Air pollution is associated with brainstem auditory nuclei pathology and delayed brainstem auditory evoked potentials

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 amyloid1–42. 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.

► Environmental pollutants have detrimental effects upon the developing brain.
► We assessed brainstem inflammation in children exposed to air pollutants.
► Children from polluted environments had delays in BAEPs waves III and V.
► Auditory nuclei accumulated α synuclein and/or β amyloid1–42.
► Urban air pollution increases children's risk for auditory and vestibular impairment.