Calderón-Garcidueñas Lilian, D'Angiulli Amedeo, Kulesza Randy J, Torres-Jardón Ricardo, Osnaya Norma, Romero Lina, Keefe Sheyla, Herritt Lou, Brooks Diane M, Avila-Ramirez Jose, Delgado-Chávez Ricardo, Medina-Cortina Humberto, González-González Luis Oscar
Instituto Nacional de Pediatría, Mexico City 04530, Mexico.
Int J Dev Neurosci. 2011 Jun;29(4):365-75. doi: 10.1016/j.ijdevneu.2011.03.007. Epub 2011 Mar 31.
We assessed brainstem inflammation in children exposed to air pollutants by comparing brainstem auditory evoked potentials (BAEPs) and blood inflammatory markers in children age 96.3±8.5 months from highly polluted (n=34) versus a low polluted city (n=17). The brainstems of nine children with accidental deaths were also examined. Children from the highly polluted environment had significant delays in wave III (t(50)=17.038; p<0.0001) and wave V (t(50)=19.730; p<0.0001) but no delay in wave I (p=0.548). They also had significantly longer latencies than controls for interwave intervals I-III, III-V, and I-V (all t(50)>7.501; p<0.0001), consisting with delayed central conduction time of brainstem neural transmission. Highly exposed children showed significant evidence of inflammatory markers and their auditory and vestibular nuclei accumulated α synuclein and/or β amyloid(1-42). Medial superior olive neurons, critically involved in BAEPs, displayed significant pathology. Children's exposure to urban air pollution increases their risk for auditory and vestibular impairment.
我们通过比较来自高污染城市（n = 34）和低污染城市（n = 17）的96.3±8.5个月大儿童的脑干听觉诱发电位（BAEP）和血液炎症标志物，评估了暴露于空气污染物的儿童的脑干炎症。还检查了9名意外死亡儿童的脑干。来自高污染环境的儿童在波III（t(50)=17.038；p<0.0001）和波V（t(50)=19.730；p<0.0001）有明显延迟，但在波I没有延迟（p = 0.548）。他们在波间期I-III、III-V和I-V的潜伏期也明显长于对照组（所有t(50)>7.501；p<0.0001），这与脑干神经传导的中枢传导时间延迟一致。高暴露儿童显示出炎症标志物的明显证据，并且他们的听觉和前庭核积累了α突触核蛋白和/或β淀粉样蛋白（1-42）。对BAEP至关重要的内侧上橄榄核神经元出现了明显病变。儿童暴露于城市空气污染会增加他们出现听觉和前庭损伤的风险。
