Department of Pediatrics, Emory University, Atlanta, Georgia; Division of Pulmonary Medicine, Children's Healthcare of Atlanta, Atlanta, Georgia.
Department of Pediatrics, Emory University, Atlanta, Georgia.
Ann Allergy Asthma Immunol. 2024 Oct;133(4):393-402.e4. doi: 10.1016/j.anai.2024.07.019. Epub 2024 Jul 27.
Epidemiologic studies have revealed associations between traffic-related pollutants such as diesel particulate matter (PM) and asthma outcomes in children, but the inflammatory features associated with diesel PM exposure in children with asthma are not understood.
To evaluate symptoms, exacerbations, and lung function measures in children with uncontrolled asthma and their associations with residential proximity to major roadways and to determine associations between diesel PM exposure and systemic inflammatory cytokines, circulating markers of T-cell activation and exhaustion, and metabolomic features using biomarker studies.
Children 5 to 17 years of age with physician-diagnosed, uncontrolled asthma despite treatment with an asthma controller medication completed a research visit involving questionnaires, lung function testing, and venipuncture for biomarker studies. Geocoding was performed to quantify residential proximity to major roadways and pollutant exposure.
A total of 447 children with uncontrolled asthma were enrolled. Children living closer to highly trafficked roadways were more disadvantaged and had more exposure to diesel PM, more exacerbations prompting an emergency department visit, and lower lung function measures. Children with the highest diesel PM exposure, compared with children with the lowest diesel PM exposure, also had blunted cytokine secretion and evidence of T-cell exhaustion, including disturbances in several metabolites associated with glutathione formation and oxidative stress.
Traffic-related diesel PM exposure in children with poorly controlled asthma is associated with poorer clinical outcomes and unique patterns of inflammation and oxidative stress. These findings argue for continued mitigation efforts to improve traffic-related air quality and health equity in children with asthma.
流行病学研究表明,交通相关污染物(如柴油颗粒物[PM])与儿童哮喘结局之间存在关联,但哮喘儿童接触柴油 PM 后与炎症相关的特征尚不清楚。
评估未得到控制的哮喘儿童的症状、加重情况和肺功能指标,及其与居住在主要道路附近的相关性,并通过生物标志物研究确定柴油 PM 暴露与全身炎症细胞因子、循环 T 细胞激活和衰竭标志物以及代谢组学特征之间的相关性。
5 至 17 岁患有经医生诊断的、未得到控制的哮喘的儿童,尽管接受了哮喘控制药物治疗,但仍完成了一项研究访问,包括问卷调查、肺功能测试和静脉采血以进行生物标志物研究。进行地理编码以量化居住与主要道路的接近程度和污染物暴露情况。
共纳入 447 名未得到控制的哮喘儿童。居住在交通繁忙道路附近的儿童处境较差,接触的柴油 PM 更多,哮喘加重导致急诊就诊的情况更多,肺功能指标也更低。与接触柴油 PM 最低的儿童相比,接触柴油 PM 最高的儿童细胞因子分泌能力减弱,且存在 T 细胞衰竭的证据,包括与谷胱甘肽形成和氧化应激相关的几种代谢物紊乱。
在未得到控制的哮喘儿童中,交通相关的柴油 PM 暴露与较差的临床结局以及独特的炎症和氧化应激模式有关。这些发现表明,需要继续采取缓解措施来改善与交通相关的空气质量和哮喘儿童的健康公平。