@Article{Sjgren1998, author = "Sjögren, Bengt", title = "A possible connection between furnace dust exposure, plasma fibrinogen levels and cardiovascular disease", journal = "Scandinavian Journal of Work, Environment & Health", year = "1998", month = "Jun", day = "24", number = "3", pages = "236--237", abstract = "
In a very well-written and informative study Hobbesland and his co-workers found an increased mortality from sudden death among ferromanganese/silicomanganese furnace workers (1). In 1955 an interesting observation was made by Rodier (2) when studying manganese-exposed Moroccan miners. The clinical signs of manganese pneumonia were first those of acute alveolar inflammation. Dyspnea was marked, the respiration was shallow, and there was gasping. The illness was altered after the 3rd day from a frank case of pneumonia to less well-defined localization and discrete pleural involvement. Death from heart failure was possible between the 5th and the 10th day. It could also occur suddenly for patients regarded as cured. Thus it seems as if sudden death occurred in some of the patients regarded as cured. During the last decade fibrinogen has emerged as an important risk factor for ischemic heart disease (IHD) (3, 4). Increased concentrations of plasma fibrinogen have also been associated with myocardial infarction and sudden death among patients with angina pectoris (5). Three deaths due to pneumonia occurred during active occupational exposure among Norwegian ferromanganese/silicomanganese furnace workers (6). Manganese pneumonia is an inflammatory disease and was associated with a marked rise in erythrocyte sedimentation rate among the Moroccan miners (2). The sedimentation rate can be influenced by several serum proteins, for example, fibrinogen, haptoglobin, immunoglobins, and ceruloplasmin (7). In other words plasma fibrinogen may be increased in this condition. In a Belgian factory producing manganese oxides and salts, the exposed workers more often had respiratory symptoms such as cough, sputum, and acute bronchitis than a reference group did. The median exposure of manganese airborne dust was 0.97 mg/m3. The exposed group also had an increased prevalence of chronic bronchitis, but the difference was not significant (8). It has recently been shown that persons with chronic bronchitis have an increased risk for coronary disease and coronary deaths (9). The mentioned manganese-exposed Belgian workers had decreased lung function for several spirometric parameters, for example, forced vital capacity (FVC), forced expiratory volume in 1 second (FEV