The chromium content was measured in the lungs of chromate workers, obtained at necropsy in six patients and at surgery in two. The mean chromium content of peripheral lung tissue was 36-7 gg per gm wet weight (range 0 50 to 130-2 jg) and that of the large airways was 0-51 jg per gm wet weight (range 0-22 to 0 99 jg). These mean values were high compared with those from control lungs of a non-chromate exposed lung cancer patient-respectively 0-21 gg per gm in lung tissue and 0-1 Igg per gm in the large bronchi. The longer the exposure period, the higher was the chromium content in the lungs. The concentration of chromium in the upper lobes was sigfificantly higher than that in the lower lobes, suggesting regional differences either in clearance from or deposition in the lung. Moreover, it was apparent that the metal remained in the lungs long after exposure to chromate had ceased.Chromate lung cancer has been recognised as one of the occupational diseases since the first report by Pfeil in 19351 and other reports in Germany and America. In Japan, chromate lung cancer was reported by Ohsaki in 1978.2 Although chromate compounds have been incriminated as carcinogens details of the exposure period for induction of lung cancer and of the chromate content in the body are not well documented. We measured the chromium content of the lungs, obtained at surgery and necropsy, of lung cancer patients who had worked in the chromate industry. MethodsThe lungs of eight chromate workers were obtained, in two cases at surgery and in six at necropsy (table 1). All the patients were men and the average age was 58 5 years (range 50 to 72 yr). All but one patient had nasal perforation. Histology revealed squamous cell carcinoma in six cases, small cell anaplastic carcinoma in one case, and adenocarcinoma in one case. The mean latent period between the occurrence of lung cancer and leaving work was five years, ranging from 0 to 27 years.

To investigate whether interleukins are involved in the formation of alveolitis in pulmonary sarcoidosis, interleukin-1 (IL-1) production by LPS-stimulated alveolar macrophages (AM) and interleukin-2 (IL-2) production by PHA-stimulated lung and blood T-cells were determined in 35 untreated patients with pulmonary sarcoidosis. The amount of IL-1 produced by AM (BAL IL-1) was significantly increased in patients with pulmonary sarcoidosis compared with that in 18 control subjects. BAL IL-1 showed a significant positive correlation with the intensity of alveolitis assessed by the proportion of lymphocytes in bronchoalveolar lavage fluid (BALF) and the absolute number of lymphocytes per milliliter of BALF. However, the amount of IL-2 produced by lung T-cells (BALT IL-2) showed a significant negative correlation with the intensity of alveolitis. BALT IL-2 was significantly lower than the amount of IL-2 produced by blood T-cells (PBT IL-2). There was no correlation between PBT IL-2 and the intensity of alveolitis. These results suggest that IL-2 contributes to the formation and maintenance of alveolitis in pulmonary sarcoidosis, whereas IL-2 production by lung T-cells is suppressed to down-regulate the enhanced immune processes at the site of disease. The possibility that this hyporesponsiveness of lung T-cells to PHA has resulted from the modulation of the T3-T cell receptor complex remains to be determined.

An autopsy case of primary esophageal choriocarcinoma in a 42‐year‐old Japanese male Is reported. The tumor was pure choriocarcinoma typical hemorrhagic and necrotic nature occupying almost the entire circumference of the mid‐esophagus. The choriocarcinoma had metastasized to the liver, lung and lymph nodes. In the esophageal tumor, immunohistochemical staining showed the presence of mainly human chorionic gonadotropin (HCG), with human placental lactogen (HPL) in a few syncytiotrophoblastic cells. Only 3 cases of extragonadal choriocarcinoma originating in the esophagus have been reported up to now. The possible pathogenesis and pathological characteristics of primary esophageal choriocarcinoma are discussed.

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