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Query: UMLS:C0037116 (silicosis)
 1,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Workers from smelter plants are at high risk from lung injuries due to exposure to quartz sand, clay, resin, loams, airborne metals etc. The aim of this study was to investigate the relevance of the problem and the risk of occupational pathology in metallurgy at "ELMA" plant--Troyan. The study revealed decreased number of occupational lung diseases but the percentage rate (about 10%) of registered new cases with occupational lung diseases was maintained. No new cases with mixed silicosis were recorded. The results were compared to respective national data. Slowly evolving forms of diffusely outlined lung chart with late functional breathing disturbances were prevailing. Chronic bronchitis are presented as a polyetiologic paraoccupational disease.
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PMID:Disturbance of respiratory system in workers in smelter plants. 1112 79

Chronic bronchitis frequently accompanies silicosis in metallurgy workers. Association of the two diseases significantly lowers life quality and disables the patients. Prophylactic measures for the diseases are elimination of the etiologic factors and detection of genetic markers for propensity and insusceptibility to silicosis and chronic bronchitis. Phenotypes of Lewis a-b- system, of Hp2-1 haptoglobin and of group-specific component Gc2-2 could be risk factors for chronic bronchitis in silicosis patients. Those of Lewis a-b+ system, of Hp2-2 haptoglobin and group-specific component Gc1-2 are resistant to chronic bronchitis on silicosis background.
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PMID:[Hereditary polymorphism features in patients with silicosis associated with chronic bronchitis]. 1150 37

In 1997, the International Agency for Research on Cancer (IARC) upgraded its evaluation of crystalline silica to a Group 1 human carcinogen. Criticism against such decision is based on the lack of consistency in experimental results across animal species, violation of an important principle for causality, such as the replication of findings under different circumstances of exposure, and the lack of a clear dose-response curve. The most recent epidemiological literature on the silica-silicosis-lung cancer link replicates the inconsistent findings that have been characterising 50 years of scientific debate in the occupational arena. Exposure circumstances capable of modifying the silica-lung cancer association include chronic bronchitis, composition of the dust mixing, particularly concerning co-occurrence of other known or probable lung carcinogens, total respirable dust, concentration of silica in respirable dust, type of crystalline silica and particle surface characteristics. The hypothesis of a silicosis-mediated pathway points toward an unspecific mechanism shared with other fibrotic conditions, for which silica might be just one of the triggers. In envisaging a multivariate multistep model of lung cancer among silica-exposed workers, silica might be considered as a "passive components of the sufficient cause", i.e., one of the associated risk factors, concurrent or subsequent to the "active component(s) of the sufficient cause" (including, for instance, smoking, asbestos, radon-daughters, arsenic, hexavalent chromium, nickel, polycyclic aromatic hydrocarbons (PAH), and diesel exhausts among the external risk factors; and DNA repair enzymes polymorphism and spontaneous inactivation of tumour suppressor genes among the internal risk factors), which adds up in modulating the tumoral development in not easily predictable directions. If silica acts as a human lung carcinogen depending on certain occupational exposure circumstances, perhaps those circumstances and not silica itself should be classified for their human carcinogenicity potential.
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PMID:Multifactorial aetiology of lung cancer among silica-exposed workers. 1160 27

Occupational exposure to crystalline silica dust is associated with an increased risk for pulmonary diseases such as silicosis, tuberculosis, chronic bronchitis, chronic obstructive pulmonary disease (COPD) and lung cancer. This review summarizes the current knowledge about the health effects of amorphous (non-crystalline) forms of silica. The major problem in the assessment of health effects of amorphous silica is its contamination with crystalline silica. This applies particularly to well-documented pneumoconiosis among diatomaceous earth workers. Intentionally manufactured synthetic amorphous silicas are without contamination of crystalline silica. These synthetic forms may be classified as (1) wet process silica, (2) pyrogenic ("thermal" or "fumed") silica, and (3) chemically or physically modified silica. According to the different physicochemical properties, the major classes of synthetic amorphous silica are used in a variety of products, e.g. as fillers in the rubber industry, in tyre compounds, as free-flow and anti-caking agents in powder materials, and as liquid carriers, particularly in the manufacture of animal feed and agrochemicals; other uses are found in toothpaste additives, paints, silicon rubber, insulation material, liquid systems in coatings, adhesives, printing inks, plastisol car undercoats, and cosmetics. Animal inhalation studies with intentionally manufactured synthetic amorphous silica showed at least partially reversible inflammation, granuloma formation and emphysema, but no progressive fibrosis of the lungs. Epidemiological studies do not support the hypothesis that amorphous silicas have any relevant potential to induce fibrosis in workers with high occupational exposure to these substances, although one study disclosed four cases with silicosis among subjects exposed to apparently non-contaminated amorphous silica. Since the data have been limited, a risk of chronic bronchitis, COPD or emphysema cannot be excluded. There is no study that allows the classification of amorphous silica with regard to its carcinogenicity in humans. Further work is necessary in order to define the effects of amorphous silica on morbidity and mortality of workers with exposure to these substances.
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PMID:Health hazards due to the inhalation of amorphous silica. 1187 95

Human individual sensitivity to health-hazardous occupational factors and probability of developing chronic lung diseases depend on genetic variation of serum and erythrocytic proteins. The present work was aimed at studying the phenotypes of serum and erythrocytic proteins in patients with occupational respiratory diseases. We studied 7 highly polymorphic genetic systems the varieties of which may be connected with development of bronchopulmonary pathology (BPP) and the immune status of the body: proteinase inhibitor (Pi), third component of the complement (C3), transferrin (Tf), group-specific component of blood serum (Gc), haptoglobin (Hp), erythrocytic glyoxalase (Glo) and phosphoglucomutase (PGM) in patients with chronic bronchitis, silicosis, occupational bronchial asthma and in the control group consisting of Moscow population not exposed to occupational hazards and apparently healthy workers of an engineering plant. Considerable differences were revealed in genetic structure of the patients with bronchopulmonary pathology as compared with the apparently healthy people along a series of Integrated system: proteinase inhibitor (Pi), C3, Tf, Gc, PGM. Comparison of the study groups by significant differences in the aggregate of the genetic information obtained suggests that 5 (HP, C3, Tf, Pl, PGM1) of the 7 studied systems showed the hereditary features of silicosis. The gene carriers Hp*2, C3*F, PGM1*2-, TF*D, GC*R due to peculiar biochemical processes appear to have less adaptive potentialities and a greater likelihood of the disease on exposure to industrial factors. The examined patients with chronic bronchitis showed an increase in the variant of GC*2 and of a rare variants of proteins GC*R and Pi*S, the patients with occupational bronchial asthma showed an increase in the variant of Hp*2 and of a rare variant Pi*S. Such studies could be useful for assessment and forecast of individual risk of occupational diseases.
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PMID:Genetic-biochemical criteria for individual sensitivity in development of occupational bronchopulmonary diseases. 1209 83

Occupational exposure is an important risk factor for chronic obstructive pulmonary disease (COPD), and silica dust is one of the most important occupational respiratory toxins. Epidemiological and pathological studies suggest that silica dust exposure can lead to COPD, even in the absence of radiological signs of silicosis, and that the association between cumulative silica dust exposure and airflow obstruction is independent of silicosis. Recent clinicopathological and experimental studies have contributed further towards explaining the potential mechanism through which silica can cause pathological changes that may lead to the development of COPD. In this paper we review the epidemiological and pathological evidence relevant to the development of COPD in silica dust exposed workers within the context of recent findings. The evidence surveyed suggests that chronic levels of silica dust that do not cause disabling silicosis may cause the development of chronic bronchitis, emphysema, and/or small airways disease that can lead to airflow obstruction, even in the absence of radiological silicosis.
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PMID:Chronic obstructive pulmonary disease due to occupational exposure to silica dust: a review of epidemiological and pathological evidence. 1266 Mar 71

The long-term exposure to dust in the hard coal mining industry can lead to various pathological lung changes, especially to chronic bronchitis without and with obstructive ventilation disorder, lung emphysema, pneumoconiosis (coal miner's pneumoconiosis, in Germany categorized as silicosis) and silicotuberculosis. These health disorders show a close pathogenetic and pathophysiological association and should not necessarily be regarded as individual entities. Most exposed subjects demonstrate more or less all of these pathological disorders. On account of individual (genetic?) susceptibility, their degree differs greatly. Some individuals are largely resistent, other subjects show severe effects like emphysema, progressive massive pneumoconiosis, or the Caplan syndrome. Several studies showed that the pathologically verified degree of lung fibrosis is associated with lung crystalline SiO(2) content whereas the emphysema score is inversely correlated with the coal content. With regard to diagnostics and medical expert opinion, it is important that conventional radiology has a low sensitivity. Further, health impairments of miners engaged for longtime which are insurance relevant (MdE) exist in cases without (BK 4111 if beginning after 12/31/1992) or with coalworkers' pneumoconiosis even for categories < 2/3.
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PMID:[Effects on the lung due to underground coal mining work]. 1496 33

Mining production has accounted for around 50% of the gross industrial product in Mongolia since 1998. Dust-induced chronic bronchitis and pneumoconiosis currently account for the largest relative share (67.8%) of occupational diseases in Mongolia, and cases are increasing annually. In 1967-2004, medically diagnosed cases of occupational diseases in Mongolia numbered 7,600. Of these, 5,154 were confirmed cases of dust-induced chronic bronchitis and pneumoconiosis. Lung diseases and other mining-sector health risks pose major challenges for Mongolia. Gold and coal mines, both formal and informal, contribute significantly to economic growth, but the prevalence of occupational lung diseases is high and access to health care is limited. Rapid implementation of an effective national program of silicosis elimination and pneumoconiosis reduction is critical to ensure the health and safety of workers in this important sector of the Mongolian economy.
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PMID:Occupational lung diseases and the mining industry in Mongolia. 1771 77

The study covers comparative analysis of silicosis course in males and females engaged into iron industry. Findings are more frequent combination of silicosis and chronic bronchitis in the females, without smoking habit. Some other differences in silicosis course and development were seen dependent on sex.
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PMID:[Peculiarities of silicosis course in women engaged into metallurgy]. 2218 Sep 69

Coal mining remains a sizable industry, with millions of working and retired coal miners worldwide. This article provides an update on recent advances in the understanding of respiratory health issues in coal miners and focuses on the spectrum of disease caused by inhalation of coal mine dust, termed coal mine dust lung disease. In addition to the historical interstitial lung diseases (coal worker's pneumoconiosis, silicosis, and mixed dust pneumoconiosis), coal miners are at risk for dust-related diffuse fibrosis and chronic airway diseases, including emphysema and chronic bronchitis. Recent recognition of rapidly progressive pneumoconiosis in younger miners, mainly in the eastern United States, has increased the sense of urgency and the need for vigilance in medical research, clinical diagnosis, and exposure prevention. Given the risk for disease progression even after exposure removal, along with few medical treatment options, there is an important role for chest physicians in the recognition and management of lung disease associated with work in coal mining.
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PMID:Coal mine dust lung disease. New lessons from old exposure. 2359 Feb 67


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