Airborne copper exposure in school environments associated with poorer motor performance and altered basal ganglia

Pujol, Jesús; Fenoll, Raquel; Macià, Dídac; Martínez‐Vilavella, Gerard; Álvarez-Pedrerol, Mar; Rivas, Ioar; Forns, Joan; Deus, Joan; Blanco‐Hinojo, Laura; Querol, Xavier; Sunyer, Jordi

doi:10.1002/brb3.467

Cited by 73 publications

(59 citation statements)

References 48 publications

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“…Of all air pollutants, particles are thought to be the most important inhaled toxicants in urban air, particularly in relation to brain damage . Among the various particle types, we found airborne copper to be associated with tissue modifications and functional connectivity in the caudate nucleus in children . Other metals, such as iron, have been linked to structural changes in mice brain, and environmental Fe nanoparticles were found in brain tissue .…”

Section: Why To Investigate Air Pollution?mentioning

confidence: 76%

Pre‐natal brain development as a target for urban air pollution

Sunyer

Dadvand

2019

Basic Clin Pharma Tox

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Air pollution is the main urban‐related environmental hazard and one of the major contributors to the global burden of disease based on its cardiovascular‐respiratory impacts. In children, exposure to urban air pollution is associated, among others, with decelerated neurodevelopment early in life and increased risk of neurodevelopmental problems such as attention‐deficit hyperactivity disorder, autism spectrum disorders, academic failure and the start of Alzheimer's pathogenesis. However, the evidence of the effects of air pollution on brain development is still inadequate, mainly due to the limitations in (a) characterizing brain development (most studies were based on subjective tools such as questionnaires or neuropsychological tests) and (b) air pollution exposure (most studies only used residential levels based on geographical modelling and also overlooking the variation in the mixture of air pollutants as well as the composition and hence toxicity of particulate pollutants in different settings), (c) the lack of studies during the most vulnerable stages of brain development (foetal and early life (first two years post‐natally)) and (d) the lack of structural and functional imaging data underlying these effects. In mice, in utero exposure to fine particles was linked to structural brain changes and there is a need to establish the generalizability of these findings in human beings. Though scarce, current evidence in children supports the importance of the pre‐natal period as a susceptible window of exposure. Two studies in schoolchildren found that pre‐natal air pollution exposure might damage brain structure while exposure during childhood was not linked to any structural alteration. Another study showed that children with higher traffic‐related air pollution at school had lower functional integration in key brain networks, but no changes in brain structure, possibly partly because of the time window of air pollution exposure (in utero versus childhood exposure). A key development is to discover the windows of greatest sensitivity of structural brain changes to air pollution exposure by incorporating the recent advances in non‐invasive imaging to characterize natal and post‐natal brain development and exploring whether and to what extend placental dysfunction could mediate such an association. Studying pre‐natal life is important because effects at this time are of a potentially irreversible nature and because the largest preventive opportunities occur during these periods.

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Section: Why To Investigate Air Pollution?mentioning

confidence: 76%

Pre‐natal brain development as a target for urban air pollution

Sunyer

Dadvand

2019

Basic Clin Pharma Tox

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“…Cu is required to support numerous biological activities, but it can exert cytotoxic effects when its concentration exceeds the body tolerance. Overexposure to Cu may produce some detrimental effects in the basal ganglia of human [28] and in the kidney [20], spleen, and thymus [29] in mice. Hepatocytes are regarded as one of the main target cells for Cu toxicity.…”

Section: Discussionmentioning

confidence: 99%

Copper Induces Oxidative Stress and Apoptosis in the Mouse Liver

Liu

Guo

Jian

et al. 2020

Oxidative Medicine and Cellular Longevity

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Copper (Cu) is an essential trace element involved in the normal physiological processes of animals. However, excessive exposure to Cu can produce numerous detrimental impacts. The aim of this study was to investigate the effects of Cu on oxidative stress and apoptosis as well as their relationship in the mouse liver. Four-week-old ICR mice (n=240) were randomly assigned to different Cu (Cu2+-CuSO4) treatment groups (0, 4, 8, and 16 mg/kg) for periods of 21 and 42 days. The high doses of Cu exposure could induce oxidative stress, by increasing the levels of reactive oxygen species (ROS) and protein carbonyls (PC) and decreasing the activities of antisuperoxide anion (ASA) and antihydroxyl radical (AHR) and content of glutathione (GSH), as well as activities and mRNA expression levels of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px). Moreover, high doses of Cu exposure induced hepatic apoptosis via the mitochondrial apoptotic pathway, as characterized by the depolarization of mitochondrial membrane potential (MMP); significantly increased mRNA and protein expression levels of cytosolic cytochrome (Cyt c), apoptosis-inducing factor (AIF), endonuclease G (Endo G), apoptosis protease-activating factor-1 (Apaf-1), cleaved caspase-9, cleaved caspase-3, cleaved PARP, Bcl-2 antagonist killer (Bak), Bcl-2-associated X protein (Bax), and Bcl-2-interacting mediator of cell death (Bim); and decreased mRNA and protein expression levels of B-cell lymphoma-2 (Bcl-2) and Bcl-extra-large (Bcl-xL). Furthermore, the activation of the tumor necrosis factor receptor-1 (TNF-R1) signaling pathway was involved in Cu-induced apoptosis, as characterized by the significantly increased mRNA and protein expression levels of TNF-R1, Fas-associated death domain (FADD), TNFR-associated death domain (TRADD), and cleaved caspase-8. These results indicated that exposure to excess Cu could cause oxidative stress triggered by ROS overproduction and diminished antioxidant function, which in turn promoted hepatic apoptosis via mitochondrial apoptosis and that the TNF-R1 signaling pathway was also involved in the Cu-induced apoptosis.

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“…Of note, children's exposure to Cu has also been linked with nononcologic conditions such as neurologic disorders [23][24][25] and obesity [22]. Significantly higher blood Cu concentrations have been found in obese children, as compared with healthy controls [88,89].…”

Section: Discussionmentioning

confidence: 99%

“…Children are particularly vulnerable, in terms of biological effects, when exposed to metal pollution [13][14][15][16][17], mainly due to oxidative damage following chronic exposure [18,19]. In pediatric age, the body burden of metals has been linked with a number of pathologic conditions including nononcologic diseases (i.e., altered growth and development [20], obesity [21,22], and neurologic [23][24][25], cognitive [26], and respiratory [19,27] disorders) and cancer [28][29][30].…”

Section: Introductionmentioning

confidence: 99%

Biomonitoring of Metals in Children Living in an Urban Area and Close to Waste Incinerators

Ciaula

Gentilini²,

Diella

et al. 2020

IJERPH

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The impact of waste incinerators is usually examined by measuring environmental pollutants. Biomonitoring has been limited, until now, to few metals and to adults. We explored accumulation of a comprehensive panel of metals in children free-living in an urban area hosting two waste incinerators. Children were divided by georeferentiation in exposed and control groups, and toenail concentrations of 23 metals were thereafter assessed. The percentage of children having toenail metal concentrations above the limit of detection was higher in exposed children than in controls for Al, Ba, Mn, Cu, and V. Exposed children had higher absolute concentrations of Ba, Mn, Cu, and V, as compared with those living in the reference area. The Tobit regression identified living in the exposed area as a significant predictor of Ba, Ni, Cu, Mn, and V concentrations, after adjusting for covariates. The concentrations of Ba, Mn, Ni, and Cu correlated with each other, suggesting a possible common source of emission. Exposure to emissions derived from waste incinerators in an urban setting can lead to body accumulation of specific metals in children. Toenail metal concentration should be considered a noninvasive and adequate biomonitoring tool and an early warning indicator which should integrate the environmental monitoring of pollutants.

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Airborne copper exposure in school environments associated with poorer motor performance and altered basal ganglia

Cited by 73 publications

References 48 publications

Pre‐natal brain development as a target for urban air pollution

Pre‐natal brain development as a target for urban air pollution

Copper Induces Oxidative Stress and Apoptosis in the Mouse Liver

Biomonitoring of Metals in Children Living in an Urban Area and Close to Waste Incinerators

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