Introduction Evidence for synergistic interaction between noise and styrene in inducing cochlear damage can be found in the literature. At present a mechanistic explanation of such an interaction is not available, although animal studies are shedding light on the phenomenon. At the aim of clarifying the effect of simultaneous exposure to noise (mild level) and styrene on the cochlear functionality, distortion product otoacoustic emissions (DPOAEs) were used as biomarkers of the cochlear status. In this work, the correlation between the DPOAE level and blood concentration of oxidative stress biomarkers is studied in a sample of subjects professionally exposed to styrene. This study is aimed at investigating the role of the oxidative stress in the inner ear damage in workers exposed to styrene.

Methods Nine subjects exposed to styrene in a fibreglass factory and eight control subjects were enrolled in this study. The mean age was the same in the exposed and control groups. The airborne concentration of styrene was evaluated by means of ambiental and personal samplers. The end shift urinary concentration of the phenylglyoxylic (PGA) and mandelic acid (MA) was also evaluated. Distortion product otoacoustic emissions were measured in the exposed workers and in a control group. The DPOAE component generated by a nonlinear mechanism, characterised by zero latency, and the long-latency component, generated by a linear reflection mechanism, were separately analysed, using a time-frequency domain wavelet filter for component unmixing.

The urinary concentration of the DNA and RNA oxidation products, namely 8-oxo-7,8-dihydroguanine (oxoGua), 8-oxo-7,8-dihydro-20-deoxyguanosine (oxodGuo), and 8-oxo-7,8-dihydroguanosine (oxoGuo), were evaluated and correlated to the DPOAE level.

Results A statistically significant negative correlation was found between the DPOAE level and the PGA and MA urinary concentration. A dose response relation was proposed correlating the styrene concentration, the exposure duration and the DPOAE level, used as outcome variables.

High levels of the oxidative damage biomarkers were found in the workers exposed to high levels of styrene. Significant negative correlation was found between the otoacoustic emission distortion component levels and the concentration of the oxoGuo biomarker.

Conclusions This experiment confirms that the styrene exposure is responsible for cochlear dysfunctionality. A quantitative relation between the styrene exposure and the reduction of cochlear functionality, expressed in terms of DPOAE amplitude, can be found. Exposure-induced damage of the cochlear amplifier is shown in the mid-frequency range, confirming the results of animal experiments, in which hair cells in the middle turn of the cochlea were damaged. Hearing damage is consistent with the outer hair cell apoptosis pathway associated with oxidative stress.