Radiological aspects of hard metal disease

Posgay, M.; Németh, László; Mester, Á.

doi:10.1055/s-2008-1032794

Cited by 13 publications

(6 citation statements)

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“…No correlation was found between intensity or duration of expo-sure and the stage and progression of pulmonary fibrosis. In 45% of the cases, there was progression of the fibrosis after cessation of the exposure (79). Death from pneumonia (80) and recurrence of giant cell interstitial pneumonitis (81) have been reported in HMD lung transplant recipients.…”

Section: Cobalt and Hard Metal Diseasementioning

confidence: 99%

Inorganic Dust Pneumonias: The Metal-Related Parenchymal Disorders

Kelleher¹,

Pacheco²,

Newman³

2000

Environmental Health Perspectives

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In recent years the greatest progress in our understanding of pneumoconioses, other than those produced by asbestos, silica, and coal, has been in the arena of metal-induced parenchymal lung disorders. Inhalation of metal dusts and fumes can induce a wide range of lung pathology, including airways disorders, cancer, and parenchymal diseases. The emphasis of this update is on parenchymal diseases caused by metal inhalation, including granulomatous disease, giant cell interstitial pneumonitis, chemical pneumonitis, and interstitial fibrosis, among others. The clinical characteristics, epidemiology, and pathogenesis of disorders arising from exposure to aluminum, beryllium, cadmium, cobalt, copper, iron, mercury, and nickel are presented in detail. Metal fume fever, an inhalation fever syndrome attributed to exposure to a number of metals, is also discussed. Advances in our knowledge of antigen-specific immunologic reactions in the lung are particularly evident in disorders secondary to beryllium and nickel exposure, where immunologic mechanisms have been well characterized. For example, current evidence suggests that beryllium acts as an antigen, or hapten, and is presented by antigen-presenting cells to CD4+ T cells, which possess specific surface antigen receptors. Other metals such as cadmium and mercury induce nonspecific damage, probably by initiating production of reactive oxygen species. Additionally, genetic susceptibility markers associated with increased risk have been identified in some metal-related diseases such as chronic beryllium disease and hard metal disease. Future research needs include development of biologic markers of metal-induced immunologic disease, detailed characterization of human exposure, examination of gene alleles that might confer risk, and association of exposure data with that of genetic susceptibility. Key words: aluminum, beryllium, cadmium, cobalt, copper, hard metal disease, iron, mercury, metal fume fever, nickel, pneumoconiosis.-Environ Health Perspect 1 08(suppl 4):685-696 (2000). http.//ehpnetl.niehs.nih.gov/docs/2000/suppl-4/685-696kelleher/abstract.html The term pneumoconiosis, first introduced in the 19th century, refers to diseases and patho-logic consequences from inhalation of particulate dusts. In recent years the greatest progress in our understanding of pneumoconioses, other than those produced by asbestos, silica, and coal, has been in the arena of metal-induced parenchymal lung disorders. As presented in Table 1, various metal dusts and fumes can induce a wide range of lung pathology , including not only parenchymal diseases but airways disorders and cancer as well. In this update we emphasize the parenchymal diseases caused by metal inhalation, including granulomatous disease, giant cell interstitial pneumonitis, chemical pneumonitis, and interstitial fibrosis, among others. Although a number of metals, in addition to those discussed in this chapter, are associated with various forms of lung injury, we have focused this discussion on those for which there has...

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Section: Cobalt and Hard Metal Diseasementioning

confidence: 99%

Inorganic Dust Pneumonias: The Metal-Related Parenchymal Disorders

Kelleher¹,

Pacheco²,

Newman³

2000

Environmental Health Perspectives

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“…An immunologic mechanism for cobalt related ILD is supported by its variable latency period, pathologic features, and risk factors, which resemble those of chronic beryllium disease (CBD) and hypersensitivity pneumonitis (HP), two well-known lung diseases caused by an adaptive immune response to an inhaled antigen [21e24]. Cobalt related ILD, much like CBD and HP, occurs in only a small percentage of exposed workers and lacks a linear dose-response relationship [10,25]. As a result, some patients are affected after just a few years of exposure, while others take decades [25].…”

Section: Pathogenesismentioning

confidence: 99%

“…Cobalt related ILD, much like CBD and HP, occurs in only a small percentage of exposed workers and lacks a linear dose-response relationship [10,25]. As a result, some patients are affected after just a few years of exposure, while others take decades [25]. This stands in contrast to pneumoconioses such as asbestosis and silicosis, which rely on a nonspecific inflammatory response rather than an adaptive immune response and have a linear dose-response relationship [26,27].…”

Section: Pathogenesismentioning

confidence: 99%

“…Further, cobalt is a known sensitizer, causing antibody production and positive skin patch testing [29]. Individual susceptibility in cobalt related ILD, HP, and CBD is clearly an important risk factor as there is no association between these diseases and either intensity or duration of exposure [10,25]. Some HLA haplotypes, such as HLA-DPB1 with a glutamic acid at position 69 of the beta-chain, can facilitate the presentation of both beryllium and cobalt to T-cells, which increases the hosts' probability of developing CBD and GIP following exposure [21,22].…”

Section: Pathogenesismentioning

confidence: 99%

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Cobalt related interstitial lung disease

Adams

Butt

Batra

et al. 2017

Respiratory Medicine

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Cobalt exposure in the hard metal and bonded diamond tool industry is a well-established cause of ILD. The primary theories regarding the underlying mechanism of cobalt related ILD include an immunologic mechanism and an oxidant injury mechanism. Cobalt related ILD may present in subacute and chronic forms and often has associated upper respiratory symptoms. The evaluation begins with a thorough occupational history and includes PFTs, HRCT, and bronchoalveolar lavage. HRCT findings are nonspecific and may resemble NSIP, UIP, sarcoidosis, or HP. The finding of cannibalistic multinucleated giant cells is diagnostic provided there is a history of exposure and appropriate changes on imaging; however, when these cells are not found on lavage, lung biopsy is required for diagnosis. Giant cell interstitial pneumonia is the classic pathologic pattern, but cobalt related ILD may also present with pathologic findings of UIP, DIP, or HP. When cobalt related ILD is suspected, removal from exposure is the most important step in treatment. Case reports suggest that treatment with steroids results in symptomatic, physiologic, and radiographic improvement.

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“…Interestingly, no correlation between the duration or intensity of exposure and progression of lung fibrosis has been described. 47 Aside from exposure cessation, no treatment has been shown to be effective, and recurrence of giant cell interstitial pneumonitis after lung transplantation has been reported. 48 Pathological findings in hard metal parenchymal lung disease include giant cell interstitial pneumonitis and desquamative interstitial pneumonitis with associated fibrotic changes.…”

Section: Cobalt and Hard Metal Lung Diseasementioning

confidence: 99%

Metal-Induced Diffuse Lung Disease

Fontenot

Amicosante

2008

Semin Respir Crit Care Med

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The number of metals that are associated with the development of diffuse parenchymal lung disease continues to expand. In addition to lung fibrosis, inhalation of metal particulates can induce a wide range of lung pathology, including reactive airways disease and cancer. This article focuses on diffuse parenchymal diseases resulting from the inhalation of beryllium and cobalt. More is known regarding the immunopathogenesis of beryllium-induced disease than is known for disease induced by any other metal. Chronic beryllium disease (CBD) is a granulomatous lung disorder caused by beryllium exposure in the workplace and is characterized by the accumulation of beryllium-specific CD4 (+) T cells in the bronchoalveolar lavage. Genetic susceptibility markers associated with increased risk have been identified for both CBD and hard metal lung disease. The mechanism for the genetic susceptibility of CBD lies in the ability of certain human leukocyte antigen (HLA)-DP molecules to bind and present beryllium to pathogenic CD4 (+) T cells. Whether the same is true for hard metal lung disease is unknown. In contrast, no HLA allelic association has been identified in nickel allergic subjects. The study of metal-induced lung disease allows the investigation of the relationship between environmental exposure and genetic susceptibility. These studies will enhance our understanding of the immunopathogenesis of metal-induced disease and how exposure to these metals results in irreversible lung fibrosis.

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Radiological aspects of hard metal disease

Cited by 13 publications

References 0 publications

Inorganic Dust Pneumonias: The Metal-Related Parenchymal Disorders

Inorganic Dust Pneumonias: The Metal-Related Parenchymal Disorders

Cobalt related interstitial lung disease

Metal-Induced Diffuse Lung Disease

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