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Public Health Statement for Asbestos Plus Asbestos MSDS Information

Complete Guide to Asbestos with specific Asbestos MSDS information



The Complete Guide to Asbestos

Below are the most commonly asked questions asked about Asbestos and Asbestos exposure including a complete public health statement and extensive Asbestos MSDS information

Closeup image of Anthophyllite-Asbestos fibers

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!

Is deadly Asbestos lurking in your home? You may be interested in our page dealing with Asbestos tips for homeowners or

our HUGE Household Chemical Guide's section on Asbestos don't miss all the other information we've included on over 100 other potentially hazardous household chemicals - It's one of the largest guides to household chemical hazards available on the internet!

This public health statement tells you about asbestos and the effects of exposure. The Environmental Protection Agency (EPA) identifies the most serious hazardous waste sites in the nation. These sites make up the National Priorities List (NPL) and are the sites targeted for long-term federal cleanup activities. Asbestos has been found in at least 83 of the 1,585 current or former NPL sites. However, the total number of NPL sites evaluated for this substance is not known. As more sites are evaluated, the sites at which asbestos is found may increase. This information is important because exposure to this substance may harm you and because these sites may be sources of exposure.

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.

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:
Gardner Wet R Dry All Weather Plastic Roof Cement (caulk) -Home maintenance -caulk tube
Gardner Lap Cement -Home maintenance -paste
Gardner Wet R Dry All Weather Plastic Roof Cement (paste) -Home maintenance -paste
Gardner Leak Stopper Rubberized Roof Patch -Home maintenance -caulk tube
Gardner Fibered Roof Coating -Home maintenance -liquid

Products containing Anthophyllite asbestos:
Glidden Ultra Hide Stain Jammer, Oil Based Interior Primer/Sealer -Home maintenance -liquid

Products containing Tremolite (nonasbestiform), aka Tremolite asbestos; Actinolite (Ca2Mg5H2(SiO3)8); Tremolite:
Zinsser Bulls Eye 1 2 3 Primer -Home maintenance -liquid
Sarak Driveway Crack Filler -Home maintenance -caulk tube
Glidden Ultra Hide Stain Jammer, Oil Based Interior Primer/Sealer -Home maintenance -liquid
DAP Blacktop Asphalt Filler & Sealant Tube -Landscaping/Yard -caulk tube - >3%

Products containg high percentage of Talc (basicly non-fibrous Asbestos):
XL Microcel Light Body Filler Putty-08/20/2001 Hobby/Craft paste 32-42 %
XL Microcel Light Body Filler Putty Home maintenance paste 32-42 %
No More Leaks Plastic Pipe Seal Home maintenance aerosol 30-35 %
Oatey Epoxy Putty Home maintenance paste 75-85 %
Shower to Shower Absorbent Powder Personal care/use powder 44 %
Johnsons Baby Powder, Original Personal care/use powder 99%
Bonide Rotenone 1% Pesticides powder 97.50 %
Bonide Rotenone 5% Insect Control Pesticides powder 85.00 %
Adams Flea & Tick Dust II Pet Care powder 10-75 %

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
Synonyms: Talc (non-fibrous); Cosmetic talc; French chalk; Magnesium silicate, hydrous; Talc powder; Talc (Mg3H2(SiO3)4); Talc (powder), containing no asbestos fibers

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
Asbestosis
Pleural Mesothelioma
PeritonealMesothelioma
Lung cancer
Esophagus cancer
Stomach cancer
Laryngeal cancer
Pneumoconioses

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.

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 Toxicology 1600 Clifton Road NE, Mailstop F-32 Atlanta, GA 30333

Information line and technical assistance:

Phone: 888-422-8737 FAX: (770)-488-4178 ATSDR 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 Service 5285 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.

1.11 ASBESTOS MSDS Information

CASRN: 1332-21-4

Human Health Effects
Emergency Medical Treatment
Animal Toxicity Studies
Metabolism/Pharmacokinetics
Pharmacology
Environmental Fate & Exposure
Environmental Standards & Regulations
Chemical/Physical Properties
Chemical Safety & Handling
Occupational Exposure Standards
Manufacturing/Use Information
Laboratory Methods
Special References
Synonyms and Identifiers

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.
[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. S7 106 (1987)]**PEER REVIEWED**

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.
[U.S. Environmental Protection Agency's Integrated Risk Information System (IRIS) on Asbestos (1332-21-4) Available from: http://www.epa.gov/ngispgm3/iris on the Substance File List as of March 15, 2000]**PEER REVIEWED**

A1; Confirmed human carcinogen. /Asbestos, all forms/
[ American Conference of Governmental Industrial Hygienists TLVs and BEIs. Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Cincinatti, OH, 2005, p. 13]**QC REVIEWED**

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.
[Selikoff IJ et al; Ann NY Acad Sci 330: 91-116 as cited in USEPA; Asbestos Health Assessment Update (Draft) p.11-13 (1984) EPA-600/8-84-003A ]**PEER REVIEWED**

/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.
[USEPA; Asbestos Health Assessment Update (Draft) p.14-16 (1984) EPA-600/8-84-003A ]**PEER REVIEWED**

/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.
[Enterline PE, Henderson V; Arch Environ Health 27: 312-17 (1973) as cited in USEPA; Asbestos Health Assessment Update (Draft) p.5 (1984) EPA-600/8-84-003A ]**PEER REVIEWED**

/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.
[Lewinsohn HC; R Soc Health J 92: 69-77 (1972) as cited in USEPA; Asbestos Health Assessment Update (Draft) p.5 (1984) EPA-600/8-84-003A ]**PEER REVIEWED**

/HUMAN EXPOSURE STUDIES/ Among female workers, ovarian cancer has been found in excess.
[Newhouse ML et al; Br J Ind Med 29: 134-41 (1972) as cited in USEPA; Asbestos Health Assessment Update (Draft) p.57 (1984) EPA-600/8-84-003A ]**PEER REVIEWED**

/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.
[Nat'l Research Council Canada; Effects of Asbestos in the Canadian Environ p.113 (1979) NRCC No. 16452 ]**PEER REVIEWED**

/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.
[Nat'l Research Council Canada; Effects of Asbestos in the Canadian Environ p.19 (1979) NRCC No. 16452 ]**PEER REVIEWED**

/HUMAN EXPOSURE STUDIES/ Asbestos fibers are toxic to macrophages, cells responsible for cleaning infectious agents and foreign material from the respiratory tract.
[Nat'l Research Council Canada; Effects of Asbestos in the Canadian Environ p.19 (1979) NRCC No. 16452 ]**PEER REVIEWED**

/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.
[Nat'l Research Council Canada; Effects of Asbestos in the Canadian Environ p.17 (1979) NRCC No. 16452 ]**PEER REVIEWED**

/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.
[International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983., p. 187]**PEER REVIEWED**

/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.
[Enterline PE et al; J Occup Med 14: 897 (1972) as cited in USEPA; Ambient Water Quality Criteria Doc: Asbestos p.C-76-77 (1980) EPA 440/5-80-022 ]**PEER REVIEWED**

/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.
[International Labour Office. Encyclopedia of Occupational Health and Safety. Volumes I and II. New York: McGraw-Hill Book Co., 1971., p. 122]**PEER REVIEWED**

/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.
[American Conference of Governmental Industrial Hygienists. Documentation of Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices for 2001. Cincinnati, OH. 2001., p. 3]**PEER REVIEWED**

/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.
[International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983., p. 189]**PEER REVIEWED**

/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.
[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V1 507]**PEER REVIEWED**

/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.
[International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983., p. 188]**PEER REVIEWED**

/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/
[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V1 506]**PEER REVIEWED**

/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.
[International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983., p. 188]**PEER REVIEWED**

/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/
[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V1 500]**PEER REVIEWED**

/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.
[American Conference of Governmental Industrial Hygienists. Documentation of Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices for 2001. Cincinnati, OH. 2001., p. 3]**PEER REVIEWED**

/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/
[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V1 500]**PEER REVIEWED**

/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.
[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. S7 106 (1987)]**PEER REVIEWED**

/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.
[Rom, W.N. (ed.). Environmental and Occupational Medicine. 2nd ed. Boston, MA: Little, Brown and Company, 1992., p. 272]**PEER REVIEWED**

/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.
[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. S7 106 (1987)]**PEER REVIEWED**

/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.
[Klaassen, C.D. (ed). Casarett and Doull's Toxicology. The Basic Science of Poisons. 6th ed. New York, NY: McGraw-Hill, 2001., p. 444]**PEER REVIEWED**

/HUMAN EXPOSURE STUDIES/ No clear excess of cancer has been associated with the presence of asbestos fibers in drinking water.
[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. S7 108 (1987)]**PEER REVIEWED**

/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).
[Hasanoglu HC et al; Arch Environ Health 58 (3): 144-50 (2003) ]**PEER REVIEWED**

/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.
[Ascoli V et al; Am J Industr Med 40 (4): 371-373 (2001) ]**PEER REVIEWED**

/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.
[USEPA/OHEA; Asbestos Health Assessment Update (Draft) p.5 (1984) EPA 600/8-84-0034A ]**PEER REVIEWED**

/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).
[Barnes R; Med J Aust 2: 221-24 (1983) ]**PEER REVIEWED**

/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.
[Nat'l Research Council Canada; Effects of Asbestos in the Canadian Environ p.138 (1979) NRCC No. 16452 ]**PEER REVIEWED**

/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.
[Rom, W.N. (ed.). Environmental and Occupational Medicine. 2nd ed. Boston, MA: Little, Brown and Company, 1992., p. 272]**PEER REVIEWED**

/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.
[International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983., p. 188]**PEER REVIEWED**

/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).
[USDHEW/NCI; Asbestos: An Information Resource p.36 (1978) DHEW Pub No. NIH 79-1681 ]**PEER REVIEWED**

/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.
[Ordonez NG, Smith JL Jr; Arch Dermatol 119 (10): 827-30 (1983) ]**PEER REVIEWED**

/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.
[Rom, W.N. (ed.). Environmental and Occupational Medicine. 2nd ed. Boston, MA: Little, Brown and Company, 1992., p. 281]**PEER REVIEWED**

/CASE REPORTS/ ...Two cases of constrictive pericarditis in subjects previously exposed to asbestos /are reported/.
[Trosini-Desert V et al; Rev Mal Respir 20 (4): 622-7 (2003) ]**PEER REVIEWED**

/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.
[Hiraoka T et al; Ind Health 39 (2): 194-7 (2001) ]**PEER REVIEWED**

/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
[Heller DS et al; Am J Ind Med 29 (5): 435-9 (1996) ]**PEER REVIEWED**

/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.
[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. S7 106 (1987)]**PEER REVIEWED**

/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.
[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. S7 107 (1997)]**PEER REVIEWED**

/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.
[Sadler TD et al; J Commun Hlth 9 (4): 285-93 (1984) ]**PEER REVIEWED**

/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.
[Kobusch AB et al; J Chron Dis 37 (8): 599-607 (1984) ]**PEER REVIEWED**

/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).
[Hodgson JT, Jones RD; Br J Ind Med 43: 158-64 (1986) ]**PEER REVIEWED**

/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.
[Kjuus H et al; Scand J Work Environ Health 12: 203-9 (1986) ]**PEER REVIEWED**

/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.
[Kelsey KT et al; JNCI 77 (2): 321-27 (1986) ]**PEER REVIEWED**

/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.
[Hammond EC et al; Arch Environ Health 29: 341 (1979) as cited in USEPA; Health and Environmental Effects Profile for Asbestos; p.12-11 (1979) EPA No 12 ]**PEER REVIEWED**

/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.
[Millette JR et al; Environ Health Perspect 53: 91-98 (1983) as cited in USEPA, Office of Drinking Water; Criteria Document (Draft): Asbestos p.VI-13 (1985) ]**PEER REVIEWED**

/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.
[Newhouse ML, Berry G; Br J Ind Med 36: 98-112 (1983) as cited in USEPA; Asbestos Health Assessment Update (Draft) p.47 (1984) EPA-600/8-84-003A ]**PEER REVIEWED**

/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.
[Froom P et al; J Occup Environ Med 42 (1): 19-24 (2000) ]**PEER REVIEWED**

/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.
[Albin M et al; : Occup Environ Med 53 (2): 87-93 (1996) ]**PEER REVIEWED**

/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.
[Glencross PM et al; Am J Ind Med 32 (5): 460-6 (1997) ]**PEER REVIEWED**

/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.
[Lohani M et al; Toxicol Lett 136 (1): 55-63 (2002) ]**PEER REVIEWED**

/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.
[Mukherjee S et al; Am J Respir Crit Care Med 162 (5): 1807-11 (2000) ]**PEER REVIEWED**

/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.
[Gennaro V et al; Am J Ind Med 37 (3): 275-82 (2000) ]**PEER REVIEWED**

/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/
[Germani D et al; Am J Ind Med 36 (1): 129-34 (1999) ]**PEER REVIEWED**

/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.
[Wilson MR et al; J Allergy Clin Immunol 60 (4): 218-22 (1977) ]**PEER REVIEWED**

/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.
[Dodson RF et al; Am J Ind Med 37 (2): 169-74 (2000) ]**PEER REVIEWED**

/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/
[Takeuchi T et al; Mutat Res 438 (1): 63-70 (1999) ]**PEER REVIEWED**

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... .
[29 CFR 1910.1001(l)(1); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from: http://www.gpoaccess.gov/ecfr as of August 20, 2004 ]**PEER REVIEWED**

...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/.
[29 CFR 1910.1001(l)(2); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from: http://www.gpoaccess.gov/ecfr as of August 20, 2004 ]**PEER REVIEWED**

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/
[29 CFR 1910.1001(l)(3); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from: http://www.gpoaccess.gov/ecfr as of August 20, 2004 ]**PEER REVIEWED**

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.
[29 CFR 1910.1001(l)(4); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from: http://www.gpoaccess.gov/ecfr as of August 20, 2004 ]**PEER REVIEWED**

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/
[USDHEW/NCI; Asbestos: An Information Resource p.93 (1978) DHEW Pub No. NIH 79-1681]**PEER REVIEWED**

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/.
[USDHEW/NCI; Asbestos: An Information Resource p.96 (1978) DHEW Pub No. NIH 79-1681]**PEER REVIEWED**

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.
[USEPA; Ambient Water Quality Criteria Doc: Asbestos p.C-99 (1980) EPA 440/5-80-022]**PEER REVIEWED**

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.
[Hammond EC et al; Health Hazards of Asbestos Exposure 473-90 (1979) as cited in USEPA; Office of Drinking Water; Criteria Document (Draft): Asbestos p.VI-21 (1985)]**PEER REVIEWED**

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.
[DHHS/ATSDR; Toxicological Profile for Asbestos p.114 (2001) ]**PEER REVIEWED**

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.
[DHHS/ATSDR; Toxicological Profile for Asbestos p.114 (2001) ]**PEER REVIEWED**

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.
[DHHS/ATSDR; Toxicological Profile for Asbestos p.115 (2001) ]**PEER REVIEWED**

Probable Routes of Human Exposure:

Asbestos /enters the human body/ from gastrointestinal and respiratory tract exposure.
[Nat'l Research Council Canada; Asbestos p.14 (1979) NRCC No. 16452]**PEER REVIEWED**

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.
[Nat'l Research Council Canada; Effects of Asbestos in the Canadian Environ p.23 (1979) NRCC No. 16452]**PEER REVIEWED**

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.
[International Labour Office. Encyclopedia of Occupational Health and Safety. Volumes I and II. New York: McGraw-Hill Book Co., 1971., p. 123]**PEER REVIEWED**

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.
[PAIK NW ET AL; AM IND HYG ASSOC J 44 (6): 428-32 (1983)]**PEER REVIEWED**

... 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.
[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V14 37 (1977)]**PEER REVIEWED**

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.
[Nat'l Research Council Canada; Asbestos p.51 (1979) NRCC No. 16452]**PEER REVIEWED**

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.
[Nat'l Research Council Canada; Asbestos p.13 (1979) NRCC No. 16452]**PEER REVIEWED**

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.
[Nat'l Research Council Canada; Asbestos p.13 (1979) NRCC No. 16452]**PEER REVIEWED**

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.
[Chen CK et al; Technological Feasibility of Controlling Asbestos and Silica at Mines and Mills. 248 pp (1983) NIOSH Contract No. PHS-NIOSH-210-81-4101]**PEER REVIEWED**

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.
[Nat'l Research Council Canada; Asbestos p.46 (1979) NRCC No. 16452]**PEER REVIEWED**

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.
[Nat'l Research Council Canada; Effects of Asbestos in the Canadian Environ p.23 (1979) NRCC No. 16452]**PEER REVIEWED**

... 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.
[USEPA, Office of Drinking Water; Criteria Document (Draft): Asbestos p.IV-8 (1985)]**PEER REVIEWED**

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.
[USEPA; Ambient Water Quality Criteria Doc: Asbestos p.63 (1980) EPA 440/5-80-022]**PEER REVIEWED**

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.
[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V14 38 (1977)]**PEER REVIEWED**

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.
[Nat'l Research Council Canada; Effects of Asbestos in the Canadian Environ p.14 (1979) NRCC No. 16452]**PEER REVIEWED**

The hazard from environmental asbestos exposure showed that mesothelioma could occur among individuals whose potential asbestos exposure con