The Experts below are selected from a list of 294 Experts worldwide ranked by ideXlab platform
James H Hull - One of the best experts on this subject based on the ideXlab platform.
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airway dysfunction in elite athletes an Occupational Lung Disease
Allergy, 2013Co-Authors: Ollie Price, Paul Cullinan, Les Ansley, Andrew Menziesgow, James H HullAbstract:Airway dysfunction is prevalent in elite endurance athletes and when left untreated may impact upon both health and performance. There is now concern that the intensity of hyperpnoea necessitated by exercise at an elite level may be detrimental for an athlete's respiratory health. This article addresses the evidence of causality in this context with the aim of specifically addressing whether airway dysfunction in elite athletes should be classified as an Occupational Lung Disease. The approach used highlights a number of concerns and facilitates recommendations to ensure airway health is maintained and optimized in this population. We conclude that elite athletes should receive the same considerations for their airway health as others with potential and relevant Occupational exposures.
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Airway dysfunction in elite athletes – an Occupational Lung Disease?
Allergy, 2013Co-Authors: Ollie Price, Paul Cullinan, Les Ansley, Andrew Menzies-gow, James H HullAbstract:Airway dysfunction is prevalent in elite endurance athletes and when left untreated may impact upon both health and performance. There is now concern that the intensity of hyperpnoea necessitated by exercise at an elite level may be detrimental for an athlete's respiratory health. This article addresses the evidence of causality in this context with the aim of specifically addressing whether airway dysfunction in elite athletes should be classified as an Occupational Lung Disease. The approach used highlights a number of concerns and facilitates recommendations to ensure airway health is maintained and optimized in this population. We conclude that elite athletes should receive the same considerations for their airway health as others with potential and relevant Occupational exposures.
Martha Stanbury - One of the best experts on this subject based on the ideXlab platform.
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The identification of Occupational Lung Disease from hospital discharge data.
Journal of Occupational and Environmental Medicine, 1991Co-Authors: Windau J, Kenneth D. Rosenman, Henry A. Anderson, Hanrahan L, Rudolph L, Martha Stanbury, Stark AAbstract:The Bureau of Labor Statistics-State Health Department Select Committee on Occupational Illnesses and Injuries conducted a study of hospital discharge records to determine their usefulness for identifying cases of Occupational Disease. Four states searched the diagnosis fields on computerized hospital discharge records for selected Occupational Lung Diseases; pneumoconiosis, extrinsic allergic alveolitis, and respiratory conditions due to chemical fumes and vapors. The hospital discharge data identified more cases of pneumoconiosis than did the BLS data systems. Numerous cases of extrinsic allergic alveolitis and respiratory conditions due to chemical fumes and vapors were also identified. Patterns evidenced in the data were generally consistent with current knowledge of the Diseases. The inclusion of industry and occupation on the hospital discharge record, further study of the quality of diagnosis coding, and the use of these data by additional states will enhance the usefulness of these data for Occupational Disease surveillance.
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surveillance of Occupational Lung Disease comparison of hospital discharge data to physician reporting
American Journal of Public Health, 1990Co-Authors: Kenneth D. Rosenman, L Trimbath, Martha StanburyAbstract:A survey of 762 New Jersey physicians showed that 35% reported seeing patients with either asbestosis, coal worker's pneumoconiosis, Occupational asthma or silicosis. Three to four times as many patients with these diagnoses were seen as outpatients as were hospitalized. The implications of these results in using hospital discharge data for Occupational Disease surveillance are discussed.
Jerry Spiegel - One of the best experts on this subject based on the ideXlab platform.
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correction to tackling injustices of Occupational Lung Disease acquired in south african mines recent developments and ongoing challenges
Globalization and Health, 2018Co-Authors: Barry Kistnasamy, Annalee Yassi, Jessica Yu, Samuel J Spiegel, Andre Fourie, Stephen Barker, Jerry SpiegelAbstract:Following publication of the original article [1], the author has request the addition of ‘Deputy’ to endnote number 1 (addition highlighted in bold):
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tackling injustices of Occupational Lung Disease acquired in south african mines recent developments and ongoing challenges
Globalization and Health, 2018Co-Authors: Barry Kistnasamy, Annalee Yassi, Jessica Yu, Samuel J Spiegel, Andre Fourie, Stephen Barker, Jerry SpiegelAbstract:South Africa’s mineral resources have produced, and continue to produce, enormous economic wealth; yet decades of colonialism, apartheid, capital flight, and challenges in the neoliberal post-apartheid era have resulted in high rates of Occupational Lung Disease and low rates of compensation for ex-miners and their families. Given growing advocacy and activism of current and former mine workers, initiatives were launched by the South African government in 2012 to begin to address the legacy of injustice. This study aimed to assess developments over the last 5 years in providing compensation, quantify shortfalls and explore underlying challenges. Using the database with compensable Disease claims from over 200,000 miners, the medical assessment database of 400,000 health records and the employment database with 1.6 million miners, we calculated rates of claims, unpaid claims and shortfall in claim filing for each of the southern African countries with at least 25,000 miners who worked in South African mines, by Disease type and gender. We also conducted interviews in Johannesburg, Eastern Cape, Lesotho and a local service unit near a mine site, supplemented by document review and auto-reflection, adopting the lens of a critical rights-based approach. By the end of 2017, 111,166 miners had received compensation (of which 55,864 were for permanent Lung impairment, and another 52,473 for tuberculosis), however 107,714 compensable claims remained unpaid. Many (28.4%) compensable claims are from Mozambique, Lesotho, Swaziland, Botswana and elsewhere in southern Africa, a large proportion of which have been longstanding. A myriad of diverse systemic barriers persist, especially for workers and their families outside South Africa. Calculating predicted burden of Occupational Lung Disease compared to compensable claims paid suggests a major shortfall in filing claims in addition to the large burden of still unpaid claims. Despite progress made, our analysis reveals ongoing complex barriers and illustrates that the considerable underfunding of the systems required for sustained prevention and social protection (including compensation) needs urgent attention. With class action suits in the process of settlement, the globalized mining sector is now beginning to be held accountable. A critical rights-based approach underlines the importance of ongoing concerted action by all.
David Rees - One of the best experts on this subject based on the ideXlab platform.
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Occupational Lung Disease in the south african mining industry research and policy implementation
Journal of Public Health Policy, 2011Co-Authors: Jill Murray, Tony Davies, David ReesAbstract:South African miners face an epidemic of Occupational Lung Diseases. Despite a plethora of research on the mining industry, and the gold mining industry in particular, research impact (including Disease surveillance) on policy implementation and Occupational health systems performance lags. We describe the gold mining environment, and research on silicosis, tuberculosis, HIV and AIDS, and compensation for Occupational Disease including initiatives to influence policy and thus reduce dust levels and Disease. As these have been largely unsuccessful, we identify possible impediments, some common to other low- and middle-income countries, to the translation of research findings and policy initiatives into effective interventions.
Kathleen Kreiss - One of the best experts on this subject based on the ideXlab platform.
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Occupational Lung Disease from case reports to prevention
Chest, 2013Co-Authors: Kathleen KreissAbstract:Flock worker’s Lung Disease presents a useful paradigm for identifying new Occupational causes of Lung Disease. It is an unusual interstitial Lung Disease characterized by lymphocytic bronchiolitis and peribronchiolitis in workers exposed to flock fibers in manufacturing velvet-like fabrics, fuzzy greeting cards and wall papers, and automotive gaskets and glove box surfaces. Flock is made by cutting short synthetic fibers from bundles of parallel monofilaments of nylon or other polymers for application to adhesive-coated substrates. Unlike respirable mineral fibers such as asbestos, synthetic flock is visible, as illustrated in its typical applications. Since 1975, published case reports have raised suspicion of a respiratory hazard associated with various synthetic fibers, including polyester, nylon, and acrylic dust.1-3 With regard to synthetic flock, early reports in 1974 and 1981 of workplace evaluations by National Institute of Occupational Safety and Health (NIOSH) investigators attributed respiratory symptoms among workers to irritant properties of nonrespirable flock fibers on the upper airways but did not pursue the possibility of Lung Disease associated with flock work.4,5 Systematic workplace investigation of Lung Disease in workers that flock with synthetic fibers awaited the recognition of case clusters of interstitial Disease in small workforces, first in Kingston, Ontario, Canada, and then in Rhode Island, as detailed in the background of the follow-up study by Turcotte et al6 published in this issue of CHEST (see page 1642). Subsequently, additional cases or subclinical morbidity have been found in relation to nylon flock in two Massachusetts plants, to polyethylene flock in Spain, to polypropylene flock in Turkey, and to rayon flock in Kansas.6 The discovery of this new cause of interstitial Lung Disease required multidisciplinary investigations. Environmental scientists found a previously unsuspected nylon dust of respirable size in the air of the Rhode Island and Massachusetts workplaces. Physician-epidemiologists identified risk factors in exposed workforces, and animal toxicologists demonstrated biologic plausibility in rodents by intratracheal instillation of workplace dusts and components thereof. Working in production and maintenance, on a flocking range, and more days and hours per week; cleaning with compressed air; and a higher current and cumulative respirable dust exposure were found to be strongly associated with symptoms of the Disease. Finally, several observations affirmed that the exposure preceded the Disease and that the Disease improved with exposure cessation and recurred in several workers with re-exposure to the implicated work environments. Together, the investigations have reasonably fulfilled Bradford Hill’s criteria for demonstrating causation.7 Thus, one lesson of flock worker’s Lung Disease is that clinical suspicion of new causes of Occupational Lung Disease requires multidisciplinary public health investigation to generate actionable preventive measures in workplaces. Another lesson is that follow-up after workplace intervention is useful in evaluating a suspected cause. In Ontario, investigators noted that the adhesive used to adhere nylon flock to backing fabric had become contaminated with a fungal growth. Knowing that flock fibers are too large to be respirable and unaware of the presence of much smaller respirable-sized nylon particles in the work environment, they initially attributed the Disease cluster to suspected mycotoxins, a previously known cause of Lung Disease. Replacing the adhesive, however, did not prevent new cases. Workforces generally lack systematic medical surveillance, and public health resources for in-depth investigations and long-term follow-up vary by agency and over time. At the Ontario plant, limited investigation and lack of intervention follow-up delayed recognition of the preventable cause for years. The reexamination of cause awaited recognition of a new outbreak in Rhode Island. This recognition depended on the vigilance and curiosity of an Occupational physician who saw two young patients within 15 months of each other who worked in the same plant, both with interstitial Lung Disease.8 Had interstitial Lung Disease been common or had this physician not recognized a common place of employment, the opportunity for motivating the company to seek assistance from NIOSH would have been missed. This temporospacial cluster was challenging to NIOSH investigators, whose initial efforts were guided by evaluating causes of hypersensitivity pneumonitis and hampered by the lack of standard methods for identifying the respirable dust found in the plant. But eventually, the dust was found to have the precise melting point of nylon, clinching its identity. Its source was discovered by examining cut ends of flock with a scanning electron microscope. In cutting nylon filament to make flock and subsequently milling the cut flock to break up clumps of flock fibers fused together during cutting, fibrils of respirable size were created and released.9 The indicated intervention then was to exhaust key operations so that respirable fragments of nylon could be eliminated from workers’ breathing zones. The company was not interested in follow-up of exposures or medical monitoring; thus, as with the Ontario plant, no public health follow-up was done for the Rhode Island plant, and no effective medical surveillance appears to have been implemented.10 In light of a report of an excess of Lung cancer in the Rhode Island cohort,10 there are two Lung Disease outcomes for which workers might be monitored. A third lesson for pulmonary physicians is that identification of a cause or a new Occupational Disease is not itself sufficient to preclude continued exposure and risk to workers. In the United States, systematic medical surveillance of workers rarely occurs in the absence of regulation by the Occupational Safety and Health Administration. Regulation of hazards is a slow and contested process, even for substances affecting many more workers than are exposed in flock operations and even when a quantitative risk assessment is available to support exposure limits. In the current study by Turcotte et al,6 the high incidences of wheeze and pulmonary function changes in unaffected workers in the up to 10-year follow-up in 2001 warrant further follow-up and remind us that we have insensitive tools for diagnosing bronchiolar Diseases.11,12 In summary, the discovery of flock worker’s Lung and its cause is a great success story seldom replicated, despite the likelihood that many Occupational Lung Disease risks remain to be identified. The ingredients for such a success are vigilance and reporting of sentinel cases by clinical practitioners, carrying out in-depth public health investigations (eg, by involving NIOSH at 1-800-232-2114), maintaining openness to new causes, and following up preventive interventions to evaluate their effectiveness. Ultimately, primary prevention requires elimination or control of causative exposures.
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beryllium a paradigm for Occupational Lung Disease and its prevention
Occupational and Environmental Medicine, 2011Co-Authors: Kathleen KreissAbstract:In this issue of the journal, Van Dyke and colleagues have shown that the supra-typic genetic marker, HLA-DPB1(E69), has an additive and independent contribution with beryllium exposure to cell-mediated beryllium sensitisation and chronic beryllium Disease in a cohort at a US nuclear weapons plant.1 This finding of statistical independence between required beryllium exposure and genetic characteristics is quantitatively consistent with an earlier finding in a small beryllia ceramics operation,2 and is extended by a concurrent publication in a second, larger nuclear weapons plant population.3 In the latter case–control study, Van Dyke et al showed that the subset of rare HLA-DPB1(E69) alleles (non-*02), most with greater electronegativity in the antigen-binding groove,4 conferred much higher risk of sensitisation and Disease than the more common *02 HLA-DPB1(E69) genotypes: Both sensitisation and chronic beryllium Disease risks were equally associated with genotype, but these two health outcomes differed with respect to exposure risk. Cumulative and average lifetime beryllium exposures were associated with chronic beryllium Disease but not with beryllium sensitisation. Other recent studies of newly exposed beryllium workers demonstrate that sensitisation often occurs within months of employment, presumably before a beryllium Lung burden sufficient for chronic beryllium Disease is attained.5–7 Although the Van Dyke paper in this issue did not have sufficient numbers to analyse beryllium sensitisation and beryllium Disease cases separately, it showed compatible results, with the beryllium-sensitised cases having much lower indices of beryllium exposure compared with the chronic beryllium Disease …
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Occupational Lung Disease risk and exposure to butter flavoring chemicals after implementation of controls at a microwave popcorn plant
Public Health Reports, 2011Co-Authors: Richard Kanwal, Greg Kullman, Kathleen B Fedan, Kathleen KreissAbstract:Objectives. After an outbreak of severe Lung Disease among workers exposed to butter-flavoring chemicals at a microwave popcorn plant, we determined whether or not Lung Disease risk declined after implementation of exposure controls. Methods. National Institute for Occupational Safety and Health staff performed eight serial cross-sectional medical and industrial hygiene surveys at the plant from November 2000 through August 2003. Medical surveys included standardized questionnaires and spirometry testing. Industrial hygiene surveys measured levels of production-related air contaminants, including butter-flavoring chemicals such as diacetyl. All diacetyl concentrations above detectable limits were corrected for the effects of absolute humidity and days to sample extraction. Results. Ventilation and isolation of the production process resulted in one to three orders of magnitude reductions in diacetyl air concentrations in different areas of the plant. Workers with past high exposures had stable chest symptoms over time; nasal, eye, and skin irritation symptoms declined. New workers had lower symptom prevalences and higher Lung function than workers with past high exposures, and they did not worsen over time. In workers who had at least three spirometry tests, those with past high exposures were more likely to experience rapid declines in Lung function than new workers. Conclusions. Implemented controls lowered exposures to butter-flavoring chemicals and decreased Lung Disease risk for much of the plant workforce. Some workers with continuing potential for intermittent, short-term peak and measurable time-weighted exposures remain at risk and should use respiratory protection and have regularly scheduled spirometry to detect rapid Lung function declines that may be work-related. Close follow-up of such workers is likely to yield additional information on risks due to peak and time-weighted exposure levels.
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Emerging opportunities to prevent Occupational Lung Disease
Occupational and Environmental Medicine, 2007Co-Authors: Kathleen KreissAbstract:How to tackle new causes of Occupational Lung Disease over the next decade New opportunities to prevent Occupational Lung Diseases require the discovery of new Occupational Lung Diseases, new settings for recognised Occupational Lung Diseases, and new approaches to their prevention. Reviewing the last decade’s discoveries, we can learn how to recognise new prevention opportunities involving emerging Occupational Lung Diseases. Since 1996, some examples of newly recognised Occupational Lung Disease include flock workers’ Lung,1 hypersensitivity pneumonitis associated with biocontaminated synthetic metal working fluids,2 severe acute respiratory syndrome (SARS), asthma associated with 3-amino-5-mercapto-1,2,4-triazole (AMT) in herbicide manufacture;3 and bronchiolitis obliterans from flavouring chemicals.4 If the past is paradigm, approaches to recognition and prevention can proceed without knowing how to measure causal agents and without regulating them. Astute clinicians can play a vital role in suspecting an emerging Occupational cause when they diagnose a rare Disease or a cluster of more common or severe Disease. For example, Dr David Kern recognised that the occurrence of interstitial Lung Disease in two young men from the same small nylon flock plant indicated a likely risk for other employees.1 Similarly, Dr Alan Parmet reviewed medical records compiled by a lawyer for eight former microwave popcorn plant workers with bronchiolitis obliterans.4 Half of these cases were on Lung transplant lists—hardly to be expected in a young worker group from one small plant—and he reported the cases to public health authorities. In automotive plants with clusters of hypersensitivity pneumonitis, labour unions pressed for investigations of work-related aetiology across the industry. At a plant in Massachusetts, herbicide workers and …
