Proposed criteria for mixed-dust pneumoconiosis: Definition, descriptions, and guidelines for pathologic diagnosis and clinical correlation

We defined mixed-dust pneumoconiosis (MDP) pathologically as a pneumoconiosis showing dust macules or mixed-dust fibrotic nodules (MDF), with or without silicotic nodules (SN), in an individual with a history of exposure to mixed dust. We defined the latter arbitrarily as a mixture of crystalline silica and nonfibrous silicates. According to our definition of MDP, therefore, MDF should outnumber SN in the lung to make a pathologic diagnosis of MDP. In the absence of confirmation of exposure, mineralogic analyses can be used to support the pathologic diagnosis. The clinical diagnosis of MDP requires the exclusion of other well-defined pneumoconioses, including asbestosis, coal workers' pneumoconiosis, silicosis, hematite miners' pneumoconiosis, welders' pneumoconiosis, berylliosis, hard metal disease, silicate pneumoconiosis, diatomaceous earth pneumoconiosis, carborundum pneumoconiosis, and corundum pneumoconiosis. Typical occupations associated with the diagnosis of MDP include metal miners, quarry workers, foundry workers, pottery and ceramics workers, and stonemasons. Irregular opacities are the major radiographic findings in MDP (ILO 1980), in contrast to silicosis, in which small rounded opacities predominate. Clinical symptoms of MDP are nonspecific. MDP must be distinguished from a variety of nonoccupational interstitial pulmonary disorders.     

Proposed criteria for mixed-dust pneumoconiosis: definition, descriptions, and guidelines for pathologic diagnosis and clinical correlation

We defined mixed-dust pneumoconiosis (MDP) pathologically as a pneumoconiosis showing dust macules or mixed-dust fibrotic nodules (MDF), with or without silicotic nodules (SN), in an individual with a history of exposure to mixed dust. We defined the latter arbitrarily as a mixture of crystalline silica and nonfibrous silicates. According to our definition of MDP, therefore, MDF should outnumber SN in the lung to make a pathologic diagnosis of MDP. In the absence of confirmation of exposure, mineralogic analyses can be used to support the pathologic diagnosis. The clinical diagnosis of MDP requires the exclusion of other well-defined pneumoconioses, including asbestosis, coal workers’ pneumoconiosis, silicosis, hematite miners’ pneumoconiosis, welders’ pneumoconiosis, berylliosis, hard metal disease, silicate pneumoconiosis, diatomaceous earth pneumoconiosis, carborundum pneumoconiosis, and corundum pneumoconiosis. Typical occupations associated with the diagnosis of MDP include metal miners, quarry workers, foundry workers, pottery and ceramics workers, and stonemasons. Irregular opacities are the major radiographic findings in MDP (ILO 1980), in contrast to silicosis, in which small rounded opacities predominate. Clinical symptoms of MDP are nonspecific. MDP must be distinguished from a variety of nonoccupational interstitial pulmonary disorders.     

Absence of significant genotoxicity in lymphocytes and urine from workers exposed to moderate levels of cobalt-containing dust: a cross-sectional study

Mortality studies have shown that, in the past, lung cancer occurred after exposure to mixtures of cobalt metal and metallic carbide particles, the main constituents of hard metals, but apparently not when exposure was to cobalt alone. The major objective of this biomonitoring study was to assess genotoxic effects as a measure for carcinogenic risk in workers from cobalt refineries and hard metal plants currently exposed to the threshold limit value/time-weighted average (TLV-TWA) for cobalt-containing dust. The study comprised three groups of workers: 35 workers exposed to cobalt dust from three refineries, 29 workers exposed to hard metal dust from two producing plants, and 35 matched control subjects recruited from the respective plants. The study design integrated complementary methodologies to assess biomarkers of effects that represent both initial DNA damage (8-hydroxydeoxyguanosine [8-OHdG] in urine and comet assay on lymphocytes) and definitive chromosome breakage/loss (micronuclei in lymphocytes). Cobalt and cotinine were determined in urine as a measure for cobalt exposure and recent smoking, respectively. No significant increase of genotoxic effects was detected in workers exposed to cobalt-containing dust as compared to controls. No difference in any genotoxicity biomarker was found between workers exposed to cobalt and hard metal dusts. Multiple regression analysis indicated that workers who smoked and were exposed to hard metal dusts had elevated 8-OHdG and micronuclei values. Because this observation is in line with a previous epidemiological study of an increased risk of dying from lung cancer in workers from the hard metal industry who smoked, it is concluded that this specific occupational group needs closer medical surveillance.     

Talc pneumoconiosis: A pathologic and mineralogic study

Seventeen cases of "talc pneumoconiosis" were examined pathologically and mineralogically to ascertain whether a true talc pneumoconiosis existed and also to compare these results in primary, secondary, and tertiary exposures. Mineralogic analyses were performed on wet tissue or tissue blocks by a variety of techniques, including analytical transmission electron microscopy and x-ray diffraction. Overall, the pathologic appearance of the tissues was similar in primary, secondary, and tertiary exposures, although ferruginous bodies and foreign body giant cells were not always present in cases caused by secondary exposures. Mixed dust fibrotic lesions were found in two cases in which there were substantial quantities of quartz present. There was great variation in the minerals found within the lung tissues. Several cases showed significant quantities of mica and kaolin in addition to talc. One case consisted predominantly of mica and in fact could be regarded as "mica pneumoconiosis"; this diagnosis was correctly attributed because of the mineralogic findings. Tremolite fibers were found in only two cases. Substantial quantities of crocidolite and amosite fibers were found in one case. This study shows that "talcosis" frequently represents disease associated with a variety of minerals and that talc is a common denominator. It shows also the usefulness of lung dust mineral analysis, particularly in secondary industries, for evaluating the cause of a pathologic reaction when exposures are especially complex.     

煤矿尘肺含铁小体的形态及尘肺病变特点观察

Ferruginous bodies were found in lung tissue collected from 105 coal miner autopsies in Beijing coal area. The incidence rate was 83.8%. Cores of the ferruginous bodies consist of black or transparent fibres partially or entirely coated with golden brown colored iron-protein. They were polymorphic in appearance, and were widely distributed in the lungs. Most of them located in the pulmonary alveoli, and some in the inflammatory or carcinomatous lesions. Besides the pneumoconiosis lesion, there were also abundant multinuclear foreign-body giant cells, and proliferation of type II alveolar cells in the alveoli. Regardless of contact history with coal dust, the average number of ferruginous bodies found in the lungs of workers with no pneumoconiosis was much lower than that with pneumoconiosis lesions (P less than 0.05). The number of ferruginous bodies tends to increase with the severity of the pneumoconiosis lesion. The authors consider that it is worth while to make a further study in elucidating the relationship between ferruginous body and the high incidence of pneumoconiosis in Beijing coal area.     

Primary pleural angiosarcoma associated with pneumoconiosis: An autopsy case

We report a case of pleural angiosarcoma in an adult male patient confirmed by autopsy and possibly associated with pneumoconiosis. The lesion was characterized by thickened pleura of both lungs with nodular tumors. Histologically, the tumor was composed of spindle‐to‐polygonal epithelioid cells that were positive for CD31, CD34, vimentin, and cytokeratin on immunohistochemical staining but were negative for calretinin. Further examination revealed mix‐dust pathological findings consistent with the existence of pneumoconiosis; dystrophic ossification, anthracosis, and fractal small dust particles were observed in the lung parenchyma and a hilar lymph node. The current case suggests that pneumoconiosis‐associated pathologies may be risk factors for the development of angiosarcoma in the pleura.     

Clinical, histopathological and mineralogical analysis findings of an unusual case of pneumoconiosis

A 43-year-old man with a long history of dyspnea which had progressively worsened over the preceding month is presented. He had worked in an antimony mine for 3 years. Radiologically, there were diffuse reticulonodular shadowing opacities in both lung parenchymas. Histopathologic examination of the open-lung biopsy specimen revealed alveolar spaces filled with dust-laden macrophages and amorphous proteinaceous semifluid, the latter being immunoreactive for Human Surfactant Apoprotein A, associated with marked interstitial accumulation of the similar-looking macrophages along the bronchovascular bundles and mild interstitial fibrosis. Silicotic nodules or mixed dust fibrosis were not seen. The patient was diagnosed as silicoproteinosis with unusual histopathological features because he had worked in an antimony mine for only 3 years and had 86% silica in a mineralogical analysis. Pneumoconiosis is a rare lung disease which may be confused with other interstitial lung diseases. Clinical, radiological and unusual histopathologic features of this rare case are presented and discussed with the differential diagnosis, especially of mixed dust pneumoconiosis.     

Morphology and pathogenesis of pneumoconiosis in dental technicians

The morphology of pneumoconiosis occurring in dental technicians could be studied by systematic light and electron microscopical investigation of 30 lung preparations from such cases. Diffuse streaky fibrosis and, in some cases, nodular fibrosis was observed together with occasional formation of silicotic nodules that may lead to extensive transformation of the alveolar structure. The etiological relationship between occupational dust exposure and pulmonary changes could be documented by element analysis of dust deposits on histologic sections, and of dusts from grinding and polishing instruments collected in the laboratory. The energy-dispersive X-ray microanalysis used in this study helps to differentiate and delimit this form of pneumoconiosis. The pathogenesis is discussed on the basis of light and electron microscopic results and physicochemical analyses.     

Giant-cell interstitial pneumonia in a gas station worker.

Giant-cell interstitial Pneumonia (GIP) is a very uncommon respiratory disease. The majority of cases of GIP are caused by exposure to cobalt, tungsten and other hard metals. In this report, we describe GIP in a patient who worked in gas station and dealt in propane gas vessels. He presented with clinical features of chronic interstitial lung disease and underwent an open lung biopsy that showed DIP-like reaction with large numbers of intra-alveolar macrophages and numerous large, multinucleated histiocytes which were admixed with the macrophages. Analysis of lung tissue for hard metals was done. Cobalt was the main component of detected hard metals. Corticosteroid therapy was started and he recovered fully.     

Impaired chemotactic responses of bronchoalveolar leukocytes in experimental pneumoconiosis

Rats were exposed to clouds of the following pneumoconiotic dusts: quartz, coal-mine dust, and chrysotile asbestos at 10 or 50 mg/m3 for 8, 32, and 75 days; for comparison, rats were also exposed to the non-pathogenic dust titanium dioxide (TiO2). The bronchoalveolar leukocytes (macrophages and neutrophils) from dust-exposed and control rats were obtained by lavage and tested for their ability to migrate toward zymosan-activated serum. Varying amounts of neutrophils were present depending on the ability of the dust to cause inflammation and the length of exposure. There was a marked loss of chemotactic ability in leukocytes from rats inhaling the pneumoconiotic dusts compared with controls; TiO2-exposed leukocytes had some impairment of chemotaxis, but this was substantially less than that found with the pneumoconiotic dusts. The loss of chemotactic activity did not correlate with the percentage of neutrophils in the lavage cells except when there were very high levels of neutrophils, and there was substantial impairment of chemotaxis with negligible numbers of neutrophils, showing that macrophage chemotaxis was impaired. A phagocytic burden within the leucocytes was not sufficient alone to inhibit chemotaxis, nor was the loss of chemotactic activity due to occupied receptors, since incubation failed to restore chemotaxis. Loss to chemotactic activity by leukocytes from pneumoconiotic dust-exposed lung could be an important factor in the development of pneumoconiosis.     

The current state of workers' pneumoconiosis in relationship to dusty working environments in Okayama Prefecture,Japan

This study involved the examination of 1,006 chest x-ray films of workers from the industries devoted to shipyard welding, stone grinding, and refractory crushing in southern Okayama prefecture. Of the reviewed films, analysis was focused on subjects with a profusion rate of 0/1 as well as pneumoconiotic subjects (exhibiting profusion rates of 1/0 or greater) in order to discover cases in the beginning stages. One-hundred-and-seventy-four films illustrated a profusion rate of 0/1 or greater, and the proportion of this profusion rate was revealed to be highest in shipyard welders. Even some workers under 40 years of age were found to have already developed pneumoconiosis. Of these 1,006 subjects, 30 volunteers permitted us to measure their personal dust exposure concentrations. The measured concentration of the shipyard welders' dust exposure (respirable dust; 3.3 86.3 mg/m3, total dust; 7.5-117.0 mg/m3) was higher than those of the other 2 industries. Statistical differences among the industries were observed in the respirable dust concentrations. A statistically significant positive correlation was demonstrated between the working duration in dusty environments and the rate of profusion. The present findings suggest the need for taking adequate measures in Okayama in order to prevent workers from developing, or to help retard the progression of, pneumoconiosis.     

Aluminum welding fume-induced pneumoconiosis

Chronic exposure to high concentrations of fumes during aluminum arc welding causes a severe pneumoconiosis characterized by diffuse pulmonary accumulation of aluminum metal and a corresponding reduction in lung function. Aluminum fume-induced pneumoconiosis is a rarely reported entity, of which the true incidence is unknown. We report the clinical, radiographic, microscopic, and microanalytic results of 2 coworkers, employed by the same aluminum shipbuilding facility, who died of complications from this disease. Scanning electron microscopy and energy dispersive x-ray analysis of the exogenous particle content in the lung tissue of these cases revealed the highest concentrations of aluminum particles (average of 9.26 billion aluminum particles per cm(3) of lung tissue) among the 812 similar analyses in our pneumoconiosis database. One patient had an original clinical diagnosis of sarcoidosis but no evidence of granulomatous inflammation.     

Labor hygiene in the fire production of nickel

Unfavorable hygienic factors, like nickel-containing dust, toxic gases, resinous sublimates, heat and hard physical labor are inherent in the modern production of nickel. A variety of occupational peculiarities results in a higher morbidity of workers. Diseases of the respiratory organs, digestive system, skin and of the subcutaneous cellular tissue are in the lead. Besides, bronchitis, pneumoconiosis, exogenous fibrosing alveolitis as well as neoplasms in the respiratory organs and stomach equally belong to occupational diseases. Preventive schemes of the general occupational and oncological morbidity of workers must rest on a comprehensive set of measures with the introduction of new technological innovations and of raw materials into all nickel-production stages being of primary importance.     

Silicosis caused by chronic inhalation of snail shell powder

A 70-yr-old woman visited our hospital for shortness of breath. Chest CT showed ground glass opacity and traction bronchiectasis at right middle, lower lobe and left lingular division. Video-assisted thoracic surgical biopsy at right lower lobe and pathologic examination revealed mixed dust pneumoconiosis. Polarized optical microscopy showed lung lesions were consisted of silica and carbon materials. She was a housewife and never been exposed to silica dusts occupationally. She has taken freshwater snails as a health-promoting food for 40 yr and ground shell powder was piled up on her backyard where she spent day-time. Energy dispersive X-ray spectroscopy of snail shell and scanning electron microscopy with energy dispersive x-ray spectroscopy of lung lesion revealed that silica occupies important portion. Herein, we report the first known case of silicosis due to chronic inhalation of shell powder of freshwater snail.     

Loss of regulatory characteristics in CD4+CD25+/hi T cells induced by impaired transforming growth factor beta secretion in pneumoconiosis

Pneumoconiosis is caused by the accumulation of airborne dust in the lung, which stimulates a progressive inflammatory response that ultimately results in lung fibrosis and respiratory failure. It is possible that regulatory cells in the immune system could function to suppress inflammation and possibly slow or reverse disease progression. However, results in this study suggest that in pneumoconiosis patients, the regulatory T cells (Tregs) and B cells are functionally impaired. First, we found that pneumoconiosis patients presented an upregulation of CD4⁺CD25⁺ T cells compared to controls, whereas the CD4⁺CD25⁺ and CD4⁺CD25^hi T cells were enriched with Th1‐ and Th17‐like cells but not Foxp3‐expressing Treg cells and evidenced by significantly higher T‐bet, interferon (IFN)‐γ, and interleukin (IL)‐17 expression but lower Foxp3 and transforming growth factor (TGF)‐β expression. Regarding the CD4⁺CD25^hi T‐cell subset, the frequency of this cell type in pneumoconiosis patients was significantly reduced compared to controls, together with a reduction in Foxp3 and TGF‐β and an enrichment in T‐bet, RORγt, IFN‐γ, and IL‐17. This skewing toward Th1 and Th17 types of inflammation could be driven by monocytes and B cells, since after depleting CD14⁺ monocytes and CD19⁺ B cells, the levels of IFN‐γ and IL‐17 were significantly decreased. Whole peripheral blood mononuclear cells and isolated monocytes and B cells in pneumoconiosis patients also presented reduced capacity of TGF‐β secretion. Furthermore, monocytes and B cells from pneumoconiosis patients presented reduced capacity in inducing Foxp3 upregulation, a function that could be rescued by exogenous TGF‐β. Together, these data indicated a potential pathway for the progression of pneumoconiosis through a loss of Foxp3⁺ Treg cells associated with impaired TGF‐β secretion.     

Possible effect of gene polymorphisms on the release of TNFα and IL1 cytokines in coal workers’ pneumoconiosis

It has been shown that coal dust exposure stimulates inflammatory response leading to increased release of cytokines from monocytes such as TNF-alpha and IL1. These released cytokines play the key role in the pathogenesis of pneumoconiosis including coal workers’ pneumoconiosis. In this study, we investigated TNFA, IL1A, IL1B and IL1RA genes variations on basal, lipopolysaccharide and coal dust-induced cytokine release from blood monocytes of homozygous allele and minor variant allele carriers in Turkish coal workers and CWP patients. According to the genotyping results, TNFA –238 gene polymorphism was found as a risk factor in CWP development (OR=3.79) and to in vitro results; release of both TNF-alpha and IL1 cytokines from the monocytes in CWP patients was significantly increased compared to the healthy workers. Also, LPS and coal dust stimulated release of TNF-alpha, which was significantly higher in allele 2 carriers compared to subjects carrying allele 1 in both the groups. These data suggest that the coal dust-induced release of TNF-alpha from monocytes may be a useful biomarker of CWP.     

Functional respiratory disorders in miners of the Lorraine coal basin at the time of their retirement

A clinical, radiological (RX) and spirographic examination and a measurement of lung transfer for CO (TCO), following the steady state method, were performed in 655 coal-miners. They had worked for an average of 30 years in the Lorraine coal-mines and their mean age was 50 years. Among the non-pneumoconiotics, 20% of non-smokers and 35% of smokers displayed ventilatory obstructive disturbances. In miners with simple pneumoconiosis, this percentage rose to 29 and 52.5% respectively. Abnormally low values of TCO were observed in 6% of non-smokers and in 22% of smokers without pneumoconiosis, while this was 35 and 41% respectively in pneumoconiotic workers. Finally, by using spirography and TCO simultaneously, we found respiratory troubles in at least 63% of pneumoconiotic miners and in 43% of those without such disturbances.     

Distribution and removal of cat, dog and mite allergens on smooth surfaces in homes with and without pets.

BACKGROUND: Removing allergen from the indoor environment should be a primary strategy for the management and treatment of allergic disease. OBJECTIVE: The aims of this study were to characterize the distribution of dog, cat, and mite allergen on hard surfaces in homes with and without pets and to evaluate the efficiency of removing allergen from hard surfaces by wiping with a dry dust cloth and by vacuum cleaning using the dustbrush attachment. METHODS: The amount of allergen collected from adjacent areas of two smooth floors, a wall, and finished furniture by wiping with a Pledge Grab-it dust cloth (S. C. Johnson & Son, Inc, Racine, WI) and by brush-vacuuming were compared for 24 homes with and without pets. In addition, the areas first wiped with the dust cloth were then brush-vacuumed and the amounts of allergen collected by the first and second cleaning were compared. RESULTS: A key finding was that 23 of the 24 homes had Can f 1 allergen on one or more of the sampled areas regardless of whether a dog was present. Most homes with pets and many homes without pets had Can f 1 and Fel d 1 allergens on walls, smooth floors, and finished furniture. Carpets were the major reservoir for pet allergens in homes with pets whereas allergen was more uniformly distributed in homes without pets. Little mite allergen was found on hard surfaces even when it was present in carpets. CONCLUSIONS: Dog and cat allergens are prevalent on walls, smooth floors, and finished furniture in homes with and without pets. Dry dusting with a Grab-it dust cloth was an effective cleaning method for removing allergen from hard smooth surfaces.