RARE DISEASE
Asbestos intoxication
Asbestos intoxication
Asbestos intoxication
Synonyms: Asbestosis
Synonyms: Asbestosis
Synonyms: Asbestosis
Drug discovery
0
drugs
With orphan designations
Overview
Asbestos intoxication refers to lung damage from inhaling asbestos fibers, causing inflammation, fibrosis, and irreversible scarring (asbestosis). Clinical features include progressive dyspnea, dry cough, and chest pain, with a latency period of 20–30 years post-exposure [1][3][16]. Complications include respiratory failure, pulmonary hypertension, and increased risk of lung cancer/mesothelioma [16][17]. Diagnosis relies on exposure history, imaging, and pulmonary function tests. Management focuses on symptom relief, slowing progression, and preventing secondary complications [3][8][13].
Burden
Global: ~255,000 annual deaths, with 91% linked to occupational exposure [4][5][14].
U.S.: ~1,300 asbestos-related deaths/year; asbestosis contributes to ~613 annual fatalities [2][7][9].
Economic impact: High costs from chronic care, lost productivity, and disability-adjusted life years (DALYs) [5][14].
Categories: rare respiratory diseases, rare transplant-related disorders
Research Papers
390 drug discovery papers about Asbestos intoxication, with 1 first-in-class emerging drug candidates forecasted to outperform the average preclinical success rate. Recent publications:
390 drug discovery papers about Asbestos intoxication, with 1 first-in-class emerging drug candidates forecasted to outperform the average preclinical success rate. Recent publications:
categories:
Small molecules
2026-06-10 | CURRENT STATUS OF GLOBAL AEROMICROBIOLOGY STUDIES
Abstract:Climate change when it had commenced due to anthropogenic activities is currently alsoinfluencing cells, propagules, environment aerosol borne, bioaerosol borne dispersal ofmicroorganisms (modes like the annual dust storms, urban and metropolitan suspended dustby vehicle plying on roads, desert storms, volcanic eruptions, silica- asbestosis, cement dustfrom building construction and industries, etc) are the major factors elevating problems likecontact dermatitis, respiratory diseases, allergies, occupational hazards (lung cancers, etc) tohumans and mammals. Thus, aeromicrobiology is concerned with health status andsocioeconomic progress of humans globally. Several species of aspergillus spores cause skinand respiratory tract infection. A. niger and A. fumigatus is the cause of otomycosis due toinfections of outer ear canal. Defeacating in open, dessication, and dispersion of faecalcontaminated soil carry airborne microorganisms (fungi, bacteria, viruses etc.,) far and wide.Tuberculosis, diphtheria, meningitis, pertusis, Streptococcus pneumonia as well as anthrax;Pandemic of Covid-19 and other virus infections spread through air. This is throughbioaerosol - aerosol transition facilitated by moisture, heat, temperature and air currents.Moreover, both natural and unnatural factors alter aeromicrobiology impact on humans. A‘solar aeromicrobiology model’ to purify air at any place have been proposed to eradicate orreducepathogenic and non-pathogenic microorganism (proposed by D.R.Saxena).The rapid Zooplane are "Machzooplane" such as birds, bats, and insects spread all types ofmicroorganisms intracontinentally if they are migratory (also fishes), if not intercontinently.The intracontinental zooplane include above stated animals as well as rodents, reptiles, etc.,that daily move in search of food, mate, etc. The slowest but ecologically significant zooplaneare bugs, ants, soil worms that disseminate the nonpathogenic and pathogenic microorganismsoccurring in air, water as well as soil borne medium.Scavengers also disseminatemicroorganisms (using various media-animal/human microbial cycle as proposed by theauthor) due to their feeding– defaecation and locomotory behaviour.Use of AI fabricated and controlled universal solar aeromicrobiology model also minidomestic models in everyresidence / flat has been hypothesized. The Prions may be a discarded protein particleofafaulty gene that is quiescent and may be accidently switched on. Now such genes maymetabolically synthesize materials such as DNA, RNA, Proteins, etc., in the bodies ofmicroorganisms, invertebrates and vertebrates including humans. This mechanism may be forslow or rapid evolution of self and non self infectious agents( this unwanted DNA, RNA,Proteins that are accidently synthesized and are not degraded and now cause diseases ),theirproduction may be accelerated manifolds triggered by continuous current climate as well asclimate changes in future and that will be the cause of global human deaths.
2026-05-11 | PREVENTIVE DIETARY NUTRITION FOR PATIENTS WITH ASBESTOSIS
This article provides a detailed overview of the basic principles of preventive dietary nutrition, the role of nutrients, and practical recommendations for patients suffering from asbestosis. A proper diet plays a crucial role in combating the progression of the disease. The article examines the role of foods rich in antioxidants, vitamins, minerals, and fiber in protecting lung tissue, based on scientific evidence.
2026-05-01 | B19-04 Pulmonary Osteoclast-like Cells in Asbestos-induced Pulmonary Fibrosis
Abstract Rationale Chrysotile asbestos inhalation drives a progressive fibrotic response in the lung, yet the cellular programs that mediate injury progression remain incompletely defined. Recent work has identified pulmonary osteoclast-like cells (POLCs) as rare, macrophage-derived effector cells that emerge in particulate lung injury and promote matrix remodeling. Whether POLCs are induced by asbestos and contribute to asbestosis pathogenesis has not been established. Here, we combined single-cell transcriptomics with histologic, molecular, and physiologic readouts to define asbestos-induced POLCs and test whether their modulation alters disease severity. Methods C57BL/6J mice received intratracheal instillation of chrysotile asbestos, and replicate whole lungs were collected at follow-up timepoints from Day 0 (control) to Day 56 post-instillation. Pulmonary function testing, lung histology, and qPCR for osteoclast-associated genes were performed in parallel. Whole-lung single-nucleus RNA sequencing was used to model longitudinal transcriptional dynamics across the injury time course. In a separate cohort, whole-lung single-cell RNA sequencing was performed to characterize cell-specific responses to treatment with zoledronic acid, a bisphosphonate that inhibits osteoclast activity. Monocle3 supported dimensionality reduction, cell state annotation, pathway analysis, and pseudotime modeling, and a beta-binomial model quantified relative changes in cell type proportions. Results Asbestos exposure results in a progressive decline in pulmonary function and produces histologic evidence of early inflammatory infiltration and fibrotic deposition by Day 28. scRNA-seq identifies more than 30 lung cell states, with strong early expansion of myeloid populations. Alveolar macrophages show increased expression of canonical osteoclast-associated genes, including Acp5, Ctsk, and Atp6v0d2, which rise sharply by Day 7 and persist through later timepoints. qPCR confirms upregulation of osteoclast-related transcripts, acquisition of capacity for bone pitting and protein staining for TRAP5b and CTSK demonstrates robust induction of osteoclast programs. TRAP+ multinucleated cells are significantly increased in BALF from asbestos-exposed mice. Pseudotime analyses indicate differentiation of POLCs along a trajectory marked by acquisition of bone-resorption, matrix-remodeling, and catabolic signatures. Intraperitoneal (i.p.) treatment with the bisphosphonate, zoledronic acid, reduced POLC abundance, and attenuated parenchymal fibrosis due to asbestos based on multiple gene expression, histologic, and physiologic measures relative to i.p. vehicle control, supporting a functional role for POLCs in disease progression. Conclusions Chrysotile asbestos induces the emergence of pulmonary osteoclast-like cells that arise from macrophage lineages and display robust osteoclast gene programs. Pharmacologic inhibition of POLCs reduces lung fibrosis, identifying POLCs as a potential therapeutic target in asbestosis. This abstract is funded by: I01 BX005128-01a (VA Merit)
2026-05-01 | REVIEW OF CURRENT AND EMERGING ANTIFIBROTIC THERAPY FOR ASBESTOSIS AND SILICOSIS
Asbestosis and silicosis are progressive occupational lung diseases driven by asbestos fiber and respirable crystalline silica inhalation, resulting in chronic inflammation and irreversible pulmonary fibrosis. While prevention and early diagnosis remain paramount due to the lack of curative options, current supportive therapies offer limited efficacy. This review examines their pathogenesis, immune mechanisms, and management strategies, with emphasis on antifibrotic agents like pirfenidone and nintedanib, alongside emerging therapies such as PDE4B inhibitors (e.g., nerandomilast) and stem cell approaches. Recent clinical data suggest slowed fibrosis progression, but occupational-specific RCTs are needed to optimize safety, efficacy, and biomarkers in high-risk cohorts like construction workers.
2026-02-19 | Asbestos Disease Initiation.
A model is developed of disease initiation and progression for asbestos related plaque deposition and mesothelioma based on prior models of wound healing and asbestos transport. The model includes short term processes such as macrophage polarization and immune system response, extending the time frame to that of detectable disease. Model results were in a biologically reasonable range. Cancer development and plaque deposition are shown to be dependent on total exposure (intensity * duration). Plaque deposition was sensitive to many systemic parameters, suggesting that assays could be developed to identify individuals with higher risk. Tumor development was sensitive only to a few parameters describing exposure and T-cell levels, indicating potential for immune system intervention.
2026-06-10 | CURRENT STATUS OF GLOBAL AEROMICROBIOLOGY STUDIES
Abstract:Climate change when it had commenced due to anthropogenic activities is currently alsoinfluencing cells, propagules, environment aerosol borne, bioaerosol borne dispersal ofmicroorganisms (modes like the annual dust storms, urban and metropolitan suspended dustby vehicle plying on roads, desert storms, volcanic eruptions, silica- asbestosis, cement dustfrom building construction and industries, etc) are the major factors elevating problems likecontact dermatitis, respiratory diseases, allergies, occupational hazards (lung cancers, etc) tohumans and mammals. Thus, aeromicrobiology is concerned with health status andsocioeconomic progress of humans globally. Several species of aspergillus spores cause skinand respiratory tract infection. A. niger and A. fumigatus is the cause of otomycosis due toinfections of outer ear canal. Defeacating in open, dessication, and dispersion of faecalcontaminated soil carry airborne microorganisms (fungi, bacteria, viruses etc.,) far and wide.Tuberculosis, diphtheria, meningitis, pertusis, Streptococcus pneumonia as well as anthrax;Pandemic of Covid-19 and other virus infections spread through air. This is throughbioaerosol - aerosol transition facilitated by moisture, heat, temperature and air currents.Moreover, both natural and unnatural factors alter aeromicrobiology impact on humans. A‘solar aeromicrobiology model’ to purify air at any place have been proposed to eradicate orreducepathogenic and non-pathogenic microorganism (proposed by D.R.Saxena).The rapid Zooplane are "Machzooplane" such as birds, bats, and insects spread all types ofmicroorganisms intracontinentally if they are migratory (also fishes), if not intercontinently.The intracontinental zooplane include above stated animals as well as rodents, reptiles, etc.,that daily move in search of food, mate, etc. The slowest but ecologically significant zooplaneare bugs, ants, soil worms that disseminate the nonpathogenic and pathogenic microorganismsoccurring in air, water as well as soil borne medium.Scavengers also disseminatemicroorganisms (using various media-animal/human microbial cycle as proposed by theauthor) due to their feeding– defaecation and locomotory behaviour.Use of AI fabricated and controlled universal solar aeromicrobiology model also minidomestic models in everyresidence / flat has been hypothesized. The Prions may be a discarded protein particleofafaulty gene that is quiescent and may be accidently switched on. Now such genes maymetabolically synthesize materials such as DNA, RNA, Proteins, etc., in the bodies ofmicroorganisms, invertebrates and vertebrates including humans. This mechanism may be forslow or rapid evolution of self and non self infectious agents( this unwanted DNA, RNA,Proteins that are accidently synthesized and are not degraded and now cause diseases ),theirproduction may be accelerated manifolds triggered by continuous current climate as well asclimate changes in future and that will be the cause of global human deaths.
2026-05-11 | PREVENTIVE DIETARY NUTRITION FOR PATIENTS WITH ASBESTOSIS
This article provides a detailed overview of the basic principles of preventive dietary nutrition, the role of nutrients, and practical recommendations for patients suffering from asbestosis. A proper diet plays a crucial role in combating the progression of the disease. The article examines the role of foods rich in antioxidants, vitamins, minerals, and fiber in protecting lung tissue, based on scientific evidence.
2026-05-01 | B19-04 Pulmonary Osteoclast-like Cells in Asbestos-induced Pulmonary Fibrosis
Abstract Rationale Chrysotile asbestos inhalation drives a progressive fibrotic response in the lung, yet the cellular programs that mediate injury progression remain incompletely defined. Recent work has identified pulmonary osteoclast-like cells (POLCs) as rare, macrophage-derived effector cells that emerge in particulate lung injury and promote matrix remodeling. Whether POLCs are induced by asbestos and contribute to asbestosis pathogenesis has not been established. Here, we combined single-cell transcriptomics with histologic, molecular, and physiologic readouts to define asbestos-induced POLCs and test whether their modulation alters disease severity. Methods C57BL/6J mice received intratracheal instillation of chrysotile asbestos, and replicate whole lungs were collected at follow-up timepoints from Day 0 (control) to Day 56 post-instillation. Pulmonary function testing, lung histology, and qPCR for osteoclast-associated genes were performed in parallel. Whole-lung single-nucleus RNA sequencing was used to model longitudinal transcriptional dynamics across the injury time course. In a separate cohort, whole-lung single-cell RNA sequencing was performed to characterize cell-specific responses to treatment with zoledronic acid, a bisphosphonate that inhibits osteoclast activity. Monocle3 supported dimensionality reduction, cell state annotation, pathway analysis, and pseudotime modeling, and a beta-binomial model quantified relative changes in cell type proportions. Results Asbestos exposure results in a progressive decline in pulmonary function and produces histologic evidence of early inflammatory infiltration and fibrotic deposition by Day 28. scRNA-seq identifies more than 30 lung cell states, with strong early expansion of myeloid populations. Alveolar macrophages show increased expression of canonical osteoclast-associated genes, including Acp5, Ctsk, and Atp6v0d2, which rise sharply by Day 7 and persist through later timepoints. qPCR confirms upregulation of osteoclast-related transcripts, acquisition of capacity for bone pitting and protein staining for TRAP5b and CTSK demonstrates robust induction of osteoclast programs. TRAP+ multinucleated cells are significantly increased in BALF from asbestos-exposed mice. Pseudotime analyses indicate differentiation of POLCs along a trajectory marked by acquisition of bone-resorption, matrix-remodeling, and catabolic signatures. Intraperitoneal (i.p.) treatment with the bisphosphonate, zoledronic acid, reduced POLC abundance, and attenuated parenchymal fibrosis due to asbestos based on multiple gene expression, histologic, and physiologic measures relative to i.p. vehicle control, supporting a functional role for POLCs in disease progression. Conclusions Chrysotile asbestos induces the emergence of pulmonary osteoclast-like cells that arise from macrophage lineages and display robust osteoclast gene programs. Pharmacologic inhibition of POLCs reduces lung fibrosis, identifying POLCs as a potential therapeutic target in asbestosis. This abstract is funded by: I01 BX005128-01a (VA Merit)
2026-05-01 | REVIEW OF CURRENT AND EMERGING ANTIFIBROTIC THERAPY FOR ASBESTOSIS AND SILICOSIS
Asbestosis and silicosis are progressive occupational lung diseases driven by asbestos fiber and respirable crystalline silica inhalation, resulting in chronic inflammation and irreversible pulmonary fibrosis. While prevention and early diagnosis remain paramount due to the lack of curative options, current supportive therapies offer limited efficacy. This review examines their pathogenesis, immune mechanisms, and management strategies, with emphasis on antifibrotic agents like pirfenidone and nintedanib, alongside emerging therapies such as PDE4B inhibitors (e.g., nerandomilast) and stem cell approaches. Recent clinical data suggest slowed fibrosis progression, but occupational-specific RCTs are needed to optimize safety, efficacy, and biomarkers in high-risk cohorts like construction workers.
2026-02-19 | Asbestos Disease Initiation.
A model is developed of disease initiation and progression for asbestos related plaque deposition and mesothelioma based on prior models of wound healing and asbestos transport. The model includes short term processes such as macrophage polarization and immune system response, extending the time frame to that of detectable disease. Model results were in a biologically reasonable range. Cancer development and plaque deposition are shown to be dependent on total exposure (intensity * duration). Plaque deposition was sensitive to many systemic parameters, suggesting that assays could be developed to identify individuals with higher risk. Tumor development was sensitive only to a few parameters describing exposure and T-cell levels, indicating potential for immune system intervention.
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0 orphan drug designations.
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