Inflammation response, oxidative stress and DNA damage caused by urban air pollution exposure increase in the lack of DNA repair XPC protein

Alves, Nilmara de Oliveira; Pereira, Guilherme Martins; Domenico, Marlise Di; Costanzo, Giovanna; Benevenuto, Sarah Gomes de Menezes; Fonoff, Adriana M. de Oliveira; Costa, Natália; Júnior, Gabriel Ribeiro; Kajitani, Gustavo Satoru; Moreno, Natália Cestari; Fotoran, Wesley Luzetti; Quiroz, Jhon; Andrade, Jaílson Bittencourt de; Veras, Mariana Matera; Artaxo, Paulo; Menck, Carlos Frederico Martins; Vasconcellos, Pérola de Castro; Saldiva, Paulo Hilário Nascimento

doi:10.1016/j.envint.2020.106150

Cited by 57 publications

(30 citation statements)

References 104 publications

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“…[ 2 ] Particularly, PM2.5 obtained from diesel exhaust can be more toxic as it can absorb chemicals including polycyclic aromatic hydrocarbons (PAHs) and nitro‐substituted PAHs (nitro‐PAHs), which enhance inflammatory responses. [ 3 ] While PM2.5 has been strongly correlated with increased risk for pulmonary and cardiovascular diseases, [ 4 ] it is now acknowledged as an enhanced risk factor for neuroinflammation that may damage the central nervous system (CNS). [ 5 ] According to significant number of epidemiological studies, individuals residing in the areas highly polluted with PM2.5 tended to have an increased neuroinflammation in the brain tissue, warning the strong association between air pollution and brain damage.…”

Section: Introductionmentioning

confidence: 99%

An Air Particulate Pollutant Induces Neuroinflammation and Neurodegeneration in Human Brain Models

et al. 2021

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Fine particulate matter (PM2.5), a major component among air pollutants, highlights as a global health concern. Several epidemiological studies show the correlation between chronical PM2.5 exposure and incidents of neurological disorders including Alzheimer's disease. However, the mechanisms have not been well understood, partly due to the lack of model systems that reflect the physiologically relevant innate immunity in human brains. Here, PM2.5‐polluted human brain models (PMBs) are created in a 3D microfluidic platform reconstituting key aspects of human brain immunity under the PM2.5 exposure. PM2.5 penetration across a blood–brain barrier (BBB) model and accumulation in the brain tissue side of the model are first validated. Second, the PMB model shows that the BBB‐penetrating PM2.5 initiates astrogliosis, resulting in slight neuronal loss and microglial infiltration. Third, it is demonstrated that the infiltrating microglia obtain M1 phenotype induced by interleukin‐1β and interferon‐γ from neurons and reactive astrocytes under the PM2.5 exposure. Finally, it is observed that additional proinflammatory mediators and nitric oxide released from the M1 microglia exacerbate neuronal damages, such as synaptic impairment, phosphoric tau accumulation, and neuronal death. This study suggests that PM2.5 can be a potential environmental risk factor for dementia mediated by the detrimental neuroinflammation.

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Section: Introductionmentioning

confidence: 99%

An Air Particulate Pollutant Induces Neuroinflammation and Neurodegeneration in Human Brain Models

et al. 2021

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“…Several studies have also investigated the cytogenetic and genotoxic effects of fine PM on in vivo human cells [ 15 , 17 , 18 , 19 ]. Particularly, studies carried out on cells derived from target tissues (e.g., pulmonary cells, mucosa cells) showed a positive association with air pollution [ 20 , 21 , 22 , 23 , 24 , 25 ].…”

Section: Introductionmentioning

confidence: 99%

Genotoxic Activity of Particulate Matter and In Vivo Tests in Children Exposed to Air Pollution

Zani

Donato

Ceretti

et al. 2021

IJERPH

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The aim of this paper was to investigate the relationship between micronuclei and DNA damage in children’s buccal mucosa cells and the genotoxicity and mutagenicity of the different sized fractions of particulate matter as well as the concentration of PAHs (polycyclic aromatic hydrocarbons) and metals in particulate matter. Air particulate matter was collected by high volume samplers located near the schools attended by the children on the same days of biological samplings. The mutagenic activity was assessed in different cells in in vitro tests (Ames test on bacteria and comet test on leukocytes). Our study showed weak positive correlations between (a) the mutagenicity of the PM0.5 fraction and PAHs and (b) the micronuclei test of children’s buccal cells and PAHs detected in PM0.5 and PM0.5–3 fractions. A positive correlation was also found between in vitro comet test on leukocytes and PAHs in the PM3–10 fraction. No correlation was observed for metal concentrations in each PM fraction.

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“…While ILC2 will further increase the type 2 cytokine production leading to airway hyperreactivity, ILC1 together with the induction of IFN-γ will be inhibited making the mice more susceptible to infections and allergens [117]. Taken it all into account PM will lead to airway inflammation, epithelial damage, DNA damage, oxidative stress, mitochondrial damage, and lung fibrosis [18,106,115,[118][119][120].…”

Section: Particulate Mattermentioning

confidence: 99%

Air Pollution and the Airways: Lessons from a Century of Human Urbanization

et al. 2021

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Since the industrial revolution, air pollution has become a major problem causing several health problems involving the airways as well as the cardiovascular, reproductive, or neurological system. According to the WHO, about 3.6 million deaths every year are related to inhalation of polluted air, specifically due to pulmonary diseases. Polluted air first encounters the airways, which are a major human defense mechanism to reduce the risk of this aggressor. Air pollution consists of a mixture of potentially harmful compounds such as particulate matter, ozone, carbon monoxide, volatile organic compounds, and heavy metals, each having its own effects on the human body. In the last decades, a lot of research investigating the underlying risks and effects of air pollution and/or its specific compounds on the airways, has been performed, involving both in vivo and in vitro experiments. The goal of this review is to give an overview of the recent data on the effects of air pollution on healthy and diseased airways or models of airway disease, such as asthma or chronic obstructive pulmonary disease. Therefore, we focused on studies involving pollution and airway symptoms and/or damage both in mice and humans.

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Inflammation response, oxidative stress and DNA damage caused by urban air pollution exposure increase in the lack of DNA repair XPC protein

Cited by 57 publications

References 104 publications

An Air Particulate Pollutant Induces Neuroinflammation and Neurodegeneration in Human Brain Models

An Air Particulate Pollutant Induces Neuroinflammation and Neurodegeneration in Human Brain Models

Genotoxic Activity of Particulate Matter and In Vivo Tests in Children Exposed to Air Pollution

Air Pollution and the Airways: Lessons from a Century of Human Urbanization

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