TWO CASES OF FATAL PMF IN AN ONGOING EPIDEMIC OF ACCELERATED SILICOSIS IN OILFIELD SANDBLASTERS: LUNG PATHOLOGY AND MINERALOGY

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1 Ann. occup. Hyg., Vol. 4, Supplement, pp , British Occupational Hygiene Society Published by Elsevier Science Ltd. All rights reserved Printed in Great Britain /97 $ Inhaled Particles VIII HI: S (96)00094-^l TWO CASES OF FATAL PMF IN AN ONGOING EPIDEMIC OF ACCELERATED SILICOSIS IN OILFIELD SANDBLASTERS: LUNG PATHOLOGY AND MINERALOGY J. L. Abraham* and S. L. Wiesenfeldf Departments of *Pathology, State University of New York, Health Science Center, 70 E Adams St, Syracuse, NY 320; and fmedicine, Texas Tech University Health Sciences Center, Odessa, Texas, U.S.A. INTRODUCTION Epidemics of silicosis have occurred repeatedly in the U.S. at intervals of a few decades (890s, 930s, 970s), during which collective memory appears to fall below a critical point of awareness (Rosner and Markowitz, 99). Sandblasting with crystalline silica has long been recognised as one of the most potentially hazardous occupations for silicosis risk and in fact, silica sandblasting has been banned in the U.K. since the 940s. Nevertheless, we have been able to study an ongoing epidemic of silicosis in West Texas Oilfield sandblasters (CDC, 990; Wiesenfeld and Abraham, 99) and to describe the clinical findings, lung pathology and mineralogy of the previously rarely described accelerated silicosis. In 988, we independently began evaluating patients (SLW) or lung biopsies (JLA) from these workers. An early fatality from acute silico-proteinosis was reported (CDC, 990). Here we present two recent fatalities from PMF in the same epidemic. The setting for the epidemic In the early 980s the price of oil rose to $34 a barrel and the Permian Basin in Texas became a magnet for oil production. Working to capacity, sandblasting provided a means for preparing metal surfaces pipes, tanks and manifolds. Working conditions were extremely dusty, little or no respiratory protection was used and in some operations, blasting sand was recirculated, becoming finer and finer until no longer useful. Workers worked in the midst of an aerosol so dense they could not see. Personal breathing zone air samples in 988 showed respirable free silica from ug m~ 3. The work was arduous and lengthy, often 6-7 days/week, 0-2 h shifts. There were no cleaning facilities, pre-employment or annual medical exams. Summer temperatures routinely exceeded 00 F. A small group of Mexicans worked in Odessa foundries in the late 970s and early 980s. As work expanded, they recruited friends and relatives to do similar work. MATERIALS AND METHODS Clinical evaluation included: history, physical examination, chest X-ray (CXR), 440

2 An ongoing epidemic of silicosis in oilfield sandblasters YEAR Of EXPOSURE ONSET AGE AT PRESENTATION Fig.. (A) Histogram showing year of onset of sandblasting for all individuals studied. The ascending line represents the cumulative frequency and the dot represents the cumulative frequency at the end of each 2 year period; (B) histogram of age at presentation to physician for all individuals studied, by year grouping. The ascending line indicates the cumulative frequency and the dot represents the cumulative frequency at the end of each year period. pulmonary function tests (PFT), CT scans, Ga scans and, in some cases, transbronchial or thoracoscopic lung biopsy. CXRs were scored using a 0-4 grading system as well as by ILO-980 B-readings. Biopsies were analyzed by brightfield and polarized light microscopy and scanning electron microscopy/energy dispersive X-ray analysis for quantification of lung inorganic particulate burden (Abraham and Burnett, 983). In 99 and 996, two men, with 36 and 48 months exposure, ceasing work at the time of diagnosis in 988 and 990, had progressed to PMF and died of respiratory failure, and 0 years after initial exposure, respectively. Both had severe disease clinically and radiologically at the time of diagnosis. Autopsies were limited to the lungs. RESULTS A brief summary of the larger group is needed to put this report in perspective; 84 patients were initially studied (Wiesenfeld and Abraham, 99). Figure (A) shows the year of first exposure, it correlates with the economic collapse in 984, when the oil price plummeted. Age at presentation ranged from years (mean 36.6 ± 0.6, median 33) [Fig. (B)]. Approximately 37% were smokers. Progressive dyspnea on exertion was insidious in onset and chest physical findings were initially mostly normal. Nearly all men had BCG vaccination as children in Mexico; no cases of M.TB were documented by sputum or biopsy cultures, although a few men years later developed atypical mycobacterial disease. Chest X-ray, gallium scans and DLCO Initially, only 3.7% of CXRs (30 of 84) showed any micronodularity or more

3 442 J. L. Abraham and S. L. Wiesenfeld advanced changes. At and 7 years of study, 9 and 8 cases or 8.7% and 33.3%, respectively, converted from normal to abnormal CXR. At years of study the mean time from initial silica exposure to CXR abnormality was 8.6 ± 4. years (range years). Biopsies confirmed accelerated silicosis and high silica burdens prior to CXR conversion. All but one had positive Ga scan prior to CXR conversion. The DLCO was reduced in these 8 cases prior to CXR conversion. The more positive CXRs and Ga scans are both associated with earlier age at presentation and shorter duration of exposure. Owing to differing work practices, patients could be divided into two cohorts: () one company in which sand was recirculated, and (2) all other companies in which sand was not recirculated. This factor of intensity of exposure apparently explains most of the at first seemingly paradoxical inverse relationship between severity of disease and age and duration of exposure. The worst initial DLCO values are seen in cohort. Even with a negative CXR, the mean initial % predicted DLCO is 7.7%. Pathology Commonly, subpleural dust and occasional nodules are seen at thoracoscopy. The most common finding is an interstitial infiltrate of dust-laden macrophages. There is a mixture of barely resolvable tiny opaque and birefringent particles with variable fibrosis. Silicotic nodules are rare and small ( mm). Many alveoli contain dusty macrophages. Caseating granulomas are not found. Polymorphonuclear leukocytes are very rare. Increased interstitial lymphocytes and many Fe-stain positive macrophages are noted. Proteinosis is not observed in any of the biopsies, although focally noted in one of the PMF autopsy cases, as has been noted by Honma and Chiyotani (99) and Shida et al. (996). In the two autopsy cases the entire lungs were greatly reduced in volume, with the tiny upper lobes being grey and stony hard (Fig. 2). The lower lobes were firm and brown, with scattered palpable nodules up to 0.4 cm. Histologically, nearly all alveoli showed interstitial inflammation and fibrosis. The transbronchial biopsy obtained from case in 988 showed severe fibrosis and high dust concentrations (see Table ). Mineralogic findings and correlations The silica concentrations in these sandblasters are among the highest seen in our analytical experience (Abraham et al., 99). The results show that pure silica exposure is rare, the more common pattern being mixed dust exposure (Table ). The geometric mean concentration of silica is higher for cohort than for cohort 2 (p < ; T-test). The geometric mean diameter of silica particles is 0.7 micrometers. The concentration of silica, but not that of other types of mineral particles, correlates with radiologic severity (Spearman Rank correlation = 0.686, p < by the Mann-Whitney U-test, for the correlation of the HRCT score with the loglo of lung silica particle concentration). Discriminant analysis (Hunt, 986) was used to assess whether the microanalysis, performed without any knowledge of the work history or histopathology, facilitated distinguishing between cohorts. Major contributions to the analysis were made by the loglo of silica, aluminum silicates, chromium and titanium, in that order. Clear separation of the workers by their cohorts is evident based on the lung burden data (Fig. 3). Analytical results in the two PMF cases demonstrate extremely high concentrations

4 An ongoing epidemic of silicosis in oilfield sandblasters 443 Fig. 2. Photograph of lungs from PMF case, showing stony grey remnant left upper and right upper and middle lobes and brown small lower lobes.

5 444 J. L. Abraham and S. L. Wiesenfeld Table. Concentrations of inorganic particulates in lungs of two sandblasters with PMF* PMF Case Biopsy upper upper middle lower PMF Case 2 upper hilar lower lower Total Silica Aluminium silicates Metals (totals) Cr Ti * All concentrations in millions of particles cm 3 lung; site of lung sampling from biopsy unknown; others from autopsy. Cr and Ti concentrations = metal particles which contain that element. of particles in the PMF lesions, and the lobar differences in dust concentration (Table ). DISCUSSION Silicosis in its accelerated form occurs in sandblasters in this outbreak, with the exception of one earlier reported case of alveolar proteinosis (CDC, 990). Two cases at least have progressed to death from PMF and respiratory failure. In accelerated silicosis the CXR is initially normal and there is little restriction on PFTs. An abnormal CXR is a late, global finding and is associated with more intense silica exposure and lung silica burden. Abnormal DLCO and Ga scan appear to be the only objective indicators of disease progression to positive CXR, while spirometry changes minimally and CXR may remain normal up to 8-2 years. In the absence of abnormal CXR, lung biopsies were of special value in demonstrating that suspect cases, based on dyspnea and impaired DLCO with or without a positive Ga scan, indeed had accelerated silicosis. The lung pathology in accelerated silicosis has not been clearly defined (Craighead et al., 988) or described in detail (Seaton, 99). Silicotic nodules in classic chronic silicosis usually measure 2-3 mm diameter. In 939, Gardner described the lung pathology in 9 cases of what the ILO in 938 termed "rapidly developing silicosis", which would now be termed acute silicosis. Nearly all these cases had complicating TB. "Microscopic examination of the lungs revealed great numbers of minute silicotic nodules of Vsth to half the size found in ordinary chronic cases." The ability of the lung particulate burden data to allow separation of workers by their employment cohorts using discriminant analysis suggests differences in workplace materials and work practices may be investigated using lung burden microanalysis to reveal a type of fingerprint of the total and frequently complex lung burden retained in a persons pre-biopsy lifetime. The finding that, of all the types of retained particles measured in the lung, only the lung silica burden related

6 An ongoing epidemic of silicosis in oilfield sandblasters " 4 _ 4-6 6,., 4 J ' + I,, I,, I,, I Discriminant Function Fig. 3. Discriminant analysis plot showing the separation of cases according to employer, based on lung concentrations of silica, aluminium silicate, chromium and titanium particulates. Groups indicated as follows: = cohort ; = workers at a second company; 6 = workers at a third company; and 4 = sandblasters from other states, not from this epidemic. to most of the measured clinical and histopathologic measures of disease severity serves to further illustrate the utility of such analyses in investigating mixed exposures and their relationship to disease outcomes. It should not be surprising, however, to demonstrate that silica dust particles are the major pathogenic particle in silicosis. As Donald Cummings pointed out at the Fourth Saranac Silicosis Symposium (939): "Among all the recognized phenomena in the realm of medicine none may be perceived with greater clarity than the true cause of silicosis." Disease paradigms in silicosis and the nature of screening The diagnosis of silicosis for clinical epidemiological and compensation purposes has been inflexibly contingent on radiological demonstration of fibrotic lesions in a +

7 446 J. L. Abraham and S. L. Wiesenfeld person with a consistent occupational history. Contemporary dust standards are based on the premise that significant disease does not exist in absence of a positive CXR. Our findings in this study do not support this requirement for a positive CXR in accelerated silicosis. Currently, if the CXR is negative, even with a history of exposure, progressive dyspnea, a positive Ga scan, a deteriorating DLCO, plus a confirming biopsy, the diagnosis is contested and benefits denied! Lung transplantation, stated by Seaton (99) to be the only possible hope for prolonged survival in accelerated silicosis, is unlikely to be available to the affected workers. CONCLUSIONS Almost a century ago, Betts (990) described an outbreak of what would now be called accelerated or acute silicosis. He examined 30 of 200 deaths at one mill where the average age at death was 30, employment.2 years and time to death 2.4 years. For every epidemic reported, Betts suspected, as we do, hundreds of silent epidemics go unreported because of industry pressures, associated litigation, reluctance of medical colleagues to get involved and difficulties in studying migrant and immigrant populations. We have shown that fatalities from PMF with brief uncontrolled silica exposure in abrasive blasting continue to occur in industrialised nations. This epidemic seems to be unique in that tuberculosis is absent, most likely related to the high prevalence of childhood BCG vaccination in these workers. The zonal distribution of silica correlates with the severity of the disease. Tissue microanalysis delineates mixed exposures and facilitates analysis of specific doseresponse relationships. There are a number of effective substitute materials for silica; issues of price, demand and safety need to be kept in mind prior to mandatory use of any specific substitutes. NIOSH in 974 proposed legislation to ban sand as an abrasive, but this was blocked by sand and related companies (Silica Safety Association, 976), mirroring similar events decades ago (Rosner and Markowitz, 993). Should similar legislation be proposed and not acted into law, the U.S.A. will be ensuring that it will continue to rediscover silicosis in the next millennium. Our cases unfortunately demonstrate the outcome of unregulated use of silica in the modern era. REFERENCES Abraham, J. L. and Burnett, B. R. (983) Quantitative analysis of inorganic particulate burden in situ in tissue sections. Scanning Electron Microscopy/983 2, Abraham, J. L. Burnett, B. R. and Hunt, A. (99) Development and use of a pneumoconiosis database of human inorganic particulate burden in over 400 lungs. Scanning Microsc., Betts, W. W. (900) Chalicosis pulmonum, or chronic interstitial pneumonia induced by stone dust. JAMA, 34, CDC (990) Silicosis: cluster in sandblasters Texas, and occupational surveillance for silicosis. MMWR 39, Craighead, J. E., Kleinerman, J., Abraham, J. L., Gibbs, A. R., Green, F. H. Y., Harley, R. A., Ruettner, J. R., Vallyathan, N. V. and Juliano, B. (988) Diseases associated with exposure to silica and nonfibrous silicate minerals. Arch. path. Lab. Med. 2, Cummings, D. E. (939) The etiology of silicosis. In Fourth Saranac Laboratory Symposium on Silicosis (Edited by B. Kuechle) p. 20. Trudeau School of Tuberculosis, Saranac Lake, NY. Gardner, L. (939) Rapidly developing silicosis. In Fourth Saranac Laboratory Symposium on Silicosis.

8 An ongoing epidemic of silicosis in oilfield sandblasters 447 (Edited by B. Kuechle), pp Trudeau School of Tuberculosis, Saranac Lake, NY. Honma, K. and Chiyotani, K. (99) Pulmonary alveolar proteinosis as a component of massive fibrosis in case of chronic pneumoconiosis: an autopsied study of 79 cases. Zentralbl. Pathol. 37, Hunt, A. (986) The application of mineral magnetic methods to atmospheric aerosol discrimination. Phys. Earth Planet. Int. 42, 0-2. Rosner, D. and Markowitz, G. (99) Deadly Dust: Silicosis and the Politics of Occupational Disease in Twentieth-Century America. Princeton University Press. Seaton, A. (99) Accelerated silicosis, In Occupational Lung Diseases, (Edited by Morgan and Seaton), 3rd edn. Saunders, p. 237, 29. Shida, H., Chiyotani, K., Honma, K., Hosoda, Y., Nobechi, T., Morikubo, J. and Wiot, J. F. (996) Radiologic and pathologic characteristics of mixed dust pneumoconiosis. RadioGraphics 6, 483--J98. Silica Safety Association (976) Silica safety association comments concerning questions proposed by the department of labor. In Federal Register, 976, 2372, Vol. 4. Stern, R. M., Pigott, G. H. and Abraham, J. L. (983) Fibrogenic potential of welding fumes. /. appl. Toxicol. 3, Wiesenfeld, S. L. and Abraham, J. L. (99) Epidemic of accelerated silicosis in Texas sandblasters: clinical, pathologic and microanalytic observations. Am. J. Resp. crit. Care Med., A70.