Noise, physical workload (later workload) and shift work are nowadays common in the work places. Life is hectic, metabolic syndrome is common due to e.g. obesity and inactivity, and coronary heart disease (CHD) is still one of the leading causes of death. This doctoral dissertation aims to evaluate the impact of these occupational exposures and of metabolic syndrome on the risk of CHD.

The research material consisted of industrial male workers who participated in the Helsinki Heart Study (HHS), primary prevention trial of a lipid-lowering drug, gem-fibrozil. The size of cohorts varied from 884 to 6 005, depending on the research problem. When the study was initialized in the early 1980’s, the men were from 40 to 55 years of age, and the longest follow-up continued until the end of 1999. The data on the exposure to noise and workload was collected from the Finnish job-exposure matrix FINJEM, and the data on shift work from a psycho-social question-naire conducted in 1987–1988. The cardiac end points were obtained from the Hos-pital Discharge Register and the Register of Deaths. The risks of CHD were estimat-ed using the Cox proportional hazards model.

The first objective of the research was to study the short-term and long-term ef-fects of occupational exposures on the risk of CHD. The workers were screened from year 1980–1982 to 1991, 1995 and 1999. Statistically, noise was a significant risk factor in all follow-ups. For subjects who were exposed to both continuous and impulse noise, the relative risks (RR) of CHD – adjusted for age and life style fac-tors (smoking, alcohol consumption and leisure-time physical activity) – at the dif-ferent follow-ups were 1.21–1.42 compared to subjects who were not exposed to noise. For studying the possible carry-over effect of occupational noise on the CHD risk after retirement, there was a follow-up for participants to start from when they turned 60 or 63 years of age. In both follow-ups, both all of the workers and the blue-collar workers only had an increased risk of CHD only if they were exposed to both continuous and impulse noise.

When the workers were divided into tertiles according to their workload, the risk of CHD was statistically significantly higher in the second and the third tertile than in the first tertile which included workers not exposed to heavy work. For those who considered their work to be physically very heavy, the age adjusted risk of CHD in the follow-ups was 1.24–1.32, at its highest in the short follow-up and at its lowest in the longest follow-up. In other words, the risk caused by heavy workload de-creased with retirement. Adjustments for occupational class (white or blue collar), age and lifestyle factors or noise lowered the risk estimates markedly. When the model was adjusted for age and lifestyle factors, the risk (1.25) was statistically sig-nificant only for those who considered their work very heavy in the follow-up that ended in 1999.

Shift work was restricted to 2- and 3-shift work and irregular work. Subjects working part-time or nights were excluded from the data. Shift work was statistical-ly significant to the CHD risk in all follow-ups and in all adjustments except for that of occupational class. The risk estimates decreased as the follow-up proceeded, i.e. the risk caused by shift work was at its highest during the period of employment. In the model adjusted for age and lifestyle factors, for example, the relative risks of CHD in the follow-ups were 1.60, 1.39 and 1.34.

The second objective of the research was to study the joint effect of these occu-pational exposures to the risk of CHD. When the workers were divided into eight (8) groups according to exposure combinations, only the joint effects of noise and shift work and of all the three factors were statistically significant in all follow-ups. The risk relations lowered with time, and in the collar color adjustment, the statisti-cal significance remained exclusively in the three-factor effect. In the 1999 follow-up the three-factor effect RR in the model adjusted for age and life style variables was 1.61 compared to the unexposed group. Subjects with many exposures had an increased risk of coronary heart disease, but all joint effects were antagonistic. It was surprising that shift work or heavy work alone caused a higher risk of CHD than those combined, i.e. heavy shift work.

The third objective was to evaluate the pathway from occupational exposures to blood pressure and further to the risk of CHD. The workers were divided into eight groups according to the exposures. In the systolic blood pressure follow-up, the highest blood pressure levels were measured among workers exposed only to work-load; the level was at its highest in the last year, 143.1 mmHg. The second highest level (140.3 mmHg) in the last year’s averages was measured among workers ex-posed to all three factors: heavy and noisy shift work. If the baseline blood pressure was high (90/140 mmHg), the CHD risk adjusted for leisure-time physical activity and noise was 2.85 times higher compared to workers with light physical workload and low baseline blood pressure.

The fourth objective was to study the joint effect of occupational exposures and the components of metabolic syndrome (MetS) – weight index, blood pressure, glu-cose levels, triglycerides and high-density lipoprotein cholesterol (HDL-C) – to the risk of CHD. When MetS was defined by high weight index, high blood pressure and glucose, the adjusted RR of subjects with MetS and heavy physical workload was 4.22 at its highest. The highest value of adjusted RR between MetS and expo-sure to noise was 2.69 compared to healthy, unexposed workers. These risk relations were compatible with the additive joint effect model. By using the more traditional definition of MetS that includes any three components of the five above-mentioned, all joint effects of MetS and occupational exposures were antagonistic i.e. they di-minished each other.