## 4 Discussion
These reactions convert, among other compounds, polynuclear aromatic hydrocarbons to their corresponding quinones as exemplified by 9,10-phenanthroquinone generation (PQ) [7] a potent biological prooxidant associated with PM [25]. Relatively higher levels of such organic prooxidants in the SB PM2.5 sample are suggested by the DTT assay data (Table 2B) that show a larger fraction of the SB PM activity not inhibited by metal chelation (i.e., DTPA-insensitive), in support of this phenomenon of atmospheric formation of organic prooxidants. Analogously, the generation of organic electrophiles such as 1,4-benzoquinone (BQ) likely contribute to the more potent SB anti-inflammatory HO-1 response in the VOC fraction (Table 3). Based on these considerations, we suggest that the higher pro- and anti-inflammatory actions of the SB sample compared to that of CM2 are due to its higher content of organic reactants generated by photochemical processes. A second consideration in determining relative biological potencies of PM and VOCs is their cellular access upon exposure. PM/metal ions' entry into cells is regulated by endocytosis and transport processes [6; 26], whereas quinones such as PQ and BQ are neutral and non-polar compounds that can readily penetrate membranes to promote oxidative stress-related reactions [27]. These biological differences underscore the complex chemical composition of PM, which limits the interpretive value of \begin{table}
\begin{tabular}{c c c c c} \hline \hline  & \multicolumn{2}{c}{**DTT**} & \multicolumn{2}{c}{**DTT + DTPA**} \\ \cline{2-5}  & **Mean** & **95\% CI** & **Mean** & **95\% CI** \\ \hline
**SB** & 0.65 & 0.55–0.75 & 0.16 & 0.11–0.20 \\
**CM2** & 0.50 & 0.47–0.55 & 0.08 & 0.03–0.13 \\
**SB/CM2 ratio** & 1.31 & & 1.89 & \\ \hline \hline \end{tabular}  
* Prooxidant content, defined by DTT activity (nmols DTT consumed/min*m3), in the presence and absence of 20 \(\upmu\)M, diethylenetriamine pentaacetic acid (DTPA), a metal chelator [16].  
\end{table} 
Table 2: Prooxidant content of SB and CM2 samples. \begin{table}
\begin{tabular}{c c c c c} \hline \hline  & \multicolumn{2}{c}{**PM2.5 TNF-\(\alpha\)**} & \multicolumn{2}{c}{**VOC HO-1**} \\ \cline{2-5}  & **Equation** & **Slope: 95\% CI** & **Equation** & **Slope: 95\% CI** \\ \hline
**SB** & Y = 413.9*X - 16.7 & 319.9–507.9 & Y = 185.2.4*X - 37.8 & 158.5–212.9 \\
**CM2** & Y = 29.88*X - 0.34 & 22.58–37.18 & Y = 42.74*X + 4.49 & 22.76–58.22 \\
**SB/CM2 ratio** & 13.8 & & 4.3 & \\ \hline \hline \end{tabular}  
* Slopes of cellular responses to three concentrations of PM2.5 from the indicated PM2.5 samples as a function of cellular protein concentration. Units: Y = TNF-\(\alpha\) pg/mg protein; Y = HO-1 ng/mg protein/m3; \(\chi\) = m3/mL.  
\end{table} 
Table 3: Biological properties of SB and CM2 samples. a general chemical assay such as the DTT assay and necessitate inclusion of parallel biological assays for more definitive evaluation of PM reactivities. Direct extrapolation of these results to potential toxicological effects in humans, i.e., PM-induced oxidative stress and VOC-induced covalent adducts, remains to be established. In one of the very few direct comparisons of 'whole' diesel exhaust (DE) and VOC components, [PERSON] et al. [28] compared the cardiovascular effects of these two samples in mice and observed major effects consistent with myocardial ischemia, attributable to VOC components. These VOC effects were also seen in vitro using isolated blood vessels. Although some of the chemical components were determined, they did not, however, assay for redox-active species or electrophiles. A second relevant study examined the role of electrophiles that included 1,2-naphthoquinone, a component of VOCs [25] in the actions of DE on mouse lungs [29]. In an intact lung model and in multiple cultured human lung cell models, they showed activation of transient receptor potential ankyrin-1, a pro-inflammatory mediator, on airway C-fibers by a variety of qualitatively and quantitatively different DE particles.