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Arsenic and compounds - 236 entries found

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  • Arsenic and compounds

2011

CIS 11-0675 Boffetta P., Fontana L., Stewart P., Zaridze D., Szeszenia-Dabrowska N., Janout V., Bencko V., Foretova L., Jinga V., Matveev V., Kollarova H., Ferro G., Chow W.H., Rothman N., van Bemmel D., Karami S., Brennan P., Moore L.E.
Occupational exposure to arsenic, cadmium, chromium, lead and nickel, and renal cell carcinoma: A case-control study from Central and Eastern Europe
The objective of this study was to investigate the risk of renal cell carcinoma (RCC) in Central and Eastern Europe in relation to exposure to known and suspected carcinogenic metals. During 1999-2003, a hospital-based study was conducted in the Czech Republic, Poland, Romania and Russia, including 1097 cases of RCC and 1476 controls. Occupational exposure to arsenic, cadmium, chromium, lead and nickel was assessed by teams of local industrial hygiene experts, based on detailed occupational questionnaires. The odds ratios (ORs) for RCC were 1.55 for exposure to lead and 1.40 for exposure to cadmium. No clear monotonic exposure-response relation was apparent for either duration of exposure or cumulative exposure to either metal, although the OR for the highest category of cumulative exposure to lead was 2.25. Exposure to other metals did not entail an increased risk of RCC.
Occupational and Environmental Medicine, Oct. 2011, Vol.68, No.10, p.723-728. 37 ref.

2008

CIS 08-1142 Garnier R., Poupon J., Villa A.
Arsenic and its inorganic compounds
Arsenic et dérivés inorganiques [in French]
Occupations that involve exposure to arsenic include the production of arsenic compounds, non-ferrous metal smelting, the production and use of arsenic-based dyes, the production of micro devices, certain glass manufacturing operations, leather tanning and CCA (chromium, copper and arsenic-based) wood treatment. Often fatal, acute poisoning results in gastroenteritis, hydroelectrolytic and haemodynamic disturbances, renal tubular damage, hepatic cytolysis, cardiomyopathy, encephalopathy (confusion, coma, convulsions) and metabolic acidosis. Long-term exposure to arsenic can cause dermatological, neurological, cardiovascular, metabolic and carcinogenic effects. Several recent epidemiological studies indicate increased risks of abortion, premature birth and in-utero deaths associated with arsenic exposure during pregnancy. The standard biological indicator of arsenic exposure is the sum of the urinary concentrations of inorganic arsenic and of its main metabolites.
Encyclopédie médico-chirurgicale, Toxicologie-Pathologie professionnelle, 2nd Quarter 2008, No.159, 13p. Illus. 104 ref.

2007

CIS 09-650 Soleo L., Gigante M.R., Antelmi A., Lovreglio P., Drago I., Gagliardi T., Sannelli G., Schiavulli N., Conversano M., Bailardi F., Greco L., Persechino B., Iavicoli S.
Exposure assessment of carcinogenic metals (Cr, As) in steel foundry workers and in the general population in Taranto (Italy)
Valutazione dell'esposizione a metalli cancerogeni (Cr, As) nei lavoratori dello stabilimento siderurgico e nella popolazione generale di Taranto (Italia) [in Italian]
Steelworks can expose workers to low concentrations of chromium and arsenic, both carcinogenic metals. These metals can also be released into the environment surrounding the industrial plants and expose the general population living near them. Non-occupational exposure to these metals also exists through the ingestion of certain foods. A total of 195 workers at an Italian steel plant with possible exposure to inorganic arsenic and chromium and two control groups consisting of 105 subjects living near the foundry, and 144 subjects living approximately 20km away, were examined. A questionnaire was administered to acquire data on personal factors, health, lifestyle and occupational and non-occupational exposure to inorganic arsenic and chromium. Urinary inorganic arsenic and chromium were tested by atomic absorption spectrophotometry. Occupational exposure to inorganic arsenic and chromium was found to be markedly below the environmental threshold limit values indicated by international organizations. No significant differences emerged among the three groups. Other findings are discussed.
Prevenzione oggi, 3rd quarter 2007, Vol.3, No.3, p.37-56. Illus. 36 ref.
http://prevenzioneoggi.ispesl.it/pdf%5Cric2007_03_3_it.pdf [in Italian]
http://prevenzioneoggi.ispesl.it/pdf%5Cric2007_03_3_en.pdf [in English]

CIS 09-319 Jones S.R., Atkin P., Holroyd C., Lutman E., Vives i Batlle J., Wakeford R., Walker P.
Lung cancer mortality at a UK tin smelter
The aim of this study was to investigate the relationship between lung cancer mortality and quantitative measures of exposure in a tin smelter. Using available records of occupational hygiene measurements, exposure matrices for arsenic, cadmium, lead, antimony and polonium-210, covering the main process areas of the smelter, were established as well as work histories from personnel record cards for the previously defined cohort of 1462 male employees. Three different methods of extrapolation were used to assess exposures prior to 1972 when no measurement results were available. Lung cancer mortality was examined in relation to cumulative inhalation exposure by Poisson regression analysis. No significant associations could be found between lung cancer mortality and simple cumulative exposure to any of the substances studied. When cumulative exposures were weighted according to time since exposure and attained age, significant associations were found between lung cancer mortality and exposures to arsenic, lead and antimony. Other findings are discussed.
Occupational Medicine, June 2007, Vol.57, No.4, p.238-245. Illus. 45 ref.

CIS 09-394 Szyman£ka-Chabowska A., Antonowicz-Juchniewicz J,, Andrzejak R.
The concentration of selected cancer markers (TPA, TPS, CYFRA 21-1, CEA) in workers occupationally exposed to arsenic (As) and some heavy metals (Pb, Cd) during a two-year observation study
Molecular epidemiology studies have lately been focused on occupational cancer associated with exposure to chemical carcinogens in the work environment. A two-year observation study was designed to investigate the relationship between arsenic, lead and cadmium concentrations and the levels of cancer markers: TPA (tissue polypeptide antigen), TPS (tissue polypeptide specific antigen), CYFRA 21-1 and CEA (carcinoembryonic antigen) in 69 male workers occupationally exposed to As and Pb, and environmentally exposed to Cd via tobacco smoking. Significant correlations were found between CEA and blood Cd concentrations or between CEA and the duration of work under exposure. All the metals examined were found to have an influence on the concentration of cancer markers, except for CYFRA 21-1. Other findings are discussed.
International Journal of Occupational Medicine and Environmental Health, 3rd quarter 2007, Vol.20, No.3, p.229-239. Illus. 30 ref.

CIS 08-764
Agency for Toxic Substances and Disease Registry (ATSDR)
Toxicological profile for arsenic (Update)
This profile has been prepared in accordance with guidelines set by the US Agency for Toxic Substances and Disease Registry and the EPA. The key literature related to the toxic effects of arsenic is identified and reviewed. Contents: public health statement; health effects; chemical and physical information; production, import, use and disposal; potential for human exposure; analytical methods; regulations and advisories; glossary. Health hazards: the acute toxicity of inorganic arsenic compounds is high; dermal exposure gives rise to skin lesions; cyanosis and cardiovascular diseases, while ingestion causes nausea; vomiting and diarrhoea. Arsenic is a known carcinogen by both inhalation and oral exposure routes. The IARC classification of arsenic is Group 1 (known carcinogen in humans). (Update of CIS 02-78).
U.S. Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry, Division of Toxicology/Toxicology Information Branch, 1600 Clifton Road NE, E-29, Atlanta, GA 30333, USA, Aug. 2007. xx, 499p. Illus. Approx. 1500 ref. Index.
http://www.atsdr.cdc.gov/toxprofiles/tp2.pdf [in English]

2006

CIS 07-1126 Liao Y.H., Hwang L.C., Kao J.S., Yiin S.J., Lin S.F., Lin C.H., Lin Y.C., Aw T.C.
Lipid peroxidation in workers exposed to aluminium, gallium, indium, arsenic, and antimony in the optoelectronic industry
The objective of this study was to investigate whether exposure to aluminium, gallium, indium, arsenic, and antimony induces lipid peroxidation in humans. Blood and urine levels of 103 exposed electronic industry workers and 67 referents were analyzed using inductively coupled plasma mass spectrometry. Malondialdehyde (MDA), the product of lipid peroxidation, was determined by high-performance liquid chromatography. The mean plasma MDA level of the exposed workers was significantly higher than that of the referents. The levels of MDA in the exposed workers were correlated significantly with the levels of urinary gallium and arsenic.
Journal of Occupational and Environmental Medicine, Aug. 2006, Vol.48, No.8, p.789-793. 35 ref.

CIS 07-642 Böcher A., Müller M., Buchter A.
Arsenic diseases of wine-growers and medical importance of environmental arsenic exposure
Die Arsenerkrankungen der Winzer und umweltmedizinische Bedeutung der Arsenbelastung [in German]
Five cases of arsenic diseases have recently been identified among elderly wine growers who had been occupationally exposed in the 1930s and 1940s to arsenic-containing pesticides and who had consumed arsenic-containing home made wine. The exposure circumstances in these cases and the diagnosed arsenic-related diseases are described. In all cases the latency period between termination of exposure and first diagnosis of an arsenic-related disease was extremely long, ranging from 40 to 60 years. In two cases a urinary transitional cell carcinoma was diagnosed in addition to typical skin diseases caused by arsenic. Based on epidemiologic data from Asian and South American countries that provided evidence of a significantly increased risk of urinary transitional cell carcinoma following long-term arsenic exposure, it is recommended that this cancer should be recognized as an occupational disease in patients with skin diseases caused by occupational arsenic exposure.
Zentralblatt für Arbeitsmedizin, Arbeitsschutz und Ergonomie, 2006, Vol.56, No.3, p.58-67. Illus. Bibl.ref.

CIS 07-369 Pakulska D., Czerczak S.
Hazardous effects of arsine: A short review
This article reviews the mechanisms by which arsine exerts its toxic effects and examines conditions of occupational exposure to this gas. Occupational exposure to arsine occurs mostly in the chemical and metallurgical industries. In these industries, arsine is often a cause of unexpected serious poisoning, affecting primarily the blood and kidneys. Acute arsine poisoning results in massive damage to red blood cells through an oxidative mechanism, probably by formation of hydrogen peroxide and adducts with oxyhaemoglobin. According to another hypothesis, arsine acts on the sodium-potassium pump mechanism, producing subsequent red blood cell swelling and haemolysis. Rapid haemolysis may lead to oliguric renal failure and death. Symptoms of chronic poisoning are similar to those observed in acute poisoning. The main difference is a longer latency period. Delayed effects of chronic exposure to low levels of arsine have not been precisely identified.
International Journal of Occupational Medicine and Environmental Health, 1st quarter 2006, Vol.19, No.1, p.36-44. 51 ref.

CIS 07-170 Lundström N.G., Englyst V., Gerhardsson L., Jin T., Nordberg G.
Lung cancer development in primary smelter workers: A nested case-referent study
The objective of this study was to evaluate the impact of work-related exposure to arsenic and lead versus smoking among lead smelter workers who had developed lung cancer. In a cohort of 3979 lead smelter workers, 46 male subjects had contracted respiratory malignancies. They were compared with 141 age-matched male referents by conditional logistic regression analysis. Cases showed a fourfold higher smoking rate compared with referents. When restricted to smokers, the cumulative air arsenic exposure index, but not the lead exposure indices, was also significantly higher among the cases. It is concluded that cumulative arsenic exposure and smoking were the main risk factors for the development of lung cancer, but not lead exposure.
Journal of Occupational and Environmental Medicine, Apr. 2006, Vol.48, No.4, p.376-380. 30 ref.

2005

CIS 06-366 Heilier J.F., Buchet J.P., Haufroid V., Lison D.
Comparison of atomic absorption and fluorescence spectroscopic methods for the routine determination of urinary arsenic
The objective of this study was to develop a rapid and robust technique for the measurement of urinary inorganic arsenic. It involves the measurement of arsenic in urine after hydride generation in acid medium and uses atomic fluorescence spectrometry (AFS) as the detection system. The AFS procedure was found to be more precise and sensitive than the atomic absorption spectroscopy (AAS) technique using a quartz cell. A variation of the procedure that allows the detection of non-directly reducible arsenic forms was also validated for samples with high arsenic concentrations.
International Archives of Occupational and Environmental Health, Feb. 2005, Vol.78, No.1, p.51-59. Illus. 23 ref.

CIS 06-137 Gawęda E.
Occupational exposure to carcinogenic metals and metalloids in refining of heavy metals
Narażenie zawodowe na rakotwórcze metale i metaloidy w procesach rafinacji metali ciężkich [in Polish]
Concentrations of carcinogenic metals (cadmium, nickel) and metalloids (arsenic) were measured in workplace air during heavy metals refining processes. The tests were conducted in two large Polish plants, a copper smelter and a non-ferrous metals smelter, at workstations for the refining of copper, zinc, cadmium, lead and silver and the production of nickel sulfate and selenium. The presence of arsenic in the workplace air was found in both plants. Exposure to cadmium occurred only in the non-ferrous metals smelter. The highest exposure was found at workstations in the lead and cadmium refining processes. The presence of nickel was found only at workstations with nickel sulfate production. The results highlight the need for routine measurements of arsenic concentrations at all workstations in the production of metals with a high degree of purity.
Medycyna pracy, 2005, Vol.56, No.2, p.161-165. 8 ref.

2004

CIS 04-577 Chlebda E., Antonowicz-Juchniewicz J., Andrzejak R.
The effect of occupational exposure to heavy metals and arsenic on the concentration of carotenoids in the serum of copper foundry workers
Wpływ ekspozycji zawodowej na ołów i arsen na stężenie karotenoidów w surowicy u pracowników huty miedzi [in Polish]
Occupational exposure to heavy metals and arsenic in moderate doses may lead to a decrease in the concentration of carotenoids in the serum of people at risk, thus reducing the efficiency of their antioxidative mechanisms.
Medycyna pracy, 2004, Vol.55, No.5, p.389-401. 40 ref.

CIS 03-1765 Grillet J.P., Adjémian A., Bernadac G., Bernon J., Brunner F., Garnier R.
Arsenic exposure in the wine growing industry in ten French departments
This study investigated exposure to arsenic from a fungicide used in French vineyards. First phase compared urinary arsenic excretion of agricultural workers after having performed the application and of a non-exposed control group. In the second phase, which included 35 subjects exposed to arsenic from ten French departments, the increase in urinary arsenic excretion after application was measured. In the first phase, urinary arsenic excretion was significantly higher in applicators than in the control group. The second phase showed a significant increase of arsenic excretion the day after the application. A closed tractor cabin provided a protective effect but efficacy of individual protective equipment could not be demonstrated.
International Archives of Occupational and Environmental Health, Feb. 2004, Vol.77, No.2, p.130-135. 16 ref.

2002

CIS 06-4
Health and Safety Executive
Arsenic and you - Arsenic is poisonous. Are you at risk?
This leaflet contains information on health hazards from exposure to dusts and fumes containing arsenic. Topics covered: sources of dusts and fumes containing arsenic; absorption routes; health hazards due to arsenic; protective measures; health checks; legal requirements and exposure limit; sources of information.
HSE Books, P.O. Box 1999, Sudbury, Suffolk CO10 2WA, United Kingdom, Sep. 2002. 6p. 1 ref.
http://www.hse.gov.uk/pubns/msa8.pdf [in English]

CIS 03-741 Apostoli P., Sarnico M., Bavazzano P., Bartoli D.
Arsenic and porphyrins
To evaluate the possible effect of arsenic and of its compounds on the urinary excretion of porphyrin homologues, the following substances were determined in the urine of 86 art glass workers exposed to arsenic and its compounds and from 54 non-exposed controls: total porphyrins and their homologues (copro, penta, hexa, hepta, uroporphyrins) and the following arsenic species: trivalent and pentavalent arsenic, monomethyl arsonic acid, dimethyl arsinic acid and arsenobetaine. A significant increase in the excretion of penta and uroporphyrins was found for workers exposed to arsenic. The best correlation with urinary porphyrin excretion was found with trivalent arsenic. The increase of urinary excretion for some porphyrin homologues is consistent with the inhibition by arsenic of uro-decarboxylase in the haeme biosynthesis pathway. The determination of urinary porphyrin homologues could be useful to assess some early effects of arsenic exposure and to demonstrate possible individual susceptibility to the element.
American Journal of Industrial Medicine, Sep. 2002, Vol.42, No.3, p.180-187. Illus. 26 ref.

CIS 03-540 Czerczak S., Fishbein L.
Inter-Organization Programme for the Sound Management of Chemicals (IOMC)
Arsine: Human health aspects
Conclusions of this criteria document: the target organ of arsine poisoning is the haematopoietic system. Arsine induces haemolysis causing haemoglobinuria and subsequent kidney damage. Myocardial and pulmonary failures are other causes of death. Aneamia and increased leucocytosis is observed at various degrees. There are no data on the carcinogenicity or mutagenicity of arsine to humans or experimental animals.
World Health Organization, Distribution and Sales Service, 1211 Genève 27, Switzerland, 2002. iv, 29p. 107 ref.
http://www.who.int/ipcs/publications/cicad/en/cicad47.pdf [in English]

CIS 97-36 Arsenic trichloride
Data sheet. May enter the body when breathed in and through the skin. May cause mutations and should be handled with extreme caution. May irritate and burn the skin and cause thickening and pigment changes. Irritates and burns the eyes. Irritates the respiratory tract. May damage the nervous system.
New Jersey Department of Health, Right to Know Program, CN 368, Trenton, NJ 08625-0368, USA, 1996, 2002. 6p.
http://www.state.nj.us/health/eoh/rtkweb/0159.pdf [in English]

2001

CIS 02-1786 Gradecka D., Palus J., Wąsowicz W.
Selected mechanisms of genotoxic effects of inorganic arsenic compounds
Chronic exposure to inorganic arsenic compounds is known to cause various tumours and diseases. In many regions of Asia and Latin America, the concentration of inorganic arsenic in drinking water considerably exceeds the standard of 50µg/L recommended by the US Environmental Protection Agency. The genotoxicity of inorganic arsenic has been confirmed in vitro and in vivo, as well as in examinations of exposed populations. Inorganic arsenic increases the frequency of micronuclei, chromosome aberrations and sister chromatid exchanges both in humans and in animals. Various studies suggest that inorganic arsenic may intensify the toxic effects of other physical and chemical agents, especially by DNA repair inhibition. Besides, it is believed that inorganic arsenic compounds may cause changes in the cell redox potential and alter DNA methylation and phosphorylation of cell-cycle control proteins. Some data also suggest that inorganic arsenic increases cellular proliferation and apoptosis. Possible cytotoxic mechanisms of inorganic arsenic compounds are discussed.
International Journal of Occupational Medicine and Environmental Health, 2001, Vol.14, No.4, p.317-328. Illus. 71 ref.

CIS 02-71
International Programme on Chemical Safety (IPCS)
Arsenic and arsenic compounds
Conclusions of this criteria document: arsenic and its compounds are highly toxic; the ingestion of large doses gives rise to gastro-intestinal symptoms and cardiovascular and neurological disorders that can lead to death. There is a causal relationship between exposure to arsenic, primarily by inhalation, and lung cancer. Chronic exposure to arsenic can cause severe peripheral vascular disease (blackfoot disease). Long-term exposure to arsenic in drinking water increases the risk of skin, lung and bladder cancer as well as other skin anomalies.
World Health Organization, Distribution and Sales Service, 1211 Genève 27, Switzerland, 2nd ed., 2001. xxviii, 521p. Illus. Approx. 1200 ref. Price: CHF 108.00 (CHF 75.60 in developing countries).

2000

CIS 02-78
Agency for Toxic Substances and Diseases Registry (ATSDR)
Toxicological profile for arsenic (Update)
This profile was prepared in accordance with guidelines set by the US Agency for Toxic Substances and Disease Registry and the EPA. The key literature related to the toxic effects of arsenic is identified and reviewed. Contents: public health statement; health effects; chemical and physical information; production, import, use and disposal; potential for human exposure; analytical methods; regulations and advisories; glossary. Health hazards include: irritation of the skin, eyes and respiratory tract; skin disorders (hyperkeratosis); gastrointestinal effects; haematotoxic effects (blood-cell anomalies); cardiovascular disorders; arrhythmia; neurotoxic effects; carcinogenic effects (skin, gastrointestinal, liver, bladder, renal and lung cancer); effects on reproduction (stillbirth); genotoxic effects. (Update of CIS 96-2217).
U.S. Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry, Division of Toxicology/Toxicology Information Branch, 1600 Clifton Road NE, E-29, Atlanta, GA 30333, USA, Sep. 2000. xx, 428p. Illus. Approx. 1440 ref.

CIS 02-169 Alguacil J., Kauppinen T., Porta M., Partanen T., Malats N., Kogevinas M., Benavides F.G., Obiols J., Bernal F., Rifa J., Carrato A.
Risk of pancreatic cancer and occupational exposures in Spain
Cases of pancreatic cancer and controls among hospital patients free of pancreatic cancer were identified during their stay in hospital. Occupational history was obtained by direct interviews with the patients. Occupational exposures to 22 suspected carcinogens associated with pancreatic cancer in previous studies were evaluated. Increased odds ratios (OR) were apparent in all pesticide groups, highest for arsenical pesticides (OR = 3.4) and "other pesticides" (OR = 3.17). ORs were also higher for high-intensity exposure to aniline derivatives, dyes and organic pigments. ORs above 3 were observed for pesticides, benzo(a)pyrene, lead, volatile sulfur compounds, and sedentary work. Results lend support to the hypothesis of an association between exposure to some pesticides and pancreatic cancer. Suggestive increases in risk from aniline derivatives, dyes and organic pigments, and benzo(a)pyrene also deserve further study.
Annals of Occupational Hygiene, Aug. 2000, Vol.44, No.5, p.391-403. 72 ref.

1999

CIS 01-1137 Subra I., Hubert G., Aubert S., Héry M., Elcabache J.M.
Occupational exposure to metals in the machining of copper-, chromium- and arsenic-treated wood
Exposition professionnelle aux métaux lors de l'usinage des bois traités au cuivre, chrome, arsenic [in French]
Exposure was measured in two workshops where impregnated wood is machined. The chromium in the treatment solution is the most toxic form (chromium VI), but due to its reducing properties the cellulose in the wood tends to transform it during impregnation into what are probably trivalent components. As a result, worker exposure to chromium VI is minimal (at the limit of analytical detection). Generally, exposure to total chromium and copper is well below the limit values, both French and American. Only exposure to arsenic reaches significant levels in the two workshops. Although well below the current French limit value of 200µg/m3, it is above the limit value recently proposed in France (50µg/m3) and that adopted by ACGIH (10µg/m3). An efficient implementation of the prevention measures related to woodworking is sufficient for a good prevention of copper, chromium and arsenic related hazards.
Cahiers de notes documentaires - Hygiène et sécurité du travail, 2nd Quarter 1999, No.175, p.61-68. Illus. 12 ref.

CIS 01-1123 Skerfving S., Bencko V., Vahter M., Schütz A., Gerhardsson L.
Environmental health in the Baltic region - Toxic metals
Recent reports on concentrations of lead, cadmium, methylmercury, arsenic and nickel in some biological media in populations of the Baltic region are reviewed. In particular, children in parts of Poland, the Czech Republic and Germany have uptakes of lead sufficient to cause adverse effects on the central nervous system and kidneys. Cadmium exposure is also high in Poland. Methylmercury uptake is dependent upon the intake of fish in Sweden and Finland, as well as along the eastern coast of the Baltic Sea. There are some indications of immunotoxic effects. However, fish also contain other immunomodulating agents. Exposure to arsenic seems to be low everywhere in the Baltic region. There is high nickel exposure in northern Russia.
Scandinavian Journal of Work, Environment and Health, 1999, Vol.25, Suppl.3, p.40-64. Illus. 199 ref.

CIS 01-134 Apostoli P., Bartoli D., Alessio L., Buchet J.P.
Biological monitoring of occupational exposure to inorganic arsenic
The study was undertaken to assess biological indicators for monitoring occupational exposure to inorganic arsenic (iAs), taking into account the possible confounding role of arsenicals present in food and drinking water. 51 glass workers exposed to arsenic (As) trioxide, a control group of 39 subjects not exposed and eight volunteers who drank water containing 45µg/L iAs for a week were monitored for total arsenic in air and urine samples, and for urinary As3, As5, monomethyl arsonic acid, dimethyl arsinic acid, and arsenobetaine. The best correlations between As in air and its urinary species were found for total iAs and As3+As5. It is proposed that urinary As3+As5 be used as an indicator for monitoring the exposure to iAs. For the current environmental limit for iAs of 10µg/m3, the limit for urinary As3+As5 was calculated to be around 5µg/L. Trivalent arsenic is the most active species and its measured concentration in urine could be the best predictor of some critical effects of the element, such as cancer.
Occupational and Environmental Medicine, Dec. 1999, Vol.56, No.12, p.825-832. Illus. 66 ref.

1998

CIS 99-1095 Potassium arsenate
Topics: carcinogens; potassium arsenate; data sheet; elimination of spills; fire hazards; first aid; glossary; health hazards; irritation; limitation of exposure; lung cancer; medical examinations; neurotoxic effects; New Jersey; personal protective equipment; skin cancer; storage; teratogenic effects; threshold limit values; USA.
New Jersey Department of Health and Senior Services, Right to Know Program, PO Box 368, Trenton, NJ 08625-0368, USA, 1998. 6p.

CIS 98-1371 Apostoli P., Giusti S., Bartoli D., Perico A., Bavazzano P., Alessio L.
Multiple exposure to arsenic, antimony and other elements in art glass manufacturing
Topics: antimony; arsenic; arts and crafts; cancer; carcinogens; lead; determination in air; determination in urine; exposure evaluation; glass industry; Italy; job-exposure relation; mixed dust; mortality.
American Journal of Industrial Medicine, July 1998, Vol.34, No.1, p.65-72. Illus. 17 ref.

1997

CIS 02-550 Arsine
Trihydrure d'arsenic [in French]
Chemical safety information sheet. Toxicity: haemoglobinaemia, which can lead to renal insufficiency with anuria; hepatotoxic effects; pulmonary disorders; neurotoxic effects. Exposure limits (France): TWA = 0.2mg/m3 (0.05ppm); ceiling value = 0.8mg/m3 (0.2ppm). EEC number and mandatory labelling codes: No.033-006-00-7; T, F+, N, R12, R26, R48/20, R50/53, S9, S16, S28, S33, S36/37, S45, S60, S61, 232-066-3. The complete datasheet collection on CD-ROM has been analysed under CIS 01-201.
Institut national de recherche et de sécurité, 30 rue Olivier-Noyer, 75680 Paris Cedex 14, France, CD-ROM CD 613, May 2000. Rev.ed. 3p. Illus. 13 ref.

CIS 00-314 Factories (Medical Examinations) (Amendment) Regulations 1997 [Singapore]
Topics: arsenic and compounds; arsenic; asbestos; benzene; bitumen; cadmium; tetrachloroethylene; pitch; lead; manganese; mercury; vinyl chloride; silica; trichloroethylene; compressed air; cotton industry; creosote; dust; exposure; law; lead and compounds; medical examinations; medical supervision; mercury and compounds; mists; noise; organophosphorus compounds; Singapore; smoke.
Photocopy, 13p. On file at CIS.

1996

CIS 97-760 Sodium arsenite
Data sheet. May enter the body when breathed in. It is a carcinogen and should be handled with extreme caution. May irritate and burn the skin, eyes and respiratory tract. May damage the nerves with numbness and weakness of the arms and legs.
New Jersey Department of Health, Right to Know Program, CN 368, Trenton, NJ 08625-0368, USA, 1996. 6p.

CIS 97-418 Arsenic pentoxide
Data sheet. May enter the body when breathed in and through the skin. It is a carcinogen and should be handled with extreme caution. May irritate the eyes, skin and respiratory tract. May cause skin rash and change of colour. May perforate the nasal septum. May damage the nerves, causing a pins and needles sensation, numbness and weakness of the arms and legs.
New Jersey Department of Health, Right to Know Program, CN 368, Trenton, NJ 08625-68, USA, 1996. 6p.

CIS 97-417 Arsenic acid
Data sheet. May enter the body when breathed in and through the skin. It is a mutagen and teratogen and should be handled with extreme caution. May irritate the eyes, skin and respiratory tract. May cause thickening of the skin and change of colour. May damage the nerves, causing a "pins and needles" sensation, numbness and weakness of the arms and legs.
New Jersey Department of Health, Right to Know Program, CN 368, Trenton, NJ 08625-68, USA, 1996. 6p.

CIS 96-1770 Morvai V.
Cardiovascular effects of metals
Studies of the toxic cardiovascular effects of metals in animals and humans are reviewed, in particular those of arsenic, barium, cadmium, cobalt, copper, iron, lead, nickel and vanadium. Despite the numerous data available, the exact mechanism of metals in the aetiology of cardiovascular disease remains obscure. Future research needs are outlined.
Central European Journal of Occupational and Environmental Medicine, 1996, Vol.2, No.2, p.115-145. 194 ref.

CIS 96-1395
International Metalworkers' Federation (IMF)
Health, safety and environment
A survey of working conditions and exposure to arsenic was carried out among copper workers in Chile. High levels of arsenic and other pollutants were found in two smelting shops and in the surrounding area; analysis of dust samples from the shop floor showed an arsenic content of 11 to 19%. Workers rarely used any form of respiratory protection. There was a high frequency of silicosis among mine workers. The role of trade unions in improving the working conditions of these workers is emphasized.
IMF Bulletin on Occupational Health and Safety - Bulletin FIOM sur l'hygiène et la sécurité au travail, 1996, No.34, p.1-8 (whole issue). Illus.

1995

CIS 99-934 Jensen G.E.
Occupational exposure to arsenic in wood workers and taxidermists
Arseneksponering ved arbejde med imprægneret træ og ved udstopning af dyr og fugle [in Danish]
Topics: arsenic; blood pressure; determination in air; determination in urine; enzyme activity; exposure evaluation; report; taxidermy; woodworking industry.
Arbejdsmiljøinstituttet, Lersø Parkallé 105, 2100 København Ø, Denmark, 1995. 72p. Illus. 114 ref.

CIS 96-1267
National Occupational Health and Safety Commission (Worksafe Australia)
Guidelines for health surveillance
These guidelines are intended for appointed medical practitioners when planning and implementing a programme of health surveillance within enterprises. Such programmes should be instituted when a workplace assessment of health risks, conducted according to the National Model Regulations for the Control of Workplace Hazardous Substances (NOHSC 1005: (1994), see CIS 95-274), has determined that workplace exposure represents a significant risk to health. Contents of the 18 booklets: 1 - Introduction (basic aspects of health surveillance, extracts from the Model Regulations and the National Code of Practice (NOHSC: 2007 (1994), see CIS 95-274 as well), list of substances subject to control, criteria for determining whether a substance should be scheduled as requiring health surveillance). 2 - sample respiratory questionnaires to be administered to workers. 3-18: Specific substances (for each substance: information on health surveillance at time of employment, during exposure to a process where the substance is present and at termination of employment; data sheet with information on substance in question). The substances are: acrylonitrile, inorganic arsenic, asbestos, benzene, cadmium, inorganic cadmium, creosote, isocyanates, inorganic mercury, MOCA, organophosphate pesticides, pentachlorophenol, polycyclic aromatic hydrocarbons, crystalline silica, thallium, vinyl chloride.
Australian Government Publishing Service, GPO Box 84, Canberra ACT 2601, Australia, 1995-1996. 18 booklets in a ring binder. Bibl.ref.
http://www.ascc.gov.au/NR/rdonlyres/481CF3F5-8C4B-4BCC-AF65-3FDBA031D43B/0/HealthSurveillance.pdf [in English]

CIS 96-1389 Enterline P.E., Day R., Marsh G.M.
Cancers related to exposure to arsenic at a copper smelter
To verify earlier findings of a supralinear dose response relation between exposure to arsenic in air and deaths from respiratory cancer, and to examine relations with other cancers, an earlier study of 2,802 men who worked at a copper smelter for a year or more during the period 1940-64 and who were followed up for deaths during the period 1941-76 was updated until 1986. Estimates of exposure for the period 1977-1984 were added. The additional follow-up confirms the earlier finding that at low doses the increments in death rates for respiratory cancer for a given increment in dose are greater than at high doses. The additional follow-up also shows significant increases in cancer of the large intestine and bone, and SMRs >150 for cancer of the buccal cavity, pharynx, rectum and kidney. There was a positive relation between exposure to airborne arsenic and kidney and bone cancer, but none for the other cancers (except respiratory cancer).
Occupational and Environmental Medicine, Jan. 1995, Vol.52, No.1, p.28-32. Illus. 26 ref.

CIS 96-309
Health and Safety Executive, Health and Safety Laboratory
Arsenic and inorganic compounds of arsenic (except arsine) in air
This method updates and replaces MDHS 41 (see CIS 85-1616). Principle: particulate arsenic and arsenic compounds are collected on a membrane filter with a sodium carbonate-impregnated back-up paper pad. Arsenic trioxide vapour is collected by reaction with the sodium carbonate on the pad. The filter, pad and sample are digested in acid and the solution is prepared for hydride generation in a continuous flow or flow injection analysis hydride generation system. Gaseous arsine and hydrogen are separated and analyzed by atomic absorption spectrometry. Scope: suitable for sampling over periods from 15 minutes to eight hours; not suitable for the determination of certain metal arsenides or in the presence of transition metals.
HSE Books, P.O. Box 1999, Sudbury, Suffolk CO10 6FS, United Kingdom, Nov. 1995. 16p. Illus. 24 ref. Price: GBP 5.00.

CIS 95-1719 de Peyster A., Silvers J.A.
Arsenic levels in hair of workers in a semiconductor fabrication facility
This study examines the relationship between total arsenic (As) levels in the hair of employees in a semiconductor fabrication facility and job responsibility, a surrogate variable for As exposure potential. Maintenance personnel who regularly worked in equipment cleaning areas were assumed to have a higher potential for occupational exposure to As than other employees. Hair samples were collected from workers with high, medium and low potential for exposure and from controls (administrative employees). Total As in hair was measured by atomic absorption spectroscopy. Exposure levels were established by taking air and wipe samples, and by evaluating returned questionnaires designed to detect nonoccupational As sources. Mean hair As, though somewhat higher than in controls, was not significantly higher in any of the exposed groups. In general, nonoccupational sources of As seemed to contribute more to hair As levels than any occupational exposure. Monitoring for low-level As exposure in this industry should only be considered if nonoccupational exposures can also be examined.
American Industrial Hygiene Association Journal, Apr. 1995, Vol.56, No.4, p.377-383. 22 ref.

CIS 95-1812 Simonsen L., Midtgård U., Lund S.P., Hass U.
Nordic Council of Ministers
Occupational neurotoxicity: Evaluation of neurotoxicity data for selected chemicals
Previously determined criteria for evaluating published data on the neurotoxicity of chemicals (see CIS 95-000) were applied to the literature on 79 common industrial chemicals. Data were too sparse to permit classification of 28. Of the rest, eight were classified as probably and 16 as possibly neurotoxic, and the following 27 as definitely neurotoxic: acrylamide, acrylonitrile, aluminium, arsenic, sodium azide, borax, boric acid, carbon monoxide, carbon disulfide, potassium cyanide, ethanol, ethylene oxide, hexachlorophene, manganese, mercury, methanol, methyl bromide, methyl butyl ketone (2-hexanone), methyl chloride, methyl methacrylate, n-hexane, nitrous oxide, styrene, thallium, toluene, trichloroethylene, triorthocresyl phosphate.
National Institute of Occupational Health, Lersø Parkallé 105, 2100 København Ø, Denmark, 1995. 119p. Bibl.ref.

1994

CIS 01-666 Javelaud B.
Arsenic and its compounds
Arsenic et dérivés [in French]
Toxicological data sheet on arsenic (As) and its compounds. Metallic arsenic is non-toxic and does not oxidize. The main toxic compounds of As are trivalent, including arsenic trioxide, sodium arsenite and potassium arsenite. The toxicity of pentavelent compounds is less than that of trivalent compounds. Main exposure routes: inhalation, ingestion. Acute toxicity: vomiting, abdominal pain and diarrhoea, followed by cardiovascular symptoms; death from ventricular fibrillation occurs within 10 hours following ingestion; lethal dose is estimated at 1-2mg/kg. Chronic toxicity: effects on the skin; neurotoxic effects; inhalation of arsenical dusts or vapours can give rise to bronchial cancer; liver cancer; cardiovascular effects; haematological effects; effects on the reproductive system. The toxicology of arsine is covered in a specific section. Tables concerning the compensation of occupational diseases caused by arsenic are included.
Encyclopédie médico-chirurgicale, Toxicologie-Pathologie professionnelle, 4th Quarter 1994, No.105, 7p. 82 ref.

CIS 96-2240 Report for 1990 of a study committee for testing the toxicity and other aspects of dangerous exotic chemicals used in the IC industry and elsewhere
Heisei 2 nendo - IC sangyō-ra de sayō sareru yūgaisei michi kagaku busshitsu ni taisuru dokusei shiken-ra no chōsa kenkyū i-inkai hōkokusho [in Japanese]
Report of a committee of academic and industrial experts. In 1990, its tasks were to determine the toxicity of phosphine and to conduct a questionnaire survey in the workforce involved in the manufacture of integrated circuits (ICs). Because of its high toxicity, a 4h LC50 (mouse) for phosphine could not be established directly; extrapolation from lethality at lower doses gives an estimate of 26.5-33.4ppm. Of 156 firms that received the questionnaire, 68 (120 sites, 47,000 workers) responded. Enterprises that provide equipment and gases to IC manufacturers were included as well as IC manufacturers themselves. The structures of the workforces by age, sex, type of contract and size of enterprise were determined. The identities and quantities of 50 chemicals used (silanes, compounds of arsenic, boron, rare earth elements, etc.) were tabulated. The existence of data sheets for these products and of systems for disposing of them as waste were also determined. Blood analyses were performed on a sample of the respondents and on controls employed outside the IC industry; all IC employees showed higher red blood cell counts, haemoglobin levels and glutamic-pyruvic transaminase activities, while those over 40 years of age also had elevated cholesterol and neutral fats. Facts on 251 accidents that occurred between Jan. 1985 and Oct. 1990 were collected.
Japan Industrial Safety and Health Association, Industrial Hygiene Inspection Centre, 5-35-1 Chiba, Minato-ku, Tokyo 108, Japan, no date. 360p. Illus.

CIS 96-787 Viren J.R., Silvers A.
Unit risk estimates for airborne arsenic exposure: An updated view based on recent data from two copper smelter cohorts
The current unit risk for chronic lifetime exposure to airborne arsenic 4.29 x 10-3, was established by the US EPA in 1984. Using updated results from a cohort mortality study on Tacoma, Washington, smelter workers and recent findings from a cohort study of 3619 Swedish smelter workers, new unit risk estimates were developed for the respective cohorts. Methods were analogous to those used by the EPA in 1984, and all estimates were derived under an absolute risk model. A new unit risk 1.28 x 10-3, was estimated for the Tacoma smelter cohort which was a factor of five less than the EPA's earlier estimate, and a direct result of radically revised exposure estimates. A unit risk of 0.89 x 10-3 was estimated from the Swedish study. Pooling these new risk estimates with the EPA's earlier estimates yielded a composite unit risk of 1.43 x 10-3. Based on this estimate, the present unit risk may overestimate the effects of airborne arsenic by a factor of 3.
Regulatory Toxicology and Pharmacology, Oct. 1994, Vol.20, No.2, p.125-138. Illus. 20 ref.

CIS 95-1737 Simonato L., Moulin J.J., Javelaud B., Ferro G., Wild P., Winkelmann R., Saracci R.
A retrospective mortality study of workers exposed to arsenic in a gold mine and refinery in France
In a mortality study among employees of a French gold mining and refining company, a twofold excess of lung cancer was found among both miners and smelters, mainly concentrated among workers who had experienced exposure to past levels of arsenic, radon and silica. The consistency of the results in the mine and the refinery are suggestive of a carcinogenic risk from both soluble and insoluble arsenic, although the potential role of other factors cannot be dismissed.
American Journal of Industrial Medicine, May 1994, Vol.25, No.5, p.625-633. 18 ref.

CIS 95-1780 Lagerkvist B.J., Zetterlund B.
Assessment of exposure to arsenic among smelter workers: A five-year follow-up
Studies of copper smelter workers exposed to arsenic dust for 13-45 years were carried out in 1982 and 1987. In both studies, peripheral nerve conduction velocities (NCVs) were significantly lower than in a matching reference group; there was a significant negative correlation between estimated total absorption of arsenic and NCVs in peripheral nerves. The differences in NCVs between the groups had increased during the follow-up period, although exposure to arsenic was lower. The data indicate that the adverse effects of arsenic on the peripheral nerves is dependent on long-term exposure rather than on short-term fluctuations in exposure levels.
American Journal of Industrial Medicine, Apr. 1994, Vol.25, No.4, p.477-488. 38 ref.

CIS 95-987 Chiba M., Kazuta T., Shinohara A., Takahashi H., Endo G., Inaba Y.
Case report: Arsenic-exposed patient with polyneuritis
Hiso bakuro sagyōsha ni mirareta tahatsu shinkeien no ichi shōrei [in Japanese]
A 50-year-old male carpenter complained of numbness in the upper and lower limbs. Because of his having been exposed to airborne dust containing arsenic pentoxide, potassium dichromate and copper sulfate as wood preservatives, he was suspected of having contracted neuritis caused by arsenic poisoning. No irregularity was found except dysaesthesia in the four limbs and light hypoaesthesia in the hands and legs. Paraneoplastic neuropathy, amyloidosis and Sjogren's syndrome were ruled out. Arsenic (As), chromium (Cr) and copper (Cu) concentrations in scalp hair, fingernail, plasma, erythrocytes and urine were determined. As and Cr concentrations were much higher than in controls. There was no difference in Cu concentration between the patient and the control. This suggests that the patient's polyneuritis was due to arsenic poisoning.
Occupational Health Journal, 25 Apr. 1994, Vol.17, No.3, p.39-41. Illus. 2 ref.

1993

CIS 96-2217
Agency for Toxic Substances and Diseases Registry (ATSDR)
Toxicological profile for arsenic: Update
Contents: public health statement; health effects; chemical and physical information; production, import, use and disposal; potential for human exposure; analytical methods; regulations and advisories; glossary. Health hazards include: irritation of the skin and respiratory tract; skin disorders (hyperkeratosis); haematotoxic effects (blood-cell anomalies); cardiovascular disorders; arrhythmia; neurotoxic effects; carcinogenic effects (skin, liver, bladder, renal and lung cancer). (Update of CIS 90-1975).
U.S. Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry, Division of Toxicology, Toxicology Information Branch, 1600 Clifton Road NE, E-29, Atlanta, GA 30333, USA, Apr. 1993. 175p. Illus. Bibl.ref.

CIS 96-1588 Lead arsenate
International Chemical Safety Card. Short-term exposure effects: affects the intestines and cardiovascular system. Long-term exposure effects: dermatitis; neurotoxic effects; affects the gastrointestinal systems, liver and kidneys; haematotoxic effects; ulceration and perforation on the nasal septum; carcinogenic effects; genetic effects. Occupational exposure limit: TLV: 0.15mg/m3 (as Pb3(AsO4)2) (ACGIH 1990-1991).
Official Publications of the European Communities, 2985 Luxembourg, Grand Duchy of Luxembourg; International Programme on Chemical Safety (IPCS), World Health Organization, 1211 Genève 27, Switzerland, 1993. 2p.

CIS 94-1304 Pan T.C., Huang C.W.
Measurement of arsenic and mercury concentrations by hydride and cold vapor atomic absorption spectrophotometry
Workplace activities in a motorcycle part manufacturing plant were observed. The processes involved were bending and pressing of metal sheets, electric welding, electroplating, machining, and motorcycle muffler assembly. Arsenic and mercury concentrations in urine specimens of student controls and workers were determined. Both methods were sufficiently precise and accurate. Total arsenic levels in the exposed workers were significantly higher than those in non-exposed controls; there is a risk of arsenic poisoning to the workers engaged in motorcycle muffler assembly. The total mercury levels in the exposed workers were no different than in the controls.
American Industrial Hygiene Association Journal, Aug. 1993, Vol.54, No.8, p.454-457. Illus. 11 ref.

CIS 93-1935 Sheehy J.W., Jones J.H.
Assessment of arsenic exposures and controls in gallium arsenide production
National Institute for Occupational Safety and Health (NIOSH) researchers conducted a study of control systems for electronics facilities using gallium arsenide. Three facilities which appeared to have effective controls were chosen for in-depth evaluation through industrial hygiene sampling. The following gallium arsenide processes were studied: Liquid Encapsulated Czochralski (LEC) and Horizontal Bridgeman (HB) crystal growing, LEC cleaning operations, ingot grinding/wafer sawing, and epitaxy. Results at one plant showed that in all processes except epitaxy, average arsenic exposures were at or above the Occupational Safety and Health Administration (OSHA) action level of 5µg/m3. While cleaning the LEC crystal pullers, the average potential arsenic exposure of the cleaning operators was 100 times the OSHA PEL. At the two other plants, personal arsenic exposures were well controlled in LEC, LEC cleaning, grinding/sawing, and epitaxy operations.
American Industrial Hygiene Association Journal, Feb. 1993, Vol.54, No.2, p.61-69. Illus. 13 ref.

CIS 93-1446 Arsenic trioxide
International chemical safety card. Short-term exposure effects: delayed effects; irritation of eyes, skin and respiratory tract; may affect the kidneys, liver and the cardiovascular, nervous and haematopoietic systems. Long-term exposure effects: may affect the lungs, skin, bone marrow, peripheral vascular and nervous systems, the heart function, and the kidneys and liver; human carcinogen; may cause birth defects. Occupational exposure limit: TLV (as As): 0.2mg/m3 (ACGIH 1989-1990).
Official Publications of the European Communities, 2985 Luxembourg, Grand Duchy of Luxembourg; International Programme on Chemical Safety (IPCS), World Health Organization, 1211 Genève 27, Switzerland, 1993. 2p.

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