Iron deficiency is very common in humans and animals. Frost et al. demonstrate that low concentrations of iron in serum, caused by the hormone hepcidin, inhibit the body's response to vaccines and infections; conversely, increasing iron can boost immunity.
Background: Work-related stress is a potential cardiovascular risk factor, but the underlying mechanism is not fully explained. The autonomic nervous system control of cardiac function might play a specific role; therefore, monitoring the QT interval in the electrocardiogram can highlight an autonomic imbalance induced by occupational stressors. The aim of our study was to explore the QT interval parameters as early indicators of imbalance of the autonomic cardiac function in relation to work-related stress. Methods: During 2015–2016 annual workplace health surveillance, we measured work-related stress in 484 workers of a logistic support company using the Health and Safety Executive (HSE) tool. We assessed the frequency-corrected QT (QTc) interval and the QT index (QTi) on the electrocardiogram of each participant, and collected demographic and clinical data. We compared the QTc values by the four Karasek’s categories (active/passive jobs, low/high strain job), and by job support (present/lacking), and conducted multivariate analysis to adjust for possible confounders. Results: The results of the multivariate regression analysis showed that QTc was prolonged among workers operating at a specific site where stress level was found to be elevated. Regular physical activity showed a beneficial effect against QTc prolongation. We did not observe an effect on QTc length by the cross-combined Karasek’s categories of job control, job demand, and job support. Conclusions: Our study suggests subclinical effects of conditions associated with work-related stress on the autonomic regulation of cardiac function. Further research is warranted to elucidate the combined effect of work organization and lifestyle factors on autonomic cardiac function.
Objectives
To test the association between occupational exposure to trichloroethylene (TCE) and risk of non Hodgkin lymphoma (NHL), we conducted a pooled analysis of four international case-control studies.
Methods
Studies were selected which included state-of-the art retrospective assessment of occupational exposure to TCE and histological information on lymphoma subtype. Overall, the pooled study population included 3788 NHL cases and 4279 controls. Summary indicators of exposure were harmonised across studies. We conducted unconditional logistic regression analysis to test the association between the harmonised TCE exposure estimates and NHL and its major subtypes, adjusting by age, gender, and study.
Results
Among the total study population, risk of follicular lymphoma, but not NHL overall or other subtypes, increased by probability (p = 0.02) and intensity level (p = 0.04) of TCE exposure. When the analysis was restricted to subjects most likely exposed to TCE, risk of NHL overall (p = 0.009), follicular lymphoma (p = 0.04), and chronic lymphocytic leukaemia (CLL) (p = 0.01) showed a linear increase by duration of exposure. No heterogeneity in NHL risk associated with high probability of exposure to TCE (all intensity levels combined) was detected.
Conclusion
With due caution because of several limitations, our pooled analysis supports the hypothesis of an increased risk of NHL, and particularly of the follicular lymphoma and CLL subtypes, associated with occupational exposure to TCE.
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