© 2007 American Public Health Association DOI: 10.2105/AJPH.2005.078873
Mika Kivimäki is with the Department of Epidemiology and Public Health, University College London, London, England. Mirka Hintsanen, Liisa Keltikangas-Järvinen, and Laura Pulkki-Råback are with the Department of Psychology, University of Helsinki, Helsinki, Finland. Mika Kivimäki and Jussi Vahtera are with the Finnish Institute of Occupational Health, Helsinki. Marko Elovainio is with the National Research and Development Centre for Welfare and Health, Helsinki. Jorma S.A. Viikari is with the Department of Medicine and Olli T. Raitakari is with the Department of Clinical Physiology, University of Turku, Turku, Finland. Correspondence: Requests for reprints should be sent to Mika Kivimäki, PhD, University College London, Department of epidemiology and public health, 1-19 Torrington Pl, London WC1E 6BT, UK (e-mail: m.kivimaki{at}ucl.ac.uk).
We examined whether preemployment influences confounded the association between job strain and atherosclerosis. We assessed biological, familial, and socioeconomic risk factors of coronary heart disease at 12 to 18 years of age and job strain and carotid artery intima-media thickness at 33 to 39 years of age for a cohort of 358 men. Adolescent risk factors predicted adult intima-media thickness but had little effect on the doseresponse relation between greater job strain and greater intima-media thickness. Pre-employment influences did not confound the association between job strain and atherosclerosis.
According to the job-strain model,1,2 increased stress and health problems are likely when high work demands coincide with low job control (i.e, lack of control over aspects of task performance and the use of skills). In accordance with this hypothesis, several epidemiological studies of adult populations have shown an association between job strain and coronary heart disease (CHD),38 but nonsignificant findings also exist.9,10 One of the problems in the evidence of job strain and CHD is that even the best-designed prospective studies have failed to take into account the cumulative effects of early life factors on the development of CHD.11 Several studies have shown that cholesterol concentration, body mass index, blood pressure, and socioeconomic position in childhood or adolescence predict atherosclerosis and CHD later in life.1214 Evidence also suggests that early-life risk factors have an effect on stress perceptions in adulthood.15,16 These early influences on both adult CHD risk and stress perception could confound evidence regarding the status of job strain as a risk factor for CHD in adult populations. Indeed, it is unclear whether part of the association between job strain and CHD may be attributable to influences from childhood or adolescence. Using data collected from men participating in the Cardiovascular Risk in Young Finns Study,17 we prospectively examined whether biological, familial, and socioeconomic risk factors in adolescence contributed to the association between job strain and adult carotid artery intima-media thickness, a marker of atherosclerosis and a valid presymptomatic predictor of CHD.1820
Participants The original sample of the Cardiovascular Risk in Young Finns Study comprised 1764 boys and 1832 girls from 6 randomly selected age cohorts of Finnish children aged 3, 6, 9, 12, 15, and 18 years at entry into the study in 1980.13,17 Our study included 358 men who had no missing data on the study variables at baseline and, at the 21-year follow-up in 2001, were free from apparent cardiovascular diseases and belonged to the 3 oldest age cohorts (n = 866). A subsidiary analysis with similar inclusion criteria involved 682 men from all 6 age cohorts. Previous attrition analyses have shown that participants lost to follow-up were younger, but differences in coronary risk factors were small between participants and dropouts.13 In the Cardiovascular Risk in Young Finns Study, adolescent risk factors were predictive of adult intima-media thickness, and among men, an association was found between adult job strain and intima-media thickness independent of adult risk factors and occupational status.8,13 For women, no association between job strain and intima-media thickness was found.8
Data Collection and Analysis In 2001, the participants aged 33 to 35 years, covered a full range of occupations from factory workers to physicians. Their level of job strain was determined from responses to the Job Demands Scale and Job Control Scale.8 As in previous studies, the distributions of demands and control were each divided into thirds.7,8,21,22 The highest 2 tertiles in job demands combined with the lowest 2 tertiles in job control (excluding the combination of the second tertile in both demands and control) formed the low-job-strain category; all other combinations were placed into the intermediate-job-strain category. Job strain was coded as an ordinal variable ranging from 1 to 3, with higher values indicating higher job strain.8 To assess intima-media thickness, the left carotid artery was scanned by ultrasound technicians in 2001 to 2002, according to a standard protocol.13 At least 4 measurements of the common carotid far wall were taken approximately 10 mm proximal to the bifurcation. The average of these measurements was used to determine carotid artery intima-media thickness. Statistical significance of the associations between each adolescent risk factor and intima-media thickness, and between adult job strain and intima-media thickness was studied by fitting separate age-adjusted linear regression models to the data. The association between job strain and intima-media thickness was adjusted additionally for adolescent risk factors so that their contribution could be evaluated.
Most of the adolescent risk factors predicted adult intima-media thickness (Table 1
Our results suggest that established biological, familial, and socioeconomic risk factors in adolescence are unlikely sources of confounding in the association between job strain and CHD risk. Our outcome was carotid artery intima-media thickness, which is a particularly suitable measure of CHD risk in healthy populations such as our sample, because it reflects general atherosclerosis, is predictive of future coronary events, and is free from potential reporting bias.1820 Because our cohort did not include employees with established CHD, prognostic factors did not complicate the interpretation. The success of organizational interventions attempting to modify job strain has thus far been modest; therefore, the question that has been raised is whether the excess health risk among employees with a high level of job strain reflects a noncausal relation attributable to confounding by preemployment effects.11 Our findings suggest that this may not be the case. Thus, our evidence should motivate the development of more systematic intervention strategies for large-scale intervention studies to confirm or refute the status of job strain as a risk factor for CHD.
The Cardiovascular Risk in Young Finns Study was supported by the Academy of Finland (grant 53392), the Social Insurance Institution of Finland, the Finnish Work Environment Foundation, Turku University Foundation, Juho Vainio Foundation, the Finnish Foundation of Cardiovascular Research, and the Finnish Cultural Foundation, Finland. M. Kivimäki, L. Keltikangas-Järvinen, and J. Vahtera were supported by the Academy of Finland (grants 117604, 105195, and 1209514). J. S. A. Viikari and O. T. Raitakari were supported by research grants from Turku University Central Hospital.
Human Participant Protection
Peer Reviewed
Contributors Accepted for publication February 14, 2006.
1. Karasek RA. Job demands, job decision latitude and mental strain: implications for job redesign. Admin Sci Q. 1979;24:285307.[CrossRef] 2. Karasek RA, Theorell T. Stress, Productivity and Reconstruction of Working Life. New York, NY: Basic Books; 1990. 3. Karasek R, Baker D, Marxer F, Ahlbom A, Theorell T. Job decision latitude, job demands, and cardiovascular disease: a prospective study of Swedish men. Am J Public Health. 1981;71:694705. 4. Steptoe A, Fieldman G, Evans O, Perry L. Control over work pace, job strain and cardiovascular responses in middle-aged men. J Hypertens. 1993;11:751759.[Web of Science][Medline] 5. Siegrist J, Peter R. Threat to occupational status control and cardiovascular risk. Isr J Med Sci. 1996;32:179184.[Web of Science][Medline] 6. Bosma H, Peter R, Siegrist J, Marmot M. Two alternative job stress models and the risk of coronary heart disease. Am J Public Health. 1998;88:6874. 7. Kivimäki M, Leino-Arjas P, Luukkonen R, Riihimaki H, Vahtera J, Kirjonen J. Work stress and risk of cardiovascular mortality: prospective cohort study of industrial employees. BMJ. 2002;325:857860. 8. Hintsanen M, Kivimäki M, Elovainio M, et al. Job strain and early atherosclerosis: the Cardiovascular Risk in Young Finns Study. Psychosom Med. 2005;67:740747. 9. Rosvall M, Ostergren PO, Hedblad B, Isacsson SO, Janzon L, Berglund G. Work-related psychosocial factors and carotid atherosclerosis. Int J Epidemiol. 2002; 31:11691178. 10. Eaker ED, Sullivan LM, Kelly-Hayes M, DAgostino RB Sr, Benjamin EJ. Does job strain increase the risk for coronary heart disease or death in men and women? The Framingham offspring study. Am J Epidemiol. 2004;159:950958. 11. Strike PC, Steptoe A. Psychosocial factors in the development of coronary artery disease. Prog Cardiovasc Dis. 2004;46:337347.[CrossRef][Web of Science][Medline] 12. Li S, Chen W, Srinivasan SR, et al. Childhood cardiovascular risk factors and carotid vascular changes in adulthood: the Bogalusa Heart Study. JAMA. 2003; 290:22712276. 13. Raitakari OT, Juonala M, Kahonen M, et al. Cardiovascular risk factors in childhood and carotid artery intima-media thickness in adulthood: the Cardiovascular Risk in Young Finns Study. JAMA. 2003;290:22772283. 14. Lynch J, Davey Smith G. A life course approach to chronic disease epidemiology. Annu Rev Public Health. 2005;26:135.[CrossRef][Web of Science][Medline] 15. Harper S, Lynch J, Hsu WL, et al. Life course socioeconomic conditions and adult psychosocial functioning. Int J Epidemiol. 2002;31:395403. 16. Meaney MJ. Maternal care, gene expression, and the transmission of individual differences in stress reactivity across generations. Annu Rev Neurosci. 2001; 24:11611192.[CrossRef][Web of Science][Medline] 17. Åkerblom HK, Uhari M, Pesonen E, et al. Cardiovascular risk in young Finns. Ann Med. 1991;23:3539.[Web of Science][Medline] 18. OLeary DH, Polak JF. Intima-media thickness: a tool for atherosclerosis imaging and event prediction. Am J Cardiol. 2002;90:18L21L. 19. Van Trijp MJ, Uiterwaal CS, Bos WJ, Oren A, Grobbee DE, Bots ML. Noninvasive arterial measurements of vascular damage in healthy young adults: relation to coronary heart disease risk. Ann Epidemiol. 2006;16:7177.[CrossRef][Web of Science][Medline] 20. Tzou WS, Douglas PS, Srinivasan SR, et al. Increased subclinical atherosclerosis in young adults with metabolic syndrome: the Bogaluza Heart Study. J Am Coll Cardiol. 2005;46:457463. 21. Green KL, Johnson JV. The effects of psychosocial work organization on patterns of cigarette smoking among male chemical plant employees. Am J Public Health. 1990;80:13681371. 22. Landsbergis PA, Schnall PL, Warren K, Pickering TG, Schwartz JE. Association between ambulatory blood pressure and alternative formulations of job strain. Scand J Work Environ Health. 1994;20:349363.[Web of Science][Medline] This article has been cited by other articles:
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