u
U.S. DEPARTMENT OF COMMERCE
National Technical Information Seivicc
PB-250 Oil
STATEMENT OF BASIS AND PURPOSE FOR THE NATIONAL
INTERIM PRIMARY DRINKING WATER REGULATIONS
ENVIRONMENTAL PROTECTION AGENCY
DECEMBER 1975
US.
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063017
PB2500.11
f
STATEMENT of BASIS and PURPOSE
for the
National Interim Primary
Drinking Water Regulations
U. S. Lnvirunmc'ilal Protection Agency
U.S. F-
JIB^ARY (7-507)
-- -
lOfJ-''- I ETHNICAL
N SERVICE
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'BIBLIOGRAPHIC DATA
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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 tins
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, ludgment, and discietion.
A. SOURCE AND FACILITIES
13. MICROBIOLOGICAL QUALITY
C. CHEMICAL QUALITY
A - SOURCE AND FACILITIES
Mounting pollution problems indicate the need for increased
attention lo the quality of source waters. Abatement and control of
pollution oi sources will significantly aid m producing drmkrig
water thai will be in full compliance with Hie provisions of these
Standards and will be esthetic-ally acceptable to the consumer, bul
Ihey will never i-limin.Uc the need lor well designed water Ireal-
menl facilities operated by competent personnel.
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Production ul water Hint poses no threat to the consumer's health
depends on continuous protection. I3e cause of liuinan fri-ilties asso-
ciated \.'Mi protection, prior-ty should be i;ivcn in selection of the
purest source1. Polluted souices should not be used unless other
sources an1 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 \\ith fragmented or cavernous rock, ha\e
been considered sulficiently protected irom bacterial contamination to
preclude need foj disinfection, this is frequently not true as ground
waters are becoming polluted with increasing frequency, and the
resulting h.i/ards require special surveillance. An illustration of
such pollution is the presence of pollut.ir.tb originating either from
sewage or industrial effluents.
Surface waters are subjected to mere-asm;; ]>ollution and sliould
never be used without bemt; effectively disinfected. Because of the
increasing li.i/.ards of pollution. Hie use of surface wiitr-rs without
coagulation aiul duration must he accompanied by adequate past
records and intensive surxeill.mcc ol the quality of the raw water
and the disinfected supply in order to assure constant protection.
This bur\eillance should include a sanitary survey of the source
and water handling, as well as biological examination of the supply.
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Thi? decree uf treatment should be dele-mined by (lio health
ha/.ards involved and the quality of th'- raw water. When in use,
tlu« source should be under continuous surveillance to assure
adequacy of treatment in meeting the ha/.ards of changing pollution
conditions. Continuous, effective disinfection shall be considered
the minimum treatment for any water supply except for ground
waters in which total cohforms can be shown to be continually
absent from the raw \\aler. 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, unproved coagulation, ;\nd/or special opera-
tion). If the pollution cannot be removed satisfactorily by treat-
ment. u--e of the source should be discontinued until the pollution
has been reduced or eliminated.
The adequacy of protection by treatment should be judged, in
part, on a record ol the quality of water produced by the treatment
plant and the relation of this quality to the requirements of these
Regulations, hvaluation 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 conlac!
time required to kill viruses in section on Microbiological Quality,
r *
.y
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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 diotribution 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 other equipment after each installa-
tion, repair, or other modification that may have subjected them to
possible contamination: pre\cntion of health ha/.ards, such as cross-
connections or loss of pressure because of ovcrdr.ilf 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. Tnc fact that the minimum number of samples are taken
and analy/cd and found to comply \\itli specilic quality requirements
of these Standards, is not sufficient evidence that protection has been
adequate. The protection procedures and physical lacilities must
be rex lowed alonj; with the results of water quality analyses to
evaluate the adequacy of the supply's protection. Knowledge of
physical dcfecis or of the existence ff oilier health hazards in the
\\atcr 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 mot, the deficiencies must
be corrected before ihe supply can be considered safe.
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D - MICROBIOLOGICAL QUALITY
Cohforin CJroup
Coliform 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 tins time, a mass of (Lita lias accumulated to permit a full
evaluation of me sensitivity and specificity of this bacterial pollution
indicator.
As defined in Standard Methods for the Examination of Water
and W.istewater (1). "the coliform group includes all of the aerobic
and facultati\e anaerobic. Gram-negative, non-spore-forming rod-
shapcd b.iL-teria which ferment lactose'with pis formation within
48 hours at 35° C." From th.s definition, it becomes immediately
apparent thai this bacterial grouping is somewhat artificial in that
it embodies a heterogeneous collection of bacterial species having
only a few broad rhai .ictcristics in common. Vet, for practical
applications to stream pollution studies, tins grouping of selected
bacterial species, which we .shall term the "total coliform group,"
has proved to be a workable arrangement.
The total colilorm group merits cun.sider.Uion as an indicator
of pollution because these bacteria are alwajs present in the normal
intestinal tract of humans and other warm-blooded animals and arc
eliminated in large numbers in fecal wastes. Thus, the absence of
total colilorm Ix'.cleria is evidence of a baclenologically safe water.
5
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Some strain:* included in the total ooliform i^r^up have a wide
distribution in the environment but aie not cununun in fecal 'iiaterial.
Enterobacter acroj;enes and K'nicrobacter cloacae are frequently found
on various types of vegetation (2-5) and in materials used in joints
ami valves (G-7).
The mlermediate-aero{;cne:3-cloacae (I.A.C) .subgroups may be
found in fecal discharges, but usually in smaller numbers than
Kscheric-lna coli that is characteristically the predominant cohform
in warm -blooded animal intestines (8-10). Entcrobactcr aero^enes
and intermediate typos of oi^'-msnis arc commonly present in soil
(11-14) and in waters polluted some time in the pas»». Arylhcr
suburoup comprises plant pathogens (15) and oilier organisms of
indefinite laxonon.y \\husi* sanitary significance is uncertain. All
of these colifurm subgroups may be found in sewage and in UK-
polluted w.iit:r environment.
Survi\al Tunes
Ori;.uusms of UK: I.A.C. f;rouj) lend to survive longer in water
than do fecal cult form organisms (1C-18). Tlie I.A.C. group also
tends to be somewhat more resistant to chloruution then E. coli or
the commonly occurring bacterial intestinal pathogens (19-22).
Hecause of lhe.sc aiu! oilier reasons, the relative survival times of (he
cohform suburoups may be useful in distin^uishim1, between recent and
less recent pollution. In waters recently contaminated with sewage,
it is expected lliat fecal coliform organisms* v. ill be present in -
numbers t;re.i(er Ilian those of the I.A.C. subgroup; but in waters that
G
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have bec-n contaminated lor a considerable length uf time or have
been insufficiently chloruiated, organisms of the I.A.C. .subgroup
may be more numerous than fecal culifurm organisms (23).
I)ifferenliation of Organisms
Because various numbers of the colilorm group normally grow
in iliver.se natural liabitats, attempts liave been made to differentiate
the population m polluted waters, with specific interest directed
toward those conforms that arc derived from warm-blooded animal
contamination. In Ins pioneering research, MacConkey (23, 24)
defined the aeroncnes group in terms of certain fermentation
characteristics, ability to produce mdole, and reaction in the
Vogcs-Proskauer lest. Oilier developments refined techniques
that progressed to differentiate the coliform group on the basis
o! mdolc production, methyl red, and Vi /es-Proskauer reactions,
and citrate utilisation (LMViC tests) into the E^ coli, Dntcrobacler
aeroi;enes, nnerniLdiatc, and irregular subgroups (24-28).
In anotlior approach to coliJorm differentiation, liajna and
Perry (29) and Vaughn, Lcvine, and Smith (30) further developed
the Liikman test (31) lo distinguish organisms of lecal origin from
those of nonfecal origin liy elevating the incubation temperature
for lactose fermentation. Gcldieich, and associates, (31, 32)
further refined the procedure and developed additional data lo
indicate the specific correlation of this clovated temperature
procedure to the occurrence of fci-al contamination.
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Feral Coliform Measurements
Tiie fcc-al cohform 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 sho\vn that 96.4
percent of the colitorms in human fcces were positive by this lest
(10). Examination of the excrement from other warm-blooded animals,
including livestock, poultry, cats, dogs, and rodents (33-34), indicate
the fecal cohforms contribute 93.0 to 98.7 percent 01 the total
coliform population. The predominant fecal coliform type most
frequently found m the intestinal flora is E. coli. Occasionally,
other coliiorm IMViC types may predominate for periods of several
Months before a shift occurs in type distribution. For tins reason,
it >s more significant to be able to measure all cohforms 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 with identification of 1£. c_oh_ by the traditional
IMVic biochemical reactions (87 2 percent).
Application to Treated Water
The presence of any type of cohform organism in treated water
.suggests eithi-i ..'ad'V.iialc treatment or com.umnation after post-
cliloniialion (ii.'Ji. It is true there are some dilfcrcnces between
various colifoiM strains with regard to natural survival and their
s
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chlonr.aMon resistance, i;i.l Miesi .ire minor oioljp,j«.;:i »ti'i.urjiis
dial are mure clearly demonstrated in the laboratory than in the*
water treatment system. The pn senee of any cohform bacteria,
focal or nonfccal, in treated water should nut be t jJeraled.
Insofar as bacterial pathogens are concerned, the cohfoun group
is considered a reliable indicator of the adequacy of treatment. As
an indicator of pollution in drinking water supply svstems, and
indiiectly as an indicator of piotcclion provided, the colilurni i-.roup
is prelerred to I real eohform organisms. Whether these considerations
can be extended to include ricketlsial and viral organisms has not
been definitely determined.
Sample Si/e
The minimum olSici.il sample volume cited ir. the earlier editions
of the Di'i'ii'.in-' Water Standards and Standard Methods for the
Kxamination 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 nil portion
of the sample. Few laboratories ever routinely employed the Jailor
portions in the multiple lube procedure because of the I'llcndanl
problems of preparing, handling and Lncubatmi; the larger sized sample
buttles that a; _ required. Thus, when the multiple lube procedure
was used, it became a practice to examine only 50 ml. With the
development ol the membrane filter procedure for routine potable
water testing, the examination of larger samplo volumes became
practical, limited only by the turbidity of water ar.-:' excessive
bacterial populations.
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Since many water supplies arc 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
low levol occurrence of coliforms. Increasing thy 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 fir control of water-
borne virus. Mack et al (35) reported poliovirus type II could be
isolated from a restaurant well water supply using a flocculant in
the 2.5 gallon samples prior to cenlrifugation to concentrate the
low density virus particles. Bacteriological examinations of 50 ml
portions of the unconcentrated water samples were negative for
colifornii... 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 coliform
standard, possibly to a one-liter base (36).
The recommendations to increase the sample size to 100 ml for
bacteriological examinations of water is supported in the 13th
Edition of Standard Methods where the larger volume is stated as
preferred. A study of Stale Health Laboratory procedures indicates
that 39 or 78 percent of these laboratory systems are currently
using 4 oz sample boll.'es to collect 100 ml of samj'lo, and 25
of these State Health Laboratory networks are exa;mning
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all public water samples uy the membrane filter procedure. These
figures suggest that 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 fecal contamination and not
subject to wide-range density fluctuation of doubtful sanitary signifi-
cance.
Although the total coliform group is the prime measurement of
potable water quality, the use ol a fecal coliform measurement in
untreated potable supplies will yield valuable supplemental infor-
mation. Any untreated potable supply that contains one or more
fecal cohforms per 100 ml should receive immediate disinfection.
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REFERENCES
1. Standard Methods '.or Hie Examination of Water and Wastcwatcr,
13th cd. APHA, AWWA, WPCF, New York (1970).
2. Thuinas, S.D. and McQuillin, J. Coli-aerogenes Bacteria
Isolated from Grass. J. Appl. Bactcriol. Iji: 41 (1952).
3. Frascr, M.H., Reid, W.B., and Malcolm, J.F. The Occurrence
of Coli-aerotfcnes Organisms on Plants. J. Appl. Bactcriol.
lj): 301 (195G).
4. Geldreich, E.E., Kenncr, B.A., and Kabler, P.W. The
Occurrence of Cohforms, Fecal Conforms, and Streptococci
on Vegetation and insects. Appl. Microbiol. \2\ 63 (1964).
5. Pnpavassiliou, J., T/.annelis, S., Ycka, H., and Michapoulos, G.
Coli-Aeroyenes Bacteria on Plants. J. Appl. Bactcriol. 30:
219 (19G7). —
6. Cnldwell. 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 Orpanics
in Human Feces. Am. J. Hyy. 27: 67 (1938).
9. Scars, H.J.. Bro\\lcs, I., and Vcluyuma. .J.K. Persistence
of Individual Strains f)f Eschericlua coli in tho intestinal Tract
of Man. J. Bactcriol. 5£: 293 (195077"
10. Geldreich. E.E., Bordncr, R.H., Huff, C.B., Clark, H.F., and
Kabler, P.W. Type-Distribution of Coliform Bacteria in the
Feces of Warm-Blooded Amnuils. JWPCF. 34; 295 (1962).
11. Frank, N. and Skinner, C.E. Coli-Acro^eiics Bacteria in Soil.
J. Daclcriol. 42: 143 (1941).
12. Taylor, C.B. Coli-Acroycncs B.'tclcria in Soils. J. Hy^. (Camb.)
49: 102 (1951).
13. Randall, J.S. Tlic Sanitary Significance of Coliform Bacilli in
Soil. J. Ilyu'.. (Camb.) 54: 365 (195G).
12
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14. Gcldrcich, E.E., Huff, C.B., Burtlncr. R.H., Kablcr, P.W.,
Clark, II. F. The Fecal Coli-Ac logcncs Flora of Soils from Various
Geographical Areas. J. Appl. Bactcriol. 25: 87 (19G2).
15 Elrod, It.P. The Erwinia-Coliform Relationslnp. J. Bactoriol.
44_: 433 (1942).
16. Parr. L.W. Viability of Coli-Acrogcnos Organisms in Cultures
and in Various Environments. J. Infect. Disease GO: 291 (1937).
17. Plait. 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.P. The Ecology and Significance of the Different Types
of Coliform Bacteria Found in Water. J. Hyg. 4JJ: 23 (1942).
19. Tonney, F.O., Grecr, F.E., and Danforth, T.F. The Minimal
"Chlorine Death Point'1 of Bacteria. Am. J. Pub. Health
18: 1259 (1928).
20. Heathman, L.S.. Pierce, S.O.. and Kabler, P.W. Resistance of
Various Strains of E. typhi and Coli-Acrot;cncs to Chlorine- and
Chloramme. Pub. Health Rpts., SJj 1367 (1936).
21. Bulterfield, C.T., et. al. Influence of pi! and Temperature on the
Surviuil of ColLforms and Enteric Pathogens when Exposed to
Free Chlorine. Pub. Health Rpts. 58: 1837 (1943).
22. Kabler, P.W. Relative Rcsislcncc 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 Focal
Coliform Organisms as Indicators of Pollution in Drinking Water.
JAWWA. 52: 1577 (I960).
24. MacConkcy. A. Lactose-Fermenting Bacteria in Fcces. J.
Hyg. 5: 333 (1905).
25. MacConkcy, A. Further Observations on the Differentiation uf
Lactose-FcniHMiting Bacteria, with Special Reference to Those oi
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. I'hc Differentiation of Bacteria
of lhe1 Colon-Aero^encs Family by tlic Use of Indicators.
J. Infect. Disease J_7: 1GO (1915).
28. Kuscr, S.A. Differential Tests for Colon-Aero^eiics Group hi
Relation to Sanitary Quality of Water. J. Infecl. Disease
35: 14 (1924).
29. Hajna, A .A . and Perry, C.A. A Comparison of the Eijkman
Test witli other Tests for Determining E. coli. J. Bacleriol.
30: 479 (1935).
30. Vaughn. 11.H.. Lcvine. M., and Smith, H.A. A Buffered Boric
Acid Lactose Medium for Enrichment and Presumptive Identifica-
tion of Eschcru-lna coli. Food Hcs. H>: 10 (1951).
31. Eijkman. C. Die Garuni;sprobc bci 4G ais Milfsmittcl bei clcr
TrinkwnssGruntersuchung. Ccnlr. Baktenol. Parasitcnk., Abl. I,
Orig., 37: 742 (1904)
32. Geldreich, E.E.. Ciark. II. F., K.iblcr, P.W.. Huff. C.B.. and
Bordncr, R.H. The Cohform Grouj). II. Read ions in EC Medium
at 45 C. AppJ. Microbiol. G: 347 (1958).
33. Geldreich. E.I-'.. Sanitary Significance of Fecal Coliforms in the
Knvironmcnl. U.S. Dept. of the Interior. FWPCA Publ. \VP 20-3
(19GG).
34. Geldrc-K-h. K.I-:.. Best, L.C.. Keiincr, B.A.. and VonDonscl. D.J.,
The Bactoriulu^ical Aspects of Slormwater Pollution. ,I\VPCF.
40- l«Gl (19G8).
35. Mack. N.M.. Tu, Y.S. and Coohon, D.B.. Isolation of Polio-
myelitis Virus from a Contaminated Well. H.S.M.H.A. Health
Reports (In press).
3G. Geldreich. i: .K. and Clarke. N.A., Tlie Colilorm Test: A
Criterion for the Viral Safety oi Water. Proc. 13tli Water
Quality Conforcnce, College of Engineering, University of Illinois.
pp. 103-113 (1971).
I1
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Substitution of Residual Chlorine Mi'asurement fur Total Cohform
Measurement
The best nicthud of assuring the 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 tlio total coliform density in the distributed water.
In the 1962 U.S. Publv Health Service Drinking Water Standards, the
major emphasis \vas on the measurement of to till coliform densities
and a sampling frequency "raph relating number of samples per month
to population served wvs included. The sampling frequency ranged
from two per month for populations <«f 2,000 .ind less to over 500 per
month, for a population ol 8 million.
The effectiveness of this approach for assuring niicrobioloiiic.il
safct> was evaluated during the 19G9 Community Water Supply Survey.
The results of tins evaluation by McCabe, et. al., (1) are paraphrased
below.
Microbiological Qua I it \
To determine the status of the bacteriological surveillance program
in each of the 9G9 water nupply systems investigated, records in the
Slate and county health departments were examined lor 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 labk
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below summarizes the results.
bacteriological Surveillance
500 or 501 Greater than All
Population Less 100,000 100,000 Populations
.Number of Systems 440 501 22 969
Percent of Systems
Met Criteria 4 15 3G 10
Did not meet
Criteria 95 85 04 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).
Kven considering a sampling rate reduced by 50 percent of that called
for in the criteria, 070 *y stems (09 percent of the survey total) still
would not have collected sufficient sample.^.
Uocommpiidaiion
The water utility should be responsible for water quality control,
but the bacteriological surveillance collection requirements arc not
bcmir met in most small water systems c\cn though only two samples
per month are 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 mi^ht be a more practical way of
characlcn/.mi; safety.
The validity of the recommendation that the measurement of chlorine
residual mi<;hl be a substitute for some total coliform measurements has
been investigated by IJucluw and Walton (2).
1G
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Because the recommended rale of sample collection could not be
or were not being used, alternative methods of indicating safety were
considered. One suggestion was to substitute ilic 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, datu
from London, U.K. Cincinnati, Ohio; and the 19G9 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 cohform determinations.
Sampling Location
During 19G5-GG, the 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 G89 samples from miscellaneous locations (complaints, hospitals,
etc.). Most of the unsatisfactory results \\cre associated \\ith reser-
voir problems. Main breaks and miscellaneous samples were
responsible for most of the remaining unsatisfactory samples.
Chlorine Residual
In Cincinnati during the 19G9-70 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 (he remaining sampling .stations showed coli-
form bacteria in only one out of the approximately 24 samples examined.
-------
At the other luur stations where 2 or moie cuhfonn-positive tests
\verc obtained from the 2-1 samples, three had no chlorine residual at
the iMHO the cohform-positive samples were collected. The question
is raised, therefore, as to the need lor examining samples routinely
collected from a large number of stations scattered throughout (he
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 cohform positives
to about 1 percent. The table below from the CWSS 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 T\pe.s of Water Supply Systems Four.cl to Have
Average Total Coliforms Greater than 1/100 ml
Non- Chlorinated With An;-
T\ pc of S\stem Chlorinated No Kcsidual Detectable Residual
f-'prmg 39 17 0
Combined Spring
and Well
Well
Surface
Combined Surface
and Well 100 1C
These findings indicate that a major port ion of ± distribution system,
exclusive of deadends, reservoirs, etc., could ho monitored for bacter-
iological safety bv the use of chlorine residual. (Emphasis added.)
IS
41
H
G4
28
5
7
0
0
2
-------
Therelore, when chlorine substitution is used, determination of
total coliluriu (.tensilities should be continued in problem areas,
and sonic .samples, as a check, should be collected in liie main
part uf the distribution system.
-------
These two sliuhos led to Hie inclusion in the Regulations uf Par.
141.2'(li) on (lie substitution uf chlorine residual tests lor a portion
of the required total coliforni determinations. Par. 141.21(h) states
thai any substitution must be approved by the State on the basis ol
a sanitary survey. The following four items sliould be specified by
the SUite:
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 nut be too difficult in larger supplies where both
of these measurements arc routinely made, but it might be quite diffi-
cult lor the sm.illcr purveyors (where the most help is needed) who have
not been making either measurement.
The Mumber and location -ul samples for which chlorine residuals
are to be substituted
-------
Total coliform measurements should continue to be made of the
finished water at> it c-nters 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
Di general, a low turbidity water with a free chlorine residual of
about 0.2 nig/l at a pli of less than 8.5 will be free from total cohforms
although these conditions may vary from water to water. However, a
higher free chlorine residual or the use of some oilier disinfectant is
requires prior to the water entering the distribution syslen., where
disinfection is practiced, :f initial disinfection is to be adequate.
Tin* frequency of Hilorinc 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 cohform test deleted. In this way wider
coverage of tne distribution system can be achieved, thereby increasing
the protection to the consumer. Since, for maximum protection,
chlormalion 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. I3y limiting
the extent of substitution to 75f^ of the required bacteriologies' samples,
-------
a sufficient number of bacteriological samples will still be taken
to cnaliJo the assessment of the adequacy of disinfection and to
abjure 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 tins reason the DPU 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 samp1' for total cohform analysis must
be taken immediately irom that point.
.
*.*-
-------
REFKRI;NCI.S
1. McCiibe, L.J., Syniuns, J.M.. Lee, H.D., iinrt Ro'jcck. G.G.
Study oi Comnuiiuty Water Supply Systems. JAWWA. 02: 670
(1970) ~~
2. Buelaw, H.W., and Will ton, G- B:ictonoloKicul Quality vs.
I Clilunnc. JAWWA. 63:28(1971).
-------
General Bacterial Population
The microbial flora in potable water supplies is highly va.-iable
in numbers and kinds of organisms. Those bacterial groups most
frequently encountered in potable waters of poor quality include:
Pscudomonas, Flavobactcrium, Achromobactcr, Proteus, Klebsiclla,
Bacillus, Serratia, Coryncbactcrium, Spirillum, Clostridium, Arth-
robactcr, Gallionclla. 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 Pscudomonas 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 ihe
elderly population of a community. These organisms can persist and
grow in water containing a minimal nutrient source of nitrogen and
carbon. If Psoudomonas 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 O.G mg/1 free chlorine rcsidunl will suppress
the development of an extensive microbial flora in all :;cctions of the
distribution network.
Flavobactcrium strains can be prevalent in drinking water and on
water taps and cirinKing-Iountam bubbler-heads. A recent study of
stored emergency water supplies indicated that 23 percent of the
samples contained Fhivoijactcrium organisms with densities ranging
-------
from 10 to 26,000 per 1 nil. Flavobarterium must be controlled in
the hospital environment because it c:m become a primary pathogen in
persons who have undergone surgery (13).
Klcbsiclla pncumoniae is another secondary invader that produces
human infection of the respiratory system, gcnito-urinary system,
nose and throat, and occasionally this organism has been reported as
the cause of meningitis and seplicema (14). Klcbsiolla pncumoniac,
like Entorobactcr acrogcncs, (15) can multiply in very minimal
nutrients that may be found in slime accumulations in distribution
pipes, water laps, 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,
Micrococcus, Flavobactorium, Proteus, Bacillus, Actmomycctcs,
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 coliform 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 9G9 public
water supplies were analyzed (Table 1) for bacterial plate count re-
lationship to detection of total cohfojms and fecal coliforms. 11 is
interesting to note that there was a significant increase in total
and Iccal coliform detection when the bacterial counts increased
up to 500 per 1 ml. However, further increase in the detection of
cither 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 wab desensitized by the occurrence of a large general bacterial
population that included organisms known to svippress coliform iccover> .
Control of the General D:)Qt"rial 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.
This necessity for monitoring the general bacterial population is
most essential ir. those supplies that do not maintain am chlorine
residual in the distribution lines and in special applicant.-
-------
TABLE: i
General Eacterial
'J"!JI
1
11
31
101
301
501
1
! '.' i'llKJO
'!:,'.
- 10
- 30
- 100
- 300
- 500
- 1.0CO
,000
CACT
lil DISTRiCUT
Peculation*
Nui..bc-r of
Samples
1013
371
396
272
120
110
164
TOTAL 2d.'.6
ERI.V. PLATE COUNT vs. t
10'! V:\TfR i.TTi.OR- S Ff>"
Total Cclif
Occurrences
47
28
72
48
30
21
31
277
:CLIFOP.H DETECTIO.:
969 PiJPLIC '..'ATEP. SUPPLIES
•Qfr.
Percent
4.6
7.5
18.2
17.6
25.0
19.1
18.9
---
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 Co-jnt (<18 lirs. incubation, 35'C)
-------
tribution lino sec-tic.ns and storage U):iks thai 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 eacli distribution system in this special study
was small, it docs reflect bacterial quality conditions in numerous
large and small water systems examined in cacli of the eight metropoli-
tan areas and the entire State of Vermont.
The.se data indicate thai the general bacterial population in
distribution lines can be controlled to a value below 500 organisms
per 1 nil by maintaining a residual chlorine level in the system.
Increasing the chlorine residual above 0.3 nig/1 to levels of 0.6 and
1.0 mg/1 did not further reduce the bacterial population b> any
appreciable amount. Restricting such bacterial densities to a limit
of 500 organisms per ml is, therefore, not only attainable in the
distribution system, but is also desirable to prevent loss in cohform
test .sensitivity definitely observed at approximate densities of
1000 organisms per ml, thereby producing a safely factor of al least
two.
-------
TABLL" 2
THE EFFECT OF VARYING LEVELS OF RESIDUAL CHLORIKE ON THE TOTAL
PLATE COUNT IN POTABLE KATE3 DISTRIBUTION SYSTEMS*
Standard Plate
Count**
< 1
1 - 10
11 - 100
10: - 500
;oi - 1000
>1000
Nu.-oer of
Samples
Residual Chlorine (r.a/l]_
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
0.1
19.7
38.2
28.9
7.9
1.3
3.9
76
0.2 0.3
12.8 16.4
*S.9 45.5
26.6 23.6
9.6 12.7
2.1 1.8
0 0
94 55
0.4
17.9
51.3
23.1
5.1
0
Z.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 corrimunity 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 (-i-ncral bacterial population
in poUible water will re-quire a dcfinitiun of medium, mcub.ilion
temperature, anci incubation time so as to standardize (lie population
to be measured. The- 13th edition of Standard Methods lor the Exam-
ination of Water and Waslewaler docs specify these require'iicnts for
a Standard Plate Count (SPC) to be used in collection • i water quality
control data. Because many organisms present in potable
watery are attenuated, initial growth in plate count a^ar frequently
is slow; thus, incubation time should be extended to 48 hours at
35 C. This lime extension will permit a more meaningful standard
count of the viable bacterial population. Samples must be collected in
bottles previously sterili/ed wjthm 30 days anci adequately protected
from dust accumulation. Examination fur a Standard Plate Count
should be initiated within 8 hours of collection. This lime may bo
extended to periods up 10 30 hours only if these samples are trans-
purled in iced containers.
With maintenance of a chlorine residual and turbidity of less than
one TurbiJii) Unit, the need for a bacteriological measurement of
the distribution system may become less critical, l-'or tins reason,
it is recommended thai such walcr supplies be monitored routinely for
bascln.e data on the c.encral bacterial population and correlated with
chlorine residual and turbidity measurements in the distribution
lines. It is also recommended thai water plant personnel he alert
lo unusual circumstances lli.-i may make it desirable lo monitor the
30-
-------
general bacterial population mure often in a check of water plant
treatment efficiencies.
For these reasons, Hie 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 thai 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.
31**-
-------
REFERENCES
1. Willis, A.T. Anaerobic Bacilli in a Treated Water Supply. J.
Appl. Dactcriol. 20: Gl (1957).
2. Lucscliow, L.A. and Mackenthun, K.M. Detection and Enumeration
of Iron Bacteria in Municipal Water Supplies. JAWWA.
54:751 (19C2).
3. Clark. F.M., Srutt, R.M. and Bone, E. Hctcrotrophic Iron Pre-
cipitating Bacteria. JAWWA. 5£: 103G (19G7).
4. Victorecn, II.T. Soil Bacteria and Color Problem in Distribution
Systems. JAWWA. 61: 429 (1969).
5. Victorecn. H.T. Panel Discussion on Bacteriological Testing of
Potable Waters. Am. Water Works Assoc. Annual Conference.
June 21-2G, 1970, Washington, D.C.
G. Gulp, R.L. Disease Due to "Non-pathogenic" Bacteria. JAWWA
GJj 157 (1969).
7. Ruuechc. B. The Annals of Medicine. Three Sick Babies.
The New Yorker, Oct. 5, 1908.
8. Hunter, C.A. and P.R. Ensign. An Epidemic of Diarrhea in
a New-born Nursery Caused by P^ aoruginosa. A . J. Pub.
Health 37: 11GG (1947).
9. Drake, C.II. and Huff, J.C. Miscellaneous Infection Section VI-
Pseudonion.is aenmimjsa Infections. pp.G35-b39.In: Diagnostic
Procedures ami Reagents, A.II. Harris and M.I>. Colcmaii,
editors. Am. Pub. Health Assoc. New York, 4th cd. (19G3).
10. Smith, W.W. Survival after Radiation Exposure - Influence of a
Distuibcd Environment. Nucleonics K)' 80 (1952).
11. Mai/.tcgui, J.I. et al. Gram-Negative Rod Dactcremia \vilh a
Discussion of Infections Caused by Hcrolla Species. Am. J .
Surgery 107: 701 (1964).
12. Cross. D.F.. Bcnchimol, A., and Dinujiul, E.G. The Faucet
Aciatur - A Source of Pscudomonas Infection. New England
J. Mcel. 274- 1430 "
32*-
-------
13. Herman, L.G. ami Ilimmclsbnrh, C.K. Detection and Control
of Hospital Sources of Flavobactcria. Hospitals. J. Am.
Hospital Assn. 39 (19657!
14. Lcigua'-da. R.H. and Polazzolo, A.Z.Q.D., Bacteria of Genus
Klebsiella in Water. Rev. Obr. Sanit . Nac., (Argent ma)
38; 169 (195G).
15. Nunez, W.J. and Colmer. A.R. Differentiation of Acrobactcr-
Klebsiella Isolated from Sugarcane. Appl. Microbiol. 1C:
1875 (1965).
16. Waksman. S.A. Antagonistic Relations of Microorganisms.
Dacteriol. Reviews £: 231 (1941).
17. Schiavone, E.L. and Passerini, L.M.D. The Genus Pscudomonas
acrugmosa in the Judgment of the I'otubility of Drinking Water.
So m. Mod., (B. Aires) III: 1151 (1957).
18. Kligler. L..J. Non-lactose Fermenting Bacteria from Polluted
Wells and Sub-soil. J. Bacterial. 4: 35 (1919).
19. Hutchmson, D.. V.'cavcr, 11. H. and Schei ago, M. The Incidence
and Significance of Microorganisms Antagonistic to Eschcrichia
coli in Water. J. Bactcnol. 4_5: 29 (1943).
20. Fi.-her, G. The Antauonistic Effect of Aerobic Sporulating
Bacteria on the Coh-Aorogcnes Group. Z. Immam l-'orsch 107:
16(1900).
21. Weaver. It.II . and Boiler, T. Antibiotic- Producing Species of
Bacillus from Well Water. Trans. Kentucky Acad. Sci. 13:
"
22. Reittcr. R. and Seli^mann, R. Pscudomonas aeruuinosa in
Dunking Water. .J . Appl. Bacteriol. 2ir~n5'TT'J57T
23. McCabc. L.J.. Svmons, J.M.. Lee. R.I)., and Robuck, G.G.
Study of Community Water Supply Systems. JAWWA .
62: 670 (1970).
-------
these 3 water supplies were really adequately treated. Only one of
the 8 poliomyelitis epidemics occurr"d in the United States, and
this was the result of cross-connccti'jn contamination. Since
Mosley's publication there have been three oilier 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 in Delhi, India, in 1955-5G (2; attributable
to a municipal water supply source heavily overloaded wil'i raw sewage.
Tins outbreak, however, was not accompanied by noticeable increase
of typhoid fever or other enterobaclerial diseases, sunneslinn 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 [>aslrociitcritiK
during the period of 194G to 1970 in which cpiccmiolo^ic evidence
suK^cstcd a waterborne nature. More than 18,000 persons were
affected in these outbreaks. Mosley (1) suspected that 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 ai e polluted with enteric viruses. Thus, water supplies
from such sources depend entirely upon the treatment processes
used to eliminate tlie.se pollutants. Even though the processes may
be perfectly effrclhe, an occasional breakdown in the plant or any
marginal practice of treatment could still allow the pollutants to
-------
reach fie finished walcr supplies. It .should be noted that Coin
and his associates (4) have reported the recovery of viruus 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 (o) reported that poliovirus
was recovered in water from a deep well in Michigan. Although tiie
well had a history of positive coliforms, conforms and virus were
not recovered from ;ui unconccntratcd walcr 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 walerborne virus disease* outbreaks have resulted
from contamination of poorly treated drinking water by sewage e thcr
directly or through cross-connections. Overt outbreaks of virus
disease from properly treated municipal water supplies are not
known to have occurred. Proper treatment ol surface water usually
means clarification followed by effective disinfection.
Chang (G), 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 hyputhvsis is true, can be
proved only by :ui intensive survey for viruses in numerous drinking
water supplies in this country, and such a survey has never been
conducted. If viruses were detected in a survey of drinking water
supplies, it would be necessary to conduct in-dcpth epidcmiological
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 asscssuig the significance of the
coliform test and the "virus safety" of water. Calculations by
Clarke ct al (7) have indicated the following virus-colilorm ratios
in feces, sewage, and polluted waters.
Calculated Virus - Coliform Ratios
Virus Colifurir. Ratio
Fcces 200/gm 13xl06/gm 1:65,000
Sewage 500/100 ml 46xlOe/100ml 1:92,000
Polluted Surface Water 1/100 ml 5xl04/100 nil 1:50,000
It is apparent that coliform organisms far outnumber human enteric
viruses in fuccs, sewage, and polluted surface water. It .should be
-------
emphasized that lhc.sc calculated ratios arc only approximations and that
ll'oy would be subject to wide variations and radical changes, particularly
during a virus disease epidemic. Additionally, both bacteria ami virus
populations in sewage and polluted waters are subject to reductions, at
different rates, from die-off, adsorption, sedimentation, dilution, and
various other 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 considc-ablc 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
iii a Committee Report. "Engineering Evaluation of Virus Hazards in
Water" (8). These reports indicate tli.il 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 liltralion
is capable of reducing virus populations up io 99.7 percent if sucli treat-
ments arc properly carried out (9). It should be noted, however, thai a
floe breakthrough, sufficient to cause a turbidity of as little as 0.5
Turbidity Units. \\as usually accompanied by a virus breakthrough in a
pilot plant unit seeded with high doses of virus (9). Dibuifeo;ion,
-------
however, is Hie 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), lias
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 stale 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 CK..-«f; "ition 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 99.9C percent of a reovirus population as
contrasted lo GO minutes to achieve the same percent inactivation
of coxsackicvirus.
Virology techniques have not yet been perfoc led 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 nauzc pad technique (1C) 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 c-T.luatini; the occurrence of human enteric viruses iii treated
waters.
As noted above, no simple and effective method for the viral
examination of water is available at this time. When such a method
is developed, and when there are sufficient data to provide the
necessary basis, a maximum contaminant level for virus \\ill be
proposed.
-------
REFERENCES
1. Moslcy, 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. Weibcl, S.R., Dixon, F.R., Wcidner, R.B., and McCabc, L.J.
Waterbornc-diseasc Outbreaks 1946-1970. JAWWA.
56: 947 (1964).
4. Coin, L., Menclrier, M.L., Labonde, J., and Hannon. 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 Coohoon, D.B. Isolation of Polio-
myelitis Virus from a Contaminated Well. Health Services Repts,
8J7: 271 (1972).
6. Chang, S.L. Walcrbornc Virus Infections ajid 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 International Conference on Water Pollution Research,
Loiu'on. 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 Chlormalion 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.. Fallal. B., Cymbalisla, S., and Goldblum, 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.D., 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 Melnick, J.L. Concentration of
Viruses from Sewage and Excreta on Insoluule Polyelcctrolytes.
Appl. Microbiol. !£: 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. (19G7).
*'."*•<
ft ^^
-------
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 participate
matter in water interferes with effective disinfection. Neefc, Daly,
Reinhold, and Stokes (1) added from 40 to 50 ppm of fcces 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 disinfection
to tl>e same concentration of total residual, produced no hepatitis
in 5 volunteers. This was repeated with 7 additional volunteers,
and again no infectious hepatitis occurred.
Chang, Woodward and Kabler (2) showed that ncmatodc worms
c.m ingest f.'iileric bacterial pathogens as well as virus, and that the
nematode-b'jrnc organisms are completely protected against chlorma-
lions even when more than 90 percent of the carrier worms are
immobili/cd.
Walton (3) analy/.cd data from three waterworks treating surface
waters by chlormation only. Coliform bacteria wc/o detected ir. the
chlui 'Mated water at only one waterworks, the one that treated a Great
La-kt.^ -..Her that usually did not have turbidities greater than 10 lurbidity
unit.-. (rUJ), but occasionally contained turbidities as great as 100 TU.
-------
Sanderson and Kelly (4) studied an impounded water supply
receiving no treatment other Hum clilorination. The concentration
of free chlorine residual in samples from household laps nftcr 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 org:uiisms. 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, arc 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 the 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 10 clearly demonstrate the facts.
-------
TABLE 1
FILTEHKn-WATKR QUALITY AND HEPATITIS INCIDENCE. 1953
City
G
C
II
13
M
A
Average
Turbulilv
TU
0.15
0.10
0.25
0.2
0.3
1.0
Final
Chlorine
Residual
ing/I
0.1
0.3 _
0.3
-
0.4
0.7
Hepatitis
cnsos/100,000 people
3.0
4.7
4.9
8.6
31.0
130.0
-------
Tracy, Camarcna, a:id Wing (6) noted that during 1963, 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
unfiltered supply was betv.'ccn 5 and 10 TU.
Finally, Robcck, Clarke, and Doslal (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.
Those 7 studies show the importance of having a low turbidity
water prior to disinfection and entrance into the distribution system.
(2) The 1969 Community Water Supply Survey (8) revealed that
unpleasant tastes and odors were among the most common customer
complaints. While organics 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.
-------
(3) 1'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 p .d maintain a
cleanliness that will help prevent rcgrowlh of bacteria and the
growth of oilier 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 difliculty in consistently producing a
finished water conforming to tins limit.
47--
-------
REFERENCES
1. Nccfe. J.R., Baty, J.B., Rcinhold. J.G., and Stokes, .1.
Inactivalion of The Virus of Infectious Hepatitis in Drmking
Water. Am.J. Pub. Health 3J7: 365 (1947).
2. Chang, S.L.. Woodward, R.L., and Kabler, P.K. Survey of
Frceliving Nematodes and Amcbas in Municipal Supplies.
JAWWA. 52: 613 (May 1960).
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.. Berg. G., Kabler, P.K.. 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. 58: 1151
(1966). ~~
7. Robock, G.G.. Clarke, N.A.. and Dostal. K.A. Effectiveness
of Water Treatment Processes in Virus Removal. JAWWA.
54: 1275-1290 (1052).
8. McCabe. !,..!.. Symons, J.M.. Lee, R.D., and Robeck, G.G.
Survey of Community Water Supply Systems. JAWWA.
62: 670 (1970).
9. llouoc-he, B. Annals of Medicine. Three Sick Babies. The
New Yorker, Oct. 5, 1968.
-------
C - CHEMICAL Ql'ALlTY
The following pages present detailed data and the reasoning used
in n-achuig the various limits.
In general, limits arc based on the fact Hint 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 lias 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
exixD.sure to man.
The Standards are regarded as a standard of quality that
is gene-rally attainable by good water quality control practices.
Poor pr.ictice is an inherent health hazard. The policy has been
to set limits that arc not so low as to be impracticable nor so
high as to encourage pollution of water.
No attempt lias been made to prescribe specific limits lor every
toxic or undesirable contaminant that might enter a public water
supply. Wliile the need for continued attention to chemical contami-
nants of water is recognized, the Regulations arc limited to need and
available scientific data or implications on winch 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 time.
-------
PERCENT OF SAMPLES IN THE COMMUNITY WATER
SUPPLY STUDY WITH VALUE EXCEEDING 75% OF EACH LIMIT
IN THE 1962 DRINKING WATER STANDARDS
Percent of
Constituent DWS Limit DWS Luiut X 0.75 Samples Exceeding
Arsenic
Barium
Cadmium
Chlui ide
Chromium
Color
Copper
Cyanide
Foaming
Agents
Iron
Lead
Manganese
Nitrate
Selenium
Silver
Sulfiitc
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/4
0.05 mg/1
45 mg''l
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 mir/i
0.225 mu'/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%
2.41%
0.00%
0.08%
15.81%
3.32%
11.91'b
3.46%
8.35%
0.00%
3.37%
0.35%
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DAILY FLUID INTAKE
For the purpose of these 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 on 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 Invc 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 getting 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?o of such
boys drink less than 8 soft drinks per day. It would probably be valid
1o stale that thn average consumption is far less than 8.
-------
Guy ton (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 75°F 2 liters or
less of fluid arc 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 +1. 09.
These men ucrc performing their normal duties including truck driving,
guard duly, 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 CO°F. To
replace their fluid tl.at day would require from 2. 3 to 5 liters of water.
In "Clinical Nutrition" (8) the normal water loss per day shown
for a normal adult ranges from 1, 500 m! - 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
41.67. This indicates that some men only drank three liters a day in
-------
a closer! environment where temperatures went as high as 105°F.
In Best and Taylor's book, "Tin: Physiological Basis of Medical
Practice, " (1945)(10) an average aduli 4s shown to require 2, 500 nil
of water from all sources under ordinary circumstances. The sources
of this water are shown as:
Solid and scmisolid 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.
I» should be noted that certain references refer to water loss per day
instead of drinking water intake. Water loss per day is approximately
1 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
\vatcr is required per caloric of food intake.
Two articles relating to the fluid intake of children might be cited
':erc. One, by G.ilagan, et al (12), used children from under one year
of aue to age ten and showed that total fluid intake per pound of body
weights was highest ainor.g infants and decreased with age. The water
intake listed average 0.40 ounces (12 ml) per day pur i*uu::d of body
•ACigln. They also found that water intake increased directly \\ilh
increases in temperature. t- -.-
-------
The second article by Bonham, el 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 Jbs.,
he would drink about one liter per day.
The "Bioastronaulics 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 man should be a reasonable
estimate. It is twice the amount listed by some authors and 30*/o higher
than other authors list as an average figure and is therefore defensible
as a rcfercMicc standard.
-------
REFERENCES
1. McDcrmott, P.M., R. L. Dclaney, J. U. Euan, and.J.F. Sull
"Myocardo-sis and Cardiac Failure in Man" JAMA 198:253 19GG
2. Morir.. Y. L., A.R. Folcy, G. Marlincau, and.I. Rousscl B«:er-
Drinkers Cardiomyopalhy: Forty-Eight Cases." Canadiaji Medical
Assoc. J. 97:881-3, 1967.
3. Boy's Life. National Readership Panel Survey, August 1970
Richard Manville Research, Inc. 1971
4. Guy tun, A.C. Textbook of Medical Physiology, Second Edition
Philadelphia, W.S. Saundcrs 1961.
5. Welch, n. E., E.R. Duskirk and P. F. lanipietro "Relation of
Climate and Temperature to Food and Water Intake" Metabolism
^7:141-8, 1958
6. Molnar, G.W., E.J. Towbin. R.E. Gosselin, A.M. Drown and
E.F. Adolph. "A Comparative Study of Water, Salt and Meat
Exchanr.es of Men in Tropical n;id Desert Environments" A. J. Hvt;
-14:411-33, 194G/
7. Wyndhan, C.M. and N. 13. Strydnm. "Th." Danger of and Inadequate
Water Intake During Marathon Running. " Suulii Afr. M. .1. 43:893-0,
19G9
8. Joliffe, N. (Editor), Clinical Nutrition, Second Edition, New York,
U-'.rpcr and Brothers, 19C2.
9. Adolph, E. F. , Physiology of Man i!'. the Desert, Now York,
Intel-science Publ. 194G."
10. Best, C.M. aiulM.B. Taylor, The Phvsioloc-icnl 'iasis of Medical
Practice. Eighth Edition, Baltimore, Williams and Wilkins Co., 19CG
11. Beck, W.S., Human Desiirn. New York, Marcuurl Brace .lovnnovich,
1971.
12. Galanan, D.J., J.R. Vcrmillion, G.A. Ncvill, Z. M. Slaclt. and
R.E. Dart. "Climate and Fluid Intake, " Pub. Health Rci;. 7^:484-90,
1957
13. Bonham, G.M.. A.S. Gray, and N. Luttrell. "Fluid Intake Patterns
of G-Yuar-Old Children in a Northern Fluoridated Community. " Canad.
Mcd. Ass. J. 21:749-51, 19G4.
-------
14. Webb, P. (Editor), ni;ja.stronaiHics Data Book, (National Aero-
nautics and Space Agency, Washington, D. C.) NASA-SP 300C,. 1904.
15. Snydor, W.S., Chairman, "Rcixjrt of the Task Group on Reference Man. "
New York, Pergamon Press, 1974.
£57 <
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ARSENIC
The high toxicity of arsenic and its widespread occurrence in
the environment necessitate the setting of a limit on (he 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 (mi; '!) 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 clement to constitute .1 risk to human wealth (1,2).
Despite the diminishing use of arscnicals as pesticides, presently
several arsciiile.^ arc usud as herbicides and some :irscnates as
insecticides. In IOG-1, farmers in the U.S. used a combined
total of approximately 15 million pounds of arscnicals (3).
The chemical forms of arsenic consist of trivalcnt and pen lava-
lent inorganic comixuinds and trivalent and pentavaleiit organic-
agents. H 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 pcntavalcnt inorganic form is the most
prevalent. Conditions that favor chemical and biological oxidation
promote the shift to the pcntavalenl specie; and conversely, iho.sc
that favor reduction will shift the equilibrium to the trivalent
state.
-------
The ixjpululion is c.\|x>scd to arsenic in a number of ways.
Arsenic is still used, albeit infrequi nlly, to treat leukemia,
certain ivpcs of anemia, and certain skin diseases (4). In the
diet, vegetables and grain contain an average of 0.44 ppm and
meats an average of 0. 5 ppm of arsenic (5). Organic arsemcals
arc 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 arscnicals on
fruits and vegetables (3. 5 mg as As}0, per kg) and in meat
(0. 5 to 2. 0 mg as As per kg) (6). Shellfish arc 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/mj (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 oecn reported from the ingeslion of water containing
0. 1 mg/1 of arsenic.
The toxicity of arsenic is well known, and the ingeslion of as
little as 100 mg can result in severe poisoning. In general, in-
organic arscnicals arc more toxic to man and experimental
animals than the organic analogs; and arsenic in the pcntavalent
state is less toxic than that in the trivalcnt form.
-------
Inorganic arsenic is absorbed readilv from the gastro-intestinal
tract, tlio lungs, and to a lesser extent from the skin, and becomes
distributed throughout the body tissues and fluids (4). Inorganic
arsoiucals appear to be slowly oxidized jn vivo from the trivalctit
to the pcntavalenl stale: however, there is no evidence that the
reduction of pentavalonl arsenic occurs within the body (5, 11-13).
Inorganic arscnicals arc potent inhibitors of the inlracellular
sulfhydryl (-SH) enzymes involved in cellular oxidations (14).
Arsenic is excreted via urine, fcccs, 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 lK>nc, muscle, and skin, and to a smaller degree in liver and
kidneys. After cessation of continuous exposure, arsenic excre-
tion P.I ay last up to 70 days (14).
A number of chronic oral loxicity studies \\ilh inorganic arscnile
and arsenate (21-25) demonstrated the minimum-effect and no-effect
levels in dogs, rats, and mice. Three generations of breeding mice
v.ere exposed to 5 ppm of arsenilc 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 (20). Arsenic is also an antagonist of selenium and has been
reported to counteract the loxicitv of sclcnifcrous foods \\hcn added
to nrgicultural animals' feed water (27, 28). Rats fed shrimp meat
GO-
-------
containing a high concentration of arsenic retain very little of the
element as compared to rats fed the same concci.'lralions of either
arsenic trioxide or calcium arsonale (29), suggesting that the
arsenic In shellfish tissues may be less toxic to mammals than
that ingested in oilier forms.
In man, subacutc 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, polyncuritis, liver cirrhosis,
bone marrow injury, and exfoliate dermatitis (30, 31). In 1902,
thirty-two school-age children developed a dermatosis associated
\ulli cutaneous cxjx>suro to arsenic trioxidc (32. 33). It has been
claimed that individuals become tolerant to arsenic. However, tins
apparent effect is probably due to the ingestion of (ho relatively
insoluble, coarse powder, since no truo tolerance lias ever been
dcmo'iM rated (M).
Since the early nineteenth century, arsenic was believed to be
a carcinogen: howcxer, evidence from animal experiments and human
experience has accumulated lo strongly suggest that arsenicals do
not produce cancer. One exception is a roport from Taiwan showing
a dose-response curve relating skin caticcr incidence lo tho arsenic
content of drinking water (-14). Somr reports incriminated arsenic
61 <
-------
as a carcinogen (34, 35), but it was later learned that agents
other than the metalloid were responsible for such cancers (30).
Sommers anH M^Manus (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 was no direct evidence that arsenic was the eliologic
agent in the production of the carcinoma.
Properly controlled studies (38, 39) have demonstrated that
industrial v.orkcrs do not have an increased prevalence of cancer
despite continued exposure to high concentrations of arsenic
trioxide. In the study by Pinto ajid 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 lo arsenic trioxide for up to 40 years,
excreted 0.82 mg of arsenic per liter, 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-
gcnic role of arsenic trioxide in the production of melhylcholan-
thrcne-induced skin tumors has been investigated and found to
have no significant effect (43).
-------
However, sonic recent evidence .supports the view that arscr1-1
is carcinogenic. Industrial workers in a plant manufacturing arsenic
powder were exposed to arsenic dust and showed n higher incidence
of skin and lung cancer than other occupational groups (44, 45, 4G).
Ulrcralion of tlio 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 \\erc "consistent \\ilh the hypothesis that exposure
t.j 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-u.xposcd employees (49).
Dactjer, 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 clue to cancer as compared to an expected number,
basr.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/1.
A similar problem has been reported in Argentina (56-58). Dermalo-
logical manifestations of arsenicism 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). Arsenicism affecting l\\o members
of a family where the arsenic content of the family's well varied between
0. 5 and 2. 75 mg/l 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 (Cl). 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
Jic production of carcinomas.
-------
Arsenic is a gcochcmical poil'.ilant, and when it occurs in an area
il can be expected to be in the air, lood, and water, but in oilier
cases it is due to industrial pollution. In some cpidemiological
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 \\ere related to exposure from this source,
but other exposures were not qumtitalcd. The Taiwan studies were
able to compare quite similar populations thai differed only in the
water intake. Deep wells contained arsenic, but persons usiii<.;
shallow wells 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.
II is estimated that the total intake of arsenic from food is an
average of 900 jjg/day (5). Al a concentration of 0.05 mg per liter
and an average intake of 2 liters of water per day, the intake from
water \\ould not exceed 100 pg per dav, or approximately 10 percent
of the total ingested arsenic.
In light of our present knowledge concerning the potential health
lia/ard from the ingcslion ol arsenic, the concentration of arsenic
in the drinking water shall not exceed 0.05 mg/1.
-------
REFERENCES
1. Umlenvood, E.J., Trace Elements in Human and Ani"T*l Nutri-
tion. New York; Academic Press, Inc., 1956, pp. 372-364.
2. Mor.ier-Williams, G.W.: Trace Elements in Food. New York:
John Wiley & Sons, Lie., 1949, pp. 1G2-20G.
3. Quantities of Pesticides Used bv Farmers in I9G4. Agriculture
Economic Report No. 131, Economic Research Service, U.S.
Department of Agriculture, 1968.
4. Sollman, T. (od.) in A Manual of Pharmacology and its Appli-
cations to Therapeutics and Toxicology. Philadelphia: W.D.
Snuitclcrs Co., 1957.
5. Schroeder, II.A., and Balassa, J.J. Abnormal Trace Metals
in Man. J. Chron. Pis. 19, 85-106, 19C6.
C. Code of Federal Reflations, Tillo 21, Sections 120.192/3/5/G
and 133^.33.
7. Coulson, E.J., Remington, R. E., and Lynch, K.M. Metabolism
in the Rate of the Naturally Occurring Arsenic of Shrimp rvs
Compared with Arsenic Trioxidc. J. Nutrition, 10, 255-270,
1935.
8. Ellis. M.M., WeslfaU, B.A., and Ellis, M.D. Arsenic in
Freshwater Fish. Indust. nnd Engineer Ciiem., 33, 1331-1332,
1911 (Experimental Station Report 87, p. 740, 1941).
9. Air Pollution Measurements of the National Air Sampling Net-
work - Analyses of Suspended Participates 19G3, U.S. Dcpt.
of Health, Education, and Welfare, Public Health Service,
Cincinnati, Ohio, 19G5.
10. McCafoc, L..J., Symons. J.M., Lee, R.D., nnd Robcck, C. G.
Survey uf Community Water Supply Systems, JAV/WA, 62,
(11), G70-G87, 1970.
11. Ovcrliy, L. II., and Frcdrickson, R. L. ,T_. A;;r. Food Chum.,
jj^, 78, 19G3.
12. Peoples. i^.A. Ann. N.Y. Acad. Sci., 111, 644, 1964.
-------
13. Winklcr.W.O. J. Assoc. Offic. Agr. Chemists, £5, 80, 10G2.
14. DuBois, K. P. and Gelling, 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, .T.W. Radiotraccr Studies
on Arsenic Injected as Potassium Arscnite: I. Excretion and
Localization of Tissues. J. Pharmacol. Expcr. Thcrap., 76
207-220, 1942.
1C. Lowry, O.H., Hunter, F.T., Kip, A. F., and Irvine, J.W.
Radiolracer Studies on Arsenic Injected as Potassium Arscnite:
II. Chemical Distribution in Tissues. J. Pharmacol. Expcr.
Tliorap. 7G, 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. 2G, 9G-118, 1942.
18. Duncoff, U.S., Neal, W.D., Slraube, R. L., Jacobson, L.O..
and Brues, A.M. Biological Studies with Arsenic: n. Excretion
and Tissue Localization. Proc. Soc. Expcr. Diol. Mod. G'J,
548, 1948.
19. Musil. J. and Dojmal, V. Experimental and Clinical Administra-
tion of Radioarsenic. Casopis tck. cosk. 9G, 1543-G, 1957;
Chom. Abslr. 1-1008, 1958.
20. Crcina, A. Distribution ct elimination dc I'arscnic 7G chez la
souris normale ct cancereuse. Arch. Internal. Phannacodyn.
)03. 57-70, 1955.
21. Soil man, 1921. Cited in Sollmann T. (eel.) in a Manual of
Pharmacology and Its Application to Therapeutics and Toxicology.
Philadelphia: W. B. Saunders Co., 1948, p. 874.
22. Srhmcder, H.A. and Balassa, J..I. Arsenic, Germanium, and
Tin in Mice. .). Nutrition. 32, 245, 19G7.
23. Kanisaua, M. and Sclirocdcr. 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. Schrocdcr, II. A., Kanisawa, M., Frost, D. V., and Milchcncr,
M.N. Nutr. 96, 37, 19G8.
/ » f
t>
-------
25. Byron, W.R., Bicrljowcr, (i.W. , Rrouwer, .J.B., and
Han.scn, W.H. Tux. Appl. Pharniacul, 10(1): 132-147, 1907.
26. Hesse, E. Klin. Wulinschr. 12, 1000, 1033.
27. DuBois, K. P. , Moxon, A. L. , and Olson, O. E. Further
Studies on the Effectiveness of Arsenic in Preventing Selenium
Poisoning. J. Nutrition 19, 477-4B2, 1940.
28. Moxon, A. L. Tlic Influence of Arsenic on Selenium Poisoning
in Hops, in Proceedings of (he South Dakota Academy of Sciences,
1941, vol. 21, pp. 34-36.
29. Calvary, 11. 0. Chronic Effects of Ingested Lead and Arsenic.
J.A.M.A. HI, 1722-1729, 1938.
30. Goodman, L. S. and Oilman, A. (ods. ) The Pharmacological
Basis of Therapeutics, 3rd Edition. Now York, N.Y. , The
Mnc-Millan Co. , 1905, pp. 944-951.
31. DiPalma, J.n. Drill's Pharmacology In Medicine, 3rd Edition.
New York, N.Y., McGraw-Hill Book Company, 1905, pp. 860-862.
32. Birmingham, D.J., Koy, M.M., aiullloladav, U. A. An
Oulhrc;ik of Dcrninlobcs m a Mining Cumr.iuuity - Report of
Environmental and Medical Survev.s. U.S. Dcpl. of Health,
Education, :tnd Welfare, TR-1I, April, 1954.
33. Birmingham, D.J., Key, M. M. , Holaday, D. A., and PC rone,
V. n. An Outbreak of Arsenical Dcrmalosiis in a M in ing
Community. Arch. Donna tol. 91, 457, 19G5.
34. Paris, .7. A. Pharmacologia: Comprchfiiding the Art of
Prescribing upon Fixed and Scientific Principles Together
With The History of Medicinal Suljstancoa, 3rd Edit. , p. 132,
London: Philips, 1820.
35. Buchanan, W.D. Toxicily of Arsenic Com|X)unds. Now Jersey:
Van Noslrand. 19G2.
3G. Frost, D. V. Arscnicals in Diolo^* - Retrospect and Prospect.
Federation Proceedings 2G, 18-1, 19G7.
37. Summers, S.C. and McManus, R.G. Multiple Arsenical Cancers
of Skui and Liternal Organs. C:uiccr G, 347-359, 1053.
38. Snegireff, L. S. , and Lombard, O. M. Arsenic and Cancer.
Arch, tndustr. ilvg. Occupational Mod. 4, 199, 1951.
lib"
-------
30. Pinto, S. S., :mcl Dennett, 13. M. Effect of Arsenic Trioxidc
Exposure on Mortality. Arcn. Environ. Health 7, 583, 1963.
•10. Baroni, C., Vnn Esch, G.J., nnd Saffiotli, U. Carcinogenesis
Tests of Two Inorganic Arsenicals. Arch. Environ. Health 7,
088, 19G3.
•11. Boutwcll, R.K. J. Agr. Food Cliom. 11, 381, 1963.
42. Huopor, W. G., and Payne, W.W. Arch. Environ. Health 5,
445, 1962.
<»3. Milncr, J.E. The Effect of Invested Arsenic on Mcthylchol-
ajithrenc-lnduccd Skin Tumors m Mice. Arch. Environ. Health,
_18, 7-11, 1969.
44. Hill. A.B., Failing, E. L., Perry, F., Bowler, R. G.,
Ducknell, II. M., Druott, H.A., and Schilling, R.S. F.
Studies in the Incidence of Cancer in a Factory Handling Inorganic
Compounds of Arsenic. Brit.- J. In dust. Mod. 5: 1 (1948).
45. Doll, R. Occupational Lung Cancer: A Review. 'Brit. J.
Indus. Mod. H5: 181 (1959).
4G. Morcwelher, E. R. A. Industrial Medicine and Hygiene.
Vol. 3, Butterworlh & Co., London, pp. 196-205(1956).
47. Ncubaucr, O. Arsenical Cancer: A Review. Brit, J. Cancer
Jh 192 (1947).
48. Lee, A.M. and Fraumcni, J. F. , Jr. Arsenic and Respiratory
Cancer in Man—an Occupational Study. J. Natl. Cancer
Iiihl. 42: 1045 (1969)...
.*
49. Ott, M.. Holrlor. B., Gordon, H. Respiratory Cancer and
Occupational Exposure to Arscnicals. to be published in
Archives of Environmental Health, Cited In: Federal Register,
40FR PI. 3, p 3395, January 21, 1975.
50. Bacljcr, A., Levin, M., Lillcnfeld, A. Analysis of Mortality
Experience of Allied Chemical Plant. Cited In: Federal Register,
40FR 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 Arscnicism in Taiwan. J. Nat. Cancer Inst. , 40, 454, 1968.
-------
52. Cli'1!!, K. P. , Wu, U., and V.'u, T. EpidcmioIoi'U' Studies on
Bl'ickfoot Disease in Taiwan1 3. Physiochemical Characteristics
of Drinking Water in Endemic Blackfoot Disease Areas. Memoirs
of the College of Medicine, National Taiwan University, Vol. Ill,
Nu. 1, 2, pp. 1 1C- 129, 1962.
53. Wu, H. , and Chen, K. Epidcmiulopc Studies on Dlackfoot
Disease: 1. Prevalence and Incidence of the Disease by A
-------
BARIUM
Barium is recogni/cd as a general muscle stimulant, including
especially the heart muscle (1). The fatal dose for mail 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 vasocunstriction (3). Aspirated barium sulfatc has been reported
to result in granuloma of the lung (4) and other sites in man (3).
Thus, evidence exists for high acute toxicity of ingested soluble
barium salts, and lor chronic irreversible changes in tissues result-
ing from the actual deposlion 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 (G). Most of
the administered dose appeared in the li\cr 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, irore 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 shuwn to go to
the skeleton of animals when tracer amounts of barium-140 were used
(9), but no determinations of barium have been made ui animals to
which barium had been repeatedly administered for long periods.
71'-
-------
No .study appears to luive been made of the amounts of barium
tli.il may be tolerated in drinking water or of effects from prolonged
feeding of barium salts from which an acceptable \vaier guideline
may be set. A rational basis for a walei 'ruidelinc may be derived
from the tliresliold limit of 0.5 mi; Da/m3 iiir set by the American
Conference of Governmental Industrial Hygicnisls (10) by procedures
that have been discussed (11). Dy assuming that 15r"o of tlic barium
inhaled is absorbed into the blood stream and tuat 90'o is a reason-
able factor for absorption via the i;aslrointcstinal tract, a value of
2 mg/1 can be derived as an approximate limiting concemration for
a healthy adult population. The introduction of a safety factor to
account for heterogeneous populations results in the derivation of
1 mi;'1 as a limit that should constitute a "no eflrct" level in
water. Decau.sc of the seriousness of the toxic effects of barium
on the heart, blood vessels, and nerves, drinking water shall not
com.iin barium in a concentration exceeding 1
-------
RKFERI:NCI-.S
1. Sollinan. T.H. (Ed.) A Manual of Pharmacology. W. B. Saundcrs
Co., PhiLiu-'lphia. pp. GG5-667 (1957).
2. Lorcnto do No. R.. and Feng, T.P. Analysis of Effect of
Barium upon Ncrvo with Particular Reference to Rhythmic
Activity. J. Cell Comp. Physiol. 2£: 397 (1946).
3. Gotsev. T. Bluldruck und Hcrzlaligkeit. Ill Milteilung:
Kroislaufwirkung von Barium. Naunyn Schiedebcrg Arch.
Expcr. Path. 203: 2G4 (1944).
4. File, F. Granulonia of Lung Due to Radiugraphic Contrast
Medium. AMA Arch. Path. 59: 673 (1955).
5. Kay S. Tissue Reaction to Barium Sulfalc Contrast Medium.
A MA Arch. Path. £7: 279 (1954). Ibid: Kay S.. and
Chay. Sun Hak: Resultj of Intrapcritoncal Injection of Barium
Sulfate Contrast Medium 59: 388 (1955).
6. A molt, R.I. Fijacion y determm.icion quimica del bario en
ori;:mos. Rev. Col. Farm. Nac. (Rosano) 7: 75 (1940)
7. Gerlach, W., and Mullcr, R. Occurrence of Strontium and
Barium in Human Organs and Excreta. Arch. Pain. Anal.
(Virchows) 294: 210(1934).
8. So\v,-'o:*.. W., ami Stitch, S.R. Trace Elements in Human Tissue.
Kstiiralion of th.e Conccnlrutions of Stable Strontium and Barium
in Human Bone. Biochem. J. 67_: 104 (1957).
9. Bauer, G.C.H.. C.irlsson. A., and Luulquist. B. A Compara-
tive Sludv ol Metabolism of 140 Ba and 4o Ca in Rats. Biochcm.
J. C3: 535 (195G).
10. American Conference of Governmental Iir.lustrial Hv^icmsls.
Tlieshold Limit Values of 19ob. A.M.A. Arch. Indust.
Health Ui: 178 (1958).
11. Stoki-iger. H.E.. and Woodward. R.L. Toxicologio Methods
lor Kslabiislung JJrinking Water Standards. .IA\V\VA
50: 5If) (l'J58;
-------
CADMIUM
As far as is known, cadmium is biologically a noncssential, nun-
beneficial clement of high toxic potential. Evidence for the serious
to::ic po*cntinl of cadmium is provided by: (a) poisoning from cadmium-
contaminated food (1) and beverages (2); (b) c;ndemiologic evidence
that cadmium may be associated with renal arterial hypertension
under certain conditions (3); (c) epidennologic association of cadmium
with "Itai-ilai" disease in Japan (4); and (d) long-term oral to.xicity
studies in animals.
The possibility of cadmium being a water contaminant has been
reported in 1954 (5); seepage of cadmium into ground water from
clcclropla'mg plants h: s resulted in cadmium concentrations ranging
Irom 0.01 (o 3.2 mg/1. Other sources of cadmium contamination in
water arise from zinc-galvanized iron in which caJmium is a con-
taminant. The average concentration of cadmium in drinking water
from community supplies is 1.3 ug per liter in the United Stales.
Slight amounts arc.- common, with G3 percent of samples taken at
household tai*.-. showing 1 ug per liter or morn. Only 0.3 percent
of tap samples would be expct-ti-c1 to exceed the limits of 10 ug
per liter (G).
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 1*5 mg/1 cadmium (1).
-------
Tliis is commonly considered the emetic threshold concentration
for cadmium. It has been stated (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, ana 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 loxicily. A maximal "no effect" level was
thus not established in the above studies (8). A dietary relation 1o
cadmium toxicity has been reported by otiiurs (0).
Fifty mg/1 of cadmium administered as cadmium chloride in food
and drinking wator to rats resulted in a reduction of blood hemoglobin
ami lessened dcnril pigmentation. Cadmium did not decrcasr; 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 Jivcr 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/l (11). Later
work lias confirmed the virtual absence of turnover of absorbed
cadmium (12). More recently, the accumulation of cadmium in rona!
and hepatic tissue \\illi age has been documented in man (13).
Recent cpidcmiologic.il evidence strongly suggests that cadmium
ingcstion is associated with a disease syndrome referred to as
"Itai-itai" in Japan (4). The disease syndrome is characterized
by clccalrificalion of bones, protcinuria, glycosuria and increased
serum alkaline phosphatase, .1.1 d other more subjective symptoms.
Similar clinical manifestations hr.vc been noted in cadmium workers
(14). Yamagalla and Shigcmatsu (15) have estimated the current
daily mtako of cadmium in an endemic "Ilai-itai" area as GOO/ug.
The authors from a ideological and topographical survey as well as
knowledge of local customs, concluded that the daily cadmium intake
in the r.Midc.im: area was probably higher in the past. They concludcc1
that GOO ug per day would not cause "Ilai-itai" disease. The average
ingcstion of c.'unp.'-im is 59 ^ig/day in non-polluted areas of Japan.
-------
-The association of cardiovascular disease, particularly hyper-
tension, with inmost ion of cadmium remains unsettled. Conflicting
evidence has been found both in man (3, 1C) and in animals (17, 18).
II 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. Duggan and P. E. Corncliusscn (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 ;ig in 1969 and 30 ;ug in 1970. Each
market basket represented 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 ;.ig as :• reasonable
estimate of average daily dietary intake (22, 23, 2-\, 25).
Cigarette smoking has also been .shown to be important. Twenty
cigarettes per day will probably cause the inhalation of 2--1 jjg of
cadmium (20). However, the absorption rale associated with cigarette
smoke inhalation is much larger than that associated with food ingest ion.
Lewis (27) has .shown in autopsy studies that men who smoke one
or more packages of cigarettes per clay 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 front 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
proleinuria. (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 59o gastrointestinal absorption,
rapid excretion of lOTbof the absorbed dose, and 0. 05% daily excretion
of the total body burden, it would take 50 years with a daily ingcslion
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 really is about
3'/',, it would probably take about 500-600 jug ingested per day to
cause protcinuria.
Concentration of cadmium shall be limited to 0.010 mg/1 in drinking
water. At this level it would contribute 20 /ag per day to the diet of a
person ingesting 2 liters of water per day. Added to an assumed diet
of 75jLig/day, this would provide about a four-fold safety factor. This
docs not, however, lake cigarette smoking into account.
8 <
-------
REFERENCES
1. Fr:int, S. , and Klccman, I. Cadmium "Food Poisoning" J. A. M. A.,
117,80 (19-11).
2. Cancolusi, J.T. Acute Cadmium Metal Poisoning. U.W. Nav.
Mod. Dull., pp. 39 and 408 (1941).
3. Sc-hroeder, H.A. Cadmium as a Factor in Hypertension, J.
Chron. Dis. 18, C47-r,;.G (19G5).
4. Murala, I., Hirono, T., Sacki, Y., and Nakagawa, S. Cadmium
Entcropathy, Renal Osteomalacia ("llai-itai" Disease in Japan).
Dull. Soc. Int. Chir. 1, 34-42 (1970).
5. Licbcr, M., and Welsch, W. F. Contamination of Ground Water
by Cadmium. J.A.W.W. A., 46, p. 51 (1954).
G. McCabc, L.J., Problem of Trace Me'.nls in Water Supply.
Proceedings of IGtli Annual Sanitary Engineering Conference,
University of Illinois (1974).
7. Polls, A.M., Simon. F. P., Tobias, J.M., Postel, S., S-vift, M.N.,
Pall, .T.M., and Gcrlad, R.W. Distribution and Fate of Cadmium
in the Body. Arch. Ind. Hvg. 2, p. 175 (1950).
8. Fit/hugh, O. G., and Mcillo", F..I. Chronic Toxicily of Cadmium.
J. Pharm. 72 p. 15 (1941).
9. Wilson. R.H., and DC Eds, F. Importance of Diet in Studies
of Chronic Toxicitv. Arch. Ind. Hyp. 1, p. 73(19500).
10. Ginn, J. T., and, Volkcr, J. F. Effect of Cd and F on Rat Dentition.
Proc. Soc. E.xptl. Piol. Mod. 57, p. 189 (1944).
11. Decker, L. E., Byerrum, R. II., Decker. C. F.. Hopporl. C.A.,
ar.d Langham, R. F. Chronic To.xicity Studies, I. Cadmium
Administered in Drinking Water !~ Rats. A.M. A. Arch. Ind.
Health, 18, p. 228 (1958).
12. Col/.ias, G.C.. Born, D.C., and Sellcck, B. Virtual Absence
of Turnover in Cadmium Metabolism: Cd Studies in the
Mouse. J. Pl.ysiol. 201, 927-930 (1961).
13. Schrocdor, H.A., Balassa, J.J., and Hogcncamp, J.C.
Abnormal Trace Metals in Man: Cadmium. J. Chron. Dis.
14, 236-258 (19G1).
-------
14. Picsalnr, M. Protoinuria in Chronic Cadmium Poisoning.
I. An Elcclrophorclic and Clicmicnl Study of Urinary and Scrum
Proteins ,'roni Workers with C'ironic Cadmium Poisoning.
Arch. Environ. Health 4, 607-621 (19G2).
15. Ynmagata, N., and Shi^oniatsu, I. Cadmium Pollution in
Perspective. Bui. lust. Public Health 19, 1-27 (1970).
1C. Morgan, J. M. Tissu Cadmium Concentration in. Man. Arch.
Intern. Mod. 123, 405-408 (1969).
17. Kamsawa, M. and Schrocder, J.A. Rcn.il Artcriolar Changes
in Hypertensive Rals Given Cadmium in Drinking Water.
Exp. & Mole. Path. 10, 81-98 (1969).
18. Lcncr, J. and Bibr, B. Cadmium Content in Some Foodstuffs
In Respect of It.', Biological Effects. Vilalstoffe Zivilisations-
drnnkhcitcn 15, 139-141 (1970).
19. Nogawa, K. , and Kawann, D. A Survey of The Blood Pressure
of Woni»n Suspected of Itai-itai Disease. Juzcn Med. Soc. J.
77, 357-3C3 (1969).
20. Du^aii, R. E. and Corncliusscn, P. E. , Dietary Intake cf Pesticide
Chemicals in the United Slates (III), June 1968-Apri! 1970, Pest.
MOM. Journal. , J3, No. 4, 331-341 (March 1972).
21. Murthy, G.K., Rhca, 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. ? . The Trace Metal Content
of Representative Canadian Diets in 1970 and 1971. Can. "fiist.
Food Sci. Tcchnol. J. J7: 56 (1974).
23. Morani;cr, J. , and Smith, D. C. The Heavy Mctai Content of
a Typical Canacliann Diet. Can. J. Of Pub. Health. , i63: 53 (1972).
24. Schroederm, H.A., Nason, A. P., Tiplon, I. H. , and Balassa, J..J. ,
i_sscnli:il 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 Ihc
Determination of Trace Elements-Standard Man Series. Proc.
Univ. Missouri 3rd Ann. Conf. on Trace Substances in Environmental
Health, 1909, Univ. of Missouri, Columbia, Mo. (1970).
26. Friberfj, L. , Piscalor, M. , and Nordrl'wrj*, D. , Cadmium in l';c
Environment, Cli'jmical Rubber Company Press, Cleveland, Ohio
p. 25 (1971).
-------
27. Lewis, G. P., .lusko, W.J., Cou^hlm, L. L. and Hnrlz, S. ,
Cadmium Accumulation in Man: Im'luencc of Smokini;, Occupation,
Alcoholic Habit and Disease. J. Cliron. Pis. , 2J3, 717 (1972).
28. Hammer, D. I., Calocci, A.V., Hnssclblad, V., Williams, M. E.
and Pinkerlon, C. Cadmium and Lead in Autopsy Tissues, Jour.
Occ. Mccl., Jj>, No. 12 (Dec. 1973).
29. Friberg, L., Piscator, M. and Nordbcrg, G., Cadmium in
The Environment, Chemical Rubber Company Press (1971), p. 85.
-------
CHROMIUM
Chromium, particularly in the hexavalcnt stale, is toxic to man,
produces lung turners when inhaled, and readily induces skin sensiti/.a-
tions. Chromium occurs in some foods, in air including cigarette
smoke, and in some water supplies (see Table I). 11 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 conversativc total value is used lor this guideline.
TABLE 1
U.S. urban air concentrations range, 19G5 £1)' 0-0.028 >ig/m3
Chromium content in cigarette tobacco (2) 1.4 ^/cigarette
Chromium in foods cooked in stainless-steel ware (3) 0-0.35 nig/100
Chromium concentration range in water supplies 11)69 (4). .. .0-0.08 mg/i
Comparatively little data arc 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
ant! other elements sn institutional diets. In that investigation, the
concentrations of chromium ill foods ranged from 0.175 to 0.470 mg/kg.
Chromium has 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 ninute quantities (5,6,7). At present, Lie
levels of chromium thai can be tolerated by man foi1 a lifetime without
adverse effects on health arc still undetermined. A family of four
b-
-------
inclh ic.uals is known to li;ivc drunk \v;iicr for periods or 3 years at a
level as high a.s 0.45 milligrams chromium per liter without known
effects on their health, as determined by a single medical examina-
tion (8).
A study by MacKen/.ie cl[ a_l (8) was designed to determine the
toxicit> to rals of chromate (Cr+Ll) 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 diehromate per kg enhances (he secretory
and motor activity of the intestines of the dog (10).
From these and other studies of toxictty (11-15), it would
appear that a concentration of 0.05 mg/1 of chromium incorporates
a reasonable factor of safety to avoid any hazard to huni.m health.
In addition, the possibility of dermal effects from batlm," in
water containing 0.05 nig/1 uould likewise appear remote.
although chromium is recognized as a potent sensitizer of the
skin (3). Therefore, drinking water :«h:ill not contain more than
0.05 mg/1 of chromium.
-------
REFERENCES
1. U.S. I»ublic Health Service, National Air Pollution Control
AdnuiUMration. Preliminary Air Pollution Survey of Chromium
and its Compounds. A Literature Review. U.S. Dept. of
Commerce, National Bureau of Standards, Clcannnlum.se of
Federal Scientific and Technical Information, Sprmj;licld, VA,
22151.
2. Coiibill. E.C.. and Hobbs. M.E. Transfer uf Metallic Con-
stituents of Cmareltes to thu Main-stream Smoke. Tobacco
Sci. 144: G8 (1957).
3. Demon, C.R.. Keennn, R.G.. and Birmingham, D.U. Tlie
Chromium Content of Cement and Its Simuficance in Cement
Dermatitis. .1. Invest. Derm. 23- 184 (1954).
4. Mc-Cabo, L..I., Symons. J.M., Lee, R.D., and Robcck, G.G.
Survev of Community Water Supply Systems. JAWWA.
02: G70 (1970).
5. Murtlu, G.K.. Rhea. U.. and Peeler. .I.T. Levels of Aiitimony,
Cadmium. Chromium, Cobalt, Manganese, and Zinc in Institu-
tional Diets. Envir. Sci. Technol. 5_: 43G (1971).
G. Schroeder. H.A.. Balassa. .J.J., and Tipton, I.II. Abnormal
Trace Metals in Man - Chromium. J. Chr'jn. Disease 15: 941
(19G2). ~
7. Hopkins. L.L. Chromium Nutrition in Man. Proceedings of
Univ. of Missouri's 4ih Annual Conference on Trace Substances
in Environmental Health, pp. 285-289 (1970).
8. D.i\ids. M.W.. and Lieber, M. Underground Water Contamina-
tion 1)\ Cliromium Wastes. Water Sc\vaj;e V/urks 98- 528
(195U. ~
9. MacKen/ie, R.I).. Byerrum. R.U.. Decker. C.F.. Hoppert. C.A..
,md Ijani^ham, R.F. C'liror.ic Toxicity Studios II llexavalent
and Trivalent Chromium Administered in Drinking Water to
Rats. A.M.A. Arch. Industr. Health 1_8: 232(1958).
10. N'aumova, M.K. Effect of Potassium Bichromate on Secretory
iiiid Motor Activity of Intestine. C-inicna Truda I Professional
'nye Zabolcvaniya 9: 52 (1965).
-------
11. Gross. W.G., and Heller, V.G. Chromalus in Animal Nutrition.
J. Indust. Hyg. Toxicol. 28_: 52 (1946).
12. Brard, M.D. Study of Toxicology of Some Cliromium Compounds.
J. Pharm. Chim. 2l_: 5 (1935).
13. Conn, L.W., Webster, H.L., and Johnson. A.11. Chromium
Toxicology. Absorption of Chromium by The Rat When Milk
Containing Chromium Lactate was Fed. Fed. Am. J. Hyg. 15:
760 (1932).
14. Schrocder, H.A.. Vinton, W.H., and Balassa, J.J. Effect
of Chromium, Cadmium, and Other Trace Metals on The
Growth and Survival of Mice. J. Nutrition 80: 39 (1965).
15. Schrooder. H.A., Vinton, W.H. and Balassa. J.J. Effects
of Chromium. Cadmium, and Lead on The Growth and
Survival of Rats. J. NutriUon 80: 48 (1965).
-------
CYANIDE
Cyanide in reasonable doses (1'J INK or loss) is readily converted
to thiocyanate 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 toxicily of cyanide
for man is shown in the following tablo.
Oral Toxicily of Cyanide for Man
Literature
Response Citations
2. 9—1.7mg/l Noninjurious (1)
10 nm, single dose Noninjurious (2)
13 mg/1 in water Calculated from threshold (3)
limited for air to be safe
50-GO nig. single dose Fatal (4)
Proper chlorination to a free chlorine residual under neutral
or alkaline conditions will reduce cy:mide to very low levels.
The acute oral loxicity of cyanogen chloride, the chlorination
product of hydrogen cy:\nide, is approximately o:>e-twcntiplh that
of hydrogen cvanido (5). It should be noted that at a pH of 8. 5
cyanide is readily converted to oymr.ite which is much less toxic.
Because of the above considerations, and because cyanide occurs,
however rarely, in drinking water primarily as the result of spiils
or other accidents, there appeals to be no justification for establish-
ing a maximum contaminant level for cyanide.
-------
REFERENCES
1. Smith, O.M. The Detection of Poisons in Public Water Supplies.
Water Works Ens. l»7: 1293 (19-J4).
2. Bodansky. M., and Levy, M.D. I: Some Factors Influencing
the Di'loxication of Cyanides in Health and Disease. Arch. Int.
Mod. 31; 373 (1923).'
3. Stokinger. H.E., and Woodward. R.L. Toxicologic Metliods
for Establishing Drinking Water Standards. JAWWA
50: 515 (1958).
4. Annon. The Merck Index. Ed. C. Merck & Co. Die., Railway, N.J.
p. 508 (1952).
5. Spec-tor, W.S. Handbook of Toxicologv. Tech. Rpt. No. 55-16,
Wright^-Patterson Air Force Base, Ohio, Wright Air. Devcl.
Center. Air Res. and Devcl. Coinir.ttul, (1955).
-------
FLUOK1DJ-:
The Food and Nutrition Board of Hie Nation.il Research Council
has stated that fluoride is a normal constituent .:" all diets and is
an essential nutric'it (1). In addition, fluoride in drinking water
will prevent cental caries. Wnen 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 ui drinking water s.ipplics produces
objectionable dental fluorosis which increases witli increasing
fluoride concentration above the recommended upper control limits.
In the United Slates, this is the only harmful effect observed to
result from fluoride found in drinking water (4,5, 0,7,3.9,10,11).
Oilier expected effects from excessively high intake levels arc:
(a) bone changes when water containing 8-20 n\u lluoridc per liter
(8-20 m^/1) is consumed ovor a Jon^ period of time (7): (b) crippling
fluorosis when 20 or more m^ of fluoride from all sources is con-
sumed per day for 20 or more ycanj (12); (c) death when 2,250-
4.500 my of fluoride (5.000-10,000 my sodium lluoridc) is consumed
in a single dose (7).
The optimum Ilroride level (sec Table 1) for a c.ivcn community
depends on climatic conditions because the amount of water (and
consequently the amount of fluoride) invested by children is primarily
influenced by air temperature. This rel.ition.ship was lirsl studied
and reported by Gala^an and Associates in Ihc 1950's (13,14,15,16),
-------
but has been further investigated and supported by Richards, et al
(17) in 19G7. 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,
DHE\V, from the data cited, plus or minus 0.1 nig/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 dc-
fluoridation and by change to a water source with more acceptable
f'uoride conceiv.rauon (22,23,24).
Richards, cl al (17) reported the degree of fluorosis among
children \\here the community water supply fluoride content was
somewhat above the optimum v?lue. From sucli evidence, it is
apparent that an approval limit (see Table 1) slightly higher than
the optimum range can b
-------
Table 1
Annual Average of Recommended Control
Maximum Daily Air Limits Fluoride
Temperatures Concentralions in mg/1
50
53
58
63
70
79
.0
.8
.-1
.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
Approval
Limit
Upper mg/1
1
1
1
1
0
0
.3
.2
.1
.0
.9
.8
2
2
2
1
1
1
.4
.2
.0
.8
.6
A
II 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 cxpcrienci-d at optimal fluoride concentrations will be
diminished by as much as 50'o when the fluoride concentration
is 0.2 mj;/l below the optimum. (25,26)
-------
REFERENCES
1. National Research Council, Food Nutrition Board, Recommended
Daily Allowance, Seventh Revised Edition, Publication 1964,
National Academy of Sciences, Washington, D.C. p. 55 (19Gb).
2. Dean, II.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. ARC 12 to 14 Years, of 13 Cities in
4 Stales. Pub. Health Rep. 57: 115S (1942).
3. DcanH.T., Jay, P., Arnold, F.A., Jr. and Elvove, E.
Domestic Water and Dental Caries, il. A Study of 2,832 White
Chil'ircn Aged 12 10 14 Years of 8 Suburban Chicago Communi-
ties, Including Lactobacillus Acidoplnlus Studies of 1,761 Child-
ren. Pub. Health Hep. 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. C-ll (J946).
5. Dean, H.T. The Investigation of Physiological Effects by The
Epidemioiogiral Method. In: Moulton, F.R., (Ed.) Fluorine
and Dcnu.l Health, A.A.A.S. Pub. No. 19, Washington, D.C.,
pp. 23-31 (1940).
6. Dean II.T. Chronic Endemic Dental Fluorosis (Molded Enamel).
JAMA. 107: 1269 (1930).
7. Hodge, H.C., and Smith, F.A. Some Public Health Aspects
of Water Fluoridalion, In: Shaw, J.H., (Ed.) Fluoridation
as a Public Health Measure. A.A.A.S. Pub. No. 38,
Washington, D.C., pp. 79-109 (1954).
8. Heyroth, F.F. To.Mcologic EUdence for the Safety of Fluori-
dation of Public Water Supplies. Am. J. Pub. Health 42-
1568 (1952).
9. McClurc. F.J. Fluorine in Food and Drinking Water. J.Am.
Diet. Assn. 29: 560 (1953).
10. U.S. Public Hoallh Service National Institutes of Health,
Division of Dental Health. Natural Fluoride Content, of
Community Water Supplies, Bethcsda, MD. (1969).
-------
11. Leone, N.C., .Sliimkin, M.I3., Arnold, F.A., Slevcr.son, C.A.,
Zimmerman, K.N., Gcisor, P. II., and Lumberman, -I.E.
Medical Aspects of Excessive Fluoride in :i Water Supply.
Pub. Health Rep. U9: 925-936 (O=l. 1954).
12. Roliulni, K. Fluorine Intoxication. A Clinical-Hygienic Study.
U.K. Lewis & Co., Ltd., London (1937).
13. Galn^an, D.J. and Lamscn, G.G. Climate and Endemic Denial
Fluorosis. Pub. Hcallli Rep. G8i: 497 U
14. Gala^an, D.J. Climate and Controlled Fluoridation. J. Am.
Dent. Assn. 47: 159 (1953).
15. Gala^ati, D.J., Vermillion, J.R. DclcrnumiiK Optimum
Fluoride Concentrations. Pub. Health Rep. 72: 491
(1957).
17. Richards, L.F., ct 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. SaundcrsCo.. Philadelphia pp. 13G-1G2 (1949).
19. Arnold. F.A.. Jr., Dean, H.T.. Jay, I'., and Knutson, J.W.
Fifteenth Year of The Grand Rapids Fluoridation Study.
J. Am. Dental As>sn. 05: 780 (1962).
20. U.S. Public Health Service. Flouridation Census 1UG9.
National Institutes uf Health, Division of Denial lit-alll).
U.S. Government Printing Office, VVaslunnton, D.C. (1970).
21. Maier, F.J. Twenty-five Y"ars of Fluoridation. JAWWA
(1970).
22. Dean, IF .T. and McKa> , F.S. Production of Mottled Kiumel
Halted by A Change in Common Water Supply. Am. J. I*ub.
Henllli 2£: 590 (1939).
23. Dcan.~H.T., McKay, F.S. .mcl F.lvovc. E. Mottled Enamel
Survey of rfciu.xile, Ark. 10 Years After A Change In The
Common Water Supply, l^ib. Health Rop. 53: 173G
(1938). ~"
24. Maier, F.J. Partial Defluoridation of Water. Public Works
(I960)..
-------
25. Chriel/borf;, .I.E. and Lewis, l-'.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.
Kchoc (1) has pointed out Hint in technologically developed countries,
the widespread use of lead multiplies the risk of exposure of the
population to excessive lead le\els. For thi^ reason, the necessity
of constant surveillance of the lead exposure of the general popula-
tion via food, air, and water is imperative.
The clinical piciure of lead intoxication lias been well dcvumentoj
(2). Unfortunately, the general piciure of the symptoms is not
unique (i.e., gastrointestinal disturbances, loss of appetite, fatigue,
anemia, motor nerve paralysis, and enccphalopalhy) to lead inloxi-
cati'Ui and often this has resulted in niisdiagnosis (3,4). Several
laboratory tests thai are sensitive to increased lead blond levels
have been developed for diagnostic purposes, but their relationship
to the effects of Jcad intoxication are incompletely understood.
The most sensitive of these is the inhibition of red coll-aminolevu-
linic acid dehydrasc (ALAD) which correlates well with blood lead
levels from 5-95^ig/100 g blood (5,6). Because this is not the
rale-limiting step in porphyrin biosynthesis, accumuiPtinn of
aminolcvulinic acid (ALA) does not occur unlil nigh blood loud
levels are readied. Other sucli tests, which correlate with blood
\
lead to a lesser degree and at higher levels, arc the measurement
of urinar) coproporpiiyrins, the number of coarsely stippled red
-------
blood colls and the basophilic quotient (G). These changes, in hcm-
selves, have little known significance in terms of tlic clanger 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 mloxicatioi. (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
ia terms of the tolerated intake and the severity of the symptoms
(8). Lead enceph'.ilopathy is most common in children up to three
years of age (12). The most prevalent source of lead in these
cases of childhood poisoning has been lead-conUiinmg paint still
found m many older homes (1,12). Prognosis of children with
lead cnccphaJopathy is poor, will: or without treatment. Up to
94'.o of the survivors have been foui.d to have psychological abnor-
malities (13). It is still unknown whether smaller intakes ol lead
without enccphalopalhy 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 load (18); however, the significance
of this finding to liumans is unknown. Some groups of individuals
-------
who rxperu-nced lend intoxication at an early age and survived
have dcmonstrated a high Incidence of chronic nephritis in later
life (19). Recent work has demonstrated a high incidence of
nminoaciduriu 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 ;ug/100 ml to be common (20). There is evidence that lead
in high doses in animals affects the immunological system (21,22,
23.2-1): this, however, has 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 rug- Data obtained subsequent
to 19-10 indicate that the intake of lead appears to have decreased
slightly since that time (1,26). Inhaled lead contributes about
40'6 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 lo bone, while soft tisssuc levels vary only
slightly from normal even with hii^Ii 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 l«j -JO pg/100 g and average about
2G jug/100 ^ (i). The U.S. !\,L;ic Health Service (31) considers
-------
40 jug'100 g lead or over in whole blood in older children and
adults on two separate occasions as e\ idencc suggestive of undue
absorption, either past or present. Levels of 50-79 jig/100 g
require iininediatc evaluation as a potential poisoning case.
iCighty jig/100 g or greater is considered to be unequivocal lead
poisoning. The 40;jg/100 £ lead level in blood probably has 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 jig/100 g
of blood signifies inhibition of ALAD that 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 epulcmiologically been implicated in increased blood lead in
children (40).
The World Health Organization Committee (41), assuming lO'-o
of lead from food and water is absorbed, established in adults a
"Provi.sion.tl tolerable weekly intake" of 3 mg of lead per person
(the maximum lead exposure the average person can tolerate without
increased body burden). (Kchoc considers GOO jig per day the limit).
-------
Assuming lO'.r absorption from the gastrointestinal tract, approxi-
mately 40 ug of lead per day would bo 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 up/mj of air,
the average urban man would absorb 1C to 48 ug of lead per day.
(The contribution from 1 u^/m1 lead in air at 20 m respiratory
volume with 30^c absorption is 6 ug). Just Irom food and 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 the
ground (44,45). Rural children have significantly less exposure
than do iirban children to these sources. Additionally, children
have increased risk, because they have food and air intakes
proportionally greater than their si/,c and they might absorb a
larger percentage from their gut, possibly 50'c, of ingested lead
(4G). Lead Might also have a greater effect on their developing
neurological, hematological, and immunological systems (18,
20-24,47,49). Likewise, fciuscs 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 inlrauterine ex-
posure to increased lead in maternal blood (52).
-------
The lead concent rations in finished water ranged fron; 0 to
O.G-1 mg/liter in tlie Community Water Supply Study conducted in
1909 (53). Of the 9G9 water supplies surveyed, 1.4'« 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 (GOOpg/day) without considering
(lie additional contribution to the total intake bj other routes of
exposure. Under certain conditions, (acidic soft water, in particular)
water can possess .sufficient plumbosolvcncy to result in appreciable
concentrations of lead in water standing in leaci pipes overnight (54).
As a result of the narrow range between the lead exposure of
the average American in everyday life and exposure which is con-
sidered excessixe (especially in children) it is imperative that
lead in water bo maintained within rather strict limits. Since a
surve\ (55) uf lead in surface water of the U.S.A. and Puerto Hico
found only 3 of 726 surtac-e waters to exceed 0.05 mg/1; the standard
of 0.05 :ug''l .should be obtainable. For a child one to three years
old drinking one liter of water a clay (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 down the average
adult's diet to be 150-200jug (56). Assuming the fraction of lead
absorbed is the same for lead in food and water, water would
contribute 25 to 33'.7> 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'.r 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 reemphasizcd that the major risk of lead in water is
i« 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 (60,61), toys,
newsprint ink (62, 63), and air. Although paint is most strongly
implicated epidemiologically, there is growing evidence that others,
such as dust, are important (40). There is a serious problem with
excess load in children; it is v.ell documented. It can lead to load
S>oisor.ing. Lead poisoning docs cause dcatli and morbidity in
children. A survey of 21 screening programs (64) testing 344,657
children between 1969 and 1971 found 26. l?«or over 80,000 childi en
with blood leads of over 40 ug/l (which is considered evidence of
excess-ivo exposure.) Several recent studios suggest that the
frequency of intellectual and psychological impairment i:. increased
among children overexposed to lead who were not thought to have-
had overt clinical lead poisoning (14,15,16,17). With the wide-
spread prevalence of undue exposure to lc..d in children, its
serious potential sequelae, and studies suggesting increased lead
absorption in children (chronic brain or kidney damage, as well
100<
-------
as acute brain damage); it would seem wise at tins time to continue
to limit the lead in water to as low a level as practicable. Data
from the Community Water Supply Study and oilier sources indicate
thai 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 arc due to stability (corrosion)
problems not due to naturally occurring lead content in the raw
wat'.-rs.
10 ;<
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HKFKRENCKS
1. Kchoe. R.A.. The Ilarhc'i) Lectures 1900. The.1 Metabolism of
Lead in Man in Health and Disease. Lecture 1. Tlie Normal
Metabolism of Load. Lecture 2. The Metabolism of Lead Under
Abnormal Conditions. Lecture 3: Present Hygiemc Problems
Relating to The Absorption of Load. J. Roy. List. Pub. Health
24j 81 (I960).
2. Goodman, L.S. and Oilman. A. The Pharmacological Basi1-:
of Therapeutics. The MacMilhan Co., London and Toronto,
pp. 977-982 (1970).
3. Hardy. II.L.. Lead. Symposium on Environmental Lead
Contamination. PUS /.-R40",~bccember 13-15, (1965).
4. Jain, S., O'Brien, 13.. Fothcringill, R.. Morgan, H.V. and
Gedcles, A.M.. Lead Poisoning Presenting as Infectious
Disease. The Praclioner, 205: 784 (1970).
5. Hernberg, S.. Nikkanen. J.. Moiling, G. and Lilius, H.
A -aminolevulmic Acid Dehydrasc as a Measure of Lead
K.xposurc. Arch. Environ. Health 21^: 140(1970).
G. dc I3rum. A. and Hoolboom, H., I-Jarh Signs of Li?ad-c.\])osure.
A Comp.iraiivr- Study of Laboratory Tests. Brit. J. Industr.
Med. 22, 203 (19C7).
7. Wcsterm.in. M.P.. Pfit/cr. E.. Ellis, L.D., and Jensen, W.N.
Concentrations of Lead in Bone in Plumbism. New Eng. J. Mcd.
273. I24G (19G5).
8. Chisolm. .!..].. Jr. Disturbances in The Biosynthesis of Heine
in Lead Intoxication. J. Pediat. Gj_, 174 (19G4").
9. Cramer. K. and Selandcr, D., Studies in Lead Poisoning,
Comparison of Different Laboratory Tests. Brit. .1.
Indu: lr. Mcd. 22, 311 U9G5).
10. Sel.indcr, .-.., Cramer. L. and Hallberg, L. Studies in Lead
Poisoning: Or'il Thcrajiy with Pemcillamme. Relationship
Between Lead n. Blood and Other Laboratory Tests. Brit.
J. Industr. Med. 23: 282 (19GG).
to;;--
-------
11. Airborne Lead in Perspective. The Committee on Biological
Effects of Atmospheric Pollutants. National Rese.irch 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.B., and .Jenkins, C.C. Epideimological and
Psychological Study ol Lead Poisoning in Children.
J. Am. Mod. Assn. 158: 15 (1355).
14. Moncrirff, A.A., Koumidcs, O.P. and Clayton, B.E.
Lead Poisoning in Children. Arch. Dis. Child. 39: 1-13 (19G4).
15. David, O., Clark, .[.. and Vocller, K., Lead and Hvper-
activity. Lancet 2: 900 (1972).
1C.* dc la Burde. B., and Choalc, M.S., Jr., Does Asymptomatic
Lead E.xposure in Cliildrcn Have Latent Sequelae? J. Pcchal.,
81_. 1088 (1972).
17. Pueschel, S.M.. Kopito, L., and Schwachman, I!. Children
with An Increased Lead Burden- A Screening and Follow-up
Study. J. Am. Med. Assn. 222: 4C2 (1972).
18. Millar, .J.A., Baflistini, V., Gumming, R.L.C., Carswcll, F.,
and Goldberg, A. Lead and -aminolacvulnuc Acid Dehydrase
Levels in Mentally Retarded Cliildrcn air.! in Lead-poisoned
Suckling Rats. Lancet, 2: G95 (1970).
19. Hei.derson, D.A. Follow-up of Cases of Plumbism in
Children. Aust. Ann. Med. 3, 219 (1954).
20. Belts. P.R., Asllry, R., Raine, D.N. Load Intoxication in
Children in BirniiiiL-liam, British Med. J. 1_: 402 (1973).
21. Solve. 11., Tuchwever. B.. and Berlok, L. Effect of Liaci
Acetate un the Susceptibility of Rats to Bacterial Encloioxins.
J. Baclcriol. 9J_: 884 (196GJ.
22. Hcmplull. F.E., Kacberle, M.A., and Buck, W.B. Lead
Suppression of Mouse Resistance to Salmonella Typlumurium .
Science 127- 1031 (1971).
-------
23. Gaiiu;r. J.II. Effects of Metals on Viral Infections in Mice.
Env. Health Pcrsp. _ : 98-999 (June 1973).
24. Holper. K., Trcjo. R.A., Bretlschneider, L., DiLuzio, N.R.
Eiiluwceiuent of Encioloxin Shock in The Lead-sensitized Subhumuj)
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. Liduslr. Hyg.
Toxicol. 22: 381 (1940).
26. Schroeder, H.A. and Dalas.^a, J..I. Abnormal Trace Elements
in Man: Lead. .1. Cliron. Diseases U; 408 (19G1).
27. Kclioe, R.A. Under Whal Circumstances is Ingcslion of Lead
Dangerous. Symposium on Environmental Lend Contamination.
(1>HS »1440), (December 13-15, 1965).
28. Hardy, H.L.. Chamberlain. R.I., Maloof. C.C., Boylen, G.W.,
and Howell, M.C.. Lead as An Environmental Poison, Clin.
Pharmocol. 1_2: 982 (1971).
29. Schroeder, M.A. and Tipton. .I.M.. The Human Body Burden
of Lead. Arch. Envoiron. Health V7: 9U5 (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. HSMHA Health
Repls. 86: MO (197J).
32. Coyer. R.A.. Moore, J. F. and Krc£m:in, M.R. Lead Dosage
and the Role of the Intranuclear Inclusion Body. Arch.
Environ Health 2J): 703 (1970).
33. Blokker. P.C. A Literature Survey of Some Health Aspects
of Load Emissions from Gasoline Engines. Atmospheric
Environ. 6: 1 (1972).
34. Hofrciitcr, I).II., ctal. The Public Health Significance of
Atmospheric Lead. Arch. Environ. Health 3: 82 (1961)
35. Anonymous. Lead in the Environment and Its Eflccl 0:1 Humans,
State of California Public Health Department. (1967).
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3G. Thomas, II. V.. Milmore, 13. K.. Heidbredcr, G.A.and
Kui;;ui, 1J.A. Ulood Lead of Pei ^-ons Living Ni'ur Freeways
Ari-h. Environ. Health 1J3: 695 (1967).
37. Hammond. P.B. Lead Poisoning: An Old Problem with a
New Dimension Essays in Toxicol. !_: 115 (19G9).
38. Anonymous. Survey of Lead in The Atmosphere of Three Urban
Communities, U.S. Public Health Service Publication 999-AP-12,
(19C5).
39. Tola. S., et al. Occupational Lead Exposure in Finland.
II. Service Stations and Garages. Work Environ. Health
9: 102 (1»G5).
40. Fiarcv. F.S. and Gray, J.W. Soil Lead and Pediatric Lead
Poisoning in Charleston, S.C., .J. Soutli Carolina Ivied. Assn.
GO: 79 (1970).
41. Evaluation of Certain Food Additives and Of ihc Contaminants
Mercury. Lead :•:»etruva, A.. Dalakmanski. Y.. and Dakalov. I). Study of
Contamination uf ihc Atmosphere in Injurious Hoad Transjxjrt
.mcl Industrial Products. J. Hytf. Edpidemio. Microbiol.
Immunol. (Pr.iha) K): 383 (19GG).
45. n.ixell. K..J. Luadpoisomn^' Combaluif- the Threat From
The Air. Science 174: 574 (1971).
4G. Alexander. F.W.. Delves, H.T., and Clayton. 13. E. The Uptake
and Excretion bv Children of Lead and Oilier Contaminants.
Proceedings of the International Symposium of Environmental
Health Aspects of Lead. Luxembourg Commission of the European
Communities, Amsterdam, October 2-6, 1973 pp. 319-331
(1973).
K;.rS--
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47. Lead: 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 Febitferer, Philadelphia (I(j70).
49. Lin-Fu, J.S. Undue Absorption of Load Amoni; Children -
A Now Look at an Old Problem. New Engl. J. Mod. 2H6
702 (1972).
50. Scanlon, .1. Human Fetal Hazards froin Envinuinicntal
Pollution with Certain Non-essential Trace Elements. Clin.
Pediatr. l\_: 135 (1972).
51. Chatterjce, P. and Gcltmnn, J.H., Lead Poisoning;: Subculture
as a Facilitating A^enl? Am. J. Clin. Nutr. _2§: -*24 (1972).
52. Annie, C.R. and Mclnlirc, M.S. Lead Poifoniim During Preg-
nancy, Am. J. Dis. Child 103: 436 (1904).
53. McC.'ibc, L.J., Symons, J.M., Lee, R.D., and Robcc.k, G. G. ,
Survey of Community Water Supply Systems. 62: 670 (1970).
54. Crawford, M. D. rind Morris, J.N. Lead in Drinking \Valer.
Lancet _: 1087 (18, 1967).
55. Hem, J.D. and Durum, V/.1I. Solubility and Occurrence of Lead
in Surface Water, 65, 562 (1973).
56. Kinu, D. 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
Tu.\icily. New, Fn». J. Mccl. 289: 1229 (1973).
58. Barltrop, D. , Sources and Significance of Environment:1! Lead
for Children. Proceeding; of Hie International Symjxjsium on
Environmental Health Aspects of Lead. Amsterdam, October 2-6,
1972. Luxembourg Commission of the Europcar. Communilics,
pp. 675-681 (May 1973).
59. Murlhy, G.R. and Rhca, U.S. Cadmium, Copper, Iron, Lend,
Manganese* and Zinc in Evajxjraled Milk Infant Products, and
Human Milk J. of Dairy Sci. 54: 1001 (1971).
IC.K'-
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GO. Berman, E.. and McKiol, K. Is That Toothpaste Safe? Arch.
Environ. Health 25: G4 (1972).
Gl. Shapiro, I.M., Cohen, G.H., and NcccUcniun, H.L. Th?
Presence of Lead in Toothpaste. J. Am. Dent. Assn. 86:
394 (1973).
G2. Jose low, M.N., Lead Content ol Printed Media. Am. J.
Pub. Health (in press).
G3 Louric. R.S., Pica and Poisoning. Am. J. Ortliopsychialry
41.: G97 (1971).
G4. Gilsmin, J.. Estimates of the Nature and Extent of Lead
Paint Poisoning in The United States (NDS TN-746)
Dcpt. of Commerce, National Bureau of Standards,
Washington, D.C. (1972).
107<
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MERCURY
Environmental exposure of the population to mcicury and its
compounds puses 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 shmicides primarily in the paper-pulp industry
and mercurial seed treatment.
Mercury is used in the metallic form, as inorganic mercurous
(monovalcnt) 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, Slock (5,6)
found mercury in lap water, springs, ram water, and beer. In all
water, the concentration of mercury was consistently I'.'ss than
one jjg/1; however, beer occasionally contained up to 15 jig/1. A
recent survey (7) demonslraled that most U.S. streams and rivers
contain 0.1 ^ig of dissolved mercury or less per liter.
-------
PresL'iUly the concentration of mi'rcury in :iir is ill-defined for
hick of analytical data. In one study (8) (lie coin duration of mercury
contained in particulalcs in the atmosphere of 2 U.S. cities was
measured and ranged from 0.03 to 0.21 jig/mj. One review (9)
cited values up to 41 jug/m1 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 Us tri-cily study and reported levels
between 10 and 70 jjg of mercury per kg of meats, fruits, and
vegetables. In 1970, it was discovered that several types of fresh
ami sail water fish contained mercury (mostly in the alkyl form)
in excess of the FDA guideline of 0.5 ppm (500pg/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 mgestion of mercury-treated seeds or of smaller animals that
had ingested such seeds. The Food and Drug Adnumsi/alion lias
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 bo acute or chronic. Generally mercurous
sails are less soluble than mercuric salts and are consequently less
toxic acutely. Acute inloxicatvm is usually the result of suicidal or
accidental exposure. For man the fatal oral dose of mercuric suits
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-hcmorrhagic
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 bronchopneumomji. Inhalation
of mercury in concentrations of 1,200 to 8,500jjg/mJ results in acute
intoxication (10). In severe cases, signs of delajcd ncurotoxic effects,
such as muscular tiomors and psychic disturbances, are observed.
The Threshold Limit Value for all forms of mercury except alkyl
is 0.05 mn'mj in the U.S. (11).
Chronic mercury poisoning results from exposure to small
amounts of mercury over extended periods ol time. Chronic
poisonmg from inorg.inic mercurials has been most often
associated with industrial exposure, vlr.-rcas that from the organic
derivative's has been the result of accidents or environmental
contamination.
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Workers continually exposed to inorganic mercury are particularly
susceptible to chronic mcrcurialism. Usually the absorption of a
single large dose by such individuals is sufficient to precipitate the
chronic disease thai is characterized mainly by ci.-ntral nervous
system toxicily (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.
IM 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 (eretlusmus mercurialis)
appears and is characterized by psychic and emotional distress and
in some cases hysteria. Although the kidney is less frequently
affected in this t>pe of poisoning, chronic neplirosis is occasionally
observed.
Several of the compounds used in agriculture and industry (such
as alkoxyalkyls and aryls) can be grouped, on the basis of then-
effects on man, with inorganic mercury to which the former com-
pounds are usually metabolized.
-------
Alkyl compounds arc the derivative^ of mercuiy most toxic to man,
producing illness from the ii.gestion of only a few milligrams (21, 24).
Chronic alkyl mercury poisoning, also known as Minamala Disease,
is an insidious form of mcrcurialism whose onset may appear alter
only a fow weeks of exposure or may not appear until after a few
years of exposure. Poisoning by those agents is characterized
mainly bv major neurological symptoms and leads to permanent
damage or death. The clinical features in children and adults
include numbness and tingling of the extremities, incoordnulion,
loss of vision and hearing, and intellectual deterioration. Autopsy
of the 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 18G5, 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 Mmamata Day, Japan, from 1953 through
I960. At lei-sl 121 children and adults were affected (of uhom
40 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 winch was referred to as
Congenital (or Fe'.al) Minamala Disease. Similarly, in 19C4
-------
and IflGS, the'diseaso was rej)orted among 47 persons, G of whom died,
in Niigata, Japan. Hunter e_t al (1C) icported 4 cases of industrial
intoxication from handling of these agents. In Guatemala, Iraq,
Pakistan, and the United States, the human consumption of grain
treated with alkyl mercurials for seed purposes has led to '.!ic
poisoning of more than 450 persons, some of whom died (17-20).
The congenital (fetal) disease observed in Mmamata 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 behoved to be the etiologic basis for
tins disease, thus indicating the greater susceptibility of infants
to alk> 1 mercury.
Absorption is a (actor important in determining the toxicitj
of alk\l mercurials. Berglund and Berlin (21) estimated that methyl
mercury is absorbed at more than a 90'o rate via gastro-inteslmal
tract as compared with 2'c, mercuric ion (22). In audition, methyl
mercury crosses the placenta into the fetus and achieves a ZQ'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 ol melhjl mercury
is::--
-------
into (he fetal i;'-;iin is as yet unknown. AJkyl mercury can cross
the bluo(l-br:nn barrier more easily than other mercurials, so that
brain levels of mercury arc much higher alter a dose of alkyl
mercury than after a corresponding dose of any other mercurial.
Excretion is of ccjual importance in determining the health
ha/ard. Unlike inorganic mercury, alkyl mercury is excreted
mainly in the fecus. 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 in^t-sled mercury can be estimated from data
presented in "Methyl Mrrcury in Ki»h" (24). From cpidemiological
evicler.ee1, the lowest whole-blood concentration of methyl mercury
associated with toxic symptoms is 0.2jj|jj/g. This blood concentration
can be compared to 00 u<; Hg/t; hair. These values, in turn, corres-
pond lu prolonged, continuous exposure at approximately 0.3 mtc Hg/70
kg/day. By usinn M safety factor of 10. the maximum dietary intake
should be 0.03 mg H^/person/day (30 Aig/70 ku/day). Although the
safety factor is computed for adults, limiting ingcstiun by children
to 30 ufj Un/day is believed to afford some, albeit smaller, dcyrcc of
safety. If exposure l
-------
containing 0.5 mg Hg/kg. In a given situation, if the total daily
intake from all sources, air, water, and food, is approaching 30
UK/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 \vatcrbornc 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 safely gained from the restricted intake of mercury in drinking
ualer can be applied to the total intake with minimal economic
impact.
I", .'i
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KE/EKKNCES
1. Proust. J.L. On the Existc ice of Mercury in The Waters
of Tlio Ocean. J. Phys. 49, 153, 1799.
2. Garri[;ou, F. Sur la Presence du Morcure clans du Rocher.
Compt. Rend. 04_, 963-965, 1877.
3. Willm. E. Sur la Presence du Mercure clans les Eaux de Sainl-
Nectairc. Compt. Rend. 88, 1032, 1879.
4. Barclct, J. Etude Spectroi',raphicc|uc des Kau\ Mmerales Fran-
caiscs. Compl. Rend. 157, 224-226, 1913.
5. Stock, A. and Cucucl, F. Die Vcrbreitunu dcs Quecksilbers.
Naturwisbcnschaften "J2/24, 390-393, 1934.
6. Stock, A. Die Mikro: nalytische Hestimmunn des Quecksilbers
and ilirc Anueiulunp; auf Hyi;ienische and Madi/.inischc Fra^ea.
Svcnsk Kern Tici^kr :j), 242-250, 1938.
7. U.S. Geological Suivey. Water Resources Review. July 70. p.7.
8. Choluk, J. The Nature of Atmospheric Pollution in a Number
of Industrial Communities. Proc. N'atl. Air Pollution Symp.,
2nd. Pasadena, California 19~5~2~
9. Nalion.il Air Pollution Control Administration, D.H.E.W.
Preliminary Air Pollution Survey of Mercury and Its Com-
pounds, A Literature Review. NAPCA Publication No. APTD
G9-40, Raleigh, No. Carolina, p. 40.
10. S'.okmner, U.K. "Mercury, Iltf " in Industrial Hv^irnc
and ToM<-olot;v. Vol. 2. 2ndcd., F.A. P.ifty, Ed. (New York:
Duel-science, p. 1090. 1963).
11. Threshold Limit Values ul Airborne Contaminants for 1970,
Adopted by The American Conference of Government;1.!
Industrial II
12. Bidslrup, L.P. 'I'o.\icitv of Mercury and Its Compounds,
(New York: AmcTIcan Lls"evjcr PublibTiTiiiTTTo., 1TJG4).
13. Wliitfjhcad, K.P. Chronic Mercury Poisoning - Organic
Mercury Compounds. Ann. Occup. Hyu. 8, 85-89, 1965.
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14. Greco, A.11. Elective Effects f»f Some Mercurial Compounds
on Nervous System Estimation of Mercury in Blood and Spinal
Fluid of Animals Treated with Diothyl Mercury .uid With
Common Mercurial Compounds. Riv. Neurol. 3, 51b-539, 1930.
IS. Study Group of Minamata Disease. Minamata Disease.
Kumamoto University, Japan, 19G8.
16. Hunter, D., Domford, R.R., and Russell, D.S. Poisoning
by Methyl Mercury Compounds. Quart. .J. Mod. 9,
193-213, 1940. ' ~ ~
17. Ordonez, J.V., Carrillo, J.A., Miranda, C.M., ct al. Esiudio
Epidemiologico de Una Enfcrmedad Considcrada Comb Enccfahlis
en la Region dc Altos do Guatemala. Dull. Pan Amor. Sanit.
Bur. 60, 510-517, I960.
18. Jalili. M.A._, and Abbasi, A.H. Poisoning by E'liyl Mercury
Toluene Sulphonanilide. Brit. J. Lid. Mcd. HJ, 303-308, 19G1.
19. Haw. I.U. Agrosan Poisoning in Man. Brit. Mcd. J.
1579-1582, 19G3.
20. Likosky, W.H.. Pierce, P.E., Hmmaii. A.H., cjlal. Organic
Mercury Poisoning, New Mexico. Presented at the Meeting of
the American Academy of Neurology, Dal Harbour, Fla.,
April 27-30, 1970.
21. Berglund, F.. and Berlin, M. Risk of Mcthylmercury Cummululion
in Men and Mammals and the Relation Between Body Burden of
Methyl-mercury and TO.VIC Effects. In "Chemical Fallout"
(M.W. Miller and G.C. Berg, etc.) (Springfield, 111.: Thomas
Publishing Co., 1969), pp. 258-273.
22. Clark.-ion, T.W. Epidcnnological 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. Tcjnmg, S. The Mcrcurv Contents of Blood Corpuscles and in
Blood Plasma in Mothers and Their New-born Children. Report
70-05-20 from Dcpt. Occupational Mc-u., Univ. Hosp., S-221 85
Lund, Sweden, 1970.
24. Methyl Mercury nn Fish, A Toxicologic-Epidemiologic Evaluation
of Risks. Report from An Expert Group. Noi d. Hvg. Tidskr.
Suppl. 4, 1971.
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NIT11ATE
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 ing/1 as nitrogen. This is about
45 ing/1 of Hie nitrate ion.
Nitrate in drinking water was first associated in 1945 with a
temporary blood disorder in infants called mclhenioglobiuemia (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 4G7 and 249 cases
tend to confirm these findings. Frequently, however, writer was
sampled and analy/.ed retrospectively and therefore the concentration
of nitrate which caused illness was nol 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 Stales
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 melhem'jglobiiieniia, 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-
moglobm. Because the altered pigment can no longer transport oxygen,
the physiologic effect of methcmoglobincmia is thai of oxygen deprivation,
or suffocation.
The ingcslion of nitrite directly would have a more immediate and
direct effect on the infant bc-cause the bacterial conversion step in the
stomach would 'KI eliminated. Fortunately, nitrite rarely occurs in
water in sigmfi-ant amounts, but waters with nitrite nitrogen concen-
trations over 1 mg/1 should not be used for infant feeding. Waters \vilh
a significant nitrite concentration would usually be heavily polluted and
would be unsatisfactory on a bacteriological basis as well.
There arc several physiological and biochemical features of early
infancy that rxplain the susceptibility of the infant less then thrve
months of age to this disorder. First, the infant's total lluid intake
per body weight is approximately three times thai of an adult (G).
In addition, the infant's incompletely developed capability to secrclo
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
1-* O*-
-'_.J ~
-------
tract. In ihis location, the- bacteria arc ablo to reduce the nitrate 'icforc
it is absorbed into tlie circuhition (7). To further predispose the infant,
the predominant form of hemoglobin at birth, hemoglobin F (fetal hemo-
globir.), is mere suscc])tible to mclliemn^lobin 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 (NADU-dependent nieUiemoi;lobin rcduclasc; (9).
Wiiiton reports on a study (10) where melhemoglobm levels in blood
were measured on infants to determine subclimcal 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 met hemoglobin
concentration is slightly elevated ovei normal. The melhcmoylobm
levels returned to normal when the b.ibics were changed to bottled 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 o! 2.2 my NO j-N/kilogram can be reached if the water contains
10 r.ig/1 nitrate nitrogen. To determine1 if a slight elevation of an infant's
melhemoglobm concentration has an adverse health effect will i squire a
large and elabo-'ilc study.
In some circumstances, winch arc not understood, the standard does
not have a safety factor. Cases of illness might occur, but for the usual
situation the limit of 10 my/1 NO-j-N will protect the majority of infants.
mo---
-------
Older children and adults do not snem to be affected, but the Russian
literature reports (11) 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 NO 3-N concentration below Ihe limit, diligent elforls
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'flay may result in the occurrence of melhemoglobincmia.
-------
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 Mcthcmo-
globinemia Due to Nitrate Contaminated Water." Am. J. Pub.
Health, 41: 98G-996.
3. S'Utelr-iachor, P.G., "Mcthemoglobinemia from Nitrates in
Drinking Water." Schriftcnrcichc dcs Vcrcins fur Wasscr Doden
und Lufthygiene. No. 21, 1962.
4. Simon, C., Ma/.ko, M., Kay, II. and Mrowitz, G., "Uber Vorkommen,
Pathogcnes and Moglichkeilen zur Propnylaxe dor durch Nitrit
Verusachtcn Melhamoglobinamia." A. Kindcrhcilk. 91^: 124 (19G4).
5. Vigil, Joseph, ct al. "Nitrates in Municipal Water Supply Cau&e
Melhemoglobinemia in Infant, " Public Hca.th Reports, 80
(12) 1119-1121 (1965).
6. Hanson, H.E. and Dennett. M.J. in Textbook of Pediatrics.
Nelson, W.E., W.B. Saunders Company, l9G4~7 p. 109.
7. Cornblalh, M. and Harlmann, A.F., '•Mclhemuglobincmia in
Young Infants," J. Pediat., 33_: 421-425 (1948).
8. Bclkc, K., Klcihaucr, E.andLipps, M., "Vergleichendc Unler-
suchugen ubcr die Spontano.xydation von Nabclsclmur und
Erwachsenenliamoglobin." Ztschr. Kmdcrh., 77:549 (1956).
9. Ross, J.D. and DCS Forges, J.F. "Reduction of Metlicmoglobin
by Erythrocyles Irom Cord Blood. Further Evidence of Deficient
Enzyme Activity in Newborn Period." Pediatrics, £3:218 (1959).
10. Winlon, E.F.. Tardiff, R.G., and McCabc, L.J. Nitrate in
Drinking Water. J_. Am. Water Works Assn. 03:95-98 (1971)
11. Diskalcnko, A. P. "Mclhcmoplobincmia of Water-Nitrate Origin
in Muldavian SSR", Hygiene and Sanitation 33:32-38 (1968).
-------
ORGAN 1CS-CARBON ADSORBABLE
The possibility ol the presence of taste and odor producing substances
and toxic organic chemicals in drinking water arc- of concern to all
connected with the provision of safe, esthetic-ally pleasing water to the
American consumer. If the quality of drinking water is to be protected,
monitoring of organics 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, .ier 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 (CAK)(1) concentrations. These extracts have an opera-
tional definition and arc a mixture of organic compounds that can be
absorbed into activated carbon under prescribed conditions and then
dcsorbcd 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-r.nr of 0.25 gallons
(945 ml) per minute, called the high-flow CAM .- ..nplcr (Note,
because the recovery of organics from water is influenced by the
i:.3<
-------
collection and extraction method, lower-case letters are used to distin-
guish the analytical procedures. Caibon-Chlorolonn Extracts collected
with the high-flow CAM sampler are hereafter called CCE-lif).
Middlcton and Rosen (3) detected substituted benzene compounds,
kerosene, polycyclic hydrocarbons, phenylether, acrylonitrilc and
insecticides in various CCE-hf's. Tins list has been expanded by many
investigators in the subsequent years, for example, by Klcopfcr and
Fairless (4). In 1903, Heupcr and Payne (5) rcix>rtcd the carcinogenic
properties of finished water CCE-hf's.
In 1905, Booth, English and McDermoll (G) developed a CAM sampler
similar to the High-Flow CAM Sampler, but witli 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 tins procedure are called
CCE-lf and CAE-lf. No drinking water standard was promulgated for
these parameters. Rosen, Mashni, and Safferman (7) isolated odorous
orgamcs 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 mure reliable, less
expensive, smaller, and more convenient, has been developed (8).
In addition, the Mini-sampler uses a type of coal-based granular
activated carbon that enhances organic collection, thereby increasing
-------
the yield of the method. The extraction apparatus has also been mina-
turi/.ed to bo mure convenient and less expensive and the procedure has
been modified to be more vigorous, thereby increasing desorplion and
further increasing organic recovery (10). The extract from this
procedure is called CCE-m.
Tardiff and Dciiizer (9) tested the- loxiciiy of a CCE-m collected
from the finished water of a river supply. The resulting LD50 of
32 mg'kg would classify this extract as extremely toxic on a typical
toxic-ological scale.
Symons, Love, Buelow and Robeck (10) reported the identification
of £-Caprolactam and 2-Uydroxyadiponilrile by gas chromatography
and mass spectrometry in a CCE-m collected Irom a fijnslied water
from a dilferenl river supply. Tins indicates the presence of .synthetic:
organics in this extract.
Extraction with the less polar solvent chloroform docs not dcsorb ail
of the organics adsorbed onto the activated carbon. Extraction with other
solvents has been proposed as a method of monitoring these materials.
The use of the polar solvent 05Vo ethyl alcohol does extract different
organics, but it also recovers inorganic salts lint were adsorbed on
the activated carbon. At this time no reliable technique has been
developed lor measuring these other organic:.,.
:><
-------
in an effort j0 determine the range of CCE-m concentrations in
finished water, as vas done by Ettinger (11), for raw water and Taylor
(12), the Interstate Carrier Surveillance Program (121 and the 19G'J
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 :ind
from 2 to 34 Camples at tho 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 arc 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 arc 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 licalth-
bascd 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
O.G
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.G
4.0
3.2
2.4
1.6
0.8
0.0
*I3asccl 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.f the volume of water sampled,
and it does not measure organic compounds of greatest concern, such
as the volatile halomelhancs. 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 witli 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 ami a false sense of alarm to persons
served by systems which exceed the level. It also would divert
resources and attention from elforls to fuid morn effective ways
of dealing with the organic chemical problem.
Total organic carbon (TOO and chemical oxygen demand (COD)
are surrogates that have been considered, but they ha\e limitations
also. TOC lias the advantage of being quicker and cheaper (on a per
sample basis) than CCE, bul the avaliability of sensitive instruments
for this measurement is questionable. More investigation oi the
-------
significance of any TOC number as a la-alth effects limit is al.su
needed. COD is easily determined with readily available laboratory
equipment, but COO is not limited to organic commands, 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 the 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 une or more surrogate te.sls for organic
chemicals or opuauic chemical groups, and will also study in dcptli
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 lor 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. Middk'ton. F.M.. "Nomenclature for Referring to Organic
Extracts Obtained from Carbon with Chloroform or Other
Solvents," JAWWA. 53, 749 (June 1961).
2. Anon., "Tentative Mot hod for Carbon Chloroform Extract
(CCE) in Water." .JAWWA, 54, 2, 223-227 (Feb. 19G2).
3. MiddlPton, F.M. and Rosen, A.A., "Organic Contaminants
Affecting, the Quality of Water," Public Health Reports, 71,
1125-1133 (November 195C).
4. Kleopfer. R.D. and Fairless, 3.J., "Characterization of
Organic Components in A Municipal Water Supply,"
Environmental Science and Technology, G, 1036-37 (November 1972)
5. Heupcr, W.C. and 1'ayne, W.'V., "Carcinogenic Effects os
Adsorbatos of Raw .ind Fuushcd Water Supplies," The Am.
Jour, of Clinical Pathology. 39, 5, 475-481 (May 19631.
6. Booth. R.L.. English, J.N.. and MrDcrmott, G.N. "Evaluation
of Sampling Conditions in the Carbon Adsorption Method,"
.JAWWA, 57, 215-220 (Feb. 19G5).
7. Rosen, A.A., Machni. C.I. and Saffcrman, R.S., "Recent
Dexelupmcnts in The Chemistry of Odor in Water: The Cause
of Earthv/Musty Odor, " Water Treatment and Examination, 19,
1, 106-119(1970). ~~
8. Buelow, R.W., Carswcll, .J.K. and Symons, J.M.. "An Improved
Method for Determining Orgamcs in Water by Activated Caruon
Adsorption and Solvent Extraction," .JAWWA GJJ, 57-72,
195-190 (January and February 1973).
G. Tardiff. R.G. and Deinzcr. M., "Toxicity of Organic Compounds
in Drinking Water," In Proceedings: Fifteenth Water Quality
Conference. Feb. 7-8, 1973. University ol 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 witli 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).
-------
11. Eltinj'.er. M.H.. "Proposed Tnxicity Screening Procedure for
Use in Protecting Drinking Water Quality." .JAWWA, 52,
689-694 (June I960).
12. Taylor, F.D., "Effectiveness of Water Utility Quality Control
Practices," JAWWA, 54_, 1257-12G4 (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 Agency,
1971, Washington. D.C.
14. McCabe, L.J., gym-ins, J.M., Lee, R.'). and Robcck G.G.,
"Survey of Commun.ty Water Supply Systems," JAWWA, 62,
670-GM7 (Nov. 1970).
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PESTIC1M.S
A . ChloriiKited Hydrocarbon Insecticides
The chlorinated hydrocarbons arc one of the most important groups
of synthetic organic insecticides because of their wide use, great
stability in I lie environment, and toxicily to mammals and insects.
When absorbed into the body, some of the chlorinated hydrocarbons arc
not metabolized rapidly but are stored in the fat.
As a general group of insecticides, the chlorinated hydrocarbons
can be absorbed into (lie body through the lungs, the Castro-intestinal
tract, or the skin. The symptoms of poisoning, regardless of the
compound involved or the route of entry, arc similar but may vary
in severity. Mild cases of poisoning are characterized by headache,
dizziness, Castro-intestinal disturbances, numbness and weakness of
the extremities, apprehension, and hypcrirritabilily. In severe cases,
tiicrc 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, prima-ily the brain (1).
Criteria Dased on Chronic Toxicity
Except as noted below, the approval limits (AL's) for chlorinated
hydrocarbons in drinking water have been calculated primarily on the
basis of the extrapolated human intake that would be equivalent to trial
-------
causing minimal toxic effects in mammals (rats and dogs). Tablj I
lists the levels of several chlorinated hydrocarbons fed chronically
to cloj;s and rats (2. 3,4) that produced minimal toxicity or no effects.
For comparison, the dietary levels are converted to mgAg body
weight/day. Endrin ami lindano had lower minimal cffect/no-effect
levels in dogs than in rats; whereas, for toxpphcnc 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 watei, by adjusting for factors thai
influence toxicity such as inter- and intra- species variability, length
of exposure, and exlcnsivencss of the studies. To determine a "safe"
exposure level for man, conventionally a factor ol 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 loss as is the case for the human melhoxychlor data cileH. 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 data are available. The minimal effect
-------
levels of endrin, lindane, and to.vipJienc are adjusted by 1/500 since
no adequate data are available for comparison. These derived values
are considered tlie maximum saf-1 exixjsure levels from all sources.
Since these values arc expressed as mgAg/day, they are then readjusted
for body weight to deter mine 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 vvith
another. The choice of a level on which to ba:>e an AL for water requires
Hie selection of the lowest value from animal experimentation, provided
that the human data are within the same order of magnitude. T'IUS the
human data should substantiate the fact that man is no more sensitive
to .1 particular agent than is the rat or the dog.
To set a standard for n 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 chcmicils has been determined by the
investigations of the Food and Drug Administration from ''market basket"
samples of food and water. Duggan and Corneliussen (C) report un this
activity from 1964-1970. The average dietary intakes (mg/man/day)
arc listed in Table I. Comparing the intake from the diet \\itli what
arc considered acceptable safe levels of these pesticides, it is
apparent that only traces of melhoxychlor and toxaphene are prof
-------
in the diet. Less than 10'.b of the maximum safe level of endrin or
lindane arc invested 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 toxaphcne was lowered because of
organoleptic effects (7, 8) at concentrations above 0.005 mg/1.
The approval limits for the chlorinated hydrocarbon insecticides
are listed in Table 1. These limits arc meant to serve only in the
event tliat these chemicals are inadvertently present in the water.
Deliberate addition of these compounds is neither implied nor
sanctioned.
-------
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-------
Criteria Based on Potential Carcinc^onicity
To establish AL's for DDT, nldrin, and diehlrin, a different
method for deriving AL's must be used, since there is evidence
that 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 microorpajiisms, and insects, and thus the potential carcin-
ogcnicily 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
uill be derived by estimating the health risk associated with
various concentrations and comparing these concentrations with
ambient levels to assess the attainability of the proposed limits
with presently knoHii means of technology.
-------
Monitoring Ai\\:i available from Uin Community Water Supply
Studies Program (CWSS) carried out during 19G9 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 drirJcing water supplies is a survey by
the Federal Water Pollution Control Administration published
in 1909 as "Pesticides in Surface Waters of the United Slates —
A Five Year Summary (1964-1968)". Obviously one cannot make
the assumption that all of the surface waters analyzed in tins
survey were utilized as drinking water supplies, and no definite
conclusions can be readied on ambient levels in drinking water
based on these data.
Since so little information is available concerning the concen-
trations of aidrin, dieldrm 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 survc\, limits for aldrin, dicldrin
and DDT will be proposed, based upon an :uialysis of the health
risks associated with low levels of intake of these pesticides and
available information concerning attainability. Risk estimates
;:l very low levels of exposure arc subject to great uncertainties,
but the bost available methods for making sucli 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
lar more stringent than those considered in the past should be
promulgated.
Aldrin-Dieldrm
Experiments carried out on mice (strain CF1) fed dicldrin in
their daily diet, at levels varying from 0.1 to 20 ppm during their
normal life span, resulted m significant increases in the 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 dicldrin in drinking water.
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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, Dines ct al (15) produced
significantly increased incidences of tumors will) the administration
of large doses of DDT (40.4 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 geneialions (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 t\\o consecutive
generations. Exposure to all four levels of DD'l resulted in a
significant increase of liver tumors in males, this being most
evident at the lushest level used. In females, the incidence of
h\cr 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 0<
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liver tumors, all occurriiif; in DDT-li rated mice, jyivc niclaslasos.
Histolo}',iiMlly, liver tumors were either well-differentiated nodular
growths, pressing but not in fill ruling the surrounding parenchyma,
or nodular growths in which the architecture of the liver was
obliterated showing {•landular or trabeeular patterns. The results
of this study app'T.r to be, at present, the most appropriate to use
as a basis for extra po La tint; the risk associated with a ran^c of
concentrations of DbT in drinking water.
Chlordane and Hcptaclilor
Because recent evidence also implicates chlordane ;md hcplachlor
as potential carcinogens, csUibhslimcnt of limits lor these pesticides
must be based on considerations similar to those for a Id r in, dicldrin
and DDT.
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REFERENCES
1. Dale, W.E., Gaincs, T. D., Hayes. W. M. , Jr., and Pcarce, G.W.,
Poisoning by DDT: Relationship Between Clinical Si\y\s and Con-
centrations in Rat Brain, Science 142:1474 (19G3).
2. Lehman, A..I., Summaries of Pesticide Toxicity. Association
of Food and Drug Officials of the U. S., Topeka. Kansas, 19C5,
pp. 1-40.
3. Treon, J.F., Cleveland, F. P., and Cappel, J., Toxicily of
Endrin for Laboratory Animals, J. Agr. Food Chcm 3,
842-848, 1955.
4. Unpublished Report of Kcllcring Laboratory, University of Cincinnati,
Cincinnati, Ohio. Ci'ed in ''Critical Review of Literature Pertaining
to the Insecticide Endrin, " a dissertation for the Master's Decree
at the University of Cincinnati by J. Cole, 1966.
5. Stein, A. A., Scrrone, D. M., and Coulston, F., Safev Evaluation
of Molhoxychlor in Human Volunteers. Toxic Appl. Pharmacol. 7:
499, 1965.
G. Du|ij;an, R.E. and Corneliusscn, P. E. Dietary Intake of Pesticide
Chemicals in the United Stales (in), June 1968-April 1970.
Pesticides Monitoring Journal 5 (4): 331-341, 1P72.
7. Cohen, J. M., Rourkc, G. A., and Woodward, R. L. : Effects of
Fish Poisons on Water Supplies. J. Amor. Water Works Assn.
53(1): 49-62, 19G1.
8. Siptorth, E.A., Identification and Removal of Herbicides and
Pesticides. J. Amor. Water Works Assn. J7(8):1016-1022,
19G5.
9. Fit/.hui;li, O. G. , Nelson, A. A., and Quaifc, M. L. Chronic Oral
Toxicity of Aldrin and Dieldrin in Rats and Do^s. Fed. COM-.'..
Toxk'ol. 2:551, 1964.
10. Walker, A.I. T. , Stevcn.son, D.E., Robinson, J., Thorpe, E.,
and Roberts, M. Pharmacodvnamics of Dieldrin OlEOD)-3:
T\^o Year Oral Exposures of Rats and Do§;s. Toxicology and
Applied Pharmacology, 15:345, 1969.
t'c' <
• ¥1^1
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11. Walker, A.I.T., Thorpe, E., and Stevenson, D.E. The Toxicology
of Die Id rin (IIEOD): Long-Term Oral Toxicity Experiments in Mice,
Fd. Cosmct. TOMCO! Vol. 11. pp. 415-432," 1972.
12. Tomalis, L., Turusov, V., Day, N., Charles, R.T.
The Effect of Long-Term Exposure to OUT on CF-1 Mice.
Int. J. Cancer 10, 489-500, 1972.
13. Men/ic, Calvin M. Metabolism of Pesticides Publ. b> Bureau
of Sport Fisheries and Wildlife, SSR-Wildhfe 127, Washington,
D.C.: 24, 1969.
14. Mantel, N., and Bryan, W.R. "Safely" Toslin^ of Carcinogenic
Agents. J. Nat. Cancer lust. 27:455, 19G1.
15. Innes, J.R.M., Ulland, B.M.. Valerio, M.G., Pctrucelli, L.,
Fishbein, L., Har', E.R.. Pallotta, A.J.. Bates. R.R..
Falk, H.L., Carl. .I.J., Klein, M., Mitchell, I., and Peters. J.,
Bioassay of Pesticides and Industrial Chemicals for Tumorigeiu-
city in Mice: A Preliminary Note, J. Nat. Cancer Inst. 42
1101, 1909.
10. Tarjan. R. and Kemeny, T., Multii;cneration Studies on DDT in
Mice. Fd. Cosmet Toxicol. 7:215,1909.
1« r*
•*o<
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13. Chlorophi'iioxy Herbicides
Aquatic weeds have become substantial problems in (he U.S. in
recent years, uiid chemical control of this vegetation has won wide
acceptance. Since waters to which applications of herbicides arc 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-dichlorophenoxyacelic
acid) and 2,4,5-TP (silvex) [2-(2, 4, 5-trichlorophenoxy) propionic acidj.
[A closely related compound, 2,4,5-T (2,4,5-tnchlorophenoxyacetic
acid) had been extensively used at one time, but lias been banned for
major aqua'.ic 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 h>drolyzcd rapidly to the corresponding
acid in the body.
The acute loxicity following oral admmislralion to a number of
experimental animals is moderate. Studies (1-4) of the acute oral
loxicily of the chlorinated phcnoxyaLkyl ..jids indicate that there is
approximately a three-fold variation between the species of animals
studied. It appears that acute oral toxicily 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).
-------
The subaculc oral toxicily of chl'»rophcnoxy herbicides has been in-
vestigated in a number of species of experimental animals (1-C). The
dot; was the most sensitive species sludicd and oiicn displayed mild
injury in response lo doses of 10 mjjAn/day for 90 days, and serious
effects from a dose of 20 mf.;AK/day for 90 days. Lehman (G) reported
that the no-effect level of 2, 4-D is 50* m^Atf/day in the rat, and
8. 0 mg/ky/day in the do};.
Although 2,4, 5-T has been banned for all aquatic uses there is con-
siderable interest as to wl:y this action was taken, so for informational
purposes, a discussion of the toxicity oi this herbicide is included. In
a study of various pesticides and related compounds for lerp.to^enic1
effects, Corlney, et al. (7) noted terata and cmbryotoxicily from
2, 4, 5-T. These effects were evidenced by statistically increased
proportions of litters affected and of abnormal fetuses within the litters
(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 m{;Ag produced no harmful effects in mice,
wliilo a level of 4.6 mgAtf caused minimal, but statistically significant,
effects in the rat. More recent \\ork (8) has indicated that a contaminant
(2, 3, 7, B-tetrachlun-diben/.u-p-dioxin) which \\as present at approximately
30 ppm in the 2,4, 5-T formulation originally tested was highly toxic lo
experimental animals and produced fetal and maternal toxicity al levels
as low as 0.0005 m\r./kg. However, purified 2,4, 5-T has also produced
*In the March 14, 1975, issue of this document, this fij^urc was erroneously
written as 0. 5. . . ,.
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leralogemc effects in both hamsters :md rats at relatively high dosage
rales (9). Current production sani|,:'-s of 2,4,5-T thai contain less tlian
1 ppm of clioxm did not produce embryotoxicity or terala in rats at
levels as high as 24 me/kg/day (10).
The subaculc and rhronic toxicily 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 arc 2 nig/kg/day in rats, and 13 ing/kg/day in dogs. In
2-year feeding studies with these same salts, the no-effect levels were
2.C nig/kg/day in rats and 0.9 nig/kg/day in dogs.
Some data arc available on the toxicily 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 2,4-1) was investigated
as a possible treatment for disseminated coccidioidomycosis, the
patient had nu .side effects from 18 intravenous doses during 33 ti'iys'
each of the l:\sl 12 doses in (lie 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 nig (G7 mg/kg) produced mild symptoms.
The acute oral close of 2,4-D required to produce symptoms in man
is probably 3UOO to 4000 mg (or about 45 to GO mg/kg). A comparison
of other loxiciiy values for 2,4,5-TP indicates that the toxioty of these
two agents is of the same order of magnitude. Thus, in the absence of
any specific loxicologic data for 2,4,5-TP in man, it might be estimated
that the acute oral close 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 inst:mccs of any illness due to ingestions (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
chloropheno.xy 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, 20r/b of the safe
exposure level cvn be reasonably allocated to water without jeopardizing
the health of the consumer.
The approval limits for these herbicides arc meant to serve m I he
event that these chemicals inadvertently occ-ir in the water. Deliberate
addition of these compounds to drinking water sources is neither
implied nor sanctioned.
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TABLE I. DERIVATIOf. OF APPROVAL LIMITS (AL) FOR CHLOROPKEKOXY HERBICIDES
Compound
2,4-3
2,4,5-TP
Lowest Long-Tern
Levels with
Mini.-al or No Effects
Species
Rat
Dog
'Rat
Dog
irgAg/day*
50 (6)
8.0 (6)
2.6 (12)
0.9 (12)
Calculated Maximum Safe Levels
Fron: all Sources of Exposure
Safety
Factor (X)
1/500
1/500
1/500
1/500
-g/kg/day
0.1
0.016
0.005
0.002
ng/nan/day
7.0
1.12d
0.35
0.14d
Water
°< of
Safe Level
20
20
AL
(mg/Dc
0.1
0.01
a ASSU.TB weight of rat = 0.3 kg and of dog = 10 kg; essu~e average daily food consumption
of rat, = O.G5 kg and of dog = 0.2 kg.
b Assure average weight of hunan adult = 70 kg.
c AssuTe average daily intake of water for nan = 2 liters.
d Choser as basis on which to derive AL.
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REFERENCES
1. Hill, E.G. and Carlisle, II. Toxicity of 2,4-Dichlorophenoxy-
acclic Acid for Experimental Animals. J. Industr. Hyg. Voxicol.
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. Dull. 15, 122-133,
1951. ~~
3. Rowc, 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. Amor. J.
Vet. Res. 15. 622-G29, !954.
4. Drill, V.A. and Hiralzka, T. Toxicity of 2,4-Dichloropheno.xya':etic
Acid and 2. 4, 5-Trichlorophenoxyacetic Acid. A Report of Their
Acute and Chronic Toxicily in Dogs. Arch. Industr. Hyg. Occup.
Mcd. 7. G1-G7, 1953.
5. Palmer, J.S. and Raclelcff, R.D. The Toxicologic Effects of Certain
Fungicides and Herbicides on Sheep and Cattle. Ann N.Y. Acad.
Sci. Ill, 729-736, 1964.
G. Lehman, A.J. Summaries of Pesticide Toxicily. Association of
Food and Drug Officials of the U.S., Topeka, Kansas. 19G5, pp 13-14.
7. Courlney, K.D., Gaylor, D.W.. Hogan, M.D., and ralk, H.L.
Teralogenic Evalualion of 2,4,5-T. Science 168, 8G4, 1970.
8. Courtney, K.D., and Moore, J.A. Terratulogy Studies with 2, 4, 5-
Trifhlorophenoxyacelic Acid and 2, 3, 7,8-Tetrachlorodibcn/o-p-dioxin.
Toxicology and Applied Pharmacology 20. 39G, 1971.
9. Collins, T.F.X. and Williams, C.H. Tcratogcmc Studies-with
2,4.5-T and 2,4-D in Hamsters. Dull, of Environmental Con-
tamination and Toxicology 6 (0):559-567, 1971.
10. Lmerson, J.L., Thompson, D.J., Gcibm. C.G., and Robinson, V.D.
Teralogciiic Slucly of 2, 4, 5-Trichloruphcnoxy Acelic Acid in the Rat.
Tox. Appl. Pharmacol. J/7, 311, 1970.
11. Mullison, W.R. Some Toxicological Aspects of Silvex. Paper
Presented at Southern Weed Conference, .Jacksonville, Fla., 1966.
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12. Kraus. as cited by Mitchess, J.W., Hogson, H.E., and
GaeljLMis, C.F. Tolerance of Farm Animas to Teed Containing
2,4-Dichlorophcnoxyacetic Acid. J. Animal. Sci. 5,
226-232, 1946. "
13. Seabury, J.H. To.xicity of 2, 4-Diclilorophcnoxyacctic Acid for
Man and Doy. Arch. Envir. Health 7, 202-209, i9G3.
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. Nic-ison, K.. Kacmpe. D., and Jensen-Holm, J. Fatal Poisoning
in Man by 2, 4-Dichlorophcno.\yacclic Acid (2,4-D): Determination
of the A«;cnt in Forensic Materials. Acta Pliarmacol. Tox. 22.
224-234, 1965.
16. Berwick, P., 2,4-Uichloroplicnoxyacctic Acid Poisoning in Man.
J.A.M.A. 214 (6):114-117, 1970.
150<
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SELENIUM
The 1962 Drinking Water Standai ds Committee lowered the limit for
selenium in drinking water primarily out of concern over the possible
carcinogenic properties of the element. Data supporting the
carcinoi;enicity 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
Follz (2) that the clement vas an integral part of "factor 3," recognized
for some time as essential in animal nutrition. While definite evidence
is still kicking 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 eflicacy 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
1 r-f <
J..J &
-------
of arsenic in selenium to.Mcity (1, 7, ft, 12). He h:is found that arsenic
in drinking water accentuates the tuxli-ity 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" level:;
of selenium in drinking water, consideration must also be given to the
variability in these other factors which are certain to occur in any given
population.
The current limit of 0.01 mg/litcr 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 solenitc or selcnate before it has appreciable solubility in water (13),
one \\ould prcciift that these would be the principal inorganic forms thai
occur in water. Organic forms of selenium occur in relenifcrous soils
;uul 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
yf plant sources of selenium lias revealed that selenium present in
bdcnilcrous grams 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), Hie results do not apply well to
environmental exposures since the only studies that made ;u* 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 f.inuly developed loss of hair, weakened nails,
and hstlcssncss after only 3 months' exposure to well-water containing
9 mg''l. The children in llic family showed increased mental alertness
after use of water from the selonifcrous well was discontinued, as
evidenced by better work in school (22).
Smith and co-workers (23, 24) reported the results of ihcir studies
dealing with human exposure to high environmental selenium concentra-
tions in the 1930's. They reported a high incidence of ga-jivointcslinal
problems, oaii teeth, and an icteriod skin color in sclcmfcrous 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/lilcr that Glover
(19) indicates to be the normal range. The gastrointestinal disturbances
and the icteriod discoloration of the skin apparently have their counter •
15. •<
-------
parts m (lie anorexia (23) and bilirubincmia (7), respectively, in rats
fed selenium. The effect of selenium on teeth has had some marginal
documentation in rats (20); and has been supported by Hadjimarkos (27)
and refuted by Cadell and Cousins (23) in epidomio logic studies.
From urinary concentrations of selenium, Smith and Wcslfall (24)
estimated that the individuals displaying these symptoms were ingesting
0.01 to 0.10 nig An/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/clay. Smith (24, 29) also presented the range of selenium
concentrations found in various food classes in the areas in which »he
field studies had been conducted. With the use of the table provided in
Dietary Levels of Households in (he U.S., Spring 1905 (U.S. D.A. Agri.
Res. Service), calculations Irom 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. Tinslcy et nl. (25) found that an intake of 0.125 mgAg/day
adversely affected early growth m rats. 1.1 mg/kg, administered
twice weekly (ca. 0.3 mgAg/day), has 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 sclcmtc: the ewes sodium sclcnatc. Although these levels
arc slightly higher than those reported for the human exposures, it must
be remembered (!!.-•! the parameters measured would not be acceptable
either in terms .,! severity or incidence in the human population.
-------
Few studies have been performed to specifically examine the loxicity
of .selenium administered in drinking water. PlcUiikova (31) found lhe-
rabbit ti> be very sensitive to selenium as sclcnitc. Ten pg/1 in drinking
water resulted in a 4Qr~o reduction in the elimination of bromosulphalcin
by the liver. Since no apparent consideration was given to the selenium
content of the diet of those 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 Ihe dietary require-
ment for selenium. The duration of the study was 71/2 months. Schrocder
(32) has indicated that intake of selenitc from drinking water is more toxic
than when mixed with food. However, this suggestion was not based on a
direct experimental comparison. Rosenfcld and Death (33) studied the
effects of sodium selcnale in drinking water on reproduction in rats.
Selenium concentrations of 2. 5 mg/1 reduced tiic number of young reared
by the second generation of mothers, and 7. 5 mg/1 prevented reproduction
in females.
Early work (34), using both naturally occurring, and a .selenitic salt,
indicated the formation of adenomas and low-grade non-mclaslasizing 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 .selcnilc
and sclenatc sails, found no evidence of neoplasms tha4 could be attributed
to the addition of these selenium compounds to the diet at 0.5 - 16 ppm.
Volgancv and Tschcnkes (35) negated their earlier results, which had
-------
indicated thai 4.3 ing/1 selenium as solcnitc ii tlic diet gave rise to tumors,
but had not used proper controls. II should be noted dial 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 sclc-nile and sclcnate, 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 selenitc), in reducing papillomas induced by
various.chemicals in mice (3C).
Any consideration of a maximum allowable concentration oi selenium
must include the evidence that the element is an essential dietary requi'-e-
mcnt. 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 Lcvandcr (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 meals. Since no
deficiency diseases of selenium have been reported to daic in the U.S.,
it may be assumed th.il 200 ug/day of selenium is nutritionally adequate.
-------
Si^ns of selenium toxicily havi.1 been scon at an c -timatcd level of
selenium intake of 0. 7-7 nig/clay according 1o the data of Smith et al.
(23, 24). At the present limit on selenium content of drinking water,
water would increase the basal 200 u^/cLiy intake of selenium by only
10':', if otic assumes a 2-litcr inuestion of walcr per day. This results
in a minimum safely factor of 3, considering the lower end of the ranj;e
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 safely brought about by selenium contained
in tlie.dict, selenium concentrations above 0.01 -my;/litcr shall not be
permitted in the drinking water.
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RKFERKNCKS
1. Frost, Douglas V. (19G7) Significance of The-Symposium. In
Symposium: Selenium in Biomedicine, O.1I. Mutli. Ed. AVI
Publishing Co.. Inc., Westport, Conn. p. 7-2G.
2. Si-h war/., K. and Foil/., C.M., Selenium As An Integral Part of
Factor 3 Against Dietary Ncciotic Liver Degeneration. J. Am.
Chcm. Soc. 79:3292.
3. Hopkins, L.L.. Jr.. and Majaj. A.S. (19G7) Selenium in Human
Nutrition in Symixj.sium: Selenium in Biomedicmc. O.H. Mulli, Ed.
AVI Publishing Co., Lie., Wcstport, Conn. p. 203-214.
4. Schwa r/.. K. and Fvedga, A. (1909) Biological Patlerny of Organic
Selenium Compounds. I. Aliphatic Moneseleno .uicl Diseleno Di-
carboxilic Acids. J. Biol. Chcm. 244, 2103-2110.
5. Smith, M.I. (1939) The Influence of Diet on The Chronic To.xicity
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 Homogciiales From Rats Fed
Diets Containing Kit her Casein or Casein Plus Linseed Oil Meal.
To.MCol. and Appl. Pharmacol. 1C, 79-87.
7. Halvcr:>on, A.W., Tsay, Duig-Tsair, Tricbevasscr. K.C. and
\VhileIiead, K.I. (1970) Development of Hcmolytic Anemia in
Rats Fed Selenite. To.xicol. and Appl. Ph.irmacol. 17, 151-159.
8. Lcvandur. O.A. and Bauman, C.A. (19GG) Selen.'um Metabolism VI.
Effect of Arsenic on The Excretion of Selenium in the Bile. Toxicol.
and Appl. Pharmacol. 9, 10G-115.
9. Levander, O.... and Morris, V.C. (1970) Ijiteractions of Mcthionme,
Vitamin JJ, and AnlioMclants in Selenium Toxicity m tlic Rat. J.
Nutrition 100.1111 -1118.
10. Schwa r/, K. (19GO) Factor 3, Selenium, and Vitamin E. Nutrition
Reviews. 18, 193-197.
11 Soiulcc.uard, Ebbo. (19G7) Selenium and Vitamin E. Interrelationslups
In S\ mposium: Selenium in Biomedicmc AVI Publishing Co., Inc.,
Weslport, Conn. O.H. Mucli Ed. pp. 3G5-381.
158-
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12. Moxon. A.L., DuD-jis, K.P. and Potter, R.L. (1941) The
ToMcily of Optically Inactive d, .ind 1-SeKnium Cyslme.
J. Pharm. and Exp. Tlier. 72, 184-195.
13. Liikir., Hub-jrl W. and Davidson, David F. (1907) The Relation
of Tne Geo-Chcmistry of Selenium to Its Occurrence in Soils.
In Symposium: Selenium in Biomedicine p. 27-56.
14. Hamilton, John W. and Bcalh, O.A. (1904) Amount and Chemical
Form of Selenium in Vegetable Plants, Agr. and Food Cliem. 12,
371-374.
15. Olson, O.E. (1907) Soil, Plant, Animal Cycling of Excessive Levels
of Selenium. In Symposium: Selenium m Hiomcdicme (AVI Pub-
lishing Co., Inc., Westport, Conn.)O.II. Mulh, Ed. pp. 297-312.
10. Frankc and Potter (1935) J. Nutr. 10, 213.
17. Cer.vcnka, Edward, A.. Jr.. and Cooper. W. Charles (1961) Toxi-
cology of Selenium on Tellurium and Their Compounds. Arch.
Environ. Illth. 3, 71-82.
18. Cooper. W. Charles (1907) Selenium Toxicity in Man. In Symposium:
Selenium in Biomedicine. (AVI Publishing Co., Inc., Westport,
Conn.) O.II. Much. Ed. pp 185-199.
19. Glover. J.R. (1907) Selenium m Human Urine: A Tentative Maxium
Allowable Concentration for Industrial and Rural Populations.
Ann Occup.Hjg. 10. 3-14.
20. Schwar/.. K. and Foil/.. C.M. M958) Factor 3 Activity of Selenium
Compounds. J. Biol. Chcm. 233, 245.
21. Death, O.A. (1902) Selenium Poisons Indians. Science News
Letter 81. 254.
22. Roscnfeld. I. and Death, O.A. (1904) Selenium. Geobotany, Bio-
chemistry, Toxicicity and Nutrition. Academic Press, N.Y. and
London.
23. Smith, M.I.. Frankc. K.W. and Westfim, 13.B. (193G) The
Selenium Problem in {{elation to Public Health. Public Health
Reports. (U.S.) 51, 1490-1505.
24. Smith, M .1. and Woslfall, D.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., Marr. .I.R., Don*-, J.F., Weswig. P.M. and
Yamamolo, U.S. (1907) Selenium Toxicity in Hals I. Growth and
Logevity. In Symposium: SGlrmum in Diomedicinc (AVI
Publishing Co.. Inc., Woslport, Conn.)O.II. Mulh, Ed. pp. 141-152.
26. Wheatcraft, M.G.. English, J.4. and Schlack, C.A. (1051) Effects
of Selenium on The uicidence of Denial Caries in While Rals. J.
Dental Res. 30, 523-524.
27. Hadjimarkos, D.M. (1965) Effect of Selenium on Denial Caries.
Arch. Environ. Health 10, 893-899.
28. Cadell, P.O. and Cousins, F.D. (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: Sclcmuri in Biomeclicinc (AVI Publishing
Co., Lie., Weslport, Conn.)O.II. Mulh, Ed. pp. 127-140.
31. Pletnikova, I. P. (1970) Biological Effect and Safe Concentration of
Selenium in Drinking Water. Hygiene and Santilation 35, 176-181.
32. Schrocdcr. Henry A. (1967) Effects of Selenale, Selcnitc and Tcll-
urite on TliL> Growth and Early Survival of Mice and Huts. J. Nuiri.
92, 334, 333.
33. Rosenfolcl, I. and Death, O.A. (1954) Effect of Selenium on Repro-
duction in Hals. Proc. Soc. Expl Bio.) and Mod. 87, 295-299.
34. Fil7.hugh, O.G., Nelson. A.A. and Bliss, C.I. (1944) The Chronic
Oral Toxicily of Se'enium. J. Pharmacol. 80. 289-299.
35. Volgancv. M.N. and Tschcnkcs, L.A. (1967) Further Studies in
Tissue Changes Associated With Sodium Selenale. In Symposium:
Selenium in Diomedicinc (AVI Publishing Co., Inc., Wcstporl,
Conn.)O.II. Mulh, Ed. pp. 179-184.
36. Shambcrgcr, II.J. (1970) Relationship of Selenium to Cancer I.
Inhibitory Effect of Selenium on Carcinogcnsis J. Nail. Cancer
Iiibt. 44, 931-936.
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37. Nushoini, M.C. and Scott, M.L. (19G1) Nutritional Effects of
Selenium Compounds in Chicks and Turkeys. Fed. Proc. 20,
C74-G78.
38. Oldfield, J.E., Schubert, J.R., and Mulh. O.H. (1963) Implica-
tions of Selenium in Large Animal Nutrition. J. Agr. Food Clicm.
11, 388-390.
39. Morris, V.C. and Levamler, O.A. (1970) Selenium Content of
Food.s.J. Nutn. 100, 1383-1388.
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SILVER
The ncod to sol a water standard for silver (Ag) arises irom 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 mucous membranes which is un-
sightly and disturbing to the observer as well as to the victim. The
amoi . '. of colloidal silver required ..o produce tins 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-
arphciiaminc, 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 closes. 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 unknovn,
but individuals concurrently receiving bismuth medication developed
argyria more readily. Although there is no evidence that gradual dcposi-
t-ion of sil"er in the body produces any significant alteration in physiologic
function, authorities arc of the opinion that occasional mild systemic
effects fro n silvc-r may have been overshadowed b> the striking external
changes. In this connection, there is a report (3) of implanted silver
-------
amalgams, resulting in localized iirgyria restricted
-------
A smdy (9) of the resorption of silver througli human skin using radio-
silver Ag"f has shown none passing the dermal barrier from either
solution (2 percent AgNOj) or ointment, within limits of experimental
error (^ 2 percent). This would indicate no significant addition of
silver to the body from battling 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 vcglablcs belonging
to the family Drassicoceae, such as cabbage, turnips, cauliflower,
and onions, would combine with residual silver in (\\o cooking water.
The silver content of several liters of water could thus be ingested.
llccausc 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 sihcr bound to sulfur components of food cooked in silver-containing
Maters (the intake for which absorption was reported m 1940 to amount
to 00-80 .ug per clay (10)|, the concentration of silver in drinking water
shall nut exceed 0.05 mg/1.
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HEFEKENCKS
1. Hill, W.B., and Pillsbury, D.M. Argyria. The Pharmocology of
Silver. Baltimore, Mel., Williams and Wilkms, 1939, 172pp.
2. Ibid., Argyria Invcsligation-Toxicologic Properties of Silver, Am.
Silver Producers Res. Proj. Report. Appendix II, (1957).
3. Bell, C.D., Cookcy, D.B., and Nickel, W.R. Amalgam Tatoo-
localized Argyria. A.M.A. Arch Derm. Syph. 66: pp. 523-525 (1952).
4. Joscpli, M., and Van Devcntcr, J.B. Atlas of Cutaneous Morbid
Histology. W.T. Klmcr&Co., Chicago, 1906.
5. Scott, K.G., and Hamilton, J.G. The Metabolism ol 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. 454-46U (1956).
7. Aub, .I.C. and Fairhall, L.T. Lxcrclion of Silver in Uruic. J.A.M.A.
118: p. 319 (1942).
8. .Just. J. and Szniolis, A. Germicidal Proi)ertie.s of Silver in Water.
.1. Am. Water Works A., 28: 492-50G, April 1936.
9. Norgaard, O. Investigations with Radio Ag Into the Rcsorption
of Silver Through Human Skin. Acts Dcrmatovener 34: 415-41*9
(1945).
10. Kclioc, R.A., Cliolak, J., and Storv, 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 sudium is mostl> 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 1COO to 'JGOO mg per diy. 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 add salt to the food at the table and the individuals
who always add salt even before lasting.
The taste threshold of .sodium in water depends on several factors (3).
The predominant nn«'>n lias 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 sulfale. A heavy salt user had a threshold of
taste that was 50 percent higher, and the taste was less delectable
in cold water.
-------
Six uf 14 infants exposed to ;i .sodium concentration of 21,140 mg/1
died when salt was mistakenly used for sugar in their formuln (4). Sea
water would have about 10,000 mg/l uf sodium.
Severe exacerbation of chronic congestive heart failure due lo sodium
in water has been documented (3). One patient required hospitalization
when lie changed his source of domestic water to one that had 4200 inn/I
sodium. Another patient was readmitted at two-to-lhree-wcck intervals
\vhen using a source of drinking water of 3500 my/I 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 dic'j 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
p.dmimMratioii of these therapeutic agents, and sodium-restricted diets
:irc require'!, especially for long periods of treatment. More recent
medical te.xl books continue to point out the usefulness of sodium-restricted.
diets for these se\eral diseases where fluid retention is a problem (C).
When disease causes fluid retention in the body, with subsequent edema
and ascites, there is a diminished urinary excretion of sodium and of
water. If the sodium intake is restricted in these circumstances, further
1G7--
-------
fluid retention will usually not occui . and the excess water invested will
be excreted in (lie urine bocau.se the mechanisms that maintain the con-
centration of sodium in the extracellular fluid do not permit (lie 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 CO mi: that \\ould
increase the intake to the widely used restricted diet of 500 mg per day
must arcount for all non-nutrition intake that occurs from drugs, water
and incidental intakes. A concentration of sodium in drinking water up
to 20 mg per liter is considered compatible with this diet. When the
social in content exceeds 20 mg/1, the physician n«:.sl Like this into
account to modify the diet or prescribe that distilled water be used.
Water utilities 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
arc kno-.ui to exceed 20 mg/1 and would *ic 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 n routine basis and a/c now informing physicians in
their jurisdiction (B). If change of source or a treatment change such
as softening occurs that \vill significantly increase the sodium concen-
tration, (ho utility must be sure that all physicians that care for
-------
consumers arc aware of the impending change. Diets prescribing int:ikc.s
of loss titan 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 ilie 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 are also regional differences that probably
result from physician training. i'he American Heart Association (AHA)
(9) feels that diuretics may allow for less need of very restricted diets
and that diuretics arc necessary for quick results in acute conditions.
For long-term use, a sodium-restricted diel is simpler, safer, and
more economical for the patient. It is preferable, especially when a
moderate or mild sudium-restnr'od Jiet will effectively control the
patient's hypertension and water retention. Literature is provided to
physicians by the AT.A to distribute to their paticrts explaining the
sodiuni-restrictcd .licls. These cover the "strict" restriction - 500 mg
sodium, "moderate" restriction - 1000 mg sodium, and Jhe "mild"
restricted diet - 2400 io -1500 mg sodium. From 19.18 through June
1971, there were 2,305,000 pieces of t'us literature distributed:
37'o - 500 mg; 34r.r, - 1000 mg; and 29'/o - "mild" (10). There are many
ways a physician can counsel his patients other than using this literature,
so the total distribution docs not reflect the extent of the problem, but
the proixjrtion of booklets distributed may provide an estimate of the
-------
ix>rlion of diets that arc proscribed. The "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 a/fecls more the 21 million
Americans, and in mure 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 sonic unknown portion
of the 27 million persons with cardiovascular disease. Thus, from 21
to 27 million Americans would be concerned with sodium intake.
Toxemias .of pregnancy arc common complications of gestation and
occur in G to 7 percent of all pi eyiiancies 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
int:ike, but no estimate can be made on the number of peop'e involved.
Questions about salt usage were asked on the ninth biennial cxamin.i-
don of the National Heart Institute's Frimingham, Massachusetts
Study (13). The study population was free of coronary heart disease
when the .study be^an in 1949 and now arc over 45 years of aj;c. There
were 3, cJ33 respondents. Forty-five percent of the males and 30 percent
of the females reported that they add salt routinely to their food before
tasim;;. Hdl at Hie other extreme, 9 percent of the men and 14 percent
of the women avoid salt intake. More of !ic people GO and over avoid
salt intake than the -15 to 59 population. It is not determined if the salt
restriction was medically prescribed nor how extensively the sodium
intake was restricted. i/"»'"•
-------
It can be seen lli:it a significant piojx>rtion of the 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. Tins
is particularly true of locations where many of the people usini; the water
would be susceptible to adverse health effects, such as hospitals, nursing
homes, and retirement communities. The use of sodium liypochloritc
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 mijjit cause a
significant increase, and .softening by either tho 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 \sould 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 mu/1 to 2G9 mu/l sodium on the average
after softenm;; (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 lias been reported where a replacement element type
softener was not flushed, and the drinking water had a sodium content
nf 3, 700 nig/l when the unit was put back in service.
17 i
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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 \vater hardness is kncwn, and because of the
increase in sodium content of softened waters, utilities should carcfuly
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 dciced highways
may increase the sodium pollution of surface water (15). The problem
is most acute when i;round water is polluted with sodium (1C, 17) because
it remain:; for a long time. Removal of .sodium Irom water requires
processes being developed by the Office of Saline Water (18) and aie
economically feasible only in certain situations.
The person who is required to maintain a restricted sodium intake
below 500 mg per clay can use a water supply that contains 20 nig 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 clay the food in Like is essentially the same, but the diet is liberalized
to allow (lie use of 1/4 teaspoon of salt, some regular bakery bread,
and/or some salted butter. II persons on the moderately restricted diet
17- <
-------
found it necessary to use a water with a significant sodium content (.hey
could still maintain their limited sodium intake with a water containing
270 mg/liter. Tins would require allocating all the liberalised 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 t'lat the sodium content ol public water supplies l:e uiown
and tins information be disseminated to physicians who have patients in
the service area. Thus, diets for those who must restrict theii 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 lor supplirs
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:
Raiu;e of Sodium Ion Percc'iit of Total
Concentration Samples
mg/1 'c
0 - 19.9 53.2
20 - 49.9 19.0
50 - 99.9 9.3
100 -249.9 8.7
250 -399.9 3.C
400 --499.9 0.5
500-999.9 0.7
Over 1000 0.1
17,----
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While llic question of a maximum ci'iiUiminant level fur sodium
is still under consideration by tlie National Academy of Sciences and
others, no specific level will be proposed for the Interim Primary
Drinking Water Regulations. Tl.c Environmental Protection Agency
believes that the available data do not support any particular level
for sodium in drinking water, and that the regulation of scdium by a
maximum contaminant le\el 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. D.ilil, I..K. Possible Role of S;ilt Intake in The Development ul
Essential Hypertension, From Essential Hypertension: An Inter-
national Sunposuim. P. Collier and K.D. Bock, Lierne (Eds.)
Springer Yerlut;, Ncidolbcrg pp. 53-65 (19GO).
2. Bureau of Radiological Health. California Stale Department of
Public Health, Estimated Daily Intake of Radionuclidcs in
Calilonua Diets, April-December 19C9, and January-June 1970.
California State Deplinent of Health, Radiological Health Data and
Reports, G250G32, November 1970 (1970).
3. Elliott, G.B., and Alexander, E.A. Sodium from Drinking Water
as An Unsuspected Cause ol Cardiac Decompensation. Circulation
M: 5G2 (1961).
4. Finbert;, L.., Kiley, J., and Luttrcl, C.N. Mass Accidental Salt
Poison in t; m Infancy. Med Assn. 184: 187 (19G3).
187-190 (April 20, 19G3).
5. Food and Nutrition lioard-NAS-NRC, Sodium-Restricted Diets,
Publication 325, National Research Council, Washumton, D.C. (1954).
G. Wmtrobc. M.M., Thorn, G.W., Adams, R.D.. Dennett, I.L.,
Drauuald, E., Isselbaeher, K.J., and I'etersdorf, R.CJ., (hds.)
Harrison's Principles ol Internal Medicine, (Gtl» ed.) McGraw-Hill
book Co., New York. (1970).
7. White, J.M., Wir.uo, J.G., Alli^ood, L.M., Cooper, G.R.,
Gutriduc, J., H\d.iker, W., Benacl:, R.T., Demnn, .J.V.'. and
Ta\lor, F.D. Sodium Ion in Drinkmi; Water 1. Propertios,
Anahsis, and Occurcnce, Dietetic Assn., 50: 32 (1967).
8. Review of .State .Somum-in-Drinkun;-\Valer Arthities. Bureau
of Water Hv^iene, U.S. Public Health, Service, Washington,
D. C. (1071).
9. Pollack, H. Note to The Physician (inserted with diet booklets)
Your 500 m-!. Sodium Diet-Strict Sodium Restriction, Your
1000 i:v.'. Sodium Diet - Moderate Sociium Restriction, and Your
Mild .Sodium-Restricted Diet, American Hei'rt Association
(19GO).
10. Cook, L.P. American Heart Assn. Personal Communication
(1971).
11. American Heart Assn. Heart Facts 1972. A.H.A., New York (1971).
•e f~j: ,
1 /.> -
-------
12. KasiiiKui, N.J. and Ilcllinan, L.M. Willuims Oustrelics. (13th cd.)
Appli'ton-Century-Crofts, New
13. Kannel, W.B. Personal Communication (1971).
14. Cinrriaun, -G.E., :i:ui Ader, O.L. Sodium 111 Drinking Water.
Lnviron. llraltli, 13: 5S1 (10GC).
15. JUibc-L-k, U.C., Dimc-nl, W.U., Deck, D.L., Hald".ui, A.L., and
Lij)(un, ,'j.U. Runuff of Ocicinc Salt: Effect on Iroiidcquuit Day,
Rorhestcr, New York. Science 172: 1128(1971).
1C. Joycr, D.F., and Sutclilfe, II. Jr. Salt-Water Conlaniii.aUon in
Wells in ilic Sara-Sands Area of SiesUi Key, Sara .sola County,
Florida. JAWWA . 59: 1504 (19G7).
17. Parks, W. W. l^rconl:tmuiation of Ground Water at LvJian Hill.
JAWWA. 51: G-14 (1959).
18. U.S. IJcpartnienl of the Diterior. Saline \Vatcr Conversion Report
for 19G9-1970. Govcrnincnl J'rmtuiy Office, Washington, D.C.
(1970).
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SULFATE
The presence of sulfalc ion in drinking water can result in a
cathartic effect. Doth sodium sulinte and magnesium suLfatc arc
well-known laxatives. The laxative dose for both Glauber salt
(Na2SO;10H2G* ajid Epsom salt (!UgSO;7H2O) is about two grains. Two
liters of water with about 300 "ig/1 of sulfalc derived from Glauber
salt, or 390 mg/1 of sulfatc from Epsom salt, would provide this dose.
Calcium sulfale is much less active in this respect.
This laxative effect is commonly noted by newcomers and casual
users of waters high in sullalcs. One evidently becomes acclimated
to use of these waters in a relatively short time.
The North Dakot;> Stale Department of Health has collected inlorma-
tion on the laxative effects of water as i elated to mineral quality. This
has been obtained by having individuals submitting water samples for
mineral analysis complete a questionnaire that asks about the taste and
odor of the water, its laxative effect (particularly on thusi; not accustomed
to using it), its effect on colfce, and its effect on potatoes cooked in it.
Peterson (1) and Moore (2) have analyzed part of the data collected,
particularly with regard lo the laxative effect of the water.
Pet( i .fii foaiid II,.u, in general, the waters containing more Mian
750 mg/! . i siilfate showed a laxative effect and those with less than
GOO mg/! j'C'nei'ally did not. If the water w.-s high in magnesium, the
17V-
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eflcc't was shown at Io\vcr snlfatc concentrations than if utlicr cations
were dominant. Moore showed that laxative effects wore experienced by
the must sensitive persons, nut accustomed to the water, when magnesium
wns about 200 ing/l and by the average person when magnesium was 500-
1,000 mti/1. Moore analyzed the data as shown in Table 1. When suJJatcs
plus magnesium exceed 1,000 mg/1, a majority uf those who ujive a definite
reply indicated a laxative effect.
Table 2 presents some data collected by Lockliart, Tucker and
Merrill (3) and \Vhipplo (4) on the influence of sulkile on (.he taste oi
water :uut coffee. Because of the milder taste of sullale over chloride
(5)IG) a taste standard for sulfate would probably be in the 300-400 mg/l
range. The Peterson data il} and Table 1 ^2), however, indicate Hint
From GOO to 1000 nig/1 of sullale lias a laxative el foci on a majority of
users.
\Vlulo a limit for sullatc may be included in Secondary Drinking
Water Regulation:?, on the basis of the effect of sulUuc on water taste,
no maximum contaminant level is being proposed at this time. As
noted above, a re.'auvrly lu^li concentration of sullato in drinking
water l»as little or no J.nown effect, on regular users of liio water, but
transients usino; iui;U sulfatr watfi- somc'times exiH?nonce a laxative
effect. Whether this effect will occur, and its .si-verity, varies
j-reatly with bu«_h r.iL'tors as llu: le\el of sulfalc in the \\ator being
consumed ami the level of MiLfaie to which the tr.msionl is accustomed.
Because of this threat variability, Ihc available data vlo not support
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the establishment uf any given maximum contaminant level. The
Environmental Protection Agency recommends tlial Hie Slates institute
monitoring programs for sulfates, and Hint the transients be notified
if the sulfalc content of the water is high. Such notification should
include an assessment uf the possible physiological effects of con-
sumption of the water.
In the meantime, research is being undertaken to determine if
the health effects of sullatc 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 Hevisecl Interim Primary
Water Regulations.
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HKFKRKNClS
1. Peterson, N.L. .Suliales in Drinking Water. Official Bulletin
No: ill Dakota Water awl Sewage Works Conference. HJ: (1951).
2. Moore, t.W. Physiological Effects of The Consumption of Saline
Drinking Water. tt'.illclui of tjubcommitee on Water Supply,
National Hi ^oarih Council, Jan. 10, 1952, Appendix B, pp. 221-227
(1952).
3. Lockiiart, E.E., Tucker, C.L., and Merritt, M.C. The Kffccl
of Water Impurities on The Flavor of 13ro\\od Coflee. Food 20:
i>98 (1905).
4. Wlnpplc, G.C., The Value of Pure Water. John Wiley, New
Yoik 11907).
5. Bruvold, W.H., and Gafley, W.R., Evaluation Ilaluij; of Mineral
. Taste in Water, J. I'cn-ejmial Motor Skills 2£: 179 (1969).
(j. Bruvold, W.H., and Gal fey, W.ll., Hated Acceptability of Mineral
Tasle in Water. II Coinbuutorial Effects of Ions on Quality and
Action Tendency Ratings. J. Applied Psychol. 53: 317 (1969).
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