关键词: COVID-19 lockdown Electronic waste HMGB1 Insulin resistance PM2.5 Pb

Mesh : Humans Child Lead / blood COVID-19 / blood epidemiology Child, Preschool Particulate Matter Insulin Resistance Male Female Environmental Exposure Electronic Waste Blood Glucose / analysis Inflammation / blood Recycling HMGB1 Protein / blood Insulin / blood Air Pollutants SARS-CoV-2

来  源:   DOI:10.1007/s10653-024-02066-4

Abstract:
Fine particular matter (PM2.5) and lead (Pb) exposure can induce insulin resistance, elevating the likelihood of diabetes onset. Nonetheless, the underlying mechanism remains ambiguous. Consequently, we assessed the association of PM2.5 and Pb exposure with insulin resistance and inflammation biomarkers in children. A total of 235 children aged 3-7 years in a kindergarten in e-waste recycling areas were enrolled before and during the Corona Virus Disease 2019 (COVID-19) lockdown. Daily PM2.5 data was collected and used to calculate the individual PM2.5 daily exposure dose (DED-PM2.5). Concentrations of whole blood Pb, fasting blood glucose, serum insulin, and high mobility group box 1 (HMGB1) in serum were measured. Compared with that before COVID-19, the COVID-19 lockdown group had lower DED-PM2.5 and blood Pb, higher serum HMGB1, and lower blood glucose and homeostasis model assessment of insulin resistance (HOMA-IR) index. Decreased DED-PM2.5 and blood Pb levels were linked to decreased levels of fasting blood glucose and increased serum HMGB1 in all children. Increased serum HMGB1 levels were linked to reduced levels of blood glucose and HOMA-IR. Due to the implementation of COVID-19 prevention and control measures, e-waste dismantling activities and exposure levels of PM2.5 and Pb declined, which probably reduced the association of PM2.5 and Pb on insulin sensitivity and diabetes risk, but a high level of risk of chronic low-grade inflammation remained. Our findings add new evidence for the associations among PM2.5 and Pb exposure, systemic inflammation and insulin resistance, which could be a possible explanation for diabetes related to environmental exposure.
摘要:
细小物质(PM2.5)和铅(Pb)暴露可引起胰岛素抵抗,提高糖尿病发病的可能性。尽管如此,潜在的机制仍然模棱两可。因此,我们评估了PM2.5和铅暴露与儿童胰岛素抵抗和炎症生物标志物的相关性.在2019年冠状病毒病(COVID-19)封锁之前和期间,共有235名3-7岁的儿童在电子垃圾回收区的一所幼儿园入学。收集每日PM2.5数据并用于计算个体PM2.5每日暴露剂量(DED-PM2.5)。全血铅的浓度,空腹血糖,血清胰岛素,测定血清高迁移率族蛋白1(HMGB1)水平。与COVID-19之前相比,COVID-19封锁组的DED-PM2.5和血铅水平较低,较高的血清HMGB1和较低的血糖和稳态模型评估胰岛素抵抗(HOMA-IR)指数。所有儿童中DED-PM2.5和血铅水平的降低与空腹血糖水平的降低和血清HMGB1的升高有关。血清HMGB1水平升高与血糖和HOMA-IR水平降低有关。由于COVID-19防控措施的实施,电子垃圾拆解活动和PM2.5和Pb的暴露水平下降,这可能降低了PM2.5和铅对胰岛素敏感性和糖尿病风险的关联,但慢性低度炎症的风险仍然很高。我们的发现为PM2.5和铅暴露之间的关联增加了新的证据,全身炎症和胰岛素抵抗,这可能是与环境暴露有关的糖尿病的可能解释。
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