During the winter of 1989-1990, influenza type A(H3N2) circulated widely, causing excess morbidity and mortality nationwide. From November through April, 1989-1990, hospitalized cases of pneumonia and influenza occurring among noninstitutionalized individuals 65 or more years of age were identified by 20 acute care hospitals in southern lower Michigan. These cases were group matched on age, sex, race, and zip code to randomly sampled, community-based controls from a comprehensive listing of Medicare beneficiaries residing in the study area. Self-reported data were collected from cases and controls on influenza vaccine status for the 1989-1990 season and on a number of other factors which could have influenced vaccination status or outcome. Questionnaires were completed by 1,907 individuals, 449 of whom were cases, resulting in an overall response rate of 76%. A community-based influenza surveillance system was implemented to determine the timing and intensity of viral activity and influenza-like illness. Vaccine effectiveness in preventing overall pneumonia and influenza hospitalizations was estimated by logistic regression. During the 3-month period of surveillance-confirmed peak influenza type A(H3N2) circulation, vaccine effectiveness was 45% (95% confidence interval 14-64, p = 0.009). However, during the 3-month period of low or absent virus activity, identical methodology and model specification resulted in an effectiveness estimate of 21% that was not statistically different from zero (p = 0.36). The effectiveness determined during the peak period of virus circulation is felt to be a conservative estimate, since agents other than influenza are responsible for pneumonia and influenza hospitalizations, even during times of peak influenza activity.
Psychological stress can contribute to health disparities in populations that are confronted with the recurring stress of everyday life. A number of biomarkers have been shown to be affected by psychological stress. These biomarkers include allostatic load, which is a summary measure of the cumulative biological burden of the repeated attempts to adapt to daily stress. Allostatic load includes effects on the hypothalamic-pituitary axis, the sympathetic nervous system and the cardiovascular system. These in turn affect the immune system via bidirectional signaling pathways. Evidence is also building that psychological stress, perhaps via heightened inflammatory states, can increase oxidative stress levels and DNA damage. The inter-relationships of ethnicity, genotype, gene expression and ability to adequately mitigate stress response are just starting to be appreciated. The need to conduct these studies in disadvantaged populations is clear and requires methods to address potential logistical barriers. Biomarkers can help characterize and quantify the biological impact of psychological stress on the etiology of health disparities.
The social status of groups is key to determining health vulnerability at the population level. The impact of material and psychological stresses imposed by social inequities and marginalization is felt most intensely during perinatal/early childhood and puberty/adolescent periods, when developmental genes are expressed and interact with social-physical environments. The influence of chronic psychosocial stresses on gene expression via neuroendocrine regulatory dysfunction is crucial to understanding the biological bases of adult health vulnerability. Studying childhood biology vulnerabilities to neighborhood environments will aid the crafting of multifaceted, multilevel public policy interventions providing immediate benefits and compounded long-term population health yields.
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