RESUMEN
Samples of airborne particles from Sapporo, the capital of Hokkaido, Japan, were collected between 1975 and 2000. Major polycyclic aromatic hydrocarbons (PAHs) included in the extracts of airborne particles were investigated for their mutagenicity and potential for inducing drug-metabolizing enzyme cytochrome P450 (CYP)1A1, which is considered to be responsible for the activation of PAHs in airborne particle extracts, as well as in cigarette smoke, to carcinogens and is associated with risk of several cancers. There was a dose-related increase in CYP1A1 activity in human lymphoblastoid cells after exposure to airborne particulates containing PAHs. The mutagenicity of the airborne particles collected in summer was lowest and for those collected in spring was lower than in autumn or winter. Likewise, the winter sample had the strongest CYP1A1 inducing potential while the summer sample had the weakest. CYP1A1 inducing potency was strongly related to the amount of benzo(k)fluorathene (Spearman's rank correlation coefficient (gamma) = 0.97), benzo[a]pyrene g = 0.96), benzo[g,h,i]perylene (gamma = 0.94), benz[a]anthracene (g = 0.93), chrysene (gamma = 0.93) in the extracts during the 25-year period, while the enzyme activity was measurably related to the amount of pyrene (gamma = 0.64) and fluorathene (gamma = 0.54). During the 25-year period, CYP1A1 inducing potential decreased every year together with a decrease in PAHs in the airborne particle extracts. CYP1A1 inducing potential may be one of the most convenient biomarkers with which to estimate the overall carcinogenicity/mutagenicity of airborne particle extracts.