In vitro biological effects of airborne PM2.5 and PM10 from a semi-desert city on the Mexico–US border

Osornio-Vargas, Álvaro; Serrano, Jose Iran Bojorquez; Rojas-Bracho, Leonora; Miranda, J.; García-Cuéllar, Claudia M.; Reyna, Marco A.; Flores, Geraldine; Zuk, Miriam; Quintero, Margarito; Vázquez, Inés; Sánchez-Pérez, Yesennia; López, Tania; Rosas, Irma

doi:10.1016/j.chemosphere.2010.11.073

Cited by 70 publications

(35 citation statements)

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“…To determine the relative inflammatory potency of PM, we measured the expression of the proinflammatory gene IL-8 in HAECs exposed to a range of concentrations of PM 10 and PM 2.5 collected from urban and semiurban locations in Mexicali, Mexico (Osornio-Vargas et al 2010). Levels of IL-8 mRNA increased in a dose-dependent manner after exposure to each particle type (Figure 1).…”

Section: Resultsmentioning

confidence: 99%

“…Previous studies on Mexicali PM have associated particle size with specific chemical composition, source, and biological effects (Mendoza et al 2010; Osornio-Vargas et al 2010). However, in the present study, PM 2.5 and PM 10 collected in urban and semiurban locations in Mexicali were of comparable potency in inducing IL-8 expression in HAECs.…”

Section: Discussionmentioning

confidence: 99%

“…PM 2.5 (PM ≤ 2.5 µm in aerodynamic diameter) and PM 10 size fractions were collected between October 2005 and March 2006 at urban and semiurban locations in Mexicali, Mexico (Osornio-Vargas et al 2010). For additional methodological details and PM 10 elemental composition and size, see Supplemental Material, p. 2 and Table 1 (http://dx.doi.org/10.1289/ehp.1103594).…”

Section: Methodsmentioning

confidence: 99%

“…To characterize relevant mechanisms that lead to inflammatory responses to PM inhalation, we examined the activation of signaling events involved in IL-8 expression in a model of human airway epithelium exposed to PM obtained from Mexicali, a city in Mexico that experiences some of the highest PM levels in North America (Osornio-Vargas et al 2010). Exposure of cultured HAECs to PM ≤ 10 μm in aerodynamic diameter (PM 10 ) collected from Mexicali ambient air induced NF-κB–dependent transcriptional expression of IL-8 through an alternate signaling pathway involving direct phosphorylation of p65.…”

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confidence: 99%

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Ambient Particulate Matter Induces Interleukin-8 Expression through an Alternative NF-κB (Nuclear Factor-Kappa B) Mechanism in Human Airway Epithelial Cells

Silbajoris

Osornio-Vargas

Simmons

et al. 2011

Environ Health Perspect

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Background: Exposure to ambient air particulate matter (PM) has been shown to increase rates of cardiopulmonary morbidity and mortality, but the underlying mechanisms are still not well understood.Objective: We examined signaling events involved in the expression of the inflammatory gene interleukin-8 (IL-8) in human airway epithelial cells (HAECs) exposed to ambient PM collected in an urban area of Mexicali, Mexico.Methods: We studied IL-8 expression and regulatory signaling pathways in cultured HAECs exposed to Mexicali PM suspended in media for 0–4 hr.Results: Exposure resulted in a dose-dependent, 2- to 8-fold increase in IL-8 mRNA expression relative to controls. PM exposure induced IL-8 transcriptional activity in BEAS-2B cells that was dependent on the nuclear factor-kappa B (NF-κB) response element in the IL-8 promoter. Chromatin immunoprecipitation (ChIP) assays showed a 3-fold increase in binding of the p65 (RelA) NF-κB isoform to the IL-8 promoter sequence in HAECs exposed to PM. Western blot analyses showed elevated levels of phosphorylation of p65 but no changes in IκBα phosphorylation or degradation. IL-8 expression was blunted in a dose-dependent manner in BEAS-2B cells transduced with a lentivirus encoding a dominant negative p65 mutant in which phosphorylation sites were inactivated.Conclusion: Taken together, these findings show that the increase in IL-8 mRNA expression in HAECs exposed to PM10 (PM ≤ 10 μm in aerodynamic diameter) is mediated through an NF-κB–dependent signaling mechanism that occurs through a pathway involving direct phosphorylation of the transcription factor p65 in the absence of IκBα degradation. These data show that exposure to PM10 in ambient air can induce inflammatory responses by activating specific signaling mechanisms in HAECs.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Ambient Particulate Matter Induces Interleukin-8 Expression through an Alternative NF-κB (Nuclear Factor-Kappa B) Mechanism in Human Airway Epithelial Cells

Silbajoris

Osornio-Vargas

Simmons

et al. 2011

Environ Health Perspect

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“…However, the cytotoxicity of the prominent occupational exposure (particulate matter from welding fumes) on the target tissue was not assessed due to the obvious practical limitations of population-based epidemiological studies. However, PM 2.5 has been shown in observational studies to be associated with increased inflammatory response, in addition to being shown in laboratory studies to induce cytotoxic cell death [41] [42] [43].…”

Section: Discussionmentioning

confidence: 99%

The Relationship between Inflammatory Biomarkers and Telomere Length in an Occupational Prospective Cohort Study

et al. 2014

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BackgroundChronic inflammation from recurring trauma is an underlying pathophysiological basis of numerous diseases. Furthermore, it may result in cell death, scarring, fibrosis, and loss of tissue function. In states of inflammation, subsequent increases in oxidative stress and cellular division may lead to the accelerated erosion of telomeres, crucial genomic structures which protect chromosomes from decay. However, the association between plasma inflammatory marker concentrations and telomere length has been inconsistent in previous studies.ObjectiveThe purpose of this study was to determine the longitudinal association between telomere length and plasma inflammatory biomarker concentrations including: CRP, SAA, sICAM-1, sVCAM-1, VEGF, TNF-α, IL-1β, IL-2, IL-6, IL-8, and IL-10.MethodsThe longitudinal study population consisted of 87 subjects. The follow-up period was approximately 2 years. Plasma inflammatory biomarker concentrations were assessed using highly sensitive electrochemiluminescent assays. Leukocyte relative telomere length was assessed using Real-Time qPCR. Linear mixed effects regression models were used to analyze the association between repeated-measurements of relative telomere length as the outcome and each inflammatory biomarker concentration as continuous exposures separately. The analyses controlled for major potential confounders and white blood cell differentials.ResultsAt any follow-up time, each incremental ng/mL increase in plasma CRP concentration was associated with a decrease in telomere length of −2.6×10−2 (95%CI: −4.3×10−2, −8.2×10−3, p = 0.004) units. Similarly, the estimate for the negative linear association between SAA and telomere length was −2.6×10−2 (95%CI:−4.5×10−2, −6.1×10−3, p = 0.011). No statistically significant associations were observed between telomere length and plasma concentrations of pro-inflammatory interleukins, TNF-α, and VEGF.ConclusionsFindings from this study suggest that increased systemic inflammation, consistent with vascular injury, is associated with decreased leukocyte telomere length.

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Polycyclic aromatic hydrocarbons within airborne particulate matter (PM_2.5) produced DNA bulky stable adducts in a human lung cell coculture model

Abbas¹,

Garçon²,

Saint-Georges³

et al. 2011

J of Applied Toxicology

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To extend current knowledge on the underlying mechanisms of air pollution particulate matter (PM(2.5))-induced human lung toxicity, the metabolic activation of polycyclic aromatic hydrocarbons (PAH) within PM(2.5) and PAH-DNA bulky stable adduct patterns in human alveolar macrophage (AM) and/or human lung epithelial L132 cells in mono- and cocultures were studied. In the coculture system, only human AM were exposed to air pollution PM(2.5), unlike L132 cells. Particles, inorganic fraction and positive controls [i.e. TiO(2), thermally desorbed PM (dPM) and benzo[a]pyrene, B[a]P, respectively] were included in the experimental design. Cytochrome P450 (CYP) 1A1 gene expression, CYP1A1 catalytic activity and PAH-DNA bulky stable adducts were studied after 24, 48 and/or 72 h. Relatively low doses of PAH within PM(2.5) induced CYP1A1 gene expression and CYP1A1 catalytic activity in human AM and, thereafter, PAH-DNA bulky stable adduct formation. Adduct spots in PM(2.5) -exposed human AM were higher than those in dPM-exposed ones, thereby showing the incomplete removal of PAH by thermal desorption. PAH within air pollution PM(2.5) induced CYP1A1 gene expression but not CYP1A1 catalytic activity in L132 cells. However, despite the absence of PAH-DNA bulky stable adduct in L132 cells from human AM/L132 cell cocultures exposed to dPM(2.5) or PM(2.5), reliable quantifiable PAH-DNA bulky stable adducts were observed in L132 cells from human AM/L132 cell coculture exposed to B[a]P. Taken together, these results support the exertion of genotoxicity of highly reactive B[a]P-derived metabolites produced within human AM not only in primary target human AM, but also in secondary target L132 cells.

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In vitro biological effects of airborne PM2.5 and PM10 from a semi-desert city on the Mexico–US border

Cited by 70 publications

References 37 publications

Ambient Particulate Matter Induces Interleukin-8 Expression through an Alternative NF-κB (Nuclear Factor-Kappa B) Mechanism in Human Airway Epithelial Cells

Ambient Particulate Matter Induces Interleukin-8 Expression through an Alternative NF-κB (Nuclear Factor-Kappa B) Mechanism in Human Airway Epithelial Cells

The Relationship between Inflammatory Biomarkers and Telomere Length in an Occupational Prospective Cohort Study

Polycyclic aromatic hydrocarbons within airborne particulate matter (PM_2.5) produced DNA bulky stable adducts in a human lung cell coculture model

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In vitro biological effects of airborne PM2.5 and PM10 from a semi-desert city on the Mexico–US border

Cited by 70 publications

References 37 publications

Ambient Particulate Matter Induces Interleukin-8 Expression through an Alternative NF-κB (Nuclear Factor-Kappa B) Mechanism in Human Airway Epithelial Cells

Ambient Particulate Matter Induces Interleukin-8 Expression through an Alternative NF-κB (Nuclear Factor-Kappa B) Mechanism in Human Airway Epithelial Cells

The Relationship between Inflammatory Biomarkers and Telomere Length in an Occupational Prospective Cohort Study

Polycyclic aromatic hydrocarbons within airborne particulate matter (PM2.5) produced DNA bulky stable adducts in a human lung cell coculture model

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Polycyclic aromatic hydrocarbons within airborne particulate matter (PM_2.5) produced DNA bulky stable adducts in a human lung cell coculture model