- December 6, 2022
- Newsletter
- 617-430-5616
Menu
» Home » CAD » Pulmonology » Pulmonary Diseases » Asbestosis
ADVERTISEMENT
ADVERTISEMENT
» Home » CAD » Pulmonology » Pulmonary Diseases » Asbestosis
Background
Asbestosis is an inflammatory lung cancer brought on by asbestos fiber inhalation. These fibers are various mineral silica, primarily hydrated magnesium silica, and can be divided into amphibole and serpentine based on morphology. Chrysolites, a type of flexible, curly fiber found in serpentine, are less harmful than amphibole filaments.
Chrysolite settles in the upper portion of the respiratory system due to its increased flexibility, curvature, and solubility. Chrysolite filaments are easily eliminated because the upper airway has a more prominent mucociliary activity. Anthophyllite, amosite, crocidolite, and tremolite are examples of amphiboles, which are straight, rigid, and more fragile fibers.
Because they are more straight and less soluble than serpentine fibers, they are more poisonous. They often align with the airstream and penetrate the epithelium to travel farther into the interstitium and lungs. Because of their excellent electrical and thermal resistance and low price, asbestos fibers have historically been preferred for commercial application in the fields of shipping, construction, aerospace, and mining engineering.
Epidemiology
In those fields where exposure is high in intensity, the disease is more common. According to a survey among construction workers in Okayama, Japan, those who install asbestos boards have the highest incidence of instances (39.1 percent), followed by those who spray asbestos (38.5 percent). Additionally, the likelihood of developing asbestosis increases with exposure time.
The highest danger of asbestosis in the UK is for insulation employees, accompanied by asbestos removal. Around 55000 deaths worldwide are attributed to asbestos use each year, according to estimates. More common among construction personnel. Compared to other pulmonary problems, benign illness has a shorter lag phase. Instances of pulmonary effusion are related to the place of exposure and were found to be 9 instances per 1000 in groups that had been exposed to high levels of radiation.
Even though mesothelioma is less common than lung cancer, the USA reported around 2000 instances per year in the 21st century. Comparatively speaking, pulmonary cancer occurs more frequently than mesothelioma. The usage of asbestos in wealthy countries has been decreased but use in poor countries like Nepal and Pakistan still substantially high.
Anatomy
Pathophysiology
Asbestosis’ primary pathogenic mechanism is thought to be interstitial fibrosis. There is thought to be a buildup of fibroblasts & macrophages after the transmigration & deposition of asbestos fibers in the lung, which creates the groundwork for fibrosis. Oxidative damage is caused when immune and phagocytic cells react to asbestos fibers by producing reactive oxygen radicals. The type 1 alveoli cells are harmed by these oxygen radicals & transepithelial movement of fibers.
Additionally, fibroblast growth factor-beta, which causes fibrosis, is produced by damaged epithelial. Macrophages release inflammatory cytokines, including interleukins, tissue necrosis factor, and activation of the phospholipase C axis in an effort to phagocytose the foreign object. Additional cells, including lymphocytes and myofibroblasts, are stimulated in a significant way by these transmitters. As a result, fibroblasts multiply, and the cells in the matrices rise by nearly twofold.
Additionally, fibroblast growth hormones, platelet-derived growth regulators, & insulin-like growth regulators are also produced by macrophages and contribute to fibrosis. The structural glycoproteins are broken down by the macrophage-produced plasminogen activation, further harming the interstitium. Fibrosis progresses throughout time due to the disease’s progressive nature. Serum supplement C5a, a chemotactic protein for macrophages, is also activated by asbestos fibers.
Reactive oxygen molecules are typically produced as a result of other poisons, such as metallic elements, coating asbestos fibers. These fibers’ iron coatings play a part in the production of hydroxide radicals in one cell-free condition, which leads to free radical damage. According to a recent study, pathogenesis and fiber length are directly related. In terms of NF-kB cascade & specific genomic activity stimulation, long fibers are more effective than short fibers.
The development of autoantibodies is connected to amphibole exposure. According to popular belief, patients who test positive for antinuclear antibodies are more likely to experience interstitial & pulmonary abnormalities. Asbestos may have cellular & fibrotic effects in addition to acting as a tumor promoter and initiator. Pleura carcinogenesis is more likely to occur in amphibole types. The recommended dosage of exposure to asbestos influences the severity of pulmonary fibrosis.
Etiology
There are 3 primary ways to be exposed to asbestos. Workers in industries like shipbuilding, mining, aircraft, etc., frequently have direct occupational pollution connected to their jobs. The second type of exposure is frequently observed in certain professions like painters, masons, and electricians.
The usage of asbestos in landfills, chemical paint coatings, playground equipment, and roadways is the third and the most prevalent type of exposure to asbestos.
The condition is dose-dependent; the first group receives larger exposure doses, while the second and third groups receive lower exposure doses. Additionally, compared to serpentine asbestosis fibers, the amphibole form carries a higher chance of contracting the disease.
Genetics
Prognostic Factors
Clinical History
Physical Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
Medication
Future Trends
References
https://www.ncbi.nlm.nih.gov/books/NBK555985/
ADVERTISEMENT
» Home » CAD » Pulmonology » Pulmonary Diseases » Asbestosis
Asbestosis is an inflammatory lung cancer brought on by asbestos fiber inhalation. These fibers are various mineral silica, primarily hydrated magnesium silica, and can be divided into amphibole and serpentine based on morphology. Chrysolites, a type of flexible, curly fiber found in serpentine, are less harmful than amphibole filaments.
Chrysolite settles in the upper portion of the respiratory system due to its increased flexibility, curvature, and solubility. Chrysolite filaments are easily eliminated because the upper airway has a more prominent mucociliary activity. Anthophyllite, amosite, crocidolite, and tremolite are examples of amphiboles, which are straight, rigid, and more fragile fibers.
Because they are more straight and less soluble than serpentine fibers, they are more poisonous. They often align with the airstream and penetrate the epithelium to travel farther into the interstitium and lungs. Because of their excellent electrical and thermal resistance and low price, asbestos fibers have historically been preferred for commercial application in the fields of shipping, construction, aerospace, and mining engineering.
In those fields where exposure is high in intensity, the disease is more common. According to a survey among construction workers in Okayama, Japan, those who install asbestos boards have the highest incidence of instances (39.1 percent), followed by those who spray asbestos (38.5 percent). Additionally, the likelihood of developing asbestosis increases with exposure time.
The highest danger of asbestosis in the UK is for insulation employees, accompanied by asbestos removal. Around 55000 deaths worldwide are attributed to asbestos use each year, according to estimates. More common among construction personnel. Compared to other pulmonary problems, benign illness has a shorter lag phase. Instances of pulmonary effusion are related to the place of exposure and were found to be 9 instances per 1000 in groups that had been exposed to high levels of radiation.
Even though mesothelioma is less common than lung cancer, the USA reported around 2000 instances per year in the 21st century. Comparatively speaking, pulmonary cancer occurs more frequently than mesothelioma. The usage of asbestos in wealthy countries has been decreased but use in poor countries like Nepal and Pakistan still substantially high.
Asbestosis’ primary pathogenic mechanism is thought to be interstitial fibrosis. There is thought to be a buildup of fibroblasts & macrophages after the transmigration & deposition of asbestos fibers in the lung, which creates the groundwork for fibrosis. Oxidative damage is caused when immune and phagocytic cells react to asbestos fibers by producing reactive oxygen radicals. The type 1 alveoli cells are harmed by these oxygen radicals & transepithelial movement of fibers.
Additionally, fibroblast growth factor-beta, which causes fibrosis, is produced by damaged epithelial. Macrophages release inflammatory cytokines, including interleukins, tissue necrosis factor, and activation of the phospholipase C axis in an effort to phagocytose the foreign object. Additional cells, including lymphocytes and myofibroblasts, are stimulated in a significant way by these transmitters. As a result, fibroblasts multiply, and the cells in the matrices rise by nearly twofold.
Additionally, fibroblast growth hormones, platelet-derived growth regulators, & insulin-like growth regulators are also produced by macrophages and contribute to fibrosis. The structural glycoproteins are broken down by the macrophage-produced plasminogen activation, further harming the interstitium. Fibrosis progresses throughout time due to the disease’s progressive nature. Serum supplement C5a, a chemotactic protein for macrophages, is also activated by asbestos fibers.
Reactive oxygen molecules are typically produced as a result of other poisons, such as metallic elements, coating asbestos fibers. These fibers’ iron coatings play a part in the production of hydroxide radicals in one cell-free condition, which leads to free radical damage. According to a recent study, pathogenesis and fiber length are directly related. In terms of NF-kB cascade & specific genomic activity stimulation, long fibers are more effective than short fibers.
The development of autoantibodies is connected to amphibole exposure. According to popular belief, patients who test positive for antinuclear antibodies are more likely to experience interstitial & pulmonary abnormalities. Asbestos may have cellular & fibrotic effects in addition to acting as a tumor promoter and initiator. Pleura carcinogenesis is more likely to occur in amphibole types. The recommended dosage of exposure to asbestos influences the severity of pulmonary fibrosis.
There are 3 primary ways to be exposed to asbestos. Workers in industries like shipbuilding, mining, aircraft, etc., frequently have direct occupational pollution connected to their jobs. The second type of exposure is frequently observed in certain professions like painters, masons, and electricians.
The usage of asbestos in landfills, chemical paint coatings, playground equipment, and roadways is the third and the most prevalent type of exposure to asbestos.
The condition is dose-dependent; the first group receives larger exposure doses, while the second and third groups receive lower exposure doses. Additionally, compared to serpentine asbestosis fibers, the amphibole form carries a higher chance of contracting the disease.
https://www.ncbi.nlm.nih.gov/books/NBK555985/
Asbestosis is an inflammatory lung cancer brought on by asbestos fiber inhalation. These fibers are various mineral silica, primarily hydrated magnesium silica, and can be divided into amphibole and serpentine based on morphology. Chrysolites, a type of flexible, curly fiber found in serpentine, are less harmful than amphibole filaments.
Chrysolite settles in the upper portion of the respiratory system due to its increased flexibility, curvature, and solubility. Chrysolite filaments are easily eliminated because the upper airway has a more prominent mucociliary activity. Anthophyllite, amosite, crocidolite, and tremolite are examples of amphiboles, which are straight, rigid, and more fragile fibers.
Because they are more straight and less soluble than serpentine fibers, they are more poisonous. They often align with the airstream and penetrate the epithelium to travel farther into the interstitium and lungs. Because of their excellent electrical and thermal resistance and low price, asbestos fibers have historically been preferred for commercial application in the fields of shipping, construction, aerospace, and mining engineering.
In those fields where exposure is high in intensity, the disease is more common. According to a survey among construction workers in Okayama, Japan, those who install asbestos boards have the highest incidence of instances (39.1 percent), followed by those who spray asbestos (38.5 percent). Additionally, the likelihood of developing asbestosis increases with exposure time.
The highest danger of asbestosis in the UK is for insulation employees, accompanied by asbestos removal. Around 55000 deaths worldwide are attributed to asbestos use each year, according to estimates. More common among construction personnel. Compared to other pulmonary problems, benign illness has a shorter lag phase. Instances of pulmonary effusion are related to the place of exposure and were found to be 9 instances per 1000 in groups that had been exposed to high levels of radiation.
Even though mesothelioma is less common than lung cancer, the USA reported around 2000 instances per year in the 21st century. Comparatively speaking, pulmonary cancer occurs more frequently than mesothelioma. The usage of asbestos in wealthy countries has been decreased but use in poor countries like Nepal and Pakistan still substantially high.
Asbestosis’ primary pathogenic mechanism is thought to be interstitial fibrosis. There is thought to be a buildup of fibroblasts & macrophages after the transmigration & deposition of asbestos fibers in the lung, which creates the groundwork for fibrosis. Oxidative damage is caused when immune and phagocytic cells react to asbestos fibers by producing reactive oxygen radicals. The type 1 alveoli cells are harmed by these oxygen radicals & transepithelial movement of fibers.
Additionally, fibroblast growth factor-beta, which causes fibrosis, is produced by damaged epithelial. Macrophages release inflammatory cytokines, including interleukins, tissue necrosis factor, and activation of the phospholipase C axis in an effort to phagocytose the foreign object. Additional cells, including lymphocytes and myofibroblasts, are stimulated in a significant way by these transmitters. As a result, fibroblasts multiply, and the cells in the matrices rise by nearly twofold.
Additionally, fibroblast growth hormones, platelet-derived growth regulators, & insulin-like growth regulators are also produced by macrophages and contribute to fibrosis. The structural glycoproteins are broken down by the macrophage-produced plasminogen activation, further harming the interstitium. Fibrosis progresses throughout time due to the disease’s progressive nature. Serum supplement C5a, a chemotactic protein for macrophages, is also activated by asbestos fibers.
Reactive oxygen molecules are typically produced as a result of other poisons, such as metallic elements, coating asbestos fibers. These fibers’ iron coatings play a part in the production of hydroxide radicals in one cell-free condition, which leads to free radical damage. According to a recent study, pathogenesis and fiber length are directly related. In terms of NF-kB cascade & specific genomic activity stimulation, long fibers are more effective than short fibers.
The development of autoantibodies is connected to amphibole exposure. According to popular belief, patients who test positive for antinuclear antibodies are more likely to experience interstitial & pulmonary abnormalities. Asbestos may have cellular & fibrotic effects in addition to acting as a tumor promoter and initiator. Pleura carcinogenesis is more likely to occur in amphibole types. The recommended dosage of exposure to asbestos influences the severity of pulmonary fibrosis.
There are 3 primary ways to be exposed to asbestos. Workers in industries like shipbuilding, mining, aircraft, etc., frequently have direct occupational pollution connected to their jobs. The second type of exposure is frequently observed in certain professions like painters, masons, and electricians.
The usage of asbestos in landfills, chemical paint coatings, playground equipment, and roadways is the third and the most prevalent type of exposure to asbestos.
The condition is dose-dependent; the first group receives larger exposure doses, while the second and third groups receive lower exposure doses. Additionally, compared to serpentine asbestosis fibers, the amphibole form carries a higher chance of contracting the disease.
https://www.ncbi.nlm.nih.gov/books/NBK555985/
Founded in 2014, medtigo is committed to providing high-quality, friendly physicians, transparent pricing, and a focus on building relationships and a lifestyle brand for medical professionals nationwide.
USA – BOSTON
60 Roberts Drive, Suite 313
North Adams, MA 01247
INDIA – PUNE
7, Shree Krishna, 2nd Floor, Opp Kiosk Koffee, Shirole Lane, Off FC Road, Pune 411004, Maharashtra
Founded in 2014, medtigo is committed to providing high-quality, friendly physicians, transparent pricing, and a focus on building relationships and a lifestyle brand for medical professionals nationwide.
MASSACHUSETTS – USA
60 Roberts Drive, Suite 313,
North Adams, MA 01247
MAHARASHTRA – INDIA
7, Shree Krishna, 2nd Floor,
Opp Kiosk Koffee,
Shirole Lane, Off FC Road,
Pune 411004, Maharashtra
Both our subscription plans include Free CME/CPD AMA PRA Category 1 credits.
On course completion, you will receive a full-sized presentation quality digital certificate.
A dynamic medical simulation platform designed to train healthcare professionals and students to effectively run code situations through an immersive hands-on experience in a live, interactive 3D environment.
When you have your licenses, certificates and CMEs in one place, it's easier to track your career growth. You can easily share these with hospitals as well, using your medtigo app.