Abstract
The purpose of this study was to investigate the neurological integrity and physiological
status of the auditory brainstem tracts and nuclei in children with chronic lead (Pb)
exposure using non-invasive acoustic stapedius reflex (ASR) measurements of afferent
and efferent-neuromuscular auditory function. Following audiological examinations,
uncrossed (ipsilateral) and crossed (contralateral) brainstem ASR responses were evoked
by pure tone (500, 1000, and 2000 Hz), and broadband noise (bandwidth: 125–4000 Hz) stimulus activators. The ASR threshold (ASRT), amplitude growth, and decay/fatigue
were measured by conventional clinical middle ear immittance methods in a group of
Andean children (age range: 2–18 years) with a history of chronic environmental Pb exposure from occupational Pb glazing.
Blood lead (PbB) levels of the study group (n=117) ranged from 4.0 to 83.7 μg/dL with a mean PbB level of 33.5 μg/dL (SD: 23.6; median: 33.0: CDC III Classification). The PbB distribution data
indicated that 77.8% (n=91) of the children had PbB levels greater than the CDC action line of 10 μg/dL. Repeatable, normal ASRTs were elicited for ipsilateral (mean: ≤90 dB HL) and contralateral (mean: ≤97 dB HL) stimulation for each acoustic activator. Spearman Rho correlation analysis
indicated no significant association between PbB level and ipsilateral or contralateral
ASRT for any of the stimulus activators. The ASR amplitude growth results showed typical
growth functions with no Pb-associated aberrations. No statistical association was
found between ASR decay/adaptation (ASRD) and PbB level for any of the stimulus activators.
The results of stapedius muscle reflex testing using several stimulus activators showed
no significant relationship between PbB level and the physiological integrity of the
auditory brainstem mediated ASR responses in children with chronic Pb exposure and
elevated PbB levels.
Keywords
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Article info
Publication history
Published online: May 06, 2011
Accepted:
April 1,
2011
Received in revised form:
March 29,
2011
Received:
December 19,
2010
Identification
Copyright
© 2011 Published by Elsevier Inc.
