Virkkunen H, Kauppinen T, Tenkanen L. Long-term effect of occupational noise on the risk of coronary heart disease. Scand J Work Environ Health 2005;31(4):291-199.Objectives The aim of the study was to investigate the short-and long-term effects of occupational exposure to continuous and impulse noise on the risk of CHD. MethodsThe effect of noise on CHD was studied among 6005 Finnish middle-aged industrially employed men (part of the screeners in the Helsinki Heart Study) in a prospective 18-year follow-up study. The CHD end points (codes 410-414 in the ninth revision of the International Classification of Diseases and codes I20-I25 in the tenth revision) were obtained from official Finnish registers. The Finnish job-exposure matrix FINJEM provided estimates of the proportion of exposed persons and the mean level of exposure among those exposed by occupation. The relative risks (RR) of CHD and the 95% confidence intervals (95% CI) for noise exposure were calculated from Cox's proportional hazard models with adjustment for some other risk factors of CHD. ResultsThe short-term (9-year follow-up) relative risk of CHD for the combined noise (continuous noise exceeding 80 decibels and impulse noise) was 1.38 (95% CI 1.04-1.82), and the long-term (18-year follow-up) RR was 1.54 (95% CI 1.28-1.86). For blue-collar workers the corresponding estimates were 1.11 (95% CI 0.82-1.51) and 1.29 (95% CI 1.05-1.57). Adjustment for other relevant risk factors did not materially change the results. ConclusionsIn our long-term follow-up of industrially employed men, exposure to noise, especially to impulse noise, was associated with a moderate, but statistically significant increase in CHD risk that persisted even after the workers had passed the age of retirement.

Background: Shift work, noise, and physical workload are very common occupational exposures and they tend to cluster in the same groups of workers. Objectives: To study the short and long term effects of these exposures on risk of coronary heart disease (CHD) and to estimate the joint effects of these factors. Methods: The study population in this prospective 13 year follow up study of 1804 middle aged industrially employed men was collected at the first screening for the Helsinki Heart Study. The CHD end points (ICD-9 codes 410-414 and ICD-10 codes I20-I25) were obtained from official Finnish registers. The Finnish job-exposure matrix FINJEM provided information on occupational exposures. Relative risks (RR) of CHD for the exposures were estimated using Cox's proportional hazard models adjusting for classical risk factors of CHD. Results: The RR in the five year follow up for continuous noise combined with impulse noise was 1.28; for shift work it was 1.59, and for physical workload 1.18, while in the 13 year follow up the RRs were 1.58, 1.34, and 1.31, respectively. When adjusted for white-collar/blue-collar status the RRs decreased markedly. The RR in the 13 year follow up for those exposed to two risk factors was close to 1.7 and for those exposed to all three, 1.87. Conclusion: Shift work and continuous noise entailed an excess risk for CHD in the shortest follow up with only a few retired workers but a decreasing risk during the longer follow up. For physical workload and impulse noise the trend was opposite: the CHD risk was increasing with increasing follow up time despite increasing numbers of retired workers.

Abstract-Heat shock protein 60 (Hsp60) and Chlamydia pneumoniae infection have both been associated with cardiovascular diseases. Our aim was to study the role of Hsp60 antibodies as coronary risk predictors and their association with C pneumoniae infection and inflammation. This was a prospective, nested, case-control study. The cases consisted of 239 middle-aged Finnish men who developed myocardial infarction or coronary death during the follow-up. Baseline levels of IgA and IgG antibodies to human-specific and C pneumoniae-specific Hsp60 were measured by enzyme immunoassay. Human Hsp60 IgA, but not IgG or C pneumoniae Hsp60, antibodies were a significant risk factor for coronary events (odds ratio 2.0, 95% CI 1.1 to 3.6, when the fourth and first quartiles are compared). When an elevated human Hsp60 IgA antibody level (above the second quartile) was present simultaneously with a high C pneumoniae IgA antibody level (the third quartile) and an elevated C-reactive protein level (the second quartile), compared with all factors at low levels, the risk was 7.0 (95% CI 2.6 to 19.1) without adjustment and 5.0 (95% CI 1.8 to 14.2) when adjustment was made for age and smoking. In conclusion, an elevated human Hsp60 IgA antibody level was a risk factor for coronary events, especially when it was present together with C pneumoniae infection and inflammation.

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Background-Given the role of chronic infections, autoimmunity, and inflammation in atherosclerosis, we studied the joint effect of chronic Chlamydia pneumoniae infection, persistently elevated human heat-shock protein 60 (hHsp60) antibodies, and C-reactive protein (CRP) on coronary risk. Methods and Results-The participants for this prospective nested case-control study were obtained from the Helsinki Heart Study, during which 241 nonfatal myocardial infarctions or coronary deaths occurred among 4081 dyslipidemic middle-aged men. Serum samples taken at baseline and 3 to 6 months before the coronary events that occurred during the 8.5-year period were analyzed for antibodies to C pneumoniae and hHsp60 and the CRP concentration. Compared with persistently low levels, the risk of coronary events was 2-fold for persistently elevated immunocomplex (IC)-bound and/or serum IgA antibodies to C pneumoniae (OR, 1.96; 95% CI, 1.14 to 3.36) and also for serum IgA antibodies to hHsp60 (OR, 2.11; 95% CI, 1.08 to 4.13). The risks associated with elevated antibodies were much higher when CRP was also elevated. Compared with low or transiently elevated levels, the risk of coronary events, with adjustment for age and smoking, was 4.