Exposure to particulate matter (PM) in the ambient air and its interactions with APOE alleles may contribute to the acceleration of brain aging and the pathogenesis of Alzheimer's disease (AD). Neurodegenerative effects of particulate air pollutants were examined in a US-wide cohort of older women from the Women's Health Initiative Memory Study (WHIMS) and in experimental mouse models. Residing in places with fine PM exceeding EPA standards increased the risks for global cognitive decline and all-cause dementia respectively by 81 and 92%, with stronger adverse effects in APOE ɛ4/4 carriers. Female EFAD transgenic mice (5xFAD+/−/human APOE ɛ3 or ɛ4+/+) with 225 h exposure to urban nanosized PM (nPM) over 15 weeks showed increased cerebral β-amyloid by thioflavin S for fibrillary amyloid and by immunocytochemistry for Aβ deposits, both exacerbated by APOE ɛ4. Moreover, nPM exposure increased Aβ oligomers, caused selective atrophy of hippocampal CA1 neurites, and decreased the glutamate GluR1 subunit. Wildtype C57BL/6 female mice also showed nPM-induced CA1 atrophy and GluR1 decrease. In vitro nPM exposure of neuroblastoma cells (N2a-APP/swe) increased the pro-amyloidogenic processing of the amyloid precursor protein (APP). We suggest that airborne PM exposure promotes pathological brain aging in older women, with potentially a greater impact in ɛ4 carriers. The underlying mechanisms may involve increased cerebral Aβ production and selective changes in hippocampal CA1 neurons and glutamate receptor subunits.

An emerging hypothesis in the field of air pollution is that oxidative stress is one of the important pathways leading to adverse health effects of airborne particulate matter (PM). To advance our understanding of sources and chemical elements contributing to aerosol oxidative potential and provide global comparative data, we report here on the biological oxidative potential associated with size-segregated airborne PM in different urban areas of the world, measured by a biological (cell-based) reactive oxygen species (ROS) assay. Our synthesis indicates a generally greater intrinsic PM oxidative potential as well as higher levels of exposure to redox-active PM in developing areas of the world. Moreover, on the basis of our observations, smaller size fractions are generally associated with higher intrinsic ROS activity compared with larger PM size fractions. Another important outcome of our study is the identification of major species and sources that are associated with ROS activity. Water-soluble transition metals (e.g., Fe, Ni, Cu, Cr, Mn, Zn and V) and water-soluble organic carbon (WSOC) showed consistent correlations with the oxidative potential of airborne PM across different urban areas and size ranges. The major PM sources associated with these chemical species include residual/fuel oil combustion, traffic emissions, and secondary organic aerosol formation, indicating that these sources are major drivers of PM-induced oxidative potential. Moreover, comparison of ROS activity levels across different seasons indicated that photochemical aging increases the intrinsic oxidative potential of airborne PM.

The recent economic crisis in Greece resulted in a serious wintertime air pollution episode in Thessaloniki. This air quality deterioration was mostly due to the increased price of fuel oil, conventionally used as a source of energy for domestic heating, which encouraged the residents to burn the less expensive wood/biomass during the cold season. A wintertime sampling campaign for fine particles (PM2.5) was conducted in Thessaloniki during the winters of 2012 and 2013 in an effort to quantify the extent to which the ambient air was impacted by the increased wood smoke emissions. The results indicated a 30% increase in the PM2.5 mass concentration as well as a 2-5-fold increase in the concentration of wood smoke tracers, including potassium, levoglucosan, mannosan, and galactosan. The concentrations of fuel oil tracers (e.g., Ni and V), on the other hand, declined by 20-30% during 2013 compared with 2012. Moreover, a distinct diurnal variation was observed for wood smoke tracers, with significantly higher concentrations in the evening period compared with the morning. Correlation analysis indicated a strong association between reactive oxygen species (ROS) activity and the concentrations of levoglucosan, galactosan, and potassium, underscoring the potential impact of wood smoke on PM-induced toxicity during the winter months in Thessaloniki.

Background:Rodent models for urban air pollution show consistent induction of inflammatory responses in major brain regions. However, the initial impact of air pollution particulate material on olfactory gateways has not been reported.Objective:We evaluated the olfactory neuroepithelium (OE) and brain regional responses to a nanosized subfraction of urban traffic ultrafine particulate matter (nPM, < 200 nm) in vivo, ex vivo, and in vitro.Methods:Adult mice were exposed to reaerosolized nPM for 5, 20, and 45 cumulative hours over 3 weeks. The OE, the olfactory bulb (OB), the cerebral cortex, and the cerebellum were analyzed for oxidative stress and inflammatory responses. Acute responses of the OE to liquid nPM suspensions were studied with ex vivo and primary OE cultures.Results:After exposure to nPM, the OE and OB had rapid increases of 4-hydroxy-2-nonenal (4-HNE) and 3-nitrotyrosine (3-NT) protein adducts, whereas the cerebral cortex and cerebellum did not respond at any time. All brain regions showed increased levels of tumor necrosis factor-α (TNFα) protein by 45 hr, with earlier induction of TNFα mRNA in OE and OB. These responses corresponded to in vitro OE and mixed glial responses, with rapid induction of nitrite and inducible nitric oxide synthase (iNOS), followed by induction of TNFα.Conclusions:These findings show the differential time course of oxidative stress and inflammatory responses to nPM between the OE and the brain. Slow cumulative transport of inhaled nPM into the brain may contribute to delayed responses of proximal and distal brain regions, with potential input from systemic factors.Citation:Cheng H, Saffari A, Sioutas C, Forman HJ, Morgan TE, Finch CE. 2016. Nanoscale particulate matter from urban traffic rapidly induces oxidative stress and inflammation in olfactory epithelium with concomitant effects on brain. Environ Health Perspect 124:1537–1546; http://dx.doi.org/10.1289/EHP134

The increasing popularity of electronic cigarettes (e-cigarettes) and, more recently, the new "heatnot-burn" tobacco products (iQOS) as alternatives to traditional tobacco cigarettes has necessitated further documentation of and research into the composition and potential health risks/benefits of these devices. In a recent study, we compared second-hand exposure to particulate metals and organic compounds from e-cigarettes and traditional cigarettes, by conducting continuous and time-integrated measurements in an indoor environment, followed by computing the emission rates of these species using a single-compartment mass balance model. In this study, we have used a similar approach to further expand our previous analyses by characterizing black carbon, metal particles, organic compounds, and size-segregated particle mass and number concentrations emitted from these devices in addition to the newly marketed iQOS. Analysis of the iQOS sidestream smoke indicated that the particulate emission of organic matter from these devices is significantly different depending on the organic compound. While polycyclic aromatic hydrocarbons (PAHs) were mostly non-detectable in the iQOS smoke, certain n-alkanes, organic acids (such as suberic acid, azelaic acid, and n-alkanoic acids with carbon numbers between 10 and 19) as well as levoglucosan were still emitted in substantial levels from iQOS (up to 2-6 mg/h during a regular smoking regimen). Metal emissions were reduced in iQOS smoke compared to both electronic cigarettes and conventional cigarettes and were mostly similar to the background levels. Another important finding is the presence of carcinogenic aldehyde compounds, including formaldehyde, acetaldehyde, and acrolein, in iQOS smoke, although the levels were substantially lower compared to conventional cigarettes. EDITORYifang Zhu