U.S. DEPARTMENT OF COMMERCE
National Technical Information Service
PB-250 Oil
STATEMENT OF. BASIS AND PURPOSE FOR THE NATIONAL
INTERIM PRIMARY DRINKING WATER REGULATIONS
ENVIRONMENTAL PROTECTION AGENCY
DECEMBER 1975
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STATEMENT of BASIS and PURPOSE
for the
National Interim Primary
Drinking Water Regulations
U. S. Environmental Protection Agency
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BIBLIOGRAPHIC
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Tlif Statcnu-Mt (•'" Kissis ar.d I'urposi: I'nr the National Interim Primary
Drinkini,' V.'atcr Hcyi.'Iations rontains the cnnr'-pts and rationale for arriving
at the specific Maximum Contaminant Levels in the Regulations which were
promulgated on Decemiier 2-1, 11)75. In addition to the material in support of
the Maximum (.'ontarninant Levels for Id inorganic chemicals, six organic
chemicals, turhiditv and microlii:iio»ic-a! contaminants, [Material is also
included which provides the basis for the lack of maximum contaminant levels
for certain other contaminants. Am'ony the latter are sodium, sulfate,
oryunics-carbon absorbable, cyanide, certain pesticides and general bacterial
•.jopulati-.ms. Xumei-ous literature citations are pro\'ided in support of the
•larrative mate-rial.
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APPENDIX
BACKGROUND USED IN DEVELOPING THE
PROPOSED INTERIM PRIMARY DRINKING WATER REGULATIONS
The Proposed Interim Primary Drinking Water Regulations have been
predicated on. the best and latest information available at the time of
their promulgation. The concepts and rationale included in this
Appendix were used in arriving at specific limits and should enable
those whose responsibility it is to interpret, apply, or enforce the
Regulations to do so with understanding, judgment, and discretion.
A. SOURCE AND FACILITIES
D. MICROBIOLOGICAL QUALITY
C. CHEMICAL QUALITY
A - SOURCE AND FACILITIES
Mounting pollution problems indicate the need for increased
attention to the quality of source waters. Abatement and control of.
pollution of sources will significantly aid in producing drinking
water that will be in full compliance with the provisions of those
Standards and will be esthetic-ally acceptable to the consumer, but
they will never eliminate the need lor well designed water treat-
ment facilities operated by competent personnel.
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Production of water that puses no threat to the consumer's health
depends on continuous protection. Because of human fnulties asso-
ciated \.:''i protection, priority should be given to selection of the
purest source. Polluted sources should not be used unless other
sources are economically unavailable, and then only when personnel,
equipment, and operating procedures can be depended on to purify and
otherwise continuously protect the drinking water supply.
Although ground waters obtained from aquifers beneath impervious
strata, and not connected with fragmented or cavernous rock, have
been considered sufficiently protected from bacterial contamination to
preclude need for disinfection, this is frequently not true as ground
waters are becoming polluted with increasing frequency, and the
resulting ha/ards require special surveillance. An illustration of
such pollution is the presence of pollutants originating either from
sewage or industrial effluents.
Surface waters are subjected to increasing pollution and should
never be used without being effectively disinfected. Because of the
increasing ha/ards of pollution, the use of surface waters without
coagulation and filtration must be accompanied by adequate past
records and intensive surveillance of the quality of the raw water
and (lie disinfected supply in order to assure constant protection.
This surveillance should include a sanitary survey of the source
and water handling, as well as biological examination of the supply.
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The decree uf treatment sliould be dele-mined by (ho health
hazards involved and the quality of tin- raw water. Wlien in use,
the source should be under continuous surveillance to assure
adequacy of treatment in meeting the hazards of changing pollution
conditions. Continuous, effective disinfection shall be considered
the minimum treatment for any water supply except for ground
waters in which total coliforms can be shown to be continually
absent from the raw water. During times of unavoidable and ex-
cessive pollution of a source already in use, it may become
necessary to provide extraordinary treatment (e.g., exceptionally
strong disinfection, improved coagulation, and/or special opera-
tion). If the pollution cannot be removed satisfactorily by treat-
ment, use of the source should be discontinued until the pollution
lias been reduced or eliminated.
The adequacy of protection by treatment should be judged, in
part, on a record of the quality of water produced by the treatment
plant and the relation of this quality to the requirements of these
Regulations. Evaluation of adequacy of protection by treatment
should also include frequent inspection of treatment works and their
operation. Conscientious operation by well-trained, skillful, and
competent operators is an essential part of protection by treatment.
Operator competency is encouraged by a formal program leading
to operator certification or licensing.
1 See reference to relationship of chlorine residual and contact.
time required to kill viruses in section on Microbiological Quality,
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Delivery of a safe water supply depends on adequate protection
by natural means or by treatment, and protection of the water in
tho distribution system. Minimum protection should include pro-
grams that result in the provision of sufficient and safe materials
and equipment to treat and distribute the water: disinfection of water
mains, storage facilities, and oilier equipment after each installa-
tion, repair, or other modification that may have subjected them to
possible contamination; prevention of health hazards, such as cross-
connections or loss of pressure because of overdraft in excess of
the system's capacity: and routine analysis of water samples and
frequent survey of the water system to evaluate the adequacy of
protection. The fact that the minimum number of samples are taken
and analy/ed and found to comply with specific quality requirements
of these Standards, is not sufficient evidence that protection has been
adequate. The protection procedures and physical facilities must
be re viewed .along with the results oi water quality analyses to
evaluate the adequacy of the supply's protection. Knowledge of
physical defects or of the existence of other health hazards in the
water supply system is evidence of a deficiency in protection of the
water supply. Even though water quality analyses have indicated
that the quality requirements have been met, the deficiencies must
be corrected before ihe supply can be considered safe.
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B - MICROBIOLOGICAL QUALITY
Coliform Group
Culiforin bacteria traditionally have been the bacteriological
tool used to measure the occurrence and intensity of fecal contam-
ination in stream-pollution investigations for nearly 70 yea-s.
During this time, a mass of data lias accumulated to permit a full
evaluation of the sensitivity and specificity of this bacterial pollution
indicator.
As defined in Standard Methods for the Examination of Water
and Was to water (1), "the coliform group includes all of the aerobic
and facultative anaerobic, Gram-negative, non-spore-form ing rod-
shaped bacteria which ferment lactosirwith pis formation within
48 hours at 35° C." From this definition, it becomes immediately
apparent that this bacterial grouping is somewhat artificial in that
it embodies a heterogeneous collection of bacterial species having
only a few broad characteristics in common. Yet, for practical
applications to stream pollution studies, this grouping of selected
bacterial species, which we shall term the "total coliform group,"
lias proved to be a workable arrangement.
The total coliform group merits consideration as an indicator
of pollution because these bacteria are always present in the normal
intestinal tract of humans and other warm-blooded animals and are
eliminated in large numbers in fecal wastes. Thus, the absence of
total coliform bacteria is evidence of a bacteriologically safe water.
5
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Some strains included in the total ooliform group have a wide
distribution in the environment but are not common in fecal material.
Enterobacter acrogenes and Kntcrobacter cloacae are frequently found
on various types of vegetation (2-5) and in materials used in joints
ajid valves (G-7).
The intermediate-acrogcnes-cloacae (l.A.C) subgroups may be
found in fecal discharges, but usually in smaller numbers than
Escherichia coli that is characteristically the predominant coliform
in warm-blooded animal intestines (8-10). Enterobacter aerogencs
and intermediate types of 01 ganisms are commonly present in soil
(11-14) and in waters polluted some time in the past. Another
subgroup comprises plant, pathogens (15) and other organisms of
indefinite (.a.\onon;y whose sanitary significance is uncertain. All
of these coliform subgroups may be found in sewage and in Un-
polluted water environment.
Survival Times
Organisms of the l.A.C. group tend to survive longer in water
than do fecal coliform organisms (16-18). The l.A.C. group also
lends to be somewhat more resistant to chlorination then E. coli or
the commonly occurring bacterial intestinal pathogens (19-22).
Because of these and other reasons, the relative survival times of the
coliform subgroups may be useful in distinguishing between recent and
less recent pollution. In waters recently contaminated with sewage,
it is expected Unit fecal coliform organisms" will be present in •
numbers greater than those of the-I.A.C. subgroup; but in waters that
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have been contaminated for a considerable length of time or have
been insufficiently chlorinated, organisms of the I.A.C. subgroup
may be more numerous than fecal coliform organisms (23).
Differentiation of Organisms
Because various numbers of the coliform group normally grow
in diverse natur.il habitats, attempts have been made to differentiate
the population in polluted waters, with specific interest directed
toward those coliforms that are derived from warm-blooded animal
contamination. In his pioneering research, MacConkey (23, 24)
defined the aerogenes group in terms of certain fermentation
characteristics, ability to produce indole, and reaction in the
Vogcs-Proskauer test. Oilier developments refined techniques
that progressed to differentiate the coliform group on the basis
of indole production, methyl red, and Vt ^es-Proskauer reactions,
and citrate utilization (LMViC tests) into the E^_ coU, Entcrobacter
aerogenes, intermediate, and irregular subgroups (24-28).
In another approach to coliform differentiation, Hajna and
Perry (29) and Vaughn, Levine, and Smith (30) further developed
the Lijkman test (31) to distinguish organisms of fecal origin from
those of nonfccal origin by elevating the incubation temperature
for lactose fermentation. Geldreich, and associates, (31, 32)
further refined the procedure and developed additional data to
indicate the specific correlation of this elevated temperature
procedure to the occurrence of fecal contamination.
7'=
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Fecal Coliform Measurements
The fecal coliform bacteria, a subgroup of the total coliform
population, does have a direct correlation with fecal contamination
from warm-blooded animals. The principal biochemical character-
istic used to identify fecal coliform is the ability to ferment lactose
with gas production at 44.5 C. Research data have shown that 96.4
percent of the colilorms in human feces were positive by this test
(10). Examination of the excrement from other warm-blooded animals,
including livestock, poultry, cats, dogs, and rodents (33-34), indicate
the fecal coliforms contribute 93.0 to 98.7 percent or the total
coliform population. The predominant fecal coliform type most
frequently found in the intestinal flora is 1C. co'i. Occasionally,
other colilorm JMViC types may predominate for periods of several
months before a shift occurs in type distribution. For this reason,
it is more significant to be able to measure all coliforms common
to the intestinal tract. In man, particularly, there is a significantly
greater positive correlation with the broader fecal coliform concept
(96.4 percent) than witli identification of 1C. c_ol£ by (lie traditional
IMVic biochemical reactions (87.2 percent).
Application to Treated Water
The presence of any type of coliform organism in treated water
suggests either ;aadoquate treatment or contamination after post-
chlorination (23). It is true there are some differences between
various colifoiM strains with regard to natural survival and their
8<
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chlonr.ation resistance, i;ut i.liesi- are minor oiul
that arc; niore clearly demonstrated in the laboratory than in the
water treatment system. The pn-.sem'e of any coliform bacteria,
fecal or nonfccal, in treated water should not be tolerated.
Insofar as bacterial pathogens are concerned, the coliforui group
is considered a reliable indicator of the adequacy of treatment. As
an indicator of pollution in drinking water supply systems, and
indirectly as an indicator of protection provided, the colilorm group
is preferred to fecal coliform organisms. Whether these considerations
can be extended to include rickettsial and viral organisms has not
been definitely determined.
Sample Si/c
The minimum olJicial sample volume cited in the earlier editions
of the Drinking Water Standards and Standard Methods for the
Examination of Water and Wastewatcr was either stated or implied
to be 50 ml because of the requirement to inoculate a series of 5
lactose broth fermentation tubes, each with a 10 nil or 100 ml portion
of the sample. Few laboratories ever routinely employed the larger
portions in the-multiple lube procedure because of the attendant
problems of preparing, handling and incubating the larger sized sample
bottles that a; _• required. Tims, when the multiple tube procedure
was used, it became a practice to examine only 50 ml. With the'
development of the membrane filter procedure for routine potable
water testing, the examination of larger sample volumes became
practical, limited only by the turbidity of water and excessive
bacterial populations.
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Since many water supplies are sampled infrequently during the
month, it is statistically more meaningful to examine a large sample
for greater lest precision with reduced risk of failing to detect some
I-.'-
low levol occurrence of coliforms. Increasing U:y sample portion
examined will tighten the base line sensitivity and is particularly
important for measuring the coliform reduction capacity of disin-
fection that approaches the magnitude essential for control of water-
borne virus. Mack et al (35) reported poliovirus type II cuuld be
isolated from a restaurant well water supply using a flocculant in
the 2.5 gallon samples prior to centrifugation to concentrate the
low density virus particles. Bacteriological examinations of 50 ml
portions of the unconcentrated water samples were negative for
coliformc. However, coliforms were found in the concentrated
sediment pellets. Future studies on coliform to virus occurrence
in potable water may require further tightening of the colilorm
standard, possibly to a one-liter base (36).
The recommendations to increase the sample size to 100 ml for
bu jleriological examinations of water is supported in the 13th
Edition of Standard Methods where the larger volume is stated as
preferred. A study of State Health Laboratory procedures indicates
that 39 or 78 percent of these laboratory systems are currently
using 4 oz sample bottles to collect 100 ml of sample, and 25
of these State Health Laboratory networks are examining
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all public water samples by the membrane filter procedure. These
figures suggest thai the stronger position now being proposed on a
minimum sample size of 100 ml for statistically improved coliform
monitoring is not unrealistic in terms of current practice.
Application to Source Waters & Untreated Potable Supplies
In the monitoring of source water quality, fecal coliform measure-
ments are preferred, being specific for focal contamination and not
subject to wide-range density fluctualion of doubtful sanitary signifi-
cance.
Although the total coliform group is the prime measurement, of
potable water quality, the use of a fecal coliform measurement in
untreated potable supplies will yield valuable supplemental infor-
mation. Any untreated potable supply that contains one or more
fecal colifornis per 100 ml should receive immediate disinfection.
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REFERENCES
1. Standard Methods for the Examination of Water and Wastcwatcr,
13th cd. APHA, AWWA, WPCF, New York (1970).
2. Thomas, S.B. and McQuillm, J. Coli-aerogenes Bacteria
Isolated from Grass. J. Appl. Bactcriql. 1_5: 41 (1952).
3. Fraser, M.H., Reid, W.B., and Malcolm, J.F. The Occurrence
of Coli-aerogenes Organisms on Plants. J. Appl. Bacteriol.
19: 301 (195G).
4. Geldreich, E.E., Kenncr, B.A., and Kablcr, P.W. The
Occurrence of Cohforms, Fecal Coliforms, and Streptococci
on Vegetation and Insects. Appl. Microbiol. 1_2: 63 (1964).
5. Papavassiliou, J., T/.annetis, S., Yeka, H., and Michapoulos, G.
Coli-Aerogenes Bacteria on Plants. J. Appl. Bacteriol. 30:
219(1967). ~
6. Caldwell, E.L.. and Parr, L.W. Pump Infection Under Normal
Conditions in Controlled Experimental Fields. JAWWA.
25: 1107 (1933).
7. Rapp, W.M. and Weir, P. Cotton caulking yarn. JAWWA.
26: 743 (1934).
8. Pan-, L.W. The Occurrence ami Succession of Coliform Organics
in Human Feces. Am. J. Hyg. 27: 67 (1938).
9. Sears, II.,I.. Browlcs, I., and Vchiyama, J.K. Persistence
of Individual Strains of Eschcrichia coli in the intestinal Tract
of Man. J. Bacteriol. 59; 293 (l
10. Geldreich, E.E., Bordner, R.H., Huff, C.B., Clark, H.F., and
Kablcr, P.W. Type-Distribution of Coliform Bacteria in the
Feces of Warm-Blooded Animals. JWPCF. 3_4: 295 (1962).
11. Frank, N. and Skinner, C.E. Coli-Aerogenes Bacteria in Soil.
J. Bacteriol. 4_2: 143 (1941).
12. Taylor, C.B. Coli-Aerogenes Bacteria in Soils. J. Hyg. (Camb.)
4_9: 162 (1951).
13. Randall, J.S. The Sanitary Significance of Coliform Bacilli in
Soil. J. Ilyg., (Camb.) 54: 365 (1956).
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14. Gcldrcich, E.E., Huff, C.B., Durdncr, R.H., Kabler, P.W.,
Clark, II. F. The Fecal Coli-Aerogcnes Flora of Soils from Various
Geographical Areas. J. Appl. Bacteriol. 25: 87 (1962).
15 Elrod, R.P. The Erwinia-Coliform Relationship. J. Bacleriol.
44: 433 (1942).
16. Parr, L.W. Viability of Coli-Aerogcnes Organisms in Cultures
and in Various Environments. J. Infect. Disease 60_: 291 (1937).
17. Platt, A.E. The Viability of Pact, coli and Pact, aerogcnes in
Water: A Method for The Rapid Enumeration of These Organisms.
J. Hyg. 35: 437 (1935).
18. Taylor, C.B. The Ecology and Significance of the Different Types
of Coliform Bacteria Found in Water. J. Hyg. 42: 23 (1942).
19. Tonney, F.O., Greer, F.E., and Dajiforth, T.F. The Minimal
"Chlorine Death Point" of Bacteria. Am. J. Pub. Health
1£: 1259 (1928).
20. Heathman, L.S., Pierce, S.O., and Kabler, P.\V. Resistance of
Various Strains of E_. typhi and Coli-Acrogenes to Clilorine and
Chloramine. Pub.TieaTtlTRpts., 5L- 1367 (1936).
21. Bulterficld, C.T., el. al. Influence of pll and Temperature on the
Survival of Coliforms and Enteric Pathogens when Exposed to
Free Clilorine. Pub. Health Rpts. 58; 1837 (1943).
22. Kabler, P.W. Relative Resistcnce of Coliform Organisms and
Enteric Pathogens in the Disinfection of Water with Chlorine.
JAWWA. 43: 553 (1951).
23. Kablcr, P.W. and Clark, H.F. Coliform Group and Fecal
Coliform Organisms as Indicators of Pollution in Drinking Water.
JAWWA. 52: 1577 (1960).
24. MacConkcy. A. Lactose-Fermenting Bacteria in Feces. J.
Hyg. 5: 333 (1905).
25. MacConkey, A. Further Observations on the Differentiation of
Lactose-Fermenting Bacteria, with Special Reference to Those of
Intestinal Origin. J. Hyg. 9:86 (1909).
26. Rogers, L.A., Clark, W.M., and Davis, B.J. The Colon Group
of Bacteria. J. Infect. Disease 14: 411 -'(1914).
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27. Clark, W.M.. and Lubs, W.A. The Differentiation of Bacteria
of the Colon-Aerogcnes Family by the Use of Indicators.
J. Infect. Disease 1J7: 1GO (1915).
28. Koscr, S.A. Differential Tests for Colon-Aerogenes Group in
Relation to Sanitary Quality of Water. J. Infect. Disease
35: 14 (1924).
29. Hajna, A.A. and Perry, C.A. A Comparison of the Eijkman
Test with other Tests for Determining E. coli. J. Bacteriol.
30: 479 (1935).
30. Vaughn, R.H., Levine, M., and Smith, H.A. A Buffered Boric
Acid Lactose Medium for Enrichment and Presumptive Identifica-
tion of Eschcrichia coli. Food Res. H3: 10 (1951).
31. Eijkman, C. Die Garungsprobe bei 46 ais Hilfsmittel bei dor
Trinkwasscruntcrsuchung. Centr. Bakteriol. Parasilcnk., Abt. I,
Orig., 37: 742 (1904)
32. Geldreich, E.E., Ciark, H.F., Kabler, P.W., Huff, C.B., and
Bordner, R.H. The Coliform Group. II. Reactions in EC Medium
at 45 C. Appl. Microbiol. G: 347 (1958).
33. Geldreich, E.E. Sanitary Significance of Fecal Coliforms in the
Environment. U.S. Dept. of the Interior, FWPCA Publ. WP 20-3
(19GG).
34. Geldreich. E.E., Best, L.C., Kenner, B.A.. and VonDonsel, D.J.,
The Bacteriological Aspects of Stormwatcr Pollution. JWPCF.
40: 18C1 (19G8).
35. Mack. N.M.. Tu, Y.S. and Coohon, D.B., Isolation of Polio-
myelitis Virus from a Contaminated Well. H.S.M.ll.A. Health
Reports (In press).
36. Geldreich, E.E. and Clarke. N.A ., The Coliform Test: A
Criterion for the Viral Safety of Water. Proc. 13th Water
Quality Conference, College of Engineering, University of Illinois,
pp. 103-113 (1971).
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Substitution of Residual Chlorine Measurement for Total C'oliforni
Measurement
The best method of assuring ihe microbiological safety of drinking
water is to maintain gcod clarity, provide adequate disinfection, in-
cluding maintenance of a disinfectant residual, and to make frequent
.measurements of tljo total col if or m density in the distributed water.
In the 1962 U.S. Publ.v Health Service Drinking Water Standards, the
major emphasis was on the measurement of total coliform densities
and a sampling frequency -.'.raph relating number of samples per month
to population served was included. The sampling frequency ranged
from two per montli for populations of 2,000 and less to over 500 per
month, for a population of 8 million.
The effectiveness of this approach for assuring microbiological
safety was evaluated during the 1969 Community Water Supply Survey.
The results of this evaluation by McCabe, et. al.., (1) are paraphrased
below.
Microbiological Quality
To determine the status of the bacteriological surveillance program
in each of the 969 water supply systems investigated, records in the
State and county health departments were examined for the number of
bacteriological samples taken and their results during the previous 12
months of record. Based on this information, only 10 percent had
bacteriological surveillance programs that met the "criteria," while
90 percent either did not collect sufficient samples, or collected
samples that showed poor bacterial quality, or both. The table
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below .sunuiiarix.es the results.
Bacteriological Surveillance
500 or 501 Greater than All
Population Less 100,000 100,000 Populations
Dumber of Systems 446 501 22 969
Percent of Systems
Met Criteria 4 15 36 10
Did not meet
Criteria 95 85 G4 90
Sampling Frequency"
Insufficient samples were taken in more than one of the previous
12 months of record from 827 systems (85 percent of the survey total).
Even-considering a sampling rate reduced by 50 percent of that called
for in the criteria, 670 systems (69 percent of the survey total) still
would not have collected sufficient samples.
Recommendation
The water utility should be responsible for water quality control,
but the bacteriological surveillance collection requirements arc not
being met in most small water systems even though only two samples
per month arc required. A more practical technique must be developed
if the public's health is to be protected. If all systems were chlorinated.
a residual chlorine determination might be a more practical way of
characterizing safety.
The validity of the recommendation that the measurement of chlorine
residual might bo a substitute for some total coliform measurements has
been, investigated by Buclow and Walton (2).
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Because the recommended rate of sample collection could not be
or were not being used, alternative methods of indicating safety were
considered. One suggestion was to substitute the measurement
of chlorine residual for some of the bacteriological samples.
Since this method has the advantage of being easy to perform, and
thus providing an immediate indication of safety. Further, data
from London, U.K. Cincinnati, Ohio; and the 1969 Community Water
Supply Survey (CWSS) lias shown that present sampling locations do not
protect all consumers and that chlorine residual can be used to
replace some coliform determinations.
Sampling Location
During 1965-66, (he London Metropolitan Water Board using its
Standards, made bacteriological examinations of 11,371 samples of
water entering the distribution system, 947 samples taken from dis-
tribution reservoirs, 2,720 samples taken following pipeline breaks,
and 689 samples from miscellaneous locations (complaints, hospitals,
etc.). Most of the unsatisfactory results were associated with reser-
voir problems. Main breaks and miscellaneous samples were
responsible for most of the remaining unsatisfactory samples.
Chlorine Residual
In Cincinnati during the 1969-70 period of free chlorine residual,
approximately 24 samples were collected from each of 143 sampling
stations. None of the samples from 116 of these stations showed pre-
sence of coliform, and 23 of (lie remaining sampling stations showed coli-
form bacteria in only one out of the approximately 24 samples examined.
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At (hi! other lour stations where 2 or more coliform-positivc tests
were obtained from the 24 samples, three had no chlorine residual at
the time the coliform-positivc samples were collected. The question
is raised, therefore, as to the need for examining samples routinely
collected from a large number of stations scattered throughout the
system without regard to the water's residual chlorine content.
Maintaining a free chlorine residual of 0.2 mg/1 in the Cincinnati,
Ohio, distribution system reduced the percentage of coliform positives
to about 1 percent. The table below from the CVVSS data, shows that
the presence of a trace or more of chlorine residual drastically re-
duced or eliminated total coliforms from distribution system samples.
Percent of Various Types of Water Supply Systems Fou::d to Have
Average Total Coliforms Greater than 1/100 ml
Non- Chlorinated With Air/
Type of System Chlorinated No Residual Detectable Re.sidual
Spring
Combined Spring
and Well
Well
Surface
Combined Surface
and Well
39
41
8
64
100
.•ate that a major
reservoirs, etc.
17
28
5
7
1C
portion of
, could be
0
0
0
2
3
a distribution system,
monitored for bacter-
iological safety bv the use of chlorine residual. (Emphasis added.)
18 <
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Therefore, wlien chlorine substitution is used, determination of
total I'olUurm deasitities should be continued in problem areas,
and sonic samples, as a check, should be collected in the main
part of the distribution system.
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These two studies loci to the inclusion in the Regulations of Par.
141.21(h) on the substitution of chlorine residual tests for a portion
of the required total coliform determinations. Par. 141.21(hj stales
that any substitution must be approved by the State on the basis o(
a sanitary survey. The following four items should be specified by
the State:
1. The number and location of samples for which chlorine
residuals are to be substituted.
2. The form and concentration of chlorine residual to be
maintained;
3. The frequency of chlorine residual determinations; and
4. The analytical method to be used!
While each approval must be made individually, taking into
account individual circumstances, the following may offer some
guidance. The first requirement is the establishment of the relation-
ship between chlorine residual and the absence of total coliforms in any
given water. This may not be too difficult in larger supplies where both
of these measurements are routinely made, but it might be quite diffi-
cult for the smaller purveyors (where the most help is needed) who have
not been making either measurement.
The Dumber and location ^f samples for which chlorine residuals
are to be substituted
20-
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Total culifurm measurements should continue to be made of the
finished water as it enters the distribution system and at known
trouble spots such as reservoirs and dead ends. Substitution can be
considered in the free-flowing portion of the distribution system.
The chlorine residual to be maintained
In general, a low turbidity water with a free chlorine residual of
about 0.2 mg/1 at a pH of less than 8.5 will be free from total coliforms
although these conditions may vary from water to water. However, a
higher free chlorine residual or the use of some oilier disinfectant is
required prior to the water entering the distribution systcn., where
disinfection is practiced, if initial disinfection is to be adequate.
The frequency of chlorine residual determinations
Because the chlorine residual test is so easy to perform, it is
reasonable to expect the substitution of several chlorine residual deter-
minations for each total col if or m test deleted. In this way wider
coverage of the distribution system can be achieved, thereby increasing
the protection to the consumer. Since, for maximum protection,
chlorination must be continuous, it is also reasonable to expect that
a minimum of one daily determination of chlorine residual be performed
whenever the chlorine residual option has been chosen. By limiting
the extent of substitution to 75'c of the required bacteriologies' samples,
-------
a sufficient number of bacteriological samples will still be taken
to cnaliic tlie assessment of the adequacy of disinfection and to
at>uuvc the continuity of water quality records.
The analytical method to be used
An analytical method free of interferences to eliminate lalse
residuals must be recommended. For this reason the DPD method
is specified.
Finally, when the chlorine residual option is in use and a free
chlorine residual concentration less than that agreed to is measured
at a sampling point, then a samp.1' for total coliform analysis must
be taken immediately from that point.
-------
REFERENCES
1. lUcCabe, L.J., Symons, J.M.. Lee, R.D., and Rojock, G.G.
Study of Community Water Supply Systems. JAWvVA. C2: 670
(1S70)
2. Buelow, R.W., and Walton, G. Bacteriological Quality vs.
Residual Chlorine. JAWWA. 63:28(1971).
-------
General Bacterial Population
The microbial flora in potable water supplies is highly variable
in numbers and kinds of organisms. Those bacterial groups most
frequently encountered in potable waters of poor quality include:
Pscudomonas, Flavobacterium, Achromobacter, Proteus, Klebsiella,
Bacillus, Serratia, Corynebacterium, Spirillum, Clostridium, Arth-
robactcr, Gallionella, and Lcptothrix (1-5). Substantial populations
of some of these organisms occurring in potable water supplies may
•
bring a new area of health risk to hospitals, clinics, nurseries, and
rest homes (6-11). Although Pseudomonas organisms are generally
considered to be non-pathogenic, they can become a serious "secondary
pathogenic invader" in post-operation infections, burn cases, and
intestinal-urinary tract infections of very young infants and the
elderly population of a community. These organisms can persist and
grow in water containing a minimal nutrient source of nitrogen and
carbon. If Pseudomonas becomes established in localized sections of
the distribution lines, it may persist for long periods and shed irreg-
ularly into the consumer's potable water supply (12). A continual
maintenance of 0.3 to 0.6 mg/1 free chlorine residual will suppress
the development of an extensive microbial flora in all sections of the
distribution network.
Flavobacterium strains can be prevalent in drinking water and on
water taps and clrinlying-fountain bubbler-heads. A recent study of
stored emergency water supplies indicated that 23 percent of the
t
samples contained Flavobacterium organisms with densities ranging
24
-------
from 10 to 26,000 per 1 nil. Fhivolxuttcriuin must be controlled in
the hospital environment because it can become a primary pathogen in
persons who have undergone surgery (13).
Klobsiclla pncumoniae is another secondary invader that produces
human infection of the respiratory system, genito-urinary system,
nose and throat, and occasionally this organism has been reported as
the cause of meningitis and septicema (14). Klebsiclla pncumoniae,
like Entcrobactcr acrogcncs, (15) can multiply in very minimal
nutrients that may be found in slime accumulations in distribution
pipes, water taps, air chambers, and aerators.
Coliform Suppression
The inhibitory influence of various organisms in the bacterial
flora of water may be important factor that could negate detection
of the coliform group (16-17). Strains of Pscudomonas, Sarcina,
Microcuccus, Flavobactcrium, Proteus, Bacillus, Actinomycetes,
and yeast have been shown to suppress the detection of the coliform
indicator group (18-21). These organisms can coexist in water, but
when introduced into lactose broth they multiply at a rapid rate,
intensifying the factor of colil'orm inhibition (22). Suspensions of
various antagonistic organisms in a density range of 10,000 to 20,000
per 1 ml, added to lactose tubes simultaneously with a suspension of
10 E. coli per 1 ml, resulted in reduction in coliform detection (19).
This loss of test sensitivity ranged from 28 to 97 percent, depending
on the combination of the mixed strains.
-------
Data from the National Community Water Supply Survey (23) on
bacteriological quality of distribution water from the 969 public
water supplies were analyzed (Table 1) for bacterial plate count re-
lationship to detection of total conforms and fecal coliforms. Jt is
interesting to note that there was a significant increase in total
and fecal coliform detection when the bacterial counts increased
up to 500 per 1 ml. However, further increase in the detection of
either coliform parameter did not occur when the bacterial count
per 1 ml was beyond 500 organisms. There was, in fact, pro-
gressively decreased detection of both coliform parameters as the
bacterial count continued to rise. This could indicate an aftergrowth
of bacteria in distribution system water or a breakpoint where coliform
detection was desensitized by the occurrence of a large general bacterial
population that included organisms known to suppress coliform recovery.
Control of the General Bacterial Population
Density limits for the general bacterial population must be related,
in part, to a need to control undesirable water quality deterioration
and practical attainment for water throughout the distribution system.
Tliis necessity for monitoring the general bacterial population is
most essential in those supplies that do not maintain any chlorine
residual in the distribution lines and in special application.- .involving
dcsalinization. This bacteriological measurement would serve as a
quality control on water treatment processes and sanitation of dis-
-------
TABLE 1
BACTERIAL PLATE COUNT
vs. CCLIFORM DETECTION
IN DISTRIBUTION WATER NETWORKS F03 969 PUHLIC WATER SUPPLIES
General Bacterial
Ofps, si tv MtTiuje
po- 1 nl
1 - 10
11-30
31 - 100
101 - 300
301 - 500
501 - 1,000
1,000
TOTAL
Population*
Ntiniber of
Samples
1013
371
395
272
120
110
164
2446
Total
Occurrences
47
28
72
48
30
21
31
277
Col iforn
Percent
4.6
7.5
18.2
17.6
25.0
19.1
18.9
c
Fecal
Occurrences
22
12
23
20
11
9
5
107
Col i form
Percent
2.2
3.2
7.1
7.4
9.2
8.2
3.0
—
*Standard Plate Count (48 hrs. incubation, 35CC)
-------
tr Unit ion line sections and storage (auks that could be shedding various
quantities of organisms into the system, thereby degrading the water
quality.
Practical attainment of a low general bacterial population can best
be judged by a study of data from the National Community Water
Supply Survey. Data presented in Table 2 demonstrate the effectiveness
of chlorine residual in controlling the general bacterial population
in a variety of community water supply distribution systems. Although
the number of samples on each distribution system in tins special study
was small, it does reflect bacterial quality conditions in numerous
large and small water systems examined in each of the eight metropoli-
tan areas and the entire State of Vermont.
These data indicate that the general bacterial population in
distribution lines can be controlled to a value below 500 organisms
per 1 ml by maintaining a residual chlorine level in the system.
Increasing the chlorine residual above 0.3 mg/1 to levels of 0.6 and
1.0 mg/1 did not further reduce the bacterial population by any
appreciable amount. Restricting such bacterial densities to a limit
of 500 organisms per ml is, therefore, not only attainab.'e in the
distribution system, but is also desirable to prevent loss in coliform
test sensitivity definitely observed at approximate densities of
1000 organisms per ml, thereby producing a safety factor of at least
two.
-------
TABLE 2
THE EFFECT OF VARYING LEVELS OF RESIDUAL CHLORINE ON THE TOTAL
PLATE COUNT IN POTABLE WATER DISTRIBUTION SYSTEMS*
Standard Plate
Count**
< 1
1-10
n - 100
101 - 500
501 - 1000
>1000
Number of
Samples
0.0
8.1***
20.4
37.3
18.6
5.6
10.0
520
0.01
14.6
29.2
33.7
11.2
6.7
4.5
89
Residual Chlorine
0.1
19.7
38.2
28.9
7.9
1.3
3.9
76
0.2
12.8
48. 9
26.6
9.6
2.1
0
94
(ng/1)
0.3
16.4
45.5
23.6
12.7
1.8
0
55
0.4
17.9
.51.3
23.1
5.1
0
2.6
39
0.5 0.6
4.5 17.9
59.1 42.9
31.8 28.6
4.5 10.7
0 0
0 0
22 28
*Data from a survey of community water supply systems in 9 metropolitan areas (23)
**Standard Plate Count (48 hrs. incubation, 35°C)
***A11 values are percent of samples that had the indicated standard plate count.
-------
Any application of a limit for the general bacterial population
in potable water will require a definition of medium, incubation
temperature, and incubation lime so as to standardize the population
to be measured. The 13th edition of Standard Methods for the Exam-
ination of Water and \Vaste\vater does specify these rcquire'iients for
a Standard Plate Count (SPC) to be used in collection • i water quality
control data. Because many organisms present in potable
waters are attenuated, initial growth in plate count agar frequently
is slow; thus, incubation time should be extended to 48 hours at
35 C. This time extension will permit a more meaningful standard
count of the viable bacterial population. Samples must be collected in
bottles previously sterilized within 30 days and adequately protected
from dust accumulation. Examination for a Standard Plate Count
should be initiated within 8 hours of collection. This time may be
extended to periods up to 30 hours only if these samples are trans-
ported in iced containers.
With maintenance of a chlorine residual and turbidity of less than
one Turbidity Unit, the need for a bacteriological measurement of
the distribution system may become less critical. For this reason,
it is recommended that such water supplies be monitored routinely for
baseline data on the general bacterial population and correlated with
chlorine residual and turbidity measurements in the distribution
lines. It is also recommended that water plant personnel be alert
to unusual circumstances lh::i may make it desirable to monitor the
30--
-------
general bacterial population more often in a check of water plant
treatment efficiencies.
For these reasons, the general bacterial population should be
limited to 500 organisms per 1 ml in distribution water. In theory,
the limitation of the general bacterial population to some practical
low level would also indirectly and proportionally limit any anta-
gonistic organisms that could suppress coliform detection and reduce
the exposure and dosage level for health effect organisms that might
be present.
While no maximum contaminant level for general bacterial popula-
tions is included in the Interim Primary Drinking Water Regulations,
it is recommended that the limit mentioned above be used as an
operational guide in assessing the quality of drinking water delivered.
31T-
-------
REFERENCES
1. Willis, A.T. Anaerobic Bacilli in a Treated Water Supply. J.
Appl. Bacteriol. 20: 61 (1957).
2. Lueschow, L.A. and Mackenthun, K.M. Detection and Enumeration
of Iron Bacteria in Municipal Water Supplies. JAWWA.
54:751 (1962).
3. Clark. P.M., Scott, R.M. and Bone, E. Heterotrophic Iron Pre-
cipitating Bacteria. JAWWA. 5£: 1036 (1967).
4. Victorccn, 11.T. Soil Bacteria and Color Problem in Distribution
Systems. JAWWA. (U: 429 (1969).
5. Victorccn, H.T. Panel Discussion on Bacteriological Testing of
Potable V.'aters. Am. Water Works Assoc. Annual Conference.
June 21-26, 1970, Washington, D.C.
6. Culp, R.L. Disease Due to "Non-pathogenic" Bacteria. JAWWA
61; 157 (1969).
7. Roueche, B. The Annals of Medicine. Three Sick Babies.
The New Yorker, Oct. 5, 1968.
8. Hunter, C.A. and P.R. Ensign. An Epidemic of Diarrhea in
a New-born Nursery Caused by P. acruginosa. A.J. Pub.
Health 37: 1166 (1947).
9. Drake, C.II. and Hoff, J.C. Miscellaneous Infection Section VI -
Pseudomonas aerugiiiosa Infections, pp.635-039.In: Diagnostic
Procedures and Reagents, A.II. Harris and M.B. Coleman,
editors, Am. Pub. Health Assoc. New York, 4th ed. (1963).
10. Smith, W.W. Survival after Radiation Exposure - Influence of a
Di.stuibecl Environment. Nucleonics K): 80 (1952).
11. Maiztegui, J-I- et al, Gram-Negative Rod Baclercmia with a
Discussion of Infections Caused by Herclla Species. Am. J.
Surgery 107: 701 (1964).
12. Cross, D.F., Benchimol, A., and Dimond, E.G. The Faucet
Aerator - A Source of Pseudomonas Infection. New England
J. Med. 274: 1430 (196~6TT
-------
13. Herman, L.G. and Ilimmelsbnch, C.K. Detection and Control
of Hospital Sources of Flavobactcria. Hospitals. J. Am.
Hospital Assn. 39 (1965T
14. Leiguarda, R.H. and Polazzolo, A.Z.Q.D., Bacteria of Genus
Klebsiella in Water. Rev. Obr. Sanit . Nac., (Argentina)
38: 169 (1956).
15. Nunez, W.J. and Colmer. A.R. Differentiation of Acrobacter-
KJebsiella Isolated from Sugarcane. Appl. Microbiol. 1C:
1875 (1965).
16. Waksman, S.A. Antagonistic Relations of Microorganisms.
Bacteriol. Reviews 5; 231 (1941).
17. Schiavone, E.L. and Passerini, L.M.D. The Genus Pscudomonas
acruginosa in the Judgment of the Potability of Drinking Water.
Scm. Mcd., (B. Aires) 111: 1151 (1957).
18. Kliglcr, L.J. Non-lactose Fermenting Bacteria from Polluted
Wells and Sub-soil. J. Bacteriol. 4: 35 .(1919).
19. Hutchinson, D., Weaver, R.H. and Scherago, M. The Dicidence
and Significance of Microorganisms Antagonistic to Escherichia
coli in Water. J. Bacteriol. 45_: 29 (1943).
20. Fi.-:her, G. Tlic Antagonistic Effect of Aerobic Sporulating
Bacteria on the Coli-Aerogenes Group. Z. Immam Forsch 107:
16 (1950).
21. Weaver. R.H. and Bolter, T. Antibiotic- Producing Species of
Bacillus from Well Water. Trans. Kentucky Acad. Sci. 13:
"
22. Reittcr, R. and Scligmann, R. Pscudomonas aeruginosa in
Drinking Water. J. Appl. Bacteriol. 2(FT4S7T9S7r
23. McCabe, L.J., Symons, J.M.. Lee. R.D., and Robcck, G.G.
Study- of Community Water Supply Systems. JAWWA .
62: 670 (1970).
33<
-------
these 3 water supplies were really adequately treated. Only one of
the 8 poliomyelitis epidemics occurred in the United States, and
this was the result of cross-connccti'jn contamination. Sir.ce
Mosley's publication there have been three other reports of water-
borne infectious hepatitis outbreaks in this country, all reportedly
due to either sewage pollution of well water or cross-connection
contamination. An estimated 20,000 - 40,000 cases of infectious
hepatitis were reported m Delhi, India, in 1955-56 (2) attributable
to a municipal water supply source heavily overloaded with raw sewage.
This outbreak, however, was not accompanied by noticeable incrcasc-t
of typhoid fever or other cnterobacterial diseases, suggesting that,
in practice, the virus(cs) of infectious hepatitis may be more
resistant to chlorine or chloramines than are vegetative bacteria.
Weibcl and co-workers (3) listed 142 outbreaks of gastroenteritis
during the period of 194G to 1970 in which ephiemiologic evidence
suggested a waterborne nature. More than 18,000 persons were
affected in these outbreaks. Mosley (1) suspected Unit a signifi-
cant portion of these cases must have been caused by viruses.
It is well recognized that many raw water sources in this
country arc polluted with enteric viruses. Thus, water supplies
from such sources depend entirely upon the treatment processes
used to eliminate those pollutants. Even though the processes may
be perfectly effective, an occasional breakdown in the plant or any
marginal practice of treatment could still allow the pollutants to
35--
-------
reach the finished water .supplies. It should be noted that Coin
and his associates (4) have reported the recovery of viru^js from
raw and finished waters in Paris, France. Coin estimated that the
Paris water probably contained one tissue culture unit of virus pei
250 liters. Very recently, Mack et al (5) reported that poliovirus
was recovered in water from a deep well in Michigan. Although the
well had a history of positive coliforms, coliforms and virus were
not recovered from on unconcentrated water sample; only after a
2.5 gallon sample of water was subjected to high speed centrifuga-
tion were both virus and coliforms recovered. This study would seem
to indicate that the present method of using the coliform test is not
adequate to indicate the presence of viruses. In summary, in the
United States, most water borne virus disease outbreaks have resuJted
from contamination of poorly treated drinking water by sewage e:.ther
directly or through cross-connections. Overt outbreaks of virus
disease from properly treated municipal water supplies are not
known to have occurred. Proper treatment of surface water usually
means clarification followed by effective disinfection.
Chang (6), however, has theorized that some water supplies that
practice only marginal treatment may contain low levels of human
viruses, and that this small amount of virus might initiate infection
or disease in susceptible individuals. He believes that such individuals
might thus serve as "index cases" and further spread the virus by
-------
person-to-person contact. Whether this hypothesis is true, can be
proved only by :m intensive survey for viruses in numerous drinking
water supplies in this country, and such a survey lias never been
conducted. If viruses were detected in a survey of drinking water
supplies, it would be necessary to conduct in-depth epideniiological
studies to determine if actual infection or disease was being caused
by these agents. Additionally, it would be necessary to determine
what modifications would be required in the water treatment pro-
cesses to eliminate these viruses.
The relative number of viruses and coliform organisms in
domestic sewage is important in assessing the significance of the
coliform test and the "virus safety" of water. Calculations by
Clarke et al (7) have indicated the following virus-colilorm ratios
in feces, sewage, and polluted waters.
Calculated Virus - Coliform Ratios
Virus Coliform Ratio
Feces 200/gm 13xl06/gm 1:65,000
Sewage 500/100 ml 46xlOe/100ml 1:92,000
Polluted Surface Water 1/100 ml SxloVlOO ml 1:50,000
It is apparent that coliform organisms far outnumber human enteric
viruses in feces, sewage, and polluted surface water. It should be
-------
emphasized that these calculated ratios are only approximations and that
they would be subject to wide variations and radical changes, particularly
during a virus disease epidemic. Additionally, both bacteria and virus
populations in sewage and polluted waters are subject to reductions, at
different rates, from die-off, adsorption, sedimentation, dilution, and
various oilier undetermined causes; thus, the coliform-virus ratio
changes, depending upon conditions resulting from the combined effect
of all factors present. Thus, one must take into consideration the
most unfavorable conditions although they may be encountered very
infrequently. Such conditions may impose considerable demands on
the indicator system and treatment processes.
The efficacy of various water treatment processes.in removing or
inactivating viruses has recently been reviewed by Chang (G) and also
in a Committee Report, "Engineering Evaluation of Virus Hazards in
Water" (8). These reports indicate that natural "die-off" cannot be
relied upon for the elimination of viruses in water. Laboratory pilot
plant studies indicate that combination of coagulation and sand filtration
is capable of reducing virus populations up to 99.7 percent if such treat-
ments arc properly carried out (9). It should be noted, however, that a
floe breakthrough, sufficient to cause a turbidity of as little as 0.5
Turbidity Units, was usually accompanied by a virus breakthrough in a
pilot plant unit seeded with high doses of virus (9). Disinfcolion,
-------
however, is the only reliable process by which water can be made free
of virus. In the past, there have been numerous studies conducted on
the chlorination of viruses. Recent work by Liu, et al (10), has
confirmed early observations and has reemphasized two possible weak-
nesses in these early reports: (a) the number of virus types studied was
very small, thus generalization on such results is not without pitfalls,
/•
(b) the early chlorination studies were usually conducted with reasonably
pure virus suspensions derived from tissue cultures or animal tissue and
may not represent the physical state of the virus as it exists under
natural conditions (clumped, embedded in protective material, etc.)
which would make the virus much more resistant to disinfectants.
Thus, it is imperative that good cu..vf; Cation processes be used on
turbid waters to reduce their turbidity levels that will ensure effective
disinfection. Additionally, Liu's data show the wide variation in
resistance to chlorine exhibited by viruses, e.g., four minutes were
required to inactivate 99.99 percent of a reovirus population as
contrasted to GO minutes to achieve the same percent inactivation
of coxsackicvirus.
Virology techniques have not yet been perfected to a point where
they can be used to routinely monitor water for viruses. Considerable
progress on method development, however, has been made in the past
decade. The methods potentially useful include: two-phase polymer
-------
separation (11), membrane filtration (12), adsorption on and elution
from chemicals (13, 14, 15), and the gauze pad technique (16) to
name a few. From the concerted efforts of virus-water laboratories
throughout the world, it is hoped that a simple and effective method
will become available for viral examination of water. In the interim,
control laboratories having access to facilities for virus isolation
and identification should be encouraged to use available procedures
for evaluating the occurrence of human enteric viruses in treated
waters.
As noted above, no simple and effective method for the viral
examination of water is available at this tJme. When such a method
is developed, and when there are sufficient data to provide the
necessary basis, a maximum contaminant level for virus will be
proposed.
40<
-------
REFERENCES
1. Mosley, J.W. Transmission of Viral Diseases by Drinking Water.
Transmission of Viruses by the Water Route, edited by G. Berg,
John Wiley and Sons, New York, pp. 5-25, 1968.
2. Viswanathan, R. Epidemiology. Indian J. Med. Res. 45: 1,
(1957). ~~
3. Weibel, S.R., Dixon, F.R., Weidner, R.B., and McCabe, L.J.
Waterbornc-disease Outbreaks 1946-1970. JAWWA.
56: 947 (1964).
4. Coin, L., Mcnetrier, M.L., Labonde, J., and Harmon. M.C.
Modern Microbiological and Virological Aspects of Water Pollution.
Second International Conference on Water Pollution Research,
Tokyo, Japan, pp. 1-10. (1964).
5. Mack, N.W., Lu, Y.S., and Cophoon, D.B. Isolation of Polio-
myelitis Virus from a Contaminated Well. Health Services Repts,
87; 271 (1972).
6. Chang, S.L. Walerbornc Virus Infections and Their Prevention.
Bull. Wld. Hlth. Org. 38: 401 (1968).
7. Clarke, N.A., Berg, G., Kabler, P.W., and Chang, S.L. Human
Enteric Viruses in Water: Source, Survival, and Removability.
First bucrnational Conference on Water Pollution Research,
London, England, pp. 523-542 (1962).
8. Committee Report "Engineering Evaluation of Virus Hazard in
Water," JASCE, SED, pp. 111-161 (1970).
9. Robcck. G.G., Clarke, N.A., and Dostal, K.A. Effectiveness
of Water Treatment Processes in Virus Removal. JAWWA,
54: 1275 (1962).
10. Liu, O.C. Effect of Chlorination on Human Enteric Viruses in
Partially Treated Water from Potomac Estuary. Progress
Report. Environmental Protection Agency, Division of Water
Hygiene, 1970.
11. Shuval, II.I., Fattal, B., Cymbalista, S., and Golclblum, N.
The Phase-Separation Method for The Concentration and Detection
of Viruses in Water. Water Res. 3: 225 (1969).
-------
12. Rao, N.U. and Labzoffsky, N.A. A Simple Method for Detection
of Low Concentration of Viruses in Large Volumes of Water by
the Membrane Filter Technique. Can. J. Microbiol., 15: 399
(19G9). ~~~
13. Rao, V.C., Sullivan, R., Read, R.B., and Clarke, N.A. A
Simple Method lor Concentrating and Detecting Viruses in Water.
JAWWA. CO: 1283 (19G8).
14. Wallis, G. and Mclnick, J.L. Concentration of Viruses on
Aluminum Phosphate and Aluminum Hydroxide Precipitates.
Transmission of Viruses by the Water Route, Edited by G. Berg,
J. Wiley and Sons, pp. 129-138, 1968.
15. Wallis, G-, Gristein, S., and Mclnick, J.L. Concentration of
Viruses from Sewage and Excreta on Insoluble Polyelectrolytes.
Appl. Microbiol. _13: 1007 (1969).
16. Hoff. J.C., Lee, R.D., and Becker, R.G. Evaluation of a
Method for Concentration of Microorganisms in Water. APHA.
Proc. (1967).
A'^<
*-»fr«/
-------
Turbidity
Drinking water should be low in turbidity prior to disinfection
and at the consumer's tap for the following reasons:
(1) Several studies have demonstrated that the presence of particulate
matter in water interferes with effective disinfection. Neefe, Baty,
Reinhold, and Stokes (1) added from 40 to 50 ppm of feces containing;
the causative agent of infectious hepatitis to distilled water. They then
treated this water by varying techniques and fed the resultant liquid
to human volunteers. One portion of the water that was disinfected
to a total chlorine residual after 30 minutes of 1.1 mg/1 caused
hepatitis in 2 of the 5 volunteers. A similar experiment in which
the water was first coagulated and then filtered, prior to disinlection
to (lie same concentration of total residual, produced no hepatitis
in 5 volunteers. This was repeated with 7 additional volunteers,
and again no infectious hepatitis occurred.
Cluing, Woodward and Kabler (2) showed that nematode worms
can ingest enteric bacterial pathogens as well as virus, and that the
neniatodc-borne organisms are completely protected against chlorina-
tions even when more than 90 percent of the carrier worms are
immobilized.
Walton (3) analyzed data from three waterworks treating surface
waters by chlorination only. Colilorm bacteria were detected in the
chlorinated water at only one waterworks, Hie one that treated a Great
Lakes water that usually did not have turbidities greater than 10 turbidity
units (TU), but occasionally contained turbidities as great as 100 TU.
-------
Sanderson and Kelly (4) studied an impounded water supply
receiving no treatment other than chlorination. The concentration
of free chlorine residual in samples from household taps after a
minimum of 30 minutes contact time varied from 0.1 to 0.5 mg/1
and the total chlorine residual was between 0.7 and 1 mg/1. These
samples consistently yielded confirmed coliform organisms. Tur-
bidities in these samples varied from 4 to 84 TU, and microscopic
examination showed iron rust and plankton to be present. They
concluded ".. .coliform bacteria were imbedded in particles of
turbidity and were probably never in contact with the active agent.
Viruses, being smaller than bacteria, are much more likely to
escape the action of chlorine in a natural water. Thus, it would
be essential to treat water by coagulation and filtration to nearly
zero turbidity if chlorination is to be effective as a viricidal
process."
Hudson (5) reanalyzed the data of Walton, above, relating
them to the hepatitis incidence for some of Uie cities that Walton
studied plus a few others. A summary of his analysis is shown
in Table I. Woodward docs, however, in a companion discussion
warn against over interpreting such limited data and urges more
fuld and laboratory research to clearly demonstrate the facts.
44<
-------
TABLE I
F1LT.EHFD-WATFR QUALITY AND HEPATITIS INCIDENCE. 1953
Final
Average Chlorine
Turbidity Residual Hepatitis
City TU mg/1 cases/100,OOP people
G 0.15 0.1 3.0
C 0.10 0.3 4.7
II 0.25 0.3 4.9
B 0.2 - 8.6
M 0.3 0.4 31.0
A 1.0 0.7 130.0
45:
-------
Tracy, Camarena, and Wing (6) noted that during 19G3, in San Fran-
cisco, California, 33 percent of all the coliform samples showed 5
positive tubes, in spite of the presence of chlorine residual. During
the period of greatest coliform persistence, the turbidity of this
unfiitered supply was between 5 and 10 TU.
Finally, Robeck, Clarke, and Dostal (7) showed by laboratory
demonstration that virus penetration through a granular filter was
accompanied by a breakthrough of floe, as measured by an increase
in effluent turbidity above 0.5 turbidity unit in a pilot unit seeded
with an extremely high dose of virus.
These 7 studies show the importance of having a low turbidity
water prior to disinfection and entrance into the distribution system.
(2) The 19G9 Community Water Supply Survey (8) revealed that
unpleasant, tastes and odors were among the most common customer
complaints. While orgnnics and inorganics in finished water do cause
tastes and odors, these problems are often aggravated by the reaction
of chlorine with foreign substances. Maintenance of a low turbidity
will permit distribution with less likelihood of increasing taste and
odor problems.
46
-------
(3) P.egrowth of microorganisms in a distribution system is
often stimulated if organic matter (food) is present. An example of
this possibility occurred in a Pittsburgh hospital (9). One source
of this food is biological forms such as algae which may contribute
to gross turbidity. Therefore, the maintenance of low turbidity
water will reduce the level of this microbial food r.;;d maintain a
cleanliness that will help prevent regrowth of bacteria and the
growth of other microorganisms.
(4) The purpose of maintaining a chlorine residual in a dis-
tribution system is to have a biocidal material present through-
out the system so that the consumer will be protected if the in-
tegrity of the system is violated. Because the suspended material
that causes turbidity may exert a chlorine demand, the main-
tenance of a low turbidity water throughout the distribution system
will facilitate the provision of proper chlorine residual.
For these reasons, the limit for turbidity is one (1) Turbidity
Unit (TU) as the water enters the distribution system. A properly
operated water treatment plant employing coagulants and granular
filtration should have no difficulty in consistently producing a
finished water conforming to this limit.
47'-
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REFERENCES
1. Ncofe, J.R., Duty, J.B., Reinhold, J.G., and Stokes, .1.
Inactivation of The Virus of Directions Hepatitis in Drijiking
Water. Am. J. Pub. Health 37: 365 (1947).
2. Chanj;, S.L., Woodward, R.L., and Kablcr, P.K. Survey of
Frceliving Nematodes and Amcbas in Municipal Supplies.
JAWWA. £2: 613 (May I960).
3. Walton, G. Effectiveness of Water Treatment Processes As
. Measured by Coliform Reduction. U.S. Department of Health,
Education and Welfare, Public Health Service, Publ. No. 898,
68 p. (1961).
4. Sanderson, W.W. and Kelly, S. Discussion of "Human Enteric
Viruses in Water: Source, Survivial and Removability" by Clarke.
N.A., Deri;, G., Kabler, P.K.r and Chang, S.L. Internal. Conf.
on Water Poll. Res., pp. 536-541, London, September 1962,
Pergamon Press. (1964).
5. Hudson, H.E., Jr. High-quality Water Production and Viral
Disease. JAWWA. 54/1265-1272 (Oct. 1962).
6. Tracy, H.W., Camarena, V.M., and Wing, F. Coliform Per-
sistence in Highly Chlorinated Waters. JAWWA. ^8: 1151
(1966).
7. Robeck. G.G., Clarke, N.A., and Dostal, K.A. Effectiveness
of Water Treatment Processes in Virus Removal. JAWWA.
54: 1275-1290 (1062).
8. McCabe, L.J.. Symons, J.M., Lee, R.D., and Robeck, G.G.
Survey of Community Water Supply Systems. JAWWA.
62: 670 (1970).
9. Roucche, B. Annals of Medicine. Three Sick Babies. The
New Yorker, Oct. 5, 1968.
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C - CHEMICAL QUALITY
The following pages present detailed data and the reasoning used
in reaching the various limits.
In general, limits are based on the fact that the substances
enumerated represent hazards to the health of man. In arriving at
specific limits, the total environmental exposure of man to a stated
specific toxicant has been considered. An attempt has been made to
set lifetime limits at the lowest practical level in order to minimize
the amount of a toxicant contributed by water, particularly when other
sources such as milk, food, or air are known to represent the major
exposure to man.
The Standards are regarded as a standard of quality that
is generally attainable by good water quality control practices.
Poor practice is an inherent health hazard. The policy has been
to set limits that are not so low as to be impracticable nor so
high as to encourage pollution of water.
No attempt has been made to prescribe specific limits for every
toxic or undesirable contaminant that might enter a public water
supply. While the need for continued attention to chemical contami-
nants of water is recognized, the Regulations are limited to need and
available scientific data or implications on which judgments can be
made. Standards for innumerable substances which are rarely
found in water would require an impossible burden of analytical
examination.
-------
The following table indicates the percent of samples analyzed in
the Community Water Supply Study which exceeded 75% of the 1962
PUS Drinking Water Standards limits. This table shows the re-
lationship of the existing quality of water analyzed during the study
to the drinking water standards in effect at that lime.
-------
PERCENT OF SAMPLES IN THE COMMUNITY WATER
SUPPLY STUDY WITH VALUE EXCEEDING 75% OF EACH LIMIT
IN THE 1962 DRINKING WATER STANDARDS
Constituent
DWS Limit
DWS Limit X 0.75
Percent of
Samples Exceeding
Arsenic
Barium
Cadmium
Chloride
Chromium
Color
Copper
Cyanide
Foaming '
Agents
Iron
Lend
Manganese
Nitrate
Selenium
Silver
Sulfate
Zinc
0.05 mg/1
1 mg/1
0.010 mg/1
250 mg/1
0.05 mg/1
15 C.U.
1 mg/1
0.2 mg/1
0.5 mg/1
0.3 mg/1
0.05 mg/;
0.05 mg/1
45 mg/1
0.01 mg/1
0.05 mg/1
250 mg/1
5 mg/1
0.0375 mg/1
0.75 mg/1
0.0075 mg/1
187.5 mg/1
0.0375 mg/1
11.25 C.U.
0.75 mg/1
0.15 mg/1
0.375 mg/1
0.225 m-i/l
0.0375 mg/1
0.0375 mg/1
33.75 mg/1
0.0075 mg/1
0.0375 mg/1
187.5 mg/1
3.75 mg/1
1.24%
0.03%
1.45%
1.56%
1.43%
3.54%
2.47%
0.00%
0.08% .
15.81% .
3.32%
11.91%
3.46%
8.35%
0.00%
3.37%
0.35%
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DAILY FLUID INTAKE
For the purpose of those Regulations, a daily intake of water or
water based fluids of two liters was assumed. This figure was taken
as being representative of the fluid consumption of a normal adult
male, and was obtained by consulting standard textbooks oh physiology
and numerous journal articles concerning water consumption.
It was realized that tremendous variation in individual consumption
would exist, but since women and children drink less than the average
man, it was decided that a large percent of the population would consume
less than two liters a day.
There have been numerous reports of individuals or groups of
persons who consume abnormally large quantities of water or water-
based fluids. For example, the consumption of six liters of beer in
a day (1, 2) is not unknown. However, it should be noted that anyone
who consumes this quantity of beer would be yetting more than 240 ml
(1/2 pint) of pure alcohol which is close to the maximum tolerable dose
for a day.
The Boy's Life Magazine (1971)(3) survey indicated that 8% of 10-17
year-old boys drink more than 8 soft drinks per day. This survey can
be viewed from another angle and a statement made that 92% of such
boys drink less than 8 soft drinks per day. It would probably be valid
to state that the average consumption is far less than 8.
-------
Guyton (1951)(4) properly indicates that diseased persons having
diabetes insipidus consume great quantities of water a day but even
raising the "daily fluid intake" to 6 liters a day would not protect
these individuals who excrete up to 15 or more liters of urine per day.
It might also be pointed out that diabetes insipidus is a relatively rare
disease and that these patients could not be considered average consumers.
Welch, et al (5) show that at temperatures up to 75T 2 liters or
less of fluid are drunk per day by adult males.
Molnar, et al (6) found that average fluid intake in the desert was 5.90
liters per day with a standard deviation of +2.03 whereas average fluid
intake in the tropics was 3.26 liters with a standard deviation of 4-1.09.
These men were performing their normal duties including truck driving,
guard duty, hiking, etc. Five percent of the men in the tropics drank as
little as 1 liter a day.
Wyndham and Strydom (7) indicated that marathon runners lost between
1, 500 and 4, 200 ml of sweat in 20 miles of running at about 60eF. To
replace their fluid that day would require from 2. 5 to 5 liters of water.
In "Clinical Nutrition" (8) the normal water loss per day shown
for a normal adult ranges from 1, 500 ml - 2,100 ml. The breakdown for
a 2, 600 ml water intake is shown as 1, 500 from fluids, 800 ml from food
and 300 ml from metabolism. .
In "Physiology of Man in the Desert"(9) the average intake of fluid
for 91 men in the desert was 5.03 liters with a standard deviation of
+1.67. This indicates that some men only drank three liters a day in
-------
a desert environment where temperatures went as high-as 105°F.
In Best and Taylor's book, "Tho Physiological Basis of Medical
Practice, " (1945)(10) an average adult is shown to require 2, 500 ml
of water from all sources under ordinary circumstances. The sources
of this water arc shown as:
Solid and semisolid food 1200 cc
Oxidation of food 300 cc
Drinks (water, milk, coffee, beer, etc.) 1000 cc
This reference points out that cooked lean meat contains from 65 to 70
percent water.
It should be noted that certain references refer to water loss per day
instead of drinking water intake. Water loss per day is approximately
I 1/2 liters higher Hum the drinking water intake figure would be.
'Human Designs" (11) by Beck (1971) indicates that between 2200 ml
and 2800 ml are required for an average adult with an average 2500 ml
daily fluid intake. This author, however, reverses the food and drink
quantities shown above. Both of these references indicate that 1 cc of
water is required per calorie of food intake.
Two articles relating to the fluid intake of children might be cited
here. One, by Galagan, et al (12), used children from under one year
of age to age ten and showed Uiat total fluid intake per pound of body
weights was highest among infants and decreased with age. The water
intake listed average 0. 40 ounces (12 ml) per day per pound of body
wcighv. They also found that water intake increased directly with
increases in temperature. r- ?,._.
-------
The second article by Bonham, et al (13) concerns six-year old
children and lists 0.70 ounces (21 ml) per day per pound. This is
total fluid and includes milk. If a child of this age weighed 50 Ibs.,
he would drink about one liter per day.
The "Bioastronautics Data Book" (14) lists an average of 2400 ml
total water intake but indicates the breakdown as 1, 500 ml from drinking
water, 600 ml from food and 30 ml from oxidation of food.
More recently, the Task Group on Reference Man (1974)(15) estimated
the water-based fluid intake of an adult man to be 1650 ml/day, with
corresponding values for an adult woman of 1200 ml/day and for a
child of 950 ml/day.
Considering all the information we have available, two liters per day
drinking water consumption for the average mail should be a reasonable .
estimate. It is twice the amount listed by some authors and 309o higher
than other authors list as an average figure and is therefore defensible
as a reference standard.
5S<
-------
REFERENCES
1. McDcrmott, P. H., R. L. Delaney, J.D. Egan, and .1. F. Sull
"Myocardosis and Cardiac Failure in Man" JAMA 198:253 19GG
2. Morin, Y. L., A.R. Folcy, G. Martincau, nndJ. Rousscl Beer-
Drinkers Cardiomyopathy: Forty-Eight Cases." Canadian Medical
Assoc. J. 97:881-3, 1967.
3. Boy's Life, National Readership Panel Survey, August 1970
Richard Manville Research, Lie. 1971
4. Guyton, A.C. Textbook of Medical Physiology, Second Edition
Philadelphia, W.S. Saunders 196TT ' "**"
5. Welch, B.E., E.R. Buskirk and P. F. lampietro "Relation of
Climate and Temperature to Food and Water Intake" Metabolism
J7:141-8, 1958
6. Molnar, G. W. , E.J. Towbin. R. E. Gosselin, A.M. Brown and
E. F. Adolph. "A Comparative Study of Water, Salt and Heat
Exchanges of Men in Tropical and Desert Environments" A. J. Hyg
44:411-33, 1946/
7. Wymlhan, C. H. andN.B. Strydom. "Til*? Danger of and Inadequate
Water Intake During Marathon Running. " South Afr. M. J. 43:893-G,
19G9
8. Joliffc, N. (Editor), Clinical Nutrition, Second Edition, New York,
Harper and Brothers, 19G2.
9. Adolph, E. F. , Physiology of Man in the Desert, New York,
Interscicnce Publ. 194G.
10. Best, C.H. andll.B. Taylor, The Physiolocicr.l Basis of Medical
Practice, Eighth Edition," Baltimore, Williams and Wilkins Co., 19CG
11. Beck, W. S., Human Design, New York, Harcourt Brace Jovanovich,
1971.
12. Galagan, D.J., J.R. Vcrmillion, G.A. Ncvitt, Z. M. Sladt. and
R.E. Dart. "Climate and Fluid Intake, " Pub. Health Ret;. 7^:484-90,
1957
13. Bonham, G. H. , A.S. Gray, and N. Luttrcll. "Fluid Intake Patterns
of G-Year-Old Children in a Northern Fluoridated Community. " Canad.
Mcd. Ass. J. 01:749-51, 1964.
-------
14. Webb, P. (Editor). Bitjnstronaulics Data Book, (National Aero-
nautics and Space Agency, Washington, D. C.) NASA-SP 300G,. 19G4.
15. Snyder, W.S., Chairman, "Rejxjrt of the Task Group on Reference Man. "
New York, Per^amon Press, 1974.
57-
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ARSENIC
The high toxicily of arsenic and its widespread occurrence in
the environment necessitate the setting of a limit on the concentration
of arsenic in drinking water.
The presence of arsenic in nature is due mainly to natural
deposits of the metalloid and to its extensive use as a pesticidal
agent. Arsenic concentrations in soils range from less than one
part per million (nig/I) to several hundred mg/1 in those areas
where arsenical sprays have been used for years. Despite rela-
tively high concentrations of arsenic in soils, plants rarely take up
enough of '.he element tci constitute a risk to human realth (1,2).
Despite the diminishing use of arscnicals as pesticides, presently
several arscnites are used as herbicides and some ra-senatcs as
insecticides. In 19G4, farmers in the U.S. used a combined
total of approximately 15 million pounds of arsenicals (3).
The chemical forms of arsenic consist of trivalcnt and pentava-
lent inorganic compounds and trivalent and pentavalen't organic
agents. K is not known which forms of arsenic occur in the drinking
water. Although combinations of all forms are possible, it can be
reasonably assumed that the penlavalent inorganic form is the most
prevalent. Conditions that favor chemical and biological oxidation
promote the shift to the penlavalent specie; and conversely, ihose
that favor reduction will shift the equilibrium to the trivalcnt
state.
-------
The population is exposed to arsenic in a number of ways.
Arsenic is still used, albeit infrequently, to treat leukemia,
certain typos of anemia, and certain skin diseases (4). In (lie
diet, vegetables and grain contain an average of 0.44 ppm and
meats an average of 0. 5 ppm of arsenic (5). Organic arsenicals
are deliberately introduced into the diet of poultry and pigs as
growth stimulators and pesticides. The Food and Drug Admin-
istration has set tolerance limits for residues of arsenicals on
fruits and vegetables (3. 5 mg as As,03 per kg) and in meat
(0. 5 to 2. 0 mg as As per kg) (6). Shellfish are the dietary com-
ponents that usually contain the highest concentrations of arsenic,
up to 170 mg/kg (2,7,8).
For the entire U.S. , the arsenic concentrations in air range
from a trace to 0. 75 ug/m3 (9). Airborne arsenic is usually the
result of operating cotton gins, manufacturing arsenicals, and
burning coal.
Arsenic content of drinking-water ranges from a trace in most
U.S. supplies to approximately 0.1 mg/1 (10). No adverse health
effects have been reported from the ingestion of water containing
0. 1 mg/1 of arsenic.
The toxicity of arsenic is well known, and the ingestion of as
little ns 100 mg can result in severe poisoning. In general, in-
organic arscnicnls are more toxic to man and experimental
animals than the organic analogs; and arsenic in the pcntavalent
state is less toxic than that in the trivalent form.
59 <
-------
Inorganic arsenic is absorbed readily from the Castro-intestinal
tract, the lungs, and to a lesser extent from the skin, and becomes
distributed throughout the body tissues and fluids (4). Inorganic
.•> . •* '"
arschicais appear to be slowly oxidized in vivo from the trivaletit
to the pcntavalent state; however, there is no evidence that the
reduction of pcntavalent arsenic occurs within the body (5, 11-13).
Inorganic arsenicals are potent inhibitors of the intracellular
sulfhydryl (-SH) enzymes involved in cellular oxidations (14).
Arsenic is excreted via urine, feces, sweat, and the epithelium of
the skin (15-20). A single dose is usually excreted largely i.i the
urine during the first 24 to 48 hours after administration: but
elimination of the remainder of the dose continues for 7 to 10 days
thereafter. During chronic exposure arsenic accumulates mainly
in bone, muscle, and skin, and to a smaller degree in liver and
kidneys. After cessation of continuous exposure, arsenic excre-
tion may last up to 70 days (14).
A number of chronic oral loxicity studies with inorganic arsenile
and arsenate (21-25) demonstrated (he minimum-effect and no-effect
levels in dogs, rats, and mice. Three generations of breeding mice
were exposed to 5 ppm of arsenite in the diet with no observable
effects on reproduction. At high doses (i.e. , 200 mg/1 or greater)
arsenic is a physiological antagonist of thyroid hormones in the
rat (2G). Arsenic is also an antagonist of selenium and lias been
reported to counteract the toxicily of sclcniferous foods when added
to argicultural animals' feed water (27, 28). Rats fed shrimp meat
60-
-------
containing a high concentration of arsenic retain very little of the
clement as compared to rats fed the same concentrations of either
arsenic trioxide or calcium arsenale (29), suggesting that the
arsenic In shellfish tissues may be less toxic to mammals than
|
that invested in other forms.
In man, subacute and chronic arsenic poisoning may be insidious
and pernicious. In mild chronic poisoning, the only symptoms
present are fatigue and loss of energy. The following symptoms may
be observed in more severe intoxication: gastrointestinal catarrh,
kidney degeneration, tendency to edema, polyncurilis, liver cirrhosis,
bone marrow injury, and exfoliate dermatitis (30, 31). In 19G2,
thirty-two school-age children developed a dermatosis associated
with cutaneous exposure to arsenic trioxide (32, 33). It has been
claimed that individuals become tolerant to arsenic. However, this
apparent effect is probably due to the ingestion of the relatively
insoluble, coarse powder, since no true tolerance has ever been
demonstrated (14).
Since the early nineteenth century, arsenic was believed to be
a carcinogen: however, evidence from animal experiments and human
experience has accumulated to strongly suggest that ar.senicals do
not produce cancer. One exception is a report from Taiwan showing
a close-response curve relating skin cancer incidence to the arsenic
content of drinking water (44). Some reports incriminated arsenic
-------
as a carcinogen (34, 35), but it was later learned that agents
other than the metalloid were responsible for such cancers (3G).
Sonuners anH McManus (37) reported several cases of cancer
in individuals who had at some time in their lives been exposed
to therapeutic doses of arsenic trioxide (usually in Fowler's
Solution). Patients displayed characteristic arsenic keratosis,
but there \\as no direct evidence that arsenic was the etiologic
agent in the production of the carcinoma.
Properly controlled studies (38, 39) have demonstrated that
industrial workers do not have an increased prevalence of cancer
despite continued exposure to high concentrations of arsenic
trioxide. In the study by Pinto and Bennett (39), the exposure
was estimated by comparing the arsenic excreted in urine of
control and exposed populations. In the experimental group, some
workers who had been exposed to arsenic trioxide for up to 40 years,
excreted 0.82 mg of arsenic per liler, or more than six times the
concentration of the control population. In addition, attempts to
demonstrate through animal studies that arsenic is tumorigenic
have met with failure (23, 35, 40-42). The possible co-carcino-
genic role of arsenic frioxide in the production of methylcholan-
thrcnc-induccd skin tumors has been investigated and found to
have no significant effect (43).
-------
However, sonic recent evidence supports the view that urscr"'
is carcinogenic. Liciustri.il workers in a plant manufacturing art'-onic
powder were exposed to arsenic dust and showed n. higher incidence
of skin and lung cajicer than other occupational groups (44, 45, 46).
Ulceration of the nasal septum appears to be a common finding among
workers exposed to inorganic arsenic. The incidence of skin cancer
has also been reported to be unusually high in areas of England where
arsenic was present in drinking water at a level of 12 mg/1 (47).
More recently Lee and Fraumeni found that the mortality rate of white
male smelter workers exposed to both arsenic trioxide and sulfur
dioxide exceeded the expected mortality rale by a statistically significant
margin and found that lung cancer deaths among these workers increased
with increasing lengths of exposure to arsenic trioxide. They concluded
that their findings were "consistent with the hypothesis that exposure
to high levels of arsenic trioxide, perhaps in interaction with sulfur
dioxide or unidentified chemicals in the work environment, is
responsible for the three-fold excess of respiratory cancer deaths
among smelter workers" (48).
Similarly, Ott, et al., found, in a. study lor the Dow Chemical
Company, that exposed employees in a dry arsenical manufacturing
plant experienced a three-fold increase in lung cancer over the rate
for non-exposed employees (49).
Bactjer, ct al., in a study for the Allied Chemical Company,
found that 19 of the 27 deaths occuring in this population between i960
-------
and 1972 were due to cancer as compared to an expected number,
bas',d on fibres adjusted for age, race, and sex, of 7. 3 cancer-
related deaths (50)-.
Additional medical problems relating to arsenic content of drinking
water have been reported from several other countries. Several
epidemiological studies in Taiwan (51-55) have reported the correlation
between increased incidence of hyperkeratosis and skin cancer with
the consumption of water with arsenic content higher than 0. 3 mg/i.
A similar problem has been reported in Argentina (56-58). Dermato-
logical manifestations of arscnicism were noted in children of .Antofagasto,
Chile, who used a water supply with 0. 8 mg/1. A new water supply
was provided, and preliminary data show that arsenic levels of hair
have decreased, and further study will be made of the health of persons
born since the change in supply (59). Arscnicism affecting two members
of a family where the arsenic content of the family's well varied between
0. 5 and 2. 75 mg/1 over a period of several months, was reported
in Nevada (GO). A study in California found that a greater proportion
of the population had elevated concentrations of arsenic in the hair
when the drinking water had more than 0.12 mg/1 than when it was
below this concentration, but illness was not noted (61). In none of
the cited incidents of apparent correlation of arsenic in drinking water
with increased incidence of hyperkeratosis and skin cancer has there
been any confirmed evidence that arsenic was the etiologic agent in
the production of carcinomas.
-------
Arsenic is a geochemical pollutant, and when it occurs in an area
it can be expected to be in the air, food, and water, but in other
cases it is due to industrial pollution. In some epidemiological-
studies it is difficult to determine which exposure is the greater
problem. A recent study (62) of metallic air pollutants showed that
arsenic levels of hair were related to exposure from this source,
but other exposures were not qur.ntitated. The Taiwan studies were
able to compare quite similar populations that differed only in the
water intake. Deep wells contained arsenic, but persons using
shallow welts were not exposed.
The change in water supply in Chile provided a unique experience
to demonstrate the effect of arsenic in drinking water in spite of
other arsenic exposures.
It is estimated that the total intake of arsenic from food is an
average of 900 ug/day (5). At a concentration of 0.05 mg per liter
and an average intake of 2 liters of water per day, the intake from
water would not exceed 100 pg per clay, or approximately 10 percent
of the total ingested arsenic.
Di light of our present knowledge concerning the potential health
hazard from the ingeslion of arsenic, the concentration of arsenic
bi the drinking water shall not exceed 0.05 mg/1.
-------
REFERENCES
1. Underwood, E.J., Trace Elements in Hum.'ui and Animal Nutri-
tion. New York; Academic Press, Inc., 195G, pp. 372-364.
2. Mor.ier-Williams, G.W.: Trace Elements in Food. New York:
John Wiley & Sons, Inc., 1949, pp. 1C2-20G.
3. Quantities of Pesticides Used by Farmers in 19G4. Agriculture
Economic Report No. 131, Economic Research Service, U.S.
Department of Agriculture, 1968.
4. Sollman, T. (ed.) in A Manual of Pharmacology and its Appli-
cations to Therapeutics and Toxicology. Philadelphia: W. D.
Saunders Co., 1957.
5. Schroeder, H.A., and Balassa, J.J. Abnormal Trace Metals
in Man. J. Chron. Pis. 19, 85-106, 1966.
6. Code of Federal Regulations, Title 21, Sections 120. 192/3/5/S
and 133g. 33.
7. Coulson, E.J., Remington, R. E. , and Lynch, K.M. Metabolism
in the Rate of (lie Naturally Occurring Arsenic of Shrimp as
Compared with Arsenic Trioxide. J. Nutrition, 10, 255-270,
1935.
8. Ellis, M.M., Westfal!, B.A., and Ellis, M. D. Arsenic iji
Freshwater Fish. Indust. and Engineer Ciioin., 33, 1331-1332,
1941 (Experimental Station Report 87, p. 740, 1941).
9. Air Pollution Measurements of the National Air Sampling Net-
work - Analyses of Suspended Parliculates 1963, U.S. Depl.
of Health, Education, and Welfare, Public Health Service,
Cincinnati, Ohio, 1965.
10. McCabe, L.J. , Symons, J.M., Lee, R.D., and Robcck, G. G.
Survey of Community Water Supply Systems, JAWWA, 62,
(11), 670-G87, 1970.
11. Overby, L.R., and Fredrickson, R. L. J_. Agr. Food Chom.,
\\_t 78, 1963.
12. Peoples. S.A. Ann. N. Y. Acad. Sci. , 111, 644, 1964.
66-
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13. Winkler.W.O. J. Assoc. Offie. Agr. Chemists, 4£, 80, 19G2.
14. DuBois, K.P. and Ceiling, E.M.K. Textbook of Toxicology.
Now York, N.Y., Oxford University Press, 1959, pp. 132-135.
15. Hunter, F.T., Kip, A. F., and Irvine, J.W. Radiotracer Studies
on Arsenic Injected as Potassium Arsenite: I. Excretion and
Localization of Tissues. J. Pharmacol. Expcr. Thcrap., ]Q
207-220, 1942.
1C. Lowry, O.H., Hunter, F.T., Kip. A. F., and Irvine, J.W.
Radiotraccr Studies on Arsenic Injected as Potassium Arsenile:
II. Chemical Distribution in Tissues. J^ Pharmncol. Exper.
Thcrap. 76, 221-225, 1942.
17. Dupont, O., Ariel, I., and Warren, S. L. The Distribution of
Radioactive Arsenic in Normal and Tumor-Bearing Rabbits.
Am. J. Syph. 26, 96-118, 1942.
18. Duncoff, U.S., Neal, W.B., Straube, R. L., Jacobson, L.O.,
and Brues, A.M. Biological Studies with Arsenic: n. Excretion
and Tissue Localization. Proc. Soc. Expcr. Biol. Med. 69,
548, 1948.
19. Musil, J. and Dejmal, V. Experimental and Clinical Administra-
tion of Radioarsenic. Casopis lek. ccsk. 06, 1543-6, 1957;
Chcm. Abstr. 14008, 1958.
20. Creina, A. Distribution et elimination de 1'arsenic 76 chez la
souri.s normale ct cancereusc. Arch. Internal. Pharmacodyn.
103. 57-70, 1955.
21. Sollmnn, 1921. Cited in Sollmann T. (cd.) in a Manual of
Pharmacology nnd Its Application to Therapeutics and Toxicology.
Philadelphia: W.B. Saunders Co., 1948, p. 874.
22. Schroedcr, H.A. nnd Bainssa, J.J. Arsenic, Germanium, and
Tin in Mice. .). Nutrition, j)2, 245, 1967.
23. Kanisawa, M. and Scliroeder, H.A. Life Term Studies on the
Effects of Arsenic, Germanium, Tin, and Vanadium on Spon-
taneous Tumors in Mice. Cancer Research 27, 1192, 1967.
24. Scliroeder, H.A., Kanisawa, M., Frost, D. V., and Milchcner,
M.N. Nutr. 96, 37, 1968.
-------
25. Byron, W.R., Bicrlx)\vor, Ci. \V., Brouwer, J.B., and
Hansen, W.H. Tux. Appl. Pliarmacol, 10(1): 132-147, 19G7.
26. Hesse, E. Klin. Wehnschr. 12, 10GO, 1933.
27. DuDois, K. P., Moxon, A. L., and Olson, O. E. Further
Studies on the Effectiveness of Arsenic in Preventing Selenium
Poisoning. J. Nutrition 19, 477-482, 1940.
28. Moxon, A. L. The Influence of Arsenic on Selenium Poisoning
in Hops, in Proceedings of the South Dakota Academy of Sciences,
1941, vol. 21, pp. 34-36.
29. Calvary, H.O. Chronic Effects of Ingested Lead and Arsenic.
J.A.M.A. Ill, 1722-1729, 1938.
30. Goodman, L. S. and Oilman, A. (eds.) The Pharmacological
Basis of Therapeutics, 3rd Edition. New York, N. Y., The
MacMillan Co., 19G5, pp. 944-951.
31. DiPalma, J.R. Drill's Pharmacology in Medicine, 3rd Edition.
New York, N.Y., McGraw-Hill Book Company, 1965, pp. 860-862.
32. Birmingham, D.J. , Key, M.M., and Holaday, D. A. An
Outbreak of Dcrmatoses in a Mining Community - Report of
Environmental and Medical Surveys. U.S. Dcpt. of Health,
Education, and Welfare, TR-11, April, 1954.
33. Birmingham, D.J., Key, M.M., Holaday, D. A., and PC rone,
V.B. An Outbreak of Arsenical Dermatosiis in a Mining
Community. Arch. Dermatol. 91, 457, 19G5.
34. Paris, J.A. Pharmacologia: Comprehending (lie Art of
Prescribing upon Fixed and Scientific Principles Together
With The History of Medicinal Substances, 3rd Edit., p. 132,
London: Philips, 1820.
35. Buchanan, W. D. Toxicity of Arsenic Compounds. New Jersey:
Van Nostrand, 1962.
36. Frost, D.V. Arscnicals in Biology - Retrospect and Prospect.
Federation Proceedings 26, 184, 1967.
37. Sommers, S.C. and McManus, R. G. Multiple Arsenical Cancers
of Skin and Internal Organs. Cancer G, 347-359, 1953.
38. Snegireff, L. S., and Lombard, O.M. Arsenic and Cancer.
Arch. Industr. t'lyg. Occupational Mcd. 4, 199, 1951.
-------
39. Pinlo, S.S. , and Dennett, B. M. Effect of Arsenic Trioxidc
Exposure on Mortality. Arcn. Environ. Health 7, 583, 1963.
•10. Daroni, C. , Van Esch, G. J., nnd Saffiotti, U. Carcinogenesis
Tests of Two Inorganic Arsenicals. Arch. Environ. Health 7,
C88, 1963.
41. Boutwcll, R.K. J. Agr. Food Chom. II, 381, 1963.
42. Hucper, W. G., and Payne, W.W. Arch. Environ. Health 5,
445, 1962.
<1J. Milner, J.E. The Effect of Ingested Arsenic on Methylchol-
anthrene-Induced Skin Tumors in Mice. Arch. Environ. Health,
18, 7-11, 1969.
44. Hill, A. B., Failing, E. L., Perry, F., Bowler, R. G.,
Buckncll, H.M., Druett, H.A., and Schilling, R.S.F.
Studies in the Incidence of Cancer in a Factory Handling Inorganic
Compounds of Arsenic. Brit. J. Indust. Mcd. J5: 1 (1948).
45. Doll, R. Occupational Lung Cancer: A Review. "Brit. J.
Indus. Med. JM3: 181 (1959).
4G. Merewethcr, E. R. A. Industrial Medicine and Hygiene.
Vol. 3, Butterworth & Co., London, pp. 196-205(1956).
47. Neubauer, O. Arsenical Cancer: A Review. Brit, J. Cancer
J_: 192 (1947).
48. Lee, A.M. and Fraumeni, J.F., Jr. Arsenic and Respiratory
Cancer in Man--an Occupational Study. J. Natl. Cancer
Inst. 42: 1045 (1969)..
.*
49. Ott, M., Holder, B. , Gordcn, H. Respiratory Cancer and
Occupational Exposure to Arsenicals. to be published in
Archives of Environmental Health, Cilcd In: Federal Register,
40FR Pt. 3, p 3395, January 21, 19T5~!
50. Baeljer, A., Levin, M. , Lillcnfeld, A. Analysis of Mortality
Experience of Allied Chemical Plant. Cited In: Federal Register,
4OFF. Part 3, p. 3395, January 21, 1975.
51. Tseng, W. P., Chu, H.M., How, S.W., Fong, J.M., Lin, C. S.,
and Ych, S. Prevalence of Skin Cancer in an Endemic Area of
Chronic Arsenicism in Taiwan. J. Nat. Cancer Inst., 40, 454, 1968.
-------
52. Clion, K. P., Wu, H. , and V.'u, T. Epidcriuologic Studies on
Dlackfoot Disease in Taiwan: 3. Physiochemical Characteristics
of Drinking Water in Endemic Blackfoot Disease Areas. Memoirs
of the College of Medicine, 'National Taiwan University, Vol. Ill,
No. I, 2, pp. 116-129, 1962.
53. Wu, H., and Chen, K. Epidemiologic Studies on Blackfoot
Disease: 1. Prevalence and Dicidence of the Disease by Ag£,_
Sex, Year, Occupation, and Geographic Distribution. Memoirs
of the College of Medicine, National Taiwan University, Vol. Ill,
No. 1, pp 33-50, 1961.
54. Yell, S., How., S.W., and Lin, C. S. Arsenical Cancer of the
Skin. Cancer 21, 312-339, 1968.
55. Chen. K., and Wu, H. Epidemiologic Studies on Blackfoot
Disease: 2. A Study of Source of Drinking Water in Relation
to the Disease, J. Formosan Mcd. Assoc. 61, (7), 611-617, 1962.
56. Arquello, R.A., Ccnget, D. D., and Telo, E. E. Cancer y
arscnicismo regional endemico el Cordoba. Rev, argent.
dcsmoltosif, 22, 461-487 (1938).
57. Bergoglio, R.M. Mortalidad por cancer cn/onas do aquas
arsenicales dela Pro vine ia do Cordoba, Rcpublica Argentina.
Prcnsa. Mcd. Agent, 5±, 99-998 (1964).
58. Trelles, Larghi and Daiz. El problema sanilarro do las aquas
destinadas a In bebida humana con contenidos elcvades de
arsenico, vanadio, y flos, Saneamienta. Jan-March 1970.
59. Borgono, J.M., and G-'cibcr, R. Epidemiological Study of
Arsenicism in tlie City of Antofagasto. Proceedings of the
University of Missouri's 5th Annual Conference on Trace Sub-
stances in Environmental Health (in press).
60. Craun, G. and McCabc, L. J. Waterbornc Disease Outbreaks,
1961-1970. Presented at the Annual Meeting of the American
Water Works Association, June 1971.
61. Goldsmith, J.R., Deane, M. , Thorn, J., and Gentry, G. ,
Evaluation of Health Implications of Elevated Arsenic in Well
Water. Water Research, 6, 1133-1136, 1972.
62. Hammer, D. I. , Finklca, J. F. , Hendricks, R. H., Shydral, C. M. ,
and Horton, R. J. M. Hair Trace Metals Levels and Environmental
Exposure. Am. Jour, of Epidemiology, 93, 84-92 (1971).
70 <
-------
BARIUM
Barium is recognized as a genera! muscle stimulant, including
especially the heart muscle (1). The fatal dose for man is considered
to be from 0.8-0.9 g as the chloride (550-600 mg Ba). Most
fatalities have occurred from mistaken use of barium salts incorporated
in rat poison. Barium is capable of causing nerve block (2) and in
small or moderate doses produced transient increase in blood pressure
by vasoconstriction (3). Aspirated barium sulfate has been reported
to result in granuloma of the lung (4) and other sites in m;ui (5).
Thus, evidence exists for high acute toxicity of ingested soluble
barium salts, and for chronic irreversible changes in tissues result-
ing from the actual dcpostion of insoluble forms of barium in sufficient
amounts at a localized site. On the other hand, the recent literature-
reports no accumulation of barium in bone, muscle, or kidney from
experimentally administered barium salts in animals (6). Most of
the administered dose appeared in the liver with far lesser amounts
in the lungs and spleen. This substantiates the prior finding of no
measurable amounts of barium in bones or soft tissues of man (7).
Later, more accurate analysis of human bone (British) showed 7 ug
Ba/g ashed sample (8), but no increase in bone barium occurred from
birth to death. Small amounts of barium have been shown to go to
the skeleton of animals when tracer amounts of barium-140 were used
(9), but no determinations of barium have been made in animals to
which barium had been repeatedly administered for long periods.
71.'-
-------
No study appears to have been made of the amounts of barium
that may be tolerated in drinking water or of effects from prolonged
feeding of barium salts from which an acceptable water guideline
may be set. A rational basis for a watei guideline may be derived
from the threshold limit of 0.5 mg Da/m3 ;ar set by the American
Conference of Governmental Industrial Hygienists (10) by procedures
that have been discussed (11). By assuming that 75f/o of the barium
inhaled is absorbed into the blood stream and that 90'c is a reason-
able factor for absorption via the gastrointestinal tract, a value of
2 ing/1 con be derived as an approximate limiting concentration for
a healthy adult population. The introduction of a safety factor to
account for heterogeneous populations results in the derivation of
1 mg'1 as a limit that should constitute a "no effect" level in
water. Because of the seriousness of the-toxic effects of barium
on the heart, blood vessels, and nerves, drinking water shall not
contain barium in a concentration exceeding 1 mg/1.
f C"-
-------
REFERENCES
1. Sollman. T.H. (Ed.) A Manual of Pharmacology. W. B. Saundcrs
Co.. Philadelphia, pp. G65-667 (1957).
2. Lorcntc do No, K.. and Feng, T.P. Analysis of Effect of
Barium upon Nerve with Particular Reference to Rhythmic
Activity. J. Cell Comp. Physiol. 28: 397 (1946).
3. Gotscv. T. Bluldruck und Hcrztatigkeit. Ill Mitteilung:
Kreislaufwirkung von Barium. Naunyu Schiedebcrg Arch.
Expcr. Path. 203: 2G4 (1944).
4. File, F. Graiiulorna of Lung Due to Radiographic Contrast
Medium. AMA Arch. Path. 59: 673 (1955V
5. Kay S. Tissue Reaction to Barium Sulfatc Contrast Medium.
A MA Arch. Path. 5_7: 279 (1954). Ibid: Kay S., and
Chay. Sun Hak: Results of Intrapcritoncal Injection of Barium
Sulfate Contrast Medium 59: 388 (1955).
6. Arnolt, R.I. Fijacion y determinacion quimica del bario en
organos. Rev. Col. Farm. Nac. (Rosario) 7: 75 (1940)
7. Gcrlach, W., and .Muller, R. Occurrence of Strontium and
Barium in Human Organs and Excreta. Arch. Paiii. Anat.
(Virchows) 294: 210(1934).
8. Sowc'e:'., W., anci Stitch, S.R. Trace Elements in Human Tissue.
Estimation of the Concentrations of Stable Strontium and Barium
in Human Bone. Biochem. J. Ql_: 104 (1957).
9. Bauer. G.C.H.. Carlsson. A., and Lindquist, B. A Compara-
tive Study oi Metabolism of 140 Ba and 45 Ca in Rats. Biochem.
J. G3: 535 (195G).
10. American Conference of Governmental Industrial Hy^icnists.
Theshold Limit Values of 195b. A.M.A. Arch. Indust.
Health 18: 178 (1958).
11. SlokiMiAcr. H.E:. and Woodward, R.L. Toxicolo^ic Methods
for E:;(abiis!iintr Drinking Water Standards. JAWWA
50: 5l!i (1U58J
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CADMIUM
As far as is known, cadmium is biologically a noncsscntial, non-
beneficial element of high toxic potential. Evidence for the serious
to:;ic potential of cadmium is provided by: (a) poisoning from cadmium-
contaminated food (1) and beverages (2); (b) euidemiologic evidence
that cadmium may be associated with renal arterial hypertension
under certain conditions (3); (c) epidemiologic association of cadmium
with "Itai-itai" disease in Japan (4); and (d) long-term oral toxicity
studies in animals.
The possibility of cadmium being a water contaminant has been
reported in 1954 (5); seepage of cadmium into ground water from
electroplating plants h;.s resulted in cadmium concentrations ranging
from 0.01 to 3.2 mg/1. Other sources of cadmium contamination in
water arise from zinc-galvanized iron in which cadmium is a con-
taminant. The average concentration of cadmium in drinking water
from community supplies is 1.3 ug per liter in (lie United Stales.
Slight amounts are common, with G3 percent of samples taken at
household taps showing 1 ug per liter or more. Only 0.3 percent
of lap samplus would be expectc-d to exceed the limits of 10 ug
per liter (6).
Several instances have been reported of poisoning from eating
substances contaminated with cadmium. A group of school children
were made ill by eating popsiclcs containing 13 to 15 mg/1 cadmium (1).
\
7-i -
-------
This is commonly considered the emetic threshold concentration
for cadmium. It has been slated (7) that the concentration and not
the absolute amount determines the acute cadmium toxicity; equivalent
concentrations of cadmium in water are likewise considered more
toxic than equivalent concentrations in food probably because of the
antagonistic effect of components in the food.
Chronic oral toxicity studies in rats, in which cadmium chloride
was added to various diets at levels of 15, 45, 75, and 135 ppm
cadmium, showed marked anemia, retarded growth, and in many
instances death at the 135 ppm level. At lower cadmium levels,
anemia developed later; only one cadmium-fed animal had marked
anemia at the 15 ppm level. Bleaching of the incisor teeth occurred
in rats at all level.-,, except in some animals at 15 ppm. A low protein
diet increased cadmium toxicity. A maximal "no effect" level was
thus not established in the above studies (8). A dietary relation to
cadmium toxicity has been reported by others (9).
Fifty mg/1 of cadmium administered as cadmium chloride in food
and drinking water to rats resulted in a reduction of blood hemoglobin
ami lessened dental pigmentation. Cadmium did not decrease experi-
mental caries (10).
In a study specifically designed to determine the effects of drinking
water contaminated \vith cadmium, five groups of rats were exposed
to drinking water containing levels from 0. 1 to 10 mg/1. Although
-------
no effects of cadmium toxicity were noted, the content of cadmium
in the kidney and lii-er increased in direct proportion to the dose
at all levels including 0.1 mg/1. At the end of one year, tissue
concentrations approximately doubled those at six months. Toxic
effects were evident in a three-month study at 50 mg/1 (11). Later
work has confirmed the virtual absence of turnover of absorbed
cadmium (12). More recently, tho accumulation of cadmium in ronal
and hepatic tissue with age has been documented in man (13).
Recent epidemiological evidence strongly suggests that cadmium
ingestion is associated with a disease syndrome referred to as
"Itai-itai" in Japan (4). The disease syndrome is characterized
by tlecalcification of bones, proteinuria, glycosuria and increased
serum alkaline phosphatase, and other more subjective symptoms.
Similar clinical manifestations have been noted in cadmium workers
(14). Yamagatta and Shigematsu (15) have estimated the current
daily intake of cadmium in an endemic "Ilai-Hai" area as 600 >ug.
The authors from a geological and topographical survey as well as
knowledge of local customs, concluded that the daily cadmium intake
in the endc.viic area was probably higher in the past. They concluded
(.hat GOO ug per day would not cause "ftai-itai" disease. The average
ingestion of cadmium is 59 ^ig/day in non-polluted areas of Japan.
-------
The association of cardiovascular disease, particularly hyper-
tension, with ingest ion of cadmium remains unsettled. Conflicting
evidence has been found both in man (3, 1C) and in animals (17, 18).
It is notable that hypertension has not been associated with "Itai-itai"
disease (19).
The main sources of cadmium exposure in the United States to
the general population appear to be the diet and cigarette smoking.
R.E. Duggnn and P. E. Corneliussen (20) of the FDA in a market
basket survey of five geographic regions in the U.S. found the "daily
intake" of cadmium to be 50 pg in I960 and 3C^ig in 1970. Each
market basket represented1 a 2-week diet constructed for a 16-19 year-
old male. Murtl;y and associates found the cadmium intake of children
to be 92 ug per day from a study of institutional diets (21). Other
estimates are also generally higher than FDA's — ranging from 67 to
to 200,ug/day. A review of these data suggest 75 jug as a reasonable .
estimate of average daily dietary intake (22, 23, 24, 25).
Cigarette smoking has also been shown to be important. Twenty
cigarettes per day will probably cause the inhalation of 2-4 ^g of
cadmium (26). However, the absorption rate associated with cigarette
smoke inhalation is much larger than that associated with food ingestion.
Lewis (27) has shown in autopsy studies that men who smoke one
or more packages of cigarettes per day have a mean cadmium
concentration in the renal cortex (wet weight) double the level in a
control group of non-smokers. Hammer (24) in similar studies also
77--
-------
found renal wet weight concentrations for those smoking 11/2 or
more packages of cigaretts per day to be more than twice as high as
for non-smokers. In terms of effective body burden, then, cigarette
smoking may double the level derived from food intake alone.
Exactly what exposure to cadmium will cause proteinuria, the
earliest manifestation of chronic cadmium poisoning, is unknown.
From animal experiments and very limited human observation in
cases of industrial exposure, it is believed that a cadmium level
of 200 ppm wet weight in the renal cortex will be associated with
proteinuria. (However, it should be noted that in one case a level
of 446 ppm was found by Axelsson and Piscator without proteinuria)
(29). It has been estimated that with 5% gastrointestinal absorption,
rapid excretion of 10% of the absorbed dose, and 0. 05% daily excretion
of the total body burden, it would take 50 years with a daily ingeslion
of 352 ^g of Cd to attain the critical level of 200 ppm wet weight
in the renal cortex. The percentage absorption in man is unknown.
If the gastrointestinal absorption of cadmium in man roally is about
3%, it would probably take about 500-600 .ug ingested per day to
cause proteinuria.
Concentration of cadmium shall be limited to 0.010 mg/1 in drinking
water. At this level it would contribute 20/ig per day to the diet of a
person ingesting 2 liters of water per day. Added to an assumed diet
of 75 jug/day, this would provide about a four-fold safety factor. This
does not, however, take cigarette smoking into account.
-------
REFERENCES
1. Frant, S. , and Kleeman, I. Cadmium "Food Poisoning" J. A. M. A.,
117,86 (1941).
2. Cangelosi, J.T. Acute Cadmiuin Metal Poisoning. U.W. Nav.
Mod. Bull., pp. 39 and 408 (1941).
3. Schroeder, H.A. Cadmium as a Factor in Hypertension, J.
Chron. Dis. 18, G47-G.M5 (1965).
4. Murata, I., Hirono, T., Saeki, Y., and Hakagawa, S. Cadmium
Enteropalhy, Renal Osteomalacia ("llai-ilai" Disease in Japan).
Bull. Soc. Int. Chir. 1, 34-42 (1970).
5. Liebcr, M., and Wclscli, W. F. Contamination of Ground Water
by Cadmium. J. A.W. W. A., 46, p. 51 (1954).
G. McCabc, L. J., Problem of Trace Metals in Water Supply.
Proceedings of IGth Animal Sanitary Engineering Conference,
University of Illinois (1974).
7. Potts, A.M., Simon, F. P. , Tobias, J.M. , Postel, S. , S-.vift, M.N.,
Pntt, J.M., and Gcrlad, R.W. Distribution and Fate of Cadmium
in the Body. Arch. Ind. Hyg. 2, p. 175 (1950).
8. Fit/.hugh, O. G., and Mcillp", F.J. Chronic Toxicity of Cadmium.
J. Pharm. 72 p. 15 (1941).
9. Wilson, R.H. , and De Eds, F. Importance of Diet in Studies
of Chronic Toxicity. Arch. Ind. Hyg. 1, p. 73(19500).
10. Ginn, J.T., and, Volker, J.F. Effect of Cd and F on Rat Dentition.
Proc. Soc. Exptl. Biol. Mecl. 57, p. 189 (1944).
11. Decker, L. E., Bycrrum, R. U., Decker. C. F. . Hoppcrl, C.A.,
ar.d Langham, R. F. Chronic Toxicity Studies, I. Cadmium
Administered in Drinking Water 1. Rats. A.M.A. Arch. Ind.
Health, 18, p. 228(1958). >-,-
12. • Col/.ias, G.C., Borg, D.C., and Selleck, B. Virtual Absence
of Turnover in Cadmium Metabolism: Cd Studies in the
Mouse. J. Physiol. 201, 927-930 (1961).
13. Schroeder, H.A., Balassa, J.J., and Hogencamp, J.C.
Abnormal Trace Metals in Man: Cadmium. J. Chron. Dis.
14, 236-258 (19G1).
75)-
-------
14. Picsnlor, M. Protoinuria in Chronic Cadmium Poisoning.
I. An Electrophoretic and Chemical Study of Urinary and Scrum
Proteins Troni Workers with Clironic Cadmium Poisoning.
Arch. Environ. Health 4, 607-G21 (19G2).
15. Yamaha-la, N., and Shigematsu, I. Cadmium Pollution in
Perspective. Bui. Inst. Public Health 19, 1-27 (1970).
16. Morgan, .I. M. Tissu Cadmium Concentration in. Man. Arch.
Intern. Med. 123, 405-408 (1969).
17. Kanisawa, M. and Schroeder, J.A. Renal Arteriolar Changes
in Hypertensive Rats Given Cadmium in Drinking Water.
Exp. & Mole. Path. 10, 81-98 (1969).
18. Lener, J. and Dibr, B. Cadmium Content in Some Foodstuffs
bi Respect of It.', Biological Effects. Vitalstoffe Zivilisations-
drankhoitcn 15, 139-141 (1970).
19. Nogawa, K., and Kawano, D. A Survey of The Blood Pressure
of Wom»n Suspected of Itai-itai Disease. Juzen Med. Soc. J.
77, 357-363 (1969).
20. Duggan, R. E. and Corncliusscn, P.E., Dietary Intake, cf Pesticide
Chemicals in the United Slates (HI), June 1968-Apri! 1970, Pest.
Mon. Journal. , _5, No. 4, 331-341 (March 1972).
21. Murthy, G. K., Rhea, U. and Peeler, J.T. , Levels of Antimony,
Cadmium, Chronium, Cobalt, Manganese and Zinc in Institutional
Total Diets, Env. Sc. and Tech. , 5 (5): 436-442 (May 1971).
22. Kirkpatrick, D. C., and Coffin, D. ? . 7"hc Trace Metal-Content
of Representative Canadian Diets in 1970 and 1971. Can. ~fiist;
Food Sci. TcchnoL J. T. 56 (1974).
23. Merangcr, J., and Smith, D. C. The Heavy Metai Content of
a Typical Canadiann Diet. Can. J. Of Pub. Health., i6_3: 53 (1972).
24. Schrocderm, H.A., Nason, A.P., Tipton, I.H., and Balnssa, J.J.,
essential Trace Metals in Man: Zinc Relation to Environmental
Cadmium, J. Chron. Diseses ^0: 179 (1967).
25. Tipton, I.H., and Stewart, P. L., Analytical Methods for the
Determination of Trace Elements-Standard Man Series. Proc.
Univ. Missouri 3rd Ann. Conf. on Trace Substances in Environmental
Health, 1969, Univ. of Missouri, Columbia, Mo. (1970).
26. Fribcrg, L., Piscator, M., and Nordrlberg, D., Cadmium in Pie
Environment, Chemical Rubber Company Press, Cleveland, Ohio
p. 25 (1971).
-------
27. Lcnvis, G. P., Jusko, W.J., Om^hlin, L. L. and Hartz, S. ,
Cadmium Accumulation in Man: Im'lucncc of Smoking, Occupation,
Alcoholic Habit and Disease. J. Chron. Pis., 25, 717 (1972).
28. Hammer, D. I., Calocci, A.V. , Hasselblad, V., Williams, M. E.
and Pinkerton, C. Cadmium and Lead in Autopsy Tissues, Jour.
Occ. Mcd., _lj>, No. 12 (Dec. 1973),
29. Fribcrg, L., Piscator, M. and Nordberg, G., Cadmium in
The Environment, Chemical Rubber Company Press (1971), p. 85.
-------
CHROMIUM
Chromium, particularly in the hexavalent stale, is toxic to mail,
produces lung turners when inhaled, and readily induces skin sensitiza-
tions. Chromium occurs in some foods, in air including cigarette
smoke, and in some water supplies (see Table I). It is usually in
an oxidized state in chlorinated or aerated waters, but measurements
for total chromium are easily made by atomic absorption,/so the some-
what conversative total value is used for this guideline.
.-.
TABLE I
U.S. urban air concentrations range, 1965 ^1)'.........'.. .0-0.028 >ig/ms
Chromium content in cigarette tobacco (2) 1.4 ug/cigarette
Chromium in foods cooked in stainless-steel ware (3) 0-0.35 mg/100 g
Chromium concentration range in water supplies 1969 (4). . . .0-0.08 mg/i
Comparatively little data are available on the incidence and frequency
of distribution of chromium in foods. Although most information has
limited applicability, one study (5) determined the occurrence of chromium
and oilier elements in institutional diets. In that investigation, the
concentrations of chromium in foods ranged from 0.175 to 0.470 mg/kg.
9
Chromium lias not been proved to bo an essential or a beneficial
element in the body. However, some studies suggest that chromium
may indeed by essential in minute quantilies (5,6,7). At present, the
levels of chromium that can be tolerated by man for a lifetime without
adverse effects on health arc still undetermined. A family of four
-------
individuals is known to have drunk water for periods of 3 years at a
level as high as 0.45 milligrams chromium per liter without known
effects on their health, as determined by a single medical examina-
tion (8).
A study by MacKenzie et a_l (8) was designed to determine the
toxicity to rats of chromate (Cr+t') and chromic (Cr*3) ion at
various levels in the drinking water. This study showed no evidence
of toxic responses after one year at levels from 0.45 to 25 mg/1
by the tests employed, viz., body weight, food consumption, blood
changes, and mortality. Significant accumulation of chromium in
the tissues occurred abruptly at concentrations above 5 mg/1;
however, no study has been made of the effects of chromium on a
cancer-susceptible strain of animal. Recent studies demonstrated
that 0.1 mg of potassium dichromate per kg enhances the secretory
and motor activity of the intestines of the dog (10).
From these and other studies of toxicity (11-15), if. would
appear that a concentration of 0.05 mg/1 of chromium incorporates
a reasonable factor of safety to avoid any hazard to human health.
In addition, the possibility of dermal effects from bathi;;::: in
water containing 0.05 mg/1 would likewise appear remote,
although chromium is recognized as :\ potent sensitizer of the
skin (3). Therefore, drinking water shall not contain more than
0.05 mg/1 of chromium.
-------
REFERENCES
1. U.S. l>ublic Health Service, National Air Pollution Control
Administration. Preliminary Air Pollution Survey of Chromium
and its Compounds. A Literature Review. U.S. Dept. of
Commcrc-e, National Bureau of Standards, Clearinghouse of
Federal Scientific and Technical Information, Springfield, VA,
22151.
2. Cogbill, E.C.. and Hobbs, M.E. Transfer of Mctullic Con-
stituents of Cigarettes to the Main-stream Smoke. Tobacco
Sci. 144: 68 (1957).
3. Demon, C.R.. Keenan, R.G.. and Birmingham, D.G. The
Chromium Content of Cement and Its Significance in Cement
Dermatitis. J. Invest. Derm. 23: 184 (1954).
4. McCabo, L..J., Symons, J.M., Lee, R.D., and Robcck, G.G.
Survey of Community Water Supply Systems. JAWWA.
62: 670 (1970).
5. Murthy, G.K.. Rhoa, U., and Peeler, J.T. Levels of Antimony,
Cadmium, Chromium. Cobalt, Manganese, and Zinc in Institu-
tional Diets. Envir. Sci. Technol. 5: 436 (1971).
6. Schroeder. H.A., Dalassa. J.J., and Tipion, I.H. Abnormal
Trace Metals in Man - Chromium. J. Chron. Disease 15: 941
(1962). . ~"
7. Hopkins. L.L. Chromium Nutrition in Man. Proceedings of
Univ. of Missouri's 4th Annual Conference on Trace Substances
in Environmental Health, pp. 285-289 (1970).
8. Davids. H.W., and Liebcr, M. Underground Water Contamina-
tion by Chromium Wastes. Water Sewage Works £8: 528
(1051). ~
9. MacKon/.ic, R.D., Bycrrum. R.U., Decker, C.F., Hoppcrt. C.A.,
and Langham, R.F. Chronic Toxicity Studies II Hexavalent
and Trivalent Clu-omium Administered in Drinking Water to
Rats. A.M.A. Arch. Industr. Health 18: 232(1958).
10. Naumova, M.K. Effect of Potassium Bichromate on Secretory
and Motor Activity of Intestine. Gigicna Truda I Professional
'nye Zabolcvaniya 9: 52 (1965).
-------
11. Gross, W.G., and Hcllor, V.G. Chromates in Animal Nutrition.
J. Imlust. Hyg. Toxicol. 28: 52 (1946).
12. Brarcl, M.D. Study of Toxicology of Some Chromium Compounds.
J. Pharm. Chim. 21_: 5 (1935).
13. Conn, L.W., Webster, H.L., and Johnson, A.II. Chromium
Toxicology. Absorption of Chromium by The Rat When Milk
Containing Chromium Lactate was Fed. Fed. Am. J. Hyg. 15:
7GO (1932). ~~
14. Schroeder, H.A., Vinton, W.H., and Dalassa, J.J. Effect
of Cliromium, Cadmium, ajid Oilier Trace Metals on The
Growth and Survival of Mice. J. Nutrition 80: 39 (1965).
15. Schroeder, H.A., Vinton, W.H. ;md Balassa, J.J. Effects
of Chromium, Cadmium, and Lead on The Growth and
Survival of Rats. J. Nutrition 80: 48 (1965).
-------
CYANIDE
Cyanide in reasonable doses (10 mg or loss) is readily converted
to Ihiocyanate in the human body and is thus much less toxic for man
than fish. Usually, lethal toxic effects occur only when the de-
toxifying mechanism is overwhelmed. The oral toxicity of cyanide
for man is shown in the following table.
Oral Toxicity of Cyanide for. Man
Literature
Dosage Response Citations
2.9-4.7 mg/1 Noninjurious (1)
10 nig, single dose Noninjurious (2)
10 mg/1 in water Calculated from threshold (3)
limited for air to be safe
50-GO nig, single dose Fatal (4)
Proper clilorination to a free chlorine residual under neutral
or alkaline conditions will reduce cyanide to very low levels.
The acute oral loxicity of cyanogen chloride, (lie clilorination
product of hydrogen cyanide, is approximately o:
-------
REFERENCES
1. Smith, O.M. The Uctccticn of Poisons in Public Water Supplies.
Water Works Eng. i/7: 1293 (1944).
2. Dodansky, M., and Levy, M.D. I: Some Factors Influencing
the Deloxication of Cyanides in Health and Disease. Arch. Int.
Mod. 3J_: 373 (1923)."
3. Stokinger, II.E., and Woodward, R.L. Toxicologic Methods
for Establishing Drinking Water Standards. JAWWA
50: 515 (1958).
4. Aimon. The Merck Index. Ed. 6. Merck & Co. Die., Railway, N.J.
p. 508 (1952).
5. Spec-tor, W.S. Handbook of Toxicology. Tech. Rpt. No. 55-16,
Wright-Patterson Air Force Base, Ohio, Wright Air, Devel.
Center, Air Res. and Devcl. Comnnnd, (1955).
-------
FLUORIDI-:
The Food and Nutrition Board of the National Research Council
has stated that fluoride is a normal constituent _•: all diets and is
an essential nutrie'.U (1). In addition, fluoride in drinking water
will prevent denial caries. When the concentration is optimum,
no ill effects will result, and the caries rate will be GO-U5 percent
below the rates in communities with little or no fluoride (2,3).
Excessive fluoride in drinking water sjpplics produces
objectionable dental fluorosis which increases with increasing
fluoride concentration above the recommended upper control limits.
/
In the United States, this is the only harmful effect observed to
result from fluoride found in drinking water (4,5,6,7,0.9,10,11).
Oilier expected effects from excessively high intake levels are:
(a) bone changes when water containing 8-20 mg fluoride per liter
(8-20 mg/1) is consumed over a long period of time (7); (b) crippling
fluorosis when 20 or more mg of fluoride from all sources is con-
sumed per day for 20 or more years.(12); (c) death when 2,250-
4, 500 mg of fluoride (5,000-10,000 mg sodium fluoride) is consumed
in a single dose (7).
The optimum llvoride level (see Table 1) for a given community
depends on climatic conditions because the amount of water (and
consequently tiie amount of fluoride) ingested by children is primarily
influenced by air temperature. This relationship was first studied
and reported by Galagan and Associales in the 1950's (13,14,15,16),
-------
but has been further investigated and supported by Richards, et al
(17) in 1967. The control limits for fluoride supplementation, as
shown in Table 1, are simply the optimum concentrations for a
given temperature zone, as determined by the Public Health Service,
DHEW, from the data cited, plus or minus 0.1 mg/liter.
Many communitie ; with water supplies containing less fluoride
than the concentration shown as the lower limit for the appropriate
air temperature range have provided fluoride supplementation
(18,19,20,21). Other communities with excessively high natural
fluoride levels have effectively reduced flucrosis by partial de-
fluoridation and by change to a water source with more acceptable
f.'uoridc concentration (22,23,24).
Richard?, et al (17) reported the degree of fluorosis among
children where the community water supply fluoride content was
somewhat above the optimum v?.lue. From such evidence, it is
apparent that an approval limit (see Table 1) slightly higher than
the optimum range can be tolerated without any mottling of teeth,
so where fluoride:; arc native to the water supply, this concentra-
tion is acceptable. Higher levels should be reduced by treatment =
or blending with other sources lower in fluoride content. In such
a case, the optimum value should be sought and maintained.
-------
Annual Average of
Maximum Daily Air
Temperatures
Table 1
Recommended Control
Limits Fluoride
Concentrations in ing/1
Approval
Limit
50
53
58
63
70
79
.0
.8
.4
.9
.7
.3
F
- 53
- 58
- 63
- 70
- 79
- 90
Lower
.7
.3
.8
.6
.2
.5
1
1
0
0
0
0
.1
.0
.9
.8
.7
.6
Optimum
1.
1.
1.
0.
0.
0.
2
1
0
9
8
7
Upper
1
1
1
1
0
0
.3
.2
.1
.0
.9
.8
mg/1
2
2
2
1
1
1
.4
.2
.0
.8
.6
.4
It should be noted that, when supplemental fluoridation is
practiced, it is particularly advantageous to maintain a fluoride
concentration at or near the optimum. The reduction in dental
caries experienced at optimal fluoride concentrations will be
diminished by as much as 50?o when the fluoride concentration
is 0.2 mg/1 below the optimum. (25,26)
90<
-------
REFERENCES
1. National Research Council, Food Nutrition Board, Recommended
Daily Allowance, Seventh Revised Edition, Publication 1964,
National Academy of Sciences, Wasliington, D.C. p. 55 (19Gb).
2. Dean, H.T., Arnold, F.A., Jr. and Elvove, E. Domestic
Water and Dental Caries. V. Additional Studies of the Relation
of Fluoride Domestic Waters to Denial Caries Experience in
4,425 White Children, Age 12 to 14 Years, of 13 Cities in
4 States. Pub. Health Rep. 57: 1155 (1942).
3. DeanH.T., Jay, P., Arnold, F.A., Jr. and Elvove, E.
Domestic Water and Dental Caries. II. A Study of 2.832 White
Children Aged 12 to .14 Years of 8 Suburban Chicago Communi-
ties, Including Lactobacillus Acidophilus Studies of 1,761 Child-
ren. Pub. Health Rep. 56: 761 (1941).
4. Dean, H.T. Geographic Distribution of Endemic Dental Fluorosis
(Mottled Enamel), In: Moulton, F.R. (Ed.) Fluorine and
Dental Health, A.A.A.S. Pub. No. 19, Washington, D.C.,
pp. 6-11 (1946).
5. Dean, H.T. The Investigation of Physiological Effects by The
Epiciemioiogical Method, In: Moulton, F.R., (Ed.) Fluorine
.and DcnuJ Health, A.A.A.S. Pub. No. 19, Washington, D.C.,
pp. 23-31 (1946).
6. Dean H.T. Chronic Endemic Dental Fluorosis (Moitlcd Enamel)^
JAMA. 107: 1269 (1936).
7. Hodge, H.C., and Smith, F.A. Some Public Health Aspects
of Water Fluoridation, In: Shaw, J.M., (Ed.) Fluoridation
as a Public Health Measure, A.A.A.S. Pub. No. 33,
Washington, D.C., pp. 79-109 (1954).
8. Hey roth, F.F. Toxicologic Evidence for the Safely of Fluori-
dation of Public Water Supplies. Am. J. Pub. Health 42:
1568 (1952).
9. McClure. F.J. Fluorine in Food and Drinking Water. J.Am.
Diet. Assn. 29: 560 (1953).
10. U.S. Public Health Service National Institutes of Health,
Division of Denial Health. Natural Fluoride Content o.r
Community Water Supplies, Bethesda, MD. (1969).
-------
11. Leone, N.C., Shimkin, M.D., Arnold, F.A., Stevenson, C.A.,
Zimmerman, K.R., Geiser, P.R., and Liebermah, .I.E.
Medical Aspects of Excessive Fluoride in a Water Supply.
Pub. Health Rep. 69: 925-936 (Oct. 1954).
12. Ronolm, K. Fluorine Intoxication. A Clinical-Hygienic Study.
H.K. Lewis & Co., Ltd., London (1937).
13. Gala^an, D.J. and Lamscn, G.G. Climate and Endemic Denial
Fluorosis. Pub. Health Rep. 68: 497 (1953).
14. Gala<;an, D.J. Climate and Controlled Fluoridation. J. Am.
Dent. Assn. 47; 159 (1953).
15. Galagan, D.J., Vermillion, J.R. Determining Optimum
Fluoride Concentrations. Pub. Health Rep. 72: 491
(1957).
17, Richards, L.F., et al. Determining Optimum Fluoride Levels
for Community Water Supplies in Relation to Temperature.
J. Am. Dental. Assn. 75: (1967).
18. Peiton, W.J., and Wisan, J.M. Dentistry in Public Health
W.B. Saundcrs Co., Philadelpliia pp. 136-162(1949).
19. Arnold, F.A., Jr., Dean, H.T., Jay, P., and Knutson, J.W.
Fifteenth Year of The Grand Rapids Fluoridation Study.
J. Am. Dental Assn. G5_: 780 (1962).
20. U.S. Public Health Service. Flouridation Census 1969.
National Institutes of Health, Division of Dental Health.
U.S. Government Printing Office, Washington, D.C. (1970).
21. Maier, F.J. Twenty-five Y'»ars of Fluoridation. JAWWA
: (1970).
22. Dean, H.T. and McKay, F.S. Production of Mottled Enamel
Halted by A Change in Common Water Supply. Am. J. I>ub.
Health 29: 530 (1939).
23. Dcan,~H.T., McKay, F.S. and Klvovc, E. Mottled Enamel
Survey of Bauxite, Ark. 10 Years After A Change In The
Common Water Supply. Pub. Health Rep. 53_: 1736
(1938).
24. Maier, F.J. Partial Defluoridaiion of Water. Public Works
: (I960)..
-------
25. Chrielzberg, J .E. and Lewis, F.D., Jr. Effect of Inadequate
Fluorides in I*ublic Water Supply on Dental Caries. Ga.
Dental J. (1957).
26. Chrietzberg, J.E. and Lewis, J.F. Effect of Modifying Sub-
Optimal Fluoride Concentration in Public.Water Supply.
J. Ga. Dental Assn. : (1962).
-------
LEAD
Lead is well known for its toxicity in both acute and chronic exposures.
Kehoe (1) has pointed out that in technologically developed countries,
the widespread use of lead multiplies the risk of exposure of the
population to excessive, lead le\els. For this reason, the necessity
of constant surveillance of the lead exposure of the general popula-
tion via food, air, and water is imperative.
The clinical picture of lead intoxication has been well documented
(2). Unfortunately, the general picture of the symptoms is not
unique (i.e., gastrointestinal disturbances, loss of appetite, fatigua,
anemia, motor nerve paralysis, and encephalopathy) to lead inloxi-
cati-.m and often this has resulted in rnisdiagnosis (3,4). Several
laboratory tests that are sensitive to increased lead blood levels
have been developed for diagnostic purposes, but their relationship
to the effects of lead intoxication are incompletely understood.
The most sensitive of these is the inhibition of red cell-aminolevu-
linic acid dehydra.se (ALAD) which correlates well with blood lead
levels from 5-95/ig/lOO g blood (5,6). Because this is not the
rale-limiting step in porphyrin biosynthesis, accumulation of
aminolevulinic acid (ALA) does not occur until iiigh blood loud
levels are readied. Other such tests, which correlate with blood
"\
lead to a lesser degree and at higher levels, arc the measurement
of urinary coproporpiiyrins, the number of coarsely stippled red
.
*-,/ If
-------
blood colls and the basophilic quotient (6). These changes, in hem-
selves, have little known significance in terms of the danger to the
health of the normal individual, for although red cell life-time
can be shown to decrease (7), high lead concentrations are required
for the development of the anemia typical of lead intoxication (8).
Urinary ALA, however, has been shown to be closely related to
elevated lead levels in soft tissues (9,10) and is considered to be
indicative of a probable health risk (11).
Young children present a special case in lead intoxication, both
in terms of the tolerated intake and the severity of the symptoms
(8). Lead enccphalopathy is most common in children up to three
years of age (12). The most prevalent source of lead in these
cases of childhood poisoning lias been lead-containing paint still
found in many older homes (1,12). Prognosis of children with
lead encephalopathy is poor, with or without treatment. Up to
94f.o of the survivors have been found to have psychological abnor-
malities (13). It is still unknown whether smaller intakes of lead
without enccphalopathy or subclinical lead poisoning causes mental
retardation or psychological abnormalities. Several studies in
man and animals suggest this, (14,15, 16,17), but a well-controlled
prospective study in man lias yet to be done. ALAD in baby rats'
brains is suppressed by excess lead (18); however, the significance
of this finding to humans is unknown. Some groups of individuals
-------
who experienced lead intoxication at an early age and survived
have demonstrated a high incidence of chronic nephritis in later
life (19). Recent work has demonstrated a high _incidence of
aminoaciduria and other biochemical changes of kidney disease in
children in Boston with excessive lead exposure (17). A recent
study found anemia in children with blood levels from
37-60 ^ig/100 ml to be common (20). There is evidence that lead
in high doses in animals affects the immunological system (21,22,
23,24); this, however, lias not yet been demonstrated in man.
The average daily intake of lead via the diet was 0.3 mg in
1940 (25) and rarely exceeded O.G mg. Data obtained subsequent
to 1940 indicate that the intake of lead appears to have decreased
slightly since that time (1,26). Inhaled lead contributes about
40ro to total body burden of lead (1,27) in the average population.
Cigarette smoking in some studies in the past has also been
associated with slightly elevated blood lead levels (3).
Accumulation of lead with age in non-occupalionally exposed
individuals has been demonstrated (20,28,29). The bulk of
this lead distributes to bone, while soft tisssue levels vary only
slightly from normal even with high body burdens (30). Blood
levels vary only slightly from normal even with high body
burdens (30). Blood levels of lead in persons without unusual
exposure to lead range up to 40 ^ig/100 g and average about
2G;ug/100 g (i). The U.S. Public Health Service (31) considers
-------
40 jug/100 g lead or over in whole blood in older children and
adulis on two separate occasions as evidence suggestive of undue
absorption, either past or present. Levels of 50-79 ug/100 g
require immediate evaluation as a potential poisoning case.
Eighty jig/100 g or greater is considered to be unequivocal lead
poisoning. The 40^ig/100 g lead level in blood probably lias a
biological effect as the National Academy of Science Lead Panel
(11) concluded:
".. .the exponential increase in ALA excretion associated
with blood lead content above approximately 40/ig/lOO g
of blood signifies inhibition of ALAD thai is significant
physiologically in vivo."
In addition animal experiments show beginning renal injury at
about the same exposure level causing urinary ALA increase (32).
Blood lead is increased in urban vs. surburban (28,33,34), near
to vs. distant from large motorways (35,36) and in occupational
exposure to areas of high traffic density (37,38,39). Lead in soil
has epidemiologically been implicated in increased blood lead in
children (40).
The World Health Organization Committee (41), assuming 10r/o
of lead from food and water is absorbed, established in adults a
"Provisional tolerable weekly intake" of 3 mg of lead per person
(the maximum lead exposure the average person can tolerate without
increased body burden). (Kehoe considers 600 ug per day the limit).
-------
Assuming 10'/c absorption from the gastrointestinal tract, approxi-
mately 40 ug of load per day would be absorbed, by the WHO
standard. With the average diet containing 100-300 ug lead per
day, and the average urban air containing 1 to 3 ug/m* of air,
the average urban man would absorb 1C to 48 ug of lead per day.
(The contribution from 1 ug/m3 lead in air at 20 m respiratory
volume with 30*^ absorption is 6 ug). Just from food ajid air
alone, some urban dwellers would have excessive exposure by the
WHO standard. Urban children are further exposed by dust with
levels of over 1000 ug/g (40, 42, 43) and because airborne lead
particles vary in density inversely from the distance from tiie
ground (44,45). lUiral children have significantly less exposure
than do urban children to these sources. Additionally, children
have increased risk, because they have food and air intakes
proportionally greater than their size and they might absorb a
larger percentage from their gut, possibly 50% of ingested lead
(46). Lead might also have a greater effect on their developing
neurological, hematological, and immunological systems (18,
20-24,47,48). Likewise, fetuses of mothers unduly exposed may
be at risk (49, 51), and Mclntire concluded that there is a definite
fetal risk maximal in the first trimester from intrauterine ex-
posure to increased lead in maternal blood (52).
-------
The lead concentrations in finished water ranged from 0 to
O.G4 ing/liter in the Community Water Supply Study conducted in
19G9 (53). OI the 969 wilier supplies surveyed, 1.4'.o exceeded
0.05 mg/'Uter of lead in drinking water. Five of the water supplies
in this sample had sufficient lead to equal or exceed the estimated
maximum safe level of lead intake (G00,ug/day) without considering
the additional contribution to the total intake by oilier routes of
exposure. Under certain conditions, (acidic soft water, in particular)
water can possess sufficient plumbosolvency to result in appreciable
concentrations of lead in water standing in lead pipes overnight (54).
As a result of the narrow range between the lead exposure of
the average American in everyday life imd exposure which is con-
sidered excessive (especially in children) it is imperative that
lead in water be maintained within rather strict limits. Since a
survey (55) of lead in surface water of the U.S.A. and Puerto Rico
found only 3 of 726 surface waters to exceed 0.05 mg/1; the standard
of 0.05 mg/1 should be obtainable. For a child one to three years
old drinking one liter of water a day (probably the most a child
would drink), the contribution would be 0.05 mg/1 x 1.0 liter equals
0.050 mg. The diet is estimated by scaling clown the average
adult's diet to be 150-200;ug (56). Assuming the fraction of lead
absorbed is the same for lead in food and water, water would
contribute 25 to 33% of the lead normally ingested. For an adult
-------
drinking 2 liters per day, the contribution would be 0.1 mg/0. 3 mg,
or 33^.' of food. At lower concentrations, for example, 0.015 mg/1,-
the average concentration in drinking water, the contribution of water
in an adult or child would be less than 10% of that of food.
It should be reemphasized that the major risk of lead in water is
to small children (50). The potentially significant sources of lead
exposure to children which have been documented include paint,
dust (40, 42,43), canned milk (58, 59), tooth paste (GO, 61), toys,
newsprint ink (62, 63), and air. Although paint is most strongly
implicated epiclemiologically, there is growing evidence that others,
such as dust, are important (40). There is a serious problem with
excess lead in children; it is well documented. It can lead to lead
poisoning. Lead poisoning does cause death and morbidity in
children. A survey of 21 screening programs (64) testing 344, 657
children between 19G9 and 1971 found 26. l^oor over 80,000 children
with blood leads of over 40 ug/1 (which is considered evidence of
excessive exposure.) Several recent studies suggest that the
frequency of intellectual and psychological impairment i:; increased
among children overexposed to lead who were not thought to have
had overt clijiical lead poisoning (14, 15,16,17). With the wide-
spread prevalence of undue'exposure to le;:d in children, its
serious potential sequelae, and studies suggesting increased lead
absorption in children (chronic brain or kidney damage, as \vell
10 0<
-------
as acute brain damage); it would seem -.vise at this time to continue
to limit the lead in water to as low a level as practicable. Data
from the Community Water Supply Study and other sources indicate
that a lead concentration of 0.05 mg/1 or less can be attained in
most drinking water supplies. Experience indicates that less than
four percent of the water samples analyzed exceed the 0.05 mg/1
limit and the large majority of these are due to stability (corrosion)
problems not due to naturally occurring lead content in the raw
wui'jrs.
101<
-------
REFERENCES
1. Kchue, It.A., The Harben Lectures 1960. The Metabolism of
Lead in Man in Health and Disease. Lecture 1. The Normal
Metabolism of Lead. Lecture 2. The Metabolism of Lead Under
Abnormal Conditions. Lecture 3: Present Hygienic Problems
Relating to The Absorption of Lead. J. Roy. List. Pub. Health
24: 81 (I960).
2. Goodman, L.S. and Oilman, A. The Pharmacological Basis
of Therapeutics. The MacMillian Co., London and Toronto,
pp. 977-982 (1970).
3. Hardy, H . L.. Lead. Symposium on Environmental Lead
Contamination. PUS .<; f4W,~becember 13-15, (1965).
4. Jain, S., O'Brien, B., Fothcringill, R., Morgan, II.V. and
Geddes, A.M., Lead Poisoning Presenting as Infectious
Disease. The Practioner, 205: 784 (1970).
5. Hernberg, S.. NLkkanen, J., Melling, G. and Lilius, H.
A -aminolevulinic Acid Dehydrase as a Measure of Lead
Exposure. Arch. Environ. Health 21: 140(1970).
G. de Bruin. A. and Hoolboom, H., Early Signs of Lead-exposure.
A Comparative Study of Laboratory Tests. Brit. J. Inclustr.
Med. 2:2, 203 (1907).
7. Westerman. M.P., Pfitxcr, E., Ellis, L.D., and Jensen, W.N.
Concentrations of Lead in Bone in Plumbism. New Eng. J. Med.
273: 124G (19G5).
8. Chisolm. J.J.. Jr. Disturbances in The Biosynthesis of Heine
in Lead Intoxication. J. Pcdiat. (34, 174 (19G4").
9. Cramer, K. and Selandcr, D., Studies in Lead Poisoning,
Comparison of Different Laboratory Tests. Brit. J.
Indu::lr. Med. 22, 311 U9G5).
10. Selandcr, £., Cramer, L. and Hallberg, I.,. Studies in Lead
Poisoning: Ornl Therapy with Pcnicillamine. Relationship
Between Lead it: Blood and Other Laboratory Tests. Brit.
J. Industr. Med. 23: 282 (19GG).
-------
11. Airborne Lead in Perspective. The Committee on Biological
Effects of Atmospheric Pollutants. National Research Council,
National Academy of Sciences. Washington, D.C. (1972).
12. Dyers, R.K. Lead Poisoning. Review of The Literature and
Report on 45 Cases. Pediatrics 23_: 585 (1959).
13. Mellins, R.D., and Jenkins, C.C. Epidemiological and
Psychological Study of Lead Poisoning in Children.
J. Am. Mod. Assn. 158: 15 (1355).
14. Moncrieff, A.A., Koumidcs, O.P. and Clayton, B.E.
Lead Poisoning in Children. Arch. Dis. Child. 39: 1-13 (1964).
15. David, O., Clark, J., and Vocller, K., Lead and Hyper-
activity. Lancet 2: 900 (1972).
1G. dc la Burde, B., and Choatc, M.S., Jr., Docs Asymptomatic
Lead Exposure in Children Have Latent Sequelae? J. Pediat.,
81_: 1088 (1972).
17. Pueschel, S.M.. Kopito, L., and Scliwachm:m, H. Children
with An Increased Lead Burden: A Screening ajid Follow-up
Study. J. Am. Mod. Assn. 222: 462 (1972).
18. Millar, J.A., Battistini, V., Gumming, R.L.C., Carswell, F.,
and Goldberg, A. Lead and -aminolaevulinie Acid Dehydrase
Levels in Mentally Retarded Children and in Lead-poisoned
Suckling Rats. Lancet, 2: 695 (1970).
19. Henderson, D.A. Follow-up of Cases of Plumbism in
Children. Aust. Ann. Med. 3, 219 (1954).
20. Belts. P.R., Asllcy, R., Raine, D.N. Lead Intoxication in
Children in Birmingham, British Med. J. Ij. 402 (1973).
21. Selyc, H., Tuchwever. B., and Bertok, L. Effect of Lead
Acetate on the Susceptibility of Rats to Bacterial Endoioxins.
J. Bacleriol. 91_: 884 (1966).
22. Hemphill, F.E., Kaeberle, M .A ., and Buck, W.B. Lead
Suppression of Mouse Resistance to Salmonella Typhimurium.
Science 127: 1031 (1971).
-------
23. Gainer, J.ll. Effects of Metals on Viral Infections in Mice.
Env. Health Persp. _ : 98-999 (June 1973).
24. Ilolper, K., Trejo, R.A., Brcttschneidcr, L., DiLuzio, N.R.
Enluxncement of Endotoxin Shock in Tlie Lead-sensitized Subhuman
Primate, Surg. Gynecol., Obstr. 136: 594 (1973).
25. Kehoc, R.A., Cholak, Hubbard, D.M., Bambach, K.,
McNary, R.R. and Story, R.V. Experimental Studies
on the Digestion of Lead Compounds. J. Industr. Hyg.
Toxicol. 22: 381 (1940).
26. Schroeder, 11.A. and Balas.ia, J.J. Abnormal Trace Elements
in Man: Lead. J. Chron. Diseases 14: 408 (19G1).
27. Kchoe, R.A. Under What Circumstances is Invest ion of Lead
Dangerous. Symposium on Environmental Lead Contamination.
(PUS »1440), (December 13-15, 1965).
28. Hardy, H.L.. Chamberlain, R.I., Malocf. C.C., Doylen, G.W.,
and Howell, M.C., Lead as An Environmental Poison, Clin.
Pharmocol. 1^: 982 (1971).
29. Schroeder, M.A. and Tipton, .J.M.. The Human Body Burden
of Lead. Arch. Envoiron. Health 17; 965 (1968).
30. Barry. P.S.I, and Mossman, D.B. Lead Concentrations in
Human Tissues. British Indus. Med. 27; 339 (1970).
31. Medical Aspects of Childhood Lead Poisoning. HSMILA Health
Repts. 86: MO (1971).
32. Coyer, R.A., Moore, J. F. and Krcgman, M.R. Lead Dosage
and the Role of the Ditranurlcar Inclusion Body. Arch.
Environ Health 2_0: 705 (1970).
33. Blokker. P.C. A Literature Survey of Some Health Aspects
of Lead Emissions from Gasoline Engines. Atmospheric
Environ. 6: 1 (1972).
34. Hofrcuter, D.H., ct al. The Public Health Significance of
Atmospheric Lead. Arch. Environ. Health 3: 82 (1961)
35. Anonymous. Lead in the Environment and Its Effect 0:1 Humans,
State of California Public Health Department. (1967).
10
1*-
-------
3G. Thomas, H.V.. Milmore, O.K.. Heidbredcr, G.A.and
Kogan, 13.A. Blood Load of Persons Living Near Freeways
Arch. Environ. Health 1_5: G95 (1967).
37. Hammond, P.B. Lead Poisoning: An Old Problem with a
New Dimension Essays in Toxicol. 1^ 115 (19G9).
38. Anonymous, Survey of Lead in The Atmosphere of Three Urban
Communities, U.S. Public Health Service Publication 999-AP-12,
(19G5).
39. Tola, S., et al. Occupational Lead Exposure in Finland.
II. Service Stations and Carafes. Work Environ. Health
9: 102 (US5).
40. Fiarey, F.S. and Gray, J.W. Soil Lead and Pcdiatric Lead
Poisoning in Charleston, S.C., J. South Carolina IVied. Assn.
GG: 79 (1970).
41. Evaluation of Certain Food Additives and Of the Contaminants
Mercury, Lead and Cadmium. Sixteenth Report of The Joint
FAO/WHO Expert Committee on Food Additives, Geneva,
April 4-12, 1972. Published by FAO and WHO, Rome (1972).
42. Needlcman, H.L., and Scanlon, J., Getting the Lead Out.
New Engl. J. M-xi. 288: 4GG (1973).
43. Hunt, W.F., Jr.. Pinkcrlon, C., McNully, O., et al.
A Study in Trace Element Pollution of Air in Seventy-seven
Midwestern Cities. Trace Substances in Environmental
Health IV. University of Missoure Press, D.D. Hemplu'll (Ed.)
Col-.ur.bia, pp. 5G-G8 (1971).
44. Petrova, A., Dnlakmanski, Y., and Bakalov, D. Study of
Contamination uf the Atmosphere in Injurious Road Transport
and Industrial Products. J. Hyg. Edpidcmio. Microbiol.
Immunol. (Praha) U): 383 (19GG).
45. Buzell, R.J. Leadpoisoning: Combating the Threat From
The Air. Science 174: 574 (1971).
4G. Alexander. F.W., Delves, H.T., and Clayton, B.E. The Uptake
and Excretion by Children of Lead and Other Contaminants.
Proceedings of the Ditcrnalional Symposium of Environmental
Health Aspects of Lead. Luxembourg Commission of the European
Communities, Amsterdam, October 2-6, 1973 pp. 319-331
(1973).
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47. Load: Airborne Load in Perspective. National Academy of
Sciences, Washington, D. C. (1972).
48. Grollman, A., and Grollman, F. F. Pharmacology and Therapeu-
tics. 7tli Ed. Lea and Febigerer, Philadelphia (1970).
49. Lin-Fu, J.S. Undue Absorption of Lead Among Children -
A Now Look at an Old Problem. New Engl. J. Mod. 286
702 (1972).
50. Scanlon, J. Human Fetal Hazards from Environmental
Pollution with Certain Non-essential Trace Elements. Clin.
Pcdiatr. U_: 135 (1972).
51. Chatterjee, P. and Gettman, J.H., Lead Poisoning: Subculture
as a Facilitating Agent? Am. J. Clin. Nutr. ^: 324 (1972).
52. Angle, C.R. and Mclntire, M.S. Lead Poisoning During Preg-
nancy, Am. J. Dis. Child 103: 436 (19G4).
53. McCabc, L.J., Syrnons, J.M., Lee, R.D., and Robeck, G. G. ,
Survey of Community Water Supply Systems. §2: 670 (1970).
54. Crawford, M. D. and Morris, J.N. Lead in Drinking Water.
Lancet _: 1087 (18, 19G7).
55. Hem, J.D. and Durum, V.'.H. Solubility and Occurrence of Lead
in Surface Water, G5, 562 (1973).
56. King, B. G. Maximum Daily Intake of Lead Without Excessive
Body Lead Burden in Children. Am. J. Dis. Child. 122: 337
(1971).
57. Lin-Fu, J.S. , Vulnerability of Children to Lead Exposure and
Toxicity. New Fug. J. Mod. 289: 1229 (1973).
58. Barltrop, D. , Sources and Significance of Environment:!! Lead
for Children. Proceedings of the International Symjxjsium on
Environmental Health Aspects of Lead. Amsterdam, October 2-6,
1972. Luxembourg Commission of the European Communities,
pp. 675-681 (May 1973).
59. Murthy, G. R. and Rhea, U.S. Cadmium, Copper, Iron, Lead,
Manganese and Zinc in Evaporated Milk Infant Products, and
Human Milk J. of Dairy Sci. 54: 1001 (1971).
1C(>'-
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60. Bornuui, E., and McKiol, K. Is That Toothpaste Safe? Arch.
Environ. Health 25: 64 (1972).
61. Shapiro, I.M., Colien, G.H., and Necdleman, H.L. The
Presence of Lead in Toothpaste. J. Am. Dent. Assn. 86:
394 (1973). . ~
62. Joselow, M.N., Lead Content of Printed Media. Am. J.
Pub. Health (in press).
63. Lourie, R.S., Pica and Poisoning. Am. J. Orthopsychiatry
4_1: 697 (1971).
64. Gilsinin, J., Estimates of the Nature and Extent of Lead
Paint Poisoning in The United States (NBS TN-746)
Dept. of Commerce, National Bureau of Standards,
•Washington, D.C. (1972).
107<
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MERCURY
Environmental exposure of the population to mercury and its
compounds poses an unwarranted threat to man's health. Since
conditions indicate an increasing possibility that mercurials may
be present in drinking water, there is a need for P. guideline that
will protect the health of the water consumer.
Mercury is distributed throughout the environment. And as 2
result of industrial and agricultural applications, large increases
in concentrations above natural levels in water, soils, and air may
occur in localized areas around chlor-alkali manufacturing plants
and industrial processes involving the use of mercurial catalysts,
and from the use of slimicides primarily in the paper-pulp industry
and mercurial seed treatment.
Mercury is used in the metallic form, as inorganic mercurous
(monovalent) and mercuric (divalent) salts, and in combination with
organic molecules (viz. alkyl, alkoxyalkyl, and aryl).
The presence of mercury in fresh and sea water was demonstrated
more than 50 years ago (1-4). In early studies in Germany, Stock (5,6)
found mercury in tap water, springs, rain water, and beer. In all
water, the concentration of mercury was consistently less than
one ug/1; however, beer occasionally contained up to 15 jag/1. A
recent survey (7) demonstrated that most U.S. streams and rivers
contain 0.1 ug of dissolved mercury or less per liter.
108<'
-------
Presently the1 concentration of mvrcury in air is ill-defined for
lack of analytical data. In one study (8) the concentration of mercury
contained in particulales in the atmosphere of 2 U.S. cities was
measured and ranged from 0.03 to 0.21 jig/m3. One review (9)
cited values up to 41 jug/m3 of particulate mercury in one U.S.
metropolitan area.
Outside of occupational exposure, food, particularly fish, is
the greatest contributor to body burden of mercury. In 1967 a
limited study of mercury residues in foods was conducted, involving
6 classes of foods. The results indicated levels of mercury in the
order of 2 to 50 ^ig/kg. The Atomic Energy Commission sampled
various foods for mercury in i'.s tri-cily study and reported levels
between 10 and 70 jjg of mercury per kg of meats, fruits, and
vegetables. Di 1970, it was discovered that several types of fresh
and salt water fish contained mercury (mostly in the alkyl form)
in excess of the FDA guideline of 0.5 ppm (500.ug/kg). Mercury
in bottom sediments had been converted by micro-organisms to the
alkyl form, entered the food chains, and had accumulated in the
higher members of the chains. Game birds were also discovered
to have high levels of mercury in their tissues, persumably from
.the ingestion of mercury-treated seeds or of smaller animals that
had ingested sucli seeds. The Food and Drug Administration has
established a guideline of 0.5 ppm for the maximum allowable
concentration of mercury in fish for human consumption; but for
all other foodstuffs, no tolerances have been established.
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Mercury poisoning may be acute or chronic. Generally mercurous
salts are less soluble than mercuric salts and are consequently less
toxic acutely. Acute intoxication is usually the result of suicidal or
accidental exposure. For man the fatal oral dose of mercuric salts
ranges from 20 mg to 3 g. The acute syndrome consists of an initial
phase referable to local effects (viz. pharyngitis, gastroenteritis,
vomiting, and bloody diarrhea) followed later by symptoms of systemic
poisoning (viz. anuria with uremia, stomatitis, ulcerative-hemorrhagic
colitis, nephritis, hepatitis, and circulatory collapse) (10).
Acute intoxication from the inhalation of mercury vapor or dusts
leads to the typical symptoms of mercury poisoning coincident with
lesions of the mucous membranes of the respiratory tract which may
ultimately develop into bronchitis and bronchopneumonki. Inhalation
of mercury in concentrations of 1,200 to 8,500 jug/m3 results in acute
intoxication (10). In severe cases, signs of delayed neurotoxic effects,
such as muscular tremors and psychic disturbances, are observed.
The Threshold Limit Value for all forms of mercury except alkyl
is 0.05 mg/mj in the U.S. (11).
Chronic mercury poisoning results from exposure to small
amounts of mercury over extended periods of time. Chronic
poisoning from inorganic mercurials lias beer, most often
associated with industrial exposure, whoreas that from the organic
derivatives has been the result of accidents or environmental
contamination.
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Workers continually exposed to inorganic mercury arc particularly
susceptible to chronic mercurialism. Usually the absorption of a
single large dose by such individuals is sufficient to precipitate the
chronic disease that is characterized mainly by central nervous
system toxicity (10, 12, 13). Initially, non-specific effects, such
as headaches, giddiness, and reduction in the power of perception,
are observed. Fine tremors gradually develop primarily in the
hands and arc intensified when a particular movement is begun.
In prolonged and severe intoxication, fine tremor is interspersed
with coarse, almost chorcatic, movements. Excessive salivation,
often accompanied by a metallic taste and stomatitis, is common. As
the illness progresses, nervous restlessness (erethismus mercurialis)
appears and-is characterized by psychic and emotional distress and
in some cases hysteria. Although the kidney is less frequently
affected in this type of poisoning, chronic nephrosis is occasionally
observed.
Several of the compounds used in agriculture and industry (such
as alkoxyalkyls and aryls) can be grouped, on the basis of their
effects on man, with inorganic mercury to which the former com-
pounds are usually metabolized.
• 111."-
-------
Alky! compounds are the derivatives of mercury most toxic to man,
producing illness from the digestion of only a few milligrams (21, 24).
Chronic alkyl mercury poisoning, also known as Minamata Disease,
is an insidious form of mercurialism whose onset may appear after
only a few weeks of exposure or may not appear until after a few
years of exposure. Poisoning by those agents is characterized
mainly by major neurological symptoms and leads to permanent
damage or death. The clinical features in children and adults
include numbness and tingling of the extremities, incoordination,
loss of vision and hearing, and intellectual deterioration. Autopsy
of live clinical cases reveals severe brain damage throughout the
cortex and cerebellum. There is evidence to suggest that compensa-
tory mechanisms of the nervous system can delay recognition of the
disease even when partial brain damage exists.
Several episodes of alkyl mercury poisoning have been recorded.
As early as 1865, two chemists became ill and died as a result of
inhaling vapors of ethyl mercury (14). One of the largest outbreaks
occurred in a village near Minamata Bay, Japan, from 1953 through
19GO. At least 121 children and adults were affected (of whom
46 died) by eating fish containing high concentrations of methyl
mercury (15). Of the population affected, 23 infants and children
developed a cerebral palsy-like disease which was referred to as
Congenital (or Fetal) Minamata Disease. Similarly, in 1964
-------
and 19G5, the'disease was reported among 47 persons, G of whom died,
in Niigata, Japan. Hunter et al (16) reported 4 cases of industrial
intoxication from handling of these agents. In Guatemala, Iraq,
Pakistan, and the United States, the human consumption of groin
treated with alkyl mercurials for seed purposes has led to f.!ie
poisoning of more than 450 persons, some of whom died (17-20).
The congenital (fetal) disease observed in Minamata and Niigata
emphasize the devastating and insidious nature of these agents. Of
particular significance are the facts that (1) the affected children
had not eaten contaminated fish and shellfish, and (2) the mothers
apparently were not affected although they had consumed some con-
taminated food. Exposure of the fetus to mercury via the placenta
and/or the mother's milk is believed to be the eliologic basis for
this disease, thus indicating the greater susceptibility of infants
to alkyl mercury.
Absorption is a factor important in determining the toxicity
of alkyl mercurials. Berglund and Berlin (21) estimated that methyl
mercury is absorbed at more than a 90r-o rate via gastro-intestinal
tract as compared with 2'.o mercuric ion (22). In audition, methyl
mercury crosses the placenta into the fetus and achieves a 30r.o
higher concentration in fetal erythrocyles than in maternal red blood
cells (23). However, the fetal plasma concentration of mercury is
lower than that of the mother. The rate of uptake of methyl mercury
1,« *"., • ~i
J.O ~ JL '..-
-------
into (he fetal brain is as yet unknown. Alkyl mercury can cross
the bluocl-brain barrier more easily than other mercurials, so that
brain levels of mercury are much higher after a dose of alkyl
mercury than after a corresponding dose of any other mercurial.
Excretion is of equal importance in determining the health
hazard. Unlike inorganic mercury, alkyl mercury is excreted
mainly in the feces. After exposure to methyl mercury, approxi-
mately 4',o of the dose is excreted within the first few days, and
about l^o per day thereafter (24). The biological half-life of methyl
mercury in man is approximately 70 days.
Safe levels of ingested mercury can be estimated from data
presented in "Methyl Mercury in Fish" (24). From epidcmiological
evidcr.cc, the lowest whole-blood concentration of methyl mercury
associated with toxic symptoms is 0.2,ug/g. This blood concentration
can be-compared to GO ug Hg/g hair. These values, in turn, corres-
pond to prolonged, continuous exposure at approximately 0.3 mg Hg/70
kg/day. By using a safety factor of 10, the maximum dietary intake
should be 0.03 mg Hg/person/day (30 ^ig/70 kg/day). Although the
safety factor is computed for adults, limiting ingestion by children
to 30 ug Hg/clay is believed to afford some, albeit smaller, degree of
safety. If exposure to mercury were from fish alone, the limit would
allow for a maximum daily consumption of 60 grams (420 g/week) of fish
11-1'
-------
containing 0. 5 mg HgAg. In a given situation, if the total daily
intake from all sources, air, water, and food, is approaching 30
ug/person/day, the concentration of mercury and/or the consumption
of certain foods will have to be reduced if a safety factor of 10 is
to be maintained. Fortunately, since only a small fraction of the
mercury in drinking water is in the alkyl form, the risk to health
from waterborne mercury is not nearly so great as is the risk
from mercury in fish. Also fortunately, mercury in drinking water
seldom exceeds 0.002 mg/1. Drinking water containing mercury at
the approval limit of 0. 002 mg/1 will contribute a total of 4 ug Hg
to the daily intake, and will contribute less than 4 ng methyl mercury
to the total intake. (Assuming that less than 0.1% of the mercury
in water is in the methyl mercury form.) Since the Regulations
approval limit is seldom exceeded in drinking water, the margin
of safety gained from the restricted intake of mercury in drinking
water can be applied to the total intake with minimal economic
impact.
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HE/EKENCES
1. Proust, J.L. On the Existence of Mercury in The Waters
of The Ocean. J. Phys. 49, 153, 1799.
2. Garrigou, F. Sur la Presence du Mercure clans du Roc her.
Compt. Rend. 84, 963-965, 1877. -
3. Willni, E. Sur la Presence du Mercure dans les Eaux de Saint-
Neciaire. Compt. Rend . £8, 1032, 1879.
4. Bardct, J. Etude Spectrographicquc des Eaux Minerales Fran-
caises. Compt. Rend . 157, 224-226, 1913.
5. Stock, A. and Cucuel, F. Die Verbreitung des Quecksilbers.
Naturwissenschaftcn ~>2/24, 390-393, 1934.
6. Stock, A. Die Mikro: nalytische Bestimmung des Quecksilbers
and iiire Amvendung :iuf Hygienische and Madiziiiische Fragen.
Svcnsk Kcm Tidskr ::0, 242-250, 1938.
7. U.S. Geological Survey. Water Resources Review, July 70, p. 7.
8. Cholak, J. The Nature of Atmospheric Pollution in a Number
of Industrial Communities. Proc . Natl. Air Pollution Syrup.,
2nd. Pasadena, California 195~2T" ~
9. National Air Pollution Control Administration, D.H.E.W.
Preliminary Air i'ollution Survey of Mercury and Its Com-
pounds, A Literature Review. NAPCA Publication No. APTD
69-40, Rrleitfh, No. Carolina, p. 40.
10. S'.okin^er, II. E. "Mercury, UK " in Industrial Hygiene
and Toxicology. Vol. 2, 2nded., F.A. Patty, Ed. (New York:
Intel-science, p. 1090, 1963).
11. Threshold Limit Values of Airborne Contaminants for 1970,
Adopted by The American Conference of Government;1.!
Industrial Hygienists.
12. Bidstrup, L.P. Toxicily of Mercury and Its Compounds,
(New York: American Elsevier Publishing Co., 1964) .
13. Whitchcad, K.P. Chronic Mercury Poisoning - Organic
Mercury Compounds. Ann. Occup. Hyg. 8, 85-89, 1965.
1.-- t • -
.• O'-
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14. Greco, A.II. Elective Effects of Some Mercurial Compounds
on Nervous System Estimation of Mercury in Blood and Spinal
Fluid of Animals Treated with Diethyl Mercury and With
Common Mercurial Compounds. Riv. Neurol. 3, 515-539, 1930.
15. Study Group of Minamata Disease. Minamata Disease.
Kumamoto University, Japan, 1968]
10. Hunter, D., Bomford, R.R., and Russell, D.S. Poisoning
by Methyl Mercury Compounds. Quart. ,±. Mcd. 9,
193-213, 1940. " ~
17. Ordonez, J.V., Carrillo, J.A., Miranda, C.M., et aJL Esiudio
Epidemiologico do Una Enfermedad Considerada Como Encefalitis
en la Region de Altos de Guatemala. Bull. Pan Amcr. Sanit.
Bur. 60, 510-517, I960.
18, Jalili. M.A., and Abbasi, A.II. Poisoning by E'liyl Mercury
Toluene Sulphonanilide. Brit. J. Ind. Mcd. 18^, 303-308, 19G1.
19. Haw, I.U. Agrosan Poisoning in Man. Brit. Mcd. J.
1579-1582, 19G3. ~
20. Likosky, W.H., Pierce, P.E., Hinman. A.H., etal. Organic
Mercury Poisoning, New Mexico. Presented at the Meeting of
the American Academy of Neurology, Bal Harbour, Fla.,
April 27-30, 1970.
21. Berglund, F., and Berlin, M. Risk of Methylmercury Cummulation
in Men and Mammals and the Relation Between Body Burden of
Methyl-mercury and Toxic Effects. In "Chemical Fallout"
(M.W. Miller and G.C. Berg, etc.) (Springfield, 111.: Thomas
Publishing .Co., 1969), pp. 258-273.
22. Clarkson, T.W. Epidemiological Aspects of Lead and Mercury
Contamination of Food. Canadian. Food and Drug Directorate
Symposium, Ottawa, June 1970 (to be published in Food and
Cosmetic Toxicology in 1971).
23. Tcjning, S. The Mercury Contents of Blood Corpuscles and in
Blood Plasma in Mothers and Their New-born Children. Report
70-05-20 from Dept. Occupational Meci., Univ. Hosp., S-221 85
Lund, Sweden, 1970.
24. Methyl Mercury iin Fish, A Toxicologic-Epidemiologic Evaluation
of Risks. Report from An Expert Group. Nord. Hyg. Tidskr.
Suppl. 4, 1971. ~~~~
-------
NITKATE
Serious and occasionally fatal poisonings in infants have occurred
following ingestion of well waters shown to contain nitrate (NO, )
at concentrations greater than 10 mg/1 nitrate nitrogen. This has
occurred with sufficient frequency and widespread geographic distribution
to compel recognition of the hazard by assigning a limit to the concentra-
tion of nitrate in drinking water at 10 mg/1 as nitrogen. This is about
45 mg/1 of the nitrate io:i.
Nitrate in drinking water was first associated in 1945 with a
temporary blood disorder in infants called methemoglobinemia (1).
Since then, approximately 2000 cases of this disease have been reported
from North America and Europe, and about 7 to 8 percent of the infants
died (2,3,4). Evidence in support of the limit for nitrate is given in
detail by Walton (2) in a survey of the reported cases of nitrate
poisoning of infants before 1951. The survey shows that no cases of
poisoning were reported when the water contained less than 10 mg/1
nitrate nitrogen. More recent surveys (3,4) involving 467 and 249 cases
tend to confirm these findings, frequently, however, water was
sampled and analyzed retrospectively and therefore the concentration
of nitrate which caused illness was not really known. Many infants have
drunk water when the nitrate nitrogen was greater than 10 mg/1 without
developing the disease. Many public water supplies in the United States
have levels of nitrate that routinely exceed the standard, but only one
case associated with a public water supply has been reported (5).
-------
A basic knowledge of the development of the disease is essential to
understanding the rationale behind protective measures. The develop-
ment of methenvjglobinemia, largely confined to infants less than three
months old, is dependent upon the bacterial conversion of the relatively
innocuous nitrate ion to nitrite. Nitrite then converts hemoglobin, the
blood pigment that carries oxygen from the lungs to the tissues, to melhe-
moglobin. Because the altered pigment can no longer transport oxygen,
the physiologic effect of methcmoglobincmia is that of oxygen deprivation,
or suffocation.
The ingestion of nitrite directly would have a more immediate and
direct effect on the infant because the bacterial conversion step in the
stomach would be eliminated. Fortunately, nitrite rarefy occurs in
water in significant amounts, but waters with nitrite nitrogen concen-
trations over 1 mg/1 should not be used for infant feeding. Waters with
a significant nitrite concentration would usually be heavily polluted and
would be unsatisfactory on a bacteriological basis as well.
There are several physiological and biochemical features of early
infancy that explain the susceptibility of the infant less then three
months of age to this disorder. First, the infant's total fluid intake
per body weight is approximately three times that of an adult (G).
In addition, the infant's incompletely developed capability lo secreto
gastric acid allows the gastric pH to become high enough (pH of 5-7)
to permit nitrate-reducing bacteria to reside high in the gastrointestinal
-------
tract. In this location, the bacteria arc able to reduce the nitrate before
it is absorbed into the circulation (7). To further predispose the infant,
the predominant form of hemoglobin at birth, hemoglobin F (fetal hemo-
globin)! is mere susceptible to methemoglobin formation than the adult
form of hemoglobin (hemoglobin A) (8). Finally, there is decreased
activity in the enzyme predominantly responsible for the normal methe-
moglobin reduction (NADH-dependent methemoglobin rcductasc) (9).
Win ton reports on a study (10) where methemoglobin levels in blood
•were measured on infants to determine subclinical effects. He
indicates that at intakes over 1C mg of nitiate ior per kilogram of body
weight (2.2 mg/kg measured as nitrate nitrogen) the methemoglouin
concentration is slightly elevated over normal. The methemoglobin
levels returned to normal when the babies were changed to bottlnd water
free of nitrate nitrogen. When a baby is fed a dehydrated formula that
is made with water that the mother boils, (increasing the concentration),
the intake of 2.2 mg NO -j-N/kilogram can be reached if the water contains
10 ing/1 nitrate nitrogen. To determine if a slight elevation of an infant's
methemoglobin concentration has an adverse health effect will require a
large and elaborate study.
In some circumstances, which are not understood, the standard does
not have a safety factor. Cases of illness might occur, but for the usual
situation the limit of 10 mg/1 NO-j-N will protect the majority of infants.
-------
Older .children and adult's do not seem to be affected, but the Russian
literature reports (il) elevated methemoglobin in school children
where water concentrations of NO3-N were high, 182 mg/1.
Treatment methods to reduce the nitrate content of dr'nking water
arc being developed and should be applied when they are ready if
another source of water cannot be used. If a water supply cannot
maintain the NO3-N concentration below the limit, diligent efforts
must be made to rssure that the water is not used for infant feeding.
Consumption of water with a high concentration of NO 3-N for as short
a period as a'day may result in the occurrence of methemoglobinemia.
l£i
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REFERENCES
1. Conily, H .H., "Cyanosis in Infants in Well Water, " J. AM
Med. Assn. 129:112-116 (1945).
2. Walton, G., "Survey of Literature Relating to Infant Methemo-
globinemia Due to Nitrate Contaminated Water." Am. J. Pub.
Health, 41: 986-996.
3. SrUtelmacher, P.G., "Methemoglobinemia from Nitrates in
Drinking Water." Schriftcnrcichc dcs Vcrcins fur Wasser Boden
und Lu ft hygiene. No. 21, 1962.
4. Simon, C., Ma/.ke, M., Kay, II. and Mrowitz, G., "Uber Vorkommen,
Pathogenes and Moglichkeiten zur Propnylaxe der durch Nitrit
Verusachten Methamoglobinamia." A. Kindcrhcilk. 91: 124 (1964).
5. Vigil, Joseph, et al. "Nitrates in Municipal Water Supply Cause
Methemoglobinemia in bifant," Public Health Reports, 80
(12)1119-1121(1965). ~~
6. Hansen, H.E. and Bennett, M.J. in Textbook of Pediatrics.
Nelson, W.E., W.B. Saunders Company, T964"7p. 109-
7. Cornblath, M. and Hartmann, A.F., "Methemoglobinemia in
Young Infants," J. Pcdiat., 33: 421-425(1948).
8. Betke, K., Kleihauer, E. and Lipps, M., "Vergleichende Unter-
suchugen uber die Spontanoxydation von Nabclschnur und
Er\vachsenenhamoglobin." Ztschr. Kindcrh., 77:549 (1956).
9. Ross, J.D. and DCS Forges, J.F. "Reduction of Methemoglobin
by Erythrocytes from Cord Blood. Further Evidence of Deficient
Enzyme Activity in Newborn Period." Pediatrics, 23_:218 (1959).
10. Win ton, E.F., Tardiff, R.G., and McCabe, L.J. Nitrate in
Drinking Water. ,J. Am. Water Works Assn. G3_:95-98 (1971)
11. Diskalenko, A.P. "Methemoglobinemia of Water-Nitrate Origin
in Moldavian SSR", Hygiene and Sanitation 33:32-38 (1968).
1*~- o«-
A,^.
-------
OKGANICS-CAR13ON ADSORBADLE
The possibility of the presence of (aste and odor producing substances
and toxic organic chemicals in drinking water art- of concern to all
connected with the provision of safe, esthetically pleasing water to the
American consumer. If the quality of drinking water is to be protected,
monitoring of organies should be part of any quality control program.
Difficulties arise, however, since monitoring for many specific organics
is beyond the capabilities of most water supplies at this time (1973).
This problem can be overcome somewhat, however, by monitoring for
the general organic content of \v-icr and assuming, as is done with the
total coliform test as the indicator test for pathogens, that if this
indicator parameter is below a certain limit, the likelihood of odorous
or toxic organics causing problems is reduced.
Historically, the general organic content of drinking water has been
determined by measuring the Carbon Chloroform Extract (CCE) and Carbon
Alcohol Extract (CAE)(1) concentrations. These extracts have an opera-
tional definition and are a mixture of organic compounds that can be
absorbed into activated carbon under prescribed conditions and (hen
desorbecl with organic solvents under prescribed conditions.
The 19G2 Public Health Service Drinking Water Standards contained
a limit of 0.2 mg/1 for CCE collected with the Carbon Adsorption
Method (CAM) sampler (2) operated at a flow-nnr: of 0.25 gallons
(945 ml) per minute, called the high-flow CAM s'tnipler . (Note,
because the recovery of organics from water is influenced by the
*"•• "7 <
„•»-.«..;•
-------
collection and extraction method, lower-case letters are used to distin-
guish the analytical procedures. Carbon-Chloroform Extracts collected
with the high-flow CAM sampler are hereafter called CCE-lif).
Middle ton and Rosen (3) detected substituted benzene compounds,
kerosene, polycyclic hydrocarbons, phenylether, acrylonitrile and
insecticides in various CCE-hf's. This list lias been expanded by many
investigators in the subsequent years, for example, by Kleopfer and
Fairless (4). In 1963, Heuper and Payne (5) reported the carcinogenic
properties of finished water CCE-hf's.
In 19G5, Boclh, English and McDermott (6) developed a CAM sampler
similar to the High-Flow CAM Sampler, but with a longer contact time
between the sample and the activated carbon. This sampler, called the
low-flow CAM sampler, increased organic adsorption and, therefore,
overall yield of the determination. In addition, measurement of CAE
was included in this method. Extracts from this procedure are called
CCE-lf and CAE-lf. No drinking water standard was promulgated for
these parameters. Rosen, Mashni, and Safferman (7) isolated odorous
organics from a CCE-lf.
Since that time, a CAM sampler, called the "Mini-Sampler," with
the advantages of the low-flow CAM s;u:ipler, but more reliable, less
expensive, smaller, and more convenient, has been developed (8).
lii addition, the Mini-sampler uses a type of coal-based granular
activated carbon that enhances organic collection, thereby increasing
124-
-------
the yield of the method. The extraction apparatus has also been mina-
turized to be more convenient and less expensive and the procedure lias
been modified to be more vigorous, thereby increasing desorption and
further increasing organic recovery (10). The extract from this
procedure is called CCE-m.
Tardiff and Dt-inzer (9) tested the toxiciiy of a CCE-m collected
from the finished water of a river supply. Tiie resulting LD50 of
32 mg/kg would classify this extract as extremely toxic on a typical
lexicological scale.
Symons, Love, Duelow and Robcck (10) reported the identification
of £-Caprolaclam and 2-Hydroxyadiponitrile by gas chromatography
and mass spectrometry in a CCE-m collected from a finished water
from a different river supply. This indicates the presence of synthetic
organics in this extract.
Extraction with the less polar solvent chloroform does not desorb all
of the organics adsorbed onto the activated carbon. Extraction with other
solvents lias been proposed as a method of monitoring these materials.
The use of the polar solvent 95f/o ethyl alcohol does extract different
organics, but it also recovers inorganic salts that were adsorbed on
the activated carbon. At this time no reliable technique has been
developed lor measuring these other organics.
-------
In an effort (o detc»'niine the range of CCE-m concentrations in
finished water, as was done by Ettinger (11), for raw water and Taylor
(12), the Interstate Carrier Surveillance Program (12) and the 19G9
Community Water Supply Survey (14) for finished water, using the
high-flow CAM technique, studies were made with the Mini-sampler at
128 locations. These were all surface water sources, and had varying
histories of raw water contamination by organics and taste and odor
problems. These sources were in 31 states, the District of Columbia,
and Puerto Rico. Single samples were collected at 122 locations and
from 2 to 34 samples at the other six locations. These latter data
were averaged.
The data were pooled and grouped by extract concentration and the
percentage in each concentration category calculated. From these
data the percentage of locations with CCE-m concentrations greater
than a given concentration was calculated. These are shown in Table n.
The proposed use of a CCE maximum contaminant level was an
attempt to deal with gross organic pollution as soon as possible pending
the results of further research, and surveys that are planned by EPA
and of the NAS study that is required in the Safe Drinking Water Act.
CCE was initially used as a means of taste and odor control. As con-
cern over adverse health effects of organic chemicals grew, CCE was
turned to as a rough surrogate for organics to be used as a health-
based standard rather than as an esthetic standard. Unfortunately,
-------
TABLE II
% of Locations*
CCE-ni with Concentration
Concentration Greater Than
Given Concentration
0.0
0.1
0.2
0.3
0.4
0.5
0.6
0.7
0.8
0.9
1.0
1.1
1.4
1.5
2.3
100.0
97.7
86.8
63.4
39.2
24.4
14.2
7.9
5.6
4.0
3.2
2.4
1.6
0.8
0.0
"Based on 128 locations.
-------
as more is learned about organic chemical pollution of drinking
water, CCE looks less and less effective as a surrogate for harmful
organics.
The principal difficulty with CCE is that it includes only about
one-fifth of the total organic content u.r the volume of water sampled,
and it does not measure organic compounds of greatest concern, such
as the volatile halomethanes. Thus, a high CCE lest result does not
necessarily mean that the water tested may pose a hazard to health,
and a low CCE test result may be obtained from water with a high
level of potentially harmful organic compounds. In short, there is
no sound basis of correlation between CCE test results and the level
of harmful organic chemicals in the water tested.
To establish a maximum contaminant level under these circum-
stances would almost certainly do more harm than good. It could
give a false sense of security to persons served by systems which
are within the established level and a false sense of alarm to persons
served by systems which exceed the level. It also would divert
resources and attention from efforts to find more effective ways
of dealing with the organic chemical problem.
Total organic carbon (TOC) and chemical oxygen demand (COD)
are surrogates that have been considered, but they have limitations
also. TOC lias the advantage of being quicker and cheaper (on a per
sample basis) than CCE, but the availability of sensitive instruments
for this measurement is questionable. More investigation of the
-------
significance of ;my TOC number as a health effects limit is also
needed. COD is easily determined with readily available laboratory
equipment, but COD is not limited to organic compounds, and besides
a COD number also cannot be adequately related to health significance
at this time.
EPA is diverting substantial resources to research into the
health effects of specific organic chemicals and groups of organic
chemicals. Also, it is expected that the study of tiie National Academy
of Sciences will produce further data on health effects. However,
in view of the significance of the potential health problem, it is not
enough to wait for this additional health effects data. EPA therefore
will undertake to identify one or more surrogate tests for organic
chemicals or o^'inic chemical groups, and will also study in depth
the presence of specific organic chemicals in drinking water supplies.
It is anticipated that this effort will result in the development of an
additional MCL or MCL's for organic chemicals by amendment of
the Interim Primary Drinking Water Regulations without having to
wait, for a more complete resolution of the organic chemicals question
in the Revised Regulations.
-------
REFERENCES
1. Middlelon, F.M., "Nomenclature for Referring to
Extracts Obtained from Carbon with Chloroform or Other
Solvents," JAWWA, 53, 749 (June 1961).
2. Anon., "Tentative Method for Carbon Chloroform Extract
(CCE) in Water." .JAWWA, 54, 2, 223-227 (Feb. 19G2).
3. Middlrton, F.M. and Rosen, A.A., "Organic Contaminants
Affecting the Quality of Water," Public Health Reports, 71.,
1125-1133 (November 195G).
4. Kleopfer, R.D. and Fairlcss, 3.J., "Characterization of
Organic Components in A Municipal Water Supply,"
Environmental Science and Technology, 6, 1036-37 (November 1972)
5. Heiipor, W.C. and Payne, W.'.V., "Carcinogenic Effects os
Adsorbatcs of Raw and Finished Water Supplies," The Am.
Jour, of Clinical Pathology, 39, 5, 475-481 (May lWT)~.
6. Booth, R.L.. English, J.N., and McDcrmott, G.N. "Evaluation
of Sampling Conditions in (he Carbon Adsorption Method, "
JAWWA, 57, 215-220 (Feb. 1965).
7. Rosen, A.A., Maclini, C.I. and Safferman, R.S., "Recent
Developments in The Chemistry of Odor in Water: The Cause
of Earthv/Musty Odor," Water Treatment and Examination, 19,
1, 106-119(1970). ~~
8. Buclo'.v, R.W., Carswell, J.K. and Symons, J.M.. "An Improved
Method for Determining Organics in Water by Activated Carbon
Adsorption and Solvent Extraction," JAWWA., #3, 57-72,
195-199 (January and February 1973).
G. Tardiff, R.G. and Deinzer, M., "Toxicity of Organic Compounds
in Drinking Water, " Di Proceedings:. Fifteenth Water Quality
Conference, Feb. 7-8, 1973. University of Illinois Bulletin, 70,
122, 23-37 (June 4, 1973). ~~
10. Symons, J.M., Love, O.T., Jr., Buelow, R.W. and
Robeck, G.G-, "Experience with Granular Activated Carbon
in the United States of America," In Proceeding: Activated
Carbon in Water Treatment, Water Research Association,
University of .Reading, U.K., April 3-5, 1973 (In Press).
iao<
-------
11. Eltinger. M.D., "Proposed Toxicity Screening Procedure for
Use in Protecting Drinking Water Quality," JAWWA, 52,
689-694 (June I960).
12. Taylor, F.B., "Effectiveness of Water Utility Quality Control
Practices," JAWWA, 54, 1257-1264 (Oct. 1962).
13. Unpublished data from Interstate Carrier Surveillance Program,
Water Supply Division, Office of Water Programs, Office of Air
and Water Programs, U.S. Environmental Protection Agepcy,
1971, Washington. D.C.
14. McCabc, L.J., Sym_,ns, J.M., Lee, R.O. and Robcck G.G.,
"Survey of Community Water Supply Systems," JAWWA, 62,
670-687 (Nov. 1970). " ~~
-------
PEST1C1M-.S
A. Chlorinated Hydrocarbon Insecticides
The chlorinated hydrocarbons are one of the most important groups
of synthetic organic insecticides because of their wide use, great
stability in the environment, and toxicity to mammals and insects.
When absorbed into the body, some of the chlorinated hydrocarbons are
not metabolized rapidly but are stored in the fat.
As a general group of insecticides, the chlorinated hydrocarbons
can be absorbed into the body through the lungs, the gastro-inlestinal
tract, or the skin. The symptoms of poisoning, regardless of the
compound involved or the route of entry, are similar but may vary
in severity. Mild cases of poisoning are characterized by headache,
dizziness, gastro-intestinal disturbances, numbness and weakness of
the extremities, apprehension, and hyperirritability. In severe cases,
there arc muscular fasciculations spreading from the head to the extre-
mities, followed eventually by spasms involving whole muscle groups,
leading finally to convulsions and death from cardiac or respiratory
arrest. The severity of symptoms is related to the concentration
of the insecticides in the nervous system, primarily the brain (1).
Criteria Based un Chronic. Toxicity
Except as noted below, the approval limits (AL's) for chlorinated
hydrocarbons in drinking water have been calculated primarily on thn
basis of the extrapolated human intake that would be equivalent to liuit
1 ''•*'-
JL O'-
-------
causing minimal toxic effects in mammals (rats and dogs). TablJ I
lists flic levels of. several chlorinated hydrocarbons fed chronically
to dogs and rats (2. 3,4) that produced minimal ioxicity or no effects.
For comparison, the dietary levels are converted to nig/kg body
weight/day. Endrin and lindano had lower minimal effect/no-effect
love-Is in dogs ihan in rats; whereas, for toxnphcnc and methoxychlor
the converse was observed.
Human studies have also been conducted for methoxychlor, although
they were of short duration (8 weeks). The highest level tested for
methoxychlor was 2 mg/kg/day (5). No illness was reported in these
subjects.
Such data from human and animal investigations may be used to derive
exposure standards, as for drinking water, by adjusting for factors that
influence toxicity such as inter- and intra- species variability, length
of exposure, and exlensiveness of the studies. To determine a "safe"
exposure level for man, conventionally a factor of 1/10 is applied to the
data derived from human exposure studies conducted longer than 2 months
at which no effects have been observed; whereas, a factor of 1/100 is
applied to data derived from human exposure studies conducted for 2 months
or less as is the case for the human methoxychlor data citer'. A 1/100
factor is applied to animal data when adequate human data are available for
corroboration and a factor of 1/500 is generally used on animal data when
no adequau and comparable human dala are available. The minimal effect
-------
levels of endrin, lindane, and to:<:tp;iene are adjusted by 1/500 since
no adequate data are available for comparison. These derived values
are considered the maximum saf~> exnosure levels from all sources.
Since these values are expressed as mg/kg/day, they are then readjusted
for body weight to determine the total quantity to which persons may
be safely exposed.
Analysis of the maximum safe levels (mg/man/day) reveals that
these levels are not exactly the same when one species is compared with
another. The choice of a level on which to base an AL for water requires
(he selection of the lowest value from animal experimentation, provided
that the human data are within the same order of magnitude. Thus the
human data should substantiate the fact that man is no more sensitive
to a particular agent than is the rat or the dog.
To set a standard for a particular medium necessitates that account
be taken for exposure from other media. In case of the chlorinated
hydrocarbons, exposure is expected to occur mostly through the diet.
Occasionally, aerial sprays of these agents will result in their inhalation.
Dietary intake of pesticide chemicals has been determined by the
investigations of the Food and Drug Administration from "market basket"
samples of food and water. Duggan and Corncliussen (6) report on this
activity from 1964-1970. The average dietary intakes (mg/man/day)
arc listed in Table I. Comparing the intake from the diet with what
are considered acceptable safe levels of these pesticides, it is
apparent that only traces of methoxychlor and toxaphene are present
-------
in the diet. Less thau lO'/b of the maximum safe level of endrin or
linclane are ingested with the diet.
The AL's for chlorinated hydrocarbon Insecticides reflect only a
portion of man's total exposure to the compounds. In general; 20%
of the total acceptable intake is taken to be a reasonable apportionment
to water. However, the AL for toxaphene was lowered because of
organolepiic effects (7, 8) at concentrations above 0.005 mg/1.
The approval limits for the chlorinated hydrocarbon insecticides
are listed in Table I. These limits are meant to serve only in the
event that these chemicals are inadvertently present in the water.
Deliberate addition of these compounds is neither implied nor
sanctioned.
-------
I. OKICIVATIGN Oi' APi'ilOVAL LIMITS CAL's! FOR CHLORINATED UVUIiOCAHliO." INSECTICIDES
I.ouv..; Long-TVr::: I .eveIs
V.'it:'. Y.::ii:r..i: or :'.u :•_':':°o».ts
Cnlc-i:'.:itcJ Mjxi.'iuiir. S:;iV Levels
Intake fro"i Diet
Water
.--.*.--». ,~,i c
\. -J . , . -J J ., . ,^' J
En--:r
Metho.vychlor
Toxu?hc.-.c
a > •
A = 5u:r.c \vei
b x
d _.
"0"'0i
R.it
Dog
M-.T
p V
Rat
Doi;
R-t
Mar.
p;x~
in riiot
5.0(3)
N. A.
5 0 . C '.' 2 1
N. A.
100. 0(2)
4000. o;:i
10.0(2)
N. A.
„ , . n T '. ,
ra . ^- U. J isb
v.- e : L
0
C
N
S
0
X
17
80
S
k",bojn
c-
02
. A.
.A.
0
0
0(5)
7
0
.A.
•'• - 70
r for .--.
;AL.
Safetv
K.-.ctor
-------
Criteria Based on Potential Carcinogonicity
To establish AL's for DDT, aldrin, and dieldrin, a different
method for deriving AL's must be used, since there is evidence
Uiat DDT, aldrin, and dieldrin represent a potential carcinogenic
hazard to humans, based on experiments with rats and mice
(9, 10, 11, 12). Aldrin is readily converted to dieldrin by animals,
soil microorganisms, and insects, and thus the potential carcin-
ogenicity of aldrin will be considered to be equivalent to that of
dieldrin (13).
It is recognized that scientists have yet to determine if there
is any level of exposure to chemical carcinogens that is completely
free of risk of cancer. For the purpose of setting these standards
we will assume that the risk of inducing cancer decreases with
decreasing dose. Thus, the limits for these possible carcinogens
will be derived by estimating the health risk associated with
various concentrations and comparing these concentrations with
ambient levels to assess (he attainability of the proposed limits
with presently known means of technology.
-------
Monitoring data available from tho Community Water Supply
Studies Program (CWSS) carried out during 1969 to 1971 are too
questionable to be used as a basis for any conclusions. Original
records of the analyses were lost during Hurricane Camille.
The only other record which might indicate the ambient level of
chlorinated pesticides in drinking water supplies is a survey by
the Federal Water Pollution Control Administration published
in 1969 as "Pesticides in Surface Waters of the United Stales --
A Five Year Summary (1964-1968)". Obviously one cannot make
the assumption that all of the surface waters analyzed in this
survey .were utilized as drinking water supplies, and no definite
conclusions can be reached on ambient levels in drinking water
based on these data.
Since so little information-is available concerning the concen-
trations of aldrin, dieldrin and DDT currently ui the nation's
drinking waters, EPA has decided to delay the proposal of limits
for these compounds pending the completion of a survey of
selected water supplies to estimate the extent of current pesticide
levels in U. S. drinking water supplies. This survey should be
completed within six months.
-------
Upon the completion of this survey, limits for aldrin, dicldrin
and DDT will be proposed, based upon an analysis of the health
risks associated with low levels of intake of these pesticides and
available information concerning attainability. Risk estimates
at very low levels of exposure are subject to great uncertainties,
but the best available methods for making such estimates will be used.
Extrapolation techniques such as the "one-hit" model and the
Mantel-Bryan use of the probit model (14) are being intensively
reviewed by several agencies of the federal government. Every
effort will be made to set the limits for these pesticides at
concentrations which will adequately protect public health without
imposing economic hardship. The Agency believes that limits
far more stringent than those considered in the past should be
promulgated.
Aldrin-Dieldrin
Experiments carried out on mice (strain CF1) fed dieldrin in
their daily diet, at levels varying from 0.1 to 20 ppm during their
norir.nl life span, resulted in significant increases in (lie incidence
of liver tumors (11). The results of this study appear to be, at
present, the most appropriate for calculating the risk associated
with a range of concentrations of dieldrin in drinking water.
-------
DDT:
Although earlier studies of the carcinogenic effect of DDT have
yielded generally negative results, three recent studies in experi-
mental animals conflict with these previous findings. Using tumor-
susceptible hybrid strains of mice, Lines et al (15) produced
significantly increased incidences of tumors with the administration
of large doses of DDT (46.4 mg/kg/day). In a separate study in
mice extending over five generations, a dietary level of 3 ppm of
DDT produced a greater incidence of leukemia and malignancies
beginning with the F2 and F3 generations (16).
More recent information (12) on the effect of DDT on long-term
exposure in mice indicated a higher incidence of liver tumors in the
treated population. CF-1 minimal inbred mice were given technical
DDT mixed into the diet at the dose levels at 2, 10, 50 and 250 parts
per million (ppm) for the entire life span for two consecutive
generations. Exposure (o all four levels of DDT resulted in a
significant increase of liver tumors in males, this being most
evident at the highest level used. In females, the incidence of
liver tumors was slightly increased following exposure to
250 ppm. In DDT-treated animals the liver tumors were observed
at an earlier age than in untreated controls. The age at death with
liver tumors and the incidence of liver tumors appear to be directly
related to the dose of DDT to which the mice were exposed. Four
14 C
-------
liver tumors, all occurring in DDT-ln ated mice, c/ive metastases.
Histologieally, liver tumors were either well-differentiated nodular
growths, pressing but not infiltrating the surrounding parenchyma,
or nodular growths in which the architecture of the liver was
obliterated showing ('lanclular or trabecular patterns. The results
of this study app'T.r to be, at present, the most appropriate to use
as a basis for extrapolating the risk associated with a range of
concentrations of DDT in drinking water.
Chlordanc and Heptachlor
Decau.se recent evidence also implicates chlordane and hcptnchlor
as potential carcinogens, establishment of limits for these pesticides
must lie based on considerations similar to those for aldrin, dicldrin
and DDT.
-------
REFERENCES
1. Dale, W.E., Gaines, T. B., Hayes, W. M. , Jr., and Pcarco, G.W.,
Poisoning by DDT: Relationship Between Clinical Signs and Con-
centrations in Rat Brain, Science 142:1474 (1963).
2. Lehman, A.J., Summaries of Pesticide Toxicity. Association
of Food and Drug Officials of the U.S., Topeka. Kansas, 1965,
pp. 1-40.
3. Treon, J. F., Cleveland, F. P., and Cappel, J., Toxicity of
Endrin for Laboratory Animals, J. Agr. Food Chcm 3,
842-848, 1955.
4. Unpublished Report of Kettering Laboratory, University of Cincinnati,
Cincinnati, Ohio. Ci'ed in ''Critical Review of Literature Pertaining
to the Insecticide Endrin, " a dissertation for the Master's Degree
at the University of Cincinnati by J. Cole, 1966.
5. Stein, A. A., Serrone, D.M., and Coulston, F., Safey Evaluation
of Mcthoxychlor in Human Volunteers. Toxic Appl. Pharmacol. 7:
499, 1965.
6. Duggan, R. E. and Corneliusscn, P. E. Dietary Intake of Pesticide
Chemicals in the United States (in), June 1968-April 1970.
Pesticides Monitoring Journal 5 (4): 331-341, 1972.
7. Cohen, J.M. , Rourkc, G.A., and Woodward, R. L. : Effects of
Fish Poisons on Water Supplies. J. Amcr. Water Works Assn.
53(1): 49-62, 1961.
8. Sigworth, E. A., Identification and Removal of Herbicides and
Pesticides. J. Amcr. Water Works Assn. {,7(8):1016-1022,
19G5.
9. Fitzhugh, O. G., Nelson, A. A., and Quaife, M. L. Chronic Oral
Toxicity of Aldrin and Dieldrin in Rats and Dogs. Fed. Cosm.
Toxicol. 2:551, 1964.
10. Walker, A.I. T., Stevenson, D. E., Robinson, J. , Thorpe, E.,
and Roberts, M. Pharmacodynamics of Dieldrin (HEOD)-3:
Two Year Oral Exposures of Rats and Dogs. Toxicology and
Applied Pharmacology, 15:345, 1969.
-------
11. Walker, A.I.T., Thorpe, E., and Stevenson, D.E. The Toxicology
of Dieldrin (HEOD): Long-Term Oral Toxicity Experiments in Mice,
Fd. Cosmet. Toxicol Vol. 11. pp. 415-432," 1972.
12. Tonuitis, L., Turusov, V., Day, N., Charles, R.T.
The Effect of Long-Term Exposure to DDT on CF-1 Mice.
Int. J. Cancer 10, 489-50G, 1972.
13. Men/ic, Calvin M. Metabolism of Pesticides Publ. b> Bureau
of Sport Fisheries and Wildlife, SSR-Wildlife 127, Washington,
D.C.: 24, 1969.
14. Mantel, N., and Bryan, W.R. "Safety" Trsting of Carcinogenic
Agents. J. Nat. Cancer Inst. 27:455, 19G1.
15. Innes, J.R.M., Ulland, B.M., Valerio, M.G., Petrucelli, L.,
Fishbein, L., Hari, E.R., Pallotta, A.J., Bates, R.R..
Falk, H.L., Cart, .I.J., Klein, M., Mitchell, I., and Peters, J.,
Bioassay of Pesticides and Industrial Chemicals for Tumorigeni-
city in Mice: A Preliminary Note, J. Nat. Cancer Inst. 42
1101, 19G9. "
1G. Tarjan, R. and Kemeny, T., Multigeneration Studies on DDT in
Mice. Fd. Cosmet Toxicol. 7:215,1969.
143<
-------
13. Chlorophenoxy Herbicides
Aquatic weeds have become substantial problems in the U.S. in
recent years, and chemical control of this vegetation has won wide
acceptance. Since waters to which applications of herbicides are made
are sometimes employed as raw water sources of drinking water, there
is the possibility that herbicides may enter potable source water. Con-
sequently, a standard is needed for the more extensively used herbicides
so as to protect the health of the water consumer.
Two widely used herbicides are 2, 4-D (2,4-dichlorophenoxyacetic
acid) and 2,4,5-TP (silvex) [2-(2, 4, 5-trichloroplienoxy)propionic acid],
(A closely related compound, 2,4,5-T (2,4, 5-trichlorophenoxyacetic
acid) had been extensively used at one time, but lias been banned for
major aquatic uses. | Each of these compounds is formulated in a variety
of salts and esters that may have a marked difference in herbicidal
properties, but all of which are hydrolyzed rapidly to the corresponding
acid in the body.
The acute toxicity following oral administration to a number of
experimental animals is moderate. Studies (1-4) of the acute oral
toxicity of the chlorinated phenoxyalkyl ..jids indicate that there is
approximately a three-fold variation between the species of animals
studied. It appears that acute oral toxicity of the three compounds
is of about the same magnitude within each species (e.g., in the rat,
an oral LD of about 500 mg/kg for each agent).
14 4 <
-------
The subacutc oral toxicity of chl»rophcnoxy herbicides has been in-
vestigated in a number of species of experimental animals (1-G). The
dot; was the most sensitive species studied and often displayed mild
injury in response to doses of 10 mgAg/day for 90 days, and serious
effects from a dose of 20 mg/kg/day for 90 days. Lehman (G) reported
that the no-effect level of 2,4-D is 50* mgAg/day in t')C ra*) a»d
8.0 mg/kg/day in the dog.
Although 2,4, 5-T has been banned for all aquatic uses there is con-
siderable interest as to wl;^ this action was taken, so for informational
purposes, a discussion of the toxicity of this herbicide is included. Ii\
a study of various pesticides and related compounds for leratogenic
effects, Cortney, et al. (7) noted terata and embryotoxicily from
2, 4, 5-T. These effects were evidenced by statistically increased
proportions of litters affected and of abnormal fetuses within the liilers
(notably, cleft palate and cystic kidneys). Effects were noted in both
mice and rats, although the rat appeared to be more sensitive to this
effect. A dosage of 21.5 mg/kg produced no harmful effects in mice,
while a level of 4.6 mgAg caused minimal, but statistically significant,
effects in the rat. More recent work (8) has indicated that a contaminant
(2, 3, 7, 8-letrachlorodibenzo-p-dioxin) which was present at approximately
30 ppm in the 2,4, 5-T formulation originally tested was highly toxic to
experimental animals and produced fetal and maternal toxicity at .levels
as low as 0.0005 mg/kg. However, purified 2,4, 5-T has also produced
*In the March 14, 1975, issue of this document, this figure was erroneously
written as 0. 5. . t
1 •>..>"-'
-------
leratogenic effects in both hamsters :md rats at relatively high dosage
rates (9). Current production sampi-vs of 2,4,5-T that contain less than
1 ppni of dioxin did not produce enibryotoxicity or tcrata in rats at
levels as high as 24 mg/kg/day (10).
The subacute and chronic toxicity of 2,4,5-TP lias been studied in
experimental animals (11). The results of 90-day feeding studies
indicate that the no-effect levels of the sodium and potassium salts of
2,4,5-TP are 2 mg/kg/day in rats, and 13 mg/kg/day in dogs. In
2-year feeding studies with these same salts, the no-effect levels were
2.G mg/kg/day in rats and 0.9 mg/kg/day in dogs.
Some data are available on the toxicity of 2,4-D to man. A daily
dosage of 500 mg (about 7 mg/kg) produced no apparent ill effects in
a volunteer over a 21-day period (12). When 2,4-U was investigated
as a possible treatment for disseminated coccidioidomycosis, the
patient had no side effects from 18 intravenous doses during 33 tiiys:
each of the last 12 doses in the series was 800 mg (about 15 mg/kg)
or more, the last being 2000 mg (about 37 mg/kg) (13). A nineteenth
and final dose of 3GOO mg (67 mg/kg) produced mild symptoms.
The acute oral close of 2,4-D required to produce symptoms in man
is probably 3000 to 4000 mg (or about 45 to GO mg/kg). A comparison
of other toxiciiy values for 2,4,5-TP indicates that the toxicity of these
two agents is of the same order of magnitude. Thus, in the absence of
any specific toxicologic data for 2,4,5-TP in man, it might be estimated
that the acute oral dose of 2,4,5-TP required to produce symptoms in
man would also be about 3000 to 4000 mg.
-------
In addition to these specific data, the favorable record of use exper-
ience of 2,4-D is also pertinent. Sixty-three million pounds of 2,4-D
were produced in 1965 while- there were no confirmed cases of occupational
poisoning and few instances of any illness due to ingest ions (14, 15).
One case of 2,4-D poisoning in man has been reported by Berwick (1C).
Table I displays the derivation of the approval limits for the two
chlorophenoxy herbicides most widely used. The long-term no-effect
levels (mg/kg/day) are listed for the rat and the dog. These values arc
adjusted by 1/500 for 2,4-D and 2.4.5-TP. The safe levels are then
readjusted to reflect total allowable intake per person. Since little
2, 4-D or 2,4, 5-TP are expected to occur in foods, 20% of the safe
exposure level ciui be reasonably allocated to water without jeopardizing
the health of the consumer.
The approval limits for these herbicides are meant to serve in the
event that these chemicals inadvertently occ-.ir in the water. Deliberate
addition of these compounds to drinking water sources is neither
implied nor sanctioned.
14 7<
-------
TABLE I. DERIVATION OF APPROVAL LIMITS (AL) FOR CHLOROPKENOXY HERBICIDES
Compound
2,4-0
2,4,5-TP
Lowest Long-Tern
Levels with
Minimal or No Effects
Species
Rat
Dog
Rat
Dog
mg/kg/da/
50 (6)
8.0 (6)
2.6 (12)
0.9 (12)
Calculated MaxiT.um Safe Levels
From all Sources of Exposure
Safety
Factor (X)
1/500
1/500
1/500
1/500
:rg/kg/day
0.1
0.016
0.005
0.002
mg/r.an/day
7.0
1.12d
0.35
0.14d
Water
% of
Safe Level
20
20
AL
(mg/l)c
0.1
0.01
a Assume weight of rat = 0.3 kg and of dog = 10 kg; assume average daily food consumption
• of rat = 0.05 kg and of dog = 0.2 kg.
b Assune average weight of hurian adult = 70 kg.'
c Assume average daily intake of water for man = 2 liters.
d Chosen as basis on which to derive AL.
-------
REFERENCES
1. Hill, E.G. and Carlisle, H. Toxicity of 2,4-Dichlorophenoxy-
acelic Acid for Experimental Animals. J. Inclustr. Hyg. Toxicol.
29, 85-95, 1947. !
2. Lehman, A.J. Chemicals in Foods: A Report to The Association
of Food and Drug Officials on Current Development. Part II.
Pesticides. Assoc. Food Drug Off. U.S., Quart. Bull. 15, 122-133,
1951. ~
3. Ro\ve, V.K. and Hymas, T.A. Summary of Toxicological Informa-
tion on 2,4-D and 2,4,5-T Type Herbicides and an Evaluation of
the Hazards of Livestock Associated with Their Use. Amer. J.
Vet. Res. 15, 622-G29, ?954.
4. Drill, V.A. and Hiratzka, T. Toxicity of 2, 4-Dichloropheno.xyacetic
Acid and 2.4, 5-Trichlorophenoxyacetic Acid: A Report of Their
Acute and Chronic Toxicily in Dogs. Arch. Industr. Hyg. Qccup.
Mcd. 7, 61-G7, 1953. ! '.
5. Palmer, J.S. and Radeleff, R.D. The Toxicologic Effects of Certain
Fungicides and Herbicides on Sheep and Cattle. Ann N.Y. Acacl.
Sci. Ill, 729-730, 1964.
6. Lehman, A.J. Summaries of Pesticide Toxicity. Association of
Food and Drug Officials of the U.S., Topeka, Kansas, 19G5, pp 13-14.
7. Courtney, K.D., Gaylor, D.W., Hogan, M.D., and Falk, ILL.
Teratogenic Evaluation of 2,4,5-T. Science 168, 8G4, 1970.
8. Courtney, K.D., and Moore, J.A. Terratology Studies with 2, 4, 5-
Trichlorophcnoxyacelic Acid and 2, 3, 7, 8-Tetrachlorodibenzo-p-dioxin.
Toxicology and Applied Pharmacology 20, 39G, 1971.
9. Collins, T.F.X. and Williams, C.H. Teratogcnic Studies -with
2,4. 5-T and 2, 4-D in Hamsters. Dull, of Environmental Con-
tamination and Toxicology 6 (G):559-567, 1971.
10. Emerson, J.L., Thompson, D.J., Gerbig, C.G., and Robinson, V.B.
Teratogenic Study of 2, 4, 5-Trichlorophcnoxy Acetic Acid in the Rat.
Tox. Appl. Pharmacol. _17, 311, 1970.
11. Mullison, W.R. Some Toxicoiogical Aspects of Silvex. Paper
Presented at Southern Weed Conference, Jacksonville, Fla., 1966.
14 5) <
-------
12. Kraus, as cited by Mitchcss, J.W., Hogson, H.E., and
Gaetjons, C.F. Tolerance of Farm Animus to Feed Containing
2,4-Dichlorophcnoxyacetic Acid. J. Animal. Sci. 5,
226-232, 1946. "
13. Seabury, J.II. Toxicity of 2, 4-Dichlorophcnoxyacetic Acid for
Man and Dog. Arch. Envir. Health 7, 202-209, i963.
14. Hayes, W.J., Jr. Clinical Handbook on Economic Poisons.
PUS Pub. No. 476, U.S. Government Printing Office,
Washington, D.C., revised 1963.
15. Nielson, K., Kaenipe, D., and Jensen-Holm, J. Fatal Poisoning
in Man by 2,4-Dichlorophcnoxyacetic Acid (2,4-D): Determination
of the Agent in Forensic Materials. Acta Pharmacol. Tox. 22.
224-234, 1965.
16. Berwick, P., 2,4-Dichloroplienoxyacetic Acid Poisoning in Man.
J.A.M.A. 214 (6):114-117. 1970.
150"
-------
SELENIUM
The 1962 Drinking Water Standards Committee lowered the limit for
selenium in drinking water primarily out of concern over the possible
carcinogenic properties of the element. Data supporting the
carcinofjCnicity of selenium has not been forthcoming, and more recent
findings concerning the nutritional requirement for selenium has required
a comprehensive review of the data available concerning the toxicity of
selenium and its compounds.
The controversy over the present limits of selenium acceptable in the
environment is largely the result of the demonstration by Schwarz and
Foltz (2) that the element vas an integral part of "factor 3," recognized
for some time as essential in animal nutrition. While definite evidence
is still lacking for a nutritional requirement for selenium in man, certain
cases of protein-resistant kwashiorkor have been shown to be responsive
to administration of the element (3).
Consideration of a maximal concentration of selenium allowable in .
drinking water is further complicated by the many secondary factors known
to affect both the efficacy of selenium in alleviating deficiency syndromes
and the intakes associated with toxicity. The chemical form of selenium
(4), the protein content of the diet (5), the source of dietary protein (G),
the presence of other trace elements (1, 7, 8), and the vitamin E intake
(9, 10, 11) all affect the beneficial and/or adverse effects of selenium in
experimental animals. The fact that these interactions are not simple
is illustrated by the comments of Frost (1) on the well-known antagonism
-------
of arsenic in selenium tuxicity (1, 7, ft, 12). Me has found Uial arsenic
in drinking water accentuates the toxirity of selenium in drinking water
in contrast to the protective effect of arsenic seen when selenium was
administered via the diet. Consequently, when considering "safe" levels
of selenium in drinking water, consideration must also be given to the
variability in these oilier factors which are certain to occur in any given
population.
The current limit of 0.01 nig/liter of selenium in drinking water is
based on the total selenium content. No systematic investigation of the
forms of selenium in drinking water sources with excessive concentrations
has ever been carried out. Since elemental selenium must be oxidized
to solenite or selenatc before it has appreciable solubility in water (13),
one would predict that these would be the principal inorganic forms that
occur in water. Organic forms of selenium occur in seleniferous soils
and have sufficient mobility in an aqueous environment to be preferen-
tially absorbed over selenate in certain plants (14). However, the extent
to which these compounds might occur in source waters is essentially
unknown.
There is considerable difficulty involved in determining what the
required level and toxic levels of selenium intake in humans might be.
The basic problem is that dietary selenium includes an unknown variety
of selenium compounds in varying mixtures. Toxicologic examination
uf plant sources of selenium lias revealed that selenium present in
seleniferous grains is more toxic than inorganic selenium added to the
-------
diet (1C). Although there is a fairly extensive literature on industrial
exposures to selenium (see Cerwenka and Cooper, 19G1 (17), and Cooper,
19G7 (18) for reviews of this subject), the results do not apply well to
environmental exposures since the only studies that made an attempt
to document systemic absorption involved elemental selenium (19).
Elemental selenium is virtually non-toxic to plants and animals that
have been shown to be very sensitive to the water soluble forms of
selenium.
Only one documented case of human selenium toxicity for a water
source uncomplicated with selenium in the diet has been reported (21).
Members of an Indian family developed loss of hair, weakened nails,
and listlcssncss after only 3 months' exposure to well-water containing
9 mg./l. The children in the family showed increased mental alertness
after use of water from the selenifcrous well was discontinued, as
evidenced by better work in school (22).
Smith and co-workers (23, 24) reported the results of Iheir studies
dealing with human exposure to high environmental selenium concentra-
tions in the 1930's. They reported a high incidence of gastrointestinal
problems, bail teeth, and an icteriod skin color in scleniferous areas.
The individuals exhibiting these symptoms had urinary selenium levels
of 0.2-1.98 jug/liter as compared to the 0.0-0.15 ug/litcr that Glover
(19) indicates to be the normal range. The gastrointestinal disturbances
and the icteriod discoloration of the skin apparently have their counter-
-------
parts in (ho anorexia (23) and bilirubineniia (7), respectively, in rats
fed selenium. The effect of selenium on teeth has had some marginal
documentation in rats (2G); and has been supported by Hadjimarkos (27)
and refuted by Cadell and Cousins (28) in epidomiologic studies.
From urinary concentrations of selenium, Smith and Weslfall (24)
estimated that the individuals displaying these symptoms were ingesting
0.01 to 0.10 mgAg/day, and possibly as much as 0.20 mgAg/day.
For the 70 kg man, this would amount to a daily intake of 700 to
7000 ug/day. Smith (24, 29) also presented the range of selenium
concentrations found in various food classes in the areas in which the
field studies had been conducted. With the use of the table provided in
Dietary Levels of Households in the U.S. , Spring 19G5 (U. S. D.A. Agri.
Res. Service), calculations from these data result in a range of intake
of GOO-G300 ug/day, very close to the estimates made from urinary
concentrations of selenium. These intakes of selenium correspond in
the main with the levels producing adverse effects in other mammalian
species. Tinsley et al. (25) found that an intake of 0.125 mgAg/day
adversely affected early growth in rats. 1.1 mgAg, administered
twice weekly (ca. 0.3 mgAg/day), lias been found to adversely affect
growth and to increase mortality in Hereford steers (30). Mortality
in ewes was increased at 0.825 mgAg/day. The steers were adminis-
tered sodium selcnitc; the ewes sodium selcnale. Although these levels
arc slightly higher than those reported for the human exposures, it must
be remembered thru the parameters measured would not be acceptable
either in terms i,f severity or incidence in the human population.
15 •!<
-------
Few studies have been performed to specifically examine the toxlcity
of selenium administered in drinking water. Pletnikova (31) found the
rabbit to be very sensitive to selenium as selenite. Ten pg/1 in drinking
water resulted in a 40*) reduction in the elimination of bromosuiphalein
by the liver. Since no apparent consideration was given to the selenium
content of the diet of these animals, the meaning of this result in terms
of liver function is obscure. If the sole intake of selenium were from
the water in these studies, the controls had to be deficient and the
experimental group marginal, at best, in terms of the dietary require-
ment for selenium. The duration of the study was 7 1/2 months. Schroeder
(32) has indicated that intake of selenite from drinking water is more toxic
than when mixed with food. However, this suggestion was not based on a
direct experimental comparison. Roscnfcld and Death-(33) studied the
effects of sodium selcnalc in drinking water on reproduction in rats.
Selenium concentrations of 2. 5 mg/1 reduced the number of young reared
by the second generation of mothers, and 7. 5 mg/'l prevented reproduction
in females.
Early work (34), using both naturally occurring, and a sclenide salt,
indicated the formation of adenomas and low-grade non-metastasizing hepatic
cell carcinomas in 11 of 53 rats surviving 18 months of diets containing
selenium. Harr el al. (24), in a much more extensive study using .selenite
and sclenate salts, found no evidence of neoplasms that could be attributed
to the addition of these selenium compounds to the diet at 0. 5 - 16 ppm.
Volgancv and Tschenkcs (35) negated their earlier results, which had
-------
indicated that 4.3 mg/1 soieiiiuni as sclcnite ii. the diet gave rise to tumors,
but luid not used proper controls. It should be noted that these studies
are not a direct negation of the earlier studies implicating selenium as
a carcinogen, since entirely different compounds of selenium were used
in the early work. Consequently, the possibility that other compounds
of selenium, besides selenitc and selenalc, possess carcinogenic pro-
perties cannot be strictly ruled out. The carcinogenic properties of
selenium are further complicated by recent reports of the effectiveness
of selenium, 1 mg/1 (as selenite), in reducing papillomas induced by
various chemicals in mice (36).
Any consideration of a maximum allowable concentration of selenium
must include the evidence that the element is an essential dietary require-
ment. A range of 0.04 to 0.10 mg/1 in the diet is considered adequate
to protect animals from the various manifestations of selenium deficiency
(10, 37, 38). Using the recent data on Morris and Levander (39), an
estimate of the present average daily intake of selenium by the American
population may be calculated. This figure approximates 200 ug/day and
some variation around this figure would be anticipated primarily as
the result of individual preferences, particularly in meats. Since no
deficiency diseases of selenium have been reported to date in the U.S..
it may be assumed that 200 ug/day of selenium is nutritionally adequate.
-------
Signs of selenium toxicity have been seen at an estimated level of
selenium intake of 0.7-7 mg/day according to the data of Smith et al.
(23, 24). At the present limit on selenium content of drinking water,
water would increase the basal 200 tig/day intake of selenium by only
10r-y, if one assumes a 2-liler ingestion of water per day. This results
in a minimum safety factor of 3, considering the lower end of the range
of selenium intakes that have been associated with minor toxic effects
in man. In view of the relative scarcity of data directly applicable to
the apparent small margin of safety brought about by selenium contained
in the diet, selenium concentrations above 0.01 mg/liter shall not be
permitted in the drinking water.
-------
REFERENCES
1. Frost, Douglas V. (19G7) Significance of The Symposium. In
Symposium: Selenium in Biomedicine, O.H. Mutli. Ed. AVI
Publishing Co., Inc., Westport, Conn. p. 7-2G.
2. Schwaiv,, K. and Foltz, C.M., Selenium As An Integral Part of
Factor 3 Against Dietary Nccrotic Liver Degeneration. J. Am.
• Chem. Soc. 79:3292.
3. Hopkins, L.L., Jr., and Majaj. A.S. (19C7) Selenium in Human
Nutrition in Symixjsium: Selenium in Biomedicine. O.H. Mulh, Ed.
AVI Publishing Co., Lie., Westport, Conn. p. 203-214.
4. Schwar/., K. and Fvedga, A. (19G9) Biological Patlerny of Organic
Selenium Compounds. I. Aliphatic Moneseleno and Diseleno Di-
carboxific Acids. J. Biol. Chem. 244, 2103-2110.
5. Smith, M.I. (1939) The Influence of Diet on The Chronic Toxicity
of Selenium. Public Health Report (U.S.) 54, 1441-1453.
G. Levander. O.A., Young, M.L. and Meeks, S.A. (1970) Studies
on The Binding of Selenium by Liver Homogcnates From Rats Fed
Diets Containing Either Casein or Casein Plus Linseed Oil Meal.
Toxicol. andAppl. Pharmacol. 16, 79-87.
7. Halverson, A.W., Tsay, Ding-Tsair, Tricbevasscr, K.C. and
Whilehead, E.I. (1970) Development of Hemolytic Anemia in
Rats FedSclenite. Toxicol. andAppl. Pharmacol. 17, 151-159.
8. Levander. O.A. and Bauman, C.A. (196G) Selenium Metabolism VI.
Effect of Arsenic on The-Excretion of Selenium in the Bile. Toxicol.
andAppl. Pharmacol. 9, 10G-115.
9. Levander, O..'.. and Morris, V.C. (1970) Interactions of Methionine,
Vitamin E, and Antioxidants in Selenium Toxicily in the Rat. J.
Nutrition 100:1111 -1118.
10. Schwar/., K. (19GO) Factor 3, Selenium, and Vitamin E. Nutrition
Reviews. 18, 193-197.
11. Sondegaarcl,' Ebbe. (1967) Selenium and Vitamin E. Interrelationships
In Symposium: Selenium in Biomedicine AVI Publishing Co., Die.,
Weslport, Conn. O.H. Much Ed. pp. 365-381.
158 <
-------
12. MoxoiL.A.L., DuB'-iis, K.P. and Potter, R.L. (1941) The
Toxicity of Optically Inactive d, and 1-Seltnium Cysline.
J. Pharm. and Exp. Ther. 72, 184-195.
13. Lakin, Hubert W. and Davidson, David F. (1967) The Relation
of Tne Geo-Chemistry of Selenium to Its Occurrence jn Soils.
In Symposium: Selenium in Biomedicine p. 27-56.
14. Hamilton, John W. and Death, O.A. (19G4) Amount and Chemical
Form of Selenium in Vegetable Plants, Agr. and Food Cliem. 12,
371-374.
15. Olson, O.E. (1967) Soil, Plant, Animal Cycling of Excessive Levels
of Selenium. In Symposium: Selenium in Biomcdicine (AVI Pub-
lishing Co., Lie., Westport, Conn.)O.II. Muth, Ed. pp. 297-312.
16. Frankc and Potter (1935) J. Nutr. 10, 213.
17. Cerwenka, Edward. A., Jr. and Cooper, W. Charles (1961) Toxi-
cology of Selenium on Tellurium and Their Compounds. Arch.
Environ. Hlth. 3, 71-82.
18. Cooper. W. Charles (1967) Selenium Toxicity in Man. In Symposium:
Selenium in Biomcdicine. (AVI Publishing Co., Inc., Westport,
Conn.) O.H. Much. Ed. pp 185-199.
19. Glover, J.R. (19G7) Selenium in Human Urine: A Tentative Maxium
Allowable Concentration for Industrial and Rural Populations.
Ann Occup.Hyg. 10, 3-14.
20. Schwarz, K. and Foil/, C.M. (1958) Factor 3 Activity of Selenium
Compounds. J. Biol. Chem. 233, 245.
21. Death, O.A. (19G2) Selenium Poisons Indians. Science News
Letter 81, 254.
22. Rosenfeld. I. and Heath, O.A. (19G4) Selenium. Geobotany, Bio-
chemistry, Toxicicity and Nutrition. Academic Press, N.Y. and
London.
.23. Smith, M.I., Frankc, K.W. and Wcstfaii, D.B. (193G) The
Selenium Problem in Relation to l\iblic Health. Public Health
Reports. (U.S.) 51, 1496-1505.
24. Smith, M.I. and Wcstfaii, B.B. (1937) Further Field Studies on
The Selenium Problem in Relation to Public Health. Public Health
Report (U.S.) 52, 1375-1384.
-------
25. Tinsley, I.J., Harr, J.R., Bone, J.F., Weswig, P.H. and
Yamamoto, R.S. (1967) Selenium Toxicity in Rats I. Growth and
Logevity. In Symposium: Selenium in Biomedicine (AVI
Publishing Co., Inc., Westport, Conn.) O.H. Muth, Ed. pp. 141-152.
26. Wheatcraft, M.G.. English, J.A. and Schlack, C.A. (1951) Effects
of Selenium on The Incidence of Dental Caries in White Rats. J.
Dental Res. 30, 523-524.
27. Hadjimarkos, D.M. (1965) Effect of Selenium on Dental Caries.
Arch. Environ. Health 10, 893-899.
28. Caclell, P.B. and Cousins, F.B. (1960) Urinary Selenium and
Dental Caries Nature 185, 863.
29. Smith, M.I. (1941) Chronic Endemic Selenium Poisoning. J.A.M.A.
116, 562-567.
30. Magg, D.D. and Glenn, M.W. (1967) Toxicily of Selenium: Farm
Animals. In Symposium: Selenium in Biomedicinc (AVI Publishing
Co., Die., Westport, Conn.) O.H. Muth, Ed. pp. 127-140.
31. Pletnikova, I. P; (1970) Biological Effect and Safe Concentration of
Selenium in Drinking Water. Hygiene and Saittitation 35, 176-181.
32. Schrocdcr, Henry A. (1967) Effects of Selenate, Selcnite and Tell-
urite-on The Growth and Early Survival of Mice and Rats. J. Nutri.
92, 334, 338.
33. Rosenfeld, I. and Death, O.A. (1954) Effect of Selenium on Repro-
duction in Rats. Proc. Soc. Expl Bio.) and Med. 87, 295-299.
34. Fitzhugh, O.G., Nelson. A.A. and Bliss, C.I. (1944) The Chronic
Oral Toxicity of Se.'cnium. J. Pharmacol. 80, 289-299.
35. Volganev, M.N. and Tschenkes, L.A. (1967) Further Studies in
Tissue Changes Associated With Sodium Selenate. Li Symposium:
Selenium in Biomedicine (AVI Publishing Co., Inc., Westport,
Conn.) O.H. Muth, Ed. pp. 179-184.
36. Shamberger, R..J. (1970) Relationship of Selenium to Cancer I.
Inhibitory Effect of Selenium on Carcinogensis J. Natl. Cancer
Inst. 44, 931-936.
-------
37. Noshcim, M.C. and Scott, M.L. (1961) Nutritional Effects of
Selenium Compounds in Chicks and Turkeys. Fed. Proc. 20,
G74-G78.
38. Oldfield, J.E., Schubert, J.R., and Mulh, O'.H. (1963) Implica-
tions of Selenium in Large Animal Nutrition. J. Agr. Food Chem.
11, 388-390.
39. Morris, V.C. and Levander, O.A. (1970) Selenium Content of
Foods J. Nutri. 100, 1383-1388.
-------
SILVER
The need to set a water standard for silver (Ag) arises i'rom its
intentional addition to waters as a disinfectant. The chief effect of
silver in the body is cosmetic. It consists of a permanent blue-grey
discoloration of the skin, eyes, and mucous1 membranes which is un-
sightly and disturbing to the observer as well as to the victim. The
amor::* of colloidal silver required i.o produce this condition (argyria,
argyrosis), and to serve as a basis of determining the water standard,
in not known, however, but the amount of silver from injected Ag-
arphenamine, which produces argyria is precisely known. This value
is any amount greater than 1 gram of silver, 8g Ag-arsphenamine,
in an adult (1, 2).
From a review (2) of more than 200 cases of argyria, the following
additional facts were derived. Most common salts of silver produce
argyria when ingested or injected in sufficient doses. There is a long-
dolayed appearance of discoloration. No case lias been uncovered that has
resulted from an idiosyncrasy to silver. There was, however, consider-
able variability in predisposition to argyria; the cause of this is unknown,
but individuals concurrently receiving bismuth medication developed
argyria more readily. Although there is no evidence that gradual deposi-
tion of silver in the body produces any significant alteration in physiologic
function, authorities are of the opinion that occasional mild systemic
effects fro n silver may have been overshadowed by the .striking external
changes. In this connection, there is a report (3) of implanted silver
-------
amalgams resulting in localized argyria restricted to the elastic fibers
and capillaries. The hislopalhologic reaction resembed a blue nevus
simulating a neoplasm with filamentous structures and globular masses.
Silver affinity for elastic fibers had been noted a half-century earlier (5).
A study (5) of the metabolism of silver from inlragastric intake in
the rat, using radio-silver in carrier-free tracer amounts, showed
absorption to be less than 0.1-0. 2 percent of the silver administered;
but this evidence is inconclusive because of the rapid elimination of silver
when given in carrier-free amounts. Further study indicated, however,
that silver is primarily excreted by the liver. This would be particularly
true if the silver were in colloidal form. Silver in the body is transported
chiefly by the blood stream in which the plasma proteins and the red
cells carry pratically all of it in extremely labile combinations. The
half-time of small amounts of silver in the blood stream of the rat was
about 1 hour. A later report (G), using the spectrographic method on
normal human blood, showed silver unmistakably in the red blood cell
and questionably in the red cell ghosts and in the plasma. Once silver
is fixed in tiie tissues, however, negligible excretion occurs in the
urine (7).
A study (8) of the toxicologic effects of silver added to drinking water
of rats at concentrations up to l,000^ig/l (nature of the silver salt
unstated) showed pathologic changes in kidneys, liver, and spleen at
400, 700, and 1,000 jug/1, respectively.
•1 *:';.
.JLv^ ^._*
-------
A study (9) of the resorption of silver through liunum skin using radio-
silver Ag1" lias shown none passing the dermal barrier from either
solution (2 percent AgNO,) or ointment, within limits of experimental
error (+_ 2 percent). This would indicate no significant addition of
silver to the body from bathing waters treated with silver.
Uncertainty currently surrounds any evaluation of the amount of
silver introduced into the body when silver-treated water is used for
culinary purposes. It is reasonable to assume that vegtables belonging
to the family Brassicoceae, such as cabbage, turnips, cauliflower,
and onions, would combine with residual silver in the cooking water.
The silver content of several liters of water could thus be ingested.
Because of the evidence (7) that silver, once absorbed, is held
indefinitely in tissues, particularly the skin, without evident loss
through usual channels of elimination or reduction by transmigration
to other body sites, and because of the probable high absorbability
of silver bound to sulfur components of food cooked in silver-containing
waters [the intake for which absorption was reported in 1940 to amount
to GO-80 .ug per day (10)|, the concentration of silver in drinking water
shall not exceed 0.05 mg/1.
16-1 <
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REFERENCES
1. Hill, W.D., and Pillsbury, D.M. Argyria. Tlie Pharmocology of
Silver. Baltimore, Md., Williams and Wilkins, 1939, 172pp.
2. Ibid., Argyria Investigation-Toxicologic Properties of Silver, Am.
Silver Producers Res. Proj. Report. Appendix II, (1957).
3. Bell, C.D., Cookey, D.B., and Nickel, W.R. Amalgam Tatoo-
localized Argyria. A.M.A. Arch Derm. Syph. 66: pp. 523-525 (1952).
4. Joseph, M., and Van Deventer, J.B. Atlas of Cutaneous Morbid
Histology. W.T. Kliner&Co., Chicago, 1906.
5. Scott, K.G., and Hamilton, J.G. The Metabolism oi Silver in The
Rat With Radiosilver Used As Indicator. U. of Cal. Publ. in
Pharm. 2: pp. 241-262 (1950).
6. Wyckoff, R.C.. and Hunter, F.R. Spectrographic Analysis of Human
Blood. Arch. Biochem. 63: pp. 454-460 (1956).
7. Aub, J.C. and Fairhall, L.T. Excretion of Silver in Urine. J.A.M.A.
118: p. 319 (1942).
8. .Just. .1. and Szniolis, A. Germicidal Properties of Silver in Water.
J. Am. Water Works A., 28: 492-506, April 1936.
9. Norgaard, O. Investigations with Radio Ag Into the Rcsorplion
of Silver Through Human Skin. Acts Dermatovener 34: 415-4119
(1945).
10. Kehoe, R.A., Cholak, J., and Story, R.V. Manganese, Lead, Tin,
Copper and Silver in Normal Biological Material. J. Nutr. 20:
85-98 (1940).
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SODIUM
Man's intake of sodium is mostly influenced by the use of salt. Intake
of sodium chloride for American males is estimated to be 10 grams per
day, with a range of 4 to 24 prams (1). This would be a sodium intake
of 1 GOO to UGOO mg per day. Intake of these amounts is considered by
most to have no adverse effect on normal individuals. Even Dahl, who
has been one of the strong advocates of the need for restricting salt intake,
has felt that an intake of 2000 mg of sodium could be allowed for an adult
without a family history of hypertension. Intake of sodium from hospital
"house" diets has been measured recently (2). The sodium content of a
pool of 21 consecutive meals that were seasoned by the chef or the
dietitian from twenty selected general hospitals was determined each
quarter. The average sodium intake per capita per day was 3G25 _+
971 (SD) milligrams. The intake could be greatly changed between
individuals who never acid salt to the food at the table and the individuals
who always acid salt even before tasting.
The taste threshold of sodium in water depends on several factors (3).
The predominant anum has an effect; the thresholds for sodium were
500 mg/1 from sodium chloride, 700 mg/1 from sodium nitrate, and
1000 mg/1 from sodium sulfatc. A heavy salt user had a threshold of
taste that was 50 percent higher, and the taste was less delectable
in cold water.
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Six of 14 infants exposed to a sodium concentration of 21,140 mg/1
died when salt was mistakenly used for sugar in their formula (4). Sea
water would have about 10, 000 mg/1 of sodium.
Severe exacerbation of chronic congestive heart failure due to sodium
in water has been documented (3). One patient required hospitalization
when he changed his source of domestic water to one that had 4200 mg/1
sodium. Another patient was readmitted at tv/o-to-three-week intervals
when using a source of drinking water of 3500 mg/1 sodium.
Sodium-restricted diets are used to control several disease conditions
of man. The rationale, complications, and practical aspects of their
use were reviewed by a committee on food and nutrition of the National
Research Council (5). Sodium-restrictive die's are essential in treating
congestive cardiac failure, hypertension, renal disease, cirrhosis of the
liver, toxemias of pregnancy, and Meniere's disease.
Hormone therapy with ACTH and cortisone is used for several diseases.
Sodium retention is one of the frequent metabolic consequences following
administration of these therapeutic agents, and sodium-restricted diets
are required, especially for long periods of treatment. More recent
medical text books continue to point out the usefulness of sodium-restricted.
diets for these several diseases where fluid retention is a problem (G).
When disease causes fluid retention in the body, with subsequent edema
and ascite.s, there is a diminished urinary excretion of sodium and of
water. If the sodium intake is restricted in these circumstances, further
1G7<
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fluid retention will usually not occur, and the excess water invested will
be excreted in the urine because the mechanisms that maintain the con-
centration of sodium in the extracellular fluid do not permit the retention
of water witho.it sodium.
Almost all foods contain some sodium, and it is difficult to provide
a nutritionally adequate diet without an intake of about 440 mg of sodium
per day from food; this intake would be from the naturally occurring
sodium in food with no salt added. The additional 60 mg that would
increase the intake to the widely used restricted diet of 500 nig per day
must account for all non-nutrition intake that occurs from drugs, water
and incidental intakes. A concentration of sodium in drinking water up
to 20 nig per liter is considered compatible with this diet. When the
sodium content exceeds 20 mg/1, the physician mi:st lake this into
account to modify the diet or prescribe that distilled water be used.
Water uiilities that distribute water that exceeds 20 mg/1 must inform
physicians of the sodium content of the water .so that the health of
consumers can be protected. About 40 percent of the water supplies
are known to exceed 20 mg/1 and would "io required to keep physicians
informed of the sodium concentration (7). Most of the State health
departments have made provision for determining the sodium content of
drinking water on a routine basis and a/e now informing physicians in
their jurisdiction (8). If change of source or a treatment change such
as softening occurs that will significantly increase the sodium concen-
tration, the utility must be sure that all physicians that care for
-------
consumers are aware of the impending change. Diets prescribing inUikcs
of less than 500 mg per day must use special foods such as milk with the
sodium reduced, or fruits that arc naturally low in sodium.
It is not known how many persons are on sodium-restricted diets and
to what extent the sodium intake is restricted. To reduce edema or
swelling, the physician may prescribe a diuretic drug, a sodium-restricted
diet, or a combination of the two. Therapy, of course, depends on the
patient's condition, but there arc also regional differences that probably
result from physician training. i'he American Heart Association (AIlA)
(9) feels that diuretics may allow for less need of very restricted diets
and that diuretics are necessary for quick results in acute conditions.
For long-term use, a sodium-restricted diet is simpler, safer, and
more economical for the patient. It is preferable, especially when a
moderate or mild sodium-restrir.cd Jiet will effectively control the
patient's hypertension and water retention. Literature is provided to
physicians by the AKA to distribute to their paticr.ts explaining the
sodium-restricted diets. These cover the "strict" restriction - 500 mg
sodium, "moderate" restriction - 1000 mg sodium, and ihe "mild"
restricted diet - 2400 to 4500 ing sodium. From 1958 through June
1971, there were 2, 305, 000 pieces of this literature distributed:
31% - 500 mg; 34r,o - 1000 mg; and 29% - "mild" (10). There are many-
ways a physician can counsel his patients other than using this literature,
so the total distribution does not reflect the extent of the problem, but
the proportion of booklets distributed may provide an estimate of the
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tion of diets that arc proscribed. Tlio "mild" restricted diet could
require just cutting down on the use of salt, and literature for the
patient would not be as necessary.
The AHA estimates that hypertension affects more the 21 million
Americans, and in more than half of these cases put enough strain on
the heart to be responsible for the development of hypertensive heart
disease (11). Congestive heart failure is a sequelae of several forms
of disease that damage the heart and would affect some unknown portion
of the 27 million persons with cardiovascular disease. Thus, from 21
to 27 million Americans would be concerned with sodium intake.
Toxemias,af pregnancy arc common complications of gestation and
occur in G to 7 percent of all pregnancies in the last trimester (12).
Thus, about 230,000 women would be very concerned with sodium
intake each year. Other diseases are treated with restricted sodium
intake, but no estimate can be made on the number of peop!c involved.
Questions about salt usage were asked on the ninth biennial examina-
tion of the National Heart Institute's Framingham, Massachusetts
Study (13). The study population was free of coronary heart disease
when the study began in 1949 and now arc over 45 years of age. There
were 3,833 respondents. Forty-five percent of the males and 30 percent
of the females reported that they add salt routinely to their food before
tasting. But at the other extreme, 9 percent of the men and 14 percent
of the women avoid salt intake. More of .he people GO and over avoid
salt intake than the 45 to 59 population. It is not determined if the salt
restriction was medically prescribed nor how extensively the sodium
intake was restricted. 1.7 (/~
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It can be seen that a .significant proportion of (lie population needs to
and is trying to curtail its sodium intake. The sodium content of drinking
water should not be significantly increased for frivolous reasons. This
is particularly true of locations where many of the people using the water
would be susceptible to adverse health effects, such as hospitals, nursing
homes, and retirement communities. The use of sodium hypochlorite
for disinfection, or sodium fluoride for control of tooth decay, would
increase the sodium content of drinking water but to an insignificant amount.
The use of sodium compounds for corrosion control might cause a
significant increase, and softening by either the base exchange or lime-
soda ash process would significantly increase the sodium content of
drinking water. For each milligram per liter of hardness removed as
calcium carbonate by the exchange process, the sodium content would be
increased about one-half mg per liter. The increase in excess lime
softening would depend on the amount of soda ash added. A study in
North Carolina found that the sodium content of 30 private well-water
.supplies increased from 110 mg/1 to 2G9 mg/l sodium on the average
after softening (14). The sodium content of the softened water was much
higher shortly after the softener had been regenerated than later in the
cycle. A case has been reported where a replacement element type
.softener was not flushed, and the drinking water had a sodium content
of 3, 700 mg/1 when the unit was put back in service.
171-
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As a further deterrent to softening of water, it should be noted that
there is considerable evidence of an inverse relationship between water
hardness and certain cardiovascular diseases. Research in the area
is being accelerated to determine ca-.:se and effect relationships. Until
the full significance of water hardness is known, and because of the
increase in sodium content of softened waters, utilities should carefuly
consider the consequences of installing softening treatment.
All consumers could use the water for drinking if the sodium
content was kept below 20 mg per liter, but about 40 percent of the
U.S. water supplies have a natural or added sodium content above this
concentration (7). Many industrial wastes and runoff from deiced highways
may increase the sodium pollution of surface water (15). The problem
is most acute when ground water is polluted with sodium (1C, 17) because
it remain:; for a long time. Removal of sodium from water requires
processes being developed by the Office of Saline Water (18) and are
economically feasible only in certain situations.
The person who is required to maintain a restricted sodium intake
below 500 mg per day can use a water supply that contains 20 mg or less
sodium per liter. If the water supply contains more sodium, low sodium
bottled water or specially treated water will have to be used. In the
moderately restricted diet that allows for a consumption of 1000 mg sodium
per day the food intake is essentially the same, but the diet is liberalized
to allow the use of 1/4 teaspoon of salt, some regular bakery bread,
and/or some salted butter. If persons on the moderately restricted diet
-------
found it necessary to use a water witli a significant sodium content they
could still maintain their limited sodium intake with a water containing
270 mg/litcr. This would require allocating all the liberalized intake
to water (the original 20 mg/1 and 250 mg/1 more with two liter domestic
use, drinking or cooking, per day). High sodium in water causes some
transfer of sodium to foods cooked in such water (5).
It is essential that the sodium content of public water supplies be Known
and this information be disseminated to physicians who have patients in
the service area. Thus, diets for those who must restrict their sodium
intake can be designed to allow for the sodium intake from the public
water supply or the persons can be advised to use other sources of drinking
water. Special efforts of public notification must be made for supplies
that have very high sodium content so that persons on the more restricted
sodium intakes will not be overly stressed if they occasionally use these
water supplies.
The 1963 Sodium Survey (7) had the following percent distribution of
sodium concentration from 2100 public water supplies:
Ilange of Sodium Ion Percent of Total
Concentration Samples
mg/1 (',o
0 - 19.9 58.2
20 - 49.9 ' 19.0
50-99.9 9.3
100-249.9 8.7
250 -399.9 3.G
400 -499.9 0.5
500-999.9 0.7
Over 1000 0.1
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While the question of a maximum ciMiUunmiuU level for sodium
is still under consideration by the National Academy of Sciences and
others, no specific level will be proposed for the Interim Primary
Drinking Water Regulations. Tl.e Environmental Protection Agency
believes that the available data do not support any particular level
for sodium in drinking water, and that the regulation of sodium by a
maximum contaminant level is a relatively inflexible, very expensive
means of dealing will: a problem which varies greatly from person to
person.
17-1 <
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REFERENCES
1. Dahl, I...K. Possible Role of Salt Intake in The Development of
Essential Hypertension, From Essential Hypertension: An Inter-
national Symposium. P. Cottier and. K.D. Bock, Berne (Eds.)
Springer Verlag, Neidelberg pp. 53-65 (I960).
2. Bureau of Radiological Health. California State Department of
Public Health, Estimated Daily Intake of Radionuclidcs in
California Diets, April-December 1909, and January-.June 1970.
California State DejUnient of Health, Radiological Health Data and
"Reports, G250G32, November 1970 (1970).
3. Elliott, G.B., ami-Alexander, E.A. Sodium from Drinking-water
as An Unsuspected Cause of Cardiac Decompensation. Circulation
23: 502 (1901).
4. Finberg, L., Kiley, J., ami Luttrel, C.N. Mass Accidental Salt
Poisoning m Infancy. Mecl Assn. 184: 187 (1903).
187-190 (April 20, 1963).
5. Food and Nutrition Board-NAS-NRC, Sodium-Restricted Diets,
Publication 325, National Research Council, Washington, D.C. (1954).
G. Wintrobe. M.M., Thorn, G.W., Adams, R.D., Bennett, I.L.,
Brauwald, E., Isselbacher, K.J., and Petersdorf, R.G., (Eds.)
Harrison's Principles of Liternal Medicine, (6th ed.) McGraw-Hill
Book Co., New York. (1970).
7. White, J.M., Wingo, J.G., Alligood, L.M., Cooper, G.R.,
Cutridgc, •/., Hvclakcr, W., Benack, R.T., Dening, J.W. and
Taylor, F.B. Sodium Ion in Drinking Water 1. Properties,
Analysis, and Occurence, Dietetic Assn., 50: 32 (1907).
8. Review of State Sodium-in-DrinkLng-Waler Activities. Bureau
of Water Hygiene, U.S. Public Health, Service, Washington,
D. C. (1071)'.
9. Pollack, II. Note to The Physician (inserted with diet booklets)
Your 500 ing. Sodium Diet-Strict Sodium Restriction, Your
1000 nig. Sodium Diet - Moderate Sodium Restriction, and Your
Mild Sodium-Restricted Diet, American Heart Association
(I960).
10. Cook, L.P. American Heart Assn. Personal Communication
(1971).
11. American Heart Assn. Heart Facts 1972. A.H.A., New York (1971).
I'—/; --.-
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12. E:\sliiuui, N.J. and Hellman, L.M. Williams Obstrelics. (13th ed.)
Appleton-Century-Crofts, New York (19GG).
13. Kannel, W.B. Personal Communication (1971).
14. Garrison, G.E., a:ul Adcr, O.L. Sodium in Drijiking Water. Arch.
Environ. Health, 13: 551 (19GG).
15. Bubeck, R.C., Diment, W.H., Deck, B.L., Bakhviii, A.L., and
Lipton, 5j.D. Runoff of Dcicing Salt: Effect on Iroudequoit Bay,
Rochester, N'ew York. Science 172: 1128 (1971).
1C. Joyer, B.F., and Sutclil'fe, H. Jr. Salt-Water Contamination in
Wells in the Sara-Sands Area of Siesta Key, Sarasota County,
Florida. JAWWA. 59: 1504 (19G7).
17. Parks, W. W. Decontamination of Ground Water at Indian Hill.
JAWWA. 51: G44 (1959).
18. U.S. Department of the Interior. Saline Water Conversion Report
for 19G9-1970. Government Printing Office, Washington, D.C.
(1970).
t**i ' *
/<:>
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SULFATE
The presence of sulfate ion in drinking water can result in a
cathartic effect. Both sodium suUate and magnesium sulfate are
well-known laxatives. The laxiitive dose for both Glauber salt
(Na^SOaOH^G) and Epsom salt (MgSO-71^0) is about two grams. Two
liters of water with about 300 mg/1 of sulfate derived from Glauber
salt, or 390 mg/l of sulfate from Epsom salt, would provide this dose.
Calcium sulfate is much less active in this respect.
This laxative effect is commonly noted by newcomers and casual
users of waters high in suliates. One evidently becomes acclimated
to use of these waters in a relatively short lime.
The North Dakota State Department of Health has collected informa-
tion on the laxative effects of water as related to mineral quality. This
has been obtained by having individuals submitting water samples for
mineral analysis complete a questionnaire that asks about the Uiste and
odor of the water, its laxative effect (particularly on those not accustomed
to using it), its effect on coffee, and its effect on potatoes cooked in it.
Peterson (1) and Moore (2) have analyzed part of the data collected,
particularly with regard to the Laxative effect of the water.
Peter.sun found that, in general, the waters containing more than
750 nig/! ->i sulfate showed a laxative effect and those with less than
600 mg/l generally did not. If the water was high in magnesium, the
1 •—!!-••(.
< • •-
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effect was shown at lower sulfate concentrations than if other cations
were dominant. Moore showed that laxative effects were experienced by
the most sensitive persons, not accustomed to the water, when magnesium
was about 200 nig/'l and by the average person when magnesium was 500-
1,000 my/1. Moore analyzed the data as shown in.Table 1. When sulfatcs
plus magnesium exceed 1,000 mg/1, a majority of those who gave a definite
reply indicated a laxative effect.
Table 2 presents some data collected by Lockhart, Tucker and
Merritt (3) and Whipple (4) on the influence of sulfate on the taste ol
water and coffee. Because of the milder taste of sulialc over chloride
(5)(G) a taste standard for sulfate would probably be in the 300-100 mg/l
range. The Peterson data (1) and Table 1 (2), however, indicate that
from GOO to 1000 mg/l of sulfate has a laxative effect on a majority of
users. .
While a limit for sull'atc may be included in Secondary Drinking
Water Re (filiations, on the basis of the effect of sulfate on water taste,
no maximum contaminant level is being proposed at this time. As
noted above, a relatively high concentration of sulfate in drinking
water has little or no known effect on regular users of the water, but
transients using high sulfate watrt- sometimes experience a laxative
effect. Whether this effect will occur, and its severity, varies
greatly with sucli factors as the level of sulfate in the water being
consumed and the level of sulfate to which the transient, is accustomed.
Because of this great variability, the available dala do not support
178-
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the establishment of any given maximum contaminant level. The
Environmental Protection Agency recommends that the Stales institute
monitoring programs for sulfates, and that the transients be notified
if the sulfate content of the water is high. Such notification should
include an assessment of the possible physiological effects of con-
sumption of the water.
In the meantime, research is being undertaken to determine if
the health effects of sulfate in drinking water warrant further con-
sideration. If data are generated to support a maximum contaminant
level, this level will be proposed for inclusion in Revised Interim Primary
Water Regulations.
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REFERENCES
1. .Peterson, N.L. Sulfates in DriJiking Wal.er. Official Bulletin
Noi ill Dakota Water ajui Sewage Works Conference. 18: (1951).
2. Moore, E.W. Physiological Effects of The Consumption of Saline
Drinking Water. Bulletin of Subcommitce on Water Supply,
National Rt-^jarch Council, Jaji. 10, 1952, Appendix B, pp. 221-227
(1952).
3. Lockiiart, E.E., Tucker, C.L., and Merrill, M.C. The Effccl
of Water Impurities on The Flavor of Brewed Coffee. Food 20:
598 (1955). ~
4. Whipple, G..C., The Value of Pure Water. John Wiley,. New
York (1907).
5. Bruvuld, W.H., and Gaffcy, W.R., Evaluation Rating of Mineral
Taste in Water, J. Perceptual Motor Skills 2£: 179 (1969).
6. Bruvold, W.H., and Gaffey, W.R., Rated Acceptability, of Mineral
Taste in Water. II Combinatorial Effects-of Ions on Quality and
Action Tendency Ratings. J. Applied Psychol. 53: 317 (1969).
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