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Alfred Bernard - One of the best experts on this subject based on the ideXlab platform.
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Effects of ultrafine particles-induced oxidative stress on Clara Cells in allergic lung inflammation.
Particle and Fibre Toxicology, 2010Co-Authors: Francesca Alessandrini, Alfred Bernard, Ingrid Weichenmeier, Erik Van Miert, Shinji Takenaka, Erwin Karg, Cornelia Blume, Martin Mempel, Holger Schulz, Heidrun BehrendtAbstract:Background Clara Cell Protein (CC16), the main secretory product of bronchiolar Clara Cells, plays an important protective role in the respiratory tract against oxidative stress and inflammation. The purpose of the study was to investigate the role of elemental carbon ultrafine particles (EC-UFP)-induced oxidative stress on Clara Cells and CC16 in a mouse model of allergic lung inflammation.
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Clara Cell Protein (CC16) in serum and bronchoalveolar lavage fluid of subjects exposed to asbestos
Biomarkers, 2008Co-Authors: Martin Petrek, Cedric Hermans, Vítězslav Kolek, Jarmila Fialová, Alfred BernardAbstract:The Clara Cell Protein (CC16) is a small and readily diffusible Protein of 16 kDa secreted by bronchiolar Clara Cells in the distal airspaces. These epithelial Cells are altered in several pulmonary pathological processes induced by various lung toxicants. In the search for a new biomarker of asbestos-induced lung impairment, we used a sensitive immunoassay to determine the levels of CC16 in bronchoalveolar fluid (BALF) and serum of subjects exposed to asbestos compared with a group of healthy controls. In the BALF of asbestos-exposed subjects there was an insignificant trend towards CC16 elevation compared with controls, with a (mean +/- SD of 0.81 +/- 0.65 mg l-1 for asbestos-exposed subjects (n = 23) versus 0.39 +/- 0.19 mg l-1 for controls (n = 11) (p = 0.09). In serum, CC16 concentration was significantly increased among asbestos-exposed subjects, with values of 27.2 +/- 24.0 micrograms l-1 for asbestos-exposed subjects (n = 34) versus 16.1 +/- 7.6 micrograms l-1 for controls (n = 34) (p = 0.01). Regarding the effects of smoking, there were significant differences between generally lower CC16 levels in serum and BALF (p = 0.05 and 0.001, respectively) of smokers compared with the higher levels in non-smokers. Serum CC16 levels positively correlated with those in BALF, which is consistent with a diffusional transfer of CC16 from the bronchoalveolar space into the serum. No association, however, emerged between the levels of CC16 in serum or BALF and either the duration of asbestos exposure or the severity of the lung impairment as assessed by chest X-ray. These findings suggest that exposure to asbestos elicits early changes in the local and, importantly, also the systemic levels of CC16. This pneumoProtein therefore appears as a promising non-invasive biomarker of asbestos-induced lung injury and occupational disease in both smoking and non-smoking exposed subjects.
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Serum Clara Cell Protein (CC16) in healthy young smokers.
Biomarkers, 2008Co-Authors: Marco Dell'omo, Alfred Bernard, Cedric Hermans, Giacomo Muzi, Vincent Haufroid, Patrizia Carrieri, Giuseppe AbbrittiAbstract:The CC16 microProtein is the main secretory product of Clara Cells, which are epithelial Cells lining lung airways. In crossing through the bronchoalveolar/blood barrier, CC16 diffuses passively into plasma. Serum CC16 (sCC16) has recently been proposed as a biomarker for detecting Clara Cell impairments. The aim of this study was to assess if sCC16 concentrations are reduced in a group of healthy young smokers. A group of 118 healthy young males volunteered to take part in the study. Each subject answered a questionnaire, and provided blood and urine samples. Serum CC16, urinary cotinine and creatinine were measured. Median serum CC16 concentrations were lower in smokers than in non-smokers (11.3 mug l(-1) vs 14.6 mug l(-1); p = 0.005; N = 89 and 29, respectively) but did not correlate with either the daily or the life-time cigarette consumption, or with urinary cotinine concentrations. sCC16 did not correlate with age or body mass index in the whole study population or in the groups of smokers and non-smokers. These results suggest the reduction in sCC16 concentrations in a group of healthy young smokers may be an early effect of cigarette smoking.
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cord blood Clara Cell Protein cc16 predicts the development of bronchopulmonary dysplasia
European Journal of Pediatrics, 2008Co-Authors: Alexandra J J Schrama, H M Berger, Alfred Bernard, Ben J H M Poorthuis, Aeilko H. Zwinderman, Frans J WaltherAbstract:Clara Cell Protein (CC16) is an anti-inflammatory Protein and a biomarker of pulmonary epithelial Cells and alveolocapillary membrane injury in adults. We investigated whether low cord blood concentrations of CC16 are associated with the development of respiratory distress syndrome (RDS) and bronchopulmonary dysplasia (BPD) in preterm infants and the relationship between CC16 and its pro-inflammatory counterpart, the secretory phospholipase A(2) (sPLA(2)) enzyme. CC16 concentration, sPLA(2) activity and IL-6 concentration were measured in cord blood plasma from 79 preterm infants (25 controls, 37 infants who developed RDS and 17 infants who developed BPD). After adjustment for gestational age and Apgar score at 5 min, the CC16 concentration was lower in BPD infants than in preterm controls (p < 0.01). sPLA(2) activity was similar in all groups and the IL-6 concentrations were increased in both RDS and BPD infants (p < 0.01 and p < 0.05, respectively, vs. controls). We conclude that low cord blood CC16 concentrations in preterm infants independently predict the development of BPD. Low CC16 levels may reflect early lung injury, which contributes to the severity of RDS and progress towards BPD. Future studies are needed to assess whether the early administration of recombinant human CC16 in preterm infants with low cord blood CC16 prevents the development of BPD.
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Lung epithelial injury markers are not influenced by use of lower tidal volumes during elective surgery in patients without preexisting lung injury.
American Journal of Physiology-lung Cellular and Molecular Physiology, 2007Co-Authors: Rogier M. Determann, Alfred Bernard, Esther K. Wolthuis, Goda Choi, Paul Bresser, René Lutter, Marcus J. SchultzAbstract:Clara Cell Protein levels are elevated in plasma of individuals with mild or subclinical lung injury. We studied the influence of two mechanical ventilation strategies on local and systemic levels ...
Robert Lauwerys - One of the best experts on this subject based on the ideXlab platform.
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potential role of Clara Cell Protein an endogenous phospholipase a2 inhibitor in acute lung injury
European Respiratory Journal, 1995Co-Authors: Philippe G. Jorens, Wout De Backer, Frans J. Van Overveld, Yves Sibille, Robert Lauwerys, Roderick J. Flower, N. J. Goulding, Leo Bossaert, A. G. Herman, Alfred BernardAbstract:It is now recognized that epithelial Cells lining airways and alveoli are capable of releasing various mediators, which have the potential to modulate local inflammatory reactions. The amount of the 16 kDa Clara Cell Protein (CC16), an inhibitor of phospholipase A2 activity produced by pulmonary epithelial Cells, was measured by means of a sensitive immunoassay in the unconcentrated bronchoalveolar lavage fluid (BALF) of 13 control subjects, and in patients with acute lung injury (14 with the full-blown adult respiratory distress syndrome (ARDS); 21 after standard cardiopulmonary bypass surgery, a known risk factor for ARDS). The level of CC16 was compared with other markers of inflammation with a wide range of molecular weights: albumin (nephelometry); total Protein (spectrophotometry); beta 2-microglobulin (latex immunoassay); cystatin C (latex immunoassay); alpha 1-antitrypsin (immunoradiometry), and lipocortin-1 (enzyme-linked immunosorbent assay (ELISA)). The Clara Cell Protein (CC16) was detectable in all BALF, and significantly higher levels of this Protein were observed in BALF from patients with acute lung injury. Changes in BALF Clara Cell Protein levels differed from those of alpha 2-macroglobulin and the natural phospholipase inhibitor lipocortin-1. Alpha 2-macroglobulin levels were not significantly enhanced in patients at risk for ARDS, but were increased in patients with ARDS; whereas, lipocortin 1 levels were not elevated in either group. Pretreatment of patients at risk for ARDS with high dose methylprednisolone did not alter the amount of Clara Cell Protein recovered in BALF. The mean CC16 level in BALF from patients with ARDS who died was significantly lower than from those who survived. The data presented in this study suggest that pulmonary epithelial Cells secrete a natural anti-inflammatory Protein during acute lung injury, which might have a protective and immunosuppressive role.
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Clara Cell Protein cc 16 induces a phospholipase a2 mediated inhibition of fibroblast migration in vitro
American Journal of Respiratory and Critical Care Medicine, 1995Co-Authors: Olivier Lesur, Robert Lauwerys, K Arsalane, Alfred Bernard, R Begin, Andre M Cantin, Denis LaneAbstract:Clara Cell Protein (CC-16, also designated CC-10) is synthesized by the bronchiolar epithelium and has been suggested as an inhibitor of phospholipase A(2) (PLA(2)) activity. Therefore, CC-16 is a candidate for controlling inflammatory events in the lung. Because CC-16 amounts and function may be altered in fibrosing lung diseases in which bronchiolar injury has been reported, it was measured in alveolar fluids and sera. Secretory PLA(2) activity in alveolar fluids and the influence of CC-16 on platelet-derived growth factor-induced human fibroblast chemotaxis and cytosolic PLA(2) activity were also explored. CC-16 content was decreased in alveolar fluids from idiopathic pulmonary fibrosis (IPF: 1.3 +/- 0.1 mg/L) and bleomycin lung (1.1 +/- 0.2 versus 2.1 +/- 0.2 mg/L in controls, p < 0.05), whereas there was a three- to ninefold increase in secretory PLA(2) activity (p < 0.05 versus controls). CC-16 inhibited fibroblast chemotaxis in a dose-dependent manner (90% inhibition at 30 mu g/ml CC-16). This inhibition was reversed by reducing CC-16. CC-16 was also able to lower fibroblastic cytosolic PLA(2) activity by 50% in vitro. In summary, CC-16 is able to inhibit fibroblast chemotaxis in vitro by mechanisms that may be related to a blockage of cytosolic PLA(2) activity. It can be postulated that CC-16 deficiency may contribute to fibroblast burden activity in fibrosing lung diseases.
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Clara Cell Protein in human amniotic fluid: a potential marker of fetal lung growth.
Pediatric Research, 1994Co-Authors: Alfred Bernard, Robert Lauwerys, N. Thielemans, Jean Paul Langhendries, M. Van Lierde, M M FreundAbstract:Clara Cell Protein (CC16) is a 16-kD Protein secreted at the surface of respiratory airways by nonciliated bronchial and bronchiolar Cells, including Clara Cells. Using the same immunoassay as that recently developed for CC16 in lung lavage, we have measured CC16 in amniotic fluid samples from 100 normal fetuses and 51 fetuses with various pathologies. Ouchterlony immunodiffusion analysis showed a complete identity between CC16 in amniotic fluid and the Protein in lung lavages of adults. CC16 was detectable in amniotic fluid from about the 15th wk of pregnancy, then progressively increased until delivery, with a tendency to reach a plateau after the 30th wk. Between the 15th and the 39th wk of pregnancy, the concentration of CC16 in amniotic fluid increased on average 25 times. The sex of the fetus did not influence the concentration of CC16 in amniotic fluid. Compared with expected values, levels of CC16 in amniotic fluid were on average not significantly altered in cases of spina bifida (n = 9), anencephaly (n = 7), and trisomy 21 (n = 6). In contrast, CC16 was on average significantly decreased in cases of diaphragmatic hernia (n = 6), trisomy 18 (n = 14), Turner syndrome (n = 4), and diabetic pregnancy (n = 5). In cases of diaphragmatic hernia, a relation emerged between the concentration of CC16 in amniotic fluid and both the weight of the lungs and the survivorship of the fetuses. The time course of CC16 in amniotic fluid during normal pregnancy and its reduction in pathologies associated with lung hypoplasia suggest that CC16 in amniotic fluid might serve as a marker of bronchial epithelium growth.
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early decrease of serum Clara Cell Protein in silica exposed workers
European Respiratory Journal, 1994Co-Authors: Alfred Bernard, Eduard Siles, J M Gonzalezlorenzo, G Trujillano, Robert LauwerysAbstract:Clara Cell Protein (CC16) is a 16 kDa Protein secreted by nonciliated Cells of the tracheobronchial tree; it has recently been proposed as a peripheral marker of respiratory epithelial injury. The concentration of CC16 was measured in the serum and, when available, in the sputum of 86 miners exposed to silica and of 86 control subjects matched for age, body mass index and smoking status (26 lifelong nonsmokers and 60 current smokers in both groups). Workers were exposed to silica-rich dust in a quarry for 15.2 months on average. No difference between exposed and control workers could be detected with regard to respiratory symptoms, chest radiographs or lung function tests. By contrast, the concentration of CC16 in serum was decreased in silica-exposed workers (geometric mean 12.3 micrograms.l-1) compared to controls (16.3 micrograms.l-1). The decrease was found both in lifelong nonsmokers (14.7 vs 21.9) and current smokers (11.3 vs 14.5). In the latter, tobacco smoking caused a decrease of serum CC16 that was additional to that associated with silica exposure. The determination of CC16 in sputum samples, judged to be reliable on the basis of the CC16/alpha-amylase concentration ratio (mostly from smokers), also revealed a reduction of CC16 following silica exposure (46.2 vs 106 mg.l-1). We conclude that alterations in the serum concentrations of CC16 probably reflect very early toxic effects of silica particles on the respiratory epithelium. This reinforces the view that serum CC16 is a sensitive marker, which might improve our ability to detect exposure to chemicals potentially harmful to the respiratory tract.
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Urinary Protein 1 or Clara Cell Protein: a new sensitive marker of proximal tubular dysfunction.
Kidney International, 1994Co-Authors: Alfred Bernard, N. Thielemans, Robert LauwerysAbstract:Protein 1 or Clara Cell Protein (CC16) is a 16 kD Protein secreted predominantly by Clara Cells in terminal bronchioles and from puberty on in the male urogenital tract. The sensitivity of CC16 in urine as an index of proximal tubule dysfunction was compared to that of retinol-binding Protein, beta 2-microglobulin and alpha 1-microglobulin. These microProteins were measured by latex immunoassay in the urine from 114 pregnant women, 126 diabetics (65 men and 61 women), 80 workers exposed to cadmium (36 men and 44 women), and from healthy subjects matched for age and sex. In women, CC16 appeared consistently as a much more sensitive index of tubular dysfunction than other microProteins. In female diabetics, for instance, the prevalence of elevated values of CC16 in urine (53%) largely exceeded that of other microProteins (< 30%) and even of albumin (35%). In men, however, the existence of a post-renal secretion contaminating the urine limits the sensitivity of CC16 which was revealed to be higher than that of other microProteins, in diabetics only. The assay of urinary CC16 has the potential, especially in women, to detect very subtle defects of the proximal tubule which pass completely unseen with other microProteins. We postulate that this unique sensitivity of CC16 is due to its very low concentration in tubular fluid which, combined with its anionic character, strongly hinders its access to brush border binding sites.
Cedric Hermans - One of the best experts on this subject based on the ideXlab platform.
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Serum Clara Cell Protein (CC16) in healthy young smokers.
Biomarkers, 2008Co-Authors: Marco Dell'omo, Alfred Bernard, Cedric Hermans, Giacomo Muzi, Vincent Haufroid, Patrizia Carrieri, Giuseppe AbbrittiAbstract:The CC16 microProtein is the main secretory product of Clara Cells, which are epithelial Cells lining lung airways. In crossing through the bronchoalveolar/blood barrier, CC16 diffuses passively into plasma. Serum CC16 (sCC16) has recently been proposed as a biomarker for detecting Clara Cell impairments. The aim of this study was to assess if sCC16 concentrations are reduced in a group of healthy young smokers. A group of 118 healthy young males volunteered to take part in the study. Each subject answered a questionnaire, and provided blood and urine samples. Serum CC16, urinary cotinine and creatinine were measured. Median serum CC16 concentrations were lower in smokers than in non-smokers (11.3 mug l(-1) vs 14.6 mug l(-1); p = 0.005; N = 89 and 29, respectively) but did not correlate with either the daily or the life-time cigarette consumption, or with urinary cotinine concentrations. sCC16 did not correlate with age or body mass index in the whole study population or in the groups of smokers and non-smokers. These results suggest the reduction in sCC16 concentrations in a group of healthy young smokers may be an early effect of cigarette smoking.
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Clara Cell Protein (CC16) in serum and bronchoalveolar lavage fluid of subjects exposed to asbestos
Biomarkers, 2008Co-Authors: Martin Petrek, Cedric Hermans, Vítězslav Kolek, Jarmila Fialová, Alfred BernardAbstract:The Clara Cell Protein (CC16) is a small and readily diffusible Protein of 16 kDa secreted by bronchiolar Clara Cells in the distal airspaces. These epithelial Cells are altered in several pulmonary pathological processes induced by various lung toxicants. In the search for a new biomarker of asbestos-induced lung impairment, we used a sensitive immunoassay to determine the levels of CC16 in bronchoalveolar fluid (BALF) and serum of subjects exposed to asbestos compared with a group of healthy controls. In the BALF of asbestos-exposed subjects there was an insignificant trend towards CC16 elevation compared with controls, with a (mean +/- SD of 0.81 +/- 0.65 mg l-1 for asbestos-exposed subjects (n = 23) versus 0.39 +/- 0.19 mg l-1 for controls (n = 11) (p = 0.09). In serum, CC16 concentration was significantly increased among asbestos-exposed subjects, with values of 27.2 +/- 24.0 micrograms l-1 for asbestos-exposed subjects (n = 34) versus 16.1 +/- 7.6 micrograms l-1 for controls (n = 34) (p = 0.01). Regarding the effects of smoking, there were significant differences between generally lower CC16 levels in serum and BALF (p = 0.05 and 0.001, respectively) of smokers compared with the higher levels in non-smokers. Serum CC16 levels positively correlated with those in BALF, which is consistent with a diffusional transfer of CC16 from the bronchoalveolar space into the serum. No association, however, emerged between the levels of CC16 in serum or BALF and either the duration of asbestos exposure or the severity of the lung impairment as assessed by chest X-ray. These findings suggest that exposure to asbestos elicits early changes in the local and, importantly, also the systemic levels of CC16. This pneumoProtein therefore appears as a promising non-invasive biomarker of asbestos-induced lung injury and occupational disease in both smoking and non-smoking exposed subjects.
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determinants of serum levels of surfactant Proteins a and b and Clara Cell Protein cc16
Biomarkers, 2003Co-Authors: Cedric Hermans, Alfred Bernard, Ping Dong, Marjorie Robin, Michel Jadoul, Andrew D Bersten, Ian R DoyleAbstract:Increased leakage of surfactant Proteins A and B (SP-A and SP-B) and Clara Cell secretory Protein (CC16) from the air spaces into the circulation occurs in a range of respiratory conditions. However, circulating levels depend not only on the rate of entry into the circulation, but also on the rate of clearance. In order to clarify the role of the kidney in the clearance of these Proteins, serum levels were related to markers of glomerular filtration in 54 non-smoking patients with varying degrees of renal dysfunction, none of whom had respiratory disease or were receiving dialysis at the time of sampling. Serum SP-A was related to SP-B (r = 0.53, p < 0.001) and to CC16 (r = 0.33, p < 0.02). Similarly, SP-B was related to CC16 (r = 0.39, p < 0.004). Stepwise multiple linear regression analysis suggested that serum SP-A and SP-B are influenced by age (approximately 20 and approximately 25% of variance, respectively), whereas CC16 is determined by renal function and, to a lesser extent, by body weight (approximately 63% of variance in total). We conclude that CC16 is cleared from blood by the renal route, whereas SP-A and SP-B are not. Serum SP-A and SP-B are influenced by age, which we speculate reflects increased damage to the alveolocapillary barrier.
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serum Clara Cell Protein a sensitive biomarker of increased lung epithelium permeability caused by ambient ozone
Environmental Health Perspectives, 2000Co-Authors: F Broeckaert, K Arsalane, Enrico Bergamaschi, Angelita Brustolin, Antonio Mutti, Cedric Hermans, Alfred BernardAbstract:Ozone in ambient air may cause various effects on human health, including decreased lung function, asthma exacerbation, and even premature mortality. These effects have been evidenced using various clinical indicators that, although sensitive, do not specifically evaluate the O(3)-increased lung epithelium permeability. In the present study, we assessed the acute effects of ambient O(3) on the pulmonary epithelium by a new approach relying on the assay in serum of the lung-specific Clara Cell Protein (CC16 or CC10). We applied this test to cyclists who exercised for 2 hr during episodes of photochemical smog and found that O(3) induces an early leakage of lung Clara Cell Protein. The Protein levels increased significantly into the serum from exposure levels as low as 0.060-0.084 ppm. Our findings, confirmed in mice exposed to the current U.S. National Ambient Air Quality Standards for O(3) (0.08 ppm for 8 hr) indicate that above the present natural background levels, there is almost no safety margin for the effects of ambient O(3) on airway permeability. The assay of CC16 in the serum represents a new sensitive noninvasive test allowing the detection of early effects of ambient O(3) on the lung epithelial barrier.
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Clara Cell Protein as a marker of Clara Cell damage and bronchoalveolar blood barrier permeability
European Respiratory Journal, 1999Co-Authors: Cedric Hermans, Murielle Wiedig, K Arsalane, Gerard Toubeau, Paul Falmagne, Bernard Knoops, Alfred BernardAbstract:The 16 kDa Clara Cell Protein (CC16), an abundant component of airway secretions, has recently been proposed in humans as a pulmonary marker measurable not only in bronchoalveolar lavage fluid (BALF) but also in serum. The aim of the present study was to investigate the changes and determinants of CC16 concentrations in these fluids in normal rats and rats with lung injury. Female Sprague-Dawley rats were given a single i.p. injection of arachis oil (n=20) or chemicals in arachis oil (n=10) that mainly damage Clara Cells (4-ipomeanol (IPO) 8 mg x kg(-1) and methylcyclopentadienyl manganese tricarbonyl (MMT) 5 mg x kg(-1)) or endothelial Cells (alpha-naphthylthiourea (ANTU) 5 mg x kg(-1)). CC16 concentration (mean+/-sD in microg x L(-1)), measured by a sensitive latex immunoassay, was significantly reduced in BALF of all treated groups (IPO 380+/-100; MMT 730+/-200; ANTU 1,070+/-200; controls 1,700+/-470). The same pattern of decrease was observed in the labelling of Clara Cells with an anti-CC16 antiserum as well as in the CC16 messenger ribonucleic acid levels assessed by Northern enzyme-linked immunosorbent assay. In serum, by contrast, CC16 was significantly increased in all treated groups (IPO 31+/-7; MMT 22+/-12; ANTU 52+/-24; controls 15+/-6). This rise of CC16 in serum was associated with an elevation of albumin in BALF which is an index of increased bronchoalveolar/blood barrier permeability. In conclusion, lung injury induces a decrease of the 16 kDa Clara Cell Protein in bronchoalveolar lavage fluid owing to a reduced production by damaged Clara Cells, and an increase in serum Protein levels resulting from its enhanced leakage across the bronchoalveolar/blood barrier. This study provides new insights into the understanding of the changes of lung secretory Proteins in bronchoalveolar lavage fluid and serum.
Philipp Hotz - One of the best experts on this subject based on the ideXlab platform.
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Clara Cell Protein and surfactant Protein B in garbage collectors and in wastewater workers exposed to bioaerosols
International Archives of Occupational and Environmental Health, 2005Co-Authors: D Steiner, S Jeggli, Alois Tschopp, Anne Oppliger, Silvia Hilfiker, A. Bernard, Philipp HotzAbstract:Objectives: Inhalation of bioaerosols has been hypothesised to cause “toxic pneumonitis” that should increase lung epithelial permeability at the bronchioloalveolar level. Serum Clara Cell Protein (CC16) and serum surfactant Protein B (SPB) have been proposed as sensitive markers of lung epithelial injury. This study was aimed at looking for increased lung epithelial permeability by determining CC16 and SPB in workers exposed to bioaerosols from wastewater or garbage. Methods: Subjects (778 wastewater, garbage and control workers; participation 61%) underwent a medical examination, lung function tests [American Thoracic Society (ATS) criteria], and determination of CC16 and SPB. Symptoms of endotoxin exposure and several potential confounders (age, gender, smoking, kidney function, obesity) were looked for. Results were examined with multiple linear or logistic regression. Results: Exposure to bioaerosols increased CC16 concentration in the wastewater workers. No effect of exposure on SPB was found. No clue to work-related respiratory diseases was found. Conclusions: The increase in CC16 in serum supports the hypothesis that bioaerosols cause subclinical “toxic pneumonitis”, even at low exposure.
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Clara Cell Protein and surfactant Protein b in garbage collectors and in wastewater workers exposed to bioaerosols
International Archives of Occupational and Environmental Health, 2005Co-Authors: D Steiner, S Jeggli, Alois Tschopp, Anne Oppliger, Silvia Hilfiker, Alfred Bernard, Philipp HotzAbstract:Objectives: Inhalation of bioaerosols has been hypothesised to cause “toxic pneumonitis” that should increase lung epithelial permeability at the bronchioloalveolar level. Serum Clara Cell Protein (CC16) and serum surfactant Protein B (SPB) have been proposed as sensitive markers of lung epithelial injury. This study was aimed at looking for increased lung epithelial permeability by determining CC16 and SPB in workers exposed to bioaerosols from wastewater or garbage. Methods: Subjects (778 wastewater, garbage and control workers; participation 61%) underwent a medical examination, lung function tests [American Thoracic Society (ATS) criteria], and determination of CC16 and SPB. Symptoms of endotoxin exposure and several potential confounders (age, gender, smoking, kidney function, obesity) were looked for. Results were examined with multiple linear or logistic regression. Results: Exposure to bioaerosols increased CC16 concentration in the wastewater workers. No effect of exposure on SPB was found. No clue to work-related respiratory diseases was found. Conclusions: The increase in CC16 in serum supports the hypothesis that bioaerosols cause subclinical “toxic pneumonitis”, even at low exposure.
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Lungenerkrankungen bei müllstaubexponierten Personen
Praxis Journal of Philosophy, 2003Co-Authors: D Steiner, S Jeggli, Alfred Bernard, Philipp HotzAbstract:The current cohort study in the canton of Zurich is investigating respiratory diseases in waste collectors. Therefore, a clinical history was taken and lung function tests and measurement of the Clara Cell Protein concentration were carried out. The first results show no elevation of the prevalence of asthma or other lung diseases in waste collectors. Compared with control subjects, waste collectors have a lower forced expiratory volume in the first second and a higher mean Clara Cell Protein concentration. The prevalence of cardiovascular risk factors such as smoking, obesity and arterial hypertension which are not caused by the occupation is high. Indeed, about 50% of all participants are hypertensive.
D Steiner - One of the best experts on this subject based on the ideXlab platform.
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Clara Cell Protein and surfactant Protein B in garbage collectors and in wastewater workers exposed to bioaerosols
International Archives of Occupational and Environmental Health, 2005Co-Authors: D Steiner, S Jeggli, Alois Tschopp, Anne Oppliger, Silvia Hilfiker, A. Bernard, Philipp HotzAbstract:Objectives: Inhalation of bioaerosols has been hypothesised to cause “toxic pneumonitis” that should increase lung epithelial permeability at the bronchioloalveolar level. Serum Clara Cell Protein (CC16) and serum surfactant Protein B (SPB) have been proposed as sensitive markers of lung epithelial injury. This study was aimed at looking for increased lung epithelial permeability by determining CC16 and SPB in workers exposed to bioaerosols from wastewater or garbage. Methods: Subjects (778 wastewater, garbage and control workers; participation 61%) underwent a medical examination, lung function tests [American Thoracic Society (ATS) criteria], and determination of CC16 and SPB. Symptoms of endotoxin exposure and several potential confounders (age, gender, smoking, kidney function, obesity) were looked for. Results were examined with multiple linear or logistic regression. Results: Exposure to bioaerosols increased CC16 concentration in the wastewater workers. No effect of exposure on SPB was found. No clue to work-related respiratory diseases was found. Conclusions: The increase in CC16 in serum supports the hypothesis that bioaerosols cause subclinical “toxic pneumonitis”, even at low exposure.
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Clara Cell Protein and surfactant Protein b in garbage collectors and in wastewater workers exposed to bioaerosols
International Archives of Occupational and Environmental Health, 2005Co-Authors: D Steiner, S Jeggli, Alois Tschopp, Anne Oppliger, Silvia Hilfiker, Alfred Bernard, Philipp HotzAbstract:Objectives: Inhalation of bioaerosols has been hypothesised to cause “toxic pneumonitis” that should increase lung epithelial permeability at the bronchioloalveolar level. Serum Clara Cell Protein (CC16) and serum surfactant Protein B (SPB) have been proposed as sensitive markers of lung epithelial injury. This study was aimed at looking for increased lung epithelial permeability by determining CC16 and SPB in workers exposed to bioaerosols from wastewater or garbage. Methods: Subjects (778 wastewater, garbage and control workers; participation 61%) underwent a medical examination, lung function tests [American Thoracic Society (ATS) criteria], and determination of CC16 and SPB. Symptoms of endotoxin exposure and several potential confounders (age, gender, smoking, kidney function, obesity) were looked for. Results were examined with multiple linear or logistic regression. Results: Exposure to bioaerosols increased CC16 concentration in the wastewater workers. No effect of exposure on SPB was found. No clue to work-related respiratory diseases was found. Conclusions: The increase in CC16 in serum supports the hypothesis that bioaerosols cause subclinical “toxic pneumonitis”, even at low exposure.
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Lungenerkrankungen bei müllstaubexponierten Personen
Praxis Journal of Philosophy, 2003Co-Authors: D Steiner, S Jeggli, Alfred Bernard, Philipp HotzAbstract:The current cohort study in the canton of Zurich is investigating respiratory diseases in waste collectors. Therefore, a clinical history was taken and lung function tests and measurement of the Clara Cell Protein concentration were carried out. The first results show no elevation of the prevalence of asthma or other lung diseases in waste collectors. Compared with control subjects, waste collectors have a lower forced expiratory volume in the first second and a higher mean Clara Cell Protein concentration. The prevalence of cardiovascular risk factors such as smoking, obesity and arterial hypertension which are not caused by the occupation is high. Indeed, about 50% of all participants are hypertensive.