Extracts of filter-collected urban airborne particulate matter contain compounds which can competitively inhibit 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) binding to the rat liver TCDD-receptor protein. The concentration of conventional polycyclic aromatic hydrocarbons (PAHs) or chlorinated dioxins and dibenzofurans cannot account for more than 1%-30% of the observed competition for TCDD-binding to the receptor protein. Chemical fractionation of an extract of a well-characterized particulate air sample collected in Washington, DC showed the highest activity residing in the hexane/benzene fraction, although significant levels of activity were found also in other fractions. Analysis of extracts of gasoline exhaust particulate matter and fractions thereof gave similar results. A series of pure PAHs and nitro-and chloroderivatives of PAHs was tested for competition with TCDD for receptor binding. Among the most potent compounds with EC50-values similar to tetrachlorodibenzofuran were 1- and 3-nitrobenzo(a)-pyrene. Other highly active compounds included dibenzo(a,h)anthracene, benzo(j)fluoranthene, benzo(k)fluoranthene, picene, indeno(1,2,3-cd)pyrene, 3-nitroperylene, and 3,9-and 3,10-dinitroperylene. the EC50-value for aryl hydrocarbon hydroxylase induction in hepatoma cells and the EC50-value for TCDD-receptor binding were similar for dibenzo(a,h)anthracene and for a PAH-containing fraction of an extract of gasoline exhaust particulates. The presence of active TCDD-receptor ligands in extracts of urban particulate matter and their ability to be taken up by cells and cause biological alterations represent a potential health risk. The identity of these compounds are largely unknown although certain PAHs and possibly some nitroderivatives of PAHs are likely to play a role.
ASJC Scopus subject areas
- Environmental Science(all)