Abstract
Clarified slurry oil (CSO) is the heavy residual material produced in the fluidized catalytic cracking unit of a petroleum refinery. CSO was adm in istered via gavage or dermal application to male C3H mice (10/ group) at a dose of 1000 mg/ kg/ d, 5 d/ wk, for up to 10 weeks. Interim sacrifices were performed after 2, 4, 8, and 10 weeks of treatment for orally exposed and control mice; dermally exposed mice were sacrificed after 10 weeks. Fifty percent of the “dermal” mice died prior to scheduled sacrifice. Deaths observed in the “oral” group were attributed to apparent misintubations, not to CSO exposure. Mice exposed orally for 2, 4, or 8 weeks (but not 10 weeks) exhibited significantly increased absolute (A) and relative (R) liver weights, while all “oral” mice (including those sacrificed after 10 weeks) had significantly decreased A and R thymus weights when compared to controls. “Dermal” mice had significantly increased R liver weights and significantly decreased A and R thymus weights. After 2 weeks most “oral” mice showed hepatocyte hypertrophy. A few mice showed liver necrosis. Liver findings increased in incidence and severity until 8 weeks of exposure. After 10 weeks, the liver of most “oral” mice showed the same or less discern ible morphologic pathology than was observed after 2 weeks. At 10 weeks, “dermal” mice showed the previously described liver effects, except that liver necrosis was severe, and evidence of fibrosis was observed. In summary, although CSO was hepatotoxic, “oral” mice showed signs of liver recovery after 10 weeks of exposure despite continued treatment. Thus, CSO appears to be more toxic to mice when administered dermally than orally. Humans are more likely to come into contact with these lipids by dermal rather than by oral exposure.