ACES Phase 3 study reported that animals exposed to concentrated exhaust from a 2007-complaint diesel engine for 16 hours per day, 5 days per week, for up to 12 months have experienced virtually no health effects (http://pubs.healtheffects.org/getfile.php?u=708). The full report also shows that particle emissions were below detection limits except during DPF regeneration (http://pubs.healtheffects.org/getfile.php?u=709, Figure 2, page 19)

Many studies, including one by CARB (NOT a diesel proponent) have shown that particulate emissions are indistinguishable from background levels. The particulate emissions are at least 2 orders of magnitude lower than gasoline engines, and gasoline engines have been shown to have particle emissions which EXCEED those of “old tech” diesel engines (i.e., unfiltered) under some common driving conditions (rapid acceleration, high speeds).

Opposition to diesel technology on health/environmental grounds is no longer legitimate.

Abstract
1-Nitropyrene (1-NP) is a nitro-polycyclic aromatic hydrocarbon (nitro-PAH) present in diesel exhaust and bound to particular matter in urban air. We show that 1-NP and the referent PAH benzo(a)pyrene (BP) induce apoptosis and a lipid accumulation dependent on cytochrome P450 1A1-metabolites in mouse hepatoma cells, whereas 1-amino-pyrene had no effect. The caspase inhibitor, N-benzyloxycarbonyl-Val-Ala-Asp(O-Me) fluoromethyl ketone (Z-VAD-fmk), inhibits 1-NP-induced apoptosis, but failed to alter 1-NP-triggered lipid accumulation determined by Nile red staining. We further show that cholesterol and fatty acid contents are modified after nitro-PAH exposure and that 1-NP-induced cholesterol level is partially involved in related apoptosis. In parallel, the activity of the stearoyl-CoA desaturase 1 (SCD1), determined by fatty acid analysis, and its expression are reduced by 1-NP. The role of SCD1 in 1-NP-induced apoptosis is demonstrated in cells down-expressing SCD1, in which an increased apoptosis is observed, whereas the SCD1 overexpression elicits the opposite effects. In contrast, changes in SCD1 gene expression have no effect on the induced lipid accumulation. Moreover, 1-NP increases the activity of the AMP-dependent protein kinase (AMPK) leading to a caspase-independent apoptosis. Overall, our study demonstrates that the 1-NP-induced apoptosis is caspase- and AMPK-dependent, and is associated to a decrease of SCD1 expression which results in an alteration of lipid homeostasis.
Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.
PMID: 21872649 [PubMed - indexed for MEDLINE]
Publication Types, MeSH Terms, Substances

Source info:
Toxicol Lett. 2011 Oct 30;206(3):289-99. Epub 2011 Aug 18.
Mechanisms involved in lipid accumulation and apoptosis induced by 1-nitropyrene in Hepa1c1c7 cells.
Podechard N, Tekpli X, Catheline D, Holme JA, Rioux V, Legrand P, Rialland M, Fardel O, Lagadic-Gossmann D, Lecureur V.
Source
EA4427-SeRAIC, Team Toxicity of Polycyclic Aromatic Hydrocarbons, IFR140, Université de Rennes 1, Faculté des Sciences Pharmaceutiques et Biologiques, IRSET, France.