A recent animal experiment suggests that gasoline exposure may be a cause of human kidney cancer. This is a literature review to see whether there is any epidemiologic support for these animal findings. Trends and geographic patterns in gasoline consumption and kidney cancer mortality are moderately supportive of a relationship, although this cannot be considered important evidence for a causal relationship. Most other ecological correlations are not supportive of a relationship. Eleven oil refinery populations and one population of petroleum products distribution workers have been studied. These studies taken as a group do not appear to support the notion of a relationship between gasoline exposure and kidney cancer. However, most were not designed or analyzed with this hypothesis in mind. An examination of these data which attempts to consider the ages of the populations studied provides some evidence of a small kidney cancer excess among older workers or among workers exposed for long periods. Because of the importance of gasoline and the potential for exposure by the public further study of exposed populations is needed. A chronic inhalation study has shown that unleaded gasoline vapor caused kidney carcinomas and sarcomas in male rats with some evidence of a dose-response relationship (1). Also observed was an increase in liver

Following discovery that the type of kidney neoplasm in-duced in protein-deprived Wlstar rats by a single dose of dimethylnitrosamine (DMN) was age-dependent, this study aimed to refine the system In order to develop a high fre-quency model for the induction of cortical epithelial tumors with low mesencfaymal tumor incidence. Using outbred fe-male Crl:(W)BR (Charles River Wlstar) rats, DMN at a dose of 30 mg/kg was administered at 9- 1 0 weeks of age follow-ing a 5-day period of high-carbohydrate/no-protein diet. From a total of 49 rats, 43 survived the early toxkdty and 91% of these developed renal tumors. Mesenchymal tumors were present in only 9 % of the tumor-bearing animals, in contrast, 70 % of the rats developed epithelial tumors of the tubules classifiable on a size and hlstological basis as adenocard-nomas/cardnomas hi response to DMN. A further 21 % of rats had smaller proliferative lesions designated as adenomas, making the total cortical epithelial tumor incidence hi excess of 90%. The malignant potential of the epithelial tumors was underscored by the presence of metastatic invasion, mainly involving the lungs, in 15 % of the tumor-bearing rats. Meta-statfc behavior correlated with progressive growth of the car-dnomas over a period of time exceeding 1.5 years to dimen-sions usually exceeding 2.9 cm diameter. Of the tumors approaching or exceeding this size, the metastatic rate was almost 50%. Thus, the administration of DMN to 65-70 days old, protein-deprived Wlstar rats provides a potent, single dose model for the study of renal epithelial cardnogen-esis with insignificant mesenchymal tumor induction and without the continuing toxidty which perturbs regimens based on repeated or continuous exposures.