A perplexing question about noise-induced hearing loss is why some persons seem to be more affected by high intensity noise than others. Hawkins (1971) has shown noise-induced vasoconstriction to be implicated in noise-induced hearing loss in animals as evidenced by vascular changes within the inner ear and he asks the question: Are these changes caused by the noise itself or mediated by the autonomic nervous system (ANS)? Our research employed a plethysmograph to measure ANS mediated vasoconstriction during noise exposure. The subjects were stress prone males and females (Pattern A) whose behavior in noise was compared to non-stress prone males and females (Pattern B). The results indicated Pattern A males showed marked vasoconstriction in the presence of noise whereas Pattern B males did not. Pattern A females performed very much like Pattern A males with no statistical difference between these two groups. However, Pattern B females demonstrated a significant increase in vasoconstriction in the presence of noise and in this respect Pattern B females are different from Pattern B males. This difference possibly resulted from the use of a test to assess personality type which was intended for use with male subjects. The authors conclude there is strong evidence to suggest that being prone to stress in the presence of noise is a contributing factor to noise-induced hearing loss.

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Previous research found a relationship between stressprone personality (pattern A) and noise-induced vasoconstriction in normal-hearing adult subjects. The present research sought evidence for a possible relationship between susceptibility to high-frequency noise-induced permanent threshold shift (NIPTS) found among industrial workers and the vasoconstrictive behavior of the same workers when they were exposed to high-intensity noise. It was hypothesized that pattern A workers would show more vasoconstriction in the presence of high-intensity noise, and hence more susceptibility to NIPTS, than pattern B (non-stress-prone) workers. The 35 male subjects tested were divided into two groups. Group I contained 16 subjects who showed significant vasoconstriction in noise; group I subjects were clearly pattern A types. Group II contained 19 subjects who did not show significant vasoconstriction in noise. Group II contained mostly pattern B but a few pattern A subjects. Unexpectedly, it was the group II subjects who showed the most susceptibility to NIPTS; the difference between the means of the two groups was statistically significant ( p 2 0.001). The explanation for this unexpected finding is obscure.

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