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

In two mines, "A"--in Lower Silesia with low, inclined coal seam and lesser degree of output mechanization and "B"--in the Silesia-Dabrowa Basin with high coal seams and a great degree of output mechanization), work conditions were examined (dust concentration, chemical composition of dust, and microclimate) and medical examinations of underground miners were done. The examinations involved: mine "A"--2094 miners, mine "B"--1846 miners. The two examined populations were almost identical as regards age and length of employment. The number of miners working in bad conditions in the "A" mine was twice as great as that of miners working in bad conditions in the "B" mine. In dust collected on work--stands in the "A" mine the amount of copper, chromium and vanadium was 3 times that in the "B" mine and in the "A" mine approximately 40% more nickel was found in the dust than in the "B" mine. Average dust concentration on work stands was 10 times greater in the "B" mine than in the "A" mine. The rate of pneumoconiosis was on average 3.7% in both populations, in the "A" mine--6.2% and in the "B" mine--0.8%. In currently working miners no nodular changes, like PMF, were found. The rate of pneumoconiosis significantly varied with the length of employment. In 71.7% miners changes in EKG were found, in the "B" mine the number of those with changes being about 10% greater than in those in the "A" mine. In miners from the "A" mine, mostly changes in conduction (17.1%) were found; in the "B" mine these changes were twice less frequent.
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PMID:[Respiratory tract diseases in coal miners. I. Pneumoconiosis]. 51 72

Sintered permanent magnets are made from the powdered metals of cobalt, nickel, aluminium, and various rare earths. During production, exposure to respirable crystalline silica and asbestos may also occur. Reported here is a cross sectional study of 310 current and 52 retired hourly employees who worked 10 or more years making sintered magnets. Each participant had a chest radiograph, spirometry, and completed a respiratory questionnaire. Illness logs were also reviewed to calculate the incidence of recorded respiratory disorders. The prevalences of abnormalities in pulmonary function and respiratory symptoms were not higher than found in an external referent population. Although the prevalence of diffuse parenchymal opacities consistent with pneumoconiosis (four workers) was similar to the referent population, one worker had radiographic findings consistent with silicosis and two workers had profusion scores of 1/2 or above, not seen in the referent group. The incidence of reported respiratory conditions in the log, including asthma, was 10 times that of other manufacturers in the same industrial classification category. Excessive exposures to cobalt, nickel, and respirable silica were shown by environmental measurements.
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PMID:Characterisation of respiratory health and exposures at a sintered permanent magnet manufacturer. 191 3

The authors provide the results of clinical, x-ray, functional and specific allergological examinations made in 396 cutters. Characterize the main forms of occupational respiratory pathology--pneumoconiosis and chronic bronchitis. Haptene metals (chromium, nickel, manganese) contained by the industrial aerosol were established to produce a sensitizing action on the body. The data obtained may be of importance for the diagnosis and prevention of occupational diseases in cutters, expert medical evaluation of the working capacity and follow-up of the patients.
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PMID:[Occupational lung pathology in gas cutters]. 215 Jul 23

The type of lung disease caused by metal compounds depends on the nature of the offending agent, its physicochemical form, the dose, exposure conditions and host factors. The fumes or gaseous forms of several metals, e.g. cadmium (Cd), manganese (Mn), mercury (Hg), nickel carbonyl (Nl(CO)4, zinc chloride (ZnCl2), vanadium pentoxide (V2O5), may lead to acute chemical pneumonitis and pulmonary oedema or to acute tracheobronchitis. Metal fume fever, which may follow the inhalation of metal fumes e.g. zinc (Zn), copper (Cu) and many others, is a poorly understood influenza-like reaction, accompanied by an acute self-limiting neutrophil alveolitis. Chronic obstructive lung disease may result from occupational exposure to mineral dusts, including probably some metallic dusts, or from jobs involving the working of metal compounds, such as welding. Exposure to cadmium may lead to emphysema. Bronchial asthma may be caused by complex platinum salts, nickel, chromium or cobalt, presumably on the basis of allergic sensitization. The cause of asthma in aluminium workers is unknown. It is remarkable that asthma induced by nickel (Ni) or chromium (Cr) is apparently infrequent, considering their potency and frequent involvement as dermal sensitizers. Metallic dusts deposited in the lung may give rise to pulmonary fibrosis and functional impairment, depending on the fibrogenic potential of the agent and on poorly understood host factors. Inhalation of iron compounds causes siderosis, a pneumoconiosis with little or no fibrosis. Hard metal lung disease is a fibrosis characterized by desquamative and giant cell interstitial pneumonitis and is probably caused by cobalt, since a similar disease has been observed in workers exposed to cobalt in the absence of tungsten carbide. Chronic beryllium disease is a fibrosis with sarcoid-like epitheloid granulomas and is presumably due to a cell-mediated immune response to beryllium. Such a mechanism may be responsible for the pulmonary fibrosis occasionally found in subjects exposed to other metals e.g. aluminium (Al), titanium (Ti), rare earths. The proportion of lung cancer attributable to occupation is around 15%, with exposure to metals being frequently incriminated. Underground mining of e.g. uranium or iron is associated with a high incidence of lung cancer, as a result of exposure to radon. At least some forms of arsenic, chromium and nickel are well established lung carcinogens in humans. There is also evidence for increased lung cancer mortality in cadmium workers and in iron or steel workers.
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PMID:Metal toxicity and the respiratory tract. 217 66

A hygiene study of a hard metal factory was conducted from 1981 to 1984. All workers exposed to hard metal were medically examined and their exposure to cobalt measured. Eighteen employees had occupational asthma related to exposure to hard metal, a prevalence rate of 5.6%. Nine had a positive bronchial provocation test to cobalt and reactions of the immediate, late, or dual type were elicited. Exposure measurements suggest that asthma may be caused by cobalt at a mean time weighted average concentration below 0.05 mg/m3. Only two of the nine individuals with cobalt asthma had a positive patch test to cobalt. Chest radiographs of three workers showed diffuse shadows of category 1 or over. X ray microanalysis of lung biopsy specimens from two of these three workers showed the presence of tungsten, titanium, cobalt, nickel, and some minerals. One of the two was diagnosed as having pneumoconiosis due to exposure to silica in a steel industry and the other was suspected of having pulmonary fibrosis caused by dust generated from the carborundum wheels used to grind hard metal. There were no cases with interstitial pneumonitis in the factory.
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PMID:Respiratory diseases in hard metal workers: an occupational hygiene study in a factory. 371 95

To investigate the pathogenicity of nickel oxide (NiO), hamsters received life-span exposures to that compound (approximately 55 mg/m3) seven hours per day, five days per week. Heavy pulmonary nickel oxide burdens resulted in pneumoconiosis but in no significant carcinogenicity, specific toxicity, or mortality. Two-month exposures of hamsters to nickel-enriched fly ash (NEFA) or fly ash (FA) aerosols (approximately 185 mg/m3) resulted in a deep lung burden of about 5.7 mg, dark discoloration of lungs, heavily dust-laden macrophages, and significantly higher lung weights than in controls, but only minimal inflammatory reaction and no deaths. The NEFA contained 9% nickel; FA contained 0.03% nickel. Exposure to aerosols of NEFA (70 or 15 mg/m3; 6% nickel) or FA (70 mg/m3; 0.3% nickel) for 20 months had no effect on body weight or life-span of the animals. Lung weights and volumes of the high-NEFA- and FA-exposed animals were higher than those of the low-NEFA group and controls. The incidence and severity of interstitial reaction and bronchiolization were significantly higher in the dust-exposed groups than in the controls. The severity of dust deposition, interstitial reaction, and bronchiolization was significantly lower in the low-NEFA group than in the high-NEFA and FA groups. Our findings revealed no significant nickel-specific toxicity/carcinogenicity in hamsters exposed to aerosols of nickel oxide or NEFA, but exposure to high concentrations of the oxide resulted in nonspecific dust pneumoconiosis.
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PMID:Pathogenicity of inhaled nickel compounds in hamsters. 653 79

A historical prospective mortality study was conducted at a nickel company with mines, mills, and a smelter in Ontario, Canada. All men were included in the study who worked for a total of at least 6 months and were employed at some time between 1950 and 1976. Mortality was ascertained and observed number of deaths (O) were compared with expected number of deaths (E), on the basis of the person-years method with the use of rates for Ontario males. There were 804 O compared to 743 E (P less than .001). However, the excess was more than accounted for by the increase in accidental and violent deaths (O = 242; E = 150). Deaths from circulatory diseases and all cancers were roughly equal to E. Laryngeal cancer mortality was significantly increased due to an excess in miners (O = 4; E = 1.00). Lung cancer mortality was somewhat increased (O = 46; E = 37.5); no nasal cancers were observed. Three deaths were due to pneumoconiosis. Sinter plant workers showed a significant increase of cancer deaths (O = 13; E = 6.7; P = .015).
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PMID:A mortality study of 11,500 nickel workers. 659 36

Quantitative determination of 10 minor and 8 trace elements in respirable coal dust by atomic absorption spectrophotometry is described herein. The coal dust samples were collected in the mine atmosphere during drilling in coal seams. A "Hexhlet" apparatus specially designed and fitted with a horizontal elutriator was used to collect the respirable coal dust fraction. After destruction of organic matter by wet oxidation and filtering off the clay and silica, iron, calcium, magnesium, sodium, potassium, manganese, zinc, copper, cadmium, and nickel were determined directly in the resulting solution by atomic absorption spectrophotometry. The studies relate to the respiratory disease-pneumoconiosis-affecting coal mine workers. X-Ray diffraction studies have shown the presence of kaolin, quartz, pirrsonite and beidellite clay minerals in the coal dust.
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PMID:Atomic absorption spectrophotometric and X-ray studies of respirable dusts in Indian coal mines. 705 29

The aim of this study was to determine whether occupational exposure to chromite, trivalent chromium (Cr(3+)) or hexavalent chromium (Cr(6+)) causes respiratory diseases, an excess of respiratory symptoms, a decrease in pulmonary function or signs of pneumoconiosis among workers in stainless steel production. Altogether, 203 exposed workers and 81 referents with an average employment of 23 years were investigated for indicators of respiratory health on two occasions, in 1993 and in 1998. Data collection with a self-administered questionnaire, flow volume spirometry, measurement of diffusing capacity, chest radiography and laboratory tests were carried out by a mobile research unit. Exposure to different chromium species and other metals was monitored regularly and studied separately. No adverse respiratory health effects were observed in the group exposed to Cr(6+), either in comparison with the control group in the first cross-sectional study or during the additional 5 year follow-up. Among the Cr (3+) exposed people, the production of phlegm, shortness of breath and breathlessness on exertion were significantly more frequent than in the control group, but the frequency of the symptoms did not increase during the follow-up; no differences were observed in the lung function tests and the radiographic findings did not progress. In the chromite group, the prevalence of breathlessness on exertion was higher than in the control group. However, in the follow-up, the occurrence of symptoms did not differ from 1993 to 1998. In the first study, most parameters of lung function were lower among the smokers in the chromite group than among the smoking controls, but in 1998 the difference was less marked. An average exposure time of 23 years in modern ferrochromium and stainless steel production and low exposure to dusts and fumes containing Cr(6+), Cr(3+), nickel and molybdenum do not lead to respiratory changes detectable by lung function tests or radiography. The workers exposed to Cr(3+) had more respiratory symptoms than those in the control group. The workers in the chromite mine had lower lung function test results than the control group due to earlier exposure to higher dust concentrations.
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PMID:Respiratory health effects of long-term exposure to different chromium species in stainless steel production. 1209 86

Nickel is a common cause of pneumoconiosis. Here, we show that nickel inactivates aquaporin (AQP)-3, the water channel expressed apically in epithelial cells of human terminal airways. Human AQP3 was transiently transfected into human lung cells, and water permeability was measured in transfected and neighboring untransfected cells. Incubation with NiCl2 rapidly, dose-dependently, and reversibly decreased water permeability in AQP3-expressing cells. Acidification of the extracellular medium also caused rapid, dose-dependent, and reversible inhibition of AQP3. Sensitivity of AQP3 to nickel was lower at alkaline pH than at neutral and acidic pH. Cells transfected with human AQP4 and AQP5, which are also expressed in airway epithelia, were insensitive to nickel and extracellular acidification. Zinc and cadmium, other common causes of pneumoconiosis, had no effect on the water permeability of AQP3. Three extracellular residues, Trp128, Ser152, and His241, were responsible for the blocking effect of nickel on human AQP3. Ser152 was identified as a common site for nickel and pH sensitivity. His53, Tyr124, and His154 were also involved in regulation of AQP3 by extracellular pH. In addition, the aromatic side chain of His154 was shown to be important for the water permeability of AQP3. Our results imply that nickel and extracellular pH may modulate lung water clearance and that defective water clearance may be an early component of nickel-induced lung disease.
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PMID:Nickel and extracellular acidification inhibit the water permeability of human aquaporin-3 in lung epithelial cells. 1277 42


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