The effects of early lead exposure on auditory function in rhesus monkeys $ Robert E. Lasky a, *, Melissa L. Luck b , Peter Torre III c , Nellie Laughlin b a Center for Clinical Research and Evidence-Based Medicine, University of Texas –Houston Medical School, 6431 Fannin Street, MSB 2.106, Houston, TX 77030-1503, USA b Harlow Center for Biological Psychology, University of Wisconsin– Madison, 22 North Charter St., Madison, WI 53715, USA c Department of Preventive Medicine, University of Wisconsin–Madison, 610 Walnut Street, 707 WARF, Madison, WI 53705, USA Received 1 June 2001; received in revised form 11 September 2001; accepted 11 September 2001 Abstract Thirty-one female rhesus monkeys were randomly assigned to three lead exposure conditions (none, birth to 1 year, and birth to 2 years). Blood lead levels were maintained at 35 – 40 mg/dl beginning shortly after birth and continuing for 1 or 2 years postnatally. Auditory function was assessed in these monkeys at least 1 year after exposure to lead. The outcome measures included tympanometry to assess middle ear function, otoacoustic emissions (OAEs) to assess cochlear function, and auditory brainstem-evoked responses (ABRs) to assess the auditory nerve and brainstem pathways. There were no significant differences among the three experimental groups for any of the tympanometric variables measured suggesting no effect of lead exposure on middle ear function. Suprathreshold and threshold distortion product OAEs (DPOAEs) were comparable among the three groups. Finally, the auditory-evoked response at levels from the auditory nerve to the cerebral cortex did not significantly differ as a function of lead exposure. The lead exposure in this study had little effect on auditory function. D 2001 Elsevier Science Inc. All rights reserved. Keywords: Lead; Rhesus monkeys; Tympanometry; Distortion product otoacoustic emissions; Auditory-evoked potentials 1. Introduction Lead is a potent neurotoxin at high body burden levels [15]. At lower body burdens, lead is associated with adverse outcomes including central nervous system deficits [3,8,13,15,38,42,43]. Legislation over the last three decades has effectively reduced lead exposure and body burdens in developed countries such as the United States [47]. How- ever, over that same time interval, threshold levels asso- ciated with insult have been revised downward consistent with ongoing research showing adverse effects at lower exposures. The Center for Disease Control has reduced the blood lead level (PbB) considered elevated from 60 mg/dl prior to 1971 to 10 mg/dl in 1991 [54]. Human studies suggest that the negative relationship between PbB and cognitive performance extends below 10 mg/dl to the limits of measurement [3,55]. Lead exposure has been associated with elevated hearing thresholds in children [56,57]. These results are apparent at very low levels of lead exposure with significant but small elevations in threshold at all frequencies tested. Other researchers have also reported elevated auditory thresholds in children with low levels of blood lead including concen- trations below 10 mg/dl [44]. In contrast, Buchanan et al. [4] and Counter et al. [6] have reported that two cohorts of Ecuadoran children with high PbB (mean of 40 mg/dl in one cohort and mean of 52 mg/dl in the other) had normal hearing thresholds. This lack of consistency of results also characterizes the small-sample-size studies concerning industrial lead exposure in adults [49]. There are several reasons these data are difficult to interpret. Children exposed to dangerous levels of envi- ronmental lead are likely to come from disadvantaged backgrounds. The reported relationship between lead and hearing may be explained in part or wholly by confounding 0892-0362/01/$ – see front matter D 2001 Elsevier Science Inc. All rights reserved. PII:S0892-0362(01)00175-1 $ This study was supported by NIH Grant No. RO1 ES0 6918 and a grant from the Center for Clinical Research and Evidence-Based Medicine. This study was conducted in accordance with national and institutional guidelines for the protection of animal welfare. * Corresponding author. Tel.: +1-713-500-5770; fax: +1-713-500-0519. E-mail address: robert.e.lasky@uth.tmc.edu (R.E. Lasky). Neurotoxicology and Teratology 23 (2001) 639– 649