Document KRZODvGG4gBZdxJ0ennOQeqXr

t IPAI International Primary Aluminium Institute Health Committee Review The Measurement of Employee Exposures in Aluminium Reduction Plants Part I: Chemical Exposures ii i*r July 1982 TX TINSR RMC0021442 * Published by the International Primary Aluminium Institute 9th Floor. New Zealand House. Haymarket. London SW1Y 4TQ United Kingdom TEL; 071 930 0528 FAX: 071 321 0183 Telex. 917837 IPAILN G International Primary Aluminium Institute 1982 A connw*/ ;irui try guarantee Registered in London no. 106200/ RegnlrieU 0ll<e U C'r0OC Lonoon 6C2V 6AO United Kingdom Oevynen Or W'lkam Walton AiSoc-aieS Old Or.nied -n England Or Rjiii'Ov Unrence b Comoany Limited at live Oe Momlort Press; ie<es:e* and uv>oon iPai 1 11 82 TX TINER RMC0021443 ' * * * * \*e Preface Preface to first edition This review has been prepared by the Health Committee of the International Primary Aluminium Institute under the authority of the Board of Directors of the Institute. Special recognition is due to the members of the working group who produced the detailed text. The group was led by Mr. Thomas B. Bonney of Aluminum Company of America and also included Mr. Homer M. Cole of Reynolds Metals Company. Mr. Eirik Nordheim representing Norwegian Smelters. Mr. Jan Rob of Elkem a/s. Dr. Alfred Steinegger of Swiss Aluminium Limited and Mr. Thomas J. Walker formerly of Kaiser Aluminum and Chemical Corporation. Preface to second edition The revised version wo? prepared by the working group led by Dr. Alfred Steinegger of Alusuisse-Lonza Services Ltd., and also included Mr. Homer Cole of Reynolds Metals Company, Dr. Peter Cook of Dubai Aluminium, Mr. Joe Damiano of Aluminum Company of America, Mr. Serge Friar of Alcan Smelters &. Chemicals Ltd., Mr. Eirik Nordheim representing Norwegian smelters. TX TINE* HMCOO2I444 3 Contents Section 3 \ir sampling and analysis Ur sampling sample analysis The significance of ampling/analytical rrors References 7lb ~tluH appendix 1 Sampling and 70 nalytical procedures appendix 2 Additional discussion on <33 j ure assessment strategies with pecial refence to recent developments n this field Section 4 Occupational exposure limits for airborne toxic substances Introductory remarks Risk evaluation on the bases of limit values Overview of different SS' occupational exposure limits (OELs) Maximum allowable 100 concentration (MAC) Threshold limit value (TLV) Biological Limits for cancerogens 40ir Exposure limits for airborne contaminants found primary aluminium industry References MO v TX TINER RMC0021445 Introduction 7 Section 1 Principal contaminants in the workplace introduction 9 Prebake process 9 Poiroom 9 Carbon plant 9 Soderberg process 9 Potroom 9 Paste plant 10 Principal contaminants 10 Potrooms 10 Carbon plants 11 Cathode relining 1% Maintenance 1^ Cast house (ingot) 1^ Section 2 Toxicology of principal environmental contaminants Introduction ity Chemical exposures in the aluminium industry categories of exposure ity IPAI industrial hygiene guides 4$ Aluminium metal dust 4& Aluminium oxide iff Ammonia *5 Asbestos lO Beryllium Carbon monoxide 23 Chlorine IS Coal tar pitch volatiles Copper dust fume/mists T9 Fluorides 30 Hydrogen chloride 31 Hydrogen fluoride 3-J Lead, inorganic dusts/fumes 3 s Lithium carbonate 3 Magnesium oxide *4 Manganese dust/fume ^ Man-Made Mineral Fibre (MMMF) 4T Oil mist WW Ozone Particulates Not Otherwise Classified (PNOC) Phosphine Silica, crystalline Sulphur dioxide 50 Welding fumes S'! Appendix: Definitions and toxicological concepts S3 TX TINER RMCOO21446 The advances in industrial technology and biological sciences have played a major part in social and economic progress in recent years. These changes have influenced governments, industry and labour both on a national and international scale. The industrial hygienist as a member of the occupational health team has been a pan of this change for a number of years. The preventive approach, which today is prominent in legislation from governments and governmental agencies, has been practised by industrial hygienists for some time. Modern technology may generate health hazards: some of which are easy to identify, but others are only discovered after years of careful study. For each type of industry, it is important to identify and analyse the health factors to determine their biological effects and to develop methods of prevention, both technical and medical. In this situation, cooperation within an industry is essential if the required knowledge is to be accumulated in a timely and efficient manner. The aluminium industry has been able to cooperate on a world-wide basis, and two of the best examples of this in the field of occupational health are the' IPAI seminars. 'Health Protection m Primary Aluminium Production', held in Copenhagen m 1977 and m Montreal in 1981. In these seminars, the various aspects of health protection in the aluminium industry were considered with reference to the various pollutants and physical factors encountered in this industry. One fact that has emerged during these seminars is that, in order to make a detailed study of the environmental conditions and related health problems at a particular working place, there is a definite need for accurate and generally acceptable methods of sampling and analysis. This is particularly important where official limits have to be met and where the question of modernization of a plant may depend on the outcome of the measurements. The present document, which has been prepared by the Health Committee of IPAI. is intended to give a review of the sampling and analytical techniques in general use in the aluminium industry. It is not the intention to give a detailed description and critical review of all known techniques, but there is an extensive list of references which can be consulted for more detailed information. The document will give a description of the most common pollutants found in the various departments of an aluminium plant. Further, it will deal with the actual sampling and analytical techniques, giving a description of the various sampling strategies and methods for sampling and analysis of the principal contaminants. Progress and innovations in the technology of aluminium production on the one hand, new results / knowledge gained in measuring technology and assessment of possible health hazards on the other made, in the opinion of the Health Committee, a partial upgrading of the first edition necessary. Essential changes and additions have been made in Section 1 "Principal contaminants at the workplace" and Section 4 "Occupational exposure limits of airborne toxic substances". Section 3 "Air sampling and analysis" was re-written. In Section 2 "Toxicology of principal environmental contaminants" no classification into substances of different importance was made any more. Part two to be published will describe the measurement of employee exposure to physical agents. TX TINER RMC0021447 1- ASBESTOS Recognized human carcinogen CAS: 1332-2!-4 Amosiie--CAS: 12172-73-5: 1987 TLV = 0.5 flbcr/ml Chrysolite--CAS: 12001-29-5: 1987 TLV = 2 llbers/ml Crocidolile--CAS: I200I-28-4: 1987 TLV = 0.2 llber/m! Olher forms: 1987 TLV = 2 fibers/ml Synonyms: Asbestos is a generic term applied to a number of hydrated mineral silicates. Physical Form. Fibers of various sizes, colors, and textures Uses. Thermal arni-eloctrical insulation* firoproofing: <omont-products Exposure. Inhalation Toxicology. Asbestos causes chronic lung disease (asbestosis), inflammation of the pleura, and certain cancers of the lungs and digestive tract. Asbestosis is a disorder characterized bv a diffuse interstitial pulmonary fibro sis, at times including pleural changes of fibrosis and calcification.1 Chest x-ray reveals a granular change chiefly in the lower lung fields; as the condition pro gresses, the heart outline becomes shaggy, and irregular patches of mottled shadowing may be seen. Typically, the patient exhibits restrictive pulmonarv function. Accompanying clinical changes may include fine rales, finger clubbing, dyspnea, dry cough, and cy anosis. The onset of asbestosis probably de pends upon asbestos dust concentra tion, fiber morphology, and the length of exposure. There may also be some factors of individual susceptibility, al though it is not possible to identify persons who may have undue sus ceptibility or resistance to developing asbestosis.2 It is a progressive disease that may develop fully in 7 to 9 years and may cause death as early as 13 years after first exposure. Usually, pneumo coniosis becomes evident 20 to 40 years after the first exposure to asbestos. Once established, asbestosis progresses even after exposure has ceased. There is often thickening of the vis ceral pleura from extension of the pa renchymal inflammation. The parietal pleura may show patches of severe thickening, particularly over the dia phragm and the lower portions of the chest wall, resulting in the so-called pleural hyaline plaques. These may be seen by x-ray, especially if calcified. Pleural plaques, which produce no symptoms, may develop from asbestos oronenogeme carcinoma <mu meso thelioma of the pleura and perito neum are causally associated with as bestos exposures; excesses of cancer of the stomach, colon, and rectum have also been observed.4 Among 632 asbes tos workers observed from 1943 to 1967, there were 99 excess deaths (above that expected on the basis of the US white male population) for three types of ma lignancies: (1) bronchogenic (63), (2) gastrointestinal, (26) and (3) ail other sites combined (10).1 Mesothelioma, a relatively rare and rapidly fatal neoplasm seen chiefly in crocidolite workers, may occur without radiologic evidence of asbestosis at ex posure levels lower than those required for prevention of radiologically evident asbestosis.1 Mesothelioma can occur after a short intensive exposure; cases in patients younger than 19 years of age indicate that the latent time period for development may be shorter than first estimated, although the disease may occur following a very limited exposure 20 to 30 years earlier. Cigarette smoking is strongly impli cated as a cocarcinogen among asbestos workers.5 The incidence of lung carci noma among nonsmoking asbestos workers is not significantly greater than that of nonasbestos workers, whereas asbestos workers who smoke have a much higher incidence. Cigarette-smok ing asbestos workers have approxi mately 15 times the risk of developing lung cancer compared with nonsmoking asbestos workers.6 REFERENCES 1. National Institute for Occupational Safety and Health, US Department of Health, Education, and Welfare: Criteria fora Recommended Stan dard . . . Occupational Exposure to Asbestos. DHEW (HSM) 72-10267. Washington, DC. US Government Printing Office. 1972 2. Parkes WR: Occupational Lung Disorders, 2nd ed, p 255. London, Butterworths, 1982 3. Asbestos. Documentation of TLVs and BEls. 5th ed, pp 40-42. Cincinnati, American Con ference of Governmental Industrial Hygienists (ACC1H), 1986 4. Selikoff 1J. Churg J, Hammond EC: Asbestos exposure and neoplasia. JAMA 188:22-28,1968 5. Selikoff Ij, Hammond EC. Churg j: Asbestos exposure, smoking and neoplasia. JAMA 204:106-112. 1968 6. Selikoff IJ, Lee DHK: Asbestos and Disease, p 327. New York, Academic Press, 1978 )t Sources Electrical insulators between pot anodes and catnodes. or ground: thermocouple wire: Mannue: spacers in casting furnaces: brake "n'ngsJ RMC0 0 214 5 6 v (remainder of outdated technology)