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

Inhalation of dust containing graphite can cause lung disease in foundry workers and workers in graphite mines or mills. Mixed dust pneumoconiosis caused by long-term occupational exposure to graphite dust is a rare disease. Only a few cases of graphite pneumoconiosis have been reported in literature, and these were usually diagnosed post mortem. Our report is of an 80-year-old male patient who had worked in an iron foundry for 20 years and whose work had entailed regular contact with ground graphite and foundry vapors. Chest x-rays revealed both a reticular and nodular pattern in the lung, moderate apical distractions and pleural scarring, all of which were confirmed by high-resolution computed tomography. Bronchoalveolar lavage and transbronchial biopsies were also consistent with mixed dust pneumoconiosis, and due to the long-term dust exposure, graphite pneumoconiosis was strongly suspected. To confirm this diagnosis, the chemical composition of the dark granules in the semi-thin histological sections of the transbronchial biopsies were analyzed using laser microprobe mass spectroscopy. The mass spectra of these black particles were consistent with those of natural graphite powder. Comparative analyses of normal lung tissue did not produce similar spectral patterns. We conclude that histology and cytology does not always suffice to confirm a diagnosis of graphite pneumoconiosis, because black particles are also found in conditions resulting from other exposures, such as heavy smoking or coal mining. Analysis of the composition of particles deposited in the lung tissue offers more precise information, which can be used as evidence in occupational and forensic medicine. Laser microprobe mass spectroscopy can assess the mineral dust load in lung samples.
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PMID:Detection of graphite using laser microprobe mass analysis of a transbronchial biopsy from a foundry worker with mixed dust pneumoconiosis. 1223 12

Exposures in the workplace result in a diverse set of diseases ranging from the pneumoconiosis to other interstitial lung diseases to acute lung injury. Physician awareness of the potential disease manifestations associated with specific exposures is important in defining these diseases and in preventing additional disease. Most occupational diseases mimic other forms of lung disease, including pulmonary fibrosis, sarcoidosis, adult respiratory distress syndrome (ARDS), and bronchiolitis. A "sarcoidosis"-like syndrome, usually limited to the lungs, may result from exposure to bioaerosols and a number of metals. Exposure to beryllium in the workplace produces a granulomatous lung disease clinically indistinguishable from sarcoidosis, chronic beryllium disease (CBD). Beryllium's ability to produce a beryllium-specific immune response is used in the beryllium lymphocyte proliferation tests to confirm a diagnosis of CBD and exclude sarcoidosis. Exposure to other metals must also be considered in the differential diagnosis of sarcoidosis. When an individual presents acutely with ARDS or acute lung injury, an acute inhalational exposure must be considered. Exposure to a number of irritant substances at high levels may cause a "chemical pneumonitis" or acute lung injury, depending on the solubility and physicochemical properties of the substance. Some of the most notable agents include nitrogen and sulfur oxides, phosgene, and smoke breakdown products. Ingestion of paraquat may also result in an ARDS syndrome, with pulmonary fibrosis eventually resulting. Bronchiolitis is a rare manifestation of inhalational exposures but must also be considered in the clinical evaluation of inhalational exposure.
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PMID:Clinical approach to chronic beryllium disease and other nonpneumoconiotic interstitial lung diseases. 1236 66

A great deal of study has gone into the assessment of the epidemiology of NTM infection and disease in many different parts of the world. Review of the available studies provides insight into the frequency of this clinical problem as well as important limitations in current data. Study methods have varied greatly, undoubtedly leading to differing biases. In general, reported rates of infection and disease are likely underestimates, with the former probably less accurate than the latter, given that people without significant symptoms are not likely to have intensive investigations to detect infection. Pulmonary NTM is a problem with differing rates in various parts of the world. North American rates of infection and disease have been reported to range from approximately 1-15 per 100,000 and 0.1-2 per 100,000, respectively (see Table 1). Rates have been observed to increase with coincident decreases in TB. MAC has been reported most commonly, followed by rapid growers and M kansasii. Generally similar rates have been reported in European studies, with the exception of extremely high rates in an area of the Czech Republic where mining is the dominant industry (see Table 2). These studies have also shown marked geographic variability in prevalence. The only available population-based studies have been in South Africa and report extremely high rates of infection, three orders of magnitude greater than studies from other parts of the world (see Table 3). This undoubtedly reflects the select population with an extremely high rate of TB and resultant bronchiectasis leading to NTM infection. Rates in Japan and Australia were similar to those reported in Europe and North America and also show significant increases over time (see Table 3). Specific risk factors have been identified in several studies. CF and HIV, mentioned above, are two important high-risk groups. Other important factors include underlying chronic lung disease, work in the mining industry, warm climate, advancing age, and male sex. Aside from HIV and CF, mining with associated high rates of pneumoconiosis and previous TB may be the most important historically, reported in studies worldwide [63]. A recurring observation is the increase in rates of infection and disease. The reason for this is unclear but may be caused by any of several contributing factors. The possibility exists that the apparent increase is either spurious or less significant than studies would suggest. Changes in clinician awareness leading to increased investigations, or laboratory methods leading to isolation and identification of previously unnoticed organisms, could play a role in this trend, and studies have been published that support [67] and refute [31] this argument. We believe such factors may contribute to but do not explain the significant increases that have been observed. A true increase could be related to the host, the pathogen, or some interaction between the two. Host changes leading to increased susceptibility could play an important role, with increased numbers of patients with inadequate defenses from diseases such as HIV infection, malignancy, or simply advanced age [31]. An increase in susceptibility could also relate to the decrease in infection with two other mycobacteria. It has been speculated that infection with TB [29,38] and Bacillus Calmette-Guerin (BCG) [19,68] may provide cross-immunity protecting against NTM infection. Many investigations have observed decreasing rates of TB concomitant with the increases in NTM. In addition, studies from Sweden [68] and the Czech Republic [19] have found that children who were not vaccinated with BCG had a far higher rate of extrapulmonary NTM infection. Potential changes in the pathogens include increases in NTM virulence, and it has been argued that this should be considered as a possible contributing factor [69]. Finally, an interaction between the host and pathogen could involve a major increase in pathogen exposure or potential inoculum size. This may be occurring secondary to the increase in popularity of showering as a form of bathing [66], a habit that greatly increases respiratory exposure to water contaminants. Several limitations of our review should be noted. We reviewed English-language reports and abstracts, probably leading to fewer data from non-English speaking regions, which may explain the paucity of studies from Africa, Eastern Europe, and most Asian nations. The heterogeneity of study methods in identifying cases and the lack of a uniformly applied definition of disease makes it difficult to compare rates between studies. Finally, the lack of systematic reporting of NTM infection in most nations limits the ability to derive accurate estimates of infection and disease. Regardless, there are more than adequate data to conclude that NTM disease rates vary widely depending on population and geographic location. NTM disease is clearly a major problem in certain groups, including patients with underlying lung disease and also in individuals with impaired immunity. The rates of NTM infection and disease are increasing, so the problem will likely continue to grow and become a far more important issue than current rates suggest.
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PMID:Epidemiology of human pulmonary infection with nontuberculous mycobacteria. 1237 Sep 92

This article reviews the high-resolution computed tomography imaging features of miliary pattern, a characteristic radiologic manifestation of diffuse micronodular lung disease. The most common entities with this pattern are miliary tuberculosis, pneumoconiosis, sarcoidosis, metastases, and hypersensitivity pneumonia. According to the distribution of the nodules in relation to the secondary lobule, high-resolution computed tomography findings divide miliary patterns into 3 groups: centrilobular, perilymphatic, and random presentation. The radiologic features that help in the differential diagnosis are discussed.
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PMID:Miliary lung disease revisited. 1241 99

A 72-year-old male painter, who complained of his "lungs burning" for 2 weeks, died suddenly. Autopsy examination revealed severe coronary atherosclerosis with plaque rupture as the cause of death. Examination of the lungs revealed emphysema, interstitial fibrosis, and multinucleated giant cells with intra- and extracellular brown-black, crystalline, polarizable foreign material. Energy-dispersive X-ray microanalysis showed the material to contain titanium, aluminum, silicon, and iron. An increased incidence of respiratory disease has been reported in professional painters. Titanium is widely used as a pigment in the manufacturing of commercial paints. Cases of pneumoconiosis and alveolar proteinosis have been described in painters in which analysis of lung tissue revealed increased levels of titanium. This case is presented as an example of a rarely reported phenomenon, which may have clinical implications for evaluation and management of lung disease in painters.
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PMID:Titanium particles identified by energy-dispersive X-ray microanalysis within the lungs of a painter at autopsy. 1274 5

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

Even in the twenty-first century, welding is still a common and a highly skilled occupation. The hazardous agents associated with welding processes are acetylene, carbon monoxide, oxides of nitrogen, ozone, phosgene, tungsten, arsenic, beryllium, cadmium, chromium, cobalt, copper, iron, lead, manganese, nickel, silver, tin, and zinc. All welding processes involve the potential hazards for inhalation exposures that may lead to acute or chronic respiratory diseases. According to literature described earlier it has been suggested that welding fumes cause the lung function impairment, obstructive and restrictive lung disease, cough, dyspnea, rhinitis, asthma, pneumonitis, pneumoconiosis, carcinoma of the lungs. In addition, welding workers suffer from eye irritation, photokeratitis, cataract, skin irritation, erythema, pterygium, non-melanocytic skin cancer, malignant melanoma, reduced sperm count, motility and infertility. Most of the studies have been attempted previously to evaluate the effects of welding fumes. However, no collectively effort illuminating the general effects of welding fumes on different organs or systems or both in human has not been published. Therefore, the aim of this review is to gather the potential toxic effects of welding fumes documented by individual efforts and provide informations to community on hazards of welding.
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PMID:Health hazards of welding fumes. 1464 49

The relationship between silicosis and tuberculosis is well known. Also other mycobacteria such as Mycobacterium kansasii often occur in association with pneumoconiosis. However, there are few reports describing an association of M. avium-intracellulare complex (MAC) lung disease and pneumoconiosis. The purpose of the present study is to describe clinical features of MAC respiratory infection associated with pneumoconiosis. Eleven patients with MAC respiratory infection associated with pneumoconiosis (all men, 6 with silicosis and 5 with welders' pneumoconiosis) were collected. A determination of whether or not MAC caused pulmonary disease was made using the 1997 criteria required by the American Thoracic Society. Radiologically, cavity formation as well as upper lung field predominance of MAC disease were observed in 8 of 11 cases (72.7%). Two of 11 patients died of respiratory failure. Our present study clearly demonstrates that clinical features of MAC respiratory infection associated with pneumoconiosis were different from MAC without underlying diseases.
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PMID:Clinical features of eleven cases of Mycobacterium avium-intracellulare complex pulmonary disease associated with pneumoconiosis. 1530 35

Even in the 21st century, millions of people are working daily in a dusty environment. They are exposed to different types of health hazards such as fume, gases and dust, which are risk factors in developing occupational disease. Cement industry is involved in the development of structure of this advanced and modern world but generates dust during its production. Cement dust causes lung function impairment, chronic obstructive lung disease, restrictive lung disease, pneumoconiosis and carcinoma of the lungs, stomach and colon. Other studies have shown that cement dust may enter into the systemic circulation and thereby reach the essentially all the organs of body and affects the different tissues including heart, liver, spleen, bone, muscles and hairs and ultimately affecting their micro-structure and physiological performance. Most of the studies have been previously attempted to evaluate the effects of cement dust exposure on the basis of spirometry or radiology, or both. However, collective effort describing the general effects of cement dust on different organ and systems in humans or animals, or both has not been published. Therefore, the aim of this review is to gather the potential toxic effects of cement dust and to minimize the health risks in cement mill workers by providing them with information regarding the hazards of cement dust.
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PMID:Health hazards of cement dust. 1544 58

A large and diverse group of pathologic conditions manifests clinically and radiologically as diffuse parenchymal lung disease. Diffuse interstitial lung diseases (ILDs) encompass mainly inflammatory processes that involve the structural elements of this organ. Some ILDs are caused by infections, but most are the result of immunologic, environmental, or toxic mechanisms. Currently, less morbid sampling techniques have increased dramatically the probability that pulmonologists will be faced with establishing a specific and clinically relevant diagnosis using surgical lung biopsy material. Most of the concepts presented in this article have been established using this type of specimen. In the early years of surgical lung biopsy, a small number of diffuse inflammatory conditions came to light that exclusively involved the lungs and did not seem to be caused by infection, toxin, sarcoidosis, pneumoconiosis, or neoplasm. In this article, these idiopathic disorders are discussed in the context of their dominant pathologic findings rather than presented as a separate group of entities.
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PMID:Pathology of interstitial lung disease. 1556 15


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