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Occupational Medicine 2008 58(8):594; doi:10.1093/occmed/kqn137
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© The Author 2008. Published by Oxford University Press on behalf of the Society of Occupational Medicine. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Monitor

Agent, host and environmental interactions

Peter Noone

Agent, host and environmental factors provide an approach to elucidating causes of incident outbreaks of infectious disease. They are less helpful in predicting when and why outbreaks arise. As public health focus moves to non-infectious health problems such as obesity or mental health, limitations of this traditional approach become clearer. The agents associated with non-infectious diseases are invariably non-specific, often there are no necessary causal factors; host susceptibility cannot be measured, and the environment has complex, interacting layers of influence. In such circumstances agent, host and environment explanations have significant limitations. McDowell reviews alternative approaches to considering these public health problems and connections among causes, explanations and understanding [1].

Population health deals with health determinants including factors from genetics to social inequities. Too often the precise nature of determinants remains obscure and lists of odds ratios provide little overall explanation. Interventions must be based on coherent explanations, and slow progress in resolving these problems suggests that current explanations are lacking.

Nielsen et al.[2] in a recent Danish study indicates that self-reported stress increases all-cause mortality over the subsequent 20 years. Gender differences were found between stress and mortality (P = 0.02). Men with high stress had higher all-cause mortality (hazard ratio (HR) = 1.3, 95% CI: 1.15, 1.5), that was highest for respiratory disease deaths (high vs. low stress: HR = 1.8, 95% CI: 1.1, 2.9), external causes (HR = 3.1, 95% CI: 1.65, 5.7), and suicide (HR = 5.9, 95% CI: 2.5, 14.2). ‘High stress’ was associated with a 2.6 (95% CI: 1.2, 5.6) higher risk of ischaemic heart disease mortality for younger, but not older, men. Interestingly younger women with high stress experienced lower cancer mortality (HR = 0.5, 95% CI: 0.3, 0.9).

Hotopf et al.[3] reviewing the results cautions that stress effects cannot be causally attributed to external exposure. The subject's personal experience, likely confounding by personality, coping styles and common mental disorders like depression or anxiety are relevant. Confirmation of these results in studies using more comprehensive stress measurements may highlight stress prevention as important risk reduction for premature death in young and middle-aged men.

Observational studies measure associations; however causal interpretation depends on study validity. Stressed, depressed, and anxious folk can have different risk factor profiles. They may exercise less, smoke more, or be more obese than the general population. Stress and depression are associated with physiologic changes like greater platelet aggregation, inflammatory markers, reduced heart rate variability, and overactivity of the hypothalamic-pituitary-adrenal system. Lastly, ‘upstream’ variables increase susceptibility to both stress or depression and mortality. Perhaps this reflects a shared genetic liability as the same genes may be associated with depression and mortality through regulation of inflammatory or serotonergic pathways. Susceptibility to stress and depression are moderately heritable [4], like many traditional mortality risk factors [5].

Nurse shortage and retention is an international problem. Josephson et al. [6] studied whether individual factors, working conditions and health problems increased the probability of leaving as well as long-term sickness absence in Swedish nurses over 3 years. Work in elderly care, bullying by superiors and/or workmates, negative effects of organizational changes and poor self-rated general health were predictive of leaving jobs and long-term sick leave. Resigning and changing employers was a way of coping with an unhealthy work environment.

Long-term stress should be reduced or prevented regardless of the possible consequences for mortality.


    References
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 References
 

  1. McDowell I. Thesis, From risk factors to explanation in public health. J Public Health (2008) 30:219–223.[CrossRef]

  2. Nielsen N, Kristensen ST, Schnohr P, et al. Perceived stress and cause-specific mortality among men and women: results, from a prospective cohort study. Am J Epidemiol (2008) 168:481–491.[Abstract/Free Full Text]

  3. Hotopf M, Henderson M, Kuh D. Invited commentary: stress and mortality. Am J Epidemiol (2008) 168:492–495.[Abstract/Free Full Text]

  4. Sullivan PF, Neale MC, Kendler KS. Genetic epidemiology of major depression: review and meta-analysis. Am J Psychiatry (2000) 157:1552–1562.[Abstract/Free Full Text]

  5. Souren NY, Paulussen AD, Loos RJ, et al. Anthropometry, carbohydrate and lipid metabolism in the East Flanders Prospective Twin Survey: heritabilities. Diabetologia (2007) 50:2107–2116.[CrossRef][Web of Science][Medline]

  6. Josephson M, Lindberg P, Voss M, et al. Employment and sickness absence, the same factors influence job turnover and long spells of sick leave, 3-year follow-up of Swedish nurses. Eur J Public Health (2008) 18:380–385.[Abstract/Free Full Text]


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This Article
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