Under the auspices of the National Institute of Environmental Health Sciences (NIEHS) and in conjunction with other Drosophila laboratories, we are assaying environmental compounds for mutagenic activity in a blind test evaluating initially for gene/point mutations in the sex-linked recessive lethal test and, if positive, for chromosome breakage in the heritable translocation test to detect translocations between chromosomes 2 and 3 and between the Y chromosome and chromosome 2 and/or 3. One of the first compounds tested proved positive in both assays. The compound bears the code designation 024474 or 623474. For the recessive lethal test, males 24 h old and starved 6 h were permitted to feed for 72 h (solutions renewed at 24-h intervals) on 0.0, 2.5, 5.0 and 7.5 mg/ml of the compound in 5% sucrose. Results were, respectively (number of lethals/numbers of tests), 1/3349 (0.03%), 10/1040 (0.96%), 16/1088 (1.47%) and 39/2509 (1.55%). Only males treated with 7.5 mg/ml were tested for translocations. No translocations were found in 8335 control genomes and 4/6210 and 7.5 mg/ml distributed as follows: 0/2645 following 7-9 days of sperm storage, 4/3416 (10-12 days) and 0,/149 (13-15 days); shorter periods of storage (1-6 days) were not tested. Regarding tests for chromosome breakage, Zimmering and co-workers have demonstrated improved chromosome-breakage detection capability of conventional F1 tests for chromosome loss by substituting repair-deficient mei-9 a for ordinary repair-proficient PI females in mutagenicity assays of 5 monofunctional alkylating agents including MMS, DMN, DEN, procarbazine (see Zimmering, 1981) and MNU (Zimmering and Moberg, unpublished). More recently, females from the repair-deficient strain designated s t mus302 have been employed and shown to confer even greater sensitivity on the chromosome loss test in assays of the above compounds (Zimmering, 1982, and unpublished). Accordingly, X c2, y f / B S y y +