To examine the risk of lung cancer associated with theMspI-restriction fragment length polymorphism and Exon7-Val polymorphisms ofCYP1A1, a meta-analysis of published case–control studies was undertaken using a random effects model. The principal outcome measure was the odds ratio for the risk of lung cancer, using homozygosity of the `wild-type allele' as the reference group. Fifteen reports detailing the relationship between the lung cancer and theMspI andIle-Valpolymorphisms ofCYP1A1were identified. The odds ratio of lung cancer associated with theMspI combined variant and homozygous genotypes were 1.09 (0.94–1.25) and 1.27 (0.91–1.77), respectively. The odds ratio of lung cancer associated with theIle-Valcombined variant and homozygous genotypes were 1.16 (0.92–1.48) and 1.62 (0.93–2.82), respectively. The hypothesis that the modulation of carcinogen metabolism is under genetic control is a plausible and attractive mechanism for explaining inter-individual susceptibility of lung cancer. However, the results from this analysis provide little support for the role of variation in theCYP1A1gene defined by either polymorphisms represents as lung cancer risk factor. Additional well-designed studies based on sample sizes commensurate with the detection of small genotypic risks may allow a more definitive conclusion.