The assessment of human cancer risk using molecular epidemiological te
chniques involves determining the relative contributions of inherited
and acquired genetic predispositions, in the context of environmental
exposures. Recently described genetic polymorphisms for CYP1A1, a gene
involved in the metabolic activation of polycyclic aromatic hydrocarb
ons, have been associated with lung cancer risk in a Japanese populati
on. We report herein findings from a United States case-control study
of lung cancer (56 cases; 48 controls). The polymerase chain reaction
followed by an Msp1 restriction enzyme digestion was used to analyze c
onstitutive DNA but no association between the restriction fragment le
ngth polymorphism and lung cancer risk was found (odds ratio, 0.7; 95%
confidence interval, = 0.3-1.6). Analysis of genotype by cumulative s
moking status did not reveal an elevated risk among lesser or greater
smokers. The presence of the CYP1A1 Msp1 site-present allele, which wa
s previously found to be associated with Japanese lung cancer risk, wa
s statistically increased in African compared to Caucasian Americans (
odds ratio, 2.9; 95% confidence interval, 1.2-2.7). When stratified by
race, however, no association between case status and the polymorphis
m was observed, but the small number of study subjects within each rac
ial group limited the statistical power. Larger studies are required t
o evaluate the risk of the CYP1A1 Msp1 polymorphism in African America
ns.