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.
The fact that one sample (A-DEPs) has been used extensively in pulmonary toxicity studies but never studied previously for mutagenicity, and virtually the opposite situation pertains for the other sample (SRM 2975), illustrates the need for scientists to engage in collaborative, multidisciplinary research efforts in this area.
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.
For all these end points, A-DEPs and SRM 2975 DEPs were quite different.
SEM images of A-DEPs and SRM 2975 at 500x magnification showed the presence of aggregated particles (> 50 [micro]m) in both samples (Figure 2).
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).
The differences between A-DEPs and SRM 2975 in size, texture, and color were not surprising considering the different types of engines used to produce the particles and the different collection methods used to obtain the samples.
A-DEPs and SRM 2975 produced similar levels of acute pulmonary injury and IL-6 but induced distinctly different cellular inflammatory responses.