BERYLLIUM DISEASE by I

Total Page:16

File Type:pdf, Size:1020Kb

BERYLLIUM DISEASE by I Postgrad Med J: first published as 10.1136/pgmj.34.391.262 on 1 May 1958. Downloaded from 262 BERYLLIUM DISEASE By I. B. SNEDDON, M.B., Ch.B., F.R.C.P. Consultant Dermatologist, Rupert Hallam Department of Dermatology, Sheffield It is opportune in a symposium on sarcoidosis monary berylliosis which fulfilled the most to discuss beryllium disease because it mimics so stringent diagnostic criteria. closely the naturally occurring Boecks sarcoid and A beryllium case registry set up at the Massa- yet carries a far graver prognosis. chusetts General Hospital by Dr. Harriet Hardy Beryllium was first reported to possess toxic had collected by 1956 309 examples of the disease, properties by Weber and Englehardt (I933) in of whom 84 had died. The constant finding of Germany. They described bronchitis and acute beryllium in autopsy material from the fatal cases respiratory disease in workers extracting beryllium had proved beyond doubt the association between from ore. Similar observations were made by the granulomatous reaction and the metal. Marradi Fabroni (I935) in Italy and Gelman It is difficult to reconcile the paucity of accounts (I936) in Russia. Further reports came from of beryllium disease in this country with the large Germany in I942 where beryllium poisoning was amount of beryllium compounds which have been recognized as a compensatable disease. Towards used in the last ten The in the end of World War II the production and use years. only reports the medical literature are those of Agate (I948),copyright. of beryllium salts increased greatly in the United Sneddon (i955), and Rogers (1957), but several States, and in 1943 Van Ordstrand et al. reported others have reached public notice in the daily the first examples of chemical pneumonia in men press by reports of coroners' inquests and medico- extracting beryllium oxide from ore in Ohio. In legal actions. It is possible that there are others addition to the acute respiratory disease, it had undiagnosed which are at present labelled Boeck's also been recognized that an acute contact derma- sarcoidosis. titis and ulcers resembling chrome ulcers occurred workers in extraction amongst beryllium plants, http://pmj.bmj.com/ but it was not until 1946 that the first examples Pathology of delayed chemical pneumonitis were described The basic pathological change seen in material by Hardy and Tabershaw. from three autopsies by Chesner (1950) was an They drew attention to a slowly progressive intra-alveolar nodular granulomatous lesion which sarcoid-like change which involved the lungs, involved all the lung fields. The nodules were liver and other organs in workers who had been composed of a preponderance of large endothelial exposed sometimes for a very short time to cells with plasma cells, mononuclears and lympho- beryllium compounds. The striking feature of cytes. There was no caseation at any stage. on September 28, 2021 by guest. Protected the condition was the long latent period between Giant cells of both foreign body and Langhan's exposure to beryllium and the onset of symptoms. type were seen in large numbers. Inclusion This delay at first lead to doubt that beryllium bodies were seen within the giant cells in some itself was responsible for the pathological changes but not all cases. Spread occurred by aggregation and even as recently as I95I an annotation in the of nodules in a more diffuse fashion throughout Lancet suggested that the case against beryllium the alveolar septa. The diffuse reaction was at was not proven, though this was later contradicted first a polymorphous cellular one with later by Harriet Hardy (1951) who has so vigorously fibrosis and hyalinization. campaigned for better recognition of the danger. Hilar lymph nodes were invariably affected by It is in deference to her that the condition is the same granulomatous process. The liver was called beryllium disease in this article. involved in two of the three cases, but there were Since that time more and more cases have been no other visceral lesions. Similar granulomatous described in the United States of America. In reactions have been described in skin lesions I953 Denardi et al., in an authoritative review of associated with beryllium disease of the lung by the subject, reported 35 examples of chronic pul- Grier et al. (I948), who also gave the first account Postgrad Med J: first published as 10.1136/pgmj.34.391.262 on 1 May 1958. Downloaded from May 1958 SNEDDON: Beryllium Disease 263 of skin nodules due to accidental implantation of when attempting to differentiate the two con- beryllium in the skin. ditions. Lederer and Savage (1954), who have described Equally, respiratory function studies which the only example of beryllium granuloma of the show diminished vital capacity and slowing of skin in this country, noted pathological changes alveolar diffusion in beryllium disease are merely indistinguishable from sarcoidosis in part of the a measurement of the severity of the lung damage. lesion but extensive caseation in other areas. Impairment of respiratory function is, however, Although most investigators have failed to pro- found earlier and is more severe in beryllium duce pulmonary granulomata in animal experi- disease than in sarcoidosis. ments with beryllium compounds, Davies and Wilson (1948) has described the radiographic Harding (1950) succeeded in causing pulmonary appearance of the lungs as being in three stages: granulomata in rats after intra-tracheal injection (I) A fine ground-glass granularity through the of a mixture cf beryllium oxide and manganese whole of the lung fields; dioxide. (2) A superimposed recticular pattern; and (3) Very characteristic nodulation. The nodules Clinical Features varying in size from small to quite large, but not Symptoms may arise after a latent period from all cases progress through these stages. the last exposure to beryllium, of a few months Hilar gland enlargement does occur but never to over ten years, and the exposure time need without densities in the lung fields. It is note- only be a few weeks. Although the majority of worthy that the early changes may be so finely patients have worked in contact with beryllium granular that miniature mass radiography may compounds, Sterne and Eisenbud (I951) have not show them. recorded beryllium disease in residents in the near Many of the American articles do not refer to neighbourhood of beryllium extraction plants the results of tuberculin skin tests, but Hardy where the air contained less than ix±g. of beryllium states that in her series of cases, in contrast to million and was as low as sarcoidosis, the responses have not differed from per parts probably those of the On the other o.I ,ug. per million. The disease has also affected general population. copyright. relatives of beryllium workers whose only contact hand, Agate's patient showed a change from a was with soiled working clothes. positive Mantoux reaction of I/I,OOO to negative The onset is insidious with dyspnoea on exer- during the course of the illness, and in Rogers' tion, one of the first complaints. A dry paroxysmal (1957) patient and in two of the author's cases the cough, fatigue and loss of weight associated with Mantoux test was negative. anorexia are usual and periods of fever may occur. The Kveim test has only been performed on a As in sarcoidosis, quite advanced changes may few patients with beryllium disease, and the be present in the lungs without symptoms, and results have either been negative or a non-specific http://pmj.bmj.com/ such cases are discovered on routine chest radio- foreign body reaction. graphy. Biopsy of the liver may reveal a sarcoid-like Physical signs are usually minimal though club- granulomatous reaction indistinguishable from bing of the fingers and crackling rales throughout sarcoidosis. both lung fields and pleural friction have been The Differential described. Enlargement of the liver and spleen Diagnosis be but The differential diagnosis of beryllium disease may found, enlarged superficial lymph on September 28, 2021 by guest. Protected glands are very rare. Skin nodules of the same includes miliary tuberculosis, miliary carcino- type as those seen in sarcoidosis have occurred matosis, pneumoconiosis and haemosiderosis, but occasionally, and in the author's case linear sarcoid above all else it resembles Boeck's sarcoidosis and infiltrations in the site of previous skin damage the majority of reported cases were first thought by beryllium copper strip were a presenting and to be that condition. unusual feature. There are some differences between the two. For instance, no lesions of the eye, parotid or tonsil have been found in beryllium disease, and Investigative Procedure cervical and axillary node enlargement is rare. As Hardy (1956) has pointed out, many of the No cystic bone changes have ever been reported. laboratory procedures such as total serum proteins The course of beryllium disease tends to be more and globulin, electrophoretic pattern of serum, rapidly downhill than that of sarcoidosis, but these liver function studies, urinary and serum calcium slight differences are not of sufficient importance and urinary steroids may show abnormalities in to tip the scale when faced with a patient. beryllium disease just as they may in sarcoidosis, The original criteria of diagnosis of beryllium and therefore they are of little or no assistance disease established by American workers were: Postgrad Med J: first published as 10.1136/pgmj.34.391.262 on 1 May 1958. Downloaded from 264 POSTGRADUATE MEDICAL JOURNAL May 1958 (I) History of exposure to dusts and fumes of beryllium compounds. (2) Clinical course of the pulmonary syndrome including studies of pulmonary function. (3) Radiographic evidence of granuloma of the :":,;;.....::.,.. lung. (4) Lung biopsy and analysis for beryllium. In 1953, Denardi et al. reported the reliability of skin patch tests carried out with dilute solutions of beryllium salts in distinguishing between * .....
Recommended publications
  • Differential Diagnosis of Granulomatous Lung Disease: Clues and Pitfalls
    SERIES PATHOLOGY FOR THE CLINICIAN Differential diagnosis of granulomatous lung disease: clues and pitfalls Shinichiro Ohshimo1, Josune Guzman2, Ulrich Costabel3 and Francesco Bonella3 Number 4 in the Series “Pathology for the clinician” Edited by Peter Dorfmüller and Alberto Cavazza Affiliations: 1Dept of Emergency and Critical Care Medicine, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan. 2General and Experimental Pathology, Ruhr-University Bochum, Bochum, Germany. 3Interstitial and Rare Lung Disease Unit, Ruhrlandklinik, University of Duisburg-Essen, Essen, Germany. Correspondence: Francesco Bonella, Interstitial and Rare Lung Disease Unit, Ruhrlandklinik, University of Duisburg-Essen, Tueschener Weg 40, 45239 Essen, Germany. E-mail: [email protected] @ERSpublications A multidisciplinary approach is crucial for the accurate differential diagnosis of granulomatous lung diseases http://ow.ly/FxsP30cebtf Cite this article as: Ohshimo S, Guzman J, Costabel U, et al. Differential diagnosis of granulomatous lung disease: clues and pitfalls. Eur Respir Rev 2017; 26: 170012 [https://doi.org/10.1183/16000617.0012-2017]. ABSTRACT Granulomatous lung diseases are a heterogeneous group of disorders that have a wide spectrum of pathologies with variable clinical manifestations and outcomes. Precise clinical evaluation, laboratory testing, pulmonary function testing, radiological imaging including high-resolution computed tomography and often histopathological assessment contribute to make
    [Show full text]
  • European Respiratory Society Classification of the Idiopathic
    This copy is for personal use only. To order printed copies, contact [email protected] 1849 CHEST IMAGING American Thoracic Society– European Respiratory Society Classification of the Idiopathic Interstitial Pneumonias: Advances in Knowledge since 20021 Nicola Sverzellati, MD, PhD David A. Lynch, MB In the updated American Thoracic Society–European Respira- David M. Hansell, MD, FRCP, FRCR tory Society classification of the idiopathic interstitial pneumonias Takeshi Johkoh, MD, PhD (IIPs), the major entities have been preserved and grouped into Talmadge E. King, Jr, MD (a) “chronic fibrosing IIPs” (idiopathic pulmonary fibrosis and id- William D. Travis, MD iopathic nonspecific interstitial pneumonia), (b) “smoking-related IIPs” (respiratory bronchiolitis–associated interstitial lung disease Abbreviations: H-E = hematoxylin-eosin, and desquamative interstitial pneumonia), (c) “acute or subacute IIP = idiopathic interstitial pneumonia, IPF = IIPs” (cryptogenic organizing pneumonia and acute interstitial idiopathic pulmonary fibrosis, NSIP = nonspe- cific interstitial pneumonia, RB-ILD = respi- pneumonia), and (d) “rare IIPs” (lymphoid interstitial pneumonia ratory bronchiolitis–associated interstitial lung and idiopathic pleuroparenchymal fibroelastosis). Furthermore, it disease, UIP = usual interstitial pneumonia has been acknowledged that a final diagnosis is not always achiev- RadioGraphics 2015; 35:1849–1872 able, and the category “unclassifiable IIP” has been proposed. The Published online 10.1148/rg.2015140334 diagnostic interpretation of
    [Show full text]
  • Occupational Lung Disease - American Lung Association Site
    Lung Disease Data at a Glance: Occupational Lung Disease - American Lung Association site Sick Building Syndrome Racial Disparity Prevention: Monitor Safety and Recognize Breathing Hazards Changing the Face of Occupational Lung Disease Research ● Occupational lung disease is the number-one cause of work-related illness in the United States in terms of frequency, severity and preventability. ● Worldwide, about 20 percent to 30 percent of the male and five percent to 20 percent of the female working-age population may have been exposed to agents that cause cancer in the lungs during their working lives. ● Occupational asthma is the most prevalent occupational lung disease in the United States. Approximately 15 percent of asthma cases in the United States are due to occupational exposures. ● The cost of occupational injuries and illnesses in the United States totals more than $170 billion. In 2002, there were about 294,500 newly reported cases of occupational illness in private industry. ● A total of 2,591 work-related respiratory illnesses with days away from work (2.4 per 100,000 workers) occurred in private workplaces in 2000. The highest total for days away from work due to respiratory illnesses was in the manufacturing sector. ● In 2002, African Americans made up 18.8 percent of the 800,000 textile workers. Exposure to dusts generated while processing cotton can cause byssinosis, a chronic condition that results in blocked airways and impaired lung function. Between 1990 and 1999, African-American males had an age-adjusted mortality rate due to byssinosis that was 80 percent greater than White males. ● It is estimated that African Americans accounted for 20.7 percent of the 3.1 million cleaning and building service jobs, which involve exposure to noxious chemicals and biological contaminants.
    [Show full text]
  • Chemical Pneumonia in Workers Extracting Beryllium Oxide1
    Commentary and update: Chemical pneumonia in workers extracting beryllium oxide1 Merril Eisenbud, Sc.D. Nearly 1,000 cases of beryllium-related disease have leading to much published information dealing been reported in the United States since the first three with the many ramifications of beryllium disease. cases were reported by VanOrdstrand and his associ- Although similar subject material in the Euro- ates in 1943. In addition to acute chemical pneumoni- pean literature had called attention to the occur- tis, beryllium exposure has also resulted in berylliosis, rence of a disease resembling chemical pneumo- a chronic granulomatous disease. The largest number nitis among workers employed in the extraction of berylliosis cases was reported in the fluorescent 1 lamp industry where beryllium was used in phosphors of beryllium, the reports lacked continuity and until 1949. Other cases occurred due to air pollution the etiologic factors given to explain the disease in the vicinity of beryllium-producing factories and were problematic. The publication in the January exposure of family members to beryllium dust brought 1943 issue of the CLEVELAND CLINIC QUARTERLY home on contaminated work clothes. Many of the pe- culiar epidemiologic features of both the acute and was the first published in the United States and chronic forms of beryllium disease can be explained was followed by publications in other journals, by its sensitizing characteristics. The standards that not only by VanOrdstrand and his associates, but were established for the control of beryllium disease in also by investigators from other parts of the the later 1940s have been remarkably effective and United States and Europe.
    [Show full text]
  • Chronic Beryllium Disease
    Chronic Beryllium Disease Chronic beryllium disease (CBD) is a disease that primarily affects the lungs, causing inflammation, characteristic scars called granulomas and, in more severe cases, scarring called fibrosis. CBD is immune-mediated, meaning that CBD can develop only in individuals who have developed an immune response or “allergy” to beryllium metal, ceramic or alloy, termed beryllium sensitization (BeS). Beryllium sensitization occurs after a susceptible person breathes beryllium dust or fumes or if beryllium particles penetrate the skin. People are more likely to develop beryllium sensitization and CBD if they are susceptible or when they have (carry) certain genes, such as the HLA-DPB Glu69 gene. How do you develop CBD? It is important to know that no one develops CBD unless they are exposed to beryllium and develop an immune response (BeS) to it. Most people who are exposed to beryllium will not experience health effects. Studies have shown that on average, 1 – 6 percent of exposed workers develop beryllium sensitization, although the rates can be as high as 16 percent among workers with the highest exposures, such as beryllium machinists. Most workers who develop sensitization tend to do so early, but follow-up testing over the years continues to identify sensitization in individuals who were exposed up to 30 years earlier. What is beryllium? Beryllium is a naturally occurring element found in rock and soil in the form of beryl and bertrandite, respectively. Beryllium is lighter than aluminum, yet stiffer than steel. These properties make it useful in many industrial applications. While beryllium occurs naturally in soil, rocks and coal, it is because this beryllium is often bound up in solid rock and soil composition that naturally occurring air concentrations are extremely low, even in major urban areas.
    [Show full text]
  • Pneumoconioses
    Review Article Pneumoconioses Vinaya S. Karkhanis and J.M. Joshi Department of Pulmonary Medicine, T. N. Medical College and B.Y.L. Nair Hospital, Mumbai, India ABSTRACT Occupational lung diseases are caused or made worse by exposure to harmful substances in the work-place. “Pneumoconiosis” is the term used for the diseases associated with inhalation of mineral dusts. While many of these broad- spectrum substances may be encountered in the general environment, many occur in the work-place for greater amounts as a result of industrial processes; therefore, a range of lung reactions may occur as a result of work-place exposure. Physicians in metropolitan cities are likely to encounter pneumoconiosis for two reasons: (i) patients coming to seek medical help from geographic areas where pneumoconiosis is common, and (ii) pneumoconiosis caused by unregulated small-scale industries that are housed in poorly ventilated sheds within the city. A sound knowledge about the various pneumoconioses and a high index of suspicion are necessary in order to make a diagnosis. Identifying the disease is important not only for treatment of the individual case but also to recognise and prevent similar disease in co-workers. [Indian J Chest Dis Allied Sci 2013;55:25-34] Key words: Pneumoconiosis, Occupation, Fibrosis. INTRODUCTION without such a reaction. Silicosis, coal worker pneumoconiosis, asbestosis, berylliosis and talcosis History of mining goes far back to pre-historic times are examples of fibrotic pneumoconiosis. Siderosis, as far back as ancient Greece and Rome, when men stannosis and baritosis are non-fibrotic forms of mined for salts, flint and ochre.
    [Show full text]
  • ABIM Pulmonary Disease Certification Exam Blueprint
    Pulmonary Disease Certification Examination Blueprint Purpose of the exam The exam is designed to evaluate the knowledge, diagnostic reasoning, and clinical judgment skills expected of the certified pulmonologist in the broad domain of the discipline. The ability to make appropriate diagnostic and management decisions that have important consequences for patients will be assessed. The exam may require recognition of common as well as rare clinical problems for which patients may consult a certified pulmonologist. Exam content Exam content is determined by a pre-established blueprint, or table of specifications. The blueprint is developed by ABIM and is reviewed annually and updated as needed for currency. Trainees, training program directors, and certified practitioners in the discipline are surveyed periodically to provide feedback and inform the blueprinting process. The primary medical content categories of the blueprint are shown below, with the percentage assigned to each for a typical exam: Medical Content Category % of Exam Obstructive Lung Disease 17.5% Critical Care Medicine 15% Diffuse Parenchymal Lung Disease (DPLD) 10% Sleep Medicine, Neuromuscular and Skeletal 10% Epidemiology 2% Infections 12% Neoplasia 9.5% Pleural Disease 5% Quality, Safety, and Complications 5% Transplantation 2% Vascular Diseases 6% Respiratory Physiology and Pulmonary Symptoms 4% Occupational and Environmental Diseases 2% 100% Exam questions in the content areas above may also address clinical topics in general internal medicine that are relevant to
    [Show full text]
  • Berylliosis As an Auto-Immune Disorder ANDREW L
    ANNALS OF CLINICAL AND LABORATORY SCIENCE, Vol. 6, No. 3 Copyright © 1976, Institute Cor Clinical Science Berylliosis as an Auto-Immune Disorder ANDREW L. REEVES, Ph.D. Wayne State University, School of Medicine, Department of Occupational and Environmental Health, Detroit, MI 48201 ABSTRACT Exposure to compounds of beryllium can cause dermatitis, acute pneumonitis and chronic pulmonary granulomatosis (“berylliosis”) in hu­ mans. These syndromes seem to have an allergic-immunologic component in common. Hypersensitivity to beryllium is of the delayed (cell-mediated) type and can be measured as skin reactivity to patch test; lymphocyte blast transformation; and macrophage migration inhibition. There is good corre­ lation between the results of these tests in exposed populations, but the degree of hypersensitivity is not necessarily a measure of either extent of exposure or severity of berylliosis. In animal experiment, inhalation expo­ sure has suppressed a previously established cutaneous hypersensitivity, and degree of hypersensitivity and degree of berylliosis were in significant inverse correlation. Introduction considerable mortality. It is associated Beryllium is a light metal widely used with inhalation of various, including in­ in fatigue-resistant alloys, nuclear reac­ soluble, beryllium compounds, some­ tors, space vehicle and missile parts, times in very low concentration. Occupa­ electronics and for other specialized pur­ tional as well as “neighborhood” cases poses. Exposure to compounds of beryl­ (the latter having occurred in the general lium has caused dermatitis, acute population living within about a mile pneumonitis and chronic pulmonary from a beryllium plant) are on record; granulomatosis (“berylliosis”) in hu­ they are collected in a “Beryllium Case mans. The dermatitis is of the allergic Registry.” 13 type with edematous lesions following The allergic nature of beryllium skin contact with soluble salts or with lesions was recognized by Curtis,8 who granulomatous ulceration following the developed a patch test.
    [Show full text]
  • Clinical Guideline for the Diagnosis of Beryllium Sensitization and Chronic Beryllium Disease
    WASHINGTON STATE DEPT. OF LABOR AND INDUSTRIES OFFICE OF THE MEDICAL DIRECTOR JULY 2015 CLINICAL GUIDELINE FOR THE DIAGNOSIS OF BERYLLIUM SENSITIZATION AND CHRONIC BERYLLIUM DISEASE PURPOSE This Guideline provides the clinical diagnostic criteria for beryllium sensitization and chronic beryllium disease (CBD; old term = berylliosis), based on the latest available medical literature and consultation with leading experts in the field. This Guideline does not address exposure prevention, workplace safety, or treatment. In addition, this Guideline is not intended to supplant all adjudicative decisions in cases that meet the case definition and which are crucial to the administration of the Washington workers’ compensation system. BACKGROUND Beryllium is a lightweight alkaline metal occurring naturally in soils and in coal; [1] it is processed into metals oxides, alloys, and composite materials. [2] It has high strength, light weight, high heat and electrical conductivity, a high melting point, is neutron-moderating and transparent to x-rays, and is non-sparking and non-magnetic.[2-5] Exposure to beryllium usually occurs through the inhalation of beryllium-containing dust, particles, vapor, liquids or fumes, though skin contact can also manifest as dermatitis and ulcerations with poor wound healing. [1] Chronic disease is due to a cell-mediated sensitization response.[2, 6, 7] There is currently no vaccine or post-exposure prophylaxis for beryllium exposure. ESTABLISHING WORK-RELATEDNESS Beryllium sensitization and chronic beryllium disease as an industrial injury: An injury is defined as “a sudden and tangible happening, of a traumatic nature, producing an immediate or prompt result, and occurring from without, and such physical conditions as result therefrom.” The only requirement for establishing work-relatedness for an injury is that it occur “in the course of employment.” For example, exposure to beryllium may be an acute, traumatic episode at work, such as a puncture wound from beryllium metal.
    [Show full text]
  • 1 Smith Seminars Online Continuing Education AARC-Approved For
    Smith Seminars Online Continuing Education AARC-Approved for 2 CRCE Air Pollution Effects on the Lungs Objectives Identify how pollution affects health and welfare Be familiar with tools to help the patient decrease the effects of air pollution Become aware of the impact of environmental pulmonary diseases due to exposure to air pollution. Learn the current diagnosis and treatment for inhalation pulmonary diseases due to exposure to air pollution. Exposure to air pollution is associated with numerous effects on human health, including pulmonary, cardiac, vascular, and neurological impairments. The health effects vary greatly from person to person. High-risk groups such as the elderly, infants, pregnant women, and sufferers from chronic heart and lung diseases are more susceptible to air pollution. Children are at greater risk because they are generally more active outdoors and their lungs are still developing. Exposure to air pollution can cause both acute (short-term) and chronic (long-term) health effects. Acute effects are usually immediate and often reversible when exposure to the pollutant ends. Some acute health effects include eye irritation, headaches, and nausea. Chronic effects are usually not immediate and tend not to be reversible when exposure to the pollutant ends. Some chronic health effects include decreased lung capacity and lung cancer resulting from long-term exposure to toxic air pollutants. The scientific techniques for assessing health impacts of air pollution include air pollutant monitoring, exposure assessment, dosimetry, toxicology, and epidemiology. Although in humans pollutants can affect the skin, eyes and other body systems, they affect primarily the respiratory system. Air is breathed in through the nose, which acts as the primary filtering system of the body.
    [Show full text]
  • Current Challenges in Pharmacovigilance: Pragmatic Approches
    CIOMS Current Challenges in Pharmacovigilance: Pragmatic Approches CIOMS Current CIOMS publications may be obtained directly from CIOMS, c/o World Health Organization, Avenue Appia, 1211 Geneva 27, Current Challenges Switzerland or by e-mail to [email protected] in Pharmacovigilance: Both CIOMS and WHO publications are distributed by the World Health Organization, Marketing and Dissemination, Avenue Appia, 1211 Geneva 27, Switzerland and are available Pragmatic Approaches from booksellers through the network of WHO sales agents. A list of these agents may be obtained from WHO by writing to the above address. Report of CIOMS Working Group V Price: CHF 30.– GenevaGeneva 20012005 GGroup5_Pharmacovigilance-cov.inddroup5_Pharmacovigilance-cov.indd 1 99.8.2007.8.2007 110:08:520:08:52 Current Challenges in Pharmacovigilance: Pragmatic Approaches Report of CIOMS Working Group V Geneva 2001 Copyright # 2001 by the Council for International Organizations of Medical Sciences (CIOMS) ISBN 92 9036 074 7 Printed in Switzerland Acknowledgements he Council for International Organizations of Medical Sciences is T grateful to the members of CIOMS Working Group V, on Current Challenges in Pharmacovigilance: Pragmatic Approaches, and to the drug regulatory authorities, pharmaceutical companies and other organizations represented, for their patience and hard work in bringing this project to its successful conclusion. Special thanks are due to the co-chairs, Drs. Murray Lumpkin and Win Castle, for their capable leadership, to Ms. Susan Roden, the secretary of the group, and to the editorial committee comprised of Drs. Lumpkin and Castle along with Dr. Arnold J. Gordon and Dr. Hugh Tilson. We wish to express our special thanks to Dr.
    [Show full text]
  • Pulmonary and Hepatic Granulomatous Disorders Due to the Inhalation of Cement and Mica Dusts
    Thorax: first published as 10.1136/thx.33.2.219 on 1 April 1978. Downloaded from Thorax, 1978, 33, 219-227 Pulmonary and hepatic granulomatous disorders due to the inhalation of cement and mica dusts J. CORTEZ PIMENTEL AND A. PEIXOTO MENEZES' From the Department of Pathology of Sanatorio D. Carlos I and Institute of Pathology, University of Lisbon, Faculty of Medicine, Lisbon, Portugal Cortez Pimentel, J., and Peixoto Menezes, A. (1978). Thorax, 33, 219-227. Pulmonary and hepatic granulomatous disorders due to the inhalation of cement and mica dusts. Hepatic and pulmonary granulomas were recognised in two workers exposed respectively to Portland cement and to muscovite dusts. The pulmonary lesions in the patient exposed to cement consisted of histiocytic granulomas and irregular fibrohyaline scars, and in the patient exposed to mica of a diffuse thickening of all interalveolar septa due to new formation of reticulin and collagen fibres and proliferation of fibroblasts and histiocytes. In the liver the following pathological findings were observed: focal or diffuse swelling of sinusoidal lining cells, sarcoid-type granulomas, and, in the case of mica exposure, perisinusoidal and portal tract fibrosis. Abundant inclusions of the inhaled material were identified within the pulmonary and hepatic lesions by histochemical and x-ray diffraction techniques. The inhalation of dusts containing silicon is known mental pathogenic effects of cement and mica to produce different kinds of pneumoconiosis. (Lemon and Higgins, 1935; Baetjer, 1947; King http://thorax.bmj.com/ Although free silica is sometimes the only patho- et al., 1947, 1950; Einbrodt and Hentschel, 1966; genic dust inhaled, in most situations there is Tripsa and Rotaru, 1966; Pimentel and Gomes, exposure to silicates (for example, mica, asbestos, 1973).
    [Show full text]