To elucidate immune pathogenic mechanisms in asbestosis, lung and spleen lymphoid cell populations were analyzed at defined time intervals (1, 2, 3, 6, and 12 weeks during exposure and 4, 24, and 48 weeks post-exposure) in asbestos-exposed and unexposed (control) mice. Polymorphonuclear leukocytes and macrophages were increased in the lung tissue histologic sections of asbestos-exposed mice compared to controls. No consistent changes were observed in percentages of lung or spleen helper, suppressor, or total lymphocyte populations after asbestos exposure. The numbers of B cells (identified by anti-IgG) in minced lung preparations of asbestos-exposed animals were increased after 12 weeks of exposure. There also was an increase in IgG production in asbestos-exposed mice after 12 weeks exposure and at 4 weeks post-exposure with a return to near baseline levels 24 and 48 weeks after initial exposure. Collectively, these studies demonstrate stimulatory effects of inhaled asbestos fibers on B cells and IgG production after 12 weeks of continuous inhalation of asbestos fibers in a dust generation chamber.

Results of isocyanate challenge tests performed on 63 workers referred with a diagnosis of probable isocyanate asthma between 1974 and 1988 were reviewed. Thirty (48 percent) had an acute episode of asthma with a greater than 20 percent decline in FEV1 following subirritant exposure to isocyanates. No difference in the frequency or type of respiratory complaints between isocyanate reactors and nonreactors was found. No differences in lung function results were present when comparing smoking and ex-smoking reactors and nonreactors. In never-smokers with complaints consistent with isocyanate-induced asthma, the presence of obstructive lung disease increased the likelihood that isocyanate-induced asthma was present. Bronchial responsiveness to methacholine occurred in nearly all isocyanate reactors but predicted isocyanate-induced asthma in only 68 percent of the workers. In nearly all cases of challenge-confirmed toluene diisocyanate (TDI)-induced asthma, a 15-min exposure to 20 ppb of the commercial TDI mixture (80:20 2,4:2,6) provoked asthma. Conversely, in the absence of an asthmatic response following exposure to this dose for this duration, a second exposure at this concentration for a longer time would be reasonable to confirm the absence of isocyanate-induced asthma. Among workers employed in the production of polyurethane foam and confirmed to have TDI-induced asthma by inhalation challenge to the different TDI isomers, there appeared to be increased airway reactivity to the 2,6 isomer. This may have relevance to the frequency and intensity of respiratory symptoms that workers with TDI-induced asthma develop in differing industrial settings.

Journal Article Effect of Chemical Composition on Pulmonary Clearance of Man-Made Mineral Fibres Get access Y. Hammad, Y. Hammad Tulane Medical Center1700 Perdido Street, New Orleans, LA 70112, U.S.A. Search for other works by this author on: Oxford Academic PubMed Google Scholar W. Simmons, W. Simmons Tulane Medical Center1700 Perdido Street, New Orleans, LA 70112, U.S.A. Search for other works by this author on: Oxford Academic PubMed Google Scholar H. Abdel-Kader, H. Abdel-Kader Tulane Medical Center1700 Perdido Street, New Orleans, LA 70112, U.S.A. Search for other works by this author on: Oxford Academic PubMed Google Scholar C. Reynolds, C. Reynolds Tulane Medical Center1700 Perdido Street, New Orleans, LA 70112, U.S.A. Search for other works by this author on: Oxford Academic PubMed Google Scholar H. Weill H. Weill Department of Earth Sciences, University of New OrleansNew Orleans, LA 70148, U.S.A. Search for other works by this author on: Oxford Academic PubMed Google Scholar The Annals of Occupational Hygiene, Volume 32, Issue inhaled_particles_VI, January 1988, Pages 769–779, https://doi.org/10.1093/annhyg/32.inhaled_particles_VI.769 Published: 01 January 1988

Prolonged asbestos inhalation results in pulmonary inflammation and fibrosis. Since alveolar macrophages are active in regulation of immune responses in lung and appear to be involved in the pathogenesis of asbestosis, we evaluated the effects of asbestos exposure on the ability of these cells to regulate lymphocyte function. Alveolar macrophages obtained by lung lavage from BALB/C mice were treated in vitro with either UICC amosite or chrysotile asbestos and the effects on lymphocyte cytostasis compared with those of macrophages incubated with latex beads or zymosan. Macrophages (10%) incubated either alone or with latex beads for 48 hr effectively inhibited lymphocyte mitogenesis. However, alveolar macrophages incubated with either amosite or chrysotile asbestos did not demonstrate intact cytostatic activity. Decreased viability of chrysotile asbestos-treated macrophages correlated with loss of cytostatic effects, but alveolar macrophages exposed to amosite remained viable. We conclude, therefore, that exposure of alveolar macrophages to asbestos can result in loss of their ability to down-regulate lymphocyte proliferation, a finding which may be important in the pathogenesis of asbestos-related disease.

Balb/c mice were exposed to aerosolized chrysotile fibers and evaluated as a host for the study of asbestos-induced pulmonary disease. Histologically, an initial macrophage reaction was found to progress to "asbestos body" formation and diffuse focal interstitial fibrosis within 1 year of a chronic exposure period. This reaction was most intense in areas adjacent to respiratory bronchioles and alveolar ducts. Two morphologically distinct tumors at the pulmonary visceral surface were also discovered among a high percentage of asbestos-exposed mice. Bronchoalveolar lavage demonstrated an eventual alteration of the retrievable cell populations among the dusted animals. Evaluation of systemic B-lymphocyte activity suggested a stimulation of this cell subset following chrysotile inhalation. These results demonstrate that subsequent to chronic asbestos exposure, the mouse develops pulmonary and immunologic changes very similar to those noted in human asbestosis.

The lung retention of man-made mineral fibres by rats, sacrificed 5 days after the end of a 6 day period of exposure to the airborne fibre, has been examined as a function of fibre length, diameter and aerodynamic equivalent diameter. The retention of fibres < 0.5 μm dia. showed a peak of about 7.6% at 21 μm fibre length and was significantly higher than the retention (< 1%) of fibres in the diameter categories 0.5-0.7 μm and 0.7-1.0 %mUm. In terms of aerodynamic equivalent diameter, retention was a maximum, ca. 7%, at de = 1 μm, but decreased rapidly to about 0.5 % at de between 1.5 and 2.5 μm amd 0.01% at ca. 4 μm. When fibre length only was considered, irrespective of diameter, retention fell sharply as length increased from 2 to 10 μm, then more slowly to < 0.05% at ca. 40 μm.

The results of an industry-wide study to determine the exposure of workers to man-made mineral fibers are summarized. The purpose of the study was to determine current employee exposures to airborne fibers and to utilize results to estimate past exposures. Measured exposures of workers to airborne total particulate matter and fibers are presented; samples were evaluated by phase contrast and electron microscopy. Results of the three year study, which encompassed 16 facilities and over 1500 eight hour samples, show that although there is a wide variation in concentrations of airborne fibers and particulate matter between and within the facilities surveyed, the concentrations of airborne particulate matter and fibers are generally less than 2.5 mg/m3 and 0.5 fibers/cm3, respectively. The norminal fiber size of the fibers manufactured and average airborne fiber concentration were highly correlated.

In the statistical analysis of the environmental sampling data the empirical observation of the best representation of the data by a log‐normal distribution is theoretically proved. The consequences of this proof in the data analysis is discussed and an example utilizing data from a field study is given to illustrate the appropriateness of using the log‐normal statistics.

Two facilities, one producing rock wool by retort melting with subsequent fiber formation by spinning (Plant A), and the other utilizing slag, glass scrap, and fly ash in a reverbatory furnace to form a melt which is spun (Plant B), were surveyed for dust exposures of employees. A variety of products was manufactured in each plant. The surveys were performed by dividing each facility into “dust zones” on the basis of the processing operations, ventilation methods, or employee jobs. Representative men in each job title associated with each “dust zone” wore personal dust sampling filters and air pumps for an entire work shift. A total of 63 samples was collected in Plant A and 72 in Plant B. Samples of dust on filters were analyzed to determine weight of total dust in the air, expressed as milligrams per cubic meter, and fiber concentrations, expressed as fibers per cubic centimeter in two diameter ranges, greater than 1 μm and less than 1 μm. Phase contrast and electron microscopic methods were utilized for the latter two analyses, respectively. Fiber length and diameter distributions were also determined. Electron microscopic analyses followed ashing of samples; each fiber observed was subjected to an intense beam to determine crystalline or amorphous structure by the presence or absence of a diffraction pattern. The ranges of Total Suspended Particulate Matter (TSPM) concentrations in Plants A and B were 0.53–23.64 and 0.045–6.88 mg/m3, respectively. In Plant A, Tile Finishing and Warehouse were the dustiest zones; in Plant B, Maintenance and Main Plant zones were the dustiest. Average fiber concentrations (>1 μm diameter) determined by phase contrast microscopy ranged from 0.20–1.4 fibers/cm3 in Plant A and from 0.011–0.43 fibers/cm3 in Plant B. The average concentrations of fibers less than 1 μm diameter, as determined by electron microscopy, ranged from 0.0056 to 0.16 fibers/cm3 in Plant A and from 0.0059 to 0.089 fibers/cm3 in Plant B. The percentage of respirable fibers, those less than 3 μm diameter, as determined by phase contrast microscopy, was approximately 75% of all airborne fibers in both plants. Estimates of fiber weight suggest that fibers contribute from 0.11 to 4.3% of TSPM for samples collected in Plant A, and from 0.8 to 57.8% of TSPM for samples collected in Plant B. Thus, fibers, defined to be particles with at least a 3:1 aspect ratio, represent a small fraction of airborne particles to which employees in these plants are exposed. In both facilities the weight concentration of total airborne dust, expressed as milligrams per cubic meter, was a poor indicator of airborne fiber concentration, expressed as fibers per cubic centimeter and determined by either phase contrast microscopy (fibers > 1 μm diameter) or electron microscopy (fibers < 1 μm diameter).

This investigation was aimed at establishing procedures for obtaining data relative to the physical and chemical characterization of respirable coal mine dust for utilization in epidemiological studies of incidence of coal workers' pneumoconiosis in different United States mines. In this paper the dust sampling and analytical procedures are briefly described and results are presented for three samples of approximately 4 grams each collected in each of two United States coal mines representing two different coal seams. Analyses were performed to determine the extent of differences ijn dust properties between (1) samples collected in the same mine and (2) samples collected in each of the two mines.

Annals of the New York Academy of SciencesVolume 200, Issue 1 p. 17-30 PHYSICAL AND CHEMICAL CHARACTERISTICS OF "RESPIRABLE" COAL MINE DUST* Morton Corn, Morton Corn Department of Occupational Health Graduate School of Public Health, University of Pittsburgh Pittsburgh, Pennsylvania 15213Search for more papers by this authorFelix Stein, Felix Stein Department of Occupational Health Graduate School of Public Health, University of Pittsburgh Pittsburgh, Pennsylvania 15213Search for more papers by this authorYehia Hammad, Yehia Hammad Department of Occupational Health Graduate School of Public Health, University of Pittsburgh Pittsburgh, Pennsylvania 15213Search for more papers by this authorSarosh Manekshaw, Sarosh Manekshaw Department of Occupational Health Graduate School of Public Health, University of Pittsburgh Pittsburgh, Pennsylvania 15213Search for more papers by this authorWilliam Bell, William Bell Department of Occupational Health Graduate School of Public Health, University of Pittsburgh Pittsburgh, Pennsylvania 15213Search for more papers by this authorStanley J. Penkala, Stanley J. Penkala Department of Occupational Health Graduate School of Public Health, University of Pittsburgh Pittsburgh, Pennsylvania 15213Search for more papers by this authorRobert Freedman, Robert Freedman Health Research Branch United States Bureau of Mines Pittsburgh, Pennsylvania 15213Search for more papers by this author Morton Corn, Morton Corn Department of Occupational Health Graduate School of Public Health, University of Pittsburgh Pittsburgh, Pennsylvania 15213Search for more papers by this authorFelix Stein, Felix Stein Department of Occupational Health Graduate School of Public Health, University of Pittsburgh Pittsburgh, Pennsylvania 15213Search for more papers by this authorYehia Hammad, Yehia Hammad Department of Occupational Health Graduate School of Public Health, University of Pittsburgh Pittsburgh, Pennsylvania 15213Search for more papers by this authorSarosh Manekshaw, Sarosh Manekshaw Department of Occupational Health Graduate School of Public Health, University of Pittsburgh Pittsburgh, Pennsylvania 15213Search for more papers by this authorWilliam Bell, William Bell Department of Occupational Health Graduate School of Public Health, University of Pittsburgh Pittsburgh, Pennsylvania 15213Search for more papers by this authorStanley J. Penkala, Stanley J. Penkala Department of Occupational Health Graduate School of Public Health, University of Pittsburgh Pittsburgh, Pennsylvania 15213Search for more papers by this authorRobert Freedman, Robert Freedman Health Research Branch United States Bureau of Mines Pittsburgh, Pennsylvania 15213Search for more papers by this author First published: December 1972 https://doi.org/10.1111/j.1749-6632.1972.tb40174.xCitations: 5 * This work was supported by United States Bureau of Mines grant No. G 010 1742. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume200, Issue1Coal Workers' PneumoconiosisDecember 1972Pages 17-30 RelatedInformation