DOCSLIB.ORG

Neurological and Neuroimaging Signs of Reversible Parkinsonism Associated with Manganese Exposure

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

Editorial

Neurological and neuroimaging signs of reversible Parkinsonism associated with manganese exposure

Basant K. Puri

Department of Imaging, Hammersmith Hospital, London, UK

Address for correspondence:

Prof. Basant K. Puri, Department of Imaging, Hammersmith Hospital, Du Cane Road, London W12 0HS, UK. E-mail: [email protected]

Received Review completed : 03-02-2014 Accepted : 03-02-2014
: 03-02-2014

In this month’s issue of Neurology India, Han et al. present an unusual case entitled ‘Reversal of pallidal magnetic resonance imaging (MRI) T1 hyperintensity in a welder presenting as reversible parkinsonism’.[1] Parkinsonism is a syndrome of multiple different etiologies and among the toxic causes of parkinsonismarealcohol(ethanol)withdrawal, methanol, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyrodine, inhalant abuse, metals (including manganese, iron and copper), cyanide poisoning, agricultural chemicals (including rotenone, paraquat, maneb and atrazine), isoquinoline derivatives, 6-hydroxydopamine, cycad seeds (which are associated with the amyotrophic lateral sclerosis-parkinsonism dementia complex of Guam), annonacin and carbon monoxide poisoning.[2,3] In the case reported in this month’s issue, the cause of parkinsonism was manganese intoxication as a result of working as a welder. The association of parkinsonism with manganese exposure, sometimes referred to as manganism, was noted in a paper published as early as 1837 by Couper in pyrolusite ore grinding workers.[4]
The heavy metal manganese (atomic number 25, relative atomic mass 54.938) lies in group 7 of the periodic table and has a natural abundance in the earth’s crust that, among the heavy metals, is second only to that of iron, with which it is roughly similar in terms of many of its physical and chemical properties (although manganese is harder and more brittle but less refractory).[5] It has one of the highest industrial uses of all metals, being important in the production of steel and batteries, in water purification, the manufacture of bactericidal and fungicide compounds and as part of a knockout compound for petrol.[3] In commonly used welding methods, such as flux-cored arc welding and shielded manual metal arc welding, manganese may be present in the flux material and in the metal electrodes used.[6] Thus, as in the accompanying case report, those who perform routine welding jobs may be exposed to manganese-containing fumes, for example as mixed oxidation state oxides formed in the high temperature oxidizing environment in which this procedure takes place.[5,6]

Racette et al. carried out a case-control study in which they compared the clinical features of parkinsonism in 15 career welders with two control groups of idiopathic Parkinson’s disease, one of which was ascertained sequentially to compare the frequency of clinical features and the second age- and sex-matched to compare the frequency of motor fluctuations.[7] Parkinsonism in welders was distinguished clinically from idiopathic Parkinson’s disease only by an earlier

Access this article online

Quick Response Code:

Website:

www.neurologyindia.com

PMID:

***

DOI:

10.4103/0028-3886.128210

Neurology India | Jan-Feb 2014 | Vol 62 | Issue 1
1

Puri: Reversible parkinsonism

  • age of onset (mean 46 years compared with 63 years in
  • A key finding in the case report in this month’s issue

of Neurology India is that the manganism was found to be reversible, with respect to both neurological signs and neuroimaging findings.[1] I strongly recommend the reader to compare the before and after structural MRI figures provided in that report. This reversibility holds out some hope for potential treatment of manganism. Finally, this case emphasizes the important point made by Professor David Moore that, ‘although Parkinson’s disease is the most common cause of parkinsonism, it must always be kept in mind that this is but one of many possible causes and the physician must dutifully consider the other causes before deciding that a patient with parkinsonism has Parkinson’s disease’.[2] the sequentially ascertained controls), with no significant differences being found in respect of frequency of tremor, bradykinesia, rigidity, asymmetric onset, postural instability, family history, clinical depression, dementia, drug-induced psychosis, response to levodopa, motor fluctuations or dyskinesias; furthermore, 6-[18F] fluorodopa positron emission tomography was carried out in two of the welders and showed findings typical of idiopathic Parkinson’s disease.[7]

In the United States, the San Francisco/Oakland Bay Bridge was damaged by the 1989 earthquake and reconstruction of a vulnerable part of the bridge began to be carried out in 2003; this afforded Bowler et al. the opportunity to study the relationship between fume exposure in confined space welding and neurological and neuropsychological sequelae.[8] The researchers reported that ‘[In] 43 eligible welders, 11 cases of manganism were identified presenting with the following symptoms: Sleep disturbance, mood changes, bradykinesia, headaches, sexual dysfunction, olfaction loss, muscular rigidity, tremors, hallucinations, slurred speech, postural instability, monotonous voice and facial masking. Significant associations between outcome variables and cumulative exposure index (CEI) or blood Mn (MnB) were obtained with CEI for variables implicating attention and concentration, working and immediate memory, cognitive flexibility and verbal learning; and with MnB for executive function, cognitive flexibility, visuo-spatial construction ability and visual contrast sensitivity. This study strongly suggests that neuropsychological features contribute in a dose-effect related way to the portrait of manganism usually characterized by tremor, loss in balance, diminished cognitive performance and signs and symptoms of parkinsonism’.[8]

References

1. Han SH, Ahn SW, Youn YC, Shin HW. Reversal of pallidal MRI T1 hyperintensity in a welder presenting as reversible parkinsonism. Neurol India 2014;62:118-9.
2. Moore DP, Puri BK. Textbook of Clinical Neuropsychiatry and
Behavioral Neuroscience. 3rd ed. London: Hodder Arnold; 2012.
3. Lev N, Melamed E, Offen D. Toxic causes of parkinsonism. Handb Clin
Neurol 2007;84:385-98.
4. Couper J. On the effects of black oxide of manganese when inhaled into the lungs. Br Ann Med Pharmacol 1837;41-2.
5. Cotton FA. Advanced Inorganic Chemistry. 6th ed., Vol. xv. New York:
Wiley; 1999. p. 1355.
6. Dale Marcy A, Drake PL. Development of a field method for measuring manganese in welding fume. J Environ Monit 2007;9:1199-204.
7. Racette BA, McGee-Minnich L, Moerlein SM, Mink JW, Videen TO,
Perlmutter JS. Welding-related parkinsonism: Clinical features, treatment, and pathophysiology. Neurology 2001;56:8-13.
8. Bowler RM, Nakagawa S, Drezgic M, Roels HA, Park RM, Diamond E, et al. Sequelae of fume exposure in confined space welding: A neurological and neuropsychological case series. Neurotoxicology 2007;28:298-311.

How to cite this article: Puri BK. Neurological and neuroimaging

signs of reversible Parkinsonism associated with manganese exposure. Neurol India 2014;62:1-2.

Source of Support: Nil, Conflict of Interest: None declared.

Neurology India | Jan-Feb 2014 | Vol 62 | Issue 1
2

Copyright of Neurology India is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.

Recommended publications
  • Manganese Toxicity May Appear Slowly Over Months and Years

    Manganese Toxicity May Appear Slowly Over Months and Years

    MANGANESE 11 2. RELEVANCE TO PUBLIC HEALTH 2.1 BACKGROUND AND ENVIRONMENTAL EXPOSURES TO MANGANESE IN THE UNITED STATES Manganese is a naturally occurring element and an essential nutrient. Comprising approximately 0.1% of the earth’s crust, it is the twelfth most abundant element and the fifth most abundant metal. Manganese does not exist in nature as an elemental form, but is found mainly as oxides, carbonates, and silicates in over 100 minerals with pyrolusite (manganese dioxide) as the most common naturally-occurring form. As an essential nutrient, several enzyme systems have been reported to interact with or depend on manganese for their catalytic or regulatory function. As such, manganese is required for the formation of healthy cartilage and bone and the urea cycle; it aids in the maintenance of mitochondria and the production of glucose. It also plays a key role in wound-healing. Manganese exists in both inorganic and organic forms. An essential ingredient in steel, inorganic manganese is also used in the production of dry-cell batteries, glass and fireworks, in chemical manufacturing, in the leather and textile industries and as a fertilizer. The inorganic pigment known as manganese violet (manganese ammonium pyrophosphate complex) has nearly ubiquitous use in cosmetics and is also found in certain paints. Organic forms of manganese are used as fungicides, fuel-oil additives, smoke inhibitors, an anti-knock additive in gasoline, and a medical imaging agent. The average manganese soil concentrations in the United States is 40–900 mg/kg; the primary natural source of the manganese is the erosion of crustal rock.
  • Manganese and Its Compounds: Environmental Aspects

    Manganese and Its Compounds: Environmental Aspects

    This report contains the collective views of an international group of experts and does not necessarily represent the decisions or the stated policy of the United Nations Environment Programme, the International Labour Organization, or the World Health Organization. Concise International Chemical Assessment Document 63 MANGANESE AND ITS COMPOUNDS: ENVIRONMENTAL ASPECTS First draft prepared by Mr P.D. Howe, Mr H.M. Malcolm, and Dr S. Dobson, Centre for Ecology & Hydrology, Monks Wood, United Kingdom The layout and pagination of this pdf file are not identical to the document in print Corrigenda published by 12 April 2005 have been incorporated in this file Published under the joint sponsorship of the United Nations Environment Programme, the International Labour Organization, and the World Health Organization, and produced within the framework of the Inter-Organization Programme for the Sound Management of Chemicals. World Health Organization Geneva, 2004 The International Programme on Chemical Safety (IPCS), established in 1980, is a joint venture of the United Nations Environment Programme (UNEP), the International Labour Organization (ILO), and the World Health Organization (WHO). The overall objectives of the IPCS are to establish the scientific basis for assessment of the risk to human health and the environment from expos ure to chemicals, through international peer review processes, as a prerequisite for the promotion of chemical safety, and to provide technical assistance in strengthening national capacities for the sound management
  • 10Neurodevelopmental Effects of Childhood Exposure to Heavy

    10Neurodevelopmental Effects of Childhood Exposure to Heavy

    Neurodevelopmental E¤ects of Childhood Exposure to Heavy Metals: 10 Lessons from Pediatric Lead Poisoning Theodore I. Lidsky, Agnes T. Heaney, Jay S. Schneider, and John F. Rosen Increasing industrialization has led to increased exposure to neurotoxic metals. By far the most heavily studied of these metals is lead, a neurotoxin that is particularly dangerous to the developing nervous system of children. Awareness that lead poison- ing poses a special risk for children dates back over 100 years, and there has been increasing research on the developmental e¤ects of this poison over the past 60 years. Despite this research and growing public awareness of the dangers of lead to chil- dren, government regulation has lagged scientific knowledge; legislation has been in- e¤ectual in critical areas, and many new cases of poisoning occur each year. Lead, however, is not the only neurotoxic metal that presents a danger to children. Several other heavy metals, such as mercury and manganese, are also neurotoxic, have adverse e¤ects on the developing brain, and can be encountered by children. Al- though these other neurotoxic metals have not been as heavily studied as lead, there has been important research describing their e¤ects on the brain. The purpose of the present chapter is to review the neurotoxicology of lead poisoning as well as what is known concerning the neurtoxicology of mercury and manganese. The purpose of this review is to provide information that might be of some help in avoiding repeti- tion of the mistakes that were made in attempting to protect children from the dan- gers of lead poisoning.
  • Manganese Exposure and Toxicity

    Manganese Exposure and Toxicity

    tion Ef llu fec o ts P f & o l C a o n n r Mirmohammadi, J Pollut Eff Cont 2014, 2:2 t r u o o l Journal of Pollution Effects & Control J DOI: 10.4172/2375-4397.1000116 ISSN: 2375-4397 ReviewResearch Article Article OpenOpen Access Access Manganese Exposure and Toxicity Seyedtaghi Mirmohammadi* Department of Occupational Health, Faculty of Health, Mazandaran University of Medical Sciences, Mazandaran, Sari, Iran Abstract One of the main essential elements for human is Manganese (Mn). Furthermore Mn is a row material for many king of ferrous foundry and there is a working exposure to Mn for workers in the workplaces. High exposure to Mn can result in increase in human tissues levels and neurological effects. Though, there should be some threshold limit value for Mn exposure related to adverse effects may occur and increase with higher exposures further than threshold limit. Conclusions from scientific literatures related to Mn toxicity revealed that this pollutant can effect on brain system and create some neurological disorders or neurological endpoints which measured in many of the occupational health assessments. Many researches have tried to show a relationship regards to biomarkers with neurological effects, such as neurological changes or magnetic resonance imaging (MRI) changes have not been founded for Mn. More precise study need for Mn risk assessment for industrial pollution exposure and it will be used to recognize situations that may guide to understand Mn accumulation on brain and Mn metabolism in different exposed workers. Workplace evaluations for Mn will prepare valuable scientific information for the development of more scientifically sophisticated guidelines, regulations and recommendations for future study and for Mn occupational toxicity control and exposure prevention in the related workplaces.
  • Alberta Environment

    Alberta Environment

    Chemical Fact Sheets Manganese, Mn CAS No. 7439-96-5 WHAT IS MANGANESE? Manganese is a gray-pink metal. USES Manganese is used in the manufacture of ceramics, matches, glass, dyes and welding rods. It is a component of steel, steel alloys, cast iron, superalloys & nonferrous alloys, as well as a chemical intermediate for high purity salts. Manganese is used as a purifying & scavenging agent in metal production. SOURCES Manganese is a naturally occurring substance found in many types of rock; it is ubiquitous in the environment and found in low levels in water air, soil, and food. It is commonly found in the environment as a result of its use in the manufacture of the above-noted materials. ENVIRONMENTAL LEVELS AND EXPOSURE Exposure to manganese might include: • Inhaling it in ambient air, particularly near industries involved in the manufacture of manganese-containing materials. Occupational exposure via inhalation is most common. Ambient air concentrations of manganese were not reported in 1997 or 1998 in Alberta. ENVIRONMENTAL FATE AND BEHAVIOUR • Manganese, as an aerosol, may dissolve upon contact with water on a time scale of a few minutes. TOXICITY • Manganese is an element considered essential to human health. • Inhalation of manganese compounds in aerosols or fine dusts may cause "metal fume fever”. MANGANESE Page 1 of 2 • Early symptoms of chronic manganese poisoning may include languor, sleepiness and weakness in the legs. Emotional disturbances such as uncontrollable laughter and a spastic gait with tendency to fall in walking are common in more advanced cases. • Chronic manganese poisoning is not a fatal disease.
  • Drinking Water Health Advisory for Manganese Drinking Water Health Advisory for Manganese

    Drinking Water Health Advisory for Manganese Drinking Water Health Advisory for Manganese

    Drinking Water Health Advisory for Manganese Drinking Water Health Advisory for Manganese Prepared by: U.S. Environmental Protection Agency Office of Water (4304T) Health and Ecological Criteria Division Washington, DC 20460 http://www.epa.gov/safewater/ EPA-822-R-04-003 January, 2004 January 2004 Acknowledgments This document was prepared under the U.S. EPA Contract Number 68-C-02-009. Lead Scientist, Julie Du, Ph.D., Health and Ecological Criteria Division, Office of Science and Technology, Office of Water, U. S. Environmental Protection Agency. January 2004 CONTENTS ABBREVIATIONS ........................................................... ii FOREWORD................................................................ iii EXECUTIVE SUMMARY......................................................1 1.0 INTRODUCTION .......................................................3 2.0 MANGANESE IN THE ENVIRONMENT ...................................3 2.1 Water...........................................................4 2.2 Soil.............................................................4 2.3 Air .............................................................5 2.4 Food............................................................5 2.5 Environmental Fate ................................................7 2.6 Summary ........................................................8 3.0 CHEMICAL AND PHYSICAL PROPERTIES ................................8 Organoleptic Properties...................................................8 4.0 TOXICOKINETICS .....................................................9
  • Welding-Related Parkinsonism Clinical Features, Treatment, and Pathophysiology

    Welding-Related Parkinsonism Clinical Features, Treatment, and Pathophysiology

    Articles CME Welding-related parkinsonism Clinical features, treatment, and pathophysiology B.A. Racette, MD; L. McGee–Minnich, BSN; S.M. Moerlein, PhD; J.W. Mink, MD, PhD; T.O. Videen, PhD; and J.S. Perlmutter, MD Article abstract—Objective: To determine whether welding-related parkinsonism differs from idiopathic PD. Back- ground: Welding is considered a cause of parkinsonism, but little information is available about the clinical features exhibited by patients or whether this is a distinct disorder. Methods: The authors performed a case-control study that compared the clinical features of 15 career welders, who were ascertained through an academic movement disorders center and compared to two control groups with idiopathic PD. One control group was ascertained sequentially to compare the frequency of clinical features, and the second control group was sex- and age-matched to compare the frequency of motor fluctuations. Results: Welders were exposed to a mean of 47,144 welding hours. Welders had a younger age at onset (46 years) of PD compared with sequentially ascertained controls (63 years; p Ͻ 0.0001). There was no difference in frequency of tremor, bradykinesia, rigidity, asymmetric onset, postural instability, family history, clinical depression, dementia, or drug-induced psychosis between the welders and the two control groups. All treated welders responded to levodopa. Motor fluctuations and dyskinesias occurred at a similar frequency in welders and the two control groups. PET with 6-[18F]fluorodopa obtained in two of the welders showed findings typical of idiopathic PD, with greatest loss in posterior putamen. Conclusions: Parkinsonism in welders is distinguished clinically only by age at onset, suggesting welding may be a risk factor for PD.
  • (+)-DTBZ (18F-AV-133) Brain PET Scan

    (+)-DTBZ (18F-AV-133) Brain PET Scan

    Journal of the Neurological Sciences 353 (2015) 102–106 Contents lists available at ScienceDirect Journal of the Neurological Sciences journal homepage: www.elsevier.com/locate/jns Chronic manganism: A long-term follow-up study with a new dopamine terminal biomarker of 18F-FP-(+)-DTBZ (18F-AV-133) brain PET scan Chu-Yun Huang a,b, Chi-Hung Liu a,c, Eusden Tsao d,e, Chia-Ju Hsieh f,g,Yi-HsinWenga,h, Ing-Tsung Hsiao f,g, Tzu-Chen Yen f,g, Kun-Ju Lin f,g, Chin-Chang Huang a,h,⁎ a Department of Neurology, Chang Gung Memorial Hospital, Taoyuan, Taiwan b College of Pharmacy, Taipei Medical University, Taipei, Taiwan c Graduate Institute of Clinical Medical Sciences, Division of Medical Education, College of Medicine, Chang Gung University, Taoyuan, Taiwan d Department of Family Medicine, Chang Gung Memorial Hospital, Taoyuan, Taiwan e Department of Environmental and Occupational Medicine, Chang Gung Memorial Hospital, Chiayi, Taiwan f Molecular Imaging Center and Nuclear Medicine, Chang Gung University, Chang Gung Memorial Hospital, Taoyuan, Taiwan g Healthy Aging Research Center Medical Imaging and Radiological Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan h Department of Neurology, College of Medicine, Chang Gung University, Taoyuan, Taiwan article info abstract Article history: Recent experimental studies revealed that dopamine neuron dysfunction in chronic manganism may be due to a Received 12 January 2015 reduced capacity of dopamine release in the striatum. The findings imposed further difficulty in the differential Received in revised form 8 April 2015 diagnosis between manganism and IPD. We conducted a long-term clinical follow-up study of 4 manganism pa- Accepted 9 April 2015 tients, applying a new tracer 18F-9-fluoropropyl-(+)-dihydrotetrabenazine (18F-AV-133) with positron emission Available online 17 April 2015 tomography (PET).
  • Preliminary Observations on Glucose Tolerance and Serum Proteins M

    Preliminary Observations on Glucose Tolerance and Serum Proteins M

    Br J Ind Med: first published as 10.1136/oem.23.1.67 on 1 January 1966. Downloaded from Brit. J. industr. Med., I966, 23, 67. Chronic Manganism: Preliminary Observations on Glucose Tolerance and Serum Proteins M. HASSANEIN, H. A. GHALEB, E. A. HAROUN, M. R. HEGAZY, and M. A. H. KHAYYAL From the Department of Medicine and the Department of Pharmacology and Therapeutics, Faculty of Medicine, Cairo University An intravenous glucose tolerance test was carried out in i i patients with chronic manganese poisoning. Prolonged reactionary hypoglycaemia was observed. The underlying mechanism is discussed. It may be due to a disturbance of the hypothalamo-pituitary-adrenal axis. In seven of these patients total serum proteins were estimated and were separated electro- phoretically. The albumin: globulin ratios were lower in patients than in controls. There were significant reductions in serum albumin concentrations and increases in concentrations of cxl and ,B globulins. Since the early discovery of chronic manganese explore factors which may help to elucidate these poisoning among workers manufacturing chlorine mechanisms. We have studied the effects of chronic gas in France using manganese ore (Couper, I837), manganism on glucose tolerance and on liver many other reports from Europe, North Africa, function, as shown by the electrophoretic pattern of India, and America have appeared (see, e.g., Nazif, serum proteins. The latter study was suggested by copyright. 1936; Flinn, Neal, Reinhart, Dallavalle, Fulton, and the similarities with Parkinsonism, the relation Dooley, 1940; Fairhall, I945; Boyer and Rodier, between which and impairment of liver finction is 1954; Rodier, I955; and Pefialver, I955, I957).
  • Late-Breaking Supplement

    Late-Breaking Supplement

    2017 Annual Meeting Abstract Supplement LATE-BREAKING ABSTRACT SUBMISSIONS These abstracts are available via the Mobile Event App, Online Planner, and a downloadable PDF from the SOT website. All Late-Breaking Abstracts are presented on Thursday, March 16, from 8:30 am–11:45 am. www.toxicology.org THURSDAY POSTER SESSION MAP March 16, 2017—8:30 AM to 11:45 AM—Hall A Poster Set Up—7:30 AM to 8:30 AM Late-Breaking Poster #s: P196-P540 (highlighted in gray) P540 P539 P538 P537 P533 P534 P535 P536 P532 P531 P530 P529 P528 P527 P526 P525 P524 P523 P522 P521 P520 P519 P518 P517 P516 P515 P497 P498 P499 P500 P501 P502 P503 P504 P505 P506 P507 P508 P509 P510 P511 P512 P513 P514 P496 P495 P494 P493 P492 P491 P490 P489 P488 P487 P486 P485 P484 P483 P482 P481 P480 P479 P461 P462 P463 P464 P465 P466 P467 P468 P469 P470 P471 P472 P473 P474 P475 P476 P477 P478 P460 P459 P458 P457 P456 P455 P454 P453 P452 P451 P450 P449 P448 P447 P446 P445 P444 P443 P425 P426 P427 P428 P429 P430 P431 P432 P433 P434 P435 P436 P437 P438 P439 P440 P441 P442 P424 P423 P422 P421 P420 P419 P418 P417 P416 P415 P414 P413 P412 P411 P410 P409 P408 P407 P389 P390 P391 P392 P393 P394 P395 P396 P397 P398 P399 P400 P401 P402 P403 P404 P405 P406 P388 P387 P386 P385 P384 P383 P382 P381 P380 P379 P378 P377 P376 P375 P374 P373 P372 P371 P353 P354 P355 P356 P357 P358 P359 P360 P361 P362 P363 P364 P365 P366 P367 P368 P369 P370 P352 P351 P350 P349 P348 P347 P346 P345 P344 P343 P342 P341 P340 P339 P338 P337 P336 P335 P317 P318 P319 P320 P321 P322 P323 P324 P325 P326 P327 P328 P329 P330 P331
  • Health Hazard Evaluation Report No

    Health Hazard Evaluation Report No

    Health Hazard Evaluation HETA B0-073-1589 ~~P.ION POWER SHOVEL Report NARIOfL OHIO . _,____ - ~- .... - ·-·--·-- ·-- - ...\ PREFACE The Hazard Evaluations ·and Tecfinical-Assistance Branch of NIOSH conducts field investigations of possible health hazards in the workplace. T~ese investigations are conducted under the authority of Section 20(a)(€) of the Occupational Safety and Health Act of 1970, 2S U.S.C. 669(a)(6) which authorizes the Secretary of Health and Human Services, following a written request from any employer or authorized representative of employees, to determine whether any substance normally found in the place of employment has potentially toxic effects in such concentrations as used or found. The Hazard Evaluations and Technical Assistance Branch also provides, upon request, medical, nursing, and industrial hygiene technical and consultative assistance (TA) to Federal, state, and local agencies; labor; industry and other groups or individuals to control occupational health hazards and to prevent related trauma and disease. ~\enti on of cornpany narr.es or products does not constitute endorsement by the National Institute for Occupational Safety and Health. - . "' HETA BO-o73-1569 NIOSH INVESTIGATORS: April 1985 Richard L. Stephenson, I.H. MARION POWER SHOVEL Gary M. Lfss, M.D., M.S. I~AFUON, OHIO I. SUMt~ARY In March 1960, the National Institute for Occupational Safety and Health (NIOSH) was requested to evaluate exposures throughout Marion Power Shovel Foundry, Marion, Ohio. The primary concern involved the core and mold areas where methylene bisphenyl isocyanate (MDI) binders are used. Reported employee symptoms included eye irritation, headache, chest pain and respiratory problems. Long-term personal and area air sampling was performed to characterize coreroom and molding department employees' exposure to MDI, triethylamine, and mineral spirits.
  • Manganese – the Silent Poison

    Manganese – the Silent Poison

    Manganese – the silent poison Dr. W.M. Coombs, INTRODUCTION possibility of excess exposure to hazardous chemi- Tel: 083 653 9859, Manganese was first discovered by Sheele in cals in South Africa. e-mail: mcoombs@ iafrica.com Sweden in 1774, and named ‘manganese’ by Guyton de Marveau in 1785. South Africa, with more EXPOSURE LEVELS Volker R. Schillack, than 50 million tons of alumino-silicates, contains Exposure levels differ worldwide; TLV – ACGIH: Analytical toxicologist, Ampath, around 40% of the world’s known reserves of these 0,2 mg/m3, OSHA 5,0 mg/m3 respectively from the Drs Du Buisson minerals and accounts for nearly half of the West- US and SA. SA has a level 25 times higher than the & Partners, P.O. Box 4419, ern world’s production. With manganese reserve in US. Arcadia, 0007. excess of 4000Mt, 80% of the world’s known man- Tel: 012 427 1738/ ganese ore deposits are located in the Northern ABSORPTION, DISTRIBUTION AND EXCRETION 012 427 1858 e-mail: schillackv@ Cape and North West Province. The country’s annual Manganese is an essential element for humans and ampath.co.za output in 1999 was 3122Kt, of which 1569Kt was is absorbed via food and water intake. It is part of exported. the enzyme mitochondrial super oxide dismutase Couper first described industrial manganese (SOD) in rats and is essential for many animal poisoning in 1837 in five workers in France, who made species for the formation of bone and connective bleaching powders using manganese dioxide. He tissue, as well as the metabolism of carbohydrates found that long-term exposure to manganese dust and lipids.