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Table 1.

Mass fraction of the elements and metals (ng/μg PM) during exposures.

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Table 2.

Size distribution of the aerosol during exposures.

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Fig 1.

nPM exposure results in an inflammatory microglia response in the corpus callosum.

(A) Iba-1+iNOS microglia in the corpus callosum of mice exposed to filtered air and nPM, with representative image of a positive cell at high magnification. (B) Iba-1+Arg microglia in the corpus callosum of mice exposed to filtered air and nPM, with representative image of a positive cell at high magnification. (C) Iba-1 positive microglia cell counts were significantly increased in the corpus callosum of mice exposed to nPM (n = 17) compared to filtered air (n = 18) (p<0.0001). (D) iNOS positive microglia cell counts were significantly increased in the corpus callosum of mice exposed to nPM (n = 17) compared to filtered air (n = 18) (p<0.0001). (E) Arginase-1 positive microglia cell counts were not significantly different in the corpus callosum of mice exposed to nPM (n = 18) compared to filtered air (n = 18) (p = NS). Data presented as mean ± standard deviation. Scale bars represent 10 μm. Error bars represent standard deviation. **** signifies p<0.0001.

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Fig 2.

nPM exposure results in myelin injury and axonal damage in the corpus callosum.

(A) dMBP in the corpus callosum of mice exposed to filtered air and nPM. Analysis was performed on both right/left sides. Right side location is marked in C. (B) dMBP immunofluorescent density was significantly increased in the corpus callosum of mice exposed to nPM (n = 18) compared to filtered air (n = 18) (p<0.001). (C) Representative images of regions analyzed (Top: Right side corpus callosum is marked. Bottom: Right side internal capsule and left side optic tracts are marked). Analysis was performed on both right and left sides. (D) dMBP in the internal capsule of mice exposed to filtered air and nPM. Analysis was performed on both right/left sides. Right side location is marked in C. (E) dMBP immunofluorescent density was significantly increased in the internal capsule of mice exposed to nPM (n = 6) compared to filtered air (n = 6) (p<0.01). (F) dMBP in the optic tract of mice exposed to filtered air and nPM. Analysis was performed on both right/left sides. Left side location is marked in C. (G) dMBP immunofluorescent density was not significantly different in the optic tract of mice exposed to nPM (n = 6) compared to filtered air (n = 6) (p = 0.65). (H) Oligodendrocytes in the corpus callosum of mice exposed to filtered air and nPM. (I) Oligodendrocyte cell counts were significantly decreased in the corpus callosum of mice exposed to nPM (n = 12) compared to filtered air (n = 12) (p<0.05). (J) SMI-312 in the corpus callosum of mice exposed to filtered air and nPM. Analysis was performed on both right/left sides. (K) SMI-312 immunofluorescent density was significantly decreased in the corpus callosum of mice exposed to nPM (n = 12) compared to filtered air (n = 12) (p<0.05). Data presented as mean ± standard deviation. Scale bars represent 10 μm. Error bars represent standard deviation. *signifies p<0.05, **signifies p<0.01, *** signifies p <0.001.

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Fig 2 Expand

Fig 3.

Microglial reactivity is correlated with myelin injury in the corpus callosum.

(A) Iba-1 positive cell count was positively correlated with dMBP immunofluorescent density (r(33) = 0.438, p = 0.009). (B) iNOS-expressing microglia cell count was positively correlated with dMBP immunofluorescent density (r(33) = 0.445, p = 0.007). (C) Iba-1 positive cell count was positively correlated with iNOS-expressing microglia cell count (r(33) = 0.560, p<0.001).

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