Diagnosis: Pneumoconiosis with a mixed dust lesion (black pigment, probable silicates, and silica), and chronic bronchiolitis. Mild thickening of walls of muscular pulmonary arteries. Mild emphysema.

Comment: This woman has a domestically-acquired pneumoconiosis that has been designated "hut lung." The black pigment is from the unvented indoor smoke from cooking, and the silicates/silica from outdoor dust, probably related in part to making clay pots. Complications of progressive massive fibrosis and cor pulmonale have occurred.

Course: Bronchodilators have relieved the cough.

Discussion: Hut Lung

Introduction: Domestic air pollution is a world-wide problem. As a result of inhaling smoke from cooking fires in poorly ventilated houses and "nuisance dust" from hand grinding corn or from exposure to outdoor dusty environments, respiratory problems such as chronic bronchitis, chronic airflow obstruction, and pneumoconiosis may develop [1]. The patient presented here had progressive cough and dyspnea, evidence of airflow obstruction and cor pulmonale, radiographic small opacities, and a conglomerate lesion consistent with complicated silicosis. When a biopsy confirmed a diagnosis of pneumoconiosis but with a mixed dust lesion, further history revealed the cause to be exposure for many years to an indoor biomass-fueled, unvented cooking stove and work making clay pots. Although the dust content of the lung was not analyzed, the mixed dust lesion is of the type associated with exposure to silica and other dusts--smoke and silicates--that modify its histologic effect in the lung. The mixed dust lesion is stellate, more cellular, and less fibrotic than the round, fibrotic, silicotic nodule, which results from inhalation of dust with a high content of silica. In a domestic situation, the disease has been termed "hut lung" to distinguish it from occupational silicosis, which predominates in men [1].

Epidemiologic and clinical features: In 1967, a condition called Transkei silicosis was described in women of the Transkei area in eastern South Africa. Radiographs showed pneumoconiosis, and histologically the lesions showed black silicotic nodules. The cause was attributed to manual grinding of corn between stones [2]. In a report in 1991, Grobbelaar and Bateman investigated 25 women, mostly from the Transkei area, who were seen at a respiratory clinic [1]. All subjects had been exposed to smoke from cooking fires and most had ground maize manually, all had no industrial exposure, and all had radiographs consistent with pneumoconiosis, evidence of pneumoconiosis on lung biopsy, and no evidence of tuberculosis. The mean age of the patients was 43 (range 20-84) and 17 were non-smokers. Of the 25, 8 were asymptomatic, 13 had mild, purulent bronchitis, and 4 had a chronic productive cough and dyspnea. Pulmonary function tests were normal in 4 and showed FEV1/FVC <70% or RV >140% in 16/22, and DLCO <80% in 13/17. One patient had cor pulmonale [1]. BAL cell numbers and percentages were normal, but alveolar macrophages had large black inclusions. The major differential diagnosis was tuberculosis.

Radiographic changes: The radiographic picture was identical to that of pure silicosis. Radiographs of patients in the two studies showed diffuse, fine to coarse, irregular nodules, which tended to predominate in the upper lung zones [1, 2]. One patient had foci of dense consolidation (progressive massive fibrosis) [1].

Histologic changes: Exposure to mixtures of silica and less fibrogenic dusts produces a lesion with more cellularity and less fibrosis than that which occurs after exposure to silica alone. Typically, a stellate lesion is composed of macrophages, lymphocytes, plasma cells, and a variable amount of black pigment. Birefringent crystals are present. Usual silicotic nodules can also be found [3]. Grobbelaar and Bateman found the mixed dust lesion in lung biopsies from 7 women. Other changes included deposition of black pigment around bronchioles, expanded black macules of dust-containing macrophages around respiratory bronchioles as in coal workers, and conglomerates of progressive massive fibrosis [1]. The mixed dust lesion is located around the respiratory bronchiole or in the pleura.

Conclusions: Hut lung is a form of pneumoconiosis characterized by mixed dust lesions containing black pigment, silicates, and silica. It is domestically acquired by persons living in primitive, rural areas. Smoke from cooking fires in poorly ventilated houses is one factor in developing disease. Grobbelaar and Bateman measured quartz dust from grinding maize and found safe levels, but total dust generated by grinding and the smoke concentrations in the huts were unacceptably high. Further, exposure begins as an infant as women carry babies around with them as they work [1]. As noted in the history of the patient presented here, making clay pots was a dusty task that could have contributed the silica and silicates. Silicates from the soil have been implicated in causing pneumoconiosis in vineyard workers and zoo animals in Southern California [4, 5]. Also, silicosis with mixed dust lesions was described in Himalayan villagers, who were exposed to frequent dust storms as well as indoor, unvented cooking stoves [6]. Two reports from Mexico, one epidemiologic and one clinical, describe features of chronic bronchitis and COPD including cases with cor pulmonale in non-smoking women with prolonged exposure to indoor biomass smoke [7, 8].


1. Grobbelaar J, Bateman E. Hut lung: a domestically acquired pneumoconiosis of mixed aetiology in rural women. Thorax 1991; 46:334-340.

2. Palmer P, Daynes G. Transkei silicosis. S A Med J 1967; 41:1182-1188.

3. Silicosis and Silicate Disease Committee. Diseases associated with exposure to silica and nonfibrous silicate minerals. Arch Pathol Lab Med 1988; 112:673-720.

4. Sherwin R, Barman M, Abraham J. Silicate pneumoconiosis of farm workers. Lab Invest 1979; 40:576-582.

5. Brambilla C, Abraham J, Brambilla E, Benirschke K, Bloor C. Comparative pathology of silicate pneumoconiosis. Am J Pathol 1979; 96:149-170.

6. Norboo T, Angchuk P, Yahya M, Kamat S, Pooley F, Corrin B, Kerr I, et al. Silicosis in a Himalayan village population: role of environmental dust. Thorax 1991; 46:341-343.

7. Sandoval J, Salas J, Martinez-Guerra M, Gómez A, Martinez C, Portales A, Palomar A, et al. Pulmonary arterial hypertension and cor pulmonale associated with chronic domestic woodsmoke inhalation. Chest 1993; 103:12-20.

8. Pérez-Padilla R, Regalado J, Vedal S, Paré P, Chapela R, Sansores R, Selman M. Exposure to biomass smoke and chronic airway disease in Mexican women. A case-control study. Am J Respir Crit Care Med 1996; 154:701-706.

Clinical summary

Comments: mw6825@itsa.ucsf.edu

Table of Contents

Last revised 10/1/98

Copyright 1998 by Martha L. Warnock. All rights reserved.
































Fuels of wood, grass, crop residues, corn cobs, or animal dung