ALDH2　is　involved　in　the　metabolism　of　styrene,　a　widely　used　industrial　material,　but　no　data　are　available　regarding　the　influence　of　this　enzyme　on　the　metabolic　fate　as　well　as　toxic　effects　of　this　chemical.　In　this　study,　we　recruited　329　workers　occupationally　exposed　to　styrene　and　152　unexposed　controls.　DNA　strand　breaks,　DNA-base　oxidation　in　leukocytes　and　urinary　8-hydroxydeoxyguanosine　(8-OH-dG)　were　assayed　as　biomarkers　to　measure　genotoxic　effects.　Meanwhile,　we　examined　the　genetic　polymorphisms,　including　ALDH2,　EXPH1,　GSTM1,　GSTT1　and　CYP2E1,　and　also　analyzed　the　levels　of　styrene　exposure　through　detecting　urinary　styrene　metabolites　and　styrene　concentration　in　air.　In　terms　of　DNA　damage,　the　three　genotoxic　biomarkers　were　significantly　increased　in　exposed　workers　as　compared　with　controls.　And　the　styrene-exposed　workers　with　inactive　ALDH2　*2　allele　were　subjected　to　genotoxicity　in　a　higher　degree　than　those　with　ALDH2　*1/*1　genotype.　Also,　lower　levels　of　urinary　styrene　metabolites　(MA　+　PGA)　were　observed　in　styreneexposed　workers　carrying　ALDH2　*2　allele,　suggesting　slower　metabolism　of　styrene.　The　polymorphisms　of　other　enzymes　showed　less　effect.　These　results　suggested　that　styrene　metabolism　and　styrene-induced　genotoxicity　could　be　particularly　modified　by　ALDH2　polymorphisms.　The　important　role　of　ALDH2　indicated　that　the　accumulation　of　styrene　glycoaldehyde,　a　possible　genotoxic　intermediate　of　styrene,　could　account　for　the　genotoxicity　observed,　and　should　be　taken　as　an　increased　risk　of　cancer.