Record Display for the EPA National Library Catalog


Main Title Aerosol Formation from Diesel Exhaust and SO2. A Chamber Study.
Author Anderson, R. J. ; Hanley, J. T. ;
CORP Author Calspan Advanced Technology Center, Buffalo, NY.;Environmental Sciences Research Lab., Research Triangle Park, NC.
Year Published 1980
Report Number EPA-68-02-2987; EPA-600/3-80-095;
Stock Number PB81-121147
Additional Subjects Air pollution ; Exhaust emissions ; Sulfur dioxide ; Photochemical reactions ; Aerosols ; Urban area ; Test chamber ; Oxidation ; Mutagens ; Ozone ; Ultraviolet radiation ; Diesel engine exhaust
Library Call Number Additional Info Location Last
NTIS  PB81-121147 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 110p
Dilute diesel emission systems were studied in a 600 cu m indoor smog chamber under various conditions likely to be encountered in an urban environment. Aerosol formation and growth in an irradiated diesel emission/SO2/propylene system was primarily attributed to sulfate formation. During irradiated experiments, the rate of SO2 oxidation experienced a maximum of about 5 percent/hr in the period when the O3 concentration was increasing rapidly. Following the peak in the O3 concentration, the rate of SO2 oxidation decreased to about 1 percent/hr. The presence of the primary diesel aerosol appeared to increase the rate of SO2 oxidation and the amount of aerosol sulfate formed as well as minimize the formation of new aerosols in irradiated experiments. In most irradiated experiments, the production of organic and nitrate aerosols represented minimal contributions to aerosol formation and growth. The results of the Ames tests were as follows: (1) UV irradiation produced no significant changes, (2) UV irradiation in conjunction with ozone production decreased mutagenicity and resulted in a change in mutagen type demonstrated by increases in direct acting response over that requiring metabolic activation, (3) dark reaction of the exhaust gas with the aerosols resulted in increased mutagenicity, both with and without metabolic activation.