Erratum to: Biological Effects in Lung Cells In Vitro of Exhaust Aerosols from a Gasoline Passenger Car With and Without Particle Filter

Erratum to: Emiss. Control Sci. Technol. (2015) 1:237–246

DOI:10.1007/s40825-015-0019-6

This article contains an error in Figure 2B and 3 as well as in Table 1. The corrected figures, text and Table 1 appear below.

Oxidative stress and anti-oxidative response

Interestingly, according to the gene SOD2 and GSR (Figure 2B), filtered exhaust overall appears to have resulted in a lower response to oxidative stress than unfiltered exhaust: SOD2-expression was increased 1.5 ± 0.5-fold by unfiltered exhaust but suppressed to 0.7 ± 0.1-fold activity by filtered exhaust. The according values for GSR are: 3.9 ± 2.8 (no GPF) and 1.3 ± 0.2 (GPF). HMOX1 expression was induced 3.1 ± 1.3-fold by unfiltered exhaust and 0.9 ± 0.2-fold by filtered exhaust.

Fig. 2

B Oxidative stress. Transcriptional response to oxidative stress of three oxidative stress- responsive genes indicates increased oxidative stress upon exposure to unfiltered exhaust for SOD2 and GSR. Error bars indicate SEMs. Experimental repetitions are for no GPF (n = 3) and GPF (n = 4). The respective controls are shown as white bars.

Pro-inflammation

In contrary to the observed oxidative stress, no pro-inflammation was measured. Both filtered and unfiltered exhaust did not increase the assessed genes, TNFα and IL8. While filtered exhaust resulted in a baseline expression (0.95 ± 0.38 and 0.73 ± 0.21- fold for TNFα and IL8), unfiltered exhaust decreased the expression of both genes (to 0.5 ± 0.2-fold and 0.7 ± 0.1) (Figure 3).

Fig. 3

Exhaust-related changes in the transcriptional activity of two pro-inflammatory genes, i.e. TNFα and IL8. No upregulation of pro-inflammatory genes was observed. Error bars indicate SEMs. Experimental repetitions are for no GPF (n = 3) and GPF (n = 4). *p > 0.05 no GPF vs. GPF. The respective controls are shown as white bars.

Table 1 Summary of the effects induced by non-filtered as well as filtered gasoline exhaust emissions in lung cells in vitro. The term oxidative stress is related to the gene expression analysis while anti-oxidative stress is related to level of the anti-oxidative protein GSH. The table indicates differences in response compared to filtered air exposures.

1 Conclusions

The biological tests showed that the removal of the particulate fraction decreased significantly the AhR- activation in human lung cells in vitro, also the Ames test suggested a lower genotoxicity for filtered gasoline exhaust. However, the GPF exhaust increased GSH oxidation in the lung cell cultures.