In a lifetime (29-month) carcinogenicity study, rats were treated with lead arsenate (PbHAsO4) or sodium arsenate (Na2HAsO4·7H2O) and the possibility that diethylnitrosamine (DENA) may exert a synergistic or additive action on the effects of these compounds was studied. Lead arsenate was fed in the diet at levels of 1850 or 463 ppm, while sodium arsenate was fed at a level of 416 ppm. Additional groups of rats were fed 463 ppm lead arsenate or 416 ppm sodium arsenate in combination with DENA given in an intubated dose of 5 μg/day on 5 days/wk. The rats receiving these diets were weaned by mothers receiving the same diet during lactation. Food intake levels (for the first 12 wk) and body weights were recorded, haematological studies were carried out after 12 months and complete gross and microscopic examinations were conducted at autopsy.At level of 1850 ppm, lead arsenate was toxic and caused intra- and extrahepatic bile-duct lesions. Intranuclear inclusions due to the ingested lead were present in the kidneys and liver, but only for the first 12 months. Other histopathological changes, commonly found in these rats, were equally divided between the groups. No differences were apparent either in the tumour incidence of the different groups or in the times at which tumours were detected. An adenoma in the renal cortex and a bile-duct carcinoma, both found in the group fed 1850 ppm lead arsenate, may have been indicative of a very weak carcinogenic action of this compound, but no definite conclusion used in this study. No additive or synergistic effect could be attributed to DENA, which also failed to induce tumours at the low dose level used, suggesting the possible existence of a no-effect level for this carcinogen.