Does smoking affect cortical auditory evoked potentials in young adults?

Cigarette smoking has vascular and neurotoxic effects that may influence auditory function, and cortical auditory evoked potentials (CAEPs) can reveal subtle central auditory changes even when peripheral hearing thresholds remain within reference limits.

To investigate whether smoking influences CAEP responses in young adults with pure-tone hearing thresholds within reference limits.

This cross-sectional comparative study included 47 young adults (18-25 years) with bilateral air-conduction thresholds ≤20 dB HL, divided into smoker (n = 26) and non-smoker (n = 21) groups. All participants were right-handed and had type A tympanograms. CAEPs were recorded using 1 kHz tone-burst stimuli at 65 dB nHL, and absolute latencies (P1, N1, P2) and peak-to-peak amplitudes (P1-N1, N1-P2) were analyzed for each ear. Group differences were assessed using independent samples tests (p < 0.05).

Compared to non-smokers, smokers had significantly prolonged right-ear P1 latency (p = 0.024) and reduced P1-N1 and N1-P2 amplitudes bilaterally (Right: p < 0.001 and p = 0.007, respectively; Left: p = 0.003 and p = 0.009, respectively).

In normal-hearing young adults, cigarette smoking is associated with prolonged P1 latencies and reduced P1-N1/N1-P2 amplitudes. This indicates early thalamocortical disruption, highlighting CAEPs as sensitive markers for subclinical tobacco-induced auditory dysfunction.