asbestos : Environmental Chemical
1. EXPOSURE
People may be exposed to asbestos in their workplace, or their homes. If products containing asbestos are disturbed, tiny asbestos fibers are released into the air. When asbestos fibers are breathed in, they may get trapped in the lungs and remain there for a long time. Over time, these fibers can accumulate and cause scarring and inflammation, which can affect breathing and lead to serious health problems.
asbestos has been classified as a known human carcinogen.
1.1. Inhalation Exposure
When asbestos fibers are inhaled, many are deposited on the epithelial surface of the respiratory tree. The number of fibers that are deposited, and the location within the airway where deposition occurs, is a function of the aerodynamic properties of the fibers. In humans, the fibers depositing in the upper airway consist mainly of relatively thick fibers (greater than about 3 µm), with thinner fibers being carried deeper into the distal airways and alveolar regions. In rats, about 30–40% of typical fibers of chrysotile, amosite, and crocidolite, are retained, with most of these (about 60%) being deposited in the upper airways (nose, throat, and trachea). The median length for these fibers was 1–2 µm, while the median diameter was 0.2–0.4 µm. After intratracheal administration of chrysotile and amosite asbestos fibers in hamsters, chrysotile fibers were found to be primarily located near air duct bifurcations, while amosite fibers tended to be more distributed over the bronchial surface. Many of these smaller fibers deposit preferentially at bifurcations in the terminal bronchioles and alveolar ducts, with the number of fibers deposited at each location decreasing in proportion to the preceding airway path length and the number of preceding branch points.
1.2. Oral Exposure
Animal studies indicate that most asbestos fibers that are ingested are not absorbed across the walls of the gastrointestinal tract. However, electron micrographic studies indicate that some fibers penetrate into the gastrointestinal epithelium. In addition, some fibers pass through the gastrointestinal wall and reach blood, lymph, urine, and other tissues .The mechanism by which asbestos fibers pass through the gastrointestinal wall is not known with certainty, but it has been noted that a wide variety of very small particles (i.e., 1 µm or less; e.g., starch granules, cellulose particles, pollen) can cross the gut by passing between (not through) the cells of the epithelial layer in a process termed persorption, and it seems likely that this may account for uptake of asbestos fibers as well. Available data are not sufficient to make a precise estimate of the fraction of ingested fibers that pass through the gastrointestinal wall, but there is agreement that it is a very small amount. Several researchers have found that the average length of fibers in extra-gastrointestinal tissues or fluids is shorter than the average length of the fibers ingested, suggesting that short fibers pass through the gastrointestinal epithelium more easily than long fibers.
1.3. Dermal Exposure
As discussed above, asbestos fibers can penetrate into the skin, producing asbestos warts. No studies were located that indicate that asbestos fibers can pass through the skin into the blood
see
[ Asbestosis: A Medical Dictionary, Bibliography, And Annotated Research Guide To Internet References. San Diego,Calif. 2004 ]
[ Diagnosis and initial management of nonmalignant diseases related to asbestos. 2004 ]
[ Fibrosis of the Lungs due to the Inhalation of Asbestos Dust. 1924 ]
2. RISK FACTORS
Several factors can help to determine how asbestos exposure affects an individual, including:
• Dose (how much asbestos an individual was exposed to).
• Duration (how long an individual was exposed).
• Size, shape, and chemical makeup of the asbestos fibers.
• Source of the exposure.
• Individual risk factors, such as smoking and pre-existing lung disease.
Although all forms of asbestos are considered hazardous, different types of asbestos fibers may be associated with different health risks. For example, the results of several studies suggest that amphibole forms of asbestos may be more harmful than chrysotile, particularly for mesothelioma risk, because they tend to stay in the lungs for a longer period of time.
see
[ Asbestosis: A Medical Dictionary, Bibliography, And Annotated Research Guide To Internet References. San Diego,Calif. 2004 ]
[ Fibrosis of the Lungs due to the Inhalation of Asbestos Dust. 1924 ]
3. SMOKING SINERGIES
Many studies have shown that the combination of smoking and asbestos exposure is particularly hazardous. Smokers who are also exposed to asbestos have a risk of developing lung cancer that is greater than the individual risks from asbestos and smoking added together. There is evidence that quitting smoking will reduce the risk of lung cancer among asbestos-exposed workers. Smoking combined with asbestos exposure does not appear to increase the risk of mesothelioma. However, people who were exposed to asbestos on the job at any time during their life or who suspect they may have been exposed should not smoke.
see
[ TOXICOLOGICAL PROFILE FOR ASBESTOS. 2001. ]
4. SYMPTOMS
Individuals who have been exposed (or suspect they have been exposed) to asbestos fibers on the job, through the environment, or at home via a family contact should inform their doctor about their exposure history and whether or not they experience any symptoms. The symptoms of asbestos-related diseases may not become apparent for many decades after the exposure. It is particularly important to check with a doctor if any of the following symptoms develop:
- Shortness of breath, wheezing, or hoarseness.
- A persistent cough that gets worse over time.
- Blood in the sputum (fluid) coughed up from the lungs.
- Pain or tightening in the chest.
- Difficulty swallowing.
- Swelling of the neck or face.
- Loss of appetite.
- Weight loss.
- Fatigue or anemia.
see
[ Fibrosis of the Lungs due to the Inhalation of Asbestos Dust. 1924 ]
5. DIAGNOSIS
A thorough physical examination, including a chest x-ray and lung function tests, may be recommended. The chest x-ray is currently the most common tool used to detect asbestos-related diseases. However, it is important to note that chest x-rays cannot detect asbestos fibers in the lungs, but they can help identify any early signs of lung disease resulting from asbestos exposure.
Studies have shown that computed tomography (a series of detailed pictures of areas inside the body taken from different angles; the pictures are created by a computer linked to an x-ray machine) may be more effective than conventional chest x-rays at detecting asbestos-related lung abnormalities in individuals who have been exposed to asbestos .
A lung biopsy, which detects microscopic asbestos fibers in pieces of lung tissue removed by surgery, is the most reliable test to confirm the presence of asbestos-related abnormalities. A bronchoscopy is a less invasive test than a biopsy and detects asbestos fibers in material that is rinsed out of the lungs. It is important to note that these tests cannot determine how much asbestos an individual may have been exposed to or whether disease will develop. Asbestos fibers can also be detected in urine, mucus, or feces, but these tests are not reliable for determining how much asbestos may be in an individual’s lungs.
Studies have shown that exposure to asbestos may increase the risk of lung cancer and mesothelioma (a relatively rare cancer of the thin membranes that line the chest and abdomen). Although rare, mesothelioma is the most common form of cancer associated with asbestos exposure. In addition to lung cancer and mesothelioma, some studies have suggested an association between asbestos exposure and gastrointestinal and colorectal cancers, as well as an elevated risk for cancers of the throat, kidney, esophagus, and gallbladder. However, the evidence is inconclusive.
asbestos exposure may also increase the risk of asbestosis (an inflammatory condition affecting the lungs that can cause shortness of breath, coughing, and permanent lung damage) and other nonmalignant lung and pleural disorders, including pleural plaques (changes in the membranes surrounding the lung), pleural thickening, and benign pleural effusions (abnormal collections of fluidbetween the thin layers of tissue lining the lungs and the wall of the chest cavity). Although pleural plaques are not precursors to lung cancer, evidence suggests that people with pleural disease caused by exposure to asbestos may be at increased risk for lung cancer.
see
[ TOXICOLOGICAL PROFILE FOR ASBESTOS. 2001. ]
[ Fibrosis of the Lungs due to the Inhalation of Asbestos Dust. 1924 ]
6. METABOLISM
6.1. Inhalation
Asbestos fibers are not metabolized in the normal sense of the word, and amphibole fibers that are retained in the lung do not appear to undergo any major changes. However, chrysotile fibers appear to undergo some type of breakdown or alteration in the lung. This conclusion is based primarily on measurements of asbestos levels in the lung as a function of exposure duration. With continuing exposure of animals, amphibole levels tend to rise linearly, whereas chrysotile levels reach a steady-state concentration within several months. These data from animal studies are supported by a number of human studies in which the ratio of amphibole to chrysotile concentration in lung tissue was much higher than
expected based on the composition of the inhaled fibers.
Long chrysotile fibers (>10 or 18 µm) are expected to accumulate in humans with continued exposure, based on observations of an association between duration of exposure of chrysotile miners and millers and lung chrysotile fiber concentrations >18 µm in length and estimations of long clearance half times (>8 years) for lungsequestered fibers in chrystotile miners and millers. Finkelstein and Dufresne discerned patterns in their data suggestive that lung concentrations of chrysotile fibers would reach plateaus in humans after decades of exposure under occupational conditions.
The basis of this apparent loss of chrysotile fibers is not clear, but it may be related to a slow dissolution of the fibers in tissue fluids or in macrophages, or to a separation of the fibers into much finer component fibrils. In the latter case, the apparent loss of fibers could be an artifact due to the inability of normal methods for fiber isolation and quantification in tissues to detect very fine fibrils. Loss of chrysotile has been reported to be related to the fragmentation of long fibers, resulting in the formation of smaller fibers. There appears to be preferential clearance of short asbestos fibers compared to long ones. For example, based on an analysis of lung fiber concentrations in 72 chrysotile miners and millers, years of exposure, and time since last exposure, long-term clearance half-times were estimated to be about 4 and 8 years for chrysotile fibers <5 µm and >10 µm in length, respectively. In contrast, clearance half-times were about 8 and 16 years for tremolite fibers <5 µm and >10 µm in length, respectively. (Short-term clearance times could not be measured in this analysis of lung fiber concentrations in chronically exposed miners and millers.) Long fibers that reside in the lung can form asbestos bodies.
The formation of asbestos bodies might represent an attempt by macrophages to digest these fibers extracellularly.
6.2. Oral Exposure
No studies were located regarding any changes in asbestos fibers in the gastrointestinal tract. However, chrysotile fibers incubated in simulated gastric juice underwent leaching of magnesium ion from the silica framework, with a resultant change in net fiber charge from positive to negative, and chrysotile fibers with altered appearance and x-ray diffraction patterns were detected in the urine of. These observations, although limited, suggest that chrysotile fibers undergo some metal ion exchange and alterations in gross structure in biological fluids after oral exposure. Asbestos bodies have been detected is tissues such as the colon (Ehrlich et al. 1992), suggesting that this process may occur in extrapulmonary tissues as well.
6.3. Dermal Exposure
No studies were located regarding any changes in asbestos fiber composition or structure after dermal exposure.
see
[ Asbestos Toxicity. ATSDR Case Studies in Environmental Medicine. U.S. 2010 ]
[ TOXICOLOGICAL PROFILE FOR ASBESTOS. 2001. ]
[ Fibrosis of the Lungs due to the Inhalation of Asbestos Dust. 1924 ]
7. WAY OF ACTION
If you breathe asbestos fibers into your lungs, some of the fibers will be deposited in the air passages and on the cells that make up your lungs. Most fibers are removed from your lungs by being carried away or coughed up in a layer of mucus to the throat, where they are swallowed into the stomach. This usually takes place within a few hours. Fibers that are deposited in the deepest parts of the lung are removed more slowly. In fact, some fibers may move through your lungs and can remain in place for many years and may never be removed from your body.
Amphibole asbestos fibers are retained in the lung longer than chrysotile asbestos fibers. If you swallow asbestos fibers (either those present in water or those that are moved to your throat from your lungs), nearly all of the fibers pass along your intestines within a few days and are excreted in the feces. A small number of fibers may penetrate into cells that line your stomach or intestines, and a few penetrate all the way through and get into your blood. Some of these become trapped in other tissues, and some are removed in your urine. If you get asbestos fibers on your skin, very few of these fibers, if any, pass through the skin into your body.
see
[ Diagnosis and initial management of nonmalignant diseases related to asbestos. 2004 ]
[ Fibrosis of the Lungs due to the Inhalation of Asbestos Dust. 1924 ]
8. THERAPY
Treatment options for patients diagnosed with nonmalignant lung or pleural disease from chronic exposure to asbestos are few. Preventing of further exposure and ceasing any tobacco smoking activities are the most important steps individuals can take to minimize development of health problems. Once established, these diseases may remain stable or progress in severity in the absence of further exposure. The diseases rarely regress. Treatment options for patients diagnosed with asbestos-related cancer of the lung or pleura are restricted to resection and/or chemotherapy.
Pleural effusions are early manifestations of inhalation exposure to high concentrations of asbestos; the fluid contains varying amounts of red blood cells, macrophages, lymphocytes, and mesothelial cells. Pleural effusions may be an early indication of mesothelioma and warrant further evaluation. Early identification of mesothelioma and intervention may increase chances of survival.
Additional research may help to develop therapeutic methods to interfere with the development of asbestos-induced lung and pleural disorders and to cause the disorders to regress once they are established
see
[ Diagnosis and initial management of nonmalignant diseases related to asbestos. 2004 ]
[ Asbestos Toxicity. ATSDR Case Studies in Environmental Medicine. U.S. 2010 ]
9. Bibliography
1 - Icon Health Publications. (2004). Asbestosis: A Medical Dictionary, Bibliography, And Annotated Research Guide To Internet References. San Diego, Calif.
2 - American Thoracic Society. (2004). Diagnosis and initial management of nonmalignant diseases related to asbestos. Am. J. Respir. Crit. Care Med , 170.
3 - Department of Health and Human Services. (s.d.). Asbestos Toxicity. ATSDR Case Studies in Environmental Medicine. U.S.
4 - GROUP, A. W., G. Douglas Hanley, M. R., Susan Kess, M. M., Yee-Wan Stevens, M., Sharon Wilbur, M., & Malcolm Williams, D. P. (2001, September). TOXICOLOGICAL PROFILE FOR ASBESTOS. Tratto da Agency for Toxic Substances and Disease Registry.
5 - WE, C. (s.d.). Fibrosis of the Lungs due to the Inhalation of Asbestos Dust. Br Med J , 140-147. 752865
