The effects of lead on otoacoustic emissions and auditory evoked potentials in monkeys.

Neurology Department, University of Wisconsin-Madison Medical School, 53792-5132, USA.
Neurotoxicology and Teratology (Impact Factor: 2.76). 01/1995; 17(6):633-44.
Source: PubMed


Auditory functioning was assessed in two groups of adult rhesus monkeys (11 years of age). One (n = 11) received modest exposure to lead early in life and the other (n = 8) served as controls and did not receive any lead supplementation. Two lead-exposed monkeys had abnormal distortion product otoacoustic emissions (DPEs) and smaller amplitude or absent evoked potentials. These monkeys had abnormal distortion product otoacoustic emission (DPEs) and smaller amplitude or absent evoked potentials. These monkeys had the highest blood levels recorded in their respective groups. For the remaining lead-exposed monkeys there was little difference between their DPEs and the DPEs of the control monkeys with one exception. DPE amplitudes of the control monkeys increased more rapidly as a function of stimulus level than those of the lead-exposed monkeys at most frequencies. There was also a significant but modest effect of lead exposure on the auditory brain stem evoked responses (ABRs) of these lead-exposed monkeys. There was no apparent effect on the middle latency evoked responses (MLRs), although that result could be due to the relatively greater variability of the MLR.

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    • "There are several nonhuman primate experimental studies that are relevant to the issue of whether Pb exposure produces sensory hearing impairment. Lasky et al. (1995) investigated DPOAE in monkeys (Macaca mulatta) exposed to Pb early in life and found that only 2 of 11 Pb-exposed monkeys had abnormal DPOAE (1 of the 2 monkeys was later discovered to have a conductive hearing loss [Lasky et al., 2001a]). In follow-up investigations, using DPOAE and other physiologic auditory measures with monkeys, no evidence was found for Pb effects on middle ear, auditory sensory or auditory neural functioning (Lasky et al., 2001a, 2001b). "
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    ABSTRACT: Studies relating sensory hearing impairment to lead (Pb) exposure in children have presented inconsistent results. The objective of this study was to measure distortion product otoacoustic emissions (DPOAE), sounds emanating from the outer hair cells of the inner ear, in Pb-exposed children to determine the effects of Pb poisoning on the inner ear. DPOAE were recorded for 9 f(2) frequencies from 1187 to 7625 Hz on 102 ears of 53 Pb-exposed children (aged 6-16 yr) residing in Pb-contaminated environments in the Andes Mountains of Ecuador where Pb glazing of ceramics is the primary livelihood. Blood lead (PbB) levels ranged from 4.2 to 94.3 μg/dl (mean: 37.7; SD: 25.7; median: 36.4). The median PbB level was markedly higher than the Centers for Disease Control and Prevention (CDC) and World Health Organization (WHO) 10-μg/dl action level. Spearman rho correlation analyses of the relation between PbB level and DPOAE amplitude and between PbB level and DPOAE signal-to-noise ratio revealed no significant associations at any of the f(2) frequencies tested. In addition, no significant correlation (Spearman rho) between PbB level and hearing sensitivity for 6 pure-tone test frequencies from 1000 to 8000 Hz was found. Although the study group was found to have abnormally elevated PbB levels, in contrast to some earlier reports, the results of the current study showed no consistent Pb-induced sensory effects on the cochlea of Pb-intoxicated children.
    Journal of Toxicology and Environmental Health Part A 10/2011; 74(19):1280-93. DOI:10.1080/15287394.2011.587106 · 2.35 Impact Factor
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    • "Lead exposure is known to generate ROS (Ahamed et al., 2007; Gurer et al., 2000): (a) inhibition of delta-aminolevulinic acid dehydratase by lead can cause accumulation of delta-aminolevulinic acid, which can be readily oxidized to generate ROS; (b) high affinity for sulfhydryl groups by lead may lead to depletion of glutathione and protein-bound sulfhydryl groups, resulting in the production of ROS; (c) lead can provoke ferrous ion-initiated membrane lipid peroxidation. Other potential mechanisms have been proposed, such as neuro-ototoxic effects of lead on the auditory brainstem and cochlea (Bertoni et al., 1988; Lasky et al., 1995; Yamamura et al., 1989). Lead also has the ability to inhibit ion flow through calcium channels (Audesirk, 1993; Garza et al., 2006), and disrupted plasma membrane calcium pump is associated with loss of sensory hair cells and hearing loss (Brini, 2009; Schultz et al., 2005; Shull et al., 2003; Spiden et al., 2008). "
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    ABSTRACT: Although lead has been associated with hearing loss in occupational settings and in children, little epidemiologic research has been conducted on the impact of cumulative lead exposure on age-related hearing loss in the general population. We determined whether bone lead levels, a marker of cumulative lead exposure, are associated with decreased hearing ability in 448 men from the Normative Aging Study, seen between 1962 and 1996 (2264 total observations). Air conduction hearing thresholds were measured at 0.25-8 kHz and pure-tone averages (PTA) (mean of 0.5, 1, 2 and 4 kHz) were computed. Tibia and patella lead levels were measured using K X-ray fluorescence between 1991 and 1996. In cross-sectional analyses, after adjusting for potential confounders including occupational noise, patella lead levels were significantly associated with poorer hearing thresholds at 2, 3, 4, 6 and 8 kHz and PTA. The odds of hearing loss significantly increased with patella lead levels. We also found significant positive associations between tibia lead and the rate change in hearing thresholds at 1, 2, and 8 kHz and PTA in longitudinal analyses. Our results suggest that chronic low-level lead exposure may be an important risk factor for age-related hearing loss and reduction of lead exposure could help prevent or delay development of age-related hearing loss.
    Hearing research 10/2010; 269(1-2):48-55. DOI:10.1016/j.heares.2010.07.004 · 2.97 Impact Factor
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    • "With a maximum life expectancy of approximately 40 years in captivity (Tigges et al., 1988), rhesus monkeys are a long-lived species that experience many of the same age-related diseases as humans do (Roth et al., 2004). Auditory function in the monkeys also approaches that of humans, including middle ear (Fowler et al., 2008; Torre, Lasky, and Fowler, 2000), cochlear, (Lasky, Beach, and Laughlin, 2002), and neural function (Fowler, Torre, and Kemnitz, 2002; Lasky, Maier, Snodgrass, Hecox, and Laughlin, 1995). "
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    ABSTRACT: Caloric restriction (CR) slows aging in many species and protects some animals from age-related hearing loss (ARHL), but the effect on humans is not yet known. Because rhesus monkeys are long-lived primates that are phylogenically closer to humans than other research animals are, they provide a better model for studying the effects of CR in aging and ARHL. Subjects were from the pool of 55 rhesus monkeys aged 15-28 years who had been in the Wisconsin study on CR and aging for 8-13.5 years. Distortion product otoacoustic emissions (DPOAE) with f2 frequencies from 2211 to 8837 Hz and auditory brainstem response (ABR) thresholds from clicks and 8, 16, and 32 kHz tone bursts were obtained. DPOAE levels declined linearly at approximately 1 dB/year, but that rate doubled for the highest frequencies in the oldest monkeys. There were no interactions for diet condition or sex. ABR thresholds to clicks and tone bursts showed increases with aging. Borderline significance was shown for diet in the thresholds at 8 kHz stimuli, with monkeys on caloric restriction having lower thresholds. Because the rhesus monkeys have a maximum longevity of 40 years, the full benefits of CR may not yet be realized.
    Hearing research 03/2010; 261(1-2):75-81. DOI:10.1016/j.heares.2010.01.006 · 2.97 Impact Factor
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