Mutagenic particulate matter in air pollutant source emissions and in ambient air.

摘要

Procedures are developed and demonstrated that can be used to investigate biological changes caused by fine particulate air pollution exposure, and to focus attention on the origin of those chemical components in the ambient fine particle mixture that are capable of causing genetic damage.;The human cell mutagenicity of the 1993 Los Angeles area particulate matter was examined by bioassay-directed chemical analysis. A composite consisting of a portion of all the urban filter samples was created and separated into fractions of varying polarity. Subfractions containing the ordinary polycyclic aromatic hydrocarbons (PAH) were responsible for a large portion of the ambient human cell mutagenic potency. Six ordinary PAH (cyclopenta(cd) pyrene, benzo (a) pyrene, benzo (ghi) perylene, benzo (b) fluoranthene, indeno (1,2,3-cd) pyrene, and benzo (k) fluoranthene) accounted for most of the mutagenic potency assigned to specific compounds. Important semipolar mutagens that were identified include 2-nitrofluoranthene and 6H-benzo (cd) pyren-6-one.;The contribution of specific particle emissions sources to the 1993 Los Angeles area airborne fine particle organic compound mass concentration was determined using a chemical mass balance receptor model based on organic compound tracers. These source contributions are used with measurements of the mutagenic potencies of the primary particles emitted from sources in the Los Angeles area to predict the mutagenic potency that would prevail if those primary particle emissions were transported without further chemical reaction. The predicted mutagenicity of the calculated source mixture was statistically indistinguishable from that of the actual atmospheric sample modeled.;Ambient fine particulate matter samples were collected throughout 1993 at four urban sites in Southern California, and at an upwind background site on San Nicolas Island. No systematic seasonal or spatial variation in mutagenic potency was observed in the urban ambient air samples. This suggests that the mutagenicity of the ambient particulate matter is due to ubiquitous primary emissions sources and that if atmospheric chemical reactions contribute important atmospheric mutagens then these reactions must proceed in the winter as well as in the photochemically more active summer season. The mutagen density in Los Angeles urban air was 1 order of magnitude greater that at the background site, showing that the city is indeed a source of mutagenic organic chemicals.