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Objectives: The inspiration of cobalt containing dust leads to various respiratory symptoms, including asthma and interstitial lung disease. Occupational asthma caused by cobalt chloride has been diagnosed in a 35-year-old patient, who worked as a diamond polishing disc former. The patient presented a 2-year history of dyspnea, cough and symptoms of rhinitis. Materials and Methods: The patient underwent a medical history interview, skin prick tests with common and occupational allergens (cobalt and nickel chloride),and pulmonary function testing both before and after the nasal provocation with 0.05% cobalt chloride. Additionally, the authors analyzed morphological and biochemical changes before and after the specific nasal challenge test. Cell proliferation analysis was also carried out. Results: Skin prick tests (SPTs)with common environmental allergens were found to be negative, while SPTs with cobalt chloride were positive for all applied solutions. The provocation with cobalt chloride caused a significant increase in the proportion of eosinophils, basophils and albumin during the late allergic reaction. The positive lymphocyte transformation caused by cobalt was also observed. Conclusions: Cobalt salts may induce occupational asthma. The mechanism of this asthma may be IgE-mediated. The cobalt-sensitized lymphocytes may play an important role in this disease. [ABSTRACT FROM AUTHOR]

Introduction: Fire smoke inhalation is a well-recognized aetiological factor of airway injuries. The objective of this study was evaluation of Clara cell protein (CC16) and myeloperoxidase (MPO) concentrations in serum of patients after exposure to uncontrolled fire smoke., Methods: The study group consisted of 40 consecutive patients admitted to the Toxicology Unit after exposure to fire smoke. CC16 and MPO concentrations in their serum samples was measured on the day of admission to hospital and rechecked at the 2nd day and on the day of discharge. Patients also underwent routine toxicological diagnostic procedures applied in case of exposures, such as carboxyhaemoglobin (COHb) levels and blood lactate and urinary thiocyanate concentrations. The same diagnostic tests were performed in the control group consisting of 10 healthy subjects not exposed to fire smoke., Results: The average concentration of CC16 in the serum of subjects exposed to toxic factors was significantly higher at the day of admission in comparison with the respective values recorded on the 2nd day and on the day of discharge. The mean level of CC16 in the serum of the exposed group was also significantly higher than that in the control group. Tests for MPO concentrations in the serum did not reveal any significant changes in patients exposed to fire smoke., Conclusions: As indicated, acute exposure to smoke induces injury at the alveolar level, which results in a transient increase of CC16 in serum of exposed subjects.