Key result
Occupational noise exposure linked to ~2-mmHg higher SBP in female workers.
Why the study?
Occupational noise exposure may activate stress-related hormone pathways and increase cardiovascular risk in women, leaving uncertain whether stress hormones mediate the associations between occupational noise exposure and blood pressure and HR in female workers.
Does occupational cumulative noise exposure increase blood pressure and alter heart rate via stress hormone mediation in female manufacturing workers?
Cross-Sectional (n=906)
Does occupational cumulative noise exposure increase blood pressure and alter heart rate via stress hormone mediation in female manufacturing workers?
Occupational noise exposure is independently associated with elevated systolic and diastolic blood pressure and reduced heart rate in female workers, especially above ~80 dB(A)-year, though this association is not statistically mediated by circulating stress hormones.
Answers are grounded in this paper and cite their sources.
Occupational noise was associated with higher BP and lower HR in female workers independent of stress hormones; hypothesis-generating and should not yet change practice.
BACKGROUND: Occupational noise exposure may activate stress-related hormone pathways and increase cardiovascular risk in women. This study aimed to investigate whether stress hormones mediate the associations between occupational noise exposure and blood pressure and heart rate (HR) in female workers. METHODS: A total of 906 female manufacturing workers in Tianjin, China, were enrolled, including 299 controls and 607 noise-exposed workers. The associations between cumulative noise exposure (CNE) and systolic blood pressure (SBP), diastolic blood pressure (DBP), and HR were evaluated using generalized additive models and restricted cubic splines (RCS). Threshold effects were further assessed. A subsample of 140 participants was selected for the measurement of six stress hormones: dopamine, norepinephrine, epinephrine, cortisol, antidiuretic hormone (ADH), and oxytocin. Mediation analyses were conducted to determine whether these hormones mediated the associations between occupational noise exposure (noise-exposed vs. control) and blood pressure or HR. RESULTS: Compared with the control group, the noise-exposed group exhibited significantly higher SBP ( β = 2.34, 95% confidence interval [CI]: 0.01-4.59) and DBP ( β = 1.90, 95% CI: 0.22-3.57), as well as a significantly lower HR ( β = -2.44, 95% CI: -4.17 to -0.71). RCS analyses revealed significant increases in both SBP and DBP as CNE exceeded the threshold values of 80.69 and 79.49 dB(A)-year, respectively. In addition, compared with the control group, the noise-exposed group had significantly higher levels of dopamine ( β = 61.17, 95% CI: 47.30-75.05) and norepinephrine ( β = 0.92, 95% CI: 0.80-1.03), but significantly lower levels of ADH ( β = -80.40, 95% CI: -90.19 to -70.61) and oxytocin ( β = -75.48, 95% CI: -81.80 to -69.17). Mediation analyses showed that none of the six stress hormones exerted a statistically significant indirect effect on the associations between occupational noise exposure and blood pressure or HR (all P > 0.05). CONCLUSION: Occupational noise exposure was independently associated with elevated blood pressure and reduced HR among female workers. However, no statistically significant mediating effects of the six stress hormones were identified in the associations between occupational noise exposure and blood pressure or HR.
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Bai et al. (2026) conducted a cross-sectional in Occupational noise exposure (n=906). Occupational cumulative noise exposure (CNE) vs. Unexposed control workers (n=299) was evaluated on Systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) (β 2.34 for SBP, 95% CI 0.01-4.59). Occupational noise exposure was associated with higher SBP (β=2.34, 95% CI 0.01-4.59) and DBP (β=1.90, 95% CI 0.22-3.57) and lower HR (β=-2.44) in female workers.
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