| Autor: |
Sininger, Yvonne S., Condon, Carmen G., Gimenez, Lissete A., Shuffrey, Lauren C., Myers, Michael M., Elliott, Amy J., Thai, Tracy, Nugent, James D., Pini, Nicolò, Sania, Ayesha, Odendaal, Hein J., Angal, Jyoti, Tobacco, Deborah, Hoffman, Howard J., Simmons, Dwayne D., Fifer, William P. |
| Zdroj: |
Developmental Neuroscience; 2021, Vol. 43 Issue 6, p358-375, 18p |
| Abstrakt: |
Prenatal exposures to alcohol (PAE) and tobacco (PTE) are known to produce adverse neonatal and childhood outcomes including damage to the developing auditory system. Knowledge of the timing, extent, and combinations of these exposures on effects on the developing system is limited. As part of the physiological measurements from the Safe Passage Study, Auditory Brainstem Responses (ABRs) and Transient Otoacoustic Emissions (TEOAEs) were acquired on infants at birth and one-month of age. Research sites were in South Africa and the Northern Plains of the U.S. Prenatal information on alcohol and tobacco exposure was gathered prospectively on mother/infant dyads. Cluster analysis was used to characterize three levels of PAE and three levels of PTE. Repeated-measures ANOVAs were conducted for newborn and one-month-old infants for ABR peak latencies and amplitudes and TEOAE levels and signal-to-noise ratios. Analyses controlled for hours of life at test, gestational age at birth, sex, site, and other exposure. Significant main effects of PTE included reduced newborn ABR latencies from both ears. PTE also resulted in a significant reduction of ABR peak amplitudes elicited in infants at 1-month of age. PAE led to a reduction of TEOAE amplitude for 1-month-old infants but only in the left ear. Results indicate that PAE and PTE lead to early disruption of peripheral, brainstem, and cortical development and neuronal pathways of the auditory system, including the olivocochlear pathway. [ABSTRACT FROM AUTHOR] |
| Databáze: |
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