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At least 613 records · Page 34Linked to original sources
PubMed1980

Experimental silicosis: morphologic and biochemical abnormalities produced by intratracheal instillation of quartz into guinea pig lungs.

Six months after intratracheal instillation of silica, histologic, ultrastructural, cytologic, and biochemical studies were performed on the lungs of guinea pigs. The tissue response consisted of both diffuse alveolar septal infiltration with interstitial fibrosis and granulomatous infiltration with nodular fibrosis. Ultrastructural studies confirmed the presence of a mixed inflammatory exudate in the alveolar interstitium (histiocytes, neutrophils, eosinophils, and lymphocytes) and the Type II lining of cell hyperplasia. The number of lung cells recovered by lavage and the proportions of neutrophils and multinucleated cells in bronchoalveolar cells were significantly greater in experimental animals (P < .05) than in controls (intratracheal saline). Total lung collagen and collagen synthesis by cultured lung tissue were also increased in the experimental animals. Since the response of guinea pig lung to intratracheal silica included pathologic features common to human silicosis and idiopathic pulmonary fibrosis, this model has the potential for improving our understanding of both of these important clinical disorders.

Animals↗
PubMed1983

Angiotensin converting enzyme in the serum of rats with experimental silicosis.

The development of silicosis in rats given an intratracheal dose of silica was followed both by normal histological procedures and by measuring the level of angiotensin converting enzyme in the serum. The histological changes demonstrated a variable response due to the uneven deposition of material given by the intratracheal route. While the enzyme activity in the serum increased in the treated group it was not well correlated with the histological changes.

Animals↗
PubMed1984

[Is scleroderma without silicosis also an occupational disease?].

Clinical, roentgenological and lung-physiological findings in 5 patients with progressive scleroderma are reported. All of them showed an intensive exposure to crystalline silica of many years however without evidence of a silicosis. Criteria for legal recognition as an occupational disease are intensity and duration of quartz dust exposure. Legal recognition in the G.D.R. can be achieved in a special procedure called "Sonderentscheidverfahren".

Aged↗
PubMed1983

[Pleural mesothelioma, asbestosis and silicosis following long-term exposure to talc dust].

A case report with pleural mesothelioma, asbestosis and silicosis after long time exposure to talc dust has been given. Pathological findings, professional exposure, diagnostic aspects, and medical assessment of disablement are described. The relationship between the diseases of lungs and the professional exposure to talc dust as well as the possibility of cause-distinction by co-working of pathologist and industrial hygienist are discussed.

Aged↗
PubMed1978

[Experimental silicosis. I. Fibrogenic effect of synthetic amorphous silica].

Fibrogenic properties of two dusts of synthetic hydrated amorphous silicas, Ze-O-Sil (French production) and Arsil (Polish production) were studied. Experimental silicosis was induced by intratracheal administration to rats of a single dust dose (50 mg in 0.6 ml NaCl). Fibrogenic properties were tested 3, 6, 9 months after administration of the dust. X-ray diffraction and chemical tests did not reveal any form of crystalline. Si02 in the composition of the investigated dusts. The dusts tested as compared with quartz, were characterized by a great solubility up to 211 mg/l, which made the dust excretion from the lungs easy; after 6 month-experiment approximately 1.2 mg of Arsil dust and about 28 mg of quartz dust residue was found. Fibrogenic properties of Arsil dust, represented by wet lungs weight increase and hydroxyproline content in lungs, were more pronounced than those of Ze-O-Sil. Hydroxyproline content 3 months after administration of Arsil, Ze-O-Sil, TiO2 and weak quartz amounted to 7.3 mg, 5.1 mg, 3.8 mg and 6.0 mg, respectively. Histological and ultrastructural investigations demonstrated that disseminated, multifocal granulomas were the basic reaction to both dusts; no clear histological signs of cytolytic action on the cells of dust granulomas were found. In the lungs no silicotic nodules or degeneration of changes were revealed. Neither biochemical tests nor histological examinations revealed a progressive development of fibrous connective tissue. In result of the studies the authors suggest 2 mg/m3 as a MAC value for Arsil dust instead of 10 mg/m3--the value which has been hitherto used.

Animals↗
PubMed1982

Acute experimental silicosis. Lung morphology, histology, and macrophage chemotaxin secretion.

The acute inflammatory reaction in the lungs of guinea pigs produced by the intratracheal injection of silica was assessed by histologic studies and whole-lung lavage 1, 2, 4, 7, and 14 days after the intratracheal instillation of quartz particles or saline. In addition, lavaged macrophages were cultured in vitro, and the media were assayed for chemotactic factors. This exposure to silica produced a neutrophilic inflammatory response around terminal bronchioles that was well developed within 1 day after injection. Four days after injection, neutrophils were replaced by mononuclear cells; and by 7 days, loosely organized granulomas and collagen deposition were detected in the interstitium. The number of neutrophils (PMNs) recovered by lavage from experimental animals was greatest 1 day after injection and was significantly greater (P less than 0.01) than that for controls at all time points. In contrast, the number of macrophages recovered by lavage did not exceed control levels until 7 days after injection and remained elevated thereafter. Thus, the cells recovered by lavage tended to mirror the changes seen in the inflamed lung. In experiments utilizing blind-well chemotactic chambers, both peritoneal exudate neutrophils and macrophages migrated toward supernatants from cultures of alveolar macrophages lavaged from silica-exposed animals in greater numbers (P less than 0.02) than toward supernatant from control animal macrophage cultures at each time point. Migration of normal alveolar macrophages toward supernatants from all cultures was minimal. Thus, exposure to silica in vivo appears to be a potent stimulus for the release of neutrophil and monocyte chemotactic factors by alveolar macrophages in vitro. The correlation between the types of inflammatory cells identified in the lung both microscopically and by lavage and the chemotactic factors released in vitro by alveolar macrophages from these lungs suggests that alveolar macrophages play a role in mediating pulmonary inflammation in this form of experimental silicosis.

Acute Disease↗
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

Studies on structural changes of collagen in silicosis.

In order to provide scientific information on the prevention and treatment of silicosis, studies about changes of silicotic collagen in lungs were carried out. In this paper, we present experiments about the structural changes of collagen in silicotic lungs of rats and patients. These included electron microscopy, circular dichroism and infrared spectroscopy studies of collagen fibers. The results indicated that fibers of silicotic collagen were shorter in length, smaller in diameter and decreased in alpha-helix content. The -Si-O-R- group and -OH group were found increased and -C-C- backbone shortened. The increase of -Si-O-R- group indicated that silica formed linking bridges between collagens which may be the cause of progressive enlargement of nodules.

Animals↗
PubMed1995

Workers, industry, and the control of information: silicosis and the Industrial Hygiene Foundation.

This essay focuses on the early history of industry and professional relationships around silicosis, the debilitating occupational lung disease, through a study of the role of the Industrial Health Foundation, an industry-sponsored group which has played a critical role in shaping the nation's agenda regarding industrial disease. From its start during the Depression, it has portrayed itself as an industry-sponsored agency that depended upon detached, disinterested professionals and experts to develop effective programs to address occupational disease. As an organization that brought together professional industrial hygienists, business groups, government officials, academics and researchers it serves as a means for understanding the intertwining of industrial and academic agendas. We explore some of the issues that arose regarding public policy and scientific investigations, asking: Under what conditions is it appropriate for professionals and scientists to work together with industrially sponsored organizations? What are the pressures that shape research questions, the range of possible solutions, and the control of scientific data? How can technically trained individuals avoid real or perceived conflicts of interest? At what point does the ostensibly disinterested goals of professionalism conflict with the self-interest of the sponsoring organizations?

Foundations↗
PubMedDate not supplied

[Pulmonary silicosis associated with MacLeod syndrome: a case report].

The paper reports a case of silicosis associated with idiopathic unilateral hyperlucent lung--MacLeod's disease (ML)--in a 65-year old miner. ML had not been diagnosed before this clinical observation and the patient had been exposed to silica dust for about 15 years as a truck operator in water supply tunnelling work in central Italy. Impaired ventilatory function due to left pulmonary dystrophy was the favouring or even the causal factor of dust accumulation in the functionally active right lung and of the tissue reaction to the dust, leading to interstitial fibrosis. A radiological diagnosis of p 1/0 pneumoconiosis was made according to the 1980 International Labour Office classification. Clinical, radiological and functional findings indicated the presence of respiratory failure as a result of the sum of silicotic and dystrophic lesions. Two combined pulmonary scintigraphic examinations with Tc99 perfusional and mTc-DPTA inhalatory methods revealed peculiar alterations: absence of ventilation associated with severe vascular impairment in the left lung, inequality of the ventilation/perfusion rate, due to pneumoconiosis, in the right lung. MacLeod's disease is rare, but must be considered as a mandatory contra-indication for work involving dust exposure risk since it is one of the predisposing factors which can cause an occupational disease even if environmental exposure standards are observed.

Aged↗
PubMed1993

[Anatomo-radiologic definition of minimal interstitial silicosis and diagnostic contribution of high-resolution computerized tomography].

Minimal interstitial silicosis (MIS) is a histologic entity characterized by questionable radiologic findings--i.e., the p/p 0/1 and 1/0 classes of the International Labour Office (ILO) 1980 classification. Thus, the condition may be responsible for borderline radiologic findings ("suspect" phase of pneumoconiosis). In order to test an alternative method to conventional radiology (CR), HRCT was performed on 35 workers exposed to silica and with histologic diagnosis of MIS: HRCT scans were compared with posteroanterior chest radiographs by using the ILO classification. Histology was the gold standard. HRCT identified many more MIS lesions. Moreover, the superiority of HRCT over CR was also proved by its better correlation with pathologic findings. HRCT provided pieces of information which could not always be obtained by means of conventional chest films. Thus, HRCT can be considered the method of choice in MIS before transbronchial lung biopsy.

Adult↗
PubMed1993

[Silicosis and systemic diseases].

We present case histories of 5 patients with silicosis who developed systemic lupus erythematosus and microscopic polyarteritis in two cases each, and rapidly progressive glomerulonephritis (limited Wegener's granulomatosis) in one case. An association between silica exposure and autoimmune disease is emphasized.

Aged↗
PubMedDate not supplied

How silicosis and coal workers' pneumoconiosis develop--a cellular assessment.

In vitro and in vivo animal studies, as well as human investigations, strongly support the role of macrophage products in the development and progression of silicosis and coal workers' pneumoconiosis. Such products include enzymes and reactive oxygen species which may cause lung damage; cytokines which recruit and/or activate polymorphonuclear leukocytes and thus result in further oxidant damage to the lung; and fibrogenic factors which induce fibroblast proliferation and collagen synthesis. This mechanistic understanding of pulmonary disease should assist in developing strategies for prevention and treatment.

Animals↗
PubMed1993

Triple lung cancers in a patient with silicosis.

A case of pulmonary silicosis associated with triple lung cancers is presented. Two of the three tumors were unexpected clinically. The discussion deals with the diagnostic difficulty in radiological differentiation between the pneumoconiotic mass lesion and superimposed tumor shadows, as well as the possible causal relationship between the two conditions. From the practical point of view, elderly patients with pneumoconiosis should be carefully monitored for the development of lung cancer.

Adenocarcinoma, Bronchiolo-Alveolar↗
PubMedDate not supplied

Clinical aspects of coal workers' pneumoconiosis and silicosis.

Coal workers' pneumoconiosis and silicosis are two important respiratory disorders that result from the inhalation of respirable particles in mining. This chapter focuses on the clinical aspects of these disorders, including their pathogenesis and pathology, and approaches to their evaluation and management.

Coal Mining↗
PubMedDate not supplied

Demonstration of the neutrophil granulocyte functional capacity in silicosis, using the NBT test.

The functional capacity of neutrophils was studied using the NBT test in 68 patients with silicosis in various evolutive stages, comparatively with a group of 35 controls. The NBT test showed an initial increase of nonspecific cellular reactivity which decreased as the disease evolved. The results in the control group showed 9 +/- 5% NBT positive neutrophils. The highest proportion of NBT positive neutrophils (17.6 +/- 2.3, p < or = 0.05) was found in stage I of the disease and then decreased gradually with the evolution of the disease. The proportion of NBT positive neutrophils may be considered as a biochemical marker of neutrophil functionality.

Biomarkers↗
PubMed1995

A biochemical study on combined treatment of experimental silicosis with tetradrine-PVNO and tetradrine-QOHP in rats.

A better understanding is needed to explain the mechanism of therapeutic effect of combined use of tetradrine-PVNO and tetradrine-QOHP which play very important roles in treatment of silicosis. Blood prolidase (PLD), monamine oxidase (MAO) and plasminogen (PLG) in silicotic rats after treatment with tetradrine-PVNO or tetradrine-QOHP were measured. The values obtained were compared with the untreated silicotic rats. It was found that the silicotic rats that received tetradrine-PVNO showed significant increase in PLD and decrease in PLG, but no significant change in MAO. The PLD in plasma of silicotic rats that received tetradrine-QOHP were elevated significantly, but PLG and MAO did not change appreciably. These findings suggest that the combined use of tetradrine-PVNO and tetradrine-QOHP can accelerate the degradation of collagen in silicotic rats.

Alkaloids↗