LETTERS TO THE EDITOR 1175

The third study was performed in seven printing work-era after a colleague had developed aplastic anemia. All cytogenetic studies were completely normal, al-though evidence of bone marrow damage was noted, presumably as a result of exposure to a variety of organic compounds (9). Review of studies in nonleu-kemic subjects (7, 10-17) reveal one of 50 patients studied with banding techniques and zero of 263 pa-tients with unhanded studies to have evidence of a clonal abnormality. These data are insufficient to permit any assessment of point 4 above, but they are consistent with the causal hypothesis. The issue of whether particular abnormalities are caused by specific agents has been raised (3, 4). If there is a strict one-to-one relation, then strong asso-ciations could be detected using case-control study designs. On the other hand, if an abnormality such as plus chromosome 8 can be caused by a variety of exposures or if the same exposure can cause several different abnormalities, the associations would be weak and difficult to detect. Preliminary data from several sources (18-20) have suggested that loss of all or part of chromosomes 5 and/or 7 is associated with environmental exposures or prior cytotoxic therapy in acute nonlymphocytic patients, but information on more patients will be required to evaluate these rela-tions. Unfortunately, unless other etiologic agents are identified for leukemia, a test of the one exposure-one abnormality hypothesis will be difficult. We believe that these issues can be examined by carefully designed studies of exposed populations. As noted by Sandier and Collman, other laboratory assayB which correlate with marrow chromosome damage such as sister chromatid exchanges or chromosome breaks in lymphocytes would facilitate such studies. Further refinements would include careful exposure histories supplemented by biologic markers or other indicators of exposure. The authors should be congratulated for a stimu-lating and thought-provoking review