Circulating IL-33 level is associated with the progression of lung cancer.

OBJECTIVES: Interleukin (IL)-33 protects against infection and inflammation; however, few studies have explored the relevance of IL-33 in lung cancer patients. We evaluated relation of plasma IL-33 levels with development and progression of lung cancer. MATERIALS AND METHODS: A total of 160 patients with lung cancer and 160 controls with normal lungs were enrolled. Plasma IL-33 levels were measured using a specific sandwich ELISA; these levels were followed-up in 18 patients who underwent surgery and in 14 patients treated with chemotherapy. Malignant lesions and normal lung tissues from 10 cancer patients were subjected to immunohistochemical staining for IL-33. RESULTS: IL-33 levels were significantly lower in cancer patients than normal controls (0.08 vs. 0.38 ng/mL, p=0.005). Among cancer patients, IL-33 decreased in a stage-dependent manner from 0.76 ng/mL in stage I patients to 0.25 ng/mL in those with stage II, 0.08 ng/mL in those with stage III, and 0.08 ng/mL in those with stage IV (p=0.002). The levels were higher at stage I (p=0.041) and markedly lower at stages III and IV than those of controls (p=0.005 and p=0.001, respectively). A similar pattern was observed when IL-33 levels were analyzed by T stage; the levels were 0.39 ng/mL at T1/T2 vs. 0.08 ng/mL at T3/T4 (p=0.001). However, no difference was noted when stage N1 levels were compared with N2 and N3 levels (p=0.058), or between stage M0 and M1 levels (p=0.147). IL-33 levels gradually decreased after surgical resection of malignant lesions (from 1.075 to 0.756 ng/mL, p=0.006), but were unchanged after chemotherapy (0.705 vs. 0.829 ng/mL, p=0.875). On immunohistochemical staining, bronchial epithelial and vascular endothelial cells of normal lung tissues mainly expressed IL-33. CONCLUSIONS: Plasma IL-33 levels are associated inversely with progression of lung cancer. The observed decreases may be attributed to lung volume reduction containing bronchial epithelium and vascular endothelium as the sources of IL-33.

Acute health effects of accidental chlorine gas exposure.

OBJECTIVES: This study was conducted to report the course of an accidental release of chlorine gas that occurred in a factory in Gumi-si, South Korea, on March 5, 2013. We describe the analysis results of 2 patients hospitalized because of chlorine-induced acute health problems, as well as the clinical features of 209 non-hospitalized patients. METHODS: We analyzed the medical records of the 2 hospitalized patients admitted to the hospital, as well as the medical records and self-report questionnaires of 209 non-hospitalized patients completed during outpatient treatment. RESULTS: Immediately after the exposure, the 2 hospitalized patients developed acute asthma-like symptoms such as cough and dyspnea, and showed restrictive and combined pattern ventilatory defects on the pulmonary function test. The case 1 showed asthma-like symptoms over six months and diurnal variability in peak expiratory flow rate was 56.7%. In case 2, his FEV1 after treatment (93%) increased by 25% compared to initial FEV1 (68%). Both cases were diagnosed as chlorine-induced reactive airways dysfunction syndrome (RADS) on the basis of these clinical features. The most frequent chief complaints of the 209 non-hospitalized patients were headache (22.7%), followed by eye irritation (18.2%), nausea (11.2%), and sore throat (10.8%), with asymptomatic patients accounting for 36.5%. The multiple-response analysis of individual symptom revealed headache (42.4%) to be the most frequent symptom, followed by eye irritation (30.5%), sore throat (30.0%), cough (29.6%), nausea (27.6%), and dizziness (27.3%). CONCLUSIONS: The 2 patients hospitalized after exposure to chlorine gas at the leakage site showed a clinical course corresponding to RADS. All of the 209 non-hospitalized patients only complained of symptoms of the upper airways and mucous membrane irritation.