Chicago Western Electric Study

Background:

The Chicago Western Electric Study was initiated in 1957 by Oglesby Paul to identify factors associated with risk of CHD. [1]

Methods:

A sample of 3,102 men was randomly selected from the population of men 40-55 years of age and employed for at least 2 years at the Hawthorne Works of the Western Electric Company near Chicago. The total initially examined was 2,107. The group included white- and blue-collar occupations associated with the manufacture of telephonic equipment. About 75% were first- or second-generation Americans of German, Polish or Bohemian ancestry while most of the remaining participants were descendants of earlier immigrants from the British Isles.

Initial examinations, conducted from October 1957 to December 1958, included a detailed family and medical history, complete physical examination, 12-lead plus V4R ECG, chest x-ray, urinalysis, and measurements of blood hemoglobin, serum total cholesterol, serum lipoprotein lipase (the measurements of which were subsequently determined to be invalid), height, weight, subscapular and triceps skinfold thicknesses, somatotype by Sheldon’s method, diet by Burke’s method, personality using the Minnesota Multiphasic Personality Inventory, physical activity on the job according to codes developed by the Company for each occupation, and physical activity away from work using a questionnaire method (subsequently deemed insufficiently reliable). No prescriptive care was given, but results were sent to personal physicians with the participant’s consent.

Men continuing in the study were re-examined and medical histories updated annually through 1969, primarily to detect incident cases of CHD. Additional data on diet, personality, social status, and pulmonary function were obtained at the second, third, and fourth annual examinations. The diagnosis of Heberden’s angina was based on published criteria, and required the concurrence of two or more internists in each case. The diagnosis of myocardial infarction was based on the clinical history plus characteristic electrocardiographic findings. Where opinions differed, decision as to diagnosis rested with the senior investigator (O.P.), who undertook an additional interview and physical examination. The assumption of death from coronary disease was made on the basis of the most reasonable conclusion to be drawn from information obtained from the family, physicians, and hospital records, death certificates, and coroners’ reports.

Data on incidence of disease were not collected after 1969, but follow-up for mortality was started in 1975. Death certificates were obtained for all decedents. All follow-up data were evaluated and coded without reference to any baseline information. Vital status was positively determined for each of the 2,107 participants on the 25th anniversary of his initial examination. [2]

Analyses based on 5 years of follow-up included angina pectoris as an endpoint and excluded sudden unexplained death. [1] The situation was reversed in analyses based on 10 years of follow-up; angina was excluded as an endpoint and sudden unexplained death was included. [3] CHD death was the endpoint for analyses based on more than 10 years of follow-up.

Results and comments:

Antecedent variables associated with risk of CHD have been listed below. Unless otherwise noted, these associations were positive in direction. Details have been omitted but can be found by consulting the referenced publications.

• Cigarette smoking, blood pressure, and serum cholesterol concentration. [1,3] Comment: Together with the other cohort studies that participated in the Pooling Project, these results helped to establish the consistency, strength, and graded nature of the associations of cigarette smoking, high blood pressure, and hypercholesterolemia to risk of CHD in American men.
• Lipid composition of the diet as summarized by the formulas of Keys et al. and of Hegsted et al., i.e., higher intake of saturated fatty acids and cholesterol and lower intake of polyunsaturated fatty acids. [4] Comment: Although effects of changes in lipid composition of the diet on serum cholesterol concentration in humans had been demonstrated experimentally, these effects had not been reliably seen in observational studies. Reasons for this were statistical in nature and unconvincing to investigators who were skeptical of the idea that dietary factors were important in the etiology of CHD. The effects were seen in the present study because Burke’s labor-intensive 28-day diet history procedure for assessment of usual diet decreased the intra-individual variation in comparison to the 24-hour diet recall procedure that was used in other studies.
• Inconsistencies in social status, e.g., class of origin not equal to present class or educational status different from occupational status. [5] Comment: The idea that psychological and social factors might be important in the etiology of CHD was common in the 1950’s and 60’s, and substantial effort went into using standardized and validated instruments to measure these variables. This result supported the idea, but neither a biological mechanism nor a way to use the information for prevention could be clearly seen and interest waned.
• Persistent, minor, nonspecific ST-T wave abnormalities. [6] Comment: This result gave clinical significance to these nonspecific ECG findings and indicated the importance of effective intervention on the major modifiable risk factors for patients who had them.
• Large fluctuations in self-reported body weight during young adulthood. [2] Comment: Ancel Keys had suggested that large, rapid gains in weight that commonly occurred after cessation of weight-reduction regimens might accelerate atherogenesis. This result supports that idea and emphasized possible risks of “yo-yo” dieting.
• Increase in body weight during young adulthood (estimated from the body mass index calculated from self-reported weight at age 20 and measured height and weight at the initial examination) was positively associated with risk of CHD death in never smokers but not in current smokers. [7] Comment: This result may explain some of the inconsistent results obtained in studies of body fatness and risk of CHD.

The following results do not concern risk of CHD directly but are related to other issues in CVD epidemiology:

• Body fatness modified the effect of change in dietary cholesterol on change in serum cholesterol concentration; a decrease of 150 mg/1000 kcal in dietary cholesterol was associated with mean changes of -0.46, -0.18, and 0.13 mmol/L in serum cholesterol, respectively, for men with body mass index <24.2, 24.2-26.6, and >26.6 kg/m2. [8] Comment: The effect of change in intake of dietary cholesterol and change in serum lipids in man has been controversial. This result provided a possible explanation for some of the otherwise unexplained variation in results observed among studies of the question.
• The serum cholesterol concentration at the initial examination affected change in diet from the first to second examination – i.e., hypercholesterolemic men were more likely than others to have reduced consumption of saturated fatty acids and cholesterol. [9] As a result, at the second examination the cross-sectional linear association between the Keys diet score and serum cholesterol concentration was significantly positive for men with initial levels of serum cholesterol less than 250 mg/dl, significantly negative for men with initial levels of 250 mg/dl or higher, and not significantly different from zero for all men together. Comment: This result provided yet another example of problems facing observational studies of diet and serum lipids in human populations. The sum of 2 MMPI variables, HsK+Hy, was positively associated with risk of uncomplicated angina pectoris as the first manifestation of CHD but not significantly associated with risk of MI or CHD death. However, among men with uncomplicated angina, HsK+Hy was inversely associated with risk of CHD death. The association between HsK+Hy and CHD death was positive among men who had nonfatal MI as the first manifestation of CHD. [10] Comment: Analysis after 5 years of follow-up had shown that the HsK and Hy variables were positively associated with risk of uncomplicated angina pectoris as the first manifestation of CHD but were not associated with risk of MI or CHD death. The basis for this association was unclear. Later, the development of coronary angiography showed that some persons with classic symptoms of Heberden’s angina did not have clinically significant occlusive coronary artery disease. Based on this new knowledge, we predicted that the HsK+Hy score would be inversely associated with mortality subsequent to diagnosis of uncomplicated angina, and the result was consistent with this hypothesis. The inverse association of HsK+Hy score with risk of subsequent CHD death was not anticipated. (RS)