Arian Saffari

Increased biomass burning due to the economic crisis in Greece and its adverse impact on wintertime air quality in Thessaloniki.

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.

Particulate air pollutants, APOE alleles and their contributions to cognitive impairment in older women and to amyloidogenesis in experimental models.

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.

Global Perspective on the Oxidative Potential of Airborne Particulate Matter: A Synthesis of Research Findings

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.

Seasonal and spatial variation of trace elements and metals in quasi-ultrafine (PM0.25) particles in the Los Angeles metropolitan area and characterization of their sources

Year-long sampling campaign of quasi-ultrafine particles (PM₀.₂₅) was conducted at 10 distinct locations across the Los Angeles south coast air basin and concentrations of trace elements and metals were quantified at each site using high-resolution inductively coupled plasma sector field mass spectrometry. In order to characterize sources of trace elements and metals, principal component analysis (PCA) was applied to the dataset. The major sources were identified as road dust (influenced by vehicular emissions as well as re-suspended soil), vehicular abrasion, residual oil combustion, cadmium sources and metal plating. These sources altogether accounted for approximately 85% of the total variance of quasi-ultrafine elemental content. The concentrations of elements originating from source and urban locations generally displayed a decline as we proceeded from the coast to the inland. Occasional concentration peaks in the rural receptor sites were also observed, driven by the dominant westerly/southwesterly wind transporting the particles to the receptor areas.

Seasonal and spatial variation in dithiothreitol (DTT) activity of quasi-ultrafine particles in the Los Angeles Basin and its association with chemical species

A year-long sampling campaign of quasi-ultrafine particles (dp < 0.25 μm) was conducted at 10 distinct sites representing source, urban and/or near-freeway, rural receptor and desert locations across the Los Angeles air basin. Redox activity of the PM samples was measured by means of the Dithiothreitol (DTT) assay and detailed chemical analysis was performed to measure the concentrations of chemical species. DTT activity per unit air volume and unit PM mass (expressed in nmol min−1 m−3 and nmol/min/μg PM, respectively) showed similar trends across sites and seasons. DTT activity was generally higher during cold seasons (winter and fall) compared to warm seasons (summer and spring). Noticeable peaks were observed at urban near-freeway locations representing “source” sites impacted by fresh traffic emissions. Regression analysis indicated strong association (R > 0.7) between the DTT activity and the concentrations of carbonaceous species (OC, EC, WSOC and WIOC) across all seasons and strong winter-time correlations with organic tracers of primary vehicular emissions including polycyclic aromatic hydrocarbons (PAHs), alkanes, hopanes and steranes. Strong correlations were also observed, particularly during winter, between DTT activity and transition metals (e.g., Cr, Mn, V, Fe, Cu, Cd and Zn), which share similar vehicular sources with primary organics. A multivariate linear regression analysis indicated that the variability in DTT activity is best explained by the variability in concentrations of WSOC, WIOC, EC and hopanes. Combined contributions from these species explained 88% of the DTT activity. The appearance of WSOC as a typical tracer of secondary organic aerosol, along with EC, WIOC and hopanes, all markers of emissions from primary combustion sources, emphasizes the contributions of both primary and secondary sources to the overall oxidative potential of quasi-ultrafine particles. Supplemental materials are available for this article. Go to the publishers online edition of the Journal of Environmental Science and Health, Part A, to view the supplemental file.

Effect of exposure to atmospheric ultrafine particles on production of free fatty acids and lipid metabolites in the mouse small intestine.

Background: Exposure to ambient ultrafine particulate matter (UFP) is a well-recognized risk factor for cardiovascular and respiratory diseases. However, little is known about the effects of air pollution on gastrointestinal disorders. Objective: We sought to assess whether exposure to ambient UFP (diameter < 180 nm) increased free fatty acids and lipid metabolites in the mouse small intestine. Methods: Ldlr-null mice were exposed to filtered air (FA) or UFP collected at an urban Los Angeles, California, site that was heavily affected by vehicular emissions; the exposure was carried out for 10 weeks in the presence or absence of D-4F, an apolipoprotein A-I mimetic peptide with antioxidant and anti-inflammation properties on a high-fat or normal chow diet. Results: Compared with FA, exposure to UFP significantly increased intestinal hydroxyeicosatetraenoic acids (HETEs), including 15-HETE, 12-HETE, 5-HETE, as well as hydroxyoctadecadienoic acids (HODEs), including 13-HODE and 9-HODE. Arachidonic acid (AA) and prostaglandin D2 (PGD2) as well as some of the lysophosphatidic acids (LPA) in the small intestine were also increased in response to UFP exposure. Administration of D-4F significantly reduced UFP-mediated increase in HETEs, HODEs, AA, PGD2, and LPA. Although exposure to UFP further led to shortened villus length accompanied by prominent macrophage and neutrophil infiltration into the intestinal villi, administration of D-4F mitigated macrophage infiltration. Conclusions: Exposure to UFP promotes lipid metabolism, villus shortening, and inflammatory responses in mouse small intestine, whereas administration of D-4F attenuated these effects. Our findings provide a basis to further assess the mechanisms underlying UFP-mediated lipid metabolism in the digestive system with clinical relevance to gut homeostasis and diseases. Citation: Li R, Navab K, Hough G, Daher N, Zhang M, Mittelstein D, Lee K, Pakbin P, Saffari A, Bhetraratana M, Sulaiman D, Beebe T, Wu L, Jen N, Wine E, Tseng CH, Araujo JA, Fogelman A, Sioutas C, Navab M, Hsiai TK. 2015. Effect of exposure to atmospheric ultrafine particles on production of free fatty acids and lipid metabolites in the mouse small intestine. Environ Health Perspect 123:34–41; http://dx.doi.org/10.1289/ehp.1307036

Nanoscale Particulate Matter from Urban Traffic Rapidly Induces Oxidative Stress and Inflammation in Olfactory Epithelium with Concomitant Effects on Brain.

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

Environmental pollution and emission factors of electronic cigarettes, heat-not-burn tobacco products, and conventional cigarettes

ABSTRACT The increasing popularity of electronic cigarettes (e-cigarettes) and, more recently, the new “heat-not-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 side-stream 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. Copyright

Development and Evaluation of a High-Volume Aerosol-into-Liquid Collector for Fine and Ultrafine Particulate Matter

This study presents a novel high-volume aerosol-into-liquid collector, developed to provide concentrated slurries of fine and/or ultrafine particulate matter (PM) to be used for unattended, in situ measurements of PM chemistry and toxicity. This system operates at 200 liters per minute (L/min) flow and utilizes the saturation–condensation, particle-to-droplet growth component of the versatile aerosol concentration enrichment system (VACES), growing fine or ultrafine PM to 3–4-μm droplets, in conjunction with a newly designed impactor, in which grown particles are collected gradually forming highly concentrated slurries. Laboratory evaluation results indicated an excellent overall system collection efficiency (over 90%) for both monodisperse and polydisperse particles in the range of 0.01 to 2 μm. Field evaluations illustrated that overall a very good agreement was obtained for most PM2.5 species between the new aerosol collection system and the VACES/BioSampler tandem as well as filter samplers operating in parallel. Very good agreement between the new system and the VACES/BioSampler was also observed for reactive oxygen species (ROS) in ambient PM2.5 samples, whereas lower ROS values were obtained from the water extracts of the filter, likely due to incomplete extraction of water insoluble redox active species collected on the filter substrate. Moreover, the field tests indicated that the new aerosol collection system could achieve continuous and unattended collection of concentrated suspensions for at least 2 to 3 days without any obvious shortcomings in its operation. Both laboratory and field evaluations of the high-volume aerosol-into-liquid collector suggest that this system is an effective technology for collection and characterization of ambient aerosols. Copyright 2013 American Association for Aerosol Research

Exposure to ambient ultrafine particulate matter alters the expression of genes in primary human neurons

HighlightsAqueous ultrafine particles change expression of noncoding RNAs in human neurons.Metallothionein 1A and 1F expression was increased by exposure to particulate matter.Particle‐induced genetic changes may lead to neurodevelopmental abnormalities. Abstract Exposure to ambient particulate matter (PM) has been associated with the onset of neurodevelopmental and neurodegenerative disorders, but the mechanism of toxicity remains unclear. To gain insight into this neurotoxicity, this study sought to examine global gene expression changes caused by exposure to ambient ultrafine PM. Microarray analysis was performed on primary human neurons derived from fetal brain tissue after a 24 h exposure to 20 &mgr;g/mL of ambient ultrafine particles. We found a majority of the changes in noncoding RNAs, which are involved in epigenetic regulation of gene expression, and thereby could impact the expression of several other protein coding gene targets. Although neurons from biologically different lot numbers were used, we found a significant increase in the expression of metallothionein 1A and 1F in all samples after exposure to particulate matter as confirmed by quantitative PCR. These metallothionein 1 proteins are responsible for neuroprotection after exposure to environmental insult but prolonged induction can be toxic. Epidemiological studies have reported that in utero exposure to ultrafine PM not only leads to neurodevelopmental and behavioral abnormalities, but may also predispose the progeny to neurodegenerative disease later in life by genetic imprinting. Our results pinpoint some of the PM‐induced genetic changes that may underlie these findings.