BackgroundManagement of solid waste (mainly landfills and incineration) releases a number of toxic substances, most in small quantities and at extremely low levels. Because of the wide range of pollutants, the different pathways of exposure, long-term low-level exposure, and the potential for synergism among the pollutants, concerns remain about potential health effects but there are many uncertainties involved in the assessment. Our aim was to systematically review the available epidemiological literature on the health effects in the vicinity of landfills and incinerators and among workers at waste processing plants to derive usable excess risk estimates for health impact assessment.MethodsWe examined the published, peer-reviewed literature addressing health effects of waste management between 1983 and 2008. For each paper, we examined the study design and assessed potential biases in the effect estimates. We evaluated the overall evidence and graded the associated uncertainties.ResultsIn most cases the overall evidence was inadequate to establish a relationship between a specific waste process and health effects; the evidence from occupational studies was not sufficient to make an overall assessment. For community studies, at least for some processes, there was limited evidence of a causal relationship and a few studies were selected for a quantitative evaluation. In particular, for populations living within two kilometres of landfills there was limited evidence of congenital anomalies and low birth weight with excess risk of 2 percent and 6 percent, respectively. The excess risk tended to be higher when sites dealing with toxic wastes were considered. For populations living within three kilometres of old incinerators, there was limited evidence of an increased risk of cancer, with an estimated excess risk of 3.5 percent. The confidence in the evaluation and in the estimated excess risk tended to be higher for specific cancer forms such as non-Hodgkin's lymphoma and soft tissue sarcoma than for other cancers.ConclusionsThe studies we have reviewed suffer from many limitations due to poor exposure assessment, ecological level of analysis, and lack of information on relevant confounders. With a moderate level confidence, however, we have derived some effect estimates that could be used for health impact assessment of old landfill and incineration plants. The uncertainties surrounding these numbers should be considered carefully when health effects are estimated. It is clear that future research into the health risks of waste management needs to overcome current limitations.
Psychological stress-related processes are thought to contribute to the development and progression of type 2 diabetes, but the biological mechanisms involved are poorly understood. Here, we tested the notion that people with type 2 diabetes experience chronic allostatic load, manifest as dynamic disturbances in reactivity to and recovery from stress across multiple (cardiovascular, neuroendocrine, inflammatory, metabolic) biological systems, coupled with heightened experience of chronic life stress. We carried out an experimental comparison of 140 men and women aged 50-75 y with type 2 diabetes and 280 nondiabetic individuals matched on age, sex, and income. We monitored blood pressure (BP) and heart rate, salivary cortisol, plasma interleukin (IL)-6, and total cholesterol in response to standardized mental stress, and assessed salivary cortisol over the day. People with type 2 diabetes showed impaired poststress recovery in systolic and diastolic BP, heart rate and cholesterol, and blunted stress reactivity in systolic BP, cortisol, cholesterol, and IL-6. Cortisol and IL-6 concentrations were elevated, and cortisol measured over the day was higher in the type 2 diabetes group. Diabetic persons reported greater depressive and hostile symptoms and greater stress experience than did healthy controls. Type 2 diabetes is characterized by disruption of stress-related processes across multiple biological systems and increased exposure to life stress. Chronic allostatic load provides a unifying perspective with implications for etiology and patient management.ype 2 diabetes has a heterogeneous pathophysiology in which β-cell dysfunction and insulin resistance play pivotal roles (1). Stress-related factors may contribute to risk of type 2 diabetes through their impact on inflammatory, metabolic, cardiovascular, and neuroendocrine regulation (2). Socioeconomic adversity over the life course predicts type 2 diabetes in later life (3), whereas stress at work and more general indicators of perceived stress are associated with future diabetes (4, 5). There appears to be a bidirectional relationship between type 2 diabetes and depressive symptoms (6), and people with type 2 diabetes may report greater social isolation and more limited social support (7).These diverse associations between stress-related processes and diabetes are only partly accounted for by lifestyle factors such as physical inactivity, alcohol consumption, or adiposity, suggesting that direct psychobiological pathways may be involved. A helpful concept in this regard is allostatic load. Allostasis refers to the dynamic process of adaptation to environmental challenges through adjustments in multiple biological systems, including the hypothalamic-pituitary-adrenocortical (HPA) axis, autonomic nervous system, and metabolic and immune systems (8). Allostasis is essential for maintaining homeostasis, but repeated or sustained stimulation leads to allostatic load, the wear-and-tear that results from dysregulation of mediating processes. Allostatic load is freque...
BackgroundThe purpose of this study was to test whether lower socioeconomic status (SES) augments the effect of psychological distress on mortality from stroke or coronary heart disease (CHD).MethodsWe prospectively linked data from 66,500 participants 35 years or older in the Health Survey for England, selected using stratified random sampling from 1994 to 2004, and free of cardiovascular disease and cancer at baseline, with mortality records. The median follow-up time was 7.9 years. SES was indexed by occupational class, and psychological distress was assessed using the 12-item General Health Questionnaire (GHQ-12).ResultsAfter adjustment for demographic and clinical variables, both psychological distress and low SES were associated with increased mortality: the hazard ratios (HR) for one-category increase in low SES (three categories in total) were 1.15 for stroke-death (95% confidence interval [CI] = 1.00–1.31, p = .043) and 1.24 for CHD-death (95% CI = 1.09–1.41, p = .001); the HR for one-category increase in GHQ-12 (three categories in total) was 1.18 for stroke-death (95% CI = 1.07–1.30, p = .001) and 1.24 for CHD-death (95% CI = 1.13–1.36, p < .001). In stratified analyses, the strongest associations were found in the lowest SES categories: the HR for GHQ-12 toward stroke-death was 1.15 in high-SES participants (95% CI = 0.97–1.37, p = .107) and 1.31 in low-SES ones (95% CI = 1.13–1.51, p < .001); the HR for GHQ-12 toward CHD-death was 1.10 in high-SES participants (95% CI = 0.97–1.25, p = .129) and 1.33 in low-SES ones (95% CI = 1.19–1.48, p < .001).ConclusionsPeople in low socioeconomic circumstances are more vulnerable to the adverse effect of psychological distress. This pattern should be taken into account when evaluating the association between psychosocial variables and health outcomes.
ObjectivesThe objective of this study was to examine the association between cortisol response to mental stress and high-sensitivity cardiac troponin T (hs-cTnT) in healthy older individuals without history of cardiovascular disease (CVD).BackgroundMental stress is a recognized risk factor for CVD, although the mechanisms remain unclear. Cortisol, a key stress hormone, is associated with coronary atherosclerosis and may accentuate structural and functional cardiac disease.MethodsThis cross-sectional study involved 508 disease-free men and women aged 53 to 76 years drawn from the Whitehall II epidemiological cohort. We evaluated salivary cortisol response to standardized mental stress tests (exposure) and hs-cTnT plasma concentration using a high-sensitivity assay (outcome). We measured coronary calcification using electron-beam dual-source computed tomography and Agatston scores.ResultsAfter adjustment for demographic and clinical variables associated with CVD as well as for inflammatory factors, we found a robust association between cortisol response and detectable hs-cTnT (odds ratio [OR]: 3.98; 95% confidence interval [CI]: 1.60 to 9.92; p = 0.003). The association remained when we restricted the analysis to participants without coronary calcification (n = 222; OR: 4.77; 95% CI: 1.22 to 18.72; p = 0.025) or when we further adjusted for coronary calcification in participants with positive Agatston scores (n = 286; OR: 7.39; 95% CI: 2.22 to 26.24; p = 0.001).ConclusionsWe found that heightened cortisol response to mental stress was associated with detectable plasma levels of cTnT using high-sensitivity assays in healthy participants, independently of coronary atherosclerosis. Further research is needed to understand the role of psychosocial stress in the pathophysiology of cardiac cell damage.
We reviewed the literature concerning the innate response from nasal and oral epithelial cells and their reaction to hydrogen peroxide (H 2 O 2 ). Hydrogen peroxide is produced physiologically by oral bacteria and plays a significant role in the balance of oral microecology since it is an important antimicrobial agent. In the epithelial cells, the enzyme superoxide dismutase catalyzes a reaction leading from hydrogen peroxide to the ion superoxide. The induced oxidative stress stimulates a local innate response via activation of the toll-like receptors and the NF-κB. Those kinds of reactions are also activated by viral infections. Virus-induced oxidative stress plays an important role in the regulation of the host immune system and the specific oxidant-sensitive pathway is one of the effective strategies against viral infections. Therefore, nose/mouth/throat washing with hydrogen peroxide may enhance those local innate responses to viral infections and help protect against the current coronavirus pandemic. We strongly encourage the rapid development of randomized controlled trials in both SARS-CoV-2 positive and negative subjects to test the preliminary findings from the in-vitro and in-vivo observational studies that we identified.
In cases of maxillary constriction and nasal airway obstruction, RME has proved to be efficient for the improvement of nasal respiration in children via a widening effect on the nasopharyngeal cavity.
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