^/  «	              WASHINGTON. 0 C  2W60
                               AUG 251988
  SUBJECT:  Transmital  of  "Guide  to Drinking water Healtn
  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.


 cc:  J. OrM

                    f t

 U.S. Environmental  Protection  Agency
        Office  Of  Orinking  Water
    Criteria  and Standards  Olvision
         Health Effects  Branch

                        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?)  .
                         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

             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).


      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  
 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.

     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.

 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

                                    - J-
      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

       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

       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' -*
 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

Immediate action may be
warranted for exposures
greater than about 10

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.
•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
                              of the contaminant in drinking
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

 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^   
        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

    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

 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.


      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.


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.

 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.

                             APPENDIX  I

                        from  US  EPA (1987)

  *t»arb«d dose.  The amount  of  a chemical  that entari the body of en

                  uptake  of  water or  dissolved chemicals by a cell or  an

 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

 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

»ioa«*ay.  1%«t which determine* the effect  of  a  cheeical  on a living

 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.

 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

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

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

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.

 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
 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

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.

 Boute  of  exposure.  The avenue by which a chemical comes  into  contact
     with an  organism  (e.g., inhalation, ingestion,  dermal  contact,

 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

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.

                                       APPENDIX  II

                OF  DRINKING WATER  CONTAMINATION." US  EPA  (1987).


       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


      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

              HATER	211-263


      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


         Outline for Videotape)	436-446