Correlation between selected environmental exposures and karyotype in acute myelocytic leukemia.
Many bone marrow cytogenetic abnormalities in acute myelogenous leukemia (AML) are tumor specific, clonal, nonrandom, and related to prognosis; it has been hypothesized that they may be markers of exposure to etiological agents. A previous report from our institution revealed several such associations; the purpose of the current study was to determine whether previous findings were present in a new group of patients. Subjects included 84 newly diagnosed AML patients (French-American-British M1 and M2); exposure data were gathered using self-report questionnaires at the time of registration. Two sets of comparisons were made: (a) patients with all (AA) or some (AN) cytogenetically abnormal cells versus those with normal karyotypes (NN) and (b) patients with specific abnormalities [-5/5q-, -7/7q-, +8, t(8;21)] versus all others. Odds ratios (ORs) were 4.64 for the association between prior cytotoxic therapy and -5/5q- and 6.38 for the association with -7/7q-, but were <1.00 for +8 and t(8;21). There were no ORs > 2.0 for specific abnormalities in any of the other exposures evaluated (cigarette smoking, alcohol use, occupational exposure to organic chemicals, paints, or pesticides/herbicides), with the exception of exposure to paints and -7/7q- (OR, 7.50). The ORs for AA/AN versus NN patients were 1.43 and 3.81 for smoking and alcohol use, and weak dose-response trends were present. The most consistent positive associations between the two series were for prior cytotoxic therapy (-5/5q-; -7/7q-), cigarette smoking (AA/AN versus NN) and alcohol use (AA/AN versus NN). Reasoning from the known association between prior cytotoxic therapy and -7/7q-, we would have predicted relatively high ORs (> 4.0) if specific abnormalities acted as markers for the exposures assessed, but none were present. However, in both series, AA/AN patients were more likely to smoke and use alcohol than were NN patients, and weak dose-response patterns were present for both. This finding suggests that both smoking and alcohol use may play a role in the pathogenesis of cytogenetic abnormalities in AML-M1/M2; however, the mechanism by which they work and whether they are involved in the etiology of these diseases remain unclear.
Crane
M M
MM
Division of Medical Education and Research, Greenville Hospital System, South Carolina 29605, USA.
Strom
S S
SS
Halabi
S
S
Berman
E L
EL
Fueger
J J
JJ
Spitz
M R
MR
Keating
M J
MJ
D000328:Adult; D000428:Alcohol Drinking; D001853:Bone Marrow / Q000473:pathology; D002869:Chromosome Aberrations; D025063:Chromosome Disorders; D002895:Chromosomes, Human, Pair 5; D002897:Chromosomes, Human, Pair 7; D004781:Environmental Exposure; D004785:Environmental Pollutants; D005260:Female; D006801:Humans; D007621:Karyotyping; D015470:Leukemia, Myeloid, Acute / Q000209:etiology* / Q000235:genetics / Q000473:pathology*; D016015:Logistic Models; D008214:Lymphocytes / Q000473:pathology; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D012907:Smoking
D004785:Environmental Pollutants