Project at a Glance
Title: Monitoring of mutagens and carcinogens in community air
Principal Investigator / Author(s): Flessel, P.
Contractor: Air and Industrial Hygiene Laboratory, California Department of Health
Contract Number: A1-029-32
Research Program Area: Health & Exposure
Topic Areas: Health Effects of Air Pollution, Toxic Air Contaminants
This field and laboratory study has measured the mutagenic activity of ambient air particulate extracts collected in Contra Costa County, California, identified and quantitated a number of specific organic compounds, which contribute to the mutagenicity and determined the major contributing sources. Intensive air sampling for source identification was carried out at four locations (Pittsburgh, Richmond, Concord and Martinez) during seasonal pollution episodes. Sampling was done over 360-hour periods in August and October 1981 and in January 1982. Organic extracts of air particulate matter were analyzed for mutagenic activity in the Ames Salmonella test and for selected polycyclic aromatic hydrocarbons (PAH) by high pressure liquid chromatography (HPLC) coupled with fluorescence detection. Ames testing was performed with and without added rat liver (S9) extract in order to measure both indirect (+S9) and direct-acting (-S9) mutagens. Nine polycyclic hydrocarbons were identified by HPLC and their sum used as a surrogate for total PAH. Air samples were also analyzed for trace metals (including Pb, Ni and Fe), secondary particulate (N03- and SO4 =) and pollutant gases (03, CO, NO, N02, S02). Multivariate statistical techniques were used to provide insights to sources of mutagens and PAH. Factor analysis helped identify types of emission sources and select source tracers. Using tracers for automobiles (Pb,), industry (Ni,) crystal material (Fe), secondary aerosols N03-, S04 = linear regression models were developed of the form Mutagenicity = a(Pb) + b(N03-) + where a and b were the regression coefficients determined from data collected during intensive sampling episodes.
The results suggested the following interpretation: During the August episode, automobile related pollutants accounted for 60-70 percent of the mutagenicity (indirect and direct) and the PAH. About one third of the mutagenicity was attributed to nitrate-associated secondary aerosols; however this conclusion is based on uncertain N03- measurements and is therefore not very firm. During the October episode, automotive sources accounted for essentially all of the indirect- and half of the direct-acting mutagenic activity, as well as more than half of the PAH. Sulfate-associated secondary sources contributed the other half of the direct-acting muta-genicity. Industrial (Ni-associated) sources added about one-fifth of the PAH and about 20 percent of the PAH could not be accounted for. The source pattern during the January episode was very complex and quantitative source apportionment was not successful. However qualitative results suggested contributions to mutagenicity from -6. vehicular traffic and contributions of residential wood combustion to PAH during the winter. Chronic air sampling for seasonal variations and trends was also carried as part of the study. Twenty-four hour hi-vol samples were collected in Contra Costa every sixth day between November 1979 and June 1982 and four-month seasonal composites prepared and analyzed for mutagenic activity, PAH and other particulate pollutants. Mutagen and PAH concentrations showed dramatic seasonal variations and were highest in the winter months (November - February). No annual trends in levels of mutagens, PAH and other pollutants, were apparent over the 32-month study period. Information was obtained about the nature of the chemicals, which contribute to the mutagenic activity of air particulate extracts. Contra Costa aerosol extracts contained both direct acting and indirect-acting mutagens. Direct-acting mutagens predominated during warm weather months, while both types were significant contributors during cold-weather months. Polycyclic aromatic hydrocarbons were among the indirect-acting mutagens found. However, the nine polycyclic hydrocarbon species measured accounted for only a small amount (ca. 1%) of the observed mutagenic activity. Indirect measurements in bacterial nitroreductase-deficient mutants suggested that nitroorganic compounds (e.g. highly mutagenic N02PAH) may contribute half of the mutagenic activity of aerosol extracts. Direct chemical identification and quantitation of these compounds in Contra Costa air remains for future research.
For questions regarding research reports, contact: Heather Choi at (916) 322-3893
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