Also, when appropriate, the role of rENP was tested as an additional independent factor.
rENP induced a statistically significant (p < 0.0001) reduction on TNF-[alpha] levels for all doses and PM fractions tested (Figure 3B).
In this case, rENP noticeably blocked the secretion of IL-6 stimulated by P[M.sub.10] from the southeastern zone (p < 0.0001) (Figure 5B).
Southeastern P[M.sub.10] strongly induced the secretion of TNF-[alpha] and IL-6 (Figures 3 and 5), and this was due at least in part to endotoxin, because the rENP reduced cytokine release in response to these particles.
Endotoxin content on P[M.sub.10] from the southeastern region could explain the proinflammatory potential of these particles because the cytokine stimulatory effects of these particles on confluent cell cultures were blocked by rENP. Moreover, the endotoxin level extracted from P[M.sub.10] from the southeastern region (59.34 EU/mg) was 2-fold higher than the endotoxin level from P[M.sub.10] from the northern region (Table 3).