Document Mn75b3kjYELE8reaVv213x7L

638 Reprinted from the Archives of Bnvironmental Health April 1968, Volume 16 Copyright 1968. American Medical Association PLAINTIFF'S EXHIBIT Experimental Studies on the Progressiveness of the Pulmonary Fibrosis Caused by Chry6otile Dust Paul Gran. MD, and Robert T. P. dr Trrrillc. PUltburgh unreliability of symptoms as a crite rion for the progression of pulmonary fibro sis was underlined in a medical and psychi atric study of coal miners with respiratory complaints. Here, a very significant associa tion was observed between a recognizable psychoneurotic factor and an apparent worsening of the clinical condition: of 40 patients studied, only 12.5% had disability on "physical" grounds alone; 35% had dis ability on psychiatric grounds alone; and the remainder on both.1 Furthermore, discerning clinicians recog nize that opinions concerning the progres sion of a pulmonary fibrosis based upon the symptomatology (eg, shortness of breath) and a roentgenologic evaluation, even when reenforced by lung function studies may be quite erroneous. In the presence of a superadded coincidental pulmonary illness, such signs and symptoms may be reversible in whole or in part between such episodes, which include covert and overt acute pneumonitides, pulmonary edema, and allergic or chronic bronchitis--with or without em physema, or emphysema without bronchitis. Such diagnostic difficulties were the subject of a recent symposium on emphysema in >n- dustry. As uncertain as are the clinical criteria of progression of pneumoconiosis, very little help has come from postmortem studies of human lungs or those of experimental ani mals in defining the criteria by which progression of pneumoconiosis may be de- Submitled lor publication Aug 9. 1966; accepted Aug 15. From the Industrial Hygiene Foundation. Mellon Institute. Pittsburgh. Read before the Hatch Symposium. Graduate School of Public Health, University of Pittsburgh, Julv IB-19. 1966. Reprint requests to the Industrial Health Foundslion, Mellon Institute, 4400 Fifth Ave. Pittsburgh 15213 (Dr. Gross). termined. This is particularly true of asbestosis. It is the purpose of this paper to define some of the anatomic stigmata of progres sion of asbeslosis and to determine whether or not asbestosis caused by chrysotile dust is progressive. Methods and Materials Lung burdens of chrysotile asbestos dust were imposed upon rats, hamsters, and guinea pigs by exposure in inhalation chambers as well as by intratracheal injection. Most of the ani mals exposed to dust in an inhalation chamber and reported in this study were part of a larger investigation that will be reported separately. The inhalation chamber in which all animals (except four guinea pigs) were exposed to dust, measured 8x8x8 feel. The animals were housed in wire cages that were suspended in racks. Periodically, these cages were rotated so that inequalities in dust exposure caused by po sition were largely obviated. The exposures were for Bix hours per day, five days per week. The total exposure varied, as listed in the table. The chrysotile asbestos was ballmilled and then Ted into a hammennill (modified from a design by Holt and Young:). This was provided with inlet and outlet tubing so arranged that the comminuted asbestos was fed back continu ally into the hammennill. At the same time, the ultrafines were allowed to waft upward into the inhalation chamber. Two of these hammermills provided the chamber with sufficient dust to av erage 86 mg/cu m with a range of 42 mg/cu m to 146 mg/cu m. The asbestos dust cloud was evaluated by sampling with a two-stage sire se lective device, similar in design to that pro posed by Wright3 and operated at 20 li ters/minute. The first stage of the instrument was a horizontal elutriator with selector char acteristics recommended by the Johannesburg Pneumoconiosis Conference of 1959, namely acceptance of all particles having terminal set tling velocities greater than that of a 7.1s sphere of density 1 gm/cu cm. 50% acceptance Arch Environ Health--Vol 15. Nov 1957 SCF-FA-5980 8005 1458 PRODUCED BY FORD