Stress hormones as potential mediators of air pollutant effects on the brain: Rapid induction of glucocorticoid-responsive genes

Thomson, Errol M.; Filiatreault, Alain; Guénette, Josée

doi:10.1016/j.envres.2019.108717

Cited by 49 publications

(20 citation statements)

References 77 publications

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“…In a study of mice exposed to air pollution, expression of the gene underlying the oxidative stress response was attenuated when the mice were injected with an inhibitor of cortisol production. However, when they were injected with cortisol itself, the oxidative stress-causing gene was activated (40). These results suggest that cortisol level is a key player in the effect of air pollution on depression.…”

Section: Depressionmentioning

confidence: 88%

“…When HPA is activated by air pollution and glucocorticoid binds to the glucocorticoid receptor (GR), the associated neurotrophic factor and the genes associated with inflammatory reactions, apoptosis, and metabolism are expressed, resulting in impaired neurogenesis, neurotoxicity, and glial cell reactivity. This eventually leads to cognitive decline, dementia, and depression (17,40,44).…”

Section: Depressionmentioning

confidence: 99%

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Air Pollution and Central Nervous System Disease: A Review of the Impact of Fine Particulate Matter on Neurological Disorders

Kim

et al. 2020

Front. Public Health

125

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Background: It is widely known that the harmful effects of fine dust can cause various diseases. Research on the correlation between fine dust and health has been mainly focused on lung and cardiovascular diseases. By contrast, the effects of air pollution on the central nervous system (CNS) are not broadly recognized.Findings: Air pollution can cause diverse neurological disorders as the result of inflammation of the nervous system, oxidative stress, activation of microglial cells, protein condensation, and cerebral vascular-barrier disorders, but uncertainty remains concerning the biological mechanisms by which air pollution produces neurological disease. Neuronal cell damage caused by fine dust, especially in fetuses and infants, can cause permanent brain damage or lead to neurological disease in adulthood.Conclusion: It is necessary to study the air pollution–CNS disease connection with particular care and commitment. Moreover, the epidemiological and experimental study of the association between exposure to air pollution and CNS damage is critical to public health and quality of life. Here, we summarize the correlations between fine dust exposure and neurological disorders reported so far and make suggestions on the direction future research should take.

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Section: Depressionmentioning

confidence: 88%

Section: Depressionmentioning

confidence: 99%

Air Pollution and Central Nervous System Disease: A Review of the Impact of Fine Particulate Matter on Neurological Disorders

Kim

et al. 2020

Front. Public Health

125

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“…Recent experimental animal research has shown that a neuroendocrine stress response is among the early biological responses triggered by exposure to fine particulate matter with an aerodynamic diameter ≤ 2.5 μm (PM 2.5 ) and exposure to nitrogen dioxide (NO 2 ) [11]. The biological stress response includes activation of the hypothalamic-pituitaryadrenal (HPA) axis and release of glucocorticoid stress hormones, with the glucocorticoid cortisol as its main downstream effector in humans [12]. The relevance of these experimental observations to humans has been confirmed in a few recent studies [13,14].…”

Section: Introductionmentioning

confidence: 99%

Residential exposure to air pollution and access to neighborhood greenspace in relation to hair cortisol concentrations during the second and third trimester of pregnancy

et al. 2021

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Background Exposure to air pollution during pregnancy has been associated with adverse pregnancy outcomes in studies worldwide, other studies have described beneficial effects of residential greenspace on pregnancy outcomes. The biological mechanisms that underlie these associations are incompletely understood. A biological stress response, which implies release of cortisol, may underlie associations of air pollution exposure and access to neighborhood greenspaces with health. Methods We explored residential exposure to air pollution and residential access to neighborhood greenspaces in relation to hair cortisol concentrations of participants in a prospective pregnancy cohort study in Flanders, Belgium. Hair samples were collected at the end of the second pregnancy trimester (n = 133) and shortly after delivery (n = 81). Cortisol concentrations were measured in 3-cm scalp-near hair sections, to reflect second and third pregnancy trimester cortisol secretion. We estimated long-term (3 months before sampling) residential exposure to fine particulate matter (PM2.5), nitrogen dioxide (NO2) and black carbon (BC), assessed residential distance to major roads and residential access to neighborhood greenspaces (NHGS). Associations between residential exposures and hair cortisol concentrations were studied using linear regression models while adjusting for season of sampling. Results Three-month mean residential NO2 and BC concentrations were positively associated with third pregnancy trimester hair cortisol concentrations (p = 0.008 and p = 0.017). Access to a large NHGS (10 ha or more within 800 m from residence) was negatively associated with third trimester hair cortisol concentrations (p = 0.019). Access to a large NHGS significantly moderated the association between residential proximity to major roads and second trimester hair cortisol concentrations (p = 0.021). Residential distance to major roads was negatively associated with second trimester hair cortisol concentrations of participants without access to a large NHGS (p = 0.003). The association was not significant for participants with access to a large NHGS. The moderation tended towards significance in the third pregnancy trimester (p < 0.10). Conclusions Our findings suggest a positive association between long-term residential exposure to air pollution and biological stress during pregnancy, residential access to neighborhood greenspaces may moderate the association. Further research is needed to confirm our results. Trial registration The IPANEMA study is registered under number NCT02592005 at clinicaltrials.gov.

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“…Therefore, these data suggest that the stress-hormone-mediated activation of ARs and GRs likely leads to the pulmonary and systemic effects of ozone [85]. Ozone-induced upregulation of Tsc22d3, metallothionein 1 (Mt-1), and Fkbp5 in the lungs following increases in stress hormone levels suggests the activation of GR-responsive genes by increased corticosterone [4,6,14,85,117].…”

Section: βAr and Gr Activation Contribute To Ozone-induced Lung Inflammationmentioning

confidence: 85%

Adrenergic and Glucocorticoid Receptors in the Pulmonary Health Effects of Air Pollution

Hodge

Henriquez

Kodavanti

2021

Toxics

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Adrenergic receptors (ARs) and glucocorticoid receptors (GRs) are activated by circulating catecholamines and glucocorticoids, respectively. These receptors regulate the homeostasis of physiological processes with specificity via multiple receptor subtypes, wide tissue-specific distribution, and interactions with other receptors and signaling processes. Based on their physiological roles, ARs and GRs are widely manipulated therapeutically for chronic diseases. Although these receptors play key roles in inflammatory and cellular homeostatic processes, little research has addressed their involvement in the health effects of air pollution. We have recently demonstrated that ozone, a prototypic air pollutant, mediates pulmonary and systemic effects through the activation of these receptors. A single exposure to ozone induces the sympathetic–adrenal–medullary and hypothalamic–pituitary–adrenal axes, resulting in the release of epinephrine and corticosterone into the circulation. These hormones act as ligands for ARs and GRs. The roles of beta AR (βARs) and GRs in ozone-induced pulmonary injury and inflammation were confirmed in a number of studies using interventional approaches. Accordingly, the activation status of ARs and GRs is critical in mediating the health effects of inhaled irritants. In this paper, we review the cellular distribution and functions of ARs and GRs, their lung-specific localization, and their involvement in ozone-induced health effects, in order to capture attention for future research.

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Stress hormones as potential mediators of air pollutant effects on the brain: Rapid induction of glucocorticoid-responsive genes

Cited by 49 publications

References 77 publications

Air Pollution and Central Nervous System Disease: A Review of the Impact of Fine Particulate Matter on Neurological Disorders

Air Pollution and Central Nervous System Disease: A Review of the Impact of Fine Particulate Matter on Neurological Disorders

Residential exposure to air pollution and access to neighborhood greenspace in relation to hair cortisol concentrations during the second and third trimester of pregnancy

Adrenergic and Glucocorticoid Receptors in the Pulmonary Health Effects of Air Pollution

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