British Journal of Industrial Medicine 1992;49:448-450

Pleural effusion in silicosis of the lung

Feisal A Al-Kassimi

I report pleural effusion in a patient with silicosisof the lung and pulmonary massive fibrosis. Nospecific aetiology for the effusion was detectedafter thorough investigation and a long follow upperiod. I speculate that, similar to asbestosis,'2silicosis of the lung might produce a benignpleural effusion. There are similarities in theinflammatory and exudative tissue response toboth types of dust particles.25

I am not aware of any previous reports ofassociation between silicosis of the lung andpleural effusion.

Case reportA man of 70 presented with a 30 year history ofmild cough with scanty mucoid sputum and milddyspnoea on exertion, which, three months beforepresentation, had increased rapidly to distress atthe slightest movement. He had no fever or weightloss. He had been taking INH, rifampicin, and

pyrazinamide in therapeutic doses regularly forthree years, as prescribed in another hospital forclinical suspicion of tuberculosis. He gave a his-tory of heavy exposure to dust most of his lifewhile working as a well digger. On examination hehad signs of pleural effusion on the right side.Chest x ray film (fig 1) showed, as well as rightsubpulmonic pleural effusion confirmed bydecubitus films (fig 2), bilateral interstitial shad-owing more pronounced in the upper zones withmassive pulmonary fibrosis. Arterial blood gaseswere normal at rest. A Mantoux test (using 10units tuberculin) was negative on two occasions.Sputum cultures, made on six occasions, werenegative for mycobacteria and fungi and were freeof asbestos bodies. Fibreoptic bronchoscopyshowed generalised hyperaemia and oedema ofthebronchial mucosa. Bronchoalveolar lavage wasnegative for mycobacteria and fungi by smear andculture, and a search for asbestos bodies wasnegative. Transbronchial biopsy of the lungshowed infiltration of the interstitial tissues withmacrophages and mononuclear inflammatory cellsintermixed with carbon particles. There were noferruginous bodies in several cuts. Birefringentparticles (fig 3) compatible with silicosis were seenby polarised light. Pleural aspiration produced

Figure 1 Chest x ray film showing right subpulmonicpleural effusion and massive pulmonary fibrosis.

Figure 2 Decubitusfilm confirming subpulmonic pleuraleffusion.

Medical Department, College of Medicine, KingSaud University, Riyadh, Saudi ArabiaF A Al-Kassimi

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Pleural effusion in silicosis of the lung

Figure 3 Birefringent particles compatibk with silicosis, as seen by polarised light

500 ml of fluid. The pleural fluid was clear, darkyellow in colour, and was an exudate with highprotein and lactate dehydrogenase, normalglucose concentration (4 mmol/l), and whiteblood cell count (210/mm3, 100% lymphocytes).Cytology for malignant cells and culture forbacteria, anaerobes, mycobacteria, and fungi werenegative. Pleural biopsy showed hyperplasia ofmesothelial cells as the only abnormality. Thepatient was sent home but fluid aspiration andpleural biopsy were repeated three times in thespan of six months, with negative results. Pleur-oscopy with a rigid bronchoscope showed thicken-ing of pleura with no tubercules or deposits.Multiple biopsies of the visceral pleura werehistologically similar to those obtained by Abramsneedle. A diagnosis of lung silicosis was made.Chemical pleurodesis, with 1 g of tetracyclineinjected intrapleurally, was performed eightmonths after presentation with appreciable im-provement of dyspnoea. Follow up for three and ahalf years showed no recurrence of the effusion.The pulmonary infiltrate remained unchanged.

Antinuclear factor and rheumatoid factorremained negative, with no clinical evidence ofarthritis. A repeat ofthe Mantoux test two monthsafter presentation also gave negative results.

DiscussionThe patient fulfilled all criteria for diagnosis ofsilicosis of the lung-namely, (1) history of heavyoccupational exposure; (2) chest x ray film show-ing bilateral symmetrical interstitial infiltrate; (3)negative cultures of sputum and bronchoalveolarlavage for mycobacteria and fungi9. Also, thehistopathology and examination by polarised lightof transbronchial biopsies were compatible withsilicosis.'0A thorough search for an altemative aetiology

for the pleural effusion remained consistentlynegative. Acute causes like pneumonia or pulmon-ary infarction are unlikely given the chronicnature of the pleural effusion and normal arterialblood gases. Tuberculosis was excluded by failureto respond to INH, rifampicin, pyrazinamide anda repeatedly negative Mantoux test, pleural bi-

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Al-Kassimi

opsies, and culture for mycobacteria. Rheumatoideffusion was excluded by negative serology, nor-mal glucose concentration in pleural fluid, andabsence of arthritis on follow up. He lived all hislife in a small village in the non-industrialisedcentral part of Saudi Arabia where there are no

reported sources of exposure to asbestos.To our knowledge, pleural effusion (unless

related to tuberculosis, a known complication ofexposure to silica) is not a recognised manifesta-tion of silicosis of the lung. I speculate that theeffusion in the patient was probably linked tosilicosis. Extensive adhesions between visceraland parietal pleura (without pleural effusion) are

frequently present in postmortem studies ofadvanced silicosis of the lung.'0 Although thepleural adhesions might be the sequaelae ofhealedpulmonary infections like tuberculosis, it isplausible that silicosis could cause a pleural reac-

tion similar to that which occurs in asbestosis.Such a view is supported by animal studies, whichfound that silica and asbestos fibres share a

common inflammatory mechanism3 and haveidentical abilities to release chemical mediators ofinflammation4 and induce inflammatory serum

exudation.5 The absence of previous reports ofassociation might be explained by cliniciansattributing pleural effusion to pulmonary infec-

tions, the incidence of which increases in silicosisof the lung.6

Requests for reprints to: Dr F Al-Kassimi,Medical Department (38), College of Medicine,King Saud University, PO Box 2925, Riyadh11461, Saudi Arabia.

1 Eisenstadt HB. Asbestos pleurisy. Dis Chest 1964;64:78-81.2 Robinson BWS, Musk AW. Benign asbestos pleural effusion:

diagnosis and course. Thorax 1981;36:896-900.3 Dubois CM, Bissonnette E, Rola-Pleszcynski M. Asbestos fibres

and silica particles stimulate rat alveolar macrophages torelease tumour necrosis factor-Autoregulatory role of leuko-triene B4. Am Rev Respir Dis 1989;139:1257-64.

4 Rom WN, Bitterman PB, Rennard SI, Cantin A, Crystal RG.Characterization ofthe lower respiratory tract inflammation ofnonsmoking individuals with interstitial lung diseaseassociated with chronic inhalation of inorganic dust. Am RevRespir Dis 1987;136:1429-34.

5 Le-Maho S, Bignon J, Lambre C, Jaurand MC, Masse R. Earlycellular and biochemical alveolar responses following intra-cheal inoculation with low dose of asbestos and quartz. ArchImmunol Ther Exp (Warsz) 1984;32:85-98.

6 Ziskind M, Jones RN, Weill H. Silicosis-State of the art. AmRev Respir Dis 1976;113:643-65.

7 Seaton A. Silicosis. In: Morgan WKC, Seaton A (eds). Occu-pational lung disease. Philadelphia: WB Saunders, 1984:266-77.

8 Weill H, Jones RN. Occupational pulmonary diseases. In:Fishman AP. Pulmonary diseases and disorders. New York:McGraw-Hill, 1988;1:828-34.

9 Weill H, Jones RN. Occupational pulmonary diseases. In:Fishman AP (eds). Pulmonary diseases and disorders. NewYork: McGraw-Hill, 1988;1:833.

10 Dunnill MS. Pulmonary pathology. Edinburgh: ChurchillLivingstone, 1982:399-438.

Accepted 7 October 1991

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