Biomedical subjects
Publications and source records attributed to G R Wagner.
In September 1990, a 2-day workshop was held in Chicago to discuss the current status of the NIOSH B reader certification program and to suggest modifications and improvements. This is a summary report of the proceedings of that conference.
Physicians trained in the use of the International Labour Office system for classification of radiographs of pneumoconioses who pass a competence test administered by the National Institute for Occupational Safety and Health are designated as B readers. The current certification and recertification examinations for qualification under the NIOSH B reader program are described. Details of the rationale and format of each examination are given, and information on candidates' scores provided for the years 1987-1990.
Many diseases associated with occupational exposures are clinically indistinguishable from diseases with non-occupational causes. Given this, how are fair decisions made about eligibility for compensation? This problem is discussed in relation to the federal black lung program. Conflicting definitions of terms--coal workers' pneumoconiosis as defined by the medical profession, pneumoconiosis as defined by the United States Congress, and the popular term, black lung--are important considerations in this discussion. Each is embedded in different logical interpretations of the causes of occupational disease and of disability. Alternative views are presented and critically discussed.
In the presence of peroxidase, myoglobin or hemoglobin, Tetrachlorodecaoxide (TCDO) forms an active oxygen species which is similar to the product of the polymorphonuclear leucocyte (PMNL) myeloperoxidase reaction and the 'Klebanoff Model' of phagocytosis, but it is also produced under anaerobic conditions. Randomly destructive species such as the free OH radical or singlet oxygen are not formed. The kinetics of the heme-dependent activation vary according to the heme type present. In comparison to myoglobin, blood shows a 2 h delay in the appearance of maximal activity. On the basis of known biochemical and clinical-physiological data, a hypothesis can be proposed to explain the reoxygenation observed in hypoxic tissue, induced by TCDO via this activated heme species. Under normal physiological conditions, vasodilation occurs via catalysis by xanthine oxidase or PMNL-dependent activation of fatty acids.
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Oxidation of methionine, 4-(methylthio)-2-oxobutyric acid (KMB), or 1-aminocyclopropane carbonic acid (ACC) are indicator reactions for activated oxygen species such as singlet oxygen (1O2), OH.-radical like oxidants, superoxide anion (O2.-), hydrogen peroxide (H2O2) or activated hemo-iron complexes like peroxidase- or catalase-"compound I". Methionine is oxidized by OH. as well as by 1O2 forming ethylene, but not by tetrachloro-decaoxygen complex (TCDO) in the absence or presence of catalytic hemoproteins such as peroxidase, hemoglobin or myoglobin. Both KMB and ACC are oxidized by TCDO under the catalysis of the above hemo-proteins where neither catalase nor superoxide dismutase are inhibitors. TCDO hemo-protein complex is an oxidant with similar properties as peroxidase-compound I and can clearly be differentiated from O2.-, H2O2, OH. and 1O2.
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