{"title":"Neurobehavioral and metabolic impacts of inhaled pollutants","authors":"Errol M. Thomson","doi":"10.4161/endo.27489","DOIUrl":null,"url":null,"abstract":"In addition to established effects on cardiovascular and respiratory systems, recent epidemiological studies show associations between air pollutants and impacts on the central nervous system such as depression and impaired cognitive ability, and on disease states associated with dysfunctional metabolism such as metabolic syndrome and type II diabetes. Although the relative risk attributed to air pollutants is small compared with established risk factors, the widespread exposure of the population translates into a substantial societal health burden. Controlled experimental studies support the notion that these associations have a biological basis. Recently, we reported that short-term exposure of rats to two pollutants associated with adverse health effects, particulate matter and ozone, activated the hypothalamic-pituitary-adrenal (HPA) stress response axis, resulting in increased circulating levels of the glucocorticoid corticosterone and systemic impacts on a variety of biological pathways. While effects were transient after a single exposure in this healthy animal model, chronic activation and dysfunction of the HPA axis is associated with adverse neurobehavioral, metabolic, cardiovascular, immune, reproductive, and developmental effects. Here I build upon the ideas presented in the original paper to discuss the potential role that activation and dysfunction of the stress axis, a common feature of neurobehavioral and metabolic disorders, may play in mediating adverse health effects associated with air pollution.","PeriodicalId":90159,"journal":{"name":"Endocrine disruptors (Austin, Tex.)","volume":"1 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2013-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4161/endo.27489","citationCount":"31","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Endocrine disruptors (Austin, Tex.)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4161/endo.27489","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 31
Abstract
In addition to established effects on cardiovascular and respiratory systems, recent epidemiological studies show associations between air pollutants and impacts on the central nervous system such as depression and impaired cognitive ability, and on disease states associated with dysfunctional metabolism such as metabolic syndrome and type II diabetes. Although the relative risk attributed to air pollutants is small compared with established risk factors, the widespread exposure of the population translates into a substantial societal health burden. Controlled experimental studies support the notion that these associations have a biological basis. Recently, we reported that short-term exposure of rats to two pollutants associated with adverse health effects, particulate matter and ozone, activated the hypothalamic-pituitary-adrenal (HPA) stress response axis, resulting in increased circulating levels of the glucocorticoid corticosterone and systemic impacts on a variety of biological pathways. While effects were transient after a single exposure in this healthy animal model, chronic activation and dysfunction of the HPA axis is associated with adverse neurobehavioral, metabolic, cardiovascular, immune, reproductive, and developmental effects. Here I build upon the ideas presented in the original paper to discuss the potential role that activation and dysfunction of the stress axis, a common feature of neurobehavioral and metabolic disorders, may play in mediating adverse health effects associated with air pollution.