UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
^/ « WASHINGTON. 0 C 2W60
"v.
AUG 251988
MEMORANDUM
SUBJECT: Transmital of "Guide to Drinking water Healtn
Advisories."
FROM: Robert Vanderslice, Ph.D.
lexicologist, Health Effects Branch, CSD
TO: Joseph A. Cotruvo, Ph.D.
Director, Criteria and Standards Division
THRU: Edward V. Ohanian, Ph.D. dMjjJi
Chief, Health Effects Brarfcrr, CSD
This guide Mr undergone extensive HEB review and is
in final forr al review. Your comments
of May 1983 have oeen incorporated. A copy was requested
in June by Peter Cook, but no comments have been received.
Attachment
cc: J. OrM
of
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f t
IIDE TO nRINKlNP, WATEH HEALTH ADVISORIES
U.S. Environmental Protection Agency
Office Of Orinking Water
Criteria and Standards Olvision
Health Effects Branch
August,
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Tao1e of contents
Regulating drinking water contaminants 1
providing guidance through the health advisory program . . i
Deriving health advisory values 2
Lifetime HAs and MCLGs for carcinogens A
Using HA values for risk assessment 4
R i s it characterization 5
Hazard identification *
Dose-response evaluation 6
Contaminants with a steep dose-response curve . . 7
Carcinogens 7
Exposure assessment ... 7
Riskmanagement ..... 7
Sources of information and assistance 3
References 3
Appendix I
Appendix II
Glossary of
manag .-r
risk assessment/risk
Top 'Workshops on
Asse-.. ... *:£..agement of Drinking
Water Contamination (US EPA. 198?) .
A-I
A-II
List of Tables
Table I. HA development for different durations
of exposure I
Table 2. Uncertainty factors for HA calculation , . . . . 3
Table 3. Assumptions used in developing HAs/MCLGs .... 3
Table 4. Carcinogen classification and derivation of
guidance values *
Table S. use of HAs for risk assessment 5
List of Figures
Figure 1. US EPA Regions and Regional Office Telephone
Numbers
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Gl'IOE '0 DRINKING WA'ES H£A|_~H AD'/
The US EPA Office of Drinking Water/Health Effects
Branch in the Criteria and Standards Division prepared
thrr~g"uide to explain the Healtn Advisory program, the
derivation of guidance values and tneir application to
risk management decisions. "Workshops on Assessemet
and Management of Drinking Water Contamination" (1987)
contains a more detailed discussion of these topics
(refer to Appendix II).
REGULATING DRINKING WATER CONTAMINANTS
Tap water contains many more chemicals than just water.
Some chemicals occur naturally, such as the minerals which make
water "hard." Other chemicals enter drinking water from h-iman
activity. Water treatment plants intentionally add some chemicals
to improve water quality. Disinfectants (such as chlorine) kill
bacteria and protect against disease, phosphates limit corrosion of
water pipes, and coagulants remove unwanted solids from turbid
waters. In addition, fluoride is often added as a health measure
to prevent tooth decay. Other activities, such as 1 ndustM al -arvd
municipal discharges, spills, agricultural runoff, may contaminate
drinking water supplies.
Some chemicals
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Longer-term and Lifetime HA values. like MCLGs, HA values are no*
enforceaTTTe" standards, but guidance values indicating the drinking
water concentration of a contaminant tnat are considered protect'.
of numan health for a given duration of exposure - i.e., unlikely
to result in any adverse effect on health with a margin of safety.
DERIVING HEALTH ADVISORY VALUES
To derive HA values, ODW reviews the pertinent studies describ-
ing the health effects of the contaminant. Studies are evaluated
based on their overall quality, their relevance to human exposure
via drinking Mater and their duration of exposure. Studies descnb
ing oral administration of the contaminant (especially via drinking
water) for the appropriate duration of exposure (see Table 1) are
the prefered basis for HA derivation. Other routes of exposure
and study durations may also be considered acceptable.
Typically, OOW derives HA values from toxicity studies which
describe doses to experimental animals which cause little or *\o~'
adverse health effects. The HA document describes these dose
levels as the Lowest-Observed-Adverse-Effect Level (LOAEL) or - -
No-Observed-Adverse-Effect Level (NOAEL), respectively. To
estimate doses causing no adverse effects in sensitive humans, ODM
divides these NOAELs/LOAELs by appropriate uncertainty factors
(UFs; see Table 2).
OOW calculates HA values from a dose level (either a NOAEL or
LOAEL) by making assumptions about the body weight of individuals,
and their drinking water consumption rates. The final formula
for calculating One-day, Ten-day and Longer-term HA values is:
One-day, Ten-day
or Longer-term HA
(NOAEL or LOAEL mo/kg/day)(Body wt. in kg)
(Uncertainty factor)(water consumption L/day)
Table 1. HA development for different durations of exposure.
Health
Advisory*
One-day M
Ten.day HA
Preferred study duration
1 to 5 (successive) dally doses
7 to 30 (successive) dally doses
Longer-term HA 101 of lifetime
(90 days 1n rats/mice)
Lifetime HA
or MCLG
Cancer risk
Lifetime (2 years in rats/mice);
subchrontc witn additional UF
Lifetime (oncogemci ty)
Protected individual/
duration of exposure
Child exposed 1 day
Child exposed < I month
Child & adult exposed
up to 7 years
Adult exposed 70 yrs
Adult exposed 70
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2. uncertainty factors for HA calculation3
UF HA basis Justification
£10 Human NOAEL Accounts for variation within the population ( intraspec ies, ,
100 Human LOAEL Incorporates a factor of 10 to account for lack of a MOAEL
and a factor of 10 for mtraspecies variation, or,
100 Animal NOAEL Incorporates a factor of 10 to account for interspecies
differences, and 10 for Intraspecies variation.
1,000 Animal LOAEL Incorporates factors of ten for lack of a NOAEL, mtersoecies
variation, and mtraspecies variation, or,
1,000 Animal NOAEL For Lifetime HAs, Incorporating factors of ten for interspecie
variation, sensitive individuals A less-than- lifetime exposure
Additional uncertainty factors, ranging from l to 10, may be incororated on a case-
by-case basis to account for deficiencies in the data base, quality of the data',
or severity of the effect.
^Recommended by the National Academy of Sciences (1977) and modified by OOW.
Lifetime HAs (and MClGs) are derived using a similar equation,
but the derivation is broken into a series of steps. First the
Reference Dose (RfO, formerly called the ADI or Acceptable Daily
Intake) i s calculated:
RfO (mg/kg/day) » (NOAEL or LOAEL mq/kg/day)
(Uncertainty factor)
Next, the Drinking Water Equivalent Level (DUEL) is derived:
OHEL (mg/L) - *Rf° _m9J**f***)(Body weight in kg)
(Water consumption L/day)
The Lifttlat HA Is the DUEL multiplied by the Relative Source Con-
tribution' (RSC), a factor to account for exposure to the contaminant
from otlMT sources such as food and air.
Table 3. Assumptions used in developing HAs/MCLGs
Body weight: ChlTdren weigh 10 kg;
Adults weigh 70 kg
Drinking water consumption: Children drink 1 L/day.
Adults drink 2 L/day
Relative source contribution; 201 in the absence of
(for Lifetime HAs/MCLGs only) chemical-spec 1 fie data
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Lifetime HA or MCLG (mg/Lj • OWEL x RSC
ODW assumes the RSC is 20*. *hen no
available. Otner assumptions used
given in Table 3.
specific exposure data are
in deriving HAs/MCLGs are
LIFETIME HAS AND MCLGs FOR CARCINOGENS
The methods for calculating Lifetime HA values and MC' Gs
are only followed for none arc i nogenic compounds. For probable
human carcinogens, OOH does not recommend Lifetime HAs and sets
MCLGs at zero (see Congressional recommendations [House Report,
1974]). Carcinogens are treated differently from other chemicals
based on the nonthreshold theory that any dose of a carcinogen,
no matter how small, entails some increased risk for cancer. EPA
estimates this risk using statistical models. To ensure the
protection of public health, these models are based on conservative
assumptions, making the underestimation of risks unlikely. HA
documents prov ide dr i nk i ng water concentrations that are associated
with risks of 10-4, 1C"5 and 10'6; meaning that lifetime expo-ssre
to these concentrations are unlikely to cause greater than one
additional case of cancer in populations of 10.000 (i.e., 104)V
100,000 (105) OP one million (106), respectively. Populations are
assumed to consume 2 liters of drinking water over a lifetime.
MCLs are generally set at the lowest feasible limit and usually
fall within the range of 10'4 to 10'6 risk.
For compound' -*
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Table 5. Use of HA /aluesfor risk assessment.
Contaminant level
e One-day HA
Between One-day HA
and Ten-day r.A
Between Ten-day HA
and Longer-term HA
Between Longer-term HA
and Lifetime HA or
10'6 cancer risk level*
Below Lifetime HA/
1Q-6 cancer risk level
Recommended response
Immediate action needed. Reduce further exposure
Action needed if exposure Exposures should be reduced wit-
exceeds approximately 10
days.
Immediate action may be
warranted for exposures
greater than about 10
days.
No immediate risk to
public health.
No action needed.
approximately 10 days of contan
tion incident.
Conduct a site-soeci fie risk
assessment to determine accepta-
level s/duration of exposure-.
reduce exposures accordingly.
Develop and implement strategie
for reducing contaminant levels
in drinking water if desirable.
Protective of public health.
ssaasasaasssasssasssassssssssaaaasBsaaaaaaasaasaasssaaaaaassBssBsassaaaBsaaaaassss::-
•See discussion of carcinogens, p. 4, and Table 4. For some compounds, levers'as hi
as the 10~4 level are considered protective of public health.
1) Determine the concentration
water,
of the contaminant in drinking
2)
3)
Refer to the appropriate HA document, obtained either through
EPA Regional Offices (See Figure 1), or by calling the Dnnici
Water Hotline (800-424.4791).
Compare contaminant levels to HA values
may be needed (Refe- Table S),
to determine if ac t
4) Characterize risks to e-aole risk managers to take appropriate
actions to ensure the safety of public water supplies.
If contaminant concentrations are below the Lifetime HA, no
action is needed for protection of public health. Whenever contami-
nant contffntratlons exceed the Lifetime HA some level of action is
needed. Guidance on whether Immediate action is needed can be
obtained by comparing drinking water levels to One-day, Ten.day and
Longer.tern Advisories (Table 5). Before decisions can be made on
how best to manage the risks of exposure to contaminants, these
risks must be clearly characterized.
ODU does not recommend Lifetime HA values for carcinogens
(Class A, 81 or 82), therefore carcinogenic contaminants must se
evaluated differently. Officials should compare the drinking
water levels to both theoretical Incremental cancer risk levels, ans
values for the DUEL (derived for non-carcinogenic effects), 'i.s.
both possible carcinogenic and noncarcinogenic effects must oe
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evaluated when determining tne risks posed by carcinogens. Drink-
ing *ate-T__C.onc - - - •- -jnging from the 10-4 to 10^° ns< leve1
are general! - ^ : a D1 e provided these levels are also
protective o - affects. Determining tne accept-
a 31 1 i t y of e .^rei at teveis greater than the 1 0 • * risk level
should oe maae on a case-ay-case basis.
RISK CHARACTERIZATION
There is no sharp boundary between safe and unsafe leve's of a
contaminant in drinking water. When concentrations exceed '-u
values, risk managers must make difficult decisions. EPA advocates
the use of quantitative risk assessment as a tool for this decision
making process. Quantitative risk assessment involves determining -.
1) Toxic effects associated with exposure (hazard identificati:
2) Dose associated with these effects (dose-response evaluatio-
3) Level of human exposure (exposure assessment).
Public officials should understand the uncertainties in each
of these three elements of risk characterization to effectively
use HA values for the management of drinking water contamlnantion.
A brief description of these three elements, originally described
in NAS (198^
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Contain • • Mts with staep dose-response relationships
suc^h as •ganophospha te pesticides, may cause severe
ejects jr even deatn at doses just slightly above tnose
which a:3ear safe, and may require an extra margin of
safety to ensure the puolic is not exposed to severe
hazards ,
Carcinogens are evaluated differently from non-carcinogens.
I: is assumed that no threshold dose exists for carcinogens
and any dose, no matter how small, increases the risk of
cancer.
3) Exposure Assessment: Measuring the concentration of the con.
taminant in water is the primary focus of the exposure assessment.
Often the first step in characterizing risk 1s to check the report
contaminant concentration to confirm that the population really
is exposed. Analysis of a single sample may be sufficient to
identify contamination problems, but often, multiple samples are
analyzed to verify the initial findings. Analytical techniques
can be quite accurate, but some variability is expected, even
between identical samples. FOP example, for vinyl chloride, EWf'
considers measurements within 401 of actual concentrations accept-
able for laboratory certification. In some cases, HA values
be lower than currently available analytical detection limits.
Uncertainties in expo • 'ssessment extend beyond questions
concerning chemical analy ,ater samples. Exposure estimates
include estimates of the c water consumption rate, the duration
of exposure, and estimations of exposure from other sources such as
food or air. Because the exposure assumptions used to develop HAS/
MCLGs (see Table 3) may differ from actual conditions for a given
site, site-specific exposure estimates can provide useful information
for assessing and managing risks.
The final step In risk assessment is risk characterization.
In this step, the hazard Identification and dose-response evaluation
are integrated with the exposure assessment. The risk characteri-
zation describes the estimates for the most likely outcomes from
exposure to the contaminant at the levels found in drinking water.
and provides the basis for Informed decision making.
RISK MANAGEMENT
The risk characterization should assist the manager in deciding
on both an appropriate course of action,.and how fast the action
must be taken. Appropriate responses to elevated contaminant levels
can range from drastic immediate action (e.g., providing bottled
water) to better long-range planning (e.g., adopting a monitoring
program with a remedial action plan if contamination continues).
Exposures to contaminants in drinking water can be reduced
using a variety of strategies. Providing bottled water or
pomt-of-use treatment devices are primarily short-term measures
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o f relatively high cost. Control strategies such as r e 5 j c ; r g ,•
eliminating contaminant sources, Blending, or finding ne* sojrces
fit 1 1 usuTTTy reduce contaminant exposures to acceptable levels.
Treatment strategies including conventional treatment, aeration,
absorption, b i odegrada11c- , -^vo-se osmosis, ion exchange and
eIectrodia 1 ys i s have all •-•- .sed successfully in removing
various drinking water c: : -.- -.ants. The most appropriate actions
may involve combining short-term meausures, control -aeasures. and
long-range treatment strategies to protect public rsalth and
inprove *ater quality.
SOURCES (IF INFORMATION AND ASSISTANCE
In emergency contamination incidents, the appropriate local
public health official snould be contacted immediately. If tnere
is a problem locating the proper local official, the National
Association of County Health Officials may be helpful (202-783-55SO.;
For other types of inquiries, local authorities may defer questions
to one of ten EPA regional offices throughout the country (FIGURE
Assistance can also be obtained from the EPA OOU Headquarte .
office in Washington, DC. The ODH supports a 24-hour, toll-free
drinking water Hotline (800-426-4791). I" addition, HA documents
provide answers to many questions about drinking water contaminants.
Each of the ten regional offices has a complete set of HAs, or a
personal copy can be obtained by calling the Drinking Hater Hotline.
REFERENCES
National Academy of Sciences, National Research Council. 1977.
Drinking Hater and Health, volume 1. National Academy Press,
Washington, DC.
National Academy of Sciences, National Research Council. ^983.
Risk Assessment In the Federal Government: Managing the Process.
National Academy Press, Washington, DC.
House Report. 1974. No. 93 - 185. July 10, 1974.
US EPA. Technology Transfer document "Workshops on Assessment
and Mani'gtHtnt of Drinking Hater Contamination." EPA/600/M-86/02S.
Revised March 1987.
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Region l:
Regi on 2:
Region 3:
Region 4:
Region 5:
(617) 565-3715
(212) 264-2525
(215) 597-9800
(404) 347-4727
(312) 353-2000
Region 6: (214) 655-6444
Region 7: (913) 236-2800
Region 8: (303) 293-1603
Region 9: (415) 974-8071
Region 10: (206) 442-5810
FIGURE 1. EPA Rtglons and Regional Office Telephone Numbers.
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APPENDIX I
— GLOSSARY OF RIS< A S S E S SHE N T/ R I S K MANAGEMENT TERMS
from US EPA (1987)
*t»arb«d dose. The amount of a chemical that entari the body of en
organism.
uptake of water or dissolved chemicals by a cell or an
organism.
Absorption factor. The fraction of • chemical making contact with an
organism that is absorbed by the organism.
Acceptable daily intake (API). Estimate of the largest amount of
chemical to whach a person can be exposed on a daily basis that is
not anticipated to remit in adverse effects (usually expressed
(Synonymous with
Active transport. An «nergy-expending mechanism by which a cell moves
a chemical across the cell membrane from a point of lower concen-
tration to 4 point of higher concentration, against the diffusion*7
gradient.
Acute. Occurring over a short period of time; used to describe brief
exposures end effects which appear promptly after exposure.
Additive tffeet. Combined effect of two or eore chemicals equal ti the
a urn of their individual effect*.
Adiorption. The process by which cheaieels are held on the surface of
a mineral or soil particle. Compare with absorption.
*»**•••*<• BiviroiuMnt*! or eur rounding condition*.
Aniaal studies. Investigation* u*ing aniaal* a* surrogate* for humans,
on the expectation that reault* in animal* are pertinent to huaans
Antagoniaa. Interference or inhibition of the effect of one chemical
by the action of another chemical.
*••«*» A test for a particular cheeical or effect.
to inadequacy in ecperiaental de*ign that leads to re*ult* or
liMiOM no-. pfe**ntative of the population under itudy.
BioaecMaulation. the retention and concentration of a tubatanc* by an
organiaa.
»ioa«*ay. 1%«t which determine* the effect of a cheeical on a living
organise.
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Sxffusion. The moveme.-.: cf suspended or dissolved particles fron *
•ore concentrated to a less concentrated region •• a result c* ^-«
.random novrement ot individual particl.es; the process tends t=
distntute then uniformly throughout tne available valuse.
The quantity of a chemical administered to an organism.
3ese. The actual quantity of a chemical to which an organiss n «
considered the toxic effect of greatest conesrn.
Endanqeraent assessment. A sits-specific risk assessment of the actual
or potential danger to human health or welfare and the environment
from the release of hazardous) substances or waste. The endanq«rnent
assessment document is prepared in support of enforcement actions
under C0CLA or MCRA.
Endpoint. A biological effect used a* an index of the effect of a
chemical on mn organism.
EpidesUolocUc stMdy* Study of human population* to identify causes of
III MM t Such studies often compare the health status of a group
of psmons who have been exposed to a suspect agent with that of a
non-exposed group.
Exposure. Contact with a chemical or physics*1 agent.
Exposure assessment. The determination or estimation (qualitative or
quantitative) of the magnitude, frequency, duration, route, and
extent (number of people) of exposure to a chemical.
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Human health risk. The Livelihood (or probability) that • given «xpc«--.rc
—0T~series of exposures may have or will damage the health of indi-
viduals experiencing t-*ie exposures.
Incidence off tumors. Percentage of aninals with tumors.
Ingestion. Type of exposure through the nouth.
Inhalation. Type of exposure through the lungs.
Integrated exposure assessment. A summation over time, in ail media,
of the magnitude of exposure to a toxic chemical.
Interspecies extrapolation model. Model used to extrapolate from
results observed in laboratory animals to huaans.
In vitro studies. Studies of chemical effects conducted in tissues,
cells or subcellular extracts froa an organism (i.e., not in the
living organism).
In vivo studies. Studies of chemical effects conducted in intact living
organisms.
Irreversible effect. Effect characterized by the Inability of the body*
to partially or fully repair injury caused by a toxic agent.
Latency. Time fro* the) first exposure to a chemical until the appearance
of a toxic effect.
LCcn* The concentration of a chemical in air or water which is expected
to cause death in SO percent of test animals living in that air or
water.
UJso- The doe* of a chemical taken by mouth or absorbed by the skin
which is expected to cause death in SO percent of the test animals
so treated.
Lesion. A pathological or traumatic discontinuity of tissue or loss of
function of a part.
Lethal. Deadlyi fatal.
exposure. Total amount of exposure to a substance that a
would receive in a lifetime (usually assumed to be seventy
years).
Unearned multistage eodel. Derivation of .the multistage model, where
the data are assumed to be linear at lev doses.
LOAEL. Lovest-Obeerved-Adverse-tf feet Levelj the lowest dose in an
experiment which produced an observable adverse effect.
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NOX£L. No-Ob«erved-Xdverae-Ef feet Level; the highest JOB* in an
experiment vruch did not produce an obaervable Adverse effec-.
HO EL. No-0bs«rved-£f*«c: L«v*l; dsee level it which no effects ire
noted.
VTP. National Toxicology Program.
Study of cancer.
One-hit modal. Mathematical aodel baaed on the biological tneory t.-.a-
a Jingle "hit* of «ome Binimvui critical aaount of a carc-..-.o received by an
i.ndlri.dya.1 without the expectation of • significantly haraful
result.
Pharaaeakinetics. The dynamic behavior of cheaical« inaide biological
systens; it includes the processes of uptake* distribution,
metaJsoiism, and excretion.
Population at risk. A population cubseoup that i* acre Likely to o«
exposed to a cheat ca I, or it acre sensitive to a chenical, than is
the general population.
Potency. Amount of material necessary to produce a given level of a
dele tar ioua effect.
Potentiadon. Hie effect of one chemical to increase the effect of
another chemical.
ppb. Part* per billion.
ppai. >«rta par •lllion.
Pretraieace study* An epidemiological study Mhich examines the
rtiatienchip* between diseases and expoaures aa they exist In a
definejd population at a particular point In tiae.
Prospectivej study* An epldeaiological atudy which examines the
development of disease in a «r«up of pvctona dacacminad to be
presently free of the diaeaae.
Qualicatlva. Descriptive of hind, typa or direction, aa opposed to
sue, magnitude or degree.
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Boute of exposure. The avenue by which a chemical comes into contact
with an organism (e.g., inhalation, ingestion, dermal contact,
-unction).
Safe. Condition of exposure under which there is a 'practical certaint/1
that no harn vill result in exposed individuals.
SinX. A place in the environment where 4 compound or naterial collects
(see reservoir).
Sorption. a surface phenomenon which stay be either absorption or
adsorption, or a combination of the two; often used when the
specific mechanism ij not known.
Stcihastie. Based on the assumption that the actions of a chemical
substance results from probabilistic events.
Stratification. M) The division of a population into aubpopulations
for sampling purposes! (2) the separation of environmental nedU
into layers, as in lakes.
Subchroni- • *tion, usually used to describe studiee
or 1 - - five and 90 days.
Syneraism. -;t.on of ewo or more chemicals that results in
an effect mat is greater than the sue of their effects taken
independently.
Systemic. Relating to whole body, rather then its individual parts.
Systemic effects. Effects observed at sitee distant from the entry
point of a chemical due to it* abeorption and distribution into
the body.
Teratogenesis. The induction of structural or functional development
abnormalities by exogenous factors) acting during gestation*
interference with normal embryonic development.
Tsratogenietty. TIM capacity of a physical or chemical agent to cause
non-hereditary congenital malformationa (birth defects) in offspring.
Therapsjutic ladM* The ratio of the deee required to produce toiic or
imthml effe«t to doee required to produce non-adverse or therapeutic
Thr«mm»>ld. The) lowest dose of a chemical at which a specified measurable
effect is observed and below which it is not observed.
Time-weighted Average. The average value of a parameter (e.g., concen-
tration of a chemical in air) that varies over time.
Tissue. A group of similar cells.
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APPENDIX II
TOPICS COVERED IN "WORKSHOPS ONSASSESSMENT AND
OF DRINKING WATER CONTAMINATION." US EPA (1987).
Introduction
I. EPA'S OFFICE OF DRINKING WATER'S DEVELOPMENT OF STANDARDS
AND HEALTH ADVISORY PROGRAM
A. Glossary of Terns i -i 0
B. Toxicologies 1 Approaches for Developing National
Drinking water Standards t Health Advisories 11-18
C. EPA's Health Advisor/ Program 19-28
II. RISK ASSESSMENT
A. Safety Evaluation/General Principles of Toxicology 29-34
B. Acute and Chronic Toxicity Tests 35-42
C. use of Toxicity Data In Regulations 43-44
D. Principles of Absorption, Distribution, Excretion «
Metabolism of Chemicals 45-50
E. Toxicology of inorganics 51-60
F. Toxicology of Pesticides 61-67
G. Toxicology of Solvents and Vapor* 68-71
H. Principles of Carclnogeniclty 72-78
I. -.-.-.ciples of Risk Assessment 79-130
J. J ess ing Risk/Introduction to Case Study 131-180
K. Risx Assessment Case Study of Drinking Water
Contaminated by Vinyl Chloride...... t8i-2iO
III. REGULATIONS AND ASSESSMENT OF RADIONUCLIDES IN DRINKING
HATER 211-263
ZV. RISK MANAGEMENT
A. Overview of Risk Management and Control Strategies 265-279
B. inorganics Treatment: •• Case Studies 280-310
C. Organics Treatment: Ov» -. .ase Studies 111-370
0. Case Study en Risk Management of Aldicarb, Triehloro-
ethyiene and vinyl Chloride in Drinking water 371-39'
E. Aldicarb Health Advisory 392-420
F. TrichleroetnyieiM Health Advisory 408-420
G. vinyl Oiloride Health Advisory 421-435
V. RISK CONMNXCATOM
Outline for Videotape) 436-446
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