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Epidemiological studies have mapped the occurrence of hepatitis B among health personnel with the use of specific serologic markers and thereby made rational preventive precautions possible. Follow-up studies have demonstrated the effect of this prevention, and the newly developed hepatitis B vaccine has further improved the possibilities for effective prophylaxis against occupational hepatitis B. On the other hand, there is the chemically induced occupational liver damage. Only a few of the thousands of industrially used chemicals have been sufficiently investigated for hepatotoxicity and the list of suspected and confirmed hepatotoxic agents is still growing. The worrisome example of vinylchloride-induced serious liver disease among PVC-workers, revealed after 42 years of industrial use by alert clinicians, calls for intensified activities in the field of occupational hepatotoxicity. However, the clinical, biochemical, and morphological features of liver disease are often vague and unspecific. A non-invasive, convenient quantitative liver function test is needed. Circumstantial evidence and a few epidemiological studies suggest that part of the so-called cryptogenic liver diseases, such as liver cirrhosis, may be caused by occupational exposure to chemicals. This should be further studies. Animal experiments have shown that one chemical agent may potentiate the hepatotoxic effect of another chemical agent. This should be the subject of investigations in the work environment, where exposure to various chemicals is the rule rather than the exception. Alcohol consumption may also interfere with the hepatotoxicity of occupationally used chemicals.
Epidemiological studies have mapped the occurrence of hepatitis B among health personnel with the use of specific serologic markers and thereby made rational preventive precautions possible. Follow-up studies have demonstrated the effect of this prevention, and the newly developed hepatitis B vaccine has further improved the possibilities for effective prophylaxis against occupational hepatitis B. On the other hand, there is the chemically induced occupational liver damage. Only a few of the thousands of industrially used chemicals have been sufficiently investigated for hepatotoxicity and the list of suspected and confirmed hepatotoxic agents is still growing. The worrisome example of vinylchloride-induced serious liver disease among PVC-workers, revealed after 42 years of industrial use by alert clinicians, calls for intensified activities in the field of occupational hepatotoxicity. However, the clinical, biochemical, and morphological features of liver disease are often vague and unspecific. A non-invasive, convenient quantitative liver function test is needed. Circumstantial evidence and a few epidemiological studies suggest that part of the so-called cryptogenic liver diseases, such as liver cirrhosis, may be caused by occupational exposure to chemicals. This should be further studies. Animal experiments have shown that one chemical agent may potentiate the hepatotoxic effect of another chemical agent. This should be the subject of investigations in the work environment, where exposure to various chemicals is the rule rather than the exception. Alcohol consumption may also interfere with the hepatotoxicity of occupationally used chemicals.
The amount of diazo-positive compounds in urine from workers at a chemical plant producing pharmaceuticals and explosives was determined in samples collected after work and after a holiday. Forty-five persons working with aromatic nitro-amino compounds (ANA) showed a statistically significant (p less than 0.01) increase in the exposed samples (1.21 +/- 1.40 mmol/mol creatinine) compared to the unexposed samples (0.56 +/- 0.31 mmol/mol creatinine). No increase in the level of diazo-positive metabolites was found in the 25 workers not exposed to ANA compounds. In a follow-up study, 32 trinitrotoluene (TNT) workers were divided into three exposure categories and seemed to show a dose-dependent increase in the level of urinary diazo-positive metabolites. However, there was a considerable interindividual variation. The method seems suitable for the biological assessment of exposure to ANA compounds--at least on a group level. This may be valuable, especially in situations where significant dermal uptake is expected.
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