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Asbestos MSDS Information and Complete Public Health StatementAsbestos MSDS, or Material Safety Data Sheet, plus complete health related exposure information is found on this extensive guide. I have also answered the most common questions asked about Asbestos below. There are also links to other related resources at the page bottom which will answer any questions you might possibly have, such as: Asbestos Abatement, Identification, Testing, and Removal questions.
Asbestos FAQs... 1.1 What is asbestos? 1.2 What happens to asbestos when it enters the environment? 1.3 How might I be exposed to asbestos? 1.4 How can asbestos enter and leave my body? 1.5 How can asbestos affect my health? 1.6 How can asbestos affect children? 1.7 How can families reduce the risk of exposure to asbestos? 1.8 Is there a medical test to determine whether I have been exposed to asbestos? 1.9 What recommendations has the federal government made to protect human health? 1.10 Where can I get more information? 1.11 Complete Asbestos MSDS Information - EVERYTHING you could ever want to know about Asbestos past, present, or future!
When a substance is released from a large area, such as an industrial plant, or from a container, such as a drum or bottle, it enters the environment. This release does not always lead to exposure. You are exposed to a substance only when you come in contact with it. You may be exposed by breathing, eating, or drinking the substance, or by skin contact. If you are exposed to asbestos, many factors determine whether you’ll be harmed. These factors include the dose (how much), the duration (how long), the fiber type (mineral form and size distribution), and how you come in contact with it. You must also consider the other chemicals you’re exposed to and your age, sex, diet, family traits, lifestyle (including whether you smoke tobacco), and state of health. Special Warning About Zonolite Vermiculite Attic Insulation and AsbestosIf the attic of your home contains Vermiculite Insulation, there is a high possibility the Vermiculite Insulation may contain dangerous levels of Asbestos which could be hazardous to your family's health if disturbed.To prevent Asbestos dust from becoming airborne and creating an inhalation hazard, do not attempt to move, clean-up, or disturb the Vermiculite in any way. Consult an Asbestos Expert and the EPA. Zonolite Attic Insulation was mined in Libby Montana prior to 1990 and has been widely used in tens of thousands of homes all over North America. Zonolite Insulation may contain significant amounts of Asbestos and will require professional testing and removal. Because of the number of houses affected, this is one of the most serious public health issues in history. But surprisingly, there has been very little media coverage of this very widespread public health crisis. I created the following page to help those who suspect their home may be contaminated with Zonolite Vermiculite Attic Insulation. If you live in an older home, you especially may want to pay that page a visit to see what Vermiculite Insulation looks like and find out what to do if you have it in your attic. 1.1 What is Asbestos? Asbestos is the name given to a group of six different fibrous minerals (amosite, chrysotile, crocidolite, and the fibrous varieties of tremolite, actinolite, and anthophyllite) that occur naturally in the environment. One of these, namely chrysotile, belongs to the serpentine family of minerals, while all of the others belong to the amphibole family. All forms of asbestos are hazardous, and all can cause cancer, but amphibole forms of asbestos are considered to be somewhat more hazardous to health than chrysotile. Asbestos minerals consist of thin, separable fibers that have a parallel arrangement. Nonfibrous forms of tremolite, actinolite, and anthophyllite also are found naturally. However, because they are not fibrous, they are not classified as asbestos minerals. Amphibole asbestos fibers are generally brittle and often have a rod- or needle-like shape, whereas chrysotile asbestos fibers are flexible and curved. Chrysotile, also known as white asbestos, is the predominant commercial form of asbestos; amphiboles are of minor commercial importance. Asbestos fibers do not have any detectable odor or taste. They do not dissolve in water or evaporate and are resistant to heat, fire, chemical and biological degradation. Because of these properties, asbestos has been mined for use in a wide range of manufactured products, mostly in building materials, friction products, and heat-resistant fabrics. Since asbestos fibers may cause harmful health effects in people who are exposed, all new uses of asbestos have been banned in the United States by the EPA. Please see the toxicological profile for more information on the properties and uses of asbestos. Synonyms: AT 7-1, Amianthus, Asbest [German], Asbesto [Spanish], Asbestos, Asbestos dust, Asbestos fiber, Asbestos fibers, Asbestos fibre, Asbestose [German], Ascarite, BK 6-20, BP 3-50, BP 5-65, CCRIS 56, Calidria HPP, Calidria R-G 244, Carey 4T, Caswell No. 061, Chlorobestos 25, EPA Pesticide Chemical Code 099301, FAPM 410-120, Ferodo C3C, Fibrous grunerite, HPO (mineral), HSDB 511, K 6-20, M 3-60, M 4-5, M 5-60, M 6-40, MTM, Mountain cork, Mountain leather, Mountain wood, NCI C08991, P 5-50, P 5-50 (mineral), SM 1 (mineral), SM 2 (mineral), Sepiolex 3, Sepiolex 5,Systematic Name: Asbestos, Superlist Name: Asbestos, Asbestos (friable), Asbestos, all forms, Man-made mineral fibres, Registry Numbers CAS Registry Number: 1332-21-4, Other Registry Number: 12413-45-5, 77641-59-9 1.2 What happens to asbestos when it enters the environment? Asbestos fibers do not evaporate into air or dissolve in water. However, pieces of fibers can enter the air and water from the weathering of natural deposits and the wearing down of manufactured asbestos products. Small diameter fibers and fiber-containing particles may remain suspended in the air for a long time and be carried long distances by wind or water currents before settling. Larger diameter fibers and particles tend to settle more quickly. Asbestos fibers are not able to move through soil. They are generally not broken down to other compounds in the environment and will remain virtually unchanged over long periods. However, the most common form of asbestos, chrysotile, may have some minor mineral loss in acidic environments. Asbestos fibers may break into shorter pieces or separate into a larger number of individual fibers as a result of physical processes. When asbestos fibers are breathed in, they may get trapped in the lungs. Levels of fibers in lung tissue build up over time, but some fibers, particularly chrysotile fibers, can be removed from or degraded in the lung with time. Please see the toxicological profile for more information on the behavior of asbestos in the environment. 1.3 How might I be exposed to asbestos? Asbestos minerals are widespread in the environment. They may occur in large natural deposits, or as contaminants in other minerals. For example, tremolite asbestos may occur in deposits of chrysotile, vermiculite, and talc. Asbestos may be found in soil that is formed from the erosion of asbestos-bearing rock. You are most likely to be exposed to asbestos by breathing in asbestos fibers that are suspended in air. These fibers can come from naturally occurring sources of asbestos or from the wearing down or disturbance of manufactured products including insulation, automotive brakes and clutches, ceiling and floor tiles, dry wall, roof shingles, and cement. However, these products do not always contain asbestos. Low levels of asbestos that present little, if any, risk to your health can be detected in almost any air sample. For example, 10 fibers are typically present in a cubic meter (fibers/m³) of outdoor air in rural areas. (A cubic meter is about the amount of air that you breathe in 1 hour.) Health professionals often report the number of fibers in a milliliter (mL) (equivalent to a cubic centimeter [cm³]) of air rather than in a cubic meter of air. Since there are one million cm³ (or one million mL) in a cubic meter, there typically would be 0.00001 fibers/mL of asbestos in air in rural areas. Typical levels found in cities are about 10-fold higher. Close to an asbestos mine or factory, levels may reach 10,000 fibers/m³ (0.01 fibers/mL) or higher. Levels could also be above average near a building that contains asbestos products and that is being torn down or renovated or near a waste site where asbestos is not properly covered up or stored to protect it from wind erosion. In indoor air, the concentration of asbestos depends on whether asbestos was used for insulation, ceiling or floor tiles, or other purposes, and whether these asbestos-containing materials are in good condition or are deteriorated and easily crumbled. Concentrations measured in homes, schools, and other buildings that contain asbestos range from about 30 to 6,000 fibers/m³ (0.00003–0.006 fibers/mL). People who work with asbestos or asbestos-containing products (for example, miners, insulation workers, asbestos abatement workers, and automobile brake mechanics) without proper protection are likely to be exposed to much higher levels of asbestos fibers in air. In addition, custodial and maintenance workers who are making repairs or installations in buildings with asbestos-containing materials may be exposed to higher levels of asbestos. Since vermiculite and talc may contain asbestos, occupational workers and the general population may be exposed to asbestos when using these products. You can also be exposed to asbestos by drinking asbestos fibers that are present in water. Even though asbestos does not dissolve in water, fibers can enter water by being eroded from natural deposits or piles of waste asbestos, from asbestos-containing cement pipes used to carry drinking water, or from filtering through asbestos-containing filters. Most drinking water supplies in the United States have concentrations of less than 1 million fibers per liter (MFL), even in areas with asbestos deposits or with asbestos-cement water supply pipes. However, in some locations, water samples may contain 10–300 million fibers per liter or even higher. The average person drinks about 2 liters of water per day. Please see the toxicological profile for more information on how you could be exposed to asbestos. Products containing Chrysotile asbestos: Products containing Anthophyllite asbestos: Products containing Tremolite (nonasbestiform), aka Tremolite asbestos; Actinolite (Ca2Mg5H2(SiO3)8); Tremolite: Products containg high percentage of Talc (basicly non-fibrous Asbestos): Talc is used commercially because of its fragrance retention, luster, purity, softness, and whiteness. Other commercially important properties of talc are its chemical inertness, high dielectric strength, high thermal conductivity, low electrical conductivity, and oil and grease adsorption. Many don't know Talc is chemically like a form of non-fibrous Asbestos and may be hazardous to your health. Though it's not as hazardous as fibrous Asbestos, exposure to Talc should definately be avoided. A general rule of thumb to remeber is that all particulates, no matter the nature, may be inhalation hazards. Our lungs are designed for extracting oxygen from the air, NOT particulates. CAS Registry Number: 014807-96-6 There is evidence of a few deaths in infants from the use of Talc containg products and Talc may also produce respiratory, skin, and eye irritation. Talc with <1% asbestos is mainly regarded as a nuisance dust. Prolonged or repeated exposure can produce a form of pulmonary fibrosis (talc pneumoconiosis) which may be due to asbestos content. Talc particles are smaller than 1 um. These particles are respirable and produce an intense inflammatory response characterized by cough, rhinitis, dyspnea, and vomiting. Four distinct forms of pulmonary disease caused by talc have been defined. The first form, talcosilicosis, is caused by talc mined with high silica content mineral. Findings in this form are identical with those of silicosis. Talcoasbestosis closely resembles asbestosis and is produced by crystalline talc, generally inhaled with asbestos fibers. Pathologic and radiographic abnormalities are virtually identical with those of asbestosis, including calcifications and malignant tumor formation. The third form, talcosis, caused by inhalation of pure talc, may include acute or chronic bronchitis as well as interstitial inflammation; radiographically, it appears as interstitial reticulations or small, irregular nodules, typical of small airway obstruction. The fourth form, due to iv administration of talc, is usually associated with abuse of oral medications and production of vascular granulomas manifested by consolidations, large nodules, and masses. Radiographic abnormalities associated with talc can be predicted when there is sufficient history of the nature of exposure, including the region of origin of the talc in cases of inhalation. Radiographic changes, such as diaphragmatic plaques, often attributed to both talc and asbestos have not been documented to be caused by talc alone. Acute inhalation exposure to talc causes symptoms such as cough, dyspnea, sneezing, vomiting, and cyanosis. Talc which is water insoluble dries up the mucous membranes of the tracheobronchial trees. This results in impairment of ciliary function. Inhaling large quantities of talc can result in obstruction of the small airways in addition to drying the mucous membranes, leading to respiratory distress syndrome or death. Although there have been few studies, it was estimated that there are probably a few thousand cases of infants inhaling talc each year. Creams and lotions should be used in place of sprinkling baby powder. Clinical studies of iv drug abusers ... have shown that iv injection of pills containing psychoactive agents and talc as a binder can result in microemboli forming in small pulmonary arteries, arterioles, and capillaries. This can result in granuloma formation, impaired pulmonary function, and death. Iv injection of talc containing formulations has been shown to predispose users to infections. 1.4 How can asbestos enter and leave my body? 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. Please see the toxicological profile for more information on how asbestos enters and leaves your body. 1.5 How can asbestos affect my health? Diseases related to Asbestos exposure: Asbestos-related pleural disease To protect the public from the harmful effects of toxic chemicals and to find ways to treat people who have been harmed, scientists use many tests. One way to see if a chemical will hurt people is to learn how the chemical is absorbed, used, and released by the body; for some chemicals, animal testing may be necessary. Animal testing may also be used to identify health effects such as cancer or birth defects. Without laboratory animals, scientists would lose a basic method to get information needed to make wise decisions to protect public health. Scientists have the responsibility to treat research animals with care and compassion. Laws today protect the welfare of research animals, and scientists must comply with strict animal care guidelines. Information on the health effects of asbestos in people comes mostly from studies of people who were exposed in the past to levels of asbestos fibers (greater than or equal to 5 µm in length) in workplace air that were as high as 5 million fibers/m³ (5 fibers/mL). Workers who repeatedly breathe in asbestos fibers with lengths greater than or equal to 5 µm may develop a slow buildup of scar-like tissue in the lungs and in the membrane that surrounds the lungs. This scar-like tissue does not expand and contract like normal lung tissue and so breathing becomes difficult. Blood flow to the lung may also be decreased, and this causes the heart to enlarge. This disease is called asbestosis. People with asbestosis have shortness of breath, often accompanied by a cough. This is a serious disease and can eventually lead to disability or death in people exposed to high amounts of asbestos over a long period. However, asbestosis is not usually of concern to people exposed to low levels of asbestos. Changes in the membrane surrounding the lung, called pleural plaques, are quite common in people occupationally exposed to asbestos and are sometimes found in people living in areas with high environmental levels of asbestos. Effects on breathing from pleural plaques alone are usually not serious. There is conflicting evidence as to whether their presence in a person accurately predicts more serious disease development in the future. Asbestos workers have increased chances of getting two principal types of cancer: cancer of the lung tissue itself and mesothelioma, a cancer of the thin membrane that surrounds the lung and other internal organs. These diseases do not develop immediately following exposure to asbestos, but appear only after a number of years. There is also some evidence from studies of workers that breathing asbestos can increase the chances of getting cancer in other locations (for example, the stomach, intestines, esophagus, pancreas, and kidneys), but this is less certain. Members of the public who are exposed to lower levels of asbestos may also have increased chances of getting cancer, but the risks are usually small and are difficult to measure directly. Lung cancer is usually fatal, while mesothelioma is almost always fatal, often within a few months of diagnosis. Some scientists believe that early identification and intervention of mesothelioma may increase survival. The levels of asbestos in air that lead to lung disease depend on several factors. The most important of these are (1) how long you were exposed, (2) how long it has been since your exposure started, and (3) whether you smoked cigarettes. Cigarette smoking and asbestos exposure increase your chances of getting lung cancer. Also, there is a scientific debate concerning the differences in the extent of disease caused by different fiber types and sizes. Some of these differences may be due to the physical and chemical properties of the different fiber types. For example, several studies suggest that amphibole asbestos types (tremolite, amosite, and especially crocidolite) may be more harmful than chrysotile, particularly for mesothelioma. Other data indicate that fiber size dimensions (length and diameter) are important factors for cancer-causing potential. Some data indicate that fibers with lengths greater than 5.0 µm are more likely to cause injury than fibers with lengths less than 2.5 µm. (1 µm is about 1/25,000 of an inch.) Additional data indicate that short fibers can contribute to injury. This appears to be true for mesothelioma, lung cancer, and asbestosis. However, fibers thicker than 3.0 µm are of lesser concern, because they have little chance of penetrating to the lower regions of the lung. The health effects from swallowing asbestos are unclear. Some groups of people who have been exposed to asbestos fibers in their drinking water have higher-than-average death rates from cancer of the esophagus, stomach, and intestines. However, it is very difficult to tell whether this is caused by asbestos or by something else. Animals that were given very high doses of asbestos in food did not get more fatal cancers than usual, although some extra nonfatal tumors did occur in the intestines of rats in one study. Several government offices and regulatory agencies have considered all of the evidence regarding the carcinogenicity of asbestos. The Department of Health and Human Services (DHHS) has determined that asbestos is known to be a human carcinogen. The EPA has determined that asbestos is a human carcinogen. The International Agency for Research on Cancer (IARC) has determined that asbestos is carcinogenic to humans. Please see the toxicological profile for more information on how asbestos can affect your health. 1.6 How can asbestos affect children? This section discusses potential health effects from exposures during the period from conception to maturity at 18 years of age in humans. Asbestos exposure in both children and adults may occur while breathing air in or near buildings (public or private) containing asbestos building materials or near asbestos-related industrial operations. Children breathe differently and have different lung structures than adults. It is not known if these differences may cause a greater amount of asbestos fibers to stay in the lungs of a child when they are breathed in than in the lungs of an adult. Children drink more fluids per kilogram of body weight than adults and can also be exposed through asbestos-contaminated drinking water. Eating asbestos-contaminated soil and dust is another source of exposure for children. Certain children intentionally eat soil, and all young children eat more soil than adults through hand-to-mouth activities. Historically, family members have also been exposed to asbestos that was carried home on the clothing of other family members who worked in asbestos mines or mills. Breathing of asbestos fibers may result in difficulty in breathing, lung cancer, or mesothelioma (another form of cancer associated with asbestos exposure). These diseases usually appear many years following the first exposure to asbestos and are therefore not likely to be seen in children. But since it may take up to 40 or more years for the effects of exposure to be seen, people who have been exposed to asbestos at a young age may be more likely to contract these diseases than those who are first exposed later in life. In the small number of studies that have specifically looked at asbestos exposure in children, there is no indication that younger people might develop asbestos-related diseases more quickly than older people. Developing fetuses and infants are not likely to be exposed to asbestos through the placenta or breast milk of the mother. Results of animal studies do not indicate that exposure to asbestos is likely to result in birth defects. 1.7 How can families reduce the risk of exposure to asbestos? If your doctor finds that you have been exposed to significant amounts of asbestos, ask whether your children might also be exposed. Your doctor might need to ask your state health department to investigate. The most important way that families can lower their exposures to asbestos is to be aware of the sources of asbestos in their homes and avoid exposure to these sources. The most important source of asbestos in a home is from damaged or deteriorating asbestos-containing insulation, ceiling, or floor tiles. Should you suspect that your house may contain asbestos, contact your state or local health department or the regional offices of EPA to find out how to test your home for asbestos and how to locate a company that is trained to remove or contain the fibers. Federal law requires schools to identify asbestos-containing material in school buildings and take appropriate action to control release of asbestos fibers. If you live close to where asbestos and certain other ores are mined or processed, where a building that contains asbestos products is being torn down or renovated, or a waste site where asbestos is not properly covered, then the levels of asbestos in dust and wind-blown soil may be higher. Pets can also bring asbestos into the home by carrying dust or dirt on their fur or feet if they spend time in places that have high levels of asbestos in the soil. Swallowing of asbestos in house dust or soil is a potential exposure pathway for children. This problem can be reduced in many ways. Regular hand and face washing to remove asbestos-containing dusts and soil, especially before meals, can lower the possibility of asbestos fibers on the skin being accidentally swallowed while eating. Families can lower exposures to asbestos by regularly cleaning the home of dust and tracked in soil. Door mats can help lower the amount of soil that is tracked into the home; removing your shoes before entering will also help. Planting grass and shrubs over bare soil areas in the yard can lower the contact that children and pets may have with soil and reduce the tracking of soil into the home. You can bring asbestos home in the dust on your hands or clothes if you work in the mining or processing of minerals that contain asbestos, in asbestos removal, or in buildings with damaged or deteriorating asbestos. Federal law regulates work practices to limit the possibility of asbestos being brought home in this way. Your occupational health and safety officer at work can and should tell you whether chemicals you work with are dangerous and likely to be carried home on your clothes, body, or tools, and whether you should be showering and changing clothes before you leave work, storing your street clothes in a separate area of the workplace, or laundering your work clothes at home separately from other clothes. Your employer should have Material Safety Data Sheets (MSDSs) for many of the chemicals used at your place of work, as required by the Occupational Safety and Health Administration (OSHA). Information on these sheets should include chemical names and hazardous ingredients, important properties (such as fire and explosion data), potential health effects, how you get the chemical(s) in your body, how to handle the materials properly, and what to do in an emergency. Your employer is legally responsible for providing a safe workplace and should freely answer your questions about hazardous chemicals. Either OSHA or your OSHA-approved state occupational safety and health program can answer any further questions and help your employer identify and correct problems with hazardous substances. OSHA and/or your OSHA-approved state occupational safety and health program will listen to your formal complaints about workplace health hazards and inspect your workplace when necessary. Employees have a right to seek safety and health on the job without fear of punishment. Much more information for concerned homeowners can be found in my Asbestos Tips for Homeowners page. 1.8 Is there a medical test to determine whether I have been exposed to asbestos? The most common test used to determine if you have received sustained exposure to asbestos is a chest x-ray. A chest x-ray is recommended for detecting exposure to asbestos only in persons who have sustained relatively heavy exposure. A chest x-ray is of no value for detecting evidence of asbestos exposure in a person whose exposure to asbestos has been only brief or transient. The x-ray cannot detect the asbestos fibers themselves, but it can detect early signs of lung disease caused by asbestos. While other substances besides asbestos can sometimes produce similar changes in the lungs, this test is usually reliable for detecting asbestos-related effects produced by long-term exposures at relatively high concentrations of asbestos fibers. Other tests, such as gallium-67 lung scanning and high-resolution computed tomography, are also useful in detecting changes in the lungs. However, there are currently no means of detecting exposure-related effects from commonly encountered environmental exposures. The most reliable test to determine if you have been exposed to asbestos is the detection of microscopic asbestos fibers in pieces of lung tissue removed by surgery, but this is a very invasive test. A test can also be run to determine the presence of asbestos fibers in material rinsed out of the lung. However, this test can cause some discomfort. Asbestos fibers can also be detected in mucus (sputum), urine, or feces, but these tests are not reliable for determining how much asbestos may be in your lungs. Low levels of asbestos fibers are found in these materials for nearly all people. Higher-than-average levels can show that you have been exposed to asbestos, but it is not yet possible to use the results of this test to estimate how much asbestos you have been exposed to, or to predict whether you are likely to suffer any health effects. Please see the toxicological profile for more information about how asbestos can be measured in people and in the environment. 1.9 What recommendations has the federal government made to protect human health? The federal government develops regulations and recommendations to protect public health. Regulations can be enforced by law. Federal agencies that develop regulations for toxic substances include the Environmental Protection Agency (EPA), the Occupational Safety and Health Administration (OSHA), and the Food and Drug Administration (FDA). Recommendations provide valuable guidelines to protect public health but cannot be enforced by law. Federal organizations that develop recommendations for toxic substances include the Agency for Toxic Substances and Disease Registry (ATSDR) and the National Institute for Occupational Safety and Health (NIOSH). Regulations and recommendations can be expressed in not-to-exceed levels in air, water, soil, or food that are usually based on levels that affect animals; then they are adjusted to help protect people. Sometimes these not-to-exceed levels differ among federal organizations because of different exposure times (an 8-hour workday or a 24-hour day), the use of different animal studies, or other factors. Recommendations and regulations are also periodically updated as more information becomes available. For the most current information, check with the federal agency or organization that provides it. Some regulations and recommendations for asbestos include the following: The federal government has taken a number of steps to protect citizens from exposure to asbestos. First, on July 12, 1989, EPA established a ban on new uses of asbestos. Uses established before this date are still allowable. Second, EPA has established regulations that require school systems to inspect for asbestos and, if damaged asbestos is found, to eliminate or reduce the exposure, either by removing the asbestos or by covering it up so it cannot get into the air. In addition, EPA provides guidance and support for reducing asbestos exposure in other public buildings. Third, EPA regulates the release of asbestos from factories and during building demolition or renovation to prevent asbestos from getting into the environment. EPA also regulates the disposal of waste asbestos materials or products, requiring these to be placed only in approved locations. Fourth, EPA has proposed a limit of 7 million fibers per liter on the concentration of long fibers (length greater than or equal to 5 µm) that may be present in drinking water. Fifth, FDA regulates the use of asbestos in the preparation of drugs and restricts the use of asbestos in food-packaging materials. NIOSH has recommended that inhalation exposures not exceed 100,000 fibers with lengths greater than or equal to 5 µm per m³ of air (0.1 fibers/mL). OSHA has established an enforceable limit on the average 8-hour daily concentration of asbestos allowed in air in the workplace to be 100,000 fibers with lengths greater than or equal to 5 µm per m³ of air (0.1 fibers/mL). Additional sources of information about asbestos are the 10 regional offices of the EPA. Most EPA regional offices have an asbestos coordinator. Please see the toxicological profile in the MSDS information below for more information about regulations and guidelines to protect people from exposure to asbestos. 1.10 Where can I get more information? If you have any more questions or concerns, please contact your community or state health or environmental quality department or: Agency for Toxic Substances and Disease Registry Division of Toxicology1600 Clifton Road NE, Mailstop F-32Atlanta, GA 30333 Information line and technical assistance: Phone: 888-422-8737 FAX: (770)-488-4178ATSDR can also tell you the location of occupational and environmental health clinics. These clinics specialize in recognizing, evaluating, and treating illnesses resulting from exposure to hazardous substances. To order toxicological profiles, contact: National Technical Information Service5285 Port Royal Road Springfield, VA 22161 Phone: 800-553-6847 or 703-605-6000 References Agency for Toxic Substances and Disease Registry (ATSDR). 2001. Toxicological profile for asbestos. Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service. For more information about Asbestos fibers and over 100 more hazardous household chemicals, have a look at my Hazardous Household Chemical Guide.
1.11 ASBESTOS MSDS Information CASRN: 1332-21-4 Human Health Effects Asbestos is the generic designation referring usually to six types of naturally occurring mineral fibers that are or have been commercially exploited. These fibers belong to two mineral groups: serpentines and amphiboles. The serpentine group contains a single asbestiform variety: chrysotile; five asbestiform varieties of amphiboles are known: anthophyllite asbestos, grunerite asbestos (amosite), riebeckite asbestos (crocidolite), tremolite, actinolite asbestos. Commercial products may contain one or more of the various mineral fibers. Human Health Effects: Evidence for Carcinogenicity: Classification of carcinogenicity: 1) evidence in humans: sufficient; 2) evidence in animals: sufficient. Overall summary evaluation of carcinogenic risk to humans is Group 1: The agent is carcinogenic to humans. CLASSIFICATION: A; human carcinogen. BASIS FOR CLASSIFICATION: Observation of increased mortality and incidence of lung cancer, mesotheliomas and gastrointestinal cancer in occupationally exposed workers are consistent across investigators and study populations. Animal studies by inhalation in two strains of rats showed similar findings for lung cancer and mesotheliomas. Animal evidence for carcinogenicity via ingestion is limited (male rats fed intermediate-range chrysotile fibers; i.e., greater than (>) 10 um length, developed benign polyps), and epidemiologic data in this regard are inadequate. HUMAN CARCINOGENICITY DATA: Sufficient. ANIMAL CARCINOGENICITY DATA: Sufficient. A1; Confirmed human carcinogen. /Asbestos, all forms/ Human Toxicity Excerpts: /HUMAN EXPOSURE STUDIES/ The /prospective/ study of /17,800/ USA and Canadian insulators /exposed primarily to chrysotile ...and amosite showed that/ lung tumors ...accounted for ...21% of /2271/ deaths. 8% were from mesothelioma of the pleura or peritoneum, and 7% ...from asbestos ...675 excess malignacies occurred, constituting 30% of all deaths. In addition ...the incidences of cancers of the larynx, pharynx and buccal cavity, and kidney were significantly elevated. Other tumors... as a group... were significantly in excess. /HUMAN EXPOSURE STUDIES/ Exposure-response relationship for mesothelioma /was compared/ from 3 studies /and showed that/ no deaths were seen for exposure periods <3 months. At >3 to 15.4 months exposure, the deaths/1000 person years ranged from 0.5 to 1.7 and at 57 months exposure, 1.7 deaths/1000 person years. /HUMAN EXPOSURE STUDIES/ Retirees of the largest USA asbestos manufacturer showed lung cancer risks ranging from 1.7 times that expected in the lowest exposure category to 5.6 times that exposed in the highest. /HUMAN EXPOSURE STUDIES/ Among some exposed groups, 50 to 80% of individuals employed for 20 or more years were found to have abnormal x-rays characteristic of asbestos exposure. ...The progression of asbestosis depends on both cumulative exposure and time from exposure. /HUMAN EXPOSURE STUDIES/ Among female workers, ovarian cancer has been found in excess. /HUMAN EXPOSURE STUDIES/ Death from bronchogenic carcinoma among asbestos workers was more frequent than expected in the general population, and was the leading cause of death among insulation workers (3 times more common than mesothelioma). Three cohorts were followed. Among New York-New Jersey insulation workers in the construction industry with 20 or more years of exposure to asbestos, the incidence of lung cancer was approximately 8/1000 man-years, an eightfold increase over the general USA population. /HUMAN EXPOSURE STUDIES/ Cancers of the digestive tract (stomach, colon, rectum) were also linked to asbestos exposure. In a study of 623 asbestos workers, these cancers accounted for 41 deaths while only 13 were expected from experience with the general population. During processing of rice, the Japanese add talc which usually has asbestos as an impurity. There was a positive correlation between the incidence of stomach cancer and rice consumption in the Japanese. Futhermore, chrysotile and amphibole asbestos fibers were found in the gastric tumors. /HUMAN EXPOSURE STUDIES/ Asbestos fibers are toxic to macrophages, cells responsible for cleaning infectious agents and foreign material from the respiratory tract. /HUMAN EXPOSURE STUDIES/ Respiratory exposure to high levels of asbestos in the workplace has been associated with pain in the chest, pleural frictional rubbing, rales (wheezing sound in the lower pulmonary region), cyanosis (low oxygen content of blood), loss of weight, clubbing of the fingers and formation of asbestos warts on the hands. /HUMAN EXPOSURE STUDIES/ The specific diseases associated with asbestos are: asbestosis (a form of fibrosis of the lung); cancers of the bronchi, pleura & peritoneum & probably other organs; & asbestos corns of the skin. All these, with the exception of corns, are due to the inhalation of asbestos fibers & consequently any process which gives rise to large amounts of asbestos dust may constitute a health hazard. /HUMAN EXPOSURE STUDIES/ A study of the largest factory of the company but not limited to retirees, shows a considerably different mortality pattern. All 689 maintenance and production employees on January 1, 1959, who were first employed at least 20 years earlier were followed through 1976. In this group, 274 deaths occurred, whereas 188.19 were expected. Fourteen pleural and 12 peritoneal mesotheliomas accounted for nearly 10% of the deaths, most recurring before age 65. A strong correlation with estimated dust exposure was seen in deaths from asbestosis, but not with the asbestos related malignancies. Gastrointestinal cancer was especially high in the lowest of four dust categories (11 observed versus 3.15 expected) and only elevated slightly in the higher exposure categories. In the highest dust category, the overall cancer was not dramatically increased, but 40% of the deaths were from asbestosis. Individuals in this department tended to die of nonmalignant disease before reaching the age of greatest risk for cancer. /HUMAN EXPOSURE STUDIES/ Spicules of asbestos easily penetrate the skin, especially the fingers in those bagging the fiber. Chronic irritation of the dermis occurs with the formation of corns ...Cancers of the skin are not produced. /HUMAN EXPOSURE STUDIES/ Asbestosis is a diffuse, nonuniform, interstitial fibrosis of the lungs that is generally most severe in the basilar portions. As a result of the fibrosis, some of the air spaces (alveoli) are not perfused with blood and may not be ventilated because of stiff, thickened alveolar walls. The fibrosis makes the lungs less compliant, thereby increasing the energy requirement for breathing. There is increased impairment in diffusion of gases leading to increasing breathlessness. /HUMAN EXPOSURE STUDIES/ Asbestos corns on the fingers (areas of thickened skin surrounding implanted fibers) are now much less common because much of the asbestos fiber is packed mechanically and gloves are worn. Corns do not lead to skin tumors and disappear on removal of the fibers. /HUMAN EXPOSURE STUDIES/ Diseases in nonoccupationally exposed persons living near sources of asbestos and familial exposures have occurred when the worker did not shower or wore the same clothes home that had been worn during work. Also, domestic exposures have been associated with household repairs, and do-it yourself construction using products containing asbestos or when disturbing products containing asbestos. /HUMAN EXPOSURE STUDIES/ Asbestosis is defined as a diffuse interstitial fibrosis of the lung, the result of exposure to asbestos dust. Neither the clinical features nor the pathology are sufficiently different from other causes of interstitial fibrosis to allow confident diagnosis without evidence of significant exposure to asbestos dust in the past, or the detection of asbestos fibers or bodies in the lung tissue greatly in excess of that commonly seen in the general population. ...Asbestosis is usually used to describe the parenchymal fibrosis but not that occurring in the parietal pleura. /HUMAN EXPOSURE STUDIES/ ...In 1998... the exposure response relationships between environmental exposure to crocidolite and mesothelioma /was examined/. The cohort consisted of 4,659 persons who had lived near the Wittenoom crocidolite mine and mill in Western Australia for at lease one month between 1943 and 1993. Twenty seven mesothelioma cases, 18 of whom were females, occurred in the cohort. Of these, 12 were wives of mine or mill workers, 11 were children and one was a brother of an employee. The other three cases were employees. Nine of the 27 cases were younger than 40 years at the time of diagnosis. Length of residence in the are and estimated cumulative crocidolite exposure were significantly positively associated with an increased mesothelioma risk. /Crocidolite absestos/ /HUMAN EXPOSURE STUDIES/ /Pathology of asbestosis/: The retained fibers in the alveolar region are 3 um or less in diameter but may be up to 200 um long. ...A portion of the longer fibers, especially amphiboles, become coated with an iron protein complex producing the drumstick appearance of asbestos bodies. All types of asbestos cause similar fibrosis. The fibrosis starts in the resp bronchioles with collections of macrophages containing fibers, and others lying free. These deposits organize, collagen replacing the initial reticulum web. Initially only a few respiratory bronchioles are affected, but the fibrosis spreads centrally to the terminal bronchioles and peripherally to the acinus. The areas increase in size and coalesce causing diffuse interstitial fibrosis with shrinkage. The process starts in the bases spreading upwards as the disease progresses; in advanced disease the whole lung structure is distorted and replaced by dense fibrosis, cysts, and some areas of emphysema. The pleura, both visceral and parietal surfaces, are affected by the fibrosis. ...The visceral surface may be sclerosed up to 1 cm thick. In the parietal pleura thickening starts as a basket-weave pattern of fibroblasts, the sheets of fibrosis lying along the line of the ribs especially in the lower thorax and posteriorly. The edges become rolled and crenated and, after many years, calcified. The parietal thickening may be extensive and thick with little or no parenchymal fibrosis. /HUMAN EXPOSURE STUDIES/ Crocidolite was commonly use din the production of gas mask canisters during World War II and mortality among these workers was investigated... . They found of 1,088 workers exposed between 1940 and 1945 and followed through 1976, that there were 22 pleural and 7 peritoneal mesotheliomas and that there was a linear relationship between employment duration and the risk of mesothelioma. There was also a modest excess of bronchial carcinoma. ...Similar results /were found in a study of/... a smaller cohort of gas mask workers in Canada and found that 7% of all deaths were due to mesotheliomas. /Crocidolite/ /HUMAN EXPOSURE STUDIES/ All types of asbestos are known to cause inflammatory changes in lung and pleurae ...and lung cancer. However, there is experimental and epidemiologic evidence that there may be differences in the potential of different asbestos types to produce disease. ...It has been suggested that crocidolite has greatest potential to produce disease; chrysotile, the smallest; with amosite occupying an intermediate position. /HUMAN EXPOSURE STUDIES/ ...The occurence of pleural and peritoneal mesotheliomas in the crocidolite mining areas of Northwest Cape Province, in South Africa /was investigated/. It was found that these tumors occurred in both the men working in the mines and mills and in the transporting and handling of the material as well as the nonmining population living in the vicinity. Thirty three cases (22 males and 11 females) of diffuse mesothelioma were described. All but on e of them had possible exosure to crocidolite. /Crocidolite/ /HUMAN EXPOSURE STUDIES/ Numerous reports from several countries have described cases or series of pleural and peritoneal mesotheliomas in relation to occupational exposure to various types and mixtures of asbestos (including talc containing asbestos), although occupational exposures have not been identified in all cases. Mesotheliomas of the tunica vaginalis testis and of the pericardium have been reported in persons occupationally exposed to asbestos. ...In some of these case reports and in other studies, asbestos fibers were identified in the lung. Amphibole fibers usually predominated, but in a few cases mainly or only chrysotile fibers were found. The long latency required for mesotheliomas to develop after asbestos exposure has been documented in a number of publications. An increasing proportion of cases has been seen with increasing duration of exposure. /HUMAN EXPOSURE STUDIES/ In human lung specimens asbestosis is seen first, and it is more advanced in the lower lobes, especially subpleural regions. In addition to peribronchiolar fibrosis, there is an intense peribronchiolar cellular reaction that may narrow and obstruct the airway lumen. High-resolution computed tomography (CT) demonstrates thickening of interlobular septa, parallel subpleural fibrotic lines, as well as honeycombing in more advanced cases. Asbestos bodies (AB) are characteristically observed in tissue sections. The number of bodies per gram dry lung tissue in the general population is generally fewer than 500, but twice as many are found in the lungs of blue-collar males. Persons with pleural plaques have 10,000 to 20,000 bodies per gram and persons with parenchymal asbestosis more than 100,000- and usually more than a million per gram of lung, which correlates with the dictum of observing at least one asbestos body per high power field. /It was/... estimated that recovery by bronchoalveolar lavage of 1 AB per mL correlated with 1,000 to 3,000 AB per gram dry lung parenchyma. AB form around amphibole fibers in preference to chrysotile and contain iron with the morphologic appearance of hemosiderin. Analysis of the coating identifies a ferritin core containing ferric oxyhydroxide, hydrous ferric oxides, acid mucopolysaccharides int he matrix protein, and calcium and phosphorus. Only a small proportion of the total fiber burden i the lung ever becomes coated, probably not more than 1%, and the proportion increases with fiber length. Coated fibers are less toxic to alveolar macrophages than uncoated ones. /HUMAN EXPOSURE STUDIES/ Environmental exposure either in the houses of asbestos workers or in the neighborhood of asbestos mines or factories has been noted in some of the cases. It has been est that a third of the mesotheliomas occurring in the USA may be due to nonoccupational exposure. In a study from Israel, the incidence of mesothelioma was found to be higher among those born in the USA or in Europe relative to those born in Israel. /HUMAN EXPOSURE STUDIES/ It is believed that alterations in both humoral and cell-mediated immunity occur in individuals exposed to asbestos and exhibiting asbestosis. Decreased /delayed hypersensitivity response/ (DHR) and fewer T cells circulating in the periphery as well as decreased T-cell proliferative responses have been reported to be associated with asbestosis. Autoantibodies and increased serum immunoglobulin levels have also been observed. /HUMAN EXPOSURE STUDIES/ No clear excess of cancer has been associated with the presence of asbestos fibers in drinking water. /HUMAN EXPOSURE STUDIES/ The authors investigated the prevalence of asbestos-related disorders among the inhabitants of Guzelyurt, a town in Malatya, located in eastern Turkey. ...Eighty-five patients (9.2%) had asbestos-related radiological findings; risk increased with age. Calcified pleural plaques were seen more frequently in individuals > or = 50 yr of age, compared with younger subjects (p<0.01). /HUMAN EXPOSURE STUDIES/ ...Eight cases of malignant pleural mesothelioma (MPM) in bakers, pastry cooks, and biscuit cooks engaged in making, baking/cooking and selling pastry/bread /are described/ in two hospital-based series in Italy totaling 222 cases during the period from 1990 to 1997. Field investigations revealed asbestos-containing material in ovens for baking bread manufactured prior to the 1980s. /HUMAN EXPOSURE STUDIES/ Diseases considered to be associated with asbestos exposure /eg, in insulation workers/ include ... bronchogenic carcinoma, and cancers of the /gastrointestinal tract/ including esophageal, stomach, colon, and rectum. /HUMAN EXPOSURE STUDIES/ A retrospective study of 197 workers was carried out to analyze deaths from asbestosis or asbestos-related disease. The number of deaths from mesothelioma (101) was almost double that from bronchogenic carcinoma (67), and more than 3 times that from asbestosis (29). /HUMAN EXPOSURE STUDIES/ Asbestos can cross the mammalian placental barrier. Furthermore, asbestos is a common contaminant of the talc used as a dusting powder for contraceptives from which it may enter the uterus. Research is needed to determine the level of in utero asbestos exposure and possible effects to the fetus because of inhalation or ingestion of asbestos or the use of talc-bearing contraceptives. /SIGNS AND SYMPTOMS/ The cardinal symptom of asbestosis is dyspnea, which may have a variable but progressive course. Dyspnea on climbing two flights of stairs is characteristic; however,by the time dyspnea on exertion develops, the disease has already reached a progressive stage. Cough and sputum are common, and a pleuritic chest pain or chest tightness may occur. These symptoms, however, may also herald concomitant disease such as lung cancer or pleural effusion. In the posterolateral basilar aspects of the chest, end-inspiratory, dry, crackles (rales) that do not clear with coughing may be heard with a stethoscope. /SIGNS AND SYMPTOMS/ The signs and symptoms of asbestosis are similar to those caused by other diffuse interstitial fibroses of the lung. Increased breathlessness on exertion is usually the first symptom, sometimes associated with aching or transient sharp pains in the chest. A cough is not usually present except in the late stages when distressing paroxysms occur. Increased sputum is not present unless there is bronchitis, the result of smoking. The onset of symptoms (except following very heavy exposure) is usually slow and the subject may have forgotten having any contact with asbestos. Persistent dull chest pain and hemoptysis indicate the need to investigate further the diagnosis of bronchial or mesothelial cancer. The most important physical sign is the presence of high-pitched fine crepitations (crackles) at full inspiration and persisting after coughing. They occur initially in the lower axillae and extend more widely later. ...Clubbing of the fingers and toes was formerly regarded as an important physical sign. ...Its severity does not relate well to other aspects of the diagnosis. ...It is possible that its presence relates to the rapidity of progression of the disease. /SIGNS AND SYMPTOMS/ Changes in pulmonary function considered most characteristic of asbestos are: 1) General reduction of lung volume, especially vital capacity (VC); 2) Decrease of pulmonary flow rates as indicated by forced expiratory volume in one second FEV (1.0); 3) Impaired alveolar-capillary diffusing capacity, reflected by reduced oxygenation of the arterial blood and increased alveolar-arterial partial pressure oxygen gradient (alveolar-capillary block syndrome). /CASE REPORTS/ Metastases in multiple distant sites, including the skin, developed in a 54 yr old man with diffuse malignant abdominal mesothelioma. This might represent the first reported case of cutaneous metastasis arising from malignant mesothelioma. Recent advances in diagnostic techniques, such as electron microscopy, may be helpful in differentiating this condition from metastatic adenocarcinoma. /CASE REPORTS/ A 64 yr old white male insulator had been employed from 1942-1988 (46 yr) insulating powerhouses and government buildings without wearing respiratory tract protection. He mixed asbestos "mud" as a helper in the 1940s. He had smoked one pack of cigarettes per day from age 19-53. He had no symptoms of dyspnea, cough, phlegm, or hemoptysis. Bibasilar end-inspiratory rales were auscultated, and he had no clubbing. His posteroanterior chest radiograph was read according to the 1980 International Classification of the Radiographs of the Pneumoconioses as a 2/3 profusion of irregular opacities in the four lower lung zones with bilateral circumscribed and diffuse pleural thickening with calcifications. The pulmonary parenchyma was diffusely positive on a gallium-67 lung scintigraphy. Pulmonary function tests revealed a vital capacity of 73% of predicted, total lung capacity 68%, forced expired volume in 1 second 77%, and diffusing capacity 57%; this picture was consistent with restrictive impairment. Bronchoalveolar lavage revealed 355,000 cells/mL --81% macrophages, 10% lymphocytes, 7% neutrophils, and 2% eosinophils with many asbestos bodies. After 1 year's follow-up, a solitary nodule was observed in the left upper lung field that contained adenocarcinoma cells on needle biopsy. Lobectomy was performed to remove the tumor. /CASE REPORTS/ ...Two cases of constrictive pericarditis in subjects previously exposed to asbestos /are reported/. /CASE REPORTS/ This case was a 79-year-old man with pleural plaques, which had been pointed out in the left lung field on chest X-ray six years ago. A new shadow in the right chest appeared in 1999 and was closely examined. Cytological class IV carcinoma was detected in his lung tissue obtained by broncho-fiberscope. Lobectomy of the right upper lobe was performed, and calcified pleural plaques were found on the chest wall. The clinical diagnosis was poorly differentiated squamous cell carcinoma, T1N0M0. In World War II when he was 26 years old, he had worked as a boiler man on a battle cruiser for one year. The amount of asbestos bodies (AB) was 3,348 per gram dry lung tissue. The cores of AB and asbestos fibers were examined and showed that amosite was the most prevalent and crocidolite, tremolite and chrysotile were present in that order. After leaving the navy, he had worked as a farmer throughout his life, suggesting that he had never contacted asbestos occupationally after being a boiler man. It is strongly suggested that he had been exposed to asbestos during his work as a boiler man and that produced pleural plaques and lung cancer 50 years' later. /EPIDEMIOLOGY STUDIES/ The asbestos fiber burden in the ovaries of women indirectly exposed to asbestos was examined. Ovaries were studied from 13 women in household contact with men who had documented exposure to asbestos and 17 women undergoing incidental oophorectomy. Ovarian tissue samples were prepared for analytic electron microscopic examination; assessments included fiber identity, size, and amount. Significant asbestos fiber burdens were detected in nine out of the 13 exposed subjects and in six out of the 17 subjects with no known exposure history. Three exposed women had asbestos counts over 1 million fibers per gram wet weight, versus one out of the 17 women with no history of exposure. Fibers were generally small in length and narrow in diameter. Both chrysotile and crocidolite asbestos fibers were detected. The authors conclude that asbestos fibers do reach the ovaries and appear to be present more frequently and in higher amounts in women with a documented exposure history /EPIDEMIOLOGY STUDIES/ A number of epidemiological studies of respiratory cancer and mesothelioma have been reported in relation to exposure to unspecified or complex mixtures of asbestos in shipyard work. The risk ratio for lung cancer has usually been moderately increased... in these studies and in studies on various other occupational groups with similarly job-related but unspecified or complex asbestos exposures. Risk ratios of about 2-5 have been reported in some studies, but the ratio was considerably higher in one rather small study and did not exceed unity in another. In one study, individuals suffering from asbestosis had a considerably greater risk for lung cancer, with a risk ratio of 9.0. In some of the studies referred to, a number of mesotheliomas were also observed. Abdominal mesotheliomas have been mistaken for pancreatic cancer. Mesothelioma cases have been observed to have a relatively lower fiber content in the lung than lung cancer cases. /EPIDEMIOLOGY STUDIES/ Laryngeal cancer has been considered in 2 case control studies, resulting in risk ratios of 2.4 and 2.3 that relate to shipyard work and unspecified exposure, respectively. A cohort study of insulation workers showed a relative risk of 1.9, based on 9 cases. A case series indicated a high frequency of exposure to asbestos, especially in low-grade smokers. ...Two correlation studies have also indicated a relationship between laryngeal cancer and exposure to asbestos. /EPIDEMIOLOGY STUDIES/ A group of health scientists tested the association between the use of asbestos-cement piping for drinking water supplies and the incidence of kidney and gastrointestinal cancers in Utah. The study found no consistent cancer incidence difference in communities with asbestos pipes compared to communities without the pipes. Leaching from the pipes was minimal. /EPIDEMIOLOGY STUDIES/ The prevalence of atypical cytology has been determined in relation to age, smoking and asbestos exposure for male workers employed in 3 mines in the Province of Quebec. Overall participation was 71%. Out of 867 participating workers, 626 (72%) presented a deep cough specimen within normal limits, 74 (8.5%) presented a specimen with mild atypical metaplasia and 10 (1.2%) presented a specimen with moderate atypical metaplasia. Four lung carcinomas were identified. 5% of the workers initially interviewed did not return their specimen and 12.7% had unsatisfactory test results. Proportions of cellular atypia increased with age and asbestos exposure. Using logistic regression analysis, estimated probabilities of abnormal cytology for workers aged 25 years when they started mining increased with both years of asbestos exposure and exposure index measured in fibers per cu m. /EPIDEMIOLOGY STUDIES/ The cause-specific mortality experience of 31,150 male asbestos workers in England and Wales (1971-1981) was evaluated in a retrospective cohort study. The study population was divided into workers with occupational exposure before the inception of asbestos regulations in 1969 and those who worked with asbestos only after 1969. Duration of exposure ranges from <10 to >20 yr. Information on exposure concentration was not provided. Overall mortality was lower than expected but there was a statistically significant excess of lung cancer deaths in workers exposed prior to 1969 (SMR=136, p<0.01). There was a small nonsignificant increase in lung cancer in workers exposed after 1969; however, the time from first exposure for this group is too short to exclude an excess of asbestos related disease. Insulation workers had the greatest excess of lung cancer deaths (SMR=256). There was no excess in alimentary tract cancer and the population showed a signifcant deficit in bowel cancer mortality (SMR=54). /EPIDEMIOLOGY STUDIES/ The role of asbestos exposure was studied in a case-control study of 175 lung cancer cases and 176 controls during a 5 yr period from two county hospitals in Norway. Information on asbestos exposure was obtained from personal interviews, and allocated to four exposure categories according to intensity and duration of exposure. A statistically significant (p<0.007) trend in risk ratio related to degree of exposure was observed, with a more than fourfold risk among the heavily exposed. The strongest association was found between asbestos exposure and small cell carcinoma (RR=3), and the weakest association between asbestos exposure and adenocarcinoma (RR=2.2). Very high risk ratios were observed among asbestos-exposed subjects who were heavy smokers, and the interaction conformed more closely to a multiplicative model than to an additive one. /EPIDEMIOLOGY STUDIES/ In a cross sectional study, the frequencies of baseline and benzo(a)pyrene induced sister chromatid exchanges were measured in peripheral blood lymphocytes from 22 male asbestos exposed workers and 10 nonexposed workers of comparable age. Four groups were defined for study based on asbestos exposure and cigarette smoking. Mean duration of asbestos exposure was 31.3 yr in smokers and 29.3 yr in nonsmokers. The mean pack yr history of smoking for the asbestos exposed population was 45.7 pack yr and 75 pack yr in controls. Among asbestos exposed workers, lymphocytes from those who smoked were significantly more susceptible to the induction of SCE by in vitro exposure to benzo(a)pyrene (p=0.01) than were the lymphocytes from nonsmokers. Active smoking elevated the baseline SCE frequency in both asbestos-exposed and nonexposed workers (p=0.001). Asbestos exposure alone was not associated with an enhanced susceptibility to the induction of SCE by benzo(a)pyrene or with an elevation in baseline SCE. /EPIDEMIOLOGY STUDIES/ In a study involving 17,800 insulation workers, the death rate for non-smokers was 5.17 times that of a non-smoking control population. The death rate was 53.24 times that of the non-smoking control population or 4.90 times the death rate for a comparable group of non-exposed smokers. Cancers of the larynx, pharynx, and buccal cavity in insulators were also found to be associated with cigarette smoking, together with some non-malignant asbestos effects such as fibrosis and deaths due to asbestosis. /EPIDEMIOLOGY STUDIES/ Cancer mortality for the populations was studied in 40 census tracts of Escambia County, FL that have been receiving drinking water through asbestos cement pipes for up to 40 years. Cancer mortality data from these 40 census tracts were compared with data from other tracts where asbestos cement pipe was not in use. No statistical association was observed between cancer deaths and the use of asbestos cement. /EPIDEMIOLOGY STUDIES/ The mortality of a large workforce employed to manufacture friction products was analyzed. All individuals employed after 1940 were included in the study and the mortality experience through 1979 was determined. Exposure estimates were made by reconstructing work and ventilation conditions of earlier years. Fiber measurements from these reconstructed conditions suggested that exposures before 1931 exceeded 20 fibers/ml but those afterwards seldom exceeded 5 fibers/ml. From 1970, exposures were less than 1 fiber/ml. These relatively low intensities of exposure kept the average cumulative exposure for the group to less than 50 fibers- yr/ml. The overall mortality of all study participants, 10 years and more after the onset of exposure, was no greater than expected for all causes. The number of deaths from cancer of the lung and pleura was slightly elevated in men (151 observed vs 139.5 expected) but the excess was largely accounted for by eight mesothelioma deaths. No unusual mortality was found in study participants employed 10 or more years. Using a case control analysis according to cumulative exposure, estimated that the lung cancer increased risk was 0.06% per fiber yr/ml (Kl = 0.0006) with an upper 90% confidence limit of 0.8% per fiber yr/ml. /EPIDEMIOLOGY STUDIES/ The effect of past exposure to asbestos on natural killer (NK) cell number and activity is uncertain. We measured NK cell number and activity in 1052 retired asbestos workers without symptomatic lung disease, lung cancer, or mesothelioma and with a long latency period from exposure; results were compared with those for 100 healthy age-matched controls. The exposed workers showed a decreased NK cell activity and increased NK cell number, yielding a 10.8 higher odds ratio for low NK activity per cell compared with controls (95% confidence interval 6.4 to 18.4), which was due to both a decrease in NK cell activity and an increase in NK cell number. Asbestos exposure of 10 years or more increased the risk of low NK activity per cell. We conclude that exposure to asbestos is associated with diminished effectiveness of NK cells and a concomitant increase in the number of NK circulating cells. /EPIDEMIOLOGY STUDIES/ To measure the impact on survival of being exposed to asbestos cement dust. Survival of 866 asbestos cement workers and 755 controls was studied with Cox's proportional hazards regression models with age as the basic time variable. The effect of cumulative exposure up to the age of 40 was investigated in an internal analysis of 635 asbestos cement workers who had dose estimates. The death risk was higher for the asbestos cement workers than for the controls with a hazard ratio (HR) of 1.15 (95% confidence interval was 1.00 to 1.31). The increased risk found seemed to be confined to the period 20-40 years from start of employment. The estimates of the cohort effect were almost unaffected by adjustment for smoking habits. The estimates of the exposure effect rose with increasing dose (< 4 fibre-years/ml (f-y/ml): HR = 1.00, 4-9.9 f-y/ml: HR = 1.06, > or = 10 f-y/ml: HR = 1.35, for workers with at least five years of employment), and were higher when restricted only to deaths from malignant or non-malignant respiratory disease. However, none of the point estimates were significantly increased. Median age at death was two years lower in the high than in the low, exposure group. The results indicate that even a moderate asbestos exposure may shorten the median duration of life in an exposed population. Compared with the estimated effect on duration of life from ever being a smoker, that of ever being an asbestos cement worker was less, although that of having a high exposure was similar. /EPIDEMIOLOGY STUDIES/ One hundred and twenty-two sheet metal workers in New England were examined over a 10-year interval for loss of pulmonary function and the development of asbestosis or asbestos-related pleural fibrosis. Regression models using the generalized estimating equation (GEE) approach were created to investigate the relationship between exposure and pulmonary function after adjusting for smoking status, age, height, and asbestos-related x-ray changes. A history of shipyard work was a significant contributor to the loss of forced vital capacity (FVC). Among smokers, loss in forced expiratory volume at 1 sec (FEV1) also had a significant relationship to prior shipyard work. There was a borderline significant relationship between percentage predicted FEV1 and cumulative years of asbestos exposure in smokers, as well as years-since-initial-exposure in never-smokers. This study supports previous findings of obstructive airway changes in asbestos-exposed workers and identifies shipboard work as an important predictor of loss in pulmonary function even years after shipyard exposure to asbestos has ceased. /EPIDEMIOLOGY STUDIES/ Several experimental and epidemiological studies have indicated augmentation of asbestos induced diseases by cigarette smoke by the mechanisms, which are still unknown. To determine whether smoking affects genetic system of the cells and further modifies asbestos induced genotoxicity, whole blood from non-smokers and smokers was exposed to asbestos fibres separately in vitro and micronucleus test was performed. The number of micronuclei was found to be significantly higher (P<0 05) in cases of smoker's lymphocytes, asbestos exposed non-smokers lymphocytes as well as asbestos exposed smokers lymphocytes, as compared with unexposed non-smokers lymphocytes. Further we investigated involvement of chromosome 1 in the damaging process using multicolor FISH technique. FISH is fast and reliable method, distinguishing both structural and numerical alterations. The centric/pericentric regions of chromosome 1 (cen-q12) were labeled, as the pericentric heterochromatin region 1 (q12) is quite large, highly repetitive and prone to breakage. Multicolor FISH assay suggested that the genetic damage by asbestos fibres mainly involve chromosome 1 but in case of cigarette smoking the damage is not strictly connected to chromosome 1 only, but also involves damage to other chromosomes. Further the study suggested that smoking makes genetic system of the cells more vulnerable to the deleterious effects of asbestos. /EPIDEMIOLOGY STUDIES/ Many asbestos-exposed individuals complain of chest pain for which there is no clear explanation. To determine whether chest pain is associated with the presence of benign pleural or parenchymal disease on chest radiograph, we studied 1,280 subjects undergoing surveillance because of prior asbestos exposure at Wittenoom, Western Australia. All subjects completed the Rose questionnaire on chest pain and this revealed 556 subjects (43%) who experienced some chest pain. A posterior-anterior chest radiograph was performed at the same clinic visit and was subsequently graded independently by two experienced readers for diffuse parenchymal disease and pleural disease. Logistic regression models adjusted for sex, age, and cumulative asbestos exposure indicated that the presence of chest pain was significantly associated with the presence of both benign pleural disease and diffuse parenchymal disease. Further analysis after stratification of chest pain into nonanginal and anginal pain showed that there was a significant association between anginal pain and the presence of pleural and parenchymal asbestos-induced radiologic abnormalities and an association of nonanginal pain with parenchymal disease. We conclude that radiographic evidence of either parenchymal or pleural disease in subjects exposed to asbestos is significantly related to the presence of chest pain, particularly anginal pain. /EPIDEMIOLOGY STUDIES/ Asbestos exposure has been definitively found to be associated with both mesothelioma and lung cancer. Nevertheless, in the overall population of oil refinery workers potentially exposed to asbestos, many studies clearly show a definitely increased risk of mesothelioma, but no proven excess of lung cancer after comparison to the general population. Through the presentation of new data and the re-appraisal of two recent and independent epidemiological studies conducted in Liguria, Italy, and Ontario, Canada, we attempt to shed light on this apparently paradoxical finding. Lung cancer mortality was studied among maintenance workers exposed to asbestos, and among two other subgroups of refinery employees: blue collar and white collar workers. The comparison with blue collar workers was performed in order to take into account the role of healthy worker effect, smoking habit, and the socioeconomic level. The comparison with white collar workers was performed to control for other occupational lung carcinogens. Results reveal a consistency between the two studies and show that 96-100% of the mesotheliomas and 42-49% of the lung tumors arising among maintenance workers were attributable to asbestos exposure. Our new analysis, estimating two cases of asbestos-related lung cancer for each case of mesothelioma, confirms published findings on the magnitude of asbestos-related tumors in oil refineries. /EPIDEMIOLOGY STUDIES/ ...The cause-specific mortality of all Italian women compensated for asbestosis and alive December 31, 1979, was investigated through October 30, 1997. In the total cohort, which included 631 subjects, 277 deaths occurred. Cause-specific SMRs (Standardized Mortality Ratio) were computed using the national rates for comparison. A significantly increased mortality for all diseases related to asbestos exposure was observed. Mortality for all causes, all neoplasms, lung cancer, uterine cancer, ovarian cancer, and non-neoplastic respiratory diseases was significantly increased. Separate analyses for textile (n=276) and asbestos-cement (n=278) workers were performed. Women employed in the textile industry, mainly exposed to chrysotile, who are compensated at a younger age, showed higher SMRs for lung cancer and asbestosis. Women in the asbestos-cement industry, mainly exposed to crocidolite containing asbestos mixtures, experienced higher mortality for pleural malignancies. /Chrysotile and crocidolite asbestos/ /HUMAN EXPOSURE STUDIES/ Five types of asbestos plus silica and glass wool fibers were tested for their ability to activate alternative complement pathway and generate chemotactic factor activity from fresh normal human serum. All 5 of the asbestos fibers tested (including anthophyllite and crocidolite) activated the alternative pathway. In addition it was demonstrated that chemotactic factor activity was generated when asbestos fibers were incubated with fresh normal human serum. These observations suggest that the complement system may mediate the initial inflammatory response observed upon exposure to certain types of asbestos fibers. /HUMAN EXPOSURE STUDIES/ The thoracic lymph nodes are a part of the clearance system from lung tissue. Accumulation of dust in these nodes are known to occur following some types of exposure. However, no information exists as to asbestos content in lymph nodes from the general population. The study cohort consisted of 21 individuals previously defined as nonoccupationally exposed to asbestos. Tissue burden of asbestos obtained from lung analysis by analytical electron microscopy was compared with burden in the lymph nodes. No asbestos fibers were detected in nodes from 8 cases. The majority of the fibers found in lymph nodes were short (<5 um) and most often noncommercial amphiboles. Ferruginous bodies (FBs) were detected in lymph node from only two samples. The total asbestos burden in the lung tissue from these individuals was quite low. However, in 12 of the 13 cases that had positive nodes, the tissue burden in the node was appreciably heavier per gram than in the lung. This raises the question as to whether the lymph nodes, though less efficient clearance, may be better indicators of lifetime exposure to dust than lung tissue. /OTHER TOXICITY INFORMATION/ Crocidolite, a carcinogenic asbestos in humans, specifically induces mesothelioma. ...The cytogenotoxic effects of crocidolite in a human mesothelioma cell line, MSTO211H, and a human promyelocytic leukemia cell line, HL60 /were investigated/. Using confocal laser scanning microscopy, /it was/ found that the MSTO211H cells had phagocytotic activity, whereas the HL60 cells did not. In the MSTO211H cells, crocidolite decreased the cell population and increased the numbers of polynucleated cells (PN) and tetraploid cells, and increased the coefficients of variation (CV) of DNA contents in G0/G1 cells and the formation of 8-hydroxydeoxyguanosine. In contrast, crocidolite showed none of these cytogenotoxic effects in HL60 cells. To investigate the importance of phagocytosis in the cytogenotoxicity of crocidolite, ...the crocidolite-phagocytosed cells /were sorted/ from less-phagocytosed cells by fluorescence-activated cell sorting, and ...the differences in cytogenotoxicity between these two cell groups /were studied/. ...Significant increases in the numbers of PN and tetraploid cells and the CV in the crocidolite-phagocytosed cells /were found/ compared to the less-phagocytosed cells. These findings indicate that MSTO211H cells are susceptible to the cytogenotoxic effects of asbestos due to their phagocytotic activity, and that the MSTO211H cell line is suitable for the detection of such effects on human cells by asbestos and other materials which need to be phagocytosed to exert their toxicity. /Crocidolite/ Medical Surveillance: The employer shall institute a medical surveillance program for all employees who are or will be exposed to airborne concentrations of fibers of asbestos at or above the TWA and/or excursion limit. ...All medical examinations and procedures /must be/ performed by or under the supervision of a licensed physician... . ...A pre-placement medical examination shall be provided or made available by the employer. Such examination shall include, as a minimum, a medical and work history; a complete physical examination of all systems with emphasis on the respiratory system, the cardiovascular system and digestive tract; completion of the respiratory disease standardized questionnaire in Appendix D to /the OSHA asbestos standard/, Part 1; a chest roentgenogram (posterior-anterior 14X17 inches); pulmonary function tests to include forced vital capacity (FVC) and forced expiratory volume at 1 second (FEV(1.0)); and any additional tests deemed appropriate by the examining physician. Interpretation and classification of chest roentgenogram shall be conducted in accordance with Appendix E to /the OSHA asbestos standard/. Periodic medical examinations shall be made available annually. The scope of the medical examination shall be in conformance with the protocol established in /pre-placement examination/. ...Chest roentgenogram shall be conducted in accordance with /the following schedule:/ 0-10 years since first exposure- every 5 yr for employees age 15-45 yr; 10+ years since first exposure- every 5 yr for employees age 15-35, every 2 yr for employees age 35-45, and every 1 yr for employees age 45+ years. /from table/ The employer shall provide, or make available, a termination of employment medical examination for any employee who has been exposed to airborne concentrations of fibers of asbestos at or above the TWA and/or excursion limit. The medical examination shall be in accordance with the requirements of the periodic examinations... and shall be given within 30 calendar days before or after the date of termination of employment. Pre-employment medical examinations should include the following: Medical history, family history, history of smoking, consumption of alcohol, and an occupational history. Physical examinations should include: oral cavity, cheek, and abdomen which includes a digital examination of the rectum. Spirometry: Including measurements of vital capacity, forced vital capacity, and forced expiratory volume at one second. Chest X-ray: postero-anterior and lateral views (14x17 inch), along /with/ sputum cytology /examination/. /Asbestos cmpd/ Asbestos workers with clinical symptoms of hoarseness, or pain, or soreness of the throat should be referred to an ear, nose, and throat specialist for a detailed otolaryngologic examination of the upper respiratory tract /for detection of laryngeal cancer/. Populations at Special Risk: Special groups at risk may include neonates and children; however, no data exist on the relative sensitivity to asbestos of infants and children undergoing rapid growth. Concern exists because fibers deposited in the tissues of young may have an extremely long residence time during which malignant changes could occur. In addition, risk could be influenced by differential absorption rates which have not been fully studied at this time. Individuals on kidney dialysis machines may also be at greater risk as fluids, potentially contaminated with asbestos fibers can enter the blood stream directly or, in selected instances, the peritoneal cavity (peritoneal dialysis). An increased risk is also associated with increased exposure to asbestos in water in municipalities such as San Francisco or Seattle where asbestos occurs naturally in water, in cities where there is a interaction between aggressive water and asbestos-cement pipe, or in cities whose water may be contaminated as a result of asbestos operations. Hypersusceptible individuals have not been defined for ingested exposures to mineral fibers. It is well known that smokers exposed to asbestos dusts from inhalation are at a higer risk of developing lung cancer than are nonsmokers with similar exposures. Variability in susceptibility to asbestos-induced respiratory tissue damage may be related to individual genetic differences in ability to detoxify reactive electrophilic molecules (e.g., reactive oxygen radicals and nitrogen oxide) produced during pulmonary disposition of fibers. NAT2 is another Phase II enzyme that displays genetic polymorphisms (one associated with slow acetylation and another with fast acetylation) that also may be associated with susceptibility to asbestos toxicity. Among a group of subjects exposed to high levels of asbestos, individuals who lacked the GSTM1 gene and had the slow NAT2 genotype showed a 4-fold increased risk for developing nonmalignant respiratory disorders and an 8-fold increased risk for developing mesothelioma compared with individuals with the GSTM1 gene and the fast NAT2 genotype. Recent studies have shown that a high percentage of human mesotheliomas also test positive for the presence of Simian Virus 40 (SV40). Based on this finding, it has been suggested that SV40-infected individuals who are exposed to asbestos might be at increased risk for developing mesothelioma. Probable Routes of Human Exposure: Asbestos /enters the human body/ from gastrointestinal and respiratory tract exposure. Asbestos is usually taken into the body by inhalation or ingestion and it is then distributed to most organs via the blood or lymphatic systems. ASBESTOS FIBERS MAY BE LIBERATED INTO AIR ... IN MINING, MILLING, PROCESSING, OF ASBESTOS CONTAINING PRODUCTS & DUMPING WASTE. ... FIBERS LESS THAN 3 UM IN DIAM & FROM 10-200 UM IN LENGTH ARE MOST IMPORTANT CAUSE OF ASBESTOSIS. CONTENTS & TYPES OF ASBESTOS IN FIREPROOFING INSULATION MATERIALS SPRAYED ON CEILINGS OF 127 BUILDINGS THROUGHOUT THE USA WERE STUDIED. DURING REMOVAL OF SPRAYED MATERIALS, WORKERS WERE EXPOSED TO EXTREMELY HIGH CONCENTRATIONS (AVG 16.4 FIBERS/CC) WHEN DRY METHODS WERE USED. WHEN WET METHODS WERE USED DURING REMOVAL, THE AIRBORNE FIBER CONCENTRATIONS WERE REDUCED TO LESS THAN 2 FIBERS/CC. ... EXPOSURES OCCUR DURING END-PRODUCT USE, AMONG ASBESTOS INSULATION WORKERS, AMONG BRAKE REPAIR & BRAKE MAINTENANCE WORKERS, & AS RESULT OF INDIRECT OCCUPATIONAL EXPOSURES, PARTICULARLY IN SHIP BUILDING & SHIP REPAIR, & IN CONSTRUCTION INDUSTRY. OTHER EXPOSURES OCCUR IN RELATION TO INSPECTION & MAINTENANCE WORK ON ASBESTOS CONTAINING STRUCTURES & EQUIPMENT, IN REFINERIES & CHEMICAL PLANTS, BUILDINGS, RAILWAY LOCOMOTIVES & WAGONS, SHIPYARDS & POWER PLANTS. ... BUILDING DEMOLITION & WASTE DISPOSAL. ... EXPOSURE MAY OCCUR DURING WEARING OF ASBESTOS SAFETY GARMENTS. Talc /which is often contaminated with asbestos/ is used in the following products: cosmetics, spray and dusting powder, insecticides, white shoe polishes, as a filler for soap, dusting powders for toy balloons, condoms, and contraceptive diaphragms. Insulation workers using asbestos materials and automotive brake repairmen have been exposed to airborne asbestos levels up to 133 and 72 fibers/cu m, respectively. Exposure to airborne asbestos in the home may /result from use of/ spackling compounds, certain types of insulation, and some workers may bring home some material ... on their work clothing. Exposure profiles for respirable silica dust in 15 mining industry groups that were prepared from the 1977-1981 Mine Safety and Health Administration (MSHA) MIDAS files are presented as probability distribution graphs. The dust exposure data have been organized into data sets according to industry group, operation category, and location (surface and underground) as discussed in this report. There are 15 industry groups: copper, gold and silver, iron, lead and zinc, molybdenum, uranium, other metals, limestone, other stone, clay and shale, asbestos, talc, oil shale, sand and gravel, and other nonmetals. Operation and location are classified into 14 categories: surface drilling; underground drilling, blasting, cutting and boring; surface production; surface mobile transport; surface haulageway maintenance; underground production; underground haulageway maintenance; crushing or grinding, and sizing; concentrating and finishing; non specific surface; and non specific underground. Occupational settings in which individuals who may be at risk from indirect exposure to asbestos include: gold mining, cigarette filter manufacture, automobile transmission parts manufacture, dentistry, and agriculture. Asbestos is present in the soil, water and air, and may be added to these media from mining, wearing of automobile brake linings, asbestos textile manufacturing, asbestos spraying for fireproofing, and the use of asbestos in construction materials. The multitude of uses for this non-combustible insulating material means that exposure may be both occupational and non-occupational (environmental); for most people, exposure to at least a low level of asbestos ocurs on a daily basis. ... Dietary materials that have been reported to contain, or are likely to contain, asbestos include foods such as vegetable oil, lard, mayonnaise, ketchup and meats ... and beverages such as beers, sherries, ports, vermouth and soft drinks. Currently, all major commercial asbestos varieties, chrysotile, amosite, and crocidolite, have been found to produce a significant incidence of asbestos-related disease among workers ocupationally exposed in mining and milling, in manufacturing, and in the use of materials containing the fiber. The predominant route of exposure has been inhalation, although some asbestos may be swallowed directly or after being brought up from the rspiratory tract. Not only has asbestos disease been found among individuals exposed to the fiber directly as a result of excessive work exposures in decades past, but asbestos-associated cancer has also been identified, albeit less frequently, among those with inhalation exposures of lesser intensity, including those who had worked near the application or removal of asbestos material, those with history or residing in the vicinity of asbestos plants, and those who had lived in the household of an asbestos worker. DOMESTIC EXPOSURE OF HOUSEHOLD CONTACTS TO ASBESTOS MAY OCCUR FROM DUSTS BROUGHT HOME ON WORKERS' CLOTHES, SHOES, HAIR, EQUIPMENT, ETC. ... ASBESTOS LEVELS /WERE FOUND/ RANGING FROM 100-500 NG/CU M IN THE HOUSES OF WORKMEN. Certain beverages are either made from water already containing asbestos fibers or are clarified (beer, wine) by filtration through asbestos filter pads from which fibers may be released. The asbestos fiber levels in other foods are largely unknown. The hazard from environmental asbestos exposure showed that mesothelioma could occur among individuals whose potential asbestos exposure consisted of having resided near an asbestos factory or in the household of an asbestos worker. Twenty of 76 cases from the files of the London hospital were the result of such exposures. A field study was conducted to measure asbestos fiber concentrations during brake repair for mechanics in the Federal Republic of Germany. In addition to asbestos air sampling, 210 occupational histories describing working conditions under which brake maintenance is carried out were evaluated. Ninety dust concentration measurements in 76 service stations with static and personal samplers during brake maintenance operations. Sampling times varied from less than 3 min to more than 1 hr depending on the duration of the work operation. Samples were analyzed by phase contrast microscopy and scanning transmission electron microscopy. Fiber concentrations during brake service operations were 0.1X10+6/cu m (0.1 fiber per cc) on average. Average fiber dosages (fiber concentration X sampling time) ranged from 4X10+6 fiber/cu m/min for dry brushing and grinding to 10X10+6 fibers/cu m/min for machine grinding. Electron microscopy of brake drum dust indicated very high concentrations of short fibers; fibers with lengths > 5 um constituted less than 1% of all the chrysotile fibers counted. Average Daily Intake: Assuming that asbestos is present at the highest accurate concentration, ie, > 9999.99 million fibers/liter the daily intake for a 70 kg adult male consuming 2 liters of drinking water/day would be > 20 billion fibers/day. Antidote and Emergency Treatment: Emergency and supportive measures: Emphasis should be placed on prevention of exposure. All asbestos workers should be encouraged to stop smoking and to observe workplace control measures stringently. There is no known antidote. Persons exposed to asbestos dust and those assisting victims should wear protective equipment, including appropriate respirators and disposable gowns and caps. Watering down any dried material will help to prevent its dispersion into the air as dust. Asbestos is not absorbed through the skin. However, it may be inhaled from the skin and clothing, so removal of clothes and washing the skin is recommended. Animal Toxicity Studies: Evidence for Carcinogenicity: Classification of carcinogenicity: 1) evidence in humans: sufficient; 2) evidence in animals: sufficient. Overall summary evaluation of carcinogenic risk to humans is Group 1: The agent is carcinogenic to humans. CLASSIFICATION: A; human carcinogen. BASIS FOR CLASSIFICATION: Observation of increased mortality and incidence of lung cancer, mesotheliomas and gastrointestinal cancer in occupationally exposed workers are consistent across investigators and study populations. Animal studies by inhalation in two strains of rats showed similar findings for lung cancer and mesotheliomas. Animal evidence for carcinogenicity via ingestion is limited (male rats fed intermediate-range chrysotile fibers; i.e., greater than (>) 10 um length, developed benign polyps), and epidemiologic data in this regard are inadequate. HUMAN CARCINOGENICITY DATA: Sufficient. ANIMAL CARCINOGENICITY DATA: Sufficient. A1; Confirmed human carcinogen. /Asbestos, all forms/ Non-Human Toxicity Excerpts: /LABORATORY ANIMALS: Acute Exposure/ In early experiments, it was demonstrated that guinea pigs and monkeys exposed by /inhalation/ to 4 commercial types of asbestos developed fibrotic lesions of lung and pleura... . In more recent experiments, this finding has been confirmed in rats and hamsters. /LABORATORY ANIMALS: Acute Exposure/ Benign asbestos pleurisy is a manifestation of asbestos-induced disease that is not uncommon but often is ignored. Crocidolite asbestos injected into the rabbit pleural space caused the appearance of chemotactic activity in an exudative effusion, characterized by a polymorphonuclear leukocyte response that peaked 4 hr after injection. /Crocidolite asbestos/ /LABORATORY ANIMALS: Acute Exposure/ ...C57BL/6-129 hybrid mice with genes for both the 55kd and 75kd receptors for TNF-alpha knocked out (TNF-alphaRKO) fail to develop fibroproliferative lesions after asbestos exposure. There is good evidence that TNF-alpha plays a major role in mediating interstitial pulmonary fibrosis. ...New data obtained by in situ hybridization /is presented/ showing that expression of the genes coding for transf orming growth factor alpha (TGF-alpha) and platelet-derived growth factor A-chain (PDGF-A) is reduced in the TNF-alphaRKO mice compared with control animals. In accordance with this observation, data on bromodeoxyuridine (BrdU) incorporation in the lungs of the TNF-alphaRKO mice show no increases over unexposed control animals. In contrast, wild-type control mice exposed to asbestos exhibit 15- to 20-fold increases in BrdU uptake and consequently develop fibrogenic lesions. Even though the levels of TNF-alpha gene expression and protein production were increased in the asbestos-exposed TNF-alphaRKO mice, the lack of receptor signaling protected the mice from developing fibroproliferative lesions. We agree with the view that TNF-alpha is essential for the development of interstitial pulmonary fibrosis and postulate that TNF-alpha mediates its effects through activation of other growth factors such as PDGF and TGF-alpha that control cell growth and matrix production. /LABORATORY ANIMALS: Acute Exposure/ .../It was found that an intrapleural/ dose of 40 mg asbestos dust on gelatin coated fiber-glass pledgets... /of/ 3 of the Union Internationale Contre le Cancer samples, crocidolite, amosite and Rhodesian chrysotile, all produced mesotheliomas in about 60% of Osborne Mendel rats. ...Mesotheliomas in Sprague Dawley rats treated with a single /intrapleural/ dose of 67 mg of chrysotile, amosite, or crocidolite /were observed/. /Crocidolite, amosite and Rhodesian chrysotile asbestos/ /LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ ...Groups of CD Wistar rats /were exposed/ to 5 Union Internationale Contre le Cancer asbestos samples (amosite, anthophyllite, crocidolite and Rhodesian and Canadian chrysotiles) at concentrations of about 12 mg/cu m respirable dust for 7 hr/day on 5 days/wk, for several lengths of exposure: 1 day (7 hr), 3 months, 6 months, 12 months or 24 months. At the end of exposures, the amount of dust in the lungs of animals exposed to the 2 chrysotile samples was much less than that in animals exposed to the 3 amphibole samples. However, all types of fiber produced asbestosis, which was progressive after removal from the dust. Futhermore, whereas no carcinomas of the lung were found in the control group, carcinomas of the lung and mesotheliomas were demonstrated in the groups exposed to Canadian chrysotile and to the amphiboles. Only carcinomas of the lung were seen with Rhodesian chrysotile ...an increasing incidence of neoplasms was observed with increasing exposures to each form of asbestos. Even as little as 1 day of exposure (providing the animals were allowed to survive and were observed) produced neoplasia. /LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ The effects of 3 months intermittent inhalational exposures of amphibole and serpentine asbestos on the constituents of the lower respiratory tract was studied. Bronchoalveolar lavage (BAL) analyses were performed on 3 groups of rats: 1 group was exposed to chrysotile (serpentine) asbestos, second group was exposed to crocidolite amphibole asbestos, while the third group was sham-exposed. The total BAL cell yields and macrophage content of BAL cells were significantly lower after asbestos exposure, especially in the chrysotile-exposed group. These effects persisted for as long as 1 yr after cessation of exposure. Multinucleated macrophages were seen in BAL cells from both asbestos-exposed groups. Striking ultrastructural alterations of macrophage morphology were noted in BAL cells from both groups of asbestos exposed rats. Chrysotile fibers were not seen in any BAL cells from chrysotile-exposed animals. However, 15 months after terminating the exposure regimen, a sizeable proportion of BAL macrophages from crocidolite-exposed rats contained phagocytosed asbestos fibers. /Amphibole and serpentine asbestos; chrysotile and crocidolite/ /LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Experimental coniosis was induced by intratracheal administration to rats of 25 mg or 50 mg of Portland cement, asbestos-cement, as well as chrysotile and crocidolite asbestos. The rats were sacrificed 90, 165 and 180 days after dust administration. The weight of wet lungs and hydroxyproline content in lungs were determined. Statistically significant lower values of fibrogenic effects indices following cement dust administration, as compared to those indices for the other dusts, were found. On the other hand, no significant differences were found between fibrogenic effects indices for asbestos-cement containing approx 13% of asbestos and pure asbestos dusts (chrysotile or crocidolite). Furthermore, it seems that the duration of dust action is more important than the dust dose in the development of fibrogenic asbestosis. /Chrysotile and crocidolite/ /LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ 6 week old male F344 rats were fed 10 mg of asbestos 3 times/week for 10 weeks. The animal tissues were examined at 34 weeks or after their natural death. Intestinal cancer (not significant) was observed; however, no toxic effects were reported. /LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Early lesions /similar to those reported earlier: multinucleated giant cells, lymphocytes, and fibroblasts/ were found in rats /following inhalation of asbestos fibers/ and consisted of a proliferation of macrophages and cell debris in the terminal bronchioles and alveolae. /LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ /Intrapleural administration to CD Wistar and Osborne-Mendel rats/ all commercial types of asbestos have produced mesotheliomas in C/D Wistar rats. A dose of 20 mg of the five UICC standard reference samples produced mesotheliomas in varying numbers - crocidolite 61%, amosite 36%, anthophyllite 34%, Canadian chrysotile 30% and Rhodesian chrysotile 19%. With a dose of 40 mg of asbestos dust on gelatin-coated fibre-glass pledgets, /it was/ found that three of the UICC samples, crocidolite, amosite and Rhodesian chrysotile, all produced mesotheliomas in about 60% of their Osborne-Mendel rats. Induced mesotheliomas with 60 mg of Russian chrysotile. In all these studies there was a long latent period between inoculation and appearance of the tumors. Evidence that the response was dose related. Mesotheliomas have also been produced by other workers: in rats, in hamsters and in rabbits. /LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ All commercial forms of asbestos tested are carcinogenic in mice, rats, hamsters and rabbits. ...The size and shape of fibers influence the incidence of tumors; fibers <0.5 um in diameter are more active in producing tumors. /LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ The effects of ingested asbestos on the colon of weanling F344 rats was studied. Based on results of preliminary experimentation, the dosage was established at 10% by weight of a standard laboratory diet. Two hundred forty animals comprised the test group; there were also 242 control rats fed 10% nonnutritive cellulose and a group of 121 controls was fed normal laboratory chow. The study was terminated at 32 months. Epithelial tumors of the colon (8 adenocarcinomas and 1 adenoma) were found in nine of the rats. Four tumors were in asbestos fed rats, two tumors in the nonnutritive cellulose fed group, and three tumors were found in the standard laboratory diet controls. Also, one malignant mesothelioma was found in the asbestos fed group. Although the differences in the numbers of tumors between asbestos fed animals and controls were not significant, the authors believe their experimentation suggests that ingested asbestos is not inert in the colon. Included in their result is the discovery that cyclic-AMP levels in the colon were significantly lower in asbestos fed animals vs controls. /LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ ...Ip injections of 20 mg amosite, crocidolite or chyrsotile /were given to/ groups of 11, 13, 13 Charles River CD rats, respectively. Three peritoneal mesotheliomas were observed with chrysotile, 3 with crocidolite and none with amosite, after 7-17 months. /Amosite, crocidolite or chyrsotile asbestos/ /LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ A study examined the carcinogenic effects of asbestos on groups of 22-24 animals fed 250 mg/week of amosite, crocidolite, or chrysotile in margarine for up to 25 months. No excess malignancies were found in the exposed group compared with the margarine or undosed control groups. /Amosite, crocidolite, or chrysotile asbestos/ /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Pregnant CD-1 mice /were given/ (10-12/dose) 4, 40 or 400 mg asbestos/kg bw (1.43, 14.3 or 143 mg asbestos/ml) in their drinking water during days 1-15 of gestation. Water consumption did not vary between the different dosage groups. There was also no difference in embryo survival between the treatment groups and the controls, which received only tap water. There were no signs of maternal toxicity. /GENOTOXICITY/ In Chinese hamster cells, chrysotile and crocidolite have produced genetic damage and morphologic transformation. /Chrysotile and crocidolite/ /GENOTOXICITY/ Chrysotile, amosite, and anthophyllite showed no mutagenic activity toward tester strains of Escherichia coli or Salmonella typhimurium. /Chrysotile, amosite, & anthophyllite/ /GENOTOXICITY/ This study was carried out in order to assess the genotoxic effect of in vitro exposure to commercial chrysotile asbestos. V 79 cell line, known as a well-established cellular model, was used for detection of asbestos genotoxic potency. Conventional structural chromosomal aberration analysis and sister chromatid exchange (SCE) method were both used for asbestos genotoxicity assessment. Within the experimental protocol applied, V 79 cells were treated with asbestos in concentrations of 100 and 200 ug/mL F-10 (HAM) media during 90 days, respectively. Analysis of changes in chromosome structure as well as of cell ploidy was performed each tenth day of the experimental course, consecutively. Two hundred well spread metaphases were taken into account for chromosomal aberration analysis. Frequency of sister chromatid exchanges was observed in 50 cells per sample. The results of cytogenetic tests revealed structural chromosomal damages, SCE-elevation and changes in cell ploidy. Cytogenetic effect of asbestos obviously depended on the dose applied and on the period of incubation. The results of this study suggest that significant cytogenetic changes occurring after asbestos treatment might directly or indirectly be the part of the biological events responsible for eliciting asbestos-induced carcinogenesis. /Chrysotile asbestos/ /GENOTOXICITY/ Studies of exposed asbestos workers, residentially exposed Turkish villagers, mesothelioma patients, and lung cancer patients suggest that asbestos is genotoxic. The number of chromosomal aberrations and the rate of sister chromatid exchange were significantly elevated in the peripheral blood lymphocytes of asbestos workers compared to a control population (Fatma et al. 1991). The mean sister chromatid exchange rate was significantly increased (p=0.002) in nonsmoking asbestos insulators compared to a control population. /GENOTOXICITY/ A large number of studies indicate that asbestos fibers can cause chromosomal aberrations in Chinese hamster ovary (CHO) and Syrian hamster embryo (SHE) cells. The aberrations include aneuploidy (usually polyploidy), fragmentation, breaks, rearrangements, gaps, dicentrics, inversions, and rings. /GENOTOXICITY/ ...Crocidolite induced transformations of Syrian hamster embryo cells. In cultured rodent cells, ...crocidolite induced chromosomal aberrations, ...and ...sister chromatid exchanges. /Crocidolite/ /GENOTOXICITY/ [Mutation research 76: 169 (1980)] Escherichia coli WP2,uvrA - reverse mutation studies with metabolic activation: negative. /ALTERNATIVE IN VITRO TESTS/ The hemolytic activity of short asbestos fibers was studied using rat and sheep red blood cells. The initial velocity of hemolysis is proportional to the concentration of fibers. /ALTERNATIVE IN VITRO TESTS/ The effects of Union Internationale Contre le Cancer crocidolite and chrysolite A, either oxalic acid-leached or unleached, on the viability, morphology and growth characteristics of rat pleural mesothelial cells (PMC) were examined. Addition of 5 or 10 ug/ml of crocidolite, either leached or unleached, did not significantly change the growth rate. A slight vacuolation of the cells occurred. Leached chrysotile inhibited growth at a concentration of 50 ug/ml; with 5 or 10 ug/ml, no spreading occurred, but a shrinkage of some cells was observed. Results confirm the different in vitro reactivities of the 2 kinds of unleached asbestos fibers. Leaching of chrysotile fibers decreased their reactivity; alternatively, leaching of crocidolite increased the effects on PMC. /Chrysotile and Crocidolite/ /ALTERNATIVE IN VITRO TESTS/ The ability of particulate air pollutants (and possible constituents) to alter pulmonary host defenses was examined using an in vitro alveolar macrophage cytotoxicity assay and an in vivo bacterial infectivity screening test which employed intratracheal injection of the particles. A wide range of response between particles was seen at the 1.0 mg/ml level in vitro and the 0.1 mg/mouse level in vivo. A sample of fluidized-bed coal fly ash, bentonite, asbestos, some ambient air particles and heavy metal oxides greatly increased susceptibility to pulmonary bacterial infection. Most coal fly ash samples and some air particles caused moderate increases in infectivity, while diesel particulates, volcanic ash, and crystalline silica caused only small increases. Cytotoxic effects on macrophages in vitro were observed with most of the particles. The in vivo and in vitro assays produced a similar ranking of toxicity, however, not all particles that were highly cytotoxic were potent in increasing bacterial infectivity. Increased toxicity measurable by either assay often appeared to be associated with small size or with the presence of metal in the particles. /ALTERNATIVE IN VITRO TESTS/ The ability of asbestos-elicited murine peritoneal macrophages to release superoxide anion and hydrogen peroxide, following in vitro triggering has been investigated. The asbestos-elicited macrophages produced increased levels of superoxide and hydrogen peroxide compared to control macrophages and similar levels to those produced by Corynebacterium parvum elicited macrophages. The supernatants from asbestos-elicited macrophages which had been triggered in vitro were capable of impairing the ability of alpha-1-protease inhibitor to inhibit elastase function. The catalase sensitivity of this effect showed it to be due to hydrogen peroxide. /ALTERNATIVE IN VITRO TESTS/ Enzymatic studies on asbestotic rat lungs revealed increased levels of fumarase and cytochrome C oxidase, and decreased levels of aconitase. /ALTERNATIVE IN VITRO TESTS/ Rats which received asbestos intratracheally had... decreased number of lung mitochondria, decreased activities of magnesium(2+) and calcium(2+)-activated ATPase and increased activities of cytochrome C oxidase and diaphorase. /ALTERNATIVE IN VITRO TESTS/ Treatment of calf thymus DNA with various types of asbestos fibers in the presence of hydrogen peroxide under physiological conditions (pH 7.4, 37 deg C) resulted in the hydroxylation of the C-8 position of guanine residues. DNA strand scission was also detected after these treatments. /ALTERNATIVE IN VITRO TESTS/ ... After asbestos suspension and filtrate treatment of V79 cells, the value of hue for indicating P53 protein expression was significantly lowered, and such abnormal expression was especially observed in binucleate cells and polykaryocytes. /OTHER TOXICITY INFORMATION/ Pet dogs with spontaneous mesothelioma were used to identify environmental exposures that might increase their owner's risk of asbestos-related disease. Eighteen histologically confirmed canine mesotheliomas were diagnosed at the veterinary hospital of the University of Pennsylvania, Philadelphia, from April 1977 to December 1981. Sixteen owners of cases and 32 owners of age, breed, and sex-matched controls were interviewed to determine their occupation and medical history and their dog's medical history, life style, diet, and exposure to asbestos. An asbestos-related occupation or hobby of a household member and use of flea repellants on the dog were significantly associated with mesothelioma. In addition, there was a trend indicating an increased risk of mesothelioma with an urban residence. Lung tissue from three dogs with mesothelioma and one dog with squamous cell carcinoma of the lung had higher levels of chrysotile asbestos fibers than lung tissue from control dogs. /OTHER TOXICITY INFORMATION/ ...Female Wistar rats received an intratracheal instillation of 5 mg chrysotile (0.5 mL saline) as well as intragastric garlic treatment (1% body weight (v/w); 6 days/wk). Effect of garlic treatment was evaluated after 1, 15, 30, 90, and 180 days by assaying aryl hydrocarbon hydroxylase (AHH), glutathione (GSH), glutathione S-transferase (GST), and production of thiobarbituric acid reactive substances (TBARS) in rat lung microsome. AHH and TBARS formation were significantly reduced at day 90 and day 180 in chrysotile treated garlic cofed rats; GSH recovered 15 days later to the near normal level and GST elevated significantly after treatment of garlic as compared to chrysotile alone treated rat lung microsome. National Toxicology Program Studies: Carcinogenesis studies of crocidolite asbestos were conducted with male and female F344/N rats. This form of asbestos was administered at a concentration of 1% in pelleted diet for the lifetime of the rats starting with the dams of the study animals The studies were started in January 1978 and ended in December 1980. Group sizes were 118 for male and female controls and 250 for male and female crocidolite asbestos exposed rats. Conclusions: Under the conditions of these feed studies, crocidolite asbestos was not overtly toxic and did not cause a carcinogenic response in F344/N rats for their lifetime. TSCA Test Submissions: Chronic toxicity was evaluated in 50 male Sprague-Dawley rats, and 15 male Syrian hamsters exposed to asbestos via inhalation at a nominal concentration of 85 mg/m3 for 7 months, followed by a lifetime observation period. In the exposed rat group, the pulmonary responses included alveolar adenomatous proliferation, non-progressive fibrosis, squamous metaplasia and a substantial incidence of pulmonary carcinoma formation (6/34). Mean body weight of exposed rats was significantly lower after 1 month of exposure, it remained low until 14 months post exposure. Mortality data for the rat group indicated no significant difference between exposed and control rats. Mortality in the exposed hamster group was significantly increased during the 7 month exposure period. No pulmonary neoplasms were noted in the surviving hamsters, (the ability to evaluate long-term pulmonary effects was severely limited due to early mortality of 8/15 hamsters). The mean body weight for hamsters was statistically decreased during the first month of exposure, but statistically increased and remained so for the remainder of the study. Histopathologic studies of other, non-pulmonary tissues were not significantly different from the control group for rats or hamsters. Metabolism/Pharmacokinetics: Metabolism/Metabolites: Asbestos has ... been observed to increase the levels or activities of the following enzymes: ... lactic dehydrogenase, acid phosphatase, glutamic pyruvate transaminase, lipase, cathepsin D, acid RNAase, B-glucuronidase, B-N-acetyl glucos-aminidase, sucrase, alkaline phosphatase, ATPase, and p-nitrophenyl acetate hydrolase. Absorption, Distribution & Excretion: Inhaled fibers deposit by sedimentation, diffusion, impaction, and interception in airways of the respiratory system. The mathematical model developed... for the respiratory deposition of ordered cylindrical rods showing periodic motion has been adapted to 3 rod configurations in random orientation. Their results suggest that for aerosols having distributions such as Union Internationale Contre le Cancer asbestos samples dispersed by the dispenser... straight uniform fibers may deposit in pulmonary spaces in about twice the number of irregularly shaped fibers which may be judged to be in random orientation. Actin, the contractile protein within cells, may be responsible for movement of asbestos particles through the epithelium to the lung interstitium where the fibers react with macrophages and fibroblasts. Two human studies gave evidence for the penetration and migration of asbestos. ...Amphibole asbestos /has been detected/ in the urine of Minnesota residents who ingested drinking water contaminated with 5X10+7 fibers/L. ...Amphibole asbestos in lung > liver > jejunum of persons exposed to high oral intake of the mineral /has been observed/. /Amphibole asbestos/ After intrapleural or subcutaneous inoculation, the only translocation that occurred was of a minute fraction of the finer fibers. ...Occasional asbestos fibers or bodies have been reported in other tissues, including pancreas, spleen and thyroid. There is no information on how fibers... reach these sites. Following inhalation ...fibers found in ...lung tissue are usually <3 um in diameter and <100 um in length. Thicker or longer fibers are either not inhaled or are rapidly cleared from the respiratory tract. On weight basis, only a very small proportion of inhaled fiber is retained. ...Asbestos was inoculated intrapleurally, the majority of fiber was cleared during the first 10 days; but subsequently there was a very slow elimination through the gut. In feeding experiments almost all the fiber was eliminated. In persons occupationally exposed to asbestos, smaller numbers of asbestos bodies or fibers than are seen in lung tissue have been found in extra-pulmonary tissue, including tonsils, thoracic and abdominal lymph nodes, pleura, peritoneum, liver, spleen, kidney and small intestine. The physical characteristics of asbestos fibers that penetrate to lung parenchyma /demonstrate/ fiber respirability was largely a function of fiber diameter. ...5000 asbestos fibers from lungs of 10 deceased persons who had been occupationally exposed... showed that... all /were/ <0.5 um in diameter. Studies with animals demonstrated that ingested asbestos can cross the gastrointestinal mucosa and from there can be transported to other sites in the body. Humans who consumed water containing asbestos were found to have asbestos fibers in their urine. Shorter fibers are preferentially removed /from the lungs of rats/ after one week following inhalation ... longer fibers reaching the alveolar spaces are trapped. The observation in humans of peritoneal mesothelioma, excess cancer of the stomach, colon, and rectum, and ... cancers at other non-respiratory sites ... could result from the migration of ... fibers to and across the gastrointestinal mucosa. ... Fibers may reach organs in the peritoneal cavity by transdiaphragmatic migration or lymphatic-hematogenous transport. Evidence for the human intestinal uptake ("persorption") of particles as large as 75 um is provided by the observation of starch granules in blood only minutes after ingestion. Most inhaled or directly ingested asbestos particles which pass through the gastrointestinal tract are excreted in feces. As mentioned previously, some fibers are absorbed by the gastrointestinal tract and are eventually eliminated through the urinary tract. Rats were fed a diet supplemented with an asbestos/margarine formulation for periods up to 1 yr. UICC standard reference samples of amosite were used. There was no evidence of asbestos retention within gut lumen, and no sign of cell penetration or damage to intestinal mucosa were observed. Dosages of 1-3 mg (1 mg/mL of water) were injected into the femoral vein of female Wistar rats at 2 day intervals from days 10-14 of gestation. Total dose varied from 4-12 mg of asbestos. The fetuses were removed by Caesarean section the day before parturition in a manner that prevented cross-contamination from the mother; the livers and lungs were than analyzed by electron microscopy. Asbestos fibers were found to cross the placenta but the extent of this occurrence was highly variable. The livers and lungs analyzed were selected at random and thus could have come from different fetuses in the same uterus. In the first experiment, the highest number of fibers found in fetal liver and lungs came from a dam administered four 3 mg injections (total dose= 12 mg). Numbers of fibers found in liver and lungs were 27.03X10+6 fibers/g and 139.97X10+6 fibers/g, respectively. In a second experiment, the highest number of fibers found in fetal liver and lung came from a dam administered five 2 mg injections (total dose= 10 mg). Numbers of fibers found in the liver and lung were 100.12X10+6 fibers/g and 2.90X10+6 fibers/g, respectively. The deposition and clearance of fibers from the lung suggest that most inhaled fibers (approximately 99%) are eventually cleared from the lung by ciliary or phagocytic action. Fibers were detected in beverages (beer, wine and soft drinks) and were studied to see if such fibers consumed orally can pass through the intestinal wall and enter the bloodstream. A stock solution was made to contain fibers the same length as those found in beverages (0.5-2) and determined to contain 9.4x10+6 fibers/l. An aliquot (assumed to be 350 ml) was then administered intragastrically to rats (number, species and sex not known). Asbestos fibers were found to accumulate in the omentum surrounding the small intestine, brain and lung. ... counts could not be made on the liver and kidneys. In the lower respiratory tract, fiber deposition is largely controlled by interception that is controlled by fiber length; asbestos fibers tend to be deposited in respiratory bronchioles at airway branch points. The curvature of chrysotile makes this fiber especially vulnerable to interception at bifurcations. In studies of rats using irradiated crocidolite, about 35% alveolar deposition was observed, and following a 1 hr inhalation exposure, electron microscopy demonstrated fiber deposition at bifurcations of alveolar ducts. Evaluation of lung tissue in both animals and humans after mixed asbestos exposure reveals that there is preferential clearance of chrysotile and retention of amphiboles over time. Animal models of asbestosis reveal greater retention of chrysotile in those with parenchymal rather than an airways lesion, and there are twice as many fibers longer than 5 um in the former, a finding consistent with host differences in clearance and risk for pulmonary fibrosis. Asbestos fibers are cleared by the mucociliary ladder or are transported across the type I alveolar epithelial cells into the interstitium, where their fate may be transmigration to hilar nodes or pleura or eventual dissolution. The kinetics of dissolution are most rapid for man-made mineral fibers followed in rank order by chrysotile, crocidolite, and erionite. The thoracic lymph nodes are a part of the clearance system from lung tissue. Accumulation of dust in these nodes are known to occur following some types of exposure. However, no information exists as to asbestos content in lymph nodes from the general population. The study cohort consisted of 21 individuals previously defined as nonoccupationally exposed to asbestos. Tissue burden of asbestos obtained from lung analysis by analytical electron microscopy was compared with burden in the lymph nodes. No asbestos fibers were detected in nodes from 8 cases. The majority of the fibers found in lymph nodes were short (<5 um) and most often noncommercial amphiboles. Ferruginous bodies (FBs) were detected in lymph node from only two samples. The total asbestos burden in the lung tissue from these individuals was quite low. However, in 12 of the 13 cases that had positive nodes, the tissue burden in the node was appreciably heavier per gram than in the lung. This raises the question as to whether the lymph nodes, though less efficient clearance, may be better indicators of lifetime exposure to dust than lung tissue. Asbestos fibers have been detected in blood and lymph of rats exposed to oral doses of asbestos, suggesting that fibers penetrating the gut might be carried to tissues throughout the body. In support of this, asbestos fibers have been detected in the lung, kidney, liver, brain, heart, and spleen of rats that had been exposed to asbestos in the diet. Highest levels of fibers were found in the omentum (a fold of the peritoneum connecting abdominal viscera to the stomach), supporting the idea that the fibers were emanating from the gastrointestinal tract. Although the diet fed to the animals was prepared using corn oil to minimize asbestos fiber inhalation, the possibility that some fiber inhalation took place cannot be eliminated. The principal pathway by which fibers are removed from the respiratory tract is mucociliary transport. This is mediated by ciliated epithelial cells that produce and move the layer of mucus coating the epithelial tissue upwards toward the throat, where it is swallowed. Fibers deposited in this mucus layer are swallowed into the alimentary canal and most are ultimately excreted in the feces. However, a small number of fibers may penetrate through the epithelial layers of the lung and/or the gastrointestinal tract and are transferred to the blood and eventually to the kidney, where some of them may be excreted in the urine. In addition, some fibers are not cleared from the lung, leading to a gradual accumulation with time. An autopsy study was conducted to investigate whether there is transplacental transfer of asbestos in humans. The asbestos burden of lung, liver, skeletal muscle, and placenta digests of 40 stillborn infants was determined using a bleach digestion method. The fibers detected in the tissue digests were characterized as to the type of asbestos, using electron microscopy, energy-dispersive x-ray analysis, and selected-area diffraction analysis. Placental digests of 45 full-term, liveborn infants were similarly processed as controls. Low levels of small, thin, uncoated asbestos fibers were detected in the placentas and organs of 37.5% of the stillborn infants (15 of 40). The fiber sizes ranged from 0.05 to 5.0 microns in length and 0.03 to 0.3 micron in width, with a mean length of 1.15 microns and a mean width of 0.069 micron. Maximum numbers of fibers were found in the lungs (mean 235,400 fibers/g; n = 10), followed by liver (mean 212,833 fibers/g; n = 6), placenta (mean 164,500 fibers/g; n = 4), and skeletal muscle (80,000 fibers/g; n = 1). The fibers were detected at all stages of gestation and showed no association with gestational age. A significant association was found between fiber presence and working mothers, and positive but nonsignificant associations were found with maternal history of drug abuse, previous abortions, and fetal maceration. No association was found between premature rupture of membranes and fiber presence. No fibers were detected in the 45 placentas of the liveborn control infants. There was a highly significant difference in the asbestos fiber counts of the placentas of the stillborn and liveborn infants (P < .001). The retention of different types of asbestos in rats following exposure to the same concentration of respirable dusts... /has been described/. For the amphiboles, there was a similar pattern with an almost proportional increase of lung dust with dose. Much less dust was found for the chrysotiles, and no increase of dust content was shown in the lungs. Dust in the lungs of animals with 6 months' exposure had been partially cleared 18 months after the inhalation period. About 74% of the amosite and crocidolite and 41% of the anthophyllite were eliminated. Rats fed chrysotile, crocidolite, or amosite exhibited no retention of fibers in the gut lumen and no penetration of the mucosa. The transit time for the majority of fibers was 48 hours, and there was no asbestos either in the feces or in the gut after 7-28 days. Twenty female CBA mice were injected subcutaneously in two sites. Each injection contained 10 mg fiber suspended in 0.4 ml saline. Each animal received three injections into each flank. The flank was chosen as a site well distant from the thorax. Three fiber types: crocidolite, amosite, and chrysotile, were tested to study their distribution. All three fiber types were found in the submesothelial tissues of the thorax and abdomen. In addition, extensive inflammatory changes and some sarcomas developed at the injection sites, while transport of fibers to submesothelial tissues culminated in mesothelioma. There is no evidence that inhaled or ingested asbestos is completely cleared from the body. It is likely that some fraction of the asbestos in the body is retained for long periods, if not for life. Mechanism of Action: In an effort to understand the properties of asbestos fibers that might contribute to their toxicity, ... three different varieties of asbestos /were incubated/ with phospholipid emulsions and ... evidence of lipid peroxidation /were sought/. Although all three types of asbestos were able to catalyze lipid peroxidation in the native state, this catalytic activity was inhibited by pre-washing of the asbestos with the iron chelator desferroxamine. This suggests that lipid peroxidation may be one of the mechanisms by which asbestos produces tissue injury, and treatment with iron chelators might diminish the potential to produce this injury. Animal experimentation... indicated that the important factor in the carcinogenicity was the dimensionality of the fibers rather than their chemical properties. ...Greatest carcinogenicity was related to fibers that were less than 2.5 um in diameter and longer than 10 um. In terms of carcinogen mechanisms, asbestos appears to act like a lung cancer promoting agent ... Promotional effect does not diminish with time after cessation of exposure ... Inhalation of the fibers can precede initiating events because the fibers remain continously available in the lung to act after other necessary carcinogenic processes occur. Following deposition, the initial lesion /in pulmonary asbestosis/ is an accumulation of alveolar macrophages in the alveolar ducts and peribronchiolar regions adjacent to the terminal respiratory bronchiole. These tissues are subsequently thickened by a predominance of interstitial macrophages followed by fibroblasts. The type I alveolar epithelial cells are injured by transepithelial migration of fibers from the air space to the interstitium, and by mediators (likely oxidants) released by alveolar macrophages as they phagocytose free fibers reaching the alveolar air sacs. There is a striking proliferation of alveolar epithelial type II cells to replace the injured alveolar epithelial lining, and ther are areas of cellular denudation. After rats were subjected to 1 months' inhalation of chrysotile the persisting alterations include an increased volume of interstitial macrophages, accumulations of myofibroblasts, and increased volume of interstitial matrix. These changes persisted and increased after 3 months' exposure, and after 12 months' exposure there was a substantial increase in the noncellular interstitial matrix. There was a significant (two-fold) increase in interstitial cells, including fibroblasts. Importantly, the fibrosis progressed over time, and progressive transport of asbestos fibers into airway walls and interstitium occurred. The pathogenesis of pleural plaques probably involves submesothelial cellular events because of the absence of mesothelial cell proliferation and pleural adhesions. Fibers and areas of inflammation can be identified at lymphatic pores of the parietal pleura. The plaques are composed of collagen bundles separated by irregularly arranged spaces in a basketweave pattern. Asbestos acts as a clastogen in mammalian cell systems, causing chromosome aberrations that may bear directly on asbestos carcinogenesis. Circulating lymphocytes of asbestos insulators have been shown to have increased numbers of sister chromatid exchanges. Larger chromosomes were more susceptible, and in the largest chromosome group, there was a significant interactive effect of asbestos exposure and smoking. By gaining access to the perinuclear region of cells, asbestos may cause transformation by binding to microtubules or other cytoskeletal proteins that are important in the disjunction of chromosomes during mitosis, resulting in hypoploidy, aneuploidy, and polyploidy. Natural killer (NK) lymphocytes, specialized cells that can identify and destroy malignant cells, are inhibited from performing their immune surveillance function when assessed in vitro following exposure to amosite, chrysotile, or crocidolite in a dose-dependent fashion from 1-10 ug/mL up to 100-1,000 ug/mL and is independent of cytotoxicity. NK-cell activity was reconstituted in vitro by adding recombinant interleukin 2. In 14 of 20 mesothelioma patients there was a reduction in NK-cell activity that could by partially reconstituted with interferon-gamma. Like mesothelioma patients, asbestos workers with reduced NK-cell activity had only a partial response when stimulated with interferon-gamma; this observation was consistent with the concept that depressed immune surveillance in asbestos workers may be associated with cancer risk. Tracheal organ cultures incubated with crocidolite asbestos with adsorbed 3-methylcholanthrene for 1 month and implanted subcutaneously into syngeneic hamsters produced carcinomas in 12 to 52 weeks, whereas neoplasms did not occur after implantation with organ cultures exposed to crocidolite alone. Both crocidolite and amosite promote epithelial hyperplasia and an increase in the incorporation of [3H]thymidine by tracheal epithelium in vitro. Furthermore, crocidolite asbestos with adsorbed polycyclic aromatic hydrocarbon is transported into the cell, where it induces the aryl hydrocarbon hydroxylase (AHH) system. The AHH system produces active metabolites of the hydrocarbon that can interact with DNA facilitating the process of carcinogenesis. Adsorption of polycyclic aromatic hydrocarbons on asbestos fibers is probably an indirect process whereby adsorption of surfactant phospholipids onto the fibers creates a continuous lipid phase along the fiber surface within which lipophilic substances such an PAHs can be solubilized. AHH is a ubiquitous enzyme involved in the early metabolism of aromatic hydrocarbons and is inducible by asbestos in vitro. Studies of blood lymphocytes from long-term asbestos workers reveal increased inducibility by 3-methylcholanthrene and dibenz(a,h)anthracene. Similarly, AHH is inducible in AM, and asbestos workers who smoked and had lung cancer had AHH in the range of what was considered high inducibility . Extensive metabolizers of cytochrome P450 debrisoquine have an enhanced risk of lung cancer following exposure to cigarette smoke and asbestos. Within the lung, alveolar macrophage activity has been implicated as playing a significant role in asbestos-induced changes in immunocompetence. Fibers of asbestos that are deposited in the lung are phagocytized by macrophages, resulting in macrophage lysis and release of lysosomal enzymes and subsequent activation of other macrophages. Recently it has been hypothesized that the development of asbestosis in animal models occurs by the following mechanism. Fibers of asbestos deposited in the alveolar space recruit the interstitial space where the complement cascade becomes activated, releasing C5a, a potent macrophage activator and chemoattractant for other inflammatory cells. Recruited interstitial and resident alveolar macrophages phagocytize the fibers and release cytokines, which cause the proliferation of cells within the lung and the release of collagen. A sustained inflammatory response could then contribute to the progressive pattern of fibrosis which is associated with asbestos exposure. Once asbestos fibers have been deposited in the lung, they may become phagocytized by alveolar macrophages. Short fibers are completely ingested and subsequently removed via the mucociliary escalator. Longer fibers are incompletely ingested, and the macrophages become unable to leave the alveoli. Activated by the fibers, macrophages release mediators such as lymphokines and growth factors, which in turn attract immunocompetent cells or stimulate collagen production. Asbestos-related lung disease thus may be mediated through the triggering of an inflammatory sequence of events or the production of changes that eventually lead to the initiation (DNA damage caused by reactive molecular species) or promotion (increased rate of cell turnover in the lung) of the carcinogenic process. The surface properties of asbestos fibers appear to be an important mechanistic element in toxicity. The protection afforded by superoxide dismutase or free radical scavengers in asbestos-related cell injury in vitro suggests that the generation of active oxygen species and concomitant lipid peroxidation are important mechanisms in asbestos toxicity. The interaction of iron on the surface of asbestos fibers with oxygen may lead to the production of hydrogen peroxide and the highly reactive hydroxyl radical, events that have been associated with asbestos toxicity. The surface properties of asbestos fibers appear to be an important mechanistic element in toxicity. The protection afforded by superoxide dismutase or free radical scavengers in asbestos-related cell injury in vitro suggests that the generation of active oxygen species and concomitant lipid peroxidation are important mechanisms in asbestos toxicity. The interaction of iron on the surface of asbestos fibers with oxygen may lead to the production of hydrogen peroxide and the highly reactive hydroxyl radical, events that have been associated with asbestos toxicity. Pleural and pulmonary fibrosis (asbestosis) are ramifications of occupational exposures to asbestos fibers, a diverse family of ubiquitous, naturally-occurring minerals. The pathogenesis of asbestos-associated fibrosis involves the participation of a number of cell types and is characterized by an early and persistent inflammatory response that involves the generation of oxidants, growth factors, chemokines, and cytokines. These mediators may also contribute directly to cell injury, proliferation, and fibrogenesis. After interaction with cells, asbestos fibers trigger a number of signaling cascades involving mitogen-activated protein kinases (MAPK) and nuclear factor kappa-B (NF-kappaB). Activation of transcription factors such as NF-kappaB and activator protein-1 (AP-1) may be linked to increases in early response genes (e.g., c-jun and c-fos) which govern proliferation, apoptosis, and inflammatory changes in the cells of the lung. Recent work has suggested potentially important mechanistic roles for a number of nuclear regulatory proteins, oncogenes, proto-oncogenes, and second messenger proteins. Among these are nuclear factor-Kbeta (NF-Kbeta) activator protein-1 (AP-1), including its subunits of c-fos, c-jun, and fra-1, p53, ras, tyrosine kinases, and protein kinase c (PKC). Interestingly, a number of these factors have been shown to influence the production of other cellular factors. Additionally, cellular oxidant status has been shown to influence the behavior of AP-1 and NF-Kbeta . The latter two observations have served to further the view that NF- and AP-1 play roles in asbestos-induced lung injury, as they would allow for the integration of several of the mechanisms proposed (i.e., asbestos-associated iron could generate oxygen radicals, leading to the increased activity of nuclear factors, which induce cytokine genes, leading to cell infiltration and proliferation). Asbestos causes asbestosis and malignancies by mechanisms that are not fully understood. Alveolar epithelial cell (AEC) injury by iron-derived reactive oxygen species (ROS) is one important mechanism implicated. We previously showed that iron-catalyzed ROS in part mediate asbestos-inducedAEC DNA damage and apoptosis. Mitochondria have a critical role in regulating apoptosis after exposure to agents causing DNA damage but their role in regulating asbestos-induced apoptosis is unknown. To determine whether asbestos causes AEC mitochondrial dysfunction, we exposed A549 cells to amosite asbestos and assessed mitochondrial membrane potential changes (delta(psi)m) using a fluorometric technique involving tetremethylrhodamine ethyl ester (TMRE) and mitotracker green. We show that amosite asbestos, but not an inert particulate, titanium dioxide, reduces delta(psi)m after a 4 hr exposure period. Further, the delta(psi)m after 4 hr was inversely proportional to the levels of apoptosis noted at 24 hr as assessed by nuclear morphology as well as by DNA nucleosome formation. A role for iron-derived ROS was suggested by the finding that phytic acid, an iron chelator, blocked asbestos-induced reductions in A549 cell delta(psi)m and attenuated apoptosis. Finally, overexpression of Bcl-xl, an anti-apoptotic protein that localizes to the mitochondria, prevented asbestos-induced decreases in A549 cell delta(psi)m after 4 hr and diminished apoptosis. We conclude that asbestos alters AEC mitochondrial function in part by generating iron-derived ROS, which in turn can result in apoptosis. This suggests that the mitochondrial death pathway is important in regulating pulmonary toxicity from asbestos. ...The accumulating evidence showing that asbestos is directly genotoxic by inducing DNA strand breaks (DNA-SB) and apoptosis in relevant lung target cells /is reviewed/. Although the exact mechanisms by which asbestos causes DNA damage and apoptosis are not firmly established, some of the implicated mechanisms include the generation of iron-derived reactive oxygen species (ROS) as well as reactive nitrogen species (RNS), alteration in the mitochondrial function, and activation of the death receptor pathway. Interactions: The cell transforming ability of asbestos dusts (amosite and crocidolite asbestos) was investigated using C3H10T1/2 murine fibroblast cultures. The dusts were capable of augmenting the oncogenic effect of benzo(a)pyrene. This synergistic effect was evident when fibers and chemicals were added to cultures as simple mixtures and when benzo(a)pyrene was adsorbed to the surface of fibers. /Amosite and Crocidolite/ After inhalation of (222)Ra at equilibrium with radon daughters, male Sprague-Dawley rats were inoculated intrapleurally with 2 mg of unleached or acid-leached asbestos fibers. ... The additive co-carcinogenic effects of this type of malignant insult were demonstrated by increased incidence of malignant thoracic tumors. In rats given mineral materials, bronchopulmonary carcinomas and mixed carcinomas were observed, as well as typical mesotheliomas and combined pulmonary pleural tumors, whereas in control rats inhaling radon alone, only bronchopulmonary carcinomas occurred. Asbestosis mortality for workers who smoked 20 or more cigaretes a day was 2.8 times higher than that for workers who never smoked regularly. ... Interactive effects between cigarette smoking and the prevalence of x-ray abnormalities have been reported. ... No relationship between cigarette smoking and the risk of death from mesothelioma or gastrointestinal cancer was found. Trace metals (beryllium, cadmium, chromium, cobalt, copper, iron, manganese, nickel, thallium) may be present as natural impurities in asbestos or may be added inadvertently during milling and handling. The release of these contaminating metals in a biologically active form when the asbestos fibers are deposited in soft tissue may be involved in the etiology of some asbestos-related diseases. The relationship between asbestos exposure and smoking indicates a synergistic effect of smoking with regard to lung cancer. Further evaluations indicate that this synergistic effect is close to a multiplicative model. ...The risk of mesothelioma appears to be independent of smoking, and a significantly decreasing trend in risk was observed with the amount smoked in 1 study. The in vitro cytotoxicity and oncogenicity of both native and acid-leached asbestos fibers were studied using the C3H10T1/2 cell model. Both native and leached fibers induced a dose-dependent toxicity. At high fiber concentrations, acid leached fibers were less toxic than their untreated counterparts. Whereas asbestos fibers alone do not induce oncogenic transformation at the concn examined, both leached and native fibers synergistically enhanced the oncogenicity of gamma irradiation. Although no significant chromosomal aberrations or sister chromatid exchanges were found in asbestos-treated cultures, a higher number of sister chromatid exchanges was observed in cells treated with both asbestos and radiation compared to cells receiving radiation alone. The enhancement in radiation induced oncogenicity by asbestos fibers may be attributed to the mere physical presence of the fibers rather than any chemical contaminants the fibers may contain. Furthermore, the carcinogenicity of asbestos may be unrelated to genotoxicity. F344 rats were gavaged with a suspension of untreated UICC anthophyllite fibers (50 mg/kg bw) and fibers which had been allowed to adsorb benzo(a)pyrene molecules from aqueous solutions. Whereas anthophyllite fibers failed to induce cytogenetic alterations,fibers pretreated with the polycyclic aromatic solutions caused dose-dependent increase in the sister chromatid exchange frequencies. The observed cytogenetic impact can be explained by a local action of carcinogen molecules accumulated and subsequently transported . The results support the hypothesis that epidemiological evidence of carcinogenicity of asbestos in potable water may be explained by the cogenotoxic action of the asbestos fibers and biologically active organic micropollutants adsorbed on their surface. /Anthophyllite asbestos/ Crocidolite asbestos plus cigarette smoke synergistically increased DNA strand breaks as measured by fluorescent spectroscopy from 4.3% (crocidolite) and 9.8% (smoking), respectively, to 78 +/- 12% together. Hydroxyl radical release was measured by electron paramagnetic resonance, and oxidant scavengers such as mannitol, catalse, iron chelators, and dimethylsulfoxide prevented the DNA damage. /Crocidolite/ Pharmacology: Interactions: The cell transforming ability of asbestos dusts (amosite and crocidolite asbestos) was investigated using C3H10T1/2 murine fibroblast cultures. The dusts were capable of augmenting the oncogenic effect of benzo(a)pyrene. This synergistic effect was evident when fibers and chemicals were added to cultures as simple mixtures and when benzo(a)pyrene was adsorbed to the surface of fibers. /Amosite and Crocidolite/ After inhalation of (222)Ra at equilibrium with radon daughters, male Sprague-Dawley rats were inoculated intrapleurally with 2 mg of unleached or acid-leached asbestos fibers. ... The additive co-carcinogenic effects of this type of malignant insult were demonstrated by increased incidence of malignant thoracic tumors. In rats given mineral materials, bronchopulmonary carcinomas and mixed carcinomas were observed, as well as typical mesotheliomas and combined pulmonary pleural tumors, whereas in control rats inhaling radon alone, only bronchopulmonary carcinomas occurred. Asbestosis mortality for workers who smoked 20 or more cigaretes a day was 2.8 times higher than that for workers who never smoked regularly. ... Interactive effects between cigarette smoking and the prevalence of x-ray abnormalities have been reported. ... No relationship between cigarette smoking and the risk of death from mesothelioma or gastrointestinal cancer was found. Trace metals (beryllium, cadmium, chromium, cobalt, copper, iron, manganese, nickel, thallium) may be present as natural impurities in asbestos or may be added inadvertently during milling and handling. The release of these contaminating metals in a biologically active form when the asbestos fibers are deposited in soft tissue may be involved in the etiology of some asbestos-related diseases. The relationship between asbestos exposure and smoking indicates a synergistic effect of smoking with regard to lung cancer. Further evaluations indicate that this synergistic effect is close to a multiplicative model. ...The risk of mesothelioma appears to be independent of smoking, and a significantly decreasing trend in risk was observed with the amount smoked in 1 study. The in vitro cytotoxicity and oncogenicity of both native and acid-leached asbestos fibers were studied using the C3H10T1/2 cell model. Both native and leached fibers induced a dose-dependent toxicity. At high fiber concentrations, acid leached fibers were less toxic than their untreated counterparts. Whereas asbestos fibers alone do not induce oncogenic transformation at the concn examined, both leached and native fibers synergistically enhanced the oncogenicity of gamma irradiation. Although no significant chromosomal aberrations or sister chromatid exchanges were found in asbestos-treated cultures, a higher number of sister chromatid exchanges was observed in cells treated with both asbestos and radiation compared to cells receiving radiation alone. The enhancement in radiation induced oncogenicity by asbestos fibers may be attributed to the mere physical presence of the fibers rather than any chemical contaminants the fibers may contain. Furthermore, the carcinogenicity of asbestos may be unrelated to genotoxicity. F344 rats were gavaged with a suspension of untreated UICC anthophyllite fibers (50 mg/kg bw) and fibers which had been allowed to adsorb benzo(a)pyrene molecules from aqueous solutions. Whereas anthophyllite fibers failed to induce cytogenetic alterations,fibers pretreated with the polycyclic aromatic solutions caused dose-dependent increase in the sister chromatid exchange frequencies. The observed cytogenetic impact can be explained by a local action of carcinogen molecules accumulated and subsequently transported . The results support the hypothesis that epidemiological evidence of carcinogenicity of asbestos in potable water may be explained by the cogenotoxic action of the asbestos fibers and biologically active organic micropollutants adsorbed on their surface. /Anthophyllite asbestos/ Crocidolite asbestos plus cigarette smoke synergistically increased DNA strand breaks as measured by fluorescent spectroscopy from 4.3% (crocidolite) and 9.8% (smoking), respectively, to 78 +/- 12% together. Hydroxyl radical release was measured by electron paramagnetic resonance, and oxidant scavengers such as mannitol, catalse, iron chelators, and dimethylsulfoxide prevented the DNA damage. /Crocidolite/ Environmental Fate & Exposure: Environmental Fate/Exposure Summary: Asbestos is a term for six naturally occurring fibrous silicate minerals that have been mined, milled and used in many commercial products. Today, only one form of asbestos, chrysotile, is used in products in the United States. Due to its high tensile strength, low cost, resistence to heat, chemical attack, and biological attack, about 3,000 types of products were previously produced using asbestos. In most of these applications, asbestos fibers were bonded with some other material such as cement, plastics, pipes, or resins. Due to health concerns, asbestos is primarily used today in roofing products, gaskets and friction parts. The mining, milling and fabrication of asbestos containing products has resulted in its release to the environment through various waste streams. The last operating US asbestos mine closed in 2002. If released to air, asbestos fibers will eventually return to soil or water through gravitational settling and wet and dry deposition. Mean airborne concentrations of asbestos in US cities are roughly 2-4 ng/cu m, but much higher levels are typically observed near source dominated areas. Movement of asbestos fibers through soils only occur during runoff or erosion. Asbestos fibers will not volatilize or degrade in soils although they may be resuspended to the air by vehicular traffic or mining operations. Asbestos may be released to water from waste water in asbestos related industries, erosion of natural deposits or waste piles, corrosion of asbestos-cemented pipes, disintegration of asbestos containing roofing materials followed by subsequent runoff. Asbestos does not volatilize or degrade from water surfaces, nor does it appear to bioconcentrate in aquatic organisms. Occupational exposure occurs through inhalation and dermal contact in workplaces where asbestos is mined, milled, and products are manufactured or used. Monitoring data suggest that the general population is exposed to asbestos through inhalation of ambient air, ingestion of drinking water, and ingestion of food sources containing asbestos. In the past, filters made from asbestos were employed in the preparation of wines, beers, cigarette filters and other consumer products; however, these practices have been discontinued and intake of asbestos through foods and drugs is now unlikely. Low levels of asbestos are present in some talc powders, but the level of exposure from this source is considered low. (SRC) Probable Routes of Human Exposure: Asbestos /enters the human body/ from gastrointestinal and respiratory tract exposure. Asbestos is usually taken into the body by inhalation or ingestion and it is then distributed to most organs via the blood or lymphatic systems. ASBESTOS FIBERS MAY BE LIBERATED INTO AIR ... IN MINING, MILLING, PROCESSING, OF ASBESTOS CONTAINING PRODUCTS & DUMPING WASTE. ... FIBERS LESS THAN 3 UM IN DIAM & FROM 10-200 UM IN LENGTH ARE MOST IMPORTANT CAUSE OF ASBESTOSIS. CONTENTS & TYPES OF ASBESTOS IN FIREPROOFING INSULATION MATERIALS SPRAYED ON CEILINGS OF 127 BUILDINGS THROUGHOUT THE USA WERE STUDIED. DURING REMOVAL OF SPRAYED MATERIALS, WORKERS WERE EXPOSED TO EXTREMELY HIGH CONCENTRATIONS (AVG 16.4 FIBERS/CC) WHEN DRY METHODS WERE USED. WHEN WET METHODS WERE USED DURING REMOVAL, THE AIRBORNE FIBER CONCENTRATIONS WERE REDUCED TO LESS THAN 2 FIBERS/CC. ... EXPOSURES OCCUR DURING END-PRODUCT USE, AMONG ASBESTOS INSULATION WORKERS, AMONG BRAKE REPAIR & BRAKE MAINTENANCE WORKERS, & AS RESULT OF INDIRECT OCCUPATIONAL EXPOSURES, PARTICULARLY IN SHIP BUILDING & SHIP REPAIR, & IN CONSTRUCTION INDUSTRY. OTHER EXPOSURES OCCUR IN RELATION TO INSPECTION & MAINTENANCE WORK ON ASBESTOS CONTAINING STRUCTURES & EQUIPMENT, IN REFINERIES & CHEMICAL PLANTS, BUILDINGS, RAILWAY LOCOMOTIVES & WAGONS, SHIPYARDS & POWER PLANTS. ... BUILDING DEMOLITION & WASTE DISPOSAL. ... EXPOSURE MAY OCCUR DURING WEARING OF ASBESTOS SAFETY GARMENTS. Talc /which is often contaminated with asbestos/ is used in the following products: cosmetics, spray and dusting powder, insecticides, white shoe polishes, as a filler for soap, dusting powders for toy balloons, condoms, and contraceptive diaphragms. Insulation workers using asbestos materials and automotive brake repairmen have been exposed to airborne asbestos levels up to 133 and 72 fibers/cu m, respectively. Exposure to airborne asbestos in the home may /result from use of/ spackling compounds, certain types of insulation, and some workers may bring home some material ... on their work clothing. Exposure profiles for respirable silica dust in 15 mining industry groups that were prepared from the 1977-1981 Mine Safety and Health Administration (MSHA) MIDAS files are presented as probability distribution graphs. The dust exposure data have been organized into data sets according to industry group, operation category, and location (surface and underground) as discussed in this report. There are 15 industry groups: copper, gold and silver, iron, lead and zinc, molybdenum, uranium, other metals, limestone, other stone, clay and shale, asbestos, talc, oil shale, sand and gravel, and other nonmetals. Operation and location are classified into 14 categories: surface drilling; underground drilling, blasting, cutting and boring; surface production; surface mobile transport; surface haulageway maintenance; underground production; underground haulageway maintenance; crushing or grinding, and sizing; concentrating and finishing; non specific surface; and non specific underground. Occupational settings in which individuals who may be at risk from indirect exposure to asbestos include: gold mining, cigarette filter manufacture, automobile transmission parts manufacture, dentistry, and agriculture. Asbestos is present in the soil, water and air, and may be added to these media from mining, wearing of automobile brake linings, asbestos textile manufacturing, asbestos spraying for fireproofing, and the use of asbestos in construction materials. The multitude of uses for this non-combustible insulating material means that exposure may be both occupational and non-occupational (environmental); for most people, exposure to at least a low level of asbestos ocurs on a daily basis. ... Dietary materials that have been reported to contain, or are likely to contain, asbestos include foods such as vegetable oil, lard, mayonnaise, ketchup and meats ... and beverages such as beers, sherries, ports, vermouth and soft drinks. Currently, all major commercial asbestos varieties, chrysotile, amosite, and crocidolite, have been found to produce a significant incidence of asbestos-related disease among workers ocupationally exposed in mining and milling, in manufacturing, and in the use of materials containing the fiber. The predominant route of exposure has been inhalation, although some asbestos may be swallowed directly or after being brought up from the rspiratory tract. Not only has asbestos disease been found among individuals exposed to the fiber directly as a result of excessive work exposures in decades past, but asbestos-associated cancer has also been identified, albeit less frequently, among those with inhalation exposures of lesser intensity, including those who had worked near the application or removal of asbestos material, those with history or residing in the vicinity of asbestos plants, and those who had lived in the household of an asbestos worker. DOMESTIC EXPOSURE OF HOUSEHOLD CONTACTS TO ASBESTOS MAY OCCUR FROM DUSTS BROUGHT HOME ON WORKERS' CLOTHES, SHOES, HAIR, EQUIPMENT, ETC. ... ASBESTOS LEVELS /WERE FOUND/ RANGING FROM 100-500 NG/CU M IN THE HOUSES OF WORKMEN. Certain beverages are either made from water already containing asbestos fibers or are clarified (beer, wine) by filtration through asbestos filter pads from which fibers may be released. The asbestos fiber levels in other foods are largely unknown. The hazard from environmental asbestos exposure showed that mesothelioma could occur among individuals whose potential asbestos exposure consisted of having resided near an asbestos factory or in the household of an asbestos worker. Twenty of 76 cases from the files of the London hospital were the result of such exposures. A field study was conducted to measure asbestos fiber concentrations during brake repair for mechanics in the Federal Republic of Germany. In addition to asbestos air sampling, 210 occupational histories describing working conditions under which brake maintenance is carried out were evaluated. Ninety dust concentration measurements in 76 service stations with static and personal samplers during brake maintenance operations. Sampling times varied from less than 3 min to more than 1 hr depending on the duration of the work operation. Samples were analyzed by phase contrast microscopy and scanning transmission electron microscopy. Fiber concentrations during brake service operations were 0.1X10+6/cu m (0.1 fiber per cc) on average. Average fiber dosages (fiber concentration X sampling time) ranged from 4X10+6 fiber/cu m/min for dry brushing and grinding to 10X10+6 fibers/cu m/min for machine grinding. Electron microscopy of brake drum dust indicated very high concentrations of short fibers; fibers with lengths > 5 um constituted less than 1% of all the chrysotile fibers counted. Average Daily Intake: Assuming that asbestos is present at the highest accurate concentration, ie, > 9999.99 million fibers/liter the daily intake for a 70 kg adult male consuming 2 liters of drinking water/day would be > 20 billion fibers/day. Natural Pollution Sources: Asbestos is a term for six naturally occurring fibrous silicate minerals that are mined and used in many commercial products(1). Asbestos is a natural contaminant of talc. ... Asbestos represents less than 1% of the samples of cosmetic talcs tested. Artificial Pollution Sources: The mining and milling of asbestos for end use in insulating products, friction parts, roofing materials and many other applications(1), has led to its release to the environment through various waste streams(SRC). Environmental Fate: TERRESTRIAL FATE: Movement of asbestos fibers only occur during runoff or erosion. Asbestos fibers will not volatilize or degrade although they may be resuspended to the air by vehicular traffic over unpaved soil surfaces containing asbestos or through mining and milling operations. AQUATIC FATE: The importance of the transport of asbestos from the surface of aquatic environments by wind-activated aerosol formation is presently indeterminate. Asbestos will not volatilize or degrade in water. ATMOSPHERIC FATE: Asbestos released to the air will eventually settle out by gravitational settling and dry deposition. Environmental Biodegradation: Asbestos is considered to be non-biodegradable by aquatic organisms. Environmental Abiotic Degradation: Certain forms of asbestos may undergo dissolution under acidic conditions. This should not be confused with solubility, which is the amount of material that dissolves in solution before it reaches chemical equilibrium. Under acidic conditions, magnesium hydroxide may leach from the outer brucite layer of amosite and chrysotile, but the basic silicate structure of the fiber remains intact (1). The other forms of asbestos are generally resistant to dissolution under acidic or alkaline conditions(1). Environmental Bioconcentration: No evidence was found regarding the bioaccumulation of asbestos in aquatic organisms. Soil Adsorption/Mobility: It appears that asbestos does not have an adsorptive affinity for the solids normally found in natural water systems; however, some materials, notably trace metals and organic cmpd, have an affinity for asbestos minerals. Volatilization from Water/Soil: Asbestos fibers will not volatilize from water or soil surfaces. (SRC) Environmental Water Concentrations: DRINKING WATER: IN 1973, AMPHIBOLE ASBESTOS FIBERS WERE DISCOVERED IN THE MUNICIPAL WATER SUPPLY OF DULUTH, MINNESOTA. THE ENTIRE CITY POPULATION OF APPROX 100,000 WAS EXPOSED FROM THE LATE 1950S THROUGH 1976 AT LEVELS OF 1-65 MILLION FIBERS/L OF WATER. DRINKING WATER: Asbestos (millions of fibers/l) in Canadian drinking water: Belleville: Bay of Quinte: 0.533; Brantford: Grand River: 0.570; Brockville: St. Lawrence River: 0.446 (no filtration plant) Chatham: Thames River: 0.595; Cornwall: St. Lawrence River: 2.11; Hamilton: Lake Ontario: 0.456; Niagara Falls: Niagara River: 2.58; North Bay: Trout Lake: 0.384 (no filtration plant); Oshawa: Lake Ontario: 0.557; Ottawa: Ottawa River: 0.136; Pembroke: Ottawa River: 2.85; Peterborough: Otonabee River: 1.86; Port Colborne: Welland Ship Canal: 0.608; Sarnia: Lake Huron: 3.87 (no filtration plant); Sault St. Marie: St. Marys River: 0.248; St. Catharines: Welland Ship Canal: 1.03; St. Thomas: Lake Erie: 1.60; Sudbury: Ramsey Lake: 0.297 (no filtration plant); Toronto: Lake Ontario: 1.90; Welland: Welland Ship Canal: 0.820. /Data derived from table/ DRINKING WATER: Asbestos content from Canadian rivers and lakes, and in drinking water /is as follows/: Ottawa, Ottawa River, tap water: 2.0x10+6 fibers/l; Toronto, Lake Ontario, tap water: 4.4x10+6 fibers/l; Montreal, St. Lawrence River, tap water: 2.4x10+6 fibers/l; Hull, Ottawa River, tap water: 9.5x10+6 fibers/l (water supply unfiltered); Beauport, St. Lawrence River, tap water: 8.1x10+6 fibers/l (water supply unfiltered); Drummondville, St. Francais River, tap water: 2.9x10+6 fibers/l; Thetford Mines, Lac a la Truite, tap water, 172.7x10+6 fibers/l (water supply unfiltered); Ottawa top 30 cm melted snow, 33.5x10+6 fibers/l; Ottawa, Ottawa River, river water, 9.5x10+6 fibers/l. /Data derived from table/ DRINKING WATER: Drinking waters from Thetford mines, Quebec, site of a major asbestos deposit and mine, contained up to 170x10+6 fibers of asbestos per l. DRINKING WATER: Water concentrations of asbestos are usually less than 1x10+6 fibers of all sizes per liter although significantly higher values (1x10+8 fibers/l) have been found in circumstances where water systems have been in contact with asbestiform minerals or where contamination of water supply exists. Fiber mass concentrations corresponding to fiber concentrations are usually less than 0.01 ug/l. Thus, direct water ingestion usually leads to exposure of less than 0.02 ug/day. DRINKING WATER: ... Data suggest that 1x10+6 fibers corresponds to from 2x10-4 to 2x10-3 ug in water systems. Data on asbestos concentrations from erosion of fibers from asbestos/cement cooling tower panels indicate that the mass of 1x10+6 fibers is from 0.01 to 0.2 ug. Samples from 365 cities have been collected and analyzed by electron microscopy by the USEPA. Of these, 45% had detectable levels of asbestos, usually of the chrysotile variety. Effluent Concentrations: In 1992, EPA estimated that air emissions from asbestos processing, including mining, milling, manufacturing, and fabrication were about 2,240 pounds annually(1). Estimated air emissions from waste disposal is about 499,000 pounds per year(1). The total amount of asbestos released to water in the US is estimated as 110,000 to 220,000 pounds per year(1). Most of these releases arise from waste water in asbestos related industries, but other sources are erosion of natural deposits and waste piles, corrosion of asbestos-cemented pipes, disintegration of asbestos containing roofing materials with subsequent runoff into cisterns sewers etc(1). Currently friable asbestos containing waste may only be deposited in landfills that are approved by the federal government. In 1999, 13,573,783 pounds of asbestos (friable) were deposited in land by 87 US facilities that produced, processed or used asbestos products(1). Sediment/Soil Concentrations: Although the serpentine and amphibole mineral groups occur over a wide range geological environments, the preponderance of these minerals are non fibrous(1). No studies were located regarding the concentration of asbestos fibers that occur in soil, however, asbestos was detected in about 80% of the samples of street dirt studied at concentrations ranging from 100 million to 1 billion fibers/g (1). Atmospheric Concentrations: URBAN/SUBURBAN: Mean airborne concentrations of asbestos in US cities are 2.1-4.3 ng/cu m(1). Measurements using electron microscopic techniques have established the presence of asbestos in the urban ambient air, usually at concentrations less than 10 ng/cu m(2). Concentrations of 100 ng/cu m to 1000 ng/cu m have been measured near specific asbestos emission sources, in schools where asbestos containing materials are used for sound control, and in office buildings where similar materials are used for fire control(2). SOURCE DOMINATED: During 1973, the dust levels from Canadian asbestos mines and mills were as high as 83 fibers/cu m. Average airborne asbestos concentrations in chrysotile mining towns in Quebec were 80,000 fibers/cu m in 1973-1974, but were reduced to 7,000 fibers/cu m in 1982(1). The geometric mean concentration of asbestos 200 meters from cement, friction parts, textile, ground tile, insulation and refractory factories in Taiwan were 6,000, 8,000, 12,000, 33,000, 12,000, and <100 fibers/cu m, respectively as measured by transmission electron microscopy(2). These levels generally declined as a function of the distance the measurements were made from the factory. MEAN AIR CONCN OF AMPHIBOLE FIBERS IN COMMUNITIES SURROUNDING MILLING OPERATIONS HAVE BEEN REPORTED TO RANGE FROM 2.6-8.9X1X10+3 FIBERS/CU M. ... CONCN OF AS HIGH AS 11X1X10+6 AMPHIBOLE FIBERS/CU M OF AIR WERE REPORTED NEAR SPECIFIC POINT EMISSION SOURCES. /AMPHIBOLE FIBERS/ SOURCE DOMINATED: The ambient air concentrations near the Union Carbide mill and waste pile in King City, CA and near the Johns-Manville mill and water dump in Coalinga, CA were 1.03 million fibers/cu m and 593 million fibers/cu m, respectively. Air concentrations over 24 hours in metropolitan areas usually are less than 5 ng/cu m but can range up to 20 ng/cu m. Values up to 50 ng/cu m are found during daytime hours in locations were construction activities and traffic can be contributing sources. A significant fraction of the fibers inhaled can be brought up from the respiratory tract and swallowed. This leads to an ingestion exposure from air sources of up to 0.1 ug/day, although most of the population exposure is from 0.01 to 0.05 ug/day. 3 different /USA/ laboratories ... found that the average fiber concn of asbestos dust in insulation work between 1968 and 1971 ranged from about 3 to 6 fibers/ml. ... In the Devonport Naval Dockyard in Great Britain ... 8.9 fibers/ml /was obtained/ for the average of long-term samples of asbestos concn. ... Peak exposures could ... exceed 100 fibers/ml /for 2 to 5 minute concn of asbestos/ during the mixing of cement. Food Survey Values: Asbestos content is specified for the following: Canadian beer: 4.3-6.6x10+6 fibers/l; USA beer: 1.1-2.0x10+6 fibers/l; Spanish sherry: 2.0x10+6 fibers/l; Canadian sherry: 4.0x10+6 fibers/l; South African sherry: 2.6x10+6 fibers/l; Canadian port: 2.1x10+6 fibers/l; French vermouth: 1.8x10+6 fibers/l; Italian vermouth: 11.7x10+6 fibers/l; French wine: 64.0x10+6 fibers/l; Ginger ale: 12.2x10+6 fibers/l; Tonic water: 1.7x10+6 fibers/l; Orange (softdrink): 2.5x10+6 fibers/l. /Data derived from table/ Fish/Seafood Concentrations: Asbestos mine tailings from a mill in Germany were dumped in a region containing large numbers of mussel beds. Mussels were examined after exposure to water containing asbestos in concentrations up to 100 mg/l. Fibers penetrated the epithelial tissue of the stomach and the intestinal tract and were present even when the mussels were kept for several weeks in unpolluted water. Other Environmental Concentrations: Measurements using electron microscopic techniques have established the presence of asbestos in the urban ambient air, usually at concentrations less than 10 ng/cu m. Concentrations of 100 ng/cu m to 1000 ng/cu m have been measured near specific asbestos emission sources, in schools where asbestos containing materials are used for sound control, and in office buildings where similar materials are used for fire control. Environmental Standards & Regulations: TSCA Requirements: The Asbestos-in-Schools Identification and Notification Rule effective June 28, 1982, required all public and private local education agencies (LEAs) to (1) inspect for friable materials; (2) sample and analyze these materials when found; (3) post notice of inspection results and notify employees and parents in schools with asbestos containing friable materials (ACFM); and (4) maintain records of the findings at the local education agencies and schools. A stratified systematic sample of 1,800 public and 800 private local education agencies was randomly selected proportionate to the square root of enrollment. A telephone survey found that 83% of the local education agencies have begun or completed inspections and 94% of all schools have been inspected. Of the schools inspected, 35% found asbestos containing friable materials. Almost all local education agencies asbestos containing friable materials have abatement programs (93%), about 1/3 of which (31%) are operations/maintenance only. Only 9% of the local education agencies were in compliance with the rule by June 28, 1983, the rule's compliance date; and 11% were by January 1984, the date of the survey. Record-keeping and notification were the major problem areas of noncompliance. QA site visits were made to 38 local education agencies and 94 schools within these local education agencies were inspected. The local education agencies data collected during the site visits agreed substantially with the telephone survey data. Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and Safety Data Reporting Rule. The section 8(d) model rule requires manufacturers, importers, and processors of listed chemical substances and mixtures to submit to EPA copies and lists of unpublished health and safety studies. Asbestos is included on this list. CERCLA Reportable Quantities: Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 1lb or 0.454 kg. The toll free number of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area (202) 426-2675. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b). /The RQ for asbestos is limited to friable forms only./ Atmospheric Standards: Asbestos has been designated as a hazardous air pollutant under section 112 of the Clean Air Act. National Emission Standards for Hazardous Air Pollutants. Asbestos air emission standards are described for asbestosmills; roadways; manufacturing; demolition and renovation; spraying; fabricating; insulating materials; waste disposal for asbestos mills; waste disposal for manufacturing, fabricating, demolition, renovation and spraying operations; inactive waste disposal sites for asbestos mills and manufacturing and fabricating operations; air-cleaning; reporting; active waste disposal sites; operations that convert asbestos-containing waste material into nonasbestos (asbestos free) material. Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Asbestos is included on this list. Clean Water Act Requirements: Toxic pollutant designated pursuant to section 307(a)(1) of the Federal Water Pollution Control Act and is subject to effluent limitations. Federal Drinking Water Standards: EPA 7 mf/l (million fibers/l) FDA Requirements: Asbestos is an indirect food additive for use only as a component of adhesives Polyester resins, cross-linked. Optional adjuvant substances employed to facilitate the production of the resins or added thereto to impart desired technical or physical properties include the following, provided that the quantity used does not exceed that reasonably required to accomplish the intended physical or technical effect and does ot exceed any limitations prescribed in this section. Asbestos use as a reinforcement in included on this list. Phenolic resins in molded articles. Optional adjuvant substances employed in the production of the phenolic resins or added thereto to impart desired technical or physical properties. Asbestos fiber is included on this list. Chemical/Physical Properties: Molecular Formula: UVCB Color/Form: FINE, SLENDER, FLAXY FIBERS Odor: ... Odorless ... Other Chemical/Physical Properties: Blue... fibrous ... solids. /Crocidolite/ Magnesium ... which occurs naturally in asbestos ... contributes to the surface charge of the asbestos fibers. Cobalt blue to lavender blue /Crocidolite/ Decomposition point: 950 deg C /Anthophylite/. 800 deg C /Crocidolite/. Index of refraction: 1.65-1.72 /Crocidolite/ Tensile strength: 1400-4600 Mpa /Crocidolite/ Of mineral origin, asbestos does not burn, does not rot, and, dependent on the variety, possesses extremely high tensile strength as well as resistance to acids, bases, and heat. Similarly, when processed into long, thin fibers, asbestos is sufficiently soft and flexible to be woven into fire resistant fabrics. Chemical composition, ((Mg,Fe)7Si8O22(OH)2)n /Anthophyllite/ Chemical composition, (Ca2(Mg,Fe)5Si8O22(OH)2)n /Actinolite/ Chemical composition, (NaFe3(2+)Fe2(3+)Si8O22(OH)2)n /Crocidolite/ Tensile strength of the asbestos fiber is an important and highly significant physical property. The tensile strength values for the different asbestos varieties should be considered as relative for the different variety rather than specific, since all these measured values are far less than the theoretical value of over 10,000 MPa (1.45X10+6 psi) attributable to silicate chain structures. Physical strengths of asbestos are adversely affected by elevated temperatures. The typical tensile strengths of asbestos fibers have the order: crocidolite > chrysotile > amosite > anthophyllite > tremolite > actinolite Commercial amphiboles are harsh fibers. They are relatively stiff, brittle, and coarser in diameter than crysotile, and rodlike in appearance under the microscope. /Amphiboles/ The structure of all the amphiboles consists of two chains or ribbons based on Si4O11 units separated by a band of cations. Seven cations form the basal unit. Two hydroxyl groups are attached to the central cation in each unit cell. These hydroxyls ... are contained entirely within the amphibole structure. The final structure is composed of stacks of these sandwich ribbons. The bonding between these ribbons is rather weak & the crystals are easily cleaved parallel to the ribbons ... If the cleavage is very facile, the result is an asbestiform mineral. /Amphiboles/ ... The amphibole asbestos fibers dehydroxylate and decompose at elevated temperatures. The presence of large quantities of iron (particularly ferrous iron) makes the decomposition or thermal analysis determinations particularly complex and very dependent on the composition of the atmosphere. ... Compared to crysotile, the amphibole fibers are relatively acid resistant. However, under boiling conditions and high acid concn the amphiboles can exhibit wt losses of approx 2-20%. ... Amphiboles fibers have a negative charge ... The magnitude of the charge exhibited by the amphiboles is substantially lower than chrysotile's. /Amphiboles/ Relative order of acid resistance is: tremolite > anthophyllite > crocidolite > actinolite > amosite > chrysotile. Amphibole fibers do not divide into fibrils as fine in diameter or as symmetrical as the chrysotile variety. Ultimate diameter of amphiboles have been reported to be about 0.1 um and the surface areas of amphibole asbestos are considerably smaller than chrysotile. /Amphiboles/ Fully fiberized commercial grades of crocidolite have surface areas by gas adsorption of 3-15 sq m/g. /Crocidolite/ Structure: lamellar, fibrous asbestiform; mineral association: in crystalline schists and gneisses; origin: metamorphic, usually from olivine; veining: slip, mass fiber unoriented and interlacing; essential composition: magnesium silicate with iron; crystal structure: prismatic, lamellar to fibrous; crystal system: orthorhombic; color: gray white, brown, gray, or green; luster: viterous to pearly; Mohs hardness: 5.5-6.0; specific gravity: 2.85-3.1; cleavage: 110%; optical properties: biaxial positive extinction parallel; index of refraction: about 1.61; Seger cones fusibility: infusible or difficult to fuse; flexibility: very brittle, nonflexible; length: short; texture: harsh; acid resistance: fairly resistant to acids; spinnability: poor; specific heat: 879 J/kg deg K or 0.210 Btu/lb deg F. /Anthophyllite/ Structure: fibrous in iron stones; mineral association: in iron rich silicious argillite in quartzose schists; origin: regional metamorphism; veining: cross fiber; essential composition: silicate of sodium and iron water; crystal structure: fibrous; crystal system: monoclinic; color: lavender, blue; luster: silky to dull; Mohs hardness: 4; specific gravity: 3.2-3.3; cleavage: 110%; optical properties: biaxial extinction inclined; index of refraction: 1.7 pleochroic; Seger cones fusibility: fusible at 3, 1145-1170 deg C; flexibility: fair to good; length: short to long; texture: soft to harsh; acid resistance: fairly resistant to acids; spinnability: fair; specific heat: 841 J/kg deg K or 0.201 Btu/lb deg F. /Crocidolite/ Structure: reticulated long prismatic crystals & fibers; mineral association: in limestone & in crystalline schists; origin: results of contact metamorphism; veining: slip or mass fiber; essential composition: calcium, magnesium, and iron silicates, water up to 5%; crystal structure: long & thin columnar to fibrous; crystal system: monoclinic; color: green; luster: silky; Mohs hardness: about 6; specific gravity: 3.0-3.2; cleavage: 110%; optical properties: biaxial negative extinction inclined; index of refraction: 1.63 weakly pleochroic; Seger cones fusibility: fusible at 4, 1165-1190 deg C; flexibility: brittle and nonflexible; length: short to long; texture: harsh; acid resistance: relatively insol in hydrochloric acid; spinnability: poor; specific heat: 908 J/kg deg K or 0.217 Btu/lb deg F. /Actinolite/ Asbestos minerals, despite a relatively high fusion temperature, are completely decomposed at temperatures of 1000 deg C. Both the dehydroxylation temperature and decompostion temperature increase with increased magnesium oxide content among the various amphibole species. ... Most materials have a negative surface charge in aqueous systems. However, since chrysotile has a positive charge, it will attract, or be attracted to, most dispersed materials. The highly reactive surface of asbestos causes many surface reactions which are intermediate between simple absorption and a true chemical reaction. The absorption of various materials on the surface of chrysotile has a greater affinity for polar molecules (eg water, ammonia) than for non-polar molecules. Amphiboles can ... occur in nonfibrous forms which may result because of structural disorder. The dominant cations are magnesium, ferrous, ferric, sodium, and calcium. Minor isomorphic substitutions of aluminum, titanium, potassium, and lithium also occur. Because of the wide compositional range, the amphiboles are often assigned to three generic series; ie, the anthophyllite cummingtonite series, the calcic amphiboles and the soda amphiboles. /Amphiboles/ Chemical Safety & Handling: DOT Emergency Guidelines: Fire or explosion: Some may burn but none ignite readily. Those substance designated with a "P" may polymerize explosively when heated or involved in a fire. Containers may explode when heated. Some may be transported hot. /Asbestos; Asbestos, blue; Asbestos, brown; Asbestos, white/ Health: Inhalation of material may be harmful. Contact may cause burns to skin and eyes. Inhalation of asbestos dust may have a damaging effect on the lungs. Fire may produce irritating, corrosive and/or toxic gases. Runoff from fire control may cause pollution. /Asbestos; Asbestos, blue; Asbestos, brown; Asbestos, white/ Public safety: CALL Emergency Response Telephone Number. ... Isolate spill or leak area immediately for at least 10 to 25 meters (30 to 80 feet) in all directions. Keep unauthorized personnel away. Stay upwind. /Asbestos; Asbestos, blue; Asbestos, brown; Asbestos, white/ Protective clothing: Wear positive pressure self-contained breathing apparatus (SCBA). Structural firefighters' protective clothing will only provide limited protection. /Asbestos; Asbestos, blue; Asbestos, brown; Asbestos, white/ Evacuation: Fire: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. /Asbestos; Asbestos, blue; Asbestos, brown; Asbestos, white/ Fire: Small fires: Dry chemical, CO2, water spray or regular foam. Large fires: Water spray, fog or regular foam. Move containers from fire area if you can do it without risk. Do not scatter spilled material with high pressure water streams. Dike fire-control water for later disposal. Fire involving tanks: Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from engulfed in fire tanks. /Asbestos; Asbestos, blue; Asbestos, brown; Asbestos, white/ Spill or leak: Do not touch or walk through spilled material. Stop leak if you can do it without risk. Prevent dust cloud. Avoid inhalation of asbestos dust. Small dry spills: With clean shovel place material into clean, dry container and cover loosely; move containers from spill area. Small spills: Take up with sand or other noncombustible absorbent material and place into containers for later disposal. Large spills: Dike far ahead of liquid spill for later disposal. Cover powder spill with plastic sheet or tarp to minimize spreading. Prevent entry into waterways, sewers, basements or confined areas. /Asbestos; Asbestos, blue; Asbestos, brown; Asbestos, white/ First aid: Move victim to fresh air. Call 911 or emergency medical service. Apply artificial respiration if victim is not breathing. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. Ensure that medical personnel are aware of the material(s) involved, and take precautions to protect themselves. /Asbestos; Asbestos, blue; Asbestos, brown; Asbestos, white/ Fire Fighting Procedures: If material involved in fire: Extinguish fire using agent suitable for type of surrounding fire. (Material itself does not burn or burns with difficulty.) Keep run-off water out of sewers and water sources. Hazardous Decomposition: Asbestos minerals, despite a relatively high fusion temperature, are completely decomposed at temperatures of 1,000 deg C. The resistance of the asbestos fibers to attack by reagents other than acid is excellent up to temperatures of approximately 100 deg C with rapid deterioration observed at higher temperatures. Immediately Dangerous to Life or Health: NIOSH considers asbestos to be a potential occupational carcinogen. Protective Equipment & Clothing: If an employee is exposed to asbestos above the /OSHA/ TWA and/or excursion limit, or where the possibility of eye irritation exists, the employer /is required to/ provide at no cost to the employee and ensure that the employee uses appropriate protective work clothing and equipment such as, but not limited to: Coverall or similar full-body work clothing; Gloves, head coverings, and foot coverings; and Face shield, vented goggles, or other appropriate protective equipment which complies with /the OSHA Asbestos standard/. Basic protection ... coveralls ... made of cotton polyester material. Cotton alone cannot be used because static build-up causes fibers to adhere to cloth. ... Provide head covering /such as/ surgical caps. Foot coverings, /such as/ canvas booties, rubber galoshes, or safety shoes /should be used/. Airborne concentration of asbestos or conditions of use: not in excess of 1 fibers/cc (10 times PEL); Required respirator: half-mask air-purifying respirator other than a disposable respirator, equipped with high efficiency filters. Airborne concentration of asbestos or condition of use: not in excess of 5 fibers/cc (50 times PEL); Required respirator: full facepiece air-purifying respirator equipped with high efficiency filters. Airborne concentration of asbestos or condition of use: not in excess of 10 fibers/cc (100 times PEL); Required respirator: any powered air-purifying respirator equipped with high efficiency filters or any supplied air respirator operated in continuous flow mode. Airborne concentration of asbestos or condition of use: not in excess of 100 fibers/cc (1,000 times PEL); Required respirator: full facepiece supplied air respirator operated in pressure demand mode. Airborne concentration of asbestos or condition of use: greater than 100 fibers/cc (1,000 times PEL) or unknown concentration; Required respirator: full facepiece supplied air respirator operated in pressure demand mode, equipped with an auxiliary positive pressure self-contained breathing apparatus. Respirator Recommendations: Escape: (Assigned protection factor = 50) Any air-purifying, full-facepiece respirator with a high-efficiency particulate filter/Any appropriate escape-type, self-contained breathing apparatus. Wear appropriate personal protective clothing to prevent skin contact. Wear appropriate eye protection to prevent eye contact. The employer shall institute engineering controls and work practices to reduce and maintain employee exposure to or below the TWA and/or excursion limit prescribed in paragraph (c) of /the OSHA asbestos standards/, except to the extent that such controls are not feasible. Wherever the feasible engineering controls and work practices that can be instituted are not sufficient to reduce employee exposure to or below the TWA and/or excursion limit prescribed in paragraph (c) of /the OSHA asbestos standard/, the employer shall use them to reduce employee exposure to the lowest levels achievable by these controls and shall supplement them by the use of respiratory protection that complies with the requirements of paragraph (g) of /the OSHA standard/. For the following operations, wherever feasible engineering controls and work practices that can be instituted are not sufficient to reduce the employee exposure to or below the TWA and/or excursion limit prescribed in paragraph (c) of /the OSHA asbestos standard/, the employer shall use them to reduce employee exposure to or below 0.5 fiber/cu cm of air (as an 8-hr time-weighted average) or 2.5 fibers/cc for 30 minutes (short-term exposure) and shall supplement them by the use of any combination of respiratory protection that complies with the requirements of paragraph (g) of /the OSHA asbestos standard/, work practices and feasible engineering controls that will reduce employee exposure to or below the TWA and to or below the excursion limit permissible prescribed in paragraph (c) of /the OSHA asbestos standard/: Coupling cutoff in primary asbestos cement pipe manufacturing; sanding in primary and secondary asbestos cement sheet manufacturing; grinding in primary and secondary friction product manufacturing; carding and spinning in dry textile processes; and grinding and sanding in primary plastics manufacturing. Respirators may always be necessary during the cleaning or repair of exhaust ductwork or during manual shakedown of collection bags in baghouses. ... This form of protection may be the only feasible method of controlling asbestos exposure during the removal of thermal insulation or the application of some asbestos products. ... The type of respirator needed ... will be indicated by the concn of airborne asbestos fiber. ... Respirators require proper fitting, maintenance, and cleaning to be effective. Local exhaust ventilation and dust collection systems shall be designed, constructed, installed, and maintained in accordance with good practices such as those found in the American National Standard Fundamentals Governing the Design and Operation of Local Exhaust Systems, ANSI Z9.2–1979. All hand-operated and power-operated tools which would produce or release fibers of asbestos, such as, but not limited to, saws, scorers, abrasive wheels, and drills, shall be provided with local exhaust ventilation systems which comply with paragraph (f)(1)(iv) of /the OSHA asbestos standard/. Insofar as practicable, asbestos shall be handled, mixed, applied, removed, cut, scored, or otherwise worked in a wet state sufficient to prevent the emission of airborne fibers so as to expose employees to levels in excess of the TWA and/or excursion limit, prescribed in paragraph (c) of /the OSHA asbestos standard/, unless the usefulness of the product would be diminished thereby. No asbestos cement, mortar, coating, grout, plaster, or similar material containing asbestos, shall be removed from bags, cartons, or other containers in which they are shipped, without being either wetted, or enclosed, or ventilated so as to prevent effectively the release of airborne fibers. Compressed air shall not be used to remove asbestos or materials containing asbestos unless the compressed air is used in conjunction with a ventilation system which effectively captures the dust cloud created by the compressed air. Sanding of asbestos-containing flooring material is prohibited. /Workers/ are required to wear a respirator when performing tasks that result in asbestos exposure that exceeds the permissible exposure limit (PEL) of 0.1 f/cc. ...Air-purifying respirators equipped with a high-efficiency particulate air (HEPA) filter can be used where airborne asbestos fiber concentrations do not exceed 2 f/cc; otherwise, air-supplied, positive-pressure, full facepiece respirators must be used. Disposable respirators or dust masks are not permitted to be used for asbestos work. For effective protection, respirators must fit your face and head snugly. ...Employers /are/ required to conduct fit tests when /employees/ are first assigned a respirator and every 6 months thereafter. Respirators should not be loosened or removed in work situations where their use is required. Preventive Measures: SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place. SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Prevention of dust prodn & its effective control at the site of prodn is the basis of technical control. Once the dust is airborne in the general atmosphere, its elimination & control become expensive & relatively ineffective. Thus, successful technical control starts with enclosing machines & applying local exhaust ventilation at points where the equipment has to be opened, for example where bags of fiber are fed into mixers or the fiber comes out of the machine at the bagging end of the mills. Damping of the fiber before mixing with other products & during spinning & weaving can greatly assist the elimination of dust prodn. ... Exhaust ventilation is required where asbestos-containing products are ground, sawn, drilled, or turned, & the cleaning up should be done by vacuum cleaners rather than brushes. The employer shall ensure that employees remove work clothing contaminated with asbestos only in /clean/ change rooms... . The employer shall provide clean change rooms for employees who work in areas where their airborne exposure to asbestos is above the TWA and/or excursion limit. The employer shall ensure that change rooms are... equipped with two separate lockers or storage facilities, so separated as to prevent contamination of the employee's street clothes from his protective work clothing and equipment. The employer shall ensure that employees who work in areas where their airborne exposure is above the TWA and/or excursion limit, shower at the end of the work shift. The employer shall provide shower facilities.../and/ ensure that employees who are required to shower... do not leave the workplace wearing any clothing or equipment worn during the work shift. The employer shall ensure that no employee takes contaminated work clothing out of the change room, except those employees authorized to do so for the purpose of laundering, maintenance, or disposal. Contaminated work clothing shall be placed and stored in closed containers which prevent dispersion of the asbestos outside the container. Containers of contaminated protective devices or work clothing which are to be taken out of change rooms or the workplace for cleaning, maintenance or disposal, shall bear labels... /including the following information: DANGER; CONTAINS ASBESTOS FIBERS; AVOID CREATING DUST; CANCER AND LUNG DISEASE HAZARD/. ...The employer shall clean, launder, repair, or replace protective clothing and equipment required by /OSHA's asbestos standard/ to maintain their effectiveness. The employer shall provide clean protective clothing and equipment at least weekly to each affected employee. The employer shall prohibit the removal of asbestos from protective clothing and equipment by blowing or shaking. Laundering of contaminated clothing shall be done so as to prevent the release of airborne fibers of asbestos in excess of the permissible exposure limits prescribed /by OSHA/. ...Contaminated clothing shall be transported in sealed impermeable bags, or other closed, impermeable containers, and labeled... . The employer shall provide lunchroom facilities for employees who work in areas where their airborne exposure is above the TWA and/or excursion limit. The employer shall ensure that lunchroom facilities have a positive pressure, filtered air supply, and are readily accessible to employees. The employer shall ensure that employees who work in areas where their airborne exposure is above the PEL and/or excursion limit wash their hands and faces prior to eating, drinking or smoking. The employer shall ensure that employees do not enter lunchroom facilities with protective work clothing or equipment unless surface asbestos fibers have been removed from the clothing or equipment by vacuuming or other method that removes dust without causing the asbestos to become airborne. The employer shall ensure that employees do not smoke in work areas where they are occupationally exposed to asbestos because of activities in that work area. The employer shall ensure that employees do not eat, drink, smoke, chew tobacco or gum, or apply cosmetics in the regulated area /where airborne concentrations of asbestos exceed, or there is a reasonable possibility they may exceed a PEL/. ... A strong corporate /policy/ should be established against the practice of eating, drinking, or smoking on the job. These activities should be restricted to a designated, clean location visited only after established decontamination procedures have been followed. Although individual asbestos removal projects vary in terms of the equipment required to accomplish the removal of the materials, some equipment and materials are common to most asbestos removal operations. Plastic sheeting used to protect horizontal surfaces, seal HVAC openings or to seal vertical openings and ceilings should have a minimum thickness of 6 mils. Tape or other adhesive used to attach plastic sheeting should be of sufficient adhesive strength to support the weight of the material plus all stresses encountered during the entire duration of the project without becoming detached from the surface. Other equipment and materials which should be available at the beginning of each project are: HEPA Filtered Vacuum is essential for cleaning the work area after the asbestos has been removed. It should have a long hose capable of reaching out-of-the-way places, such as areas above ceiling tiles, behind pipes, etc. Portable air ventilation systems installed to provide the negative air pressure and air removal from the enclosure must be equipped with a HEPA filter. ...Water spray... used to keep the asbestos material as saturated as possible during removal... . ...Water used to saturate the asbestos containing material can be amended by adding at least 15 mL ( 1/4 ounce) of wetting agent in 1 L (1 pint) of water. An example of a wetting agent is a 50/50 mixture of polyoxyethylene ether and polyoxyethylene polyglycol ester. Backup power supplies are recommended... . Shower and bath water should be with mixed hot and cold water faucets. Water that has been used to clean personnel or equipment should either be filtered or be collected and discarded as asbestos waste. Soap and shampoo should be provided to aid in removing dust from the workers' skin and hair. Warning labels shall be affixed to all raw materials, mixtures, scrap, waste, debris, and other products containing asbestos fibers, or to their containers. ...The labels shall comply with the requirements of 29 CFR 1910.1200(f) of OSHA's Hazard Communication standard, and shall include the following information: DANGER; CONTAINS ASBESTOS FIBERS; AVOID CREATING DUST; CANCER AND LUNG DISEASE HAZARD. Pollution control technology in Canadian asbestos mines and mills ... the industry has taken several steps to improve worker safety ... the amount of airborne dust in the workplace has been reduced by: 1) wet processing of fibers during textile manufacture, and 2) encapsulation of the yarn by chemical dispersing agents which inhibited small asbestos fibrils from breaking away. Sealants /are now available/ which help prevent the release of asbestos from surfaces which are flaking. Do not wear work clothing outside the work area ... this will curtail exposure of other individuals. Use a vacuum to remove asbestos fibers from work clothing. Contact lenses should not be worn when working with this chemical. If material not involved in fire: Keep material out of water sources and sewers. Personnel protection: Avoid breathing dusts. ... Do not handle broken packages unless wearing appropriate personal protective equipment. Wash away any material which may have contacted the body with copious amounts of water or soap and water. Shipment Methods and Regulations: No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./ The International Air Transport Association (IATA) Dangerous Goods Regulations are published by the IATA Dangerous Goods Board pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry carrier regulations to be followed by all IATA Member airlines when transporting hazardous materials. The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals. Detailed recommendations for individual substances and a number of recommendations for good practice are included in the classes dealing with such substances. A general index of technical names has also been compiled. This index should always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or article. Cleanup Methods: Techniques are available to minimize the concentration of asbestos fibers in drinking water. Filtration research conducted at locations on lake superior and in the cascade mountains in Washington has shown that amphibole and chrysotile fibers can be removed by granular media filtration. Pilot scale and distribution system research projects have shown that asbestos cement (AC) pipes can be protected from dissolution and leaching effects that can result in release of asbestos fibers into drinking water. Suggested techniques include modifying low pH, low alkalinity water so they are not aggressive; coating the pipe wall with a chemical precipitate; and applying a cement mortar lining to the pipe wall. Environmental considerations: Land spill: Cover solids with a plastic sheet to prevent dissolving in rain or fire fighting water. Dike surface flow using soil, sand bags, foamed polyurethane, or foamed concrete. Environmental considerations: Water spill: Use natural barriers or oil spill control booms to limit spill travel. Disposal Methods: SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations. Recommendable method: Landfill. Peer-review: No one should handle fibrous or dusty asbestos waste without a suitable ... /NIOSH approved respirator/. Asbestos waste should be put into good quality plastic bags and sealed as it is produced. These bags should then be buried at the landfill without opening, and immediately covered with 1.5-2 m of non-asbestos waste. (Peer-review conclusions of an IRPTC expert consultation (May 1985)) Asbestos is a poor candidate for incineration. Empty shipping bags can be flattened under exhaust hoods and packed into airtight containers for disposal. Empty shipping drums are difficult to clean and should be sealed. Vacuum bags or disposable paper filters should not be cleaned, but should be sprayed with a fine water mist and placed into a labeled waste container. Process waste and housekeeping waste should be wetted with water or a mixture of water and surfactant prior to packaging in disposable containers. Material containing asbestos that is removed from buildings must be disposed of in leak-tight 6-mil thick plastic bags, plastic-lined cardboard containers, or plastic-lined metal containers. These wastes, which are removed while wet, should be sealed in containers before they dry out to minimize the release of asbestos fibers during handling. Occupational Exposure Standards: OSHA Standards: The employer shall ensure that no employee is exposed to an airborne concentration of asbestos in excess of 0.1 fiber/cu cm of air as an 8-hr TWA as determined by the method prescribed in Appendix A to this section, or by an equivalent method. The employer shall ensure that no employee is exposed to an airborne concentration of asbestos in excess of 1.0 fiber/cu cm of air as averaged over a sampling period of 30 min as determined by the method prescribed in Appendix A to this section, or by an equivalent method. Occupational safety and health standard for asbestos. Defines conditions, or the adoption or use of one or more practices, means, methods, operations, or processes, reasonably necessary or appropriate to produce safe or healthful employment and places of employment. Threshold Limit Values: 8 hr Time Weighted Avg (TWA): 0.1 fibers/cc. Respirable fibers: length greater than 5 m; aspect ratio greater than or equal to 3:1, as determined by the membrane filter method at 400-450X magnification (4-mm objective), using phase-contrast illumination. /Asbestos, all forms/ Excursion Limit Recommendation: Excursions in worker exposure levels may exceed three times the TLV-TWA for no more than a total of 30 min during a work day, and under no circumstances should they exceed five times the TLV-TWA, provided that the TLV-TWA is not exceeded. /Asbestos, all forms/ A1; Confirmed human carcinogen. /Asbestos, all forms/ NIOSH Recommendations: NIOSH considers asbestos to be a potential occupational carcinogen and recommends that exposures be reduced to the lowest feasible concentration. For asbestos fibers >5 micrometers in length, NIOSH recommends a REL of 100,000 fibers per cubic meter of air (100,000 fibers/m3), which is equal to 0.1 fiber per cubic centimeter of air (0.1 fiber/cm3), as determined by a 400-liter air sample collected over 100 minutes in accordance with NIOSH Analytical Method #7400. Airborne asbestos fibers are defined as those particles having (1) an aspect ratio of 3 to 1 or greater and (2) the mineralogic characteristics (that is, the crystal structure and elemental composition) of the asbestos minerals and their nonasbestiform analogs. The asbestos minerals are defined as chrysotile, crocidolite, amosite (cummingtonite-grunerite), anthophyllite, tremolite, and actinolite. In addition, airborne cleavage fragments from the nonasbestiform habits of the serpentine minerals antigorite and lizardite, and the amphibole minerals contained in the series cummingtonite-grunerite, tremolite-ferroactinolite, and glaucophane-riebeckite should also be counted as fibers provided they meet the criteria for a fiber when viewed microscopically. Immediately Dangerous to Life or Health: NIOSH considers asbestos to be a potential occupational carcinogen. Other Occupational Permissible Levels: Regulations regarding asbestos levels in air in the workplace, ... United Kingdom: 2 fibers/cu m average over 4 hr for chrysotile, amosite, and anthophyllite also 12 fibers/cu m average over 10 min (for above mentioned fibers), crocidolite 0.2 fibers/cu m average over 10 minutes; Federal Republic of Germany: Chrysotile: 0.15 mg/cu m; Italy: 5 fibers/cu m; Denmark: 2 fibers/cu m, (ban asbestos for insulation work; special permission required to use crocidolite); USSR: 2 mg/cu m (if asbestos content > 10% of total dust; German Democratic Republic: 100 particles/cu m if asbestos content > 40%; South Africa: 2 fibers/cu m; Finland: 5 fibers/cu m (to be lowered to 2 fibers/cu m (ban crocidolite and ban spraying); Norway: 5 fibers/cu m (to be lowered to 2 fibers/cu m); Sweden: 2 fibers/cu m (special permission required to use crocidolite). /Data derived from table/ Manufacturing/Use Information: Major Uses: The largest former use of asbestos was in asbestos cement for products such as pipes, ducts, and flat and corrugated sheets. While asbestos containing corrugated sheets are still available, fiberglass or other materials have now been substituted in place of asbestos in most of these applications. Fiberglass has now been substituted in place of asbestos in most of these applications. Asbestos cement sheets were used in a wide variety of construction applications. Other uses of asbestos include fire resistant textiles, friction materials (i.e., brake linings), underlayment and roofing papers, and floor tiles. Asbestos has been widely used for thermal and electrical insulating purposes. The main characteristic properties of asbestos fibers that can be exploited in industrial applications are their thermal, electrical, and sound insulation; nonflammability; matrix reinforcement (cement, plastic, and resins); adsorption capacity (filtration, liquid sterilization); wear and friction properties (friction materials); and chemical inertia (except in acids). ... Asbestos-cement products mostly for the construction industry and sanitation (sheets, pipes). Crocidolite can be spun & woven using modified cotton industry machinery; the asbestos cloth is used for fireproof clothing & curtains. Inert filler medium (lab and commercial) Reinforcing material in vinyl and asphalt flooring products /former use/ Reinforcing pigment in surface coatings and sealants Reinforcing filler in elastomers for packing and gaskets Fire and rot resisting material in felts (eg, for roofing) Raw material for asbestos based paper Component of textiles (eg, for use in fireproof clothing) Thermal and electrical insulation medium Component of industrial talcs Filler in industrial greases Component of taping compounds Heat resisting additive to metals (eg, for spacecraft) Selected asbestos products and their end uses: Valve, flange, and pump components; clutch/transmission components; industrial friction components; automotive/truck body coatings; electronic motor components; chemical process piping; water supply piping; conduits for electric wire; commercial/industrial dryer felts; theater curtains and fireproof draperies; gas vapor ducts for corrosive compounds; table pads and heat protective mats; molten glass handling equipment; underlayment for sheet flooring; hoods, vents for corrosive chemicals; chemical tanks and vessel manufacturing; portable construction buildings; electrical switchboards and components; laboratory furniture; and cooling tower components. /Data derived from table/ About 98% of the crocidolite is used in the production of asbestos cement pipe, because of its hardness, brittleness, and high tensile strength, which add to the ridigity of the end product, and its superior filtration qualities, which enhance the drainage of water, permitting cement to dry more rapidly. ... A very large proportion of total asbestos use is accounted for by shorter length fibers. ... /Crocidolite/ Former use: Spraying of asbestos fibre mixed with cement & other binders started in about 1935 & was 1st used for insulation of railway carriages. Later it was used in greatly increased amounts for fire protection & insulation in naval ships & in storage buildings. After the Second World War its use was ... expanded for encasing structural steel in buildings to prevent rapid bending in the event of fire. ... in the late 1960s when the extent of hazards from this use of asbestos became apparent spraying decreased & is now banned in many countries. Manufacturers: There are no US manufacturers of asbestos. The last US mine was closed in 2002. Methods of Manufacturing: The mineral is mined or quarried as its ore. In dry milling operations, which are currently the most widely used, the ore is first crushed to a nominal size and then dried. Fiber extraction then begins through a series of crushing operations, each followed by a vacuum aspiration of the ore running on a vibrating screen. On the latter, the fibers released from the ore have a tendency to move to the surface and, because of their large hydrodynamic volumes (low density), they can be readily collected into a vacuum system. The fibers recovered from consecutive vibrating screens are brought to cyclone separators, and the air is filtered to remove the finer suspended fibers. ... Wet milling operations have been initiated with obvious advantages in dust control and potential advantages in the separation of mineral contaminants from the fiber product. General Manufacturing Information: USEPA/OPP Pesticide Code: 099301 The term asbestos is a generic designation referring usually to six types of naturally occurring mineral fibers which are or have been commercially exploited. These fibers are extracted from certain varieties of hydrated alkaline silicate minerals comprising two families: serpentines and amphiboles. The serpentine group contains a single fibrous variety: chrysotile; five fibrous forms of amphiboles are known: anthophyllite, amosite, crocidolite, tremolite, and actinolite. Blue asbestos (crocidolite) was discovered in South Africa about 1803 to 1806, but not until 1893 ... was this variety commercially exploited. /Crocidolite/ ... Crocidolite and amosite are the only amphiboles with significant industrial uses; ... tremolite, although having no industrial application, may be found as a contaminant in other fibers or in other industrial minerals (eg, talc). Tremolite & actinolite are of little commercial value, but may be mixed with true talc (an amorphous magnesium silicate) to make commercial talc. Cosmetic talcs are in general free of fibrous silicates. /Actinolite/ Crocidolite ... /is/ produced in significant quantities only in South Africa. Main producing areas are at Bosrand, Cornheim, Ouplaas, Owendale, the Kuruman area in the Cape Province, & the Lyndenburg District in the Transvaal. Prodn statistics vary widely with the source of information. In 1976, 178 metric tons were produced in South Africa. /Crocidolite/ The main prodn of /anthophyllite/ was in the Paakkila area of north East Finland where it has been mined since 1918. Mining has now ceased. /Anthophyllite/ The major properties of concern are length, granular content, degree of openness or effective surface area, drainage or filtration rate, color, absorption, electrical resistivity, bulk density, & strength giving properties. Materials which may serve as asbestos substitutes are: 1) polypropylene: reinforcement of cement; 2) glass: reinforcement of cement, friction materials; 3) carbon: friction materials; 4) steel: friction materials; 5) mineral wool: insulation board; 6) vermiculite: fire protection, friction materials; 7) silicon nitride: friction materials; 8) ceramic paper: dental castings; 9) alumina and zirconia: high temperature insulation, filtration. /Data derived from table/ The US Navy tested shipboard transformers, one with asbestos and one without. Among the tests conducted, the transformer containing asbestos surpassed all others by 300 deg F in the determination of failure temperature on various overloads. Also, air emission tests demonstrated that little, if any, asbestos fiber was emitted during actual operating conditions. A neoprene spray process was developed for coating asbestos fibers to prevent their escape from construction components used in building interiors. A promising substitute for asbestos for cement reinforcement is glass fiber made from slate & limestone. /SRP 60: Former/ Asbestos /was/ commercially mined and milled in... states of California, Arizona, and Vermont. The Consumer Product Safety Commission has banned general use garments containing asbestos. The use of asbestos in special garments such as fire fighting suits is permitted, ...only if they are constructed so that asbestos fibers will not become airborne under normal conditions of use. In Beshada vs Johns-Manville Products Corp, the Supreme Court of New Jersey held that a state of art defense is unavailable in cases brought under a theory of strict liability for failure to warn. The court indicated that asbestos producers may be held liable for their products' harm even if the health hazards of asbestos were unknown and not discoverable when the products were /sold/. The material from the separating mill was largely unopened bundles of fibers. For many purposes it was necessary to open the fiber by separating the bundles into their constituent fibers, which greatly increases the bulk of the material. ... Parenteral drugs may be contaminated during their manufacture if asbestos is used as a filtration medium. Asbestos content of product is not necessarily indication of its relative health risk, for in many products fibers are tightly bound to matrix or encapsulated. Potential health risk arises when asbestos fibers are set free, eg, during drilling or sawing of asbestos cement sheets. /Asbestos products/ ... only chrysolite is used in or imported into the United States today, and only in a few products in which the fibers are firmly encapsulated in a matrix. Canadian chrysotile crudes are classified as follows: crude #1: 1.9 cm staple & longer; crude #2: 0.95 cm to 1.9 cm staple; crude run of mine: unsorted crudes. Milled Canadian fibers sold from Quebec are classified by a dry screen technique known as the Quebec Standard Asbestos Test. This test method grades fibers roughly by fiber or staple length. Minimum test values are guaranteed for each grade & a numerical classification system has been estabilished for fibers ranging from Group 3, the longest grade, to Group 7, the shortest grade. Chrysotile fibers produced outside Quebec are graded or controlled by screening test methods differing from the Quebec Screen Test; however, these basically identify grade by staple length. Formulations/Preparations: Typical chemical compositions of amphibole asbestos: silicon dioxide, 49-53%; magnesium oxide, 0-3%; ferrous oxide, 13-20%; ferric oxide, 17-20%; aluminum oxide, 0 to 0.2%; calcium oxide, 0.3-2.7%; potassium oxide, 0 to 0.4%; sodium oxide, 4 to 8.5%; & water, 2.5-4.5%. /Crocidolite/ Typical chemical compositions of amphibole asbestos: silicon oxide, 56-58%; magnesium oxide, 28-34%; ferrous oxide, 3-12%; aluminum oxide, 0.5-1.5%; & water, 1-6%. /Anthophyllite/ Typical chemical compositions of amphibole asbestos: silicon oxide, 51-52%; magnesium oxide, 15-20%; ferrous oxide, 5-15%; ferric oxide, 0-3%; aluminum oxide, 1.5 to 3%; calcium oxide, 10-12%; potassium oxide, 0 to 0.5%; sodium oxide, 0.5-1.5%; & water, 1.5-2.5%. /Actinolite/ Impurities: ... During preparation of the fiber by the separation of the bundles, contamination by oils & other substances can readily occur. Virgin asbestos may also contain small amounts of oils & waxes. Trace amounts of a number of metals, including nickel, chromium, cobalt & manganese are present in many samples. Samples of commercially used asbestos, especially chrysotile, are frequently contaminated by small amounts of other fibrous minerals. Among these are tremolite and brucite. Trace metals (beryllium, cadmium, chromium, cobalt, copper, ... manganese, nickel, and thallium) may be present as natural impurities in asbestos. Consumption Patterns: (1983) COMPONENT OF FRICTION MATERIALS, 21%; REINFORCING MATERIAL IN FLOORING PRODUCTS, 20%; REINFORCING MATERIAL IN CEMENT FOR PIPES, 15%; FOR SHEETS, 4%; REINFORCING PIGMENT IN SURFACE COATINGS & SEALANTS, 10%; REINFORCING FILLER IN ELASTOMERS FOR PACKING & GASKETS, 6%; FIRE & ROT RESISTING MATERIAL IN FELTS, 3%; RAW MATERIAL FOR ASBESTOS-BASED PAPER, 1%; OTHER USES, 20% (1973) Construction materials: 30%; floor tiles: 21%; friction products: 8%; paper: 10% asphalt felts: 5%; packing and gaskets: 3%; insulation: 1.5%; textiles: 1.5%; others: 20%. (1975) 550,900 metric tons Between 1974 and 1975 asbestos consumption declined 27% from 856,000 to 629,000 tons. Replacement of asbestos by other materials believed to be safer has been widespread since the mid 1970s. Man-made mineral fibers & other insulating materials are rapidly replacing asbestos for heat insulation. But for other uses ... /such as/ asbestos cement, friction materials & some felts & gaskets, substitution is not ... /yet/ practicable. (1986) Friction products, 22%; asbestos cement pipe, 18%; coatings and compounds, 15%; packing and gaskets, 9%; asbestos cement sheet, 8%; and other, 28% (1985) FRICTION PRODUCTS, 22%; FLOORING PRODUCTS, 21%; ASBESTOS CEMENT PIPE, 16%; COATINGS AND COMPOUNDS, 10%; PACKING AND GASKETS, 6%; ASBESTOS CEMENT SHEET, 5%; ROOFING PRODUCTS, 3%; PAPER AND TEXTILES, 1%; AND OTHER, 16% /FOR ASBESTOS/ (1988) Asbestos was consumed in roofing products, 28%; friction products, 26%; asbestos cement pipe, 14%; packing and gaskets, 13%; paper, 6%; and other 13%. (1999) 16,000 metric tons, estimated (2000) 15,000 metric tons, estimated (2001) 13,000 metric tons, estimated (2002) 7,000 metric tons, estimated (2003) 6,000 metric tons, estimated (2003) Asbestos was consumed in roofing product, 80%; gaskets, 8%; friction products, 4%; and other, 8%. U. S. Production: (1977) 9.26X10+10 G (1982) 6.36X10+10 G (1985) 5.7X10+4 metric tons (1986) 5.1X10+4 metric tons (1987) 5.1X10+4 metric tons (1999) Production (sales), mine: 7,000 metric tons (2000) Production (sales), mine: 5,000 metric tons (2001) Production (sales), mine: 5,000 metric tons (2002) Production (sales), mine: 3,000 metric tons (2003) There was no asbestos production in the United States. U. S. Imports: (1977) 5.51X10+11 G (1982) 2.42X10+11 G In 1974, 96.5% of the asbestos imported ... was from Canada. (1985) 1.42X10+5 metric tons (1986) 1.08X10+5 metric tons (1987) 9.4X10+4 metric tons (1999) 16,000 metric tons (2000) 15,000 metric tons (2001) 13,000 metric tons (2002) 7,000 metric tons (2003) 6,000 metric tons, estimated U. S. Exports: (1977) 3.45X10+10 G (1982) 5.90X10+10 G (1985) 4.6X10+4 metric tons (1986) 4.7X10+4 metric tons (1987) 6.0X10+4 metric tons (1999) 22,000 metric tons (probably includes nonasbestos materials and reexports) (2000) 19,000 metric tons (probably includes nonasbestos materials and reexports) (2001) 22,000 metric tons (probably includes nonasbestos materials and reexports) (2002) 8,000 metric tons (probably includes nonasbestos materials and reexports) (2003) 4,000 metric tons, estimated (probably includes nonasbestos materials and reexports) Laboratory Methods: Clinical Laboratory Methods: Method: Transmission Electron Microscopy; Analyte: asbestos; Matrix: urine; Sample Detection Limit: 0.1-0.3X10-6 fibers per liter. /From table/ Method: Transmission Electron Microscopy; Analyte: asbestos; Matrix: feces; Sample Detection Limit: 0.15X10+6 fibers per gram. /From table/ Method: Transmission Electron Microscopy; Analyte: asbestos; Matrix: lung tissue; Sample Detection Limit: 0.1X10+6 fibers per gram. /From table/ Method: Phase Contrast Electron Microscopy; Analyte: asbestos; Matrix: lung tissue; Sample Detection Limit: 5,000 fibers per gram. /From table/ Analytic Laboratory Methods: METHODS OF CONFIRMING ASBESTOS CAN INCLUDE OPTICAL TESTING USING POLARIZED LIGHT, FIRST ORDER RED OR OTHER RETARDATION PLATES, ANGLES OF EXTINCTION, DISPERSION STAINING. BULK SAMPLES MAY BE ANALYZED BY X-RAY DIFFRACTION OR IR ABSORPTION OF DIFFERENTIAL THERMAL ANALYSIS. Method: NIOSH 7402, Asbestos by TEM (Transmission Electron Microscopy); Analyte: asbestos fibers; Matrix: air; Estimated Limit of Detection: 1 confirmed asbestos fiber above 95% of expected mean blank value. Method: NIOSH 7400, Issue 2, Asbestos and Other Fibers by PCM (Phase Contrast Microscopy); Analyte: fibers (manual count); Matrix: air; Estimated Limit of Detection: 7 fibers/sq mm filter area. Method: NIOSH 9002, Issue 2, Asbestos (bulk) by PLM (Polarized Light Microscopy); Analyte: asbestos; Matrix: bulk samples; Estimated Limit of Detection: less than 1% asbestos. Method: OSHA ID-160, Asbestos in Air (phase contrast microscopy at 400X); Analyte: asbestos; Matrix: air; Detection Limit: 5.5 fibers/sq mm or 0.001 fibers/cc (2,400 L air volume). Method: OSHA ID-191, Polarized Light Microscopy of Asbestos; Analyte: asbestos; Matrix: bulk; Detection Limit: less than 1% by area. ... The number and size distribution of fibers in a sample can only be determined by direct microscopic examination. This may be performed using either light or electron microscopy. Sampling Procedures: Matrix Air: Collection procedure: A known volume of air is drawn through a 25-mm diameter cassette containing a mixed-cellulose ester filter. The cassette must be equipped with an electrically conductive 50-mm extension cowl. The sampling time and rate are chosen to give a fiber density of between 100 to 1,300 fibers/sq mm on the filter. Recommended sampling rate: 05 to 5.0 liters/minute (L/min). Recommended air volumes: minimun - 25 L; maximum - 2,400 L. Special References: Special Reports: 40 CFR 1910.1001. Occupational safety and health standard for asbestos. U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from: http://www.gpoaccess.gov/ecfr as of February 10, 2004. Defines conditions, or the adoption or use of one or more practices, means, methods, operations, or processes, reasonably necessary or appropriate to produce safe or healthful employment and places of employment. MARSH GM; ENVIRON HEALTH PERSPECT 53: 49-56 (1983). REVIEW: THIRTEEN EPIDEMIOLOGIC STUDIES OF INGESTED ASBESTOS CONDUCTED IN 5 AREAS OF THE USA & CANADA WERE REVIEWED & EVALUATED FOR THE DEFINITIVENESS & APPLICABILITY REGARDING THE DEVELOPMENT OF AMBIENT WATER QUALITY STANDARDS. USDHEW/NIOSH; Revised Recommended Asbestos Standard (1976) DHEW (NIOSH) Pub No. 77-169 USDHEW/NIOSH; Occupational Exposure to Talc Containing Asbestos (1980) DHEW (NIOSH) Pub No. 80-115 USEPA; Ambient Water Quality Criteria Doc: Asbestos (1980) EPA 440/5-80-022 Nat'l Research Council Canada; Effect of Chromium, Alkali Halides, Arsenic, Asbestos, Mercury in the Canadian Environment (1980) NRCC No. 17585 Nat'l Research Council Canada; Asbestos (1979) NRCC No. 16452 USEPA/ECAO; Asbestos Health Update (1984) EPA 600/8-84-003A Becklake MR; Amer Rev Resp Dis 126 (2): 187-94 (1982). Asbestos-related diseases of the lungs and pleura /are reviewed along with/ current clinical issues. Canadian Center for Occupational Health and Safety; A Review of Four Major Reports on the Health Hazards of Asbestos 93 pp. (1981) Bishop K et al; Bull Environ Contam Toxicol 34 (3): 301-8 (1985). Identification of asbestos and glass fibers in municipal sewage sludges. WHO; Environ Health Criteria: Asbestos and Other Natural Mineral Fibers (1986) USEPA; Health and Environmental Effects Profile for Asbestos (1979) U.S. Dept Health & Human Services/Agency for Toxic Substances Disease Registry; Toxicological Profile for Asbestos (Update) (1995) NTIS # PB/95-264305 DHHS/NTP; Toxicology & Carcinogenesis Studies of Crocidolite Asbestos in F344/N Rats (Feed Studies) Technical Report Series No. 280 (1988) NIH Publication No. 89-2536 U.S. Department of Health & Human Services/National Toxicology Program; Tenth Report on Carcinogens. National Institutes of Environmental Health Sciences. The Report on Carcinogens is an informational scientific and public health document that identifies and discusses substances (including agents, mixtures, or exposure circumstances) that may pose a carcinogenic hazard to human health. Asbestos (1332-21-4) was listed in the First Annual Report on Carcinogens (1980) as known to be a human carcinogen . DHHS/ATSDR; Toxicological Profile for Asbestos PB/2001/109101 (2001) Synonyms and Identifiers: Related HSDB Records: 2957 [AMOSITE] (mineral class) 2966 [CHRYSOTILE ASBESTOS] (mineral class) 4212 [TREMOLITE ASBESTOS] (mineral class) Synonyms: ASBESTOSE (GERMAN) ASBESTOS FIBER ASBESTOS FIBRE ASCARITE Associated Chemicals: Anthophyllite;17068-78-9 Formulations/Preparations: Typical chemical compositions of amphibole asbestos: silicon dioxide, 49-53%; magnesium oxide, 0-3%; ferrous oxide, 13-20%; ferric oxide, 17-20%; aluminum oxide, 0 to 0.2%; calcium oxide, 0.3-2.7%; potassium oxide, 0 to 0.4%; sodium oxide, 4 to 8.5%; & water, 2.5-4.5%. /Crocidolite/ Typical chemical compositions of amphibole asbestos: silicon oxide, 56-58%; magnesium oxide, 28-34%; ferrous oxide, 3-12%; aluminum oxide, 0.5-1.5%; & water, 1-6%. /Anthophyllite/ Typical chemical compositions of amphibole asbestos: silicon oxide, 51-52%; magnesium oxide, 15-20%; ferrous oxide, 5-15%; ferric oxide, 0-3%; aluminum oxide, 1.5 to 3%; calcium oxide, 10-12%; potassium oxide, 0 to 0.5%; sodium oxide, 0.5-1.5%; & water, 1.5-2.5%. /Actinolite/ Shipping Name/ Number DOT/UN/NA/IMO: UN 2590; White asbestos UN 2212; Blue asbestos; Brown asbestos Return to top of page Is deadly Asbestos lurking in your home? To learn where to look, what to do, what NOT to do, or who to call - you may be interested in our page dealing with Asbestos tips for homeowners. My extensive Household Chemical Guide also has a section dealing with Asbestos, as well as 100 other potentially hazardous household chemicals. It is one of the most extensive guides to household chemical hazards on the internet. Return to Home Air Purifier Expert Index Page from Asbestos MSDS
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