Changes in the type and prevalence of human diseases have occurred during shifts in human social organization, for example, from hunting and gathering to agriculture and with urbanization during the ...Industrial Revolution. The recent emergence and reemergence of infectious diseases appears to be driven by globalization and ecological disruption. We propose that habitat destruction and biodiversity loss associated with biotic homogenization can increase the incidence and distribution of infectious diseases affecting humans. The clearest connection between biotic homogenization and infectious disease is the spread of nonindigenous vectors and pathogens. The loss of predators and hosts that dilute pathogen transmission can also increase the incidence of vectorborne illnesses. Other mechanisms include enhanced abiotic conditions for pathogens and vectors and higher host-pathogen encounter rates. Improved understanding of these causal mechanisms can inform decisionmaking on biodiversity conservation as an effective way to protect human health.
Increasing evidence shows that elevated levels of particulate matter (PM) can exacerbate existing asthma, while evidence that PM can promote the induction of asthma is limited. PM in ambient air has ...been associated with increased emergency room visits and medication use by asthmatics. Controlled human exposure studies of acid aerosols suggest increased responses among adolescent asthmatics. Increased ambient and indoor levels of bioaerosols (e.g., house dust mite, fungal spores, endotoxin) have been associated with exacerbation of asthma. Environmental Protection Agency (EPA) studies focus on the effects of exposing humans and animal models to a combination of various PM samples (e.g., diesel exhaust particles, oil fly ash) and allergens (e.g., house dust mite, ovalbumin). These research efforts to understand the mechanisms by which PM exposure can promote allergic sensitization and exacerbate existing asthma concentrate on the role of transition metals. Exposure of animal models to combined PM and allergen promotes allergic sensitization and increases allergic inflammation and airway hyperresponsiveness. Exposure of healthy human volunteers to emission source PM samples promotes inflammation and increased indices of oxidant formation correlating with the quantity of transition metals in the samples. Results of these studies suggest that transition metals in ambient PM promote the formation of reactive oxygen species and subsequent lung injury, inflammation, and airway hyperresponsiveness leading to airflow limitation and symptoms of asthma.
“Health is a state of complete physical, mental and social well-being and not merely the absence of disease or infirmity” states the WHO. However, the current focus in this important area seems to be ...on reducing diseases, while less attention is paid on aspects how to increase the well-being of populations.
This paper reviews three examples where well-being has drawn attention of the public and policy makers, and compares the policies of two wealthy countries. The first example is noise. Noise can reduce sleep quality and cause physiological, mental, and social effects. In Switzerland, noise receives a lot of attention by the public. Swiss laws are extensive, e.g., they prohibit trucks and planes from traveling at night. In the USA, there is little public attention and no national strategy against environmental noise. The second example is aesthetics and recreation. Many humans seek contact with the beauty of nature. The USA and Switzerland have similar strategies for achieving clear waters, while the protection of scenic views is approached very differently. Lifestyle is the last example. In the USA, the desire for individual freedom is a leading cause for suburban sprawl, a car-dependent sedentary lifestyle resulting in obesity, asthma and loss of community spirit. In Switzerland, a strict land use planning seeks to balance individual and public interests and stresses public transportation, which seems to be a more promising approach.
Paying attention to aspects of well-being while developing political strategies might be a promising model to tackle environmental problems. Successful strategies employed so far seem to include the public, local authorities, politicians and scientists in this process, which might have been a key for their success.
This article categorizes four kinds of adverse effects to human health caused by ecosystem change: direct, mediated, modulated, and systems failure. The effects are categorized on their scale, ...complexity, and lag-time. Some but not all of these can be classified as resulting from reduced ecosystem services. The articles also explores the impacts that different socioeconomic-ecologic scenarios are likely to have on human health and how changes to human health may, in turn, influence the unfolding of four different plausible future scenarios. We provide examples to show that our categorization is a useful taxonomy for understanding the complex relationships between ecosystems and human well-being and for predicting how future ecosystem changes may affect human health.
Despite that a significant body of published literature exists in the complex area of interconnection among the environment, ecosystems, and human activity, relatively little attention has been paid ...to the integration and analysis of ecological and human health data in the form of a conceptual model. Human and ecological health protection generally have been treated as separate domains of policy, with significant differences in both the analytic methods used to characterize risks and the policies developed for risk reduction. Understanding the relationships among population growth, development, natural resource use, the environment, human health, and ecosystems is an important area of both scientific inquiry and environmental policy. The present paper focuses on the development of a conceptual model for understanding disease causation, particularly infectious disease, and the implications of such a model for public policy. The conceptual model incorporates ecological and human health risk assessment information applied to case studies of two infectious diseases. This article takes an initial step toward formalizing the conceptual model so that research and assessment procedures can be developed.
An acute (2 h) exposure of humans to 0.4 ppm ozone initiates biochemical changes in the lung that result in the production of components mediating inflammation and acute lung damage as well as ...components having the potential to lead to long-term effects such as fibrosis. However, many people are exposed to lower levels of ozone than this, but for periods of several hours. Therefore, it is important to determine if a prolonged exposure to low levels of ozone is also capable of causing cellular and biochemical changes in the lung. Nonsmoking males were randomly exposed to filtered air and either 0.10 ppm ozone or 0.08 ppm ozone for 6.6 h with moderate exercise (40 liters/min). Bronchoalveolar lavage (BAL) was performed 18 h after each exposure, and cells and fluid were analyzed. The BAL fluid of volunteers exposed to 0.10 ppm ozone had significant increases in neutrophils (PMNs), protein, prostaglandin E2 (PGE2), fibronectin, interleukin-6 (IL-6), and lactate dehydrogenase (LDH) compared with BAL fluid from the same volunteers exposed to filtered air. In addition, there was a decrease in the ability of alveolar macrophages to phagocytize yeast via the complement receptor. Exposure to 0.08 ppm ozone resulted in significant increases in PMNs, PGE2, LDH, IL-6, alpha 1-antitrypsin, and decreased phagocytosis via the complement receptor. However, BAL fluid protein and fibronectin were no longer significantly elevated. We conclude that exposure of humans to as low a level as 0.08 ppm for 6.6 h is sufficient to initiate an inflammatory reaction in the lung.
Acute exposure of humans to ozone results in reversible respiratory function decrements and cellular and biochemical changes leading to the production of substances which can mediate inflammation and ...acute lung injury. While pulmonary function decrements occur almost immediately after ozone exposure, it is not known how quickly the cellular and biochemical changes indicative of inflammation occur in humans. Increased bronchoalveolar lavage (BAL) fluid levels of neutrophils (PMNs) and prostaglandins (PGE2) have been reported in humans as early as 3 hr and as late as 18 hr after exposure. The purpose of this study was to determine whether a broad range of inflammatory mediators are elevated in BAL fluid within 1 hr of exposure. We exposed eight healthy volunteers twice: once to 0.4 ppm ozone and once to filtered air. Each exposure lasted for 2 hr during which the subjects underwent intermittent heavy exercise (66 liters/min). BAL was performed 1 hr after the exposure. Ozone induced rapid increases in PMNs, total protein, LDH, α-1 antitrypsin, fibronectin, PGE2, thromboxane B2, C3a, tissue factor, and clotting factor VII. In addition, there was a decrease in the recovery of total cells and alveolar macrophages, and decreased ability of alveolar macrophages to phagocytizeCandida albicans.A comparison of these changes with changes observed in an earlier study in which subjects underwent BAL 18 hr after an identical exposure regimen indicates that IL-6 and PGE2levels were higher 1 hr after exposure than 18 hr after exposure, fibronectin and tissue-plasminogen activator levels were higher 18 hr after exposure, and that PMNs, protein, and C3a were present at essentially the same levels at both times. These results indicate that (i) several inflammatory mediators are already elevated 1 hr after exposure; (ii) some mediators achieve their maximal levels in BAL fluid at different times following exposure. These data suggest that the inflammatory response is complex, depending on a cascade of timed events, and that depending on the mediator of interest one must choose an appropriate sampling time.
Air Pollution and Health Maynard, Robert L; Holgate, Stephen T; Koren, Hillel S ...
1999, 1999-04-21
eBook
Concern about the impact of air pollution has led governments and local authorities across the world to regulate, among other things, the burning of fossil fuels, industrial effluence, cigarette ...smoke, and aerosols. This legislation has often followed dramatic findings about the impact of pollution on human health. At the same time there have been significant developments in our ability to detect and quantify pollutants and a proliferation of urban and rural air pollution networks to monitor levels of atmospheric contamination. Air Pollution and Health is the first fully comprehensive and current account of air pollution science and it impact on human health. It ranges in scope from meteorology, atmospheric chemistry, and particle physics to the causes and scope of allergic reactions and respiratory, cardiovascular, and related disorders. The book has substantial international coverage and includes sections on cost implications, risk assessment, regulation, standards, and information networks. The multidisciplinary approach and the wide range of issues covered makes this an essential book for all concerned with monitoring and regulating air pollution as well as those concerned with its impact on human health. * Only comprehensive text covering all the important air pollutants and relating these to human health and regulatory bodies * Brings together a wide range of issues concerning air pollution in an easily accessible format * Contributions from government agencies in the US and UK provide information on public policy and resource networks in the areas of health promotion and environmental protection
Interleukin (IL)-1beta, IL-6, IL-8, tumor necrosis factor (TNF)-alpha, and the secreted form of the IL-1 receptor antagonist (sIL-1RA) are involved in the inflammatory response to inhaled grain dust. ...Previously, we found considerable production of these cytokines in the lower respiratory tract of workers exposed by inhalation to aqueous extracts of corn dust extract. Alveolar macrophages (AM) have long been considered the cell type responsible for producing these cytokines, and only recently has it been realized that airway epithelial cells may also be involved in cytokine production. In order to determine whether airway epithelia are involved in the inflammatory response to inhaled corn dust extract and to compare the magnitude of response of bronchial epithelial cells (BE) and bronchoalveolar lavage (BAL) cells, we used the reverse transcriptase/polymerase chain reaction (RT/PCR) technique in a semiquantitative manner to evaluate the concentration of IL-1beta, IL-6, IL-8, TNF-alpha, and sIL-1RA. Alveolar cells were obtained by BAL, and BE were obtained by endobronchial brush biopsy from 15 grain handlers 6 h after experimental inhalation of saline or an aqueous corn dust extract. After inhalation of saline, BE expressed low but detectable levels of IL-6, IL-8, and IL-1beta (> 1 complementary DNA cDNA molecule/cell). After inhalation of corn dust extract, the expression of messenger RNA (mRNA) for IL-1beta and IL-8 in the BE were significantly increased, whereas no change was seen in IL-6, sIL-1RA, and TNF-alpha mRNA expression. Comparing cytokine mRNA levels in BE and BAL cells from the same subjects after inhalation of corn dust extract, BE and BAL cells expressed equivalent amounts of IL-8 mRNA; IL-1beta was 11-fold higher in BAL cells; and TNF-alpha and sIL-1RA were expressed exclusively by BAL cells. Immunostaining for the cytokines in BAL cells showed cytokine protein expression in AMs but not in polymorphonuclear cells (PMNs). On the other hand, sIL-1RA was strongly expressed in both AMs and PMNs. Analysis of cytokine protein levels in endobronchial lavage (EBL) fluid demonstrated that only IL-8 was released in detectable amounts into the airway lumen, whereas all the other cytokines of interest were exclusively found in the BAL fluid. Thus, within 6 h after inhalation exposure to corn dust extract, BE appear to contribute to airway inflammation by producing IL-8. AMs are responsible for most of the IL-1beta and IL-6 production in the alveolar region, whereas AMs and PMNs both produce sIL-1RA. Our findings suggest that the inflammatory response to inhaled grain dust is compartmentalized, involving specific mediators of inflammation released by macrophages, neutrophils, and airway epithelial cells.
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