Our plain-English summary of Inorganic dust pneumonias: the metal-related parenchymal disorders, by P. Kelleher, K. Pacheco, L.S. Newman (Environmental Health Perspectives, 2000).
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The study
- Authors: P. Kelleher, K. Pacheco, L.S. Newman
- Journal: Environmental Health Perspectives
- Published: 2000;108 Suppl 4(Suppl 4):685-96
- Type of article: Review
- Cited by: 109 articles, as counted by NIH iCite
- Read it: PubMed · Publisher · Free full text
Abstract
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.
In plain English
This article was a review, which the authors call an update, of lung diseases from breathing metal dusts and fumes. It focused on disease of the lung tissue itself. It covered aluminum, beryllium, cadmium, cobalt and hard metal disease, copper, iron, mercury and nickel, and also metal fume fever. It was not a study of asbestos: the authors set asbestos, silica and coal aside. Beyond that, asbestos came up only in the iron section, where the authors noted that iron is suspected to help asbestos produce reactive oxygen species in the lung. Drawing on other studies, the review reported that chronic beryllium disease occurs on average in 2-6% of exposed individuals. A genetic marker, Glu69, was found in 85-95% of patients versus 30-45% of controls. In one workforce the marker carried about a 10-fold risk of disease, and machining carried about an 8-fold risk. Surveys of hard metal plants reported lung tissue disease in 0.7 to 13% of workers. The authors noted that studies were hard to compare. They concluded that better understanding of disease mechanisms and exposure-response relationships may help prevent metal-induced disorders.
We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.
What the study did and found
- Design: Narrative review (described by the authors as an update) of published research on metal-induced lung disorders
- Who was studied: No study population of its own; the review covered published human, animal and laboratory studies of disorders from aluminum, beryllium, cadmium, cobalt, copper, iron, mercury and nickel exposure, organized by metal
- Exposure: Inhaled metal dusts and fumes, mostly at work; lung diseases from asbestos, silica and coal were explicitly outside the scope
- Main results:
- From the studies reviewed: chronic beryllium disease occurs on average in 2-6% of beryllium-exposed individuals
- From studies cited: the genetic marker Glu69 was found in 85-95% of chronic beryllium disease patients compared with 30-45% of controls
- In a cited population-based study at a beryllium ceramics plant (Richeldi et al.), the Glu69 marker conferred approximately a 10-fold risk of beryllium disease
- In the same cited study, a history of machining conferred an approximately 8-fold risk of beryllium disease
- From cited cross-sectional surveys: prevalence of lung tissue (parenchymal) disease among hard metal plant workers ranged from 0.7 to 13%
- In a cited retrospective study of hard metal workers (Posgay et al.), lung fibrosis progressed after exposure stopped in 45% of cases
- Apart from the scope statement in the introduction, the review's only asbestos-related statement: iron is suspected to be a mediator in catalyzing asbestos-induced production of reactive oxygen species in the lung (citing another study)
- A cited controlled human exposure study concluded that 2 hours of breathing zinc oxide fume at the threshold limit value of 5 mg/m3 still produced fever and symptoms of metal fume fever
- The authors' conclusion: The authors concluded that better understanding of both disease mechanisms and exposure-response relationships may make it possible to better prevent metal-induced disorders. They called for research on biologic markers, human exposure and gene alleles that may confer risk.
- Limitations the authors state:
- The review covered only those metals for which knowledge had grown significantly in recent years, not all metals linked to lung injury
- Comparison across hard metal studies is difficult because exposure history, diagnostic criteria and comparison populations varied
- Most genetic marker studies in beryllium disease used a case-control design
Topics
Medical terms in this study, explained in our Lexicon: Pathology, Interstitial, Pneumonitis, Interstitial Fibrosis, Epidemiology, Reactive Oxygen Species (ROS).
Related studies
- Increased mortality from infectious pneumonia after occupational exposure to inorganic dust, metal fumes and chemicals — K. Torén, I. Qvarfordt, et al. (2011)
- In vitro genotoxicity data of nanomaterials compared to carcinogenic potency of inorganic substances after inhalational exposure — M. Roller (2011)
- Desquamative interstitial pneumonia induced by metal exposure. A case report and literature review — T. Blin, A. De Muret, et al. (2020)
- The legacy of World Trade Center dust — J.M. Samet, A.S. Geyh, et al. (2007)
- Inorganic materials and living organisms: surface modifications and fungal responses to various asbestos forms — S. Daghino, E. Martino, et al. (2005)
- Environmental exposure to asbestos and other inorganic fibres using animal lung model — E. Fornero, E. Belluso, et al. (2009)
Browse more research in Environmental Health Perspectives, or return to medical research.
Cited on this site
How to cite it
Cite the study
P. Kelleher, K. Pacheco, L.S. Newman. Inorganic dust pneumonias: the metal-related parenchymal disorders. Environmental Health Perspectives 2000;108 Suppl 4(Suppl 4):685-96. doi:10.1289/ehp.00108s4685. PMID: 10931787.
Cite our summary
“Inorganic dust pneumonias: the metal-related parenchymal disorders.” AsbestosClaims.Law Library. https://asbestosclaims.law/library/research/inorganic-dust-pneumonias-the-metal-related-parenchymal-disorders.
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