As the cause of leukemia remains obscure, epidemiology has assumed an importance in two directions: first, the incidence, age, and sex differences in the various forms of the disease related to their geographic presentation, and second, the hunt for etiologic clues.

One of the first epidemiology studies on leukemia was by W. R. Gowers, based upon 154 cases and published in London in 1879. The study comprised age and sex data collected at a time when leukemia was recognized only as a chronic disease. It offered few etiologic clues other than exposure to malaria, which was then not confined to tropical countries.

Toward the close of the nineteenth century, a small number of cases of leukemia in its acute form were reported in Europe, and attention was focused on this new form of the disease, particularly in America. George Dock of the University of Michigan was a leading investigator of the complicated aspects of acute leukemia and its rapid onset. The literature, which Dock reviewed extensively in 1903, regarded infection and "some microscopic germ" as suspects.

The infective theory of acute leukemia was further discussed in a 1917 publication in the British Journal of Children's Diseases by G. Ward, who had collected a series of 1,457 cases of leukemia. This work added to the knowledge of the age-sex distribution of the disease and suggested that although acute leukemia resembled an infectious disease in many respects (e.g., the feverlike symptoms it caused), there was little evidence to suggest that it was by nature infectious or that it was hereditary.

Leukemia tends to present in an irregular pattern, evidenced by the number of "clusters" of cases that are regularly reported, clusters being defined as more cases of the disease than would be expected to occur in a specific area. The first report of a cluster of leukemia cases came from Paris in 1922, where four patients living within a short distance of one another were diagnosed with acute leukemia in a period of 7 weeks. It was the commonly held view that the cause was the water from a canal in the area. In this event, as with most clusters, the pattern was of normal or less than normal incidence of the disease both before and after the appearance of the cluster of cases.

Because of the sudden presentation of clusters of the disease, investigations are often launched to find a cause. The identification of possible contributory factors within the environment is one approach, although the prime concentration is on what influences the basic cells and genes to change and begin the malignant process. The most established etiologic factor in human leukemias is ionizing radiation. The atom bombs dropped on Hiroshima and Nagasaki in 1945, for example, brought a rise in the incidence of leukemia, which began about 3 years after the atomic attack and reached a peak at 6 years, but then slowly declined to a normal incidence of the disease at 20 years. On investigation it was found that the greatest incidence was among those closest to the explosion, whereas at 2,000 meters or more the risk of leukemia was no greater than among unirradiated people.

Altogether some 250 cases of leukemia occurred between 1946 and 1965 in the 183,000 people exposed to radiation in Hiroshima and Nagasaki. From this information it followed that only a small proportion of those irradiated developed leukemia, and this led to the suggestion of individual susceptibility. Later, public concern about nuclear power causing leukemia was heightened by the number of clusters of cases of the disease reported in areas surrounding nuclear power stations. Indeed many questions have been raised on this issue, particularly because childhood cases appear to be more prominent in these reported clusters. The pattern — which became apparent in the aftermath of the attacks on Hiroshima and Nagasaki - seems to emerge in these clusters as well; for if nuclear power stations are emitting radiation, relatively few people are actually affected - again raising the etiologic question of possible susceptibility.

The issue of genetic susceptibility was studied by Frederick Gunz, a distinguished research physician at Sydney Hospital in Australia, whose biological approach to epidemiology resulted in his publications in 1974 and 1975 on the genetics of human leukemia. Gunz concluded that evidence from family studies reinforced the theory of a genetic basis in some people for chronic lymphatic leukemia in particular. Gunz also reported that certain chemicals, notably benzene along with viruses, were identified as triggering factors in some animal leukemias, but evidence for such a conclusion in human leukemia remained elusive.

A major epidemiology study embracing a population base of some 20 million people was started in 1984 in England and Wales, at the University of Leeds, by the Leukaemia Research Fund. This computerized program with diagnostic check controls will be of major importance in assessing current trends in the presentation of the disease.

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