Diurnal variation in the proinflammatory activity of urban fine particulate matter (PM2.5) by in vitro assays

Background: Ambient particulate matter (PM) smaller than 2.5 µm in diameter (PM2.5) undergoes diurnal changes in chemical composition due to photochemical oxidation. In this study we examine the relationships between oxidative activity and inflammatory responses associated with these diurnal chemical changes. Because secondary PM contains a higher fraction of oxidized PM species, we hypothesized that PM2.5 collected during afternoon hours would induce a greater inflammatory response than primary, morning PM2.5. Methods: Time-integrated aqueous slurry samples of ambient PM2.5 were collected using a direct aerosol-into-liquid collection system during defined morning and afternoon time periods. PM2.5 samples were collected for 5 weeks in the late summer (August-September) of 2016 at a central Los Angeles site. Morning samples, largely consisting of fresh primary traffic emissions (primary PM), were collected from 6-9am (am-PM2.5), and afternoon samples were collected from 12-4pm (pm-PM2.5), when PM composition is dominated by products of photochemical oxidation (secondary PM). The two diurnally phased PM2.5 slurries (am- and pm-PM2.5) were characterized for chemical composition and BV-2 microglia were assayed in vitro for oxidative and inflammatory gene responses. Results: Contrary to expectations, the am-PM2.5 slurry had more proinflammatory activity than the pm-PM2.5 slurry as revealed by nitric oxide (NO) induction, as well as the upregulation of proinflammatory cytokines IL-1β, IL-6, and CCL2 (MCP-1), as assessed by messenger RNA production. Conclusions: The diurnal differences observed in this study may be in part attributed to the greater content of transition metals and water-insoluble organic carbon (WIOC) of am-PM2.5 (primary PM) vs. pm-PM2.5 (secondary PM), as these two classes of compounds can increase PM2.5 toxicity.

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Diurnal variation in the proinflammatory activity of urban fine particulate matter (PM2.5) by in vitro assays

F1000Research ◽

10.12688/f1000research.14836.2 ◽

2018 ◽

Vol 7 ◽

pp. 596 ◽

Cited By ~ 2

Author(s):

Christopher Lovett ◽

Mafalda Cacciottolo ◽

Farimah Shirmohammadi ◽

Amin Haghani ◽

Todd E. Morgan ◽

...

Keyword(s):

Particulate Matter ◽

Chemical Composition ◽

Los Angeles ◽

Messenger Rna ◽

Inflammatory Responses ◽

Photochemical Oxidation ◽

In Vitro Assays ◽

Diurnal Changes ◽

Proinflammatory Activity

Background: Ambient particulate matter (PM) smaller than 2.5 µm in diameter (PM2.5) undergoes diurnal changes in chemical composition due to photochemical oxidation. In this study we examine the relationships between oxidative activity and inflammatory responses associated with these diurnal chemical changes. Because secondary PM contains a higher fraction of oxidized PM species, we hypothesized that PM2.5 collected during afternoon hours would induce a greater inflammatory response than primary, morning PM2.5. Methods: Time-integrated aqueous slurry samples of ambient PM2.5 were collected using a direct aerosol-into-liquid collection system during defined morning and afternoon time periods. PM2.5 samples were collected for 5 weeks in the late summer (August-September) of 2016 at a central Los Angeles site. Morning samples, largely consisting of fresh primary traffic emissions (primary PM), were collected from 6-9am (am-PM2.5), and afternoon samples were collected from 12-4pm (pm-PM2.5), when PM composition is dominated by products of photochemical oxidation (secondary PM). The two diurnally phased PM2.5 slurries (am- and pm-PM2.5) were characterized for chemical composition and BV-2 microglia were assayed in vitro for oxidative and inflammatory gene responses. Results: Contrary to expectations, the am-PM2.5 slurry had more proinflammatory activity than the pm-PM2.5 slurry as revealed by nitric oxide (NO) induction, as well as the upregulation of proinflammatory cytokines IL-1β, IL-6, and CCL2 (MCP-1), as assessed by messenger RNA production. Conclusions: The diurnal differences observed in this study may be in part attributed to the greater content of transition metals and water-insoluble organic carbon (WIOC) of am-PM2.5 (primary PM) vs. pm-PM2.5 (secondary PM), as these two classes of compounds can increase PM2.5 toxicity.

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Urban Air Pollution Nanoparticles from Los Angeles: Recently Decreased Neurotoxicity

Journal of Alzheimer s Disease ◽

10.3233/jad-201577 ◽

2021 ◽

pp. 1-10

Author(s):

Hongqiao Zhang ◽

Carla D’Agostino ◽

Henry Jay Forman ◽

Mafalda Cacciottolo ◽

Max Thorwald ◽

...

Keyword(s):

Air Pollution ◽

Los Angeles ◽

Inflammatory Responses ◽

Urban Air Pollution ◽

Ambient Air ◽

Brain Regions ◽

Ambient Air Pollution ◽

In Vitro Assays

Background: Air pollution is widely associated with accelerated cognitive decline at later ages and risk of Alzheimer’s disease (AD). Correspondingly, rodent models demonstrate the neurotoxicity of ambient air pollution and its components. Our studies with nano-sized particulate matter (nPM) from urban Los Angeles collected since 2009 have shown pro-amyloidogenic and pro-inflammatory responses. However, recent batches of nPM have diminished induction of the glutamate receptor GluA1 subunit, Iba1, TNFα, Aβ 42 peptide, and white matter damage. The same methods, materials, and mouse genotypes were used throughout. Objective: Expand the nPM batch comparisons and evaluate archived brain samples to identify the earliest change in nPM potency. Methods: Batches of nPM were analyzed by in vitro cell assays for NF-κB and Nrf2 induction for comparison with in vivo responses of mouse brain regions from mice exposed to these batches, analyzed by PCR and western blot. Results: Five older nPM batches (2009–2017) and four recent nPM batches (2018, 2019) for NF-κB and Nrf2 induction showed declines in nPM potency after 2017 that paralleled declines of in vivo activity from independent exposures in different years. Conclusion: Transcription-based in vitro assays of nPM corresponded to the loss of in vivo potency for inflammatory and oxidative responses. These recent decreases of nPM neurotoxicity give a rationale for evaluating possible benefits to the risk of dementia and stroke in Los Angeles populations.

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Chemical and Biological Characterization of Particulate Matter (PM 2.5) and Volatile Organic Compounds Collected at Different Sites in the Los Angeles Basin

Applied Sciences ◽

10.3390/app10093245 ◽

2020 ◽

Vol 10 (9) ◽

pp. 3245

Author(s):

Arthur K. Cho ◽

Yasuhiro Shinkai ◽

Debra A. Schmitz ◽

Emma Di Stefano ◽

Arantza Eiguren-Fernandez ◽

...

Keyword(s):

Particulate Matter ◽

Volatile Organic Compounds ◽

Los Angeles ◽

Organic Compounds ◽

Inflammatory Responses ◽

Biological Properties ◽

Heme Oxygenase 1 ◽

Tnf Α ◽

Volatile Organic

Background: Most studies on air pollution (AP) exposure have focused on adverse health effects of particulate matter (PM). Less well-studied are the actions of volatile organic compounds (VOCs) not retained in PM collections. These studies quantified chemical and biological properties of both PM2.5 and VOCs. Methods: Samples were collected near the Port of Los Angeles (Long Beach, LB), railroads (Commerce, CM), and a pollution-trapping topography-site (San Bernardino, SB). Quantitative assays were conducted: (1) chemical—prooxidant and electrophile content, (2) biological—tumor necrosis factor-α (TNF-α) and heme oxygenase-1 (HO-1) expression (3), VOC modulation of PM effects and (4), activation of the antioxidant response element (ARE) using murine RAW 264.7 macrophages. Results: SB site samples were the most potent in the chemical and biological assays, followed by a CM railroad site. Only PM2.5 exhibited significant proinflammatory responses. VOCs were more potent than PM2.5 in generating anti-inflammatory responses; further, VOC pretreatment reduced PM-associated TNF-α expression. VOCs significantly increased ARE activation compared to their corresponding PM2.5 which remained at background levels. Conclusion: Ambient VOCs are major contributors to adaptive responses that can modulate PM effects, in vitro, and, as such, need to be included in comprehensive assessments of AP.

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In vitro particulate matter toxicity relates to seasonal variability in chemical composition

Toxicology Letters ◽

10.1016/j.toxlet.2013.05.171 ◽

2013 ◽

Vol 221 ◽

pp. S108

Author(s):

Alvaro Osornio Vargas ◽

Natalia Manzano-Leon ◽

Raul Quintana-Belmares ◽

Brisa Sanchez ◽

Alexandra Sitarik ◽

...

Keyword(s):

Particulate Matter ◽

Chemical Composition ◽

Seasonal Variability

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HIF-1α is a key mediator of the lung inflammatory potential of lithium-ion battery particles

Particle and Fibre Toxicology ◽

10.1186/s12989-019-0319-z ◽

2019 ◽

Vol 16 (1) ◽

Cited By ~ 4

Author(s):

Violaine Sironval ◽

Mihaly Palmai-Pallag ◽

Rita Vanbever ◽

François Huaux ◽

Jorge Mejia ◽

...

Keyword(s):

Inflammatory Responses ◽

Hypoxia Inducible Factor ◽

Lithium Ion ◽

In Vitro Assays ◽

Inhalation Toxicity ◽

Cobalt Nickel ◽

Occupational Settings

Abstract Background Li-ion batteries (LIB) are increasingly used worldwide. They are made of low solubility micrometric particles, implying a potential for inhalation toxicity in occupational settings and possibly for consumers. LiCoO2 (LCO), one of the most used cathode material, induces inflammatory and fibrotic lung responses in mice. LCO also stabilizes hypoxia-inducible factor (HIF) -1α, a factor implicated in inflammation, fibrosis and carcinogenicity. Here, we investigated the role of cobalt, nickel and HIF-1α as determinants of toxicity, and evaluated their predictive value for the lung toxicity of LIB particles in in vitro assays. Results By testing a set of 5 selected LIB particles (LCO, LiNiMnCoO2, LiNiCoAlO2) with different cobalt and nickel contents, we found a positive correlation between their in vivo lung inflammatory activity, and (i) Co and Ni particle content and their bioaccessibility and (ii) the stabilization of HIF-1α in the lung. Inhibition of HIF-1α with chetomin or PX-478 blunted the lung inflammatory response to LCO in mice. In IL-1β deficient mice, HIF-1α was the upstream signal of the inflammatory lung response to LCO. In vitro, the level of HIF-1α stabilization induced by LIB particles in BEAS-2B cells correlated with the intensity of lung inflammation induced by the same particles in vivo. Conclusions We conclude that HIF-1α, stabilized in lung cells by released Co and Ni ions, is a mechanism-based biomarker of lung inflammatory responses induced by LIB particles containing Co/Ni. Documenting the Co/Ni content of LIB particles, their bioaccessibility and their capacity to stabilize HIF-1α in vitro can be used to predict the lung inflammatory potential of LIB particles.

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Design Considerations and Assays for Hemocompatibility of FDA-Approved Nanoparticles

Seminars in Thrombosis and Hemostasis ◽

10.1055/s-0039-1688491 ◽

2019 ◽

Vol 46 (05) ◽

pp. 637-652

Author(s):

Amit K. Saha ◽

Min-Yi S. Zhen ◽

Folarin Erogbogbo ◽

Anand K. Ramasubramanian

Keyword(s):

Biomedical Applications ◽

Inflammatory Responses ◽

Mode Of Delivery ◽

Systemic Circulation ◽

In Vitro Assays ◽

Cardiovascular Tissues ◽

Wide Range ◽

The Us ◽

Imaging Sensors

AbstractNanoparticles have numerous biomedical applications including, but not limited to, targeted drug delivery, diagnostic imaging, sensors, and implants for a wide range of diseases including cancer, diabetes, heart disease, and tuberculosis. Although the mode of delivery of the nanoparticles depends on the application and the disease, the nanoparticles are often in immediate contact with the systemic circulation either because of intravenous administration or their ability to enter the bloodstream with relative ease or their longer survival time in circulation. Once in circulation, the nanoparticles may elicit unintended hemostatic and inflammatory responses, and hence the design of nanoparticles for therapeutic applications should take broad hemocompatibility concerns into consideration. In this review, we present the principles underlying the structural and functional design of various classes of nanoparticles that are currently approved by the US Food and Drug Administration, categorize these particles based on their interactions with cardiovascular tissues and ensuing adverse events, and also describe various in vitro assays that may be used evaluate their hemocompatibility.

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