Bar i jego związki rozpuszczalne. Dokumentacja dopuszczalnych wielkości narażenia zawodowego

• Autorzy: Sapota A. , Skrzypińska-Gawrysiak M

Warianty tytułu

EN

Barium and its soluble compounds. Documentation

• Języki publikacji: PL

Abstrakty

PL

Bar jest srebrzystobiałym metalem alkalicznym reaktywnym chemicznie, który występuje w stanie naturalnym w skorupie ziemskiej. Do rozpuszczalnych związków baru należą głównie jego sole – chlorek, azotan, octan i węglan. Sole baru są klasyfikowane jako związki szkodliwe. Bar i jego związki mają powszechne zastosowanie przemysłowe (m.in. w przemyśle chemicznym, szklarskim, ceramicznym i elektrotechnicznym), są także stosowane jako topniki w elektrodach spawalniczych. Narażenie zawodowe na bar i jego związki rozpuszczalne (w postaci pyłów i dymów) występuje głównie w przemyśle stalowym, szklarskim, metalurgicznym i wydobywczym. Minimalna doustna dawka letalna dla człowieka wynosi około 10 mg/kg dla chlorku baru i około 60 mg/kg dla węglanu baru. Węglan baru w dawce 20 mg/kg powoduje już osłabienie mięśni, parestezje i porażenia wiotkie. Związkami najczęściej powodującymi ostre zatrucia są: węglan, chlorek, azotan i octan baru. W klinicznym obrazie zatrucia związkami baru zwykle występują ostre zaburzenia żołądkowo-jelitowe, osłabienie odruchów głębokich i zmniejszenie napięcia mięśniowego oraz osłabienie siły mięśniowej i postępujące porażenie mięśni. Śmierć zwykle następuje w wyniku zatrzymania oddechu (porażenia mięśni oddechowych) i krążenia. Objawom tym towarzyszy zmniejszenie stężenia potasu w surowicy i częstoskurcz komorowy, który przechodzi w migotanie komór. W wyniku ostrego zatrucia związkami baru wystąpić może także ostra niewydolność nerek, rabdomioliza, dysfagia i nadciśnienie tętnicze. Wartość NDS baru i jego związków rozpuszczalnych została przyjęta przez Komisję, która wnioskowała o jej wprowadzenie do wykazu wartości najwyższych dopuszczalnych stężeń i natężeń czynników szkodliwych dla zdrowia w środowisku pracy.

EN

Barium is a metallic, alkaline, chemically reactive element found in soil. Its salts – chloride, nitrate, acetate and carbonate – belong to soluble barium compounds. Barium salts are classified as harmful compounds. Barium and its compounds have broad industrial application (e.g. in chemical, glass-making, ceramic and electrotechnical industries); they are also used as fluxes in welding electrodes. Occupational exposure to barium and its soluble compounds (dust, smoke) takes place mainly in steel, glass-making, metallurgical and mining industries. The minimal oral, lethal dose for a human is about 10 mg/kg for barium chloride and about 60 mg/kg for barium carbonate. Barium carbonate in a dose of 20 mg/kg causes muscular weakness, paraesthesia and flaccid paralysis. Barium: carbonate, chloride, nitrate and acetate are compounds most frequently causing acute intoxication. Acute gastrointestinal disorders, weakening of deep reflex and decreased muscle tone as well as reduction of muscle strength and flaccid paralysis are usually observed in the clinical picture of barium compound intoxication. Death is usually the result of respiratory arrest (respiratory muscles paralysis) and circulatory arrest. These symptoms are accompanied by a decrease in the concentration of serum potassium and ventricular tachycardia which then transform into ventricular fibrillation. Acute renal failure, rhabdomyolysis, dysphagia and arterial hypertension may also result from acute intoxication with barium compounds. DL50 values for soluble barium compounds are within the range of 118 – 800 mg/kg. Barium compounds demonstrate weak irritating action and no allergy reaction. The subchronic and chronic investigations carried out on different animal species have mainly demonstrated a decrease in body mass and the mass of some organs, and a renal defect which intensified depending on the applied doses. Barium and its soluble compounds do not demonstrate mutagenic, genotoxic or carcinogenic activity. There is no sufficient evidence on the effect of barium and its compounds on reproduction. Barium and its soluble compounds have a toxic effect on the cardiovascular system causing mainly hypertension and arrhythmia. Such effects have been observed both in humans and in animals. Furthermore, on the basis of the results of chronic experiments on animals, kidneys have been demonstrated to be the critical organ. To calculate MAC values, the results of Zschiesche et al. (1992) were accepted. The concentration of 4.4 mg Ba/m3 was assumed for the NOAEL value. The following uncertainty factors were accepted in calculating the MAC value: A=2, individual sensitivity differences, B=2, resulting from short- to long-term investigations, C=2, a modifying coefficient associated with the lack of data concerning absorption efficiency in the respiratory tract. Thus, the calculated MAC value is 0.55 mg/m3. On the basis of the presented calculations we suggest the concentration of 0.5 mg Ba/m3 to be accepted as the MAC value for barium and its soluble compounds. The suggested MAC value should protect workers against any effects of the systemic action of barium and it should protect against changes in the cardiovascular system. The MAC value, which has been valid so far in Poland is also 0.5 mg/m3 but it concerns barium and all its inorganic compounds. There are no grounds for accepting STEL values for barium. Due to the lack of data, the determination of BEI values is not suggested, either.

Słowa kluczowe

PL

bar; rozpuszczalne związki baru; układ sercowo-naczyniowy; najwyższe dopuszczalne stężenie (NDS)

EN

barium; barium soluble compounds; cardiovascular system; MAC value

• Wydawca: Centralny Instytut Ochrony Pracy - Państwowy Instytut Badawczy
• Czasopismo: Podstawy i Metody Oceny Środowiska Pracy
• Rocznik: 2006
• Tom: Nr 1 (47)
• Strony: 39--64
• Opis fizyczny: Bibliogr. 72 poz., tab.

Twórcy

autor

Sapota A.

• Uniwersytet Medyczny 90-151 Łódź ul. J. Muszyńskiego 1

autor

Skrzypińska-Gawrysiak M

• Uniwersytet Medyczny 90-151 Łódź ul. J. Muszyńskiego 1

Bibliografia

• 1.ACGIH (2002) Barium and soluble compounds. CD-ROM
• 2.ACGIH (2005) Threshold limit values for chemical substances and physical agents and biological exposure indices.
• 3.Apostoli N.R. i in. (1998) Multiple exposure to arsenic, antimony and other elements in art. Glass manufacturing. Amer. J. Ind. Med. 34, 65-72 (cyt. za CICAD 2001).
• 4.ATSDR (1992) Toxicological profile for barium. US Department of Health and Human Services. Public Health Service. Agency for Toxic Substances and Disease Registry.
• 5.Borzelleca J.F., Condie L.W., Egle J.L. (1988) Short-term toxicity (one- and ten-day gavage) of barium chloride in male and female rats. J. Amer. Coll. Toxicol. 1, 675-685.
• 6.Brenniman G.R., Levy P.S. (1984) Epidemiological study of barium in Illinois drinking water supplies. W: Calabrese EJ (ed) Advances in modern toxicology. Princeton, NJ, Princeton Scientific Publications, 231-249 (cyt. za IRIS 1998; EPA 1998; CICAD 2001).
• 7.CICAD (2001) Concise International Chemical Assessment Document 33. Barium and barium compounds. Geneva, WHO.
• 8.Clary J.J., Tardiff R.G. (1974) The absorption, distribution and excretion of orally administered 133BaCl2 in weanling male rats. Toxicol. Appl. Pharmacol. 29, 139.
• 9.Cuddihy R.G., Ozog J.A. (1973) Nasal absorption of CsCl, SrCl2, BaCl2 and CeCl3 in Syrian hamsters. Health Phys 25, 219-224 (cyt. za EHC 1990; EPA 1998).
• 10.Cuddihy R.G., Hall R.P., Griffith W.C. (1974) Inhalation exposures to barium aerosols. Physical, chemical and mathematical analysis. Health Phys. 26, 405-416 (cyt. za EHC 1990; EPA 1998).
• 11.Dare P.R. i in. (1984) Barium in welding fume. Ann. Occup. Hyg. 28, 445-448 (cyt. za EHC 1990; CICAD 2001).
• 12.Deng J.F., Jan I.S., Cheng H.S. (1991) The essential role of poison center in handling an outbreak of barium carbonate poisoning. Vet. Hum. Toxicol. 33, 173-175 (cyt. za streszcz. w PubMed).
• 13.Dietz D. i in. (1992) Subchronic toxicity of barium chloride dihydrate administered to rats and mice in the drinking water. Fund. Apel. Toxicol. 19, 527-537.
• 14.EHC (1990) Environmental Health Criteria 107. Barium, IPCS/WHO, Geneva.
• 15.EPA (1998) Toxicological review of barium and compounds. Washington, US Environmental Protection Agency, DC.
• 16.Hicks R.i in. (1986) Cardiotoxic and bronchoconstriction effects of industrial metal fumes containing barium. Arch. Toxicol. Suppl. 9, 416-420.
• 17.HSDB (2001), (komputerowa baza danych).
• 18.IRIS (1998) Integrated Risk Information System: barium and compounds.
• 19.Jeske J., Musiałowicz E. (1978) Ostre doustne zatrucia solami baru. Pol. Tyg. Lek. 33, 1617-1618.
• 20.Johnson C.H., Van Tassel V.J. (1991) Acute barium poisoning with respiratory failure and rhabdomyolysis. Ann. Emerg. Med. 20, 1138-1143 (cyt. za streszcz. w PubMed).
• 21.Kanematsu N., Hara M., Kada T. (1980) Rec assay and mutagenicity studies on metal compounds. Mutat Res 77, 109-116 (cyt. za CICAD 2001).
• 22.Kołaciński Z. (1987) Samobójcze zatrucie azotanem barowym. Pol. Tyg. Lek. 42, 339-341.
• 23.Kopp S.J. i in. (1985) Cardiovascular dysfunction and hypersensitivity to sodium pentobarbital induced by chronic barium chloride ingestion. Toxicol. Appl. Pharmacol. 77, 303-314 (cyt. za ATSDR 1992; CICAD 2001).
• 24.Lengeman F.W. (1959) The site of action of lactose in the enhancement of calcium utilization. J. Nutr. 69, 23-27 (cyt. za ATSDR 1992).
• 25.Liniecki J., Witkowska D., Karniewicz W. (1971) Kinetics of calcium, strontium, barium and radium In rabbits. Health Phys. 21, 367-376.
• 26.Matczak W., Przybylska M. Gromiec J. (2003) Ocena narażenia spawaczy na dymy powstające podczas stosowania drutów proszkowych. Streszczenia IX Sympozjum „Zagrożenia zdrowotne w środowisku pracy”. Łódź, IMP.
• 27.Matilla M.J., Anyos K., Puisto E.L. (1986) Cardiotoxic action of doxepin and barium chloride in conscious rabbits. Arch. Toxicol. Suppl. 9, 205-208 (cyt. za CICAD 2001).
• 28.McCauley P.T., Washington I.S. (1983) Barium bioavailability as the chloride, sulfate or carbonate salt in the rat. Drug. Chem. Toxicol. 6, 209-217.
• 29.McCauley P.T. i in. (1985) Investigations into the effect of drinking water barium on rats. W: E.J. Calabrese (ed). Advances in modern toxicology. Vol. IX, Princeton NJ, Princeton Publishing Co 197-210 (cyt. za EHC 1990; EPA 1998; CICAD 2001).
• 30.Monaco M. i in. (1990) Mutagen activity of barium chloride in salmonella typhimurium. Med. Lav 81, 54-64 (cyt. za EPA 1998, CICAD 2001).
• 31.Monaco M. i in. (1991) The evaluation of the presumed mutagenic activity of barium nitrate. Med. Lav. 82, 439-445 (cyt. za EPA 1998; CICAD 2001).
• 32.NIOSH (1976) Health hazard evaluation and determination report. B.F. Goodrich Company, Koroseal Division, Marietta, Ohio. Cincinnati, National Institute for Occupational Safety and Health, Centre for Disease Control (NIOSH Report No 75-24-273), (EHC 1990).
• 33.NIOSH (1978) Health hazard evaluation determination report. Mark Steel Corporation, Salt Lake City, Utah. Cincinnati, OH, National Institute for Occupational Safety and Health, Center for Disease Control (NIOSH Report No 78-93-536), (cyt. za EHC 1990),
• 34.NIOSH (1979) Health hazard evaluation and technical assistance report: Kentile Floors Inc., South Plainfield, New Jersey. Cincinnati, OH, National Institute for Occupational Safety and Health, Center for Disease Control (NIOSH Report No 78-72-618 (cyt. za EHC 1990).
• 35.NIOSH (1980) Technical assistance report. Cincinnati, OH, National Institute for Occupational Safety and Health, Center for Disease Control (NIOSH Report No. 79-022-789), (cyt. za EHC 1990),
• 36.NIOSH (1982) Health hazard evaluation determination report. Shervin Williams Company, Coffeyville, Kansas. Cincinnati, OH, National Institute for Occupational Safety and Health, Centers for Disease Control (NIOSH Report No. HETA/81-356-1183 (cyt. za EHC 1990; EPA 1998; CICAD 2001).
• 37.NIOSH (1984) Industrial hygiene survey report of Dorchester Refining Company. Cincinnati, OH, National Institute for Occupational Safety and Health, Center for Disease Control (NIOSH Report No 124-11), (cyt. za EHC 1990).
• 38.NIOSH (1985) Health hazard evaluation report: General Motors Corporation, Dayton, Ohio. Cincinnati, OH, National Institute for Occupational Safety and Health, Centers for Disease Control (NIOSH Report No HETA/84-060-1645), (cyt. za EHC 1990).
• 39.NIOSH (1987) Health hazard evaluation report: Wellman Dynamics Corporation, Creston, Iowa. Cincinnati, OH, National Institute for Occupational Safety and Health, Centers for Disease Control (NIOSH Report No HETA/83-015-1809), (cyt. za EHC 1990).
• 40.Nishioka H. (1975) Mutagenic activities of metal compounds in bacteria. Mut. Res. 31, 186-189 (cyt. za EHC 1990; CICAD 2001).
• 41.NTP (1994) National Toxicology Program, Public Health Service, US Department of Health and Human Services. NTP technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no 1032-27-9) in F 344?n rets and B6C3F1 mice (drinking water studies). NTP TR 432 Research Triangle Park, NC, NIH pub. no 94-3163. NTIS pub PB94-214179 (cyt. za EPA 1998; IRIS 1998; CICAD 2001).
• 42.Penington G.R. (1993) Severe complications following a “barium swallow” investigation for dysphagia. Med. J. Aust. 159, 764-765 (cyt. za streszcz. w PubMed).
• 43.Perry H.M. i in. (1983) Cardiovascular effects of chronic barium ingestion. In: Hemphill DD (ed) Trace substances in environmental health. Columbia MO, University of Missouri, 155-164 (cyt. za ATSDR 1992; EPA 1998).
• 44.Perry H.M. i in. (1985) Barium induced hypertension. In: Calabrese E (ed) Inorganics in drinking water and cardiovascular disease. Princeton, NJ, Princeton Publishing Co, 221-229 (cyt. za EPA 1998; CICAD 2001).
• 45.Perry H.M. i in. (1989) Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding. J. Toxicol. Environ. Health. 28, 373-388 (cyt. za ATSDR 1992; EPA 1998; CICAD 2001).
• 46.Poradnik fizykochemiczny (1976) Warszawa, WNT.
• 47.Reeves A.L. (1986) Barium W: Handbook on the toxicology of metals. Vol. II. Specific metals. Amsterdam, Elsevier Science Publishers, 84-93.
• 48.Ridgeway L.P., Kanofsky D.A. (1952) The effects of metals in chick embryo. An. NY. Acad. Sci. 55, 203-215 (cyt. za CICAD 2001).
• 49.Roig-Navarro A.F. i in. (1997) An assessment of heavy metals and boron contamination in workplace atmospheres from ceramic factories. Sci. Total. Environ. 201, 225-234 (cyt. za CICAD 2001).
• 50.Rossman T.G. i in. (1991) Performance of 133 compounds in the lambda propgage induction endpoint of the microscreen assay and comparison with s. typhimurium mutagenicity and rodent carcinogenicity assays. Mut. Res. 260, 349-367 (cyt. za CICAD 2001).
• 51.Roza O., Berman L.B. (1971) The pathophysiology of barium: Hypokalemic and cardiovascular effects. J. Pharmacol. Exp. Ther. 177, 433-439 (cyt. za EPA 1998; CICAD 2001).
• 52.Rozporządzenia ministra zdrowia z dnia 28 września 2005 r. w sprawie wykazu substancji niebezpiecznych wraz z ich klasyfikacją i oznakowaniem – aktu wykonawczego do ustawy z dnia 11 stycznia 2001 r. o substancjach i preparatach chemicznych (DzU 2001, nr 11, poz. 84, z późniejszymi zmianami).
• 53.Rozporządzenie ministra zdrowia w sprawie substancji niebezpiecznych wraz z ich klasyfikacją i oznakowaniem. DzU 2002 nr 11, poz. 84, z późniejszymi zmian.
• 54.Rozporządzenie ministra pracy i polityki społecznej w sprawie najwyższych dopuszczalnych stężeń i natężeń czynników szkodliwych dla zdrowia w środowisku pracy. DzU 2002 nr 217, poz. 1833.
• 55.RTECS (2005), (komputerowa baza danych).
• 56.Schorn T.F. i in. (1991) Barium carbinate intoxication. Intensive Care Ned. 17, 60-62 (cyt. za streszcz. w PubMed).
• 57.Schroeder H.A., Tipton L.H., Nason A.P. (1972) Trace metals an man strontium and barium. J. Chron. Dis. 25, 491-517 (cyt. za EHC 1990; CICAD 2001).
• 58.Schroeder H.A., Mitchener M. (1975a) Life-term studies in rats. Effects of aluminum, barium, beryllium and tungsten. J. Nutr. 105, 421-427.
• 59.Schroeder H.A., Mitchener M. (1975b) Life-term effects of mercury, methyl mercury and nine other trace metals on mice. J. Nutr. 105, 452-458.
• 60.Shankle R., Keane J.R. (1988) Acute paralysis from inhaled barium carbonate. Arch. Neurol. 45, 579- 580 (cyt. za EHC 1990; streszcz. w PubMed).
• 61.Stewart D.W., Hummel R.P. (1984) Acute poisoning by a barium chloride burn (cyt. za streszcz. W PubMed).
• 62.Sutton A. i in. (1972) Reduction in the retention of radioactive barium in rats following the addition of sodium alginate derivatives to the diet. Int. J. Radiat. Biol. 22, 297-300 (cyt. za ATSDR 1992).
• 63.Tarasenko N.Y., Pronin O.A., Silayev A.A. (1977) Barium compounds as industrial poisons (an experimental study). J. Hyg. Epidemiol. Microbiol. Immunol. 21, 361-373.
• 64.Tardiff R.G. Robinson M., Ulmer N.S. (1980) Subchronic oral toxicity of BaCl2 in rats. J. Enviro. Pathol. Toxicol. 4, 267-275.
• 65.Taylor D.M., Blight P.H., Duggan M.H. (1962) The absorption of calcium, strontium, barium and radium from the gastrointestinal tract of the rat. Biochem. J. 83, 25-29.
• 66.Tenenbein M. (1985) Severe cardiac dysrhythmia from bariu acetate ingestion. Pediatr Emerg Care 1, 34-36 (cyt. za streszcz. w PubMed).
• 67.Tipton I.H., Stewart P.L., Dickson J. (1969) Patterns of elemental excretion in long term balance studies. Health. Phys. 16, 455-462.
• 68.Verhage M. i in. (1995) Ba2+ replaces Ca2+/calmodulin in the activation of protein phosphates and in exocytosis of all major transmitters. Eur. J. Pharmacol. 291, 387-398 (cyt. za EPA 1998).
• 69.Wang P.Y. i in. (1989) Occupational endermatic intoxication of barium – 2 case report. Chim. J. Ind. Hyg. Occup. Dis. 7, 86-87 (cyt. za EHC 1990).
• 70.Wetherill S.F., Guarino M.J., Cox R.W. (1981) Acute renal failure associated with barium chloride poisoning. Ann. Intern. Med. 95, 187-188 (cyt. za streszcz. w PubMed).
• 71.Wones R.G., Stadler B.L., Frohman L.A. (1990) Lack of effect of drinking water barium on cardiovascular risk factors. Environ. Health. Persp. 85, 1-13.
• 72.Zschiesche W., Schaller K.H., Weltle D. (1992) Exposure to soluble barium compounds: an interventional study in arc welders. Int. Arch. Occup. Environ. Health. 64, 13-23.