Background Noise exposure is the main cause of preventable hearing loss worldwide. Findings from animal studies suggest that even moderate noise exposure can cause substantial damage to the cochlear nerve without any noticeable hair cell damage. Crucially, such damage need not affect sensitivity to quiet sounds and therefore may be difficult to diagnose. It is currently unclear which are the most sensitive physiological measures for early identification of noise-induced damage to the auditory system. The NExpo Study is a cross-sectional cohort study focussing on physiological, behavioural, and magnetic resonance imaging (MRI) measures of the effects of noise exposure. Objective This paper introduces the NExpo Study, which aims to determine the functional and structural consequences of damage to the human peripheral and central auditory system resulting from cumulative lifetime noise exposure. The primary objective is to determine the neural correlates of noise exposure in the peripheral (cochlear nerve) and central (auditory brainstem and auditory cortex) auditory system. Secondary objectives are to assess the relative contributions of age and elevated audiometric thresholds to these observed neural correlates of damage, and the degree of association between structural and functional MRI measures of the auditory pathways and measures of peripheral and central auditory function. Methods and Analysis Lifetime noise exposure is estimated using the Noise Exposure Structured Interview. Auditory function is assessed using extended high-frequency audiometry, distortion-product otoacoustic emissions, middle ear muscle reflexes, the auditory brainstem response, and speech reception thresholds in noise. MRI measures include magnetic resonance neurography and Diffusion Tensor Imaging (DTI) of the cochlear nerve, and central measures of T1 myelination mapping, brain morphometry, DTI, and resting state functional MRI. The primary analyses employ between-group comparisons for these measures. Sample Description The project plans to recruit 200 healthy adult volunteers, in four groups of 50 participants, based on their pure-tone hearing thresholds and lifetime noise exposure. Group 1: 18-19 years, normal hearing and low noise exposure; Group 2: 30-50 years, normal hearing for their age and low noise exposure; Group 3: 30-50 years, normal hearing for their age and high noise exposure; Group 4: 30-50 years, suspected noise-induced hearing loss and high noise exposure. Conclusion Our comprehensive study, combining behavioural, physiological, and neuroimaging data, will contribute to the understanding of the mechanisms of auditory damage due to noise exposure. Results may inform diagnostic procedures, enabling the early identification of noise-induced auditory damage by detecting early changes in central auditory structure and processing. This approach could facilitate the provision of personalised advice regarding ear defence and monitoring for further damage, thus reducing the global impact of noise-induced auditory damage.