The following factors have been implicated: 

missing acoustic reflex
previous sensorineural hearing loss
a bad general health state: bad cardiovascular function, insufficient intake of oxygen, a high platelet aggregation rate; and most importantly, a high viscosity of the blood
cigarette smoking
exposure to ototoxic chemicals (medication or environmental chemicals that can damage the ear), including certain solvents and heavy metals
type 2 diabetes

Diagnosis
Both NIHL caused by acoustic trauma and gradually-developed-NIHL can often be characterized by a specific pattern presented in audiological findings. NIHL is generally observed to decrease hearing sensitivity in the higher frequencies, also called an audiometric notch, especially at 4000 Hz, but sometimes at 3000 or 6000 Hz. The symptoms of NIHL are usually presented equally in both ears.This typical 4000 Hz notch is due to the transfer function of the ear. As does any object facing a sound, the ear acts as a passive filter, although the inner ear is not an absolute passive filter because the outer hair cells provide active mechanisms. A passive filter is a low pass: the high frequencies are more absorbed by the object because high frequencies impose a higher pace of compression-decompression to the object. The high frequency harmonics of a sound are more harmful to the inner-ear.However, not all audiological results from people with NIHL match this typical notch. Often a decline in hearing sensitivity will occur at frequencies other than at the typical 3000–6000 Hz range. Variations arise from differences in peoples ear canal resonance, the frequency of the harmful acoustic signal, and the length of exposure.
While healing, an over-expression of glutamate receptors can result in temporary tinnitus, or ringing in the ears. Repeated ruptures at the same synapse may eventually fail to heal, leading to permanent hearing loss.Prolonged exposure to high intensity noise has also been linked to the disruption of ribbon synapses located in the synaptic cleft between inner hair cells and spiral ganglion nerve fibers, leading to a disorder referred to as cochlear synaptopathy or hidden hearing loss. This disorder is cumulative and over time, leads to degeneration of the spiral ganglion cells of the inner ear and overall dysfunction in the neural transmission between auditory nerve fibers and the central auditory pathway. The most common symptom of cochlear synaptopathy is difficulty understanding speech, especially in the presence of competing noise. However, this type of hearing impairment is often undetectable by conventional pure tone audiometry, thus the name "hidden" hearing loss. Acoustic over-exposure can also result in decreased myelination at specific points on the auditory nerve. Myelin, an insulating sheath surrounding nerve axons, expedites electrical impulses along nerves throughout the nervous system. Thinning of the myelin sheath on the auditory nerve significantly slows the transmission of electrical signals from hair cell to auditory cortex, reducing comprehension of auditory stimuli by delaying auditory perception, particularly in noisy environments. Individual susceptibility towards noise
There appear to be large differences in individual susceptibility to NIHL.