THE AUTHORS REPLY

We thank Dr. Nordström for his observations (1). In the “Conclusion” section of our article, we stated, “[O]ur data support the hypothesis that loud noise exposure is a risk factor for acoustic neuroma. Further research is needed to validate self-reports of loud noise exposure and to evaluate the effect of potential detection bias” (2, p. 333). Thus, we did not conclude that loud noise exposure is a risk factor for acoustic neuroma; additional research is needed to draw such a firm conclusion.

In our article, we discussed in detail possible sources of bias, as well as potential biologic mechanisms based on animal-model experiments. Our study was not the first to suggest that loud noise might influence acoustic neuroma risk; a previous study using somewhat different methods, focusing on occupational loud noise exposure assessed by an occupational hygienist, reported risk increases of a similar or even higher magnitude (3). The authors of that study suggested a biologic mechanism for the development of acoustic neuroma following loud noise exposure, based on acoustic trauma research in birds.

Our study adds to the evidence suggesting a possible effect of loud noise exposure on acoustic neuroma development. However, further research is needed in which specific attention is paid to the potential sources of bias discussed. Whether hearing tests would be the best approach is not obvious; loud noise exposure—from a machine or explosion, for example—may occur primarily on one side of the head. A valid and objective measure of hearing loss would necessitate a prospective study, requiring an exceptionally large sample in order to evaluate a rare disease such as acoustic neuroma.

Note that loud noise was erroneously defined as >80 dB in our article; as the Journal stated in a subsequent erratum, the correct definition is ≥85 dB (4).

Conflict of interest: none declared.

References