PubMed Health⌕ Search

Biomedical subjects

R Bégin

Publications and source records attributed to R Bégin.

At least 37 records · Page 2Linked to original sources
PubMed1995

Further information on aluminium inhalation in silicosis.

OBJECTIVES: In previous studies, a significant reduction in biological activity of quartz by the surface chemistry of aluminium was noted. Aluminium lactate inhalation one month after quartz exposure significantly suppressed silicosis. In a recent study, it was noted that aluminium inhalation failed to alter the silicosis process after disease was recognised by standard chest radiography in the first year after monthly treatment. METHODS: That study was extended with the same groups of sheep, the aluminium treated group received weekly aerosol of 100 mg of aluminium lactate for an additional two years. All sheep were evaluated at three-month intervals by chest radiography, lung function, and lung lavage. RESULTS: The sheep with silicosis had significantly reduced lung functions, increased cellularity, phospholipids, and hyaluronan. These changes persisted for several years without significant differences between the silicotic sheep with or without the aluminium aerosol treatment. CONCLUSION: Aluminium aerosol treatment of silicosis after radiographic recognition of disease and the end of exposure did not alter the disease process.

Administration, Inhalation↗
PubMed1995

Respiratory health of workers exposed to metal dusts and foundry fumes in a copper refinery.

OBJECTIVES: To assess airflow limitation in workers exposed long term to metal dust, the prevalence of pleural plaques in those workers exposed in the past to asbestos, the influence of pleural plaques on lung function, and the possible association with airway disease caused by asbestos. METHODS: A cross sectional and longitudinal (seven year) survey of 494 long term (mean (SEM) 21(1) years) workers in a copper refinery was carried out from medical questionnaires, chest radiographs, and forced spirometry. RESULTS: The prevalence of lifetime non-smokers was 19%, current smokers 39%, and ex-smokers 42%. The prevalence of chronic obstructive pulmonary diseases (COPD) (forced expiratory volume in one second (FEV1) < 80% predicted) was 5%, small airway dysfunction (SAD) (maximal mid-expiratory flow (MMEF) < 60% predicted) was 7%, and this did not differ from the control population. The COPD and SAD were associated with cumulative smoking index but not with the cumulative work years at the plant or with any type of work at the plant. The mean (SEM) reduction of FEV1 was 20(7) ml in non-smokers, 26(4) ml in smokers, and 26(5) ml in ex-smokers (P > 0.05). In the smokers and ex-smokers with COPD, the loss of FEV1 was 53(10) (P < 0.02). The prevalence of pleural plaques was 11% (P < 0.0001); pleural plaques were found in older workers with known exposure to asbestos. The pleural plaques were circumscribed and associated with a non-significant 196 ml reduction in forced vital capacity (FVC) and non-significant reduction of FVC over time. The pleural plaques were not associated with COPD or SAD. The cumulative smoking index obtained by a technician did not differ from that by a chest physician. CONCLUSIONS: Despite exposures to asbestos that produced pleural plaques and exposures to metal dusts and foundry fumes the long term workers of this plant did not have excessive prevalence of COPD or SAD. The data suggest that low level long term exposure to metal dusts, gases, and foundry fumes do not necessarily cause respiratory dysfunction, circumscribed pleural plaques with low grades of width and extent do not reduce FVC significantly, and exposure to asbestos dust that produced pleural plaques does not necessarily produce airway dysfunction.

Adult↗
PubMed1995

Clara cell protein (CC-16) induces a phospholipase A2-mediated inhibition of fibroblast migration in vitro.

Clara cell protein (CC-16, also designated CC-10) is synthesized by the bronchiolar epithelium and has been suggested as an inhibitor of phospholipase A2 (PLA2) 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 PLA2 activity in alveolar fluids and the influence of CC-16 on platelet-derived growth factor-induced human fibroblast chemotaxis and cytosolic PLA2 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 PLA2 activity (p < 0.05 versus controls). CC-16 inhibited fibroblast chemotaxis in a dose-dependent manner (90% inhibition at 30 micrograms/ml CC-16). This inhibition was reversed by reducing CC-16. CC-16 was also able to lower fibroblastic cytosolic PLA2 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 PLA2 activity. It can be postulated that CC-16 deficiency may contribute to fibroblast burden activity in fibrosing lung diseases.

Adult↗
PubMed1995

Emphysema in silica- and asbestos-exposed workers seeking compensation. A CT scan study.

It has been established that coal pneumoconiosis and confluent silicosis are associated with emphysematous changes in the lungs. In the present study, we addressed the concept of emphysema in simple silicosis and asbestosis and in workers exposed to these minerals without the pneumoconiosis. The study was done on 207 consecutive workers evaluated for possible pneumoconiosis at Québec Workman Compensation Board, who had a radiographic reading of pneumoconiosis in the category 0 or 1 of the ILO scale, and in 5 control subjects. Emphysema was detected, typed, and graded on high-resolution CT scans by three independent experienced readers. Age, work experience and industry, smoking habits, and pulmonary function test results were analyzed for possible associations. The subjects were 59 +/- 1 years of age and had mineral dust exposure averaging 26 +/- 1 years; 31 were lifetime nonsmokers and the others were either ex- or current smokers. Ninety-six workers were from primary and 111 from secondary industries and did not differ in any parameter. The CT scan readings for emphysema yielded a 63% complete agreement. In lifetime non-smokers, emphysema was seen in 1 of 20 subjects without pneumoconiosis but in 8 of 11 patients with pneumoconioses. In smokers without pneumoconioses, emphysema was present in 55% of patients with silica exposure, but 29% of patients with asbestos exposure but comparable smoking (p = 0.04). Emphysema type was equally distributed among the groups except for more paracicatricial type in confluent silicosis. Regression analyses documented that age, smoking, exposure type, and presence of pneumoconiosis were significant contribution factors. In the workers without pneumoconiosis, age, smoking, and exposure type (silica) were significant. Emphysema related best with FEV1/FVC ratio, MMEF, and DCO reductions. The prevalence of abnormality of FEV1/FVC ratio was two to five times normal and that of reduced DCO two times normal. We conclude that, in our population, there was a significant excess of CT scan emphysema, associated with lung dysfunction, in those with pneumoconioses and in smokers with silica exposure. In the absence of smoking, it took a patient with pneumoconiosis to have emphysema. These changes contributed to the lung function impairment of these subjects with ILO category 0 or 1 pneumoconioses.

Analysis of Variance↗
PubMed1995

Alterations of surfactant lipid turnover in silicosis: evidence of a role for surfactant-associated protein A (SP-A).

Type II cell hypertrophy with surfactant accumulation in the lung is a common observation in silicosis. Mechanisms leading to these alterations are poorly understood. By using silica dusts and alveolar fluids from saline and silica exposed sheep, we explored four different pathways of surfactant turnover in vitro: (1) synthesis and (2) secretion of lipids by rat type II cells; and dipalmitoylphosphatidylcholine (DPPC) uptake/reuptake by (3) type II cells and (4) alveolar macrophages. Silica had no direct specific effect on type II cell lipid metabolism. Alveolar fluids from both saline and silica exposed animals induced several alterations compared to control medium: (a) an increase in lipid synthesis (60 to 130%, P < 0.05); (b) a decrease in lipid secretion (25 to 70%, P < 0.05); (c) a 50 to 75% increase in DPPC reuptake by type II cells (P < 0.05); (d) a 65 to 75% decrease in DPPC uptake by alveolar macrophages (P < 0.05). DPPC uptake by in vivo silica exposed alveolar macrophages was reduced. Alterations of surfactant lipid metabolism induced by alveolar fluids from silicotic animals was more pronounced than in those treated with control fluids. Anti SP-A antibodies significantly suppressed most of the alveolar fluid induced effects on surfactant turnover. From these in vitro data, silica-induced type II cell hypertrophy seems to result from an increase in lipid synthesis activity and an imbalance in the lipid secretion/reuptake ratio.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1994

Partial characterization of the proliferative activity for fetal lung epithelial cells produced by silica-exposed alveolar macrophages.

The proliferation of lung epithelial cells is a prominent feature of lung tissue response following silica-induced lung injury and alveolar macrophages are recognized as a major contributing cell to the lung inflammatory processes. In previous studies, a growth-promoting activity for fetal rat lung epithelial cells was observed in silicotic alveolar fluids and in supernatants from in vitro and in vivo silica-exposed alveolar macrophages. In the present work, the biological and physicochemical properties of the macrophage-derived growth-promoting activity for fetal lung epithelial cells were explored. Four peaks of growth-promoting activity for lung epithelial cells ranging from 32 to 7 kDa were found in both in vitro and in vivo silica-exposed macrophage supernatants. The investigations were coupled with biochemical treatments of the mitogenic peaks and blocking antibodies or antisera were used to specify further the nature of the proliferative activities. Among the established growth factors, alveolar macrophage-derived growth fractions had characteristics consistent with platelet-derived growth factor-, insulin-like growth factor 1-, and fibroblast growth factor-like molecules. The cytokine production following in vitro exposure, which reflects very early events in the pathogenesis of silicosis, was more strongly related to the high-molecular-weight PDGF-like molecules, whereas the cytokine production following in vivo exposure, which reflects later events in the pathogenesis of silicosis, was more influenced by intermediate-molecular-weight FGF- and IGF-like molecules.

Animals↗
PubMed1993

Silica-exposed macrophages release a growth-promoting activity for type II pneumocytes.

This study addresses the hypothesis that silica-activated alveolar macrophages could release soluble factors stimulating type II cell proliferation. Macrophages from control sheep were exposed or not in vitro to silica, aluminum-treated silica (Si-Al), or titanium dioxide (TiO2). In addition, macrophages from a model of chromic silica-exposed sheep were studied. Supernatants from unstimulated macrophages were found to double basal type II cell DNA synthesis. Alveolar macrophage-conditioned media (AMCM) collected from cells exposed in vitro to silica induced an additional growth-promoting activity for type II cells. Supernatants from Si-Al- or TiO2 dust-exposed alveolar macrophages had the same effects as unstimulated AMCM. In addition, AMCM from in vivo silicotic sheep cells also contained elevated levels of type II cell mitogenic activity. These results suggest that in vitro as in vivo, silica-activated macrophages produce a type II cell growth factor(s) for type II epithelial cells.

Animals↗
PubMed1993

Surfactant-associated proteins (SP-A, SP-B) are increased proportionally to alveolar phospholipids in sheep silicosis.

In silicosis, a profile of surfactant overproduction associated with type II epithelial cell hypertrophy and hyperplasia has been documented. In addition, enhanced accumulation of surfactant-associated protein A (SP-A) has been seen in the rat model of acute silicosis by 2 independent groups, but the exact role of these surfactant changes in silicosis are incompletely understood. In this study we measured in lung lavage surfactant total phospholipids and surfactant-associated proteins A and B (SP-A, SP-B). In addition, the surface tension reducing activities of lipid extracts of bronchoalveolar lavage fluids (BALFs) in the sheep silicosis model were examined using a pulsating bubble surfactometer. Two groups of animals (n = 18) were investigated: a saline-exposed (PBS-PBS) group and a silica-exposed (Si-PBS) group. Total surfactant phospholipids in the silicotic sheep increased 2-fold over the control sheep values (p < 0.05), as previously reported. In addition, we found a substantial rise in total surfactant-associated proteins, with significant increase in SP-A (1.16 +/- 0.22 micrograms/ml Si-PBS group vs. 0.70 +/- 0.07 micrograms/ml PBS-PBS group, p < 0.05) and a parallel but not significant increase in SP-B (2.68 +/- 0.90 micrograms/ml Si-PBS group vs. 1.10 +/- 0.30 micrograms/ml PBS-PBS group). The surface-tension-reducing activities of alveolar fluid lipid extracts did not differ significantly between the groups (Si-PBS group at maximal bubble radius [Rmax]: 27.0 +/- 1.6 and at minimal bubble radius [Rmin]: 1.0 +/- 0.7 milli Newton/m, vs. PBS-PBS group Rmax: 27.0 +/- 2.2 and Rmin: 0.7 +/- 0.3 milli Newton/m at 4 min pulsation). The ratios of SP-A and SP-B to lipid phosphorus levels document a proportional enhancement of surfactant-associated proteins and phospholipids, thus suggesting a co-ordinated upregulation of both surfactant-associated proteins and phospholipids in this model of silicosis. However, on an individual basis, these changes were not related, suggesting a more complex model of regulation. This study documents significant increases of the surfactant apoproteins proportional to changes in phospholipids in the lung of silicotic sheep. In spite of these alterations of surfactant components, organic solvent lipid extracts of BAPLFs surfactant remained equally effective in reducing surface tension.

Animals↗
PubMed1993

Pulmonary dust retention in a silicon carbide worker.

This paper reports on pulmonary dust retention in a man who worked 42 years in the vicinity of an Acheson furnace of a silicon carbide plant and had a carborundum pneumoconiosis. Special attention is paid to the retained silicon carbide fibers in the lung parenchyma. The concentration of silicon carbide fibers longer than 5 microns is 39,300 fibers/mg dry lung. These fibers have a similar morphology to fibers observed in the working environment. The result is compared to pulmonary retention of workers exposed to asbestos.

Carbon↗
PubMed1993

Effects of phosphorylation of chrysotile on pleuropulmonary fibrogenicity and carcinogenicity.

As well as fibre size, fibre chemistry is a determinant of toxicity of mineral fibres. On these grounds, a few years ago, the asbestos industry in Québec developed a process to modify the surface chemistry of chrysotile asbestos by fixing phosphorous atoms. The pleuropulmonary fibrogenicity and carcinogenicity of the native and surface treated chrysotile, called chrysophosphate, were tested. Both products initiated similar pulmonary fibrogenicity in rats exposed by inhalation and sheep exposed by injection in the tracheal lobe. Tumour production in rats after long term inhalation or intrapleural injection was not different between chrysotile and chrysophosphate. These findings clearly show that modification of the phosphate surface of chrysotile fibres does not appear to alter the pleuropulmonary activities of the mineral, thus arguing against the earlier contention of less biological activity for chrysophosphate, a contention essentially based upon results of in vitro tests. This study strongly argues for in vivo testing of new fibrous materials before making definite conclusions about their biological activities.

Animals↗
PubMed1993

Computed tomography in the early detection of asbestosis.

Computed tomography (CT; both conventional (CCT) and high resolution (HRCT)) scans of the thorax were evaluated to detect early asbestosis in 61 subjects exposed to asbestos dust in Québec for an average of 22(3) years and in five controls. The study was limited to consecutive cases with chest radiographs of the International Labour Organisation categories 0 or 1 determined independently. All subjects had a standard high kilovoltage posteroanterior and lateral chest radiograph, a set of 10-15 1 cm collimation CCT scans and a set of three to five 2 mm collimation HRCT scans in the upper, middle, and lower lung fields. Five experienced readers independently read each chest radiograph and sets of CT scans. On the basis of three to five readers agreeing for small opacities of the lung parenchyma, 12/46 (26%) negative chest radiographs were positive on CT scans, but 6/18 (33%) positive chest radiographs were negative on CT scan. On the basis of four to five readers agreeing on a chest radiograph, 36/66 (54%) subjects were normal (group A), 17/66 (26%) were indeterminate (group B), and 13/66 (20%) were abnormal (group C). By the combined readings of CCT and HRCT, 4/31 (13%) asbestos exposed subjects of group A were abnormal (p < 0.001), 6/17 (35%) of group B were abnormal, and in group C, 1/13 (8%) was normal, 2/13 were indeterminate, and 10/13 (77%) were abnormal. Separate readings of CCT and HRCT on distinct films in 14 subjects showed that all cases of asbestosis were abnormal on both CCT and HRCT. Inter-reader analyses by kappa statistics showed significantly better agreement for the readings of CT than the chest radiographs (p < 0.001), and for the reading of CCT than HRCT (p < 0.01). Thus CT scans of the thorax identifies significantly more irregular opacities consistent with the diagnosis of asbestosis than the chest radiograph (20 cases on CT scans v 13 on chest radiographs when four to five readers agreed, 13% of asbestos exposed subjects with normal chest radiographs or 21% of asbestos exposed subjects with normal or near normal chest radiographs. It decreased the number of indeterminate cases significantly from 17 on chest radiographs to 13 on CT scans. All cases of asbestosis detected only on CT scans were similarly seen on CCT and HRCT and did not have significant changes in lung function. The CT scans significantly reduced the inter-reader variability, despite the absence of ILO type reference films for these scans.

Adult↗
PubMed1993

Phospholipid content of bronchoalveolar lavage fluid in granite workers with silicosis in Quebec.

BACKGROUND: Some of the prominent features of silicosis are hyperplasia and hypertrophy of epithelial type II cells, which in experimental animals are often accompanied by accumulation of phospholipids in the lung. METHODS: The total phospholipid content of lung lavage fluid and its composition in 28 granite stone cutters with long term exposure to silica dust (23 with radiological silicosis) was compared with that of lavage fluid in 15 normal volunteers, 15 patients with untreated idiopathic pulmonary fibrosis, and 19 patients with untreated stage 2 or 3 sarcoidosis. All lavage fluid was obtained at the time of first pulmonary investigation, which also included lung function tests. RESULTS: In the normal subjects total phospholipid content was 1.13 (0.16) micrograms phosphorus/ml of lung lavage, in the patients with idiopathic pulmonary fibrosis 0.52 (0.07) microgram/ml (p < 0.05), and in the patients with sarcoidosis 1.02 (0.20) microgram/ml composition being in the range reported in humans. In the patients with silicosis total phospholipid content was significantly decreased to an average of 0.46 (0.08) microgram/ml compared with the findings in normal subjects and patients with sarcoidosis. Within the group exposed to silica changes in total phospholipid content did not correlate with the severity of the radiographic disease, changes in lung function, the cellularity of lung lavage fluid, or hyaluronate concentrations. The secretory capacity of rat epithelial type II cells was not significantly different when cultured with bronchoalveolar lavage fluid from all four groups of subjects. CONCLUSIONS: Total phospholipid content in lung lavage fluid was significantly reduced in granite workers with radiological evidence of lung disease, but showed no correlation with radiological or functional markers of disease severity.

Adolescent↗
PubMed1993

Farmer's lung. Long-term outcome and lack of predictive value of bronchoalveolar lavage fibrosing factors.

This study evaluates the long-term outcome of farmer's lung (FL), adding high-resolution computed tomograms (HRCT) to previously reported procedures and verifying whether bronchoalveolar lavage (BAL) fluid markers or substrates of fibrosis (hyaluronic acid, Type III procollagen, fibronectin, and fibroblast growth factors) (FF) predict outcome. A total of 33 subjects with a history of FL dating back at least 6 yr were evaluated with pulmonary function tests, chest x-ray (CXR), and HRCT. All subjects had an initial evaluation, which included a BAL, 6 yr before the current study. Subjects were then either in acute FL (n = 19) or in clinical remission despite continued contact (n = 14). In the current study, pulmonary function tests revealed an obstructive profile in 13 subjects, restrictive changes in 1, an isolated decrease in lung diffusion capacity in 3, and normal values in 16. Chest radiographs (CXR) were normal in 22 subjects, abnormal with interstitial or reticulonodular changes in 6, and suggestive of emphysema in 5. HRCT revealed emphysema in 9 subjects; 3 had localized fibrotic changes, 2 a ground-glass pattern, and 19 were normal. There was a good correlation between the findings on pulmonary function tests and HRCT; however, CXR alone did not suggest the existence of emphysema in 4 subjects who had such findings on HRCT. No correlations were found between most outcome parameters and the level of the BAL FF measured 6 yr previously. We conclude that airflow obstruction with or without emphysema is an important long-term sequela of FL and that BAL FF do not predict outcome in this disease.

Acute Disease↗
PubMed1993

Fibrogenic activities in bronchoalveolar lavage fluid of farmer's lung.

Hyaluronic acid (HA), type III procollagen, fibronectin, and fibroblast growth factors (FGF) were measured in 43 bronchoalveolar lavage fluid (BALF) specimens obtained from 38 patients with farmer's lung (FL) and in BALF of 9 nonexposed normal control subjects. Bronchoalveolar lavage was done in 21 farmers with acute FL (acute) and in 22 with a history of previous FL (Ex) who were still in daily contact with dairy barns. All farmers from the acute and Ex groups had a lymphocytic alveolitis, respectively, 62.7 (3.5) percent (mean [SEM]) and 48.1 (4.3) percent. Hyaluronic acid, type III procollagen, fibronectin, and FGF were all highly increased in acute disease. These substances were also increased in the BALF of subjects of the Ex group who had no clinical symptoms or signs of acute disease at the time of lavage, but were actively farming. The increase in type III procollagen, however, was less in this group than in the subjects with acute disease. These observations suggest that the fibrosing activities and potentialities of the allergic alveolitis of FL are fully expressed at the time of clinical presentation and also in the subclinical phase of the disease in susceptible farmers who remain exposed after an initial acute phase of the disease.

Adult↗
PubMed1993

Aluminium inhalation in sheep silicosis.

In prior studies, we and others have documented a significant reduction by surface chemistry modification in the biological activity of quartz. We further documented that aluminium lactate inhalation one month after quartz exposure significantly suppressed the silica-induced alveolitis, reduced the pathological process and decreased the retention of quartz in the lung tissue. In the present study, we evaluated the efficacy of aluminium inhalation in altering the silicosis process after disease was recognized by standard chest radiography. Twenty-four sheep were enrolled in the study. The 14 silica exposed sheep had an abnormal chest radiograph of the ILO category 1 or above after 3 years of 100 mg Minusil-5 in 100-ml saline intratracheal injections. Ten control sheep were exposed to saline intratracheal injections. All sheep were evaluated at 3-month intervals by chest radiography, lung function and lung lavage. At month 36 of the study, all 14 sheep had an abnormal chest radiograph while the radiographs of controls remained normal. The sheep with silicosis had significantly reduced lung functions and increased cellularity, phospholipids and hyaluronan. These changes persisted during the next 12 months without exposure or treatment. At month 48 and at monthly intervals after, for 12 months, aerosol inhalations were carried out with saline alone for control and seven silicotic sheep and with 100 mg of aluminium lactate in 10 ml saline generated with a Bird Mark 8 pressure ventilator for the other seven silicotic sheep. All sheep were evaluated at 3-month intervals by chest radiography, lung function and lung lavage.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1992

Work-related mesothelioma in Québec, 1967-1990.

Prior surveys of malignant mesothelioma in Québec have noted that almost all the excess in occupational exposure related mesothelioma was in the manufacture and industrial application of asbestos rather than in the mining and milling operations. To evaluate the current status of malignant pleural mesothelioma in the Québec workforce, we reviewed all cases of pleural mesothelioma seen and accepted by the Québec Workman's Compensation Board (CSST) for work related compensation of industrial disease. We identified 120 cases, 7 of whom were females. They were of an average age of 59 +/- 8.5 yrs (sd) (range 42-84); they were exposed to asbestos dust in the workplace for an average of 26 +/- 14.3 yrs (range 0.5-50). The cases were subdivided into 3 groups according to workplace asbestos exposures. There were 49 cases originating in the mines and mills of the Québec Eastern Township region (primary industry, group 1), 50 cases from the manufacture and industrial application sector (secondary industry, group 2), and 21 cases from industries where asbestos was not a major work material, often an "incidental" material (tertiary industry, group 3). Group 1 was of an average age of 62 +/- 8 years, exposed to asbestos dust 31 +/- 14 years and the distribution of exposure time was as follows: 15% cases with < or = 10 year-exposure and 77% > or = 25 year-exposure. In group 2, the age was significantly lower at 57 +/- 9 years; the exposure time was also significantly lower at 22 +/- 14 years, and the distribution of exposure time differed from the above (29% cases with < or = 10 year-exposure and 48% > or = 25 year-exposure). In group 3, the average age was 58 +/- 7 years, the exposure time was also significantly lower at 28 +/- 12 years and the distribution of exposure time differed from the above (33% cases with < or = 10 year-exposure and 62% > or = 25 year-exposure). Analyses of the yearly incidence of new cases in each group documented the general incremental trend in all groups, with the sharpest rises in group 3. In the mining towns of Thetford and Asbestos, the incidence of mesothelioma was proportional to the workforce, thus suggesting that the tremolite air contamination, which is 7.5 x higher in Thetford, may not be a significant determinant of the disease in these workers.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1992

Hyaluronan (hyaluronic acid) in lung lavage of asbestos-exposed humans and sheep.

The concentration of hyaluronan was measured in the bronchoalveolar lavage fluid (BALF) of 18 control subjects and 27 workers from the asbestos mills and mines of Québec, 9 without asbestosis and 18 with asbestosis. Hyaluronan was also measured in the BALF of 9 control sheep exposed to 100 ml phosphate-buffered saline (PBS) at 10 day intervals for 39 months, and 13 sheep exposed at the same intervals to 100 mg chrysotile in 100 ml PBS for 24 months. At month 24, the asbestos-exposed sheep were classified into 3 groups: (A) 4 sheep exposed to PBS alone, (B) 4 sheep exposed to 10 mg chrysotile asbestos every 10 days, and (C) 5 sheep exposed to 100 mg chrysotile asbestos every 10 days for 15 months. The BALF hyaluronan averaged 53.9 +/- 7.4 ng/ml in human controls, 67.5 +/- 10.3 ng/ml in asbestos-exposed workers without asbestosis, and 206 +/- 83 ng/ml in workers with asbestosis (p less than 0.05 vs. normal). In the control sheep, BALF hyaluronan was 34.7 +/- 6.9 ng/ml, and it was 31.5 +/- 17.8 ng/ml in the low-dosage asbestos-exposed group (A), 83.0 +/- 27.7 ng/ml in the intermediate-dose group (B), and 248.0 +/- 134.7 ng/ml in the high-dosage group (C) (p less than 0.05 vs. controls). In contrast, the release of plasminogen activator, a protease that may play a role in limiting the fibrotic process, was increased in group A, but not in groups B and C. In conclusion, BALF hyaluronan constitutes an indicator of lung interstitial tissue changes that may reflect the activity of the fibrosing alveolitis associated with chronic asbestos exposure.

Adult↗