NYC-WTC_000195068

NYC 9/11 Public Portal Document

■ ASBESTOS MEDITEXT ® - Medical Management Page 9 of 15

fiber-year/mL of exposure (Albin et al, 1990). 2. The rate of mesothelioma continues to rise, with estimated lifetime risks of 1.3 percent in British persons bom between 1893 and 1948, 1.0 percent in those bom between 1943 and 1948, and 0.6 percent for those bom between 1948 and 1953. 3. According to one model, deaths from mesothelioma will peak in approximately the year 2020, and may account for 1 percent of all deaths for men bom in the 194O's (Peto et al, 1995). 2. CONSISTENCY/RISK ESTIMATES includes the following - a. Risk estimates for bronchogenic cancer among workers with asbestosis or significant exposure to asbestos have not been consistently high. This variability can be due to methodological differences. b. Although persons exposed to asbestos by inhalation have a twofold greater risk of colorectal cancer than unexposed individuals, data were conflicting and insufficient to clearly relate GI tumors or peritoneal mesotheliomas to direct ingestion of asbestos fibers (Albin et al, 1990; ATSDR, 1990; Edelman, 1988; Weiss, 1990). c. A 3.4-fold increase in mortality from malignancy (compared to expected rates) has been noted among workers in a factory where the average asbestos level was 80 particles/mL and where crocidolite-containing cigarette filters were manufactured (Talcott et al, 1989). d. In one study of mesothelioma cases among miners and millers, amphibole (crocidolite and amosite), chrysotile, and tremolite were found in lung fibers and were highest among workers with mesothelioma (Dufresne et al, 1995). 3. TEMPORALITY is shown as follows - a. Reports of asbestosis and colorectal cancer showed only temporality of association and not causality (Weiss, 1990). 4. BIOLOGIC SENSE is shown as follows - a. Asbestos fibers have been identified within some human specimens of colorectal adenocarcinomas and in extrapulmonary tissues, including tonsils, thoracic and abdominal lymph nodes, small intestines, pancreas, kidneys, and bone marrow (ATSDR, 1990; Finkel, 1983; Smith et al, 1989). This establishes only site­ specific evidence of exposure, not causation (Weiss, 1990). b. Lung cancer patients had significantly higher levels of ferruginous bodies in lung digests than did controls, even though only one cancer patient had any known exposure to asbestos (Warnock & Churg, 1975). This finding suggests that asbestos may be commonly involved in lung cancer. c. Animal studies revealed that asbestos fibers can penetrate the GI tract (ATSDR, 1990). Tumorigenesis has also been noted in animal bioassays (Smith et al, 1989). 5. OZONE effects are shown as follows - a. Prolonged exposure to low levels of ozone appears to impair clearance of asbestos from the lungs. In a study of rats exposed to low levels of ozone for 6 weeks and then exposed to aerosolized asbestos fibers for 5 hours, fiber mass and fiber number were significantly greater (P<0.05) than that of a control group of rats exposed only to aerosolized asbestos (Pinkerton et al, 1989). D. MESOTHELIOMA 1. Mesothelioma is a rapidly invasive and fatal malignancy associated with asbestos exposure (ATSDR, 1990; Neuberger & Kundi, 1990; Newhouse, 1983; Roggli et al, 1993). a. Andersson & Toren (1995) suggested that in Sweden there may be an under

http;//www.tomescps.com/DATA/TM/TM356-3.htm 1/4/2002

CITY_21MC100_011105059

NYC-WTC_000195077