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Updated: Aug 6, 2026

Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model
Published on: December 10, 2021
Occupational noise exposure and ischaemic heart disease mortality
R McNamee1, G Burgess, W M Dippnall
1Biostatistics Group, Division of Epidemiology and Health Sciences, University of Manchester, UK. rmcnamee@manchester.ac.uk
Aims:
To investigate the hypothesis that long term exposure to excessive noise can increase the risk of ischaemic heart disease.
Methods:
A case-control design, nested within a cohort of nuclear power workers employed at two sites in England over the period 1950-98, was used. Cases were men who died from ischaemic heart disease (ICD-9: 410-414) aged 75 or under; each was matched to a surviving control of the nearest age who joined the same site at the same time. Personal noise exposure was assessed retrospectively for each man by hygienists using (1) company work histories, (2) noise survey records from 1965-98, and (3) judgements about likely use of hearing protection devices. Men were classified into four groups according to their cumulative exposure to noise, with men whose exposure at the company never exceeded 85dB(A) for at least one year being considered "unexposed". Risks were compared via odds ratios (ORs) using conditional logistic regression and adjusted for systolic and diastolic blood pressure, height, BMI, and smoking, as measured at recruitment to the company.
Results:
Analysis was based on 1101 case-control pairs. There was little difference between the exposure groups at recruitment. There was no evidence of increased risk at site A: the ORs for ischaemic heart disease mortality among low, medium, and high exposure categories, compared to unexposed men, being 1.04, 1.00, and 0.77. The corresponding ORs (95% CIs) at site B were 1.15 (0.81-1.65) 1.45 (1.02-2.06), and 1.37 (0.96-1.96). When the comparison was confined to men with at least five years of employment, these dropped to 1.07 (0.64-1.77), 1.33 (0.88-2.01), and 1.21 (0.82-1.79) respectively.
Conclusions:
The authors did not find statistically robust evidence of increased risk but the estimates at site B are consistent with those in a major cohort study. A strength of the present study is that the validity of noise estimation at site B has been demonstrated elsewhere.
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