Gene expression changes in rat brain after short and long exposures to particulate matter in Los Angeles basin air: Comparison with human brain tumors

Ljubimova, Julia Y.; Kleinman, Michael T.; Karabalin, Natalya; Inoue, Satoshi; Konda, Bindu; Gangalum, Pallavi R.; Markman, Janet L.; Ljubimov, Alexander V.; Black, Keith L.

doi:10.1016/j.etp.2013.04.002

Cited by 23 publications

(9 citation statements)

References 57 publications

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“… 18 Furthermore, gene expression patterns similar to that seen in human brain tumors were found in rats after exposure to concentrated particles, in particular the coarse fraction. 19 However, epidemiological evidence is sparse, consisting of 2 ecological studies, 20 , 21 3 cohort studies, 22–24 and a case-control study. 25 A US study found association between airborne toxicant volatile organic compound emissions at a county level and the incidence of brain cancer, 20 while a recent nationwide study found no association of brain cancer incidence and mortality at country level with any of 30 different hazardous air pollutants examined.…”

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confidence: 99%

Long-term exposure to ambient air pollution and incidence of brain tumor: the European Study of Cohorts for Air Pollution Effects (ESCAPE)

et al. 2017

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BackgroundEpidemiological evidence on the association between ambient air pollution and brain tumor risk is sparse and inconsistent.MethodsIn 12 cohorts from 6 European countries, individual estimates of annual mean air pollution levels at the baseline residence were estimated by standardized land-use regression models developed within the ESCAPE and TRANSPHORM projects: particulate matter (PM) ≤2.5, ≤10, and 2.5–10 μm in diameter (PM2.5, PM10, and PMcoarse), PM2.5 absorbance, nitrogen oxides (NO2 and NOx) and elemental composition of PM. We estimated cohort-specific associations of air pollutant concentrations and traffic intensity with total, malignant, and nonmalignant brain tumor, in separate Cox regression models, adjusting for risk factors, and pooled cohort-specific estimates using random-effects meta-analyses.ResultsOf 282194 subjects from 12 cohorts, 466 developed malignant brain tumors during 12 years of follow-up. Six of the cohorts also had data on nonmalignant brain tumor, where among 106786 subjects, 366 developed brain tumor: 176 nonmalignant and 190 malignant. We found a positive, statistically nonsignificant association between malignant brain tumor and PM2.5 absorbance (hazard ratio and 95% CI: 1.67; 0.89–3.14 per 10–5/m3), and weak positive or null associations with the other pollutants. Hazard ratio for PM2.5 absorbance (1.01; 0.38–2.71 per 10–5/m3) and all other pollutants were lower for nonmalignant than for malignant brain tumors.ConclusionWe found suggestive evidence of an association between long-term exposure to PM2.5 absorbance indicating traffic-related air pollution and malignant brain tumors, and no association with overall or nonmalignant brain tumors.

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confidence: 99%

Long-term exposure to ambient air pollution and incidence of brain tumor: the European Study of Cohorts for Air Pollution Effects (ESCAPE)

et al. 2017

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“…After 16 months of exposure to the MC atmosphere v controls, the DVC exhibited significant inflammation in MC mice (COX-2 and IL-1β P < 0.001) along with the olfactory bulb upregulation of CD14 ( P = 0.002) and significant DVC imbalance in genes for antioxidant defenses, apoptosis, and neurodegeneration. Similar gene cluster changes are seen upon exposure to diesel PM or a combination of PM +ozone (Gerlofs-Nijland et al, 2010 ; Levesque et al, 2011a , b , 2013 ; Ljubimova et al, 2013 ).…”

Section: Introductionmentioning

confidence: 69%

“…Extensive literature supports human and animal, breakdown of the nasal/olfactory blood-brain-barrier, alveolar-capillary, and intestinal barriers, as well as the brain expression of detrimental genes associated to urban air pollution (Thomson et al, 2007 ; Gerlofs-Nijland et al, 2010 ; Villarreal-Calderon et al, 2010 ; Bolton et al, 2012 ; Calderón-Garcidueñas et al, 2012a , 2013c , 2015g ; Bergin and Witzmann, 2013 ; Carson et al, 2013 ; Kish et al, 2013 ; Ljubimova et al, 2013 ; Win-Shwe et al, 2014 ; Rossner et al, 2015 ; Tsamou et al, 2016 ). Specifically, inductively coupled plasma mass spectrometry for metal analysis and real time PCR in frontal samples of Mexico City children and young adults showed higher concentrations of metals associated with PM: manganese ( p = 0.003), nickel and chromium ( p = 0.02) along with higher frontal COX2 mRNA ( p = 0.008) and IL1β ( p = 0.0002) and COX2 ( p = 0.005) olfactory bulb indicating neuroinflammation.…”

Section: Introductionmentioning

confidence: 99%

Chocolate, Air Pollution and Children's Neuroprotection: What Cognition Tools should be at Hand to Evaluate Interventions?

et al. 2016

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Millions of children across the world are exposed to multiple sources of indoor and outdoor air pollutants, including high concentrations of fine particulate matter (PM2.5) and ozone (O3). The established link between exposure to PM2.5, brain structural, volumetric and metabolic changes, severe cognitive deficits (1.5-2 SD from average IQ) in APOE 4 heterozygous females with >75 − < 94% BMI percentiles, and the presence of Alzheimer's disease (AD) hallmarks in urban children and young adults necessitates exploration of ways to protect these individuals from the deleterious neural effects of pollution exposure. Emerging research suggests that cocoa interventions may be a viable option for neuroprotection, with evidence suggesting that early cocoa interventions could limit the risk of cognitive and developmental concerns including: endothelial dysfunction, cerebral hypoperfusion, neuroinflammation, and metabolic detrimental brain effects. Currently, however, it is not clear how early we should implement consumption of cocoa to optimize its neuroprotective effects. Moreover, we have yet to identify suitable instruments for evaluating cognitive responses to these interventions in clinically healthy children, teens, and young adults. An approach to guide the selection of cognitive tools should take into account neuropsychological markers of cognitive declines in patients with Alzheimer's neuropathology, the distinct patterns of memory impairment between early and late onset AD, and the key literature associating white matter integrity and poor memory binding performance in cases of asymptomatic familial AD. We highlight potential systemic and neural benefits of cocoa consumption. We also highlight Working Memory Capacity (WMC) and attention control tasks as opened avenues for exploration in the air pollution scenario. Exposures to air pollutants during brain development have serious brain consequences in the short and long term and reliable cognition tools should be at hand to evaluate interventions.

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“…Leached metals trigger the production of reactive oxygen species via Fenton-like reactions 21 and soluble toxins can activate molecular signaling cascades that trigger tissue inflammation 22 . Pro-inflammatory cytokines, monocytes and macrophages are subsequently released into the systemic circulation 3 , and if sustained, can trigger BBB damage 23 , 24 , nervous system inflammation 25 and the expression of cancer-related genes in brain tissue 26 . Many studies that have investigated PM effects on organ health defined PM 10 , as per regulation, as any particulate matter sized ≤10 μm.…”

Section: Introductionmentioning

confidence: 99%

Coarse particulate matter (PM2.5–10) in Los Angeles Basin air induces expression of inflammation and cancer biomarkers in rat brains

Ljubimova

Braubach

Patil

et al. 2018

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Air pollution is linked to brain inflammation, which accelerates tumorigenesis and neurodegeneration. The molecular mechanisms that connect air pollution with brain pathology are largely unknown but seem to depend on the chemical composition of airborne particulate matter (PM). We sourced ambient PM from Riverside, California, and selectively exposed rats to coarse (PM2.5–10: 2.5–10 µm), fine (PM<2.5: <2.5 µm), or ultrafine particles (UFPM: <0.15 µm). We characterized each PM type via atomic emission spectroscopy and detected nickel, cobalt and zinc within them. We then exposed rats separately to each PM type for short (2 weeks), intermediate (1–3 months) and long durations (1 year). All three metals accumulated in rat brains during intermediate-length PM exposures. Via RNAseq analysis we then determined that intermediate-length PM2.5–10 exposures triggered the expression of the early growth response gene 2 (EGR2), genes encoding inflammatory cytokine pathways (IL13-Rα1 and IL-16) and the oncogene RAC1. Gene upregulation occurred only in brains of rats exposed to PM2.5–10 and correlated with cerebral nickel accumulation. We hypothesize that the expression of inflammation and oncogenesis-related genes is triggered by the combinatorial exposure to certain metals and toxins in Los Angeles Basin PM2.5–10.

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Gene expression changes in rat brain after short and long exposures to particulate matter in Los Angeles basin air: Comparison with human brain tumors

Cited by 23 publications

References 57 publications

Long-term exposure to ambient air pollution and incidence of brain tumor: the European Study of Cohorts for Air Pollution Effects (ESCAPE)

Long-term exposure to ambient air pollution and incidence of brain tumor: the European Study of Cohorts for Air Pollution Effects (ESCAPE)

Chocolate, Air Pollution and Children's Neuroprotection: What Cognition Tools should be at Hand to Evaluate Interventions?

Coarse particulate matter (PM2.5–10) in Los Angeles Basin air induces expression of inflammation and cancer biomarkers in rat brains

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