Emerging Mechanistic Targets in Lung Injury Induced by Combustion-Generated Particles
Marc W. Fariss, M. Ian Gilmour, Christopher A. Reilly, Wolfgang Liedtke, and Andrew J. Ghio
Toxicological Sciences 132(2), 253–267 (2013)
The second sentence of the third paragraph in column two on page 255 should have read as follows (updated text in bold). The authors regret the error.
Two ditert-butylphenol analogues, presumably arising on diesel PM from their use as a fuel/oil preservative, activated TRPA1 via the propofol/menthol binding site (S873/T874) (Fig. 2A), and the fully extracted residual “stripped” DEP mass activated TRPA1, V1, and M8 equivalently and to the same level as the authentic coal fly ash PM, whose potency at TRPA1 was unaffected by solvent extraction (Figs. 2A–C).