8 research outputs found

    Environmental exposures: an underrecognized contribution to noncommunicable diseases

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    Previous attempts to determine the degree to which exposure to environmental factors contribute to noncommunicable diseases (NCDs) have been very conservative and have significantly underestimated the actual contribution of the environment for at least two reasons. Firstly, most previous reports have excluded the contribution of lifestyle behavioral risk factors, but these usually involve significant exposure to environmental chemicals that increase risk of disease. Secondly, early life exposure to chemical contaminants is now clearly associated with an elevated risk of several diseases later in life, but these connections are often difficult to discern. This is especially true for asthma and neurodevelopmental conditions, but there is also a major contribution to the development of obesity and chronic diseases. Most cancers are caused by environmental exposures in genetically susceptible individuals. In addition, new information shows significant associations between cardiovascular diseases and diabetes and exposure to environmental chemicals present in air, food, and water. These relationships likely reflect the combination of epigenetic effects and gene induction. Environmental factors contribute significantly more to NCDs than previous reports have suggested. Prevention needs to shift focus from individual responsibility to societal responsibility and an understanding that effective prevention of NCDs ultimately relies on improved environmental management to reduce exposure to modifiable risks

    Profili gestionali e di controllo delle aziende vitivinicole

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    Background: Waste from end-of-life electrical and electronic equipment, known as e-waste, is a rapidly growing global problem. E-waste contains valuable materials that have an economic value when recycled. Unfortunately, the majority of e-waste is recycled in the unregulated informal sector and results in significant risk for toxic exposures to the recyclers, who are frequently women and children. Objectives: The aim of this study was to document the extent of the problems associated with inappropriate e-waste recycling practices. Methods: This was a narrative review that highlighted where e-waste is generated, where it is recycled, the range of adverse environmental exposures, the range of adverse health consequences, and the policy frameworks that are intended to protect vulnerable populations from inappropriate e-waste recycling practices. Findings: The amount of e-waste being generated is increasing rapidly and is compounded by both illegal exportation and inappropriate donation of electronic equipment, especially computers, from developed to developing countries. As little as 25% of e-waste is recycled in formal recycling centers with adequate worker protection. The health consequences of both direct exposures during recycling and indirect exposures through environmental contamination are potentially severe but poorly studied. Policy frameworks aimed at protecting vulnerable populations exist but are not effectively applied. Conclusions: E-waste recycling is necessary but it should be conducted in a safe and standardized manor. The acceptable risk thresholds for hazardous, secondary e-waste substances should not be different for developing and developed countries. However, the acceptable thresholds should be different for children and adults given the physical differences and pronounced vulnerabilities of children. Improving occupational conditions for all e-waste workers and striving for the eradication of child labor is non-negotiable

    Health consequences of environmental exposures: causal thinking in global environmental epidemiology

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    The 2010 Global Burden of Disease estimates indicate a trend toward increasing years lived with disability from chronic noncommunicable diseases (NCDs). Risk factors examined included smoking, diet, alcohol, drug abuse, and physical inactivity. By contrast, little consideration was given to accumulating evidence that exposures to environmental chemicals, psychosocial stress, and malnutrition during fetal development and across the life span also increase risk of NCDs. To address this gap, we undertook a narrative review of early-life environmental contributions to disease. We documented numerous etiologic associations. We propose that future GBD estimates use an expanded approach for assessing etiologic contributions of environmental exposures to recognized disease risk factors. We argue that broadening the definition of environmental disease, together with improved methods of assessing early life exposures and their health outcomes across the life span, will allow better understanding of causal associations and provide the incentives required to support strategies to control avoidable exposures and reduce disease risk

    Developmental origins of health and disease: Integrating environmental influences

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    There are now robust data supporting the Developmental Origins of Health and Disease (DOHaD) paradigm. This includes human and animal data focusing on nutrition or environmental chemicals during development. However, the term DOHaD has not been generally accepted as the official term to be used when one is concerned with understanding the pathophysiological basis for how environmental influences acting during early development influence the risk of later noncommunicable diseases. Similarly, there is no global research or public health program built around the DOHaD paradigm that encompasses all aspects of environment. To better inform the global health efforts aimed at addressing the growing epidemic of chronic noncommunicable diseases of environmental origin, we propose a two-pronged approach: first, to make it clear that the current concept of DOHaD comprehensively includes a range of environmental factors and their relevance to disease occurrence not just throughout the life span but potentially across several generations; and second, to initiate the discussion of how adoption of DOHaD can promote a more realistic, accurate, and integrative approach to understanding environmental disruption of developmental programming and better inform clinical and policy interventions

    Workgroup Report: Public Health Strategies for Reducing Aflatoxin Exposure in Developing Countries

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    In response to consecutive outbreaks of acute aflatoxicosis in Kenya in 2004–2005 (responsible for over 150 deaths) a workshop of international experts and health officials was convened in Geneva, July 2005, by the United States Centers for Disease Control and Prevention and the World Health Organization. The goals of the workshop were to identify public health strategies for the reduction of morbidity and mortality associated with the consumption of aflatoxin-contaminated food in the developing world and to outline an integrated plan that more effectively combines public health and agricultural approaches to the control of aflatoxins. Following discussions concerning what is known about aflatoxins, participants were able to identify gaps in current knowledge about acute and chronic human health effects of aflatoxins, surveillance and food monitoring, analytic methods, and the efficacy of intervention strategies. Four themes emerged from the workshop and warrant immediate attention: 1) quantify the human health impacts and the burden of disease due to aflatoxin exposure; 2) compile an inventory, evaluate the efficacy, and disseminate results of on-going intervention strategies; 3) develop and augment the disease surveillance, food monitoring, laboratory, and public health response capacity of affected regions; and 4) develop a response protocol that can be used in the event of an outbreak of acute aflatoxicosis. This report summarizes the workshop findings.JRC.D.8-Food safety and qualit

    Long-term survival of patients with CLL after allogeneic transplantation: A report from the European Society for Blood and Marrow Transplantation

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    Even with the availability of targeted drugs, allogeneic hematopoietic cell transplantation (allo-HCT) is the only therapy with curative potential for patients with CLL. Cure can be assessed by comparing long-term survival of patients to the matched general population. Using data from 2589 patients who received allo-HCT between 2000 and 2010, we used landmark analyses and methods from relative survival analysis to calculate excess mortality compared with an age-, sex- and calendar year-matched general population. Estimated event-free survival, overall survival and non-relapse mortality (NRM) 10 years after allo-HCT were 28% (95% confidence interval (CI), 25-31), 35% (95% CI, 32-38) and 40% (95% CI, 37-42), respectively. Patients who passed the 5-year landmark event-free survival (N=394) had a 79% probability (95% CI, 73-85) of surviving the subsequent 5 years without an event. Relapse and NRM contributed equally to treatment failure. Five-year mortality for 45- and 65-year-old reference patients who were event-free at the 5-year landmark was 8% and 47% compared with 3% and 14% in the matched general population, respectively. The prospect of long-term disease-free survival remains an argument to consider allo-HCT for young patients with high-risk CLL, and programs to understand and prevent late causes of failure for long-term survivors are warranted, especially for older patients
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