In Vivo Comparative Study on Acute and Sub-acute Biological Effects Induced by Ultrafine Particles of Different Anthropogenic Sources in BALB/c Mice

Farina, Francesca; Lonati, Elena; Milani, Chiara; Massimino, Luca; Ballarini, E; Donzelli, E; Crippa, Luca; Marmiroli, P; Botto, Laura; Corsetto, Paola Antonia; Sancini, Giulio; Bulbarelli, Alessandra; Palestini, Paola

doi:10.3390/ijms20112805

Cited by 24 publications

(39 citation statements)

References 83 publications

(106 reference statements)

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“…To date, reactive oxygen species (ROS) generation and oxidative stress induced by DEP are frequently reported [ 47 , 48 ]. Chronic DEP exposure induces inflammatory conditions in mice [ 24 , 49 ], subsequently inflammatory and epithelial cells release ROS which gives rise to DNA damage [ 46 ]. Considering that oxidative stress and inflammation response after DEP exposure can be somewhat attributed to our positive results of the comet assay.…”

Section: Discussionmentioning

confidence: 99%

Age and Gender Effects on Genotoxicity in Diesel Exhaust Particles Exposed C57BL/6 Mice

et al. 2021

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There is growing evidence that the accumulation of DNA damage induced by fine particulate matter (PM2.5) exposure is an underlying mechanism of pulmonary disease onset and progression. However, there is a lack of experimental evidence on whether common factors (age, gender) affect PM2.5 induced genomic damage. Here, we assessed the DNA damage potency of PM2.5 using conventional genotoxicity testing in old male and female mice aged 8 and 40 weeks. Mice were intratracheally instilled with diesel exhaust PM2.5 (DEP, NIST SRM 1650b), twice a week for 4 weeks. Exposure to DEP was not associated with an increase in the frequency of micronucleated polychromatic erythrocytes and did not induce a systemic genotoxic effect in the bone marrow. Meanwhile, the results from the comet assay showed a significant increase in DNA damage in DEP exposed mouse lung specimens. The positive relationship between DEP exposure and DNA damage is stronger in the older than in the younger group. Statistical analysis showed that there was a modifying effect of age on the association between PM2.5 exposure and DNA damage. Our results suggest that the age factor should be considered to better understand the cellular adverse effects of PM2.5.

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Section: Discussionmentioning

confidence: 99%

Age and Gender Effects on Genotoxicity in Diesel Exhaust Particles Exposed C57BL/6 Mice

et al. 2021

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“…In vivo animal studies also offered insights on wood smoke exposure induced inflammatory responses locally and systemically. Exposure of BALB/c mice to an organic wood smoke extract from emissions derived from spruce combustion significantly increased inflammatory responses (COX-2, MPO) in both respiratory and cardiovascular systems [ 46 ]. Serum collected from C57BL/6 mice exposed to oak wood smoke (PM 2.5 at 380 μg/m 3 ) for 24 h was able to induce pro-inflammatory responses (IL-6 and CXCL1), and elevated expression of adhesion molecules (VCAM1 and ICAM1) in murine endothelial cells [ 15 ].…”

Section: Mechanisms Of Cardiovascular Impacts Of Wildfire Smokementioning

confidence: 99%

Cardiovascular health impacts of wildfire smoke exposure

et al. 2021

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In recent years, wildland fires have occurred more frequently and with increased intensity in many fire-prone areas. In addition to the direct life and economic losses attributable to wildfires, the emitted smoke is a major contributor to ambient air pollution, leading to significant public health impacts. Wildfire smoke is a complex mixture of particulate matter (PM), gases such as carbon monoxide, nitrogen oxide, and volatile and semi-volatile organic compounds. PM from wildfire smoke has a high content of elemental carbon and organic carbon, with lesser amounts of metal compounds. Epidemiological studies have consistently found an association between exposure to wildfire smoke (typically monitored as the PM concentration) and increased respiratory morbidity and mortality. However, previous reviews of the health effects of wildfire smoke exposure have not established a conclusive link between wildfire smoke exposure and adverse cardiovascular effects. In this review, we systematically evaluate published epidemiological observations, controlled clinical exposure studies, and toxicological studies focusing on evidence of wildfire smoke exposure and cardiovascular effects, and identify knowledge gaps. Improving exposure assessment and identifying sensitive cardiovascular endpoints will serve to better understand the association between exposure to wildfire smoke and cardiovascular effects and the mechanisms involved. Similarly, filling the knowledge gaps identified in this review will better define adverse cardiovascular health effects of exposure to wildfire smoke, thus informing risk assessments and potentially leading to the development of targeted interventional strategies to mitigate the health impacts of wildfire smoke.

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“…125 It is believed that exposure to smaller particles (PM 2.5 and UFPs) is of greater health concern since they can deposit deeper into the lungs and adsorb more chemicals onto their surfaces because of larger surface-tovolume ratios. In fact, the toxic effects of PM exposure on human health are believed to be largely mediated by UFPs because of their ability to activate inflammation and oxidative stress at the cellular and systemic levels [126][127][128][129] Diesel exhaust particles (DEPs) are composed of PM 2.5 and UFPs. Below, we focus on mechanisms by which PM, NO 2 , and O 3 could affect SARS-CoV-2 infection and COVID-19 pathogenesis.…”

Section: Coronavirus Pathogenesismentioning

confidence: 99%

SARS‐CoV‐2 infection, COVID‐19 pathogenesis, and exposure to air pollution: What is the connection?

Woodby

Arnold

Valacchi

2020

Annals of the New York Academy of Sciences

125

113

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Exposure to air pollutants has been previously associated with respiratory viral infections, including influenza, measles, mumps, rhinovirus, and respiratory syncytial virus. Epidemiological studies have also suggested that air pollution exposure is associated with increased cases of SARS-CoV-2 infection and COVID-19-associated mortality, although the molecular mechanisms by which pollutant exposure affects viral infection and pathogenesis of COVID-19 remain unknown. In this review, we suggest potential molecular mechanisms that could account for this association. We have focused on the potential effect of exposure to nitrogen dioxide (NO 2), ozone (O 3), and particulate matter (PM) since there are studies investigating how exposure to these pollutants affects the life cycle of other viruses. We have concluded that pollutant exposure may affect different stages of the viral life cycle, including inhibition of mucociliary clearance, alteration of viral receptors and proteases required for entry, changes to antiviral interferon production and viral replication, changes in viral assembly mediated by autophagy, prevention of uptake by macrophages, and promotion of viral spread by increasing epithelial permeability. We believe that exposure to pollutants skews adaptive immune responses toward bacterial/allergic immune responses, as opposed to antiviral responses. Exposure to air pollutants could also predispose exposed populations toward developing COIVD-19associated immunopathology, enhancing virus-induced tissue inflammation and damage.

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In Vivo Comparative Study on Acute and Sub-acute Biological Effects Induced by Ultrafine Particles of Different Anthropogenic Sources in BALB/c Mice

Cited by 24 publications

References 83 publications

Age and Gender Effects on Genotoxicity in Diesel Exhaust Particles Exposed C57BL/6 Mice

Age and Gender Effects on Genotoxicity in Diesel Exhaust Particles Exposed C57BL/6 Mice

Cardiovascular health impacts of wildfire smoke exposure

SARS‐CoV‐2 infection, COVID‐19 pathogenesis, and exposure to air pollution: What is the connection?

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