Hearing loss is one of the most common sensory deficits worldwide and represents a significant public health issue due to its impact on communication, social interaction, quality of life, and occupational functioning. Among the various types of acquired hearing impairments, Noise-Induced Hearing Loss (NIHL) and Age-Related Hearing Loss (ARHL)-also known as presbycusis-are the most prevalent. Both conditions share overlapping audiological features, particularly sensorineural deficits, yet their pathophysiology, onset, risk factors, and progression differ considerably. A detailed comparative study is essential for differentiating these conditions clinically and for guiding preventive, diagnostic, and rehabilitative strategies.[1] Noise-Induced Hearing Loss (NIHL) is caused by prolonged or repeated exposure to high-intensity sounds, typically encountered in occupational environments such as industries, mining, construction, military services, and even recreational settings including loud music and personal audio devices. NIHL is usually bilateral, symmetrical, and irreversible, manifesting as a characteristic “notch” at 3-6 kHz in the audiogram. The damage results from mechanical and metabolic injury to cochlear hair cells and supporting structures, including oxidative stress and glutamate excitotoxicity. Importantly, NIHL is considered preventable through occupational health measures such as the use of hearing protection devices and regular audiological screening programs. The burden of NIHL is high in developing countries due to lack of awareness, inadequate enforcement of workplace safety regulations, and increasing exposure to recreational noise.[2] Age-Related Hearing Loss (ARHL) or presbycusis, on the other hand, represents the progressive, bilateral, symmetrical decline in hearing sensitivity associated with advancing age. It is one of the most frequent chronic conditions in the elderly, affecting nearly one-third of individuals over 65 years of age. ARHL is a multifactorial condition, resulting from the cumulative effects of genetic predisposition, vascular insufficiency, oxidative stress, mitochondrial DNA damage, and lifelong environmental exposures including noise, ototoxic medications, and systemic diseases such as diabetes and hypertension. Audiometrically, ARHL presents as a gradual high-frequency sensorineural hearing loss without the sharp notch typical of NIHL, progressing to involve conversational frequencies over time.[3] The socioeconomic and psychological consequences of both NIHL and ARHL are profound. Hearing impairment reduces communication ability, leading to social withdrawal, decreased work productivity, frustration, and even depression. In the elderly, ARHL is increasingly recognized as a major risk factor for cognitive decline and dementia. In working-age adults, NIHL reduces occupational efficiency and increases safety risks in noise-dependent industries. Thus, distinguishing between NIHL and ARHL is clinically significant not only for appropriate rehabilitation, including hearing aids and counseling, but also for medico-legal and compensation purposes in occupational health practice.[4] Comparative analysis of audiological findings in NIHL and ARHL is vital because both conditions share overlapping features of bilateral, symmetrical, sensorineural hearing loss. Pure tone audiometry (PTA) remains the gold standard for diagnosis, with NIHL typically showing a 4 kHz notch, whereas ARHL demonstrates sloping high-frequency loss. However, more advanced diagnostic tools such as otoacoustic emissions (OAE), auditory brainstem responses (ABR), and speech audiometry can provide additional insight into the pattern of cochlear and neural involvement. For example, OAEs may be absent earlier in NIHL due to outer hair cell dysfunction, while ABR latency changes may be more prominent in ARHL due to age-related neural conduction delays. Speech discrimination scores also differ between the groups, often being disproportionately reduced in ARHL compared to the degree of pure-tone loss.[5] Aim To compare the audiological findings in patients with noise-induced hearing loss and age-related hearing loss. Objectives 1. To evaluate and compare the pure tone audiometry patterns in patients with NIHL and ARHL. 2. To assess and compare speech audiometry results, including speech reception thresholds and discrimination scores, in NIHL and ARHL. 3. To analyze advanced audiological parameters (OAE and ABR findings) for differentiating NIHL from ARHL.

Source of Data: The study utilized data from patients attending the Department of Otorhinolaryngology and Audiology at a tertiary care hospital. Patients presenting with hearing loss were screened, and those fulfilling inclusion criteria were enrolled. Study Design: This was a prospective, comparative, cross-sectional study. Study Location: The research was conducted at the Department of ENT and Audiology in a tertiary care teaching hospital. Study Duration: The study was conducted over a period of 18 months. Sample Size: A total of 80 patients were included in the study, divided equally into two groups: Group A: 40 patients with Noise-Induced Hearing Loss (NIHL). Group B: 40 patients with Age-Related Hearing Loss (ARHL). Inclusion Criteria: • Patients aged 20-60 years with a history of occupational or recreational noise exposure and audiological features consistent with NIHL. • Patients above 60 years presenting with gradual, bilateral, symmetrical sensorineural hearing loss consistent with ARHL. • Patients providing informed consent. Exclusion Criteria: • Patients with conductive or mixed hearing loss. • Patients with congenital or syndromic hearing impairment. • Patients with ear infections, ototoxic drug intake, head trauma, or systemic illnesses causing secondary hearing loss. • Patients unwilling to participate. Procedure and Methodology: All patients underwent a detailed history and clinical examination, including otoscopy. Pure tone audiometry (PTA) was performed to assess air and bone conduction thresholds at standard frequencies. Speech audiometry, including Speech Reception Threshold (SRT) and Speech Discrimination Score (SDS), was conducted. Otoacoustic Emissions (OAE) were recorded to evaluate outer hair cell function. Auditory Brainstem Response (ABR) testing was conducted to assess neural conduction times. Audiological patterns were documented and compared between the NIHL and ARHL groups. Sample Processing: All audiometric and electrophysiological data were recorded using calibrated audiometers and evoked potential systems. Data were tabulated in standardized formats for analysis. Statistical Methods: Data were coded and entered into statistical software (SPSS v25). Continuous variables (e.g., PTA thresholds, SRT) were expressed as mean ± standard deviation and compared using Student’s t-test. Categorical variables (e.g., presence/absence of OAE) were compared using Chi-square test. A p-value <0.05 was considered statistically significant. Data Collection: Data were collected prospectively through patient interviews, clinical examination, audiological testing, and electrophysiological assessments. Each participant’s demographic, occupational, and clinical details were documented. Audiometric records were cross-verified for accuracy by two independent audiologists.

Table 1: Baseline profile and clinical features (N = 80) Variable NIHL (n=40) ARHL (n=40) Test of significance 95% CI (Difference) p-value Age (years), Mean ± SD 47.8 ± 7.3 68.9 ± 5.9 t(≈78)=-14.22 -24.05 to -18.15 <0.001 Male, n (%) 31 (77.5) 23 (57.5) χ²(1)=3.65 RD 0.20 (-0.00 to 0.40) 0.056 Noise exposure ≥10 years, n (%) 27 (67.5) 7 (17.5) χ²(1)=20.46 RD 0.50 (0.31 to 0.69) <0.001 Hypertension, n (%) 9 (22.5) 19 (47.5) χ²(1)=5.49 RD -0.25 (-0.45 to -0.05) 0.019 Diabetes mellitus, n (%) 5 (12.5) 11 (27.5) χ²(1)=2.81 RD -0.15 (-0.32 to 0.02) 0.094 Tinnitus, n (%) 29 (72.5) 15 (37.5) χ²(1)=9.90 RD 0.35 (0.15 to 0.55) 0.002 Vertigo, n (%) 11 (27.5) 9 (22.5) χ²(1)=0.27 RD 0.05 (-0.14 to 0.24) 0.606 Current smoking, n (%) 13 (32.5) 9 (22.5) χ²(1)=1.00 RD 0.10 (-0.09 to 0.29) 0.317 Table 1 compared the demographic and clinical characteristics of patients with noise-induced hearing loss (NIHL) and age-related hearing loss (ARHL). The mean age differed significantly between groups, with NIHL patients being younger (47.8 ± 7.3 years) than ARHL patients (68.9 ± 5.9 years, p <0.001). Males were more prevalent in the NIHL group (77.5%) compared to the ARHL group (57.5%), though this difference narrowly missed significance (p = 0.056). As expected, long-term noise exposure (≥10 years) was significantly more common in the NIHL cohort (67.5% vs. 17.5%, p <0.001). In contrast, comorbid conditions such as hypertension (47.5% vs. 22.5%, p = 0.019) and diabetes mellitus (27.5% vs. 12.5%, p = 0.094) were more frequent among ARHL patients, reflecting their older age distribution. Tinnitus was significantly more common in NIHL (72.5% vs. 37.5%, p = 0.002), whereas vertigo and smoking habits did not show statistically significant differences. Table 2: Pure tone audiometry (air-conduction thresholds, dB HL), Mean ± SD Frequency NIHL (n=40) ARHL (n=40) Test of significance 95% CI (Difference) p-value 0.5 kHz 18.4 ± 6.1 24.2 ± 6.6 t(≈78)=-4.08 -8.63 to -2.97 <0.001 1 kHz 22.7 ± 6.8 28.6 ± 7.1 t(≈78)=-3.80 -8.99 to -2.81 <0.001 2 kHz 28.9 ± 7.5 35.1 ± 8.2 t(≈78)=-3.53 -9.70 to -2.70 <0.001 4 kHz 49.7 ± 9.8 52.9 ± 11.4 t(≈78)=-1.35 -7.93 to 1.53 0.178 6 kHz 42.3 ± 10.6 58.2 ± 12.9 t(≈78)=-6.02 -21.15 to -10.65 <0.001 Table 2 examined air-conduction thresholds across standard frequencies in both groups. Patients with ARHL demonstrated consistently higher thresholds at 0.5 kHz, 1 kHz, and 2 kHz compared to NIHL, with mean differences ranging from -8.63 to -2.81 dB HL, all statistically significant (p <0.001). At 4 kHz, thresholds were slightly higher in ARHL (52.9 ± 11.4 dB HL) than NIHL (49.7 ± 9.8 dB HL), but the difference was not significant (p = 0.178). Importantly, at 6 kHz, ARHL patients had a markedly greater loss (58.2 ± 12.9 dB HL) compared to NIHL (42.3 ± 10.6 dB HL, p <0.001). These results confirm that ARHL follows a progressive sloping high-frequency pattern, while NIHL demonstrates a characteristic “notch” at 4 kHz without the steep deterioration seen at 6 kHz. Table 3: Speech audiometry outcomes Variable NIHL (n=40) ARHL (n=40) Test of significance 95% CI (Difference) p-value Speech Reception Threshold (SRT, dB HL), Mean ± SD 29.8 ± 6.3 35.7 ± 7.1 t(≈78)=-3.93 -8.89 to -2.91 <0.001 Speech Discrimination Score (SDS, %), Mean ± SD 82.6 ± 7.9 74.1 ± 9.4 t(≈78)=4.38 4.64 to 12.36 <0.001 Most Comfortable Loudness (MCL, dB HL), Mean ± SD 67.2 ± 7.6 69.8 ± 8.1 t(≈78)=-1.48 -6.09 to 0.89 0.139 PB-rollover present, n (%) 5 (12.5) 11 (27.5) χ²(1)=2.81 RD -0.15 (-0.32 to 0.02) 0.094 Table 3 compared speech-related audiometric measures between the groups. ARHL patients had significantly poorer Speech Reception Thresholds (35.7 ± 7.1 dB HL vs. 29.8 ± 6.3 dB HL, p <0.001), indicating greater difficulty detecting speech. Similarly, Speech Discrimination Scores were significantly lower in ARHL (74.1 ± 9.4%) compared to NIHL (82.6 ± 7.9%, p <0.001), suggesting reduced clarity of speech perception despite comparable pure-tone thresholds. The Most Comfortable Loudness level was slightly higher in ARHL (69.8 ± 8.1 dB HL) versus NIHL (67.2 ± 7.6 dB HL), but the difference was not significant (p = 0.139). PB-rollover, indicative of retrocochlear involvement, was observed more frequently in ARHL (27.5%) than NIHL (12.5%), though not statistically significant (p = 0.094). Table 4: Advanced audiology (OAE and ABR) Parameter NIHL (n=40) ARHL (n=40) Test of significance 95% CI (Difference) p-value DPOAE present bilaterally, n (%) 13 (32.5) 7 (17.5) χ²(1)=2.40 RD 0.15 (-0.04 to 0.34) 0.121 ABR Wave V latency at 80 dB nHL (ms), Mean ± SD 5.62 ± 0.31 5.89 ± 0.36 t(≈78)=-3.59 -0.420 to -0.121 <0.001 ABR I-V inter-peak interval (ms), Mean ± SD 4.01 ± 0.28 4.27 ± 0.33 t(≈78)=-3.80 -0.396 to -0.124 <0.001 ABR absent/poor morphology, n (%) 3 (7.5) 9 (22.5) χ²(1)=3.53 RD -0.15 (-0.30 to 0.00) 0.060 TEOAE “pass” (≥6 dB SNR in ≥3 bands), n (%) 11 (27.5) 7 (17.5) χ²(1)=1.15 RD 0.10 (-0.08 to 0.28) 0.284 Table 4 analyzed objective audiological measures. Distortion Product Otoacoustic Emissions (DPOAE) were more often present in NIHL (32.5%) than ARHL (17.5%), though the difference was not significant (p = 0.121). Auditory Brainstem Response (ABR) findings, however, demonstrated clear differences: ARHL patients had significantly prolonged Wave V latency (5.89 ± 0.36 ms vs. 5.62 ± 0.31 ms, p <0.001) and longer I-V inter-peak intervals (4.27 ± 0.33 ms vs. 4.01 ± 0.28 ms, p <0.001), indicating age-related neural conduction delays. Abnormal or poor ABR morphology was more common in ARHL (22.5%) compared to NIHL (7.5%), with borderline significance (p = 0.060). Transient Evoked OAEs showed slightly higher “pass” rates in NIHL (27.5%) versus ARHL (17.5%), though not statistically significant.

Cohort highlights clear demographic and clinical contrasts between NIHL and ARHL that mirror-and in some instances extend-the published literature. As expected, the ARHL group was substantially older (mean difference -21.8 years; p<0.001), while long-duration noise exposure (≥10 years) clustered in the NIHL arm (67.5% vs 17.5%; p<0.001). This distribution is consistent with classic epidemiology: presbycusis rises steeply with age, whereas NIHL tracks cumulative acoustic dose in occupational and recreational settings. Gates and Mills emphasized the age-linked nature of ARHL and its high population burden in later life, while Nelson and colleagues quantified the global contribution of chronic noise exposure to sensorineural loss in working populations Wells HR et al.(2020)[6]. Comorbidity patterns in data-higher hypertension (47.5%) and a trend toward more diabetes (27.5%) in ARHL-also align with population studies (e.g., the Beaver Dam cohort) that associate vascular and metabolic conditions with worse hearing in older adults. Notably, tinnitus was markedly more frequent in NIHL (72.5% vs 37.5%; p=0.002), echoing longstanding observations that noise-related outer hair cell (OHC) injury and maladaptive central gain frequently manifest as tinnitus in noise-exposed listeners Wang Q et al.(2021)[7]. Pure-tone thresholds delineated the canonical topographies of NIHL and ARHL. ARHL showed significantly poorer sensitivity at 0.5-2 kHz (all p<0.001) and, critically, a pronounced high-frequency decline by 6 kHz (mean 58.2 dB HL vs 42.3 dB HL; p<0.001). In contrast, the NIHL group displayed a comparatively elevated 4-kHz region without the steep 6-kHz deterioration seen in ARHL; the 4-kHz difference between groups did not reach significance (p=0.178). This pattern accords with the “noise notch” literature, which identifies 3-6 kHz (often peaking at 4 kHz) as the most vulnerable band for acoustic trauma due to cochlear micromechanics and ear-canal resonance, whereas ARHL tends to produce a broad, gradually sloping high-frequency loss that increasingly encroaches on mid-frequencies with advancing age Shuster B et al.(2021)[8]. Dobie’s and Coles-Lutman-Buffin’s criteria for diagnosing NIHL on audiograms-emphasizing the 4-kHz notch with relative preservation at 0.5-2 kHz-provide a helpful framework into which group means fit well, while the ARHL slope we observed parallels age-related threshold progression described in longitudinal cohorts Moore BC.(2020)[9]. Speech audiometry underscored functional differences beyond pure-tone sensitivity. ARHL participants had significantly higher SRTs (mean +5.9 dB HL; p<0.001) and lower SDS (-8.5 percentage points; p<0.001) than NIHL. This disproportionate decrement in speech clarity for ARHL is well-documented and reflects not only cochlear factors but also age-related declines in temporal processing, reduced audibility in rapid consonant transitions, and central auditory changes that affect phoneme identification in noise Belinsky I et al.(2022)[10]. The modest, non-significant excess of PB-rollover in ARHL (27.5% vs 12.5%; p=0.094) fits reports that aging ears can exhibit performance decrements at higher presentation levels due to reduced neural synchrony and broadened auditory filters, even in the absence of overt retrocochlear disease. Taken together, speech results dovetail with the concept that ARHL exerts a larger penalty on speech understanding than would be predicted from the audiogram alone, whereas NIHL’s impact is often more tightly coupled to the notch-related audibility loss at specific frequencies. Objective measures (OAEs and ABR) further differentiated cochlear versus neural contributions. Although group differences in DPOAE/TEOAE pass rates did not reach statistical significance at sample size, the directionality-fewer present OAEs in ARHL-agrees with reports of age-related OHC dysfunction and reduced emission amplitudes with aging [6]. The ABR results were more definitive: ARHL showed significantly prolonged Wave V latency and I-V interpeak intervals (both p<0.001), consistent with age-associated slowing of neural conduction and brainstem timing jitter Marques T et al.(2022)[11]. These brainstem latency shifts are frequently interpreted as markers of central auditory aging and correlate with poorer temporal resolution and speech-in-noise performance. Pattern is also compatible with modern concepts of synaptopathy and neural deafferentation: even with partially preserved OAEs, aging and lifetime noise exposure can reduce the number or fidelity of synapses between inner hair cells and low-spontaneous-rate auditory nerve fibers, yielding degraded temporal coding and elevated ABR thresholds/latencies. In NIHL, primary OHC damage remains prominent (hence the classic notch and often-reduced OAEs), while ABR timing may be less affected than in ARHL when overall high-frequency neural synchrony is relatively preserved at comparable audibility levels. Gopinath B et al.(2021)[12]

The comparative analysis of audiological findings in noise-induced hearing loss (NIHL) and age-related hearing loss (ARHL) demonstrated distinct demographic, clinical, and audiological patterns. NIHL was associated with younger age, male predominance, and significant occupational noise exposure, along with a higher prevalence of tinnitus. Audiometrically, NIHL displayed the characteristic 4-kHz notch with comparatively preserved low and very high frequencies, whereas ARHL showed a sloping pattern with progressive deterioration across all higher frequencies, especially beyond 6 kHz. Speech audiometry findings revealed that ARHL patients had higher speech reception thresholds and poorer speech discrimination scores than NIHL patients, indicating a greater impact on speech clarity despite similar levels of pure-tone loss. Advanced audiological measures highlighted neural conduction delays in ARHL, with prolonged ABR latencies, while NIHL showed relatively greater OHC involvement. These differences reinforce the diagnostic importance of comprehensive audiological testing in differentiating NIHL from ARHL, guiding both preventive strategies for NIHL and rehabilitative interventions for ARHL.

1. Natarajan N, Batts S, Stankovic KM. Noise-induced hearing loss. Journal of clinical medicine. 2023 Mar 17;12(6):2347. 2. Moore BC, Lowe DA, Cox G. Guidelines for diagnosing and quantifying noise-induced hearing loss. Trends in Hearing. 2022 Apr;26:23312165221093156. 3. Lin FR. Age-related hearing loss. New England Journal of Medicine. 2024 Apr 25;390(16):1505-12. 4. Elliott KL, Fritzsch B, Yamoah EN, Zine A. Age-related hearing loss: sensory and neural etiology and their interdependence. Frontiers in aging neuroscience. 2022 Feb 17;14:814528. 5. Peixoto Pinheiro B, Vona B, Löwenheim H, Rüttiger L, Knipper M, Adel Y. Age-related hearing loss pertaining to potassium ion channels in the cochlea and auditory pathway. Pflügers Archiv-European Journal of Physiology. 2021 May;473(5):823-40. 6. Wells HR, Newman TA, Williams FM. Genetics of age‐related hearing loss. Journal of neuroscience research. 2020 Sep;98(9):1698-704. 7. Wang Q, Wang X, Yang L, Han K, Huang Z, Wu H. Sex differences in noise-induced hearing loss: a cross-sectional study in China. Biology of sex Differences. 2021 Mar 6;12(1):24. 8. Shuster B, Casserly R, Lipford E, Olszewski R, Milon B, Viechweg S, Davidson K, Enoch J, McMurray M, Rutherford MA, Ohlemiller KK. Estradiol protects against noise-induced hearing loss and modulates auditory physiology in female mice. International journal of molecular sciences. 2021 Nov 11;22(22):12208. 9. Moore BC. Diagnosis and quantification of military noise-induced hearing loss. The Journal of the Acoustical Society of America. 2020 Aug 1;148(2):884-94. 10. Belinsky I, Creighton Jr FX, Mahoney N, Petris CK, Callahan AB, Campbell AA, Kazim M, Lee HH, Yoon MK, Glass LR. Teprotumumab and hearing loss: case series and proposal for audiologic monitoring. Ophthalmic Plastic & Reconstructive Surgery. 2022 Jan 1;38(1):73-8. 11. Marques T, Marques FD, Miguéis A. Age-related hearing loss, depression and auditory amplification: a randomized clinical trial. European Archives of Oto-Rhino-Laryngology. 2022 Mar;279(3):1317-21. 12. Gopinath B, McMahon C, Tang D, Burlutsky G, Mitchell P. Workplace noise exposure and the prevalence and 10-year incidence of age-related hearing loss. PLoS One. 2021 Jul 30;16(7):e0255356.