Abstract

The effects of impulse noise of a relatively low peak level were examined to develop damage risk criteria for impulse noise. Eight to 13 normal male students (age: 20-24 years) were exposed to impulse noise. Peak levels of impulse noise were 100 dB (S.P.L.) and 105 dB (S.P.L.), B-duration of impulse noise being 10 ms, 50 ms, and 100 ms, and the repetition rates of impulse noise were 3 per 1 s and 1 per 3 s. Exposure time was 8 h in all exposure conditions. Exposure conditions of long B-duration induced greater TTS2 than those of short B-duration (P less than 0.05). Impulse noise exposure at a high peak level induced slightly larger TTS2 than that at a low peak level. TTS2 increased proportionally to the logarithm of the amount of impulse noise. Exposure to impulse noise induced smaller TTS2 than that of steady-state noise of an equal energy level. In addition, exposure to large amounts of impulse noise induced slightly greater urinary 17 OHCS levels than small amounts of impulse noise, and exposure to impulse noise induced smaller urinary 17 OHCS levels than steady-state noise of an equal energy level (P less than 0.05). The decreasing effect of the acoustic reflex on the acoustic energy of impulse noise was considered to be the reason for the results obtained. This experiment supported the modified CHABA Limit of Damage Risk Criteria of impulse noise proposed by the US Environmental Protection Agency.

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