Document 7MwXqrO3D8n0bk5MjV0Z6N2Oa
Interim Report
lead
Physiological Aspects of
"Water Quality Criteria" with regard to Man March, 1957
Appendix to ueport on the Recommended Physiological! Safe Limit
for Continued Human Consumption of Lea in Water (January 28, 1953)
(
s Prepared as part of the
Toxicity Project
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of the
Ohio River Valley Water Sanitation Commission
N35512
From The Kettering Laboratory in the Department of Preventive Medicine
ana Industrial Health, College of Medicine, University of Cincinnati
Cincinnati, Ohio.
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Original report prepared by Jules S. Cass, D.V.M., Assistant Professor of Industrial Health
Appendix by Paul E. Foldes, M.D., Responsible Investigator Lilli B. Lange, Research Assistant
Approved:
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Date: March, 1957
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Bibliography
1. Am. Pubo Health Assoc-: Occupational lead exposure and lead poisoning. Kept, by Indust. Hyg. Sect. Am. Public Health Assoc., 1-61., 1943.
2. Bambach, K., Kehoe, R.A. and Logan, M.A.: The plasma-cell partition of blood lead. J. Pharmacol. Exp. Therap. 76:326-37, 1942.
3. Bloomfield, J.J. and Isbell, H.S.s The presence of lead dust and fumes in the air of streets, automobile repair shops, and industrial establishments of large cities. J. Ind. Hyg. 15:144-49, 1933.
4. Chambers, L.A., Foter, M.J. and Cholak, J.: A comparison of particulate loadings in the atmospheres of certain American cities. Proc. 3rd Natl. Air Pollution Symposium, April 1955:24-32.
5. Cholak, J.: Measurement of air pollution. Arch. Ind. Hyg. Occup. Med. 10:203-09, 1954.
5. Cholak, J., Schafer, L.J. and Hoffer, R.F.: Results of a five-year
investigation of air pollution in Cincinnati. Arch. Ind. Hyg. Occup.
Med. 6:314-25, 1952.
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7. Cant, V.A.: Le&d Poisoning. Chicago, 111., Chicago Book Company, 1939.
y8. liansmann, G.H. and Perry, M.C.s Lead absorption and intoxication in man unassociated with occupations, or industrial hazards. Arch. Path. 30:226-39, 1940.
9. Harrold, G.C. and Meek, S.F.: Solubility and particle size in lead poisoning. Proc. Lead Hyg. Conf., Lead Indus. Assoc. Chicago, Illinois, Nov. 11-24, 1948.
10. Ingleson, H.: determination of lead in drinking water. Analyst 63s 546-59, 1938.
11. Kehoe, R.A.: Exposure to lead. Occup. Med. 3:156-71, 1947.
12. Kehoe, R.A.: Lead absorption and lead poisoning. Med. Clinics of N. Amer. 26:1261-79, 1943.
13. Kehoe, R.A.:'The diagnosis of lead poisoning in the light of recent information. J. Med. (Cincinnati) 16:527-32, 1935.
14. Kehoe, R.A. and Ashe, W.F.: Lead poisoning. Mimeographed Rept. Kettering Laboratory, June 2, 1941.
15. Kehoe, R.A., Cholak, J., Hubbard, D.M., Bambach, K., MeNary, R.R. and Story, R.V.: The fate of lead in human blood. Proc. 6th Pacific Sci. Cong. 6:193-204, 1939.
16 zvehoe. *"veiU-, Oiioiak, J ., riuobard, D.ri. , rancach. } mar'.' R.R, and Stoiy, IUV. Experimental studies on the ingestion of lea compounds. J. Ind. Hyg. Toxicol. 22:381-400. 1940,
17. Kehoe, R.A, Cholak, J.. Hubbard, D.M., Bambacn, ii. and MeJiaiy, 1.1,? Experimental studies on lead absorption, and excretion, and their relation to the diagnosis and treatment of lead poisoning, J Ind, Hyg. Toxicol, 25:71, 1943.
18. Kehoe, R.A., Cholak, J, and Largent, 2.J. : The concentralions of certain
trace metals in drinicing water, J, Am, Water 'Works Assoc. 16:637-44,
1944.
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19, Kehoe, R.A., Cholak. J, and Story, R.V.: A spectrochemical study of the normal ranges of concentration of certain trace metals in biological materials. J. Nutrition 19s579-92, 1940.
20. Kehoe, R.A., Cholak, J. and Story, R.V.: Editorial review. Manganese, lead, .. tin, aluminum, copper, and silver in normal biological material. J. Nutrition 20:85-98, 1940.
21. Kehoe, R.A,, Thamann F. and Cholak, J.: On the normal absorption and excretion of lead. J. Ind. Hyg. 5:257-72, 1933.
99 Kehoe. R.A., Thamann F. and Cholak, J.: On the normal absorption and excretion of lead. J. Ind. Hyg. 15:273-38, 1933.
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y K. W O
Kehoe, R.A., Thamann F. and Cholak, J.: On the normal absorption and
excretion of lead. J. Ind. Hyg. 15:301-05, 1933.
/ 24. Kehoe, R.A., Thamann, F. and Cholak, J.: On the normal absorption and excretion of lead. J. Ind. Hyg. 15:306-19, 1S33. (
25. Kehoe, R.A., Thamann, F. and Cholak, J.: On the normal absorption and excretion of lead. J. Ind. Hyg. 15s320-40, 1933.
26. Kehoe, R.A . T h a m a n n , F. and Cholak*, J.s An appraisal of the lead hazards associated with the distribution and use of gasoline containing tetra ethyl lead.' II. The occupational lead exposure of filling station attendants and garage mechanics. J, Ind. Hyg. Toxicol. 18:42-68, 1936.
27. Kehoe, R.A, Thamann, F. and Cholak, J,: Normal absorption and excretion of lead. J. Am. Med. Assoc. 104:90-2, 1935.
28. Kruse, W.: Was lehren uns die Leipziger Bleivergiftungen durch Trinkwasser? (What can we learn from the cases of lead poisoning caused by the drinking water in Leipzig?) Ztsch. f. Hyg. und Infektionskr. 118: 143, 1956. .
29. Lead Industries Assoc.: Lead in Modern Industry. New York, Lord Baltimore Press, 1952: 230 pp.
30. Lorraine, N,: A case of severe lead poisoning from drinking water. Lancet 2:1347, 1930.
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32. McClure, F.J.: Ingestion of fluoride and dental caries. Am. J. Lis. Children 66:362-69, 1943.
33. Monier-Williams, G.W.: Trace Elements in Food. New York, John Wiley and Sons, Inc., 1949: Chapt. 2:64-106.
34. Neal, P.A., Dressen, W.C., Edwards. T.R., Reinhart, W.H., Webster, S.H., Castberg, H.T. and Fairhall, L.T.: A study of the effect of lead arsenate exposure on orchardists and consumers of sprayed fruit. Pub. Health Bull. 267:181 pp., 1941.
35. Pardoe, A.U.: Renal function in lead poisoning. Brit. J. Pharm. Chemotherap. 7:349-57, 1952.
36. Vogt, E.C.: Roentgenologic diagnosis of lead poisoning in infants and children. J. Am. Med. Assoc. 125:129, 1932.
37. Weber, H.J.: Lead hygiene in the plant - the industrial hygiene aspect.
Hygiene Conf., Metallic Lead Products Div., Lead Industries Ansoc.
12-21, 1948.
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38. Whitaker, P.J.: The absorption, excretion, and retention of ingested lead by human experimental subjects. Dissertation, ^University of Cincinnati,
1951.
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LIAD*ION ` I-JlN
SAFE RANGE Long Period:
in water all sources
0.05 ppm 0.5 - 0.6 mg per day total intake
Short Period:
in water
2 - 4 ppm
HARMFUL RANGE Borderline:
in water
2.31 mg per day, short period (calc: 0.92 ppm in 2500 ml -water) 2 - 4 ppm, 3 months
Toxic:
in water
2.31 mg per day, 2 years 8 - 1 0 ppm, several weeks
Lethal:
no data given in report
PERCEPTIBLE RANGE laste: Odor: Color: Texture:
in water in water in water in water
no information does not apply does not apply does not apply
METABOLISM Essential Nutrient: Beneficial Nutrient Daily Intake:
Daily Output:
urine feces
no
no
average 0.3 mg from food and water
average 0.04 mg from/ inhaled air
average 0.03 mg/liter
average 0.3 mg
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RANGES IN THE ENVIRONMENT
WATER Drinking Water Surface Water:
Ground Water: Sea Water:
0.003 - 0.05 ppm 0.001 - 0.004 ppm Ohio River: 0.12 ppm (1 analysis) 0.001 - 0.06 ppm 0.001 - 0.008 ppm
AIR Suburban: 0.1 - 21.0 pg/cu.m.; average 2.0 pg/cu.m Rural: trace - 1.3 pg/cu.m.; average 1.0 pg/cu.m. Industrial Areas: 3.0 - 4.1 pg/cu.m. average 2.7 pg/cu.m.
PLANT Food: traces - 1.83 ppm occasional values considerably higher Non-food: 0.02 - 1.60 ppm
S0IL 0.6 - 25.0 pprn.
ANIMAL Food: traces - 1.60 ppm generally; occasional values, i.e., fcone and cartilage, higher
EXPLANATORY NOTES
S--.NE :tHi.GE Lons Period: Short Period:
The range of concentration or dosage within which a substance causes no recognised h arm
A defined period of exposure to a subs ounce in norths, years, or over a lifetime.
Gne day, up to a week or two, or an unknown out Dried period of exposure to a subsoance.
NAENFUL rai:c-b Borderline:
T b xic: Lethal:
Die range of concentration or dosage of a substance within wh.ich (in a specified tine) recognised effects on bodily function or structure are induced.
A range of concentration- or dosage of a substance which causes temporary discomfort, or which induces physio logical adaptation (e,,g,,, transient diarrhea, or increased frequency of urination -which disappears even though there is continued exposure to the sane concentration and dose).
A range of concentration or dosage of a substance which causes a harmful change in bodily function or structure that does not disappear with continued exposure to the same concentration and dose.
Tne concentration or dose of a subs canoe which has caused death in a defined or unknown period of exposure.
PERCEPTIBLE RANGE
Taste:
Odor: Color: 'Texture:
.
The range of concentration within which certain charac teristics imparted by a substance to water affect its physiological or esthetic acceptability,
Hie range of concentration of a substance which can be recognized by the sense of taste (bitter, street,, salty, sour).
Hie range of concentration of a substance which can be recognized by the sense of smell.
Hie range of concentration of a substance -which can be recognized by the sense of sight.
The range of concentration of a substance which can be recognized by the sense of touch or feeling.
ITSTABOLISH Essential Nutrient: Beneficial Nutrient:
Daily Intake:
Daily Output:
The significance and the equilibrium of a substance in the body.
A dietary substance without which the body dies. A dietary substance which in defined amounts contributes
to the optimal function of the body, but may or may not be necessary for life. The amount of a substance which the body normally -obtains daily from all sources (including food, drink and air). Hie amount of a substance which the body normally eliminates daily by various paths.
RANGES IN THE ENVIRONMENT
The various amounts of a substance present in the environment which may contribute to the total daily intake by the body,
This IKTEEIL: 5T-.'.2:.v.lY is one of a seri.es of reporte devoted to the CRITICAL SVALATIOI! of the PIIY5I0LCOECAI, ASILCIC of '`'later Quality Criteria,
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The basis of this summary report is a critical evaluation of available information from published and unpublished sources.' The purpose is to define ranges of concentration and dosage which, for a designated substance or group of substances, are safe or unsafe, desirable or undesirable, in raters rich, otherwise, are potable for nan and domestic animals.
From tine to time, as additional information ,.-y warrant, revisions of this summary report will be published. There can be no claim to completeness, but rather there is a need for additional source information which nay not have been noted in 'die preparation of this report.
Information, references and critique will be gratefully received by:
. The Kettering Laboratory
Department of Preventive medicine and Industrial Health
College of medicine
University cf Cincinnati
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Cincinnati, Ohio