Relative contributions of a major international airport activities and other urban sources to the particle number concentrations (PNCs) at a nearby monitoring site

Pirhadi, Milad; Mousavi, Amirhosein; Sowlat, Mohammad H.; Janssen, Nicole; Cassee, Flemming R.; Sioutas, Constantinos

doi:10.1016/j.envpol.2020.114027

Cited by 23 publications

(24 citation statements)

References 59 publications

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“…The size distribution of the exposure aerosol is presented in Table 2 . According to the table, the mode diameter is around 50 nm which is typical of particulate matter in the urban areas impacted by traffic emissions [ 42 , 43 ].…”

Section: Resultsmentioning

confidence: 99%

Nanoparticulate matter exposure results in white matter damage and an inflammatory microglial response in an experimental murine model

et al. 2021

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Exposure to ambient air pollution has been associated with white matter damage and neurocognitive decline. However, the mechanisms of this injury are not well understood and remain largely uncharacterized in experimental models. Prior studies have shown that exposure to particulate matter (PM), a sub-fraction of air pollution, results in neuroinflammation, specifically the upregulation of inflammatory microglia. This study examines white matter and axonal injury, and characterizes microglial reactivity in the corpus callosum of mice exposed to 10 weeks (150 hours) of PM. Nanoscale particulate matter (nPM, aerodynamic diameter ≤200 nm) consisting primarily of traffic-related emissions was collected from an urban area in Los Angeles. Male C57BL/6J mice were exposed to either re-aerosolized nPM or filtered air for 5 hours/day, 3 days/week, for 10 weeks (150 hours; n = 18/group). Microglia were characterized by immunohistochemical double staining of ionized calcium-binding protein-1 (Iba-1) with inducible nitric oxide synthase (iNOS) to identify pro-inflammatory cells, and Iba-1 with arginase-1 (Arg) to identify anti-inflammatory/ homeostatic cells. Myelin injury was assessed by degraded myelin basic protein (dMBP). Oligodendrocyte cell counts were evaluated by oligodendrocyte transcription factor 2 (Olig2). Axonal injury was assessed by axonal neurofilament marker SMI-312. iNOS-expressing microglia were significantly increased in the corpus callosum of mice exposed to nPM when compared to those exposed to filtered air (2.2 fold increase; p<0.05). This was accompanied by an increase in dMBP (1.4 fold increase; p<0.05) immunofluorescent density, a decrease in oligodendrocyte cell counts (1.16 fold decrease; p<0.05), and a decrease in neurofilament SMI-312 (1.13 fold decrease; p<0.05) immunofluorescent density. Exposure to nPM results in increased inflammatory microglia, white matter injury, and axonal degradation in the corpus callosum of adult male mice. iNOS-expressing microglia release cytokines and reactive oxygen/ nitrogen species which may further contribute to the white matter damage observed in this model.

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Section: Resultsmentioning

confidence: 99%

Nanoparticulate matter exposure results in white matter damage and an inflammatory microglial response in an experimental murine model

et al. 2021

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“…Individual exposures to UFP emissions from aviation emissions (total, take-off only and landing only), non-aircraft airport vehicles (such as passenger buses, fuel tankers, baggage trucks and local airport traffic) and non-airport (urban background and road) sources were calculated as a 5h average for each exposure date using a Positive Matrix Factorization (PMF) source apportionment model. Details of the model and instruments used to collect the input data are provided by Pirhadi et al. (2020) ( Pirhadi et al., 2020 ) and Lammers et al.…”

Section: Methodsmentioning

confidence: 99%

“…Encouraged by our developing understanding of road emissions toxicity, concern has developed over the impacts that aviation and other airport emissions could have on human health. In addition to manoeuvring aircraft, auxiliary power units, ground service equipment and ground access vehicles are strong sources of nitrogen oxides (NO x ), carbon monoxide (CO), volatile organic compounds (VOCs), sulphur oxides (SO x ) and particulate matter (PM) at airports ( Yang et al., 2018 ; Winther et al., 2015 ; Pirhadi et al., 2020 ; Simonetti et al., 2015 ).…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…Much of airport-originating PM falls within the ultrafine size range (PM < 0.1 μm) ( Pirhadi et al., 2020 ) and is dominated by particles <20 nm in diameter based on the particle number concentrations (PNC) counts. This fraction is apportioned to primarily aircraft emissions ( Pirhadi et al., 2020 ; Keuken et al., 2015 ). Concentrations of aviation-related PNCs have been detected at significantly elevated levels as far as 18 km downwind of airports ( Keuken et al., 2015 ; Hudda et al., 2014 , 2018 ; Rivas et al., 2020 ) affecting both total indoor and outdoor PNCs ( Hudda et al., 2014 , 2018 ).…”

Section: Introductionmentioning

confidence: 99%

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Alterations to the urinary metabolome following semi-controlled short exposures to ultrafine particles at a major airport

Selley

Lammers

Guennec

et al. 2021

International Journal of Hygiene and Environmental Health

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Background Inflammation, oxidative stress and reduced cardiopulmonary function following exposure to ultrafine particles (UFP) from airports has been reported but the biological pathways underlying these toxicological endpoints remain to be explored. Urinary metabolomics offers a robust method by which changes in cellular pathway activity can be characterised following environmental exposures. Objective We assessed the impact of short-term exposures to UFP from different sources at a major airport on the human urinary metabolome. Methods 21 healthy, non-smoking volunteers (aged 19–27 years) were repeatedly (2–5 visits) exposed for 5h to ambient air at Amsterdam Airport Schiphol, while performing intermittent, moderate exercise. Pre- to-post exposure changes in urinary metabolite concentrations were assessed via 1 H NMR spectroscopy and related to total and source-specific particle number concentrations (PNC) using linear mixed effects models. Results Total PNC at the exposure site was on average, 53,500 particles/cm 3 (range 10,500–173,200) and associated with significant reductions in urinary taurine (−0.262 AU, 95% CI: −0.507 to −0.020) and dimethylamine concentrations (−0.021 AU, 95% CI: −0.040 to −0.067). Aviation UFP exposure accounted for these changes, with the reductions in taurine and dimethylamine associating with UFP produced during both aircraft landing and take-off. Significant reductions in pyroglutamate concentration were also associated with aviation UFP specifically, (−0.005 AU, 95% CI: −0.010 – <0.000) again, with contributions from both landing and take-off UFP exposure. While non-aviation UFPs induced small changes to the urinary metabolome, their effects did not significantly impact the overall response to airport UFP exposure. Discussion Following short-term exposures at a major airport, aviation-related UFP caused the greatest changes to the urinary metabolome. These were consistent with a heightened antioxidant response and altered nitric oxide synthesis. Although some of these responses could be adaptive, they appeared after short-term exposures in healthy adults. Further study is required to determine whether long-term exposures induce injurious effects.

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Particulate matter exposure and chronic cerebral hypoperfusion promote oxidative stress and induce neuronal and oligodendrocyte apoptosis in male mice

Lamorie‐Foote

Liu

Shkirkova

et al. 2022

J of Neuroscience Research

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Chronic cerebral hypoperfusion (CCH) may amplify the neurotoxicity of nanoscale particulate matter (nPM), resulting in white matter injury. This study characterized the joint effects of nPM (diameter ≤ 200 nm) and CCH secondary to bilateral carotid artery stenosis (BCAS) exposure on neuronal and white matter injury in a murine model. nPM was collected near a highway and re‐aerosolized for exposure. Ten‐week‐old C57BL/6 male mice were randomized into four groups: filtered air (FA), nPM, FA + BCAS, and nPM + BCAS. Mice were exposed to FA or nPM for 10 weeks. BCAS surgeries were performed. Markers of inflammation, oxidative stress, and apoptosis were examined. nPM + BCAS exposure increased brain hemisphere TNFα protein compared to FA. iNOS and HNE immunofluorescence were increased in the corpus callosum and cerebral cortex of nPM + BCAS mice compared to FA. While nPM exposure alone did not decrease cortical neuronal cell count, nPM decreased corpus callosum oligodendrocyte cell count. nPM exposure decreased mature oligodendrocyte cell count and increased oligodendrocyte precursor cell count in the corpus callosum. nPM + BCAS mice exhibited a 200% increase in cortical neuronal TUNEL staining and a 700% increase in corpus callosum oligodendrocyte TUNEL staining compared to FA. There was a supra‐additive interaction between nPM and BCAS on cortical neuronal TUNEL staining (2.6× the additive effects of nPM + BCAS). nPM + BCAS exposure increased apoptosis, neuroinflammation, and oxidative stress in the cerebral cortex and corpus callosum. nPM + BCAS exposure increased neuronal apoptosis above the separate responses to each exposure. However, oligodendrocytes in the corpus callosum demonstrated a greater susceptibility to the combined neurotoxic effects of nPM + BCAS exposure.

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Relative contributions of a major international airport activities and other urban sources to the particle number concentrations (PNCs) at a nearby monitoring site

Cited by 23 publications

References 59 publications

Nanoparticulate matter exposure results in white matter damage and an inflammatory microglial response in an experimental murine model

Nanoparticulate matter exposure results in white matter damage and an inflammatory microglial response in an experimental murine model

Alterations to the urinary metabolome following semi-controlled short exposures to ultrafine particles at a major airport

Particulate matter exposure and chronic cerebral hypoperfusion promote oxidative stress and induce neuronal and oligodendrocyte apoptosis in male mice

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