# Noise matters: assessing non-auditory health impacts of occupational noise exposure among factory workers

**Authors:** S. Krishnan, K. Priyasha, Manasi Bhattacharjee, Abhishek Sinha, Benzamin Hanse, Saklain Mustak Alam, Jyotirmoy Kalita

PMC · DOI: 10.3389/fpubh.2026.1753715 · Frontiers in Public Health · 2026-02-18

## TL;DR

This study shows that industrial noise not only harms hearing but also raises blood pressure, stress, and cognitive delays in factory workers.

## Contribution

The study provides empirical evidence of non-auditory health impacts of occupational noise exposure in an under-researched Indian industrial context.

## Key findings

- Occupational noise exposure significantly increases blood pressure, heart rate, and cortisol levels in factory workers.
- Noise exposure is associated with delayed visual and auditory reaction times, indicating impaired cognitive processing.
- Elevated blood glucose levels were observed in a significant proportion of workers after shifts in noisy environments.

## Abstract

Industrial noise exposure is a global occupational hazard, with increasing recognition of its deleterious non-auditory effects. Although the auditory consequences of excessive noise are well-known, an emerging body of evidence suggests significant impacts on cognition, cardiovascular and metabolic functions. India with a burgeoning industrial workforce and limited occupational health surveillance, remains under-researched in this domain.

This study investigates the physiological and sensory processing impact of occupational noise exposure among industrial workers in Guwahati, a rapidly industrializing region in Northeast India.

A longitudinal study was conducted involving 590 workers from various factories in Guwahati. Ambient noise levels were recorded using calibrated sound level meters. Workers were assessed before and after their work shifts for sensory processing (via reaction time tests), cardiovascular health (blood pressure and heart rate), metabolic health (blood glucose levels), and stress markers (blood cortisol). Ethical clearance was obtained from the Institutional Ethics Committee.

Noise levels across the industrial settings ranged from 62.2 dB(A) to 91.8 dB(A). High noise levels were particularly noted in batch manufacturing rooms and weighing machine areas. Significant post-shift increases were observed in systolic and diastolic blood pressure (mean increases of 13.2 mmHg and 9.3 mmHg respectively, p < 0.001), heart rate (mean increase of 4.5 bpm, p < 0.001), visual reaction time (mean increase of 50 ms, p < 0.001), and auditory reaction time (mean increase of 50 ms, p < 0.001). Cortisol levels also rose significantly (mean increase of 15.8 ng/mL, p < 0.001), and elevated blood glucose was observed in a substantial proportion of workers post-shift. Regression analysis demonstrated moderate positive associations between noise exposure and reaction times (visual reaction time: R2 = 0.48; auditory reaction time: R2 = 0.32), indicating delayed cognitive responses with increasing noise levels.

The study demonstrates significant non-auditory impacts of occupational noise exposure, suggesting impaired cognition, heightened physiological stress, and acute alterations in metabolic markers among industrial workers. These findings highlight the need for preventive noise management strategies and short-term occupational health monitoring, engineering controls, and routine health surveillance to mitigate these effects.

Our findings demonstrate the need for factories to adopt effective noise control measures such as engineering modifications, administrative controls, and mandatory hearing protection. These steps can reduce workers’ noise exposure, minimizing physiological stress and cognitive impairments, and thus improve overall occupational health and productivity.

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}
- **Diseases:** fatigue (MESH:D005221), cardiovascular strain (MESH:D013180), metabolic disorders (MESH:D008659), hearing loss (MESH:D034381), metabolic dysregulation (MESH:D021081), sleep disturbances (MESH:D012893), metabolic disturbances (MESH:D024821), hyperglycemia (MESH:D006943), metabolic disruption (MESH:D019958), responses (MESH:D018746), auditory damage (MESH:D001304), noise (MESH:D014012), neurological, psychiatric, or cardiovascular disorders (MESH:D001523), diabetic (MESH:D003920), dysfunction (MESH:D006331), type 2 diabetes (MESH:D003924), NIHL (MESH:D006317), cognitive dysfunctions (MESH:D003072), blood pressure (MESH:D006973), insulin insensitivity (MESH:D007333), cardiovascular dysfunction (MESH:D002318), attention deficits (MESH:D001289), ischemic heart disease (MESH:D017202)
- **Chemicals:** blood glucose (MESH:D001786), adrenaline (MESH:D004837), Cortisol (MESH:D006854), glucose (MESH:D005947), catecholamines (MESH:D002395)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

21 references — full list in the complete paper: https://tomesphere.com/paper/PMC12957204/full.md

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Source: https://tomesphere.com/paper/PMC12957204