Asbestosis is caused by long-term inhalation of asbestos fibers. Persons with occupational mining, manufacturing, manipulation or removal of asbestos exposure are at risk for asbestosis. There is an increased risk of lung cancer and mesothelioma associated with an increased risk of lung cancer and " mesothelioma " risk associated with the risk for asbestosis asbestosis.
There is risk
is related to the total dose received and the duration of exposure to
asbestos in asbestos. In general, microorganisms, dust and other foreign
particles from the air we breathe to be filtered by the nose hair,
causing coughing reflex.
Because asbestos particles (amphibole) long,
very thin, microscopic and light enters the nose cannot be filtered by
the nose hair, causing asbestos particles can enter the respiratory
occupational exposure is the most common cause asbestosis but also
provided at the entrance of the airways of these particles in the
alveolar gas and existing gas exchange 300 million.
Each cell has a
large number of cells called cells macrophages ingest cleaning airborne
particles. The alveoli are very thin elastic walls that allow the
exchange of gases vital to your health - the flow of oxygen from the
alveoli into the blood to nourish the body and the flow of carbon
dioxide waste from the blood into the alveoli and the lungs to be
expelled .
Alveoli very thin elastic that allows gas exchange is
important for health. The oxygen passes from the blood cells in the body
to the power source, and carbon dioxide from the blood to the alveoli
and bronchi unwrapped. Asbestos fibers can be easily separated and are
small enough to be inhaled deep into the asbestos to be removed easily
lungs.
Fiber and small enough to be inhaled into the lungs. When inhaled
into the lungs, the lung defense cells try to destroy asbestos fibers,
but the defense mechanisms of the body can not break asbestos. If the
inhaled into the lungs and the fibers reach the alveoli (air sacs) -
lung in the Lungs where oxygen is transferred into the blood, foreign
bodies (asbestos fibers) cause the activation of the lungs.
Lung defense cells try to destroy asbestos fibers, but the defense mechanisms of the body can not destroy asbestos, including macrophages. Macrophages trying to swallow a fiber of asbestos, often fails because the fiber is too long.
In prose that macrophages secrete substances to
destroy foreign objects, but they can also damage cells. This leads to
the appearance of scar tissue in the wound and form of the cells is a
process called fibrosis. Then, the asbestos fibers to remain can't be
filtered in and cause lung inflammation and scarring.
The lung tissue causing thickened alveolar walls reduces the elasticity and the ability to exchange oxygen and carbon dioxide. Therefore, decreased lung capacity, reduces the exchange of oxygen and is felt increasingly short of breath time. More than 50% of people who develop asbestosis exposed with plaques in the parietal pleura, the space between the chest wall and the lung.
Patients dry crackling inspired club, and the mode of
propagation in the lower lobe pulmonary fibrosis, which is the case more
often affected with asbestosis. The fibers are inhaled, ingested
by alveolar macrophages reach the alveoli, C5a stimulates the release of
the trailer and chemicals (chemoattractant) in second place.
Ambifol
(hetero hard) into the lungs in the fiber coil, which results in an
increase in pathogenicity. More asbestos inhaled by macrophages, the
remaining to reach the interstitium and lymph vessels. Some fibers are inhaled surrounded by hemosiderin and glycoproteins to form a dumbbell Jicin asbestos, pearls and features.
The accumulation of inhaled fibers in a given period of time, the type
and resistance, and the effect of fiber size and fibrogenisitas
carcinogenicity. Early asbestosis varies cumulative levels of inhaled
fibers, more levels of accumulation, the greater the incidence of
asbestosis.
The mechanism of progressive fibrosis of lung injury may include :
• Release of toxic or free by macrophages / neutrophils radical enzymes were attracted to the place of deposit of asbestos.
• Fibrogenik release of cytokines and growth by alveolar macrophages after the phagocytosis of the fibers factors.
• Stimulation of collagen formation by fibroblasts asbestos.
All types of fibers comprising asbestos fibers in the lungs. Amphibole
crocidolite asbestos fibers in a particularly clear and significantly
more cancer in the pleura. The diameter of the fibers is less than 3
microns because fibrogenik can penetrate the cell membrane.
The existence imflamasi stimulate macrophages in the alveoli. Asbestos activates macrophages to produce a variety of growth factors including fibronectin and platelets, which are interconnected to affect the growth of fibroblasts.
Free oxygen (eg, superoxide anion, hydrogen peroxide, hydroxyl) released by macrophages destroy proteins and lipids that support the inflammatory process. A plasminogen activator, which is released by macrophages, which causes damage to the lung interstitium, and glycoproteins of the matrix is reduced.
In addition to pulmonary fibrosis, pleural asbestos stimulates reactions such as :
1. Efusi
benigna
2. Adhesi Pleura Fibrosa
3. Fibrokalsifik Pleural Plaques in solid or diaphragm.
Plates calcification times; jisim not contain asbestos. Asbestos exposure is also associated with an increased risk of lung cancer and malignant mesothelioma .
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