However, when the mutagenic potencies of the EOM were combined with the percent EOM of the particles, the mutagenic potency of the A-DEPs per mass of particle was greater in all strains than that of the SRM 2975 DEP regardless of S9 (Table 3).
2004) for greater amounts of PAH-type mutagenicity and PAHs in the A-DEPs compared with SRM 2975.
Differences in percentages of EC and OC in the A-DEP and SRM 2975 samples may be explained by the sample collection methods, as well as by differences in engine design and operation.
Compound A-DEP SRM 2975 Carbon analysis (% of total mass) EC 9 60 OC 50 5 Carbonate <1 <1 Remaining fraction 41 35 PAH ratios Phenanthrene:anthracene 1 >20 Fluoranthene:pyrene 1 >20 EOM (%) 26.
A-DEPs have been tested extensively for their effects on pulmonary inflammation and exacerbation of allergic asthmalike responses.
In the present study, mice were exposed by involuntary aspiration to 0, 25, or 100 [micro]g of A-DEPs or SRM 2975 or to a dose of an organic extract of these DEP equivalent to the proportional mass of the fraction present in a 100-[micro]g dose of the particle sample.
The generation and collection conditions of the A-DEPs have been described previously (Kobayashi and Ito 1995; Sagai et al.
Mice were anesthetized using vaporized halothane (Sigma) and exposed to 25 or 100 [micro]g of either A-DEPs or SRM 2975 in 50 [micro]L saline (Sigma) vehicle by involuntary aspiration for whole-particle exposures.
By contrast, A-DEPs produced significant increases in total numbers of MACs in the BALF at 4 hr, which reduced to control levels by 18 hr (not shown).
SRM 2975 (only at 25 [micro]g), A-DEPs (25 and 100 [micro]g), and endotoxin (10 [micro]g) significantly increased concentrations of microalbumin in the BALF 4 hr after exposure (Figure 4A).
Instillation of 100 [micro]g of A-DEPs significantly increased the concentration of the proinflammatory cytokines IL-6 and TNF-[alpha] and the chemokine MIP-2 in BALF at 4 hr compared with instillation of saline (Figure 5A-C).
A-DEPs and SRM 2975 produced similar levels of acute pulmonary injury and IL-6 but induced distinctly different cellular inflammatory responses.