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Query: UMLS:C0032273 (pneumoconiosis)
 1,578 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diagnosis of pneumoconiosis was made in 2 dental technicians presenting with interstitial lung disease. The occupational origin of inhaled dust was confirmed by mineralogic analyses, which disclosed mainly large amounts of chromium-cobalt-molybdenum particles originating from Vitallium prostheses, but also showed abrasives (silica and silicon carbide) and asbestos in 1 patient. The presence of Vitallium and its chemical stability in bronchoalveolar lavage and lung several years after cessation of exposure confirm the resistance of this alloy to corrosion by body fluids. This contrasts with the high solubility of cobalt described in cobalt or hard metal disease. We suggest that dental technician's pneumoconiosis is a complex pneumoconiosis distinct from silicosis, asbestosis, or hard metal disease and that Cr-Co-Mo alloys play a role in its pathogenesis.
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PMID:Dental technician's pneumoconiosis. A report of two cases. 394 27

One hundred and seventy-eight dental laboratory technicians and 69 non-exposed controls participated in an epidemiological respiratory study. Eight technicians who had a mean of 28 years' grinding nonprecious metal alloys were diagnosed as having a simple pneumoconiosis by chest radiograph. Mean values for per cent predicted FVC and FEV1 were reduced among male nonsmoker technicians compared to male nonsmoker controls; after controlling for age, there was also a reduction in spirometry with increasing work-years. An industrial hygiene survey was conducted in 13 laboratories randomly selected from 42 laboratories stratified by size and type of operation in the Salt Lake City, Utah metropolitan area. Personal exposures to beryllium and cobalt exceeded the Threshold Limit Values (TLVs) in one laboratory. Occupational exposures in dental laboratories need to be controlled to prevent beryllium-related lung disorders as well as simple pneumoconiosis.
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PMID:Pneumoconiosis and exposures of dental laboratory technicians. 649 19

The clinical heterogeneity of hard metal disease lung with its two basic forms, i.e. hart metal pneumonitis and hard metal asthma, supports the view of different pathogenetic mechanisms. Cobalt, which is generally considered the noxious agent in hard metal diseases, is cytotoxic on the one hand and allergenic on the other. Four typical, extensively investigated cases are presented, i.e. hard metal pneumoconiosis, hypersensitivity pneumonitis, toxic-irritative hard metal asthma and allergic cobalt asthma. The immunological results were negative in the patient with hard metal pneumoconiosis. A hard metal grinder with typical occupational hypersensitivity pneumonitis showed a high level of precipitating antibodies against Aureobasidium pullulans, a well-known antigen in humidifier fever and sequoiosis. The inhalative provocation test induced on both patients with hard metal asthma an immediate and prolonged, i.e. a dual asthmatic reaction. Only the patient with allergic contact eczema due to cobalt and a positive epicutaneous test of the delayed type and a positive scratch tests of the immediate type with cobalt chloride.
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PMID:[Occupation-related lung diseases in hard metal production and manufacturing. An allergic process?]. 713 42

Experimental pneumoconiosis was induced by intratracheal injection of dusts of presintered cemented tungsten carbide, G2 (WC : Co=98 : 2) and TX20 (WC : Co : TiC : TaC=64 : 16 : 6 : 14) into the lungs of rats in order to document the pathological changes in lung tissues associated with environmental cobalt and tungsten. The following results were obtained. 1) Six months after the administration of G2 and TX20 dusts, marked fibrotic foci were noted and tungsten was detected in the lung tissues of all of the experimental animals. 2) Twelve months after the administration of both dusts, both the fibrotic changes and the tungsten levels were reduced in both test groups, but the reduction was more notable in the G2 group. The cases with fibrotic changes were relatively concomitant with the cases in which tungsten was detected. 3) On examination of tissue levels of cobalt derived from the dust, the cobalt levels in the lungs and bone tissues were less influenced by the dust of the G2 group at any point of investigation, whereas only the pulmonary cobalt levels at six months after the administration of the TX20 group showed a remarkable influence from the dust cobalt (p less than 0.01). 4) In the cases where tungsten was detected six months after the administration of both groups and twelve months after the administration of the TX20 group, pulmonary cobalt levels had not reached the value that should have been gained by the addition of expected values (dust cobalt levels calculated from the tungsten levels) to the control values. 5) The above results indicate that both G2 and TX20 dusts induced marked fibrotic changes in rat pulmonary tissues. However, these changes were reversible to some extent. In addition, a portion of the dust cobalt was dissolved in the body fluid and disappeared from the pulmonary fields.
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PMID:[Experimental pneumoconiosis induced by cemented tungsten and sequential concentrations of cobalt and tungsten in the lungs of the rat (author's transl)]. 727 46

A cross-sectional study, with 1,237 employees solely exposed to hard alloy dust and 502 controls in four hard metal works and two tool and grinder manufacturers in China, was conducted. Results showed prevalence of symptoms of respiratory system, and abnormalities in lung function and serum level of ceruloplasmin and urine cobalt content in exposed group were significantly higher than those in controls. Eight cases of pneumoconiosis were detected by chest X-ray films with a prevalence of 0.65% and an average length of employment in dust environment of 25.2 years. It suggested hard alloy dust could cause pulmonary fibrosis and pneumoconiosis in exposed workers.
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PMID:[An epidemiologic study on pulmonary fibrosis caused by hard alloy dust]. 779 83

Exposure to cobalt can give rise to adverse health effects related to various organs or tissues, such as the respiratory organs, the skin, the hematopoietic tissues, the myocardium, the thyroid gland, as well as teratogenic and carcinogenic effects. In occupational and environmental health, it is important to identify effects that occur at relatively low exposure, i.e. the critical effects which are crucial for preventive action. The limited database available on cobalt toxicity makes it difficult to select critical effects. For dermal exposures, allergic dermatitis may be regarded as such an effect, even if this is a reversible condition and dose-response relationships need to be defined. For inhalation exposures, effects on the respiratory tract can be considered as critical effects. Evidence of cobalt carcinogenicity in humans is inadequate and cannot be evaluated quantitatively but an extra safety factor to be added on exposures estimated from other effects may well be needed. Risks for development of pneumoconiosis are likely to be dependent on physical and chemical characteristics of airborne cobalt containing particles, but such information is lacking in most studies. It has been recognised for many years that there is an excess risk of pneumoconiosis when exposure to cobalt containing dust exceeds 100 micrograms/m3. Recently considerably lower concentrations occurring in the cobalt diamond industry have given rise to such effects. Irritation of mucous membranes may occur at 5-10 micrograms/m3.
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PMID:Assessment of risks in occupational cobalt exposures. 793 97

Hard metal lung disease is usually easy to diagnose, on the basis of occupational history, chest X-ray appearance of interstitial lung disease and, if necessary, by bronchoalveolar lavage (BAL). However, other interstitial lung diseases may affect patients with an occupational history of exposure to cobalt. In hard metal disease, the hylar lymphnodes may enlarge due to high draining of hard metals from the lung tissue via lymphatic vessels. Also, the presence of Giant Cells (even if Langhan's type) in the BAL fluid of sarcoid patients may be high. We present four patients with a history of exposure to hard metals and whose chest X-rays suggest sarcoidosis, stage II; in each, a pulmonary biopsy was necessary to confirm the diagnosis. Final diagnosis was sarcoidosis in one (showing typical granulomata in the lung tissue), and hard metal disease in three: two of these had foreign body-type granulomata in the lung tissue. Neutron activation analysis (NAA) study was carried out on these four patients using specimens of BAL fluid, blood, urine, toenails, pubic hair and sperm. In the light of available data, the concentration of elements may not be useful in differentiating between sarcoidosis and hard metal pneumoconiosis. However, NAA on BAL fluid or other specimens may be helpful in confirming the presence of the offending agent in suspected cases when the occupational history is not clear.
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PMID:The differential diagnosis of hard metal lung disease. 793 13

Dental technician's pneumoconiosis (DTP) is a rather recent finding in subjects exposed to the dust generated in dental laboratories producing metal-framed removable partial dentures from alloys based on cobalt, chromium, and molybdenum. This study presents details of the first three Swedish cases of DTP with some emphasis on the diagnostic procedures and the dust exposure. A follow-up of at least 5 years from diagnosis is included.
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PMID:Three cases of dental technician's pneumoconiosis related to cobalt-chromium-molybdenum dust exposure. 861 99

This article reports on a case of pneumoconiosis in a dental laboratory technician with a history of respiratory exposure to dental materials. Special attention is paid to the mineralogical analysis of the lung biopsy. The abundance of chromium, cobalt, and silica particles suggests that the dental technician's pneumoconiosis is the result of the combined effects of hard metal dusts and silica particles generated during finishing dental frameworks. Adequate technical protection such as a local ventilation system should be considered in dental laboratories to prevent respiratory exposure of dental technicians to airborne contaminants.
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PMID:Mineralogy of lung tissue in dental laboratory technicians' pneumoconiosis. 1078 86

Pneumoconiosis was diagnosed by open lung biopsy in two dental technicians who had interstitial lung disease. Mineralogical analysis was performed to investigate the origin of the dust that had been inhaled. A marked accumulation of silicon and phosphorus was found in both cases. The hard metals chromium and cobalt were also found. Dental technician's pneumoconiosis is a complex pneumoconiosis in which such dust and hard metals may play a role.
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PMID:Dental technician's pneumoconiosis: mineralogical analysis of two cases. 1261 95


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