26 shared non-person entities · 1 shared topics · similarity 0.989
machine-extracted · confidence unavailable · Check page ↗NYC-WTC_000195068
Label derived from the City's folder field. The City does not supply document titles.NYC-WTC_000195068–000195119
OCR status: ok · source: pdftotext
NYC 9/11 Public Portal Document
ASBESTOS MEDITEXT ® - Medical Management Page 3 of 15
capacity, and clinical symptoms of interstitial fibrosis (rales, clubbing and cyanosis) (Markowitz et al, 1997). B. PLEURALPLAQUES 1. DEFINITION - Pleural plaques are focal, irregular thickenings composed of dense bands of avascular collagen occurring predominantly in the submesothelial parietal pleura (Gefter & Conant, 1988). 2. SITES - Plaques may be bilateral and asymmetrical, and are usually located on the parietal pleura of the thorax, diaphragm, mediastinum, or pericardium (Dark & Pingleton, 1983; Mossman & Gee, 1989). Less often, they may occur on the visceral pleura within the interlobar fissure (Gefter & Conant, 1988). 3. CAUSES - Although plaques are the most common chest radiographic manifestation of asbestos exposure, no such exposure can be established for 22 percent of autopsy-proven cases (Gefter & Conant, 1988). While the overall incidence of plaques increases with dose, there is no linear correlation between plaque severity and total dust exposure (Gefter & Conant, 1988). 4. CLINICAL MANIFESTATIONS - Plaques by themselves are not symptomatic until they become calcified and large enough to restrict chest wall movements and thus affect vital capacity (ATSDR, 1995; Dark & Pingleton, 1983; Dunn, 1989; Gefter & Conant, 1988; Mossman & Gee, 1989). 5. MALIGNANCY - Pleural plaques are not lung cancer precursors, although persons with pleural plaques have an increased incidence of lung cancer (ATSDR, 1990; Gefter & Conant, 1988; Mossman & Gee, 1989) and possibly malignant mesothelioma (Bianchi et al, 1997). C. PLEURAL EFFUSION 1. INCIDENCE of BENIGN ASBESTOS PLEURAL EFFUSIONS - The overall incidence of benign asbestos-related pleural effusions was 3.1 percent, with a 7 percent incidence in the heavily exposed group and a 0.2 percent incidence in the indirectly exposed group in one report (Gefter & Conant, 1988). Of all the asbestos-related diseases, it has the shortest latency period, with detection within the first 10 years after exposure (Dunn, 1989; Gefter & Conant, 1988). 2. CLINICAL MANIFESTATIONS - Acutely, fever, chest pain, leukocytosis, and an increased erythrocyte sedimentation rate (ESR) may be seen (Dark & Pingleton, 1983; Dunn, 1989). 3. Chronically, there are few, if any, signs or symptoms (Dunn, 1989). 4. The effusions are mostly exudative, sterile, and frequently blood-tinged (Dunn, 1989; Gefter & Conant, 1988; ILO, 1983). 5. Most effusions identified were asymptomatic and small (and often overlooked); as many as 28 percent may recur (Gefter & Conant, 1988). D. DIAGNOSIS - Benign asbestos-related pleural effusion is a diagnosis of exclusion. The differential diagnosis includes mesothelioma, metastatic tumor, tuberculosis, and disease involving the superior vena cava, mediastinal nodes, thoracic duct, or pericai’dium (Gefter & Conant, 1988). E. CLINICAL COURSE - Although termed "benign, asbestos-related effusions may precede the development of mesothelioma in a small number of patients, necessitating long-term follow-up (Gefter & Conant, 1988). Benign pleural effusions may also lead to functional respiratory impairment because of ensuing fibrosis and pleural thickening (Gefter & Conant, 1988).
o PLEURAL THICKENING
http://www.tomescps.com/DATA/TM/TM356-3.htm 1/4/2002
CITY_21MC100_011105053
NYC-WTC_000195071
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