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NSIP in a curry sauce factory worker
  1. S Ando1,
  2. T Arai1,
  3. Y Inoue1,
  4. M Kitaichi2,
  5. M Sakatani3
  1. 1Department of Respiratory Medicine, National Hospital Organization, Kinki-chuo Chest Medical Center, Osaka, Japan
  2. 2Department of Pathology, National Hospital Organization, Kinki-chuo Chest Medical Center, Osaka, Japan
  3. 3Department of Respiratory Medicine, National Hospital Organization, Kinki-chuo Chest Medical Center, Osaka, Japan
  1. Correspondence to:
    Dr Y Inoue
    National Hospital Organization Kinki-chuo Chest Medical Center, Nagasone-cho, Kita-ku, Sakai, Osaka 591-8555, Japan; giichi{at}

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Curry powder and ground pepper are commonly used spices in many countries of the world. Although a case of bronchiolitis obliterans organising pneumonia has been reported in a worker who inhaled spice dust in a potato chip factory,1 we report the first case of non-specific interstitial pneumonia (NSIP)2 with bronchiolar lesions associated with curry powder and ground pepper.

A 50 year old male smoker (20 pack-years) developed a cough with sputum and shortness of breath on both working days and non-working days and was admitted to our hospital 1 month after developing the symptoms. He had worked in a factory that produced curry sauce for 13 years. His job was to carry sacks filled with curry powder (containing a mix of ground spices) and ground pepper on his shoulders and to empty them into a large curry sauce cooker without any equipment to protect against dust inhalation.

Physical examination on admission revealed inspiratory crackles in the bilateral lower lungs without digital clubbing. Serum markers for interstitial pneumonia, surfactant protein D (SP-D), and KL-6 were raised to 2410 ng/ml and 5570 U/ml, respectively. A high resolution computed tomographic (HRCT) scan of the chest revealed multiple irregular consolidations along with bronchovascular bundles and, in the subpleural lesions, trivial pleural effusion and cystic air spaces in the bilateral apex portions (fig 1A). Bronchoalveolar lavage was performed; the total cell count was 4.1×106/ml with 23.8% macrophages, 70.4% lymphocytes, 0.2% neutrophils, 2.6% eosinophils, and 3.0% basophils. The CD4+/CD8+ lymphocyte ratio was 0.94 and pathogenic organisms were not detected.

Figure 1

 Radiological findings during the clinical course of lung disease in a patient who worked with curry powder and ground pepper. (A) HRCT scan at the onset of lung disease showing multiple peribronchovascular consolidations and pleural thickening. (B) After 14 months the consolidations in the lung fields had almost completely resolved, but the subpleural cystic air spaces had increased in size and number.

Specimens obtained by video assisted thoracoscopic surgery from the right lung (S3 and S8) 2 months after the onset of disease revealed a cellular and fibrosing NSIP pattern with polypoid granulation tissues in a few respiratory bronchioles and alveolar ducts. The bronchioles showed reparative proliferation of the bronchiolar epithelium and infiltration of eosinophils, lymphocytes, and multinucleated giant cells, together with stenosis with intraepithelial infiltration of lymphocytes. These findings suggest an association between the patient’s disease and the particles he inhaled while working.3

Four months after the onset of disease his serum SP-D and KL-6 levels had fallen and the consolidations seen on the HRCT scan had spontaneously resolved. Lymphocyte stimulation tests (LST) using the patient’s peripheral blood lymphocytes were positive for the curry powder, ground black pepper, and ground white pepper used in the factory, with stimulation indices of 311%, 244% and 2459%, respectively. The LST were negative for curry powder and ground pepper used in another curry sauce factory. LST using blood samples from three healthy volunteers and the three substrates were negative. We therefore concluded that the patient’s lung disease was associated with the spices used in his factory and we advised him not to return to work. Prednisolone and azathioprine were administered but both drugs were discontinued owing to the occurrence of bilateral pneumothoraces which were surgically treated. Although the consolidations on the HRCT scan did not recur after his isolation from the factory, the subpleural cystic lesions—thought to be caused by a check valve mechanism with bronchiolar constriction—increased in size and number and post-inflammatory pleural thickening progressed (fig 1B). Fourteen months after onset of the disease the patient died from ventilatory insufficiency with hypercapnia.

Although fungi or bacilli in the spices may have induced the lung disease4 and further investigation is needed to determine the exact elements responsible, we wish to draw attention to the possibility of this type of lung disease. Progressive pulmonary cysts and respiratory failure may happen even after avoidance of pathogenic antigens, as found in pigeon breeder’s lung,5 and early diagnosis is necessary to improve its prognosis.


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