Articles / Case Studies on Peritoneal Mesothelioma

Peritoneal mesothelioma in a 17-year-old boy with evidence of previous exposure to chrysotile and tremolite asbestos.

Abstract: We describe a case of malignant peritoneal mesothelioma arising in a 17-year-old boy. The diagnosis was based on a comprehensive study including light microscopy, histochemistry, immunohistochemistry, evaluation of the clinical course, and autopsy examination. Analytical transmission electron microscopy showed a concentration of 510,000 asbestos fibers/g dry lung tissue. The fibers were represented by chrysotile (62%) and tremolite (38%) asbestos. About 40% of the total fibers were longer than 5 microns. The presence of tremolite fibers was probably due to environmental exposure to contaminated cosmetic talc. This is the first reported case of pathologically proven exposure to asbestos dust in malignant mesothelioma of childhood and adolescence.

Andrion A and Bosia S
Division of Pathological Anatomy, City Hospital, Asti, Italy.
Hum Pathol
1994 Jun, vol. 25, pages 617-622
UNITED STATES

Intraperitoneal cisplatin and etoposide in peritoneal mesothelioma: favorable outcome with a multimodality approach.

Abstract: Ten patients with histologically documented peritoneal mesothelioma were treated with intraperitoneal cisplatin 200 mg/m2, sodium thiosulfate rescue and etoposide 65-290 mg/m2 every 4 weeks for a maximum of six cycles. All had epithelial or mixed epithelial-fibrous histology. Toxicity was tolerable, with 50% sustaining grade 3 or 4 granulocytopenia. There was one episode of neutropenic fever. Grade 2 peripheral neuropathy occurred in one patient, grade 1 in five patients. Complete remission occurred in one of five patients with measurable disease. Median survival for patients whose tumors were surgically debulked to < 2 cm residua prior to treatment was 22 months, while it was 5 months for those with measurable, surgically inaccessible disease (P = 0.0731 by Cox regression proportional hazard model). These data suggest that patients who present with resectable disease may benefit from an aggressive adjuvant approach. This possibility warrants prospective testing in a randomized clinical trial.

Langer CJ and Rosenblum N
Department of Medical Oncology, Fox Chase Cancer Center,
Philadelphia, PA 19111.
Cancer Chemother Pharmacol
1993, vol. 32, pages 204-208
GERMANY

Intestinal obstruction due to diffuse peritoneal fibrosis at 2 years after the successful treatment of malignant peritoneal mesothelioma with intraperitoneal mitoxantrone [published erratum appears in Cancer Chemother Pharmacol 1992;30(3):249]

Abstract: A 44-year-old man who had achieved a complete remission of malignant peritoneal mesothelioma after the intraperitoneal administration of 25mg/m2 mitoxantrone presented with clinical and radiological signs of intestinal obstruction suggestive of recurrent disease at about 2 years following the initial treatment. However, laparotomy revealed extensive adhesive fibrosis but no sign of malignant mesothelioma. The peritoneal complications of intraperitoneal cytostatic treatment are discussed.

Vlasveld LT and Taal BG
Department of Medical Oncology, The Netherlands Cancer Institute,
Antoni van Leeuwenhoek Huis, Amsterdam.
Cancer Chemother Pharmacol
1992, vol. 29, pages 405-408
GERMANY

Malignant peritoneal mesothelioma in childhood with long-term survival.

Abstract: A diffuse, well-differentiated, malignant peritoneal mesothelioma (MPM) developed in a nine-year-old girl. She received limited chemotherapy and radiation therapy and is alive and well without clinical evidence of disease 109 months after diagnosis. The neoplastic cells stained immunohistochemically for cytokeratin and epithelial membrane antigen but were unreactive with B72.3, anti-carcinoembryonic antigen, and anti-Leu-M1. Ultrastructurally, the tumor cells had abundant desmosomes, numerous tonofilament bundles, and variable-length microvilli. These findings confirm the mesothelial nature of the cells. Features consistent with malignancy included DNA aneuploidy by flow cytometric analysis and diffuse peritoneal involvement. The three previously described survivors with MPM were also premenarchal girls. Some MPMs in premenarchal girls have an indolent biologic behavior similar to that of low-grade peritoneal serous neoplasia or well-differentiated papillary mesothelioma in adult women.

Geary WA, Mills SE and Frierson HF, Jr
Department of Pathology, University of Virginia Health Sciences Center, Charlottesville 22908.
Am J Clin Pathol
1991 Apr, vol. 95, pages 493-498

Successful therapy of peritoneal mesothelioma with intraperitoneal chemotherapy alone. A case report.

Abstract: Malignant peritoneal mesothelioma is a disease that remains relatively refractory to conventional intravenous chemotherapy with currently available agents. Single-agent and combination chemotherapy offer a response rate of 20%. Direct intraperitoneal administration of some chemotherapeutic agents results in a significant pharmacologic advantage with much greater area under the concentration versus time curve (AUC). We report a case of a patient with peritoneal mesothelioma treated with combination intraperitoneal cisplatin and Ara-C who achieved a pathologic complete remission. This patient is still alive and has been in complete remission for 53 months. This combination of intraperitoneal chemotherapy deserves further evaluation in malignant mesothelioma.

Garcia Moore ML
Section of Medical Oncology, University of Miami School of Medicine,
Florida 33121.
Am J Clin Oncol
1992 Dec, vol 15, pages 528-530
UNITED STATES

Intraperitoneal chemotherapy for malignant peritoneal mesothelioma [published erratum appears in Eur J Cancer 1991;27(12):1717]

Abstract: 4 patients with malignant peritoneal mesothelioma have been treated with intraperitoneal chemotherapy in the Netherlands Cancer Institute in the recent years. 1 patient achieved a complete remission for 36+ months and another patient had a partial remission that lasted for 10 months. Intraperitoneal chemotherapy alone or in combination with other treatment modalities may yield a response rate of 58% with 24% complete remissions in 70 patients reviewed in the literature. Although these data should be considered with caution because of the heterogenicity of the patient group treated, cisplatin-based intraperitoneal chemotherapy seems to be the best available treatment for malignant peritoneal mesothelioma at present.

Vlasveld LT
Department of Medical Oncology, Netherlands Cancer Institute, Amsterdam.
Eur J Cancer
1991, vol. 27, pages 732-734
ENGLAND

Efficacy of cisplatin-based intraperitoneal chemotherapy as treatment of malignant peritoneal mesothelioma.

Abstract: In an effort to examine the potential clinical utility of intraperitoneal (i.p.) therapy in the management of patients with malignant peritoneal mesothelioma, 19 individuals with this disease were treated with a cisplatin-based i.p. treatment regimen. All but 1 patient also received i.p. mitomycin. The treatment was generally well tolerated, although a maximum of only four or five courses of cisplatin (100 mg/m2 every 28 days) and mitomycin (5-10 mg/treatment given 7 days after each i.p. cisplatin administration) could be administered, the treatment principally being stopped because of disease progression or catheter failure. Of 15 patients with malignant ascites, 7 (47%) experienced control of fluid reaccumulation ranging from 2 months to 73+ months (median 8 months). While the median survival for the 19 patients was only 9 months, 4 (21%) patients survived for more than 3 years from the initiation of therapy, and 2 patients are currently alive and clinically disease-free more than 5 years from the start of the i.p. treatment program. We conclude that a subset of patients with peritoneal mesothelioma, principally those with small-volume residual disease following surgical tumor debulking, can benefit from a cisplatin-based i.p. treatment strategy with control of ascites and prolonged disease-free survival.

Markman M and Kelsen D
Breast/Gynecology Oncology Service, Memorial Sloan-Kettering Cancer Center, New York, New York 10021.
J Cancer Res Clin Oncol
1992, vol. 118, pages 547-550
GERMANY

Articles / Case Studies on Pericardial Mesothelioma

Primary pericardial mesothelioma:

Yuko Kobayashi1, , Ryusuke Murakami1, Junko Ogura1, Kanae Yamamoto1, Taro Ichikawa1, Kouichi Nagasawa2, Masaru Hosone3 and Tatsuo Kumazaki4
(1) Department of Radiology, Tama-Nagayama Hospital, Nippon Medical School, 1-7-1 Nagayama, Tama-shi, Tokyo 206-8512, Japan
(2) Department of Internal Medicine, Tama-Nagayama Hospital, Nippon Medical School, 1-7-1 Nagayama, Tama-shi, Tokyo 206-8512, Japan
(3) Department of Pathology, Tama-Nagayama Hospital, Nippon Medical School, 1-7-1 Nagayama, Tama-shi, Tokyo 206-8512, Japan
(4) Department of Radiology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8603, Japan

Abstract. The imaging features of primary pericardial mesothelioma have rarely been described. Herein we present a case report of its diagnostic-pathologic features. Chest computed tomography (CT) revealed an irregularly enhanced mass occupying the entire pericardial space and surrounding the superior vena cava. At autopsy, the tumor was found to fill the pericardial space completely, and to extend to the superior vena cava through the superior pericardial sinus. The CT features of the tumor were correlated well with those revealed at autopsy, and provided satisfactory information regarding the presence and the extension of the tumor.

Article/Cases Studies on Desmoplastic Malignant Mesothelioma or Malignant Mesothelioma

Desmoplastic malignant mesothelioma is the growth of fibrous or connective tissues around the tumor of the lining of the lung or chest cavity. The term "desmoplastic" refers to the growth of fibrous or connective tissue. "Desmo-" comes from the Greek "desmos" meaning "a fetter or band" and "-plastic" is also borrowed from the Greek, from "plassein" meaning "to form" = to form a band or fetter

Kannerstein M, Churg J: Desmoplastic diffuse mesothelioma. In: Progress in Surgical Pathology, Vol. II (Fenoglio CM, Wolff M, eds.), New York: Masson Pub., 1980, pp. 19-29.

Machin T, Mashiyama ET, Henderson JAM, McCaughey WTE: Bony metastases in desmoplastic pleural mesothelioma. Thorax 43:155-156, 1988.

Hillerdal G: Malignant mesothelioma 1982: Review of 4710 published cases. Br J Dis Chest 77:321-343, 1983.

McCaughey Wte: Criteria for diagnosis of diffuse mesothelial tumors. Ann NY Acad Sci 132:603-613, 1965.

Adams VI, Unni KK, Muhm JR, Jett JR, Ilstrup DM, Bernatz PE: Diffuse malignant mesothelioma of pleura: Diagnosis and survival in 92 cases. Cancer 58:1540-1551, 1986.

Obers VJ, Leiman G, Girdwood RW, Spiro FI: Primary malignant pleural tumors (mesothelioma) presenting as localized masses: Fine needle aspiration cytologic findings, clinical and radiologic features and review of the literature. Acta Cytolog 32:567-575, 1988.

Solomons K, Polakow R, Marchand P: Diffuse malignant mesothelioma presenting as bilateral malignant lymphangitis. Thorax 40:682-683, 1985.

Alexander E, Clark RA, Colley DP, Mitchell SE: CT of malignant pleural mesothlioma. AJR 137:287-291, 1981.

Mirvis S, Dutcher JP, Haney PJ, Whitley NO, Aisner J: CT of malignant pleural mesothelioma. AJR 140:665-670, 1983.

Lorigan JG, Libshitz HI: MR imaging of malignant pleural mesothelioma. J Comput Asst Tomogr 13:617-620, 1989.

Harwood TR, Gravey DR, Yokoo H: Pseudomesotheliomatous carcinoma of the lung: A variant of peripheral lung cancer. Am J Clin Pathol 65:159-167, 1976.

Whitaker D, Shilkin KB: Diagnosis of pleural malignant mesothelioma in life: A practical approach. J Pathol 143:147-175, 1984.

Roberts GH, Campbel GM: Exfoliative cytology of diffuse mesothelioma. J Clin Pathol 25:577-582, 1972.

Sterrett GF, Whitaker D, Shilkin KB, Walters MNI: Fine needle aspiration cytology of malignant mesothelioma. Acta Cytologica 31:185-193, 1987. Churg J, Rosen SH, Moolten S: Histological characteristics of mesothelioma associated with asbestos. Ann NY Acad Sci132:614-622, 1965.

Adams VI, Unni KK: Diffuse malignant mesothelioma of pleura: Diagnostic criteria based on an autopsy study. AM J Clin Pathol 82:15-23, 1984.

Yousem SA, Hochholzer L: Malignant mesotheliomas with osseous and cartilaginous differentiation. Arch Pathol Lab Med 111:62-66, 1987.

The onset of pleural diffuse malignant mesothelioma is usually insidious. Chest pain and dyspnea are the most frequent initial complaints; cough, weight loss, and asthenia tend to develop somewhat later. Infrequently, diffuse malignant mesothelioma may present as recurrent pneumothorax. (Situnayake RD, Middleton WG.

Recurrent pneumothorax and malignant pleural mesothelioma. RespirMed 1991;85:255-6.) , miliary dissemination in the absence of clinically identifiable pleural- based tumor. (Musk AW, Dewar J, Shilkin KB, Whitaker D. Miliary spread of malignant pleural mesothelioma without a clinically identifiable pleural tumor. Aust NZ J Med 1991;21:460-2.) , or enlargement of ipsilateral supraclavicular lymph nodes (Sussman J, Rosai J. Lymph node metastasis as the initial manifestation of malignant mesothelioma: report of six cases. Am J Surg Pathol 1990;14:819-28.)

The most distressing symptom as the disease progresses is pain due to infiltration of the chest wall. The pain is often of an aching, nonpleuritic type and may be referred to the abdomen or shoulder. Evidence of pleural effusion is the most frequent finding on initial physical and radiographic examination.
(Legha SS, Muggia FM.

Pleural mesotheliomas. Clinical features and therapeutic implications. Ann Intern Med 1977;87:613-21.) , and a small proportion of diffuse malignant mesotheliomas are preceded for periods ranging from 1 to 7 years by recurrent pleural effusions. Close to 10 percent of patients have radiologic evidence of tumor without effusion.

Asbestos workers may have recurrent pleural effusions with associated fibrous pleurisy (asbestos pleurisy) in the absence of any tumor. (Gaensler EA, Kaplan AI. Asbestos pleural effusion. Ann Int Med 1971;74:178-91.) Chest roentgenogram and computerized tomographic (CT) scan may show a diffusely nodular or irregularly thickened pleura , hilar or mediastinal masses, or masses of apparent pulmonary origin. (Heller RM, Janower ML, Weber AL. The radiological manifestations of malignant pleural mesothelioma. Am J Roentgenol 1970;108:53-9.) .

The radiologic appearance may change markedly within a short time . Radiologic evidence of asbestosis is uncommon, whereas pleural plaques are seen quite frequently. Effusions are often blood stained, and may be massive and require frequent tapping.

They tend to disappear in the later stages of the disease with advancing neoplastic thickening of the pleura and obliteration of the pleural cavity. Contraction of the affected hemithorax often occurs in the late stages, with pulling of the mediastinal structures to the affected side.

Subcutaneous tumor nodules may appear in the chest wall, especially in relation to aspiration needle or thoracoscopy tracts and thoracotomy scars The tumor may occasionally present as a mass in the chest wall or mimic Pancoast's tumor.

Tumors of the Serosal Membranes.
Battifora H, McCaughey WT. Tumors of the serosal membranes.
Atlas of Tumor Pathology, 3rd Series Fascicle 15.
Washington, D.C., Armed Forces Institute of Pathology, 1995.
key words: AFIP, serosa, peritoneum, peritoneal, pleura, pleural

Packet No.: 2
68658

Nodules of fibrous tumor sometimes infiltrate alveolar spaces in the adjacent lung or the soft tissues of the chest wall. In most instances, cellular areas with sarcomatous characteristics can be found in parts of the tumor, although a careful search is sometimes necessary.

In about one third of cases, epithelial- type tumor elements, usually of tubular or papillary form, are seen at least focally and may be accompanied by obvious sarcomatous areas. Zones of bland infarct-like necrosis are quite common. As such zones are rarely seen in inflammatory fibrosis, they help to distinguish desmoplastic mesothelioma from fibrous pleurisy.

It has been suggested that the most cellular tissue found in desmoplastic mesothelioma is at the mediastinal aspect of the pleura. (Henderson DW, Shilkin KB, Whitaker D, et al. Unusual histological types and anatomic sites of mesothelioma. In: Henderson DW, Shilkin KB, Langlois SL, Whitaker D, eds.

Malignant mesothelioma. New York: Hemisphere Publishing, 1992:140-63.) A feature frequently seen in desmoplastic mesothelioma and rarely, if ever, in fibrosing pleuritis is focal invasion into the underlying pulmonary parenchyma along interlobular septa and fissures and into subserosal adipose tissue in the parietal pleura . Such areas of focal invasion may be made apparent by immunostaining with antibodies to low molecular weight cytokeratins . (Battifora H. The pleura. In: Sternberg SS, ed. Diagnostic surgical pathology. New York: Raven Press, 1989:829-55.)

Nonetheless, even when abundant decortication material is available, and numerous samples are taken, confident differentiation between desmoplastic mesothelioma and fibrous pleurisy may be difficult or impossible.

It should be remembered that there are many causes of benign diffuse pleural fibrosis, one of which is asbestos. (Gaensler EA, Kaplan AI. Asbestos pleural effusion. Ann Int Med 1971;74:178-91.) Asbestos is also the main cause of the discrete fibrous plaques that are frequently seen on the parietal pleura in persons exposed to asbestos.

Tumors of the Serosal Membranes.
Battifora H, McCaughey WT. Tumors of the serosal membranes.
Atlas of Tumor Pathology, 3rd Series Fascicle 15.
Washington, D.C., Armed Forces Institute of Pathology, 1995.
key words: AFIP, serosa, peritoneum, peritoneal, pleura, pleural

Packet No.: 4
68659

In cases in which only small biopsy specimens are available, localized malignant fibrous tumors of the pleura (so-called malignant localized mesothelioma) may enter into the differential diagnosis because of the dense fibrosis that occurs in some of them.

Immunostaining for low molecular weight keratins helps in diagnosis since desmoplastic mesotheliomas nearly always express keratin, whereas benign localized fibrous tumors do not. Ultrastructurally, desmoplastic mesothelioma is similar to conventional sarcomatoid mesothelioma, but with more cells with the appearance of myofibroblasts. (d'Andiran G, Gabbiani GA. Metastasizing sarcoma of the pleura composed of myofibroblasts. In: Fenoglio CM, Woolf M, eds. Progress in surgical pathology. New York: Masson Publishing, 1980:34-40.)

However, the frequent expression of cytokeratins by the cells of desmoplastic mesothelioma sets them apart from myofibroblasts. (Battifora H. The pleura. In: Sternberg SS, ed. Diagnostic surgical pathology. New York: Raven Press, 1989:829-55.) .

Tumors of the Serosal Membranes.
Battifora H, McCaughey WT. Tumors of the serosal membranes.
Atlas of Tumor Pathology, 3rd Series Fascicle 15.
Washington, D.C., Armed Forces Institute of Pathology, 1995.
key words: AFIP, serosa, peritoneum, peritoneal, pleura, pleural.

What Caused Mesothelioma Information on Asbestos

Information on Asbestos FAQ's

What is asbestos?

Asbestos is a mineral. It is mined in much the same way that other minerals, such as iron, lead, and copper, are. Asbestos is composed of silicon, oxygen, hydrogen, and various metal cations (positively charged metal ions). There are many varieties of asbestos: the three most common are chrysotile, amosite, and crocidolite. Chrysotile fibers are pliable and cylindrical, and often arranged in bundles. Amosite and crocidolite fibers are like tiny needles.

The first commercial asbestos mine -- a chrysotile mine -- opened in Quebec, Canada, in the 1870's. Crocidolite asbestos was first mined in South Africa during the 1980's. Amosite asbestos also comes from Africa and was first mined in 1916. Unlike most minerals, which turn into dust particles when crushed, asbestos breaks up into fine fibers that are too small to be seen by the human eye. Often individual fibers are mixed with a material that binds them together, producing asbestos containing material (ACM).

What type of asbestos causes mesothelioma?

Chrysotile asbestos is the main cause of malignant pleural mesothelioma. The three most common forms of asbestos are chrysotile, amosite, and crocidolite. Chrysotile asbestos or white asbestos accounts for approximately 95% of the asbestos used in US production of asbestos products and is the only member of the serpentine group of minerals.

Why has asbestos been so widely used?

Asbestos appealed to manufacturers and builders for a variety of reasons. It is strong yet flexible, and it will not burn. It conducts electricity poorly, but insulates effectively. It also resists corrosion. Asbestos may have been so widely used because few other available substances combine the same qualities.

How many products contain asbestos?

One study estimated that 3,000 different types of commercial products contained asbestos. The amount of asbestos in each product varied from as little as one percent to as much as 100 percent. Many older plastics, paper products, brake linings, floor tiles and textile products contain asbestos, as do many heavy industrial products such as sealants, cement pipe, cement sheets, and insulation. The final Asbestos Ban and Phaseout Rule prohibits the manufacture, processing and importation of most asbestos products.

How long has asbestos been in use?

Asbestos was first used in the United States in the early 1900's, to insulate steam engines. But until the early 1940's, asbestos was not used extensively. However, after World War II, and for the next thirty years, people who constructed and renovated schools and other public buildings used asbestos and asbestos -containing materials (ACM) extensively. They used ACM primarily to fireproof, insulate, soundproof, and decorate. The Environmental Protection Agency (EPA) estimates that there are asbestos containing materials in most of the nation's approximately 107,000 primary and secondary schools and 733,000 public and commercial buildings.

How are people exposed to asbestos? When asbestos fibers are in the air, people may inhale them. Because asbestos fibers are small and light, they can stay in the air for a long time. People whose work brings them into contact with asbestos—workers who renovate buildings with asbestos in them, for example— may inhale fibers that are in the air: this is called occupational exposure. Workers' families may inhale asbestos fibers released by clothes that have been in contact with ACM: this is called paraoccupational exposure. People who live or work near asbestos-related operations may inhale asbestos fibers that have been released into the air by the operations: this is called neighborhood exposure. The amount of asbestos a worker is exposed to will vary according to:

• The concentration of fibers in the air
• Duration of exposure
• The worker's breathing rate (workers doing manual labor breathe faster)
• Weather conditions
• The protective devices the worker wears

It is estimated that between 1940 and 1980, 27 million Americans had significant occupational exposure to asbestos. People may also ingest asbestos if they eat in areas where there are asbestos fibers in the air.

When is ACM most likely to release asbestos fibers?

Damaged ACM is more likely to release fibers than non-damaged ACM. In a 1984 survey, EPA found that approximately 66 percent of those buildings that contained asbestos contained damaged ACM. If ACM, when dry, can be crumbled by hand pressure -- a condition known as "friable" -- it is more likely to release fibers than if it is "non-friable." Fluffy, spray-applied asbestos fireproofing material is generally considered "friable." Some materials which are considered "non-friable," such as vinyl-asbestos floor tile, can also release fibers when sanded, sawed or otherwise aggressively disturbed. Materials such as asbestos cement pipe can release asbestos fibers if broken or crushed when buildings are demolished, renovated or repaired. ACM which is in a heavy traffic area, and which is therefore often disturbed, is more likely to release fibers than ACM in a relatively undisturbed area.


How can asbestos be identified?

While it is often possible to "suspect" that a material or product is/or contains asbestos by visual determination, actual determinations can only be made by instrumental analysis. Until a product is tested, it is best to assume that the product contains asbestos, unless the label, or the manufacturer verifies that it does not.

The EPA requires that the asbestos content of suspect materials be determined by collecting bulk samples and analyzing them by polarized light microscopy (PLM). The PLM technique determines both the percent and type of asbestos in the bulk material. EPA Regional Offices can provide information about laboratories that test for asbestos.

Does asbestos exposure cause health problems?

Some people exposed to asbestos develop asbestos-related health problems; some do not. Once inhaled, asbestos fibers can easily penetrate body tissues. They may be deposited and retained in the airways and lung tissue. Because asbestos fibers remain in the body, each exposure increases the likelihood of developing an asbestos-related disease. Asbestos related diseases may not appear until years after exposure. Today we are seeing results of exposure among asbestos workers during World War II.

A medical examination which includes a medical history, breathing capacity test and chest x-ray may detect problems early. Scientists have not been able to develop a "safe" or threshold level for exposure to airborne asbestos. Ingesting asbestos may be harmful, but the consequences of this type of exposure have not been clearly documented. Nor have the effects of skin exposure to asbestos been documented. People who touch asbestos may get a rash similar to the rash caused by fiberglass.

What illnesses are associated with asbestos exposure?

Asbestosis

Asbestosis is a serious, chronic, non-cancerous respiratory disease. Inhaled asbestos fibers aggravate lung tissues, which causes them to scar. Symptoms of asbestosis include shortness of breath and a dry crackling sound in the lungs while inhaling. In its advanced stages, the disease may cause cardiac failure.

There is no effective treatment for asbestosis; the disease is usually disabling or fatal. The risk of asbestosis is minimal for those who do not work with asbestos; the disease is rarely caused by neighborhood or family exposure. Those who renovate or demolish buildings that contain asbestos may be at significant risk, depending on the nature of the exposure and precautions taken.

Lung Cancer

Lung cancer causes the largest number of deaths related to asbestos exposure. The incidence of lung cancer in people who are directly involved in the mining, milling, manufacturing and use of asbestos and its products is much higher than in the general population. The most common symptoms of lung cancer are coughing and a change in breathing. Other symptoms include shortness of breath, persistent chest pains, hoarseness, and anemia.

People who have been exposed to asbestos and are also exposed to some other carcinogen — such as cigarette smoke — have a significantly greater risk of developing lung cancer than people who have only been exposed to asbestos. One study found that asbestos workers who smoke are about 90 times more likely to develop lung cancer than people who neither smoke nor have been exposed to asbestos.

Mesothelioma

Mesothelioma is a rare form of cancer which most often occurs in the thin membrane lining of the lungs, chest, abdomen, and (rarely) heart. About 3000 cases are diagnosed each year in the United States. Virtually all cases of mesothelioma are linked with asbestos exposure. Approximately 2 percent of all miners and textile workers who work with asbestos, and 10 percent of all workers who were involved in the manufacture of asbestos-containing gas masks, contract mesothelioma.

People who work in asbestos mines, asbestos mills and factories, and shipyards that use asbestos, as well as people who manufacture and install asbestos insulation, have an increased risk of mesothelioma. So do people who live with asbestos workers, near asbestos mining areas, near asbestos product factories or near shipyards where use of asbestos has produced large quantities of airborne asbestos fibers.

The younger people are when they inhale asbestos, the more likely they are to develop mesothelioma. This is why enormous efforts are being made to prevent school children from being exposed.

Other Cancers

Evidence suggests that cancers in the esophagus, larynx, oral cavity, stomach, colon and kidney may be caused by ingesting asbestos. For more information on asbestos-related cancers, contact your local chapter of the American Cancer Society.

Who regulates asbestos?

The U.S. Environmental Protection Agency and the Occupational Safety and Health Administration (OSHA) are responsible for regulating environmental exposure and protecting workers from asbestos exposure. OSHA is responsible for the health and safety of workers who may be exposed to asbestos in the work place, or in connection with their jobs. EPA is responsible for developing and enforcing regulations necessary to protect the general public from exposure to airborne contaminants that are known to be hazardous to human health.

The EPA's Worker Protection Rule (40 CFR Part 763, Subpart G) extends the OSHA standards to state and local employees who perform asbestos work and who are not covered by the OSHA Asbestos Standards, or by a state OSHA plan. The Rule parallels OSHA requirements and covers medical examinations, air monitoring and reporting, protective equipment, work practices, and record keeping. In addition, many State and local agencies have more stringent standards than those required by the Federal government. People who plan to renovate or remove asbestos from a building of a certain size, or who plan to demolish any building, are required to notify the appropriate federal, state and local agencies, and to follow all federal, state, and local requirements for removal and disposal of regulated asbestos-containing material (RACM).

EPA's advice on asbestos is neither to rip it all out in a panic nor to ignore the problem under a false presumption that asbestos is "risk free." Rather, EPA recommends a practical approach that protects public health by emphasizing that asbestos material in buildings should be located, that it should be appropriately managed, and that those workers who may disturb it should be properly trained and protected. That has been, and continues to be, EPA's position. The following summarizes the five major facts that the Agency has presented in congressional testimony:

FACT ONE:
Although asbestos is hazardous, human risk of asbestos disease depends upon exposure.

FACT TWO:
Prevailing asbestos levels in buildings -- the levels school children and you and I face as building occupants -- seem to be very low, based upon available data. Accordingly, the health risk we face as building occupants also appears to be very low.

FACT THREE:
Removal is often not a school district's or other building owner's best course of action to reduce asbestos exposure. In fact, an improper removal can create a dangerous situation where none previously existed.

FACT FOUR:
EPA only requires asbestos removal in order to prevent significant public exposure to asbestos, such as during building renovation or demolition.

FACT FIVE:
EPA does recommend in-place management whenever asbestos is discovered. Instead of removal, a conscientious in-place management program will usually control fiber releases, particularly when the materials are not significantly damaged and are not likely to be disturbed.

What are EPA's regulations governing asbestos?

TSCA

In 1979, under the Toxic Substances Control Act (TSCA), EPA began an asbestos technical assistance program for building owners, environmental groups, contractors and industry. In May 1982, EPA issued the first regulation intended to control asbestos in schools under the authority of TSCA; this regulation was known as the Asbestos-in-Schools Rule. Starting in 1985, loans and grants have been given each year to aid Local Education Agencies (LEAs) in conducting asbestos abatement projects under the Asbestos School Hazard Abatement Act (ASHAA).

AHERA

In 1986, the Asbestos Hazard Emergency Response Act (AHERA; Asbestos Containing Materials in Schools, 40 CFR Part 763, Subpart E) was signed into law as Title II of TSCA. AHERA is more inclusive than the May 1982 Asbestos-in-Schools Rule. AHERA requires LEAs to inspect their schools for asbestos containing building materials (ACBM) and prepare management plans which recommend the best way to reduce the asbestos hazard. Options include repairing damaged ACM, spraying it with sealants, enclosing it, removing it, or keeping it in good condition so that it does not release fibers.

The plans must be developed by accredited management planners and approved by the State. LEAs must notify parent, teacher and employer organizations of the plans, and then the plans must be implemented. AHERA also requires accreditation of abatement designers, contractor supervisors and workers, building inspectors, and school management plan writers. Those responsible for enforcing AHERA have concentrated on educating LEAs, in an effort to ensure that they comply with the regulations. Contractors that improperly remove asbestos from schools can be liable under both AHERA and NESHAP. For more information on AHERA, request the pamphlet entitled "The ABC's of Asbestos in Schools" from the EPA Public Information Center.

ASBESTOS BAN & PHASEOUT RULE

In 1989 EPA published the Asbestos: Manufacture, Importation, Processing, and Distribution in Commerce Prohibitions; Final Rule (40 CFR Part 763, Subpart I). The rule will eventually ban about 94 percent of the asbestos used in the U.S. (based on 1985 estimates). For example, asbestos containing drum brake linings and roof coatings will be banned. The rule will be implemented in three stages between 1990 and 1997.

NESHAP

The Clean Air Act (CAA) of 1970 requires EPA to develop and enforce regulations to protect the general public from exposure to airborne contaminants that are known to be hazardous to human health. In accordance with Section 112 of the CAA, EPA established National Emission Standards for Hazardous Air Pollutants (NESHAP). Asbestos was one of the first hazardous air pollutants regulated under Section 112. On March 31, 1971, EPA identified asbestos as a hazardous pollutant, and on April 6, 1973, EPA promulgated the Asbestos NESHAP in 40 CFR Part 61, Subpart M. The Asbestos NESHAP has been amended several times, most recently in November 1990. For a copy of the Asbestos NESHAP contact the Asbestos NESHAP Coordinators listed in the Appendix.

What are the basic requirements of the Asbestos NESHAP?

The Asbestos NESHAP is intended to minimize the release of asbestos fibers during activities involving the handling of asbestos. Accordingly, it specifies work practices to be followed during renovations of buildings which contain a certain threshold amount of friable asbestos, and during demolitions of all structures, installations, and facilities (except apartment buildings that have no more than four dwelling units). Most often, the Asbestos NESHAP requires action to be taken by the person who owns, leases, operates, controls, or supervises the facility being demolished or renovated (the "owner"), and by the person who owns, leases, operators, controls or supervises the demolition or renovation (the "operator").

The regulations require owners and operators subject to the Asbestos NESHAP to notify delegated State and local agencies and/or their EPA Regional Offices before demolition or renovation activity begins. The regulations restrict the use of spray asbestos, and prohibit the use of wet applied and molded insulation (i.e., pipe lagging). The Asbestos NESHAP also regulates asbestos waste handling and disposal.

Why was the Asbestos NESHAP recently amended?

The Asbestos NESHAP was amended for several reasons. EPA wanted to clarify existing regulatory policies, and to add regulations which explicitly address monitoring and record keeping at facilities which mill, manufacture, and fabricate asbestos. Also, because of the high risk associated with the transfer and disposal of ACM, EPA also wanted to strengthen the requirements which govern asbestos waste disposal by requiring tracking and record keeping. Furthermore, EPA determined that the Asbestos NESHAP needed to take into account the availability of improved emission controls. EPA also wanted to make the NESHAP consistent with other EPA statutes that regulate asbestos.

What sources are now covered by the asbestos NESHAP?

The following activities and facilities are currently regulated by the Asbestos NESHAP:

• The milling of asbestos.
• Roadways containing ACM.
• The commercial manufacture of products that contain commercial asbestos.
• The demolition of all facilities.
• The renovation of facilities that contain friable ACM.
• The spraying of ACM.
• The processing (fabricating) of any manufactured products that contain asbestos.
• The use of insulating materials that contain commercial asbestos.
• The disposal of asbestos-containing waste generated during milling, manufacturing, demolition, renovation, spraying, and fabricating operation.
• The closure and maintenance of inactive waste disposal sites.
• The operation of and reporting on facilities that convert asbestos containing waste material into non-asbestos material.
• The design and operation of air cleaning devices.
• The reporting of information pertaining to process control equipment, filter devices, asbestos generating processes, etc.
• Active waste disposal sites.

What were the major changes to the Asbestos NESHAP?

Milling, Manufacturing, and Fabricating Sources
Businesses which are involved in asbestos milling, manufacturing, and fabricating now must monitor for visible emissions for at least 15 seconds at least once a day (during daylight hours), and inspect air cleaning devices at least once a week. The facilities must maintain records of the results, and submit each quarter a copy of the visible emissions monitoring records if visible emissions occurred during the quarter. Facilities that install fabric filters (to control asbestos emissions) after the effective date of the revision must provide for easy inspection of the bags.

Demolition and Renovation
All facilities which are "demolished" are subject to the Asbestos NESHAP. The definition of demolition was expanded to include the intentional burning of a facility, in addition to the "wrecking or taking out . . . any load-supporting structural member of a facility." Owners and operators of all facilities which are to be demolished, and of facilities that contain a certain amount of asbestos which are to be renovated, must now provide more detailed information in notifications, including the name of the asbestos waste transporter and the name of the waste disposal site where the ACM will be deposited.

Owners and operators must give a 10-day notice for planned renovations and demolitions. They must renotify EPA in advance of the actual start date if the demolition or renovation will begin on a date other than the one specified in the original notification. Telephone re-notifications are permitted, but must be followed by written notice.

Starting one year after promulgation of the regulation, a person trained in the provisions of the Asbestos NESHAP, and in the methods of complying with them, must supervise operations in which ACM is stripped, removed or otherwise handled. This supervisor is responsible for all on-site activity. Before wetting is suspended, the EPA administrator must approve. When wetting of asbestos during its removal is suspended due to freezing temperatures, owners or operators must measure the air temperature in the work area three times during the workday, and must keep those records for at least two years.

The revisions also clarify EPA's position regarding the handling and treatment of non- friable asbestos material. The owner and operator must inspect the site for the presence of non-friable ACM, and include in the notification an estimate of how much non-friable ACM is present. Also, the owner and operator must describe the procedures to be followed if unexpected ACM is found in the course of demolition or renovation, and if non-friable asbestos becomes friable in the course of renovation or demolition.

Waste Transport and Disposal

Vehicles used to transport ACM must be marked according to new guidelines during loading and unloading. Labels indicating the name of the waste generator and the location where the waste was generated must be placed on containers of RACM. When ACM waste is transported off-site, a waste shipment record (WSR) must be given to the waste site operator or owner at the time that the waste is delivered to the waste disposal site. The owner or operator must send a signed copy of the WSR back to the waste generator within 30 days, and attempt to reconcile any discrepancy between the quantity of waste given on the WSR and the actual amount of waste received. If, within 15 days of receiving the waste, the waste site owner or operator cannot reconcile the discrepancy, he or she must report that problem to the same agency that was notified about the demolition or renovation.

New disposal sites must apply for approval to construct, and must notify EPA of the startup date. Existing disposal sites must supply EPA with certain information concerning their operations, such as the name and address of the owner or operator, the location of the site, the average weight per month of the hazardous materials being processed, and a description of the existing emission control equipment.

If a copy of the WSR signed by the waste site owner or operator is not received by the waste generator within 35 days of the date that the waste was accepted by the initial transporter, the waste generator must contact the transporter and/or disposal site owner or operator to determine the status of the waste shipment. If a signed copy of the WSR is not received within 45 days of the date that the waste was accepted by the initial transporter, the waste generator must submit a written report to the same agency that was notified about the demolition or renovation.

Owners of disposal sites must record on the deed to the disposal site that the property has been used for ACM disposal. They must also keep records that show the location, depth, area and volume of the asbestos waste; they must indicate on the deed that these records are available. Owners of inactive disposal sites must obtain written approval before they excavate or otherwise disturb ACM waste that has been deposited on the site.

Where can I get more information?

There are ten EPA Regional Offices around the country. You can obtain more information about the Asbestos NESHAP by contacting your EPA Regional Office's NESHAP coordinator or the appropriate State or local agency.

You can obtain more information about AHERA by contacting your EPA Regional Asbestos Coordinator (RAC). You may also call the EPA Toxic Substances Control Act (TSCA) Hotline to ask general questions about asbestos, or to request asbestos guidance documents. The Hotline number is (202) 554-1404.

The EPA Public Information Center can send you information on EPA regulations. You can reach the center at (202) 382-2080 or (202) 475-7751.

The Office of the Federal Register (202-382- 5475) can send you copies of any regulations published in The Federal Register, including the Asbestos NESHAP.

Finally, the EPA has an Asbestos Ombudsman to provide information on the handling and abatement of asbestos in schools, the work place and the home. Also, the EPA Asbestos Ombudsman can help citizens with asbestos-in-school complaints. The Ombudsman can be reached toll-free at (800) 368-5888, direct at (703) 557-1938 or 557-1939.