at least one pack/day. For example, during the second trimester, the odds ratio for smoking <5 cigarettes/day was 1.0 (95% confidence interval [CI] 0.6, 1.8), but the odds ratio (OR) for smoking 15 or more cigarettes/day was 1.6 (95% CI 0.9, 2.8), after adjustment for maternal age, education, race-ethnicity, sub-fertility, parity, folic acid supplement intake, body mass index, and study center. Among women who did not smoke, adjusted odds ratios suggested that secondhand smoke exposure at home, but not at work/school, was associated with modestly increased risk; the OR for home exposure was 1.3 (95% CI 0.9, 1.9). Results followed a similar pattern for some, but not all, specific suture types, but numbers for some groupings were small. CONCLUSIONS: The results suggest moderately increased risk of craniosynostosis among mothers who were the heaviest smokers and who continued to smoke after the first trimester. Results are somewhat equivocal, given that most confidence intervals included one. Birth Defects Research (Part A), 2008. © 2007 Wiley-Liss, Inc. [source] Prenatal and postnatal parental smoking and acute otitis media in early childhoodACTA PAEDIATRICA, Issue 1 2010SE Håberg Abstract Aim:, To explore the associations between acute otitis media in early childhood and prenatal and postnatal tobacco smoke exposure. Methods:, Subjects were 32 077 children born between 2000 and 2005 in the Norwegian Mother and Child Study with questionnaire data on tobacco smoke exposure and acute otitis media up to 18 months of age. Multivariate regression models were used to obtain adjusted relative risks for acute otitis media. Results:, Acute otitis media was slightly more common in children exposed to parental smoking. The incidence from 0 to 6 months was 4.7% in unexposed children and 6.0% in children exposed both prenatally and postnatally. After adjusting for postnatal exposure and covariates, the relative risk for acute otitis media 0,6 months when exposed to maternal smoking in pregnancy was 1.34, 95% confidence interval: 1.06,1.69. Maternal smoking in pregnancy was associated with acute otitis media up to 12 months of age. Compared with non-exposed children, there was a slightly increased risk of recurrent acute otitis media for children exposed both prenatally and postnatally with a relative risk of 1.24, 95% confidence interval: 1.01,1.52. Conclusion:, Even in a cohort with relatively low exposure levels of parental smoking, maternal smoking in pregnancy was associated with an increased risk of acute otitis media in early childhood. [source] | |||||||||||||||||||||||||||||||