Document kaEX5kx4pgERoQMyyqyQkb6On

Wfiiii.fWTftW-*'*' HASKELL LABORATORY FOR DU PONT USE ONLY L1M1TEV DISTRIBUTION TkU Aevteitf n.&ilect6 the available toxietty LitenatuAe, both published and unpubZt&hed. Studies have, not Seen evaluated ion. xcientiiic meA.it. Contact WaxkzLl Labcnatony you. have question*. Common Name; Lead Saifate Chemical Name: Sulfuric Acid, lead (2+) salt Synonyms: Oil, Pigment White 3, Anglislite CAS Registry Np,: 7446-i4~2 Chemical Structures (1:1) 0 -O- S 0 I! 0 +2 Pb / Physical Properties: Description Molecular Weight Boiling Point Melting Point Density/Specific Gravity Vapor Pressure Flash Point/Flammability Explosive Limits Solubility Conversion Factors White solid 303.2:5 1170C 4.25 mg/100 mL water @ 25C 5.6 mg/100 mL water @ 40C Slightly soluble in concentrated sulfuric acid See Reference 16 for additional information Exposure Standards OSHA PEL = SOtg/m3 (la) DOT Classification Lead sulfate containing more than 3% sulfuric acid is con sidered a corrosive material (lc). DUP040011151 2E.PA Status Lead sulfate is listed as a hazardous substance under the Federal Water Pollution Control Act (lb). FDA Status None TSCA Inventory Yes DUP040011152 -3 TOXICITY A. Acute I* Oral LD50 (guinea pigs) = 35 grams/kg (11) a l d (dog) = 2000-3000 mg/kg (4) 2. Skin No information -was found 3. Eye Lead sulfate., placed in the anterior chamber of rabbit eyes, caused a moderate purulent reaction and general inflammation (4.). 4. Inhalation Related Reference 14 contains some information on inhalation exposure to lead sulfate containing 32% lead oxide (white lead). 5, injection Studies a) Intraperitoneal Lb10 (guinea pigs) - 146 mg/kg (3) LD75 (guinea pigs) = .290 mg/kg (3) S,, Extended. Studies 1. Oral Lead sulfate was administered orally to groups of four rats at doses of 25 and 37,5 mg/day for four consecutive days. On day two each animal received 100 mg/kg of phenobarbital. No change in body weight,liver weight and microsomal protein and blood hemoglobin levels was observed. The lead con tent of the liver was four times that In control animals. Slight decreases in the induction of Cytochrome and aminopyrine demethylase was seen (10). DUP040011153 4 Severe lead poisoning was produced in a eat by the administration of 167 mg/kg/day for 12 days (8). Eight-month-old dogs were maintained on a high fat, low calcium diet containing a mixture of lead chloride, lead bromide and lead sulfate at four dose levels. Dogs on high levels of lead . showed marked weight loss and gastrointestinal y- symptoms followed by death. Dogs on low levels of lead developed neurological signs. Highest tis sue lead levels were found in bones followed by liver and kidney, Drain and spinal cord (5). A group of seven cats was administered 1.8-13,5 mg Pb*/kg,/day for from 56 to 215 days. Effects from the lead administration included loss of weight and cramps. All the animals died as a result of the lead administration. Autopsy usually showed a somewhat bluish-black coloration of the appendix and of the upper rectum. No histological examinations were made (9). 0 A group of three cats was administered 15, 19.2 and 23.1 mg Pb*/kg/day, respectively. The animals died after 57, 50 and 18 days, respectively. Another group of three was administered 50, 47 and 48 mg Pb*/ kg/day. These animals died after 42,32 and 61 days, respectively (9). A group of three rabbits was administered 43, 44 and 47 mg Pb*/kg/day, respectively. The animals died after 92, 49 and 46 days on test, respectively (9). A group of two rabbits was administered 50 mg of lead sulfate* if. their diet for up to 79 weeks. One aiiimal was sacrificed after 28 weeks for analy sis of body tissues for lead. This rabbit con tained 42.9 mg of lead. The other rabbit continued on test. The animals seemed to tolerate the lead without difficulty. They were lively, well nourished and gained weight. When sacrificed the rabbit was well and did not appear to have any com pound-related effects. However, lead content of the body had increased three-fold to 121 mg (9). *64% PbS04, 32% P;bO DUP040011154 5 See Belated Beference 13 for additional informa tion C. Carcinogenic Potential No information available D. . Mutagenic Potential .# Sister chromatid exchanges (SCEs) in cultured hu man lymphocytes were increased by 10"^ molar lead sulfate (12). E. . Embryotoxic Potential n o information available F. Other Beproduction Studies None G. higuafic/Environmental Studies Twenty-six (26) mg/L of lead sulfate has been reported as the lethal concentration for goldfish (6) . In distilled water, 25 mg/L of lead sulfate killed goldfish in four days and killed minnows in two to three hours (2) . H. . Clinical Beports of Human intoxication None I Epidemiology No information available J. Metabolism No information available K. Bioehemical Studies See Belated Beference 15 DUP040011155 -- 6-- REFERENCES 1. Code of Federal Regulations (a) Title 29, Section 1910.1025 (b) Title 40, Sections 116.4a and 117.3 (c) Title 49, Section 172,101 2. Ellis, M, M. , "Detection and Measurement of Stream Pollu tion" United States Department of Bur, of Fisheries Bull, 22 (1937) (From McKee and Wolf, Water Quality Criteria, p, 209 (1963). S- 3. Fairhall, L, T,, et al., U.S. Pub. Health Bull., No. 253, 1-40 (1940) (CA34;: 5563) (" Ft ^ ~ ~~r~ 4. Flury, F., Abderhalden'S Hdb,, 4(7b):1289-1314 (1935) (ESECS). 5. Hamir, A.N., et al,, Aust. Vet. J. 57(9):401-406 (1981) (CA96:63858) (J- ), 6. Jones. J, R. E., "Fish and River Pollution", Chapter 7 of Aspects of River Pollution L. Klein, ed. Butterworth Science Publication, London (1957) (From McKee and Wolf, Water Quality Criteria, p, 209 (1963). 7. Leber, T. , Die Entstehung der Entzundung und die Wirkung der Entzundung-erregenden Schadlichkelten: Nach vorzugsweise am Auge angestellten Untersuchungen. Leipzig, Wilhelm Englemann (1891) (from Grant, W., Tox. of the Eye"(1974)). 8. Lehmann, K, B*, Arch. Hyg,, 16 (1893) (Ref. from Lehmann, K. B., Arch. Hyg., 101;197-204 (1929) (J-3867). 9. Lehmann, K. B,, Arch Hyg., 101:197-204 (1929) (Verified CA23;505D) (J-3867). 10. Norpoth, K,, et al., Int. Arch. Arbeitsmed 33:139-151 (1974) (Verified CA84:160262), 11. Tartler, G.Arch, Hyg, , 125:273-292 (1941) (CA36:49U) 12. Wulf, H. C., Dan, Med. Bull., 27(l):40-42 (1980) (CA93: 1976) (,J- JT DUP040011156 -7 RELATED REFERENCES Oral 13- Gage, J. C. and M. H. Litchfield/ Pood COsmet. Toxicol., 6:32 9-338 (1968) {Verified CA69:104754) . "Migration of lead from polymers in the rat gastrointes tinal tract" Inhalation 14. Koelsch, P. , et al. , Arch. Hvcr. , 101:234-256 (1929) (CA23: 5050). "Comparative investigations on the toxicity of basic lead sulfate and basic lead carbonate" Biochemical Studies 15. Granata, A. and D. Germano, Boll. Soc. Ital. Biol. Sper., 39(16):928-931 (1963) (CA60:4564c)* "Action of lead and its principal inorganic salts on red blood cells" Solubility 16. Horiguchi, S. , et al., Sumitomo Sangyo Eisei, 13:48-51 (1977) (CA88:99845) . ' '"Studies on occupational lead poisoning. I. An experiment on the solubility of several lead compounds in water, stimu lated gastric and intestinal juice" Richard C. Graham:mjh December 14, 1982 DUP040011157