United States
Environmental Protection
Agency
Effluent Guidelines Division
WH-552
Washington DC 20460
Development
I!
Document f|>r Effluent
Limitations Guidelines
and Standards for the
ii
Organic Chemicals
and Plastics! and
Synthetic Fibers
EPA 440/1-83/009-b
February 1983
Point Source Category
Volume III (BAT)
-------
DEVELOPMENT DOCUMENT
for
PROPOSED EFFLUENT LIMITATIONS GUIDELINES
AND
NEW SOURCE PERFORMANCE STANDARDS
FOR THE
ORGANIC CHEMICALS AND PLASTICS AND SYNTHETIC FIBERS INDUSTRY
VOLUME III (BAT)
Anne M. Burford
Administrator
Frederic A. Eidsness, Jr.
Assistant Administrator for Water
Steven Schatzow, Director
Office of Water Regulations and Standards
Jeffery D. Denit, Director
Effluent Guidelines Division
Devereaux Barnes, Acting Branch Chief
Organic Chemicals Branch
Elwood H. Forsht
Project Officer
FEBRUARY 1983
EFFLUENT GUIDELINES DIVISION
OFFICE OF WATER REGULATIONS AND STANDARDS
U.S. ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON, DC 20460
U.S. Environmental Protection Agency
?J*ion 5.Library (PJ.-12J)
522 «?%&12th
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NOTICE MAR 31 1983
On February 28, 1983, EPA proposed effluent limitations guidelines and
standards for the organic chemicals and plastics and synthetic fibers (OCPSF)
point source category. The Federal Register notice of this proposal was printed
on March 21, 1983 (48 F£ 11828 to 11867).
Information received by the Agency after proposal indicates that the total
OCPSF industry estimated annual discharges of toxic pollutants are too high.
The Agency will be Devaluating these estimates when additional information
becomes available prior to promulgation of a final regulation. In the interim,
the Agency advises that there should be no reliance on the annual total toxic
pollutant discharge estimates presented in the Federal Register notice, the
February 1983 OCPSF Development Document, and February 10, 1983 OCPSF Regulatory
Impact Analysis.
n^T Protection
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VOLUME III (BAT)
TABLE OF CONTENTS
APPENDIX
PAGE
APPENDIX A:
APPENDIX B:
APPENDIX C:
SAMPLE 308 QUESTIONNAIRES
CHEMICAL PRIORITY LIST FOR SCREENING
AND VERIFICATION SAMPLING PROGRAMS
ANALYTICAL METHODS DEVELOPMENT
AND REVIEW OF DATA
I. INTRODUCTION C-1
A. General C-1
B. Quality Assurance/Quality Control C-1
C. Wastewater Analysis in the OCPSF Industry C-2
D. Available Analytical Methods C-3
II. ANALYTICAL METHODOLOGIES AND QA/QC
FOR THE BAT STUDY C-3
A. Screening Phases I and II C-9
1. Analytical Methods C-9
2. Quality Assurance/Quality Control C-10
B. Verification Phase C-13
1. Background C-13
2. Analytical Methods C-14
3. Quality Assurance/Quality Control C-20
C. CMA Five-Plant Study C-22
REVIEW OF DATA FROM SAMPLING STUDIES
A. Introduction
B. Screening Phases I and II
1. Description of the Review
2. Use of Phase I and II Data
C-23
C-23
C-24
C-24
C-25
Ill-i
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APPENDIX
APPENDIX D:
APPENDIX E:
APPENDIX F:
TABLE OF CONTENTS
(continued)
C. Verification Phase
1. Background
2. 1982 Data Review by Original Contract
Laboratories
3. Results of the Review
4. Effect of the Review on the OCPSF
Industry Database
D. CMA Five-Plant Study
1. Description of the Review
2. Transcribing and Encoding Errors
3. Errors from Improper Application of
GC/CD Methods
REFERENCES
ACTIVATED CARBON AND STEAM
STRIPPING QUESTIONNAIRES
TREATABILITY STUDIES
STATISTICAL DETAILS AND DEVELOPMENT
OF VARIABILITY FACTORS
A. Formulas and Definitions
B. Rationale for Using Daily Sample Averages
in Modeling -Effluent Variability
C. Goodness-of-Fit Tests
D. Derivation of Variability Factors
E. Example of Variability Factor
Calculations
F. Subcategorization
References
PAGE
C-25
C-25
C-25
C-26
C-27
C-27
C-27
C-27
C-28
C-33
F-1
F-2
F-8
F-9
F-14
F-18
F-32
APPENDIX G:
APPENDIX H:
CHEMICAL TREES OF THE GENERALIZED
PLANT CONFIGURATIONS (GPCs)
HEALTH AND ENVIRONMENTAL EFFECTS OF
PRIORITY POLLUTANTS
A. General
B. Priority Pollutants
1. Volatile Organic Compounds
2. Acid Extractable Organic Compounds
3. Base/Neutral Extractable Organic
Compounds
4. Metals and Cyanide
H-l
H-1
H-1
H-28
H-38
H-74
Ill-ii
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APPENDIX
APPENDIX I:
APPENDIX J:
TABLE OF CONTENTS
(continued)
FATE OF PRIORITY POLLUTANTS IN PUBLICLY
OWNED TREATMENT WORKS: EXECUTIVE SUMMARY
TREATMENT CATALOGUE FOR THE CATALYTIC
COMPUTER MODEL
PAGE
APPENDIX K: DESCRIPTION OF MODEL COMPONENTS AND USE
A. Permanent Files
1. Master Process File
2. Parameter and Treatment Selection File
3. Effluent Target File
4. Unit Process Sequence Rules File
5. Plant Adder File
6. Capital Costs File
7. Operating Costs File
8. Cost Allocation Rules File
B. Treatment Technology Program Modules
C. Model Logic Control Programs
1. Model Run Modes
a. Model Selection Run Mode
b. Specified Unit Process Train
(SUPT) Mode
2. Subsequent Steps for Both Modes
K-1
K-1
K-2
K-3
K-3
K-3
K-3
K-4
K-4
K-4
K-7
K-11
K-11
K-11
K-11
Ill-iii
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LIST OF TABLES
TABLE TITLE PAGE
C-1 Characteristics of Analytical Methods Used
for the OCPSF Industry Sampling Phases C-4
C-2 Analytical Methods Used During the Verification
Phase C-17
F-1 Comparison of Standard Deviations Estimated by
Two Methods F-6
F-2 Goodness-of-Fit Tests for Variability Data:
Log (C-D) for Daily Averages C over D yg/fc F-10
F-3 Values of C and X for 1,2-Dichloroethane Results F-15
F-4 Principal Component Weights for Organics Data F-25
F-5 Principal Component Weights for
Metals/Cyanide Data F-27
F-6 Comparison of Plastics-Only Plants with
Other Plants F-28
F-7 Comparison of Organics-Only Plants with Mixed
Organics/Plastics Plants F-30
F-8 Comparison of Three BPT Subcategories for
Not Plastics-Only Plants F_3-j
K-1 Cost Factor for Each Element in Operating
Cost File K_5
K-2 Operating Cost File Unit Costs K_g
K-3 Cost and Scale Factors for Each Unit Process _
Ill-iv
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LIST OF FIGURES
FIGURE TITLE PAGE
C-1 Comparative Chronologies of OCB and EMSL Method
Validation Programs C-15
C-2 Verification Quality Assurance/Quality Control
Program C-21
K-1 Schematic of Major Model Components K-9
Ill-v
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LIST OF EXHIBITS
EXHIBIT TITLE PAGE
C-1 Organic Chemicals Verification (OCV) Program C-29
Ill-vi
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APPENDIX A
SAMPLED .308_QUESTJONNAI RES
-------
308 BPT QUESTIONNAIRE
A-l
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UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON. D.C. 20460
OFFICE OF WATER AND
HAZARDOUS MATERIALS
As you may be aware, we are in the process of reconsidering
and re-issuing regulations with respect to water pollutants
discharged as a result of the manufacture of organic
chemicals and plastics and synthetics. The earlier
regulations were issued as 40 C.F.R. Parts 414 and 416,
respectively.
The reconsideration of organic chemicals is a result of a
joint stipulation filed in the Fourth Circuit Court of
Appeals entered into on behalf of companies in the industry
and the Environmental Protection Agency. The stipulation
requires the Agency to obtain new and more reliable data and
requires the industry to cooperate in the gathering and
furnishing of data necessary to formulate regulations for
the organic chemicals manufacturing point source category.
The reconsideration of plastics and synthetics results from
the remand by the Fourth Circuit Court of Appeals of the EPA
regulations promulgated on April 5, 1974. The Court ordered
the EPA to restudy areas where the record was ruled to be
inadequate.
To complete these reconsiderations, the Agency is collecting
additional information on the production processes, raw
waste loads, treatment methods and cos'«, and effluent
quality associated with the manufacture of these materials.
The Environmental Protection Agency is no* soliciting your
cooperation in obtaining the necessary information.
A-2
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According to our records/ your Corporation produces one or
more of the products on the attached list(s) (Part I), which
were covered by the referenced regulations. For the
plastics and synthetics category, plants that solely
purchase polymer, resin or fiber to manufacture finished
plastic components should return the enclosed forms
unanswered and state this reason. Plants that manufacture
plastic components in addition to the polymer, resin or
fiber should list the manufactured components as "other
products" in the appropriate section and complete} the forms.
The information requested shall be provided for each plant
of your firm in the format of the attached portfolios. This
will allow the Agency to correlate and make available to
interested parties the results of the data gathered. If our
records are incorrect and you do not feel that the requested
information is related to your plant (i.e., you no longer
manufacture the products listed or do not produce them at
this site), please inform us as soon as possible. In order
to expedite the process we have sent a copy of this letter
to those individuals and plants of your firm as noted on the
attached list.
The information requested in this letter and the enclosed
data collection portfolio is sought pursuant to Section 308
of the Federal Water Pollution Control Act Amendments of
1972. That section authorizes this Agency, whenever
required for developing any effluent limitation, or other
limitation, prohibition, or effluent standard, pretreatment
standard, or standard of performance under this Act, to
require the owner or operator of any point source to
establish and maintain such records, make such reports,
install, use and maintain such monitoring equipment or
methods (including where appropriate, biological monitoring
methods), sample such effluents (in accordance with such
methods, at such locations, -at such intervals, and in such
manner as the Administrator shall prescribe), and provide
such other information as the Agency may reasonably require,
and to have access to and copy any records, inspect any
monitoring equipment and sample any effluents.
A-3
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Information requested pursuant to Section 308 may not be
withheld from EPA on the ground that it is considered to be
confidential or proprietary. Section 308(b), however, does
accord protection to trade secrets. Accordingly, please
indicate clearly on your response any information which you
consider to be confidential or to constitute a trade secret,
BO tnat the Agency may take appropriate protective measures.
Any information not so identified in your response will not
be accorded this protection by the Agency. Effluent data
cannot be protected as trade secrets. Any data may be
disclosed to officers, employees, or authorized
representatives of the United States concerned with carrying
out the Act or when relevant in any proceeding under the
Act.
For your convenience, a data collection portfolio has been
enclosed with this letter. This form is divided into
several parts. Those parts that are applicable to your
operations should be filled out and returned to the Agency
as soon as possible but in no event later than sixty days
after receipt of the letter.
The parts contained in the data collection portfolio are as
follows:
Part X. General Information
Part II. Water Use, Reuse and Discharge
Part III. Treatment Technology
Please answer all items. Also, please provide a separate
set of responses for each plant. The purpose of this
request is to gather all available, pertinent information
and is not designed to create an undue burden of sampling
requirements on your plant personnel. If a question is not
applicable to a particular facility, indicate by writing
"Not Applicable". If an item is not known, indicate unknown
and include an explanation of the reason for not knowing
such information. If an item seems ambiguous, complete as
best as possible and state your assumptions in clarifying
the apparent ambiguity. Also, submit copies of the summary
A-4
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data sheets compiled or used in completing the tables in
this form.
The Agency will review the information submitted and may, at
a later date, require site visits and additional sampling in
order to complete the data base.
Thank you in advance for the cooperation of your company.
The Environmental Protection Agency is committed to
promulgating effluent regulations which are in accordance
with the Federal Water Pollution Control Act and which are
reasonable. The Agency has found that only with complete
cooperation of all parties concerned can thoughtful and fair
regulations be published. Z am confident that we can
anticipate your assistance in carrying out that goal.
Should you have any questions regarding this request, please
do not hesitate to contact Lamar Miller with respect to
organic chemicals at (202) 426-2582 or Michael Kosakowski at
(202) 426-4617 with respect to plastics and synthetics.
Sincerely yours,
Robert B. Schaffer
Director
Effluent Guidelines Division (WH 552)
Enclosures
A-5
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ORGANIC CHEMICALS OR PLASTICS AND SYNTHETICS (Identify Category)
PART Z GENERAL INFORMATION
To be returned within 60 days of receipt to:
Robert B. Schaffer, Director
Effluent Guidelines Division
U.S. EPA (WB-552)
Washington, D. C. 20460
1. Name of Corporation
2. Address of Corporation Headquarters
Street:
City:
State; Zip Code
3. Name of Plant
4. Address of Plant
Street:
City:
State: 2ip Code
5. Name(6) of corporation personnel to be contacted for information
pertaining to this data collection portfolio.
Name Title fArea Code) Telephone
6. Plant NPDES Permit Number (s)
Date of expiration ____
If no permit, application number
Date of application
A-6
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Corporation
Plant
Citv State
7. Products produced at this plant site.
a. Indicate which of the products in list 1 (Plastics and Synthetics-
page 3) or list 2 (Organic Chemicals-page 4) that you produce at this
site and the production rate during the period January 1, 1975 to
September 30, 1976. If there is more than one process type for a
given product, identify and list each separately. The average daily
production while operating should match with the waste water data
tables in Part II.
Avg. Daily
Production Year
Design While Process
Product Process Capacity Operating Installed
Ibs/day Ibs/day
Attach additional pages, if necessary.
A-7
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LIST 1
PIASTICS g SYNTHETICS
ABS/SAN
Acrylic Resins
ADcyds and Unsaturated Polyester Resins
Cellulose Acetate Fiber/Resin
Cellulose Derivatives
Cellulose Nitrate
Cellophane
Epoxy Resins
£thylene-Vinyl Acetate Copolymers
Fluorocarbon Polymers
Melamine Resins
Nylon Resins/Fiber
Phenolic Resins
Polyamides
Polyester Resin/Fiber
Polyethylene
Polypropylene Resin/Fiber
Polystyrene
Polyurethane Resins
Polyvinyl Acetate
Polyvinyl Chloride
Rayon
Si li cones
rea Resins
A-8
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LIST 2
ORGANIC CHEMICALS
Aeetaldehyde
Acetic Acid
Acetone
Acetylene
Acrylates (includes acrylic add,
methacrylie acid, and esters)
Acrylonitrile
Adiponitrile
Aniline
Benzene
Benzole Acid
Bisphenol A
Caprolactam
Chloromethanes (Methyl Chloride,
Dichloromethyl, Chloroform, and
Carbon tetrachloride)
Citronellol
Coal Tar
Cumene
Cyclohexane
Dimethyl Terephthalate
Diphynylamine
Ethyl Acetate
Ethyl Benzene
Ethylene
Ethylene Dichloride
Ethylene Glycol
Ethylene Oxide
Formaldehyde
Bexamethylenedianine
Isobutylene
Isopropanol
Maleic Anhdride
Methanol
Meta-Xylene
Methyl Amines (including mono,
di, and tri methyl amine)
Methyl Ethyl Ketone
Methyl Salicylate
Ortho-Nitroaniline
Ortbo-Xylene
OxoChemicals
Para-Ajninophenol
Para-Cresol
Para-Mi troaniline
Para-Xylene
Phenol
Pbthalic Anhydride
Plasticizers (esters of
phthalic acid)
Propylene
Sec-butyl-alcohol
Styrene
Tannic Acid
Terephthalic Acid
Tetraethyl Lead
Toluene
Vinyl Acetate
Vinyl Chloride
A-9
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Corporation
Plant "m
City
State
c. Indicate which of the products in list 3 (Organic Chemicals - page
6) that you produce at this site and the production rate during the
period January 1r 1975 to September 30, 1976. If there is more than
one process type for a given product, identify and list separately.
The average daily production while operating should natch with the
waste water data tables in Part II.
Avg. Daily
Production Year
Design While Process
Product Process Capacity Operating Installed
Ibs/day Ibs/day
Attach additional pages, if necessary.
A-10
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LIST 3
ORGANIC CHEMICALS
Proplyene Oxide
Acetic Anhydride
Ethyl Alcohol, Synthetic
Adipic Acid
Cyclohexanone
Nitrobenzene
Tetrachloroethylene (Perchloroetbylene)
Propylene Glycol (1,2-Propanediol)
Diethylene Glycol
Tri chloroethy1ene
N-Butyl Alcohols (N-Propylcarbinol)
Di chlorodifluoromethane
Ethanolamines, Total
Trichlorofluoromethane
4,U-Isopropylidenediphenol (Bisphenol A)
2-Methoxyethanol (Ethylene Glycol
Monomethyl Ether)
2-Aminoethano1 (Monoe thanolamine)
Cresols, Total
Epoxidized Esters, Total
2,2-Zminodiethanol (Diethanolamine)
Trietbylene Glycol
Pentaerythritol
Eexamethylenetetramine, Tech*
Ortho-Dichlorobenzene
a-Chlorotoluene (Benzylchloride)
Funaric Acid
Dipropylene Glycol
Glutamic Acid, Monosodium Salt
Choline Chloride (All Grades)
Para-Nitrophenol and Sodium Salt
Pentachloropbenol (PCP)
Propionic Acid
Xylenesulfonic Acid, Sodium Salt
Aspirin
Acetic Acid Salts, Total
Methyl Bromide
Dodecyl Mercaptans
Salicylic Acid
Benzole Acid Salts: Sodium Benzoate, tech.
and U.S.P.
5-Nitro-Ortho-Toluenesulfonic Acid (SO3H-1)
Benzyl Alcohol
Benzoyl Peroxide
Castor Oil, Ethoxylated
2-Ethylhexanoic Acid (a-Ethylcaproic Acid)
2-£imethylaminoethanol
A-ll
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Corporation
Plant "
City State.
,-. List below all other products (not appearing on lists 1, 2 or 3}
manufactured at this sane site that account for at least one percent
of the plant* s total production. Minor products may be grouped in
this listing if the products are similar in nature and made by a
similar process. The products should be listed individually with a
total production indicated for the group in all instances where
grouping is used to report.
Avg. Daily
Production
Design While
Product Process Capacity Operating
Ibs/day Ibs/day
A-12
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Corporation
Plant "
City State.
d. List below products not in items 7a, b and c if they account for
an inordinate pollution load either in terms of pounds discharged per
1,000 pounds of production (RWL) or difficult treatment problems.
8. For each product indicated in response to Questions 7a and 7b of
Part I, attach a process flow diagram which identifies the unit
operations involved in each product manufacturing process and all
sources and quantities of waste waters from the process
operations. Show recycle loops for both process water and non-
contact cooling water and specify the blowdown control systems.
Indicate raw materials used and contact and non-contact water
entering each operation. Identify pollution control devices
associated with the process that have wastewater streams. Use
consistent units throughout; for example, gallons per hour or
pounds per hour. Supplement the diagram with a narrative
description for clarity or completeness where necessary.
The respondent may use process flow diagrams from EPA Development
Documents if representative of the process. The process diagrams
should be modified to include all requested information.
On each process flow diagram, clearly state whether the process
operational mode is batch, continuous or other. If the answer is
•other*1 the operational mode should be specified. If the process
is batch or semi-continuous, describe the length of cycle and
frequency.
9. Describe major process modifications made (to each process
described in response to Question 6) since January 1, 1972 that
significantly affect either the volume of flow, or the amount of
waste water pollutants per unit of production originating from
that process. Explain the purpose behind each of these
modifications. Give your best estimate as to the technological
age of each process installation as it now exists.
-------
Corporation
Plant
ttty State.
Give an analysis of the effect of mafcing the modification, i.e.r
describe the load and flow prior to the modification and after the
modification. Do you have future modifications for in-plant
control of waste water pollutants scheduled, if so, on which
processes? Specifically highlight any process changes that would
not be made except for pollution control. Include all such
changes in the process flow diagram of Item 8 using a separate
block wherever feasible.
A-14
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Corporation
Plant
City State.
*GANIC CHEMICALS OR PLASTICS AMD SYNTHETICS (Identify Category)
iRT II HATER USE, RE-USE, AND DISCHARGE
:> be returned within 60 days of receipt to:
Robert Scbaffer, Director
Effluent Guidelines Division
U.S. EPA (WH-552)
Washington, D. C. 20460
• Hater Use. Total Plant Needs During the Period
January 1. 1975 to September 30. 1976
List below for your plant the sources and quantities of water used
and describe the disposition of waste waters. If a time period of
less tban January 1, 1975 to September 30, 1976 is used, state the
reason that the values used are representative of that period.
Hater Source:
Time Period
of Calculation
Municipal mgd (average value)
Surface mgd
Ground ________ »gd
Other (specify) mgd
3. Uses:
Non-contact cooling mod
Direct process contact (as diluent, solvent,
carrier, reactant, by-product,
cooling, etc.) mgd
Indirect process contact (pumps,
seals, etc.) mgd
Non-contact ancillary uses (boilers,
utilities, etc.) mgd
Maintenance, equipment cleaning
and work area washdown mqd
Air pollution control mod
Sanitary and potable mod
Other (specify) mgd
A-15
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Corporation
Plant
Citv State.
j. Source of waste water flows:
Non-contact cooling mgd ________
Direct process contact mad _____
Indirect process contact mod __.____.____,
Won-contact ancillary uses mad _______
Maintenance, equipment cleaning
and work area wasbdown mod _______
Air pollution control mad ________
Sanitary/Potable water mad _______
Storm water (collected in
treatment system) mod ________
Other (specify) mod _______
D. Process or Process Contaminated Waste Water Discharged To:
(Do not include cooling water, boiler blowdown, etc.)
Surface water or storm sewer
Treated mad __________
Untreated mod __________
Municipal Sewage Treatment Plant mod _________
Deep well mod _________
Other (Specify and describe »od ____________
briefly)
2. Quality of Water Discharged;
For the period January 1, 1975 to September 30, 1976, summarize
your influent, effluent and raw waste loads in Tables A, fi, C, D
and £. If data for individual waste streams are not available,
information for combined waste streams should be furnished which
represents the greatest degree of detail available. The tables
are located at the end of this section.
Instructions for Completing Tables AX B^ C^. D and jg:
For Tables A, fi, C, D and £, use the following definitions and
notes. The period covered should correspond with that used for
Part I question 7 to calculate average daily production.
Flow - Do not include rainfall runoff, unless it is collected
in the treatment system. If, collected, estimate the percent
of total flow which is attributed to this source.
Average day - Should represent the average of the data period
covered.
Significant parameters - Those potential pollutants not
specifically listed, but which are introduced into the waste
streams as a result of materials used, product produced,
process used and for which you have test data.
A-16
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Corporation.
Plant
City State,
Identify all data which results from abnormal operating or
other conditions.
If use of a different time period (a portion of the time
period January 1, 1975 to September 15, 1976) results in more
adequate representation of the pollution loads, you may do so
if the time period is not less than six months. You should
specify the time period and explain why that period is more
re pr e sen tati ve.
Table A - Complete Table A for the combined influent to
each treatment facility.
Table B - Complete Table fi for each untreated waste
discharge point (to surface waters, deep veils, land
application, etc.)
Table C - Complete Table C for the treated effluent from
each treatment facility. Hot applicable to plants that
have not yet installed waste treatment facilities. This
section is not restricted by type of treatment.
Table D - Complete Table 0 for the process wastewaters
from each of the product/process lines identified in
Part I, items 7a and 7b. Do not include non-contact
cooling waters but do include all contact cooling
waters. If measured values are not known or not
available, ' supply the best estimate available and
specify the basis for the estimate. The production
basis should be the same as the average daily production
while operating that was given din Part Z.
Table £ - Complete Table £ for the plant intake water.
3. Attach the water analysis data summary sheets shoving the daily
water analyses that were used to compute Tables A through £, e.g.
monthly summary tables. Also include any data for the period
January 1, 1975 to September 30, 1976 that was omitted in Tables A
through £ as not being representative.
4. The method of sample collection for the data supplied in response
to Question 2, Tables A, B, C, D and £, should be specified (e.g.,
daily grab sample, 8 hour flow composited, 24 hour continuous,
etc.).
5. Indicate all parameters listed in Part II, tables A through Z,
which were not measured by EPA approved methods.
A-17
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A-18
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A-19
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CltT *lBt»-
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•• i
-------
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Mica)
(*C) -
(*C) -
(Ik./l.OOO ih.)»«
ee* (iks/i.eeo ik»)
TOC (Ifc./l.OOO lk«)
XSS (lk«/i.OOO Iks)
TVS Uk
-------
TABI.C I
IRTAKt VAlik
rt»c*»*
TIM »•
Calendar
CMC»)
CM M
Alt
COD
T»C
TS8
TBS Uk»/4«y>
TU •• K
•tk«r«
A-22
-------
Corporation
Plaint
City State.
6. fias the seed used in the BOD5 test been acclimated to the waste
waters that have been tested?
Yes No
If yes, what is the source of the seed?
A ___ sewage treatment plant
fi __ plant treatment facility
C __ laboratory acclimation
D __ other explain ______.______________«.
A-23
-------
Corporation
Plant "
City State.
ORGANIC CHEMICALS^OR PIASTICS AND SYNTHETICS (Identify Category)
PART III TREATMENT TECHNOLOGY
To be returned within 60 days of receipt to:
Robert B. schaffer. Director
Effluent Guidelines Division
U.S. EPA (WH-552)
Washington, D. C. 20460
have a treatment system(s) at this plant?
If yes, complete the following and attach a separate flow sheet for
each distinct treatment facility indicating waste streams treated,
unit sizes of treatment equipment, detention times, recycle rates,
effluent concentration or design criteria and other pertinent
engineering information for operation of the treatment facility.
Include treatment of storm runoff, where applicable.
*ndicate the process lines for which any portion of the waste water
xow is diverted to separate treatment, pretreatment or disposal (e.g.
deep well, solvent recovery, incineration, etc.). Which portions are
so diverted and which portions are combined for joint treatment?
For each treatment facility complete the following:
Name of Facility
Source(s) of Haste Water
Cost f1976 dollars)
1 a. Original installation
(Battery limits of treatment plant only)
b. Other costs (include collection
system, piping, pumping, etc.)
2 Estimated replacement cost
3 Estimated total capital expenditure
for this facility to date
Annual cost of operation and maintenance
(exclude depreciation and debt service cost)
last major modifications or additions since original installation and
A-24
-------
Corporation
Plant "
City State
state the purpose of the modification or addition.
Treatment Cost Pur;
•iodification-Addition Facility Year (1976 Dollars)
6 List scheduled modifications or additions and estimated date of complei
and state the purpose of the modification or addition.
Treatment Cost Purj
Codification-Addition Facility Year H976 Dollars)
7 is nutrient addition practiced:
Yes No
8 Bow many employees (equivalent man-years/year) are primarily engaged
as operators of the waste water treatment facility? (exclude maintenanc
Bow many employees (equivalent man-years/year) are engaged as support
personnel for the waste water treatment facility?
9 Is an operator always present?
Yes No
10 Quantity of wastewater treatment facility solid wastes disposed
of at present (dry basis)
Ibs/dav
A-25
-------
Corporation
Plant "
City State.
11 Moisture content of waste solids disposed of at present
% moisture
12 Present disposition of solids
13 Estimated annual cost of solids handling and disposal (1976 dollars)
S/ton dry basis
14 Planned future disposition of solids:
15 What are the total annual energy requirements for the treatment
facility?
Electrical Kwhr
Other (e.g. Beat) Btu
16 For discharges of industrial wastes to municipal treatment plants
are there local pretreatment regulations applying to you?
Yes NO .
Zf yes, reference those regulations and attach a copy.
A-26
-------
Corporation
Plant "
City State
j. carbon Sorption Technology.
Jave you determined carbon sorption isotherms
>n your waste waters? . ___
Yes No
lave carbon sorption isotherms been determined
:or waste waters from your plant(s) by a person(s)
>ther than company personnel? _ —_
iave you or anyone else evaluated carbon
:olumns on waste waters from this plant? __ ___
>o you have carbon sorption data from
rour plant (s) on:
raw wastes _ ___
biologically treated wastes ___ ___
individual process lines ___ __
combined process lines ___ __
pilot plant studies ^__ ^^^
contractor evaluations ___ __
cost evaluations ^^ _-
plant scale evaluations ___ ___
operational units ___ __—>
or each question above which was answered affirmatively*
ive a brief description of the data (source and types of wastes,
eriod of time covered, plant involved, extent of data base and
ontact personnel suggested) in the space below.
A-27
-------
Corporation
Plant
Citv State
w. Filtration
fiave you done filtration studies on your waste waters
(sand, multi-media, etc.) beyond what was described
in Section A, Part III? _ Yes ___ Ho
If yes, give a brief description of the data (source and types of
wastes, period of time covered, process stream involved, extent of
data base and contact personnel suggested) in the space below.
Biological Treatment
~~ive biological treatability studies been
^nducted on your wastewaters beyond what was
described in Section A, Part III? Yes No
If yes, give a brief description of the data and results (source and
types of wastes treated, duration of the study, extent of data base,
conclusions of study, and contact personnel suggested) in the space belov
£. Save other treatability studies, beyond what
vas described in Section A, Part III, employing
treatment processes such as sedimentation, neutral-
ization, hydrolysis, precipitation, oxidation/
reduction, ion exchange, phenol recovery, etc,,
heen run on any of the process wastewater streams
om the plant? __ Yes
If yes, list on a separate sheet those product/process
streams from which such treatability studies were conducted.
Identify the sheet as response to III-E.
A-28
-------
308 BAT QUESTIONNAIRE
A-29
-------
,yp UNITED STATES ENVIRONMENTAL PROTECTION AG€NCY
^ WASHINGTON. D C. 20460
Dear Sir:
As you may be aware, we are in the process of reconsidering and re-
issuing regulations with respect to water pollutants discharged as a
result of the manufacture of organic chemicals and plastics and
synthetics. The earlier regulations were issued as 40 C.F.R. Parts
414 and 416, respectively.
The reconsideration of organic chemicals is a result of a joint stipu-
lation filed in the Fourth Circuit Court of Appeals entered into on
behalf of companies in the industry and the Environmental Protection
Agency. The stipulation requires the Agency to obtain new and more
reliable data and requires the industry to cooperate in the gathering
and furnishing of data necessary to formulate regulations for the
organic chemicals manufacturing point source category.
The reconsideration of plastics and synthetics results from the remand
by the Fourth Circuit Court of Appeals of the EPA regulations promul-
gated on April 5, 1974. The Court ordered the EPA to restudy areas
where the record was ruled to be inadequate.
To Implement these reconsiderations, the Agency collected additional
information on the production processes, raw waste loads, treatment
methods and costs and effluent quality associated with the manufacture
of these materials in a data portfolio mailed to your company on
October 18, 1976. The Environmental Protection Agency is again solic-
iting your cooperation in obtaining information to supplement those
data previously requested. This portfolio seeks Information not
requested 1n the prior portfolio, particularly with regard to the
presence or absence of the priority pollutants.
According to our records, your Corporation produces one or more of the
products on the attached list(s) (Part I) which were covered by the
referenced regulati ons.
The information requested shall be provided for each plant of your
firm in the format of the attached portfolios. This will allow the
Agency to correlate and make available to interested parties the re-
sults of the data gathered. If our records are incorrect and you do
not feel that the requested information is related to your plant
(i.e., you no longer manufacture the products listed or do not produce
them at this site), please inform us as soon as possible. If you have
supplied EPA previously with the information requested, you need not
do so again, however, please indicate to whom you submitted the data.
A-30
-------
The purpose of this request is to gather all available, pertinent in-
formation and is not designed to create an undue burden on your plant
personnel. Please return the portfolio to the Agency as soon as
possible, but in no event later than sixty days after receipt of the
letter.
For your convenience, the form is divided into three parts, with
descriptive headings and instructions for completing the portfolio.
Please answer all items in each part of the portfolio. If a question
is not applicable to a particular facility, indicate by writing "Not
Applicable". If an item is not known, indicate unknown and include an
explanation of the reason for not knowing such information. If an
item seems ambiguous, complete as best as possible and state your
assumptions in clarifying the apparent ambiguity. Also, submit copies
of the summary data sheets compiled or used in completing the tables
in this form.
The Agency will review the information submitted and may, at a later
date, require site visits and additional sampling in order to complete
the data base.
Addenda A and B attached are a part of this letter. They provide you
with information regarding the legal authority for requiring the com-
pletion of the portfolio and your options for requesting that certain
information be held confidential.
Thank you in advance for the cooperation of your company. The
Environmental"Protection Agency is committed to promulgating effluent
regulations which are in accordance with the Federal Water Pollution
Control Act and which are reasonable. The Agency has found that only
with complete cooperation of all parties concerned can thoughtful and
fair regulations be published. I am confident that we can anticipate
your assistance 1n carrying out that goal.
Should you have any questions regarding this request, please do not
hesitate to contact Paul Fahrenthold with respect to organic chemicals
at (202) 426-2497 or Michael Kosakowski at (202) 426-2497 with respect
to plastics and synthetics.
Sincerely yours,
Robert B. Schaffer, Director
Effluent Guidelines Division (WH-552)
Enclosures
A-31
-------
ADDENDUM A: AUTHORITY
This request for information is made under authority provided by
Section 308 of the Federal Water Pollution Control Act, 33 U.S.C.
61318. Section 308 provides that; "Whenever required to carry out the
objective of this Act, including but not limited to ... developing
or assisting in the development of any effluent limitation . . .
pretreatment standard, or standard of performance under this Act" the
Administrator may require the owner or operator of any point source to
establish and maintain records, make reports, install, use and
maintain monitoring equipment, sample effluent and provide "such other
information as he may reasonably require." In addition, the
Administrator or his authorized representative, upon presentation of
credentials, has right of entry to any premises where an effluent
source is located or where records which must be maintained are
located and may at reasonable times have access to and copy such
records, inspect monitoring equipment and sample effluents.
A-32
-------
ADDENDUM B: CONFIDENTIALITY
Information may not be withheld from the Administrator or his
authorized representative because it is confidential. However, when
recuested to do so the Administrator is required to consider
information to be confidential and to treat it accordingly if
disclosure would divulge methods or processes entitled to protection
as trade secrets. EPA regulations concerning confidentiality of
business information are contained in 40 CFR Part 2, Subpart B, 41
Fed. REG. 36902-36924 (September 1, 1976). These regulations provide
that a business may, if it desires, assert a business confidentiality
claim covering part or all of the information furnished to EPA. The
n.anner of asserting such claims is specified in 40 CFR 82.203(b).
Information covered by such a claim will be treated by the Agency in
accordance with the procedures set forth in the Subpart B regulations.
In the event that a request is made for release of information covered
by a claim of confidentiality or the Agency otherwise decides to make
a determination whether or not such information is entitled to
confidential treatment, notice will be provided to the business which
furnished the information. No information will be disclosed by EPA as
to which a claim of confidentiality has been made except to the extent
and in accordance with 40 CFR Part 2, Subpart B. However, if no claim
of confidentiality is made when information is furnished to EPA the
information may be made available to the public without notice to the
business.
Effluent data (as defined in 40 CFR 62.302(a)(2)) may not be considered
by EPA as confidential. In addition, any information may be disclosed
to other officers, employees or authorized representatives of the
United States concerned with carrying out the Federal Water Pollution
Control Act or when relevant in any proceeding under this Act.
A-33
-------
Instructions for Completing the Attached Questionnaire
Part I
1. Questions 1 through 6: You may have completed these items in response to
our previous industry survey. If these items have changed please bring them
up to date. In addition, indicate in Item 5 the location of the persons
familiar with your response to the questions.
2. Question 7: Lists 1, 2 and 3 on Pages 8, 9 and 10 represent the group of
products for which a limited data base exists. In order to insure the con-
tinued usefulness of the existing data base, current production data for
existing and new plants producing chemicals on Lists 1, 2 and 3 is necessary.
The previous questionnaire required the reporting of all "minor" products
(defined as being greater than one percent of total production). You are
now requested to report the production or use volumes of'all chemicals on
List 4, if they were not previously reported as greater than one percent of
total production, regardless of the production or usage rate.
Part II
1. Tables A through E: Place in the columns of the .tables labeled "Analytical
Results - Concentration ranges - parts per billion" the number of analytical
results which have been obtained, in the range indicated at the top of the
column. The column labeled "Method" should be filled with the analytical
methodology used for the analyses. (For example: gas chromatography,UV
spectrophotometry, IR spectrophotometry, NMR, or wet chemistry.) It is not
essential to itemize each analysis. If the number of analyses is greater than
100, estimate as accurately as possible the actual number of analyses.
Specify the concentration units used in completing the table - define all
abbreviations used.
Part III
For the purposes of Part III of the questionnaire the concept of a "set" of
effluent data will be very helpful. A "set" of effluent data contains the
following items:
(1) a list of all activated sludge plants located at a facility with the
product/process wastewater lines discharging to that facility clearly listed;
(2) a summary of long-term data in the format as requested in Tables A and C
of this part (the last two pages of Part III): and
(3) a short summary of specific wastewater parameters which are essential in
determining the effectiveness of the biological treatment plant at your facility.
A-34
-------
The questions in this part are designed to supplement data previously supplied
by requesting all or parts of Items 1, 2 and 3 above. The questions will
provide a means of effective performance evaluation of the existing waste-
water treatment plants.
1. Question 2: If you feel that recent production levels or wastewater
treatment plant data are mere representative than data included in your
previous submission you may submit a new set of data.
2. Question 3: In Part A, clarification is being requested to enable the
Agency to identify specific product/process wastewater lines entering
treatment facilities. Fart B requests summer/winter performance data from
the plant to determine the effectiveness of the biological treatment system
in place. The evaluation of treatment effectiveness is necessary to establish
the effect of operating conditions on the cost of waste treatment.
3. Question 4: For new plants or modified plants, a full set of information
is requested.
Example tables are attached for reference.
A-35
ii
-------
EXAMPLE TABLE A,B,C,D or E.
PRIORITY
POLLUTANT
BENZENE
ETHYLENE
DI CHLORIDE
CHROMIUM
CHROMIUM
UNITS
PPM
PPM
PPM
PPB
CONCENTRATION RANGES
CIO
2
3
0
6
10-100
25
2
5
1
100-1000
20
6
6
0
>1000
1
2
2
0
ANALYTICAL METHOD
GC-Flame Detector
GC-EC Detector
Atomic Absorption
Wet Chemical - SULFATE
NOTE: For Units, use standard wastewater abbreviations, such as:
parts per million - ppm
parts per billion - ppb
Line 1 indicates 48 analytical results in the ranges shown.
A-36
iii
-------
EXAMPLE RESPONSE TO QUESTION 7d
la
Product/
Process Line
Aromatics
Aklylation
Description of the Process
Modification or In-Process
Control
Steam stripper installed
on raw waste line to
treatment plant.
Intended Objective of
the Modification or
Control System
remove benzene, toluene,
xvlene, ethylbenzen* to
ppm level.
b Quantify the results of the use of the Modification or PC System
Parameter
Benzene
Toluene
Xylene
Effluent Parameter
Value Before Modification
40 ppm, 25 gpm
60 ppm, 25 gpm
10 ppm, 25 gpm
Effluent Parameter
Values After Modification
5 ppm, 20 epm
2 ppm, 20 gpm
10 ppm, 20 gpm
Repeat the above table for each modification
a
b Parameter
Effluent Parameter
Value Before Modification
Effluent Parameter
Values After Modification
+Flow and concentration if possible
A-37
-------
308 LETTER QUESTIONNAIRE FOR THE ORGANIC CHEMICALS AND PLASTICS AND
SYNTHETICS MANUFACTURING POINT SOURCE CATEGORIES
PART I
GENERAL INFORMATION AND PRODUCT-PROCESS INFORMATION
To be returned within 60 days from date of receipt to:
Robert B. Schaffer, Director
ATTN: P. D. FahrenthoLd
Effluent Guidelines Division
U.S. EPA (WH-552)
Washington, D. C. 2046-)
1. Name of Corporation
Address of Corporation Headquarters
Street:
City:
State:
Name of Plant
Zip Code:
Address of Plant
Street:
City:
State:
Zip Code:
Name(s) of personnel to be contacted for information pertaining to this data
collection portfolio
Location
Name and Title Telephone (plant or Cor?.
A-38
-------
Corporation_
Plant
City State
Plant NPDES Permit Number^
Date of Exoiration
If No Permit, Application Number_
Date of Application
This question consists of four parts, some or all of which may apply to your
facility. The parts of the question are labeled i through iv, corresponding
to questions 7a, 7b, 7c and 7d. Where questions relate to Lists 1, 2, or 3
an update of the previously submitted portfolio (October 18, 1976) is intended
The heading beside the question and the Instructions provide more detail re-
garding the intent of the questions.
Has your plant (since October 18, 1976)
i. Added new production processes for chemicals on Lists 1, 2, 3, or does it
use or produce either as a product, by-product or intermediate any
chemical on List A.
ii. Changed design production capacity or average daily production ay
means of debottlenecking, removal/replacement of process equipment,
etc.
iii. Discontinued production process(es) that is(are) on Lists 1, 2 or
3 (see Part I, Pages 7, 8 and 9).
iv. Installed any new process modifications or in-plant controls which
affect raw waste characteristics.
II None Apply. Proceed directly to Part II.
1 1 Some or all Apply. Continue through Part I.
I J The data submitted in response to the October 18, 1976, request
substantially represents current plant operations. Proceed to
Question 1, Part II.
A-39
-------
Corporation
Plant ~
City
State
7a. If your facility has added the production Of new processes for chemicals on
Lists 1, 2 or 3, please coraolete the table below using the units indicated.
Product
Process
Design
Capacity
(Ibs/day)
Avg. Daily
Production
While
Operating
(Ibs/day)
Date
Process
Installed
Ciear. Month)
Attach additional pages, if necessary.
A-40
PART I - Pace 3
-------
Corporation
Plant ~
City
Stats
7a. (Continued)
Do you produce as a product or intermediate, consume, package or use* as a
diluent, solvent, raw material (feedstock) or intermediate in any narmer
other than in laboratory research or analytical programs any of the 129
priority pollutants (see Part II, Pages 2 and 3) which were not reported
in the previous questionnaire dated October 18, 1976? If so, please list
these below.
Product
Process
Design
Capacity
(Ibs/day)
Avg. Daily
Production
While
Operating
(Ibs/day)
Date
Process
Installed
(Year. Mont
Attach additional pastes, if necessary.
*the word "use" in this context excludes uses or production of less than 1000 Ibs p<
year in any research, pilot or laboratory operation.
A-41
PART T -
-------
Corporation
Plant
City State
7b. If your plant has changed design production rate or average daily production
rate throup.h orocess modifications which involve debottlenecking of certain
unit operations by the modification or replacement of equipment, or expansion
or other similar projects, please complete the table below using the units
indicated for products on Lists 1, 2, 3 and 4.
Avg. Daily
Production Date
Design While Process
Product Process Caparity Operating Changed
(Ibs/dav) (Ibs/dav) (Year, Month)
Attach additional pages, if necessary.
A-42
-------
Corporation
Plant
City State
7c. If your plant has discontinued, since October 18, 1976, the production of any
product on List 1, 2 or 3, please complete the table below using the units
indicated.
At your discretion, you may indicate the reasons for the discontuance. For
example, was the process line technologically out of date and too costly to
update; were applicable environmental controls prohibitive; etc.
Date
Discontinued
Product Process (Year, month) Reason for Discontinuan
A-43
-------
Corporation^
Plant ~
City
State
7d. If you have installed any process modifications (reactor design, distillation
column operating conditions, etc.) or in-plant controls, (steam stripping,
solvent extraction, etc.) since October 18, 1976, which either sj.gnificantly
affected or were designed to reduce the raw waste loads (flow or composition)
of wastewater discharged to either a treatment facility or direccly to surface
waters, please complete the following table.*
I Product/Process
! line
i
la.
Description of the Process
Modification or in-Process
Control
Intended Objective of the
Modification or Control System
e.g. remove volatile organics.
b. Quantify the results of the use of the modification or process control system.
Parameter
Effluent Parameter
Values* Before Modification
Effluent Parameter
Values"*" After Modification
Repeat the above table for each modification
2a
b. Parameter
Effluent Parameter
Values Before Modification
Effluent Paramters
Values After Modification
+ Wastewater flow and pollutant concentration if possible.
*Attach additional tables, if necessary (photocopy this page).
*Attach flow diagrams or drawings, if appropriate.
A-44
PART I - Page 7
-------
LIST 1
PLASTICS & SYNTHETICS
ABS/SAN
Acrylic Resins
Alkyds and Unsaturated Polyester Resins
Cellulose Acetate Fiber/Resin
Cellulose Derivatives
Cellulose Nitrate
Cellophane
Epoxy Resins
Ethylene-Vinyl Acetate Copolymers
Fluorocarbon Polymers
Melamine Resins
Nylon Resins/Fiber
Phenolic Resins
Polyamides
Polyester Resin/Fiber
Polyethylene
Polypropylene Resin/Fiber
Polystyrene
Polyurethane Resins
Polyvinyl Acetate
Polyvinyl Chloride
Rayon
Silicones
Urea Resins
A-45
BADT T _ T>~~« 3
-------
LIST 2
ORGANIC CHEMICALS
Acc-taldehyde
Acetic acid
Acetone
Acetylene
Acrylates (includes acrylic acid,
methacrylic acid, and esters)
Acrylonitrile
Adiponitrile
Aniline
Benzene
Benzoic acid
Bisphenol A
Caprolactam
Chloromethanes (Methyl Chloride,
Methylene Chloride, Chloroform,and
Carbon tetrachloride)
Citronellol
Coal Tar
Cumene
Cyclohexane
Dimethyl terephthalate
Diphenylamine
Ethyl acetate
Ethyl benzene
Ethylene
Ethylene dichloride
Ethylene glycol
Ethylene oxide
Formaldehyde
Hexame chylened1 ami n e
Isobutylene
Isopropanol
Maleic Anhydride
Methanol
meta-Xylene
Methyl amines (including mono-
di- and tri-methyl amine)
Methyl ethyl ketone
Methyl salicylate
ortho-Nitroaniline
ortho-Xylene
Oxo-Chenicals
para-Aminophenol
para-Cresol
para-Nitro aniline
para-Xylene
Phenol
Phthalic anhydride
Plasticizers (esters of
phthalic acid)
Propylene
sec-Butyl-alcohol
Styrene
Tannic acid
Terephthalic acid
Tetraethyl lead
Toluene
Vinyl acetate
Vinyl chloride
A-46
PART I - Page 9
-------
LIST 3
ORGANIC CHEMICALS
Acetic acid salts, Total
Acetic anhydride
e<-Chlorotoluene (Benzyl chloride)
Adipic acid
2-Asinoethanol (Monoethanolamine)
Aspirin
Benzyl alcohol
Benzoyl peroxide
Benzoic acid salts: Sodium Benzoate, technical
and U.S.?. grades
Castor Oil, Ethoxylated
Choline chloride (All Grades)
Cresols, Total
Cyclohexanone
Dichlorodif luoromethane
Diethylene glycol
2-Diaethylaminoethanol
Dipropylene glycol
Dodecyl mercaptans
Ethanolamines, Total
Ethyl alcohol, Synthetic
2-Ethylhexanoic acid (ot-Ethylcaproic Acid)
Epoxidized esters, Total
Fumaric acid
Glutamic acid, Monosodium salt
Hexamethylenetetramine, Technical grade
2,2-Iminodiethanol (Diethanolamine)
4,A-Isopropylindenediphenol (Bisphenol A)
2-Methoxyethanol (Ethylene Glycol
Monomethyl Ether)
Methyl bromide
N-Butyl Alcohols (N-Propyl carbinol)
Nitrobenzene
5-Nitro-ortho-toluenesulfonic acid (S03H-1)
ortho-Dichlorobenzene
para-Nitrophenol and Sodium salt
Pentachlorophenol (PCP)
Pentaerythritol
Propionic acid
Propylene glycol (1,2-Propanediol)
Propylene oxide
Salicylic acid
Tetrachloroethylene (Perchloroethylene)
Trichloroethylene
Trichlorofluoromethane
Triethylene glycol
Xylenesulfonic acid, Sodium Salt
A-47
-------
Corporation
Plant
City State
PART II
INTRODUCTION
The objective of this part is to obtain information related to the analysis of
wastewaters, and the detection, quantification and treatment of the 129 priority
pollutants named on List 4. The logic flow of the questions in this section is
as follows:
(1) Identify which wastewater streams have been analyzed for the
129 priority pollutants.
(2) Report the analytical results for those streams where compounds
on List 4 have been detected.
(3) Describe all efforts of any scale directed toward the removal
of one or more compounds on List 4 by a wastewater treatment
or In-process control system since October 1972.
1. The identification of compounds on List 4 has been categorized into three
areas as follows: (please check the appropriate box)
I -1 a. No analyses have been conducted for any of the compounds oa
List 4. Please go to Question 4 of Part II.
I 1 b. Wastewaters have been analyzed for some of the compounds or
List 4. Please go to Question 2 of Part II.
I I c. Wastewaters have been analyzed for some of the compounds on
List 4 (e.g., metals, etc.) and part of the data was reported
in the previous Section 308 questionnaire (October 18, 1976).
Those priority pollutants previously reported are as follows:
Please go to Question 2 of Part II and report on those not included in the
previous questionnaire. If there are no additional List 4 pollutants to
those listed above, please go to Question 4 of Part II.
A-48
PART II - Page 1
-------
LIST 4
129 PRIORITY POLLUTANTS
Compound Name
acenaphthene
acrolein
acrylonitrile
benzene
benzidine
carbon tetrachloride
(tetrachlorome thane)
chlorobenzene
1,2,4-trichlorobenzene
hexachlorobenzene
1,2-dichloroethane
1,1,1-trichloroethane
hexachloroethane
1,1-dichloroethane
1,1,2-trichloroethane
1,1,2,2-tetrachloroethane
chioroethane
bis(chloromethyl) ether
bis(2-chloroethyl) ether
2-chloroethyl vinyl ether
(mixed)
2-chloronaphthalene
2,4,6-trichlorophenol
chloroform (trichloromethane)
2-chlorophenol
1,2-dichlorobenzene
1,3-dichlorobenzene
1,4-dichlorobenzene
3,3'-dichlorobenzidine
1,1-dichloroethylene
1,2-trans-dichloroethylene
2,4-dichlorophenol
1,2-dichloropropane
1,2-dichloropropylene
(1,3-dichloropropene)
2,4-dimethylphenol
2,4-dinitrotoluene
2,6-dinitrotoluene
1,2-diphenylhydrazine
ethylbenzene
fluoranthene
Compound Name
4-chlorophenyl phenyl ether
4-bromophenyl phenyl ether
bis(2-chloroisopropyl) ether
bis(2-chloroethoxy) methane
methylene chloride (dichlorometh.j.ne)
methyl chloride (chloromethane)
methyl bromide (bromomethane)
bromoform (tribromomethane)
dichlorobromomethane
trichlorofluoromethane
dichlorodifluoromethane
chlorodibrocomethane
hexachlorobutadiene
hexachlorocyclopentadiene
isophorone
naphthalene
nitrobenzene
2-nitrophenol
4-nitrophenol
2,4-dinitrophenol
4,6-dinitro-o-cresol
N-nitrosodime thylamine
N-nitrosodiphenylamine
pentachlorophenol
phenol
bis(2-ethylhexyl) phthalate
butyl benzyl phthalate
di-n-butyl phthalate
di-n-octyl phthalate
diethyl phthalate
dimethyl phthalate
benzo (at) anthracene
(1,2-benzanthracene)
benzo («) pyrene (3,4-benzopyrene)
3,4-benzofluoranthene
benzo(k)fluoranthane
(11,12-benzofluoranthene)
chrysene
acenaphthylene
anthracene
benzo(ghi)perylene (1,12-benzoperylene)
A-49
PART II - Page 2
-------
LIST 4
129 PRIORITY POLLUTANTS
(Continued)
Compound Name
fluorene
phenanthrene
dibenzo (a,h) anthracene
(1,2,5,6-dibenzanthracene)
indeno (l,2,3-cd)pyrene
(2,3-o-phenylenepyrene)
pyrene
tetrachloroethylene
toluene
trichloroethylene
vinyl chloride
(chloroethylene)
aldrin
dieldrin
chlordane (technical mixture
& metabolites)
4,4'-DDT
4,4'-DDE (p,p'-DDX)
4,4'-DDD (p,pf-TDE)
a-endosulfan-Alpha
b-endosulfan-Beta
endosulfan sulfate
endrin
endrin aldehyde
heptachlor
heptachlor epoxide
a-BHC-Alpha
b-EHC-Beta
r-BHC (lindane)-Gamma
g-BHC-Delta
PCB-1242 (Arochlor 1242)
PCB-1254 (Arochlor 1254)
PCB-1221 (Arochlor 1221)
PCB-1232 (Arochlor 1232)
PCB-1248 (Arochlor 1248)
PCB-1260 (Arochlor 1260)
PCB-1016 (Arochlor 1016)
Toxaphene
Compound Name
Antimony (Total)
Arsenic (Total)
Asbestos (Fibrous)
Beryllium (Total)
Cadmium (Total)
Chromium (Total)
Copper (Total)
Cyanide (Total)
Lead (Total)
Mercury (Total)
Nickel (Total)
Selenium (Total)
Silver (Total)
Thallium (Total)
Zinc (Total)
2,3,7,8- tetrachlorodibenzo-
p-dioxin (TCDD)
A-50
PART II - Page 3
-------
Corporation
Plant
City State_
2. Complete Tables A through £ on the following pages with the results of
analyses of wastewaters from processes at the plant site. Include in the
tables the names of priority pollutants detected and quantified by the
analyses of wastewaters, at the locations described in Tables A through E.
Table A: Complete this table with the influent raw waste loac.ings
to either on-site treatment or pre-treatment facilities.
Table B: Complete this table for those process wastewaters which are
discharged without treatment to surface waters or to municipal
treatment (POTW). Do not include storm waters or nun-contact
cooling waters.
Table C: Complete this table for treatment plant effluents discharged
to surface waters or pre-treatment facility efflue-its prior
to discharge to a POTW.
Table D: Complete this table for individual product or process waste
streams where priority pollutants have been identified as a
constituent. Express values obtained for the priority pollutar.
in terms of unit raw waste loading, e.g. (Ib priority pollutant
1000 Ib product).
Table E: Complete this table for priority pollutants found In the plant
intake raw water supply. Its purpose is to establish appropria
background levels.
PLEASE READ THESE NOTES BEFORE COMPLETING THE TABLES;
Please identify all treatment or pre-treatment plants for which Tables A
through E apply by a specific designation—especially if more than one
facility exists. Use the same name as on the previous 308 letter respons
If possible.
Tables A and C should be influent and effluent of the same facility and
identified by the same name.
Place the number of analytical results which fall within the concentratio
ranges shown in the appropriate columns of each table. Please use ap-
propriate concentration ranges such as parts per million, part per billio
A-51
PART II - Pace 4
-------
Corporation
Plant I
City
State
TABLE A
COMBINED RAW WASTE TO TREATKEOT FACILITIES
Complete this table for each treatment or pre-treatment facility at the plant site.
Report the results of analyses performed on the influent wastewater to eitne.r com-
bined on-site treatment or a pre-treatment facility, for each facility (photocopy
the blank page, if necessary).
Treatment/Pretreatment Facility Name
Treatment Unit Processes included in the Treatment/Pretreatment Facility
Identify the Product/Process lines which generated the vastevaters for which the
analytical results below apply.
Results presented in the table below were obtained from analyses made
I 1 Prior to January 1, 1973
After January 1, 1973, approximate
date
Process Wastewater Flow
(million Gal/Day)
min.
avg.
max.
Priority
Pollutant
UNITS
CONCENTRATION RANGES
<10
10-100
100-1000
>1000
Analytical Method
PART II - Page 5
-------
Corporation
Plant "
City
State
TABLE B
UNTREATED PROCESS WASTEWATER DISCHARGED TO SURFACE WATER OR TO MUNICIPAL TREATMENT
Complete this table with the results of analyses performed on each undiluted pro-
cess wastevater stream discharged without treatment to surface waters or to muni-
cipal treatment. (Photocopy the blank page, if necessary.)
Product/Process producing wastewater_
or
Wastewater Source
Discharge Point
Time Period Represented^
by the Results
Results presented in the table below were obtained from analyses made
I 1 Prior to January 1, 1973
l__l After January 1, 1973, approximate
date
Process Wastevater Flow
(million GAL/DAY)
min.
avg.
max.
FSIORTTT
POLLUTANTS
UNITS
CONCENTRATION RANGES
<10
10-100
100-1000
>1000
ANALYTICAL METHOD
A-B3
PART TT - Pawn
-------
Corporation,
Plant "
City
State
TABLE C
PROCESS WASTEWATER DISCHARGED FROM FINAL TREATMENT OR PRETREATMENT FACILITIES
Complete this table with the results of analyses performed on the effluent from each
wastewater treatment plant or pretreatment plant. (Photocopy the blank page., if
necessary.)
Treataient/Pretreatment Facility Name
Discharge Point of the Treatment/Pretreatinent facility:
Results presented in the table below were obtained from analyses made
Prior to January 1, 1973 I I After January 1, 1973, approximate
date
Process Wastewater Flow
(million GAL/DAY)
min.
avg.
max.
'RIORITY
'OLLUTANTS
UNITS
CONCENTRATION RANGES
<10
10-100
100-1000
I
>1000
ANALYTICAL METHODS
-------
Corporation
Plant '^
City
State
TABLE D
PRODUCT/PROCESS LINES RAW WASTE LOADS
Complete this table with the results of analyses on each individual product or pro-
cess wastewater stream.
Product/Process producing wastewater_
Or Wastewater Source
Results presented in the table below were obtained from analyses made
II Prior to January 1, 1973 I I After January 1, 1973, approximate
date
Process Wastewater Flow
(million GAL/DAY)
min.
avg.
max.
Does the process wastewater flow include contributions from non-contact wastewater
such as cooling tower blowdown, boiler blowdown, etc? If it does, report the per-
centage as follows: . ___________
min.
avg.
max.
PRIORITY
POLLUTANTS
UNITS
CONCENTRATION RANGES
<10
10-100
100-1000
i
i
>1000
ANALYTICAL METHOD
PART IT - Pa«» ft
-------
Corporation_
Plant ~
City
State
TABLE E
PLANT INTAKE WATER
Complete this table with the results of analyses on the raw water intake to the
facility.
Results presented in the table below were obtained from analyses made
I I Prior to January 1, 1973 L_J After January 1, 1973, approximate
date
Intake Water Flow
(million
PRIORITY
POLLUTANTS
GAL/DAY)
UNITS
min. avg.
CONCENTRATION RANGES
<10
10-100
100-100C
A-56
jj
>1000
max.
ANALYTICAL >SETHOD
PART II - Page 9
-------
Corporation
Plant
C i ty S tat e_
Describe the sampling and analytical techniques used for priority
pollutants.
Was/is EPA protocol used for the sampling?
Was/is the EPA protocol used for the analysis?
Describe other techniques by pollutant parameter, (attach
additional material if clarification of the technique is
desirable).
Pollutant Technique
4. If you have not analyzed for all of the 129 priority pollutants in various
waters and wastewaters in your plant, please answer the following questions
for those pollutants for which analyses have not been made.
A. Do you have reason to believe or would you suspect that any of the
129 priority pollutants are present In your plant's raw wastewater
or treatment plant effluent as a result of your manufacturing.
operations or as a result of the presence of your facility at
your site? (Do not list suspected presence in intake waters as a
source of priority pollutants in answering this question)..
I I No - Co to Question 6.
{ I Yes - Continue below.
B. If the answer to 4A is yes, please list the priority pollutants you
would suspect to be present and the suspected product source.
Pollutant Suspected Source
A-57
PART II - Page 10
-------
Corporation
Plant
City State
Questions 5 through 8 ask for Information on the treatment and research on the
treatment of the List A priority pollutants. If the information requested was
supplied in the previous Section 308 questionnaire, in all cases, please name
the priority pollutant and state that the information was already submitted.
5. Have treatment facilities (end-of-pipe or in-plant control) been installed
specifically for removal of any of the priority pollutants (List 4)?
1 i No - Go to Question 7.
I i Yes — Continue below.
If the answer is yes, please list the treatment unit process or processes,
the pollutant(s) removed and whether installed in-plant or end-of-pipe.
If in-plant, list the product on which installed.
Attach data, flow sheets and drawings as appropriate to define the
design criteria and process effectiveness (e.g., removal efficiency,
etc.). If this was supplied in the previous questionnaire, please
state so after listing the pollutant(s).
Indicate end-of-pipe
Treatment Pollutants or specific product
Unit Process(es) removed on which installed
Do you have any data on the removal of specific priority pollutants by
existing end-of-pipe treatment facilities or in-process pollutant control
processes which were originally designed for removal of conventional
pollutant parameters? (e.g., BODs, COD, NH, TSS, etc.)
j I No
Yes
If answer is yes, please indicate the treatment process, the priority
pollutant(s) studied, the design criteria, and the removal efficiency
by the process. Attach flow sheets or other data as appropriate to define.
PART II - Page 11 A"58
-------
Corporation
Plant
C it y S ta t e
Have vou conducted research and/or bench-scale or pilot-scale programs for
studying the treatability or removal of one or more of the 129 priority
pollutants exclusive of heavy metals?
No
Yes
If the answer is yes, please describe the studies conducted, the priority
pollutants examined, and the results of the studies. (attach extra pages
if necessary, or provide a copy of the study to complete your answer).
B. Do you have data on the adsorption capacity of activated carbon for specific
process vastewaters resulting from the production of any of the compounds
presented in Lists 1, 2, 3 or A.
I ; NO
' ! Yes
If yes, list the product/process effluents, the type of carbon tested
(granules or powdered) and the adsorption capacity.
Adsorption Capacity*
Activated (grams adsorbed/
Product/Process Carbon Tested gram carbon)
^Specify adsorbate basis (e.g., COD, TOC, phenol, butadiene, PVA) and
concentration ranges evaluated.
A-59
PART II - Page 12
-------
Corporation
Plant
City Sta-e
PART III - TREATMENT INFORMATION
PLEASE READ THE INSTRUCTIONS FURNISHED PRIOR TO PROCEEDING TO THIS PART.
1. Even though you nay not now be discharging to a municipal sewer system,
is there an adequate municipal trunk sewer close by to which you could
discharge?
CD No
I I Yes - Distance from production facilities ft.
1 I Already discharging to a municipal system
2. If the recent data from your plant production or wastewater treatment plant
operation is, in your opinion, more representative than that submitted in
the previous questionnaire, you may submit new data (since October 18, 1976)
on Tables A and C attached, being careful to:
A. Include the beginning and end dates of the period covered.
B. Show average daily production for each product corresponding to .the
time period that treatment plant and raw waste parameters are reported
In Tables A and C. You may use any of the tables in Part I, Question 7
to report production data.
C. If raw waste is discharged without treatment, describe discharge point
(e.g., municipal sewer, river, etc.).
D. Indicate where (location) the samples were taken which generated the
analytical data presented in Tables A and C.
E. Continue responding to the questions in this part.
3. Does your plant operate an activated sludge process for treatment of either
a single process wastewater effluent or a combination of two or more product/
process wastewater effluents?
! I No - It is not necessary to complete the remainder of Part III
Ii Yes - (1) If you reported data from your plant in the previous portfolio,
dated October 18, 1976, please continue below with Parts A & B.
(2) If you commenced operation or modified an activated sludge
plant since October 18, 1976,and did not report on it or its
operation, please go to Question A.
Certain areas of the previous question portfolio dated October 18, 1976, were
not adequate to provide the necessary information for an effective performance
evaluation of the existing wastewater treatment plants. The performance
evaluation is essential in determining the cost of waste treatment as a functi
of plant operating criteria, external factors such as temperature, etc.
A-60
PART III - Page 1
-------
Corporation
Plant
Ci ty S tate_
Parts A and B request supplemental or clarifying information resulting from gaps in th
previous submittals. Complete this page for each Activated Sludge System on this site
A. If the answer to Question 3 is yes, please list each activated sludge facility
operated at your plant and list the product/process effluents included In the
influent to the activated sludge process.
Activated Sludge Type of Activated Sludge Systec
Plant Name (Contact Stabilization, Conventional, etc.)
Product/Process lines discharging to this treatment plant.
Activated Sludge Type of Activated Sludge System
Plant Name (Contact Stabilization, Conventional, etc.)
Product/Process lines discharging to this treatment plant.
Activated Sludge Type of Activated Sludge System
Plant Name (Contact Stabilization. Conventional, etc.)
Product/Process lines discharging to this treatment plant.
A-61
-------
Corporation_
Plant ~
City
Stats
List the following daily average values. Please select a three-month operating
period representing typical summer conditions , and if climate changes are sig-
nificant, select a second three-month period representing winter conditions.
Unless otherwise noted below, production levels reported in your October 18,
19 76 » questionnaire will be used as representative of the data below.
Activated Sludge Plant Name or Designation (Complete for each plant)
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
Summer
Winter
Influent total BOD. concentration
Effluent total BOB, concentration
Influent soluble BOD. concentration
Effluent soluble BOD,, concentration
Influent TSS concentration
Effluent TSS concentration
Mixed liquor suspended solids concen-
tration maintained in the aeration tank
Mixed liquor volatile- suspended solids
concentration maintained in the
aeration tank
Temperature of mixed liquor
Detention time maintained in the
aeration tank
F/M ratio
Sludge production (excess biological
sludge)
Total oxygen (air) supplied
Is activated carbon added to the
activated sludge system?
mg/1
_mg/l
mg/1
"ng/1
mg/1
""mg/1
mg/1
hours
Ibs/day
Ibs/day
A-62
-------
Corporation_
Plant
City State
4. Have you modified, installed or added any wastewater treatment facilities since
submission of the October 18, 1976, portfolio.
No - If no, the balance of the portfolio does not apply.
L—J Yes - continue to the next paragraph
A. If the answer to the above questions is yes, please complete the following
items, if information is available, for each new or modified wastewater
treatment facility.
1. Please describe the modified or new facilities.
2. State the purpose of the change/new installation.
3. Give the month/year of the change/new installation.
4. State the capital costs of the change/new installation.
5. State the operating costs for the system changed or added.
6. Give the new operational parameters. (If the new unit operation is
activated sludge, the operational parameters should be listed below.)
Attach a diagram illustrating the process as it currently exists.
7. Please.complete the attached Table A (treatment plant influent raw
waste load) and Table C (treatment plant effluent characteristics) for
the new or modified facility.
8. Please complete Sections B and C for each new or modified accivated
sludge plant.
A-63
PART III - Paae 4
-------
Corporation
Plant
City State
B. Please list each activated sludge facility operated at your plant and list
the product/process effluents included in the influent to the activated
sludge process.
Activated Sludge Type of Activated Sludge System
Plant Name (Contact Stabilization. Conventional, etc.)
Product/Process lines discharged to the activated sludge plant
Activated Sludge Type of Activated Sludge Systea
Plant Name (Contact Stabilization. Conventional, etc.)
Product/Process lines discharged to the activated sludge plant
Activated Sludge Type of Activated Sludge System
Plant Name (Contact Stabilization, Conventional, etc.)
Product/Process lines discharged to the activated sludge plant
Activated Sludge Type of Activated Sludge System
Plant Name (Contact Stabilization, Conventional, etc.)
Product/Process lines discharged to the activated sludge plan;
A-64
PART III - Page 5
-------
Corporacion_
Plant
City State
C. Complete this question for each activated sludge plant indicated is Part A
above. List the following daily average values. Please select a three-
month operating period representing typical summer conditions, and if
climate changes are significant, select a second three-month period
representing winter conditions.
Activated Sludge Plant Name or Designation
(Complete for each plant)_
Summer Winter
1. Influent total BOD_ concentration mg/1
2. Effluent total BOD. concentration mg/1
3. Influent soluble BOD. concentration _______ ___________ m8/l
4. Effluent soluble BOD. concentration ________ »g/l
5. Influent TSS concentration mg/1
6. Effluent TSS concentration ________ m8/1
7. Mixed liquor suspended solids concen-
tration maintained in the aeration tank _______ _______«. m8/l
8. Mixed liquor volatile suspended solids
concentration maintained in the
aeration tank mg/1
9. Temperature of mixed liquor °C
10. Detention time maintained in the
aeration tank _ hours
11. F/M ratio ^
12. Sludge production (excess biological
sludge) Ibs/day
13. Total oxygen (air) supplied _______ _ Ibs/day
14. Is activated carbon added to the
activated sludge system?
A-65
-------
TABU A
HARK LOAM TO TttATMBIT FACILITIES
Corporation.
Plant
City
State
TmeLU.tr
Trvacant Fadlicy D*Bcrl»cloe
Sowrc«(*)_
(wo)
(°C) -
Air
low
COD (Ito/tey)
TOC
TSS (Ita/tey)
TBS
TIB M » (lba/««y)
St»»iflc«nt Hoc«ls (Idoacify)
( lb«/«Uy)
_ (lb./
-------
TABLE C
TREATED PIOCESS WASTE UUSS DISCHARGED
Corporation,
ria&t
Citv ftat»
Traataaat Facility Saaplc location (final diacharat line. «te.)
Traacaant Facility Baacrtotlaa _______^_________^___^^_______
Diacharc* Fwiat
Do you poat-chierinat* tki* BffliMat? To M y*«, do you ebloriMt* (A) fell-T
»o (j) Fart-TlM
>«ra»»t«r
Flov (NED)
pi (pM «tt»)
Ta»p«rat«r« C*C) - Uaacawatar
Air
(Ika/dar)
ODD (Ifca/day)
TOC (IWoay)
TSS (Ifca/day)
TM (laW*ay)
•B2 a* • (Ua/day)
TO) a* M (lka/4ay)
fhanol (Ika/day)
Slgnlfle«t Naeala (Zdratify)
_ (Ua/day)
_(lba/aay)
JIbt/day)
Jtta/oay)
Othara (Xaaatlfy)
(lba/daT>
(Iba/dav)
„ (Ika/day)
Uba/day)
TAXI III - Pat* 8
A-67
-------
APPENDIX B
CHEMICAL PRIORITY LIST FOR
SCREENING AND VERIFICATION SAMPLING PROGRAMS
-------
APPENDIX B
CHEMICAL PRIORITY LIST FOR
SCREENING AND VERIFICATION SAMPLING PROGRAMS
In September, 1977, the Organic Chemicals Manufacturing Industry Working
Group approved a priority list containing seven categories of products
manufactured by the industry. This Appendix lists the chemicals in each of
the top five priorities. The last two priority lists are omitted because of
their length.
The seven levels of priorities are as follows:
Priority 1: Chemicals manufactured in excess of 5 million pounds per year
(top 100 production items) that are on the list of priority
pollutants. This list contains 25 products.
Priority 2: Chemicals derived from priority pollutants that are identified
in an ORD survey (Radian report) and are manufactured in excess
of 5 million pounds per year. This list contains 19 products.
Priority 3: The organic chemicals on the list of priority pollutants, not
including Priority 1 above and not including pesticides. This
list contains 67 products.
Priority 4: Chemicals derived from priority pollutants but that are
manufactured at less than 5 million pounds per year. This list
contains 146 products.
Priority 5: All other organic chemicals manufactured in excess of 5 million
pounds per year. This list contains 81 products.
Priority 6: Organic, non-pesticide entries on the TOSCA list that are not in
Priorities 1 through 5 above. This list contains 325 products.
Priority 7: The remainder of the 20,000 commercial industrial chemicals.
B-l
-------
CHEMICALS IN PRIORITY LEVELS 1 THROUGH 5
Priority 1
Acrylonitrile
Benzene
Bis(2-ethylhexyl) Phthalate
Butyl Benzyl Phthalate
Carbon Tetrachloride
Chloroform
1,4-Dichlorobenzene
Diethyl Phthalate
Dimethyl Phthalate
Di-n-butyl Phthalate
Di-n-octyl Phthalate
Ethyl Benzene
Methyl Bromide
Methyl Chloride
Dichlorodifluoromethane
Nitrobenzene
4-Nitrophenol
Pentachlorophenol
Phenol
Tetrachloroethylene
Methylene Chloride
Toluene
Trichloroethylene
Trichlorofluoromethane
Vinyl Chloride
B-2
-------
Priority 2
Acetone
Adipic Acid
Aniline
Benzoic Acid
Benzoid Acid Salts, Sodium Benzoate
Benzyl Alcohol
Benzyl Chloride
Bisphenol A
Cumene
Cyclohexane
Cyclohexanone
Cyclohexanone/Cyclohexanol (AK oil)
Diisopropyl Benzene
D ipheny1am ine
Fumaric Acid
Maleic Anhydride
Methyl Ethyl Ketone (2-butanone)
Phthalic Anhydride
Styrene
B-3
-------
Priority 3
Acenaphthene
Acenaphthylene
Acrolein
Anthracene
1,2-Benzanthracene
Benzidine
Benzo(a)pyrene (3,4-benzopyrene)
3,4-Benzofluoranthene
11,12-Benzofluoranthene
1,12-Benzoperylene
Bis(chloromethyl) Ether
Bis(2-chloroethyl) Ether
Bis(2-chloroethoxy) Methane
Bis(2-chloroisopropyl) Ether
Bromoform (tribromomethane)
4-Bromophenyl Phenyl Ether
Chlorobenzene
Chloroethane
2-Chloroethyl Vinyl Ether (mixed)
2-Chloronaphthalene
2-Chloropheno1
m-Chlorophenol
4-Chlorophenol
4-Chlorophenyl Phenyl Ether
Chlorodib romoraethane
Chrysene
1,2,5,6-Mbenzanthracene
1,2-Dichlorobenzene
1,3-Dichlorobenzene
3,3-Dichlorobenzene
Dich1orobromomethane
1,1-Dichloroethane
1,2-Dichloroethane
1,1-Dichloroethylene
1,2-trans-dichloroethylene
2,4-Dichlorophenol
1,2-Dichloropropane
1,3-Dichloropropylene (1,3-dichloropropene)
2,4-Dimethylphenol
4,6-Dinitro-o-cresol
2,4-Dinitrophenol
1,2-DiphenyIhydrazine
Fluoranthene
Fluorene
Hexachlorobenzene
Hexachlorobutadiene
Hexachlorocyclopentadiene
Hexachloroethane
Indeno(l,2,3-C,D)pyrene
Isophorone
Napthalene
2-Nitrophenol
B-4
-------
3-Nitrophenol
4-Nitrophenol
N-Nitrosodimethylamine
N-Nitrosodiphenylamine-n-propylamine
Parachlorometa Cresol
Phenanthrene
Pyrene
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)
1,1,2,2-Tetrachloroethane
1,2,4-Trichlorobenzene
1,1,1-Trichloroethane
1,1,2-Tr ichloroethane
2,4,6-Trichlorophenol
2,4,5-Trichlorophenol
N-nitrosodiphenylamine
B-5
-------
Priority 4
Acetanilide
Acetphenone
Acetone Cyanohydrin
Acrylamide
Alkylnaphthalenes
Alkyl (Cg, C ) phenols
Allyl Alcohol
m-Aminobenzoic Acid (Anthranilic Acid)
o-Aminobenzoic Acid
p-Aminobenzoic Acid
Aminoethylenthanolamine
Aniline Hydrochloride
m-Anisidine
o-Anisidine
p-Anisidine
Anisole
Anthraquinone
Benzaldehyde
Benzamide
Benzoquinone
Benzenedisulfonic Acid
Benzenesulfonic Acid
Benzil
Benzilic Acid
Benzoin
Benzonitrile
Benzophenone
Benzotrichloride
Benzyl Chloride
Benzylamine
Benzyl Bichloride
Bromobenzene
B romonaphtha1enes
Chloranil
m-Chloroanaline
o-Chloroanaline
p-Chloroanaline
o-Chlorobenzaldehyde
p-Chlorobenzaldehyde
o-Chlorobenzoic Acid
p-Chlorobenzoic Acid
m-Chlorobenzyl Chloride
o-Chlorobenzyl Chloride
p-Chlorobenzyl Chloride
Chloronaphthalenes
m-Chloronitrobenzene
o-Chloronitrobenzene
p-Chloronitrobenzene
m-Chlorotoluene
o-Chlorotoluene
p-Chlorotoluene
Cyclohexanol
Cyclohexene
B-6
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Cyclohexylamine
Decahydronaphthalenes
Diacetone Alcohol
2, 7-Diaminobenzoic Acid
3,5-Diaminobenzoic Acid
2,4-Dichloroanaline
3,4-Dichloroanaline
m-Dichlorobenzene
o-Dichlorobenzene
p-Dichlorobenzene
Dichlorohydrin
Dicyclohexylamine
Diketene
n,n-Dimethylanaline
2,3-Dimethylanaline
2,4-Dimethylanaline
2,5-D imethy1ana1ine
2,6-Dimethylanaline
3,4-Dimethylanaline
Dimethyl Sulfide
Dimethyl Sulfoxide
2,4-Dinitrotoluene
2 ,6-Dinitrotoluene
Dinitrotoluenes (mixed 2,4/2,6)
Diphenyl
Diphenyl Sulfoxide
p-DodecyIpheno1
Ethylenediamine
Ethyl Orthoformate
Glyceraldehyde
Glycerin
Glycerol
Hexalene Glycol
Hydroqu inone
Maleic Acid
Malic Acid
1-Malic Acid
+ and - Malic Acid
Mesityl Oxide
Methacrylic Acid
n-Butyl methacrylate
Methyl methacrylate
2-Methylaniline
4-Methylaniline
3-Methylaniline
n-Methylaniline
Methylcyclohexane
MethyIcyclohexano1
Methy1cyclohexanone
Methyl Isobutyl Carbinol
Alpha-Naphthalene Sulfonic Acid, Sodium Salt, & Formaldehyde Condensate
Beta-Naphthalene Sulfonic Acid, Sodium Salt, & Formaldehyde Gondensate
Alpha-Naphthol
B-7
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Beta-Naphthol
o-Nitroanisole
p-Nitroanisole
m-Nitrobenzoic Acid
o-NitrobenzoiC Acid
p-Nitrobenzoic Acid
Nitrophenol
Nitrotoluene
Nonylphenol
Octylphenol
p-Phenetidines
Phenosulphonic Acid, Ammonium Salt, Sodium Salt, Zinc Salt, and
Formaldehyde Condensate
m-Phenylinediamine
o-Phenylinediamine
p-Phenylinediamine
Phthalimide
Phthalimide, potassium salt
Phtholonitrile
Piperazine
Resorcinol
Sodium Phenate
Succinic Acid
Sulfanilic Acid
Tetrachlorophthalic Anhydride
1,2,3,4-Tetrahydronaphthalene
Tetrahydrophthalic Anhydride
Tetramethylethylenediamine
Toluene-2,4-diamine
Toluene diamines (2,4/2,6)
p-Toluenesulfonamide
Toluenesulfonic Acid
p-Toluenesulfonyl Chloride
Trichloroaniline
1,1,2-Trichloro-1,2,-trifluorethane
Vinylidine Chloride
Xylenes (mixed)
2,4-Xylenol
Xylidine
m,p-Xylenes
B-8
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Priority 5
Acetaldehyde
Acetic Acid
Acetylene
Acrylic Acid
Adiponitrile
Amyl Acetate
Amyl Alcohols
Caprolactam
Citronellol
Dimethyl Terephthalate
Ethyl Acetate
Ethyl Amines
Ethylene
Ethylene Glycol
2-Ethylhexyl aerylate
Ethylene Oxide
Formaldehyde
Hexamethylenediamine
Isobutylene
Isopropanol
Linear alcohol ethoxylates
Methanol
M-Xylene
Mono-Methyl Amines
di-Methyl Amines
tri-Methyl Amines
Methyl Salicylate
Nylon salt
o-Xylene
n-Butanol
n-Propanol
p-Am inopheno1
o-Aminophenol
p-Cresol
p-Nitroaniline
o-Nitroaniline
p-Xylene
p-Nitrophenol and Sodium Salt
Propylene (propene)
Sec-butyl-alcohol
n-Butyl acrylate
Butylenes
Tannic Acid
Terephthalic Acid
Tetraethyl Lead
Vinyl Acetate
Acetic Acid Salts, Total
Acetic Anhydride
Aspirin
Benzoyl Peroxide
Castol Oil, Ethoxylated
B-9
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Choline Chloride (all grades)
Cresols, total
Cresote
Diethylene Glycol
Dipropylene Glycol
Diphenylisodecyl phosphate
n-Dodecyl Mercaptans
Tert-Dodecyl Mercaptans
Ethyl acrylate
Ethyl Alcohol, Synthetic
Glutamic Acid, Monosodium Salt
Hexamethylenetetramine, Tech.
Pentaerythritol
Proprionaldehyde
Propionic Acid
Propylene Glycol (1,2-Propanediol)
Propylene Oxide
Salicyclic Acid
Triethylene Glycol
Xylenesulfonic Acid, Sodium Salt
2-Aminoethanol (monothanolamine)
2-Dimethylaminoethanol
2-Ethylhexanoic Acid (a-Ethylcaproic Acid)
2-Methoxyethanol (Monomethyl Ether)
2,2-Iminodiethanol (Diethanolamine)
5-Nitro-o-Toluenesulfonic Acid (S03H-1)
n-Propanol
iso-Butyraldehyde
n-Butyraldehyde
B-10
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APPENDIX C
ANALYTICAL METHODS DEVELOPMENT
AND REVIEW OF DATA
-------
I. INTRODUCTION
A. General
Perhaps no other aspect of pollution control is more fundamental than the
definition of the pollutants to be controlled. An important early step in
developing regulations limiting the discharge of pollutants to the environment
and in designing a treatment system to meet such limitations is the
characterization of the pollutant load by sampling and analysis. After the
treatment system has been installed, the discharge must be regularly monitored
to evaluate the effectiveness of the treatment system and compliance with the
discharge limitations.
In gathering data to develop and support regulations, the reliability of
the results is more important than the specific analytical methodology
employed to characterize the wastewater. Where available, "standard" methods
should be used to eliminate the inconvenience and expense of establishing a
non-standard method suitable to the specific wastewater. However, the notion
that data of acceptable quality is inherently associated with the use of a
"standard" method is incorrect. If performed improperly, however, either a
standard or a non-standard method can yield faulty data. (Taylor 1981).
Programs to assure the reliability of analytical results should focus on
the quality of the results, not the analytical techniques employed. If the
accuracy and precision data accompanying a reported number meet the criteria
chosen, the analytical techniques are acceptable. (Amore 1979).
The data produced by all analytical techniques reflect the variations in
human and equipment performance that are inherent to the analyses. The
critical questions are: What are the precision and accuracy of a reported
value and are these acceptable for the application use of the data? These
questions are answered by emphasizing quality assurance in laboratory
operations and minimizing measurement errors to produce results appropriate to
how the data is to be used.
B. Quality Assurance/Quality Control
Quality assurance/quality control (QA/QC) includes all of the laboratory
activities necessary to determine the precision (repeatability) and accuracy
(relationship to the true value) of an analytical measurement. The accuracy
of the measurement is determined by adding (spiking) a known amount of analyte
(the pollutant of interest) to a wastewater sample. Recovery (the ratio of
the amount of spike detected to the amount that had been added) depends on the
matrix (the other pollutants and chemicals in the wastewater) and the
analytical technique, and may be used to adjust the observed value to obtain
the "true" value (observed value * recovery = true value).
An analytical method that fails to detect an organic compound spiked into
pure water (i.e., zero recovery) is inappropriate. When that method has been
modified so that substantial (>50%) recovery from pure water is consistent
and predictable, and the accuracy and precision have been established, the
method is validated. If the accuracy and precision achieved in the pure water
is also realized in varying wastewater matrices, the method can be considered
C-l
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standardized. Accuracy and precision in a wastewater sample usually differs
from that achieved in pure water.
Measurements at concentrations near the detection limit for the compound
of interest (e.g. less than 10 parts per billion for most organics), create
additional problems. The limit of detection for any pollutant is the lowest
concentration of that pollutant that is distinguishable from background
concentrations with a known degree of confidence. Below this concentration,
the pollutant is "not detected". The limit of determination for each
pollutant is the concentration at which one can state with a known degree of
confidence that the pollutant is present. Between the limit of detection and
the limit of determination, the pollutant is "detected but unconfirmed".
Two errors affect any analysis: operator inconsistency and matrix
interference. Practice should reduce operator error. Reduction of matrix
interferences is more difficult,since it is impossible to anticipate all
possible matrix interferences. In metals analysis, most of the interfering
compounds are destroyed by acidic high temperature digestion prior to
measuring the metals concentration. Digestion prior to the analysis of
specific organic compounds however, is not feasible, since it would alter the
individual compounds.
Specific methods or, if appropriate, standard methods can be utilized to
reduce the interferences from a specific matrix. Regardless of method, the
measurements should be validated with an adequate QA/AC program. This
approach is in many cases the only practical means of accurately quantifying
organic priority pollutants in a variety of wastewater matrices.
C. Wastewater Analysis in the OCPSF Industry
Each product/process employed in manufactured organic chemicals, plastics,
or synthetic fibers produces a wastewater containing priority pollutants
characteristics of the product/process. Few manufacturing facilities in the
Organic Chemicals and Plastics/Synthetic Fibers (OCPSF) industrial category
have the same combination of product/processes, so the wastewater generated at
a single plant cannot represent the entire industrial category. This
diversity creates a wastewater analysis challenge not found in those
industrial categories where the product/process mix and the associated
priority pollutants are more consistent throughout the industry.
The variability of the wastewater matrices found within the OCPSF industry
suggests that a specific analytical method may not produce the same precision
and accuracy at all plants. While an off-the-shelf "standard" method may be
more convenient to use, it may not be entirely appropriate for every
wastewater sample. In a plant manufacturing organic chemicals, for example,
the types and amount of pollutants in the process wastewater vary with the
product/process operating conditions and with the combination of
product/processes that are being operated. To minimize the impact of these
variations on the data, an analytical method should be selected that is
appropriate for the specific wastewater matrix that is being analyzed. It is
also important to ensure that the samples are collected in such a way as to be
representative of the wastewater being sampled, and that the integrity of the
C-2
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samples is protected during short-term storage, transport and preparation for
analysis at the receiving laboratory.
D. Available Analytical Methods
At the beginning of the BAT study, EPA had no validated analytical methods
for measuring organic priority pollutant concentrations in the OCPSF
Industry. Three analytical methodologies were available for measuring
individual organic priority pollutants at low concentrations in wastewaters.
These methodologies were (1) gas chromatography/mass spectrometry (GC/MS), (2)
gas chromatography/conventional detector (GC/CD), and (3) high performance
liquid chromatography (HPLC). Conventional detectors include flame ionization
(FID), electron capture (EC), photoionization (PI), and Hall
electroconductivity. HPLC is recently finding more frequent application,
especially in the pesticide industry.
Both GC/MS and GC/CD use gas chromatography to separate the individual
compounds extracted from a wastewater sample. The mass spectrometer (MS) is a
universal detector that can identify and measure organic compounds without
prior programming, whereas conventional detectors (CD) identify a particular
compound by comparing its retention time with that of a known compound under
the same column conditions.
GC/MS is a broad-spectrum technique--a large number of compounds in a
single sample can be identified and measured. It is generally used in
conjunction with a solid state microelectronic computer system; the mass
spectrometer repeatedly scans the mass spectrum. Because most of the
detectable constituents of a sample can be identified from their mass spectra,
GC/MS is a very versatile method for determining pollutants in a sample
without advance knowledge of what pollutants are there.
GC/CD is a targeted technique; it can recognize and measure only those
compounds for which it has been calibrated. The usual method for identifying
a GC peak as a specific pollutant is to measure its absolute retention time
under strictly controlled operating conditions, or its relative retention time
compared to a standard compound under the same conditions.
Sample preparation for either GC/CD of GC/MS can be quite complicated and
time-consuming if there are many organic compounds present in the sample
matrix. If only a few compounds are present, the sample may be injected
directly into the GC. If a large number of compounds are present, however,
they must be separated into broad groups by three or more extraction
procedures. Complicated sample preparation increases the degree of pollutant
loss and sample contamination.
II. ANALYTICAL METHOLODOLOGIES AND QA/QC FOR THE BAT STUDY
The analytical methodologies and QA/AC used in the BAT study are
summarized in TABLE C-l and discussed below.
C-3
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NOTES TO TABLE C-l
1. The latest EPA EMSL Cincinnati GC/CD and GC/MS methods are also shown, for
comparison.
3. Date of first publication of method.
4. Reference document for first release of method.
5. EPA method number and name of analytical technique employed.
6. The portion of sample to be analyzed by the method.
7. Data or specifications for identification of specific compounds.
8. The maximum acceptable number of mass spectrometer scans within which the
characteristic mass spectral ions must maximize for the compound to be
considered detected.
9. Maximum acceptable discrepancy in GC retention time between a peak and
that of the standard for compound identification.
10. The maximum acceptable discrepancy in the ratios of the characteristic
mass spectral ions between the standard and those of the sample.
11. The number of characteristic mass spectral ions specified by the method.
12. Information supporting the identification of a compound and the
measurement of its concentration.
13. The instrumental method used to calculate compound' concentration.
14. Relationship between mass of chemical injected and output signal.
15. The number of data points used for calibration.
16. How often the calibration is to be verified.
17. Criteria and specifications of procedures that support data validity.
18. Specific test which demonstrates instrument performance.
19. Compound(s) used for end-to-end system test.
20. Test which demonstrates mass spectrometer sensitivity and spectrum
validity, relative to EMSL standard peak intensity ratios.
21. Standard deviation obtained with multiple analyses of standards (i.e.,
replicability).
22. Requirements for initial precision evaluation.
C-7
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NOTES TO TABLE C-l
(continued)
23. Specifications for subsequent precision measurements .
24. Recovery of known masses of standards added to a standard sample (usually
reagent water) or to an OCPSF sample.
25. The compounds employed for accuracy measurement.
26. The specification levied by the method.
27. Blanks required to demonstrate freedom from contamination and
interferences.
28. Required frequency of analysis of lab blanks.
29. Blanks carried to and from the sampling site.
30. Only major differences between the methods are listed.
31. Gas chromatograph column type.
32. Analyst's flexibility in selecting alternate column.
33. Means by which sample is separated from the water.
34. Analyst's flexibility in removing interferences from sample.
35. Specified ratio of water volume to extract volume.
36. Memo from Telliard to EGD project officers through Bob Schaffer dated May
27, 1977, entitled "Sampling and Analysis Procedures for Screening of
Industrial Effluents for Priority Pollutants."
37. Analysis for compounds included in the "volatiles" fraction, containing 30
specific priority pollutants.
38. NS means "no specification given" in method.
39. Employed internal standard, which uses compounds different from the
compounds to be measured.
40. Test standard containing all compounds to be analyzed by the method in the
particular fraction specified.
41. Decafluorotriphenylphosphine used for calibration.
42. Quality control charts showing deviation of results from true or average
value chronologically for each standardization measurement.
C-8
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NOTES TO TABLE C-l
(continued)
43. Two times the standard deviation of the spike concentration that had been
added.
44. AR means as required.
45. One required with each Sample Set (SS).
46. Not applicable; the purge and trap method does not "concentrate" the
sample in a liquid phase.
47. The semi-volatiles (acid and base/neutral) fractions. Some protocols also
include GC/MS confirmation of a pesticide or PCB found by GC.
48. PGP is pentachlorophenol; Benz is benzidine. These two compounds are
employed to test GC column performance for the acid and base/neutral
fractions, respectively.
49. Not required by this method.
50. Capillary columns were permitted but were seldom used.
51. Separatory funnel extraction or continuous liquid/liquid extraction.
52. Either internal (see 39) or external (which uses the compound to be
measured) standard calibration methods could be used.
53. Required either multi-point calibration or a standard which matched
closely the concentration(s) of the compound(s) found in the sample.
54. No precision and accuracy requirement in these methods, but a quality
control/quality assurance program containing precision and accuracy
requirements was suggested in the Federal Register notice.
55. Surrogate compounds -- compounds which simulate the behavior of the
compounds being analyzed.
56. Methods were given in work statements sent by EPA to its contract
laboratories.
57. The OCV (Organic Chemicals-Verification Phase) program was directed at
testing for a given pollutant or group of pollutants at each plant. Each
analyst was allowed to fractionate the sample as seen fit in order to
successfully analyze for the pollutant(s).
58. The specifications and requirements set at each EPA contract laboratory
for each pollutant reflected the analytical judgment of the analysts and
quality assurance personnel.
59. The actual priority pollutant under investigation was tested.
C-9
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NOTES TO TABLE C-l
(concluded)
60. Analytical precision was determined by analysis of duplicate samples.
61. Each OCV analytical method specifies extraction methods. For the 5-plant
study, EPA chose the OCV methods to be used by each contract laboratory.
No flexibility in choosing and applying the method (other than that
specifically permitted in the method) was allowed.
62. As required and as permitted by the method, based on the judgment of the
analyst.
63. This GC/CD method was chosen as typical of the latest 304(h) EMSL
Cincinnati methods. Methods 601-613 are all similar.
64. Less than three times the standard deviation obtained by analysis of
standards during the sample analysis.
65. Four replicate analyses of standards.
66. Within three standard deviations, combined with analysts' judgment.
67. Cowen, W.F., and J. L. Simons (Catalytic, Inc.) Analytical Methods for
the Verification Phase of the Bat Review (for Organics and Plastics
and Synthetics Industrial Category). September, 1980.
C-10
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A. Screening Phases I and II
1. Analytical Methods
As noted in the Federal Register (3 December 1979, p. 69464), when
Congress passed the 1977 Clean Water Act, "...section 304(h) analytical
methods were not available in many cases....because only on rare occasions had
industry monitored or had EPA regulated (priority) pollutants." In the fall
of 1977, the only methodology recommended by the EPA was the GC/MS screening
protocol, which EPA had not yet validated. The Organic Chemicals Branch (OCB)
of EPA's Effluent Guidelines Division adopted this GC/MS analytical protocol
for the Screening Phase work. Introduced by the Agency in April of 1977, this
protocol was also used extensively by other branches within the Effluent
Guidelines Division, by EPA contractors and Regional laboratories, and by
private labs.
The analytical methods used during the Screening Phase are described
in "Sampling and Analysis Procedures for Screening of Industrial Effluents for
Priority Pollutants" (USEPA 1977). Since the purpose of screening was to
identify all priority pollutants among a host of other compounds that may be
present in a wastewater sample, GC/MS methodology was appropriate because it
is not as subject to interferences as other analytical alternatives. The
GC/MS screening protocol was intended for the qualitative and
semi-quantitative determination of organic priority pollutants during EPA's
initial survey of industrial effluents.
The screening protocol's procedure for extracting organic priority
pollutants from wastewater samples was either purge and trap, or liquid-liquid
extraction. Some compounds may be recovered from the wastewater by either
procedure. The efficiency of recovery depends on the vapor pressure
(volatility) and water solubility of the compound. When a compound is
efficiently recovered by both procedures, the GC conditions determine the
procedure of choice. In general, the GC conditions selected for the purge and
trap are not suitable for organic priority pollutants that elute from the GC
column later than chlorobenzene.
The purge and trap recovery procedure involves purging the wastewater
sample with an inert gas (Helium) and trapping the purged organic compounds by
adsorption on a resinous substrate (Tenax-silica gel). The trapped organic
compounds are subsequently desorbed by heating the trap and directing the
desorbate into the GC/MS system. This method detects a group of 29 priority
pollutants, which are mostly halogenated C1-C5 hydrocarbons. It was
recognized that the two priority pollutants acrolein and acrylonitrile are so
water-soluble that they cannot be efficiently recovered by the purge and trap
procedure. Direct aqueous injection was recommended for these two compounds,
as well as any of the volatiles that may be present at more than one part per
million.
For the less volatile organic priority pollutants, a liquid-liquid
extraction procedure (Webb 1978) separated them into groups that are
selectively extracted at differed pH. Extraction with methylene chloride at
pHll removes basic and neutral compounds. Included in this group are 46
priority pollutants: halogenated aromatics, nitroaromatics, nitrosamines,
Oil
-------
polyaromatics (PAH's) and phthalate esters. Extraction with 15 percent
raethylene chloride in hexane at pH7 removes neutral compounds. Included in
this group are 26 priority pollutants: organochlorine pesticides and
polychlorinated biphenyls (PCB's). Extraction with methylene chloride at pH2
removes acidic compounds. Included in this group of 11 phenolic priority
pollutants: phenol, chlorophenols and nitrophenols.
The solvent extract was dried and filtered by passing it through a
short column of sodium sulfate, which had been prewashed with methylene
chloride. After evaporating the solvent to concentrate the extract, it was
injected into the GC/MS system. Pesticides were to be initially quantified
using GC/EC (electron capture detector), since that is a much more sensitive
detector than the MS and is specific for compounds containing halogens.
Pesticide identity was to be subsequently confirmed using GC/MS, when more
than 40 nanograms of the pesticide was injected (EC detector subject to
overload).
Metals were determined by flame or flameless atomic adsorption.
Total cyanides were analyzed by a colorimetric method after distillation.
Total phenols were determined by the 4-aminoantipyrine (4-AAP) colorimetric
method, often giving values several orders of magnitude higher than the GC/MS
value for simple phenol. The 4-AAP procedure measures most phenols (not
para-substituted phenols) as well as various non-phenolic compounds found in
industrial wastewaters. The 4-AAP data accompanied metal and cyanide analyses
as part of a package of "classical pollutants". Since the 4-AAP test is not
compound specific for phenolic priority pollutants, such data had no further
use in this study.
2. Quality Assurance/Quality Control
The following discussion refers to the April 1977 revision of the
March 1977 Screening protocol (USEPA 1977).
The QA/QC procedures for the volatile fraction of the priority
pollutants that are explained next include:
a. Analysis of blanks
b. Daily calibration of the GC/MS system with priority
pollutant and internal standards. Daily MS tuning with
DFTPP (Decafluorotriphenyl phosphine).
c. Calibration procedure gave recovery-corrected data.
d. GC/MS system testing. Quality control of data precision by
replicate analyses of internal standards.
e. No tolerance specifications for compound identification
criteria.
A blank is reagent water, i.e., water in which no priority pollutants
or interfering compounds can be detected by the analytical method being used.
A trip blank septum-sealed in a vial accompanied each shipping container of
C-12
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samples. The purpose of analyzing a trip blank was to test for contamination
during sampling and sample transport. Laboratory blanks were analyzed to
demonstrate that the GC/MS system was free of interferences and contamination.
Laboratory blanks were to be analyzed each day prior to the first sample and
between samples afterward. While practices varied from one laboratory to
another, analysis of laboratory blanks between samples was frequently omitted
if the previous sample showed a low content of priority pollutants.
The GC/MS system was to be calibrated daily by spiking reagent water
at a level of 20 ppb with a "cocktail" of priority pollutants and three
internal standards. These compounds were recovered by the purge and trap
technique and analyzed by the GC/MS system. From these results, response
factors for each priority pollutant could be calculated and used to determine
concentration in the subsequent analyses. Since the priority pollutants and
internal standards were recovered together from the reagent water during the
calibration procedure, concentrations that were subsequently computed from the
calibration response factors were recovery corrected values.
The screening protocol also called for the MS to be tuned daily with
20 nanograms of DFTPP. Since the retention time of DF.TPP on the GC column
used for volatiles was too long to be practical, the tuning requirement was
met by replacing the GC column used for volatiles with the one used for
base/neutrals. Although not allowed by the screening protocol, some analysts
introduced the DFTPP directly into the MS by means of a probe. DFTPP has
since been replaced by p-Bromofluorobenzene, so that now the MS tuning
compound can be conveniently added with the other standards for the daily
calibration and avoid the GC column change necessitated by the DFTPP.
The GC/MS system was to be tested and the precision of the purge and
trap-GC/MS procedure was to be routinely determined (frequency unspecified) by
spiking reagent water with three internal standards and performing replicate
analysis. The three compounds were Bromochloromethane,
2-Bromo-l-chloropropane and 1,4-Dichlorobutane. These compounds are not
priority pollutants, but were used because they span the range of GC column
retention times of the volatile priority pollutants. Quality control charts
were to be constructed showing results as a function of time, or number of
analyses performed.
Qualitatively, a weakness of the screening protocol for volatile
priority pollutants was the lack of specifications on compound identification
criteria. Characteristic masses or mass ranges were tabulated and were the
only information afforded for qualitative determinations. No tolerances were
given for relative retention time ( + minutes), or for correspondence with
published mass spectral peak height ratios ( + percent). Most laboratories
compensated for this omission by applying the tolerance specifications that
were provided for the semi-volatile priority pollutants (see following
discussion). If the presence or absence of a compound was in doubt, the
laboratories were instructed to report the compound as being present.
C-13
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The QA/QC procedures for the semi-volatile fractions of the priority
pollutants that are explained next include:
a. Analysis of blanks
b. Calibration (frequency unspecified) at two concentrations
with priority pollutants and an internal standard (D10
anthracene). Daily MS tuning with DFTPP.
c. Calibration procedure did not give recovery-corrected
data.
d. Daily GC/MS system testing with pentachlorophenol (acid GC
column), and with benzidine (base/neutral GC column). No
quality control of data precision by replicate analysis.
e. Tolerances were specified for compound identification
criteria.
A trip blank was to be analyzed with each set of samples. This blank
was obtained in the field by pumping reagent water through the sampling pump's
system of plastic tubing. For this reason, the trip blank was also known as a
"tubing blank." To avoid unnecessary GC/MS analysis of blanks, the screening
protocol allowed the extract of the blank to be run on GC/FID, using the GC
column appropriate to the acid or base/neutral fraction. If no peaks greater
or equal to that of the D10 anthracene internal standard appeared, then a
GC/MS analysis of the blank was not required.
The GC/MS system was to be calibrated at unspecified intervals by
direct injection of a "cocktail" of priority pollutants and an internal
standard (D10 anthracene) at two concentration levels, 10 and 100 ppb. Since
the calibration standards were not carried through the extraction procedure,
the concentrations subsequently computed from the calibration response factors
were not recovery corrected. The screening protocol did not require that the
semi-volatile priority pollutant data be corrected for recovery.
The GC/MS system was to be tested each day. To test with the GC
column used for the acid fraction (Tenax-GC), 100 nanograms of
Pentachlorophenol was to be used. To test with the base/neutral GC column
(SP-2250), 40 nanograms of Benzidine was to be used. These compounds were to
be injected directly into the respective column. If the compound could not be
detected by the GC/MS system, the GC column was to be replaced. There was no
requirement to maintain Quality Control charts on the precision of this
method, as was required for the purge and trap method.
Relatively rigorous criteria were applied to the identification of
semi-volatile priority pollutants. Three conditions were specified:
a. The characteristic ions for the compound must be found to
maximize in the same mass spectral scan.
C-14
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b. The time at which the GC peak occurs must be within a
window of + 1 minute of the retention time of the
compound.
c. The ratio of three mass spectral peak heights must agree
within + 20 percent with the relative intensities given
for the compound.
If the presence or absence of a compound was in doubt, the laboratories were
instructed to report the compound as being present.
B. Verification Phase
1. Background
Although well suited for a qualitative assessment of organic priority
pollutants in wastewater samples, the GC/MS method used for the Screening
Phase--The Screening Protocol--was not appropriate for the improved
quantitation sought in the Verification Phase. Determination of extraction
efficiency (percent recovery) and replication to measure precision and
accuracy for many disparate waste streams would have made a substantial
increase in the number of analyses to be performed. The continued use of the
GC/MS method with more rigorous QA/QC would have made the analytical costs
prohibitive, and there were not sufficient qualified GC/MS-equipped
laboratories available in the fall of 1977 to handle the samples.
OCB obtained data of adequate quality at reasonable cost by
substituting conventional detectors for the mass spectrometer and modifying
existing "state-of-the-art" GC/CD methods. GC/MS was used to confirm priority
pollutant identification, and was routinely reserved for those instances when
interferences in the sample matrix so complicated the analysis that the use of
GC/CD proved impractical. By using the less expensive and widely available
GC/CD methods routinely, and by using the substantially more expensive GC/MS
method for 10 to 15 percent of the samples, OCB cost-effectively combined the
two methodologies without severely compromising QA/QC. An added benefit of
this approach was that the level of QA/QC employed and the practice of the
methods in a variety of matrices demonstrated the applicability of the GC/CD
methods for the analysis of effluents from product/processes within OCB's
assigned industries.
The 1979 Water Pollution Control Federation literature review
(Journal WPCF, Vol. 51, 'No. 6, pp. 1134-1171) of analytical methods used in
research published during 1978 (when Verification began) showed that GC/CD was
the methodology most often used for measuring organic priority pollutants. Of
186 published investigations involving a number of organic priority pollutants
in a wide range of sample types, 150 utilized GC/CD. At least part of the
reason for this dominance was the GC/CD instruments were more widely available
than GC/MS at that time.
In June of 1977, EMSL published a preliminary collection of GC/CD
methods selected from a computerized literature search by the Denver National
Enforcement Investigation Center (NEIC) of EPA. A year later EMSL let
contracts on a program to validate some of these methods. Although not yet
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validated, these methods were proposed in the Federal Register (3 December
1979, p. 69532 ff). Having already begun to use GC/CD methodology during
Verification for reasons previously discussed, OCB continued its methods
development program concurrent with the Verification Phase. The chronologies
and milestones of the two independent GC/CD method development and validation
efforts are presented in FIGURE C-l. EMSL's contracting laboratories began
delivery drafts of validated GC/CD methods six to nine months after OCB had
completed it own verification program. EMSL's validated methods will be
promulgated by EPA in 1983 as the 600 series.
Dr. C. A. Hammer of Envirodyne Engineers compiled an initial list of
proposed methods for OCB's Verification program from the EMSL selections and
the NEIC bibliography. The literature search had focused on methods suitable
for groups of priority pollutants that would have similar responses to
extraction procedures, chromatographic conditions, and detectors. A method
appropriate to each of these was assembled in a loose-leaf manual and made
available to both OCB's contractor laboratories and Verification plants.
OCB's objective was to develop site-specific (in many cases
matrix-specific) GC/CD methods by analyzing actual industry wastewater
samples. Often sampling product/processes effluents with high matrix
interference potential, OCB's experimental approach used spiked and duplicate
sample analyses to define the validity of each measurement.
2. Analytical Methods
Before the initial plant visit, a list of priority pollutants to be
verified was compiled using the analytical results of the Screening Phase (see
Section V of Volume II) and predictions from the product/processes known to be
operating at the plant. The list and a package of appropriate methods
selected from the then current GC/CD methods manual were sent to the plant
well in advance of the initial visit to allow time for their review. During
the initial visit, a grab sample of wastewater was taken from each location to
be sampled. The grab samples were used by the EPA contract laboratory to tune
the proposed analytical method to the specific wastewater matrix at each
sampling location. Extraction, cleanup, and GC conditions were modified as
necessary during three weeks of method evaluation. At the end of that time
(approximately one week before the actual Verification sampling was to
commence), the method variation found to be most appropriate in each sample
matrix was specified. EPA discouraged the contract laboratory from
subsequently modifying the method significantly, and informed the plant what
methods would be used.
The purpose of discouraging further change in the methods was
primarily to offer each plant an opportunity to replicate OCB's Verification
sampling and analysis. The benefits anticipated from replication were:
(a) A doubling of the number of data points.
(b) A chance for the plant to evaluate the analytical methods
for utility and cost-effectiveness, particularly in
comparison to GC/MS; and
C-16
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(c) An interlaboratory comparison of OCB and plant analytical
results would be compiled.
Many plants elected to do no replication or to limit their
replicative participation to samples of the final effluent, or of the combined
untreated wastewater. For self-verifying plants, the plant performed the
principal analysis and OCB's contractor performed the replicate analysis. A
potentially important contribution to the methods development effort was
reduced by the limited plant participation.
Seven contracting laboratories eventually participated in OCB's
Verification methods development: Envirodyne, Midwest Research Institute,
Southwest Research Institute, Gulf South Research Institute, Jacobs
Engineering Group (PJB Labs), Acurex Corporation, and A.D. Little. Beginning
in January 1979, the key analysts from each of these laboratories met
approximately every two months to discuss developments and update methods. As
methods were matched with the matrices at each plant, variations (usually a
change in GC conditions or column) were forwarded to all team members and
documented in the methods manual. This continuing update of successful
modifications avoided redundant effort and cost-effectively helped resolve new
matrix problems simultaneously encountered by members of the team.
Verification methods for metals and cyanides were the same as those
used during the Screening phase. For organic compounds, however, the
verification methods developed were designed to isolate, concentrate, and
quantify one or more compounds from each of the following groups of organic
priority pollutants:
(a) Pesticides, PCBs, and phthalates
(b) Phenols
(c) Volatile organics
(d) Halogenated volatile organics
(e) Polynuclear aromatic hydrocarbons
(f) Nitrosamines
(g) Acrolein and acrylonitrile
(h) Chlorobenzenes
(i) Haloethers
(j) Chlorinated hydrocarbons
TABLE C-2 lists the analytical methods used during Verification.
Details of each analytical procedure, including precision and accuracy data,
are presented in the September 1980, report by W. F. Cowen and J. L. Simons of
Catalytic, Inc., entitled "Analytical Methods for the Verification Phase of
the BAT Review", under EPA Contract No. 68-01-5011. Analytical methods were
varied as required by the sample matrix and each variation was assigned a
number. Any method used in the program was identified by a procedure code
number, a variation number, and the laboratory that was responsible for its
initial use. Several of the procedure codes include methods that were 'later
submitted for validation to EMSL contract laboratories.
Dr. W. F. Cowen of Catalytic, Inc. continually summarized and studied
the precision and recovery data to determine which methods gave the most
consistent results despite a variety of wastewater matrices. Supplementary
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TABLE C-2
ANALYTICALS METHODS USED DURING THE VERIFICATION PHASE
ANALYTICAL PROCEDURE
CODE NO.
Direct Aqueous Injection Procedure for GC
Analysis of Acrolein and Acrylonitrile
Method for Benzidine and Its Salts in Wastewater
Method for Organochlorine Pesticides and Phthalat-e
Esters in Industrial Effluents
Total Cyanide
A-26 Resin/GC-FID Method for Phenols
Analysis of Nitrosamines
Microextraction Method for Organic Compounds in
Industrial Effluents
Purge-and-Trap Procedures for Analysis of Volatile
Organic Compounds in Effluents
Method for Polychlorinated Biphenyls CPCB's) in
Industrial Effluents
Analysis of Arsenic and Selenium in Industrial Effluents by
Flameless Atomic Adsorption Spectrophotometry and
Hydride Generation
Analysis of Silver, Antimony, and Thallium in
Industrial Effluents by Flameless Atomic
Adsorption Spectrophotometry
Analysis of Beryllium, Cadmium,' Chromium, Copper,
Nickel, Lead and Zinc in Industrial Effluents by
Flame or Flameless Atomic Adsorption Spectrophotometry
Mercury in Water (Manual Cold Vapor - Atomic
Adsorption Technique)
Pentane Extraction of Organics in Wastewaters
for GC Analysis
1*
2
3*
4
5
6
7*
10*
11*
12*
13*
14*
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TABLE C-2 (Concluded)
ANALYTICAL PROCEDURE CODE NO.
Acid Extraction Procedure for Phenols 15
Analysis of Nitroaromatics, Isophorone, and 16
Chlorobenzene
Analysis of Polynuclear Aromatic Hydrocarbons 17
in Industrial Wastewater
Procedure for Vapor Equilibration (Headspace) Analysis 18
Procedure for Determination of Phenolic Compounds 19
by Solvent Extraction
Procedure for the Determination of Neutral and 20
Basic Compounds by Solvent Extraction
Procedure for Volatile Aromatic Hydrocarbons by 21
Solvent Extraction
NOTE: Code numbers 1 through 18 are the procedures initially compiled for
OCB by Envirodyne from EMSL and NEIC information. Procedures 19
through 21 are modifications of procedure Number 7 (Microextraction)
for specific groups of organic compounds. Code numbers with an
asterisk(*) are those 13 routinely used by OCB's contractor
laboratories.
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laboratory studies at A.D. Little and Greenwood Labs further developed those
methods that showed promise of general applicability. Of the methods
originally compiled, some were never practiced because the classes of priority
pollutants (e.g., pesticides, PCBs) requiring these methods were not
encountered. From the initial compilation of 18 methods used for analyzing
organic priority pollutants, 13 were routinely used by OCB's contractor
laboratories.
OCB's choice of GC/CD methodology during the Verification phase in
preference to the GC/MS Screening protocol resulted in the following
advantages:
(a) GC/CD quantification was simplified, through compound
spiking to generate recovery data. GC/MS support was used
in a number of instances for pollutant identification.
(b) For the typical case of monitoring 10 to 20 compounds by
two to three methods, the cost using conventional detectors
was less than that using the mass spectrometer. According
to information presented by W.L. Budde and J. W.
Eichelberger of EPA-EMSL in "Analytical Chemistry", Vol.
51, No. 6, May 1979, p. 567A, for 10 compounds, the cost
using conventional detectors is about one-third that using
mass spectrometry; for 20 compounds, GC/CD costs about 40%
of what GC/MS costs.
(c) The time required for a given analysis was reduced. At the
inception of the program, GC/MS laboratories were
delivering analytical results three to six months after
receipt of the samples. The GC/CD methodology reduced this
delivery time to one month.
(d) The wider availability of GC/CD instrumentation and
qualified analysts/technicians at the time facilitated the
analysis of the large number of samples from the many
product/processes studied.
A disadvantage anticipated for GC/CD was that it would require more
clean-up of the solvent extract in order to separate subclasses of priority
pollutants from each other, as well as from other organic compounds in the
sample matrix. In each of the wastewater samples that were examined, no more
than 20 priority pollutants were detected; generally 10 to 20 were detected.
Chromatographic resolution problems were less than expected, because those
subclasses of priority pollutants that are difficult to separate from one
another were rarely present in the same sample.
The traditional exhaustive solvent extraction/evaporative
concentration methods used at the beginning of the program were gradually
replaced by simplified and more expeditious extraction procedures, the most
important of which was microextraction. Volatile organic compounds were
traditionally extracted exhaustively (continuously or in multiple steps) with
excess solvent, coextracting much of the organic matrix. Subclasses of
priority pollutants then had to be separated from interfering organic
C-21
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components by sample cleanup before concentration by evaporation. For the
simpler and faster microextraction, a small aliquot of the sample was
extracted in one step with an even smaller amount of solvent (100:1).
Partitioning of many priority pollutants into the extraction solvent (aided by
salting out) left most of the GC-interfering organic compounds in the sample.
With the right choice of GC column conditions, it was frequently unnecessary
to cleanup the extract to separate interfering organics for a satisfactory GC
analysis. Because the extract was already concentrated, evaporative
concentration of the extraction solvent was unnecessary. This shortened
analysis time significantly and eliminated the potential for alteration or
loss of sample components during evaporation.
Later in the program another innovation was implemented: static
head-space analyses of volatile organic compounds. This technique's
advantages for measuring volatile organics are analogous to the advantages of
microextraction for measuring extractable organics. Its original purpose was
to prevent the loss of volatile compounds in cases where it was necessary to
open the septum-sealed vial for transfer to a purge and trap apparatus, or for
compositing.
Another change from traditional methodology was the use of liquid
crystal and capillary GC columns for separation of polycyclic aromatic
hydrocarbons.
Analysts were allowed to use any method that they considered
applicable to a particular sample, as long as it did not require routine use
of the GC/MS. The analysts were, however, required to execute QA/QC
procedures adequate to validate the method used.
3. Quality Assurance/Quality Control
The QA/QC program for verification evolved in three stages. In 1978
(Stage 1), the first six plants were verified with a QA/QC program consisting
of a blind spike on the Day 2 composite sample. In the next set of five
plants (Stage 2), spikes were added at 2 to 5 times the concentrations
detected in the grab samples taken at the pre-sampling meeting. In addition,
duplicates of 10 percent of the Day 2 and Day 3 samples were analyzed. When
plant personnel collected and analyzed the samples (self-verification), an OCB
contract laboratory collected split samples and analyzed them, spiking samples
collected on Day 1 of the verification exercise to a concentration double that
detected in the unspiked sample. Stage 3 was the program indicated in FIGURE
C-2, in which a designed set of spike and duplicate samples were taken. An
unspiked, stored control sample (taken on Day 3) was required only in cases of
prolonged storage (greater than 48 hours) before spiking. This control was
rarely required.
Before adding the spike, it was necessary to wait for the results of
the unspiked sample analyses, so that the spike level could be made
appropriate for accurate calculation of the recovery of the added spike.
Recovery was calculated as:
0/ _ ,,.,. .. [Detected in Spiked Sample] - [Detected in Unspike Sample] X
% Recovery = 100 X a — —^ , A .j j i—r,—; c c—
3 [Added as Spike]
C-22
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FIGURE C-2
VERIFICATION QUALITY ASSURANCE/QUALITY CONTROL PROGRAM
DAY 1
EXTRACT
EXTRACT
ANALYZE
ANALYZE
DAY 2
EXTRACT
HOLD,
SPIKE
ANALYZE
EXTRACT
AND
ANALYZE
EXTRACT
ANALYZE
DAY 3
HOLD,
SPIKE
HOLD
EXTRACT
AND
ANALYZE
EXTRACT
AND
ANALYZE
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where [] denotes concentration.
The formula assumes that the volume of the added spike was small
compared to the sample volume. Otherwise, corrections must be made to account
for the added volume.
During the Verification program, the recommended concentrations to
add for spiking were:
(a) Twenty times the instrument-response detection limit, if
the sample concentration was less than 10 times the
instrument-detection limit; or
(b) Two times sample concentration, if the sample concentration
was at least 10 times the instrument-detection limit.
Ten percent of the samples analyzed for metals and cyanide were
spiked, and duplicate analyses were performed on 10 percent.
The purpose of determining spike recoveries on two of the three
samples collected at each site during verification was to calculate the
efficiency of solvent extraction procedures. Measured concentration may be
adjusted for spike recovery. For example, if only 50 percent of the phenol
that had been added was detected, the unspiked sample concentration of phenol
detected was assumed to be 50 percent of the correct concentration.
Correction of the measured concentration may be made by the following equation:
... . , „ . . . -, ™ v Measured Concentration
Adjusted Concentration = 100 X - —^ 7-——
J Percent Recovery of Spike
In the case of metals and cyanides, which were not extracted by
liquid/liquid partitioning, no adjustments were made to the raw data, although
spike recovery data was reported by some of the analytical laboratories.
Recovery efficiency and consistency were useful to the analysts during
verification in judging whether or not an extraction procedure was appropriate
to the sample matrix.
It should be noted that the proposed effluent limitations are based
on measured concentrations that were reported by individual laboratories.
These concentrations were not further adjusted mathematically for recovery of
spike, as indicated above. Exceptions to this are concentration values
measured by a system that was calibrated by adding the internal standard
directly to the wastewater sample (matrix). When calibration response factors
were determined by this procedure, concentrations measured were automatically
recovery-corrected.
C. CMA Five-Plant Study
Samples were analyzed for a selected group of priority organic pollutants
that were characteristic of each plant, together with certain conventional and
nonconventional pollutants. All organic priority pollutants included in this
study were not analyzed at all five plants. Analyses were not run for
pesticides, polychlorinated biphenyls, or metals.
C-24
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EPA's contract laboratories analyzed all influent and effluent samples for
selected organic priority pollutants using GC/MS or GC/CD procedures (44 FR
69464 et. seq., December 3, 1979, or variations acceptable to the EPA
Effluent Guidelines Division). For example, one EPA laboratory used GC
coupled with flame ionization detection (GC/FID). Approximately 25 percent of
the influent and effluent samples collected at each participating plant were
analyzed by the CMA contractor using the GC/MS procedures cited above. The
variations in the analytical procedures used by the EPA contract laboratories
and the CMA laboratory during this study are summarized in Appendix A of the
April 1982 Engineering-Science report entitled "CMA/EPA Five-Plant Study," as
are the sampling protocols for each of the five plants.
Each participant provided daily analyses of the convention/nonconventional
pollutants in their influent and effluent wastewaters, using the methods found
in "Methods for Chemical Analysis of Water and Wastes," EPA 600/4-79-020,
March 1979. Additionally, four of the participants analyzed from 25 to 100
percent of the samples collected by EPA for the same organic priority
pollutants that were evaluated by the Agency. At a minimum, those analyses
included duplication of the CMA contractor's analyses.
III. REVIEW OF DATA FROM SAMPLING STUDIES
A. Introduction
In June, 1982, the EPA requested the Environmental Engineering Committee
of its Science Advisory Board (SAB) to review portions of the Contractor's
Engineering Report on the Analysis of the Organic Chemicals and
Plastics/Synthetic Fibers Industries. Such reviews help EPA realize its goal
of developing regulations based on data obtained by credible scientific
methods. The SAB was asked to address three major issues in its review of the
analytical methods and data used in developing the proposed BAT effluent
limits.
1. The adequacy of the overall experimental plan, the analytical
methods used and the application of those methods.
2. The quality of the data presented, particularly with respect to
whether compounds were adequately identified and whether
accuracy and precision were determined.
3. The adequacy of the data for drawing reasonable conclusions from
which defensible effluent guidelines could be developed.
At the time of the request, the EPA had not yet completed its summary of
the Verification data upon which the proposed BAT effluent limits are based.
The SAB was, therefore, unable to address issues (b) and (c). The material
available for SAB's review included:
1. A description of the technical approach that was used by EPA and
its contract laboratories in developing analytical methods
during Verification (see Part I of this Appendix).
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2. The analytical methods with multiple variations that were
developed and carefully documented during Verification,
accompanied by a summary of the recoveries obtained with these
methods in a wide variety of OCPSF wastewater matrices.
3. The QA/QC methodology that had been employed during Verification
to establish the precision and accuracy of the analytical
results.
The SAB criticized the dominant use of GC/CD methodology during verification
on grounds that compound identification had not been adequately confirmed.
The SAB also criticized the QA/QC methodology as being insufficient.
Subsequent to the SAB criticisms, the OCPSF Industry also criticized the
verification analytical methodology on similar grounds. At SAB meetings,
however, representatives of the OCPSF Industry have stated that during
Verification the EPA:
1. Used state-of-the-art GC/CD methods.
2. Used more QA/QC than the OCPSF Industry could have afforded.
In response to these criticisms, EPA has conducted an extensive review of
all organic priority pollutant analytical data that it has used in support of
the proposed regulations. A similar review for the metal priority pollutant
data was unnecessary, since neither the SAB nor the OCPSF Industry were
critical of that analytical methodology. The review will be completed prior
to promulgation of a final rule. All data not meeting the standards of
quality described in the following sections are being deleted from that
database being used to develop the regulations.
In the following sections, the method by which the analytical data was
reviewed and its quality assessed is described for the three data collection
programs:
1. Screening Phases I and II
2. Verification
3. CMA Five-Plant Study
B. Screening Phases I and II
1. Description of the Review
Section II.1 of this Appendix described the analytical methods
employed in Phase I and II Screening. Screening data was from one-day
composited samples of both treated and untreated wastewaters from over 143
OCPSF manufacturing plants. These studies were the first comprehensive
analysis of OCPSF Industry wastewaters and EPA's first large scale field use
of GC/MS analytical procedures. At that time, the Agency did not have an
existing database on priority pollutants for the OCPSF Industry, nor had a
predictive scheme been worked out to show the relationship between
product/process chemistry and the occurrence of priority pollutants. Thus,
there was nothing available with which the screening results could be
compared. Since QA/QC was not extensive in the screening protocol, there was
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no systematic means of detecting problems with the analytical procedures with
which the data was being acquired.
2. Use of Phase I and II Data
Screening data from a plant, plus additional priority pollutants that
were suggested by the raw materials and process chemistry of the products
being manufactured at the plant, were used during the verification program to
develop a presumptive list of priority pollutants that were to be verified at
that plant. These considerations were also part of the priority pollutant
selection criteria for plants in the EPA/CMA Five-Plant Study.
The OCPSF plants that were selected for screening during Phases I and
II, represent a broad coverage of the product classes listed under the
corresponding SIC Codes for these two industrial categories. Thus a
compilation of the priority pollutants that were identified during screening
of the combined untreated contact process wastewater of all of these plants
constitutes a universe of priority pollutants that characteristically occurs
within the industry.
The screening data were also used in a multivariate statistical
analysis to confirm subcategories. This application of the screening data
recognizes the semi-quantitative nature of the data (see Appendix F,
"Subcategorization Multivariate Analysis").
C. Verification Phase
1. Background
The Environmental Engineering Committee of EPA's Science Advisory
Board (SAB) reviewed the technical approach to wastewater analysis for
priority pollutants that had been used during Verification, but not the raw
data. The "Report of Meeting in Chapel Hill, N.C. June 24-25, 1982" included
in those minutes the findings of the SAB's analytical consultants. This
review is still underway and will be completed before publication of the final
rule.
2. 1982 Data Review by Original Contract Laboratories
EPA employed six contract laboratories to analyze samples from 29
direct discharge plants in the 1978 to 1980 Verification Study. SAB's major
concern was that all the laboratories had used GC/CD (gas chromatography with
conventional detectors) methods, which SAB felt needed confirmation by GC/MS
(gas chromatography with mass spectroscopy detection) and more extensive
QA/AC. The results from three plants were not reviewed extensively because
all GC/CD data from the EPA contract laboratories that analyzed samples from
these plants had been confirmed by GC/MS during Verification. At two of these
three plants, samples had been split and analyzed by both a laboratory under
contract to the plant and the plant laboratory. The plant laboratory data
agreed with its contract laboratory data within the limits considered normal
for these analyses, which obviated a need for extensive review of the data
from these plants.
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The remaining four EPA contract laboratories performed analyses for
samples from the remaining 26 plants. The analysts that had been responsible
for the Verification analytical work at the four laboratories met in October,
1982, to adopt a uniform approach to validating the GC/CD data and to attempt
to locate all data that might be of some use in confirming the Verification
GC/CD data.
From October, 1982, to March, 1983, all of the former EPA contract
laboratories and principal analytical chemists from the Verification program
cooperated in a review of the data, using the review procedure that had been
developed at the October meeting. The analysts examined laboratory notebooks,
chromatograms, mass spectral tapes and other information that documented the
methods that had been used during Verification. EXHIBIT C-l (at the end of
the Appendix) is a copy of the form used for this review. Every data point
obtained by the four laboratories has been or will be reviewed. Pending
completion of the review, the data bank for these proposed effluent
limitations, which was frozen in December, 1982, has been made available in
summary format as part of the public record.
3. Results of the Review
(a) GC/MS Confirmation of GC/CD Data. The presence of many
priority pollutants that had been detected by GC/CD during the analysis of
Verification Samples was confirmed by GC/MS, or had been confirmed by GC/MS in
a preliminary grab sample. These confirmations were encoded into the
December, 1982, BAT data summary. While EPA limited the use of GC/MS by its
contract laboratories during Verification, the laboratories eventually applied
GC/MS confirmation to more than 10 percent of the total samples that were
analyzed.
(b) GC/CD Data Qualitation. The criteria EPA applied during
its recent review of Verification GC data to eliminate questionable data
points were more rigorous than those that were proposed in the 600-series
methods (Federal Register, Vol. 44, No. 1233, pp. 69464 to 69552, December
3, 1979), and are nearly identical to published revisions of the 600-series
GC/CD methods (EMSL, Cincinnati, EPA-600/4-82-057, July 1982). The only major
difference is the criterion for retention time agreement between standard and
sample. The 1979 600-series methods do not specify the maximum retention time
discrepancy that is acceptable for the identification of a specific compound.
The EMSL's July, 1982 revision of these methods proposes "three times the
standard deviation of a retention time for a compound"..."based upon
measurements of actual retention time variations of standards over the course
of a day", and "... the experience of the analyst should weigh heavily in the
interpretation of chromatograms". For confirmation of Verification results,
EPA's review contractor measured the retention time difference between GC
charts with a millimeter scale (aided by overlaying the charts on a light
table at some laboratories), or by integrator. EPA's contractors thus applied
1982 criteria to their qualitative review of the GC/CD Verification data.
(c) GC/CD Data Quantitation. Quantitative measurements at
EPA's contract laboratories employed multi-point calibration over the working
range of the detection system for compounds with non-linear responses, and
single-point calibration for those compounds with a linear response. These
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calibration procedures are the same as those proposed by EPA in 1979 (Federal
Register, Vol. 44, No. 1233, pp. 69464 to 69552, December 3, 1979) and in the
July 1982 EMSL methods (EPA-600/4-82-057).
(d) Interlaboratory Comparisons. During Verification at
several plants, duplicate samples were analyzed by the plant's laboratory, by
a commercial laboratory under contract to the plant, or by the EPA contract
laboratory. The data from these analyses offers both qualitative and
quantitative comparisons between labs using the same methodology, or where one
laboratory used GC/CD while the other laboratory used GC/MS. Such comparisons
can be made, when all of the information garnered from the review has been
encoded.
4. Effect of the Review on the OCPSF Industry Database
Data for organic priority pollutants that were collected from six
plants during Verification have already been deleted from the statistical
analysis to determine BAT effluent limitations. These plants were sampled
early in the Verification program, when blind spiking was used in the QA/QC
procedure. In those instances in which an inappropriate spiking level was
used, the data would certainly be quantitatively unreliable and may often be
qualitatively suspicious. Since this data was of variable quality, a decision
was made to exclude all of it from the statistical analysis.
Since the review will provide GC/MS confirmation for many GC/CD data
points, it is expected to enhance the overall quality of the database and
justify retainage of most of those influent-effluent data pairs with a
significant difference in concentration. In general, the review of the
Verification data focused on influent-effluent data pairs where the influent
concentration was greater than about 30 ppb.
D. CMA Five-Plant Study
1. Description of the Review
Section V of Volume II describes the Five-Plant Study. Late in 1982,
EPA staff and contractors reviewed the data by comparing results from analyses
of the same samples at (1) EPA contract laboratories, (2) CMA contract
laboratories, and (3) the plant laboratory or plant contract laboratory.
Errors in transcription and encoding and in application of GC analyses were
found and corrected. This section gives details of this review.
2. Transcribing and Encoding Errors
In the Five-Plant Study, laboratories used GC/MS or GC/CD analytical
methods. The data were transcribed from instrument readouts to data sheets
and, in some cases, from data sheets to typewritten report forms. EPA then
encoded the data from the typewritten forms and data sheets into its
Five-Plant computer database. The Agency's 1982 review of printouts from this
database revealed occasional disparities between the printout and results that
had been reported by laboratories. Typical errors were the transposition of
results from treated and untreated effluent streams, typographical errors, and
encoding errors. Copies of printouts with suspect values noted were sent to
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the original EPA contract laboratories and to the original participating CMA
laboratories for confirmation. Confirmed transcription and encoding errors
were corrected. In a few instances, laboratories corrected the GC/MS results
after re-examining the original analytical data recorded on magnetic tape.
The laboratory originally responsible for each data point made the final
decision on correcting that data point.
3. Errors from Improper Application of GC/CD Methods
When the Five-Plant Study began, EPA sent samples to an EPA
contractor laboratory for analysis using GC/MS methods. From these results,
EPA determined which GC/CD methods its contractor laboratory should employ for
monitoring the treated and untreated wastewaters at three of the five plants
for the 30-day period. In contrast to the flexibility afforded EPA contractor
laboratories during the Verification Phase, EPA contractor laboratories in the
Five-Plant study were not permitted to modify the selected GC/CD methods or
employ alternate methods, if an interference was suspected. EPA now admits
this approach was faulty. The contractor laboratories should have been
permitted the same flexibility in response to GC/CD interferences, or only
GC/MS methods should have been employed.
For each plant, a technical contractor's review compared GC/CD data
from EPA's contract laboratory with GC/MS results from the CMA plant
laboratory, or CMA contract laboratory. These data showed significant
disparities. EPA was then faced with determining which data were acceptable.
Two approaches were applied: (1) the GC/CD and GC/MS results were compared
statistically; and (2) the technical contractor's review of the GC/CD data
evaluated concerns such as the potential interference with GC/CD peaks by
non-priority pollutant compounds. The EPA review staff and technical
contractor reviewed the chromatograms supporting the GC/CD data at the IFB
contractor's facility. In addition, the IFB contractor reviewed the
chromatograms and detection limits data and subsequently recommended some of
the major changes described next.
The results of the statistical comparison, a paired-sample T-test,
were inconclusive because of a shortage of both GC/CD and GC/MS analyses from
split samples. EPA's review contractor recommended removal of all GC/CD data
from the CMA Five-Plant database because of the disparities with GC/MS
results, the impossibility of determining which GC/CD data points were valid,
and the failure to use the interference elimination options which had been
employed in Verification Phase GC/CD methods.
Following the review contractor's technical recommendation and on its
own technical evaluation, EPA decided to delete all GC/CD data from the
Five-Plant database. Deletion of GC/CD data reduces the total number of data
points by approximately 60 percent. However, GC/MS data exist for all the
pollutants detected by GC/CD at all plants. EPA has determined from
interlaboratory comparisons that the remaining GC/MS data are adequately
precise and accurate for developing the proposed BAT effluent limits.
Therefore, all GC/MS data from the Five-Plant database have been retained.
C-30
-------
EXHIBIT C-l
ORGANIC CHEMICALS VERIFICATION (OCV) PROGRAM
METHOD VALIDATION FORM
LABORATORY:
1. APPLICABLE OCV DATA
METHOD PLANT
POLLUTANT
STREAM
METHOD SUMMARY
2.1 Extraction:
2.2 Column: Length _
Packing
2.3 Detector: „
I.D.
Plates
Est
CONFIRMATORY DATA
3.1 Confirmed by GCMS
Other
3.1.1 Qual confirm: Yes
3.1.2 Quant confirm: Yes
GC ug/1 GCMS
2nd Column
_ No _
_ No _
_ ug/1
2nd Temp
3.2 Describe "other" confirmatory technique
3.3 Describe how confirmatory technique was applied:
4. QUALITATIVE DETAILS (not required if results are confirmed both
qualitatively and quantitatively by GCMS)
4.1 Retention time window as compared to standard
4.1.1 Absolute ± sec Est Meas
4.1.2 Relative ± Est Meas Int Sd
4.1.3 Specification applied? Yes No Est
C-31
-------
4.2 Peak width @ half height
4.2.1 Of standard: mm
4.2.2 Before spike: mm Interference present?
4.2.3 After spike: mm Yes No
4.3 Specific detector/interferences
4.3.1 Nature of potential interferences
Responsive
Non-responsive
4.3.2 Specificity ratio (response to pollutant divided
by response to interference: FID = 1.0)
Responsive Est Meas
Non-responsive Est Meas
4.3.3 Other evidence that only a single compound was measured
4.4 Methodology to remove interferences
5. QUANTITATIVE DETAILS
5.1 Calibration
5.1.1 Int Std Ext Std
5.1.2 Number of initial calibration points
5.1.3 Frequency of calibration check
5.2 Detector Range
5.2.1 Within upper linear limit? Yes No
5.2.2 Within calibration limit? Yes No
5.2.3 Pollutant level measured: ug/1
5.2.4 Detection limit: ug/1 Est Meas
5.2.5 Signal-to-noise ratio of pollutant measurement
6. STATISTICS
6.1 Replicates
6.1.1 Initial number: % MD Est Meas .
6.1.2 Ongoing: % RSD Est Meas
6.1.3 Control limits: Upper: Lower:
C-32
-------
6.2 Inter-lab comparisons: % RSD Est Meas
List other labs
7. COMPARISON WITH 1979 FEDERAL REGISTER 600 SERIES METHODS (if method
used was 600 series method, skip this section)
7.1 Nearest 600 series method:
7.2 Expected comparison
7.2.1 Detection limit: Yes No Est Meas
7.2.2 Linear range: Yes No Est Meas
7.2.3 Specificity: Yes No Est Meas
7.2.4 Reproducibility: Yes No Est Meas
7.3 Was 600 series method available at the time this sample
was analyzed? Yes No
7.4 Do you feel that the method used produced data comparable
to the 600 series method on this sample?
Yes No
If no, why not?
8. RECONCILIATION WITH PRODUCT/PROCESS
8.1 Is pollutant presence consistent? Yes No
8.2 Was pollutant found in raw water or blanks?
Yes No
8.3 Evidence that matrix was constant:
9. REGULATORY
I believe the pollutant reported on this form was
qualitated and quantitated accurately.
Yes No
10. PERFORMANCE EVALUATION: Date
C-33
-------
11. Other comments
Signature: Date:
Print:
C-34
-------
REFERENCES
AMORE, F. 1979. Good analytical practices. Analytical Chemistry 51:1105a.
TAYLOR, J.K. 1981. Coordination for chemical measurement assurance and
voluntary standardization. Center for Analytical Chemistry, U.S. Department
of Commerce, National Bureau of Standards, Washington, B.C. From a letter to
OCB, September 3, 1981.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1977. Sampling and Analysis
Procedures for Screening of Industrial Effluents for Priority Pollutants.
USEPA, Environmental Monitoring and Support Laboratory, Cincinnati, Ohio.
March 1977 (revised April 1977).
WEBB, R.G. 1978. Solvent extraction of organic water pollutants. J.
Environmental Anal. Chem. 5 (3):239-252.
C-35
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APPENDIX D
ACTIVATED CARBON AND STEAM
STRIPPING QUESTIONNAIRES
-------
ACTIVATED CARBON QUESTIONNAIRE
D-l
-------
Company
Location
Date
U.S. ENVIRONMENTAL PROTECTION AGENCY
ORGANIC CHEMICALS BRANCH
EFFLUENT GUIDELINES DIVISION
SURVEY OF ACTIVATED CARBON WASTE WATER TREATMENT SYSTEMS
The purpose of this survey is to gather data on activated carbon
treatment for the removal of priority pollutants from waste water
discharges. Of particular interest are the procedure for design
of systems and the availability of procedures for predicting the
performance of activated carbon on priority pollutants, especi-
ally when other adsorbable or nonadsorbable compounds are present
Relatively simple and short responses to the questions will
generally suffice. However, any amplification or additional
comments will be appreciated.
D-2
-------
Company
Location
Date
PART I: SYSTEM IDENTIFICATION
1. Company
2. Location
Person responding or to whom further questions should be sent
3. Do you have an activated carbon system (ACS) operating on a
vaste water stream containing one or more of the priority
pollutants listed in Table I attached?
Yes ___ If the answer is yes, please continue with
this questionnaire. If more than one instal-
lation is involved, copy this questionnaire
and complete one set for each installation.
No ___ If the answer is no, please return the
questionnaire; no further data are required.
D-3
-------
Company
Location
Date
PART II: SYSTEM DESCRIPTION
1. Please diagram the treatment system using gross blocks for
pretreatment and post-treatment (if used) and more detail
for the activated carbon system (see examples).
2. Give flow rate of waste water Ib/hr
Temperature *F
Composition (at entrance to ACS contact)
3. Effluent composition after ACS contact.
4. AC loadings (by component, if available)
lb/100 Ib AC
5. Residual on AC after regeneration or reactivation (if used)
D-4
-------
Company
Location
Date
PART ZI: EXAMPLE DIAGRAMS
Waste
Water
Source]
off line carbon r~~T_
\bed & regeneration I {Scrubber
|| |
FIXED BED SYSTEM
.fter Burner
nace /
/
Pzetieaonsit
(Filter)
etc
rS- -
5?
^/
V ^
\ ^
_ .V..**
Carbon
Bed(s)
L
y
^.
/
/
/
/
/
/
Post-treatsnen-
(aeration
chlorination)
etc
i
Effluent
waste
Water
Source
•*—!
— \r\
v^y
|K
P
,
-------
Company
Location
Date
FAX? Ill: DESIGN BASIS
1. Has system bench scale tested or piloted before design?
Yes
No
2a. If answer to 1 is yes:
Describe tests and note whether individual components, a
synthetic mixture, or the authentic plant effluent was used,
2b. If answer to 1 is no:
Describe basis for design of plant unit.
D-6
-------
Company
Location
Date
FAST IV: COMMENTARY
Based on experience with the unit described, comment on the
following:
1. Can AC systems be specified from available design parameters
without need for tests?
2. If testing is believed necessary, describe briefly minimum
program to assure meeting effluent guidelines.
3. How does the actual performance of the unit described corre-
spond with the predicted performance? If available, give
quantitative results for individual components.
4. By hindsight, how would you modify the procedure used for
•pecif/ing and designing the subject systemr
D-7
-------
STEAM STRIPPING QUESTIONNAIRE
D-8
-------
Form Approved
OMB No. 158-R0160
Company
Location
Date
STEAK STKIPrING
Copy and answer Parts I through IV of this questionnaire for each
steam stripper used to reduce the raw waste loading prior to direct
discharge or discharge to an end-ol-pipe treatment system (wnether it
be a publicly owr.ed treatment worns, a regional industrial treatment
system, your own on-site treatment system, cr otner system such as a
nearby refinery's biological treatment system).
PART 1
1. List the names ot all process(es) whose waste water discharges
constitute a portion of the feed (charge) to the steam stripper. In
the event more than one process waste water str^ax manes up the ccarge
(feed) to the stripper, give the approximate percentage or eacn stream
on a flow or weight rate basis. Please place tne percentages or each
stream in the table below.
Stripper Feed Source *Percer.tage of feed
1. 1.
2. 2.
3. 3. „____
Total feed
tlow (gpffi) and/or weight (Ib/hr)
* Indicate whether basis is weight (Ib/hr) or flow (gpm)
D-9
-------
Company
Location
Date
Part II
This part of the survey requests information adequate to assemble a
trial material balance around the stripper. Operating data is the
preferred source of information requested in this part. Flow or
stream composition data based on lindted monitoring or calculations
(engineering estimates) is required as an alternative.
1. Please attach a process flow diagram of the steam stripper.
Kindly numoer and label all waste streams that are associated with tne
operation of the stripper such as the charge (feeJ), reflux, overhead
product, decanter water, bottoms, etc. Indicate in your drawing major
equipment items such as pumps, heat exchangers, etc. A sample sketcn
has been provided for reference.
2. Complete the attached Table I with the information requested for
each stream numbered in the sketch prepared in (1) above. Note that
two sets of information are requested. One set consists of general
Stream characterization parameters such as flow, temperature, pH, BOO,
Toe, etc. with spaces for additional or different characteristics, and
organic or inorganic compounds known to be present. The second set
labeled "component" refers to priority pollutants identified or
indicated to be present in the waste waters associated with the
stripper.
D-IO
-------
Company
Location
Dare
D-ll
-------
!
I Par* II
|
!
Sampl
e Process FT
••Steam Str-
ew 'Diagram
pping
I
!
1
!
_ J.. ...
Cujt
>S
fad1 (charge)
fred
,
I
fecoverfc* hue/ro car Joan
or
— •!- /
D-12
-------
-------
Company
Location
Date
Part III
This part of the survey requests information essential to evaluate the
operating performance of the stripper and the energy consumption of
the opera tier per unit of pollutant remove a from the waste water.,
1. Utility Requirements
A. Steam Requirements
Pressure
Temperature _ °i
Rate _ Its/hr
Is open steam used or does the coluirn utilize a reooiler?
______________ Cpen Steam Re toiler
B. Cooling Water Use
Condenser Influent Temperature _ °F
'Condenser Effluent Temperature _ °£
flow Rate _ gai/hr.
C. Other Energy Requirements
Electricity _ *wh
Compressed air scf m
Inert gas scf m
2. Column Specifics
(The sketch called for in 11(1) aoove can be expanded upon to provide
the following information) .
D-14
-------
Company
Location
Do re
Part
A.
fi.
C.
Ill (Continued)
Feed Rate
feed Temperature
Opera-ting Pressure
Top _
Bottom
D.
Operating Temperature
Top
Bottom
L.
F,
Column Diameter
Nuii.ber of Theoretical
Trays (if known)
No.
Actual Number of Installed
Trays or Packing Height,
Trays
Packing.
D-15
.Ib./hr.
usia
°F
ft.
fi.
I.
J.
K.
L.
K.
N.
O.
P.
Type of
Iray Sp
Overall
Reflux
Reflux
Reflux
Bottoms
Bottoms
Materia
Trays or Packing
acina ft.
Column Height ft.
Ratio* (if anv)
Rate Ib./hr
Temperature ° F
flow Rate Ib./hr.
Temperature °F
Is of Construction
No. or ft. (specify)
*Use overhead flow rate as the basis of this value
-------
Company
Location
Dare
Part III (Continued)
Column or Vessel
3. Specify the ultimate disposition ot column overhtaac (i.e.,
incineration, returned to process, etc.) tor both the aqueous and -the
organic phases.
4. Specify the method of disposition of column bottoms. (i.e.,
discharged to biological treatment, discharged directly to surface
waters, re use a as cooling tower max.e-up, etc.)
5. Are there any substances presenfiT* "the influer.t a LI- can -co the
steam stripper that interfere with the removal of the pollutant(&)
listed in (2) above. (i.e., maximum coiling azeotropes, pn
adjustment, foaming, scaling, necessity to equalize flow or fefei
concentration, etc.). If so, please list and exj-Iair -...- r.ature of
the interferences and any methods devised tc minimi2•=• -ir eliminate
these interferences. Also explain how successful these methods have
been.
D-16
-------
Location
Date
Part III (Continued)
6. Operating Specifics
A. Is the steam stripper operated in a continuous or uatc^ rr.cie?
If batch, explain.
B. Explain the method of treatment of th-= process was.ze»atfcr t**
as normally discnaiged to the strijper >»h2r. tnr stra:. striper i
dcwn for repair.
D-17
-------
Company
Location
Date
Part IV
your responses to the following questions will be used to determine
the desireability of additional fcllow-u{. relating to capital and
operating costs associated with the steam stripper.
A. Was the steam stripper installed as a new piece of
equipment?
Yes No
B. When was the steam stripper installed?
C. Do you have detailed cost information (both capital and
operating) relating to the steam stripper as a separate unit?
Yes No
D. Are you willing to share this cost information with ZPA to be
used to verify the cost of the installation of steam
strippers for the treatment of waste water.
Yes No
£. Operating Labor
Direct Operating work-days/yr.
Maintenance worx-days/yr.
Supervisory _woric-days/yr.
F. Do you have V-L equilibrium data which was used to design
the stripper from your own experiments, or Henry's Law
Constants, or vapor pressure data, or activity coeificient
data, or otner correlations?
No Yes Identify which one
D-18
-------
Company
Location
Dare
Part IV (Continued)
G. Do you have information regarding the cost impacts of
installing the stripper or. tne following off-site activities?
(check either Yes or No, or indicate (a) , (b) or (c) as appro-
priate)
Yes No
a. Steam generation or a
major revision in dis-
tribution
b. electrical substation
capacity
c. Instrument air capacity
d. Valve/Fiping/wiring
systems to supply a,
b, or c (a) (b) {c) (a) (h> ic)
D-19
-------
APPENDIX E
TREATABILITY STUDIES
-------
APPENDIX E
TREATABILITY STUDIES*
GENERAL
The following is a summary of treatability studies sponsored by the
Organic Chemicals Branch on activated sludge, activated carbon adsorption,
steam stripping, and organic resin adsorption processes. The intent of the
research was to collect data on biological and physical constants for specific
priority pollutants and derive methods for predicting the removal of
pollutants in single and multi-component waste streams. These data were
intended for use in benchmarking the Agency's computer Model (see Appendix
K).
BIOLOGICAL TREATMENT
Introduction
Activated sludge treatment is perhaps the most common treatment technology
practiced by industry. To determine which pollutants are effectively removed
by this technology in real systems, the Organic Chemicals Branch developed a
pollutant-based treatability model for activated sludge treatment. Beyond the
evaluation and application of existing models of biological processes, data
for specific priority pollutants were required to accurately predict their
susceptibility to removal, their effects on the biological treatment process,
and their fate during the treatment process.
*From U. S. Environmental Protection Agency. 1981. Contractors Engineering
Report Analysis of Organic Chemicals and Plastics/Synthetic Fibers Industries,
Effluent Guidelines Division, Contract No. 68-01-6024, Chapter 3.
E-1
-------
Biological treatment involves the breakdown and stabilization of organic
material by aerobic or anaerobic microorganisms. Organic matter is removed from
wastewater by microbial oxidation and cell synthesis, essentially accelerating the natural
water purification mechanisms. Bacteria are the primary organisms involved in the
transformation of waste constituents ultimately into carbon dioxide, water, cellular
building blocks, and energy. Treatment processes available for industrial application
include: variations of the activated sludge process, aerated lagoon systems, oxidation or
contact stabilization ponds, trickling filters, rotating biological discs, and anaerobic
lagoons, or digesters. Historically, the activated sludge process, in which aerobic
microorganisms are mixed with the influent wastewater and subsequently removed as a
sludge, has had the broadest application to industrial wastes. The toxicity of the waste,
the biodegradability of the waste (typically judged by the BOD/COO ratio), and the
metabolic rate of the microorganisms (i.e., the effective removal rate) all influence
process efficiency.
Basic environmental conditions (i.e., proper microbial growth conditions) must be
met for microbial metabolism and stabilization of the waste organics to occur. These
conditions include (I) oxygen availability, (2) near neutral pH, (3) available growth-limiting
nutrients, nitrogen and phosphorus, (4) absence of toxic materials, and (5) adequate
mixing. Further, biological processes can be designed to operate optimally by properly
controlling the following rate-controlling variables: (I) microorganism concentration, (2)
bacterial acclimation or adaptation, (3) temperature level, (4) contact duration and mode,
and (5) organic feed concentration.
The activated sludge process was chosen for the modeling effort conducted by
Catalytic, Inc., because it has proven to be cost-effective in treating relatively low
concentrations of organics found in industrial wastes, and can be designed to provide more
operational flexibility than other types of biological treatment. A flow diagram for a
E-2
-------
typical activated sludge process, in which aerobic microorganisms are mixed with the
influent wastewater and subsequently removed as sludge, is shown in Figure E-l.
FIGURE E-l
TYPICAL ACTIVATED SLUDGE PROCESS
ACTIVATED
SLUDGE
REACTOR
RAW
WASTE
WATER
PRIMARY
CLARIFIER
(optional)
FINAL
CLARIFIER
WASTE
.SLUDGE
TREATMENT
SLUDGE RECYCLE
SOURCE: Kinconnon and Gaudy, no date.
Biokinetic Models
The theoretical approach used in the design of biological treatment systems is to
develop mathematical models which depict relationships between parameters that control
efficiency of microbial growth and substrate removal. The purpose of these design models
is to provide predictive equations consistent with the underlying metabolic principles
governing the waste treatment process. The general approach to developing biokinetic
models is to write mass balance equations describing the mass rate of change !n substrate
(i.e., organic pollutants) and in biomass of the microorganisms. The models incorporate
various assumptions regarding fundamental relationships governing microbial growth, and
factors derived from laboratory bench scale or pilot plant studies.
Various models, or kinetic approaches, are available for use in designing
activated sludge processes. The basic formulas for four well-known models—
Eckenfelder's, McKinney's, Lawrence and McCarty's, and Gaudy's—are presented in
Table E-l. A materials balance for substrate (S) can be derived, as shown in Table E-2
from each equation.
E-J
-------
TABLE E-l
KINETIC APPROACHES FOR THE ACTIVATED SLUDGE PROCESS
Design Approoch
Eckenf elder
Basic Formula
- Se) F
S X
si
-------
TABLE E-l (Continued)
k . = Maintenance energy coefficient (all models)
6 = Sludge retention time (mean cell retention time)
a = Recycle flow rate
SOURCE: Kincannon, 1979.
E~5
-------
Gaudy
TABLE E-2
MATERIALS BALANCE FOR SUBSTRATE, S
Balance
Model
Eckenfelder
McKinney
Lawrence-
McCarty
Mass Rate
of
Change
H- -
H -v •
dS T,
dt -v -
Mass Rate
due to
Inflow
F.S. -
F.S. -
F.S. -
Mass Rate
due to
Outflow
F.Se -
F.Se -
F.Se -
Mass Rate
due to
Metabolism
KeX.Se.V
Ve'7
S.
KV .^M^^H^^ '
* • v AC *
-Pi
Where:
V
X
F
F
w
t
se
"m
K
max
f
t
Volume of the reactor
Influent BODj
Effluent BOD5
MLSS or MLVSS
Influent flow rate
Solids wastage flow rate
Eckenfelder's 1st order substrate removal rate constant
McKinney's substrate removal rate constant
Maximum substrate utilization rate (Lawrence and
McCarty)
Saturation constant (Lawrence and McCarty, Gaudy)
Maximum specific growth rate (Gaudy)
True cell yield (all models)
Recycle flow rate
SOURCE: Kincannon, 1979.
E-6
-------
Based on an comparison of these four models by Kincannon and Gaudy (no date)
and Kincannon (1979), certain relationships are held in common in each of the mass
balance equations:
I. The mass rate of change of substrate in the reactor is equal to the rate of
change in concentration of substrate (dS/dt) multiplied by the volume of
the reactor (V).
2. The rate of change of substrate concentration is increased by the inflow of
the substrate.
3. The rate of change of substrate concentration is decreased by the flow of
substrate concentration out of the reactor, and by the rate at which
substrate is utilized for growth of the microorganisms in the reactor.
E-7
-------
Eckenfelder's ond McKinney's Models
Eckenfelder's and McKinney's models are developed assuming that the irate of
substrate removal is a first order reaction. The models differ in the relationship used to
describe the substrate utilization rate. In McKinney's model, this term is dependent only
upon the substrate concentration in the reactor (Sg) and a substrate removal rate constant
0
-------
Goudy's Model
Gaudy's model, also based on Monod kinetics, differs from the above three as a
result of writing the mass balance around the bioreactor rather than around the whole
activated sludge process. This approach separates the biological unit process of biological
growth and substrate utilization occurring in the activated sludge tank from the unit
operation of physical separation accomplished in the clarifier (see Figure E-2). As a
consequence of writing the balance around the bioreactor, the effect of a (a factor
related to solids recycling) on the substrate balance is noted. The mass rate of substrate
utilization is related to the growth of the biomass and the biomass "constants", i.e., the
maximum specific growth rate (ymax), the saturation constant (K ), and the "true" cell
yield (Yf).
E-9
-------
FIGURE E-2
FLOW DIAGRAM, ACTIVATED SLUDGE PROCESS SHOWING
NOTATION AND MASS BALANCE ENVELOPES
. 1 —1
1 I
1
lS,.P.X0l
1 j
1
1
1
1
1
1
1
1
1
St,x
V
BIOREACTOR
/ — x
1 / \
n*0)p ' . f njin VIP-PW), X..S.
\ J
\ ^>*~^ ^^r
Of, X.
?m i X» , S«
I
SOURCE: Kinconnon, 1979.
Doto Development for Siokinetic Models
One feature common to all of the kinetic approaches described above is the
inclusion of biokinetic constants, or K-rates. Reliable biokinetic constants, values
determined empirically in wastewater treatability studies, are necessary if the design
models are to have an accurate predictive application.
In the Catalytic modeling approach, kinetic formulas are used to calculate
removal of organic matter by the activated sludge process. As Catalytic's approach
involved the determination of rate coefficients for each product/process waste load, two
types of treatability data were required:
I. Reaction rate constants for BOD, and
2. K-rates specific to the pollutant regardless of its product/process source.
The individual process stream data identified during field sampling were used to calculate
a weighted-average reaction rate for the summation of the BOD load from the
E-10
-------
contributing product/processes. Thus, the activated sludge process design was based on
that weighted-average BOD reaction rate (K-rate) that describes the total plant waste.
For the development of pollutant-specific K-rates, treatability data requirements were
two fold: the biological reaction rate (K-factor), and the lowest attainable
concentration.
Based on data obtained from OCB's screening and verification sampling and
analysis program, from EPA's 308 questionnaires,
and from Catalytic's laboratory test results, treatability
factors for individual pollutants were calculated using the following equation:
K - So-sose
TXSe
where:
K = Treatability factor for any priority pollutant (day~ )
S « Influent concentration (mg/l) of the priority pollutant
S s Effluent concentration (mg/l) of the priority pollutant
X = Mixed liquor volatile suspended solids (mg/l)
T s. Basin detention time (days).
For a more complete discussion of the development of the treatability factors used in
the Catalytic computer model, see the 1980 Catalytic Report. The treatability data
developed by Catalytic during the 1980 analysis of the applicability of activated sludge
appear in the Parameter and Treatment Selection file (Catalytic, 1980).
E-ll
-------
The minimum attainable value for a priority pollutant in the treated effluent was
considered to be the lowest value observed in an effluent for which data was considered
acceptable. Of the 115 organic priority pollutants, biological treatability factors for 86
pollutants were established in this manner.
For 20 other priority pollutants, the biological treatability factor was estimated
by using Eckenfelder's Modified (zero-order) Equation:
xt
where:
S = Influent concentration, mg/liter
S = Effluent concentration, mg/liter
X = Mixed liquor volatile suspended solids concentration
(MLVSS), mg/liter
t = Hydraulic retention time, days
K = Reaction rate constant, day" .
However, there were several areas where information was needed to support the
computer modeling effort relative to biological treatment. Specifically, more data were
needed on the relative treatability of certain compounds, compound groups, priority
pollutants and process raw waste loads. More work was needed relative to finding and
supporting the best predictive mathematical process model. As such, a main objective of
the Catalytic work was to refine or continue to verify the method of combining kinetic
factors of components of a mix to determine the overall treatability of the wastewater.
To have run laboratory studies in order to determine biokinetic constants for every
possible combination of organic chemicals would have been prohibitively expensive and
time consuming. However, the determination of biological constants for wastes contain-
ing single compounds was feasible; and from this data constants could be combined to give
E-12
-------
a single constant for wastes containing a mix of organic compounds. Grau-type K values
as high as 20 day" have been encountered and values between 2 and 10 day" have been
determined for other chemicals. There is, however, a lower range of K's for which data is
lacking. Systems utilizing chemicals with low K values are the most difficult to operate
because upsets are easier to provoke and the slowly degradable organic chemicals often
present handling problems.
Methodology Development
To address the problem of an inadequate data base, Catalytic, Inc., under
contract to Effluent Guidelines Division's Organic Chemical Branch has developed a
methodology for bench-scale biological studies to evaluate treatability factors (K-factors)
of selected organic compounds. The treatability of various classes of organic chemicals
had previously been grouped through the use of literature surveys according to
degradability. As such, five general classes of degradability were established, as shown
in Table E-3
TABLE E-3
CLASSES OF DEGRADABILITY
CLASS K RATE
1. Highly degradable
II. Easily degradable
III. Moderately degradable
IV. Slowly degradable
V. Biostatic or biotoxic
20
10
2
0.5
0
The best method of combining K values (e.g., straight average, rate limiting K, weighted
average, etc.) has not yet been deter-mined. Presently, the average of component K
factors is being used.
Chemicals were classified by existing degradation data or by structural analysis.
E-13
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InitiaLwork to gain more precise information on specific treatability factors and
on combining K-rates was performed by Catalytic from 1976 to 1978 (Catalytic, I979b). In
these initial experimental systems, the chemical or chemicals of interest were used as the
sole source of carbon for the bacteria. This type of laboratory operation represents an
artificial situation which is not likely to occur in a full scale chemical plant. Also,
because of the very specific biological population which develops under these conditions,
operational problems were encountered.
Thus, a new laboratory methodology was devised as part of a Phase 2 study to
overcome some of these operational problems. The new systems used sludge age as a
variable, since this parameter is required to evaluate all the current biological models.
Another significant change from the earlier work was that a portion of the feed for each
system was made up of a mixture of readily biodegradable organic compounds, in addition
to the chemical of interest. This "base mix" was composed of ethylene glycol, ethyl
alcohol, glucose, glutamic acid, acetic acid, phenol, and nutrients (ammonium sulfate,
phosphoric acid and salts) as required. In addition to stabilizing the bench scale system,
the impact of non-biodegradable and/or slightly biodegradable compounds on biokinetic
rates could then be evaluated.
The kinetic equation used in the Catalytic system is the Grau model (or
Eckenfelder's second order equation). This approach has enjoyed acceptance by industry
and allows more flexibility in predicting effluent quality under varying influent con-
centrations, which typically occur in industrial biological treatment systems, than does a
first order equation. Other kinetic models such as those utilizing solids retention time
(SRT) as a primary variable (which includes the Lawrence and McCarty models and the
Gaudy model), were considered less extensively verified. The Grau equation is shown
below:
E-14
-------
e xt
where:
K = kinetic constant
S = BOD influent concentration (mg/liter)
S = BOD effluent concentration (mg/liter)
X = MLVSS (mg/liter)
t = Aeration time (days)
Gaudy (I960) has pointed out some limitations of the Grau model; it is not a good
mechanistic relationship because it combines at least four separate biokinetic constants
known to be determining factors in characterizing the behavior of activated sludge into
one "constant", and combines separate engineering control parameters which indepen-
dently affect S . Further, operating conditions such as net specific growth rate which can
affect the performance of an activated sludge system, are not built into this model for
assessing removal of priority pollutants. However, Gaudy also noted that industrial
information expressed in terms of the Grau model was more readily available, and that
the model would prove useful for estimating effluent guidelines relating to biological
treatment for a broad group of combinations of compounds. He has recommended the
gathering of kinetic data applicable to the testing of a variety of models in order to verify
or modify values used in the Catalytic computer model; such research is presently in
progress at Oklahoma State University (see the following section).
To obtain a K value for a specific chemical based on the Grau model, Catalytic
ran several bench-scale systems to obtain different effluent BODs. The values of
o o" e were plotted versus the effluent BOD values; the slope of the resultant line
Xt
equaled the K value for the chemical in question.
E-15
-------
From Catalytic's Phase 2 experimental work came kinetic information on 15
compounds, tested with "base mix" only and in combination, and run at various loadings.
Compounds selected for study represented known raw materials, products and by-products
expected in industrial effluents, groups of chemical compounds for which little biotreat-
ability information was available, and priority pollutants where possible. Other primary
considerations in selecting compounds for study included solubility, volatility, chemical
stability in water, toxicity, carcinogenicity, odor, flammability, chemical compatibility
with the other chemicals in a mix, availability, and cost. See Table E-A for a list of
compounds studied according to the Catalytic methodology. Results of this experimental
work are present in the Catalytic files (Catalytic, I979b).
Oklahoma State University Studies
The methodology for determination of biokinetic constants in activated sludge
models developed by OCB and their contractor, Catalytic is also being applied by
researchers at Oklahoma State University. An EPA-sponsored study by Kincannon is now
in progress with objectives consistent with those of the Catalytic study:
I. To determine biokinetic constants for wastewaters containing 24 major
organic compounds
2. To determine a method for combining biological constants for evaluating
complex waste streams.
Biokinetic constants are being determined for design models developed by Eckenfelder,
McKinney, Lawrence and McCarty, and Gaudy. To develop a methodology for combining
K-rates, three compounds are run individually and in combination, with pilot plants
operated at three different sludge ages for each compound or combination. In addition,
specific compounds in the off gases from the pilot plants are being measured to determine
the strippability of volatile organic compounds. Preliminary results for four sets of
priority pollutants (three pollutants run individually and in combination) have been
E-16
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TABLE E-4
ORGANIC COMPOUNDS STUDIED IN
CATALYTIC'S PHASE II BENCH-SCALE BIOLOGICAL SYSTEM
N-Butyl Phthalate (nBP) 75%, Base Mix* 25%
0-Nitrophenol (ONP)** 75%, Base Mix 25%
Maleic Acid 75%, Base Mix 25%
Acetonitrile 75%, Base Mix 25%
Acetonitrile 25%, ONP 25%, Maleic Acid 25%, Base Mix 25%
Base Mix (with and without phenol** in the mix)
Butyl Acetate 75%, Base Mix 25%
Methyl. Cellulose 75%, Base Mix 25%
Methyl Formate 75%, Base Mix 25%
Melamine 75%, Base Mix 25%
Catechol 75%, Base Mix 25%
Formamide 75%, Base Mix 25%
Ethanol 75%, Base Mix 25%
Ethanol (denatured) 75%, Base Mix 25%
Isophorone ** 75%, Base Mix 25%
Ethylene Dichloride** 75%, Base Mix 25%
2-Naphthol-3,6-disulfonic Acid 75%, Base Mix 25%
l-Phenyl-2 thiourea 75%, Base Mix 25%
Base Mix without Glutamic Acid 100%
Base Mix without Ethanol 100%
Base Mix without Glucose 100%
Methyl Formate 25%, Formamide 25%, Maleic Acid 25%, Base Mix 25%
*Base mix is composed of ethylene glycol, ethyl alcohol, glucose,
acid, acetic acid, and phenol.
**Priority pollutant.
E-17
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reported in four quarterly reports (Kincannon, I980a and I980b, and Kincannon and Stover,
I98la and I98lb). See Table E-5 *or the list of compounds studied.
Effect of Priority Pollutants on Biological Treatment
The optimal operation of an activated sludge process is subject to change as a
result of a number of environmental conditions, including the presence of compounds toxic
to the system's microbial population. These several conditions acting simultaneously on
the biological system make it difficult to determine whether a particular chemical, or a
combination of toxic compounds, is responsible for an observed malfunction of a waste
treatment process. Such a data base is essential to the development of pre-treatment
requirements for industrial wastes containing priority pollutants to treatment works
employing the activated sludge process.
The effect of 2k priority pollutants on the performance of batch and continuous
flow bench-scale activated sludge pilot plants was studied by Gaudy et a[. (1979).
Additionally, • erght of these compounds were studied in continuous flow pilot plants
operated at a net specific growth rate (u ) of 0.2" (9 = 5 days); four of the eight were
also studied in extended aeration pilot plants. See Table 3-9 for a list of those priority
pollutants tested. Each test compound was added to the feed at dosage levels that
increased from 5 mg/liter to 20 or 25 mg/liter to 50 mg/liter. Following a period of
operation at a steady dosage level of 50 mg/liter, the unit was subjected to daily cycling
or pulsing of the concentration of test compound (e.g., 25 to 0 to 25 mg/liter).
The following conclusions with respect to the effects of the 24 priority pollu-
tants on the pilot plant performance were drawn after a two-year experimental period.
Results are also summarized in Table E-6 . An evaluation of plant performance was
based on a comparison of the residual soluble COD and effluent suspended solids in the
test unit and the control unit.
E-18
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TABLE E-5
PRIORITY POLLUTANTS STUDIED
IN OSU'S BENCH-SCALE BIOLOGICAL SYSTEM
Compounds Studied (with Percent Total COD)^
Set 1: Individual Feed
1,1,2,2-Tetrachloroethane (TCE) 9%
Nitrobenzene (NB) 33%
2,4-Dichlorophenol (DCP) 21%
Combined Feed
TCE 2%, NB 14%, DCP 75%
Set 2: Individual Feed
Acrolein (Ac) 66%
Acrylonitrile (Aery) 66%
1,2-Dichloropropane (DCP) 2%
Combined Feed
Ac 22%, Aery 22%, DCP 1%
Set 3: Individual Feed
Methylene Chloride (MC) 5%
Benzene (BEN) 67%
Ethyl acetate (EA) 67%
Combined Feed
MC 2%, BEN 22%, EA 32%
Set 4: Individual Feed
1,2-Dichloroethane (DCE) 13%
Phenol (Ph) 85%
1,2-Dichlorobenzene (DCB) 33%
Combined Feed
DEC 3%, Ph 34%, DCB 3%
remaining COD was contributed by "base mix," a readily biodegradable
synthetic wastewater.
SOURCE: Kincannon, I980aand ! 980b, and Kincannon and Stover, 1981 a and I98lb.
E-19
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TABLE E-6
SUMMARY OF EFFECTS OF PRIORITY POLLUTANTS
OSU BENCH-SCALE BIOLOGICAL SYSTEM
—
PARAMETER
BATCH UNIT
DOSAGE (rag/1)
CONTINUOUS riCM UNIT
(in » O.2 EXTENDED AERATION
DOSVZ fug/liter) DOSATE (mg/liter)
0 5 20/25 50 CYCLIC 0 5
20/25 50 CYCLIC 0 5 20/25 50 CYCLI
PENDCHLOPCPHEtCX.
1,2-OICHLCJCETHWa
NZTfOBEitEENE
TRICHLORCenniENE
JCIWLEKE CHLORIDE
PHENOL
2-CHLORQPHENOL
4^LOtO-3-MEIHtt
PHENOL
O • Performance saws
X • Performance poor
7 • Performance poor
BLank indicates par*
The following priorit
Anthracene
Benzene*
CODE 0 X X X X
nrm; OOOO OOOO
SSE 0 O X X
CODE OOOOOOOOOO
SSE O 0 0 0 X
ODE OOOOOOOOOX
SSE 0 O 0 0 X
gne OOOOOOOOOO
SSE 0 X X X X
SSE 0 X X X X
CODE OXXXOOOOOO
SSE 0 O O X X
CODE OOXX 000?
SSE OOOO
as control
compared with control
in both control and test system
inter not measured
y pollutants, tested in the batch unit, did not affect performance:
Hexacnlorobenzene
Hexactiloreetnane
O 0 0 O 0
00000
Oy v y y
A A A A
0 0 0 X X
0 O 0 O O
O O 0 O O
OOO?
OOOO
Carbon Tetrachlorioe
Chlordaenzene
Chloroform
Ethylbenzene
Fluorene
•Also >••«••* in continuous flew unit
Naphthalene
2-Nitrcphenol
Tetrachloroethane
Tetrachloroethylene
1,1,2-Trichlorcethane
Toluene
un » 0.2 day j
SOURCE: Gaudy et d., 1979
E-20
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I. Of the 24 compounds studied in batch systems, only two compounds (pentachloro-
phenol and 2-chlorophenol) gave evidence of causing metabolic stress to the
system, as judged by comparison of residual soluble COD in the test unit and
control unit at a daily feed concentration of 5 mg/l. At higher concentrations
(20 to 25 and 50 mg/l), there was evidence of metabolic disturbance for only one
additional compound, 4-chloro-3-methylphenol.
2. For the eight compounds tested in the continuous-flow activated sludge pilot
plant operated at w = 0.2 days , there was no evidence of increased soluble
COD in the effluent at the 5 mg/l dose. At this dose, however, there was an
increase in suspended solids in the effluent of pilot plants dosed with phenol and
methylene chloride. In addition, at higher dosage levels, there was an increase in
soluble COD and suspended solids in the effluent for the pilot plant dosed with
phenol. For the units dosed with 2-chlorophenol at the 50 mg/l dose, methylene
chloride at the 5 mg/l dose and dichloroethane at the 25 mg/l dose, soluble COD
in the effluent was not affected but there was an increase in effluent suspended
solids concentration. Under alternating concentration levels (daily changes from
25 to 50 to 25 mg/l followed by 0 to 25 to 0 mg/l) there was increased soluble
COD and suspended solids in the effluent for the unit dosed with trichloro-
ethylene. For the pilot plants dosed with nitrobenzene, 2-chloro-phenol,
methylene chloride and 1,2-dichloroethane, cyclic loading led to increased
suspended solids in the effluent.
3. For the four compounds tested in the extended aeration pilot plant, increased
soluble COD in the effluent was reported only for the unit dosed with phenol at
the 5 mg/l dosage level. There was no increase in effluent suspended solids in
any of the four systems at this dosage level. At the higher dose levels (20 and
50 mg/l) and during the period of cyclic loading of the test compound, the units
dosed with phenol showed increased soluble COD and suspended solids.
E-21
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FATE OF PRIORITY POLLUTANTS
Introduction
In developing predictive models for biological treatment of specific organic
compounds found in industrial effluents, an important distinction needs to be made
between treatability and removability of the specific compounds. Removability describes
the change in concentration of the compound between entering and leaving the treatment
process. Treatability is a more specific term, relating to the treatment mechanism by
which compounds can be evaluated (biodegradation, air stripping of volatile compounds,
adsorption on sludge, etc.) and compared to other compounds (Kincannon e£a[., 1981).
To date, most design models have originated from a simplified mass balance for
the substrate, represented as:
CHANGE OF MASS MASS LEAVING MASS
MASS IN = ENTERING - REACTORIN - CONSUMED
REACTOR REACTOR EFFLUENT BIOLOGICALLY
As adsorption and stripping are not included in this mass balance equation, treatability
data derived on this basis may:
I. Incorrectly determine biokinetic constants (and thus inaccurately pjredict
substrate treatability by giving biological processes credit for removal).
2. Leave unrecognized air and solid waste pollution problems, resulting from
stripping and adsorption of the various
organic compounds.
A more correct substrate mass balance would thus be (Kincannon and Stover, 1981):
CHANGE MASS MASS MASS MASS MASS
OF MASS = ENTERING - LEAVING - STRIPPED - ADSORBED - CONSUMEC
INRE- REACTOR REACTOR ON BIOLOGIC^
ACTOR IN EFFLUENT SLUDGE
E-22
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This approach, that is considering the multiple pathways by which pollutants can be
removed during biological treatment, is used in the following section.
Multimedia Models Of Biological Treotability
Hwang Model
Hwang (1980a) has developed a model describing the dynamics of substrate
removal in a continuous activated sludge process with sludge recycle, incorporating the
mechanisms of biodegradation, air stripping, and adsorption on sludge. The components of
Hwang's model are described briefly below.
Several models describing the kinetics of biological degradation were evaluated
in the development of the Hwang Model, including those using first order kinetics for the
substrate reaction (e.g., Eckenfelder and McKinney), those which apply Monod kinetics in
their material balance formulations (e.g., Lawrence and McCarty, and Gaudy), and the
Grau model (which treats the substrate removal rate as a function of the remaining
substrate concentration as compared to the original concentration). Experimental data
from several sources served as the basis for judging the suitability of each of the
treatability models to predict removal of the specific toxic compounds from waste
streams. The Grau method best described the data and, as a result, is used in the Hwang
multimedia model to describe the biodegradation of priority pollutants; this model is
represented by:
- dS [S ]n
dt " *n(s)
where:
S = substrate concentration, g/liter
t = time, days
Data were obtained from the following sources: EPA, Cincinnati, Union Carbide
Corporation, Catalytic, Inc., and the literature.
E-23
-------
'n(s)
= rate constant in the Grau equation, I/day when n=l
S = initial substrate concentration, yg/liter.
To describe air stripping kinetics in the Hwang model, experimental data on air
stripping rate constants are used where available. The expression for air stripping of
volatile components is represented as:
k s
at a
where:
k = air stripping rate constant, I/day
S = substrate concentration in the liquid, ug/liter.
Where experimental data on air stripping rate constants are not available, rates can be
determined by combining the individual liquid and gas phase mass-transfer constants as
follows:
where:
k = air stripping rate constant, I/day
k i = individual liquid mass-transfer constant
aG = individual gas mass-transfer constant
K = equilibrium distribution coefficient.
Adsorption on activated sludge provides an additional route of removal for some
organic pollutants, cyanides, and metals. Adsorbed toxic compounds are removed from
the biological system when the activated sludge is wasted. In Hwang's model, removal of
a specific toxic pollutant in sludge is represented by the multicomponent Langmuir type
E-24
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adsorption equation, which is based on the concept of binary characterization of
wastewater adsorption:
K, X1 S
IB'SJ = . ^ / e ^ t
where:
y*B*S¥z = concentration of a substrate in sludge, Ug/Iiter
S = substrate concentration in the liquid, P g/liter
S = concentration of total substrates minus substrate
S under consideration, u g/liter
K., K-j- = adsorption constants
X' = the maximum amount of the substrate adsorbed on
sludge, yg/liter.
Hwang's unified model (see Figure E-3) for removal of toxic chemicals by
multimedia pathways incorporates the above three mechanisms. The model is described
below in terms of the schematic of the activated sludge process and by the equations
which follow.
E-25
-------
FIGURE E-3
A SCHEMATIC OF THE ACTIVATED SLUDGE PROCESS
Q_ littrt/d«y
Q. - Qw liters/day
ii s£«
>
r
Biological
Treatment
V
A.
J S. //g/liter
Q liters/day
L Z ^
SOURCE: Hwang, I960.
F.-26
-------
S = substrate concentration in influent, y g/liter
o
S = substrate concentration in effluent, y g/liter
X , X , X0 = concentration of substrate on sludge in influent,
o e r\
effluent, and return sludge, respectively, y g/liter
V = bioreactor volume, liter
r = recycle ratio, volume flow rate recycle/volume flow rate
feed
Q r flow rate to biological treatment (=(kr)Qp), liter/day
Qp. = flow rate of the fresh feed
Q.II = flow rate of the waste sludge.
QFSO - UP ' Qw>se « *1(s)* Se v * ka s v
so a e
Q Kl X> Se
1 * Vr * Klse
or
_ e
Q se « e
So
Se
* K1Se Q
where:
tc = hydraulic residence time, day
X s sludge concentration in the reactor, y g/liter
X' = maximum concentration of a substrate on sludge, yg/Iiter
k./ v = rate constant in the Grau equation, I/day when n=l
kQ = air stripping rate constant, I/day
Ki and Kj = adsorption constants
S = concentration of total substrates minus substrate S under consideration,
y g/liter.
E-27
-------
Using the relationship Qp = i , one gets
SQ - (1 - W(l+r))Se , _1 ^e_ (i+r)tc + ka Se(l+r)tc
o
kl X' Se
t KTSr * KlSe
where W=Qw/Qp (waste sludge flow/fresh feed flow).
Since Hwang found the W(Ur) term to be small, the equation may be reduced to:
{so " Se} » 1(s)s £(Hr)tc + ka(l+r)Se tc
o
u y' e
Kl x se
i + KTsr * Klse
Monsanto Model
In addition to the Hwang model, a number of other models have been developed
to describe the removal of organic compounds by multiple pathways during biological
treatment. Monsanto Company has described an approach for use in predicting the rate of
air stripping and biological degradation (Freeman, 1979). Mathematical predictions based
on the Monsanto model for the treatability of the priority pollutant ccrylonitrile were
verified using an experimental activated sludge system (Freeman et a[., 1980).
In the Monsanto model, the biological oxidation component is represented by the
model of Gerber. This model involves the solution of the following three simultaneous
non-linear equations in three unknowns; solution by use of a digital computer is
recommended by the authors. Use of the Gerber model to describe biological treatability
E-28
-------
differs from the one constant Grau model used by Hwang; further, the Gerber mode!
accounts for the impact of substrate, oxygen, and biota concentrations.
r - k5Boco°o
°o * K02Ks + Co°o + K02Co
Mw
tr
where:
TQ s Rate of oxygen use, Ib/hr-ft ,
2 3
TQ s Rate of microorganism growth, Ib/hr-ft ,
r * = Rate of organic disappearance, Ib/hr-ft ,
B = Concentration of microorganisms from the basin, Ib/ft ,
CQ = Concentration of organics from the basin, Ib/ft >
0 = Oxygen concentration in the basin liquid, Ib/ft ,
k. and kc = Reaction rate constants,
KQ and K = Constants,
t = Oxygen use factor, Ib mole C^H
mole oxygen used,
S s Substrate use factor, Ib mole Ce
mole substrate consumed, and
produced/lb
produced/lb
E-29
-------
j MWg, = molecular weights of the organic compound, micro
and (V\WQ organisms, and oxygen, respectively, Ib/lb mole.
The rate of air stripping in the model is represented by the following equation, in
which the rate of stripping to the atmosphere varies with the organic concentration in the
liquid phase.
N s "... NK (X •> X *1 + fA —
Na 4 N*a lxa xa ' *
-------
The treatability of acrylonitrile was studied to verify the predictability of this
model. The model indicated that if sufficient aeration capacity is maintained (2 ppm or
above), 99 percent of the feed acrylonitrile will be biodegraded and less than I percent
will be air stripped (Freeman, 1979). These results were confirmed in series of bench-
scale continuous flow activated sludge treatment systems, in which biological treatability
efficiencies of greater than 99.9 percent were found (Freeman et aU, 1980). When the
treatment system was run under sterile conditions (i.e., no seed microorganisms were
present), it was found that 18 percent of the acrylonitrile was air stripped.
Data Development for Multimedia Models
Indicatory Fate Study
The data base for predicting the fate of individual compounds by multiple routes
is presently limited. One of the first attempts to determine the fate of specific priority
pollutants as they pass through a biological system was conducted in the EPA-sponsored
Indicatory Fate Study (EPA, I979a). Three plants belonging to the organics and plastics
industries participated in a screening study to provide an indication of the removal of
specific priority pollutants via air, water, or residuals routes. The types of treatment
processes used to treat the industrial effluents are shown in Appendix G. Analyses were
conducted for priority pollutants which had been identified in previous screening and
verification sampling under the direction of EPA's Effluent Guidelines Division, Organic
Chemical Branch. Analyses were performed on composite samples (influent, effluent, air,
and residuals) and on grab samples (influent and effluent}. The data generated from these
analyses provide only an indication of the route of removal of specific priority pollutants,
and were not intended to represent a mass balance across a biological treatment system.
Analysis for organic compounds in the three plants sampled revealed no discernible
patterns concerning the fate of specific organic compounds or classes of compounds in the
effluent, sludge/sediment, or air. Heavy metals occurred at the highest concentrations in
E-31
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all three plants in the activated return sludge or the sediment of aerated lagoons. The
heavy metals" included arsenic, copper, chromium, nickel, zinc, and lead in return sludge,
and additionally selenium, cadmium, beryllium, antimony, silver, and thallium in lagoon
sediments.
EPA-Sponsored Bench-Scale Studies
Kincannon e£ a[. (1981) and Kincannon and Stover (I98lc), in work supported in
part by the EPA, have evaluated the removal of priority pollutants by biodegradation and
stripping. Experimental results were obtained using a bench scale-continuous flow
activated sludge reactor used to treat a synthetic wastewater containing selected priority
pollutants. The reactor was operated as a nonbiological system to determine the strippa-
bility of the chemical compound, and as a biological activated sludge system to determine
biodegradation and stripping, and adsorption for a limited number of compounds. These
results are summarized in Table E-7.
Total percent removal of the specific compounds varied from 93 to 99.9 percent.
Stripping during biological treatment accounted for essentially all of the
tetrachloroethane, 1,2-dichloropropane, and 1,2-dichloroethane removed. These studies
show that volatile organic compounds can be removed by concurrent stripping and
biological oxidation. Further, the results indicate that the failure to recognize stripping
as a removal mechanism will affect the experimentally derived biokinetic constants for
pollutants.
It is interesting to note that the stripping that takes place in a nonbiological
system does not necessarily predict the degree of stripping in a biological system. While
approximately 100 percent of 1,2-dichloropropane, methylene chloride, benzene, and
1,2-dichlorobenzene are stripped in nonbiological systems, only 1,2-dichloropropcne is
highly stripped during treatment with the biological systems.
E-32
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TABLE E-7
FATE OF SPECIFIC POLLUTANTS
Compound
Tetrachloro-
ethane
Nitrobenzene
2,4-Dichloro-
phenol
Acrolein
Acrylonitrile
1,2-Dichloro-
propane
Methylene
Chloride
Ethyl Acetate
Benzene
1,2-Dichloro-
ethane
Phenol
1,2-Dichloro-
benzene
Total
Percent
Removed
93
97
94
99.9
99.9
99.9
99.5
99.8
99.9
98.5
99.9
99.9
Biological
Percent
Stripped
93
0
0
0
0
99
5
17
15
97.5
0
24
System* Nonbiological
SvstemD
Percent Percent Percent
Adsorbed Degraded Stripped
0
97.0
94.0
99.9
99.9
0 98.8
94.5 99.4
82.8 81.9
84.9 99.3
1 0 96.1
0 99.9 1.9
0 75.9 84.7
SOURCE: Kinconnon and Stover, 1981 c.
SOURCE: Kincannonetd., 1981.
E-33
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A limited evaluation of the fate of priority pollutants in batch and continous
flow bench-scale activated sludge pilot plants was performed by Gaudy et aJ. (1979) in
their study of the effects of 24 priority pollutants on the activated sludge process. S»See
Biological Treatability Studies—Toxicity of Priority Pollutants for a discussion of the test
methods used.fe The results of these analyses appear in Appendix H. Although the data
are limited, most compounds were removed effectively (with the exception of
nitrobenzene, 2-chlorophenol and 3-methylphenol under certain experimental conditions).
Anthracene and fluorene concentrations were high in the mixed liquor while
concentrations were low in the settled effluent. This indicates that the compounds were
present as part of the biological solids, possibly adsorbed to the surface. Although these
analyses do not provide specific information on the removal routes of the priority
pollutants, the results indicate there was no evidence for massive pass-through in the
effluents of any of the compounds. Small quantities of some of the compounds were
detected in the effluents, however; more detailed analytical procedures are needed to
adequately address the question of pass-through of small concentrations of the priority
pollutants.
Fate of Priority Pollutants in Publicly Owned Treatment Works
The fate of priority pollutants in publicly owned treatment works (POTW) was
presented in an interim report, in which the preliminary results from 20 of the 40 POTW's
selected by the EPA's Effluent Guideline Division were reported (Feiler, I960). The
treatment processes included among the 20 plants were conventional activated sludge and
modifications of activated sludge such as contact stabilization, Kraus, and pure oxygen, as
well as some advanced waste treatment processes, notably mixed media filters. Samples
of influent, effluent, and sludge streams were analyzed for conventional, non-
conventional, and priority pollutants. Based on their analyses of 93 priority pollutants,
E-34
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the following preliminary findings relating to the fate of priority pollutants were
reported:
I. For five of the treatment plants (four activated sludge and one trickling filter)
where the mass balances were assumed to be relatively accurate it was observed
that metallic priority pollutant mass balance was good, but some organic priority
pollutants in the influent were always not accounted for in the effluent or
sludges. This indicates that, in general, a portion of organic priority pollutants
are biodegraded or, in the case of volatiles, stripped out of the wastewater.
2. Based on the 20 POTW data base, half of secondary treatment plants achieved at
least 76 percent reduction of total priority pollutant metals, 85 percent
reduction of total volatile priority pollutants, and 70 percent reduction of total
acid-base-neutral priority pollutants. Tertiary treatment was slightly more
effective than secondary treatment in reducing priority pollutants, and primary
treatment the least effective.
3. For many conventional and priority pollutants, as influent concentrations
increased, effluent concentrations also increased. This trend held for all metals
(except for mercury) with correlation coefficients ranging from 0.204 to 0.995,
and, in general, for volatile priority pollutants, correlation coefficients ranging
from 0.262 to 0.937.
4. Some pollutants not measured in POTW influents were regularly measured at
high levels in the corresponding sludge streams. This phenomenon was observed
for 25 priority pollutants, including metals and organic compounds. This
observation was most likely due to concentration of the pollutant in the sludge
stream to detectable levels.
5. Eleven priority pollutant chlorinated hydrocarbons increased in concentration
during chlorine disinfection.
E-35
-------
Conclusions
The complexities of the removal of organic pollutants during biological
treatment are receiving greater attention, both in terms of modeling and the design of
experimental protocols to determine treatability constants for pollutants during biological
treatment. The multimedia models reflect the recognition that biological treatment not
only involves oxidation of organic compounds, but removal through air stripping and waste
sludge as well. Failure to incorporate these additional routes of pollutant removal can
result in inaccurate determination of biokinetic constants and failure to predict possible
air and solid waste pollution problems. Thus, a model of the activated sludge process
which incorporates a single biokinetic constant is not an accurate mechanistic model of
the complete treatment process. Further experimental work is required in order to
determine accurate kinetic constants for each of the competing treatability mechanisms
that occur during biological treatment.
E-36
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ACTIVATED CARBON ADSORPTION
Introduction
Adsorption processes can be used to remove contaminants from aqueous
wastewaters by the preferential adsorption (either physical or chemical) of the
contaminants on solid surfaces. Pollution parameters affected by activated carbon
include BOD, COD, TOC, specific organic priority pollutants, and to a lesser degree four
specific non-organics: cadmium, chromium, cyanide, and mercury.
There are approximately 100 large scale industrial or municipal wastewater
activated carbon treatment systems in domestic use (Hydroscience, 1981). Large scale
industrial activated carbon treatment systems require extensive pilot plant study before
scaling up to optimize the system and assure compatibility between the system and the
characteristics of the waste stream. This is due, in part, to the competition among
individual components in a multicomponent stream for active adsorption sites. For
example, the adsorptive capacity of a particular system with respect to a specific
compound may be lessened if another compound is added to the waste stream.
Additionally, system designers must consider the best economic configuration of the
adsorption process itself and, if used in conjunction with other treatment modules (e.g.,
biological treatment), the optimal configuration of the entire treatment scheme. This is
especially true for multicomponent wastestreams where target pollution parameters are
of the utmost concern. Recent EPA research efforts have been directed toward modeling
systems to assess the applicability of activated carbon treatment systems to differing
waste stream types and to provide preliminary design data for scaling up.
Background
Activated carbon adsorption treatment systems may be implemented on a
commercial scale in several differing design modes using either granulated or powdered
carbon. The most common type of system in use will be discussed here. That system uses
E-37
-------
granulated carbon in a fixed bed. The design criteria of a system are numerous:
consideration must be given to the presence of suspended solids in the wastestream, the
potential for biological growth in the adsorper, carbon regeneration costs, and cycling
time. The most critical design parameter is the adsorptive capacity of the bed which
dictates the performance of the system.
The effectiveness of granular carbon in removing a given pollutant from solution
is typically evaluated in terms of its adsorption capacity at constant temperature.
Adsorption capacity measures the amount of solute adsorbed per unit weight of adsorbent
as a function of solute (pollutant) concentration in bulk solution.
The actual selection of the adsorber configuration is dependent on the required
carbon dosage and contact time (flow rate/adsorber volume), which requires bench and/or
pilot scale testing to determine the rate of adsorption. By dynamic column testing over a
range of contact times, the concentration of solute (contaminant) remaining in solution
(C/C ) can be plotted versus volume of solution (wastewater) through the column to give
the breakthrough curve. Depending on the complexity of the wastewater, the shape of the
breakthrough curve may vary but, it is characteristically "S-shaped." The breakpoint
represents the point on the curve at which the column is in equilibrium with the influent
wastewater, and little additional removal of the contaminant(s) will occur. Generally,
time to breakpoint may be extended by increasing the carbon bed depth and lowering the
flow rate; however, several other factors, such as the characteristics and concentration of
the solute, the pH of the solution, and the characteristics of the carbon selected influence
the overall capacity of the adsorption system (i.e., height and rate of movement of the
mass transfer zone, capacity of adsorbent, etc.). The objective, in any application, is to
design a system in which the most economical, yet practicable, carbon exhaustion rates
(the time necessary to reach the breakpoint) can be achieved.
E-38
-------
Another major consideration in the design and operation of a carbon adsorption
system is the means of replacing exhausted carbon. This may be accomplished by
removing the carbon from the adsorber for permanent disposal (i.e., throwaway carbon),
or more typically, for reactivation. Reactivation is any means by which the carbon is
restored to its original adsorptive capacity. Organic impurities may be removed by
thermal, alkaline, acid, hot gas (steam), solvent, or biological regeneration. However, in
treating wastewaters containing a mixture of organics, thermal regeneration of the
carbon in either multihearth or rotary tube furnaces provides the most reliable
reactivation process and, thus, is the most widely applied. Thermal regeneration may be
carried out on-site or off-site depending on the scale of operations. As a result of
handling and reactivation, attrition losses, requiring fresh make-up carbon, will typically
range from 5 to 15 percent by weight.
Under certain conditions (e.g., the presence of biodegradable organics, favorable
pH ranges, etc.) biological activity may occur in the carbon adsorption column. In
general, anaerobic growth not only results in HUS production, but reduces the adsorption
capacity of the column and therefore should be discouraged. Aerobic bacterial activity,
depending on the concentration and composition of the waste loading, may enhance
treatment efficiency. In certain cases, biological degradation of organic contaminants
complements the adsorption process, increasing adsorption capacity and providing partial
regeneration of the carbon.
State of the Art
As indicated above, the most critical design parameter for carbon adsorption
treatment systems is the adsorption capacity of the carbon which determines the cycle
time of the adsorption bed. The length of the adsorption cycle can be determined by two
lab techniques and pilot scale tests. The lab scale tests are the use of isotherms and the
Dynamic Mini-column Adsorption Technique (DMCAT).
E-39
-------
Isotherms are usually determined under static conditions which assume the
resistance to mass transfer to be neglible. EPA (1980) has adopted an alternate approach,
DMCAT, that considers non-equilibrium effects to take into account the nature of the
driving forces which control the transport phenomena of solutes from solution.
Breakthrough curves for complex waste streams with nonlinear isotherms are usually
empirically determined. Recent efforts have focused on modeling efforts for
multicomponent wastestreams using psuedo-contaminant parameters which represent an
empirical theoretical approach to the problem of optimizing dynamic adsorbent systems.
Data gathered through isotherm and DMCAT testing can be extended in some
cases through the use of mathematic models which simulate the kinetics of adsorption in
full scale systems. The lumped parameter model combines the diffusional resistances
described by a pore diffusion model and homogeneous solid diffusion model into a single
parameter. This model has been developed based on data from full scale operations and
pilot plant data on several priority pollutants (EPA, 1980). Adsorption occurs through a
four-step process:
I. Transport of a solute from bulk liquid to solid interface
2. Transport across the interface
3. Transport from the interface into the solids
4. Adsorption on the active sites.
Each one of these steps represents a resistance to mass transfer from the bulk liquid to
the active sites. Equilibrium models assume the resistance to mass transfer due to steps
I, 2 and 3 to be neglible and that the bulk concentrations of the two phases are in
equilibrium which is unrealistic (i.e., equilibrium is not attained in practical systems).
The lumped parameter model is developed by c fundamental material balance for
each step in the adsorption process. The mass transfer equations that result from such an
analysis are solved numerically and combined into a single mass transfer coefficient. A
E-40
-------
brief treatment of this concept is presented below, the reader is referred to Appendices I
and J and to EPA (I979b) for a detailed discussion of the lumped parameter model.
In order to utilize the principles of any model it is necessary to obtain
experimental data to estimate mass transfer parameters. This requires dynamic column
testing to generate breakthrough curves which, when done in a pilot plant scale column, is
a timely and costly procedure. This is particularly true of requisite data on specific
organic compounds. The Dynamic Mini-column Adsorption Technique (DMCAT) is capable
of rapidly generating necessary design data to nominally assess the performance of an
adsorption system for single and multi-component wastestreams.
This technique, described by Beaudet et pj. (1980), utilizes a high pressure
precision metering pump to pass wastewaters through a very small column at pressures up
to 6,000 PSI. Meticulous care must be taken to avoid contamination of the absorbent
during assembly of the apparatus to assure accurate and reproducible results.
Additionally, influent and effluent samples must also be protected from contamination by
ambient airborne organics.
Beaudet e£ a[. (1980) conducted several tests with the DMCAT on several single
and multi-components, and "real world" wastestreams and them compared their results
with those from pilot scale tests. Their results were congruent with pilot scale results.
The utility of DMCAT is to rapidly obtain reproducible data that can be used to determine
the amenability of a particular wastestream to carbon adsorption and carbon usage rates
to estimate system economics.
Applications of Activated Carbon Adsorption
In one laboratory study (Walk, Haydel, I980a), two commercially available
adsorbents were tested on an unspecified industrial wastestream in a laboratory study.
The wastestream was from a multi-product effluent that contained five priority
pollutants; chlorobenzene (8.8 ppm), p-dichlorobenzene (360 ppm), nitrobenzene (166 ppm),
E-41
-------
dinitrotoluene (7.9 ppm), and phenol (30.8 ppm). Carbon adsorption was found to be
effective, exhibiting effluent concentrations of O.I ppm or less for each of the priority
pollutants. These results are based on equilibrium and dynamic testing. Walk, Haydel,
(I980b) also compiled data on commercially operating systems in a limited survey. These
data are presented in Table E-8. Hydroscience (1981) conducted a more extensive survey
of facilities using carbon absorption, to treat process wastewaters. Approximately 50
plants primarily engaged in organic chemicals or pesticide manufacture were queried.
Other facilities included in the survey were those expected to generate process
wastewaters that may be amenable to carbon adsorption treatment, such as refineries,
coke plants, and detergent manufacturers. The design characteristics of these full scale
adsorption systems are presented in Table E-9 and the performance of these systems in
removing priority pollutants is summarized in Table E-10.
The utility of these data are somewhat limited because survey respondents often
provided incomplete data. For example, most facilities reported influent streams in
terms of BOD, COD, and only one or two priority pollutants. In some survey responses,
only influent or only effluent concentrations of pollutants were reported. However, as
noted elsewhere, a particular plant in the organic chemicals industry will only have a
small number of priority pollutants in its wastestream in addition to conventional organic
pollutants. Because the specific wastestream components were not sufficiently identified
in this survey, the impact of specific priority pollutants on systems removal performance
can only be inferred. In particular, data are inadequate to assess the competition among
individual pollutants for active adsorption sites in a multicomponent stream. Of the
systems surveyed by Hydroscience (1981), many were effective in the removal of specific
priority pollutants.
E-42
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DESIGN CHARACTERISTICS AND OPERATIONAL PARAMETERS FOR
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Although carbon adsorption systems require extensive lab and scale up testing en a
particular wastestream the results of ^he survey suggest that such systems ere a vicoie
and acceptable technology for use m priority pollutant removal from multi-componenf
wastestrecms generated by full scale plants.
A daily sampling effort was conducted by EPA at an organic chemicals
manufacturing plant (5?A, l?3lc). Effluent concentrations from a carbon adsorption unit
used to treat process waste-waters are presented in Table E-ll*These results are from one
laboratory only and exhibit some pronounced variability among parameters. Parameters
were selected on the basis of the process chemistry and are expected to be present !n the
effluent. During the study, two other labs also 'conducted sample analysis which also
exhibited a degree of variability. Whether these differences are attributable to system
pertubations or ancl/tical deviations is not known because a statistical analysis of these
data is not yet available. EPA is currently conducting such en analysis which will better
define this particular system's performance.
E-52
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E-53
-------
STEAM STRIPPING
Introduction
Steam stripping is a mass transfer operation that is used to remove volatile
organic contaminants from dilute solutions. It is essentially a distillation that uses live
steam as its energy source and is typically used for liquids that ere immiscible in water.
Steam stripping may be employed for binary distillations, and is also amenable to
multicomponent streams. Design equations and criteria are well established and in some
cases there is little need for extensive pilot plant studies prior to installing a large scale
unit.
Background
Steam stripping is accomplished by injecting live steam into a vertical mass
transfer column. Steam distillation, a batch process, is commonly used to distil! organic
liquids, which might decompose if heated to temperatures high enough to cause them to
boil in the absence of steam. Stripping columns may be packed, sieve tray, or bubble cap
tray. Packed columns are preferred because they maximize the interfacial surfaces
available for mess transfer; however, they may not be the rncst economical.
Consideration must also be given to the compatibility of the mixture to be separated with
the materials used to construct the column in order to assess the expected lifetime of the
packing. Additionally, throughput rate, energy requirements, maintenance, end operating
costs may dictate a column design of either the sieve tray or valve tray type. Subble cap
tray columns ere seldom used today because they have been replaced by valve trays.
Either choice is about twice as expensive (capital cost) as sieve tray columns.
Regardless of the column design the principle cf separation of mixture
components is the same. Once the column is in a steady state condition, a temperature
gradien; and a congruent series of gas-liquid equilibrium stages are established. Standard
design equations that relate the vcpor pressure, activity coefficients, and equilibrium
E-54
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TABLE E-13
STEAM STRIPPING OF ORGANIC PRIORITY POLLUTANTS WITH AQUEOUS REFLUX
(inlet concentration = solubility limit)
STEAM STRIPPER NO OF TH~OR£TICAT
POLLUTANT OUTLET CONCENTRATION ' "
10 6 g/L(ppb)
Acrolein
Acrylonitrile
Benzene
Carbon Tetrachlor ide
(tetrachlor one thane)
Chlorobenzene
1,2, 4-Tr i.chlor obenzene
Hex a chlorobenzene
1, 2- Di chloroe thane
1,1,1-lri chloroe thane
Kexachloroe thane
1,1- Di chloroe thane
1, 1, 2 -ir i chloroe thane
1, 1,2, 2- Tetr a chloroe thane
Chloroe thane
Bis (chlorome rjyl) ether
2- Chloroe thy i vinyl
ether (mixei).
Chloroform
(trichloror thane)
1, 2-Dichior-. ,/nzene
l,3-Dichlcrcr.-,-r.zene
1,4-DichiorcLer.zene
1, 2- Tr an s-di chloroe thy lene
1,2-Dichloropropane
1,3-Dichloropropylene
(1,3-Dichloropropene)
2,4-Dinitrotoluene*
2, 6-Dinitrotoluene
Ethylbenzene
Bis (2-chloroisopropyl) ether
Kethylene chloride"
(dichlorome thane)
Methyl chloride (chlorome thane)
50
50
50
50
50
50
50
50
50
50
50
50
50
50
50
50
50
50
50
50
50
50
50
50
50
50
50
50
19
13
5
4
5
4
3
6
6
3
6
5
5
7
6
6
4
3
4
5
5
10
» V
10
3
9
g
6
E-57
-------
TABLE E-13 (Continued)
STEAK STRIPPER
POLLUTANT OUTLET CONCENTRATION
10 * 9/L(ppb)
Methyl bromide (bromoine thane)
Sronoforni (tribromomethane
Dichiorobromome thane
Trichlorofluorome thane
D i ch lor odifluorome thane
Chlorodibroror.e thane
Eexachlorobutsdiene
Kexachlorocyclopentafiiene
Nitrobenzene
Tetrachloroethylene
Toluene
Trichloroethyler.e
Vinyl chloride (chloroethylene)
SO
50
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E-58
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E-60
-------
constants to the material balance in the staged column (with and without reflux) are
presented in Appendix K.
Volatile organic components having a partial pressure at a particular
temperature evaporate or distill and are removed at the top of the column while the
"stripped" liquid phase water is discharged from the bottom. The presence of steam in the
vapor phase reduces the partial pressure of the other components at a fixed total pressure
and thus lowers the saturation temperature of the liquid to be distilled. The column tops
may be incinerated, partially condensed, or totally condensed. The water from the
column tops may be refluxed to the column depending on the economic utility of
refluxing. Refluxing offers the advantage of recovering organics as a liquid and increases
the degree of separation of the column. It also increases the steam requirements to
satisfy the overall heat balance for the column. Again, as with the column
design, selection of refluxing options are based upon economic considerations.
State-of-the-Art
Standard design equations that relate the vapor pressure, activity coefficients,
and equilibrium constants to the material balance in the staged column (with and without
reflux) can be used to predict the column performance. Hwang and Fahrenthold (1980)
have compiled thermodynamic data pertaining to 99 (of the 129) priority pollutants
potentially amenable to steam stripping. These data were extracted from the literature
or calculated from solubility and other data. Data on compounds normally subject to
steam stripping have been summarized and are presented in Table E-12 Tables E-13ond
E-14 present calculated column efficiencies, tray and steam requirements, and outlet
concentrations of the priority pollutants based upon data from five commercial steam
stripping columns, several pilot plant studies, and laboratory data. These are calculated
data assuming the inlet concentration to the stripper is the solubility limit of the specific
pollutant. Additionally, the calculations assume ideal behavior for mixtures (i.e., no
E-61
-------
intermolecular interactions among components). Pollutants that require more than 20
trays to effect an outlet concentration of 50 ppb or less were excluded because they may
not be economically justifiable for wastewater treatment.
In a recent controlled and comparatjve bench scale study, the validity of the
estimated thermodynamic data presented in Table E-12was examined (EPA, I98lb). A
water solution saturated with three nonpriority pollutants was steam stripped and the
effluent concentrations were measured. These results were compared to predicted results
that are calculated by assuming five theoretical plates. The measured and calculated
results compared favorably (see Table E-15} although the measured effluent
concentrations are slightly lower suggesting that the assumption of five theoretical plates
was incorrect (i.e., the column has more than five plates). The calculated effluent
concentrations were based on K values of these nonpriority pollutants that were derived
from published vapor-liquid equilibrium data. As noted earlier, the average K values for
priority pollutants presented in Table E-12are more or less based on solubility data rather
than vapor-liquid equilibrium data. The experiment was repeated with the calibrated
column using six priority pollutants (benzene, chlorobenzene, 1,1,2,2-tetrachlorobenzene,
chloroform, ethylbenzene, and tetrachloroethylene).
Saturated aqueous solutions of the six priority pollutants were also stripped
individually and in combination with each other. The calculated effluent concentrations,
assuming one theoretical plate, were much lower (in some cases up to four orders of
magnitude) than the measured values (see Table E-16). The calculated values in
Table E.I6 for priority pollutants were based on the estimated average K values presented
in Table E-12. The assumption of one theoretical plate reduces the system to a simple
single stage vapor-liquid equilibrium. These data suggest that, although column
efficiencies for the priority pollutant may be less than those of the nonpriority pollutants
examined in this study, the accuracy of the estimated K values presented in Table E-12
E-62
-------
TABLE E-15
CALCULATED RESULTS FOR STEAM STRIPPING OF SOLUBLE
NONPRIORITY POLLUTANTS ASSUMING A 5 THEORETICAL TRAY COLUMN
Calculated
Hole Fraction Hole Fraction Hole Fraction
Component Feed X 1CT Bottoms X 1(T Bottoms X 1CT
Acetone 2,470 .329 SI. 2
2-Propanol 2,110 .122 12.9
Methanol 4,610 1,520 2.489
E-63
-------
TABLE E-16
CALCULATED RESULTS FOR STEAM STRIPPING OF
POLLUTANTS ASSUMING A 1 THEORETICAL TRAY
Mole Fraction
Component Feed X 10
Benzene 5.53
Chloroform 39.8
1,1.2,2-Tetrachloroethane 29.1
Chlorobenzene 3.59
Ethyl Benzene 1.96
Tetrachloroethylene 15.4
Ethyl benzene .952
1,1,2,2-Tetrachloroethane 11.2
1,1,2,2-Tetrachloroethane 16.4
Benzene 3.01
Chloroform 2.53
Ethyl benzene .391
Chlorobenzene 1.51
Tetrachloroethylene .468
Chlorobenzene 1.32
Ethyl benzene .204
Tetrachloroethylene .174
1,1,2,2-Tetrachloroethane 6.79
Chlorobenzene .899
Chloroform 9.52
1,1,2,2-Tetrachloroethane 4.49
Chloroform 9.10
Ethylbenzene .170
Tetrachloroethylene .105
1,1,2,2-Tetrachloroethane 3.38
Benzene .809
Chlorobenzene .513
Ethylbenzene .117
1,1,2,2-TetracMoroethane 3.27
Benzene 3.08
Chlorobenzene .257
Ethylbenzene .199
Tetrachloroethylene .0557
Chloroform .324
Mole Fraction
Bottoms X 10 •
.303
.0876
.364
.437
.130
.365
.102
.692
.200
.0733
-.0062
.140
.0166
.315
.0296
.0129
.0693
.0175
.149
.192
.139
.00334
.00107
.118
.0859
.0184
.00372
.00258
.0555
.00876
.00297
.000357
.00364
PRIORITY
COLUMN
Calculated
Mole Fraction
Bottoms X 103
.000298
.00833
.0875
.000794
.000179
.0000905
.000101
.0446
.0452
.000138
.000431
.0000409
.000238
.00000318
.000283
.0000280
.00000162
.0222
.00000137
.00190
.0188
.00233
.0000213
.000000833
.00932
.0000374
.0000658
.00000959
.00975
.000153
.0000355
.0000176
.000000344
.0000588
E-64
-------
may be somewhat limited in the range of influent concentrations investigated in this study
and that calculations predicated oh these data should be viewed in the context of these
limitations.
Column efficiencies are among the most critical of design parameters in that
they predict the actual number of trays for a tray column or the height of the packing for
a packed column. The efficiency of any column is dependent on several phenomena: the
degree of mixing of the liquid, entrainment of liquid in the vapor phase, and the contact
time between phases. They are always empirically determined and essentially assess the
performance capabilities of the column.
More recentfy Hwang has investigated tray and packing efficiencies in a follow-
up study for mixtures at extremely low contaminant concentrations, utilizing pilot plant
data and predictive correlations to revise and expand his earlier model (Hwang, I980b). In
this latter study, Hwang has suggested the grouping of volatile organic compounds based
on common parameters (e.g., functional groups and molecular weight) to streamline the
model. EPA has solicited industry for additional data concerning priority pollutants that
are separated by steam strippers in order to assess the validity and accuracy of the
correlations used for column design and modeling. These performance data on
commercially operating wastewater steam stripping columns are presented in Table E-17.
E-65
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ORGANIC ADSORPTION RESINS
Introduction
Organic adsorption resins are a relatively new system for removing organic
chemicals from aqueous streams. Resin adsorption performs like activated carbon: a
waste stream passes through a bed of resin beads, which pick up dissolved organic
molecules and colloidally suspended organic particles from the waste stream by means of
the Van der Wools attraction between the resin and the organic molecules or particles.
Resin adsorption has been shown to reduce organic priority pollutant levels well below the
parts-per-million range, performing nearly as well as activated carbon. Its most
attractive feature is the ease with which a resin bed can be returned to its original
adsorption capabilities after use—the major disadvantages of resin adsorption are the high
capital cost of the resin units and the problems of disposing of contaminated, spent
regenerant.
Organic resin adsorption can be characterized as producing the same result as
activated carbon—removing trace organic priority pollutants from a waste stream, and
using the same equipment as ion exchange—columns of polymer resin beads. An organic
adsorption resin unit is generally a bed of small beads. Each bead is an aggregate of many
-4
tiny microbeads of resin, ranging from 10 mm to I mm in diameter. These resin beds
consist of agglomerated microbeads; the channels between these tiny spheres provide a
large surface area—between 100 and 700 m /g per bed, depending on the type of resin—on
which adsorption can occur. Some types of resin beads used in organic adsorption have
the same structure as the resin beads used in ion exchange. Resin beads which do not
have the ionic functional sites are also effective in removing organic compounds from
aqueous solution. These beads consist of a polymer framework, or matrix (generally
styrene-diviny!benzene copolymer, phenol-formaldehyde copolymer or acrylic ester
polymer) which bears ionic acidic or basic functional groups. Figure E-4 shows the most
E-70
-------
FIGURE E-4
WIDELY USED POLYMER MATRICES AND
FUNCTIONAL GROUPS
MotriCM
Styrene-
Divinylbenzene
( Ml )
-CH,- C - CH, - C -
2 I z I
c«o
OH
Formaldehyde
(M2)
I
0
i
CH,
I
0
Acrylic Ester
(M3)
Anton Eicnonqe functional Groupt
i
ru rw
Vrr»» wrlM
CH,
CH,
HydroMde
Form
Strong BOK
Quoternory Ammonium Group
(Al)
ffCHV Cl"
CH,
Chloride
Form
-N
H
Free BOM
Form
-N H*. cr
H
Acid Chloride
Form
Weak BOM
Secondary Amine Group
(A2)
Cotton E«chqnce Functionol Groupt
-SOj, H* -COOH
Stronq Acid
Sulfonote Group
Hydrogen Ion Form
( Cl )
Weak Acid
Carboxyl Group
Hydrogen Ion Form
(C2 )
-Matrixes and functional groups of resins com-
monly used for water purification.
SOURCE: Kim etoL, 1976.
E-71
-------
widely used polymer matrices and functional groups. Polymeric adsorbents have the same
basic structure without the functional groups.
In addition to polymeric adsorption resins, there is another set of adsorption
materials. These are carbonaceous adsorbents, which consist of black spheres roughly 10
mm in diameter, intermediate in composition between activated carbon and polymeric
resin adsorbents. Several types of carbonaceous adsorbents ("Ambersorb" trade name) are
included in the investigations by Rohm and Haas which are discussed later in this report.
For polymeric adsorbents the polymer matrix is the site of organic adsorption.
Organic molecules are attracted to the resin's organic matrix by Van der Waals forces.
Attractive forces between the adsorbed organic molecules and the adsorbent resin matrix
are relatively weak, weaker than the attractive forces in activated carbon adsorption.
This means that the resins can be effectively regenerated by solvent elution. The role of
the polymer's ionic functionalities, weak and strong acid and base groups, is a secondary
one of attracting particular types of polar organic molecules to the surface of the beads
to facilitate their adsorption onto the resin matrix. The actual driving force of the
adsorption process, howeve'r, is the affinity between an organic pollutant molecule and the
hydrophobic polymer resin matrix. Adsorption occurs when this affinity is greater than
the affinity between the organic pollutant molecule and the aqueous waste stream.
Therefore, organic adsorption resins are most effective in situations where a nonpolar
organic pollutant is to be removed from an aqueous stream; the presence of ionic
functional groups acts to increase the resin's affinity for slightly charged organic
molecules by introducing electrostatic attraction.
The pH of the aqueous stream being treated affects the degree to which slightly
polar organic molecules are adsorbed onto the resin matrix. pH determines the extent to
which an ionizable organic molecule will be polarized. Therefore, since a hydrophobic
molecule will be more strongly attracted to the hydrophobic resin matrix than a
E-72
-------
hydrophilic molecule, a weak organic acid (such as phenol) will be best adsorbed from an
acid solution, where the organic acid will be present in its less water soluble nonionized
form—this is the phenomenon known as "salting out."
Nonionic resins have been shown to be particularly effective in removing
chlorinated pesticides, detergent compounds, emulsifiers, wetting agents, dispersants and
all types of textile dyes. These resins consist of a polymer matrix and do not include any
functional ionic groups; they are regenerated with methanol, acetone, isopropanol and
similar solvents.
Weakly basic resins have been shown to be effective in removing phenolics,
anionic surfactants, carbpxylic acids, proteins, anionic textile dyes and kraftpaper waste
color bodies; weakly basic resins with phenol-formaldehyde polymer matrices remove
phenolic organics particularly well. Sodium hydroxide solutions regenerate these resins.
Strongly acidic and strongly basic resins do not perform as well as weakly acidic
and weakly basic resins in terms of removing organic molecules. Furthermore, strongly
ionic resins must be eluted with large amounts of acid or base; and disposing of these
eluents requires special facilities.
Organic adsorption resins generally are effective in the same situations where
activated carbon adsorption is effective. Resin adsorption differs from carbon adsorption
in that resins can be manufactured to adsorb specific types of organic molecules by
selecting the appropriate ionic functionality on the resin matrix and in that the attractive
forces between adsorbent and pollutant molecule are weaker for resin adsorption than for
activated carbon adsorption. The fact that pollutants are less strongly adsorbed onto
resin than onto activated carbon has two significant implications: first, the effluent
stream from a resin unit will have a higher concentration of residual organic pollutants
than an effluent from an equivalent activated carbon unit and secondly, resin can be
E-73
-------
regenerated with solvents or steam while activated carbon requires expensive thermal
regeneration.
Although regeneration by elution restores the resin bed to most of its original
effectiveness the elution stream presents a disposal problem. The net effect of an
adsorption-elution cycle is to transfer pollutants from the waste stream to an eluent
stream. A technique frequently used is to isolate the first portion of eluent to come out
of the resin during elution. This eluent stream is relatively concentrated and can be sent
to incineration or treated to recover the pollutant. The second portion of eluent will
emerge from the resin bed with a lower pollutant concentration. This eluent stream can
be recycled into the waste stream entering the resin bed, or it can be used as the first
portion in the next elution.
Elution regeneration, nevertheless, effectively restores resin function. Fox, of
Rohm and Haas, describes a commercial phenolic removal and recovery system using
Amerlite XAD-Aj "After 2 l/4-years of operation, the original resin performed the same
as it did during startup. Resin capacity measurements made in the laboratory show the
used resin has 98 percent of its original capacity for phenol even after 1,300 load, regen-
eration cycles" (Fox, 1978).
Rohm and Haas applications for their commercial resins are given iri-TSble E-18.
E-74
-------
TABLE E-18
ROHM AND HAAS COMMERCIAL RESIN APPLICATIONS
Adsorbent/Reoenerant in Wastewater Treatment
Waste Stream/Process
phenols (BPA and others)
brine (phenols and others)
pesticides (cl-, NO--
phenols)
nitroacromatics (TDI
and others
amines (alkyl and
aromatic)
grease (misc. hydro-
carbons
dyes
chlorinated organics
unidentified
US (14 sites)
XAD-4/Methanol
XAD-4,XAD-7/Methanol
XAD-7/Methanol
XAD-74% Caustic
XAD-2,XAD-4/Methanol
XAD-4/Methanol
XAD-4/Isopropanol
XAD-4/2% Caustic
XAD-4/Acetone
XAD-2/Methanol
XAD-2/4% Caustic
XAD-2/steam
XAD-4/acetone
XAD-7/Methanol
XAD-4/4% Caustic
Foreign (13 sites)
IRA-93/Methanol
XAD-4/Acetone (3)
XAD-2/4% Caustic
XAD-4/Methanol
XAD-4/Toluene (2)
CAD-4/steam (2)
CAD-4/Methanol
XAD-4(?)/steam (2)
E-75
-------
Rohm and Haas is a leading manufacturer and distributor of commercial organic
adsorption resins; therefore, these listings describe a significant portion of world-wide
resin use.
Organic adsorption resins are also used commercially to treat paper mill kraft
washes and are placed upstream to ion exchangers to prevent resin fouling. The latter
application exploits the affinity between resins and organic pollutants which caused the
fouling problem in the first place.
Preliminary Development of Resin Performance Data
Rohm and Haas Studies
Research aimed at developing reliable equations to predict the performance of
any synthetic resin by means of parameters easily obtained experimentally is currently
under way; no definitive design/performance equations have yet been developed. Rohm
and Haas, a major commercial manufacturer of organic adsorption resins, has undertaken
a testing program to develop a simple laboratory test which will evaluate the performance
and cost of various synthetic resins in removing organic pollutants from industrial waste
streams. This laboratory test is intended to establish applicability of synthetic resin
adsorbents for removal of organic pollutants from industrial waste streams, to identify
the most useful resin or combination of resins and suitable regenerants for them, and to
allow estimation of approximate treatment costs. Results of these tests have been
presented by Rohm and Haas as a series of quarterly reports entitled "Synthetic Resin
Adsorbents in Treatment of Industrial Waste Streams" (1980, 1981).
The test evaluated in the Rohm and Haas study was the Batch/Rate Test, which
measured both the amount of pollutant removed by a known mass of a certain resin and
the rate at which the pollutant was adsorbed onto the resin. The Batch/Rate tests were
performed on a variety of resins, including resins manufactured by Rohm and Haas,
Mitsubishi, Diamond-Shamrock, Montedison, Calgon, and Dow Chemical. Batch/Rate test
E-76
-------
results were supplemented by data from adsorption isotherm studies, and also by column
loading/regeneration studies. In the column loading/regeneration studies, the effluent
concentration of a pollutant-bearing stream passing through a resin column was
monitored. Then, when the resin had been saturated with the pollutant, regenerant was
sent through the column and analyzed as it was collected leaving the column to give the
cumulative amount of pollutant eluted as a function of the volume of eluent pumped
through the bed. The resins used in this project are listed and characterized in
Table E-12. The synthetic waste streams used were single-solute aqueous solutions of 2-
nitrophenol, tetrachloroethylene, 1,2-dichloropropane and 2,4-dinitrotoluene.
Pilot columns, routinely used to evaluate the adsorption performance of
activated carbon, cannot be effectively used to evaluate organic adsorption resins,
because synthetic resins are manufactured in a wide variety of resin types, with a broad
range of performance characteristics, amenable to regeneration with numerous eluent
solvents. Determining the optimum adsorbent/regenerant pair from all the combinations
available would require a prohibitively expensive and time-consuming set of column
experiments.
The first step in the Batch/Rate test is compiling adsorption isotherms for the
adsorbents and waste streams being studied.
The Batch/Rate studies measure the capacity of a resin to adsorb pollutants
from a stream and the rate at which this adsorption rakes place. In the Batch phase of
the Batch/Rate tests, the adsorbent is saturated with a pollutant in a stream, which is a
solution of one of the four priority pollutants studied. The saturated adsorbent is then
eluted with a regenerant solution (acetone or rnethanol), and the eluent is analyzed for the
pollutant. In the Rate part of the Batch/Rate test, the adsorbent is exposed to the waste
stream as it is in the Batch test. However, small portions of the resin are taken out of
the waste at regular intervals, while the resin is still being saturated with pollutant. The
E-77
-------
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portions of resin removed are eluted with regenerant and the eluents are analyzed for
pollutants; rate test results are presented as adsorption capacity (mg pollutant adsorbed
per g of resin) determined as a function of the length of time the resin has been exposed
to the pollutant.
The Batch/Rate tests were supplemented by column tests which were somewhat
analogous in design to the Batch/Rate tests. Columns were packed with resin to construct
a bench-scale resin adsorption unit, and column loading and column regeneration tests
were performed. Column loading tests consisted of passing pollutant streams (synthetic
single-solute solutions of one of four organic priority pollutants—2-nitrophenol, 2,4-dini-
trotoluene, 1,2-dichloropropane and tetrachloroethylene) through a resin bed and
monitoring the effluent pollutant concentration. In column regeneration tests, the
columns that were saturated with pollutant in the column loading tests are eluted with
regenerant. The regenerant leaving the column is analyzed for pollutant.
The adsorption data from isotherm, Batch/Rate, and column
loading/regeneration studies are summarized in Table E-20 . The batch test has proven to
be a very good predictor of saturation column capacity for single component streams. It
not only gives a more accurate saturation value than the isotherm test, it also is a much
simpler test, requiring a single analysis after exposure to the influent waste stream.
Equations which will predict resin effectiveness in removing organic pollutants
from industrial waste streams by means of easily determined parameters do not yet exist.
However, Rohm and Haas* study represents the first steps towards these equations. The
limitations of the body of data assembled to date (up to and including the third quarterly
report, released by Rohm and Haas in August 1981) reflect the fact that synthetic resin
adsorption is a new technology in the earliest stages of application.
The most significant limitation of the resin performance data is that no studies
have been yet published which describe the performance of systems in the course of
E-7-9
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•c 'c
CU — '
4j -a
>9 i
u ,
o-o
3
•O "
«S m
CM
E-80
-------
multiple saturation-regeneration cycles. Therefore, estimates of an adsorbent's useful
lifetime cannot be made, nor can the effectiveness of a multiply regenerated resin be
predicted as a function of the number of its regeneration cycles. Because the ease with
which resins can be regenerated is one of their most attractive features, a complete
quantitative evaluation of resin performance will include examining the performances of
resins which have been subject to more than one regeneration cycle.
A second limitation of the studies is that they were all performed on single-
solute synthetic solutions of one of four organic priority pollutants. Performance data
obtained from streams more closely resembling industrial waste streams will more
reliably characterize resin performance in industrial application.
Although no equations have yet been developed to predict resin peformance,
Rohm and Haas' investigation included a preliminary evaluation of the mathematical bases
of resin adsorption capacities and rates, considered together with capacity and rate data
from the Batch/Rate tests. This evaluation is the beginning of the development of a
theory of resin adsorption kinetics and equilibria to be applied to resin system design and
economics; it is not yet a reliable means of quantitatively predicting resin adsorption
performance.
Walk, Haydel Studies
In addition, a treatability study comparing carbon and resin adsorption was run
by Walk, Haydel (I980a) in which equilibrium and dynamic studies on organic resin systems
were performed. Five organic priority pollutants were monitored: chlorobenzene,
p-dichlorobenzene, nitrobenzene, dinitrotoluene, and phenol. The equilibrium studies
were batch operations at three pH levels; it was found that adsorption performance was
higher at pH 6 than at pH 9 and that the resin had a low adsorption capacity at low
pollutant concentrations, adsorption capacity increased with the strength of the waste
stream. Resin was found to be more effective than carbon for priority pollutant removal
E-81
-------
at high pollutant concentrations, while carbon performed better than resin with a dilute
waste stream; resin performance was more sensitive to waste stream concentration than
carbon performance.
The dynamic studies of resin adsorption consisted of six runs with methanol
regeneration between runs. Constant leakage, 3 percent of the organic components of the
waste stream, was observed almost from the beginning of the runs. Table E-21 presents
an economic analysis, based on regenerability observations. The Walk, Haydel studies
concluded that resin adsorption of organic contaminants from an industrial wastewater is
technically feasible, and that the economic justification rests on a combination of
wastewater cleanup and specific compound recovery.
Conclusion
The conclusion to be drawn from the experimental studies by Rohm and Haas and
Walk, Haydel is that synthetic resin adsorption may be equivalent to activated carbon
adsorption in effectiveness in removing organic priority pollutants from industrial waste
streams. The absence of quantitative data describing adsorption capacities and resin
regenerability prevents a direct comparison between the two methods. However, if
subsequent research indicates that resins can retain their original adsorption capacities
after multiple saturation/regeneration cycles, the demonstrated effectiveness of resin
priority pollutant adsorption plus the ease with which the regeneration operation can be
performed suggest that resin adsorption may be a valuable means of removing organic
pollutants from industrial waste streams.
E-82
-------
TABLE E-21
TREATMENT COSTS FOR RESIN ADSORPTION
Basis: 1,130 1/min (300 gpm) treatment to 1 ppm {jrdicniorobenzene.
Investment $1,700,000
Working Capital $ 370,000
Materials Cost
Streams units/vr S/unit
Resin ,
Replacement 28.3raa 1,833.92
Royalty ,
On Resin 28.3m' 424.03
Metbanol 1,239,840 1 0.17
Subtotal
Processing Cost
Labor Directed;
Direct taoor
Supervision 10% Direct Labor
Plant Overhead 100% Direct Labor
Subtotal
Investment Directed:
Amortization Cost*
Taxes ft Insurance £2% tnv.
Maintenance (§4% Inv.
Supplies I§1% to*.
Subtotal
Throughout Directed:
Steam $0.77/100 kg
Other Utilities
Subtotal
Total Treatment Cost
Treatment Costs
S/yr S/l.QOO I
290,000
12,000
213.000
47i,000 0.80
105,000
10,000
105.000
220,000 0.37
351,000
34,000
•8,000
17.000
47(T,Oub1 0.79
478,000
51,000
536.000 0.90
1,701,000 JUb .
•Based on 12 years and IS percent intent.
SOURCE: Walk, Haydel, I980a.
E-83
-------
METALS REMOVED
The two processes most widely used in industry to remove heavy metals are
precipitation, followed by coagulation and flocculation, and ion exchange; both are
effective in removing the metallic priority pollutants from waste streams. Precipitation-
cotogulation-flocculation uses relatively cheap and simple equipment and reagents to
reduce high influent metals concentrations (e.g., 100 mg/liter) to concentrations near the
ppm level. Ion exchange systems on the other hand can remove metals originally present
at low concentrations (e.g., 1-2 ppm), but is complicated and expensive. Moreover, in
many cases, the stream entering the ion exchange unit must be pretreated to remove
contaminants that would damage the ion-exchange resin.
Precipitation
Precipitation is a common metals removal process based on the solubility of
metal salts. While a particular salt of a given metal may be relatively soluble in water,
another salt of the same metal may be much less soluble in water. An example is the
silver ion: at pH 10, the silver cation in a solution of AgOH has a solubility of 10 g/liter,
while the silver cation in a solution of Ag2$ has a solubility of 10" g/liter. Therefore,
introducing sulfide to a solution of AgOH (at pH 10) reduces the solubility of silver by
17 orders of magnitude. Silver is precipated as Ag2S, an insoluble salt.
The solubility of a salt is described quantitatively by its solubility product
constant K .
For a salt solution in equilibrium with its solid precipitate, K = (M*)m(Xm~)n where m
and n are the stoichiometric coefficients of each species.
E-84
-------
Precipitation is, therefore, the process of introducing to a solution of metal ions
a particular anionic specie to form insoluble salts of those metal ions, thus removing them
from solution. The choice of the particular anionic species that will most effectively
precipitate pollutant metals, however, is rarely straightforward. Industrial waste streams
often contain many ions, each of which has a specific solubility product. Additionally,
industrial wastewaters often contain species that form water-soluble complexes with
metal ions, thus increasing their resistance to precipitation. Amphoteric metals,
berryllium, cadmium, chromium, copper, lead, nickel, and zinc, form stable, solvated
complexes at both high and low pH. There is therefore a narrow range of solution pH for
each metal in which hydroxide precipitation is most effective as shown in Figure E-5..
Four types of chemicals are widely used industrially as precipitants: hydroxides,
ferrites, sulfides and xanthates. Metal hydroxides are the most widely used precipitants.
Typically lime [Ca(OH)J and caustic soda (NaOH) are used. Though hydroxide
precipitation is a relatively simple and inexpensive procedure, it is limited by its
effectiveness in metal removal: soluble metallic complexes form at high pH and, in
general, metal concentrations range from several parts per billion to parts per million.
Other disadvantages are that hydroxide precipitates tend to form stable colloidal
suspensions and that hydroxide precipitate sludge is bulky and presents a disposal problem.
Ferrite coprecipitation can be used to precipitate zinc, cadmium, copper, nickel,
lead, and chromium from acidic wastewater. In one ferrite coprecipitation procedure, a
ferrous salt is added to the heavy metal containing waste stream; the stream is then
neutralized and the resulting heavy metal ferrous hydroxide precipitate oxidized to the
stable ferrite coprecipitate. Large particles are formed by this procedure and the
resulting sludges are stable enough for safe landfill disposal. Another more energy-
intensive ferrite-coprecipitation procedure has been used in Japan primarily for removing
E-85
-------
FIGURE E-5
METAL SULFIDE AND HYDROXIDE SOLUBILITIES
AS A FUNCTION OF pH
10
10
10
10
10
10
-10
10
-12
0 1
9 10 U 12 13 14
E-86
-------
chromium from acidic waste streams. Chromium is electrolytically reduced from Cr(VI)
to Cr(lll) in the presence of iron salts and forms insoluble chromium ferrite (iron
chromite). The magnetized ferrites can be recovered from sludge by magnetic separation.
Sulfide precipitation is similar to hydroxide precipitation in principle and
procedure. Figure E-5 and Table E-22 show that for the metal priority pollutants
cadmium, copper, lead, mercury, silver, nickel, and zinc, the metal sulfide is considerably
less soluble than the metal hydroxide; additionally, soluble metallic complexes are not
formed at high pH. Therefore, adding sulfide ions to a metal-bearing waste stream will
precipitate larger quantities of metal from solution than will hydroxide ions, and will
result in an effluent containing significantly less metal. Despite this advantage,
hydroxide precipitation is more common because lime and caustic soda are less expensive
than sodium or ferrous sulfide, and also because sulfide forms hydrogen sulfide (a severe
acute health hazard) if introduced to an acidic stream. Thus use of sulfide precipitation is
largely limited to a polishing step following hydroxide precipitation, when effluent
concentrations below those obtainable by hydroxide precipitation are required. Treatment
systems for sulfide precipitation and for hydroxide precipitation are similar, generally
consisting of a pH adjustment tank, a flash mixer, a flocculator, settling units with flash
storage, and a dual media filter. A pH adjustment to pH 7 to 8 is critical because of the
risk of hydrogen sulfide generation.
E-87
-------
TABLE E-22
SOLUBILITY PRODUCTS OF TRACE METALS AS
HYDROXIDES, SULFIDES AND XANTHATES
Solubility Product
Constant (-log K )
Metal
Cadmium, Cd
Copper, Cu
Ferrous, Fe*
Lead, Pb
Mercury, Hg
Nickel, Ni
Zinz, Zn
Chromium (VI), Cr*6
Metal
Hydroxide
13.6
18.6
15.3
16.1
25.4
14.8
15.7
8.9
Metal
Sulfide
26.1
35.2
P6.9
26.6
52.2
25.7
25.2
-
Ethyl
Xanthate
13.6
7.1
16.9
37.8
11.9
8.3
Xanthate precipitation combines aspects of ion exchange with a chemical
precipitation process. Xanthates are long-chain starch molecules that bear functional
groups capable of forming insoluble complexes with metals. They can be generated by
mixing starch or cellulose with carbon disulfide in a caustic medium. .Three types of
xanthates have been studied: soluble starch xanthate with a cationic polymer, insoluble
starch xanthate and fibrous cellulose xanthate. These were tested for their ability to
remove cadmium, chromium(III), copper, lead, mercury, nickel, silver, and zinc. In
general, xanthates were found to be effective in removing metals over a wide pH range,
from 3 to II, with optimum performance between pH 7 and 9. The studies also concluded
E-88
-------
that while cellulose xanthate and starch xanthate were similarly effective in removing
trace metals, cellulose xanthate is superior to starch xanthate in terms of sludge settling
characteristics, filterability, and handling. Xanthate may also be used as a complexing
agent to prevent insoluble hydroxides of amphoteric metals from forming soluble anions as
the pH of the stream changes.
Xanthate precipitation, however, is a new technology; reagents, therefore, are
not yet available in commercial quantities, and data has not been gathered on dosage
rates in continuous flow xanthate precipitation operations. Table E-23 presents
qualitative characterizations of the behavior of priority pollutants during treatment by
precipitation.
E-89
-------
TABLE E-23
QUALITATIVE CHARACTERIZATIONS OF
PRIORITY POLLUTANT METAL
IONS FOR PRECIPITATION
BERYLLIUM:
CHROMIUM:
ANTIMONY:
Cr*
SbH
ZINC:
SELENIUM:
ARSENIC
Se<
hydroxide is amphoteric, sulfide decomposes
aqueous solution, sulfate is water soluble
in
"hydroxide" is hydrated oxide, is amphoteric and
dissolves in excess strong base, approximate
solubility = 0.00064 mg/liter. Sulfide cannot be
made in aqueous solution, sulfate is water soluble
oxide is amphoteric, sulftde can be formed in acid
solution (to pH 6) with solubility 0.0018 g/liter
(1.3 mg/liter Sb), sulfide is soluble in neutral to
alkaline solutions and solutions with excess alkali
sulfide
amphoteric hydroxide gelatinous precipitate when
formed in aqueous solution.
Kspof ZnS = 2xlO~14
oxide is very water soluble, sulfide insoluble in
water, but dissolves in excess sulfide reagent
oxides soluble in water, As (V) sulfide
water solubility 0.0014 g/Iiter (0.6 mg/liter As)
As(lll) sulfide water solubility 0.0005 g/liter (0.3
mg/liter As). Both sulfides soluble at pH 6 and in
excess alkali metal sulfide
E-9-0
-------
Coaqulation-Flocculation
Coagulation-fiocculation is a physical treatment process designed to remove
suspended particulate matter known as colloids and as such is an integral part of metal
removal processes. Colloids exist because solids in water are always electrically charged;
one side of the solid-water interface assumes a positive or negative net electrostatic
charge. This causes an equivalent number of oppositely charged ions to form a diffuse
layer in the aqueous phase immediately surrounding the metal particle. The electrostatic
repulsion between the diffuse outer layers surrounding the metal particles keeps the metal
particles in colloidal suspension and precludes their agglomeration and subsequent
precipitation. Removing the metal species from colloidal suspension requires that the
charged cloud surrounding the metal ion be destabilized.
Coagulation is, therefore, the process of destabilizing colloids suspended in the
waste stream by neutralizing the repulsive forces between them. This destabilization is
carried out by adding certain ionic species known as chemical coagulants—generally low
molecular weight salts of multivalent inorganic ions, usually aluminum salts, iron salts or-
polyelectrolytes—and then gently stirring the suspension to facilitate contact between the
newly destabilized colloids. The result of the coagulation process is that the colloidal
particles agglomerate into floes.
Adding charged species to the waste stream destabilize colloids in two ways.
First, raising the electrolyte concentration in the aqueous medium lowers the diffuse
outer layers surrounding each metal particle, so the range of electrostatic repulsion
decreases and the short-range electrostatic attractive forces take over. Because this
phenomenon results from simple electrostatic attraction, the minimum coagulant
concentration required to destabilize the colloid is independent of the chemical
composition of the colloid. Therefore, quantitative data are not available to describe the
response of each individual priority pollutant to coagulation and flocculation. Second,
E-91
-------
cations can bring the negatively charged layers surrounding each metal ion closer together
by bridging them electrostatically. Multivalent cations are especially effective in
bridging heavy metal colloids; a trivalent ion may be 1,000 times as effective as a
monovalent ion.
Flocculation is the process of getting these floes to coalesce still further to form
settleable agglomerates. Like coagulation, this process involves adding flocculants—
cations that bridge small floes together by bridging the negatively charged layers
surrounding each floe—and then mixing the suspension intensely but not violently.
The two processes, therefore, involve the same procedure: ion addition followed
by mild agitation. Alum salts and iron salts are widely used both as coagulants and as
flocculants; cationic polyelectrolytes can be used as coagulants, but they are especially
effective as flocculants because they are long molecules containing multiple ionic groups
and are therefore structurally ideal for bridging floes. Agitation is generally
accomplished by slow stirring with long thin blades; a coagulation/flocculation unit is
usually a tank with blades arranged inside as stators and rotors, equipped with meters to
dispense measured quantities of coagulants and flocculants. TableE-24 presents a
summary (EPA, I979c) of several coagulation-flocculation-precipitation processes and
their effectiveness in treating the metal priority pollutants. Table E-25presents typical
performances for some of these treatment processes as 30-day average effluent metal
concentrations.
Ion Exchange
Ion exchange removes metal ions from water by transferring them to a solid
material, the ion exchanger, which accepts these undesirable species at acidic or basic
exchange sites, giving back to the aqueous phase an equivalent number of a similarly
charged species (usually H"1" or OH") stored on the ion exchanger skeleton. When the
exchange sites become saturated with the undesirable ions, the ion exchanger is washed
E-92
-------
TABLE E-24
PERFORMANCE DATA SUMMARIES
ANTIMONY AND ARSENIC REMOVAL
Treateent Technology
AntijTony
lire/Filter
Ferric chloride/Tilter
Alum/Filter
Arsenic
Lime Softening
Sulfide/Filter
Lime (260 ing/l) /Filter
Lowe (600 mg/1) /Filter
Ferric sulfate
Ferric sulfate
Line/Ferric Chloride/
Filter
Activated alunijia
(2 mg/1)
Activated carbon
ES
11.5
6.2
6.4
mf
6-7
10.0
11.5
5-7.5
6.0
10.3
6.8
3.1-3.6
Initial
Concen-
tration
(mg/1)
0.6
0.5
0.6
0.2
-
5.0
5.0
0.05
5.0
3.0
0.4-10
0.4-10
Final
Concen-
tration
(mg/1)
0.4
0.2
0.2
0.03
0.05
1.0
1.4
0.005
0.5
0.05
<0.4
<4.0
Rsroval
28
65
62
85
-
80
72
90
90
98
96-99+
63-97
(3
Ferric Chloride
Ferric Chloride
0.3 0.05
0.6-0.9 <0.13
98
E-93
-------
TABLE E-24 (Continued)
BERYLLIUM AND CADMIUM REMOVAL
Treat-rent Technology
Beryllium
Lire/Filter
Cadmium
Lime (260 mg/1) /Filter
Lire (600 mg/1) /Filter
Line Softening
Line/Sulfice 8
Ferrous Sulfide (Sulfex)
Ferrite coprecipitation/
Filter
pH
11.5
10.0
11.5
5-6.5
.5-11.3
8.5-9.0
neutral
Initial
Concen-
tration
•(mg/1)
0.1
5.0
5.0
0.44-1.0
0.3-10
4.0
240
Final
Concen-
tration
(irg/1)
0.006
0.25
0.10
0.008
0.006
<0.01
0.008
Reroval
(%)
99.4
95
98
92-98
98+
99+
99+
E-94
-------
TABLE E-24 (Continued)
CHROMIUM 111 AND CHROMIUM VI REMOVAL
_«-_
Chraritn
Lire (260 mg/1) /Filter
lane (600 sq/I) /Filter
Red^^rv^
Reduction/line
Lire Scfierinj
lira/niter
Line
liae
Ferrite ecpracipitaticrv'
Filter
Ferric sulf ate
Ferric sulfate/TUter
ftrarian VI
Activated na:tm
(pulverized, ?iets-
bur?ft type 1C)
Ssre as above
Acsivaud «*-» ••* • "
Ferrite ceprecipitaucn
Sulfur rfirri<> reduction
Bisulfite reduffiisr.
-
10.0
u.s
7-8
7-8
10.6-11.3
7-9
9.5
9.5
—
6.5-9.3
—
3.0
2.0
6.0
—
Initial
Conoen-
traticn
(eg/I}
5.0
5.0
140 (as
Cr VI)
1300 (as
Or VI)
—
—
IS
3.2
25
—
5.0
10
10
3
0.5
—
—
Final
Cacea-
traticn
(mg/l)
0.1
0.1
1.0
0.06 CrIIX
0.15
0.05
0.1
<0.1
0.01
—
0.05
1.5
0.4
0.05
not
detectable
0.01-0.1
0.05-1.0
Ascv.il
98
98
—
—
98*
—
98*
99
85
96
98
—
—
E-95
-------
TABLE E-24 (Continued)
COPPER REMOVAL
Treatment Technology
Line/Tilter 8
Lime (260 mg/1) /Filter
Lime (600 mg/1) /Filter
Ferric sulfate/Filter
PH
.5-9.0
10.0
11.5
6.0
Loire >8.5
Lire
Alun 6
Lire/Sulfide 5
Ferrous sulfide (Sulfex) 8
Ferrous sulfide (Sulfex) 8
Ferrite Coprecipitation/
Filter
9.5
.5-7.0
.0-6.5
.5-9.0
.5-9.0
Initial
Concen-
tration
(mg/1)
3.2
5.0
5.0
5.0
10-20
3.0
3.0
50-130
3.2
4.0
Final
Concen-
tration
(mg/l)
0.07
0.4
0.5
0.3
1-2
0.2
0.2
<0.5
0.02
0.01
0.01
Renewal
(%)
98
92
91
95
90
93
93
-
99
99+
99-1-
E-96
-------
TABLE E-24 (Continued)
LEAD REMOVAL
Treat-rent Technology
Line (260 mg/1)
Lime/filter
Lire (260 mg/1) /Filter
Lire (600 mg/1) /Filter
Ferrous sulfate/Filter
Sodium hydroxide (1 hour
settling)
Sodium hydroxide (24 hour
settling)
Sodium hydroxide/Filter
Sodium carbonate/Filter
Sodium carbonate/Filter
Sodium carbonate/Filter
Ferrous sulfide (Sulfex)
Ferrite coprecipitation/
pH
10.0
8.5-9.0
10.0
11.5
6.0
5.5
7.0
10.5
10.1
6.4-8.7
9.0-9.5
8.5-9.0
Initial
Concen-
tration
tmg/l)
5.0
189
5.0
5.0
5.0
—
— —
1700
1260
10.2-70.0
5.0
189
480
Final
Concen-
tration
(mg/1)
0.25
0.1
0.075
0.10
0.075
1.6
0.04
0.60
0.60
0.2-3.6
0.01-0.03
0.1
0.01-0.05
Removal
(%)
95.0
99.9
98.5
98.0
98.5
—
99+
99+
82-99+
99+
99.9
99.9
Filter
E-97
-------
TABLE E-24 Continued)
MERCURY II REMOVAL
Treatment Technology pH
Sulfide
Sulfide 10.0
Sulfide/Filter 5.5
Sulfide/Filter 4.0
Sulfide/Filter 5.8-8.0
Ferrite ccprecipitation/
Filter
Activated Carbon
Activated Carbon/Alum
Activated Carbon
Initial
Concen-
tration
(ng/1)
0.3-50.0
10.0
16.0
36.0
0.3-6.0
6.0-7.4
0.01-0.05
0.02-0.03
0.06-0.09
Final
Concen-
tration
(ng/1)
0.01-0.12
1.8
0.04
0.06
0.01-0.125
o.ooi-o. ops
< 0.0005
0.009
0.006
Removal
(%)
-
96.4
99
99.8
87-99.2
99.9
-
-
—
E-98
-------
TABLE E-24 (Continued)
NICKEL REMOVAL
Treatment Technology
Liiie
Lire (260 mg/1) /Filter
Lime (600 mg/1) /Filter
Caustic Soda/Filter
Ferrous sulfide (Sulfex)
Ferrite coprecipitation
PH
8.5-9.0
10.0
11.5
11.0
8.5-9.0
—
Initial
Concen-
tration
(mg/1)
75
5.0
5.0
-
75
1000
Final
Concen-
tration
(mg/1)
1.5
0.3
0.15
0.3
0.05
0.20
Removal
(%)
93
94
97
-
99.9
99.9
E-99
-------
TABLE E-24 (Continued)
SILVER REMOVAL
Treatment Technology
Scdium hydroxide
Ferric sulfate (30 ng/1)
Lime Softening
Chloride precioitation
PH
9.0
6-9
9.0-11.5
-
Initial
Concen-
tration
(mg/l)
54
0.15
0.15
105-250
Final
Concen-
tration
(mg/1)
15
0.03-0.04
0.01-0.03
1.0-3.5
Removal
(%)
72
72-83
80-93
97+
(alkaline chlorination
in the presence of
cyanide)
Ferric chloride/Filter
Sulf ide precipitation
6.2 0.5
5-11
0.04 98.2
- verv hich
* \ •"
E-100
-------
TABLE £-24 (Continued)
SELENIUM AND THALLIUM REMOVAL
Treatment Technology
Selenium
Ferric chlorice/^Tilter
Ferric chloride/Tilter
Alum/Filter
Ferric sulfate
Ferric sulfate
Lime/Filter
Lime/Filter
Thallium
Lire/Filter
Ferric chloride/Filter
AlurVFilter
PH
6.2
6.2
6.4
5.5
7.0
11.5
11.5
11.5
6.2
6.4
Initial
Concen-
tration
(ng/1)
0.1
0.05
0.5
0.10
0.10
0.5
0.06
0.5
.0.6
0.6
Final
Concen-
tration
(rrg/1)
0.03
0.01
0.26
0.02
0.03
0.3
0.04
0.2
0.4
0.4
Raraoval
(%)
75
80
48
82
75
35
38
60
30
31
E-101
-------
TABLE E-24 (Continued)
ZINC REMOVAL
Treatment Technology
Line/Filter
Lime (260 mg/1)
Lime (260 mg/D/Filter
Lime (600 mg/1)
Lime (600 mg/1) /Filter
Lime/Filter
Sodium hydroxide
Sulfide
Ferrous sulfide (Sulfex)
Ferrite coprecipitation
pH Initial
Concen-
tration
(mg/1)
8.5-9.0
10.0
10.0
11.5
11.5
-
9.0
-
8.5-9.0
-
3.6
5.0
5.0
5.0
5.0
16
33
42
3.6
18
Final
Concen-
tration
(mg/1)
0.25
0.85
0.80
0.35
1.2
0.02-0.23
1.0
1.2
0.02
0.02
Removal
(%)
93
83
84
93
77
-
97
97
99+
99+
E-102
-------
CO
>-UJ
< rj
QO
o^
ro O
15
S LU
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u-i < C
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with regenerant, a strong solution of the ion originally present on the resin—usually
mineral acid or caustic soda. The pollutant species accumulated on the resin are replaced
by the original species of ions from the regenerant and the exchanger is returned to its
original usable condition.
The ion exchanger is almost always a three-dimensionally cross-linked polymer
resin to which particular ionic function-alities are attached. There are four categories of
ion-exchange resin, each with a characteristic set of functional groups, which interact
most strongly with a particular type of charged species. First are the strongly acid
cation-exchange resins. Their general formula is Res-SO^-H"1" where "Res" represents the
polymeric resin structure. Most typically, strongly acid-cation exchange resins consist of
polystyrene sulfonic acid cross-linked with divinylbenzene. Second, there are weakly
acidic cation-exchange resins: Res-CC^-H. These are generally polyacrylic acid or
polymethacrylic acid cross-linked with divinylbenzene. Third, there are strongly basic
an ion-exchange resins: Res-NR«-OH, where R is an aliphatic or aryl-aliphatic radical.
Strongly basic an ion-exchange resins generally are polyvinylbenzyl trimethyl-ammonium
hydroxide cross-linked with divinylbenzene. And fourth, there are weakly basic anion-
exchange resins: Res-NR2« Several varieties of these are available; all contain tertiary
aliphatic or aryl-aliphatic amine function-alities on resin matrices ranging from the
polystyrene type through polyacrylate to aliphatic polyamine condensation products.
The selectivity of a particular resin is a function of the size and charge of the
ions to be exchanged—an exchange resin prefers highly charged multivalent ions.
Knowledgeable choice of a particular ion exchange material from the wide range of
selective resins commercially available can often allow selective separation of one ion
from another, allowing selective removal of an undesirable ion from a stream bearing
many other ions. The affinity of a particular ion exchange resin for a particular ion is a
function of several factors, including ion size and charge, the composition of the waste
E-105
-------
stream, and the functional group and polymer structure of the resin. Extensive
commercial literature is available for the engineer intending to design an ion-exchange
system to remove particular metals from a particular waste stream.
Commercially available ion exchangers operate in one of two modes: fixed bed
or continuous. (Figure E-6 presents their flow diagrams.) Fixed bed units perform in a
four-operation cycle. First, service wastewater flows through the ion exchange unit until
the point of exhaustion is reached where all available ion-exchange sites are occupied by
pollutant ions. Second, backwash water is pumped through the bed in the direction oppo-
site to that of the waste stream during the service phase. Third, regeneration occurs in
which a strong solution of the ion originally occupying the exchange sites on the resin is
pumped through the bed to dislodge the pollutant ions and return the resin to its original
composition. And fourth, the resin is rinsed with water. The backwash phase is necessary
to flush out extraneous particles from between the resin beads. Fixed bed units can
operate cocurrently—the regenerant is pumped through the unit in the same direction the
waste stream flowed-or counter currently—the regenerant flows in the opposite direction
from the waste stream. Countercurrent regeneration is more effective than cocurrent
regeneration because the maximum pollutant sorption occurs where the waste stream
enters the ion-exchange unit. Sorption sites become progressively less occupied by
pollutant ions along the path of the waste stream through the unit. Therefore, the
countercurrent method is better because it brings fresh regenerant into contact with the
part of the resin bearing the fewest pollutant ions and as the regenerant proceeds through
the unit and becomes less concentrated, the resin along the path of the regenerant
becomes more heavily occupied with contaminant ions—therefore a mass ratio regenerant
iontsorbed metal ion favorable to regeneration is maintained all along the regenerant
path.
E-106
-------
FIGURE E-6
ION EXCHANGE BED CONFIGURATIONS
Co-Current
Fixed Bed Mode
Service Za
1*1
Regenerant In
Service Out "III Regenerant Out|j|
Service Step Regeneration Step
Counter-Current
Fixed Bed Mode
Service In
Service Out
Regenerant Out
_ Regenerant Zn
Service Step Regeneration Step
Counter-Current
Continuous Mode
Service Zn
Service Out
Regenerant Out
1
Resin Flow
Hash To Remove
Fines
Pulse Generation
Section
~ » Regenerant Out
E-107
-------
Continuous ion-exchange operations are run countercurrentty. Figure M-6 shows
how ion-exchange resin beads are circulated through a loop. One segment of the loop is
the seryice segment, through which wastewater to be treated is sent, and another section
is the regeneration segment, through which regenerant is passed in a direction opposite to
the direction the wastewater took.
Since ion exchange is basically a method for tranferring pollutant ions from the
waste stream to the regenerant solution, there arises the problem of disposing of the
spent regenerant. In some cases, it is economical to recover the metal pollutant from the
regenerant. Disposal or recovery is simplified when the volume of regenerant is
minimized. Many fixed bed units minimize regenerant volume with the "staged" or
"proportional" regeneration technique. The first part of the regenerant leaving the ion
bed is the most enriched in the pollutant species being removed. This portion is sent to
treatment or disposal. The second portion of regenerant to leave the ion-exchange bed
leaves with a significantly lower pollutant concentration. It is stored and used as the first
portion of regenerant in the next service regeneration cycle.
Ion exchange removes metal priority pollutants with outstanding efficiency.
Table E-26 summarizes the results of treatability studies on ion exchange removal of
priority pollutants. Most removal efficiency percentages are in the high nineties.
Table E-24 summarizes ion exchange removal efficiencies for each metal priority
pollutant obtained in treatability studies with industrial wastewaters and synthetic
solutions.
One chemical company has prepared a summary of treatment and cost data for
an industrial ion-exchange system, treating a chromium-bearing waste, which it considers
to represent BAT for chromium removal. The waste stream is a cooling tower blowdown,
containing chromium added to inhibit growth of fungi and algae.
E-108
-------
TABLE E-26
TREAT ABILITY STUDIES SUMMARY FOR PRIORITY
POLLUTANT REMOVAL WITH ION EXCHANGE
METAL
As
Cd
Cr
Cu
Pb
Hg
Ag
Zn
DATA
POINTS
19
17
12
3
2
5
5
7
EFFLUENT CONC., mg/1
MEAN MED MIN
1.65
0.019
0.36
1.8
0.03
0. 0005
3.5
2.2
0.60
0. 0003
0.05
2.0
-
0.0001
0.14
0.4
0.0
0.0001
0.01
0.5
-
0
0.01
0
8.
0.
1.
3.
0.
6.
10
MAX
0
1
8 (11)
0 (4)
-
002
5 (7)
(9)
MEAN
87.1
96.8
96.7
96.5
99.85
99. 9*
93.7
97.7
REMOVAL %
MED MIN
96.5
99.9*
99.5
97
-
99.9*
95
99
21
75
88
93
-
99.9*
90
90
MAX
100
99. 9H
99.9
99*
100
100
100
*
*
*
*
*
*Data set includes results from synthetic solutions.
() s Data points used for that computation.
E-109
-------
This application for ion exchange is relatively new technology. Slowdown is
filtered and pH adjusted before passing through weak base anion exchange vessels for
chromium removal and then weak acid cation exchangers for zinc and trivalent chrome
removal. Upon regeneration of the resins, chrome and zinc can be recovered and recycled
back to the cooling towers eliminating a large percentage of the make-up chrome and zinc
solutions. Another advantage of ion exchange is the elimination of voluminuous metal
sludges formed in the precipitation technique commonly employed for chrome-and-zinc
removal in cooling tower blowdown.
Figure E-7 is the flow diagram of the system. TableE-27 summarizes operating
parameters and removal data. Tables E-28 and E-29 present daily and rolling average
chromium effluent concentrations.
The ion exchange units were installed in January 1978 and have consistently met
the NPDES permit. Installed costs were $4.7 million. The operating costs for the first
quarter of 1981 were approximately $80,000/month. This figure includes utilities services,
wages, salary and payroll overhead, maintenance, chemical requirements, laboratory
analyses, technical engineering services, catalyst (resin), fixed indirects, and unit
depreciation. Assuming an average flow of 650 gpm, at 8 ppm Cr ° removal across the
unit, this comes to roughly $W/pounds of Crtot or $2.85/1,000 gallons.
A survey of published ion exchange treatability data is presented in Tables M-3Q
These data were compiled by Calmon, Casana, and Gold of Water Purification Associates
(1980); many of these represent results obtained with synthetic solutions.
Minor drawbacks to the application of ion exchange to industrial waste
treatment exist. They include the problems of spent regenerant disposal, susceptibility to
damage by high temperatures and strong oxidants, and the tendency to contamination by
organic matter present in the waste stream. Furthermore, suspended organic solids will
foul the resin and aromatic molecules will be irreversibly adsorbed onto the resin.
E-110
-------
HI
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TABLE E-27
CHROMIUM AND ZINC REMOVAL SUMMARY
Treatment Technology: Ion Exchange
Data Source: Cooling Tower Slowdown Data Source Status:
Point Source Category: Organic Chemicals Engineering estimate
Subcategory: Bench scale
Plant: Pilot scale
References: Pull scale
Use in System: Cr Removal and Reuse
Pretreatment of Influent: Dual Media Filtration (Anthracite/Sand,
pH adjustment
Design or Operating Parameters*
Wastewater Flow: 400 gpm Avg? 1000 gpra avg design 1500 gpm max design
Solids Loading Rate: 0.50 lb/day/ft* based on 400 gpm 8 40 ppm TSS
Bed Height: Anion 44" Cation 36"
Pressure Drop:
Resin Type: Anion Rohm & Haas IRA-94 Cation Rohm & Haas DP-1
Avg. Run Length: Anion 1 regeneration/day Cation 1 regeneration/3
days (based on 400 gpm)
Regenerant Used: 5X HC1 5X NaOH
Cycle Time: 8 hrs/regeneration time
Backwash Rate:
Resin Pulse Volume:
Unit Configuration: Dual Media Filtration, pH adjustments, Anion
Exchange (.Chrome Removal), Cation Exchange
(Zinc Removal)
REMOVAL DATA
Sampling period: 7/1/79 - 7/31/30
Concentration, mg/1 Percent
Pollutant/Parameter Influent Effluent Removal
Toxic pollutants:
Chromium
Mean Concentration 10.94 .48 94
9_ath percentile 36.00 2.58 99
9.5th percentile 21.78 1.20 99
9.0th. percentlle 17.31 0.80 98
E-112
-------
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TABLE E-30
POLLUTANT REMOVAL SUMMARIES
ARSENIC REMOVAL SUMMARY
Source
Potable Well
Potable Well
Potable Well
Synthetic
As cone
Influent
1.06
0.84
0.09
Drinking Water 0.06
H
M
M
H
"
"
"
«
II
M
n
"
"
Geo thermal
1.06
24.7 *
60.1 •
104 *
12.8 •
25.4 *
34.7 •
6.54*«
13.4 ••
26.7 *•
6.75"
13.4 ••
26.7 ••
100 •
100 **
(ag/1)
Effluent
0.01
0
0
0.003
0.17
0
0.6
3.0
0.5
1.9
5.7
1.33
2.3
8.0
0.7
2.3
5.5
0
0
Removal (%)
91
100
100
99.5
21
100
99
97
96.5
92.4
83.5
79.6
73.0
70.0
88.8
83.0
79.3
100
100
Coriined Data
Source
Potable Well
Synthetic
TOTAL
Data
Points
3
16
19
As effluent cone, (aw/1)
mean aed
0.003 0
1.96 1.01
1.65 0.60
min max
0 0.01
0 8.0
0 8.0
As Removal (%)
mean aed min max
97 100 91 100
85.2 90.6 21 100
87.1 96.5 21 100
E-115
-------
TABLE E-30 (Continued)
CADMIUM REMOVAL SUMMARY
(an Cd/l)
Data
Pts. Mean Med Min Max
14 0.0018 0.0002 0.0001 <0.01
3 0.1 0.1 0.1 0.1
17 0.019 0.0003 0.0001 0.1
Jieisoval ( ^ )
HA
no.
Data.
?ts. Mean Med. Min. Max.
1« 96.2 99.9* 75* 99
3 99.7 99.8 99.5* 99
+ ^
17 96.8 99.9 75 99
.9*
.9*
4f
.9
Sours* Initial Other
woncv^AA W^OH
(ae/1 Cd) Ps
CdSO. Synthetic
solution 5
Gas Hashing
Hastevater 0.039
•esent ment Volsse (ac/1 Cd) (»)
pa adj. 8.6 500 0.
1000 0.
1600 0.
3000 0.
4800 0.
Hg;Cu pH adj. S.S. 1000 <0.
0001*
9002*
0003*
008*
0018*
01*«
Reacvel 200Q <0.01..
w.w. rrea
Phsto Plant 1.7 Organic
:> pH adj. 100 <0.
001
^••••••••^B
99.9*
99.9*
99.9*
99.9*
99.9*
75*
75*
99.9*
C Inorganic S.S. res.
Sales
WW *rea Cd
Placing 4.6 CS «
pR adj. S.S. 100 <0.
001
99.9*
Inorganics res. NaCIO
ww 5-ss Cd
Battery Plant 0.02
Flue gas
Trtatsent
rea. CK
pH adj. 9.0 100 0.
S3 rtsoved 100 0.
300 0.
Solution 0.8 Hg pH adj. 9.0 1000 0.
Cr 3000 0.
0002
0002
OOC2
0002-
0003*
99
99
99
99.9*
99.9*
?b
Inorg. Salts
in s«ri*s.
Cth«r haavy sctals r»duc«d
ta vtry low levels.
E-116
-------
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E-117
-------
TABLE E-30 (Continued)
CHROMIUM REMOVAL SUMMARY
Concentration(rag/l as Cr) _ ._
• Capacity-
Source Influent Effluent Seaoval(%) (*CrO /ft )
Plating Waste 44.8 0.025 99.9 1.7 - 2.0
(rinse water)
Cooling Tower 9.8 0.02 99.8 3.0
Slowdown
(Electroplating)
Electroplating 41.6 0.01 99.8 5.2 - 6.3
Waste (Rinse
Water)
Cooling Tower
Slowdown 17.9 1.8 90 5-6
Cooling Tower
Slowdown - 0.1
Cooling Tower
Slowdown 10 1 90 2.5 - 4.5
Cooling Tower 7.4-10.3 1 86-90
Slowdown
Coolifio Tower 20 < 0.05 99.4
Slowdown
Cooling Tower 10 0.05 99.5 0.6 - 5.2
Slowdown
Wool Dyeing
Wastewater 10-20 0.05 99.5-99.75 0.6 - 5.2
Cooling Tower
Slowdown 8.96 0.2 97.7 2.51
(Chesicai
Complex}
Pigaent 1210 <0.5 99.9+
Manufacture
Wastewater
E-118
-------
TABLE E-30 (Continued)
COPPER REMOVAL SUMMARY
Source
Synthetic
Synthetic
Synthetic
Synthetic
£ff (ma /I Cu) Removal
-
-
93
0.5 99
Rayon Wastewater 3.0 99+
Pickle Rinse
No data ?ts
3
No data ots
4
No data r>ts
4
Soln. 2.0 95
Combined Data
Effluent Cu (rag/1)
Mean Med
1.8 2.0
Removal %
Mean Hed
96.5 97
Capacity (mec/1)
Mean Med
1303 =1290
(\) Capacity (aes/1)
-
1220 (pH 4)
-
1250 (H* forr
1412
1330
Min Kax
0.5 3.0
Min Max
93 99+
Min Max
1220 1412
E-119
-------
TABLE E-30 (Continued)
LEAD REMOVAL SUMMARY
Source InfCag/1 Pb) Eff (n»c/l Pb) Removal (%) Capacity
Azssunition
Plant 6.5 0.01 99.8
Wastevaters
Synthetic 50 0.05 99.9 4.4 lb/ft3
Solution
28.5 0.03 99.85 4.4 lb/ft3
E-120
-------
^Continued)
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E-122
-------
TABLE E-30 (Continued)
SILVER REMOVAL SUMMARY
Influent
Synthetic So In.
Synthetic So In.
Sand/Carbon Treated
Effluent Cone.
(mq/1 Aq)
50
Not reported
0.01
Removal
%
90
MOO
99.4
Capacity
roeq/1 bed
90
300-1000
Not reported
Sewage
Lime/Sand Treated
Sewage
0.14
91.7
Not reported
Photographic wastes 10
Photographic wastes <1
Photographic wastes 6.5
95
>90
90
278
75
900-1300
E-123
-------
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E-126
-------
Conclusion
The vast majority of waste treatment systems in the organic chemicals and
plastics industry use coagulation-flocculation-precipitation, or ion exchange, or both, to
remove metal priority pollutants from wastewater. However, other metal-removing
systems exist and are used to some extent as in the inorganic chemicals processing
industry. These are reduction and oxidation processes, membrane processes (reverse
osmosis), and carbon adsorption.
E-127
-------
REFERENCES *
AMORE, F.. 1979. Anal. Chem. 51:1105A
BEAUDET, B.A., BILELLO, L.J., KELLAR, E.M., and ALLAN, J.M. (ESE), and TURNER,
R.J. (EPA). 1980. Removal of Specific Organics from Wastewater by Activated
Carbon Adsorption, Evaluation of a Rapid Method for Determining Carbon Usage
Patterns. Environmental Science and Engineering, Inc. (ESE). U.S. Environmental
Protection Agency, Industrial Pollution Control Division, IERL-CI, Cincinnati.
Prepared for the U.S. Environmental Protection Agency. May 1980. Presented at
the 35th Annual Industrial Waste Conference, Purdue University
BELLA, T.A., and LICHTENBERG, JJ. 1974. Determining volatile organics at rnicro-
gram-per-liter levels by gas chromatography. J. Am. Water Works 12:739-744.
December 1974 (As cited in EPA 1977)
CALMON, C.t CASANA, J., and GOLD. H. 1980. Ion Exchange and Resin Adsorption Data
for the Removal of Toxic Contaminants from Wastewaters. EPA Contract 68-01-
5052, September 1980
CATALYTIC, INC. 1975. Capabilities and Costs of Technology for the Organic
Chemicals Industry to Achieve the Effluent Limitations of P.L. 92-500. Prepared
for the National Commission on Water Quality. Contract No. WQ4ACOI5
CATALYTIC, INC. 1978. Letter of 20 September 1978 to CMA Committee for review of
proposed Treatment Catalog
CATALYTIC, INC. !979a. Analytical Methods for the Verification Phase of the BAT
Review. March 21, 1979 (Revised September 4, 1979)
CATALYTIC, INC. I979b. Laboratory Study of Biological System Kinetics. Biological
Treatability Factors—Methodology for Obtaining Data. Biological Treatability
Factors—Addenda to Methodology
CATALYTIC, INC. I979c. Letter of 22 March 1979 to CMA Committee for review of
final draft of the Treatment Catalog
CATALYTIC, INC. I979d. Letter of 16 April 1979 to selected environmental consultants
for review of final draft of the Treatment Catalog
CATALYTIC, INC. I980a. Evaluation of Organic Chemicals and Plastics and Synthetics.
Draft Final Report prepared for U.S. Environmental Protection Agency, Effluent
Guidelines Division, Washington, D.C. December 1980. Contract No. 68-01-5011
CATALYTIC, INC. I980b. Computerized Wastewater Treatment Model. Technical
Documentation. Prepared for U.S. Environmental Protection Agency
EICHELBERGER, J.W., HARRIS, L.E., and BUDDE, W.L. 1975. Reference compound to
calibrate ion abundance measurements in gas chromatography-mass spectrometry
systems. Anal. Chem. 47:995-1000 (As cited in EPA 1977)
EPA. See U.S. Environmental Protection Agency.
E-128
-------
FE1LER, H. 1980. Fate of Priority Pollutants in Publically Owned Treatment Works-
Interim Report. Prepared for Effluent Guidelines Division, Water Regulations and
Standards, Office of Water and Waste Management, U.S. Environmental Protection
Agency, Washington, D.C. EPA-440/I-80-30I
FOX. 1978. Plant uses prove phenol recovery with resins. Hydrocarbon Processing.
November 1978. P. 269
FREEMAN, R.A. 1979. Stripping of Hazardous Chemicals from Surface Aerated Waste
Treatment Basins. Monsanto Company, St. Louis, Missouri. Air Pollution Control
Federation Specialty Conference Proceedings
FREEMAN, R.A., SCHROY, J.M., KLIEVE, J.R., and ARCHER, S.R. 1980. Experimental
Studies on the Rate of Air Stripping of Hazardous Chemicals from Waste Treatment
Systems. Monsanto Company, St. Louis, Missouri, and Monsanto Research Corpora-
tion, Dayton, Ohio
GAUDY, A.F. 1980. Memo to Judy Longfield, P.E., Catalytic Corporation, dated May 19,
1980
GAUDY, A.F., KINCANNON, D.F., and MANICKAM, T.S. 1979. Treatment Compatibi-
lity of Municipal Waste and Biologically Hazardous Industrial Compounds. Bio-
environmental Engineering Laboratories, School of Civil Engineering, Oklahoma
State University, Stillwater, Oklahoma. Prepred for U.S. Environmental Protection
Agency, Office of Research and Development, Robert S. Kerr Environmental
Research Laboratory, Ada, Oklahoma. Grant No. R805242
HARRIS, L.E., BUDDE, W.L., and EICHELBERGER, J.W. 1974. Direct analysis of water
samples for organic pollutants with gas chromatography-mass spectrometry.
Anal. Chem. 46:1972 (As cited in EPA 1977)
HOTELLING, H., and PABST, M.R. 1936. Rank correlation and tests of significance
involving no assumption of normality. Ann. Mathematical Stat. 7:29-43
HWANG, S.T. I980a. Treatability and Pathways of Priority Pollutants in the Biological
Wastewater Treatment. (Draft) For presentation in the AlChE meeting, Chicago.
Organic Chemicals Branch, Effluent Guidelines Division, U.S. Environmental Pro-
tection Agency, Washington, D.C.
HWANG, S.T. I980b. Tray and Packing Efficiencies at Extreme Low Concentrations.
U.S. Environmental Protection Agency, Effluent Guidelines Division, Washington,
D.C. Prepared for presentation at the Chicago AlChE meeting, November 1980
HWANG, S.T. No date (a). Solvent Extraction of Organic Priority Pollutants. Unpu-
blished report to U.S. Environmental Protection Agency
HWANG, S.T. No date (b). Treatability of the Organic Priority Pollutants by Steam
Stripping. Unpublished report to U.S. Environmental Protection Agency
HWANG, S.T. and FAHRENTHOLD, P. 1980. Treatability of the Organic Priority
Pollutants by Steam Stripping. U.S. Environmental Protection Agency, Effluent
Guidelines Division, Washington, D.C.
E-129
-------
HYDROSCIENCE, INC. 1981. Survey of Industrial Applications of Aqueous-Phase
Activated Carbon Adsorption for Control of Pollutant Compounds from Manufacture
of Organic Compounds. Volumes I and II. Prepared for the U.S. Environmental
Protection Agency, Office of Research and Development, Industrial Environmental
Research Laborabory, Cincinnati. Contract No. 68-03-2568, Task No. T7009
KAGEL, R.O., and STEHL, RJH. 1978. Draft—Priority Validation Protocol.
February 13, 1978
KENDALL, M.G., and STUART, A. 1973. The Advanced Theory of Statistics. Vol. 2.
Hafner
KENNEDY, D.F. 1980. Vice President, Envirodyne Engineers, Inc. Personal communica-
tion to Kay Storey, U.S. EPA, September 1980
KIM ET AL. 1976. Adsorption of organic compounds by synthetic resins. JWPCF 48s 120
KINCANNON, D. 1979. Determination of Activated Sludge Biokinetic Constants for
Chemical and Plastic Industrial Wastewaters. Proposal No. EN 79-R-I23. Division
of Engineering, Oklahoma State University, Stillwater, Okla.
KINCANNON, D.F. I980a. Determination of Activated Sludge Biokinetic Constants for
Chemical and Plastic Industrial Wastewaters—First Quarterly Report for March I,
1980 to May 31, 1980. Project No. CR8068A30IO. Oklahoma State.University
KINCANNON, D.F. .1980b. Determination of Activated Sludge Biokinetic Constants for
Chemical and Plastic Industrial Wastewaters—Second Quarterly Report for June I,
I960 to August 31, 1980. Project No. CR8068430IO. Oklahoma State University
KINCANNON, D.F. and STOVER, E.L. I98la. Determination of Activated Sludge
Biokmetic Constants for Chemical and Plastic Industrial Wastewaters—Third
Quarterly Report for September I, 1980 to November 30, 1980. Project No.
CR8063430IO. Oklahoma State University
KINCANNON, D.F. and STOVER, E.L. I98lb. Determination of Activated Sludge
Biokinetic Constants for Chemical and Plastic Industrial Wastewaters—Fourth
Quarterly Report for December I, 1980 to February 28, 1981. Project No.
CR8068430IO. Oklahoma State University
KINCANNON, D.F., and STOVER, E.L. I98lc. Fate of Organic Compounds during
Biological Treatment. To be presented at the American Society of Civil Engineers
Meeting, Atlanta, Ga., July 1981
KINCANNON, D. and GAUDY, A. No date. Functional Design of Aerobic Biological
Waste Water Treatment Processes. Bioenvironmental Engineering, School of Civil
Engineering, Oklahoma State University, Stillwater, Okla.
KINCANNON, D.F., STOVER, E.L., and CHUNG, Y.P. 1981. Biological Treatment of
Organic Compounds Found in Industrial Aqueous Effluents. Presented at the
American Chemical Society National Meeting, Atlanta, Ga., March 29-ApriI 3, 1981
E-130
-------
LIPTAK, B.G. 1974. Environmental Engineers'Handbook. ChiIton, Radnor, Pa.
MACNA1R, W.H. 1980. Unpublished Bibliography on Organic Chemical Biodegradability.
Private communication, Catalytic, Inc., September 1980
PERRY, J.H., and CHILTON, C.H. 1973. Chemical Engineers' Handbook. 5th ed.
McGraw-Hill, New York
RITCHIE-SCOTT, A. 1918. The correlation coefficient of a polychoric table.
Biometrika 12:93
ROCHELEAY, R.F. No date. E. I. du Pont de Nemours and Co. Personal communication
to Catalytic, Inc.
ROHM AND HAAS. 1980 and 1981. Synthetic Resin Adsorbents in Treatment of
Industrial Waste Streams. Quarterly Progress Reports, submitted by Rohm and Haas
Company to EPA for the period I June to I September 1980, I September to
I December 1980, and I December 1980 to I March 1981
TAYLOR, JX. 1981. Coordinator for Chemical Measurement Assurance and Voluntary
Standardization, Center for Analytical Chemistry, U.S. Department of Commerce,
National Bureau of Standards, Washington, D.C. 20234. From a letter to OCB,
September 3, 1981
US. ENVIRONMENTAL PROTECTION AGENCY (EPA). 1975. Development Document
for the Interim Final Effluent Limitations Guidelines and New Source Performance
Standards for the Significant Organic Products Segment of the Organic Chemical
Manufacturing Point Source Category. EPA-440/1-75/045, Washington, D.C.
U.S. ENVIRONMENTAL PROTECTION AGENCY (EPA). I977a. Sampling and Analysis
Procedures for Screening of Industrial Effluents for Priority Pollutants. U.S. EPA
Environmental Monitoring and Support Laboratory, Cincinnati, Ohio, March 1977
(Revised April 1977)
U.S. ENVIRONMENTAL PROTECTION AGENCY (EPA). I977b. Multi-Media
Environmental Goals for Environmental Assessment. Draft Report. Industrial
Environmental Research Laboratory, Research Triangle Park, North Carolina.
January 1977
U.S. ENVIRONMENTAL PROTECTION AGENCY (EPA). I978a. Procedure for Pre-
liminary Evaluation of Analytical Methods to be used in the Verification Phase of
the Effluent Guidelines Division's BAT Review. Environmental Monitoring and
Support Laboratory, Cincinnati, Ohio. March 1978
U.S. ENVIRONMENTAL PROTECTION AGENCY (EPA). I978b. BPT Evaluation of
Organic Chemicals and Plastics and Synthetics. Draft Final Report. Washington,
D.C.
U.S. ENVIRONMENTAL PROTECTION AGENCY (EPA). I979a. Indicatory Fate Study.
Draft prepared by Industrial Sources Section, Source Management Branch, Robert S.
Kerr Environmental Research Laboratory, Ada, Okla.
E-131
-------
U.S. ENVIRONMENTAL PROTECTION AGENCY (EPA). I979b. Treatability of the
Priority Pollutants by Activated Carbon. Hwang, S.T., Organic Chemicals Branch,
Washington, D.C. June 1979
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). I979c. Coagulation and
Precipitation of Selected Metal Ions from Aqueous Solutions. Research and
Development, Washington, D. C. EPA 600/2-79-204
U.S. ENVIRONMENTAL PROTECTION AGENCY (EPA). I979d. Self-Monitoring Program
Analytical Methods Package. EPA 440/1-79/102, Washington, D.C. July 1979
U.S. ENVIRONMENTAL PROTECTION AGENCY. (EPA). I979e. Review of Existing
Conventional Pollutant BAT Effluent Guidelines (Section 73 of Clean Water Act of
1977). Action Memorandum from Assistant Administrator for Water and Hazardous
Materials to the Administrator, June 22, 1979
U.S. ENVIRONMENTAL PROTECTION AGENCY (EPA). I980a. Treatability of Priority
Pollutants in Wastewater by Activated Carbon. Hwang, S.T., Organic Chemicals
Branch, Washington, D.C. To be presented at the AlChE Philadelphia meeting. June
I960
U.S. ENVIRONMENTAL PROTECTION AGENCY (EPA). I980b. Computerized Waste-
water Treatment Model. Technical Documentation. September 1980
U.S. ENVIRONMENTAL PROTECTION AGENCY (EPA). 1981 a. EPA files, Organic
Chemicals Branch
U.S. ENVIRONMENTAL PROTECTION AGENCY (EPA). I98lb. Bench-Scale Stean,
Stripping Treatment of Organic Priority Pollutants. Office of Research and
Development, Robert S. Kerr Environmental Research Laboratory, Industrial
Sources Section, Ada, Okla.
U.S. ENVIRONMENTAL PROTECTION AGENCY (EPA). No date. Treatability of Priority
Pollutants by Coagulation/Flocculation. Research Triangle Park
WAITE, W.H. No date. Pollution Control Through Selective Ion Exchange. Rohm and
Haas Co., Philadelphia, Pa.
WALK, HAYDEL AND ASSOCIATES, INC. I980a. Laboratory Studies of Priority
Pollutant Treatcbility. Prepared for the U.S. Environmental Protection Agency,
Office of Research and Development, Industrial Environmental Research Labora-
tory, Cincinnati. Contract No. 68-03-2579, Directive 2579 WD-6
WALK, HAYDEL AND ASSOCIATES, INC. I980b. Industry Survey to Determine the
Performance of Activated Carbon Adsorption. Prepared for the U.S. Environmental
Protection Agency
WISE, H., and FARENTHOLD, P. 1981. Occurrence and Predictability of Priority
Pollutants in Wastewaters of the Organic Chemicals and Plastics/Synthetic Fibers
Industrial Categories. Effluent Guidelines Division, U.S. Environmental Protection
Agency
* References from other sections of the 1981 Contractor's Engineering Report also
in this reference list.
E-132
-------
APPENDIX F
STATISTICAL DETAILS AND DEVELOPMENT OF
VARIABILITY FACTORS
-------
APPENDIX F
STATISTICAL DETAILS AND DEVELOPMENT OF
VARIABILITY FACTORS
This Appendix presents the major statistical methodologies and data
processing procedures used in the development of the proposed effluent
limitations from the OCPSF effluent data. As explained in Section IX,
variability factors were determined using organic priority pollutant data from
the CMA study and heavy metals data from five BPT Daily Data File plants.
Organic priority pollutant data from the Verification study were used in
conjunction with the CMA data to determine median long term values for
calculating the effluent limitations. The Screening data were used to
investigate BAT subcategorizaton. Some elementary formulas and definitions
are presented first; subsequent sections discuss the rationale for using daily
sample averages to model effluent variability, goodness-of-fit tests,
derivation of variability factors, example variability factor calculations,
and the statistical methodology used to investigate BAT subcategorization.
A. FORMULAS AND DEFINITIONS
Important formulas and definitions of statistical terms used in this
appendix include the following:
1. N - number of valid observations used in a particular analysis (e.g.,
the total number of valid effluent values at a particular plant for a
particular pollutant)
F-l
-------
N
2. Mean - arithmetic average: X = I X./N
N
_ 9
3. Variance (unbiased estimate): 02 _ 1 I (X. - X)
o — i
N - 1 i=l
(The standard deviation is S = Vs .)
4. Minimum - the smallest value in a set of N observations.
5. Maximum - the largest value in a set of N observations.
6. Range - the minimum subtracted from the maximum
7. Median - the middle value in a set of N observations. If N is odd (N
= 2k - 1 for some integer k), the median is the kth order statistic,
C(k). If N is even (N = 2k), the median is
l/2[C(k) + C(k + 1)].
B. RATIONALE FOR USING DAILY SAMPLE AVERAGES IN MODELING EFFLUENT VARIABILITY
In the CMA Five-Plant Study, multiple measurements of organic pollutant
concentrations in daily samples were made by one or more laboratories. Thus,
several reported values of a specific pollutant concentration were available
for a particular daily sample. Because NPDES permits require a single
reported value, the Agency considered several alternate approaches for
characterizing the variability of the pollutant concentration of individual
daily samples. The following approaches were considered.
F-2
-------
• Arbitrarily selecting one measurement per day and
calculating a variance from the selected measurements
• Calculating daily sample averages of multiple
measurements and computing a variance of the results
• Performing a variance component analysis using
replicate measurements and adding estimates of
relevant components to estimate the variance of a
single measurement.
The first alternative was rejected because it does not use all the data and
gives different answers depending on which measurements are selected. The
second method is a way duplicate measurements can be handled in NPDES
reporting; it is more straightforward than the last alternative, which
eventually also was rejected. The variance component method is described
briefly below.
A variance component analysis of data for a given plant and pollutant
characterizes variation in effluent monitoring results at the plant by
estimating a variance component for each relevant source of variation.
Because of the way the CMA study was conducted, it was possible to estimate
variance components for the following sources:
F-3
-------
• Within-day variation attributable to short-term
replication errors within a laboratory
• Between-day variation attributable to process,
treatment, sampling, and longer-term
within-laboratory variation
• Between-laboratory variation.
The between-day and between-lab variance components generally are larger than
the within-day variance component because many more factors affect between-day
and between-laboratory variability.
Although it was possible to estimate a between-laboratory variance
component from the CMA data, it was not necessary to do so to characterize
effluent variability. In practice, a single laboratory generally performs all
monitoring analyses of a given pollutant at a given plant, so
between-laboratory differences do not affect observed effluent variation at a
plant. (Between-lab differences do contribute to between-plant differences,
which are reflected in the observed long-term performance of the industry.)
2
Given estimates of the within- and between-day variance components a
o
and of" for a specific plant and pollutant, the variance of a single
measurement is estimated from
o2 = o2 + o?.
w b
F-4
-------
9 2
Estimates of a and or" can be obtained from data for a given plant,
w b
lab and pollutant using formulas in Linear Models (Searle, 1971).
A comparison of the daily sample average and variance component approaches
resulted in selection of the daily sample average because of its relative
simplicity, its confortnance to general monitoring practice, and its tendency
to give conservative variance estimates. The conservativeness of the daily
sample average approach results from including measurements from different
laboratories in the daily average. This tends to make the variances of daily
average data larger than corresponding variance component estimates.
TABLE F-l shows a comparison of standard deviations estimated from the CMA
data by the two approaches. The variance component estimates in the table
were based on log (C-10) for individual concentrations (C) above 10 Vg/1;
6
the daily sample average estimates were based on log (C-10) for daily
G
sample averages (C) above 10. Note that in 8 out of 13 plant-pollutant
comparisons, the daily sample average result was larger. The median standard
deviation for the daily sample average method was 1.54 compared to 1.37 for
the variance component method.
Daily sample averages were computed by averaging replicate measurements
within laboratories and then averaging the results across laboratories.
Before computing daily sample averages for organic pollutants, it was
necessary to decide how to handle results below the detection limit (<10
yg/1). Alternatives considered were to exclude such values or to replace
them with some number between zero and the limit. In order to use all the
data and to be conservative from the standpoint of effluent levels plants can
F-5
-------
TABLE F-l
COMPARISON OF STANDARD DEVIATIONS
ESTIMATED BY TWO METHODS
METHOD
ORGANIC POLLUTANT
(8)
(10)
(21)
(23)
(25)
(31)
(44)
(59)
(64)
(65)
1 , 2 ,4-tr ichlorobenzene
1 , 2-dichloroethane
2 , 4 , 6 -t r ichlorophenol
Chloroform
1 , 2-dichlorobenzene
2,4-dichlorophenol
Methylene Chloride
2 , 4-dinitrophenol
Pentachlorophenol
Phenol
PLANT
P4
PI
P3
P3
PI
P4
P4
PI
P3
P3
P3
P5
LAB
8
9
1
4
3
3
6
8
1
4
8
9
9
1
6
-
-
-
Variance
Component
.95
.73
.84
2.20
2.32
2.26
1.31
1.50
.84
1.35
1.23
1.19
1.25
1.02
1.15
1.37
2.69
1.13
1.77
-
-
-
Daily
Average
.88
2.54
1.39
1.55
.92
1.54
2.12
1.07
1.80
1.48
1.25
.24
NOTE: The average standard deviation is given for the variance component
method where there are estimates for more than one laboratory.
F-6
-------
TABLE F-l
(concluded)
METHOD
ORGANIC POLLUTANT
PLANT
LAB
Variance Daily
Component Average
(66)
(68)
(70)
(86)
Bis(2-ethylhexyl) Phthalate
Di-n-butyl Phthalate
Diethyl Phthalate
Toluene
P3
P3
P3
P3
3
6
8
3
3
3
1
2
1
1
1
1
1
.54
.34
.00
.63
.29
.52
.71
1
1
1
1
.50
.20
.65
.99
F-7
-------
achieve, a replacement value equal to the detection limit was chosen. For
example, suppose duplicate measurements on a sample resulted in Cl = 20 pg/1
and C2 = ND (not detected). Setting C2 = 0 gives an average concentration of
C = 10 yg/1; setting C2 = 10 gives C^ = 15 yg/1. Note that the use of 10
not only yields a higher average, but results in counting the pollutant as
detected in the sample (with detected defined as C > 10).
C. GOODNESS-OF-FIT TESTS
The statistical distribution used to model the effluent data assumes that
X = log (C-D) is NORMAL for C > D, where C is the daily effluent
6
concentration and D is the analytical detection limit. To assess the validity
of that assumption, goodness-of-fit tests were performed using the studentized
range test based on the statistic
U = R/S,
with the range (R) and standard deviation (S) defined in A. Critical values
of the U-test are given in Biometrika Tables (Pearson and Hartley, 1969).
An upper tail test was used to guard against alternative distributions with
heavier tails than the lognormal distribution: if such alternatives were
appropriate, the lognormal distribution would tend to underestimate the 99th
percentile.
A test was run using daily sample averages above the detection limit for
each plant-pollutant data set. The criterion for distribution rejection was a
statistical significance level of a = 0.01 for each test. As the results
F-8
-------
in TABLE F-2 show, the model was rejected for only one of the 27 data sets
tested (lead at Plant 113). The Agency concluded that the lognormal
distribution is appropriate for modeling the data above the analytical
detection limit.
For organic pollutants, a detection limit of D = 10 yg/1 was used; no
metals readings were reported as being at or below a detection limit,
therefore D = 0 was used.
D. DERIVATION OF VARIABILITY FACTORS
To develop variability factors for each pollutant at each plant, the
Agency assumed that the concentration C has a delta distribution modified to
have its origin at D, the analytical detection limit (Aitchison and Brown,
1957). This assumption implies that a result under the detection limit has
probability 6 of occurring, and x = log(C - D) for C > D is normally
2
distributed with mean y and variance o . The 99th percentile value of
the concentration is then
C0.99
with
= i"1 [(.99 - 6)/(l - 6)J ,
where f (•) is the inverse of the standard normal cumulative
distribution function. The mean and variance of C for C > D are
F-9
-------
TABLE F-2
GOODNESS-OF-FIT TESTS FOR VARIABILITY DATA
LOG (C - D) FOR DAILY AVERAGES C OVER D yg/fc
(8)
(10)
(21)
(23)
(25)
(31)
(44)
(59)
(64)
(65)
(66)
(68)
(70)
(86)
(119)
(120)
(122)
(128)
(121)
POLLUTANT
1 , 2 ,4-trichlorobenzene
1,2-dichloroethane
2,4,6-trichlorophenol
Chloroform
1 , 2 -dichlorobenzene
2 ,4-dichlorophenol
Methylene chloride
2,4-dinitrophenol
Pentachlorophenol
Phenol
Bis(2-ethylhexyl) phthalate
Di-n-butyl phthalate
Diethyl phthalate
Toluene
Chromium
Copper
Lead
Zinc
Cyanide
*Critical values for the studentized
n U.99
3 2.00
4 2.44
5 2.80
6 3.10
7 3.34
8 3.54
10 3.88
11 4.01
PLANT
P4
PI
P3
P3
PI
P4
P4
PI
P3
P3
P3
P5
P3
P3
P3
P3
3
110
113
126
113
118
113
27
110
113
P5
range test
n
13
14
18
20
25
30
45
90
NDAY
11
7
7
18
14
6
5
13
7
4
3
4
26
10
24
10
46
8
90
26
145
27
13
158
8
140
27
(a =
U
4
4
4
4
5
5
5
6
U
0.01
.99
.24
.34
.67
.80
.06
.26
.67
.27
3
2
2
3
3
2
2
4
3
2
1
2
3
3
3
3
3
3
3
5
5
5
4
6
2
6
4
.00
.73
.65
.18
.05
.48
.53
.23
.02
.44
.73
.00
.64
.79
.94
.41
.14
.25
.18
.01
.42
.18
.53
.01
.63
.07
.14
upper
TEST RESULT*
N.
N.
N.
N.
N.
N.
N.
N.
N.
N.
N.
N.
N.
N.
N.
N.
N.
N.
N.
N.
N.
N.
P <
N.
N.
N.
N.
tail)
S.
S.
S.
S.
S.
S.
S.
S.
S.
S.
S.
S.
S.
S.
S.
S.
S.
S.
S.
S.
S.
S.
0.01
S.
S.
S.
S.
are:
N.S. = not significant (U value below critical level).
Pearson and Hartley, 1969
F-10
-------
and
o2 - e2v + ° (e° - 1). (3)
The Agency defined the daily variability -factor as
C y + zo
VF(1) = 0.99 = D + e (4)
yc y + 1/2 a2
D + e
Estimates of the above quantities are calculated by replacing 6 by the
2
proportion of observations below D and replacing y and o with the mean
and variance of log (C-D) for observations above D.
To obtain the variability factor for a monthly mean C of 4 samples per
month, only results above the detection limit (i.e., C > D) were averaged.
The following assumptions were made: C has a modified delta-lognormal
2
distribution with the same mean as C and with variance proportional to ac
(Barakat, 1976), and measurements are uncorrelated. The last assumption
implies that the probability of obtaining no results above D in the four
monthly samples for a month is
64 = 6- (5)
The other assumptions give
F-ll
-------
and
W4 + Z4 °4
C0.95=D+e
with
-1 [(.95 - 5 )/(! - 6 )].
L 4 4 J
z = $ |(.95 - 5 )/(! - 6 )
The Agency defined the 4-day monthly variability factor as
F V4 + Z4 °4
VF(4) = 0.95 = D + e (9)
^ y^ + 1/2 02-
D + e
Q
To estimate VF(4), it is necessary to express y, and aj- in terms
of 6, y, and o. Since y— = y , it can be shown using (2) and
(6) that
2 2
V4 = V + " 4 . (10)
2 2
To relate o, to parameters of the original distribtuion, c— must be
2
expressed as a function of a . When k out of 4 tests in a month are above
C
D (k > 0), the variance of C for that month is o^/k. In addition, k
O
varies randomly from month to month with probability distribution
• (0-
PrlK = kl = (71(1 - 6)k 64"k
F-12
-------
for k = 0, 1, 2, 3, 4 (K has a binomial distribution with parameter 1-6).
2 2
Thus o_ is a weighted average of values a /k for different k:
c c
4
= E Pr(K=k)
k=l 1 - 64
2 2
cfK~ 2u + a , a ...
= f(6)e p (e - 1)
with
f(6) = (1 - 64) I Pr(K = k)/k.
k=l
Equating the expressions in (7) and (12) and simplifying with the aid of (10)
gives
= log
1 + f(6)(e° - 1) .
Equations (5), (10), and (13) now express the parameters 6,, u , and
2 2
a, in terms of the original parameters 6, y, and o . Substituting
the values calculated earlier for these three parameters into the three
equations and substituting the results into equation (9) gives an estimate of
VF(4).
For organic priority pollutants a detection limit of D = 10 ug/1 was
used in the model. For metals and cyanide, no readings had been reported as
being at or below a detection limit.
F-13
-------
E. EXAMPLE OF VARIABILITY FACTOR CALCULATIONS
Use of the above formulas to estimate variability factors is illustrated
below with data for 1,2-dichloroethane (10) from CMA plant 3. To avoid
rounding errors and reproduce computer results, intermediate calculations were
carried out to several decimal places. Measurements of 1,2-dichloroethane
were made on samples from 33 days, but the pollutant was detected on only 7
days. The daily sample average values (C) and their corresponding values of
log (C - D) are listed in TABLE F-3.
The estimated mean and variance of x are then
A _
u = x = 1.40442
and
a2 = s2 = 1.93184
_ 2
(Definitions for x and s are given under Formulas and Definitions).
The estimated probability of obtaining a daily sample average at or below the
detection limit is
6 = 26/33 = 0.787879,
so
z = §"1(0.952857) = 1.67321.
F-14
-------
TABLE F-3
VALUES OF C AND X FOR 1,2-DICHLOROETHANE RESULTS
Daily
Sample Average _
Concentration (C)
13
25.5
50
11
12
11
15
x = loge(C - 10)
1.09861
2.74084
3.68888
0
0.69315
0
1.60944
F-15
-------
Therefore, by formulas (1), (2), and (4), the estimated 99th percentile, mean,
and daily variability factor are
S0.99 ' 10 * °* + "
= 10
and
VF(1) = c/y = 2.498
These results were rounded to 52, 21, and 2.50 and then entered into the
variability factor table.
For the four day average variability factor, formula (5) gives
thus
6 = (26/33)4 = 0.385334;
z. = $"1(0.918655) = 1.39608.
4
F-16
-------
Next, f(6) in (12) is estimated. By (11),
Pr(K = k)
Thus
I I
| 1 463(1 - £) = 0.414975 |
I I
| 2 662(1 - 6)2 = 0.167586 |
I I
| 3 4$ (1 - 6)3 = 0.030080 |
I I
| 4 (1 - £)4 = 0.002025 |
J I
A A -1 4
f(6) = (1 - 6 ) Z Pr(K = k)/k = 0.828582.
k=l
By formulas (10) and (13) then,
r -
;[l + f(6)(«
a
= logl + f(6)(e
= 1.77333
and
A A
= 1.48368.
Using equations (8), (6), and (9), respectively, the estimated 95th
percentile, mean, and variability factor for 4-day averages are
A A
A V4 + V4
CQ 95 = 10 + e* ** = 38.3,
F-17
-------
*4
y_ = 10 + e =20.7,
and
VF(4) = c"rt OC/V_ = 1.850.
The variability factor was rounded to 1.85 and then entered into the summary
table.
F. SUBCATEGORIZATION
The data selection and reduction and statistical test, procedures employed
in the subcategorization analyses are described in this section. The
wastewater characteristics examined were untreated influent concentrations of
all priority pollutants except pesticides and asbestos.
Data from the Screening study were used for subcategorization because that
study provided the most comprehensive assessment on the presence of priority
pollutants at OCPSF plants (in terms of plant coverage and number of
pollutants per plant). Untreated influent data were summarized as follows to
create one observation for each plant:
F-18
-------
• Not detected, trace, and values under 10 yg/fc
were replaced by 10.
• Since the Screening data was used, pollutant
concentration levels at a plant were usually based on
a single analysis measurement. For plants where
multiple analysis determinations were made, a sample
average was generated for that pollutant.
• The value 10 yg/fc was inserted for any compound
for which there was no measurement at a plant (i.e.,
if a value was not reported for a pollutant, it was
considered not detected).
• Natural logarithms of the resulting concentrations
were computed.
The initial data base produced by the above process continued observations for
143 plants.
Many priority pollutants were considered in the subcategorization
analysis--88 organic compounds and 14 metals plus cyanide. Furthermore, the
correlations among measurements of different pollutants caused by common
analytical, sampling, and matrix effects made one-pollutant-at-a-time analyses
inappropriate. Therefore, alternate multivariate analysis procedures were
considered.
The classical multivariate technique for comparing the means of two
populations (e.g., two possible subcategories of plants) involves comparing an
F-statistic to tabled critical values of the F distribution with p and N1 +
N_ - p - 1 degrees of freedom, where p is the number of pollutants and N-
and ti are the numbers of plants with data in the two groups (Morrison,
1967, p. 125-126). It can be seen, therefore, that the number of plants with
F-19
-------
measurements must exceed the number of pollutants measured in order to use
this technique; that is,
(since N- + N_ - p - 1 must be greater than zero). There are pollutant
measurements on 143 plants in the Screening file, but it was necessary to use
the BPT Summary file to obtain other plant characteristics such as
product/processes employed. Many of the plants in the Screening file could
not be identified or had incomplete information in the Summary file. Thus
less than 143 plants could be used in statistical comparisons based on the
classical test. For example, there are 14 Plastics-Only and 78 Not
Plastics-Only plants identifiable in the Screening file; there are 13
Organics-Only and 31 Mixed Organics/Plastics plants identifiable. It can be
seen from these examples that it was not possible to include all 102 priority
pollutants of interest (88 organics and 14 metals/cyanide) in a single
multivariate comparison of groups of plants--splitting the pollutants into
groups would have been necessary.
Another difficulty with using the classical multivariate test was the
analytical limitations of the Screening data. These we11-documented
limitations made the use of a nonparametric procedure preferable, since such
procedures are based on less restrictive assumptions than the classical
multivariate procedure. Unfortunately, the well-known nonparametric
procedures are univariate (statistical analyses of only one variable at a
time). To address these problems, another multivariate technique called
F-20
-------
principal components was used to define a few new uncorrelated variables based
on the original pollutant variables, and the nonparametric test was applied to
the new variables. The principal component analysis defined new variables as
weighted averages of the original pollutant-specific variables; weights were
selected to retain as much information as possible in the original data
(Morrison, 1967, p. 222-230). Principal components were derived separately
for organics and metals/cyanide because their measurements are based on
different analytical methods; the derivation for organics is described below
(the derivation for metals was similar).
For each plant, let X ,...., X represent the original 88 organics
1 oo
variables (logs of mean concentrations of organic priority pollutants in the
_ 2
acid, base/neutral, and volatile fractions). Let X. and s. represent the
mean and variance of the ith variable, and R = (r..) the matrix of pairwise
— 2
correlations among the 88 variables X., s., and r.. were computed from
the 143 plant-specific observations described above). The first principal
component, Y , was defined as the weighted average
88 _ (14)
Yl =
whose coefficients a., were chosen to make the sample variance
2 88 88
s.., = Z Z a. na.,r . .
Yl .=1 j=1 il jl ij
F-21
-------
as large as possible given that
88
I a. = 1.
1=1 U
The second principal component was defined as the weighted average
88 _ (15)
Y2 = .^ *i2(Xi - V/Si
whose coefficients a were chosen to make the sample variance
2 88 88
s = Z I a a.0r..
Y2 1=1 =l l2 j2 ^
as large as possible given that
88
and
88
I a.,a.. = 0.
(The last condition makes Y- and Y_ uncorrelated.) Additional principal
components were defined in similar fashion. The weights for each component
were computed by the PRINCOMP procedure in SAS (SAS Institute, 1982, p.
347-361). The value of the first principal component at a given plant was
obtained by substituting the log-mean concentrations for the 88 pollutants at
that plant for the X. in formula (14). Plant-specific values of other
F-22
-------
principal components were obtained from corresponding formulas for those
components.
When a principal component analysis is based on the correlation matrix R
2
as above, the total variation for all 88 components (the sum of the s *s)
2
equals the number of original variables, 88. Thus the ratio s /88
indicates the proportion of the total variation accounted for by the ith
component. Because of the way principal components are defined, the
proportion of variation accounted for by successive components generally
decreases (and never increases).
Principal components analysis has the following advantages as a
variable-reduction procedure:
2
• It indicates through sy./88 how many components
are needed to describe the data.
• The first few components summarize most of the
information in the data when the original variables
are highly correlated.
• The principal components themselves are
uncorrelated so interpretation of statistical
analyses based on them is straightforward.
• Principal components often have a physical meaning
that can be identified from the magnitudes of the
weights (a..).
For the organics Screening data, the first 5 components accounted for 74
percent of the total variation; for metals and cyanide the first five
components accounted for 78 percent of the total variation. Morri-son suggests
F-23
-------
that up to five principal components be retained for subsequent analysis if
those components account for at least 75 percent of the total variation.
The weights defining the first five principal components for organics and
for metals/cyanide are shown in TABLES F-4 AND F-5, respectively.
In the final stage of the statistical subcategorization analysis, the
first five principal components were evaluated for each plant, and plants
belonging to groups of interest (e.g., Plastics-Only or Not Plastics-Only
producers) were identified using information from the BPT Summary file.
Plants not classifiable were excluded from the remainder of the analysis,
which consisted of using a normal-scores test (Bradley, 1968) to compare group
medians of principal component scores.
Results of the comparison of Plastics-Only and Not Plastics-Only plants
are given in TABLE F-6. Differences between the two groups were found for the
first and fifth organics components. Based on an examination of the relative
magnitudes of the weights for individual components in Table F-4, these two
components can be roughly interpreted as the average for all 88 compounds and
the average for benzene, chlorobenzene, ethylbenzene and toluene,
respectively. The statistical test indicates that Not Plastics-Only plants
had higher median levels of these two weighted averages than the Plastics-Only
plants.
A further analysis based on subdividing Not Plastics-Only plants into
Organics-Only and Mixed Organics/Plastics producers showed no significant
F-24
-------
TABLE F-4
PRINCIPAL COMPONENT WEIGHTS FOR ORGAN ICS DATA
NAME
(001)
(002)
(003)
(004)
(005)
(006)
(007)
(008)
(009)
(010)
(011)
(012)
(013)
(014)
(015)
(016)
(017)
(018)
(019)
(020)
(021)
(022)
(023)
(024)
(025)
(026)
(027)
(028)
(029)
(030)
(031)
(032)
(033)
(034)
(035)
(036)
(037)
(038)
(039)
(040)
(041)
PRIN1
ACENAPHTHENE
ACROLEIN
ACRYLONITRILE
BENZENE
BENZIDINE
CARBON TETRACHLORIDE
CHLOROBENZENE
1 , 2, 4-TR I CHLOROBENZENE
HEXACHLOROBENZENE
1 2-DICHLOROETHANE
1 1, 1-TRICHLOROETHANE
HEXACHLOROETHANE
1 1-DICHLOROETHANE
1 1,2-TRICHLOROETHANE
1 1,2,2-TETRACHLOROETHANE
CHLOROETHANE
BIS (CHLOROMETHYL) ETHER
BIS (2-CHLOROETHYL) ETHER
2-CHLOROETHYLVINYL ETHER
2-CHLORONAPHTHALENE
2,4, 6-TR I CHLOROPHENOL
4-CHLORO-M-CRESOL
CHLOROFORM
2-CHLOROPHENOL
1 , 2-D I CHLOROBENZENE
1,3-DICHLOROBENZENE
1,4-DICHLOROBENZENE
3, 3-D I CHLOROBENZ I D I NE
1,1-DICHLOROETHYLENE
1 , 2-TRANSD I CHLOROETHYLENE
2,4-DICHLOROPHENOL
1 , 2-D I CHLOROPROPANE
1,3-DICHLOROPROPYLENE
2,4-DIMETHYLPHENOL
2,4-DINITROTOLUENE
2,6-DINITROTOLUENE
1 , 2-D I PHENYLHYDRAZ I NE
ETHYLBENZENE
FLUORANTHENE
4-CHLOROPHENYLPHENYL ETHER
4-BROMOPHENYLPHENYL ETHER
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
11832
10254
09594
03579
11649
04990
02269
12806
12283
06166
07084
13167
10759
11434
09515
08960
10805
13682
10458
13611
08193
09946
02229
07882
11444
12127
10948
13667
08101
11179
07089
11051
09710
07025
13105
11739
12806
06442
12304
13420
13231
PR1N2
-0.
0.
0.
0.
-0.
0.
0.
-0.
-0.
0.
0.
-0.
0.
0.
0.
0.
0.
-0.
0.
-0.
0.
0.
0.
0.
-0.
-0.
-0.
-0.
0.
0.
0.
0.
0.
0.
-0.
-0.
-0.
0.
-0.
-0.
-0.
09204
03237
02801
02401
06185
14408
08494
07363
06556
14630
12300
07959
17180
19300
19678
17613
14920
07077
16754
06862
02875
04933
09740
05713
04583
02829
04410
07195
13390
20678
04118
19151
19114
05421
05846
05911
05186
03413
10152
07890
07321
0.
-0.
-0.
0.
-0.
0.
0.
-0.
-0.
0.
0.
0.
-0.
-0.
-0.
-0.
-0.
-0.
0.
-0.
-0.
-0.
0.
-0.
-0.
-0.
0.
-0.
0.
0.
-0.
-0.
0.
0.
-0.
-0.
-0.
0.
0.
-0.
-0.
PRIN3
12450
13206
14006
24430
00499
09154
01713
04961
00722
03189
06478
01439
05333
01635
00526
03963
04864
03315
04113
04357
14453
11297
18054
14389
02831
01400
00434
05525
14023
02071
07943
00915
07285
05740
06753
07384
05715
13828
14610
03595
06447
0.
-0.
-0.
-0.
-0.
-0.
-0.
-0.
0.
-0.
-0.
0.
-0.
-0.
-0.
-0.
-0.
-0.
-0.
-0.
0.
0.
0.
0.
-0.
-0.
0.
-0.
0.
-0.
0.
-0.
-0.
0.
-0.
-0.
-0.
0.
0.
-0.
-0.
PRIN4
02471
07823
07650
00345
02740
04663
00106
06440
03107
05613
01088
00687
06053
05458
04839
03809
08669
05069
02569
04806
29237
30597
06215
28065
07489
06128
03403
06190
04340
05852
34257
05173
04893
28435
06536
05341
02549
05917
03246
09384
07584
PRIN5
-0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
-0.
-0.
0.
-0.
-0.
-0.
0.
-0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
-0.
0.
-0.
-0.
-0.
0.
0.
-0.
0.
-0.
0.
0.
07431
15138
15403
39891
03294
11093
39068
07410
03824
02358
08441
01359
06081
12345
15969
08165
06753
00900
05771
00417
06094
02545
05912
06125
11233
04829
03100
02805
17501
08186
05122
06060
14428
06726
03616
04886
00964
26989
08005
02231
04262
F-25
-------
TABLE F-4 (concluded)
NAME
(042)
(043)
(044)
(045)
(046)
(047)
(048)
(049)
(050)
(051)
(052)
(053)
(054)
(055)
(056)
(057)
(058)
(059)
(060)
(061)
(062)
(063)
(064)
(065)
(066)
(067)
(068)
(069)
(070)
(071)
(072)
(073)
(074)
(075)
(076)
(077)
(078)
(079)
(080)
(081)
(082)
(083)
(084)
(085)
(086)
(087)
(088)
PRIN1
BIS-(2-CHLOROISOPROPYL) ETHER
BIS-(2-CHLOROETHOXY) METHANE
METHYLENE CHLORIDE
METHYL CHLORIDE
METHYL BROMIDE
BROMOFORM
D I CHLOROBROMOMETHANE
TR I CHLOROFLUOROMETHANE
D I CHLOROD I FLUOROMETHANE
CHLOROD I BROMOMETHANE
HEXACHLOROBUTAD I ENE
HEXACHLOROCYCLOPENTADI ENE
ISOPHORONE
NAPHTHALENE
NITROBENZENE
2-NITROPHENOL
4-NITROPHENOL
2,4-DINITROPHENOL
4, 6-D I N I TRO-0-CRESOL
N-N 1 TROSOD 1 METHYLAM 1 NE
N-N 1 TROSOD 1 PHENYLAM 1 NE
N-N 1 TROSOD I-N-PROPYLAMINE
PENTACHLOROPHENOL
PHENOL
BIS-(2-ETHYLHEXYL) PHTHALATE
BUTYLBENZYL PHTHALATE
DI-N-BUTYL PHTHALATE
DI-N-OCTYL PHTHALATE
Dl ETHYL PHTHALATE
DIMETHYL PHTHALATE
BENZO( A (ANTHRACENE
BENZO(A)PYRENE
3,4-BENZOFLUORANTHENE
BENZO(K)FLUORANTHENE
CHRYSENE
ACENAPHTHYLENE
ANTHRACENE
BENZO(GHI )PERYLENE
FLUORENE
PHENANTHRENE
D IBENZO( A, H) ANTHRACENE
INDENO(1,2,3-C,D)PYRENE
PYRENE
TETRACHLOROETHYLENE
TOLUENE
TRICHLOROETHYLENE
VINYL CHLORIDE
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
12328
12994
01847
06459
11343
09996
10759
03985
10350
10936
13577
13372
12654
08261
10075
09850
09867
09247
11066
12811
13042
13280
10152
03146
07348
10984
09483
12487
11862
11160
12087
13441
13487
12990
11579
10319
09696
13456
11169
11080
13666
13549
11794
07083
03813
07514
10825
PRIN2
-0.
-0.
0.
0.
0.
0.
0.
0.
0.
0.
-0.
-0.
-0.
-0.
-0.
0.
0.
-0.
0.
-0.
-0.
-0.
0.
0.
-0.
-0.
-0.
-0.
-0.
-0.
-0.
-0.
-0.
-0.
-0.
-0.
-0.
-0.
-0.
-0.
-0.
-0.
-0.
0.
-0.
0.
0.
08636
05707
14937
14575
16426
16523
18494
18125
14501
19881
07686
07690
07552
08181
03826
04016
02423
03557
01715
10043
05853
08230
11060
04506
01975
08687
03585
05723
10368
08238
12152
05759
05981
08323
10256
10236
11007
07662
10541
06292
07228
05998
09883
12133
00456
18593
17387
-0
-0
0
-0
-0
-0
0
0
-0
-0
-0
-0
0
0
-0
-0
-0
-0
-0
-0
-0
-0
-0
0
0
0
0
0
0
0
0
0
-0
-0
0
0
0
0
0
0
-0
-0
0
0
0
0
-0
PR INS
.04923
.04904
.29997
.03850
.06482
.03763
.02639
.16554
.07459
.01253
.06010
.04000
.00808
.24327
.00322
.16553
.15526
.16634
.15425
.07234
.05274
.05791
.08187
.09045
.22260
.03570
.14928
.05483
.01156
.02932
.00108
.00831
.02084
.05720
.06777
.21682
.21446
.00658
.20816
.15200
.02773
.01665
.17964
.07433
.22582
.09676
.02209
-0.
-0.
0.
-0.
-0.
-0.
-0.
0.
-0.
-0.
-0.
-0.
0.
0.
-0.
0.
0.
0.
0.
-0.
-0.
-0.
0.
0.
0.
-0.
0.
0.
-0.
0.
-0.
-0.
-0.
-0.
0.
0.
0.
-0.
0.
0.
-0.
-0.
0.
0.
-0.
-0.
-0.
PRIN4
08711
07580
03189
08328
05632
03338
08996
00962
05124
05321
06901
09478
05459
11219
01309
26254
21177
21247
20787
08064
04155
08475
16777
18532
11881
06840
11303
00643
05015
02961
01091
08044
04020
03931
03394
10626
07784
07446
06221
02978
05851
05135
06655
03379
04796
02850
06305
PRIN5
0.
0.
0.
0.
0.
-0.
-0.
0.
0.
-0.
0.
0.
-0.
••0.
0.
0.
-0.
0.
-0.
0.
0.
0.
-0.
0.
0.
-0.
-0.
-0.
-0.
-0.
0.
-0.
-0.
0.
-0.
-0.
0.
-0.
-0.
-0.
-0.
-0.
-0.
0.
0.
-0.
-0.
02223
02963
07741
02434
06992
08045
13525
05837
06669
12406
04334
02735
04904
07097
07289
03919
01496
08969
03203
11704
05756
05837
06747
07148
04058
06570
12809
08868
09015
09997
07808
01869
02449
06108
10366
12002
01894
05279
08166
12882
03735
06193
11559
10503
28578
11590
11654
F-26
-------
TABLE F-5
PRINCIPAL COMPONENT WEIGHTS FOR METALS/CYANIDE DATA
(lit)
(115)
(117)
(118)
(119)
(120)
(121)
(122)
(123)
(124)
(125)
(126)
(127)
(128)
NAME
ANTIMONY
ARSENIC
BERYLLIUM
CADMIUM
CHROMIUM
COPPER
CYAN I DE
LEAD
MERCURY
NICKEL
SELENIUM
S I LVER
THALLIUM
ZINC
PRINT
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
30083
19453
27386
32574
23323
28649
04380
28694
24750
28106
28805
31248
31597
22166
0
0
0
0
-0
-0
0
-0
-0
-0
0
0
0
-0
PRIN2
.14570
.32669
.13534
.03418
.40820
.09643
.48968
.17496
.11203
.07280
.19861
.11945
.21691
.53631
PRIN3
-0.
0.
-0.
0.
0.
0.
0.
0.
-0.
0.
-0.
-0.
-0.
0.
06916
11624
18238
02977
31476
17821
67704
14908
42100
18551
18106
09996
20932
19460
0.
0.
-0.
-0.
0.
-0.
-0.
0.
-0.
-0.
0.
-0.
0.
0.
PRIN4
10133
61894
52114
21213
07162
04895
23871
07995
07369
05328
35473
25184
09984
10805
0.
-0.
-0.
-0.
0.
0.
0.
0.
0.
-0.
0.
-0.
0.
0.
PRIN5
23727
26333
06186
19271
03567
07541
38796
23695
51283
43498
15347
37689
01308
04248
F-27
-------
TABLE F-6
COMPARISON OF PLASTICS-ONLY PLANTS WITH OTHER PLANTS
PRINCIPAL
COMPONENT
1
2
3
4
5
ORGANICS
Cumulative
% Variation
56
63
68
72
74
Significance
Level"
<.001
.520
.125
.445
<.001
METALS/CYANIDE
Cumulative
% Variation
49
58
66
73
78
Significance
Level*
.473
.338
.130
.757
.498
Based on the Terry-Hoeffding (normal scores) test comparing medians
for principal component score for Plastics-Only and Not Plastics-Only
plants. There were 92 plants involved in the comparisons, 14
Plastics-Only and 78 Not Plastics-Only.
F-28
-------
differences (see TABLE F-7). Likewise, no significant differences were found
among the three BPT subcategories for Not Plastics-Only (TABLE F-8). These
analyses employed the same principal components as the Plastics-Only/Not
Plastics-Only comparison; they included all Screening plants that could be
identified as belonging to the groups of interest.
F-29
-------
TABLE F-7
COMPARISON OF ORGANICS-ONLY PLANTS WITH
MIXED ORGANICS/PLASTICS PLANTS
PRINCIPAL
COMPONENT
1
2
3
4
5
ORGANICS
Cumulative
% Variation
56
63
68
72
74
Significance
Level*
.717
.871
.502
.837
.738
METALS/CYANIDE
Cumulative
% Variation
49
58
66
73
78
Significance
Level*
.694
.550
.258
.948
.410
Based on the Terry-Hoeffding (normal scores) test comparing median of
principal component scores for Organics-Only and Mixed
Organics/Plastics plants. There were 44 plants involved in the
comparisons, 13 Organics-Only and 31 Mixed Organics/Plastics.
F-30
-------
TABLE F-8
COMPARISON OF THREE BPT SUBCATEGORIES
FOR NOT PLASTICS-ONLY PLANTS*
PRINCIPAL
COMPONENT
1
2
3
4
5
ORGANICS
Cumulative
% Variation
56
63
68
72
74
Significance
Level**
.575
.705
.370
.122
.342
METALS/CYANIDE
Cumulative
% Variation
49
58
66
73
78
Significance
Level**
.710
.166
.822
.978
.270
* The 3 subcategories are Type I with Oxidation (27 plants), Type I
without oxidation (8 plants), and Not Type I (9 plants).
** Based on the normal scores test comparing medians of principal
component scores for plants in the 3 subcategories (with 44 plants
involved in the comparisons). The test was run using PROC NPAR/WAY
in SAS Institute (1982), pages 205-211, with the van der Waerden
option.
F-31
-------
REFERENCES
AITCHISON, J., and J.A.C. BROWN. 1957. The Lognormal Distribution, Cambridge
University Press, London, pp. 14-15, 95-96.
BARAKAT, R. 1976. Sums of indepenent lognormally distributed random
variables. Journal Optical Society of America 66: 211-216.
Biometrika Tables for Statisticians, Vol. 1, page 200.
BRADLEY, J.V. 1968. Distribution-free Statistical Tests, Prentice-Hall,
Englewood Cliffs, NJ, 149-154, 326-330.
MORRISON, D.F. 1967. Multivariate Statistical Methods, McGraw-Hill, New York,
125-126, 222-230.
SAS INSTITUTE, INC. 1982. SAS User's Guide: Statistics, Gary, NC, 205-211,
347-361.
SEARLE, S.R. 1971. Linear Models, Wiley, New York, 473-474.
F-32
-------
APPENDIX G
CHEMICAL TREES OF THE GENERALIZED PLANT
CONFIGURATIONS (GPCs)
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APPENDIX H
HEALTH AND ENVIRONMENTAL EFFECTS
OF PRIORITY POLLUTANTS
-------
APPENDIX H
HEALTH AND ENVIRONMENTAL EFFECTS OF
PRIORITY POLLUTANTS
A. GENERAL
This appendix presents a description of the toxic human health and
environmental effects associated with each of the 108 priority pollutants (see
Table VI-1) that the Agency is considering regulating with BAT, NSPS or
pretreatment standards. The priority pollutants are listed in alphabetical
order by the fraction in which they appear -- volatile organic compounds, acid
extractable organic compounds, base/neutral extractable organic compounds,
metals and cyanide, and polychlorinated biphenyls.
B. PRIORITY POLLUTANTS
1. Volatile Organic Compounds
Acrolein
Acrolein is a potent irritant of the eyes and nose in humans. Effects
were observed within 5 minutes at levels of 0.58 mg/cu m (Albin 1962, as
reported in USEPA 1980). Vapor concentrations of 23 mg/cu m were reported to
be lethal within a short time (Henderson and Haggard 1943, as reported in
USEPA 1980). Strong skin irritation was reported to result from dermal
exposure to 10% acrolein in ethanol (Lacroix et al. 1976, as reported in
USEPA 1980). In vitro studies have shown that acrolein is a potent
inhibitor of the synthesis of human polymorphonuclear leukocytes chemotaxis
(Bridges et al. 1977, as reported in USEPA 1980). The odor threshold for
humans was reported to be 0.48 mg/cu m (Reist and Rex 1977, as reported in
USEPA 1980).
Acute inhalation studies in rats, mice, rabbits, and guinea pigs have
shown pathological changes in the lungs including edema, hyperemia,
hemorrhages, and possible degenerative changes in the bronchial epithelium
(Skog 1980, Pattle and Cullumbin 1956, Salem and Cullumbin 1960, as reported
in USEPA 1980). Hyperemia and fatty degeneration of the liver and focal
inflammatory changes in kidneys have been reported in rats administered lethal
subcutaneous doses of acrolein (Skog 1950, as reported in USEPA 1980).
Acrolein was reported to cause significant cardiovascular effects, including
tachycardia (Basu et al. 1972, as reported in USEPA 1980), and bradycardia,
and decreased blood pressure (Egle and Hudgins 1974, as reported in USEPA
1980). In acute inhalation studies, acrolein was also found to increase
respiratory resistance in guinea pigs exposed to 0.92-2.3 mg/cu m for up to 12
hours (Murphy et al. 1963, as reported in USEPA 1980); to be cytotoxic to
the airway cells of hamsters exposed to 13.8 mg/cu m for 4 hours (Kilburn and
McKenzie 1978, as reported in USEPA 1980); to reduce mucus flow rates in cats
H-l
-------
(dosage unspecified; Carson et al. 1966, as reported in USEPA 1980); and to
inhibit rabbit phagocytosis, adhesiveness, and calcium dependent ATPase
activity in in vitro tests (Low et al. 1977, as reported in USEPA 1980).
In subacute inhalation tests, dogs and monkeys continuously exposed to
2.3-4.1 mg/cu m for 90 days subsequently developed eye and respiratory tract
irritation. In the same study, dogs and monkeys exposed repeatedly to 8.5
mg/cu m for eight hours per day, five days per week, for six weeks developed
pathological changes in the lungs (squamous metaplasia and basal cell
hyperplasia of the trachea) (Lyon et al. 1970, as reported in USEPA 1980).
Hamsters, rats, and rabbits exposed by inhalation to 11.3 mg/cu m for 6
hours/day for 13 weeks showed signs of eye irritations, decreased food
consumption and decreased weight gain (Feron et al. 1978, as reported in
USEPA 1980). Epithelial metaplasia and inflammation of the nasal cavity were
observed in a chronic toxicity study in hamsters exposed to 9.2 mg/cu m for 7
hours/day for 52 weeks (Feron and Kruysse 1977, as reported in USEPA 1980).
In a subacute oral toxicity study, rats exposed to acrolein in drinking water
at concentrations up to 200 rug/liter for 90 days only showed slight weight
reduction at the highest level tested. This effect was attributed to
unpalatability of drinking water (Albin 1972, as reported in USEPA 1980).
Acrolein has been shown to be mutagenic in different short-term bacterial
assays (USEPA 1980). The carcinogenic potential of this compound has not yet
been established (USEPA 1980).
The acute toxicity of acrolein on freshwater aquatic organisms is
reflected by static 96-hour LC50 values of 0.057-0.080 mg/liter in cladoceran
(mean acute value of 0.068 mg/liter for the species), 0.09-0.10 mg/liter in
the bluegill, and 0.16 mg/liter in the largemouth bass. Aquatic macrophytes
were destroyed or badly scorched after one week of exposure to 25 mg/liter.
After 24-hour exposure to 10 mg/liter, 98% of adult snails and 100% of snail
embryos died. In a total of nine short-term exposures with seven fish
species, acute toxicity values ranged from 0.046 to 0.115 mg/liter. Flavor
impairment of rainbow trout flesh was reported to occur up to 4 days after a
4-hour exposure to 0.090 mg/liter (USEPA 1980). Toxicity to the saltwater
eastern oyster was manifested by a 50% decrease in shell growth at 0.055
mg/liter using a flow through test. Chronic toxicity was observed in
cladoceran at 21 yg/liter and the fathead minnow at 21 yg/liter. The
effects of acrolein on fresh and saltwater plants have not been studied (USEPA
1980).
EPA has established an ambient water quality criterion of 320 mg/liter for
the protection of human health from the toxic properties of acrolein ingested
through water and contaminated aquatic organisms.
EPA has not yet established an aquatic life water quality criterion for
acrolein.
Acrylonitrile
Acrylonitrile is an acute poison that is a severe skin and eye irritant
(NAS 1980). Acute toxicity can cause nasal and respiratory oppressions,
vomiting, nausea, weakness, fatigue, headache, and diarrhea (Patterson et
H-2
-------
al. 1976, as reported in USEPA 1980). Occupational studies have associated
acrylonitrile with diseases of the peripheral nervous system, stomach,
duodenum, and skin (Goncharova et al. 1977, Shirshova et al. 1975 and
Stamov et al. 1976, as reported in USEPA 1980). Other studies have shown
changes in the heart and circulation, blood methemoglobin content, and
clinical blood values; lowered blood cell counts; and mild liver injury
(Sakarai and Kusimto 1972, Ostrovskaya et al. 1976, Zotova 1975, and Shustov
and Mavrina 1975, as reported in USEPA 1980).
Acrylonitrile has been characterized as a serious hazard in inhalation
studies (Union Carbide Corporation 1970, as reported in NAS 1980). In one
study, all exposed rats died within 5 minutes while breathing saturated air;
in another study, all exposed rats died in 4 hours breathing 0.33 mg/liter.
Acute oral toxicity values for acrylonitrile range from 27 to 128 mg/kg for
mice (Benes and Cerna 1959, Zeller et al. 1969, as reported in NAS 1980) and
from 78 to 93 mg/kg for rats (Benes and Cerna 1959, Smyth and Carpenter 1948,
as reported in NAS 1980).
A 90-day oral toxicity study, incorporating 0.66 and 0.99 mg/liter of
acrylonitrile in the drinking water of rats resulted in the animals' death
before the end of the experiment (NRDC 1976, as reported in USEPA 1980).
Rabbits and rats breathing 50 mg/cu m for 6 months developed changes in
peripheral blood patterns, functional disorders in the respiratory and
cardiovascular systems, and signs of neuronal lesions in the central nervous
system (Knobloch et al. 1972, as reported in USEPA 1980).
Chronic inhalation exposures of dogs, cats, rats, guinea pigs, rabbits,
and monkeys to concentrations ranging from 0.12 mg/liter to 0.33 mg/liter
produced irritation of the eyes and nose, loss of appetite, gastrointestinal
disturbances, and incapacitating weakness of the hind legs (Dudley et al.
1942, as reported in NAS 1980). Central nervous system effects also occurred
in inhalation studies of rats exposed to 80 ppm for one year (USEPA 1980).
The mutagenicity of acrylonitrile has been demonstrated in the Salmonella
typhimurium test and in Escherichia coli W P2 strains. Fetal malformations
and maternal toxicity were observed in rats administered 65 mg/kg/day by
gavage on days 6-15 of gestation. Other embryotoxic effects included reduced
fetal body weight and crown-rump length and increased incidences of minor
skeletal variants.
Acrylonitrile was carcinogenic in rats administered 100 or 300 mg/liter
for 12 months in the drinking water. Cancer of the stomach, central nervous
system, and inner ear were reported (USEPA 1980).
The toxicity of acrylonitrile to freshwater aquatic organisms was
demonstrated in the cladoceran, fathead minnow, guppy, and bluegill, with
96-hour LC50 values ranging from 7.55 to 33.5 mg/liter. The only information
on saltwater species is a 24-hour LC50 value of 24.5 mg/liter for the
pinfish. No other data including the effects of aquatic plant life are
available (USEPA 1980).
H-3
-------
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to acrylonitrile through ingestion of contaminated water and
contaminated aquatic organisms. However, since the zero level may not be
attainable at the present time, a level of 0.058 yg/liter, corresponding to
an estimated lifetime incremental cancer risk of 0.000001, was recommended.
EPA has not yet established an aquatic life water quality criterion for
acrylonitrile.
Benzene
Single exposure to benzene at 20,000 ppm has caused death within 5-10
minutes in humans and produced acute toxic effects including nausea,
giddiness, headache, unconsciousness, convulsions, and paralysis (Browning
1965 and Eckardt 1973, as reported in NAS 1977). The chronic occupational
exposure of benzene to humans has been reported to produce thrombocytopenia,
leukopenia, and anemia. In more severe cases of benzene hematoxicity,
pancytopenia and acute myeloblastic leukemia have been observed (USEPA 1980).
Increased incidence of chromosomal aberrations with aneuploidy and breakage
has been observed in nonsymptomatic workers exposed to benzene (NAS 1980).
In chronic animal studies, leukopenia has been reported in rats exposed to
88 ppm, 7 hours per day, for up to 269 days. Below this level, no blood
changes were observed in rats, guinea pigs and rabbits (Wolf et al. 1956, as
reported in USEPA 1980). Other studies in which leukopenia developed include
a study in which rats were given 132 oral doses of 50 mg/kg over 6 months
(Wolf et al. 1956, as reported in USEPA 1980) and a study of rats exposed to
44 ppm for 5 hours/day, 4 days/week, for 5 to 7 weeks (Deichmann ejb al.
1963, as reported in USEPA 1980). Abnormalities of the spleen and lungs were
observed in rats exposed to 31-47 ppm, 20 hours per week, for 6-31 weeks
(Deichmann et al. 1963, as reported in USEPA 1980). Pregnant mice
administered 3 ml/kg gave birth to offspring with malformations and decreased
white cell counts (Watanabe and Yoshida 1970, as reported in USEPA 1980). In
another study, mice administered 0.3-1.0 ml/kg benzene by gavage during days
6-15 of gestation developed significant maternal lethality and embryonic
resorptions (Nawrot and Staples 1979 as reported in USEPA 1980). Inhalation
studies in rats conducted at various times before and during pregnancy, at
concentrations ranging from 210 mg/cu m to 1,000 mg/cu m produced no
malformations but did decrease fetal weight gain (USEPA 1980). Benzene was
not mutagenic in the Salmonella/microsome in vitro assay (Lyon 1975, Shahin
1977, Simon et al. 1977, as reported in USEPA 1980). However, it has been
reported that chromosomal abnormalities in bone marrow cells have resulted
from benzene exposure in a number of species including rats, rabbits, mice,
and amphibians (USEPA 1980). Benzene-induced leukemogenesis has not been
demonstrated in laboratory animals (USEPA 1980).
A variety of freshwater organisms are sensitive to the affects of
benzene. Static 96-hour LC50s have been reported in juvenile rainbow trout
(5.3 mg/liter), goldfish (34,42 mg/liter), fathead minnow (33.47 rag/liter),
guppy (36.6 mg/liter)> mosquitofish (386 mg/liter), bluefish (22.5 lag/liter)
and Daphnia magna (203-620 nag/liter) . A 5'0i reduction in the cell numbers
H-4
-------
of Chlorella vulgaris was seen after 48 hours of exposure to 530 mg/liter
benzene. Most saltwater organisms exposed to benzene gave 96-hour LC50 values
between 5 and 100 rag/liter. Striped bass, anchovy, and pacific herring are
more sensitive species giving values between 5.8 and 25 rug/liter. Saltwater
invertebrates appear to be less sensitive. Female pacific herring exposed to
700 mg/liter for 48 hours exhibited reduced survival of embryos at hatching
and reduced survival of larvae through yolk absorption. The 96-hour LC50
values ranged from 27 mg/liter for the grass shrimp to 450 rag/liter for the
copepod. Chronic effects for saltwater organisms have not been studied.
Benzene concentrations of 20-100 mg/liter inhibited growth in three species of
algae (USEPA 1980).
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to benzene through ingestion of contaminated water and
contaminated aquatic organisms. However, since the zero level may not be
attainable at the present time, a criterion of 0.66 yg/liter, corresponding
to an incremental lifetime cancer risk of 0.000001, was recommended.
EPA has not yet established an aquatic life water quality criterion for
benzene.
Bromoform
Bromoform is regarded as highly toxic to humans by all major routes of
exposure (lungs, GI tract, skin). However, information concerning the
compound's toxicity in humans is not extensive. Acute inhalation exposures
produce irritation of the respiratory tract, pharynx, and larynx, with
lacrimation and salivation. Mild poisoning cases may be limited to headache,
listlessness, and vertigo. In more severe cases, symptoms may include
unconsciousness, loss of reflexes, convulsions, and death resulting from
respiratory failure. Histopathological findings include fatty, degenerative
and necrotic changes in the liver (USEPA 1980). No information on chronic
toxicity in humans is available.
In studies with the mouse, LD50s of 1,820 and 1,400 mg/kg were reported
following single subcutaneous and intragastric injections, respectively (USEPA
1980). Single subcutaneous doses of 278 and 1,112 mg/kg bromoform resulted in
impaired liver function in the mouse (Kutob and Plaa 1962, as reported in
USEPA 1980), and 10 daily injections of 100-200 mg/kg/day produced liver and
kidney pathology in the guinea pig (NAS 1978, as reported in USEPA 1980).
Reticuloendothelial system function (liver and spleen phagocytic activity) was
suppressed in mice given intragastric doses of 0.3 to 125 mg/kg/day bromoform
(Munson et al. 1978, as reported in USEPA 1980). Bromoform was shown to be
mutagenic in in vitro tests with three strains of Salmonella typhimurium
(Clayton and Clayton 1981). Inconclusive evidence for potential carcinogenic
activity of bromoform has been reported by Theiss et al. (1977, as reported
in USEPA 1980) using the strain A mouse lung tumor assay system. Mice were
injected at doses of 4, 48, and 100 mg/kg 3 times/week for 6 to 8 weeks and
were sacrificed 24 weeks after the first injection. A significant increase in
lung tumors was observed only at the middle dose, and a dose-response
relationship was not evident. Epidemiological studies provide some evidence
H-5
-------
for a positive association between trihalomethane levels in drinking water
supplies and the incidence of cancer. The results of these studies are
limited, however, by inability to control for all confounding variables and
limited monitoring data (USEPA 1980).
Acute aquatic toxicity for bromoform has been evaluated in two freshwater
species. The 96-hour LC50 values reported for Daphnia magna and for the
bluegill were 46,500 and 29,300 yg/liter, respectively. In studies with the
mysid shrimp and sheepshead minnow, 96-hour LCSOs were 24,400 and 17,900
ug/liter, respectively. In an embryo-larval study with sheepshead minnow.,
chronic effects were observed at 6,400 yg/liter (USEPA 1980). In freshwater
and saltwater algae, 96-hour EC50 values of 112,000 and 12,300, respectively,
were reported (based on effects in chlorophyll a) (USEPA 1980).
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to bromoform through ingestion of contaminated water and aquatic
organisms. However, since a zero level may not be obtainable at the present
time, a level of 0.19 yg/liter, corresponding to a lifetime incremental
cancer risk of 0.000001, was recommended.
EPA has not yet established an aquatic life ambient water quality
criterion for bromoform.
Carbon Tetrachloride
Carbon tetrachloride produces acute, subacute, and chronic poisoning with
fatalities by ingestion, inhalation, and dermal routes in both humans and
animals. In humans, carbon tetrachloride has been shown to cause liver arid
kidney damage (Dume et al. 1969 and Echardt 1965, as reported in NAS 1977).
Signs and symptoms of acute toxicity include dyspnea, cyanosis, proteinuria,
hematuria, jaundice, hepatomegaly, optic neuritis, ventricular fibrillation,
eye, nose, and throat irritation, headache, dizziness, vomiting, abdominal
cramps and diarrhea (NAS 1977). Chronic exposures generally result in
gastrointestinal upset, such as nausea and vomiting, and nervous system
symptoms, such as headache, drowsiness, and excessive fatigue (Browning 1961,
as reported in NAS 1977). Hepatic cirrhosis and necrosis, renal damage,
changes in blood enzymes, and increased serum bilirubin also result from
chronic exposure (Busuttil et al. 1972, Litchfield and Garland 1974, as
reported in NAS 1977).
In a series of studies to evaluate the carcinogenic potential of carbon
tetrachloride, liver tumors were observed during lifetime exposures of mice,
hamsters, and rats using different routes of exposure: hamsters were orally
administered 6.25-12.5 yl/week for 30 weeks (Della-Porta et al. 1961, as
reported in NAS 1977); mice were orally administered 0.1 ml, twice a week for
20-26 weeks (Confer and Stenger 1965, as reported in NAS 1977), rats were
injected subcutaneously with 0.2-0.3 ml/100 g every two weeks (Kawasaki 1965,
as reported in NAS 1977) and rats were administered 1.3 ml/kg orally twice a
week for 12 weeks (Ruber and Glover 1967, as reported in NAS 1977). However,
carbon tetrachloride was not found to be mutagenic or teratogenic (NAS 1977).
H-6
-------
Carbon tetrachloride produces acute and chronic toxic effects on
freshwater vertebrates and acute toxic effects on freshwater invertebrates.
The 96-hour LC50 values for bluegill were reported as 27.3 and 125 mg/liter.
A 48-hour LC50 value of 35.2 mg/liter was reported for Daphnia magna. The
96-hour LC50 values reported for tidewater silversides and Limanda limanda
were 150 mg/liter and 50 mg/liter, respectively (USEPA 1980).
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to carbon tetrachloride through the ingestion of contaminated
water and contaminated aquatic organisms. However, since the zero level may
not be attainable at the present time, a level of 0.40 ug/liter,
corresponding to an estimated lifetime incremental cancer risk of 0.000001,
was recommended.
EPA has not yet established an aquatic life water quality criterion for
carbon tetrachloride.
Chlorobenzene
Chlorobenzene has been identified as a respiratory irritant and a central
nervous system depressant in humans (NAS 1977).
Chlorobenzene has an acute oral LD50 of approximately 3-3.4 mg/kg in rats
(Vecerek et al. 1976, as reported in USEPA 1980). The rats died about 7
days after exposure and showed signs of many metabolic disturbances such as
elevated levels of serum glutamic-oxaloacetic transaminase (SCOT), lactase
dehydrogenase, alkaline phosphatase, blood urea nitrogen, and decreased levels
of glycogen phosphorylase and blood sugars.
Chronic feeding studies administered in dogs and rats produced clinical
and pathological changes (Knapp et al. 1971, as reported in USEPA 1980).
DogS administered 272.5 mg/kg/day, by gavage, 5 days/per week for a period of
90 days, exhibited gross and/or microscopic pathological changes in the liver,
kidneys, gastrointestinal mucosa, and hematopoietic tissues. Clinical
symptoms included an increase in immature leukocytes, low blood sugar,
elevated serum glutamic-pyruvic transaminase (SGPT) and alkaline phosphatase.
In chronic inhalation studies, rats, rabbits, and guinea pigs were exposed to
200, 475, and 1,000 ppm over 44 days (Irish 1963, as reported in USEPA 1980).
Histopathological changes in the lungs, liver, and kidneys occurred in the
high-dose group. The middle dose group exhibited an increase in liver weight
and slight liver histopathology. No effects were reported in the low dose
group.
Chlorobenzene was administered orally to rats in daily doses of 14.4-228
mg/kg for a total of 137 doses over 192 days. No blood or bone marrow changes
were observed (Irish 1963, as reported in USEPA 1980). No studies have
evaluated the carcinogenic potential of Chlorobenzene, although an NCI
bioassay is in progress.
The acute toxicity of Chlorobenzene to various saltwater and freshwater
species is reflected by LC50 values for cladoceran of 86 mg/liter, the
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goldfish, 51.6 mg/liter, the fathead minnow, 29.1-33.9 mg/liter, the guppy,
45.3 mg/liter, the bluegill, 15.9-24.0 mg/liter, and the sheepshead minnow,
10.5 mg/liter. Chlorobenzene has also demonstrated acute toxic effects to
freshwater and saltwater algae with 96-hour EC50 values ranging from 22.4 to
34.1 mg/liter (USEPA 1980).
EPA has established an ambient water quality criterion of 488 yg/liter
for the protection of human health from the toxic properties of chlorobenzene
through ingest ion of water and contaminated aquatic organisms. Using
available organoleptic data for controlling undesirable taste and odor of
ambient water, the estimated level is 20 yg/liter.
EPA has not yet established an aquatic life water quality criterion for
chlorobenzene.
Chlorodibromomethane
No data are available on the toxicity of Chlorodibromomethane to humans,
animals, or aquatic organisms.
EPA has not yet established ambient water quality criteria for
Chlorodibromomethane because of the lack of sufficient information.
Chloroethane
Of the chlorinated ethanes, monochloroethane is considered to be one of
the least toxic. It is known to disturb cardiac rhythm (Goodman and Gilman
1975, as reported in USEPA 1980) and overdoses can lead to severe contractile
failure of the heart (Doering 1975, as reported in USEPA 1980). Exposure to
acute concentrations in humans has also been reported to cause neurologic
symptoms (including central nervous system depression, headache, dizziness,
incoordination, inebriation, and unconsciousness); abdominal cramps;
respiratory tract irritation and respiratory failure; and skin and eye
irritation. As a halogen-containing hydrocarbon, chloroethane is potentially
toxic to the liver (USEPA 1980).
In a series of acute inhalation studies in guinea pigs, exposure to two
percent chloroethane in air for 540 minutes produced histopathological changes
in liver and kidneys; exposure to four percent chloroethane for the same
period resulted in deaths. When guinea pigs were exposed to 23-24 percent
chloroethane for five to ten minutes, unconsciousness and some deaths weres
reported (Sayers et al. 1929, as reported in Clayton and Clayton 1981).
Repeated two-hour exposures for 60 days to 5,300 ppm chloroethane was reported
to cause a decrease in the phagocytic activity of leukocytes, lowered hippuric
acid formation in the liver, and histopathological changes in the liver,
brain, and lungs (species tested not specified) (Troshina 1964, as reporter! in
Clayton and Clayton 1981). In a study in which rats and dogs were exposed to
chloroethane at concentrations of 0, 1,600, 4,000, or 10,000 ppm for six
hours/day, five days/week for two weeks, the only observed effects were slight
liver weight increase in the 4,000 and 10,000 ppm male rats and CNS depression
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in the high dose animals (Dow Chemical Company, unpublished data, as reported
in Clayton and Clayton 1981).
No data on the toxicity of chloroethane to aquatic organisms are available.
EPA has not yet established an ambient water quality criteria for
chloroethane because of the lack of sufficient data.
2-Chloroethyl Vinyl Ether
No toxicity data for 2-chloroethyl vinyl ether in humans are available,
and only limited acute toxicity information in animals has been published.
The acute oral LD50 in the rat has been given as 250 mg/kg, and the acute
dermal LD50 in the rabbit as 3,200 mg/kg (Smyth ejt al. 1949, as reported in
USEPA 1980) . Toxic effects were observed in rats exposed to 250 ppm
2-chloroethyl vinyl ether vapor for four hours (Carpenter et al. 1949, as
reported in USEPA 1980). No chronic studies for this compound have been
conducted.
In an acute toxicity study with the bluegill, the 96-hour LC50 was
determined to be 354,000 ug/liter (USEPA 1980). No toxicity data are
available for saltwater species.
EPA has not yet established ambient water quality criteria for
2-chloroethyl vinyl ether because of the lack of sufficient data.
Chloroform
Chloroform has been reported to cause severe adverse effects on the human
body. Acute effects via skin absorption include local irritation, hyperemia,
erythemia, and moisture loss (Malten et al. 1968, as reported in USEPA
1980); central nervous system depression and gastrointestinal irritation
(Challen et al. 1958, as reported in USEPA 1980) and hepatic and renal
damage (Fuhner 1923 and Althausen and Thoenes 1932, as reported in USEPA
1980). Oral doses of 44.6 and 148.3 g have produced severe nonfatal
poisonings in humans; a dose of 296.6 g was fatal (Van Oettingen 1964, as
reported in NAS 1980). Chronic effects in humans include central nervous
system depression, loss of appetite, hallucinations, ataxia, nausea, rheumatic
pain, and delirium (NIOSH 1974, as reported in USEPA 1980).
Oral LDSOs have been estimated for male rats (0.8 ml/kg), mice (0.33
ml/kg), and dogs (1.0 ml/kg) (Kimura et al. 1971, Hill et al. 1975,
Klassen and Plaa 1966, as reported in NAS 1977). Chloroform has been shown to
produce liver tumors after oral administration of 138 mg/kg for 78 weeks. In
this same study, kidney epithelial tumors were observed when an average dose
level of 100 mg/kg was administered to rats by gavage for 78 weeks and
sacrificed at 111 weeks (NCI 1976, as reported in NAS 1977). The fetuses from
rats exposed to 489 mg/cu m (100 ppm) of chloroform 7 hours/day during the 6th
to 15th day of gestation were reported to have an increased incidence in
several abnormalities which included acaudia, imperforate anus, subcutaneous
edema, missing ribs, and delayed ossification of sternebrae. At an exposure
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of 147 mg/cu m (30 ppm) there was an increased incidence of delayed
ossification of skull bones and of wavy ribs (Schwetz 1974, as reported in
USEPA 1980). Maternal toxicity was observed in pregnant rats given oral
chloroform doses of 126 mg/kg/day and greater. Doses of 316 mg/kg/day and
greater caused acute toxic nephrosis and hepatitis and death of dams, as well
as fetotoxicity. Oral doses of 100 mg/kg/day or higher were toxic to rabbits,
dams, and fetuses (Thompson et al. 1974, as reported in USEPA 1980).
Ninety-six hour LC50 values for rainbow trout and bluegill were reported
as 43.8-66.8 mg/liter and 100-115 mg/liter, respectively. Daphnia magna had
a 48-hour LC50 value of 28.9 mg/liter. Anesthetization or death occurred at
concentrations between 97 and 207 mg/liter for stickleback, goldfish, and
orangespotted sunfish. Teratogenesis was produced in 40 percent of the embryo
of rainbow trout exposed to 10.6 mg/liter for 23 days; 1.24 mg/liter produced
50 percent mortality of the embryo larval stage after a 27 day exposure. A
96-hour LC50 for pink shrimp was reported as 81.5 mg/liter. No other
information on marine organisms or on aquatic plant life is available (USEPA
1980).
EPA has established a water quality criterion of zero for maximum
protection of human health from the potential carcinogenic effects due to
exposure to chloroform through ingestion of contaminated water and
contaminated aquatic organisms. However, since zero may not be attainable at
the present time, a criterion of 0.19 yg/liter, corresponding to a lifetime
incremental cancer risk of 0.000001, has been recommended.
EPA has not yet established an aquatic life water quality criterion for
chloroform.
Dichlorobromomethane
No information is available on human toxicity to dichlorobromomethane. As
a halomethane, it is reported that the compound is "probably narcotic in high
concentrations" (USEPA 1980).
In mice, the LDSOs for males and females administered dichlorobromomethane
by gavage is 450 and 900 mg/kg, respectively. At doses between 500 and 4,000
mg/kg, histopathological examinations revealed fatty infiltration in livers,
pale kidneys, and hemorrhage in kidneys, adrenal glands, lungs, and brain
(Bowman et al. 1978, as reported in USEPA 1980). Cambell (1978, as reported
in USEPA 1980) reported reduced water consumption and body weight in mice
given 300 mg/liter dichlorobromomethane in drinking water. Cellular and
humoral immune responses were suppressed in mice exposed by gavage to 125
mg/kg/day of dichlorobromomethane for 90 days. (Schuller et al. 1978, as
reported in USEPA 1980). Suppression of hepatic phagocytic activity has also
been reported in mice (USEPA 1980). Limited evidence for tertogenic
properties of dichlorobromomethane are presented in a study by Schwetz et
al. (1975, as reported in USEPA 1980), in which some fetal anomalies
(unspecified) were observed among mice exposed to vapors at 8,375 mg/cu m for
7 hours/day during gestation days 6 to 15. Dichlorobromomethane was reported
to be mutagenic in an in vitro test with Salmonella typhimurium (Simmon
et al. 1977, as reported in USEPA 1980). Inconclusive evidence for
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potential carcinogenic activity of dichlorobromomethane has been reported by
Theiss et al. (1977, as reported in USEPA 1980) using the strain A mouse
lung tumor assay system. Mice were injected at doses of 20, 40, and 100
rag/kg, three times/week for 6 to 8 weeks and were sacrificed 24 weeks after
the first injection. A marginally significant incidence of lung tumors was
observed only at the highest dose (p <0.067).
No aquatic toxicity data are available for dichlorobromomethane.
Available data for halomethanes indicate that acute toxicity to freshwater
aquatic life occurs at concentrations as low as 11,000 yg/liter (USEPA
1980).
EPA has established ambient water quality criterion of zero for maximum
protection of human health from the potential carcinogenic effects due to
exposure to dichlorobromomethane through the ingestion of contaminated water
and aquatic organisms. However, since the zero level may not be attainable at
the present time, a level of 0.19 yg/liter, corresponding to a lifetime
incremental cancer risk of 0.000001, was recommended.
EPA has not yet established an aquatic life water quality criterion for
dichlorobromomethane.
1,1-Dichloroethane
1,1-Dichloroethane has been shown to cause marked excitation of the heart,
central nervous system depression, respiratory tract irritation, and burning
skin in humans. Liver injury was observed in experimental animals exposed to
4,000-17,500 ppm (species, route unspecified) (Sax 1975). The oral LD50 for
the rat is 14 g/kg (Sax 1975). Retarded fetal development occurred in rats
exposed to 24,250 mg/cu m (Schwetz et al. 1974, as reported in USEPA 1980).
No information is available on the toxic effects of 1,1-dichloroethane on
aquatic organisms (USEPA 1980).
EPA has not yet established ambient water quality criteria for
1,1-dichloroethane because of the lack of sufficient data.
1,2-Dichloroethane
In humans, 1,2-dichloroethane has been shown to produce central nervous
system depression, gastrointestinal upset, and systemic injury to the liver,
kidneys, lungs, and adrenals (USEPA 1979, as reported in USEPA 1980).
Accidental oral ingestion of a single dose of 0.5-1.0 g/kg resulted in death;
autopsy revealed liver necrosis and focal adrenal degeneration and necrosis
(Wirtshafter and Schwartz 1939, Yodaiken and Babcock 1973, as reported in
USEPA 1980). Acute toxic effects include nausea, vomiting, dizziness,
internal bleeding, cyanosis, rapid but weak pulse, and unconsciousness.
Chronic exposure to 1,2-dichloroethane has been shown to cause neurological
changes, loss of appetite and other gastrointestinal problems, anemia,
irritation of the mucous membranes, liver and kidney impairment, and in some
cases death (NIOSH 1978, USEPA 1979, as reported in USEPA 1980).
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Acute and subacute inhalation studies with dogs, rabbits, guinea pigs,
rats, and mice indicate that 1,2-dichloroethane is toxic to the liver, bone
marrow, blood, kidneys, myocardium, and sometimes the adrenals (Heppel et;
al. 1946, Liola et al. 1959, Liola and Fondacaro 1959, as reported in USEPA
1980). Chronic inhalation exposures to 100-400 ppm 1,2-dichloroethane, for
5-32 weeks in the guinea pig, monkey, rabbit, dog, and cat were reported to be
toxic to the liver at concentration of 200 ppm and greater (Spencer et al.
1951, Hofman et al. 1971, as reported in USEPA 1980). Increased liver
weights were observed in guinea pigs after a 32-week exposure to 100 ppm of
1,2-dichloroethane (Spencer et aj.. 1951, as reported in USEPA 1980).
Exposure of female rats to 57 mg/cu m (4 hrs/day, 6 days/week) for 6
months before breeding and throughout gestation resulted in a reduction in
litter size, number of live births, and fetal weights (vozovaya 1974, as
reported in USEPA 1980). 1,2-Dichloroethane was found to be carcinogenic at
several sites to both rats and mice administered 50-300 mg/kg for 78 weeks by
gavage (NCI 1978, as reported in USEPA 1980).
The acute toxic effects of 1,2-dichloroethane on freshwater organisms is
reflected in 96-hour LC50 values for the fathead minnow (118 mg/liter) and the
bluegill (431-550 mg/liter). Toxic.ity to saltwater organisms was demonstrated
in the mysid shrimp at 113 mg/liter. Chronic toxicity was observed in the
fathead minnow in concentrations ranging from 14 to 29 mg/liter. Toxicity to
aquatic plants was observed in saltwater algae at concentrations ranging from
more than 126 mg/liter to more than 433 mg/liter (USEPA 1980).
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects
from exposure to 1,2-dichloroethane through ingestion of contaminated water
and contaminated aquatic organisms. However, since the zero level may not be
attainable at present, a level of 0.94 yg/liter, corresponding to a lifetime
incremental cancer risk of 0.000001, was recommended.
EPA has not yet established an aquatic life water quality criterion for
1,2-dichloroethane.
1,1-Dichloroethylene
The primary acute effect of 1,1-dichloroethylene is depression of the
central nervous system. Animal studies have shown 1,1-dichloroethylene to
produce liver and kidney damage in the rat exposed to 189 mg/cu m (Prendergast
et al. 1967, as reported in USEPA 1980) and to produce cardiac sensitization
at high concentrations (102,000 mg/cu m) for 10 minutes (Siletchnik and
Carlson 1974, as reported in USEPA 1980). Pregnant rats exposed by inhalation
to 80-160 ppm on days 6 to 15 of gestation showed decreased weight gain,
decreased food consumption, and increased water consumption. Increased liver
weight was observed at 160 ppm only. In the offspring, there was a
significantly increased incidence of skeletal alterations at 80 and 160 ppm.
In the same study, rabbits exposed to 160 ppm on days 6 to 18 days of
gestation had an increase in resorptions in the dams; in the offspring, a
significant increase in several minor skeletal variations was observed (Murray
et al. 1979, as reported in USEPA 1980). Kidney adenocarcinomas were
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produced in Swiss mice exposed to 100 mg/cu m, 4 hours per day, 4 to 5 days
per week for 52 weeks (Maltoni et al. 1977, as reported in USEPA 1980). In
another study, a small increase in hepatic hemangiosarcomas was observed in
mice exposed to 220 mg/cu m by inhalation 6 hours/day 5 days per week for 7-12
months (Lee et al. 1972, as reported in USEPA 1980). No effect was observed
in rats exposed to 200 mg 1,1-dichloroethylene in drinking water for two years
or to 100 and 300 mg/cu m by inhalation, 6 hours per day, 5 days per week for
18 months (Rampy et al. 1977, as reported in USEPA 1980). An NCI bioassay
is currently in progress (USEPA 1980). 1,1-Dichlorethylene, which has a
structure similar to vinyl chloride monomer (a known liver carcinogen in
several species including humans), is also suspected of being a human
carcinogen.
Acute toxicity of 1,1-dichloroethylene on freshwater aquatic fish life is
reflected by 96-hour LC50 values for the fathead minnow of 169 mg/liter and
for the bluegill of 73.9 mg/liter. Furthermore, the toxicity of this compound
increases with increasing chlorine content. The 48-hour LC50 value for
Daphnia magna was reported as 11.6 mg/liter. The 96-hour LC50 values were
reported in the sheepshead minnow to be 249 mg/liter, the tidewater
silversides 250 mg/liter, and the mysid shrimp 224 mg/liter. No information
is available on the chronic effects of 1,1-dichloroethylene on aquatic
organisms (USEPA 1980).
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to 1,1-dichloroethylene through ingestion of contaminated water
and contaminated aquatic organisms. However, since the zero level may not be
attainable at present, a level of 0.33 yg/liter, corresponding to a lifetime
incremental cancer risk of 0.000001, was recommended.
EPA has not yet established an aquatic life water quality criterion for
1,1-dichloroethylene.
1,2-Dichloropropane
Acute toxic effects reported in humans include vertigo, lacrimation,
irritation of the mucous membrane, and changes in the blood (St. George 1937,
as reported in USEPA 1980). Death has been reported after ingestion of a
50-ml solution containing 1,2-dichloropropane (Larcan et al. 1977, as
reported in USEPA 1980).
The oral administration of 5,700 mg/kg of 1,2-dichloropropane in dogs
produced staggering and loss of coordination in 15 minutes, complete lack of
coordination in 90 minutes, and death in 3 hours. Congestion of the lungs,
kidney, and bladder was reported along with hemorrhage of the stomach and
respiratory tract. Liver and kidney damage was also produced (Wright and
Schaffer 1932, as reported in USEPA 1980). Inhalation exposure to 400 ppm for
7 hours/day for 128-140 days was reported to cause slight fatty degeneration
of the liver in mice, but no effects were observed in rats similarly exposed
(Heppel et al. 1948, as reported in USEPA 1980). 1,2-Dichloropropane is
mutagenic in the Salmonella typhimurium assay (DeLorenzo et al. 1977, as
reported in USEPA 1980). Chromosomal aberrations in rat bone marrow were
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reported (Dragusanu and Goldstein 1975, as reported in USEPA 1980). No
information is available on the carcinogenicity of 1,2-dichloropropane in
animals (USEPA 1980).
The acute toxicity of 1,2-dichloropropane in freshwater aquatic organisms
was demonstrated in cladoceran, fathead minnows, and bluegill; 96-hour LD50
values were 52.5, 139.3, and 280-320 mg/liter, respectively. Tidewater
silverside, a saltwater organism, was affected with an LC50 of 240 mg/liter.
Growth inhibition of sheepshead minnow was observed after exposure to 164
mg/liter for 33 days. Chronic toxicity was reported in the fathead minnow in
concentrations ranging from 6 to 11 mg/liter. No information is available on
the toxic effects on aquatic plant life (USEPA 1980).
EPA has not yet established ambient water quality criteria for
1,2-dichloropropane because of the lack of sufficient data.
1,3-Dichloropropylene
No information is available on the toxic effects in humans. Daily oral
doses of up to 2.5 mg/kg of 1,3-dichloropropylene for six months caused an
increase in trypsin activity, a decrease in trypsin inhibitor, an increase in
blood lipase activity, and a decrease in amylase (Strusevich and Ekshtat 1974,
as reported in USEPA 1980). Daily oral doses of 2.2 and 55 mg/kg/day for 30
days resulted in changes in the liver function of rats (Kurysheva and Ekshtat
1975, as reported in USEPA 1980). Oral LD50 values for the rat of 140 mg/kg
and the mouse of 300 mg/kg and an LC50 for the rat and mouse of 4,530 mg/cu m
were reported (Hine et al. 1953, as reported in USEPA 1980).
1,3-Dichloropropylene was mutagenic in the Salmonella typhimurium assay
(DeLorenzo et al. 1977, as reported in USEPA 1980). The carcinogenic
potential of 1,3-dichloropropylene has not been established, although an NCI
bioassay is in progress.
Acute toxicity of 1,3-dichloropropylene in freshwater aquatic organisms is
reflected by 96-hour LC50 values in the cladoceran and the bluegill of 6.15
and 6.06 mg/kg, respectively. Acute toxicity to saltwater organisms occurred
in the mysid shrimp and sheepshead minnow with LC50 values of 0.79 and 1.77
mg/liter, respectively. Chronic toxicity was observed in the fathead minnow
in concentrations ranging from 180 to 330 yg/liter. Acute toxic effects on
fresh- and saltwater algae were reported at 4.95 and 1.0 mg/liter,
respectively (USEPA 1980).
EPA has not yet established water quality criteria for
1,3-dichloropropylene because of the lack of sufficient data.
Ethylbenzene
Although ethylbenzene has a wide environmental distribution, little
information is available on its biological effects (USEPA 1980). It has been
shown to persist in man for days after exposure (USEPA 1980). Men exposed to
4.35 mg/liter in the air experienced eye irritation, which diminished in
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intensity on continued exposure. At a concentration of 21.75 mg/liter,
however, the irritation to eye and nasal membranes was intolerable (Patty
1963).
In a 6-month study on rats, daily single oral doses of ethylbenzene were
found to produce histopathological changes in the kidney and liver (Wolf et
al. 1956, as reported in USEPA 1980). No data are available on the
teratogenicity, mutagenicity, or carcinogenicity of ethylbenzene (USEPA 1980).
Among freshwater animal species, the 96-hour LC50 ranged from 32 mg/liter
in the bluegill to 97.1 mg/liter in the guppy. The 48-hour EC50 value in
Daphnia magna is 75 mg/liter. The 96-hour LC50s in saltwater invertebrates
are 3.7 mg/liter for the bay shrimp, 87.6 mg/liter for the mysid shrimp and
1,030 mg/liter for the pacific oyster. In saltwater fish, the 96-hour LC50
for striped bass was 0.43 mg/liter, but it was 275 mg/liter for the sheepshead
minnow. The variability in fish and invertebrate data may be due to
difficulties in testing ethylbenzene in saltwater. No adverse effects were
observed in aquatic plants exposed to ethylbenzene (USEPA 1980).
EPA has established an ambient water quality criterion of 1.4 mg/liter for
the protection of human health from the toxic properties of ethylbenzene
ingested through water and contaminated aquatic organisms.
EPA has not yet established an aquatic life water quality criterion for
ethylbenzene.
Methyl Bromide
Methyl bromide is a central nervous system depressant and is regarded as
highly toxic to humans. Acute fatal intoxication can result from inhalation
of vapors at concentrations as low as 1,164 to 1,552 mg/cu m, and harmful
effects can occur at 388 mg/cu m (USEPA 1980). Minor poisoning episodes may
be limited to mild neurological and GI disturbances, with recovery in a few
days. More severe cases may involve visual and speech disturbances,
incoordination, tremors developing to convulsions, and psychic disturbances.
Neurological disorders may be persistent. Death may result from pulmonary
edema or circulatory failure, and pathological changes often include
hyperemia, edema, lung and brain inflammation, and degenerative changes in the
kidneys, liver, and stomach (Doull et aj.. 1980, and USEPA 1980). Skin
contact with methyl bromide may produce prickling, cold sensation, erythema,
vesication, blisters, damage to peripheral nerve tissue, and permanent brain
damage (USEPA 1980).
Methyl bromide is also neurotoxic to animals. Exposure to 846 to 997
mg/cu m for 22 to 26 hours was lethal to rats (Irish et al. 1940, as
reported in USEPA 1980). A 3-hour exposure to 846 mg/cu m and a 13.5-hour
exposure to 1,164 mg/cu m were lethal to rabbits and guinea pigs, respectively
(von Oettingen 1964, as reported in USEPA 1980). In rabbits, 128 mg/cu m for
8 hours/day, 5 days/week resulted in lung irritation and paralysis (Irish et
al. 1941, as reported in USEPA 1980). Dogs receiving methyl bromide by
ingestion (fumigated diet yielding residual bromide at a dose level of 150
mg/kg/day) were adversely affected (Rosenblum et al. 1960, as reported in
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USEPA 1980). Subcutaneous administration of methyl bromide (in oil) to
rabbits at 20-120 mg/kg caused paralysis, cessation of drinking, and reduced
urine excretion (Kakizaki 1967, as reported in USEPA 1980). Cattle fed methyl
bromide fumigated hay (resulting in bromide ion concentrations of 6,800 to
8,400 mg/liter) developed signs of CNS toxicity (motor incoordination) at 10
to 12 days of exposure (Knight and Reina-Guerra 1977, as reported in USEPA
1980). Bromomethane was reported to be mutagenic in an in vitro test with
Salmonella typhimurium (Simmon et al. 1977, as reported in USEPA 1980).
No chronic studies of methyl bromide toxicity are available.
For methyl bromide, the 96-hour LC50 value for the bluegill, a freshwater
species, is 11,000 ug/liter and for the tidewater silverside, a saltwater
species, is 12,000 yg/liter (USEPA 1980). No chronic toxicity data for
aquatic organisms are available.
EPA has established ambient water quality criterion of zero for maximum
protection of human health from the potential carcinogenic effects due to
exposure to methyl bromide through the ingestion of contaminated water and
aquatic organisms. However, since the zero level may not be attainable at the
present time, a level of 0.19 yg/liter, corresponding to a lifetime
incremental cancer risk of 0.000001, was recommended.
EPA has not yet established an aquatic life water quality criterion for
methyl bromide.
Methyl Chloride
Methyl chloride is not generally regarded as highly toxic in humans,
although numerous instances of poisonings have been reported. Serious or
prolonged exposures may occur because of methyl chloride's odorless and
colorless properties, low irritancy, and characteristic latency of effect
(USEPA 1980). Methyl chloride acts principally as a central nervous system
depressant. In persons exposed to levels ranging from 52 to more than 20,000
mg/cu m, the following toxic symptoms have been reported: blurred vision,
headache, nausea, loss of coordination, and personality changes, lasting from
hours to days (USEPA 1980). Severe poisonings are characterized by a latent
period followed by serious neurological disorders which may be persistent.
Renal and hepatic injury are common. Coma and death may result from cerebral
and pulmonary edema and circulatory failure (USEPA 1980). No other chronic
effects have been reported, although no epidemiological studies of populations
exposed to methyl chloride have been reported.
In acute inhalation studies in animals, methyl chloride has produced
severe neurological disturbances. The LC50 value for the mouse was 6,500
mg/cu m following a six-hour inhalation exposure (Davis et al. 1977, as
reported in USEPA 1980). Permanent muscular dysfunction was reported in mice
surviving several weeks of daily six-hour exposures at 1,032 mg/cu m, and
paralysis followed exposure to 531 mg/cu m for 20 hours (von Oettinger et
al. 1964, as reported in USEPA 1980). In dogs and monkeys, signs of
poisoning were observed after one six-hour exposure to 1,032 mg/cu m. Daily
exposure of dogs to this concentration for 2 to 4 weeks led to some deaths and
permanent neuromuscular damage in survivors (von Oettinger 1964, as reported
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in USEPA 1980). Under prolonged exposures to less severe levels, methyl
chloride increased mucus flow in cats (Weissbecker et. al. 1971, as reported
in USEPA 1980).
Little aquatic toxicity data are available for methyl chloride. Dawson
et al. (1977, as reported in USEPA 1980) reported 96-hour LC50 values for
the bluegill (a freshwater species) and the tidewater silverside (a saltwater
species) of 550,000 and 270,000 yg/liter, respectively. Data on the general
class halomethanes indicate that acute toxicity may occur at levels as low as
11,000 yg/liter (USEPA 1980). No data on toxic effects to aquatic plants
are available.
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to methyl chloride through ingestion of contaminated water and
aquatic organisms. Since the zero level may not be attainable at the present
time, a level of 0.19 yg/liter, corresponding to a lifetime incremental
cancer risk of 0.000001, was recommended.
EPA has not yet established an aquatic life water quality criterion for
methyl chloride.
Methylene Chloride
The acute toxic effects of methylene chloride on humans include decreased
psychomotor performance (Winneke 1974, as reported in USEPA 1980), central
nervous system dysfunctions and irritation of the mucous membranes (eyes,
respiratory tract, and skin) (NAS 1978, as reported in USEPA 1980). Mild
poisoning produces somnolence, lassitude, anorexia, and mild lightheadedness.
Fatal poisonings have resulted from cardiac injury and heart failure (NAS
1978, citing Hughes 1954, Stewart and Hake 1976, Collier 1936, Moskowitz and
Shapiro 1952, as reported in USEPA 1980). Upon metabolism, methylene chloride
will form carbon dioxide, which will increase carboxyhemoglobin levels in the
blood and interfere with oxygen transfer and transport (USEPA 1980).
Central nervous system functional disturbances were produced in animal
studies in which rats were exposed for 3 hours to 1,740 mg/cu m (Fodor and
Roscovanu 1976, as reported in USEPA 1980). Liver changes were reported in
mice continuously exposed for up to 2 weeks to 87-347 mg/cu m (NAS 1978 citing
Haun et al. 1972, as reported in USEPA 1980). Conjunctivitis, blepharitis,
corneal thickening, keratitis, and iritis were observed in rabbits (Ballantyne
et al. 1976, as reported in USEPA 1980). Fetotoxicity and embryotoxicity
were reported in mice and rats exposed to 4,340 mg/cu m for 7 hours on day 9
of gestation (Schwetz et al. 1975, as reported in USEPA 1980).
Methylene chloride was reported to be mutagenic in the Salmonella
typhimurium assay. No information on the carcinogenicity of methylene
chloride in animals or humans is available (USEPA 1980).
The acute toxic effects of methylene chloride on freshwater aquatic
organisms have been studied. 96-Hour LC50 values were determined for Daphnia
magna (224 mg/liter), fathead minnow (193 mg/liter), and bluegill (224
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mg/liter). Among saltwater species, mysid shrimp have reported 96-hour LC50
values of 256 mg/liter; sheepshead minnows, 331 mg/liter; and tidewater
silverside, 270 mg/liter. No information on the chronic toxicity of methylene
chloride on aquatic organisms is available. Toxicity to both freshwater and
saltwater algae was reported to occur in concentrations greater than 662
mg/liter (USEPA 1980).
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to halomethanes including methylene chloride through the ingestion
of contaminated water and contaminated aquatic organisms. However, since the
zero level may not be attainable at the present time, a level of 0.19
yg/liter corresponding to a lifetime incremental cancer risk of 0.000001 was
recommended for all the halomethanes including methylene chloride.
EPA has not yet established an aquatic life water quality criterion for
methylene chloride.
1,1,2,2-Tetrachloroethane
A number of cases of human poisonings from occupational exposure to
1,1,2,2-tetrachloroethane have been reported. Frequently noted symptoms
include vomiting, nausea, gastric pain, headache and dizziness, and in some
cases death resulting from central nervous system (CNS) depression. Chronic
exposure can result in hepatotoxic and CNS effects (ACGIH 1981, USEPA 1980).
In two occupational studies, hepatic injury and leukopenia were reported in
workers exposed to concentrations of 1,1,2,2-tetrachloroethane between 1.5 and
247 ppm for three years, and nervous complaints and gastric symptoms were
present in workers exposed to concentrations between 9 and 98 ppm (Jeney ejb
al. 1957, Lobo-Mendoca 1963, as reported in ACGIH 1981). Cases of human
deaths have also resulted from accidental or intentional
1,1,2,2-tetrachloroethane ingestion (USEPA 1980).
Acute inhalation exposure of rats and mice to 1,1,2,2-tetrachloroethane
produced anesthesia, fatty degeneration of the liver, tissue congestion, and
death; exposures in these studies ranged from 5,900 ppm (three hours) to
11,400 ppm (six hours for two days). A three-hour exposure of mice to 600 ppm
resulted in increased hepatic triglycerides and total lipids and decreased
hepatic energy stores (Tomokuni 1969, as reported in USEPA 1980). Intravenous
or intraperitorieal injection of 0.7 ml (total dose administered in five doses
over 14 days) in guinea pigs caused weight loss, convulsions, death, and fatty
degeneration of the liver and kidney (Muller 1932, as reported in USEPA
1980). Injection of 200 mg/kg was lethal to mice in seven days (Natl. Res.
Counc. 1952, as reported in USEPA 1980).
Chronic inhalation exposure of rabbits to 1,1,2,2-tetrachloroethane at
14.6 ppm, 4 hours/day for 11 months induced liver and kidney degeneration
(Navrotskiy et al. 1971, as reported in USEPA 1980). White blood cell
count, pituitary adrenocorticotropic hormone, and fat content of the liver
were affected in rats exposed by inhalation to 1.94 ppm, 4 hours/day for up to
265 days (Deguchi 1972, as reported in USEPA 1980). Monkeys exposed to 1,000
or 4,000 ppm, 2 hours/day for 190 days developed marked vacuolation of the
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liver (Horiguchi et al. 1962, as reported in USEPA 1980). A National Cancer
Institute bioassay was conducted for 1,1,2,2-tetrachloroethane in which male
and female mice received time-weighted average doses of 142 and 282 mg/kg/day
by stomach tube for 78 weeks (NCI 1978, as reported in USEPA 1980). The
incidence of hepatocellular carcinomas in both male and female mice was
positively correlated (p <0.001) with dosage level. In male and female rats
given time-weighted average doses of 62 and 108 mg/kg/day (males) and 43 and
76 mg/kg/day (females) for 78 weeks, the incidence of neoplasms was not
statistically significant. 1,1,2,2-Tetrachloroethane was shown to be
moderately mutagenic in in vitro assays with Salmonella typhimurium and
E. coli (USEPA 1980).
In freshwater species, LD50 values of 9,320-23,900 yg/liter have been
reported for the cladoceran, 20,300 ug/liter for the fathead minnow, and
19,600-21,300 yg/liter for the bluegill. In an embryo-larval study of
fathead minnow, chronic toxicity was observed at 2,400 yg/liter (USEPA
1980). Acute toxicity in saltwater species of 1,1,2,2-tetrachloroethane was
reported for mysid shrimp and sheepshead minnow with LD50 values of 9,020 and
12,300 lag/liter, respectively (USEPA 1980). No chronic studies in saltwater
species were available. In 96-hour EC50 tests with freshwater and saltwater
algae using chlorophyll a and cell number as measured responses, toxic
effects were observed at concentrations of 136,000-146,000 and 6,230-6,440,
respectively (USEPA 1980).
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to 1,1,2,2-tetrachloroethane through ingestion of contaminated
water and aquatic organisms. However, since the zero level may not be
attainable at the present time, a level of 0.17 ng/liter, corresponding to a
lifetime incremental cancer risk of 0.000001, was recommended.
EPA has not yet established an aquatic life water quality criterion for
1,1,2,2-tetrachloroethane.
Tetrachloroethylene
The acute effects of tetrachloroethylene on humans are dominated by
central nervous system depression. Lassitude, mental fogginess, and
exhilaration were observed in human volunteers exposed to 6,258 mg/cu m for 95
and 130 minutes (Carpenter 1937, as reported in USEPA 1980). When-this
concentration was raised to 10,000 mg/cu m signs of inebriation were observed
and, at 13,400 mg/cu m, all volunteers were forced to leave the chamber within
7.5 minutes. Minimal effects on the central nervous system were observed on
volunteers exposed to 1,300 mg/cu m (Rowe et al. 1952 and Stewart et al.
1961, as reported in USEPA 1980). Irritation of the mucous membranes have
also been reported (NAS 1980). Mild to severe hepatotoxicity was observed in
several instances following inhalation of tetrachloroethylene (dose and
duration unspecified; Hake and Steward 1977; Salund 1967; Stewart et al.
1961; Stewart 1969; Meckler and Phelps 1966, as reported in NAS 1980). No
consistent neurological changes were reported in a study of 12 volunteers
exposed to 168 and 670 mg/cu m tetrachloroethylene for 5.5 hours per day for
up to 53 days (Stewart et al. 1977, as reported in USEPA 1980).
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Occupational exposure to an average concentration of 400 mg/cu m (in one
worker, for up to 15 years) resulted in subjective complaints, such as
headaches, fatigue, somnolence, dizziness, and a sensation of intoxication
(Medek and Kovarik 1977, as reported in USEPA 1980). No other information on
the subacute of chronic toxicity of tetrachloroethylene on humans is available.
Few studies have been conducted to evaluate the acute toxic effects of
tetrachloroethylene on animals. A single 240-minute exposure to 1,340 mg/cu m
(200 ppm) resulted in moderate fatty degeneration of the liver of mice (Kylin
et al. 1963, as reported in NAS 1980). Levels of serum glutamic oxaloacetic
transaminase were elevated following a single oral dose of 0.75 ml/kg in rats
(Moslen et^ al. 1977, as reported in NAS 1980). Similarly, intraperitoneal
administration of 0.3 to 0.5 ml/kg tetrachloroethylene in rats resulted in
increased serum enzyme levels (Klassen and Plaa 1967, as reported in NAS
1980). The oral LD50 value for the dog and cat is 4,000 mg/kg, the rabbit,
5,000 mg/kg, and for the mouse, the values range from 195 to 8,100 mg/kg
(USDHHS 1980).
Rats, guinea pigs, rabbits, and monkeys exposed repeatedly for 7 hours per
day showed no changes in behavior at concentrations up to 2,720 mg/cu m
(duration unspecified; Rowe et al. 1952, as reported in USEPA 1980). After
a 2-week exposure to 10,999 mg/cu m for 7 hours per day, rats showed signs of
marked salivation, restlessness, irritability and loss of equilibrium and
coordination (Rowe et al. 1952, as reported in USEPA 1980). Changes in EEC
patterns were reported in rats exposed to 100 mg/cu m, 4 hours per day, for 15
to 30 days (Dmitrieva 1966; Dmitrieva and Kuleshov 1972, as reported in USEPA
1980) . Increased liver weight and mild to marked centra] fatty degeneration
of the liver were reported in guinea pigs exposed to 670-16,750 mg/cu m, 7
hours per day for up to 158 repeated exposures (Rowe el; al. 1952, as
reported in USEPA 1980). Congestion and granular swelling in the kidney was
observed in rats exposed to 1,540 mg/cu m for 8 hours per day, 5 days per week
over a period of 7 months (Carpenter 1937, as reported in USEPA 1980). A very
high incidence of nephrotoxicity and a little evidence of hepatotoxicity was
observed in a chronic oral study of mice and rats gavaged with doses of
tetrachloroethylene ranging from 386 to 1,072 mg/kg/day for 78 weeks (National
Cancer Institute 1977, as reported in NAS 1980).
Tetrachloroethylene did not induce mutations in Escherchia coli in the
presence of a microsomal activating system (Greim et al. 1975, as reported
in NAS 1980). Female rats and mice exposed to 2,000 mg/cu m for 7 hours daily
on days 6 through 15 of gestation did not produce teratogenic effects.
However, there was a decrease in the fetal body weight of mice, a small but
significant increase in fetal resorptions in the rat, subcutaneous edema in
mice pups and delayed ossification of skull bones and sternabrae in the mice
(Schwetz et al. 1975, as reported in USEPA 1980). Heptocellular carcinomas
were reported in mice, but not rats gavaged with daily oral doses of
tetrachloroethylene ranging from 386 to 1,072 mg/kg for up to 78 weeks
(National Cancer Institute 1977, as reported in NAS 1980).
The acute toxic effects of tetrachloroethylene on aquatic fish life is
reflected by 96-hour LC50 values for the cladoceran, 17.7 mg/liter; the midge,
30.8 mg/liter; the rainbow trout, 4.8-5.8 mg/liter; the fathead minnow,
13.5-21.4 mg/liter; the bluegill, 12.9 mg/liter; and the mysid shrimp, 10.2
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mg/liter. Chronic toxicity was observed in the fathead minnow in
concentrations ranging from 0.5 to 1.4 mg/liter and in the mysid shrimp in
concentrations ranging from 0.3 to 0.67 mg/liter. No adverse effects were
observed on chlorophyll a or cell number of freshwater algae exposed to
concentrations as high as 816 mg/liter. Saltwater algae, however, are more
sensitive and have EC50 values ranging from 10.5 to 509 mg/liter (USEPA
1980).
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to tetrachloroethylene through ingestion of contaminated water and
contaminated aquatic organisms. However, since the zero level may not be
attainable at present, a level of 0.80 yg/liter, corresponding to a lifetime
incremental cancer risk of 0.000001, was recommended.
EPA has not yet established an aquatic life water quality criterion for
tetrachloroethylene.
Toluene
Acute toxic effects in humans include adverse mental changes, such as
altered psychomotor performance, irritability, disorientation, and
unconsciousness (NAS 1980). Additionally, toluene abuse has been associated
with cardiac arrhythmias and with liver and kidney dysfunction (Hayden et
al. 1977, Weisenberger 1977, as reported in NAS 1980). In occupational
exposures to solvent mixtures, workers have reported myelotoxicity (NAS 1980),
minor blood cell change, and hepatomegaly (Greenburg et al. 1942, as
reported in NAS 1980), and immunoincompetence (Lange et al. 1973, as
reported in NAS 1980). These affects cannot be attributed to toluene alone.
The minimal lethal concentration of toluene was reported to be 20 mg/liter
in mice for a single 8-hour inhalation exposure. The acute oral toxicity of
toluene is greater in young rats than in adult animals (Kimura et al. 1971,
as reported in NAS 1980). Liver microsomal activity was decreased by acute
oral administration of high doses of toluene to rats (Mungikar and Pawar 1976,
as reported in USEPA 1980). Rats exposed to 1,000 ppm for 8 hours/day for 1
week had slightly elevated serum glutamic-oxaloacetic transaminase (SCOT) and
serum glutamic-pyruvic transaminase (SGPT) activities. Chronic studies in two
dogs exposed 8 hours/day for 6 months showed nervous system intoxication,
incoordination, paralysis of the hind legs, and congestive changes in the
lungs, heart, liver, kidney, and spleen (Tahti et al. 1977, as reported in
NAS 1980). Chromosome damage of bone marrow cells was reported in rats
injected with 1 g/kg of toluene (Lyapkalo 1973, as reported in NAS 1980).
Embryotoxicity was observed in rats exposed to toluene vapors at 600 mg/cu m
(Hudak et al. 1977, as reported in NAS 1980). The carcinogenic potential of
toluene has not been established (USEPA 1980).
The acute toxicity of toluene to freshwater organisms was demonstrated in
four species of fish with 96-hour LC50 values ranging from 17.5 top 59.3
mg/liter. In saltwater shrimp and oysters, 96-hour LCSOs ranged from 9.5 to
1,050 mg/liter. Striped bass and coho solmon have LC50 values of 6.3 and
10-50 mg/liter, respectively. A range of LC50 values between 17.2 and 38.1
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rag/liter were observed in a number of 24-hour tests on the grass shrimp. A
chronic toxicity effect was observed on the hatching and survival of
sheepshead larvae and embryos. Fresh and saltwater algae were adversely
affected at 245 mg/liter and 100 mg/liter, respectively. Photosynthesis and
respiration were affected in kelp at 10 mg/liter and in algae at 34-85
mg/liter (USEPA 1980).
EPA has established an ambient water quality criterion of 14.3 mg/liter
for the protection of human health from the toxic properties of toluene
ingested through water and contaminated organisms.
EPA has not yet established an aquatic life water quality criterion for
toluene.
Trans -1,2-Dichloroethylene
Humans have developed nausea, vomiting, weakness, tremor, and cramps
following exposure to high concentrations of trans-1,2-dichloroethylene vapor
(Sax 1975). The effects are rapidly reversible following removal from
exposure. No other information is available on the toxic effects of this
compound on humans.
There is limited information available from experimental studies.
Repeated inhalation exposures of 800 mg/cu m, 8 hours per day, 5 days per week
for 16 weeks of trans-1,2-dichloroethylene produced fatty degeneration of the
liver in rats (Freundt et al. 1977, as reported in USEPA 1980). In a series
of studies using 1,2-dichloroethylene, no measureable effects on growth,
mortality, organ and body weights, hematology, clinical chemistry and gross
and microscopic pathology were reported in rats, rabbits, guinea pigs, and
dogs exposed to levels as high as 4,000 mg/cu m for six months (ACGIH 1977, as
reported in USEPA 1980). Trans-1,2-dichloroethylene is not metagenic when
assayed with E_L coli K12 (Greim et al. 1975, as reported in USEPA 1980).
No information is available on the potential teratogenicity or carcinogenicity
of this compound.
The assessment of the toxicity of trans-l,2-dichloroethylene on aquatic
life is limited to one 96-hour LC50 value of 135 mg/liter for the bluegill.
No other information is available on the toxic effects of this compound on
aquatic life (USEPA 1980).
EPA has not yet established ambient water quality criteria for
trans-1,2-dichloroethylene because of the lack of sufficient data.
1,1,1-Trichloroethane
1,1,1-Trichloroethane primarily causes central nervous system disorders in
humans (USEPA 1980). Symptoms include depression; changes in reaction time,
perceptual speed, manual dexterity, and equilibrium; incoordination; and
burning and tingling sensation in the hands and feet. Other toxic effects
that have been observed in humans include hepatic cellular damage, liver
function abnormalities, nausea, vomiting, diarrhea, hypotension, bradycardia,
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cardiac arrhythmias, eye irritation, fatigue, and death (NIOSH 1978, as
reported in USEPA 1980).
Experimental studies have shown that 1,1,1-trichloroethane induces toxic
effects in a wide range of animal species. Cardiac arrhythmia, myocardial
depression, tachycardia, tremors and respiratory failure have been reported in
the monkey. Cardiac failure, pulmonary congestion, respiratory failure and
damage to the central and peripheral nervous systems have been observed in the
rat. In the mouse, liver dysfunction, pulmonary congestion, and cardia
arrhythmia have been reported. In the guinea pig, lung irritation and liver
dysfunction have been observed. Respiratory failure has been induced in the
dog and damage to the central and peripheral nervous systems has been reported
in the cat (Truhart et al. 1973, Horiguchi and Horiguchi 1971, Tsapko and
Rappoport 1972, Beleg et al. 1974, Herd et al. 1974, Torkelson et al.
1958, MacEwen and Vernot 1974, as reported in USEPA 1980). In most studies,
high concentrations were used. The lowest concentration producing toxic
effects was 73 ppm administered four hours per day for 50-120 days (Tsapko and
Rappoport 1972, as reported in USEPA 1980).
The acute toxic effects of 1,1,1-trichloroethane on freshwater aquatic
organisms is reflected by 96-hour LC50 values of 52-105 mg/liter for the
fathead minnow and 69.7 mg/liter for the bluegill. Toxicity to saltwater
organisms has been observed in the mysid shrimp, with a reported LC50 value of
31.2 mg/liter, and in the sheepshead minnow, with an LC50 value of 70.9
mg/liter. Toxicity to plants occurs in freshwater algae at levels greater
than 530 mg/liter and in saltwater algae at levels greater than 669 mg/liter.
No information is available on the chronic toxicity of 1,1,1-trichloroethane
on aquatic organisms (USEPA 1980).
EPA has established an ambient water quality criterion of 18.4 mg/liter
for the protection of human health from the toxic properties of
1,1,1-trichloroethane ingested through water and contaminated aquatic
organisms.
EPA has not yet established an aquatic life water quality criterion for
1,1,1-trichloroethane.
1,1,2-Trichloroethane
No information is available on the toxic effects of 1,1,2-trichloroethane
in humans. Kidney necrosis was reported in the mouse and dog administered
single dose intraperitoneal injections of 0.35 ml/kg and 0.45 ml/kg,
respectively (Klassen and Plaa 1967, as reported in USEPA 1980). The
effective dose that produces kidney necrosis in 50% of the animals is 0.17
ml/kg in mice and 0.4 ml/kg in the dog, both administered by intraperitoneal
injection. Centrilobular necrosis of the liver was observed in dogs treated
with a single dose of 0.35 ml/kg by intraperitoneal injection (Klassen and
Plaa 1967, as reported in USEPA 1980). 1,1,2-Trichloroethane has been found
to cause liver and adrenal cancer in mice administered 195 and 390 mg/kg/day
by gavage for 78 weeks (NCI 1978, as reported in USEPA 1980).
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The acute toxic effects of 1,1,2-trichloroethane on freshwater organisms
is reflected by 96-hour LC50 values for Daphnia magna of 18-43 mg/liter, for
the fathead minnow of 81.7 mg/liter, and for the bluegill of 40.2 mg/liter.
Chronic toxicity has been observed in the fathead minnow in concentrations
ranging from 6 to 14.8 mg/liter. No information is available on the toxicity
to saltwater organisms or the effects of 1,1,2-trichloroethane to aquatic
plants (USEPA 1980).
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to 1,1,2-trichloroethane through ingestion of contaminated water
and contaminated fish. However, since the zero level may not be attainable at
present, a level of 0.6 yg/liter, corresponding to a lifetime incremental
cancer risk of 0.000001, was recommended.
EPA has not yet established an aquatic life water quality criterion for
1,1,2-trichloroethane.
Trichloroethylene
The acute toxic effects of trichloroethylene in humans include nervous
system depression, incoordination and unconsciousness (NAS 1977). Clinical
signs and symptoms are principally those of gastrointestinal upset, narcosis,
and occasional cardiac abnormalities (NAS 1980). Controlled human clinical
studies have shown that inhalation of 100 to 200 ppm (duration unspecified)
caused complaints of the eye, throat irritation, and fatigue in several
exposed volunteers (Gamberale et al. 1976, Nomiyama and Nomiyama 1977,
Vernon and Ferguson 1969, as reported in NAS 1980). In a separate study, two
patients who drank 350 and 500 ml trichloroethylene were rendered unconscious
for four and eight days, respectively. Hypotension and cardiac arrhythmias
were delayed in onset, but were quite serious in nature (Dhuner et al. 1957,
as reported in NAS 1980).
In an epidemiology study, evidence of increased nervous system disorders
was found in workers exposed for 5 to 15 years to concentrations less than the
threshold limit value (50 ppm). (Grandjean et al. 1955, as reported in
USEPA 1980).
Insomnia, tremors, severe neurasthenic syndromes coupled with anxiety
states and progressive bradycardia have been reported in workers exposed to
concentrations of trichloroethylene ranging from 30 to 632 ppm (duration
unspecified) with disturbances of the nervous system continuing for up to 1
year following exposure (Bardodej and Vyskoch 1956, as reported in USEPA
1980). Headaches have been reported in workers exposed to concentrations as
low as 27 ppm (Nomiyama and Nomiyama 1977, as reported in USEPA 1980). Each
of these accounts of the chronic effects of trichloroethylene suffer from a
lack of accurate exposure levels and the inability to distinguish
trichloroethylene induced effects from those caused by other factors.
Behavioral studies have generally confirmed that the CNS depressant
activity of trichloroethylene observed in humans also occurs in rats following
roughly equivalent exposures (Khorvat and Formanek 1959 arid Goldberg et al.
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1964, as reported in USEPA 1980). The acute oral LD50 of trichloroethylene in
rats if 4,920 mg/kg (NIOSH 1980); and the acute intraperitoneal LD50 for the
mouse isv2.2 ml/kg (Klaasen and Plaa 1967, as reported in NAS 1980). A single
intraperitoneal injection of 0.6 ml/kg caused a loss of muscle tone,
depression of reflexes, and slowing of heart rate in guinea pigs (Mikiskova
and Mikiska 1966, as reported in NAS 1980).
In subacute toxicity studies, rabbits injected intramuscularly with 4.38
grams per animal three times a week for four weeks developed a loss of
Purkinje cells with associated basket cells in the cerebellum and other less
specific damage to the telencephalic cortex, basal gaglia and brain stem
nuclei (Bartonicek and Brun 1970, as reported in USEPA 1980). Similar effects
have been reported in rabbits exposed by inhalation to 1,889 ppm for 20 to 30
days (Bernardi eft al. 1956, as reported in USEPA 1980) and in dogs exposed
to 297-502 ppm (duration unspecified; Baker 1958, as reported in USEPA 1980).
The chronic toxicity from long term exposure to trichloroethylene is not
considered to differ significantly from the observed acute toxic effects (NAS
1980). Maximum no-effect levels have been reported in monkeys, 400 ppm,
rabbits and rats, 200 ppm and guinea pigs, 100 ppm, exposed to
trichloroethylene vapor 7 hours per day, 5 days per week for six months (Adams
et al. 1951, as reported in NAS 1980).
In another study, rats, guinea pigs, monkeys, rabbits, and dogs exposed by
inhalation to either 730 ppm, 8 hours per day, 5 days per week, for 6 weeks or
35 ppm continuously for 90 days showed no evidence of adverse effects
(Prendergast 1967, as reported in NAS 1980).
Trichloroethylene has been found to be mutagenic in a number of
microsomally activated in vitro screening systems, including Salmonella
typhimurium (NAS 1980), Excherichia coli (Greim et al. 1975, as reported
in USEPA 1980) and Saccharomyces cerevisiae (Shahin and von Barstel 1977, as
reported in USEPA 1980) . No evidence of teratogenicity was observed in mice
and rats exposed to 297 ppm on days 6 through 15 of gestation for 7 hours per
day (Schwetz et al. 1975, as reported in NAS 1977).
Trichloroethylene has been found to be carcinogenic in the liver of mice
orally administered time weighted average doses of 1,169 and 2,339 mg/kg for
males and 869 and 1,739 mg/kg for females five days per week for 78 weeks.
Some evidence of metastasis of hepatocellular carcinoma to the lungs was also
observed in the mice. No increase in the incidence of tumors was observed in
parallel experiments with rats (NCI 1976, as reported in USEPA 1980). Two
other long-term bioassays, one in rats and the other using a different strain
of mice, yielded negative results (Maltoni 1979 and Van Duuren et al. 1979,
as reported in USEPA 1980). This combined with questions about the design of
the NCI study have raised questions about the true carcinogenic potential of
trichloroethylene (NAS 1980).
The acute toxicity of trichloroethylene on aquatic fishlife is reflected
by 96-hour LC50 values for cladoceran, 39-100 mg/liter, fathead minnow,
40.7-66.8 mg/liter, and the bluegill 44.7 mg/liter. Intoxication
characterized by erratic swimming, uncontrolled movement and loss of
equilibrium was observed in grass shrimp and sheepshead minnow after several
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minutes of exposure to 2.0 mg/liter and 20 mg/liter, respectively. A loss of
equilibrium was reported in the fathead minnow exposed to 21.9 mg/liter for 96
hours. A 50 percent decrease in 14C uptake during photosynthesis was observed
in saltwater algae exposed to 8 mg/liter trichloroethylene. No information is
available one the chronic toxicity of trichloroethylene to aquatic fishlife.
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to trichloroethylene through the ingestion of contaminated water
and contaminated aquatic organisms. However, since the zero level may not be
attainable at the present time, a criterion of 2.7 ug/liter at an
incremental lifetime cancer risk of 0.000001, was recommended.
EPA has not yet established an aquatic life water quality criterion for
trichloroethylene.
Vinyl Chloride
This compound in highly flammable and volatile with high explosive
characteristics. The toxicity of this compound has been clearly described in
animals and in humans (NAS 1977 and USEPA 1980).
In humans, vinyl chloride has been shown to produce central nervous system
dysfunction, sympathetic-sensory polyneuritic and organic disorders of the
brain (Smirnova and Granik 1970, as reported in NAS 1977) In occupational
studies, vinyl chloride has been associated with scleroma-like skin
alterations, Raynaud's syndrome, acroosteolysis, thrombocytopenia, portal
fibrosis, and hepatic and pulmonary dysfunction (Juehe and Lange 1972, Juene
et al. 1974, Berk et al. 1975, Martsteller et al. 1975, as reported in
NAS 1977). In addition, hepatic angiosarcoma, one of the rarest human
malignant neoplasms, has been observed in vinyl chloride workers (Anon 1974,
Makk et al. 1976, as reported in NAS 1977 and Creech and Johnson 1974, as
reported in USEPA 1980). Lesions of the skin, bone, liver, spleen, and lungs
have also been reported after chronic exposure to this compound (Popper and
Thomas 1975, Gedigk et al. 1975, Thomas and Pepper 1975, as reported in NAS
1977).
In acute arid subchronic inhalation studies, vinyl chloride has been shown
to produce lung congestion, hemorrhaging, blood-clotting difficulties, and
congestion of liver and kidneys (species unspecified; Mastromatteo et al.
1960, as reported in NAS 1977). Numerous studies have reported its
carcinogenic effects in rats, mice, hamsters, and rabbits by both inhalation
and oral administration (USEPA 1980).
No acute or chronic data are available on the effects of vinyl chloride on
freshwater of saltwater organisms (USEPA 1980).
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to vinyl chloride through the ingestion of contaminated water and
contaminated aquatic organisms. However, since the zero level may not be
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attainable at the present time, a level of 2.0 yg/liter, corresponding to a
lifetime incremental increase of cancer risk of 0.000001, was recommended.1
EPA has not yet established an aquatic life water quality criterion for
vinyl chloride.
lln the Carcinogen Assessment Group's summary and conclusions regarding
carcinogenicity of vinyl chloride (July 14, 1978) an individual lifetime risk
of 0.00001 was associated with an intake of 1.054 mg/kg/day (0.53 mg/liter).
A risk of 0.000001 would be associated with an intake of 0.1054 mg/kg/day
(0.053 mg/liter).
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2. Acid Extractable Organic Compounds
4-Chloro-m-cresol
The only reported toxic effect of 4-chloro-m-cresol in humans is vesicular
dermatitis. In sensitive individuals, a 1.5 percent aqueous solution caused a
pruritic vesicular dermatitis within four hours of exposure which regressed
within a week (Guy and Jacobs 1941, as reported in USEPA 1980).
In animals, acute exposure to 4-chloro-m-cresol produces severe muscle
tremors, damage to renal tubules, and death in a few hours (Wein 1939, as
reported in USEPA 1980). For the mouse, Wein (1939, as reported in USEPA
1980) reported LDSOs by subcutaneous injection and by intravenous injection of
360 and 70 mg/kg. For the rat, the subcutaneous LD50 was given as 400 mg/kg.
An oral LD50 of 1,330 mg/kg has also been reported for the mouse (Schrotter
et al. 1977, as reported in USEPA 1980). In subchronic studies in which
rats were injected subcutaneously with 80 mg/kg/day for 14 days and rabbits
were injected with approximately 6.5 mg/kg/day for four weeks, the only
observed effect was mild inflammation at the site of injection in the rats
(Wein 1939, as reported in USEPA 1980). No chronic toxicity data for
4-chloro-m-cresol are available.
Limited aquatic toxicity data is available for 4-chloro-m-cresol. The
96-hour LD50 for the fathead minnow is 30 yg/liter (USEPA 1980). No data
are available for saltwater species.
EPA has not yet established ambient water quality criteria for protection
of human health and aquatic life from exposure to 4-chloro-m-cresol because of
the lack of sufficient information. However, using available organoleptic
data for control of undesirable taste and odor quality of ambient water, the
recommended criterion is 3,000 yg/liter.
2-Chlorophenol
Very little information is available on the toxic effects of
2-chlorophenol on humans. Acute toxicity has been characterized as being
"likely" to be corrosive and irritating to the eyes and skin (Doedens 1963, as
reported in USEPA 1980). 2-Chlorophenol is considered to be a weak uncoupler
of oxidative phosphorylation (Mitsuda et al. 1963, as reported in USEPA
1980) and a convulsant poison (Farquharson et al. 1958 and Angel and Rogers
1972, as reported in USEPA 1980).
Relatively few acute toxicological studies are available on laboratory
animals. Acute LD50 values have been reported as follows: the rat, 670
mg/kg-oral and 900 mg/kg-subcutaneous (Diechmann 1943, as reported in USEPA
1980); the mouse, 670 mg/kgoral (Bubnov et al. 1969, as reported in USEPA
1980); and the. blue fox, 440 mg/kg-oral (Bubnov et al. 1969, as reported in
USEPA 1980). Subcutaneous LD50 values have been reported for the rabbit, 950
mg/kg (Christensen and Luginbyhl 1975, as reported in USEPA 1980). Minimum
lethal dose values have also been reported for the rabbit, 120 mg/kg,
(intravenous administration; Kuroda 1926, as reported in USEPA 1980); for the
guinea pig 800 mg/kg, (subcutaneous administration; Christensen and Luginbyhl
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1975, as reported in USEPA); and for the albino rat, 230 mg/kg
(intraperitoneal administration; Farquharson et al. 1958, as reported in
USEPA 1980). Symptoms of acute toxicity in rats, regardless of the route of
administration, include restlessness and increased rate of respiration,
followed by the development of motor weakness, tremors and convulsions.
Eventually, dyspnea and the appearance of coma result and continue until death
(Farquharson et al. 1958, as reported in USEPA 1980). Marked kidney injury
including red blood cells casts in the tubules, fatty infiltration of the
liver, and hemorrhages in the intestine were observed in rats following fatal
poisoning (dose unspecified; Patty 1963). Similar pathological effects were
reported for the blue fox and the mouse (Bubnor et al. 1969 as reported in
USEPA 1980). A rapid onset of convulsions was observed in mice administered
2-chlorophenol intraperitoneally (dose unspecified; Angel and Rogers 1972, as
reported in USEPA 1980).
No information is available on the subacute or chronic toxicity, nor on
the mutagenic or teratogenic potential of 2-chlorophenol. Topical application
of 0.3% dimethylbenzanthracene in benzene as an initiator followed by 20%
2-chlorophenol twice weekly for 20 weeks, promoted papillomas in mice
(Boutwell and Bosch 1959, as reported in USEPA 1980).
The acute toxicity of 2-chlorophenol on aquatic fish life is reflected by
96-hour LC50 values for the cladoceran, 2.6-7.4 mg/liter, the goldfish, 12.4
mg/liter, the fathead minnow, 11.6-14.5 mg/liter, the guppy, 20.2 mg/liter,
and the bluegill, 6.6-10 mg/liter. No effect was observed in fathead minnow
exposed to 3.9 mg/liter in a chronic test using the embryo-larval method. A
reduction in chlorophyll was observed in an alga exposed to 500 mg/liter for
72 hours indicating that plants may be less sensitive to 2-chlorophenol than
fish life. 2-Chlorophenol was found to impair the flavor of fish at
concentrations as low as 2 mg/liter (USEPA 1980).
EPA has not yet established ambient water quality criteria for
2-chlorophenol because of the lack of sufficient data.
2,4-Dichlorophenol
No information is available on the toxic effects of 2,4-dichlorophenol on
humans. In vitro studies, however, indicate that 2,4-dichlorophenol is an
uncoupler of oxidative phosphorylation (Mitsuda et al. 1963, as reported in
USEPA 1980).
Relatively few studies are available on the acute or subacute toxicity of
2,4-dichlorophenal in animals. Oral LD50 values have been reported for the
rat, 580 and 4,000 mg/kg (Derchman 1943 and Kobayashi et al. 1972, as
reported in USEPA 1980) and for the mouse, 1,600 mg/kg. (Kobayashi jit al.
1972, as reported in USEPA 1980). Acute subcutaneous and intraperitoneal LD50
values for the rat have been reported to be 1,730 mg/kg and 430 mg/kg,
respectively (Deichman 1943 and Farquharson et al. 1958 as reported in
USEPA).
In a subacute study, all mice survived when 2,4-dichlorophenol was
administered orally for 10 days at a dose of 667 mg/kg body weight (Kobayashi
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e^t al. 1972, as reported in USEPA 1980). In a six-month feeding study by
the same authors, no observed adverse changes in growth rate, hematology,
serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic
transaminase (SGPT), and behavior were reported for male mice fed dietary
levels as high as 230 mg/kg/day (Kobayashi et al. 1972, as reported in USEPA
1980). However, at the 230 mg/kg/day dosage levels, slight abnormalities in
liver histopathology were observed. These authors concluded that 100
mg/kg/day was a maximum no-effect level in mice.
No information is available on the chronic toxicity, mutagenicity or
teratogenicity of 2,4-dichlorophenol. Topical application of 0.3%
dimethylbenzanthracene in benzene as an initiator followed by 20% (312 mg/kg)
2,4-dichlorophenol twice weekly for 39 weeks promoted papillomas and
carcinomas in mice (Boutwell and Bosch 1959, as reported in NAS 1980).
The acute toxic effects of 2,4-dichlorophenol on aquatic fish life is
reflected by 96-hour LC50 values of 2.6 mg/liter for cladoceran, 2.02 mg/liter
for the bluegill and 8.23 mg/liter for the juvenile fathead minnow. Chronic
toxicity was observed in the fathead minnow exposed to concentrations ranging
from 290 to 460 yg/liter. The toxicity of 2,4-dichlorophenol to aquatic
plants occurs at much higher concentrations, ranging from 50 to 100 mg/liter
depending on the species. Flavor impairment studies showed that fish flavor
became tainted in 2,4-dichlorophenol concentrations ranging from 0.4
yg/liter for the largemouth bass to 14 yg/liter for the bluegill (USEPA
1980).
EPA has established an ambient water quality criterion of 3.09 mg/liter
for the protection of human health from the toxic properties of
2,4-dichlorophenol.
EPA has not yet established an aquatic life water quality criterion for
2,4-dichlorophenol.
2,4-Dimethylphenol
No information on the toxicity of 2,4-dimethylphenol in humans is
available (NAS 1977). Acute toxicity has been observed in rats, mice, and
rabbits (NAS 1977). Irritation of mucous membranes, enlargement of blood
vessels of the ears and extremities, and excitability followed by lethargy
were observed in rats and mice exposed by inhalation to 2,4-dimethylphenol.
In the same studies, oral LD50 values for rats and mice were reported as 3,200
mg/kg and 809 mg/kg, respectively; a dermal LD50 of 1,040 mg/kg was reported
for rats (Uzhdovini et al. 1974, as reported in USEPA 1980). Topical
papillomas have been reported in mice treated with 2,4-dimethylphenol twice
weekly for 28 weeks (Boutwell and Bosch 1959, as reported in NAS 1977).
The acute toxicity of 2,4-dimethylphenol on aquatic organisms is reflected
in the 96-hour LC50 values of 2.12 mg/liter for cladoceran, 16.75 mg/liter for
the fathead minnow, and 7.75 mg/liter for the bluegill. Chronic toxicity was
observed in the fathead minnow in concentrations ranging from 1.5 to 3.2
mg/liter. Chronic tests with invertibrate species, which appear to be most
sensitive to 2,4-dimethylphenol, have not been performed (USEPA 1980). Algae
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and duckweed were affected by concentrations of 500 mg/liter and 292.8
mg/liter, respectively. No information is available on the toxic effects of
2,4-dimethylphenol on saltwater organisms (USEPA 1980).
EPA has not yet established an ambient water quality criterion for
2,4-dimethylphenol because of the lack of sufficient information. However,
using available organoleptic data for control of undesirable taste and odor
quality of ambient water, the estimated level is 400 yg/liter.
4,6-Dinitro-o-cresol
A number of human poisonings by 4,6-dinitro-o-cresol have been reported.
4,6-Dinitro-o-cresol may be absorbed in acutely toxic amounts through the
respiratory and gastrointestinal tracts and through the skin. Signs and
symptoms of both acute and chronic poisoning include profuse sweating,
malaise, thirst, lassitude, loss of weight, headache, sensation of heat, and
yellow staining of the skin, hair, sclera, and conjunctiva. Other effects
occasionally reported include kidney damage, diarrhea, disorders of the
gastrointestinal tract, cardiovascular system, and peripheral vascular and
central nervous systems (Doull et al. 1980, and USEPA 1980). It has been
estimated that 5 mg/kg may prove fatal to humans (Fairchild 1977, as reported
in USEPA 1980). A study was conducted in which five male volunteers were
given oral doses of 75 mg/day of 4,6-dinitro-o-cresol for five consecutive
days (Harvey et al. 1951, as reported in USEPA 1980). At blood levels of 20
mg/kg, an exaggerated sense of well-being was experienced. At blood levels of
40 to 48 mg/kg, headache, lassitude, and malaise were reported. In patients
who received 4,6-dinitro-o-cresol for the treatment of obesity during the
1930s, poisonings, deaths, and the development of cataracts were reported.
Signs of poisoning occurred in three people who had taken as little as 0.35 to
1.5 mg/kg/day (NIOSH 1978, as reported in USEPA 1980). In a Russian study of
agricultural workers, exposure to 0.7 to 0.9 mg/cu m produced unspecified
changes in the blood, cardiovascular, and autonomic and central nervous
systems and in the gastrointestinal tract (Burkatskaya 1965, as reported in
USEPA 1980).
Acute oral LD50 values have been reported for the rat (30-85 mg/kg), mouse
(16.4-47 mg/kg), and rabbit (24.8 mg/kg) (USEPA 1980). LD50 values for
subcutaneous administration in the rat, mouse, and goat range from 20-50
rag/kg. 4,6-Dinitro-o-cresol is less toxic by the dermal route, with LD50s for
the mouse and rabbit of 187 and 1000 mg/kg, respectively (USEPA 1980). In a
feeding study with rats, no adverse effects were observed among rats on diets
containing 100 mg 4,6-dinitro-o-cresol/kg food. At 1000 mg/kg, observed
effects included weight loss, emaciation, unkempt appearance, and minor
histopathological effects on the liver, kidneys, and spleen (Spencer et al.
1948, as reported in USEPA 1980). Ambrose (1942, as reported in USEPA 1980)
reported no observable effects in rats fed diets containing 63 mg
4,6-dinitro-o-cresol/kg food for 105 days. At dietary levels of 125 mg/kg
food, 60 percent of the animals died. Cats exposed to airborne
4,6-dinitro-o-cresol at 0.2 mg/cu m for 2-3 months had slightly increased body
temperatures and leukocyte counts and decreased hemoglobin concentrations,
erythrocyte counts, and catalase and peroxidase activities (Burkatskaya 1965,
as reported in USEPA 1980).
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No aquatic, toxicity data are available for 4,6-dinitro-o-cresol.
EPA has established an ambient water quality criterion of 13.4 yg/liter
for protection of human health from the toxic properties of
4,6-dinitro-o-cresol through ingestion of contaminated water and aquatic
organisms.
EPA has not yet established an aquatic life water quality criterion for
4,6-dinitro-o-cresol.
2,4-Dinitrophenol
2,4-Dinitrophenol is a potent uncoupler of oxidative phosphorylation.
This prevents the utilization of energy provided by cellular respiration and
glycolysis by inhibiting the formation of high energy phosphate bonds.
2,4-Dinitrophenol may also act directly on the cell membrane causing toxic
effects on cells not dependent on oxidative phosphorylation for their energy
requirements (QSEPA 1980). Acute poisoning in humans from 2,4-dinitrophenol
results in sudden onset of pallor, burning thirst, agitation, dyspnea, profuse
sweating, and hyperpyrexia (Horner 1942, as reported in USEPA 1980).
Therapeutic doses of 2,4-dinitrophenol have resulted in skin rashes with
intense itching and considerable swelling (Tainter et al. 1933, as reported
in USEPA 1980). A loss of taste for salt and sweets has been reported in some
patients treated therapeutically with 2,4-dinitrophenol (Tainter et al.
1933, as reported in USEPA 1980). The development of cataracts in humans has
been clearly demonstrated after use of 2,4-dinitrophenol (USEPA 1980). Bone
marrow effects (agranulocytosis) and neuritis have also been reported in
humans (Horner 1942, as reported in USEPA 1980).
In animals, an increase in the percentage of stillborn young and neonatal
deaths has been reported in a study of rats treated with 20 mg/kg
2,4-dinitrophenol, 8 days prior to mating (Wulff et al. 1935, as reported in
USEPA 1980).
The acute toxicity of 2,4-dinitrophenol on freshwater aquatic organisms is
reflected in LC50 values of 4.09 mg/liter for Daphnia magna, 16.7 mg/liter
for the juvenile fathead minnow, and 0.62 mg/liter for the bluegill.
Increased respiration was observed in the tadpoles of Southern bullfrogs
exposed to 5.52 mg/liter for 7 hours. A 96-hour lethal threshold value of 0.7
mg/liter has been reported for juvenile Atlantic salmon (USEPA 1980).
Saltwater organisms are also affected by 2,4-dinitrophenol. Mysid shrimp
had a 96-hour LC50 of 4.85 mg/liter; the embryo of herring, a 96-hour LC50 of
5.5 mg/liter; and sheepshead minnow, a 96-hour LC50 of 29.4 mg/liter.
Respiration and motility were reported to be inhibited in the sperm of sea
urchin exposed to 92.0 mg/liter for more than 1 hour. Abnormal cleavage in
the embryo of the sea urchin was also reported to occur at 46 mg/liter for 2
hours. At levels of 10 mg/liter, complete mortality of Lymnaeid snails was
reported within 24 hours. The chronic effects of 2,4-dinitrophenol on
hatching and survival in an early life test with the sheepshead minnow
resulted in limits of 7.9 mg/liter (USEPA 1980).
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Freshwater plants also exhibited a toxicity to 2,4-dinitrophenol.
Chlorophyll synthesis in algae was inhibited after 3 days exposure to 50
mg/liter. A 50% reduction in growth was observed in duckweed exposed to 1.47
mg/liter. Eight-day toxicity thresholds for different species of algae varied
from 16-33 mg/liter (USEPA 1980).
EPA has established an ambient water quality criterion of 70 yg/liter
for the protection of human health from the toxic properties of total
dinitrophenols through ingested water and contaminated aquatic organisms.
EPA has not yet established an aquatic life water quality criterion for
2,4-dinitrophenol.
2-Nitrophenol
The acute toxic effects of 2-nitrophenol include kidney and liver damage
and methemoglobin formation in experimental animals (Sax 1975). Experimental
studies have shown 2-nitrophenol to inhibit chloride transport in red blood
cells in rats (Motais et al. 1978, as reported in USEPA 1980) and to
increase the platelet count in rats administered 1 mg/kg by intraperitoneal
injection (Gabor et al. 1960, as reported in USEPA 1980). Oral LD50 values
are reported for the rat and mouse as 2,830 rag/kg and 1,300 mg/kg,
respectively (Vernot et al. 1977, as reported in USEPA 1980). No other
information on the toxicity of 2-nitrophenol in human or nonhuman mammals is
available.
The 24-hour LC50s of 2-nitrophenol in freshwater organisms are 210
mg/liter for Daphnia magna and 66.9 mg/liter for juvenile bluegill.
Eight-hour exposures of gold fish to 33.3 mg/liter resulted in 38% mortality.
Shrimp showed 96-hour lethal threshold values of 32.9 mg/liter. No chronic
toxicity information is available on any aquatic organisms (USEPA 1980).
Freshwater plants were reported to be more susceptible to the effects of
2-nitrophenol than aquatic fishlife. Inhibition of chlorophyll synthesis was
observed in algae treated with 35 mg/liter for 3 days and a 50% reduction in
growth was reported in duckweed exposed to 62.5 mg/liter (USEPA 1980).
EPA has not yet established ambient water quality criteria for
2-nitrophenol because of the lack of sufficient information.
4-Nitrophenol
No information is available on the acute or chronic toxicity of
4-nitrophenol to humans (USEPA 1980). The known effects of 4-nitrophenol
demonstrated by animal studies include methemoglobinemia and shortness of
breath (Von Oettingen 1949, as reported in USEPA 1980). 4-Nitrophenol
inhibited chloride transport in rat red blood cells (Motais et al. 1978, as
reported in USEPA 1980) and increased respiratory volume in rats administered
7-12 mg by stomach tube (Grant 1959, as reported in USEPA 1980). Oral LD50s
for the rat and mouse are reported as 350 and 470 mg/kg, respectively
(Fairchild 1977, Vernot et al. 1977, as reported in USEPA 1980).
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Acute toxicity of 4-nitrophenol has been demonstrated in freshwater
aquatic fishlife. 96-Hour LC50 values reported for 4-nitrophenol for
bluegills and fathead minnows are 8.28 mg/liter and 60.5 mg/liter,
respectively. The toxicity of this compound to daphnids shows a wide
variation with values ranging from 8.4 to 21.9 mg/liter. Mortality of 42% in
goldfish was reported after 8 hours exposure to 8.0 mg/liter. 4-Nitrophenol
produced 96-hour LCSOs of 7.17 mg/liter in mysid shrimp and 27.1 mg/liter in
the sheepshead minnow. 96-Hour lethal threshold values for shrimp and
soft-shell clams were reported to be 26.4 and 29.4 mg/liter, respectively
(USEPA 1980).
Chronic studies on hatching and survival in the early life stage test
showed toxic effects in concentrations ranging from 10 to 16 mg/liter for
sheepshead minnows. No other information is available on the chronic effects
on aquatic organisms (USEPA 1980).
Inhibition of chlorophyll synthesis was reported in alga exposed to 25
mg/liter after 3 days. Growth inhibition of 50% was also reported in alga
exposed to 6.95 mg/liter for 80 hours and in duckweed exposed to 9.45 mg/liter
(USSPA 1980).
EPA has not yet established ambient water quality water criteria for
4-nitrophenol because of the lack of sufficient information.
Pentachlorophenol
Exposure of pentachlorophenol in humans has been reported to cause loss of
appetite, eye irritation, respiratory difficulties, anesthesia, hyperpyrexia,
sweating, dyspnea, skin irritation, and rapidly progressive coma (Menon 1958,
as reported in NAS 1977). The minimum lethal dose for humans is estimated to
be 29 mg/kg (Toxic Substance List 1974, as reported in NAS 1977). Chronic
exposure to pentachlorophenol has been associated with the development of
chloracne, a type of acneform dermatitis (Baader and Bauer 1951 and Nomura
1953, as reported in USEPA 1980). Nonfatal chronic exposures can produce
muscle weakness, headache, anorexia, abdominal pain, and weight loss, in
addition to skin, eye, and respiratory irritation (USEPA 1980).
Acute symptoms in animals include vomiting, hyperpyrexia, elevated blood
pressure, increased respiration rate, and tachycardia (NAS 1980). The acute
oral LD50s for pentachlorophenol are reported in the ranges of 120-140 mg/kg
for the mouse, 27-100 mg/kg for the rat, 100 mg/kg for the guinea pig, 100-130
mg/kg for the rabbit, and 150-200 mg/kg for the dog (Christensen et al.
1974, Deichmanri et al. 1942, Knudsen et al. 1974, McGavack et al. 1941,
Stohlman 1951, as reported in NAS 1977). Teratogenic effects have been
reported in rats orally administered amounts up to 50 mg/kg/day during day
6-15 of gestation (Schwetz et al. 1974, as reported in NAS 1977). No
evidence of mutagenicity was found in several short-term bioassays (Anderson
et al. 1972, Fahrig et al. 1978, Vogel and Chandler 1974, Buselmaier et
al. 1973, as reported in USEPA 1980).
Dermal application of a 20% solution of pentachlorophenol dissolved in
benzene did not increase the rate of papillomas in mice pretreated with
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dimethylbenzanthracene (Boutwell and Bosch 1959, as reported in USEPA 1980).
Mice dosed with commercial pentachlorophenol at 46.4 mg/kg from 7-28 days of
age and then fed 130 ppm in the diet for the remainder of their life did not
have a significant increase in tumors (Innes et al. 1969, as reported in
USEPA, 1980) . No effect was also observed in rats fed amounts up to 30 mg/kg
for 22-24 months (Schwetz et al. 1978, as reported in USEPA 1980).
Pentachlorophenol has been shown to be acutely toxic to a wide variety of
freshwater fish. No chronic test data are available. For nine fish species
tested, the 96-hour LC50 values ranged from 37 to 340 yg/liter. Toxicity
tests gave 96-hour LC50 values ranging from 50-130 yg/liter in sockeye
salmon, from 60-77 yg/liter in the bluegill, and 340 yg/liter in fathead
minnows (USEPA 1980).
Saltwater marine life are also affected by pentachlorophenol. Adjusted
96-hour LC50 values for sheepshead minnows, pinfish, and striped mullet ranged
from 21 to 442 yg/liter. Pentachlorophenol appears to be most toxic to
molluscs; shrimp are less sensitive and oysters more sensitive than fish.
Oyster embryos develop abnormally when exposed to 55 yg/liter for 48 hours.
Lugworm feeding activity was significantly inhibited by concentrations of 80
yg/liter pentachlorophenol during a 144-hour exposure. Chronic studies of
saltwater organisms show that 195 yg/liter significantly reduced hatching of
embryos spawned by exposed parental fish and reduced survival of second
generation sheepshead minnows in a 151-day life cycle exposure (USEPA 1980).
In plant tests, pentachlorophenol caused complete destruction of
chlorophyll in algae in 72 hours at 7.5 yg/liter, and in kelp in 4 days at
2.66 rag/liter (USEPA 1980).
EPA has established an ambient water quality criterion of 1.01 mg/liter
for protection of public health from the toxic properties of pentachlorophenol
ingested through water and contaminated fish.
EPA has not yet established an aquatic life water quality criterion for
pentachlorophenol.
Phenol
The predominant effect of phenol on humans is on the central nervous
system leading to sudden collapse and unconsciousness (USEPA 1980). Numerous
cases of phenol toxicity resulting from occupational exposures have reported
symptoms including shock, collapse, coma, convulsions, cyanosis, and death
(StajduhavCaric 1968, Noury 1940, Johstone and Miller 1960, Cronin and Brauer
1949, Duvernevil and Ravier 1962, Abraham 1972, Light 1931, as reported in
USEPA 1980).
People who had consumed estimated daily doses of 10-240 mg phenol in well
water for approximately 1 month developed burning of the mouth, mouth sores,
diarrhea, headaches, skin rashes, abdominal pain, dizziness, and dark urine
(Baker et al. 1978, as reported in USEPA 1980).
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The toxic effects observed in animals are quite similar to those in
humans. The pathological changes produced by phenol in animals vary with the
route of absorption, vehicle employed, concentration, and duration of
exposure. Local damages to the skin include eczema, inflammation,
discoloration, papillomas, necrosis, sloughing, and gangrene. Following oral
ingestion, the mucous membranes of the throat and esophagus may show swelling,
corrosions, and necroses, with hemorrhage and serious infiltration of the
surrounding areas. In a severe intoxication, the lungs may show hyperemia,
infarcts, bronchopneumonia, purulent bronchitis, and hyperplasia of the
peribronchial tissues. There can be myocardial degeneration and necrosis.
The hepatic cells may be enlarged, pale, and coarsely granular with swollen,
fragmented, and pyknotic nuclei. Prolonged administration of phenol may cause
parenchymatous nephritis, hyperemia of the glomerular and cortical regions,
cloudy swelling, edema of the convoluted tubules, and degenerative changes of
the glomeruli. Blood cells become hyaline, vacuolated, or filled with
granules. Muscle fibers show marked striation (Deichman and Keplinger 1963,
as reported in USEPA 1980).
The acute toxicity of phenols in mammals ranges from an oral LD50 of 100
mg/kg in the cat (Macht 1915, as reported in USEPA 1980) to 620 mg/kg in the
rabbit (Clark and Brown 1906, as reported in USEPA 1980). Pathological
changes reported in mammals include intense congestion of the peritoneum,
abdominal viscera, kidney and adrenals, and marked degenerative changes in the
kidney. In rats fed 8,000 mg/liter in their drinking water over two
generations, there were reduced growth rates in the young with many deaths
(Heller and Pursell 1938, as reported in USEPA 1980). In another study, no
effects were observed in rats fed for 12 months at concentrations as high as
2,400 mg/liter in the drinking water (Diechmann and Oesper 1940, as reported
in USEPA 1980). Slight kidney and liver effects were reported in rats
administered 20 daily doses of 0.1 g/kg by gavage (Unpublished report of Dow
Chemical 1976, as reported in USEPA 1980). Skin painting studies of mice
exposed to 20% phenol concentrations have produced skin ulcerations, exhibited
strong promoting action on tumor development, and exhibited a weak
carcinogenic response (Salaman and Glendenning 1957, as reported in USEPA
1980).
The acute toxicity of phenol to freshwater vertebrates ranges from 44.5
mg/liter at 96 hours for the goldfish to 10.2 mg/liter for rainbow trout.
Rainbow trout was the most sensitive species tested with a 24-hour LC50 of 5.0
mg/liter for embryos. Juvenile rainbow trout were killed at 6.5 mg/liter
phenol in 2 hours. At these concentrations, there was rapid damage to gills
and severe pathology of other tissues. Typical gross pathological changes
have also been reported and include internal hemorrhages, deterioration of
gill membranes, degradation of the liver, and brain damage. Phenol appears to
act as a nerve poison causing too much blood to flow to the gills and to the
heart cavity of the fish. Pathological changes in the gills and in fish
tissue have been found at concentrations of 20-70 ug/liter. Phenol is
acutely toxic to freshwater invertebrates, although it appears to be less
toxic to fish food organisms and lower aquatic life than to fish. The 48-hour
LC50 for the freshwater flea is 9.6 mg/liter. A concentration of 2.0 mg/liter
inhibited egg development in oysters and reduced oxygen consumption
approximately 50% in the freshwater snail. Phenols inhibit chlorophyll
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synthesis, and cause complete destruction of algae at concentrations of 50 and
1,500 mg/liter, respectively (USEPA 1980).
EPA has established an ambient water quality criterion of 3.5 mg/liter for
the protection of human health from the toxic properties of phenol through
ingestion of contaminated water and contaminated aquatic organisms.
EPA has not yet established an aquatic life water quality criterion for
phenol.
2,4,6-Trichlorophenol
No information is available on the toxic effects of 2,4,6-trichlorophenol
on humans. In animal studies, a number of different adverse effects have been
observed. Convulsions were produced in rats injected intraperitoneally with
2,4,6-trichlorophenol during an acute toxicity test. The LD50 was estimated
at 276 mg/kg in this test (Farquharson et al. 1958, as reported in USEPA
1980). 2,4,6-Trichlorophenol was reported to cause inhibition of lactate
dehydrogenase and hexokinase, in. vitro, in concentrations ranging from
0.0028-0.005 Molar (species unspecified; Stockdale and Selwyn 1971, as
reported in USEPA 1980). 2,4,6-Trichlorophenol was shown to penetrate the
rabbit eye with the highest amounts concentrating in the cornea and
conjunctiva (Ismail et al. 1975, as reported in USEPA 1980). However, the
significance of this finding has not yet been established.
No information is available on the subacute or chronic effects of
2,4,6-trichlorophenol. In a mutagenicity study using a strain of
Saccharomyces cerevisiae, 400 mg of 2,4,6-trichlorophenol increased the
mutation rate (Fahrig et al. 1978, as reported in USEPA 1980). Evidence of
a genetic change in the offspring of mothers administered 50 or 100 mg/kg of
2,4,6-trichlorophenol on day 10 of gestation was reported in a mouse spot test
(Fahrig et aj.. 1978, as reported in USEPA 1980). 2,4,6-Trichlorophenol was
negative in the Salmonella-mammalian microsome Ames test (Rasanen et al.
1977, as reported in USEPA 1980). In a lifetime feeding study,
2,4,6-trichlorophenol was shown to be carcinogenic in male rats, including
lymphomas or leukemias, and in both male and female mice, including
hepatocellular carcinomas or adenomas. Both tests were conducted with dosage
levels of approximately 5,000 ppm in the diet (NCI 1979, as reported in USEPA
1980). The topical application of a 20% solution of 2,4,6-trichlorophenol in
benzene did not increase the incidence of papillomas in mice pretreated with
dimethylbenzanthracene (Boutwell and Bosch 1958, as reported in USEPA 1980).
The acute toxicity of 2,4,6-trichlorophenol on aquatic life is reflected
by the following 96-hour LC50 values for the cladoceran, 6 mg/liter, the
fathead minnow, 0.6 mg/liter, the juvenile fathead minnow, 9 mg/liter, and the
bluegill, 0.3 mg/liter. Chronic toxicity was observed in an early life stage
test using fathead minnow exposed to concentrations ranging from 0.53-0.97
mg/liter. One hundred percent mortality was observed in lymnaeid snails
exposed to 5 mg/liter for 24 hours. The highest estimated concentration (ETC)
of 2,4,6-trichlorophenol that will not impair the flavor of fish is 52
ug/liter for a 48-hour exposure of rainbow trout. Complete destruction of
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chlorophyll was observed in an alga exposed to 10 mg/liter and chlorosis was
reported in duckweed exposed to 5.9 mg/liter (USEPA 1980).
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to 2,4,6-trichlorophenol through ingestion of contaminated water
and contaminated aquatic organisms. However, since a zero level may not be
attainable at present, a level of 1.2 yg/liter, corresponding to a lifetime
incremental cancer risk of 10-6, was recommended.
EPA has not yet established an aquatic life water quality criterion for
2,4,6-trichlorophenol.
3. Base/Neutral Extractable Organic Compounds
Acenaphthene
Very little information on the toxic effects of acenaphthene in humans is
available. It is irritating to skin and mucous membranes, and may cause
vomiting if swallowed in large quantities (Sax 1975). In animals, oral
administration of 2 g/kg daily for 32 days was reported to cause loss of body
weight, changes in peripheral blood, heightened amino transferase levels in
blood serum, and mild morphological damage to both liver and kidneys in rats.
In the same studies, oral LDSOs for rats and mice were 10 g/kg and 2.7 g/kg,
respectively (Knoblock et al. 1969, as reported in USEPA 1980). Chronic
inhalation studies showed toxic effects to the blood, lungs, and glandular
constituents in rats exposed to 12 mg/cu m, 4 hours per day, six days per week
for 5 months (Reshetyuk et al. 1970, as reported in USEPA 1980).
No information is available on the teratogenicity of acenaphthene and the
only data on mutagenicity, using microoganisms as the indicator system, were
negative (USEPA 1980). Very little work has been done to determine whether
acenaphthene may have carcinogenic potential. Negative results were obtained
in the newt with acenaphthene injected subcutaneously (dosage not reported,
USEPA 1980). The only other carcinogenicity studies available involve
acenaphthene as a component of a complex mixture of polycyclic aromatic
hydrocarbons (USEPA 1980).
In one study, isolated polycyclic hydrocarbon-rich fractions from the
neutral portion of cigarette smoke condensate were applied (dose unspecified)
to the dorsal skin of female mice, five times a week for 13 months. The
acenaphthene containing extracts were applied five weeks after the animals
were painted once with 125 ug of 7,12-dimethylbenz(a)anthracene. No
significant tumor-promoting activity over controls were observed (Akin et
al., 1976 as reported in USEPA 1980). In a second study benzene extracts, of
gasoline exhaust condensates containing an unspecified concentration of
acenapthene, were reported to be carcinogenic in mouse skin painting studies
(details unspecified; Hoffman and Wynder, 1962 as reported in USEPA 1980).
The most thoroughly investigated effect of acenaphthene is its ability to
produce nuclear and cytological changes in microbial and plant species. Most
of these changes, such as an increase in cell size and DNA content, are
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associated with disruption of the spindle mechanisms during mitosis and the
resulting induction of polyploidy (USEPA 1980).
The acute toxicity of acenaphthene to aquatic organisms is reflected in a
static 48-hour LC50 of 41.2 mg/liter for Daphnia magna; and static 96-hour
LC50 values of 1.7 mg/liter in the bluegill, 0.97 mg/liter in the mysid shrimp
and 2.23 mg/liter in the sheepshead minnow. Chronic toxicity by the
embryo-larval test was observed in the sheepshead minnow. Algae were affected
at 500-530 yg/liter. Bluegill were reported to accumulate acenaphthalene
during a 28-day exposure and a bioconcentration factor of 387 was reported for
this same species (USEPA 1980).
Sufficient data were not available for EPA to establish ambient water
quality criteria that would protect human health against the potential
toxicity of acenaphthene. However, a level of 0.02 mg/liter was recommended
based on available organoleptic data, for controlling undesirable taste and
odor quality of ambient water.
EPA has not yet established an aquatic life water quality criterion for
acenaphthene.
Acenaphthylene
No information is available on the toxic effect of acenaphthylene on
humans, animals, or aquatic life. EPA has not yet established ambient water
quality criteria for acenaphthylene because of the lack of sufficient data.
However, the agency has established an ambient water quality criterion of zero
for the maximum protection of human health from the potential carcinogenic
effects due to exposure to polynuclear aromatic hydrocarbons, which include
acenaphthylene, through ingestion of contaminated water and contaminated
aquatic organisms. However, since a zero level may not be attainable at
present, a level of 2.8 ng/liter, corresponding to a lifetime incremental
cancer risk of 10-6, was recommended.
Anthracene
No information is available on the toxicity of pure anthracene to humans.
However, anthracene oils can cause headaches, nausea, loss of appetite, skin
rashes, and irritation of the mucous membranes (Encyclopedia of Occupational
Health and Safety 1971). Various oils of anthracene and substances containing
anthracene have also been associated with carcinogenesis in animals (Searle
1976). Anthracene exhibits relatively low toxicity to animals. The acute
oral toxicity in rats is greater than 3,200 mg/kg. Large oral doses in rats
caused reaction of the abdominal wall, rough coat, and diarrhea (Patty 1963).
Anthracene applied to the backs of guinea pigs caused a slight skin irritation
on the pig skin (Patty 1963). No information is available on the carcinogenic
effects of pure anthracene.
There is limited information on the toxicity of anthracene to aquatic
organisms. A 90% lethal photodynamic response was observed in protozon
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exposed to 0.1 yg/liter for 60 minutes. Bioconcentration factors ranged
from 200 in the Daphnia magna to 3,500 in the may fly (USEPA 1980).
EPA has not yet established ambient water quality criteria for anthracene
because of the lack of sufficient data. However, the agency has established
an ambient water quality criterion of zero for the maximum protection of human
health from the potential carcinogenic effects due to exposure to polynuclear
aromatic hydrocarbons, which include anthracene, through ingestion of
contaminated water and contaminated aquatic organisms. However, since a zero
level may not be attainable at present, a level of 2.8 ng/liter, corresponding
to a lifetime incremental cancer risk of 10-6, was recommended.
Benz(a)anthracene
No information is available on the toxic effects of benz(a)- anthracene on
humans. Most of the studies in animals have been conducted to evaluate the
carcinogenic potential of benz(a)anthracene. This is especially true of the
derivatives of benz(a)anthracene. Benz(a)anthracene has been shown to be
carcinogenic Ln the mouse by several routes of administration (IARC 1973).
Oral administration of 1.5 mg as a 3% solution in "methocelaerosol OF" by
stomach tube, for 15 treatments over a 5-week period, resulted in the
development of hepatomas and lung adenomas (Klein 1963, as reported in IARC
1973). Skin tumors developed when benz(a)anthracene was applied topically 3
times a week, to mice, in a 1% concentration in toluene and a 0.002%
concentration in n-dodecane (Bingham and Falk 1969, as reported in IARC
1973). Sarcomas were also produced in mice following subcutaneous injections
with as low as 50 yg administered as a single dose (Steiner and Edgecomb
1952, as repotted in IARC 1973). No information is available on the
mutagenicity or teratogenicity of benz(a)anthracene (USEPA 1980).
The only information available on the toxic effects of benz(a)anthracene
on aquatic life is a 6-month study of bluegill exposed to 1.0 mg/liter. In
this study, 87% mortality was observed (USEPA 1980).
EPA has not yet established ambient water quality criteria for
benz(a)anthracene because of the lack of sufficient data. However, the agency
has established an ambient water quality criterion of zero for the maximum
protection of human health from the potential carcinogenic effects due to
exposure to polynuclear aromatic hydrocarbons, which include
benz(a)anthracene, through ingestion of contaminated water and contaminated
aquatic organisms. However, since the zero level may not be attainable at
present, a level of 2.8 ng/liter, corresponding to a lifetime incremental
cancer risk of 10-6, was recommended.
Benzidine
Epidemiological studies show that occupational exposure to benzidine is
strongly associated with bladder cancer. A high incidence of bladder tumors
was reported in workmen exposed to benzidine or benzidine and aniline in
British chemical factories. Thirty cases of bladder tumors were reported,
with a mean latent period of ten years (Case et al. 1954, as reported in
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USEPA 1980). In a retrospective study of a single factory, 17 of 76 workmen
exposed to benzidine alone developed bladder tumors (Goldwater et al. 1965,
as reported in IARC 1972). Bladder cancer has been reported in several
studies of Italian dyestuff workers. In a study by Barsotti and Vigliani
(1952, as reported in USEPA 1980), 13 of 83 workers developed bladder
carcinomas from exposure to benzidine during the period 1931 to 1948.
Dermatitis and increased urinary fJ-glucuronidase activity have also been
reported in workers exposed to benzidine (USEPA 1980).
Benzidine is also carcinogenic to experimental animals. Cholangiomas and
liver-cell tumors were reported in lifetime feeding studies with rats fed
0.017% benzidine in the diet and hamsters fed 0.1% in the diet (Boyland et
al. 1954, Saffiotti et al. 1967, as reported in IARC 1972). Three of seven
dogs given 200-300 mg/day, 6 days/week, for 5 years developed bladder
carcinomas seven to nine years after the start of treatment (Spitz et al.
1950, as reported in IARC 1972). Benzidine administered subcutaneously to
rats at a dose of 15 rag/week for their lifespan produced liver injury,
cirrhosis, hepatomas, sebaceous gland carcinomas, and adenocarcinomas of the
rectum (Spritz et al. 1950, as reported in USEPA 1980). A cumulative dose
of 0.75 mg/kg of benzidine given subcutaneously for 15 days produced tumors in
20 of 22 rats, including hepatomas, cholangiomas, intestinal tumors, and
sebaceous gland carcinomas (Holland et al. 1974, as reported in USEPA
1980). Hepatomas have been reported in mice given subcutaneous injections of
benzidine (USEPA 1980).
In addition to its carcinogenic activity, benzidine also causes a
reduction in catalase and peroxidase activity, a reduction in erythrocytes and
thrombocytes, and an increase in leukocytes when injected in rats (Soloimskaya
1968, as reported in USEPA 1980). Neish (1967, as reported in USEPA 1980)
reported that an intraperitoneal dose of 12.7 mg/kg in rats increased liver
glutathione levels. Benzidine is mutagenic in the Ames assay with Salmonella
typhimurium and gave positive results in a DNA synthesis inhibition test with
HeLa cells (USEPA 1980).
Limited toxicity data are available for aquatic organisms. The 96-hour
LC50 for rainbow trout and lake trout, red shiner, and the flagfish range from
2,500 to 16,200 yg/liter. Chronic toxicity data for freshwater organisms
are not available. No saltwater organisms have been tested with benzidine
(USEPA 1980).
EPA has established an ambient water quality criterion of zero for maximum
protection of human health from the potential carcinogenic effects due to
exposure to benzidine through the ingestion of contaminated water and aquatic
organisms. However, since the zero level may not be attainable at the present
time, a level of 0.00012 yg/liter corresponding to a lifetime incremental
cancer risk of 0.000001 was recommended.
EPA has not yet established an aquatic life water quality criterion for
benzidine.
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3,4-Benzofluoranthene
3,4-Benzofluoranthene is a member of the class of polynuclear aromatic
hydrocarbons (PAHs). Many members of this class of chemicals are
carcinogenic. 3,4-Benzofluoranthene has produced skin tumors in mice
following repeated skin painting. Three groups of mice were painted with
0.01, 0.1, or 0.5% solutions of 3,4-benzofluoranthene in acetone three times
per week. After 8-12 months, the incidence of carcinomas in the survivors was
0%, 85%, and 90% (Wynder and Hoffman 1958, as reported in IARC 1973). In a
later study, a single dermal application of 1 mg in acetone produced no tumors
in mice after 63 weeks; the same procedure followed by repeated paintings with
croton resin produced carcinomas in 5 of 20 mice (Van Duuren et al. 1966, as
reported by IARC 1973). 3,4-Benzofluoranthene also produced sarcomas in mice
at the site of injection after 3 subcutaneous injections of 0.6 mg of the
compound over a two month period (Lacassagne et al. 1963, as reported in
IARC 1973).
No human case studies or epidemiological studies have been conducted which
establish 3,4-benzofluoranthene as a human carcinogen. Indirect evidence for
the compound's carcinogenicity comes from air pollution studies which indicate
an excess of lung cancer mortality among workers exposed to high
concentrations of PAH-containing material such as coal gas, tars, soot, and
coke oven emissions (IARC 1973, USEPA 1980).
No data are available on the aquatic toxicity of 3,4-benzofluoran- thene.
EPA has not yet established ambient water quality criteria for
3,4-benzofluoranthene itself because of the lack of sufficient data. However,
the agency has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to polynuclear aromatic hydrocarbons, which include
3,4-benzofluoranthene, through ingestion of contaminated water and aquatic
organisms. Since the zero level may not be attainable at present, a level of
2.8 ng/liter corresponding to a lifetime incremental cancer risk of 0.000001
was recommended.
Benzo(k)fluoranthene
No information is available on the toxic effects of benzo(k)fluoranthene
in humans, animals, or aquatic organisms.
EPA has not yet established ambient water quality criteria for
benzo(k)fluoranthene because of the lack of sufficient data. However, the
agency has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to polynuclear aromatic hydrocarbons, which include
benzo(k)fluoranthene, through ingestion of contaminated water and aquatic
organisms. Since a zero level may not be obtainable at present, a level of
2.8 ng/liter, corresponding to a lifetime incremental cancer risk of 0.000001,
was recommended.
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Benzo(g,h,i)perylene
Benzo(g,h,i)perylene is a member of the class of polynuclear aromatic
hydrocarbons (PAHs), many of which are known for their ability to induce
cancer.
No data are available on the aquatic or mammalian toxicity of
benzo(g,h,i)perylene. This compound has not been identified as a carcinogen;
however, benzo(g,h,i)perylene acted as a cocarcinogen when applied with
benzo(a)pyrene, a known carcinogen, to the skin of mice at a dose of 2 mg, 3
times per week, for 52 weeks (Van Duuren et al. 1973 and 1976, as reported
in USEPA 1980).
EPA has not yet established ambient water quality criteria for
benzo(g,h,i)perylene because of the lack of sufficient data. However, the
agency has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to polynuclear aromatic hydrocarbons through ingestion of
contaminated water and contaminated aquatic organisms. Since a zero level may
not be attainable at present, a level of 2.8 ng/liter corresponding to a
lifetime incremental cancer risk of 0.000001 was recommended.
Benzo(a)pyrene
Benzo(a)pyrene is a member of the class of polynuclear aromatic
hydrocarbons (PAHs) and is a well-known animal carcinogen. Administration of
50-250 ppm in the diet to mice for 122 to 197 days resulted in a greater than
70 percent incidence of stomach tumors (Neal and Ridgon 1976, as reported in
IARC 1973). Leukemias, lung adenomas, and stomach tumors were produced in
mice by dietary administration of 250 ppm benzo(a)pyrene for 140 days (Rigdon
and Neal, 1969, as reported in IARC 1973). In hamsters and rats, oral
administration of benzo(a)pyrene produced tumors of the esophagus,
forestomach, and intestine (IARC 1973).
Benzo(a)pyrene is also carcinogenic when administered by intratracheal
instillation. Instillation of 3.25 to 52 mg once weekly for 52 weeks in
Syrian golden hamsters produced a respiratory tract tumor incidence of 10 to
93 percent (Feron et al. 1973, as reported in USEPA 1980).
Many experiments have been conducted involving repeated application to the
skin or subcutaneous and intramuscular injection. In skin painting studies,
the threshold dose to induce tumors is dependent on the species and strain of
animal tested and the vehicle used. Thrice weekly applications of
benzo(a)pyrene in acetone to CAF1 mice produced papillomas and carcinomas at a
concentration as low as 0.001% benzo(a)pyrene (Wynder et al. 1957, as
reported in IARC 1973). In a subcutaneous carcinogenicity study using C57
mice, injection of benzo(a)pyrene in oil at doses of 0.00004, 0.0004, 0.004,
and 0.04 mg produced sarcomas in, respectively, 0, 1, 5, and 23 mice of groups
of 50 (Hieger 1959, as reported in IARC 1973).
Little information on other potential toxic effects of benzo(a)pyrene is
available. Benzo(a)pyrene has been shown to have little effect on fertility
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or on the developing embryo in several mammalian and nonmammalian studies
(USEPA 1980). Benzo(a)pyrene induced damage to the bronchial epithelium of
Syrian golden hamsters in animals treated intratracheally with 0.63 mg
benzo(a)pyrene (total dose) dispersed in various vehicles once weekly for life
(Reznik-Schuller and Mohr 1974, as reported in USEPA 1980).
No human case studies or epidemiologic studies have been conducted which
establish benzo(a)pyrene as a human carcinogen. Indirect evidence for the
compound's carcinogenicity comes from air pollution studies which indicate an
excess of lung cancer mortality among workers exposed to high concentrations
of PAH-containing material such as coal gas, tars, soot, and coke-oven
emissions (IARC 1973, USEPA 1980).
No data are available on the aquatic toxicity of benzo(a)pyrene.
EPA has not yet established ambient water quality criteria for
benzo(a)pyrene because of the lack of sufficient data. However, the agency
has established an ambient water quality criterion of zero for the maximum
protection of human health from the potential carcinogenic effects due to
exposure to polynuclear aromatic hydrocarbons through ingestion of
contaminated water and aquatic organisms. Since the zero level may not be
attainable at present, a level of 2.8 ng/liter corresponding to a lifetime
incremental cancer risk of 0.000001 was recommended.
Bis(2-chloroethoxy) methane
No toxicity data for bis(2-chloroethoxy) methane in humans are available,
and only limited acute toxicity information in animals has been published.
Acute LD50 values for the rat by oral administration and for the guinea pig by
dermal administration have been given as 65 mg/kg and 170 mg/kg, respectively
(NIOSH 1980). Unspecified toxic effects were observed in rats exposed to 62
ppm bis(2-chloroethoxy) methane vapors for four hours (NIOSH 1980). No
chronic studies for this compound have been conducted.
No aquatic toxicity data are available for bis(2-chloroethoxy) methane.
Available data for the class of chloroalkyl ethers indicate that acute
toxicity to freshwater aquatic life occurs at concentrations as low as 238
mg/liter (USEPA 1980).
EPA has not yet established ambient water quality criteria for
bis(2-chloroethoxy) methane because of the lack of sufficient data.
Bis(2-chloroethyl) Ether
Bis(2-chloroethyl) ether is moderately persistent and insoluble in water.
Toxic effects of exposure to bis(2-chloroethyl) ether have been observed in
humans. Exposure to 550 ppm was intolerable and caused irritation of the eyes
and nasal passages. Bis(2-chloroethyl) ether can also affect the kidney and
liver (Sax 1975).
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A wide variety of acute effects has been observed in animals. Guinea pigs
exposed to 500-1,000 ppm by inhalation immediately developed severe eye and
nasal irritation and in 3 hours developed respiratory disturbances and death
with pulmonary lesions. Autopsy revealed congestion of the lungs and upper
respiratory tract, pulmonary edema, and congestion of the liver, brain, and
kidney (Schrenk et al. 1933, as reported in USEPA 1980). Oral LDSOs have
been reported as 75-150 mg/kg for rats, 136 mg/kg for mice, and 126 mg/kg for
rabbits. Only mild physiological stress has been observed in animals exposed
chronically to bis(2-chloroethyl) ether. Bis(2-chloroethyl) ether at 300
mg/kg administered orally or by intraperitoneal injection for 80 weeks
produced an increased incidence of liver tumors in mice (Innes et al. 1969,
as reported in USEPA 1980).
No information is available on the toxic effects of bis(2- chloroethyl)
ether on aquatic fish or plant life (USEPA 1980).
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to bis(2-chloroethyl) ether through ingestion of contaminated
water and contaminated aquatic organisms. Since the zero level may not be
attainable at the present time, a level of 0.030 yg/liter, corresponding to
a lifetime incremental risk of 0.000001, was recommended.
EPA has not yet established an aquatic life water quality criterion for
bis(2-chloroethyl) ether.
Bis(2-chloroisopropyl) Ether
No evidence of human toxicity from exposure to bis(2-chloro- isopropyl)
ether is available. Acute toxicity of bis(2-chloroisopropyl) ether has been
reported in rats exposed by inhalation to 350 ppm for eight, 5-hour
exposures. Toxic effects included respiratory difficulty, lethargy, retarded
weight gain, and congestion of the liver and kidneys. Lethargy and retarded
weight gain were also observed in rats exposed to 70 ppm for 20, 6-hour
exposures (Gage 1979, as reported in USEPA 1980). An oral LD50 for the rat
was established as 240 mg/kg and a dermal LD50 for the rabbit is reported as
3,000 mg/kg (Smyth et al. 1951, as reported in USEPA 1980).
In a chronic oral toxicity study, the major toxic effects observed in the
rat exposed to 200 mg/kg/day for a total of 728 days were on the lungs, where
congestion, pneumonia, and aspiration were noted. Centrilobular necrosis of
the liver, hyperkeratosis of the esophagus, and agiectasis of the adrenal
cortex were also reported. In this same experiment, mice exposed to 10
mg/kg/day also developed centrilobular necrosis of the liver (NCI, unpublished
as reported in USEPA 1980). Bis(2-chloroisopropyl) ether is mutagenic in in
vitro assays (USEPA 1980). Tumors were induced by bis(2-chloroisopropyl)
ether in rats and mice fed 200 and 25 mg/kg/day respectively for 5 days per
week for two years. However, the significance of this result has not been
fully determined because of high tumor incidence in controls (NCI, unpublished
as reported in USEPA 1980).
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No information is available on the toxicity of bis(2-chloroisopropyl)
ether on aquatic organisms (USEPA 1980).
EPA has established a limit of 3.47 yg/liter for the protection of human
health against the toxic properties of bis(2-chloroisopropyl) ether through
ingestion of water and contaminated aquatic organisms.
EPA has not yet established an aquatic life water quality criterion for
bis(2-chloroisopropyl) ether.
Bis-2-ethylhexyl Phthalate
Toxic effects of bis-2-ethylhexyl phthalate in humans have not been
reported. In chronic animal studies, liver and kidney weights increased in
both the parental (PI) generation of rats fed 0.4% bis-2-ethylhexyl phthalate
for a maximum of 2 years and in their offspring also fed 0.4% bis-2-ethylhexyl
phthalate for 1 year; and in a second study, at 0.5% for up to 2 years
(Carpenter 1953 and Harris et al. 1956, as reported in USEPA 1980). Liver
damage was reported in monkeys exposed to bis-2-ethylhexyl phthalate
solubilized in blood (administered as transfusions) in concentrations ranging
from 6.6 to 33 mg/kg for periods ranging from 6 months to 1 year (Kevy et
al. 1978, as reported in USEPA 1980). Tubular atrophy and degeneration in
the testes were observed in rats administered bis-2-ethylhexyl phthalate in
the diet at 1.5 and 3.0% for 90 days (Shaffer et al. 1945, as reported in
USEPA 1980). Oral LD50 values have been reported in the rat as 26.0 mg/kg,
and in the rabbit as 34.0 mg/kg. A dermal LD50 has been reported in the
guinea pig as 10.0 mg/kg (Autian 1973, as reported in USEPA 1980).
Dose-related skeletal abnormalities and reduced fetal weight were reported in
rats administered 5 ml/kg bis-2-ethylhexyl phthalate by intraperitoneal
injection during days 5, 10, and 15 of gestation (Singh et al. 1972, as
reported in USEPA 1980).
In a recent National Cancer Institute/National Toxicology Program bioassay
(NTP 1982), bis-2-ethylhexyl phthalate was carcinogenic to both rats and mice
fed diets containing the test chemical at concentrations of 6,000 or 12,000
ppm (rats) and 3,000 or 6,000 ppm (mice) for 103 weeks. An increased
incidence of hepatocellular carcinomas was observed in high dose female rats
and male mice and in both groups of female mice. In addition, degeneration of
the seminiferous tubules was observed in the high-dose male rats and mice, and
hypertrophy of the cells in the anterior pituitary was found in the high-dose
male rats.
In freshwater aquatic life 48-hour LC50 values ranging from 1 to 5
mg/liter, for Daphnia magna and greater than 18 mg/liter for the midge have
been reported. The 96-hour LC50 values were reported as greater than 32
mg/liter for the scud and greater than 770 mg/liter for the bluegill.
Significant increase in total body protein catabolism was reported in rainbow
trout exposed to 14-54 yg/liter for 24 days. Bis-2-ethylhexyl phthalate at
100 yg/g in the diet of the guppy caused an increase in abortions.
Significant reproductive impairment in Daphnia magna was reported after
chronic exposure to bis-2-ethylhexyl phthalate at 3 yg/liter. No other
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information was available on the chronic toxic effects of bis-2-ethylhexyl
phthalate or on its toxic effects in aquatic plantlife (USEPA 1980).
EPA has established an ambient water quality criterion of 15 mg/liter for
the protection of human health from the toxic properties of bis-2-ethylhexyl
phthalate ingested through water and contaminated aquatic organisms.
EPA has not yet established an aquatic life water quality criterion for
bis-2-ethylhexyl phthalate.
4-Bromophenyl Phenyl Ether
No human or mammalian toxicity data are available for 4-bromophenyl phenyl
ether.
Limited aquatic toxicity data are available for 4-bromophenyl phenyl
ether. For Daphnia magna, the 48-hour EC50 is 360 ug/liter, and the
96-hour LC50 for the bluegill is 4,940 yg/liter. In an embryo-larval test
with the fathead minnow, adverse effects on survival and growth were observed
at 122 ug/liter (USEPA 1980).
EPA has not yet established ambient water quality criteria for
4-bromophenyl phenyl ether because of the lack of sufficient data.
Butyl Benzyl Phthalate
Butyl benzyl phthalate is not known to be toxic to humans. A Russian
report suggests that certain phthalate esters such as dibutyl phthalate and
butyl benzyl phthalate have caused polyneuritis in industrial workers (Milkov
et al. 1973, as reported in Doull et al. 1980); however, similar
observations have not been reported in this country (Doull et al. 1980).
Phthalate esters are considered as having a low order of acute toxicity in
animal studies. The only reported LD50 value for butyl benzyl phthalate is
that reported for the mouse by intraperitoneal injection of 3.16 g/kg (Autian
1973, as reported in USEPA 1980). When single doses of butyl benzyl phthalate
were administered to groups of rats either orally (1.8 g/kg) and
intraperitoneally (4 g/kg), the animals died after four to eight days
(Mallette and Von Hamm 1952, as reported in USEPA 1980). Histopathological
studies demonstrated toxic splenitis and degeneration of central nervous
system tissue with congestive encephalopathy. Myelin and glial proliferation
were also reported. Most phthalate esters are precluded from presenting an
acute toxic response by inhalation because of their low volatility (USEPA
1980). No chronic or subchronic toxicity data are available for butyl benzyl
phthalate.
The LC50 values for butyl benzyl phthalate have been reported for three
fish and one invertebrate species ranging from 1,700 ug/liter for the
bluegill to 92,300 ug/liter for Daphnia magna (USEPA 1980). For two
saltwater species, acute toxic values were reported for the raysid shrimp of
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900 and 9,630 yg/liter and for the sheepshead minnow of 3,000 and 445,000
ug/liter. The lower values were obtained using a solvent in which the
chemical is more soluble and thus presumably more available (USEPA 1980).
Chronic studies have been conducted with two freshwater species. In a
life-cycle study of Daphnia magna, effects were observed at 440 yg/liter,
and in an early life stage test with the fathead minnow, an acute value of 220
was reported (USEPA 1980). EC50 values for freshwater algae showed wide
variation in toxicity, with a range of 110 to 1,000,000 yg/liter (USEPA
1980).
EPA has not yet established ambient water quality criteria for butyl
benzyl phthalate because of the lack of sufficient data.
2-Chloronaphthalene
Little toxicity information is available on 2-chloronaphthalene. As a
class, chlorinated naphthalenes have been associated with the development of
chloracne in humans, and, in some cases, fatal liver disease. It has been
demonstrated, however, that monochloronaphthalenes did not produce chloracne
in a test with dermal application to the inner side of the rabbit ear (Adams
et al. 1941, as reported in Clayton and Clayton 1981).
EPA has not yet established ambient water quality criteria for
2-chloronaphthalene because of the lack of sufficient information.
4-Chlorophenyl Phenyl Ether
The only available toxicity data on 4-chlorophenyl phenyl ether is that
reported for experimental animals by Hake and Rowe (1963, as reported in USEPA
1980) for various chlorinated phenyl ethers. For an unspecified monochloro
phenyl ether, the lethal oral dose within four days of dosing in guinea pigs
was given as 700 mg/kg. The "survival dose" was reported as 200 mg/kg.
Within 30 days of the single oral dosing, the "lethal" and "survival" doses
were reported to be 600 and 100 mg/kg, respectively. Hake and Rowe also
reported that 19 daily oral doses of 100 mg/kg/day of a monochloro phenyl
ether over a 29-day period produced no effects in rabbits. Because of
inadequate experimental detail, these results are difficult to interpret
(USEPA 1980).
No aquatic toxicity information is available for 4-chlorophenyl phenyl
ether. Available data for haloethers indicate that acute and chronic toxicity
to freshwater aquatic life occur at concentrations as low as 360 and 122
yg/liter , respectively (USEPA 1980).
EPA has not yet established ambient water quality criteria for
4-chlorophenyl phenyl ether because of the lack of sufficient data.
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Chrysene
No information is available on the toxicity of chrysene in humans. In one
experimental study, Swiss mice painted three times weekly with a 1% solution
of chrysene in acetone developed skin cancer. This effect was not repeatable
in other studies however, and the carcinogenicity of chrysene has not been
clearly determined (IARC 1973).
No information is available on the toxic effects of chrysene on aquatic
organisms. However, chrysene was reported to bioconcentrate 8.2 times in
clams over 24 hours (USEPA 1980).
EPA has not yet established ambient water quality criteria for chrysene
because of the lack of sufficient data. However, the agency has established
an ambient water quality criterion of zero for the maximum protection of human
health from the potential carcinogenic effects due to exposure to polynuclear
aromatic hydrocarbons, which include chrysene, through ingestion of
contaminated water and contaminated aquatic organisms. However, since a zero
level may not be attainable at present, a level of 2.8 ng/liter, corresponding
to a lifetime incremental cancer risk of 10-6, was recommended.
Dibenzo(a,h)anthracene
Dibenzo(a,h)anthracene (DB(a,h)A) is a member of the class of polynuclear
aromatic hydrocarbons (PAHs) and was the first pure chemical compound shown to
be carcinogenic (IARC 1973). When DB(a,h)A was administered to mice as an
aqueous-oil emulsion in the place of drinking water at an average dose of
0.76-0.85 mg/day, all surviving mice at 200 days had respiratory tract tumors
and 12 of 13 females had mammary carcinomas (Snell and Stewart 1962, as
reported in IARC 1973). A single dose of 1.5 mg DB(a,h)A in polyethylene
glycol produced forestomach papillomas in 2 of 42 male mice within 30 weeks
(Berenblum and Haran 1955, as reported in IARC 1973).
Many studies have reported the induction of skin tumors from application
of DB(a,h)A. Thrice weekly paintings with solutions containing 0.001, 0.01,
and 0.1% DB(a,h)A produced skin carcinomas in one of 30 mice, 43 of 50 mice,
and 39 of 40 mice, respectively (Van Duuren et al. 1967, as reported in IARC
1973). In a subcutaneous injection study, single injections of DB(a,h)A at
doses ranging from 0.00019 to 8 mg produced incidences of local sarcomas of
2.5% to 100% (IARC 1973). In in vitro hamster embryo cell transformation
studies, DB(a,h)A at concentrations of 2.5 to 10 yg/ml did not produce any
compound-related increase in cell transformations; however, the 5,6-epoxide of
DB(a,h)A did produce a dose-related increase in cell transformations (Grover
et al. 1971, Huberman et al. 1972, as reported in USEPA 1980). High doses
of DB(a,h)A have been reported to produce an immunosuppressive effect in mice
(Malmgren et al. 1952, as reported in USEPA 1980).
No human case studies or epidemiological studies have been conducted which
establish DB(a,h)A as a human carcinogen. Indirect evidence for the
compound's carcinogenicity comes from air pollution studies which indicate an
excess of lung cancer mortality among workers exposed to high concentrations
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of PAH-containing material such as coal gas, tars, soot, and coke-oven
emiss-ions (IARC 1973, USEPA 1980).
No data are available on the aquatic toxicity of DB(a,h)A.
EPA has not yet established ambient water quality criteria for DB(a,h)A
because of the lack of sufficient data. However, the agency has established
an ambient water quality criterion of zero for the maximum protection of human
health from the potential carcinogenic effects due to exposure to polynuclear
aromatic hydrocarbons, which include DB(a,h)A, through ingestion of
contaminated water and aquatic organisms. Since the zero level may not be
attainable at present, a level of 2.8 ng/liter corresponding to a lifetime
incremental cancer risk of 0.000001 was recommended.
Di-n-butyl Phthalate
Occupational exposure to di-n-butyl phthalate has been associated with
toxic polyneuritis (Milkov et al. 1973, as reported in USEPA 1980).
Abnormal encephalographic responses were observed in three workers exposed to
0.12-0.15 mg/cu m (Men'shikova 1971, as reported in USEPA 1980).
In animal studies, testicular atrophy has been reported in rats
administered 2,000 mg/kg orally "for a period of time." Significant weight
loss of the testes was observed after 14 days. Zinc metabolism was also
affected as evidenced by increased zinc levels in the urine (Carter et al.
1977, as reported in USEPA 1980). In an inhalation experiment, a dose-related
increase in gamma globulin was observed in rats exposed to concentrations
ranging from 0.098-0.98 mg/cu m, continuously for 93 days (Men'shikova 1971,
as reported in USEPA 1980). In a feeding study, 50% of rats fed 1.25%
di-n-butyl phthalate in the diet died in the first week of administration
following one year exposure to levels up to 0.25% (Smith 1953, as reported in
USEPA 1980). A dermal LD50 for rabbits has been reported as 20 ml/kg (Autian
1973, as reported in USEPA 1980). Dose-related skeletal abnormalities and
reduced fetal weight were reported in the offspring of rats administered 1/10,
1/5, and 1/3 the LD50 value of 3.05 ml/kg di-n-butyl phthalate, by
intraperitoneal injection during days 5, 10, and 15 of gestation (Singh e_t
al. 1972, as reported in USEPA 1980).
The acute toxicity of di-n-butyl phthalate on fresh water aquatic
organisms is reflected by 96-hour LC50 values for scud (2.1 mg/liter), midge
(4.0 mg/liter), rainbow trout (6.47 mg/liter), fathead minnow (1.3 mg/liter),
and bluegill (0.73-1.2 mg/liter). Crayfish were less sensitive, having an
LC50 greater than 10 mg/liter. No information is available on the toxic
effects in saltwater organisms or the chronic effects in any aquatic
organisms. Di-n-butyl phthalate was reported to be extremely toxic to plant
life, causing toxic effects in algae in concentrations as low as 3.4
ug/liter (USEPA 1980).
EPA has established an ambient water quality criterion of 34 mg/liter for
the protection of human health from the toxic properties of di-n-butyl
phthalate ingested through contaminated water and contaminated aquatic
organisms.
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EPA has not yet established an aquatic life water quality criterion for
di-n-butyl phthalate.
1,2-Dichlorobenzene
The acute toxic effects on humans following exposure to
1,2-dichlorobenzene include eye and upper respiratory tract irritation when
inhaled (Dupont 1938, as reported in USEPA 1980), and skin irritation and
burning when absorbed through the skin (Reidel 1941, as reported in USEPA
1980). Chronic exposure to 1,2-dichlorobenzene produced weakness, fatigue,
nausea, headaches, peripheral lymphadenopathy, chronic lymphoid leukemia,
acute myeloblastic leukemia, acute hemolytic anemia, leukocytosis, and bone
marrow hyperplasia under different conditions of exposure (Girard et al.
1969 and Gadrat et al. 1962, as reported in USEPA 1980). Chronic skin
contact resulted in contact eczematoid dermatitis, erythema, and edema (Dowing
1939, as reported in U.S. EPA 1980).
Acute toxic effects were observed in rats exposed to a 4,800 mg/cu m
concentration of 1,2-dichlorobenzene (Cameron et al. 1937 in USEPA 1980).
In this study, nasal and ocular irritation, drowsiness, massive liver
necrosis, coma, and death occurred after exposure by inhalation for 11-50
hours. Rats (2,138 mg/kg), mice (2,000 mg/kg), rabbits (1,875 mg/kg), and
guinea pigs (3,375 mg/kg) exposed to different levels of 1,2-dichlorobenzene
in single doses by stomach tube developed acute poisoning manifestations
including hyperemia of the mucous membranes, adynamia, ataxia, paraparesis,
paraplegia, dyspnea, and death due to central respiratory paralysis
(Varshavskaya 1967, as reported in USEPA 1980). On necropsy, enlarged
necrotic livers, and brain, stomach, and kidney edema were observed in these
animals. Chronic exposure to 1,2-dichlorobenzene at levels of 0.0010.1
mg/kg/day predominantly affected the hematopoietic system after 5 months
(preliminary report, Varshavskaya 1967, as reported in USEPA 1980). In this
report, rats fed 0.1 mg/kg developed disturbances of higher cortical function
in the central nervous system, inhibition of erythropoiesis, thrombocytosis,
neutropenia, and inhibition of bone marrow mitotic activity. Hepatic
prophyria was induced in rats fed 455 mg/kg 1,2-dichlorobenzene by stomach
tube daily for 15 days. Severe liver damage with intense necrosis and fatty
changes were observed (Rimington and Ziegler 1963, as reported in USEPA
1980). 1,2-Dichlorobenzene was not mutagenic in the Salmonella typhimurium
assay (Anderson e_t al. 1972, as reported in USEPA 1980). No information is
available on the teratogenicity of 1,2-dichlorobenzene, and the carcinogenic
potential of 1,2-dichlorobenzene has not been established (USEPA 1980).
The acute toxicity of 1,2-dichlorobenzene to freshwater aquatic organisms
has been demonstrated in the bluegill and cladoceran with 96-hour LC50 values
of 5.59-27 and 2.44 mg/liter, respectively. Chronic toxicity was observed in
fathead minnows in concentrations ranging from 1.6 to 2.5 mg/liter. Plant
toxicity was demonstrated in freshwater algae at 91.6-98 mg/liter. Saltwater
organisms affected by 1,2-dichlorobenzene include tidewater silverside,
sheepshead minnows, and rays id shrimp. LD50 values are 7.3, 9.66, and 1.97
mg/liter, respectively. Emergence from parasitized oysters was observed in
the polychaete worm at concentrations of 100 mg/liter. Saltwater algae were
affected at 44.1 mg/liter (USEPA 1980).
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EPA has established an ambient water quality criterion of 400 yg/liter
for the protection of human health from the toxic properties of total
dichlorobenzenes including 1,2-dichlorobenzene ingested through water and
contaminated aquatic organisms.
EPA has not yet established an aquatic life water quality criterion for
1,2-dichlorobenzene.
1,3-Dichlorobenzene
No information is available on the human or animal effects which result
from exposure to 1,3-dichlorobenzene.
The acute toxicity of 1,3-dichlorobenzene to aquatic organisms is
reflected in the 96-hour LC50 values of 5.02 mg/liter for the bluegill, 7.79
mg/liter for the fathead minnow, 28.1 mg/liter for the cladoceran, 2.85
mg/liter for the mysid shrimp, and 7.77 mg/liter for the sheepshead minnow.
Chronic toxicity has been observed in the fathead minnow in concentrations
ranging from 1 to 2.27 mg/liter. Algae are affected by concentrations ranging
from 46.9 to 179 mg/liter, depending on the species (USEPA 1980).
EPA has established an ambient water quality criterion of 400 yg/liter
for the protection of human health from the toxic properties of total
dichlorobenzenes, including 1,3-dichlorobenzene, through ingestion of
contaminated water and aquatic organisms.
EPA has not yet established an aquatic life water quality criterion for
1,3-dichlorobenzene.
1,4-Dichlorobenzene
1,4-Dichlorobenzene is toxic to mammals, birds, and aquatic organisms and
imparts an offensive taste and odor to water. Human exposure to
1,4-dichlorobenzene is associated with leukemia and other blood dyscrasias,
liver necrosis, and eye irritation. Symptoms of exposure include headaches,
weakness, nausea, jaundice, and anemia (Sumers et al. 1952, Cotter 1953,
Perrin 1941, Hallowell 1959, Campbell and Davidson 1970, Nalbandian and Pierce
1965, as reported in USEPA 1980).
Acute inhalation studies in rabbits exposed to 100 gm/cu m for 30 minutes
daily caused central nervous system depression, and occular and nasal
irritation; rats similarly exposed developed irritation and narcosis while
guinea pigs exposed under the same conditions developed irritation, central
nervous system depression and deaths (Domenjoz 1946, as reported in USEPA
1980). Rats and guinea pigs administered 500 mg/kg by stomach tube developed
centrilobular hepatic necrosis and marked cloudy swelling of renal tubular
epithelium; no effects were observed at 10 and 100 mg/kg (Hollingsworth et
al. 1956, as reported in USEPA 1980).
In subchronic studies, rabbits subjected by inhalation to
1,4-dichlorobenzene at approximately 800 ppm for 8-hour periods, 5 days per
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week for as long as 12 weeks, developed tremors, weakness, nystagmus, and
reversible nonspecific eye changes (Pike 1944, as reported in NAS 1977).
Rabbits fed 1,000 mg/kg for 5 days per week developed similar toxicity
symptoms after several months (Pike 1944, as reported in NAS 1977).
Rats and guinea pigs exposed at 2,050 mg/cu m, 5 hours per day, 5 days per
week for 6 months displayed growth depression (guinea pigs); liver pathology
including cloudy swelling, fatty degeneration, focal necrosis, and cirrhosis;
and increased liver and kidney weights (rats only) (Ho11ingsworth et a1.
1956, as reported in USEPA 1980).
The acute toxicity of 1,4-dichlorobenzene on aquatic organisms is
reflected in 96-hour LC50 values of 11 mg/liter for the cladoceran, 13
mg/liter for the midge, 1.12 mg/liter for the rainbow trout, 4 mg/liter for
the fathead minnow, 4.28 mg/liter for the bluegill, 1.99 mg/liter for the
mysid shrimp, and 7.4 mg/liter for the sheepshead minnow. Chronic toxicity
was observed in the fathead minnow exposed to concentrations ranging from 5.6
to 1.04 mg/liter in the embryo-larval test. Algae were affected by
concentrations ranging from 54.8-98.1 mg/liter, depending on the species
(USEPA 1980).
EPA has established an ambient water quality criterion of 400 yg/liter
for the protection of human health from the toxic properties of total
dichlorobenzenes including 1,4-dichlorobenzene through ingestion of
contaminated water and contaminated aquatic organisms.
EPA has not yet established an aquatic life water quality criterion for
1,4-dichlorobenzene.
3,3*-Dichlorobenzidine
3,3'-Dichlorobenzidine has not been shown to be toxic in humans. Three
epidemiological studies of industrial exposure to 3,3*-dichlorobenzidine have
been conducted by Gerarde and Gerarde (1974) in the United States, by
Maclntyre (1975) and Gadian (1975) in Great Britain, and by Akiyama (1970) in
Japan (all as reported in USEPA 1980). The studies do not provide any
evidence that 3,3*-dichlorobenzidine induces bladder cancer, the
characteristic lesion induced by carcinogenic aromatic amines such as
benzidine used in the dye and pigment industry. The evidence is not, however,
conclusive since the populations studied have been small, tumors may not have
appeared at the time of the study because of a long latent period, and the
focus of the studies has been solely on bladder cancer as the lesion of
interest (USEPA 1980).
In rats, the oral LD50 for 3,3'-dichlorobenzidine is 488 for females and
676 for males (Gaines and Nelson 1977, as reported in USEPA 1980). Pliss
(1959, as reported in USEPA 1980) injected rats subcutaneously with 120 mg of
3,3*-dichlorobenzidine and observed a state of excitation and short-lived
convulsions. Exposure of rats to a concentrated atmospheric dust of
3,3*-dichlorobenzidine dihydrochloride for 14 days results in slight to
moderate pulmonary congestion; the actual concentration of the compound was
not measured (Gerarde and Gerarde 1974, as reported in USEPA 1980). However
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HC1 may have caused or contributed to the observed pulmonary effects. Freeman
et al. (1973, as reported in USEPA 1980) reported that 3,3*-dichlorobenzi-
dine at concentrations of 5 ppm or greater was cytotoxic to embryonic rat
cells in culture.
3,3'-Dichlorobenzidine has not been shown to be teratogenic. However, the
compound has been demonstrated to increase significantly the incidence of
leukemia in the offspring of pregnant female mice given doses of 8 to 10 mg by
subcutaneous injection during the last week of gestation (Golub et al. 1974,
as reported in USEPA 1980). When tested for mutagenicity in the Ames assay
using several strains of bacteria, 3,3'-dichlorobenzidine caused frameshift
and base-pair substitution mutations (USEPA 1980). 3,3*-Dichlorobenzidine. is
carcinogenic in experimental animals. Male and female rats fed the chemical
at 1,000 mg/kg diet for up to 488 days developed significantly increased
incidences (p <0.05) of mammary adenocarcinomas, granulocytic leukemia
(males only), and Zymbal's gland carcinomas (males only) (Stula et al. 1975,
as reported in USEPA 1980). 3,3'-Dichlorobenzidine added to the feed of rats
for 12 months (total dose of 4.63 g/rat) resulted in a wide variety of tumors
in 22 of 29 surviving animals (Pliss 1959, as reported in USEPA 1980).
Papillary transitional cell carcinomas of the urinary bladder and hepatic
carcinomas were induced in female beagle dogs given oral doses of 100 mg of
3,3*-dichlorobenzidine, three times per week for six weeks, then five times
per week for up to 7.1 years. Tumors of these types were not found in
controls (Stula et al. 1978, as reported in USEPA 1980).
No aquatic toxicity data are available for 3,3*-dichlorobenzidine.
EPA has established an ambient water quality criterion of zero for the.
maximum protection of human health from the potential carcinogenic effects due
to exposure to 3,3*-dichlorobenzidine through ingestion of contaminated water
and aquatic organisms. Since the zero level may not be attainable at the
present time, a level of 0.010 yg/liter, corresponding to a lifetime
incremental cancer risk of 0.000001, was recommended.
EPA has not yet established an aquatic life water quality criterion for
3,3'-dichlorobenzidine.
Diethyl Phthalate
Diethyl phthalate produces irritation of the mucous membranes of the nasal
passages and the upper respiratory tract in humans when vaporized by heat
(USEPA 1980).
In animals, diethyl phthalate produced small but significant decreases in
the growth rate of rats exposed for 2 years to 5% diethyl phthalate in the
diet, but no other effects were reported at dosages of 0.5 and 2.5%. No
adverse effects were reported in dogs fed levels up to 2.5% for 1 year (Food
Research Laboratories, Inc. 1955, as reported in USEPA 1980). An oral LD50
for rabbits has been reported as 1.0 g/kg (Autian 1973, as reported in USEPA
1980). Dose-related skeletal abnormalities and reduced fetal weight were
reported in rats administered 1/10, 1/5, and 1/3 of the LD50 value of 5.06
ml/kg diethyl phthalate, by intraperitoneal injection on days 5, 10, and 15 of
gestation (Singh et al. 1972, as reported in USEPA 1980).
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The acute toxicity of diethyl phthalate on freshwater aquatic organisms is
reflected by 96-hour LC50 values of 52.1 mg/liter for Daphnia magna and 98.2
mg/liter for bluegill. The saltwater species, mysid shrimp, gave a 96-hour
LC50 value of 7.59 mg/liter. Sheepshead minnows were also affected at an LC50
of 29.6 mg/liter (USEPA 1980).
No information is available on the chronic effects of diethyl phthalate on
aquatic organisms. Diethyl phthalate is toxic to algae in concentrations
ranging from 3.0 to 90.3 mg/liter (USEPA 1980).
EPA has established an ambient water quality criterion of 350 mg/liter for
the protection of human health from the toxic properties of diethyl phthalate
ingested through water and contaminated aquatic organisms.
EPA has not yet established an aquatic life water quality criterion for
diethyl phthalate.
Dimethyl Phthalate
Few toxic effects have been observed in humans exposed to dimethyl
phthalate (USEPA 1980). In animal studies, rats fed for 2 years at levels of
2% and 8% in the diet developed minor growth retardation. At 8%, some
indication of nephritic damage was observed. A 90-day LD50 value of 4 ml/kg
was obtained when dimethyl phthalate was applied to the skin of rabbits
(Draize et al. 1948, as reported in USEPA 1980). Oral LDSOs have been
reported for the mouse (7.2 g/kg), rat (2.4 g/kg), and guinea pig (2-4 g/kg)
(Autian 1973, as reported in USEPA 1980). Dose-related skeletal abnormalities
and reduced fetal weight were reported in the offspring of rats administered
1/10, 1/5, and 1/3 the LD50 value of 3.38 ml/kg by intraperitoneal injection
during days 5, 10, and 15 of gestation (Singh et al. 1972, as reported in
USEPA 1980).
The acute toxicity of dimethyl phthalate on freshwater aquatic organisms
is reflected by 96-hour LC50 values for Daphnia magna (33 mg/liter) and
bluegill (49.5 mg/liter). The saltwater species, mysid shrimp, gave a 96-hour
LC50 value of 73.7 mg/liter, and sheepshead minnow showed an LC50 of 58
mg/liter. Significant decreases in survival were reported in the larvae of
grass shrimp exposed to 100 mg/liter during active larvae development. No
information on the chronic effects of dimethyl phthalate on aquatic organisms
is available. The toxic effect of dimethyl phthalate on plant life occurs at
levels similar to those causing toxic effects on fishlife. Toxicity occurred
in a wide variety of algae in concentrations ranging from 26.1 to 185 mg/liter
(USEPA 1980).
EPA has established a water quality criterion of 313 mg/liter for the
protection of human health from the toxic properties of dimethyl phthalate
ingested through contaminated water and contaminated aquatic organisms.
EPA has not yet established an aquatic life water quality criterion for
dimethyl phthalate.
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2,4-Dinitrotoluene
The acute toxic effects of 2,4-dinitrotoluene in humans include
methemoglobinemia followed by cyanosis (USEPA 1980). The symptoms of
methemoglobinemia following absorption by inhalation, ingestion, or dermal
absorption of 2,4-dinitrotoluene include headache, vertigo, fatigue, nausea,
dyspnea, tremor, dizziness, loss of weight and appetite, paralysis, chest
pain, shortness of breath, and palpitations. Many of these symptoms were
observed in workers exposed to 2,4-dinitrotoluene (USEPA 1980). Acute oral
LD50s for 2,4-dinitrotoluene are 268 and 1,625 mg/kg for rats and mice,
respectively (USEPA 1980).
The 13 week subacute toxicity of 2,4-dinitrotoluene by oral administration
was studied in dogs, rats, and mice (Ellis et al. 1976 in USEPA 1980). The
dogs were fed daily doses of 1, 5, and 25 mg/kg, and the rats and mice were
fed dietary concentrations of 0.07, 0.2, and 0.7%. Toxic effects in dogs and
rats included inhibited muscle coordination in the hind legs, decreased
appetite, and weight loss. The latter two symptoms were also observed in
mice. Other symptoms observed in the test species were methemoglobinemia,
anemia with reticulocytosis, lesions in the spleen and liver, demyelination in
the brain, and aspermatogenesis. The highest dose was lethal to some animals
in all three species, and the lowest dose produced no toxic effect.
Chronic exposure to 2,4-dinitrotoluene produced benign tumors in rats
(National Cancer Institute 1978, as reported in USEPA 1980). Rats were fed
average doses of 17.6 and 440 mg/kg/day, and mice were fed doses of 16.3 and
81.5 mg/kg/day for 78 weeks. Treated male rats at both dose levels.developed
a significantly higher incidence of fibroma of the skin and subcutaneous
tissue (a benign tumor) than their controls. An increased incidence of
mammary gland fibroadenoma was observed in the high dose female rats. Certain
rare neoplasms occurred at low incidence in high dose rats, but the study
concluded that these tumors were not compound related. No tumors were
observed at a statistically significant incidence in mice. Data available in
the literature on the mutagenicity of 2,4-dinitrotoluene are "limited and
rather confusing" (USEPA 1980).
The 48-hour EC50 value for 2,4-dinitrotoluene to Daphnia magna is 35
mg/liter and is 31 mg/liter for the fathead minnow. No data are available
that describe the toxic effect of 2,4-dinitrotoluene to aquatic plants (USEPA
1980).
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to 2,4-dinitrotoluene. Since the zero level may not be attainable
at the present time, a level of 0.11 yg/liter, corresponding to an estimated
lifetime incremental cancer risk of 10-6, was recommended.
EPA has not yet established an aquatic life water quality criterion for
2,4-dinitrotoluene.
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2,6-Dinitrotoluene
The only toxicity information available on 2,6-dinitrotoluene are oral
LD50 values for the rat of 177 mg/kg and for the mouse of 1,000 mg/kg (USEPA
1980).
EPA has not yet established ambient water quality criteria for
2,6-dinitrotoluene because of lack of sufficient data.
Di-n-octyl Phthalate
Di-n-octyl phthalate is not known to be toxic to humans. A Russian report
suggests that certain phthalate esters such as dibutyl phthalate and butyl
benzyl phthalate have caused polyneuritis in industrial workers (Milkov et
al. 1973, as reported in Doull et al. 1980); however, similar observations
have not been reported in this country (Doull et al. 1980).
Phthalate esters are considered as having a relatively low order of acute
toxicity. A reported oral LD50 for di-n-octyl phthalate in the mouse is 13
g/kg. LD50 values for the rat by intraperitoneal administration and the
guinea pig by dermal exposure are reported to be 50 ml/kg and 5 ml/kg,
respectively (Autian 1973, as reported in USEPA 1980). Most phthalate esters
are precluded from presenting an acute toxic response by inhalation because of
their low volatility (USEPA 1980). In a teratogenicity study, Singh et al.
(1975, as reported in USEPA 1980) administered eight phthalic acid esters,
including dioctyl phthalate, to rats by intraperitoneal injection on days 5,
10, and 15 of gestation. Dioctyl phthalate was administered at doses of 5 and
10 ml/kg. All of the esters were reported to produce dose-related gross or
skeletal abnormalities and reduced fetal weight, although dioctyl phthalate
had the least adverse effects on embryo-fetal development. No other chronic
or subchronic data are available for di-n-octyl phthalate.
Little aquatic toxicity data are available for di-n-octyl phthalate. In a
26-day early life stage study with rainbow trout, the LC50 was reported to be
139,500 ug/liter. In 7 to 8-day early life stage studies with redear
sunfish, channel catfish, and the largemouth bass, LC50 values of 6,180, 690,
and 32,900 yg/liter were reported (USEPA 1980). Available data for the
general class of phthalate esters indicate that acute and chronic toxicity to
freshwater aquatic life can occur at concentrations as low as 940 and 3
yg/liter, respectively.
EPA has not yet established ambient water quality criteria for di-n-octyl
phthalate because of the lack of sufficient data.
1,2-Diphenylhydrazine
No information on the toxicity of 1,2-diphenylhydrazine to humans is
available.
The oral LD50 of 1,2-diphenylhydrazine in rats is 301 mg/kg (Mason
Research Institute Report 1971, as reported in NAS 1977). Studies in rats and
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mice have shown that 1,2-diphenylhydrazine produces both benign and malignant
tumors when administered subcutaneously or orally. Pliss (1974, as reported
in NAS 1977 and USEPA) administered 1,2-diphenylhydrazine by subcutaneous
injection (40 mg/week/rat and 5 mg/week/mouse) and in the diet (30 mg/mouse,
five times per week) for 588 days, and observed an increased incidence of
rhabdomyosarcomas, pulmonary adenomas, leukemia, and liver tumors in the
mouse, and tumors of the uterus, mammary glands, Zymbal's gland, liver, and
spleen, and lymphoid leukemias in rats. In a study by the National Cancel-
Institute (NCI 1978, as reported in USEPA 1980), mice were fed diets
containing 1,2-diphenylhydrazine at concentrations of 0.008 and 0.04 percent
for males and 0.004 and 0.04 percent for females for 78 weeks. Male rats were
fed diets containing 0.008 and 0.03 percent 1,2-diphenylhydrazine and females
0.004 and 0.01 percent. In rats, 1,2-diphenylhydrazine produced a
significantly increased incidence of hepatocellular carcinomas or neoplastic
nodules in males at both dose levels and females at the high dose; Zymbal's
gland squamous cell carcinomas in high dose males; adrenal tumors in high dose
males; and mammary carcinomas in high dose females. 1,2-Diphenylhydrazine
produced hepatocellular carcinomas in high dose female mice, but not in male
mice.
In a 48-hour EC50 test with Daphnia magna and a 96-hour LC50 test with
the bluegill, toxic values of 4,100 yg/liter and 270 yg/liter,
respectively, were reported (USEPA 1980). No data are available for any
saltwater species.
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to 1,2-diphenylhydrazine through ingestion of contaminated water
and aquatic organisms. Since the zero level may not be attainable at the
present time, a level of 42 ng/liter, corresponding to a lifetime incremental
cancer risk of 0.000001, was recommended.
EPA has not yet established an aquatic life water quality criterion for
1,2-diphenylhydrazine.
Fluoranthene
No information is available on the toxicity of fluoranthene in humans. In
acute toxicity studies in animals, this compound was found to present a
relatively low degree of toxicity (USEPA 1980). Fluoranthene does not appear
to be a direct acting carcinogen or mutagen, but it is a potent cocarcinogen
in animal studies (USEPA 1980). In skin painting studies, fluoranthene
increased the tumor incidence and reduced the time-to-tumor of mice treated
with benzo(a)pyrene (Van Duuren and Goldschmidt 1976, as reported in USEPA
1980).
Fluoranthene is acutely toxic to various freshwater and marine organisms.
Bluegill were found to have a 96-hour LC50 value of 3.98 mg/liter. Daphnia
magna were more resistant, with a 48-hour LC50 of 325 mg/liter. Fluoranthene
has a 96-hour LC50 value of 40 yg/liter and chronic value of 16 ug/liter
in mysid shrimp. No data are available on the chronic toxicity of
fluoranthene on freshwater organisms (USEPA 1980).
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EPA has established an ambient water quality criterion of 42 ug/liter
for the protection of human health from the toxic properties of fluoranthene
ingested through water and contaminated organisms.
EPA has not yet established an aquatic life water quality criterion for
fluoranthene.
Fluorene
No information is available on the toxic effects of fluorene on humans,
and very little information is available on the effects on animals. The
carcinogenic potential of fluorene was tested by skin painting and
subcutaneous administration in mice and by feeding and subcutaneous
administration in rats. Carcinogenicity was not established in any of these
tests (dose, duration unspecified; Hueper and Conway 1964).
Only one study is available on the toxic effects of fluorene on aquatic
life. A crude oil extract of fluorene was used in a 96-hour LC50 test on a
polychaete worm. The LC50 value determined in this test is 1.0 mg/liter
(USEPA 1980).
EPA has not yet established ambient water quality criteria for fluorene
because of the lack of sufficient data. However, the agency has established
an ambient water quality criterion of zero for the maximum protection of human
health from the potential carcinogenic effects due to exposure to polynuclear
aromatic hydrocarbons, which include fluorene, through ingestion of
contaminated water and contaminated aquatic organisms. However, since a zero
level may not be attainable at present, a level of 2.8 ng/liter, corresponding
to a lifetime incremental cancer risk of 10-6, was recommended.
Hexachlorobenzene
An outbreak of hexachlorobenzene-induced porphyria cutanea tarda occurred
in Turkey between 1955 and 1959 as a result of human consumption of seed grain
that had been treated with hexachlorobenzene (IARC 1979, USEPA 1980). More
than 3,000 people were affected by the condition, characterized by blistering
and epidermolysis of the exposed skin, loss of hair, and skin atrophy. A
mortality rate of 14% was reported within several years, and among breast-fed
infants of mothers whose milk contained hexachlorobenzene, the infant
mortality rate was greater than 95% (Cam 1960, Peters 1976, as reported in
IARC 1979 and USEPA 1980). There was no evidence of porphyria in Louisiana
residents living near an hexachlorobenzene manufacturing plant and whose
average plasma hexachlorobenzene levels were 3.6 yg/liter; however, plasma
coproporphyrin levels were abnormally high (Burns and Miller 1975, as reported
in IARC 1979 and USEPA 1980).
In experimental animals, the acute toxicity of hexachlorobenzene is
relatively low. The oral LD50 in rats varies from 3,500 to 10,000 mg/kg
(Booth and McDowell 1975, as reported in IARC 1979). With prolonged moderate
exposure, hexachlorobenzene exhibits a wide range of biological effects. In
rats given 500 mg/kg hexachlorobenzene in their diet for 4 months,
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hepatocellular hypertrophy and necrosis, spleen enlargement, prophyria, and
death were observed (Kimbrough and Linder 1974, as reported in IARC 1979).
Immunosuppression was observed in mice fed 167 mg/kg diet for 6 weeks (Loose
et al. 1977, as reported in IARC 1979). Pigs were administered
hexachlorobenzene in the diet at doses of 0.05-50 mg/kg/day for 90 days.
Porphyria and death occurred at the highest dose level, histopathological
changes of the liver at 5 mg/kg/day, and increased excretion of coproporphyrin
in the groups receiving 0.5 and 5 mg/kg/day (den Tonkelaar et al. 1978, as
reported in IARC 1979). Porphyrinuria has also been observed in rabbits,
Japanese quail, guinea pigs, and mice (USEPA 1980). Hexachlorobenzene is
fetotoxic and produces some teratogenic effects. Mice administered 100
mg/kg/day orally on gestation days 7-16 gave birth to offspring with an
increased incidence of cleft palates and kidney malformations (Courtney et
al. 1976, as reported in IARC 1979 and USEPA 1980). In a four-generation
study with rats treated with hexachlorobenzene at doses ranging from 0 to 640
mg/kg diet, the neonatal survival rate and neonatal body weight were reduced
at the 80 mg/kg level; birth weights were reduced at the 160 mg/kg level. No
gross abnormalities were found in this study (Grant et al. 1977, as reported
in USEPA 1980).
Hexachlorobenzene was shown to be carcinogenic in two studies. Groups of
male and female rats were fed diets containing 0, 50, 100 or 200 mg
hexachlorobenzene/kg diet for 120 days, and 300 mg/kg diet for 15 weeks. An
increased incidence of liver cell tumors was observed in the 100, 200 and 300
mg/kg diet groups (Cabral et al. 1978 and 1979, as reported in IARC 1979).
In a lifetime study with Syrian golden hamsters given dietary concentrations
of 0, 50, 100, and 200 mg hexachlorobenzene/kg diet (equivalent to 0,.4, 8,
and 16 mg/kg bw/day), a significantly increased incidence of hepatomas was
reported at all doses tested. Liver hemangioendotheliomas and alveolar
thyroid adenomas were found at the high dose level (Cabral et al. 1977, as
reported in IARC 1979).
Few data are available on the toxicity of hexachlorobenzene to aquatic
organisms. In 10 to 15 day studies with the largemouth bass, no effects were
observed at concentrations of 26 and 10 yg/liter (Laska et al. 1978, as
reported in USEPA 1980). In a study of saltwater protozoa, a 10-day exposure
to 1 ug/liter of hexachlorobenzene caused decreased growth (Geike and
Prasher 1976, as reported in USEPA 1980). Ninety-six hour exposure of pink
shrimp to 25 ug/liter resulted in 33 percent mortality (Parrish et al.
1974, as reported in USEPA 1980).
EPA has established an ambient water quality criterion of 0.0072
yg/liter for the protection of human health from the toxic properties of
hexachlorobenzene ingested through contaminated water and aquatic organisms.
EPA has not yet established an aquatic life water quality criterion for
hexachlorobenzene.
Hexachlorobutadiene
The acute oral toxicity of hexachlorobutadiene is moderate to high.
Schwetz et al. (1977, as reported in USEPA 1980) reported oral LD50 values
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of 200-400 mg/kg for female rats, 580 mg/kg for male rats, and 64 mg/kg for
weanling rats. Oral LD50 values reported by Gradiski et al. (1975, as
reported in USEPA 1980) for male rats and mice were 250 and 80 mg/kg; hepatic
and renal disorders and effects on the central nervous system were noted.
In chronic and subchronic studies of hexachlorobutadiene, the kidney
appears to be the most sensitive organ. In a 30-day feeding study, renal
tubular epithelial degeneration, necrosis, and an increase in the
kidney-to-body weight ratio occurred in female rats receiving 30, 65, or 100
mg/kg/day hexachlorobutadiene in their diets, but not at 3 mg/kg/day (Kociba
et al. 1971, as reported in USEPA 1980). In a two-year chronic study with
rats given 0, 0.2, 2, or 20 mg/kg/day hexachlorobutadiene in their diet, a
significant increase in renal tubular adenomas and carcinomas was observed in
both male and female rats at the 20 mg/kg/day level (Kociba et al. 1977, as
reported in USEPA 1980). Slight renal tubular epithelial hyperplasia was
noted at the 2 mg/kg/day level. A statistically significant increase in
urinary coproporphyrin was observed in male rats ingesting 20 mg/kg/day
hexachlorobutadiene and in females ingesting 2 mg/kg/day. Schwetz et al.
(1977, as reported in USEPA 1980) reported renal tubular dilation,
degeneration, and regeneration in kidneys from male and female rats given
hexachlorobutadiene in their diet at a dose level of 20 mg/kg/day for 143
days; a mottled cortex was noted at the 2 mg/kg/day level. Kidney damage has
also been induced by inhalation of hexachlorobutadiene; injury to the tubular
epithelium was reported after 15 daily six-hour exposures to 25 ppm
hexachlorobutadiene (Gage 1970, as reported in USEPA 1980). Evidence for the
teratogenic potential of hexachlorobutadiene is inconclusive. Poteryaeva
(1966, as reported in USEPA 1980) reported increased neonatal mortality,
decreased birthweight, kidney damage, and degenerative changes in red blood
cells in offspring of female rats given single subcutaneous injections of 20
mg/kg hexachlorobutadiene before breeding. Schwetz et al. (1977, as
reported in USEPA 1980) observed no effects in offspring of male and female
rats given hexachlorobutadiene in the diet at dose levels of 0.2 and 2.0
mg/kg/day for 90 days before mating, during mating, and throughout gestation
and lactation; at the 20 mg/kg/day level, a slight decrease in weanling body
weight was the only observed effect.
Acute toxicity data have been reported for four species of freshwater
fish, with LC50 values ranging from 90 to 326 yg/liter (USEPA 1980). In
static tests conducted with saltwater mysid shrimp, grass shrimp, pinfish, and
sheepshead minnow, the 96-hour LC50 values were 59, 32, 399, and 557
ug/liter, respectively. In an embryo-larval test with fathead minnow, a
chronic toxicity value of 9.3 yg/liter was reported (USEPA 1980).
EPA has established a water quality criterion of zero for the maximum
protection of human health from the potential carcinogenic effects due to
exposure to hexachlorobutadiene through ingestion of contaminated water and
contaminated aquatic organisms. Since the zero level may not be attainable at
the present time, a criterion of 0.45 yg/liter corresponding to a lifetime
incremental cancer risk of 0.000001 was recommended.
EPA has not yet established aquatic life ambient water quality criteria
for hexachlorobutadiene.
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Hexachloroethane
The acute toxic effects of hexachloroethane in humans include extensive
eye irritation including inability to close the eyelid, tearing of the eyes,
inflammation of the delicate membrane lining of the eye, and visual
intolerance to light (NIOSH 1978, as reported in USEPA 1980).
Liver degeneration and tubular nephrosis of the kidney were observed in
rabbits administered daily oral doses of 320 or 1,000 mg/kg for 12 days (Weeks
et al. 1979, as reported in USEPA 1980). Inhalation exposure of dogs,
guinea pigs, and rats to 260 ppm for 6 hours/day, 5 days per week, for 6 weeks
produced central nervous system toxicity in dogs and rats, and increased liver
size in guinea pigs and rats (Weeks et al. 1978, as reported in USEPA
1980). Rats administered 500 mg/kg/day orally from day 6 through 16 of
gestation gave birth to a significantly lower number of live fetuses (Weeks
et al. 1979, as reported in USEPA 1980). Liver cancer was produced in mice
administered 590 mg/kg/day hexachloroethane by stomach tube for 78 weeks
(National Cancer Institute 1978, as reported in USEPA 1980).
The toxicity of hexachloroethane to freshwater organisms was demonstrated
in Daphnia magna at 8.07 mg/liter, midge at 1.7 mg/liter, rainbow trout at
0.98 mg/liter, fathead minnow at 1.53 mg/liter, and the bluegill at 0.98
mg/liter. Toxicity to saltwater organisms was observed in the mysid shrimp at
0.94 mg/liter and the sheepshead minnow at 2.4 mg/liter. Chronic toxicity has
been observed in the fathead minnow in concentrations ranging from 0.41 to 0.7
mg/liter. Toxicity to aquatic plants was observed in freshwater algae at
87-93.2 mg/liter and in saltwater algae at 7.75-8.57 mg/liter (USEPA 1980)..
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects
from exposure to hexachloroethane through ingestion of contaminated water and
contaminated aquatic organisms. However, since a zero level may not be
attainable at present, a level of 1.9 ug/liter, corresponding to a lifetime
incremental cancer risk of 0.000001, was recommended.
EPA has not yet established an aquatic life water quality criterion for
hexachloroethane.
Hexachlorocyclopentadiene
Little human toxicity data is available on hexachlorocyclopenta- diene.
Occupational experience has shown that hexachlorocyclopentadiene is highly
irritating (USEPA 1980, ACGIH 1980). In a recent incidence in which
approximately 200 sewage treatment plant workers were exposed to acutely toxic
levels of hexachlorocyclopentadiene from illegal disposal of the compound,
workers reported severe irritation of the eyes, nose, throat, and lungs;
headache; nausea; and respiratory difficulty (Carter 1977 and Singal 1978, as
reported in USEPA 1980).
The acute oral toxicity of hexachlorocyclopentadiene was investigated by
Treon et al. (1955, as reported in USEPA 1980). The LD50 for rats and
rabbits was determined to be about 500 mg/kg. IRDC (1972) and Naishstein and
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Lisovskaya (1965, both as reported in USEPA 1980) have reported similar LDSOs
for rats of 584 mg/kg and 600 mg/kg, respectively. Hexachlorocyclopentadiene
appears to be as acutely toxic by dermal exposure as by oral exposure (USEPA
1980). A 7-hour inhalation exposure to 1.5 ppm hexachlorocyclopentadiene was
lethal to rabbits; five 7-hour exposures to 1.0 ppm or two 7-hour exposures to
3.2 ppm was lethal to rats (Treon et al. 1955, as reported in USEPA 1980).
To date, no adequate subchronic or chronic oral toxicity studies of
hexachlorocyclopentadiene have been performed. Hexachlorocyclopentadiene was
given orally to rats at levels ranging from 0.00002 to 20 mg/kg/day for six
months (Naishstein and Lisovskaya 1965, as reported in USEPA 1980). At the
high dose level, 2 of 10 animals died; at 0.002 mg/kg/day, the only reported
effects were neutropenia and a tendency toward lymphocytosis. Rats, rabbits,
guinea pigs, and mice exposed to vapors of hexachlorocyclopentadiene showed
irritation of the eyes and mucous membranes (Treon et al. 1955, as reported
in ACGIH 1980). At the lowest exposure level (0.15 ppm for 7 hours on each of
150 days over a 216-day period) degenerative changes in the liver and kidneys
of all species and pulmonary irritation in mice were observed.
Hexachlorocyclopentadiene has been tested for mutagenicity and reported to be
nonmutagenic in both short-term in vitro mutagenicity assays and in a mouse
dominant lethal study (USEPA 1980).
Hexachlorocyclopentadiene is highly toxic to freshwater fish. EC50 levels
for Daphnia magna of 39 and 52 yg/liter have been reported. Investigators
have reported 96-hour LC50 values for the fathead minnow ranging from 7 to 180
yg/liter. LC50 values for the channel catfish and bluegill have been
reported to be 97 and 130 yg/liter, respectively. The chronic toxicity
value for the fathead minnow in an embryo-larval test is 5.2 yg/liter.
Ninety-six-hour LC50 values for three saltwater invertebrate and three
saltwater fish species ranged from 7 to 48 yg/liter for all species except
the polychaete for which the LC50 value was 371 yg/liter (USEPA 1980).
EPA has established an ambient water quality criterion of 206 yg/liter
for the protection of human health from the toxic properties of
hexachlorocyclopentadiene through ingestion of contaminated water and aquatic
organisms.
EPA has not yet established an aquatic life ambient water quality
criterion for hexachlorocyclopentadiene.
Indeno(1,2,3-cd)pyrene
Indeno(l,2,3-cd)pyrene is a member of the class of polynuclear aromatic
hydrocarbons (PAHs) many of which are known for their ability to induce
cancer.
Limited data are available on the carcinogenicity of
indeno(l,2,3-cd)pyrene. When groups of 20 female mice were painted three
times weekly with indeno(l,2,3-cd)pyrene in acetone at concentrations of 0.01,
0.05, 0.1 and 0.5%, no tumors were produced at the 2 lower doses, 6 papillomas
and 3 carcinomas were produced at the 0.1% dose level, and 7 papillomas and 5
carcinomas were produced at the 0.5% dose level (Hoffman and Wynder 1966, as
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reported in IARC 1973). Indeno(l,2,3-cd)pyrene also produced tumors by
subcutaneous administration. Three injections of 0.6 mg indeno(l,2,3-cd)-
pyrene in olive oil at one month intervals to male and female mice resulted in
sarcomas in 10 of 14 male mice after 265 days and in only 1 of 14 females
after 145 days (Lacassagne et al. 1965, as reported in IARC 1973).
No human case studies or epidemiologic studies have been conducted which
establish indeno(l,2,3-cd)pyrene as a human carcinogen. Indirect evidence for
the compound's carcinogenicity comes from air pollution studies which indicate
an excess of lung cancer mortality among workers exposed to high
concentrations of PAH-containing material such as coal gas, tars, soot, and
coke oven emissions (IARC 1973, USEPA 1980).
No data are available on the aquatic toxicity of indeno(l,2,3-cd)- pyrene.
EPA has not yet established ambient water quality criteria for
indeno(l,2,3-cd)pyrene because of the lack of sufficient data. However, the
agency has established an ambient water quality criterion of zero for the
maximum protection to human health from the potential carcinogenic effects due
to exposure to polynuclear aromatic hydrocarbons through ingestion of
contaminated water and aquatic organisms. Since the zero level may not be
attainable at present, a level of 2.8 ng/liter corresponding to a lifetime
incremental cancer risk of 0.000001 was recommended.
Isophorone
Human exposure to isophorone vapor causes irritation of the eyes, hose,
and throat of unacclimatized workers at concentrations of 25 ppm. Workers
exposed to 5 to 8 ppm complained of fatigue and malaise (Silverman et al.
1946, as reported in Clayton and Clayton 1981 and USEPA 1980). Inhalation of
200 and 400 ppm isophorone resulted in nausea, headache, dizziness, faintness,
inebriation, and a feeling of suffocation (Smyth and Seaton 1940, as reported
in USEPA 1980).
In rats, exposure to isophorone vapors at 750 ppm for "several" hours
produced no symptoms other than slight eye and nose irritation; "some" deaths
were reported after four hours at 1,840 ppm, usually due to paralysis of the
respiratory system or lung irritation (Smyth and Seaton 1940, as reported in
USEPA 1980). Rats and guinea pigs exposed to 100 to 500 ppm isophorone 8
hours/day, 5 days/week, for 6 weeks showed weight loss and evidence of
pathologic changes in the lung, spleen, and kidney. In rats at 200 ppm and
guinea pigs at 500 ppm, conjunctivitis and nasal irritation were observed.
Exposure of rats to 50 ppm produced evidence of pathologic changes in the lung
and kidney (Smyth 1941, as reported in USEPA 1980). It has been suggested
that the material used in these two inhalation studies was an impure
commercial product containing appreciable amounts of other volative
materials. Therefore, the reported results are of uncertain reliability
(USEPA 1980).
Oral LD50s have been reported for rats and mice ranging from 1.87 to 2,37
g/kg. The LD50 reported for rabbits following acute dermal exposure to
isophorone is 1.39 g/kg (USEPA 1980) . Isophorone is weakly irritating to the
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skin of rabbits, and induces reversible irritation of the conjunctiva and
corneal opacity when applied to rabbit eyes (Truhaut et al. 1972, as
reported in USEPA 1980). In a 90-day feeding study in rats and dogs given 750
to 3,000 ppra in the diet (rats) or 35 to 150 mg/kg/day in gelatin capsules
(dogs), no significant differences between treated and control groups
regarding hematology, blood chemistry, urinalysis, or pathologic lesions were
observed (Parkin 1972, as reported in USEPA 1980).
For Daphnia tnagna and the bluegill, EC50 concentrations for isophorone
of 117,000 and 224,000 yg/liter, respectively, have been reported (USEPA
1980). For a saltwater species, the mysid shrimp, the 96-hour LC50 is 12,900
yg/liter. Chronic effects were observed in an embryo-larval test with the
sheepshead minnow, a saltwater species, at a concentration of 110,000
Vg/liter. Because this value is greater than the 96-hour LC50 for mysid
shrimp, the sheepshead minnow was not considered to be a sensitive species
(USEPA 1980). Cell number production and chlorophyll a content in a
freshwater alga were affected in a 96-hour test at concentrations of 122,000
to 126,000 ug/liter. In a saltwater alga, these effects were observed at
110,000 and 105,000 ug/liter (USEPA 1980).
EPA has established an ambient water quality criterion of 5.2 mg/liter for
protection of human health from the toxic properties of isophorone through
ingestion of contaminated water and aquatic organisms.
EPA has not yet established an aquatic life water quality criterion for
isophorone.
Naphthalene
Systemic toxicity to naphthalene in humans includes nausea, headache,
diaphoresis, hematuria, fever, anemia, liver damage, convulsions, and coma
(Sax 1975). Toxic effects have been reported in infants when the only
exposure was to the mother during pregnancy (Zinkham and Childs 1958,
Anziulewicz et al. 1959, as reported in USEPA 1980). Occupational studies
have associated laryngeal cancer with worker exposure in a coaltar naphthalene
production facility (Wolf 1976, as reported in USEPA 1980).
Acute toxicity in animals is reflected by the following toxicity values.
In the rat, oral LD50s range from 1.78 to 9.43 gm/kg. In the same species, an
inhalation LC50 of 100 ppm for 8 hours and a dermal LD50 of 2.5 gm/kg were
reported. An LD50 of 5.1 gm/kg was reported in mice injected subcutaneously
with naphthalene (Ime et al. 1973, Gaines 1969, NIOSH 1977, Union Carbide
Corporation 1968, as reported in USEPA 1980). In subacute and chronic
studies, rats fed 2% naphthalene in the diet for at least 60 days developed
early cataracts in both groups (Fitzhugh and Buschke 1949, as reported in
USEPA 1980). Lens changes and early cataracts were also observed in rabbits
fed 1,000 mg/kg naphthalene by gavage for various lengths of time up to 28
days (Van Heyningen and Pirie 1976, as reported in USEPA 1980). Bronchial
epithelial changes have been observed in mice treated by intraperitoneal
injection with 67.4 mg/kg and sacrificed at different times up to 7 days
following treatment (Mahvi et aj.. 1977, as reported in USEPA 1980).
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The offspring of rabbits administered a metabolite of naphthalene,
2-naphthol, were born with cataracts and evidence of retinal damage (Van der
Hoeve 1913, as reported in USEPA 1980). However, naphthalene was not
mutagenic in several microsomal/bacterial assay systems (McCann et al. 1975,
Kraemer et al. 1974, as reported in USEPA 1980).
Lymphatic leukemia was observed in mice treated (skin painting) with a
solution of 0.5% coal tar naphthalene in benzene, 5 days per week for life
(Knake 1956, as reported in USEPA 1980). Rats, subcutaneously injected with
500 mg/kg of coal tar naphthalene every 2 weeks for a total of seven
treatments, developed metaplastic lymphosarcoma (Knake 1956, as reported in
USEPA 1980). These studies are difficult to interpret, however, because of
the nature of the purity of the naphthalene administered. Several skin
painting studies, using pure naphthalene on mice (Kennaway 1930, Kennaway and
Hieger 1930, as reported in USEPA 1980) and rabbits (Bogdat'eva and Bid 1955,
as reported in USEPA 1980) showed no carcinogenic effect. The possible
carcinogenicity of pure naphthalene consequently has not yet been
established.
The acute toxicity of naphthalene to aquatic organisms was demonstrated in
six different species in concentrations ranging from 2.3 to 8.9 mg/liter.
Mosquitofish and pacific oysters were more resistant, having 96-hour LC50
values of 150 and 199 mg/liter, respectively. Chronic toxicity has been
demonstrated in the fathead minnow in concentrations ranging from 0.45 to 0.85
mg/liter. Algae were affected at 33 mg/liter (USEPA 1980).
EPA has not yet established ambient water quality criteria for naphthalene
because of the lack of sufficient information.
Nitrobenzene
The most characteristic acute symptom in humans, following exposure to
nitrobenzene, is cyanosis as a result of methemoglobin formation. Anemia may
develop 1 or 2 weeks after a poisoning or in more severe, cases may lead to
coma and death. The symptoms of chronic occupational exposure to nitrobenzene
include cyanosis, methemoglobinemia jaundice, anemia, sulfhemoglobinemia,
persistence of Heinz bodies in the erythrocytes, and dark-colored urine.
There have been reports of menstrual disturbances in women chronically exposed
to nitrobenzene, and changes have been observed in the tissues of the chorion
and placenta from pregnant women occupationally exposed to nitrobenzene
(USEPA 1980).
Nitrobenzene has induced methemoglobin formation in dogs, cats, and rats,
but not in guinea pigs or rabbits (Levin 1927, as reported in USEPA 1980). An
early study found that nitrobenzene fumes caused cerebellar disturbances in
dogs and birds (Dresbach and Chandler 1918, as reported in USEPA 1980).
Little information is available on the teratogenic effects of nitrobenzene.
In one study on rats, however, a subcutaneous dosage of 125 mg/kg during the
preimplantation and placentation periods was associated with delay of
embryogenesis, alteration of normal placentation, and fetal abnormalities
(Kazanina 1968, as reported in USEPA 1980). No studies are available that
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show nitrobenzene to be mutagenic or carcinogenic. Nitrobenzene is, however,
structurally related to known carcinogens (USEPA 1980).
Among freshwater animal species, the 48-hour EC50 is 27 mg/liter for
Daphnia tnagna, and the 96-hour LC50 is 42.6 mg/liter for the bluegill. A
freshwater alga, Selenastrum capricornuum, has an EC50 value for chlorophyll
a of 44.1 mg/liter. In saltwater animal species, the 96-hour LCSOs are 6.68
mg/liter for the mysid shrimp and 58.6 mg/liter for the sheepshead minnow.
The saltwater alga Skeletonema costatum had an EC50 value for chlorophyll a
of 10.3 mg/liter (USEPA 1980).
EPA has established an ambient water quality criterion of 19.8 mg/liter
for the maximum protection of human health from the toxic properties of
nitrobenzene through the ingestion of water and contaminated aquatic
organisms.
EPA has not yet established an aquatic life water quality criterion for
nitrobenzene.
N-Nitrosodimethylamine
Dialkyl N-nitrosoamines are characteristically hepatotoxic, producing
hemorrhagic centrilobular necrosis. A few cases of human poisoning from
exposure to N-nitrosodimethylamine have been reported. Symptoms included
abdominal pains, exhaustion, headaches, and distended abdomens. Clinical
examination showed signs of liver damage and bronchopneumonia in one case, and
autopsies have revealed cirrhotic livers (USEPA 1980).
Acute exposure of experimental animals to N-nitrosodimethylamine produces
liver lesions in 24 to 48 hours, peritoneal and sometimes pleural exudate, and
in some cases kidney lesions (USEPA 1980). An acute oral LD50 of 40 mg/kg has
been reported for the rat (USEPA 1980). N-nitrosodimethylamine has been
reported to induce forward and reverse mutations in several bacterial species,
gene recombination and conversion in Saccharomyces cerevisiae, recessive
lethal mutation in Drosophila melanogaster, and chromosome aberrations in
mammalian cells (Montesano and Bartsch 1976, as reported in USEPA 1980).
N-nitrosodimethylamine is carcinogenic in all species tested: mice, rats,
hamsters, guinea pigs, rabbits, ducks, mastomys, various fish, newts, and
frogs (IARC 1978). In mice, chronic administration in the drinking water at a
concentration corresponding to a dose of 0.4 mg/kg/day produced lung adenomas
and hemangiocellular tumors in 13/17 and 2/10 mice, respectively (Clapp and
Toya 1970, as reported in IARC 1978). Numerous studies in the rat have shown
that administration of 50-100 mg/kg in the diet or drinking water (or 4
mg/kg/day) leads to the development of high incidences of hepatocellular
carcinomas and cholangiocellular tumors. Kidney tumors have been produced by
short-term or single-dose treatment with high oral doses (up to 30 mg/kg body
weight) (IARC 1978). Lung adenocarcinomas and squamous-cell carcinomas have
also been observed after oral N-nitrosodimethylamine treatment (IARC 1980).
Druckrey et al. (1967, as reported in IARC 1978) reported tumors of the
nasal cavity in rats exposed by inhalation twice weekly for 30 minutes at a
concentration corresponding to 2 mg/kg body weight. Single subcutaneous
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administration of N-nitrosodimethylamine in mice at doses of 1, 2, 4, and 8
mg/kg produced lung tumor incidences of 29%, 35%, 39%, and 67%, respectively
(Cardesa et al. 1974, as reported in IARC 1978). A thorough review of the
available carcinogenicity data for N-nitrosodimethylamine is presented in IARC
(1978) and USEPA (1980).
No acute aquatic toxicity information is available for
N-nitrosodimethylamine. However, available data for nitrosamines indicates
that acute toxicity to freshwater aquatic life occurs at concentrations as low
as 5,850 ug/liter (USEPA 1980). In a 52-week feeding study with rainbow
trout, a dose-related response of hepatocellular carcinoma occurred in trout
fed 200 to 800 mg N-nitrosodimethylamine (Grieco et al. 1978, as reported in
USEPA 1980). In a study by Harshbarger et al. 1971 (as reported in USEPA
1980), crayfish exposed for six months to N-nitrosodimethylamine developed
extensive degeneration of the antennal gland at 200,000 ug/liter and
hyperplasia of the hepatopancreas at 100,000 yg/liter. No toxicity data are
available for saltwater species.
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to N-nitrosodimethylamine through ingestion of contaminated water
and aquatic organisms. Since the zero level may not be attainable at the
present time, a level of 1.4 ng/liter, corresponding to a lifetime incremental
cancer risk of 0.000001, was recommended.
EPA has not yet established an aquatic life water quality criterion for
N-nitrosodimethylamine.
N-Nitrosodiphenylamine
The dialkyl N-nitrosamines are characteristically hepatotoxic, producing
hermorrhagic centrilobular necrosis. Acute oral LD50 values in the rat have
been given as 1,650 and 3,000 mg/kg (USEPA 1980). The class of N-nitroso
compounds includes some of the most powerful chemical mutagens known.
However, N-nitrosodiphenylamine is reported to give a negative response in
both Salmonella typhimurium and E. coli mutagenicity assays after
activation with a rat liver microsomal preparation (USEPA 1980). In a recent
National Cancer Institute bioassay (Cardy et al. 1979, as reported in USEPA
1980) rats developed neoplastic and non-neoplastic urinary bladder lesions
after two years of dietary administration of N-nitrosodiphenylamine at a
dose-level of 200 mg/kg/day.
Acute toxicity from exposure to N-nitrosodiphenylamine has been reported
for Daphnia magna and the bluegill at concentrations of 7,760 and 5,850
Vg/liter, respectively. A 96-hour LC50 for the mummichog, a saltwater
species, of 3,300 mg/liter has been reported (USEPA 1980). No chronic aquatic
studies are available for N-nitrosodiphenylamine.
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to N-nitrosodiphenylamine through ingestion of contaminated water
and aquatic organisms. Since the zero level may not be attainable at the
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present time, a level of 4.9 ug/liter, corresponding to a lifetime
incremental cancer risk of 0.000001, was recommended.
EPA has not yet established an aquatic life water quality criterion for
N-nitrosodiphenylamine.
N-Nitrosodi-n-propylamine
No information on the toxicity of N-nitrosodi-n-propylamine in humans is
available.
The dialkyl N-nitrosamines are characteristically hepatotoxic, producing
hemorrhagic centrilobular necrosis. An acute oral LD50 in the rat is reported
as 480 mg/kg. The subcutaneous LD50 for the rat is given as 487 mg/kg and for
the Syrian golden hamster as 600 mg/kg (IARC 1978). N-nitrosodi-n-propylamine
is carcinogenic in experimental animals. Administration in drinking water at
doses of 4, 8, 15, or 30 mg/kg/day produced liver carcinomas in 45 of the 48
rats tested after induction times ranging from 120 to 300 days (Druckrey et
al. 1967, as reported in IARC 1978). Male and female rats injected
subcutaneously with 24.4, 48.7, or 97.4 mg/kg N-nitrosodi-n-propylamine once
weekly for life developed a high incidence of neoplasms of the nasal or
paranasal cavities (45 of 58 treated rats). In addition, 13 liver tumors, 11
lung cancers, and 11 squamous-cell papillomas of the esophagus were seen
(Althoff et al. 1973, as reported in IARC 1978). Syrian golden hamsters
were treated subcutaneously with 1.2% N-nitrosodi-n-propylamine in olive oil
once weekly for life at doses of 3.75, 7.5, 15, 30, or 60 mg/kg. A high
incidence of tumors of the nasal and paranasal cavities, laryngobronchial
tract, and lung were observed in treated guinea pigs but not in controls
(Althoff et al. 1973, as reported in IARC 1978). N-nitrosodi-n-propylamine
is mutagenic in in vitro assays with the bacteria Salmonella typhimurium
and E. coli and Chinese hamster V79 cells (IARC 1978).
No aquatic toxicity studies are available for N-nitrosodi-n- propylamine.
However, available data for nitrosamines indicate that acute toxicity to
freshwater aquatic life occurs at concentrations as low as 5,850 yg/liter
(USEPA 1980).
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to N-nitrosodi-n-propylamine through ingestion of contaminated
water and aquatic organisms. Since the zero level may not be attainable at
the present time, a level of 0.8 ng/liter, corresponding to a lifetime
incremental cancer risk of 0.000001, was recommended.
EPA has not yet established an aquatic life water quality criterion for
N-nitrosodi-n-propylamine.
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Phenanthrene
Phenanthrene is a polynuclear aromatic hydrocarbon that causes skin
photosensitization in humans and has produced cancer in animals (Sax 1975).
The oral LD50 in mice is 700 mg/kg (USDHHS 1980).
The information on the toxicity of phenanthrene to aquatic organisms is
limited to one study of a crude oil fraction of phenanthrene that produced a
96-hour LC50 value of 600 yg/liter in the polychaete worm (USEPA 1980).
EPA has not yet established ambient water quality criteria for
phenanthrene because of the lack of sufficient data. However, the agency has
established an ambient water quality criterion of zero for the maximum
protection of human health from the potential carcinogenic effects due to
exposure to polynuclear aromatic hydrocarbons, which include phenanthrene,
through ingestion of contaminated water and contaminated aquatic organisms.
However, since a zero level may not be attainable at present, a level of 2.8
ng/liter, corresponding to a lifetime incremental cancer risk of 10-6, was
recommended.
Pyrene
No information is available on the toxicity of pyrene in humans, animals,
or aquatic life. In an in vitro assay, pyrene exhibited toxicity to
transplanted rat respiratory epithelium and the submucosa of the trachea
(Topping et al. 1978). Derivatives of pyrene, however, such as
benzoCa!pyrene, are highly potent animal carcinogens.
EPA has not yet established ambient water quality criteria for pyrene
because of the lack of sufficient data. However, the agency has established
an ambient water quality criterion of zero for the maximum protection of human
health from the potential carcinogenic effects due to exposure to polynuclear
aromatic hydrocarbons, which include pyrene, through ingestion of contaminated
water and contaminated aquatic organisms. However, since a zero level may not
be attainable at present, a level of 2.8 ng/liter, corresponding to a life
time incremental cancer risk of 10-6, was recommended.
2,3,7,8-Tetrachlorodibenzo-p-dioxin
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is one of the most toxic
substances known. It produces a delayed biological response in many species
and is highly toxic at low doses to aquatic organisms and mammals, including
humans. Many human exposures to TCDD result from occupational exposure to
2,4,5-trichlorophenol (2,4,5-TCP) or 2,4,5-trichlorophenoxyacetic acid
(2,4,5-T), in which TCDD is a contaminant.
TCDD has been identified as the cause of numerous outbreaks of chloracne
in humans. In addition, investigators have reported muscular weakness, loss
of appetite and weight, sleep disturbances, hypotension, abdominal pain, liver
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impairment, peripheral neuropathy, psychopathological changes, hyperlipaemia
and hypercholesterolaemia, and porphyria cutanea tarda among exposed persons
(USEPA 1979).
TCDD is extremely toxic in all animal species tested, with oral LD50
values for several species ranging between 0.6 and 115 yg/kg (NAS 1977).
Rats given single doses of 25 and 50 yg/kg of TCDD showed moderate to severe
thymic atrophy and liver damage; rats that received 100 Vg/kg showed 43%
mortality, severe liver damage, thymic atrophy, and icterus (Gupta et al.
1973, as reported in NAS 1977). Mortality following acute oral doses may be
delayed. In female rats given single oral doses up to 300 yg/kg, delayed
mortality was observed over a 90-day period (Greig et al. 1973, as reported
in NAS 1977). McConnell et al. (1978, as reported in USEPA 1979) observed
weight loss, blepharitis, facial alopecia with acneform eruptions, and anemia
in rhesus monkeys given single oral doses of 70 to 350 yg/kg TCDD. Deaths
were also reported.
Damage to the liver and thymus are the predominant effects of subchronic
administration of TCDD. In a 13-week study conducted by Kociba et al.
(1976, as reported in NAS 1977), degenerative changes in the liver and thymus,
porphyria, altered serum enzyme concentrations, and loss of body weight were
reported in rats given 0.1 yg/kg TCDD five days a week. Young female rhesus
monkeys given a diet containing 500 ppt TCDD for up to nine months showed loss
of facial hair and eyelashes, edema, accentuated hair follicles, and dry scaly
skin (Allen et al. 1977, as reported in USEPA 1979). Five of the eight
monkeys died from severe pancytopenia.
TCDD is fetotoxic and teratogenic in various animal species. Fetuses from
rats that had received 0.125 yg/kg/day showed reduced body weight and a
slight increase in intestinal hemorrhage and edema. At 0.5 yg/kg/day, a
reduction in fetal number and increase in fetal deaths were reported (Sparschu
et al. 1971, as reported in NAS 1977). Courtney and Moore (1971, as reported
in NAS 1977) reported an increase in fetal kidney malformations in rats that
received TCDD subcutaneously at 0.5 yg/kg/day on days 9, 10 or 13 and 14 of
gestation. Increased incidences of cleft palate and kidney abnormalities were
reported in mice that received 1.0 and 3.0 yg/kg/day on days 6 to 16 of
gestation (Smith et al. 1976, as reported in USEPA 1979). The Advisory
Committee on 2,4,5-T (1971, as reported in NAS 1977) reported gastrointestinal
hemorrhage in the fetuses of hamsters that received 0.5 yg/kg/day TCDD on
days 6-10 of gestation.
TCDD is a potent carcinogen. Ingestion by rats of 2.2 ppb or 0.1
yg/kg/day induced squamous cancer of the respiratory tract and oral cavity
in males and females and liver cancer in females only (Kociba et al. 1978).
Van Miller et al. (1977, as reported in USEPA 1979) fed rats diets
containing 0.001 to 1,000 yg TCDD/kg diet. An increased incidence of liver
tumors was reported in groups of rats receiving TCDD at levels of 0.005 to 5
yg/kg of diet; animals in the higher dose groups died between the second and
fourth weeks of treatment.
TCDD has been shown to be mutagenic in three bacterial systems (Hussain
1972, as reported in USEPA 1979). However, this finding has not been
confirmed by other researchers.
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The data on aquatic toxicity of TCDD is not extensive. Miller et al.
(1973, as reported in USEPA 1979) exposed coho salmon to 0.000056 yg/liter
of TCDD for 96 hours under static conditions and then transferred the fish to
control water. Sixty days after exposure, the mortality among the exposed
fish was 12 percent compared to 2 percent among controls. An exposure of
0.056 yg/liter for 24 hours was lethal to all salmon within 40 days.
Reduced reproduction was reported in the snail, Physa sp. and worm, Paranis
sp., exposed to 0.2 yg/liter for approximately 1,175 hours (Miller e*t al.
1973, as reported in USEPA 1979).
No data on the toxicity of TCDD to saltwater organisms or to aquatic
plants are available.
EPA has proposed an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to TCDD through ingestion of contaminated water and aquatic
organisms. Since the zero level may not be attainable at the present time,
the Agency considered establishing an interim criterion of 4.55 x 10 -8
yg/liter, corresponding to a lifetime risk of 0.000001. A final criterion
will be established upon completion of a review of the carcinogenic potential
of TCDD by the, Agency.
EPA has not yet established an aquatic life water quality criterion for
TCDD.
1,2,4-Trichlorobenzene
Human exposure to 1,2,4-trichlorobenzene vapor at 3 and 5 ppm causes minor
eye and respiratory irritation (Rowe 1975 in USEPA 1980). No apparent
"serious" illness, change in liver function, or alteration of blood components
were observed over a period of 4 years in workers employed in a plant where
benzene was chlorinated. One worker inhaled a "massive" amount of
trichlorobenzene and experienced lung hemorrhaging (NAS 1977).
The single dose acute oral LD50 for 1,2,4-trichlorobenzene is 756 mg/kg in
rats and 766 mg/kg in mice (Brown et al. 1969 in USEPA 1980). The rats'
deaths occured within 5 days of exposure, and the mice died within 3 days of
exposure. For both species, decreased signs of activity were observed at low
doses, and convulsions occurred at higher doses. 1,2,4-Trichloro- benzene was
not irritating in subchronic skin irritation studies with rabbits and guinea
pigs (Brown et al. 1969 in USEPA 1980). However, skin inflammation in
rabbits was noted after 3 weeks of exposure. 1,2,4-Trichlorobenzene applied
to rabbit ears for 13 weeks produced some dermal irritation.
Rats, rabbits, and monkeys were administered 1,2,4-trichlorobenzene by
inhalation at concentrations of 25, 50, and 100 ppm for up to 26 weeks (Coate
et al. 1977 in USEPA 1980). No "exposure-related" ophthalmologic,
hematologic, pulmonary, or metabolic (blood urea nitrogen, bilirubin, serum
glutamic oxaloacetic transaminase, serum glutamic-pyruvic transaminase, lactic
dehydrogenase, and alkaline phosphatase) changes were observed. Histologic
changes were noted in the livers and kidneys of rats necropsied at 4 weeks.
The changes were dose-related and were observed in animals from each treatment
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group. However, after 20 weeks, no compound-related histopathological changes
were noted in rabbits or monkeys. Mice exposed to 600 ppm of 1,2,4-
trichlorobenzene for 6 months did not develop hepatomas. No other information
is available on the carcinogenicity, mutagenicity, or teratogenicity of
1,2,4-trichlorobenzene (USEPA 1980).
The acute toxicity of 1,2,4-trichlorobenzene to various saltwater and
freshwater species is reflected by the 96-hour LC50 values in cladoceran of
50.2 mg/liter, rainbow trout of 1.5 mg/liter, fathead minnow of 2.9 mg/liter,
mysid shrimp of 0.45 mg/liter, and sheepshead minnow of 21.4 mg/liter. The
chronic toxicity value for 1,2,4-trichlorobenzene to fathead minnow ranges
from 0.28 to 0.71 mg/liter. 1,2,4-Trichlorobenzene has also demonstrated
acute toxic effects to freshwater and saltwater algae with 96-hour EC50 values
ranging from 8.7 to 36.7 mg/liter. The whole-body, 28-day bioconcentration
factor of 1,2,4-trichlorobenzene in the bluegill is 182 (USEPA 1980).
EPA has not yet established ambient water quality criteria for
1,2,4-trichlorobenzene because of the lack of sufficient information.
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4. Metals and Cyanide
Ant imony
The major toxic symptoms that are associated with antimonial compounds in
humans involve the gastrointestinal tract, heart, respiratory tract, skin, and
liver. The most serious effects of these compounds have been observed during
antimonial therapy and during industrial exposure (National Institute for
Occupational Safety and Health 1978, as reported in NAS 1980). Symptoms
include cardiac alterations, bradycardia, and fluctuations in blood pressure
(Brieger et al. 1954, NIOSH 1978, as reported in NAS 1980). Respiratory
changes include irritation of the mucous membranes, upper respiratory tract
irritation, and, more seriously, pneumonoconiosis. Pneumonia has also been
cited as a side effect to the therapeutic use of antimony. Gastrointestinal
symptoms include cramps, nausea, pain, anorexia, diarrhea, and vomiting (NAS
1980). Chromosomal damage in human leukocytes studied in vitro occurred
with exposure to as little as 280 mg/liter of antimony (Paton and Allison
1972, as reported in USEPA 1980 and NAS 1980). A greater incidence of
spontaneous abortion, premature deaths, and gynecological problems were
reported in antimony workers at a metallurgical plant (Belyayeva 1967, as
reported in NAS 1980).
Acute poisoning of antimonial compounds in animals produce labored
breathing, general weakness, and other signs of cardiovascular insufficiency
leading to death among many animals within several days after exposure. Oral
LD50 values are 300 mg/kg (tartar emetic) for the rat and 804 mg/kg (antimony
trifluoride) for the mouse (Bradley and Fredrick 1941, as reported in USEPA
1980).
In chronic animals studies, rats fed 135 mg/kg trivalent antimony chloride
for 10 days developed toxic symptoms including myocardial degeneration
(Arzamastsev 1964, as reported in NAS 1980). Decreased hemoglobin and
increased reticulocyte count were observed in guinea pigs treated for 10 days
with 12 and 20 mg/kg trivalent antimony chloride (Arzamastsev 1964, as
reported in NAS 1980). In a longer study, rats orally fed 200 mg antimony
potassium tartrate died after 85 days (Flury 1927, as reported by NAS 1980).
Decreased fertility was reported in rats exposed to 50 mg/kg metallic antimony
by inhalation (Belyayeva 1967, as reported in NAS 1980). No evidence of
carcinogenicity was observed in mice given 5 ug of antimony potassium
tartrate per milliliter of drinking water throughout their lifetime (Kanisawa
and Schroeder 1969, as reported in USEPA 1980).
The acute toxicity of antimony compounds on aquatic organisms is reflected
by 96-hour LC50 values in cladoceran of 9 mg/liter for antimony potassium
tartrate, and 21.9 mg/liter in the fathead minnow and 18.8 mg/liter in
cladoceran for antimony trichloride. 96-Hour LC50 values for antimony
trioxide are greater than 530 mg/liter in the bluegill and greater than 4.2
mg/liter in the mysid shrimp. For this same compound the 96-hour LC50 ranges
from 6.1 to 8.3 mg/liter. Chronic toxicity was observed in cladoceran exposed
to between 4.2-7.0 mg/liter antimony trichloride; and the fathead minnow
exposed to greater than 7.5 yg/liter for antimony trioxide and between 1.1
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and 2.3 mg/liter for antimony trichloride. Freshwater algae were affected by
0.61-0.63 mg/liter antimony trioxide while freshwater algae were not affected
by levels of 4.2 mg/liter antimony trioxide (USEPA 1980).
EPA has established an ambient water quality criterion of 146 yg/liter
for the protection of human health from the toxic properties of antimony
ingested through water and contaminated aquatic organisms.
EPA has not yet established an aquatic life water quality criterion for
antimony.
Arsenic
The toxicity of arsenic varies according to the physical form and the
oxidation state of the compound. In general, soluble trivalent arsenic
compounds are more toxic than the pentavalent species, and inorganic
arsenicals are also more toxic than organic arsenicals. Inorganic arsenate
predominates in most waterways because of its stability and solubility.
Many epidemiological studies have linked the development of cancer to
exposure to inorganic arsenic compounds. Evidence has come from the use of
arsenicals as drugs, from geographical areas with high arsenic levels in the
drinking water, and from occupational exposures of workers in mining
operations, smelters, pesticide manufacture and vineyards. However, this
evidence associating inorganic arsenic compounds with lung cancer in humans is
still open to question. For skin cancer, however, a causal relationship
between incidence and high-level exposures to inorganic arsenic compounds has
been reported (Tseng et al. 1968, as reported in NAS 1977).
Symptoms of acute arsenic poisoning by ingestion include abdominal pain
and vomiting, while acute poisoning by inhalation produces giddiness,
headache, extreme general weakness, and later nausea, vomiting, colic,
diarrhea, and pains in the limbs (Browning 1961, as reported in NAS 1977).
Although no animal experiments have demonstrated carcinogenicity of
arsenic, several have shown that sodium arsenate and arsenite induce
developmental malformations in a variety of test animals including chick
embryos, hamsters, rats, and mice (USEPA 1980).
Arsenic has been shown to be toxic to both vertebrate and invertebrate
freshwater aquatic organisms and saltwater aquatic organisms. Cladocerans
have been reported to be more sensitive than fish, although certain
invertebrates such as stoneflies may be more tolerant than fish. Static
96-hour LC50 values range from 0.812 mg/liter sodium arsenite for the scud to
22 mg/liter for the stonefish. However, less sensitive static 96-hour LC50
values of 26 mg/liter and 41.76 mg/liter sodium arsenite, respectively, were
reported for goldfish and bluegill. One hundred percent of three different
strains of freshwater algae were killed in 2 weeks in 2.32 mg/liter sodium
arsenite. Arsenic has been shown to bioconcentrate in both fresh and
saltwater organisms (USEPA 1980).
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EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to arsenic through the ingestion of contaminated water and
contaminated aquatic organisms. Since the zero level may not be attainable at
the present time, a level of 2.2 ng/liter, corresponding to an estimated
lifetime incremental increase of cancer risk of 10-6, was recommended.
EPA has not yet established an aquatic life water quality criterion for
arsenic.
Asbestos
Asbestos is a term applied to numerous fibrous mineral silicates composed
of silicon, oxygen, hydrogen, and metal cations. The two major groups of
asbestos are serpentine (chrysotile) and amphibole. Numerous epidemiological
studies have shown that long-term exposure to asbestos dust can lead to
asbestosis and an increased risk of cancer.
Asbestosis is a chronic, progressive pneumoconiosis, characterized by
fibrosis of the lung parenchyma. Other symptoms of the disease include cough,
rales, finger clubbing, restrictive pulmonary dysfunction, and weight loss.
In some cases the disease can lead to death. X-rays typically reveal small,
irregular opacities in the lungs, often accompanied by pleural fibrosis,
thickening, or calcification.
An association between inhalation of asbestos and an increased rislc of
cancer has been clearly established in epidemiologic studies. In a study of
the mortality experience of 17,800 asbestos insulation workers from 1967 to
1976 by Selikoff et al. (1979, as reported in USEPA 1980), significantly
increased incidences of lung tumors, mesotheliomas, cancer of the
gastrointestinal tract, larynx, pharyxn, and buccal cavity, and renal tumors
were reported.
Several studies of cancer incidence among factory workers employed in the
manufacture of asbestos products have been reported (USEPA 1980).
Investigators have shown a significant excess in total mortality in exposed
workers, with important contributions from asbestosis, cancer of the lung,
bronchus, and trachea, and neoplasms of the digestive organs and peritoneum
(including peritoneal mesothelioma). Mesothelioma is a form of cancer that is
very rare among individuals not exposed to asbestos. Increased risks of lung
cancer and mesothelioma have also been reported among individuals exposed only
indirectly to asbestos, including shipyard workers and groups living or
working in an area of asbestos mining (USEPA 1980).
Several studies have considered the relationship between ingestion of
asbestos in drinking water and gastrointestinal cancer. The human data is,
however, inconclus ive.
The carcinogenicity of asbestos has also been demonstrated in animals.
Gross et al. (1967, as reported in USEPA 1980) reported 19 adenocarcinomas,
4 squamous cell carcinomas, and one mesothelioma among 72 rats exposed by
inhalation to 86 mg/cu m chrysotile for 16 months or longer. No malignant
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tumors were found in 39 controls. Rats exposed to various forms of asbestos
at concentrations ranging from 10 to 15 mg/cu m for periods ranging from 1 day
to 24 months showed an increased incidence of adenocarcinomas, squamous-cell
carcinomas, and mesotheliomas. No tumors appeared prior to 300 days from
first exposure, and none of these tumors appeared in control animals (Wagner
et al. 1974, as reported in USEPA 1980).
Mesotheliomas have been produced in rats by intrapleural injection of 10
mg of asbestos (Reeves et al. 1971, as reported in USEPA 1980) and by
intraperitoneal injection (Maltoni and Annoscia 1974, as reported in USEPA
1980). The carcinogenicity of asbestos administered by ingestion has not been
demonstrated.
No data were available on the potential toxicity of asbestiform material
to freshwater or saltwater organisms.
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to asbestos through ingestion of contaminated water and aquatic
organisms. Since the zero level may not be attainable at the present time, a
level of 30,000 fibers/liter, corresponding to a lifetime cancer risk of
0.000001, was recommended.
EPA has not yet established an aquatic life water quality criterion for
asbestos.
Beryllium
Beryllium is relatively nontoxic to humans when ingested in food and water
because absorption from the digestive tract is slight (NAS 1977). However,
beryllium and several beryllium compounds can cause acute and chronic effects
in humans. The most common effects of industrial exposure to beryllium are
skin lesions: dermatitis, ulceration, and granulomas. Dermatitis has been
regarded as a sensitizing reaction (Doull et al. 1980). Acute effects on
the respiratory system -- known as acute berylliosis -- may occur following
inhalation of beryllium at levels of 30 mg/cu m for the high-fired oxide, 1-3
mg/cu m for the low-fired oxide, and 0.1-0.5 mg/cu m for beryllium sulfate;
effects are usually reversible after weeks or months (Reeves et al. 1979, as
reported in IARC 1980). The acute response is characterized by
nasopharyngistis, tracheobronch.itis, and fulminating pneumonia (Doull et al.
1980).
Repeated inhalation exposure can lead to chronic berylliosis, with latent
periods of 10 to 20 years from the first exposure commonly observed. Chronic
berylliosis is characterized by dyspnea, chronic cough, weight loss, weakness,
fatigue, and chest pain. Systemic impairments include granulomatous
inflammation of the lungs; involvement of the striated muscle, liver, spleen,
kidneys, and heart; disturbances in nitrogen and calcium metabolism; and
immunological sensitization (Doull et al. 1980). Human case reports and
epidemiologic studies provide suggestive but inconclusive evidence that
beryllium is carcinogenic in humans. A positive correlation between beryllium
concentrations in drinking water and cancer deaths in 15 regions of the
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country was reported (Berg and Burbank 1972, as reported in USEPA 1980). The
results of three epidemiological studies suggest that beryllium exposure
increased the risk of cancer mortality; however, confirmatory studies are
needed to evaluate the importance of other risk factors in beryllium-
associated lung cancer cases (USEPA 1980).
In animal studies, beryllium has been shown to be acutely toxic to rats by
intravenous injection at 0.44 to 0.51 mg Be/kg (as soluble beryllium salts),
by the oral route at 9.7 mg/kg, and by inhalation at 42-194 yg/cu m (USEPA
1980). Chronic beryllium disease can be produced in experimental animals by
inhalation of low concentrations of soluble beryllium salts. Rats exposed for
up to 6 months to 35 yg/cu m of beryllium sulfate aerosol developed typical
chronic pneumonitis along with granulomatous lesions and some neoplasms
(Schepers et al. 1957, as reported in USEPA 1980). Exposure of monkeys to
35 yg/cu m of beryllium sulfate or intratracheal instillation of a 5 percent
suspension of beryllium oxide resulted in chronic pneumonitis in all animals
(Vorwald et al. 1966, as reported in USEPA 1980). Macrocytic anemia and
osteosclerotic changes have also been reported in animals following chronic
exposure to beryllium (USEPA 1980). Lung cancer and bone cancer
(osteosarcoma) are the two types of malignancies commonly induced in
experimental animals by exposure to beryllium compounds. In an inhalation
study in which rats were exposed to beryllium sulfate at 2.8, 21, and 42 yg
Be/cu m for 7 hours/day, 5 days/week, for a period of 18 months, pulmonary
cancers were found in almost all animals at the two highest doses and in 62
percent at the low dose (Vorwald et al. 1966, as reported in USEPA 1980).
Groups of rats were administered beryllium oxide calcined at temperatures of
500-1600oC by intratracheal instillation at a dose of 25 mg/kg; pulmonary
cancers were reported in 25 to 100% of the animals (Spencer et al. 1968, as
reported in USEPA 1980). Osteosarcomas have been produced in rabbits by
intravenous injections or injections into the bone by numerous investigators.
In one study, osteosarcomas were produced in 89% and 100% of the rabbits
injected with beryllium oxide into the femur at doses of 220-400 and 420-600
mg, respectively, twice weekly for 1-43 weeks (Yamaguchi and Katsura 1963, as
reported in USEPA 1980).
Acute beryllium aquatic toxicity data are available for the fathead
minnow, guppy, and bluegill at levels of hardness ranging from about 20 to 400
mg calcium carbonate/liter. For these species, acute toxic effects were
reported at concentrations ranging from 130 yg/liter to 3,200 yg/liter
(USEPA 1980). A 48-hour EC50 for Daphnia magna of 2,500 yg/liter was
reported. In a chronic life-cycle study with Daphnia magna, toxic effects
were observed at 5.3 yg/liter (USEPA 1980). Toxic effects of beryllium on
saltwater organisms have not been reported. In one study of freshwater
plants, the growth of a green alga was inhibited at a beryllium concentration
of 100,000 yg/liter (USEPA 1980).
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to beryllium through ingestion of contaminated water and aquatic
organisms. Since the zero level may not be attainable at present, a level of
3.7 ng/liter, corresponding to a lifetime incremental cancer risk of 0.000001,
was recommended.
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EPA has not yet established an aquatic life water quality criterion for
beryllium.
Cadmium
Human toxicity resulting from exposure to cadmium is well-documented, the
major effects being respiratory and renal toxicity. Numerous cases of acute
cadmium poisoning in humans have been reported. Acute lethal doses by
inhalation vary considerably depending on chemical form, particle size, and
duration of exposure; the product of concentration x time representing a
lethal dose of cadmium fumes has been estimated to be 2,600 mg/cu m. min,
i.e., 2,600 mg/cu m for one minute, 26 mg/cu m for 100 minutes, and so on
(Doull et al. 1980). The minimal toxic dose for an 8-hour inhalation
exposure is estimated to be 1 to 3 mg/cu m (CEC 1978, as reported in Doull et
al. 1980). Acute toxic effects of cadmium inhalation include irritation of
the upper respiratory tract, chest pains, nausea and diarrhea, dizziness, and
death usually due to massive pulmonary edema (Doull et al. 1980). Acute
lethal cadmium doses by oral exposure in humans are estimated to range from
350 to 8,900 mg; major toxic effects of cadmium ingestion include nausea,
vomiting, salivation, diarrhea, and abdominal cramps. Death due to shock,
dehydration or delayed systemic effects (notably renal and cardiopulmonary
failure) may occur (Doull et al. 1980).
The principal target organs following chronic exposure to cadmium are the
lungs and kidney. Chronic inhalation of cadmium fumes and dust can lead to an
emphysema-like condition with loss of ventilatory capacity, increased residual
lung volume, and shortness of breath (Lauwerys et al. 1974, as reported in
Doull et al. 1980). The kidney appears to be the most cadmium-sensitive
organ, primarily because of its prediliction for accumulation of cadmium.
Renal toxicity of cadmium was first reported in a study of industrial exposure
to cadmium oxide dust in an alkaline storage battery factory (Friberg 1948, as
reported in Doull et al. 1980). Workers exhibited consistent proteinuria
and a reduced ability to concentrate urine. Glycosuria, hypercalciuria,
aminoaciduria, and increased uric acid excretion have also been reported in
workers (Kazantzis et al. 1963, as reported in Doull et al. 1980). Based
on limited renal biopsies of affected and nonaffected workers, Friberg e_t
al. (1974, as reported in Doull et al. 1980) have proposed a threshold
concentration for renal toxicity of 200 ug Cd/g kidney cortex. An incident
of chronic cadmium poisoning resulting from dietary intake was reported in
Japan in the 1940's. The disease was named Itai-itai (or ouch-ouch). People
consuming cadmium-contaminated rice developed osteomalacia with attendant
spontaneous multiple bone fractures as well as porteinuria and glycosuria
(Doull et al. 1980).
Several epidemiologic studies provide suggestive evidence that cadmium
increases the risk of prostatic cancer in men. Lemen et al. (1976, as
reported in Clayton and Clayton 1981) found an excess of cancers of the
prostate among cadmium smelter workers. Five of eight deaths among a group of
74 alkaline cadmium battery workers who had been exposed to CdO dust for ten
or more years were due to cancer, including three carcinomas of the prostate
(Potts 1965, as reported in Clayton and Clayton 1981). In a survey of 248
workers exposed to CdO for one or more years, four deaths from prostatic
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cancer, significantly more than expected, were observed (Kipling and
Waterhouse 1967, as reported in Clayton and Clayton 1981). The evidence for
carcinogenicity of cadmium in humans is not conclusive, however, because of
the small study populations and confounding exposures to other elements which
are known to be human carcinogens (USEPA 1980).
The toxic effects of cadmium observed in humans have been reproduced in
experimental animals. The acute oral LD50 varies from approximately 100 mg/kg
for soluble salts of cadmium to several thousand mg/kg for metallic cadmium
powder or the insoluble selenide and sulfide. Rats exposed to a cadmium
aerosol for 15 days developed lung inflammation followed by emphysema and
fibrosis (Snider et al. 1973, as reported in Doull et al. 1980).
Itai-itai disease has also been reproduced experimentally in rats given an
excess of cadmium in a calcium deficient diet (Itokawa e,t al. 1974, as
reported in Doull et al. 1980). In newborn animals, cadmium has been shown
to cause cerebral and cerebellar damage. Cadmium also is toxic to the testes
of rats and mice, and causes hyperglycemia and glucose intolerance in animals
(Doull et al. 1980).
Animal studies have demonstrated that the injection of cadmium metals or
salts causes sarcomas at the site of injection and testicular tumors (Leydig
or interstitial cell tumors). Interstitial cell tumors and subcutaneous
sarcomas were reported in rats following a single subcutaneous injection of
0.03 mmol cadmium chloride (Gunn 1963, as reported in Clayton and Clayton
1981). Cadmium metal, CdO, CdS, and cadmium sulfate have also elicited
injection-site sarcomas (Clayton and Clayton 1981 and USEPA 1980). Several
long-term feeding and inhalation studies have been carried out with cadmium
compounds; the induction of tumors by these routes of exposure has not been
observed (USEPA 1980).
Predicting the impact of cadmium on aquatic organisms is complicated by
the variety of forms in which cadmium may be present, the differences in
toxicity and availability of the various forms, hardness of the water, pH,
temperature, and presence of other metal ions (USEPA 1980). The results of
acute toxicity tests on cadmium with 29 freshwater fish and invertibrate
species range from 1 to 73,500 yg/liter (as Cd); both EC50 and LD50 values
are included in this range. Chronic toxicity was observed in Daphnia magna
at concentrations ranging from 0.15 to 0.44 yg/liter, and in 12 freshwater
fish species at concentrations ranging from 1.7 to 50 yg/liter (USEPA
1980). In a 42-day study of cadmium toxicity to the bay scallop, exposure to
60 and 120 yg/liter reduced growth by 42 and 69 percent, respectively (Pesch
and Stewart 1980, as reported in USEPA 1980). A 48-day exposure of copepods
to cadmium inhibited reproduction at concentrations greater than 44 yg/liter
(D'Agostino and Finney 1974, as reported in USEPA 1980). Acute toxicity
values for 5 species of saltwater fish ranged from 577 yg/liter for larval
Atlantic silversides to 114,000 yg/liter for juvenile mummichog. Acute
toxicity values for 26 species of saltwater invertibrates ranged from 15.5
yg/liter for the mysid shrimp to 46,600 yg/liter for the fiddler crab. In
two life-cycle studies of mysid shrimp, toxic effects were observed at
concentrations of 5.5 and 8.0 yg/liter (USEPA 1980). Growth reduction was
the major toxic effect observed in several species of freshwater plants at
concentrations ranging from 2 to 7,400 yg/liter (USEPA 1980). In studies of
two species of saltwater phytoplankton, EC50 values of 160 and 175 yg/liter,
based on growth inhibition, were reported (USEPA 1980).
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EPA has established an ambient water quality criterion of 10 yg/liter
for the protection of human health from the toxic properties of cadmium
through ingestion of contaminated water and contaminated aquatic organisms.
EPA has established an aquatic life water quality criterion for freshwater
species of 0.012 yg/liter (24-hour average), with a maximum not to be
exceeded of 1.5 yg/liter. For saltwater species, the 24-hour average
criterion is 4.5 yg/liter, with a maximum not to be exceeded of 59
yg/liter.
Chromium
The toxicity of chromium varies according to its valence state. The
hexavalent and trivalent moieties are the biologically significant forms.
Hexavalent chromium has long been recognized as a toxic substance, while
trivalent chromium is considered to be relatively innocuous (NAS 1977).
Chromium has been shown to cause a variety of toxic effects. Certain
chromium (VI) compounds are carcinogenic in humans (IARC 1980, USEPA 1980, NAS
1974, as cited in USEPA 1980). In occupational exposures, dermatitis,
irritation of mucous membranes, injury to nasal tissue, changes in pulmonary
dynamics, lung cancer, and renal and hepatic toxicity have been observed (NAS
1974, Borett et al. 1977, Mancuso 1951, Bloomfield and Blum 1928, USPHS
1953, and IARC 1980, as reported in USEPA 1980).
In animals, acute toxicity has been observed only when high doses were
administered. For example, rats tolerated hexavalent chromium in drinking
water at 25 ppm for 1 year, and dogs showed no effect from chromium as
potassium chromate at 0.45-11.2 ppm over a 4-year period (NAS 1974, as
reported in NAS 1977). Chromates, however, have been shown to be mutagenic in
a wide variety of test systems (USEPA 1980). Chromium compounds also caused
terata in hamsters (IARC 1980). With regard to carcinogenicity, intraosseous,
intramuscular, subcutaneous, intrapleural, and intraperitoneal injections of
chromium compounds produced tumors at the site of administration in rabbits,
mice, and rats (NAS 1977). Intramuscular administration of lead chromate in
rats produced renal carcinomas (IARC 1980).
Acute toxicity data for hexavalent chromium are available for 13
freshwater animal species; 96-hour LC50 values range from 67 ug/liter for a
scud to 59,900 yg/liter for a midge. In saltwater species 96-hour LC50
values of hexavalent chromate range from 2,000 yg/liter for polychaete
annelids and mysid shrimp to 105,000 yg/liter for the mud snail. Soft water
96-hour LC50 values for hexavalent chromium range from 17.6 mg/liter for
fathead minnows to 118 mg/liter for bluegill; hard water 96-hour LC50 values
for hexavalent chromium range from 27.3 mg/liter for fathead minnows to 133
mg/liter for bluegill. 96-Hour LC50 trivalent chromium values (chromium
potassium sulfate) range from 3.33 mg/liter for guppies to 7.46 mg/liter for
bluegill in soft water. The LC50 for fathead minnows exposed to potassium
chromate in soft water was reported to be 45.6 mg/liter. Hexavalent chromium
was also found to significantly reduce the growth and survival of chinook
salmon at concentrations of 0.2 mg/liter. Chronic toxicity of hexavalent
chromium was observed in the polychaete worm at concentrations ranging from 17
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to 38 yg/liter; the mysid shrimp at concentrations ranging from 88 to 198
yg/liter; the rainbow and brook trout at concentrations ranging from 200 to
350 yg/liter; and the fathead minnow at concentrations ranging from 1,000 to
3,950 yg/liter. Algae and the giant kelp were affected at concentrations
ranging from 1,000 to 5,000 yg/liter (USEPA 1980).
EPA has established an ambient water quality criterion of 50 yg/liter
for the protection of human health from the toxic properties of chromium (VI)
through ingestion of water and contaminated aquatic organisms. A human health
criterion of 170 mg/liter was established for chromium III.
EPA has established an aquatic life water quality criterion for freshwater
species of 0.29 yg/liter (24-hour average) for chromium VI, and a criterion
of 2200 yg/liter (maximum level not to be exceeded) for chromium III. The
aquatic life water quality criterion for saltwater species is 18 yg/liter
(24-hour average) for chromium VI.
Copper produces a metallic taste in the mouth, nausea, vomiting,
epigastric pain, diarrhea, and depending on the severity, jaundice, hemolysis,
hemoglobinuria, hematuria, and oliguria. In severe cases, hepatic necrosis,
gastrointestinal bleeding, anuria, hypotension, tachycardia, convulsions, and
coma can occur (USEPA 1980). The toxic intake of inorganic copper for an
adult male was reported to be greater than 15 mg per dose (Burch et al.
1975, as reported in USEPA 1980). Chronic oral exposure to copper has
resulted in behavioral changes, diarrhea, and progressive marasmus in an
infant (Salmon and Wright 1971, as reported in USEPA 1980).
Chronic toxicity in animals varies considerably in different species.
Sheep are highly susceptible while rats are resistant to the effects of copper
(USEPA 1980). Copper poisoning has been reported in swine at levels of 250
yg/g in the diet (Suttle and Mills 1966, as reported in USEPA 1980).
Hepatic hemosiderosis developed in swine and rats fed copper acetate in a
chronic oral feeding study (Mailory and Parker 1931, as reported in USEPA
1980). No information is available on the teratogenicity or mutagenicity of
copper, although one report suggested that copper may increase the mutagenic
activity of other compounds. The carcinogenic potential of copper has not
been established (USEPA 1980).
Acute toxicity testing on copper has been conducted with 45 freshwater
species and chronic tests with 15 species. Acute toxicity levels range from
0.0072 mg/liter for cladocerna in soft water to 10.2 mg/liter for the bluefish
in hard water. Toxicity appears to decrease as the hardness of the water
increases. Additional data for several species indicate, that toxicity also
decreases with increasing alkalinity and total organic carbon. Among the more
sensitive species are daphnids, scuds, midges, and snails, which form the
major food webs for both warm and cold water fish (USEPA 1980).
The acute toxicity of copper to saltwater animals ranges from 17
yg/liter for a Calonoid copepod to 600 yg/liter for the shore crab. A
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chronic lifecycle test on mysid shrimp showed adverse effects at 77
Tig/liter. Saltwater algae were adversely affected in concentrations ranging
from 5 to 100 yg/liter. Oysters have been reported to bioaccumulate copper
up to 28,200 times the ambient concentration. In long-term exposures, the bay
scallop was killed at 0.005 mg/liter (USEPA 1980).
Chronic toxicity values for 15 species ranged from a low of 3.9 yg/liter
for brook trout to 6.4 yg/liter for the northern pike. The two most
sensitive species, bluntnose minnow and G. pseudolimnia, are both important
food organisms. Copper toxicity has been evaluated on a wide range of plant
species, with results similar to those for animals. Bioaccummulation does not
appear to occur often in the edible portion of freshwater aquatic species
(USEPA 1980).
EPA has not yet established ambient water quality criteria for the
protection of human health from the toxic effects of copper because of the
lack of sufficient information. However, using organoleptic data for
controlling undesirable taste and odor of ambient water, the estimated level
is 1 mg/liter.
The aquatic life water quality criterion for freshwater species is 5.6
yg/liter (24-hour average), with a level not to be exceeded of 12
yg/liter. For saltwater species, the 24-hour average criterion is 4
yg/liter; the maximum level not to be exceed is 23 yg/liter.
Cyanide
Hydrogen cyanide and its alkali metal salts are extremely toxic to humans
and other mammals (USEPA 1980). By ingestion, the mean lethal dose of these
substances is estimated to range from 50 to 200 mg for humans with death
occurring generally within 1 hour (Gosselin et al. 1976, as reported in
USEPA 1980). Inhalation of hydrogen cyanide gas at 0.1-0.3 mg/liter has
caused death in 10-60 minutes in humans (Prentiss 1937 and Fassett 1963 as
reported in USEPA 1980). The acute effects of cyanide poisoning mostly result
from inhibition of cytochrome C oxidase, resulting in a blockage of oxidative
metabolism and phosphorylation (Gosselin et al. 1976, as reported in USEPA
1980). The organ systems most profoundly affected are the heart and brain
because of their high dependence on oxidative metabolism. Cyanide poisoning
can also cause increased blood pressure (Heymans and Neil 1958, as reported in
USEPA 1980). Exposure of humans to small amounts of cyanide compounds over
long periods of time is reported to cause loss of appetite, headache, weakness
nausea, dizziness, and symptoms of toxicity in the upper respiratory tract and
eyes (Sax 1975).
Despite the high acute toxicity of cyanide, chronic exposure to sublethal
doses does not appear to have serious adverse effects (USEPA 1980). Animal
studies with dogs administered 0.5-2 rag/kg sodium cyanide once or twice each
day for 15 months showed no evidence of pathophysiological changes in organ
function or permanent alteration in intermediary metabolism (Hertting et a1.
1960, as reported in USEPA 1980). In other studies rats were fed a potassium
cyanide mixture equivalent to the LD50 for 25 days and dogs were fed 150 ppm
sodium cyanide for 30 days without observing significant adverse effects
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(Hayes 1967 and American Cyanamid 1959, as reported in USEPA 1980). No
information is available on the mutagenicity and carcinogenicity of cyanides
(USEPA 1980). However, thiocyanate, the major metabolic product of cyanide,
has produced, jji vivo, developmental abnormalities in the chick and ascidian
embryo. (Nowinski and Pandra 1946 and Ortolani 1969, as reported in USEPA
1980)
The acute toxicity of cyanide to aquatic organisms has been demonstrated
in over 35 species of fresh and saltwater animals. The 96-hour LC50 values
range from 30 yg/liter for the saltwater copopod to 2326 yg/liter for the
freshwater isopod. Most values, however, cluster between 50 and 200
yg/liter. Teratogenic effects have been observed in the Atlantic salmon,
and reproductive disturbances have occurred in the bluegill, fathead minnow,
brook trout, and rainbow trout at concentrations ranging from 5.4 to 62
yg/liter (USEPA 1980).
Chronic toxicity has been observed in the brook trout, fathead minnow, the
bluegill, the isopod, and the scud in concentrations ranging from 8 to 34
yg/liter, depending on the species. Reduced swimming capacity was observed
in the brook trout at 10 yg/liter, in rainbow trout at 20 yg/liter, and in
the Cichlasoma binaculatum at 40 yg/liter. Aquatic plants are much more
resistant to the effects of cyanide; effects are not observed until
concentrations reach 3,000 yg/liter (USEPA 1980).
EPA has established an ambient water quality criterion of 200 yg/liter
for the protection of human health from the toxic properties of cyanide
through ingestion of water and contaminated aquatic organisms.
EPA has established an aquatic life water quality criterion for freshwater
species of 3.5 yg/liter (24-hour average), with a maximum not to be exceeded
of 52 yg/liter. EPA has not yet set a criterion for saltwater species.
Lead
Acute inorganic lead intoxication is rare (Casarett and Doull 1975). The
most serious effects of chronic exposure in humans are seen in the
hematopoietic system (decreased heme synthesis), nervous system
(encephalopathy), and renal system (NAS 1977 and USEPA 1980). Blood lead
concentrations of 25-30 yg/day in children and women and 35-40 yg/day in
men have been associated with statistically significant increases in red-cell
protoporphyrin (Zielhuis 1975, as reported in USEPA 1980). The noeffect
concentration of lead in the blood on the developing human nervous system has
been estimated at 55-60 yg/day whole blood (NAS 1977). Blood-lead
concentrations in excess of about 50-60 yg/day have been associated with
spermatoxic effects in men (Lancranjan et al. 1975, as reported in USEPA
1980). Lead has not been shown to be carcinogenic in humans, although one
researcher has questioned the statistical methodology used in the
epidemiological studies (Kanj et al. 1980, as reported in USEPA 1980).
Certain lead compounds have been found to produce tumors in some species
of experimental animals. For example, in a 2-year feeding study on rats, lead
acetate at concentrations of 1,000 ppm or more was found to induce renal
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tumors; furthermore, the number of tumor bearing animals was dose dependent
(Azar et al. 1973, as reported in USEPA 1980). Lead has been associated
with teratogenic effects in chick embryos and rodents (USEPA 1980).
Teratogenic effects were seen in the offspring of rats that had received a
single intraperitoneal dose of 25-70 mg/kg on day 9 of gestation.
Administration later in pregnancy induced fetal resorption without teratogenic
effects (McClain and Beeker 1975, as reported in USEPA 1980). Chronic
administration of lead in the drinking water of pregnant rats at
concentrations up to 250 mg/liter was found to delay fetal development and
increase fetal resorption; no teratogenic effects were seen (Kimmel et al.
1976, as reported in USEPA 1980).
Lead has been shown to be acutely toxic to freshwater animals over a range
of concentrations from 124 to 542,000 yg/liter, depending on the species
tested and the hardness of the water. The acute toxicity values for saltwater
invertebrates ranged from 668 yg/liter to 27,000 yg/liter. Chronic tests
have been conducted with two invertibrate species and six fish species with
the chronic values ranging from 12 yg/liter for Daphnia magna to 174
yg/liter for the white sucker (USEPA 1980). Concentrations as low as 500
yg/liter were found to inhibit the growth of freshwater algae (USEPA 1980).
EPA has established an ambient water criterion of 50 yg/liter for the
protection of human health from the toxic properties of lead through ingestion
of water and contaminated aquatic organisms.
EPA has established an aquatic life water quality criterion for freshwater
species of 0.75 yg/liter (24-hour average), with a maximum level not to be
exceeded of 74 yg/liter.
Mercury
Elemental mercury is extremely toxic but is very poorly absorbed from the
gastrointestinal tract. The oral toxicity of inorganic mercury salts depends
on their solubility. Elemental mercury is transformed biochemically in bottom
sediments to methyl mercury or other organic mercurial compounds (USEPA
1976). The organic form readily enters the food chain with concentration
factors as great as 3,000 in fish (Hannerz 1968, as reported in USEPA 1976).
Acute poisoning in man has resulted from exposure to mercury vapor in
concentrations ranging from 1.2 to 8.5 mg Hg/cu m with symptoms related to
pulmonary effects (Casarett and Doull 1975). Chronic exposure to mercury
vapor results in central nervous system effects including psychic and
emotional disturbances, increased irritability, combativeness, defective
patterns, ocular disturbances, and tremors. Kidney and gastrointestinal
disturbances are often associated with chronic mercury exposure (AIHA 1966, as
reported by Casarett and Doull 1975).
Symptoms of acute inorganic mercury poisoning include pharyngitis,
gastroenteritis, vomiting followed by ulcerative hemorrhagic colitis,
nephritis, hepatitis, and circulatory collapse (USEPA 1976). Renal toxicity
occurs with chronic exposure to inorganic mercury (Casarett and Doull 1975).
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The toxicity of alkyl mercury compounds, particularly methyl mercury,
differs significantly from other organic mercurials. In addition to the
environmental transformation of other forms of mercury to methyl mercury, this
compound is readily absorbed through the lungs, and skin and gastrointestinal
absorption under most circumstances is nearly complete (Casarett and Doull
1975). Methyl mercury will also readily cross the placental barrier causing
fetal toxicity. In humans methyl mercury poisoning has produced fatalities,
birth defects, and severe central nervous system effects (NAS 1977). The
ingestion of fish containing mercury in Minamata, Japan, and the ingestion of
wheat seed treated with phenyl mercuric acetate resulted in similar toxic
effects including mental disturbance, ataxia, speech disturbances, hearing
impairment, constriction of visual fields, increased tendon reflex, and
involuntary movement. Hypoplasia and atrophy of the brain tissue have also
been reported (Casarett and Doull 1975).
The toxicity of inorganic mercury to freshwater aquatic organisms was
demonstrated in nine taxonomic orders from rotifers to fish. Acute toxicity
values ranged from 0.02 to 2,000 yg/liter. The acute toxicity of mercuric
chloride was reported for 26 species of saltwater animals including annelids,
molluscs, crustaceans, echinoderms, and fishes. Species mean acute values
range from 3.5 to 1,680 yg/liter. Fish are more resistant while molluscs
and crustaceans are more sensitive. The acute toxicity of methyl mercury and
other mercury compounds is available only for fish, limiting an estimate of
the range of species sensitivity to the compound. Methyl mercury is the most
toxic of the mercury compounds with chronic values for cladoceran and brook
trout being 1.0 and 0.52 yg/liter, respectively. For inorganic mercury the
chronic value for cladoceran is reported to be 1.6 yg/liter. Concentrations
that affected growth and photosynthetic activity of one saltwater diatom and
six species of brown algae range from 10 to 160 yg/liter. Adverse effects
on reproduction of the mysid shrimp occurred at a concentration of 1.6
yg/liter. A bioconcentration factor of 40,000 was reported for methyl
mercuric chloride in the oyster. In freshwater organisms, a bioconcentration
factor of 23,000 was reported for inorganic mercury (USEPA 1980).
EPA has established a water quality criterion of 144 ng/liter for the
protection of human health from the toxic effects of mercury ingested through
water and contaminated aquatic organisms.
EPA has established an aquatic life water quality criterion for freshwater
species of 0.20 yg/liter (24-hour average), with a maximum level not to be
exceeded of 4.1 yg/liter. For saltwater species, the 24-hour average
criterion is 0.10 yg/liter, with a maximum not be exceeded of 3.7
yg/liter.
Nickel
A significantly increased incidence of cancers of the lungs and nasal
cavities has been found in epidemiologic studies of workmen in nickel smelters
and refineries (NAS 1977). The implicated compounds are nickel subsulfide,
nickel oxides, nickel carbonyl vapor, and soluble aerosols of nickel sulfate,
nitrate, or chloride (NAS 1980). Toxic effects depend on the nickel compound
to which a subject is exposed. Acute nickel carbonyl poisoning results in
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immediate symptoms of headache, nausea, and insomnia, followed by constrictive
chest pains, hyperpnea, cyanosis, and severe weakness (Sunderman 1970, Vuopala
1979, as reported in USEPA 1980). Nickel carbonyl exposures have also been
associated with nephrotoxicity (Blandes 1934, Carmichael 1953, as reported in
USEPA 1980). Exposure to occupational sources of nickel and exposure to such
nickel-containing items as jewelry and tools have been associated with a
characteristic nickel dermatitis (USEPA 1980).
Animal studies have shown that the oral toxicity of nickel and nickel
salts is relatively low, but that parenteral injections of nickel salts are
much more toxic (NAS 1977). The major symptoms of acute nickel toxicity are
hyperglycemia and gastrointestinal and central nervous system effects (NAS
1977). One researcher found malformations in hamster embryos when the mother
was exposed to unidentified nickel compounds administered parenterally at
dosages ranging from 0.7 to 10.0 mg/kg (Perm 1972, as reported in USEPA
1980). No teratogenic effects were seen when either nickel chloride (16
mg/kg) or nickel subsulfide (80 mg/kg) was administered to rats (Sunderman et
al. 1978, as reported in USEPA 1980). Multigenerational reproductive
studies have linked nickel to decreases in litter size, increased numbers of
runts, and increased neonatal mortality (USEPA 1980). Male rats given daily
oral doses of nickel sulfate at 25 mg/kg were completely sterile after 120
days (Watschewa et al. 1972, as reported in USEPA 1980). Several
nickel-containing substances including nickel dust, nickel subsulfide, nickel
oxide, nickel carbonyl, and nickel bicyclopentadiene have been found to be
carcinogenic in animals upon inhalation or parenteral administration (NAS
1977).
The toxicity of nickel to freshwater animals decreases with increasing
hardness of the water. For example, the LC50 for Daphnia magna was 510
yg/liter at a water hardness of 45 mg of calcium carbonate/liter. By
comparison, the LC50 for the fathead minnow was 5.21 mg/liter at 45 mg of
calcium carbonate/liter. In several life cycle or early life stage studies in
freshwater fish, the fathead minnow, chronic toxicity was observed at
concentrations ranging from 109 to 527 yg/liter (USEPA 1980). Nickel has
also been shown to reduce the growth of several freshwater algae species at
concentration ranging from 100 to 700 yg/liter. The LC50 values for
saltwater animal species ranged from 152 yg/liter for mysid shrimp to
350,000 yg/liter for the mummichog fish. Growth reductions have been
reported for a species of saltwater algae (USEPA 1980).
EPA has established an ambient water criterion of 13.4 yg/liter for the
protection of human health from the toxic properties of nickel through
ingestion of contaminated water and contaminated aquatic organisms.
EPA has established an aquatic life water quality criterion for nickel.
For freshwater species, the 24-hour average criterion is 0.20 yg/liter, with
a maximum not to be exceeded of 4.1 yg/liter. The 24-hour average criterion
for saltwater species is 0.10 yg/liter, with a maximum not to be exceeded of
3.7 yg/liter.
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Selenium
Although elemental selenium is relatively nontoxic, the soluble salts
of selenium dioxide, selenium trioxide, some halogen compounds, and especially
hydrogen selenite are toxic in humans (NAS 1977). Acute human exposure
generally produces irritation to the eyes, skin, and mucous membranes and
nausea, headaches, and a variety of respiratory disorders (NAS 1977). Chronic
human exposures have produced such symptoms as depression, nervousness,
occasional dermatitis, and gastrointestinal disturbance (NAS 1977). In
addition, epidemiologic studies of children indicated a relationship between
increased incidence of dental caries and consumption of small amounts of
selenium while the teeth were developing; similar results have been seen in
experimental studies of rats (NAS 1977).
Acute and chronic selenium toxicity have been observed experimentally in
laboratory animals and also in domestic animals consuming plants with a high
selenium content. Selenium disease in domestic animals, in its most serious
form, first manifests itself by impaired vision, then paralysis, and
ultimately death by respiratory failure (USEPA 1980). The concentrations of
selenium in the diet which will produce chronic toxic effects depend on the
chemical form of the selenium and other dietary components. (Fishbein 1977,
as reported in USEPA 1980) . In a chronic feeding study, young rats treated
with sodium selenite showed growth depression when the diet contained 6.4 ppm
selenium or more. Animals receiving concentration of 8 ppm or more died after
the fourth week and showed enlargement of the pancreas, reduction of
hemoglobin content, and increased serum bilirubin (Halverson et al. 1966, as
reported in NAS 1977). Selenium has not been positively established as a
carcinogen. Although some studies have reported increased tumor incidences in
animals fed selenium, these results have not been sufficiently documented and
are not in accord with other studies (NAS 1977). No reports of mutagenicity
by selenium compounds are available. Selenium has been shown to be
teratogenic in chick embryo tests, even when exposure is at low concentrations
(NAS 1977). Malformations have also been seen in domestic mammals, but they
were not reproduced in the only available study on laboratory animals in which
hamsters received a near lethal intravenous dose of 2 mg/kg sodium selenite
(Holmberg and Ferm 1969, as reported in USEPA 1980 and NAS 1977). In
reproduction tests on rats, selenium has been associated with decreases in
fertility and pup survival (NAS 1977).
Selenium is acutely toxic to aquatic invertebrates and to fish. Acute
toxicity data for inorganic selenite is available for 13 species of freshwater
animals and ranges from 340 yg/liter for the scud to 42,000 yg/liter for
the midge. For selenate, acutely toxic concentrations range from 760
yg/liter for the scud to 12,500 yg/liter for the fathead minnow. Chronic
toxicity for selenite and selenate compounds in freshwater organisms range
from 88 yg/liter for rainbow trout to 690 yg/liter for Daphnia magna
(USEPA 1980). Selenium compounds have also been shown to be toxic to aquatic
and terrestial plants (USEPA 1980).
EPA has recommended an ambient water quality criterion of 10 ug/liter for
the protection of human health from the toxic properties of selenium through
ingestion of contaminated water and contaminated aquatic organisms (USEPA
1980).
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EPA has established an aquatic life water quality criterion for
freshwater species of 35 yg/liter (24-hour average), with a maximum not to
be exceeded of 260 yg/liter. For saltwater species, the 24-hour average
criterion is 54 yg/liter, with a maximum not to be exceeded of 410
yg/liter.
Silver
Silver exhibits moderate toxicity in humans. Acute oral doses of silver
nitrate can cause abdominal pain and rigidity, vomiting, and convulsions.
Exposure information for the case reports of acute poisonings is generally
scanty. However, ingestion of 10 g is usually fatal (USEPA 1980).
The most common effect of chronic human exposure to silver is argyria
(either generalized or localized) resulting from medical or occupational
exposure. Generalized argyria is characterized by slate gray pigmentation of
the skin, hair, conjunctiva of the eye, and internal organs resulting from
deposition of silver in tissue. In severe cases of argyria, the respiratory
tract may be affected. In localized argyria, only limited areas are
pigmented, and in a condition called argyrosis, the tissues of the eye are
pigmented (Clayton and Clayton 1981, Doull et al. 1980, and USEPA 1980).
With improved work conditions, no cases of argyria from industrial exposures
have been reported since the 1930's (Clayton and Clayton 1981).
Acute toxicity in experimental animals is associated predominantly with
intravenous administration. Dogs injected with approximately 32 mg Ag/kg (as
silver nitrate) in the pulmonary system developed edema, myocardial ischemia
and lesions, and hypertension. When inorganic silver compounds were injected
into animals intravenously, effects were primarily on the central nervous
system (Hills and Pillsbury 1939, as reported in USEPA 1980). Large doses of
colloidal silver administered intravenously have produced death due to
pulmonary edema and congestion (USEPA 1980).
In subchronic and chronic animal studies, the predominant effects of
silver administration have been on conditioned reflex activity and on the
kidney. Klein et al. (1978, as reported in USEPA 1980) reported hemorrhages
in the kidneys of rats given silver at 0.4 mg/liter drinking water for 100
days. At 1 mg/liter, changes in both the kidney and liver were observed (form
of the metal unspecified). Several investigators have reported effects on
conditioned reflex activity in rats given silver in drinking water (form of
the metal unspecified) at concentrations between 0.5 and 20 mg/liter for
periods of 1 to 11 months (Barkov and El'piner 1968, Kharchenko and Stepanenko
1972, and Zapadnyuk et al. 1973, as reported in USEPA 1980). Brain nucleic
acid content in rats was also reduced at 0.5 mg/liter drinking water (form of
the metal unspecified) (Kharchenko et al. 1973, as reported in USEPA 1980).
In several studies, implanted foils and disks and injected colloidal
suspensions of metallic silver have been found to produce tumors or
hyperplasia. These effects are considered to be due to the particular form of
the metal or to its being an exogenous irritant. Thus, silver is not
considered to be carcinogenic (USEPA 1980).
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In natural waters, silver exists primarily in the 0 and +1 oxidation
states; the monovalent species is the form of greatest environmental concern.
Silver is one of the most toxic metals to freshwater aquatic life. For
invertibrate species, acute toxicity values range from 0.25 yg/liter for
Daphnia magna to 4,500 yg/liter for the scud Gammarus pseudolitnnaeus.
Acute toxicity values for fish range from 3.9 yg/liter for the fathead
minnow in soft water to 280 yg/liter for rainbow trout in hard water (USEPA
1980). In an 18-month study conducted by Davies et al. (1978, as reported
in USEPA 1980) with freshwater trout, the rate of growth was decreased in fish
exposed for two months at a concentration of 0.17 yg/liter, and mortality
was 17 percent greater than the control in this dose group at the study end.
Acute toxicity values for saltwater organisms ranged from 4.7 yg/liter
for the summer flounder to 1,400 yg/liter for the sheepshead minnow (USEPA
1980). In a life-cycle toxicity study with mysid shrimp, brood size was
smaller than the control at a concentration of 33 yg/liter of silver
(Lussier and Gentile 1980, as reported in USEPA 1980).
In various strains of freshwater algae, growth inhibition has been
reported at silver concentrations ranging from 30 to 200 yg/liter (USEPA
1980). Phytotoxicity was reported in duckweed at a silver concentration of
270 yg/liter, and in waterweed at a concentration of 7,500 yg/liter (Brown
and Rattigan 1979, as reported in USEPA 1980). In saltwater algae, reduced
cell numbers were reported at 130 yg/liter (USEPA 1978, as reported in USEPA
1980).
EPA has established an ambient water quality criterion of 50 yg/liter
for the protection of human health from the toxic properties of silver through
ingestion of contaminated water and aquatic organisms.
EPA has not yet established an aquatic life water quality criterion for
silver. However, EPA has set maximum limits not to be exceeded of 1.2
yg/liter for freshwater organisms and 2.3 yg/liter for saltwater
organisms.
Thallium
Numerous cases of thallium poisonings have been recorded, largely as a
result of thallium's medicinal or rodenticidal uses. Minimum toxic doses in
humans of between 3 and 15 mg Tl/kg have been reported (Clayton and Clayton
1981). Acute poisoning is characterized by gastrointestinal irritation, acute
ascending paralysis, psychic disturbances, alopecia, and abnormalities of
cardiac function (Clayton and Clayton 1981, Doull et al. 1980, and USEPA
1980). Autopsies in fatal cases have revealed damage to the gastric and
intestinal mucosa, fatty infiltration of the liver and kidneys, and damage to
the adrenal glands and central nervous system (Clayton arid Clayton 1981). In
the few reported cases of subchronic and chronic poisoning in humans, symptoms
are similar to those for acute poisoning (USEPA 1980).
In animal studies, the acute toxicity of thallium compounds exhibits a
particularly narrow range. Of 14 inorganic thallium compounds administered by
various routes to five animal species, the lowest lethal doses or LD50 values
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ranged from about 15 to 50 mg Tl/kg (Clayton and Clayton 1981). In a 90-day
feeding study in rats, doses as low as 30 to 35 ppm in the diet produced
marked growth depression after 30 days. The major histological change at
these dietary levels was atrophy of the hair follicles and sebaceous glands of
the skin. At 15 ppm in the diet, the major effect was alopecia (Downs et
al. 1960, as reported in Clayton and Clayton 1981). Evidence for the
teratogenicity of thallium is inconclusive. Thallium was administered to
pregnant rats on gestation days 8-10 at 2.5 mg/kg/day or on days 12-14 at 2.5
and 10 mg/kg/day; both dose levels caused maternal toxicity. In the
offspring, reduced fetal weight and increased incidences of hydronephrosis and
missing or non-ossified vertibrae were reported (Gibson and Becker (1970, as
reported in USEPA 1980). Dwarfism (achondroplasia) in rats has also been
described as a teratogenic response to thallium salts (Nogami and Terashima
1973, as reported in Doull et al. 1980). Information is not available on
the carcinogenicity of thallium; however, thallium has shown some mild
anti-carcinogenic effects in experimental animals (USEPA 1980).
Acute toxicity of thallium to freshwater organisms is reflected in mean
LC50 values for Daphnia magna of 1,400 yg/liter, for the fathead minnow of
1,800 yg/liter, and for the bluegill of 126,000 yg/liter (Dawson et al.
1977, Kimball manuscript, and USEPA 1978, as reported in USEPA 1980). Chronic
effects have been observed in Daphnia magna at 100-181 yg/liter and in the
fathead minnow at 40-81 yg/liter (Kimball manuscript, as reported in USEPA
1980).
In saltwater species, an LC50 value of 2,130 yg/liter has been reported
for the mysid shrimp. The sheepshead minnow and tidewater silverside were
less sensitive to thallium with 96-hour LC50 values of 20,900 and 24,000
yg/liter, respectively (USEPA 1978 and Dawson et al. 1977, as reported in
USEPA 1980). Chronic effects were observed in the sheepshead minnow at
concentrations between 4,300 and 8,400 yg/liter (USEPA 1978, as reported in
USEPA 1980).
In freshwater algae, a 50% reduction in chlorophyll a and cell numbers
was observed at 100-110 yg/liter (USEPA 1978, as reported in USEPA 1980). A
50% inhibition of photosynthesis at 4,080 yg/liter was reported for
saltwater algae (Overnell 1975, as reported in USEPA 1980).
EPA has established an ambient water quality criterion of 13 yg/liter
for protection of human health from the toxic properties of thallium through
ingestion of contaminated water and aquatic organisms.
EPA has not yet established an aquatic life water quality criterion for
thallium.
Zinc
Zinc salts are astringent, corrosive to the skin, and irritating to the
gastrointestinal tract. Accidental oral poisonings in humans have produced
such symptoms as fever, vomiting, stomach cramps, and diarrhea (Patty 1963).
Occupational exposure to zinc oxide may result in a characteristic short-term
syndrome. It generally occurs after a lapse of exposure, for example on
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Monday mornings or after a holiday. The symptoms include chills and fever
followed by remission after 24-48 hours, despite continued exposure (Casarett
and Doull 1975). Zinc chloride fumes may give rise to a grey cyanosis,
dermatosis, and ulceration of the nasal passages and in severe cases may
result in acute pulmonary damage or death (Casarett and Doull 1975).
In feeding tests on rats, no adverse effects were observed at dosages up
to 5,000 rag/kg. At 10,000 mg/kg, however, a cessation of growth and some
deaths were seen (Rothstein 1953, as reported in CSWRCB 1963). No studies are
available showing zinc to be teratogenic, mutagenic, or carcinogenic.
Zinc has been shown to be acutely toxic to freshwater animals over a range
of concentrations from 0.090 to 58.1 mg/liter, depending on the species tested
and the hardness and temperature of the water. In saltwater animals, the
range was from 0.166 mg/ liter to 83 mg/liter. Zinc concentration from 0.030
to 21.65 mg/liter have been shown to reduce the growth of various freshwater
plant species. A range of 0.050 to 25.5 mg/liter was found to inhibit growth
in several saltwater plant species (USEPA 1980).
EPA has not yet established ambient water quality criteria for the
protection of human health from the toxic properties of zinc because of the
lack of sufficient data. However, using available organoleptic data for
controlling undesirable taste and odor of ambient water, the estimated level
is 5 mg/liter.
EPA has established an aquatic life water quality criterion for zinc. For
freshwater species, the 24-hour average criterion is 47 yg/liter, with a
maximum not to be exceeded of 180 yg/liter. The 24-hour average criterion
for saltwater species is 58 yg/liter, with a maximum not to be exceeded of
170 yg/liter.
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5. Polychlorinated Biphenyls
The toxic effects of polychlorinated biphenyls (PCBs) in humans are
well-established. Most human exposures have occurred as a result of the
episode in Japan in 1968 resulting from ingestion of rice oil contaminated
with Kanechlor 400 or from industrial exposure to PCBs (USEPA 1980). In the
Japanese poisoning incident, initial symptoms included eye discharge, acneform
eruptions, pigmentation of the skin, dermatologic problems, swelling,
jaundice, numbness of limbs, spasms, hearing and vision problems, and
gastrointestinal disturbances. Blood changes were noted and liver biopsies
revealed histopathological changes. It has been estimated that the average
amount of PCB ingested by those affected was 2 g (Kuratsune et al. 1972, as
reported in USEPA 1980). During 1968, ten live and two stillborn infants were
delivered to parents poisoned with PCBs. Nine of the ten had abnormally
pigmented skin. Birth weight and growth of the children was significantly
lower than Japanese national standards. In four babies, gingival hyperplasia,
tooth eruption at birth, bone abnormalities, facial edema, and exophthalmic
eyes were also observed (Yamashita 1977, as reported in USEPA 1980). Many
symptoms, reported in affected individuals four years after the poisoning
episode, were highly persistent.
In an occupational setting in which PCB air levels were reported to
be 5.2 to 6.8 mg/cu m, three cases of severe chloracne have been reported
(Puccinelli 1954, as reported in USEPA 1980). Laboratory workers exposed to
breathing zone concentrations of 0.014 to 0.073 mg/cu m complained of dry sore
throat, skin rash, gastrointestinal disturbances, eye irritation, and headache
(Levy et al. 1977, as reported in USEPA 1980). Changes in a liver function
test (increased antipyrene clearance) was observed in workers occupationally
exposed to PCBs for at least four years (Alvares et al. 1977, as reported in
USEPA 1980).
In acute animal studies, PCBs are only slightly toxic. Oral LD50
values for the rat range from 0.79 to 3.17 g/kg (USEPA 1980). Toxic effects
of acute doses of Aroclor 1242 include diarrhea, chromoacryorrhea, weight
loss, unusual stance and gait, CNS deterioration, and histopathologic changes
of the liver and kidney (USEPA 1980). The more significant toxic effects of
PCBs are observed as a result of repeated exposures and are similar to those
observed in humans. Adult Rhesus monkeys are particularly sensitive to PCBs.
Aroclor 1248 at 100 or 300 ppm in the diet for 2 to 3 months (total intakes of
0.8-1.0 g and 3.6-5.4 g, respectively) caused high morbidity within one month
and almost 100 percent mortality within three months (Allen 1975, as reported
in USEPA 1980). Pathological changes of the liver are the most consistent
changes occurring in mammals after exposure to PCBs. In one study by
Kimbrough et al. (1972, as reported in USEPA 1980), rats fed Aroclor 1254 or
1260 at levels between 20 and 1,000 ppm for eight months showed
histopathologic changes of the liver and porphyria. Adenofibrosis of the
liver was observed at the higher doses. Liver pathology similar to that seen
in rats has been reported in mice exposed to 1.5 mg PCB/day (Nishizumi 1970,
as reported in USEPA 1980). PCB applied dermally to rabbits results in skin
lesions and pathological changes in the liver and kidney (Vos and Beems 1971,
as reported in USEPA 1980). Female Rhesus monkeys fed low levels of Aroclor
1248 (2.5 and 5 ppm) for 52 weeks developed periorbital edema, alopecia,
erythema, and acneform lesions (Barsotti and Allen 1975, as reported in USEPA
H-93
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1980); effects in males was less pronounced. Induction of liver microsomal
enzymes has been demonstrated at dietary levels as low as 0.5 to 25 ppm.
Other systemic effects in experimental animals include porphyria, increased
thyroxin metabolism, ultrastructural changes in the thyroid,
immunosuppression, and alterations in steroid metabolism'(USEPA 1980).
Administration of PCBs has resulted in adverse reproductive effects in rats,
rabbits, mice, mink, and Rhesus monkeys. An increased estrus cycle and a
decreased rate of implantation were observed in mice treated for ten weeks
with 0.025 mg/day Clophen A60 (Orberg and Kihlstrom 1973, as reported in USEPA
1980). In a study of female Rhesus monkeys fed 2.5 or 5.0 ppm Aroclor 1248 in
the diet for six months before mating, Barsotti and Allen (1975, as reported
in USEPA 1980) observed a decreased rate of conception, live births, and
neonatal body weights and an increase in neonatal deaths. The carcinogenicity
of PCBs has been demonstrated in mice and rats. Liver tumors were reported in
mice given PCB in the diet at levels of 500 ppm for 224 days (Ito et al.
1973, as reported in USEPA 1980) and 300 ppm for 330 days (Kimbrough and
Linder 1974, as reported in USEPA 1980). Kimbrough et al. (1975, as
reported in USEPA 1980) fed Aroclor 1260 to rats at levels of 100 ppm for 21
months and found hepatocellular carcinomas in 26/184 experimental animals but
only one out of 173 controls. A 1978 National Cancer Institute bioassay (as
reported in USEPA 1980) concluded that Aroclor 1254 was not carcinogenic in
Fischer 344 rats, although a high frequency of hepatocellular proliferative
lesions and an increase in carcinomas of the gastrointestinal tract (not
statistically significant) were considered possibly associated with
treatment.
The acute toxicity of PCBs to freshwater organisms has been measured in
three invertibrate species with acute values ranging between 10 and 2,400
Vg/liter, and in four fish species with acute values ranging between 2 and
300 yg/liter (USEPA 1980). In eleven life-cycle or partial life-cycle tests
with three vertibrate and two fish species, chronic effects were reported from
0.2 to 15 yg/liter (USEPA 1980). In saltwater species, the mean acute
values for the eastern oyster, brown shrimp, and grass shrimp were 20, 10.5
and 12.5 ug/liter, respectively (USEPA 1980). Two chronic studies have been
performed on the sheepshead minnow; chronic effects were observed at 0.098 to
7.14 ug/liter (USEPA 1980). Available data for saltwater plants indicate
that unicellular plants are affected by concentrations similar to
concentrations that are chronically toxic to animals, while freshwater algae
are somewhat less sensitive to PCBs (USEPA 1980).
EPA has established an ambient water quality criterion of zero for the
maximum protection of human health from the potential carcinogenic effects due
to exposure to PCBs through ingestion of contaminated water and aquatic
organisms. Since the zero level may not be attainable at the present time, a
criterion of 0.079 ng/liter, corresponding to a lifetime incremental cancer
risk of 0.000001, was recommended.
EPA has established an aquatic life water quality criterion for freshwater
organisms of 0.014 yg/liter as a 24-hour average and for saltwater organisms
of 0.030 yg/liter as a 24-hour average.
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REFERENCES
AMERICAN CONFERENCE OF GOVERNMENT INDUSTRIAL HYGENISTS, INC (ACGIH). 1980.
Documentation of the Threshold Limit Values. Fourth Edition. Cincinnati, Ohio
CALIFORNIA STATE WATER RESOURCES CONTROL BOARD (CSWRCB). 1963. Water Quality
Criteria, 2nd ed. Publication 3-A. Sacramento, California
CASARETT, L.J., and DOULL, J. 1975. Toxicology, the Basic Science of
Poisons. New York, New York
CLAYTON, G.D., and CLAYTON, F.E., eds. 1981. Patty's Industrial Hygiene and
Toxicology. Third Revised Edition. Volume 2--Toxicology. John Wiley and
Sons, New York
DOULL, J., KLAASSEN, C.D., and AMDUR, M.O. 1980. Casarett and Doull's
Toxicology. 2nd Edition. Macmillan Publishing Company, Inc., New York
ENERGY RESEARCH AND DEVELOPMENT ADMINISTRATION. 1977. Environmental, Health
and Control Aspects of Coal Conversion: An Informational Overview. Vols. 1
and 2. Oak Ridge National Laboratory, Oak Ridge, Tennessee. ORNL/E15-95
ENCYCLOPEDIA OF OCCUPATIONAL HEALTH AND SAFETY. 1971. International Labor
Organization. McGraw-Hill, New York
HUEPER, W.C., and CONWAY, W.D. 1964. Chemical Carcinogenesis and Cancers.
Charles C. Thomas, Springfield, Illinois
INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC). 1972. IARC Monographs on
the Evaluation of the Carcinogenic Risk of Chemicals to Man. Volume 1. World
Health Organization, Lyon, France
INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC). 1972. IARC Monographs on
the Evaluation of the Carcinogenic Risk of the Chemical to Man. Volume 3.
Certain Polycyclic Aromatic Hydrocarbons and Heterocyclic Compounds. World
Health Organization, Lyon, France
INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC). 1973. IARC Monographs on
the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Vol. 2: Some
Inorganic and Organometallic Compounds. World Health Organization, Lyon,
France
INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC). 1974. IARC Monographs on
the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Vol. 3:
Certain Polycyclic Aromatic Hydrocarbons and Heterocyclic Compounds. World
Health Organization, Lyon, France
INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC). 1979. IARC Monographs on
the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Volume 20:
Some Halogenated Hydrocarbons. World Health Organization, Lyon, France
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INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC). 1978. IARC Monographs on
the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Volume 17.
Some N-Nitroso Compounds. World Health Organization, Lyon, France
INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC). 1980. IARC Monographs on
the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Vol. 23:
Some Metals and Metallic Compounds. World Health Organization. Lyon, France
KOCIBA, R.J., KEYES, D.G., BEYER, J.E., CARREON, R.M., WADE, C.E., DITTENBER,
D.A., KALNINS, R.P., FRAUSON, L.E., PARK, C.N., BARNARD, S.D., HUMMEL, R.A.,
and HUMISTON, C.G. 1978. Results of a two-year chronic toxicity and
oncogenicity study of 2,3,7,8-tetrachlorodibenzo-p-dioxin in rats. Toxicol.
Appl. Pharmacol. 46:279-303
NATIONAL ACADEMY OF SCIENCES (NAS). 1977. Drinking Water and Health.
Washington, D.C.
NATIONAL ACADEMY OF SCIENCES (NAS). 1980. Drinking Water and Health. Vol.
3. Washington, D.C.
NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH). 1980.
Registry of Toxic Effects of Chemical Substances. 1979 Edition. U. S.
Department of Health and Human Services, Cincinnati, Ohio. DHHS (NIOSH)
Publication No. 80-111
NATIONAL TOXICOLOGY PROGRAM (NTP). 1982. NTP Technical Report on the
Carcinogenesis Bioassay of Di(2-Ethylhexyl) Phthalate (CAS No. 117-81-7) in
F344 Rats and B6C3F1 Mice. Technical Report Series No. 217. U. S. Department
of Health and Human Services, NIH Publication No. 82-1773
PATTY, F.A. 1963. Industrial Hygiene and Toxicology. Vol. II. John Wiley
and Sons, New York
SAWYER, C.N., and McCARTHY, P.L. 1967. Chemistry for Sanitary Engineers.
McGraw-Hill Book Company, New York
SAX, NI.I. 1975. Dangerous Properties of INdustrial Materials, 4th ed. Van
Nostrand Reinhold Company, New York
SEARLE, C.E. 1976. Chemical Carcinogens. ACS Monograph 173, Washington, D.C.
STANDARD METHODS FOR THE EXAMINATION OF WATER AND WASTEWATER. 1971. American
Public Health Association, American Water Works Association, and Water
Pollution Control Association. 13th ed.
TOPPING, D.C., PAL, B.C., MARTIN, B.A., NELSON, F.R., and NETTESHEIM, P.
1978. Pathological changes induced in respiratory tract mucosa by polycyclic
hydrocarbons of differing carcinogenic activity. Am. J. Pathol. 93:311-324
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES (USDHHS). 1980. Registry of
Toxic Effects of Chemical Substances. Cincinnati, Ohio
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U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1976. Quality Criteria for
Water. Office of Water and Hazardous Materials. Division of Water Planning
and Standards, Washington, B.C.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1979. Ambient Water Quality
Criterion for 2,3,7,8-Tetrachlorodibenzo-p-dioxin. Draft report. Ofice of
Water Regulations and Standards, Criteria and Standards Division, Washington,
D.C.
U.S. ENVIRONMENTAL PROTECTION AGENCY (USEPA). 1980. Ambient Water Quality
Criteria. Office of Water Regulations and Standards, Criteria and Standards
Division, Washington, D.C.
WASTEWATER ENGINEERING: COLLECTION, TREATMENT DISPOSAL. 1972. Metcalf and
Eddy, Inc. McGraw-Hill Book Company, New York
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APPENDIX I
FATE OF PRIORITY POLLUTANTS IN
PUBLICLY OWNED TREATMENT WORKS
Executive Summary
-------
United States
Environmental Protection
Agency
Effluent Guidelines Division
WH-552
Washington DC 20460
EPA 440/1 -82/303
September 1982
vvEPA
Water and Waste Management
Fate of Priority Pollutants
in Publicly Owned
Treatment Works
Final Report
Volume I
1-1
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PATE OF PRIORITY TOXIC POLLUTANTS
IN
PUBLICLY OWNED TREATMENT WORKS
FINAL REPORT
VOLUME I
PREPARED FOR:
EFFLUENT GUIDELINES DIVISION
OFFICE OF WATER REGULATIONS AND STANDARDS
U.S. ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON, D.C. 20460
PREPARED BY:
BURNS AND ROE INDUSTRIAL SERVICES CORPORATION
PARAMUS, NEW JERSEY 07652
1-2
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PREFACE
This document is being issued as the Final Report on a project
initiated by the United States Environmental Protection Agency in
1978 to study the occurrence and fate of the 129 priority toxic
pollutants in 40 Publicly Owned Treatment Works (POTW) and a
supplemental study conducted at 10 additional POTW. This report
consists of two volumes. Volume I contains the background and
purpose of study, the POTW selection criteria, the sampling
program details, the overall POTW data, evaluation of analytical
results, and the preliminary conclusions of the study. Volume II
contains the Daily Analytical Results which embody the basic data
generated during the course of this study and which are the
source for all other data compilations and analyses.
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TABLE OF CONTENTS
VOLUME I
SECTION PAGE
I. SUMMARY, RESULTS AND CONCLUSIONS 1
Summary 1
Results and Conclusions 1
II. INTRODUCTION 3
Background 3
Purpose 4
III. POTW SELECTION AND DESCRIPTION 5
Selection Criteria 5
POTW Characteristics 7
IV. DESCRIPTION OF FIELD SAMPLING PROGRAM 15
Sampling Frequency 15
Sampling Techniques 16
Sample Points 17
V. DATA ORGANIZATION AND INTERPRETATION 27
Data Organization 27
Laboratory Data Reporting Protocol 27
Data Interpretation and Presentation 30
Quality Assurance Program 31
VI. EVALUATION AND DISCUSSION OF ANALYTICAL DATA 35
Overview of Priority Pollutant Occurrence 35
Summary of Influent Pollutant Concentrations 51
Impact of Industrial Contribution on Influent 51
Quality
Treatment or Removal of Priority Pollutants in 56
POTWs
Reduction of Priority Pollutants by POTW 58
Treatment Processes
POTW Priority Pollutant Mass Balances 62
Daily Variation of Influent Pollutant Concen- 64
trations
Effect of Rainfall on Influent Concentrations 66
Formation of Chlorinated Hydrocarbons 66
Pollutants Detected in Sludges When Not 70
Measured in the Influent
Correlation of Influent and Effluent Concen- 70
trations
Discussion of 10-Plant Study Results 73
1-4
iii
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TABLE OF CONTENTS (Continued)
SECTION
APPENDIX A
APPENDIX B
APPENDIX C
APPENDIX D
APPENDIX E
Flow Diagrams - Plants 1 to 40 and
51 to 60
Cumulative Distribution Curves of
Effluent Concentrations and Percent
Removals for the Twenty-four Most
Frequently Found Priority Pollutants
Summary of Analytical Data - Plants 1
to 40 and 51 to 60
Percent Occurrence of Pollutant
Parameters - Plants 1 to 40 and 51
to 60
Mass Balance in Pounds Per Day
Plants 1 to 40 and 51 to 60
PAGE
A-1 to A-52
B-1 to B-14
C-1 to C-108
D-1 to D-74
E-1 to E-102
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I.
SUMMARY, RESULTS AND CONCLUSIONS
SUMMARY
In 1978, the United States Environmental Protection Agency (EPA)
initiated a program to study the occurrence and fate of the 129
priority pollutants in 40 Publicly Owned Treatment Works (POTWs).
The first phase of this work was a two-plant pilot study designed
to set operating parameters for the remainder of the 40 POTW
study. In October 1979, EPA's Effluent Guidelines Division (EGD)
published a report summarizing "the findings of the pilot study
work, "Fate of Priority Pollutants in Publicly Owned Treatment
Works-Pilot Study," EPA 440/1-79-300. Upon completion of half of
the POTW project EGD published a report summarizing the findings
for the first 20 POTWs, "Fate of Priority Pollutants in Publicly
Owned Treatment Works-Interim Report," EPA 440/1-80-301.
In this final report, data from all 40 POTWs plus 10 supplemental
POTWs sampled under a parallel project are presented. At most of
these plants, a minimum of 6 days of 24-hour sampling of
influent, effluent and sludge streams was completed. Each sample
was analyzed for conventional, selected non-conventional, and
priority pollutants.
Beyond presenting the occurrence and concentration of priority
pollutants in the 40 POTWs (and 10 supplemental POTWs) other spe-
cific phenomena and relationships are evaluated in this report.
These items include:
o Impact of industrial contribution on influent quality
o Treatment or removal of priority pollutants in POTWs
o Reduction of priority pollutants by individual POTW treatment
processes
o POTW priority pollutant mass balances
o Daily variation of influent pollutant concentrations
o Effect of rainfall on priority pollutant levels in POTW influents
o Formation of chlorinated hydrocarbons through chlorine disin-
fection
o Quantification of pollutants found in sludges but not detected
in POTW influents
o Correlation of influent and effluent priority pollutant levels.
RESULTS AND CONCLUSIONS
1. A total of 102 priority pollutants were detected, at least
once, in POTW influents.
2. In general, the higher the industrial contribution to a POTW,
the higher the concentration of priority pollutants in the
POTW influents.
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3. Based on the 40 POTW data base, 50 percent of secondary
treatment plants achieved a minimum of 70 percent reduction
of total priority pollutant metals, 82 percent reduction of
total volatile priority pollutants, and 65 percent reduction
of the total base neutral priority pollutants.
4. Tertiary treatment processes reduced priority pollutants
slightly better than secondary processes. Primary treatment
was less effective than either secondary or tertiary pro-
cesses. Activated sludge, trickling filter, rotating biolo-
gical contactor and pure oxygen activated sludge processes
were approximately equally effective in reducing priority
pollutant concentrations.
5. At plants where the metal priority pollutant mass balance was
good, some organic priority pollutants in the influent were
not always accounted for in the effluent or sludges. This
indicates that, in general, a portion of the organic priority
pollutants are biodegraded or, in the case of volatiles,
stripped out of the wastewater.
6. The mass loading of priority pollutants in POTW influents was
higher on weekdays than on weekends. This was true for the
metals, volatiles and base neutral priority pollutants.
7. Heavy rainfall increased metallic priority pollutant mass
loading at POTWs.
8. Certain priority pollutant chlorinated hydrocarbons increased
slightly in concentration during chlorine disinfection.
9. Some pollutants not measured in POTW influents were regularly
measured at high levels in the corresponding sludge streams.
10. For many conventional and priority pollutants, as influent
concentrations increased effluent concentrations also
increased. This implies that the removal rates for the
priority pollutants are relatively constant and a fixed per-
centage of incremental loadings of these pollutants will be
removed by secondary treatment.
1-7
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APPENDIX J
TREATMENT CATALOG FOR THE
CATALYTIC COMPUTER MODEL
-------
TREATS NT CATALOG
FOR THE CATALYTIC COMPUTER MODEL
Catalytic, Inc.
Philadelphia, Pennsylvania
September 1980
J-l
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TABLE OF CONTENTS
Page
GENERAL DESCRIPTION 1
Process 2
Function 2
Parameters Affected 2
Effectiveness 2
Appl icati on L imits 3
Design Basis 3
Treatability Factor 4
Cost Parameter 4
Cost Curve Scale Factor 4
Resi dues 5
Major Equipment 5
TREATABILITY 5
TREATMENT CATALOG AND MODEL SEQUENCING RULES 11
UNIT PROCESS COST DEVELOPMENT 12
UNIT PROCESSES 14
Equalization and Surge Storage 14
Neutralizati on 16
Oil Separation and Dissolved-Air Flotation 18
Chemical Precipitation, Coagulation, and Flocculation 21
Clarification 23
Filtration, Dual-Media 27
J-2
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TABLE OF CONTENTS (Continued)
Page
Activated SIudge 29
Aeration, Biological Processes 34
Nutrients, Biological Processes 37
Nitrification, Biological 39
Denitrification, Biological 42
Ozonation 45
Chemical Oxidation 47
Activated Carbon Adsorption 49
Activated Carbon Regeneration 52
I on Exchange 54
Sludge Handling And Disposal - General 56
Gravity Thickening 58
Aerobic Digestion 60
Vacuum Filtration 62
Pressure Filtration 64
Landfill 66
Incineration 68
Ammoni a Strippi ng 72
Steam Stripping 74
So"vent Extraction 76
Cooling Tower/Heat Exchanger/Steam Injector 78
Deep-Well Disposal 81
Lime Handl ing 83
J-3
ii
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TREATMENT CATALOG
FOR THE CATALYTIC COMPUTER MODEL
The Treatment Catalog defines the basis for applying the unit pro-
cesses that are to be considered for treatment and disposal of wastewaters
and their residues. The unit processes now in the catalog are not to
be construed as an all-inclusive list of commercially available wastewater
treatment processes; however, they are sufficiently comprehensive to provide
a "typical" treatment method for any of the pollutants expected to be
encountered.
GENERAL DESCRIPTION
Each unit process is represented by a separate entry in the Catalog.
The first part is a general description of the process, with a discussion
of the design basis and applicable assumptions for simplification of the
design procedure. The second part is a design data sheet (or sheets)
in which the performance characteristics, design criteria, and key design
features are specified under the following headings:
PROCESS
FUNCTION
PARAMETERS AFFECTED
EFFECTIVENESS
APPLICATION LIMITS
DESIGN
TREATABILITY FACTOR
COST PARAMETER
COST CURVE SCALE FACTOR
RESIDUES
1
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MAJOR EQUIPMENT
The following paragraphs indicate the type of information presented
under each of these headings and provide guidelines for your review and
comment.
Process
The name of the process is shown at the top of the page. The unit
processes are arranged in the catalog in three groups: wastewater treat-
ment processes, sludge treatment processes; and special systems.
Function
The purpose of the unit process is stated in broad terms, for example,
"Removal of dissolved organics" (Activated Sludge), and "Removal of suspended
solids" (Filtration, Dual-Media). Different processes could have the,
same general function, as in the cases of Activated Sludge and Activated
Carbon Adsorption.
Parameters Affected
Pollutants which are altered by the process are listed. The list
is not necessarily all-inclusive, but includes at least the following:
1. Parameters for which effluent limitations were previously
promulgated by the U.S. Environmental Protection Agency for
the organic chemicals industry for BPT.
2. Parameters which may affect the applicability, effectiveness,
and/or cost of other (downstream) unit processes.
3. General classes of pollutants (e.g., dissolved organics) are
specified when a listing would be too lengthy. These classes
include priority pollutants.
Pollutant characteristics which do not fall into any of the foregoing
categories are generally omitted (e.g., color), even though they may be
altered by the process. In some instances, a parameter may be included
because of prevailing state regulations.
2
0-5
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Effectiveness
The effectiveness of the process in reducing the affected parameters is stated.
In some cases, this statement may consist simply of a percentage removal or some
other reliably achievable result (e.g., effluent concentration). In other cases, the
statement is more complex because the effectiveness of the process is sensitive
to various design parameters and to the relative treatability of the waste stream.
In those cases, it is necessary to relate the effectiveness of the process both to the
waste to which it is applied and to the chosen design criteria. These relationships
are expressed or implied in the effectiveness statement and are further defined under
other headings in the catalog (e.g., Design Basis).
For most unit processes there are practical limitations on effectiveness. A
"Limit of Effectiveness" statement is sometimes needed to stipulate that there is
a limit on percentage removal achievable or that the effluent concentration will
not be below a particular achievable level.
For those unit processes involving consideration of relative treatability of
the particular wastewater, a "reference case" has been included in the effectiveness
statement. This specifies the effectiveness achieved for a given wastewater with
a defined treatability and specified design basis. The design of this unit process
for other wastes with different treatability is relatable to the reference case. (See
Treatability Factor and Cost Curve Scale Factor).
Application Limits
Waste characteristics that must be controlled within certain ranges in order
for the process to function properly are described. For example, the pH of wastewater
generally must be controlled within a range of 6.0-8.5 in order that a biological proc
such as activated sludge, can be applied. (These are exceptions, however. For examp-
if the wastewater exists as a buffered solution in an aeration basin, then excursions
of pH in the influent stream can be tolerated. These exceptions are not definable
with the data available for this study.) If the waste characteristics are not within
the prescribed range, then a preceding unit process (e.g.,
3
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neutralization) is applied so as to bring the characteristic withTn the
required range.
Design Basis
The process design basis is specified. In some cases, this consists
of specifying a design loading such as' an overflow rate or hydraulic residence
time. In others, particularly when relative treatability has a major
impact upon cost, a functional relationship between design ("size") and
performance is indicated.
Treatability Factor
For each unit process, this heading will include absolute and relative
treatability information for each pollutant affected by that unit process.
This information is discussed systematically in the TREATABILITY Section
of this document.
Cost Parameter
A cost curve has been developed for each unit process, relating capital
cost to a basic parameter representative of the size (and, therefore, the
cost). In some cases, a second cost parameter is required for adequate
description of the cost of the system in terms of its size. The cost curve
will then be a family of curves on the same graph.
Cost Curve Scale Factor
For those unit processes involving a treatability factor, the cost
estimates (and cost curves) are based upon a reference case. The design
of the process and its cost were determined for a given value of the treata-
bility factor. The cost parameter, in those cases, does not fully define
the system size; it is necessary to refer to the reference case to do
so. For example, the cost parameter for activated sludge is flow rate.
However, the cost of an aeration basin is determined by the volume of
the basin, which is a function of both the flow rate and the detention
time. The detention time is directly related to the treatability of the
waste. In order to disassociate the system cost curve from the treatability
4
J-7
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of the particular waste encountered in the reference case, flow rate was
chosen as the cost parameter. Although the cost curve is based upon the
reference case (at different flow rates), the size of a basin (and therefore
the cost) can be determined for any application once the detention time
is specified. This is achieved by comparing the detention time with that
of the reference case and scaling the flow rate up or down as indicated.
The detention time in this case (activated sludge), is termed the Cost
Curve Scale Factor.
Another use of the Cost Curve Scale Factor is as a multiplier of
a unit cost. This is used, for instance, in aeration, where the cost
factor is individual-aerator horsepower and the scale factor is the number
of aerators. The cost estimate for one aerator (including associated
instrumentation, electrical connections, structural supports, etc.) appears
in the cost curves and then is multiplied by the number of aerators (of
the same horsepower) required.
Residues
Any residues (solid, gaseous, or liquid) generated by the process
are identified as to type and quantity. Either additional unit processes
are provided for their treatment and disposal, or processes already included
in the treatment scheme for some other purpose are designed to handle them.
Major Equipment
The major equipment and facilities that must be installed for this
unit process are identified. The key features that affect cost (such
as materials of construction, operating mode, and process variants) are
also indicated,
TREATABILITY
The treatability of various pollutants and product/process waste
streams had to be assessed and quantified to enable the model to predict
contaminant removals in the various unit processes. The problem of predic-
5
J-8
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tion is different for conventional parameters (e.g., BOD, TSS) than for
specific pollutants. These differences in assessment of treatabi1ity
are highlighted in the following discussion of the requirements for modeling
each treatment unit processes.
Equalization
No treatabi 1 ity factors are involved in this unit process. The function
of equalization is to lessen the variability of the raw waste load. The
average values of parameters are unaffected. The only exception is waste-
water temperature, which will move toward the ambient air temperature
during the 1-day holding time in the equalization basin.
Neutral ization
Again, there are no treatabi1ity factors involved. The size of the
basin is determined by the wastewater flow, while the chemical requirements
are determined by acidity/alkal inity values (if available) or by pH values
if acidity/alkalinity are not reported. When no data (acidity/alkalinity
or pH) are reported, a neutral pH is assumed.
Oil Separation and Dissolved Air Flotation
There are no treatability factors for oil and suspended so'lids removal.
Basin size is determined by wastewater flow rate. Oil and TSS removal are
predicted on the basis of operating experience. Organic pollutants are
assumed to be removed down to their solubility in water. (These solubilities
are taken from chemical handbooks.)
Coagulation and Flocculation
The treatability factors required for this unit process are the chemical
coagulant used, the ratio of chemical to pollutant, and the remaining
solubility of the precipitate formed for ion being removed. These factors
are obtained from operating experience and chemical handbooks, supplemented
as necessary by laboratory tests on metal-ion compounds for which the
literature provided inadequate solubility data.
6
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Clarification
Specific treatability factors are required. Different overflow rates, effluent
TSS concentrations, and underflow TSS concentrations for various types of suspended
solids are given in the design data sheet for the clarification unit process.
Activated Sludge
The treatabil ity factors required for this unit process are the biological reacti
rate coefficient (k factor) and the maximum attainable percent removal. The k
factor has been estimated by grouping chemicals according to relative biological
degradability; k rates for five classes, ranging from extremely biodegradable to
bio-static or toxic, have been assigned. The biological treatability of different che:
has been related to chemical structure and functional group. The k factors for produc
BOD's have been estimated by taking the average of the k's for the raw materials,
intermediates, and products that make up a particular product process. Other sources
of biological kinetics data and maximum percent removals are Screening/Verification
data and responses to the 308 questionnaire.
Aeration, Biological Processes
There are no treatability factors involved. The power required depends on
the oxygen transfer rate in the wastewater, oxygen solubility, and oxygen utilization
rate, which in turn depends on the amount of BOD to be removed and the amount
of MLVSS under aeration.
Nutrients, Biological Processes
There are no treatabi1ity factors involved. The amounts of nitrogen and phosphor;
to be added are the amounts necessary to maintain a BOD:N:P ratio of 100:5:1, based
on using anhydrous ammonia and 75 percent phosphoric acid.
Nitrification
The treatabil ity factor is a temperature correction, which affects the design
nitrification rate. The design data sheet includes a plot
7
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of temperature vs. percent of design nitrification rate.
Denitrification
As with nitrification, the treatability is a temperature correction.
The design data sheet includes a plot of temperature vs. percent of design
denitrification rate.
Ozonation
Three treatability parameters are involved: 1) the ozone/pollutant
ratio required for treatment; 2) the normal lower level of effluent treat-
ment achieved; and 3) the upper level of effluent treatment normally
expected. These values have been obtained for a few pollutant parameters
from surveys of the technical literature.
Chemical Oxidation
The treatability factors are similar to those for ozonation, but
the oxidation chemical must be specified in addition to the chemical/pollutant
ratio and the lower and upper expected effluent values.
Activated Carbon Adsorption
There are four treatability factors needed, and they are:
1. Isotherm constant - Langmuir constant related to the
slope of the isotherm plot.
2. Isotherm constant - Langmuir constant related to the
intercept and slope of the isotherm plot.
3. Final value - lowest attainable effluent value mg/1.
4. Peclet number.
Activated Carbon Regeneration
There is no treatability factor involved. The function of the regenera-
tion furnace is to remove the adsorbed organics from the spent activated
carbon, so that the carbon can be reused in the adsorption unit.
2
Regeneration loadings have all been given the same value: 40 Ib/hr/ft .
This rate may vary for different chemicals adsorbed onto the carbon, as
J-ll
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indicated by activated-carbon and incineration equipment manufacturers.
The value selected for the model is probably on the low side of the actual
average.
Ion Exchange
The treatability factors needed for this unit process are resin type
(cationic or anionic), resin exchange capacity, effluent concentration
attainable, regeneration chemical to be used, and regeneration chemical
dosage. These have been obtained from the literature and from vendor
data.
Gravity Thickening
There are no treatability factors. The function of this unit process
is to increase the solids concentration, and thus facilitate the operation
of the subsequent sludge-handling processes.
Aerobic Digestion
The treatability factor in this unit process is a temperature correction,
which has a significant effect on the rate of reduction of the volatile
suspended solids in waste activated sludge from biological treatment.
The equation for this effect is included in the design data sheet for
Aerobic Digestion.
Vacuum Filtration/Pressure Filtration
There are no treatabi 1 ity factors. The function of either of these
unit processes is further removal of water from the sludge to prepare
the sludge for landfill ing or incineration. Pressure filtration is the
preferred pretreatment for incineration because it yields a drier sludge.
Landfill
There are no treatability factors. This is a method of ultimate
disposal for ash residues and dewatered sludges.
I nc i ner at i on
Sludge moisture content is the treatabi1ity factor in this unit process.
9
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The moisture content determines whether the incineration of the sludge
is self-sustaining, or whether (and how much) auxiliary fuel is required.
Ammonia Stripping
There are no treatability factors. The function of this unit process
is to remove ammonia from wastewater by direct injection of steam, and
thus meeet the limitation on ammonia concentration in the effluent.
Steam Stripping
The factors required for steam stripping are pollutant latent heat,
azeotropic composition, molecular weight, achievable effluent concentration,
activity coefficient, K-value (function of the activity coefficient and
the partial pressure), stripping-steam requirements, and tray efficiency.
This information is available from chemical manufacturers and handbooks.
Steam stripping tray effieciencies at low effluent concentration must
be verified by laboratory experiment, to confirm or modify the calculated
values currently being used.
Solvent Extraction
Treatabil ity factors needed for this unit process are: the solubility,
latent heat, 'and specific heat of the pollutant; identification of the
solvent; the solvent density; and solvent-pollutant distribution coefficient.
Pollutant properties are obtained from manufacturers and chemical handbooks.
Two solvents have been chosen for solvent extraction: tricresyl
phosphate and a mixture of C,Q-C-,? paraffins (mostly straight-chain).
Solvent density can be obtained from manufacturers or from the literature.
The distribution coefficient for tricresyl phosphate was estimated from
the literature. Its affinity for phenol is estimated to be eight times
that of benzene for phenol; since the distribution coefficient for a benzene-
phenol system is about 2.5, the distribution coefficient for tricresyl
phosphate has been assumed to be 20. The distribution coefficient for
the C]Q-C-i2 paraffin has been assumed to be 30, based on textbook discussions
and examples of solvent extraction where it was used to remove chlorinated
10
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hydrocarbons. These assumptions need to be confirmed by laboratory experiment.
Cooling Tower/Heat Exchanger/Steam Injector
There are no treatability factors. A cooling tower or heat exchanger
is introduced into the unit process trail to reduce the wastewater temperature
to meet the operating requirement of a biological treatment system, or
to conform to the temperature limitation on discharge of treated wastewater
to a receiving stream or other body of surface water. A steam injector
may be required in winter to heat a waste stream for biological treatment.
Deep-Well Disposal
There are no treatability factors. The function of the deep well
is ultimate disposal of liquid wastes.
Lime Hand! ing
There are no treatability factors. The function of this unit process
is to provide lime (or caustic) for neutralization and other unit processes.
TREATMENT CATALOG AND MODEL SEQUENCING RULES
This treatment catalog and the computer model derived from it do
not include all the possible treatment unit process alternatives. The
inclusion or exclusion of specific unit-process types or configurations
does not imply that the process types included in this treatment catalog
are the only ones applicable to the treatment of the subject waste streams.
The processes that have been included were chosen because they are widely
used and provide representative treatment costs.
Chemical plants should have flow and/or contaminant equalization
someplace in the treatment system, and possibly also in connection with
storage or monitoring of the treated effluent. The cost of this unit
can be effectively represented by the rules stated herein.
Many plants will have to transfer the waste streams by means of a
lift station someplace in the treatment system. If they do not so require,
sewer complexities or other waste-hand! ing problems will add some increment
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of cost, and that increment is assumed to be equivalent in cost impact
to a lift (pumping) station.
Almost every plant requires some form of neutralization, even if
only on an intermittent basis, and some type of facilities for this purpose
will be provided.
Liners for large earthen basins will be of the synthetic-membrane
type, rather than clay. Landfill liners will also be of the synthetic-
membrane type.
UNIT PROCESS COST DEVELOPMENT
The unit process costs were developed by preparing detailed Flow
Sheets, sizing the equipment, obtaining vendor quotations for major items,
and then using standard estimating procedures to determine installed costs.
The basic design parameters appear in the Treatment Catalog. Flow Sheets
were constructed to establish the kinds of equipment required for a unit
process. Equipment was sized according to specifications in the Treatment
Catalog where specified, and by standard engineering calculations for
equipment items or processes that were not so specified. After equipment
was sized, an equipment list was prepared for estimating purposes.
This equipment list includes the identification and size of each
significant item of hardware for each size range of each treatment unit
process. It includes all mechanical equipment, basins, structures, vessels,
and piping, but does not cover labor costs or instrumentation. The Catalytic
Estimating Department estimators used this list as the basis for determination
of the installed cost of a unit process (based on costs in the St. Louis,
Mo. area as of June 1977). These installed costs included taxes, insurance,
legal fees, contingencies, and overhead. The flow diagram for each unit
process shows all instrumentation and thus serves as a basis for estimating
the instrumentation costs.
Obviously, it is not practical to prepare cost estimates for all
possible sizes of a unit process. On the other hand, it is not good practice
12
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to use one cost estimate (base case) as the basis for all sizes, 'because
the cost of a treatment facility is not necessarily directly proportional
to its size. Consequently, a compromise approach was taken, involving
four separate cost estimates generally covering a unit process size range
of three orders of magnitude. For all unit processes designed to treat
the wastewater forward flow to a treatment plant, flow rates of 0.2, 1,
5, and 20 MGD were used as the basis for the cost estimates.
The four ensuing cost estimates were used to establish the cost curves,
which indicate the installed cost of each unit process as a function of
the "cost parameter" involved. This cost parameter, for example, may
be a flow rate, basin volume, or surface area. Although there can be
only one "cost parameter" for a given unit process, there are other variables
that may affect the cost curve. Thus, the "cost parameter" may be multiplied
by a "scale factor" to provide the necessary adjustment. These scale
factors are indicated on the design data sheet for each unit process.
In addition to the costs of the individual unit processes, there
are many miscellaneous costs that must be considered such as: home office
engineering, site development work, utility and general piping, electrical
requirements, a control building, and a sanitary sewage pumping station.
These costs are introduced into the model as functions of the total capital
cost of the unit processes, the total operating horsepower, and the number
of unit processes. The overall miscellaneous cost is then allocated back
to the individual unit processes. This allocation of the miscellaneous
costs to each unit process reflects the ratio of the individual unit process
cost to the total cost of all the unit processes, as defined by the cost
curves.
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EQUALIZATION AND SURGE STORAGE
Start with an equalization basin with capacity equivalent to the 24-hour filling
volume based on average total wastewater forward flow, and with a separate surge
basin with a capacity equivalent to a similar 12-hour filling volume. Provide a pumpir
station, equipped with two pumps each with a capacity equal to 120 percent of the
daily average total wastewater forward flow.
If the ratio of the maximum daily flow to the average daily flow (or the ratio
of the average to the minimum) exceeds 2.0, increase the size of the basins in accordar
with the following formula:
New Size = Base Size x (Larger Flow Ratio - 2.0) + 1.0
If the ratio of the maximum calendar-month flow to the average daily flow
(or the ratio of the average to the minimum) exceeds 1.5, increase the size of the
basins in accordance with the following formula:
New Size = Base Size x 1.5 (Larger Flow Ratio - 1.5) + 1.0
If both ratios* are in excess of the designated limits, calculate both increases,
but use only the larger of the two.
All equalization basins are equipped with mixers. The design power demand
on the mixers is 0.01 HP per 1,000 gallons of wastewater volume, and costs are based
on floating mechanical mixers.*
In addition to reducing the flow variability and pollutant concentrations, equali;
will cause the wastewater temperature to approach ambient temperature. This change
is accounted for with a temperature balance model that includes heat gains from
influent wastewater, mechanical action, and solar radiation, and heat losses from
effluent flow, evaporation, and surface and sidewall convection/conduction.
See the attached design data sheet for additional details.
This power requirement is based on providing adequate mixing, and
is not intended to prevent all influent suspended solids from settling.
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EQUALIZATION/SURGE STORAGE
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS
APPLICATION
LIMITS:
DESIGN BASIS:
TREATABILITY
FACTOR:
COST PARAMETER:
COST CURVE SCALE
FACTOR:
RESIDUES:
MAJOR
EQUIPMENT:
Equalization of flow and concentration.
Capture of concentrated spills to process sewer.
Hourly fluctuations of flow and pollutant concentration.
Wastewater temperature
Essentially complete homogeneity of average daily
flow, excluding major spills.
Spills diverted to separate surge basin if detected
in time.
Reduces excessive temperature.
None
Equalization Basin C.apacity: 24-hour detention time
for average daily flow.*
Mixing Energy: 0.01 HP/1,000 gallons.
Surge Basin Capacity: 12-hour detention time for
average daily flow.*
Equalization will always be provided.
None
Flow rate
Based on flow variability
Solids accumulation dredged every 5 years.
Equalization Basin and Surge Basin Construction.
550,000 gal: earthen basin with membrane liner
(concrete abrasion pads under mixers)
200,000-550,000 gal: earthen basin with concrete-lined sides
** 20,000-200,000 gal: lined carbon steel tank
** 20,000 gal: stainless steel tank
Mixers:
Floating mechanical mixers
Lift Station for each basin
15
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**
Capacity will be greater if the maximum:average or average:mini mum
flow ratios exceed the limits specified in the general discussion.
No surge basin for these sizes.
NEUTRALIZATION
The basic component of the neutralization unit is a 2-chamber tank
with design retention times of 5 minutes for the first chamber and 20
minutes for the second chamber. Normally, the value of 120 percent of
the average wastewater flow is used in conjunction with these residence
times to calculate the size of the chambers. However, if neutralization
is to precede equalization for any reason (e.g., to avoid the use of expensive
corrosion-resistant materials in an oil separator, which must precede
equalization), the flow value used in this calculation is 200 percent
of the average wastewater flow.
Both chambers are equipped with mixers and with pH controllers for
acid and base addition. Facility design and capital costs for acid addition
are based on sulfuric acid addition for all ranges. The base-addition
facilities (and the related costs) are different for systems of different
sizes. Caustic is specified for small systems (less than 500 Ib/day),
hydrated lime for systems requiring 500-800 Ib/day, and quick lime for
those requiring more than 8,000 lb/d-ay. Lime storage silos and slakers,
and caustic make-up facilities are not part of this unit process; they
are included under "LIME HANDLING".
Chemical dosages are calculated whenever the acidity or alkalinity
of the raw wastewater is known. For cases where this information is not
available, a continuous demand of 200 mg/1 of sulfuric acid is assumed.
This value is considered valid for these cases where no acidity or alkalinity
information is available because it is highly likely that alkalinity or
pH data would be available if higher alkalinity were present. For systems
16
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whose data indicate an essentially neutral condition, a continuous demand
of 50 mg/1 is used, to accomodate the occasional pH swings that can be
expected in normal operation.
17
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NEUTRALIZATION
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS:
APPLICATION
LIMITS:
DESIGN BASIS:
TREATABILITY
FACTOR:
COST PARAMETER:
COST CURVE SCALE
FACTOR:
RESIDUES:
MAJOR
EQUIPMENT:
pH Adjustment
pH
Acidity
Alkalinity
Will achieve control within a pH unit range of -0.5
to +1.0 of target.
None
Dual (acid/base) titration with lime and sulfuric acid.
Dosages:
50 mg/1 of lime or H2S04 for neutral wastes
200 mg/1 of lime or H^SO* for undetermined wastes
Actual alkalinity or acidity where data are available
Two-stage reaction chamber, having five-(5) and twenty-
(20) minute detention times, based on 120 percent
of average flow.
None
Flow Rate
2.0, when neutralization precedes equalization.
To be determined on case-by-case basis.
Depending upon waste characteristics, gases may evolve
(e.g., HpS), or inert solids may be generated.
Reaction chambers with mixers:
0.2 MGD - Concrete, Acid-Brick-Lined
0.2 MGD - Fiberglass Tanks
Sulfuric Acid Storage Tank, carbon steel
Sulfuric Acid Feed Pumps (centrifugal type) with a
closed-loop recycle.
Dual pH Control Units (one for coarse controls, one
for fine control) with panel.
Caustic or Lime Storage and Feed Equipment, carbon steel
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OIL SEPARATION AND DISSOLVED-AIR FLOTATION
Since these two unit process are so frequently and so closely related, they
are discussed together. However, each process is available to the model separately.
Before selecting the unit process to be applied, determine the characteristics
of the oil, grease, and other floating and floatable materials present in the subject
product/process, to determine the applicability (effectiveness) of each of these two
treatment process. This is the basis for selection of either process or of both proce:
in series. In all cases, the design flow rate is 120 percent of the average wastewatei
flow, and a minimum of two (2) units, each at 50 percent of design capacity, will
be provided.
A chemical (coagulant) mix tank and a feed system are listed for Dissolved
Air Flotation (DAF). This equipment is to be used only with DAF and not with gravity
oil separation.
When no information is available, the following rules apply:
For oil and grease concentrations:
Greater than 150 mg/1 Oil Separation followed by Dissolved-
Air Flotation for all cases.
Between 35 and 150 mg/1
Feed to subsequent Oil Separation with effluent at 35 mg/1
activated sludge or or 50 percent removal, whichever is
chemical coagulation lower.
steps.
All others, including Oil Separation followed by Dissolved-Air
direct discharge. Flotation with effluent at 10 mg/1.
Below 35 mg/1 Oil Separation with effluent at 10 mg/1.
For floatable solids: Dissol ved-Air Flotation in all cases.
See the attached design data sheets for more details.
Disposal of separated solids and oils is described at the beginning
of the Sludge-Handling section of this treatment catalog, and the available
Sludge-treatment trains are listed in the accompanying table there.
19
J-22
-------
OIL SEPARATION
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS:
APPLICATION
LIMITS:
DESIGN BASIS:
TREATABILITY
FACTOR:
COST PARAMETER:
SCALE FACTOR:
RESIDUES:
MAJOR
EQUIPMENT:
Removal of floating oil and solids
Floati ng oil
Floatable or Floating Solids
Can achieve effluent concentration of 35 mg/1 floating oil,
or 10 mg/1 floating oil for low-influent concentrations.
None
p
Overflow Rate = 1,000 gpd/ft unless specific data
indicate otherwise.
Maximum horizontal velocity = 3 ft/min.
None
Flow rate
None
Oil and sludge
Quantity to be determined upon application
Splitter box, concrete, with acid-proof lining
*0il Separation Unit, concrete with acid-proof coating
*Skimming Mechanism
*Bottom Flight Scrapers
Sludge Removal Pumps (positive-displacement type)
Oil Sump, concrete, with acid-proof coating
Oil Pumps
Slop-Oil Tank, FRP
Minimum of two (2) units
20
J-23
-------
DISSOLVED-AIR FLOTATION
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS
APPLICATION:
DESIGN BASIS:
TREATABILITY
FACTOR:
COST PARAMETER:
RESIDUES:
SCALE FACTOR:
MAJOR
EQUIPMENT:
Removal of suspended and colloidal materials.
TSS
Free oil
80 percent removal efficiency
Limits of effectiveness:
TSS will not be reduced below 30 mg/1
Free oil will not be reduced below 10 mg/1
Flow, TSS, temperature and pH must not be highly
f luctuati ng.
50 percent recycle
Pressurized recycle aeration for 2 minutes ?@ 50 psig
Overflow rate 2 gpm/ft
Preceded by flocculation
None
Flow rate
Float: Characteristics to be defined upon application
None
Rectangular flotation clarifier with skimmer and bottom
sludge removal; pressure tank; controls (carbon
steel or concrete)
Centrifugal compressor, carbon steel
Flocculation chamber, carbon steel or concrete
Polymer storage and feed system (housed in steel-sided
building), fiber-reinforced plastic
Chemical mix tank, concrete
Chemical mix tank agitator, carbon steel
Sludge pump, carbon steel
Float sump, concrete or carbon steel
Float pump, carbon steel
21
J-24
-------
CHEMICAL PRECIPITATION, COAGULATION, AND FLOCCULATION
This unit process is used for removal of heavy metals and solids
specifically noted as requiring coagulation, and for removal of specific
dissolved materials such as sulfates or fluorides. Proper design requires
a file of solubility data for each potential parameter. (Dissolved-air
flotation has its own chemical feed system, and does not utilize this
unit process).
Coagulation/flocculation is followed by clarification or filtration,
depending upon the quantity and nature of the solids produced. The occurrence
of a large amount of good floe favors the use of clarification; conversely,
small amounts and relatively poor floe favor the use of filtration.
Separate mixing and flocculation chambers are used, with a mix time
of two (2) minutes and a floe time of twenty (20) minutes, based on 120
percent of the average flow. Since it is seldom possible in practice
to achieve theoretical levels, dissolved materials will be removed to
a level 1.5 times the solubility of the resultant precipitated material
in water. Lime and polyelectrolyte will be used as typical chemicals
for costing purposes. A polyelectrolyte dosage of 1 mg/1 is used in all
c as es.
See the attached design data sheet for more details.
22
J-25
-------
COAGULATION AND FLOCCULATION
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS:
APPLICATION
LIMITS:
DESIGN BASIS:
TREATABILITY
FACTOR:
COST PARAMETER:
SCALE FACTOR:
RESIDUES:
MAJOR
EQUIPMENT:
Conversion of dissolved, colloidal, and certain
suspended solids to settleable suspended solids.
Dissolved solids (TDS)
Heavy metals
Dissolved ion removal to 1.5 times the solubility
of the precipitated material in water.
pH, depending upon ions to be removed.
Mix time: two (2) minutes for coagulation.
Floe time: twenty (20) minutes.
Chemical dosage: 1.5 x stoichiometric requirement
for precipitation.
Polyelectrolyte dosage: 1 ppm.
None
Flow
Square root of the number of treatment chemicals used
Precipitate is removed by CLARIFICATION or DUAL-MEDIA
FILTRATION, depending upon concentration and
floe characteristics.
Influent splitter box (concrete)
*Reactor Chambers (concrete), with agitators
*Flocculation chambers (concrete), with flocculators
Polymer storage and feed systems
Minimum of two (2) units
23
J-26
-------
CLARIFICATION
The clarification process is used for removal of primary suspended
solids, chemically-produced suspended solids from coagulation and floccula-
tion, and biological suspended solids from biological unit processes.
Pollution parameters affected are total suspended solids (TSS), plus those
specific parameters made insoluble through chemical precipitation.
All clarification is categorized as one'of three types: primary
clarification without chemical treatment, primary clarification with chemical
treatment, and secondary clarification following biological treatment.
Special applications, such as lime settling prior to ammonia stripping,
may be associated with any of the three basic forms.
The design basis and effectiveness for the clarification process
are based on separate overflow rates for primary sludges, activated sludge
(based on the Food/Microorganism (F/M) ratio), other biological sludges
(nitrif ication/denitrif ication), alum sludges, iron sludges, and lime
sludges. In the case of activated sludge, correction factors for effluent
quality are included for influent MLSS concentrations and dissolved solids.
These correction factors are included in the design data sheet which follows.
In all cases, two clarifiers (in parallel) are included, to insure
continuous operation. Each clarifier has a capacity of 50 percent of
the total design flow.
The effluent suspended solids (TSS) levels indicated on the specifica-
tion sheet for activated sludge - 30 mg/1 for F/M range of 0.2-0.6 and
40 mg/1 for F/M range of 0.05-0.19 - seem well supported by the analysis
of the November 1977 308 data. (The data involved in this analysis represent
long-term averages of all the plants for which data were available.)
These data, however, do not support any consistent relationship between
influent BOD to the activated sludge system and the effluent TSS from
the clarifier. Nevertheless, there is a sound basis for a relationship
24
0-27
-------
between the solids loading in the clarifier and the effluent TSS. As
the activated sludge mixed liquor suspended solids (MLSS) increases for
a given size of clarifier, there should also be an increase in the suspended
solids concentration in the clarifier overflow. Consequently, an increase
in effluent TSS from this relationship would take into account the higher
MLSS required when the influent BOD is higher and/ or where the biological
reaction is lower because of a lower temperature.
The proposed TSS correction in the Treatment Catalog for a change
in MLSS is:
Addition to base- level effluent TSS = ^SS-IOOO
This correction, plus a TSS correction for change in Total Dissolved Solids
-* — ing would provide for a maximum clarifier effluent TSS, as shown
in the following sample calculation for a system with an F/M ratio of
0.2-0.6, an MLSS concentration of 4000 mg/1, and an influent TDS concentration
of of 10,000 mg/1:
on + 4000-1000 , 10,000-4000
- JU f f
=30+60+60
= 150 mg/1
This correction procedure is in agreement with industry's comments
on the Treatment Catalog on a previous organic chemicals study for the
National Commission on Water Quality (NCWQ).
CLARIFICATION
FUNCTION: Removal of suspended solids
PARAMETERS
AFFECTED: Suspended solids (TSS)
APPLICATION
LIMITS: None
25
J-28
-------
EFFECTIVENESS/
DESIGN BASIS:
TREATABILITY
FACTOR:
COST
PARAMETER:
COST CURVE SCALE
FACTOR:
RESIDUES:
Type of Sol ids
Primary Chemical
Alum
Iron
Lime
Sulfide
Activated Sludge*
F/M: 0.2-0.6
F/M: 0.05-0.19
Other Biological**
Overflow
Rate
800
500
700
800
500
500
500
400
*Influent MLSS correction =
Effluent
TSS
(mq/1)
50
20
20
20
50
30
40*
30
MLSS-1000
50
'Underflow
Concentration
Influent TDS correction =
_ TDS-4000
100
3
1.5
3
10
2
1
Addition to effluent
TSS as described in
the preceeding
discussion
**For biological nitrification and denitrification systems,
the lowest overflow rate will be used. Effluent and TSS
and underflow concentrations will be weighted averages.
As per design basis
Surface area
None
Depending upon application (source):
Clarifier bottom sludge of the quantity and characteristics
defined above.
26
J-29
-------
CLARIFICATION (Continued)
MAJOR Clarifiers:
EQUIPMENT: Two provided, each with capacity for 50 percent
of the waste water flow*
Concrete bottom and side walls
Clarifier mechanism with gear drive and motor
Peripheral weir and baffle
Surface skimmer and scum pit
Scum pump
Sludge pumps (applies for primary or other chemical
sludges only; for recycle pumps for activated
sludge process, see ACTIVATED SLUDGE).
Influent splitter box (concrete)
Could be more than two clarifiers. These would be equal in size,
and together would have capacity for 100% of the wastewater flow.
27
J-30
-------
FILTRATION, DUAL-MEDIA
The filtration process is used for the removal of suspended solids, such as residi
biological solids in settled effluents from secondary treatment and residual chemical
solids after alum, iron, or lime precipitation and settling. In these applications,
filtration may serve either as a necessary preliminary step to further treatment
(such as carbon adsorption or ion exchange), or as a final polishing step following
other processes. In cases where chemical treatment is used and only a small quantity
of floe is generated, filtration rather than clarification is used to remove the solids
from the wastewater.
Oil, at low influent levels, can also be removed by this unit process.
The design for filtration is based on a hydraulic loading that varies with influer
? ? 2
TSS concentration from 2.5 gpm/ft to 7.9 gpm/ft , with a backwash rate of 20 gprn/fr"
for 15 minutes per cycle. In conjunction with the water backwash, air scouring is
o
provided at a rate of 5 SCFM/ft . An agitated holding tank, to receive backwash,
is sized to hold 125 percent of the anticipated backwash from one filter. Even for
low flows, a minimum of two operating filters and one spare will be specified. For
higher flows (those requiring three or more operating filters) there will be no design;
spare, but calculation of the required surface area will be based on 120 percent of
the average wastewater flow, to facilitate switching from the operating mode to
the backwash or standby mode without sacrifice of performance.
The cost parameters are based on pressurized downflow dual-media filters.
Backwash handling could vary for different applications of dual-media filtration.
The backwash water may be recycled to the head end of the treatment plant, sent
to the sludge-treatment facilities, or handled in a separate disposal system. This
Treatment Catalog, however, specifies a separate backwash holding tank and then
incorporates the solids handling into the sludge-treatment train.
28
J-31
-------
FILTRATION, DUAL-MEDIA
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS:
APPLICATION
LIMITS:
DESIGN BASIS:
TREATABILITY
FACTOR:
COST PARAMETER:
COST CURVE SCALE
FACTOR:
Removal of suspended solids
TSS
Limits of effectiveness:
90 percent TSS removal
75 percent oil removal
Effluent TSS not less than 5 mg/1
Free oil: 35 mg/1
Influent TSS: 200 mg/1
Hydraulic loading = 8.1 x lo^0'00255) TSS
Backwash water @ 20 gpm/ft for 15 minutes per cycle
Backwash air (3 5 SCFM/ft2 for 3 minutes
None
Flow rate
None
29
J-32
-------
RESIDUES: Filter backwash waste
MAJOR Filters
EQUIPMENT: Pressurized downflow dual-medi a f il ters with
5-ft total bed depth, carbon steel
Influent collection sump, concrete
Feed pumps (centrifugal type)
Filter effluent holding tank, carbon steel (if
requi red)*
Backwash pumps (if required)*
Air compressors for backwash air
Large units can utilize filtered forward flow from adjacent
filter compartments for backwash.
30
J-33
-------
ACTIVATED SLUDGE
The activated sludge process is used to remove dissolved and colloidal
biodegradable organic material. Pollution parameters affected are BOD, COD,
TOC, TOD, and specific soluble organic materials proven to be degradable
(e.g., phenol). Other parameters, such as ammonia and suspended solids,
are affected by the installation of this process, but are not the reason
for its use.
Activated sludge is available to the sensitivity model in only two
forms: conventional activated sludge; and extended aeration. Since chemical
industry wastes tend to require long detention times, there are two elements
in the breakpoint between the two forms for the model: 12-24 hours detention
time; and 90 percent removal. The logic here is that if treatment (at
whatever degree of removal) is accomplished in 12 hours or less, then
conventional activated sludge is adequately descriptive. On the other
hand, if 90 percent removal has not been achieved in 24 hours, then extended
aeration is indeed the process in operation. Between 12 and 24 hours,
conventional activated sludge will be used with a sliding scale on operational
limits, as listed in the design data sheet.
Today, there are many forms of biological treatment, and each has
its own particular features or advantages. In general, the alternatives
to activated sludge are used either to lower the cost from that of activated
sludge for the same or better performance, or to take advantage of a particular
feature of the alternative system in order to bring the effluent of a
problem waste to the quality usually expected from activated sludge.
As an example of the second reason, some wastes will produce a biological
floe that will not settle well, thus the making effluent suspended solids
concentration high. Certain variations of the activated sludge process
enhance settleability and can be the reason for varying the process.
31
0-34
-------
These variations are available to new sources, but generally -are not readily
available to a plant that had installed a treatment plant before such variations were
invented or sufficiently tested. Therefore, both forms of this process are available
to the model in two modes. The first is the new-source mode, which involves the
assumption that proper design of pretreatment and proper selection of the specific
form of the biological treatment process can produce an effluent with "normal activate
sludge process characteristics" at equivalent activated sludge cost (plus the cost
of appropriate pretreatment). The second mode is the existing-source mode, which
includes specific allowances for those factors that have an impact on effluent qualitx
Typical examples are the effects on effluent suspended solids from influent BOD
concentration and from dissolved solids in the wastewater.
Biological treatability reaction rate coefficients are determined as accurately
as possible from actual treatment plant data in the industry. Where such data are
unavailable, pilot or laboratory-scale data are used. The values chosen represent
the treatment mode most widely used for the wastes in question. If pilot or laborator
data are used, K rates are chosen from systems with aeration-basin detention times
as close as possible to 24 hours. Only single-stage systems are used.
Application limits, as shown in the following design data pages, trigger the
need for pretreatment if exceeded. (The various unit processes used for pretreatment
and the manner of their application are detailed in other sections of this catalog).
The suspended solids limitation is intended to protect the activated sludge biomass
from becoming too heavily loaded with non-volatile solids. The ammonia limitation
is to prevent ammonia toxicity. The decision as to whether ammonia must be removed
(because of its status as a pollutant) is made elsewhere in the treatment catalog.
32
J-35
-------
ACTIVATED SLUDGE
FUNCTION: Removal of dissolved organics
PARAMETERS BOD
AFFECTED: COD (TOC, TOD)
Phenol
Other specific organic materials
EFFECTIVENESS: Soluble BOD£: removal up to 99 percent for easily de-
gradabie materials and 97 percent for those difficult
to degrade. Conventional activated sludge (CS)
will be used up to 24 hours detention or 90 percent
soluble BOD removal, whichever is greater. Beyond
that level, extended aeration (EA) will be used.
Effluent BOD5: Soluble fraction not less than 10 mg/1;
suspended solids fraction = 0.3 Ib of BOD,, per Ib
of solids leaving final clarification.
Phenol Removal: Although cases will vary, pure phenol
removal will be high (99% or greater) in steady-
load, acclimated systems, with removal dropping
off as the phenol" analysis reflects substituted
phenols and other phenolic compounds. Regardless
of removal rates, bottom level limits will, reflect
the influent concentration and expected variability.
Oil Removal: 50 percent
COD, TOC and TOD removal: Although cases will vary,
in general the removal of these parameters will
reflect the biodegradable fraction of each parameter.
33
J-36
-------
APPLICATION
LIMITS:
pH
Temperature
Oil
TDS
TSS
Heavy Metals:
Pb
Zn
Cr
Cu
Ni
CN
Phenol:
NH,:
6.0 - 9.1
50 - 1001
_35 mg/1
_10,000 mg/1
_(25
mg/1
mg/1
mg/1
mg/1
mg/1
mg/1
0 mg/1
300 mg/1
'100 mg/1
(500 + 0.
.05 MLVSS)
(steady load)
(fluctuating load)
05 BODK)
Revised 8/4/80
34
0-37
-------
ACTIVATED SLUDGE (Continued)
DESIGN BASIS:
TREATABILITY
FACTOR:
TEMPERATURE LOSS
RATE:
COST PARAMETERS:
COST CURVE SCALE
FACTOR:
RESIDUES:
MAJOR
EQUIPMENT:
vs<
where
K =
= effluent BOD concentration (dissolved), mg/1
= influent BOD concentration (dissolved), mg/1
T = reaction rate coefficient at operating temp.
T (°C), day -1
X = mixed liquor volatile suspended solids, mg/1
t = aeration time, day
F/M= v|
So
Xt
.05
.20
to 0.
to 0,
day"]
day"
0.05 to 0.2 day"
overall range
range for a conventional
system
range for extended aeration
X = 4,000 mg/1
= K
20°C
(1.06)
T-20
where T = temperature ( C)
A model that includes heat gains from the influent
wastewater flow, mechanical action, and from biological
and chemical reactions, plus solar radiation and
losses including evaporation from the liquid surface
and the sidewalls.
Flow rate
Aeration time
Excess activated sludge
Ib dry solids produced (net)/lb BOD removed =
up to 24 hours detention: 0.3 Ib/lb
24 hours detention: 0.3-(t-24)(0.003) Ib/lb
solids 80 percent volatile
Aeration basins
Two (2) basins, each with capacity for 50 percent of
35
J-38
-------
design wastewater flow; common influent splitter box,
Construction:
550,000 gallons - all concrete
_550,000 gallons - earthen basin with
membrane liner; concrete abrasion pads under
aerators (see AERATION)
Aerators - See AERATION
Clarifiers - See CLARIFICATION
Revised 8/4/80
36
J-39
-------
ACTIVATED SLUDGE (Continued)
Sludge recycle pumps: Three centrifugal pumps (including
spare), each with capacity to pump 33.3 percent of
the design wastewater flow at 1 percent solids con-
centration.
Monitoring and control devices
Sludge-wasting control
Sludge-recycle control
DO monitor, temperature monitor
pH monitor and control system
Nutrient storage and feed - See NUTRIENTS
Defoamer storage and feed
37
J-40
-------
Revised 8/4/80
AERATION, BIOLOGICAL PROCESSES
Aeration is required in a biological unit process to supply the dissolved
oxygen needed for sustaining biological growth reactions, and to provide
mixing to keep the bio-mass suspended in the system. The biological processes
requiring aeration are activated sludge, nitrification, and aerobic digestion.
Aeration requirements and the equipment for activated sludge and nitrifica-
tion are covered in this section, while the aeration facilities for aerobic
digesters are covered under AEROBIC DIGESTION.
The design basis is the power required either to supply oxygen or
to accomplish mixing, whichever is greater. The oxygen requirement for
activated sludge is based on the Ib 0~/lb BODr removed. For nitrification,
a requirement for nitrogen oxygen demand is added to the oxygen required
for BOD removal. The mixing requirement is determined on the basis of
horsepower per 1000 gallons of wastewater under aeration.
The cost parameters for these aeration systems are based on platform-
mounted surface turbine aerators. See the attached design data sheet
for a more detailed description of the design basis.
38
J-41
-------
AERATION, BIOLOGICAL PROCESSES
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS:
APPLICATION
LIMITS:
DESIGN BASIS:
Supply dissolved oxygen and mixing for activated
sludge and nitrification processes.
Dissolved oxygen (DO)
Will maintain at least 2.0 mg/1 DO in aeration basin
at 30 C (summer conditions).
lOOmg 02/1 per hour
Power Supplied = Power Required plus one extra aerator
horsepower equivalent.
Activated Sludge
Power Required (at 85% motor and gear efficiency)
NT
P = , '
r 3.0 Ib 02/hr/horsepower
subject to a minimum of 0.1 HP/1,000 gallons
(under aeration).
Required Oxygen Transfer (Ib/hr) at Standard Conditions
N.
N
CssP - CL
(1.025)
1-20 °'4756
= 0.7
= 0.9
Css = 7.63 mg/1 @ 30°C
C$ = 9.17 mg/1 9 20°C
CL = 2.0 mg/1
P - Barometric pressure at plant site _ -,
Barometric pressure at sea level
T = 30°C
Oxygen Utilization Rate (Ib/hr)
39
J-42
-------
N = a' (Ib BOD removed/hr) + b1
(Ib MLVSS under aeration)
a1 = 0.7 Ib 02/lb BOD removed
b1 = see grapn (on following page)
40
J-43
-------
TREATABILITY
FACTOR:
COST
PARAMETER:
COST CURVE SCALE
FACTOR:
RESIDUES:
MAJOR
EQUIPMENT:
Nitrification
Oxygen Utilization Rate (Ib/hr)
N =a'(lb BOD removed/hr) + b'(lb MLVSS under aeration)
+ 4.6 (Ib NH3 -N + Organic-N applied/hr)
Power Required is then computed as for activated sludge.
None
Installed horsepower per aerator
Number of aerators
None
Surface turbine-type aerators, mounting platforms,
walkways, and concrete abrasion pads.
41
J-44
-------
NITTRIENTS, BIOLOGICAL PROCESSES
A nutrient addition system is required for a biological unit process so that
sufficient nitrogen and phosphorus will be present in the wastewater to insure that
neither nutrient becomes the limiting factor in the biological growth reactions.
In some cases, a sufficient amount of either one or both nutrients may already be
present in the wastewater, which reduces or eliminates the need for a nutrient supply
system. This is determined on a case-by-case basis. Capital costs are based on stora
and feeding facilities for phosphoric acid and/or anhydrous ammonia.
42
J-45
-------
NUTRIENTS, BIOLOGICAL PROCESSES
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS:
APPLICATION
LIMITS:
DESIGN RATES:
TREATABILITY
FACTOR:
COST
PARAMETER:
COST CURVE SCALE
FACTOR:
RESIDUES:
MAJOR
EQUIPMENT:
Supply nutrients to biological processes, such as
activated sludge, if not already present in wastewater
in required amounts.
None
Supply enough nitrogen (N) and phosphorus (P) to maintain
biological unit processes.
Only enough nitrogen and phosphorus added to maintain a
small residual of nitrogen and phosphorus in effluent
from biological unit process.
BOD:N:P ratio = 100:5:1
using 75 percent phosphoric acid (H3PO.) and
anhydrous ammonia (NH,)
None
Nitrogen deficiency
Phosphate deficiency
None
None
Ammonia storage tank (carbon steel), with ammonia
feed system, including water bath, irrmersion
heater, evaporator, and ejector - if usage is
over 2 tons/week.
Ammonia cylinders and ejector - if usage is equal to
or less than 2 tons/week.
Phosphoric acid storage tank, - fiber-reinforced plastic,
(if usage is over 200 Ibs/day)
Phosphoric acid, feed pumps (metering type).
A3
J-46
-------
NITRIFICATION, BIOLOGICAL
The biological nitrification unit process is used for ammonia removal, when
required, following an activated sludge system with a detention time of less than
24 hours. Because activated sludge systems with detention times greater than 24
hours (extended aeration) operate at an F:M of 0.2 or lower, it is assumed that nitrif-
takes place concurrently with carbonaceous BOD removal, and does not always require
an additional step. In almost all cases, the nitrification unit process follows an act
sludge process. However, if the discharge from some other type of treatment unit
process has an easily biodegradable waste with a BODg of less than 125 mg/1 and
a BOD5/TKN ratio of less than 3.0, then the nitrification unit process can be considere
for direct use. The pollution parameters affected by this unit process are ammonia
nitrogen (NH3-N), organic nitrogen (TKN), BOD, COD, and TOC. Ammonia compounds
are converted biologically, first to nitrites (NOp) and then to nitrates (NO^). Nitrog
in these forms can be converted to nitrogen gas (N?) by anaerobic denitrification
(See DENITRIFICATION, BIOLOGICAL).
The design parameters are based on Ib NH--N and Ib TKN removed per Ib MLVSS
per day, with a correction factor for temperature. The cost parameter is based
on flow, with a cost-curve scale factor for aeration time.
Application limits, as shown in the specification pages, will either trigger the
need for pretreatment or rule out this unit process for ammonia removal.
44
J-47
-------
NITRIFICATION, BIOLOGICAL
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS:
APPLICATION
LIMITS:
DESIGN BASIS:
TREATABILITY
FACTOR:
Conversion of NH3-N and Organic-N to N02-N and N03-N
NFL-N
Organic-N (TKN)
BOD,
TOC
NH^-N + Organic-N removal to 2 mg/1
Soluble BOD, removal to 5 mg/1
pH
Temperature
BOD,
BOD^/TKN
TDS5
Total Nitrogen
7.5-9.0
50-100°F
125 mg/1
3.0
10,000 mg/1
2,000 mg/1
Basin configuration = complete mix
Nitrification rate = 0.3 Ib NH--N + TKN
removed/Ib MLVSS/day I 30°C and pH 8.5
MLVSS = 2000 mg/1
HT =
VN
qN
where:
HT = hydraulic detention time (days)
N = influent NH.-N + Organic-N (mg/1)
N° = effluent NH^-N + Organic^ (mg/1)
qw = nitrification rate (day " )
Xlj1 = MLVSS (mg/1)
Aeration Tank D.O. 2.0 mg/1
Temperature correction
45
J-48
-------
NITRIFICATION, BIOLOGICAL (Continued)
COST PARAMETERS: Basin volume
COST CURVE SCALE
FACTOR: Aeration time
RESIDUES: Excess sludge:
Ib dry solids produced/lb NH--N + Organic-N removed = 0.5
Ib dry solids produced/lb BOD,, removed = 0.3
MAJOR Aeration basin:
EQUIPMENT: Two provided, each @ 50 percent capacity, with
one 10'-deep influent splitter box
Construction:
550,000 gal. - all concrete
_550,000 gal. - earthen basin with membrane liner
(The number of baffles is estimated on the
basis of complete mixing.)
Aerators: See AERATION, BIOLOGICAL PROCESSES
Clarifiers: See CLARIFICATION
Sludge recycle pumps:
Three centrifugal pumps (including spare) each
@ 33.3 percent of plant design flow
Monitoring and control devices
Sludge wasting control
Sludge recycle control
DO monitor
pH monitor and control system
Defoamer storage and feed
Temperature monitor
46
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DEN ITR IF I CATION, BIOLOGICAL
The anaerobic denitrification unit process is used for the conversion
of nitrates and nitrites to free nitrogen, following a nitrification unit
process or an extended-aeration unit process. The pollution parameters
affected are nitrates (N03) and nitrites (NO-).
The design parameters are based on Ib NO.-N + NOp-N per Ib MLVSS
per day, with a correction factor for temperature. The cost parameters
are based on flow, with cost-curve scale factors for reaction time.
Effluents from nitrifying units are exceptionally free of BOD. For
this reason, denitrification is a very slow process unless a readily oxi-
dizable source of carbonaceous material is added. For the purpose of
design, methanol is used as the source of carbon because it is more completely
oxidized and produces less sludge for disposal, and is more cost effective
than other source of carbon. The effluent from the denitrification unit
is flash-aerated prior to clarification, to oxidize the excess methanol
and to strip entrapped nitrogen gas from the sludge in order to improve
its settling characteristics.
See attached specification pages for a more detailed description
of the design basis.
47
J-50
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DENITRIFI CATION, BIOLOGICAL
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS:
APPLICATION
LIMITS:
DESIGN BASIS:
TREATABILITY
FACTOR:
COST PARAMETER:
COST CURVE SCALE
FACTOR:
Conversion of NO..-N and NO^-N to free nitrogen
NO--N
NO^-N
NO--N removal to
NO^-N removal to
pH
Temperature
NO,-N + N09-N
TDS i
1.0 mg/1
1.0 mg/1
6.0 - 8.0
10 - 38°C (50 - 100°F)
500 mg/1
10,000 mg/1
Basin configuration - complete mix
Denitrification rate - 0.16 Ib NO, + NO?-N removed/lb
MLVSS/day @ 30° and pH 7.0 J *
Dissolved Oxygen 0.1 mg/1
MLVSS = 2000 mg/1
D_-D.
HT = hydraulic detention time (days)
HT =
9DxX1
D = influent NO, + N00-N
o 32
D] = effluent N03 + N02-N (mg/1)
gp = denitrification rate (day" 1\
X1 = MLVSS (mg/1)
Methanol requirements = 4 Ibs methanol/lb NO,-N + N09-N
O L-
Temperature correction
Flow rate
Reaction time
48
J-51
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DENITRIFICATION, BIOLOGICAL (Continued)
RESIDUES:
MAJOR
EQUIPMENT:
Excess sludge
Ibs dry solids produced/lb NO.+NOp-N removed = 0.7
Reaction Basins (uncovered): Two provided, each @ 50 percent
of capacity, with concrete influent splitter box.
Construction:
550,000 - all concrete
_550,000 - earthen basin with membrane liner;
concrete mixer-abrasion pads
Mixers: 0.5 HP/1000 cu ft (0.067 HP/1000 gal)
Clarifiers: See CLARIFICATION
Sludge Recycle Pumps:
Three centrifugal pumps (including spare) each
@ 33.3 percent of plant design flow.
Monitoring and Control Devices:
Sludge wasting control
Sludge recycle control
pH monitoring and control system
Temperature monitor
Methanol Feed System:
Methanol storage tank (if usage is over 350 Ib
per day), carbon steel surrounded by a
concrete dike
Methanol feed pumps (metering type)
Aerated Stabilization Chamber, concrete:
Detention time (0.5 hr)
Aerators: (0.1 HP/1000 gallons)
Acid storage tank (carbon steel) and feed pumps
49
J-52
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OZONATION
The ozonation treatment process is used for the removal of cyanide
and/or phenol, but only on individual process-unit streams or in plants
with low wastewater flow.
The two principal features of the design basis for the ozonation
process are: 7 Ib 0.,/lb cyanide and/or phenol for the ozone-generating
equipment; and 30 minutes retention time for the contactor chambers.
The concentration of ozone (03) is 1.0-2.0 percent (by weight), or
about 20 grams/cubic meter. Efficiency of usage is assumed to be 70 percent.
Waste air/ozone from the contactors will be returned to the compressor
section, with 33 percent discharged to the atmosphere as a purge stream.
Equipment considerations limit the capacity of the ozonation unit
to 2.0 MGD. PI ate-type ozonators are used.
50
J-53
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OZONATION
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS:
APPLICATION
LIMITS:
DESIGN BASIS:
TREATABILITY
FACTOR:
Removal of cyanide and phenol
Cyan i de
Phenol
Other organics
Cyanide removal - to less than or equal to 1 mg/1
Phenol removal - total
None
Ozone dosage = 7 lb,0, per lb (CN + phenol),
20 6M 03/meterJ J
Contact time - 30 minutes
None
COST PARAMETER: Ozone usage rate (Ib/day) and Flow
COST CURVE SCALE
FACTOR:
RESIDUES:
MAJOR
EQUIPMENT:
Concentration of pollutants
None
Ozone generator (air-fed) with compressor, cooler,
water knockout drum, and dryer.
Closed contact chamber (2-Stage), with venting system
51
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CHEMICAL OXIDATION
Chemical oxidation is used in removal of cyanide and other organic
and inorganic materials. This unit process is needed when the pollutant
involved is not amenable to other types of treatment, for either technological
or economic reasons. Cyanide removal by alkaline chlorination is used
on individual-process waste streams when the cyanide concentration is
too high for effective removal in a biological treatment system. To minimize
the risk of formation of chlorinated organics, chlorine is used only when
no feasible alternative is available.
Other available chemical oxidants include permanganates and hydrogen
peroxide, which can be used as required for removal of specific organic
and inorganic pollutants. However, for the purposes of preparing the
cost estimate for this unit process, it was assumed that chlorine would
be used. Oxidation by ozone, which would be generated on-site, performs
the same function as oxidation by purchased oxidants, but the costs generally
are more capital-intensive. (Ozonation is included in this Treatment
Catalog as a separate unit process).
The choice among the various types of oxidation systems is essentially
an economics decision.
52
J-55
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CHEMICAL OXIDATION
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS:
APPLICATION
LIMITS:
DESIGN BASIS:
TREATABILITY
FACTOR:
COST PARAMETER:
RESIDUES:
MAJOR
EQUIPMENT:
Removal of cyanide and/or other organic and inorganic
materi al s.
Specific organic or inorganic pollutants.
Specific for each oxidant/pollutant combination.
Total cyanide destruction by chlorine.
TSS 50 mg/1 maximum
Contact time
First stage 10 minutes
Second stage 30 minutes
Chemical requirements (CN destruction)
15 parts chlorine per part CN~
17 parts NaOH* per part CN"
pH 8-9.5
None
Basin volume
Oxidized impurities that form TSS
Two-stage, concrete reaction vessel
pH control system
ORP control system
Oxidation-chemical feed system (for chlorine: chlorine
vaporizer, chlorinator, and circulation pumps).
A chemically equivalent amount of lime can be substituted for
the 17 parts NaOH.
53
J-56
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ACTIVATED CARBON ADSORPTION
The activated carbon process is used to remove dissolved organic
material. Pollution parameters affected are COD, TOC, TOD, and specific
soluble organic material adsorbable by carbon. In most cases, activated
carbon is used as an individual-stream pretreatment process; however,
in other cases, activated carbon treatment is used as a final treatment
process following biological treatment.
Activated carbon adsorption rate coefficients are determined as accu-
rately as possible from actual treatment plant data in industry when available.
Where such data are unavailable, pilot or laboratory-scale data are used.
Values chosen represent the adsorption rate most typical of the wastes
in question for a variety of types of carbon. No attempt is made to opti-
mize a particular brand of carbon to the particular wastes in question.
The time required to reach the "breakthrough point" is one of the
most important design factors in fixed-bed adsorption processes. The
approach taken to model the activated carbon adsorption process was to
apply a method for predicting breakthrough times to yield: size, perfor-
mance, cost, and operation data for the required carbon system.
Non-equilibrium fixed-bed column dynamics is suggested as the most
applicable adsorption method for controlling water pollutants. Non-equi-
librium theories take into account the nature of driving forces which
control the transport phenomena of solutes from solution. Equilibrium
theories assume the resistance to mass transfer to be negligible.
Three models were presented which deal with the theoretical treatment
of non-equilibrium column dynamics: 1) pore diffusion; 2) homogeneous
solid diffusion; and 3) kinetic reaction (or bilinear adsorption). All
three models are based on the fundamental concept of a material balance
for the adsorbate in the liquid phase and on the solid adsorbent.' '
The model selected for analysis was the lumped parameter model (also
54
J-57
-------
called the Glueckauf Model). This model combines the diffusional -resistances
described by the pore diffusion model and homogeneous solid diffusion
model into a single parameter.
The approach taken to model the activated carbon adsorption process
was the application of a method for predicting the breakthrough time of
a pollutant from the known breakthrough time of a similar pollutant/ '
A breakthrough curve for benzene was selected as the reference case from
which all other breaktrough times were predicted for those pollutants
treatable by carbon.
Various pretreatment unit processes, such as filtration or clarification
for suspended solids removal, frequently are required prior to the use
of activated carbon. These processes are not included here, but they
are detailed in other sections of this catalogue.
On-site carbon regeneration is considered only when carbon usage
exceeds 1,000 Ib carbon/day (see ACTIVATED CARBON REGENERATION). When
carbon usage is below 1,000 Ib/day, disposal is by landfill or outside
contract regeneration.
ACTIVATED CARBON ADSORPTION
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS:
APPLICATION
LIMITS:
DESIGN BASIS:
Removal of dissolved organics.
COD, TOC, specific organic materials.
Removal of pollutant is subject to the adsorption
limits for the compounds present.
Suspended solids: 25 mg/1
Free oil: 10 mg/1
Langmuir adsorption isotherm theory for multicomponent
mixtures. Design is based on the breakthrough time
of the critical pollutant. The reference case is the
breaktrough curve for benzene.
Backwash @ 20 gpm/ft for 15 minutes/cycle.
On-site carbon regeneration only for plant using more
than 1,000 Ib carbon/day. See ACTIVATED CARBON
55
J-58
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REGENERATION.
TREATABILITY Isotherm constants
FACTOR: Q = Langmuir constant related to slope
B = Langmuir constant related to intercept and slope
Final attainable value
COST PARAMETER: Total bed volume
COST CURVE SCALE
FACTOR: None
RESIDUES: Spent carbon
If 1,000 Ib/day, see ACTIVATED CARBON REGENERATION.
If 1,000 Ib/day, disposal by landfill or contract
hauler.
Backwash effluent.
Drainage and transport water.
56
J-59
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ACTIVATED CARBON ADSORPTION (Continued)
MAJOR Moderate-Flow Unit ( 0.4 MGD)
EQUIPMENT: Adsorbers
Fixed-bed, pressurized, downflow contactors;
minimum of two in series, plus a spare (all lined
carbon steel).
Minimum depth: Diameter ratio = 1:1
Regenerated-carbon storage tank, lined carbon steel
Spent-carbon holding tank, rubber-lined carbon steel
Effluent holding tank, carbon steel
Backwash pumps
Backwash storage tank, carbon steel, (with agitator)
Backwash return pumps
Spent-carbon slurry pumps
Surface-spray pumps
If on-site carbon regeneration is involved
(1,000 Ib/day carbon), see ACTIVATED CARBON
REGENERATION.
High-Flow Unit ( 0.4 MGD)
Feed pumps
Adsorbers, lined carbon steel
Pulsed-bed, fluidized, upflow contactors; minimum
of two contactors, plus a spare.
Minimum depth: Diameter ratio = 1:1.
Regenerated-carbon storage tank
Spent-carbon storage tank
Spent-carbon slurry pumps
Regenerated-carbon loading pumps
57
J-60
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ACTIVATED CARBON REGENERATION
The activated carbon regeneration process is used only when the carbon usage
exceeds 1,000 Ib/day. The parameter affected is the adsorption capacity of the carbon
and there is a 10 percent carbon loss per cycle during regeneration. The carbon is
regenerated on a column-by-column basis when the effluent quality reaches the limiting
effluent requirement.
The design parameters are based on a mul tipie-hearth furnace with a carbon
loading of 40 lb/day/square foot, plus 20 percent for down time. The cost parameters
are based on the effective hearth area required.
Activated carbon regeneration by multiple-hearth furnace is the only regeneration
process used in the model. Other regeneration processes (such as solvent washing
and acid or caustic washing) were investigated, but were considered less desirable.
See the attached design data page for a more detailed description of the design basis.
58
J-61
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ACTIVATED CARBON REGENERATION
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS:
APPLICATION
LIMITS:
DESIGN BASIS:
TREATABILITY
FACTOR:
COST PARAMETER:
COST CURVE SCALE
FACTOR:
RESIDUES:
MAJOR
EQUIPMENT:
area
Remove and thermally oxidize adsorbed organics from
spent activated carbon, for reuse of the carbon.
Restoration of carbon adsorption capacity
Complete combustion of off-gases
None
Multiple-hearth furnace with afterburner on top hearth
Carbon loading: 40 Ib/day per ft of hearth surface a
Temperature: 1700°F to 1800?°F
Surface area required: design plus 20 percent for down time
Regeneration fuel: 8,000 Btu/lb of carbon
Carbon loss: 10 percent per cycle
None
Total hearth area
(No. of Furnaces)0'8
Clean off-gas and ash, representing the carbon losses
Regeneration furnace (multiple-hearth) w/stacks and
afterburner
Quench chamber
Venturi scrubber
Separator
Venturi recirculation tank and pumps
Caustic storage and feed system, carbon steel
Combustion and shaft cooling air blowers
Fuel-oil storage and feed system, carbon steel
Carbon transfer pumps
Feed slurry tank
Dewatering screw conveyor
Asphalt slab, surrounded by a concrete wall, for storage
of a 14-day supply of carbon during furnace downtime.
59
J-62
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ION EXCHANGE
The ion exchange process is used to remove dissolved contaminants
that are not amenable to other forms of treatment. Pollution parameters
affected are cyanide, ammonia, and specific soluble heavy metals. In
almost every case, ion exchange is used as a pretreatment process on a
single product/ process waste stream.
The design parameters are based on the ion exchange resin capacity
(Ib/cubic foot of resin) for cyanide, ammonia, and specific metals. The
values chosen represent the resin capacity most typical of the wastes
in question for the type of resin being used. No attempt is made to optimize
a particular brand of resin to the particular waste in question; thus,
values are chosen of a variety of types of resin. Other design parameters
include hydraulic loading and regeneration rates. The cost parameters
are based on the working-bed volume required to achieve the desired effluent
quality.
Various pretreatment unit processes are required preliminaries to
the use of ion exchange, e.g., filtration or clarification for suspended
solids removal. These processes are not included here, but they are detailed
in other sections of this catalogue.
Ion exchange resins are regenerated, by rinsing with clean water
and concentrated brine solutions, after the bed capacity is exhausted.
The type of treatment system to be used on the regeneration wastes depends
on the particular contaminants removed by the ion exchange.
See the attached design data page for a more detailed description
of the design basis for ion exchange.
60
J-63
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ION EXCHANGE
FUNCTION: Removal of dissolved contaminants
PARAMETERS Cyanide
AFFECTED: Ammonia
Metals
Total Dissolved Solids (TDS)
EFFECTIVENESS: Removal subject to ion-exchange rates for
compounds present
APPLICATION Suspended solids - 25 mg/1
LIMITS: Oil - 10 mg/1
DESIGN BASIS: Hydraulic 1oading:
1.5 gpm/f±J
10 gpm/fr
(12 bed volumes/hr)
Regeneration rate: ,
6 bed volumes @ 0.5 gpm/ft (4 bed volumes/hr)
Ion exchange capacity:
2 Ib cyanide/cubic ft of resin
1 Ib ammonia/cubic ft of resin
4 Ib Zn, Ni, Cu/cubic ft of resin
3 Ib Cr/cubic ft of resin
61
J-64
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TREATABILITY
FACTOR: None
COST PARAMETERS: Working bed volume and flow
COST CURVE: Number of beds
RESIDUES: Spent regenerant
Cyanide - 15% NaCl solution (precipitation with FeClJ
Ammonia - 15% NaCl,CaCl9, CaO mixed solution
(see AMMONIA STRIPPING)
Zn,Ni,Co - 5% H?SO. solution (precipitation with lime)
Cr - 10% NaOR solution (chromic acid recovery)
Backwash effluent
MAJOR Exchangers, Fiber-Reinforced Plastic (FRP)
EQUIPMENT: Fixed-bed pressurized downflow contactors,
minimum of two in series.
Minimum depth/diameter ratio = 1:1
Regenerant make-up tank, FRP
Spent regenerant collection and treatment tanks, FRP
Ion-exchange resin
Regeneration and sludge pumps
Regenerant treatment and make-up tank agitators
62
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SLUDGE/RESIDUE HANDLING AND DISPOSAL
GENERAL
Aerobic digestion, gravity thickening, vacuum filtration, pressure
filtration, landfill, and incineration are the Treatment Catalog unit
processes for handling and disposal of sludges and other residues generated
by biological and physical-chemical unit processes. A specific sludge/residue
may require only one of these specific unit processes, or it may require
treatment by a sequence of several unit processes.
Aerobic digestion is used to stabilize waste activated sludges, gravity
thickening to concentrate chemical and biological sludges, and vacuum
or pressure filtration for the dewatering of chemical and biological sludges.
Ultimate disposal of sludges is either by landfill alone or by incineration
followed by landfill. Federal and state regulations, land availability,
sludge type, and other factors affect the decision on whether to landfill
directly or to incinerate a processed sludge. Therefore, the option to
examine both landfill and incineration of a sludge/residue is available
for most of the treatment trains that will be encountered.
For each particular sludge or sludge combination from a biological
or physical-chemical unit process, there is an assigned treatment train(s)
for processing that sludge/residue. The treatment trains to be used on
all sludges/residues are summarized on the attached table, which presents
the sludge/residue type on the left and the treatment train options on
the right side for that particular sludge/residue. When the quantity
of a sludge/residue is small, the treatment train concept is not used,
for economic reasons; instead, a private contractor is utilized to handle
the sludge/residue.
In this sludge-handling section of the Treatment Catalog, the unit
pro-cesses used in the sludge/residue treatment trains are examined on
an individual basis. For each of the six sludge unit processes mentioned,
63
0-66
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there is a narrative and a design data sheet(s) detailing its applicability,
operation, design basis, association with other sludge unit processes,
and other information necessary to model the unit process under consideration
i. T
accurately.
64
J-67
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TABLE 1. SLUDGE TREATMENT SUMMARY
Disposal
Sludge/Residue Options*
Process Primary Sludge
(Primary Clarifier)
Incinerator Scrubber Sludge
Oil/Oily Solids
Floatable Chemical Solids
Waste Activated Sludge (WAS)
Chemical Sludges from Floc-
cul ation/Clarif ication and
Neutralization
Chemical plus Biological
Sludge (WAS)**
Process Primary Sludge
plus (WAS)
Extraction/Distillation
Resi dues
Inci nerator Ash
Non-Organic Filter
Backwash from Tertiary
Sand F il ter
Throw- away Activated
Carbon
L
I
O.C
L
I
O.C
L
I
O.C
L
I
O.C
L
I
O.C
L
I
O.C
L
I
O.C
L
I
O.C
L
I
O.C
L
I
O.C
L
I
O.C
L
I
O.C
Aerobic
Digestion Vacuum/
Pressure
Gravity (Bio-Sludge Filtra- Incinera- Land-
Thickening Only) tion tion fill
X XX
Option Not Avail able
Option Avail able
Option Not Avail able
X
Option Available
X X
X X
Option Available
XXX X
X XX
Option Available
X XX
Option Not Available
Ojjti on Avail able
XXX X
X XXX
Option Available
XXX X
X XX
Opti on Avail able
Opti on Not Avail able
X
Option Avai Table
X
Option Not Available
Opti on Avail able
X XX
Option Not Avail able
Opti on Avail able
XXX X
X XX
Option Avail able
X
Option Not Avail able
Option Avail able
* L = Landfills; I = Incineration; O.C. = Outside Contractor.
** For the Incineration option, biological and chemical sludges are thickened separately;
the chemical sludge is landfilled, and the bio-sludge is incinerated. For the Land-
fill option, the two types of sludge are thickened separately, the bio-sludge is
digested, and then the sludges are combined in a conditioning unit before dewatering.
65
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GRAVITY THICKENING
Gravity thickening is used to concentrate waste activated sludge, chemical
sludges, primary sludges, and certain combinations of these types of sludge. Concentr
of these sludge solids in a gravity thickener results in cost savings in subsequent
sludge dewatering.
The gravity thickener used in the model is a mechanical type with a picket
sludge-collection device used to promote thickening. Thickened sludge that collects
on the bottom of the thickener is pumped to a dewatering device as required. For
biological sludge thickeners, recycled final effluent water is available to suppress
odors associated with septic conditions. The continuous supernatant flow from sludge
thickening is pumped to the head end of the treatment plant.
Determination of the thickener surface area, which dictates associated costs,
o
is based on solids surface loading in Ib/ft /day. Typical solids loadings vary depend
on the type of sludge being thickened, as indicated on the attached design data sheet.
For sludge combinations, a weighted average approach is used to define the solids
loading to the thickener. Underflow solids concentration at the thickener depends
on the type of sludge being concentrated, as well as on the solids loading. For sludg
combinations, a weighted average technique is used to determine thickener underflow
concen-trations. For more details on the thickener, see the attached design data
sheet.
66
0-69
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GRAVITY THICKENING
FUNCTION:
PARAMETER
AFFECTED:
EFFECTIVENESS/
DESIGN BASIS:
APPLICATION
LIMITS:
TREATABILITY
FACTOR:
COST PARAMETER:
COST CURVE SCALE
FACTOR:
RESIDUES:
MAJOR
EQUIPMENT:
Increase the solids concentration
Concentration of suspended solids
Solids, underflow concentration:
Type of Sludge
Primary
Waste Activated
Lime
Alum
Iron
Combined
Overflow quality:
Solids Loading
(lb/ft/z/day)
20
5
40
24
15
Weighted Average
500 ppm TSS
Underflow Cone.
9
2.5
15
3
6
None
None
Surface area
None
Scum
Thickened sludge at various solids concentrations,
depending on the type of sludge.
Supernatant liquor - 500 mg/1 suspended solids
Thickener tank, carbon steel: 15-ft liquid depth
Thickener mechanism with skimmer (center feed,
peripheral overflow), carbon steel
Underflow sludge pumps (positive-displacement type)
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AEROBIC DIGESTION
Aerobic digestion is used to reduce the volatile suspended solids
(VSS) content of a waste activated sludge (WAS) if the sludge is to be
dewatered and hauled directly to a landfill for final disposition. When
the WAS is to be incinerated, aerobic digestion is not used, because a
digested sludge has a lowered percentage of VSS, making it less efficient
as an incinerator fuel. Aerobic digestion is preceded by gravity thickeners
in all sludge-handling systems.
The aerobic digester utilized in the model has a basin similar to
that of an activated sludge system. The digester basin is 12 feet deep
with a three-foot freeboard. Basin size determines the materials of construction
and also the number of aerators required for proper digestion of the activated
sludge. Aerobic digester basins are not covered or heated.
Digested sludge from this unit process is pumped to a dewatering
unit. The dewatering unit is not normally operated continuously (24 hr/day),
but the feed rate to the digester is relatively constant. Therefore,
the water level will vary somewhat, and fixed-mounted surface aerators
cannot be used. Floating, low-speed, surface-turbine aerators are provided.
Waste activated sludge going to the digester has a solids concentration
of 2.5 percent, of which 80 percent is volatile. In the digester, the
volatile material in the sludge will be reduced by 4 percent per day at
20°C, to a maximum reduction of 70 percent. A temperature correction
factor is included on the specification sheet for operating temperatures
different from the normal of 20°C. For further information on the aerobic
digester, refer to the attached design data sheet.
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AEROBIC DIGESTION
FUNCTION:
PARAMETER
AFFECTED:
EFFECTIVENESS:
APPLICATION
LIMITS:
DESIGN BASIS:
TREATABILITY
FACTOR:
COST PARAMETER:
COST CURVE SCALE
FACTOR:
RESIDUES:
MAJOR
EQUIPMENT:
Reduction of volatile suspended solids (VSS) in waste
activated sludge (WAS).
Stabilization of WAS.
VSS
VSS Reduction = 4 percent/day @ 20°C, to a maximum
of 70 percent
pH of basin: 6.0-9.0
Basin temperature: 55-100 F
VSS/TSS = 0.8
Influent solids concentration =2.5 percent
Hydraulic retention time = 15 days under normal conditions.
Can be varied for temperature and VSS reduction con-
siderations.
Aerators: 0.1 HP/1,000 gallons
Temperature correction;, percent reduction @ T = (% Reduction
@ 20°C) (1.06)'^°'
where T = calculation temperature ( C)
Sludge - flow rate (gpd)
Hydraulic retention time
Digested biological solids
Digester basin (12' SWD + 3' Freeboard)
300,000 gal:, steel tank, above ground
_300,000 gal: earthen basin, with plastic membrane
1 iner
Floating, 1ow-speed mechanical aerators
Sludge-transfer pumps (progressive-cavity,
vari able-speed)
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VACUUM FILTRATION
Vacuum filtration, pressure filtration, and centrifugation all are accepted sludc
dewatering techniques. The choice is usually based on technical effectiveness, and
depends on the type of sludge to be dewatered. Vacuum filtration is discussed here;
pressure filtration is covered in a separate section of this Catalog.
The rotary vacuum filter is used in the model to dewater chemical sludges,
biological sludges, and their various combinations. The sludges are fed to the vacuurr
filter at various solids concentrations from the sludge thickener. Lime and ferric
chloride are used to condition all biological sludges for dewatering; conditioning
is also required for some chemical sludges. The quantities of conditioners required
are defined as a certain weight percentage of the sludge being dewatered. (See the
attached design data sheet for the lime and ferric chloride requirements for different
sludges.) The resulting sludge cake from the vacuum filter is either sent to a centre
landfill or incinerated. Filtrate from the vacuum filtration operation is pumped
to the head end of the plant.
Filter surface area is the basis for determination of the associated costs of
a vacuum filtration system. Factors which affect filter surface areas are filter
yield and operation time. Filter yield, defined as pounds of dry sludge filtered per
hour per square foot of surface area, varies depending on the type and quantity of
sludge being filtered. Filter yields for both chemical and biological sludges are pre
on the attached design data sheet. In the case of combined sludges, weighted averages
determine filter yields. Performance of the designed vacuum filter is dependent
on the type of sludge. Cake moistures for different sludges are also presented on
the attached design data sheet. In combination sludge cases, weighted average techniq
again are used to determine sludge cake moisture.
70
J-73
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VACUUM FILTRATION
FUNCTION: Dewatering of sludge
PARAMETERS
AFFECTED: Sludge Moisture Content
EFFECTIVENESS/
DESIGN BASIS: Chemical requirements, filter yields, expected cake solids:
P r. Expected
Sludge Type Lime reu 3. Filter Yield Cake Solids
% _% Ib/hr/sq ft %
Biological 15 4 2 12
Primary 8 1.5 8 25
D.A.F. Chemical 8 1.5 8 25
Float
Sulfide 20 - 1.2 20
Incinerator 8 1.5 8 25
Scrubber Sludge
Iron 20 - 1.2 20
Alum 20 - 0.8 20
Lime 10 40
Combined Weighted Average
Filtrate Quality: 1,000 ppm TSS (maximum)
71
J-74
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TREATABILITY
FACTOR: None
COST PARAMETER: Filter media surface area
RESIDUES: Filtrate (return to head end of plant)
Filter cake - see effectiveness/design basis
MAJOR Vacuum filters (two)
EQUIPMENT: Sludge conditioning unit
Mix chamber with mixers, carbon steel
Fed- storage and feed unit, rubber-lined carbon
•'steel
Lime storage and feed system, carbon steel
Filtrate return system (receivers and pumps), carbon
steel
Cake-conveying units, carbon steel
Cake storage units, carbon steel
Hopper
Bin activator
Vacuum pumps (two) including silencers
Facilities for equipment shelter
Building sump and pumps
72
J-75
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PRESSURE FILTRATION
Pressure filtration (filter press) is available as an alternative to vacuum filtr
It is applicable to all types of sludges and is used whenever the required solids cone
for the dewatered sludge is higher than the maximum achievable by vacuum filtration.
The application of pressure filtration encountered most frequently is the dewater
of waste activated (biological) sludge prior to incineration. Filter presses are used
in this situation because they can produce a dewatered sludge with a solids concentrat
of 35 percent or more, which is high enough for self-sustained combustion (no auxiliar
fuel required). Filter presses can also be used to dewater chemical or primary sludge
that are to be disposed of in a landfill; their advantage is a greater reduction in si
volume, which could be an important factor if the landfill is small relative to demand
or if the haul distance to the landfill is significant.
The pressure filtration system is sized on the basis of 8 hours per day, 5 days
per week operation. A minimum of two filters is provided, which permits the design
sludge load to be processed by the remaining filter (or filters) over a longer period
of time (e.g., 16 hours per day for a 2-filter system) when one filter is out of servi
73
0-76
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FUNCTION:
PARAMETER
AFFECTED:
EFFECTIVENESS/
DESIGN BASIS:
PRESSURE FILTRATION
Dewatering of sludge
Sludge moisture content
Chemical requirements, filter yields, expected cake solids:
FeCl,
Lime
Sludge Expected
Loading? Cake Solids
lb/ft-/cycle
Sludge Type
Biological
Process primary
D.A.F. Chemical
float
Sulfide
Incinerator
Scrubber Sludge
Iron
Alum
Lime
*Three cycles per 8-hour shift
Diatomaceous-earth Requirement: approx. 8 lb/100 sq ft of filter area
8
5
5
30
5
_
-
-
15
10
10
-
10
30
30
-
1.5
2.2
2.2
2.2
2.2
1.6
1.6
3.6
35
45
45
40
45
40
40
50
74
J-77
-------
TREATABILITY
FACTOR: None
COST PARAMETER: Filter plate area
RESIDUES: Filtrate - to clarification
Cake - to incineration or landfill
MAJOR Feed pumps
EQUIPMENT: Contact tank, carbon steel
Surge tanks, carbon steel
Ferric chloride tank, rubber-lined carbon steel
Ferric chloride pumps
Filters, carbon steel/cast iron
Cake conveyors, carbon steel
Filtrate tank, carbon steel
Precoat blower
Bag breaker
Precoat storage bin, carbon steel
Precoat feeder
Precoat slurry tank
Precoat pumps
75
J-78
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LANDFILL
Landfill is the method of ultimate disposal for ash and dewatered sludge in
the treatment model. Depending on existing legislation and the particulars of a
given situation, an individual company may either landfill on unused land on plant
property, purchase land on a suitable site away from plant property, or utilize a
public or privately-owned landfill. For the purposes of the model, it is assumed that
a company will construct and operate a controlled landfill on a suitable site on its
own property, away from the production area. The location, design, construction,
and operation of the controlled industrial landfill are such as to minimize degradatio
of air and water quality in the immediate area of the landfill.
In the initial design of a controlled landfill, area requirements are of prime
concern. The landfill is designed to handle all dewatered sludges/residues produced
in a 20-year period; but operation is based on 2-year cells. Loading rates to the
landfill vary depending on the type of sludge being landfilled, and on the dewatering
method used (vacuum or pressure filtration). The attached design data sheets present
all landfill loadings and other design parameters.
The area and loading requirements presented are based on a mixture of sludge
and soil to a final solids concentration of 80 percent. The landfill area designated
for each landfill cell is adequately diked and has easy access for earthmoving and
dumping equipment; to account for this extra area requirement, the basic cell area
requirement for sludge and soil is increased by 25 percent. While one cell is being
utilized, the next 2-year cell is being constructed, thus providing flexibility in oper
The landfill cell area is lined with a plastic membrane liner to contain leachate flow
A 2-foot layer of sand drainage material is placed above this liner on the landfill
bottom. Any leachate that develops percolates through the landfill sludge layer,
hits the drainage material and then drains down the slightly-sloped landfill bottom
toward a central leachate collection basin. Besides collecting leachate, this basin
also collects rainwater. Central-col lection-basin water is treated by a package physic
chemical treatment system. Leachate monitoring wells are strategically placed
around the landfill to determine whether there is any leachate contamination of
groundwater. In addition, an underdrain system is provided to intercept any leachate
that leaks through the liner and prevent it from reaching the groundwater.
76
J-79
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LANDFILL
FUNCTION:
APPLICATION
LIMITS:
DESIGN BASIS:
TREATABILITY
FACTOR:
Ultimate disposal of sludge
None
Loading rate based on adding sludge and soil to 80 percent
sol ids:
Sludge
WAS
Primary
Lime
FeCl.,
Alum"3
Sulfide
Fly Ash
Sludge Solids Loading
Vacuum Pressure
F i 1 ter F i 1 ter
(Dry tons/
Acre-ft)
From Process
27
71
170
49
49
49
103
169
270
124
122
122
318
Operating time: 20 years with 2-year cells
Final area requirement: 1.25 x sludge area requirement
Landfill depth: 10 ft.
None
COST PARAMETER: Land area requirements based -on sludge application rate.
COST CURVE SCALE
FACTOR:
RESIDUES:
MAJOR
EQUIPMENT:
None
Leachate
Runoff
Membrane-lined earthern landfill cells, 2-yr capacity each
Bulldozer
Leachate monitoring wells around landfill
Wide-tire dump truck(s)
Leachate collection basin, earthern basin, membrane-lined
Leachate collection sump (concrete), with transfer pump.
Package treatment plant feed pumps in concrete sump.
Package treatment plant
Leachate-monitoring underdrain system
77
J-80
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INCINERATION
Incineration is available as a volume-reduction method for organic
primary sludges and waste activated sludges, and as a final disposal method
for oils and the liquid residues from extraction/distillation. Two types
of incinerators (the multiple-hearth and vertical liquid waste type) are
used in the model, depending on the particular type of waste to be incinerated.
If biological sludge, oil, or liquid residue quantities are below a defined
limit, the residue is handled by contractor disposal rather than by incinera-
tion.
The multiple-hearth incinerator is used to burn liquid residues from
extraction/distillation and biological sludges with or without waste oils.
Gases produced by residue combustion pass through a venturi scrubber for
particulate removal. If removal of contaminants in a vapor phase is also
required, the off gases will then be passed through a packed-tower alkaline
scrubber. Hearth area requirements are based on a loading of 8 Ib/hr/sq ft.
Depending on the calorific value of the wastes being burned in the
incinerator, auxiliary fuels may be necess.ary to support combustion.
The attached design data sheet presents typical fuel values of typical
wastes and of No. 2 fuel oil, which is the auxiliary fuel to be used when
necessary to assist combustion. Storage and feeding facilities for No. 2
fuel oil are provided even if the heat value of the wastes is high enough
to sustain combustion, because auxiliary fuel is considered necessary
for incinerator start-up.
When liquid wastes (oils, extraction/distillation residues) are burned
without being mixed with biological sludges, a liquid waste incinerator
is used. Waste gases are cleaned with a venturi scrubber, followed by a
packed-tower alkaline scrubber, which is considered mandatory for liquid
waste incineration. The combustion chamber volume is based on a heat
release value Of 40,000 Btu/hr/cu ft.
78
J-81
-------
No spare units are provided for inci neration^and scrubbing facilities.
In lieu of duplicate units, a storage vessel that has the capacity to
hold two weeks' feed (average rate) to the incinerator is provided.
Separate design data sheets are presented for Sludge Incineration
(Liquid Optional) and for Liquid Incineration.
79
J-82
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SLUDGE INCINERATION (with LIQUID OPTIONAL)
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS:
APPLICATION
LIMITS:
DESIGN BASIS:
TREATABILITY
FACTOR:
COST PARAMETER(S)
COST CURVE SCALE
FACTOR:
RESIDUES:
Volume reduction
Sludge volume
Type of Waste
Organic primary sludge
Waste activated sludge
Grease, scum, oily wastes
Ash Remaining
After Combustion
35%
35%
5%
Sludge must be dewatered before inci nceration
LjQ:iy,4.u av%Qa _ Total 1b of waste/hr
Hearth area - 8.0 ib/nr/Sq ft
Total heat release = (Ib waste/hr) x (avg Btu/lb)
+ (Ib aux fuel/hr) x (Btu/lb)
Typical fuel values of wastes
Fuel Value
Type of Waste Btu/lb dry solids
Organic primary sludge 6,500
Grease, scum, oily wastes 16,000 (pure fraction only)
Waste Activated Sludge 8,000 (volatiles only)
Typical fuel value of No. 2 fuel oil = 18,000 Btu/lb
(a 7.25 Ib/gal
Typical fuel requirements of water = 2,000 Btu/lb
Operating time: 24 hrs/day; 5 days/week
Sludge moisture content
Lb/hr of wet sludge
None
Ash (see EFFECTIVENESS for percent)
(See LANDFILL)
Venturi scrubber slurry
Spent packed-tower scrubber liquor (if liquid wastes
are present)
80
J-83
-------
SLUDGE INCINERATION (with LIQUID OPTIONAL) (Continued)
MAJOR Multiple-hearth incinerator, including cooling-air
EQUIPMENT: fan for center shaft and combustion-air blowers
(supplied as vendor package).
Sludge handling system (storage vessel, bin vibrator,
conveyors, controls), carbon steel.
Gas-scrubbing unit (Venturi type).
Exhaust blower
Separator, carbon steel.
Venturi recycle pumps.
Venturi recycle tank
Ash-handling system (conveyors, storage vessel, vibrator)
Packed tower (optional).
Caustic storage and feed system, carbon steel.
Liquid waste or auxiliary fuel system
(storage vessel, pumps, controls).
Gas-quenching system, carbon steel.
Vent stack.
Afterburner.
Feed storage tank and bin vibrator, carbon steel.
Asphalt slab, surrounded by concrete wall, for storing
a 14-day supply of sludge when the incinerator
is not in operation.
81
J-84
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LIQUID INCINERATION (OILS, EXTRACTION/DISTILLATION RESIDUE)
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS:
APPLICATION
LIMITS:
DESIGN BASIS:
Ultimate disposal
All organics
Total combustion; negligible residue
NONE
Total heat release =
+
Minimum incinerator
volume
(Ib waste/hr) x (avg Btu/lb)
(Ib aux. fuel/hr) x (Btu/lb)
_ Total heat released (Btu/hr)
40,000 Btu/cu ft/hr
Typical fuel values of wastes:
Type of Haste
Oils
Phenolics
Paraffins
Aromatics
Cyclics
01ef i ns
Fuel Value (Btu/lb)
16,000
14,000
19,000
17,500
18,700
19,500
Operating time: 24 hr/day; 5 days/week
82
J-85
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TREATABILITY
FACTOR: Moisture content of the waste
COST PARAMETER: Required heat release
COST CURVE SCALE
FACTOR: None
RESIDUE: Venturi ash scrubber slurry
Spent packed-tower scrubber liquor.
MAJOR Incinerator
EQUIPMENT: Waste injector assembly
Combustion air blower
Liquid waste storage and feed system, stainless steel
Fuel-oil storage & feed system, carbon steel
Venturi scrubber unit
Cyclone separator
Venturi recycle tank, with agitator
Venturi recycle pumps
Packed tower
Packed tower recirculation tank with agitator
Gas quenching system
Vent stack, carbon steel
Gas-emission monitoring equipment
83
J-86
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AMMONIA STRIPPING
Ammonia stripping removes ammonia from pre-limed wastewaters by using
direct-contact steam as the heat input. Two stripping towers are used, each with
an independent collection system. Each tower has the same wastewater flow rate,
with 200 gallons per minute specified as the upper limit for flow to a column.
Pre-liming is necessary to facilitate the removal of ammonia, and a pH of
10.5 or higher is specified for the system. Ammonia removal is 99 percent of the
influent rate, and the attainable effluent limit is set at 50 ppm of ammonia.
The ammonia is collected overhead and sent to a spary absorber, where it is
reacted with dilute sulfuric acid to produce ammonium sulfate, which is recovered
as a crystalline powder.
84
J-87
-------
AMMONIA STRIPPING
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS
APPLICATION
LIMITS:
DESIGN BASIS:
TREATABILITY
FACTOR:
COST PARAMETER:
COST CURVE SCALE
FACTOR:
RESIDUES:
MAJOR
EQUIPMENT:
Removal of ammonia from wastewater by direct injection
of steam into a distillation column.
Ammonia concentration
99 percent removal of ammonia, or 50 ppm of ammonia in
the effluent.
TSS: 50 mg/1
pH: 10.5
NH3-N: 500 mg/1
Flow = average of the average and high values
Stripping steam rate: 1.4 Ib/gal of feed
Bottoms temperature: 232 F
24 actual trays at 24" spacing
25 weight percent ammonia vapor leaving dephlegmator
Sulfuric acid (10%) rate = two times the stoichiometric
requirement
60-foot high column
400 gallon per minute maximum flow per column
None
Flow per stripping column
For two or more operating columns Ipjus a spare),
multiply by: (number of columns/2)
Ammonium sulfate recovered as product
Sieve-tray stripping columns, carbon steel
Bottoms cooler
85
J-88
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Bottoms flash tanks
Dephlegmators
Accumulators
Spray absorption tower
Crystal!izer
Centrifuge
Rotary drum dryer
Slurry tanks
Sulfuric acid feed tank
86
J-89
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STEAM STRIPPING
Steam stripping causes the separation of water-immiscible (or slightly water-
miscible) materials from a wastewater stream by means of direct-contact steam
as the heat input. For the purpose of this design calculation, the concentration of
the organic pollutant in the influent wastewater stream is assumed to be at or below
the solubility of the pollutant at ambient conditions.
The influent stream is preheated by the effluent stream in a counter-current
heat exchanger. It enters the stripping column near the top, and cascades down
over a number of trays. Steam, which is added at the bottom of the column, causes
the organics to vaporize, and the water/organic azeotrope exits at the top. The
vapors are condensed, and the water and organic phases separate in a decanter.
The organic phase is either recovered or incinerated. The water phase, which is
saturated with the organic contaminants, is recycled to the top of the column.
It is possible that the organics removed will be highly toxic. Therefore, the
removal efficiency of this unit process must be constant and the operation must
be uninterrupted. Accordingly, each steam stripper will be provided with a spare
unit at 100 percent of design capacity. This should insure that maintenance problems
will not adversely affect the degree of treatment provided.
87
J-90
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STEAM STRIPPING
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS:
APPLICATION
LIMITS:
DESIGN BASIS:
TREATABILITY
FACTOR:
COST PARAMETER:
COST CURVE SCALE
FACTOR:
Separation of
wastewater
specific dissolved organics from
Concentration of organics, temperature
Removal to achievable outlet concentration, usually 50 g/1
TSS:
Oil:
50 mg/1
100 mg/1
Design flow = 120 percent of the average flow
Maximum number of trays = 22
Maximum column diameter = 6 ft
Tray spacing = 2.5 ft
Organic concentration: No higher than its solubility
at ambient conditions
Pollutant molecular weight
Overall column efficiency
Pollutant latent heat of vaporization
Achievable effluent concentration (each pollutant)
Steam requirement (each pollutant)
Vapor- liquid equilibrium ratio.
Activity coefficient (deviation from ideal -
solution behavior)
Diameter of the column
Number of columns
For two or more
spare), multiply
Number of trays
operating columns (plus a
by: (number of columns/2)
,.
88
J-91
-------
RESIDUES: Distillate is decanted; water phase is returned to
column; organic phase is recovered or incinerated.
MAJOR Feed tank, carbon steel
EQUIPMENT Distillation columns with sieve trays, carbon steel
Feed preheater, carbon steel
Condensers, carbon steel
Accumulator/decanter, carbon steel
Organic-phase pumps
Water-phase recycle pumps
Column feed pumps
Bottoms pumps
89
J-92
-------
SOLVENT EXTRACTION
This unit process is used for removal of dissolved phenol ics or other
organics from a contaminated stream in cases where distillation is inapplicable
or too costly, such as with some azeotropic mixtures or with mixtures
that have components whose boiling points are very close. Extraction
is capable of 99.5 percent removal or reduction to an effluent concentration
of 10 mg/1.
The optimum solvent for extraction is selected upon consideration
of several properties, including; solubility, density (difference between
solvent and water), interfacial tension, selectivity, distribution coefficient,
chemical inertness, viscosity, flammability, pH, ease of solvent recovery,
and cost.
SOLVENT EXTRACTION
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS:
APPLICATION
LIMITS:
DESIGN BASIS:
TREATABILITY
FACTOR:
Removal of dissolved phenol ics or other organics into
a water-immiscible solvent stream.
Organic or phenolic concentration.
99.5 percent removal or 10 ppm of the pollutant and
residual solvent in the effluent.
Temperature: 50 to 150°F
pH: 6.0 to 9.0
TSS: 25 mg/1
Solute concentration must be less than the solubility
of the solute in water.
Boiling point of the organic must be less than 230 C.
Removal to 99.5 percent or 10 ppm organic.
120 percent of flow
Contact time = 20 minutes
Distribution coefficient
Solubility of the pollutant in water
Latent heat of the pollutant
90
J-93
-------
Pollutant specific heat
COST PARAMETER: Flow
COST CURVE SCALE
FACTOR: Percent removal efficiency
RESIDUES: The phenolic or other organic compound is recovered
from the solvent by distillation in a solvent-
recovery system.
MAJOR Extraction column with extract reflux, carbon steel
EQUIPMENT: Recovered-sol vent pump
Solvent storage tank
Solvent feed pump
Pre-heater (solvent and/or water stream), stainless steel
Spent solvent pump
Spent solvent filter
Solvent-recovery distillation column
Reboiler
Condenser
Effluent transfer pump
Accumul ator
Pump for removal of recovered pollutant
91
J-94
-------
COOLING TOWER/HEAT EXCHANGER/STEAM INJECTOR
Cooling towers or heat exchangers may be required to lower the temperature
of a wastewater stream for either or both of two reasons. First, if a biological syst
is used, its temperature may not exceed 105°F; therefore, the influent stream must
be cooled prior to treatment. Second, water quality criteria of the receiving stream
may place a maximum temperature limitation on the plant's wastewater discharge;
in this case, the treated effluent wastewater must be cooled.
Heat exchangers are used for small flows, and cooling towers for larger ones.
Thus, cooling towers are specified whenever the required surface area of a heat
exchanger would exceed 5,000 sq ft. Area requirements are based on she11-and-tube,
countercurrent heat exchangers. Because the tubes can be individually valved off
for maintenance purposes, no spare exchanger is provided. Cooling towers are
the mechanical-draft type, which use fans to improve the rate of heat transfer.
The water is cascaded down the tower through splash bars, causing continuous shearing
that results in maximum contact with the rising air, whose upward flow is induced
by a fan at the top of the tower. The tower generally lowers the water temperature
to within 3 to 5°F of the wet-bulb temperature of the incoming air. Multiple towers
(or cells) are provided whenever practicable.
In the winter, it may be necessary to heat a waste stream prior to biological
treatment. This is done by direct injection of steam. An energy balance is used
to determine the stean requirements. Because the cost of generating the steam
is much greater than the cost of the equipment needed to add it, no capital cost
curve (and no design data sheet) is included for this feature of the unit process;
operating costs are calculated, based on pounds of steam per day.
92
J-95
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COOLING TOWERS
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS:
APPLICATION
LIMIT:
DESIGN BASIS:
TREATABILITY
FACTOR:
COST PARAMETER:
COST CURVE SCALE
FACTORS:
MAJOR
EQUIPMENT:
To cool a wastewater stream to the operating temperature
of a subsequent unit process, or to meet receiving stream
temperature requirements
Wastewater temperature
Approach to within 3-5°F of wet-bulb temperature of air
Desired temperature cannot be lower than 5°F above
the wet-bulb temperature of air
Design flow = 110 percent of the average flow
Wet-bulb temperature = 78 F
None
Flow rate
Change in wastewater temperature
Difference between effluent wastewater temperature
and the wet-bulb temperature of the air
Cooling tower cells, wood
Top-mounted fans, steel
Hot and cold wells, concrete
Vertical feed pumps, steel
Chlorine storage and feed system, steel
93
J-96
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HEAT EXCHANGER
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS:
APPLICATION
LIMITS:
DESIGN BASIS:
TREATABILITY
FACTOR:
COST PARAMETER:
COST CURVE SCALE
FACTOR:
MAJOR
EQUIPMENT:
Cooling of a wastewater stream in an exchanger, using
cowater as the heat-transfer medium.
Wastewater temperature
Cooling normally to within 5°F of the inlet cooling water
temperature
Desired temperature cannot be lower than 5°F above
the inlet cooling water temperature.
Maximum heat transfer Area = 5,000 sq ft
Countercurrent flow
Overall heat transfer coefficient U = 100
Change in cooling water temperature is half the
change in the wastewater temperature
None
Heat transfer area
None
Concrete wet well with carbon steel feed pumps
Shell-and-tube heat exchanger, carbon steel
94
J-97
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DEEP-WELL DISPOSAL
Deep wells are used as a means of ultimate disposal of liquid wastes. This
unit process, however, is not permitted in all areas of the country, and is used only
when in compliance with state and local regulations.
All wastewater outside a pH range of 6.5 to 8.0 must be neutralized prior to
injection, and the maximum allowable suspended solids concerntration is 10 mg/1.
However, the neutralization and filtration facilities needed to meet these limits
are not included as part of this unit process.
All estimates are based on a well depth of 3,500 feet. Flow rates vary from
0.02 to 1.5 MGD, and a constant discharge pressure of 500 psi is assumed.
DEEP-WELL DISPOSAL
FUNCTION:
PARAMETERS
AFFECTED:
EFFECTIVENESS:
APPLICATION
LIMITS:
TREATABILITY
FACTOR:
COST PARAMETER:
SCALE FACTOR:
RESIDUES:
MAJOR
EQUIPMENT:
Ultimate disposal of liquid waste
None
Total disposal
Where permitted by law
Where subsurface geology is suitable
Suspended solids 10 mg/1
pH 6.5-8.0
None
Flow rate
None
None
Injection pumps, carbon steel
Deep-well, 3,500 ft
95
J-98
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LIME HANDLING
Lime (or caustic) addition is required in connection with several unit processes,
including neutralization, coagulation, vacuum filtration, pressure filtration, and
sludge incineration. If the lime requirement exceeds 8,000 Ib/day of hydrated lime,
quick lime is used instead. If less than 500 Ib/day are needed, lime is replaced by
caustic.
Both quick lime and hydrated lime are supplied by truck and unloaded by blowers
to storage silos. Automatic feeding equipment is used to slurry the lime to a 10 perc
concentration. Slakers are provided when quick lime is involved. Spares are providec
for all feeding equipment such as pumps, volumetric feeders, and slakers. Only one
lime storage silo (or one liquid caustic storage tank) is provided, since neither of
these should have to be taken out of serivce.
The lime slurry is stored in agitated pits, from which it is pumped to the other
unit processes. The slurry pipeline is operated as a loop, past all "user" unit proce
and then back to the slurry storage pits. The slurry feed pumps run continuously,
even when there is no demand for lime. This is necessary to provide a constant moveme
in the line to prevent clogging. It also provides sufficient pressure in the line to
satisfy the demand immediately.
If caustic is used, the system consists of a liquid caustic storage tank and feec
pumps.
LIME HANDLING
FUNCTION: Provide lime slurry (or caustic) to other unit
processes.
PARAMETERS
AFFECTED: None
EFFECTIVENESS: Not applicable
APPLICATION 500 Ibs/day: Caustic
LIMITS: 500-8,000 Ibs/day: Hydrated Lime
8,000 Ibs/day: Quick Lime
DESIGN BASIS: Lime silo capacity sized for two weeks storage, or
96
J-99
-------
for one week storage plus minimum bulk.delivery load,
whichever is larger.
TREATABILITY
FACTOR: None
COST PARAMETER: Lbs/day of hydrated lime
SCALE FACTOR: None
RESIDUES: None
MAJOR Caustic:
EQUIPMENT: Caustic storage tank, carbon steel
Caustic feed pumps, carbon steel
Hydrated Lime:
Storage silo, carbon steel
Bag filter, carbon steel housing
Bin vibrator, carbon steel
Lime feeder (plus warehouse spare), carbon steel
Slurry tanks with agitators, carbon steel
Feed pumps, carbon steel
Quick Lime:
Storage silo, carbon steel
Bag filter, carbon steel housing
Bin vibrator, carbon steel
Lime slakers with grit collectors, carbon steel
Lime feeders, carbon steel
Slurry tanks, carbon steel
97
J-100
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APPENDIX K
DESCRIPTION OF MODEL COMPONENTS AND USE
-------
APPENDIX K
DESCRIPTION OF MODEL COMPONENTS AND USE
This Appendix describes the computer model developed for EPA by Catalytic,
Inc. that can evaluate the costs and performance of various wastewater and
sludge treatment technology trains in treating specific wastestreams generated
in the Organic Chemicals and Plastics/Synthetic Fibers Industry. The Model
has three distinct components: (1) the permanent files which contain data on
the design criteria, costs, and performance of the treatment trains, (2) the
28 treatment technology program modules which model the design, performance,
and cost of each unit treatment process; and (3) the control programs that
sequence the treatment units and estimate the overall costs. Details of each
of these three major components are discussed in this section. The
relationships between the files and programs are depicted in Figure K-l, and
the design assumptions incorporated into each treatment technology module are
stated in Appendix J, the Treatment Catalogue.
A. PERMANENT FILES
The Model programs draw data from eight separate permanent files in
executing the design and cost estimating routines. These data files are
separate from the treatment technology modules and control programs in order
to facilitate not only updating the cost and treatment performance information
but also overriding the default values built into the Model. During each
Model run the user may override the default values with new values.
The eight data files, discussed in sequence below, are:
• Master Process File
• Parameter and Treatment Selection File
• Effluent Target File
• Unit Process Sequence Rules Files
• Plant Adder File
• Capital Costs File
• Operating Costs File
• Costs Allocation Rules File
1. Master Process File. It was not practical to evaluate regulatory
options for each of the thousands of OCPSF production plants. Using
pollutant loadings obtained during the Verification phase sampling
program, responses to Section 308 questionnaires, and engineering
judgment, a Master Process File was developed. For 176 major
product/processes, this file estimates the flow and loadings for
conventional, nonconventional and priority pollutants, as well as
rate constants for BOD 5 and COD. The user may employ the Master
Process File to simulate wastewaters from the Generalized Plant
K-l
-------
Configurations (GPC's) or from any combination of the 176
product/processes. Alternatively, the user can specify other raw
waste loads and flows.
2. Parameter and Treatment Selection File. The Parameter and Treatment
Selection File contains pollutant-specific treatability information
that is used to calculate the treatment performance of eight of the
treatment unit processes for each pollutant considered treatable by
that technology. The information tabulated for each of the various
technologies is:
• Activated Carbon Adsorption -- control constant,
two sets of the Langmuir adsorption constants Q and b
(one for influent values below the control constant
and another for influent values above the control
constant), lowest effluent concentration assumed by
the Model to be achievable, and Peclet number.
• Activated Sludge -- reaction rate constant and
lowest modeled effluent concentration.
• Chemical Oxidation -- applicable oxidizing
chemical, ratio of oxidizing chemical to pollutant,
and lowest and highest predicted effluent
concentrations assumed by the Model to be
achievable.
• Chemical Precipitation -- water solubility of the
pollutant, applicable coagulating chemical, and ratio
of coagulating chemical to pollutant.
• Ion Exchange -- type of resin (e.g., cationic or
anionic), resin exchange capacity, lowest effluent
concentration assumed by the Model to be achievable,
type of regeneration chemical, and dose of
regeneration chemical.
• Ozonation -- ratio of ozone to pollutant, lowest
and highest effluent concentrations assumed by the
Model to be achievable.
• Solvent Extraction -- distribution coefficients for
the solvents paraffin and tricresyl phosphate; water
solubility, latent heat, and specific heat of the
pollutant.
• Steam Stripping -- molecular weight (used in
calculating the molar reflux ratio), column
efficiency, latent heat of vaporization, lowest
predicted effluent concentration, steam dosage,
vapor/liquid equilibrium ratio, and activity
coefficient.
K-2
-------
The Parameter and Treatment Selection File also contains information
on how each treatment unit process is typically used (e.g.,
in-process, pretreatment of comingled streams, or end-of-pipe
treatment).
3. Effluent Target File. The Effluent Target File (ETF) contains
concentration limitations equivalent to the concentrations presented
in EPA's Multi-Media Environmental Goals for Environmental
Assessment (IERL, Research Triangle Park, N.C. 1977). Override
options allow the user to evaluate any desired set of target
concentrations for conventional, nonconventional, and priority
pollutants. This override capability facilitates analyzing the
sensitivity of treatment cost to target effluent concentration.
4. Unit Process Sequence Rules File. The Unit Process Sequence Rules
File contains rules for arranging the unit treatment processes into
sequences consistent with OCPSF industry wastewater engineering
practice. This file also contains the rules for inserting necessary
ancillary unit processes into a treatment train (e.g., addition of
nutrients where needed for activated sludge; filtration where
necessary before activated carbon adsorption).
5. Plant Adder File. If commanded to do so by the user, this file adds
wasteloads and flows from plant washdown, sanitary and utility waste
disposal, spills, and other non-process sources of plant waste load.
Only flow and conventional pollutants (e.g., suspended solids and
BOD) data are contained in this file. To simulate these non-process
flows and loadings, the file increases the total flow by 50 percent
of the estimated product/process flow calculated by the Master
Process File; the file increases the loadings of the individual
conventional pollutants by factors ranging from five to fifteen
percent.
Following user option decisions, the Model's programs design and
assess performance of various treatment systems using data from the
five files discussed above. The data in the three remaining
permanent files--the Capital Costs File, Operating Costs File, and
Cost Allocation Rules File--are utilized solely for estimating
treatment system costs.
6. Capital Costs File. The Capital Costs File contains the equations
for capital cost curves for each unit process. Each cost curve was
developed by estimating the cost of the entire unit treatment
process, including required mechanical equipment, electrical
equipment, tanks, piping, and system back-up equipment, for four
different sizes of the treatment unit process. Curves relating cost
to size were developed from these four estimates. For unit processes
where equipment requirements for small systems were significantly
different than for large systems, a second costing curve for small
units was generated. For those unit process costs described by one
curve, precision at the small-system end of the curve was increased
by defining the curve in small segments. The Capital Costs File
K-3
-------
reflects the CE Plant Cost Index from Chemical Engineering Magazine,
July 1977, of 204.7 . The user can update costs by specifying a new
Chemical Engineering Index. The July 1982 CE Plant Cost Index value
was 314.2.
7. Operating Costs File. The Operating Costs File contains two types
of costs or file elements. The first type is organized by unit
process and includes the elements listed in TABLE K-l. For each
technology, the Operating Cost File contains the wastewater-flow
dependent values for shifts per day and service water flow that are
necessary to calculate the cost for each element.
The second set of elements in the Operating Costs File are those
items consumed during operation of each treatment technology and
include chemicals, electrical energy and other utilities such as fuel
oil; the unit costs for these items are listed in TABLE K-2. For
each run, each treatment technology program module calculates the
quantity of each item consumed annually by operation of the treatment
technology. The annual cost of each item consumed is the product of
the quantity consumed and the unit cost of the item. The Model user
may override any of these unit costs.
8. Cost Allocation Rules File. This file stores the information
necessary to allocate capital and operating costs back to each
product/process in proportion to that product/process's contribution
to the overall loading of those pollutants which necessitate
treatment.
In addition to the eight permanent files just discussed, during a run the
Model stores relevant portions of the permanent files and any data calculated
in temporary working files.
B. TREATMENT TECHNOLOGY PROGRAM MODULES
Design, performance, and cost information on the 31 specific technologies
has been programmed' into the Model. This technology information differs from
the information in the Treatment Catalogue written by Catalytic in the
mid-1970's in that this version includes the following: additional unit
processes; improved specifications for each technology; allowable influent
quality and pollutant removal rates that have been revised to reflect the new
data obtained through recent treatability studies and the Section 308
questionnaires; more accurately defined capital and operating cost data and
cost scale factors for each unit process; changes incorporating current
industry design practices, observed performance, cost information and other
comments from reviews by the Chemical Manufacturers Association. The
individual treatment technology modules encoded into the computer Model are
discussed in Appendix J, The Treatment Catalogue. The 31 technologies
include: wastewater treatment technologies; processes, such as nutrient
addition to activated sludge, which are ancillary to the wastewater treatment
technologies; one wastewater disposal process (deep well injection); and
sludge treatment and disposal technologies.
K-4
-------
TABLE K-l
COST FACTOR FOR EACH ELEMENT IN OPERATING COST FILE
ELEMENT COST FACTOR
Direct Labor Shifts per Day
Supervision Percent of Direct Labor
Overhead Percent of Direct Labor
Laboratory Labor Percent of Direct Labor
Maintenance Percent of Capital Cost
Services Percent of Capital Cost
Insurance and Taxes Percent of Capital Cost
Service Water Thousand Gallons per Day
K-5
-------
TABLE K-2
OPERATING COST FILE
UNIT COSTS
UNIT
COST
Energy
Fuel
Steam
Lime
Acid
Ammonia
Phosphate
Sodium Sulfide
FeCl3
Alum
Polymer
Activated Carbon
Methanol
Waste Hauling
Residue Disposal
SoIvent-Undecane
Solvent-Tricresyl Phos
Caustic
Chlorine
P. Permanganate
H. Peroxide
NaCl
$0.02/kw-hr
0.46/gal
0.0045/lb
0.0149/lb
0.0215/lb
0.0789/lb
0.604/lb
0.1375/lb
0.045/lb
0.0645/lb
2.00/lb
0.52/lb
0.0696/lb
0.0004/lb-mile
0.018/lb
0.0137/lb
0.76/lb
0.1575/lb
0.0713/lb
0.48/lb
0.386/lb
0.0199/lb
NOTE: Costs are in July, 1977 dollars.
K-6
-------
In addition to the design criteria, sludge generation quantities, and
costing data that are generated by the treatment technology programs, limits
on allowable influent concentrations and variability are defined within each
treatment technology program. The variability (ratio of maximum to minimum
concentration) for each pollutant is determined by the values in the Master
Process File and is reduced appropriately when waste streams merge. As an
example of checking the influent limits, if activated sludge treatment is
selected, the influent is checked for temperature, pH, and concentrations of
oil and grease, ammonia, TSS, TDS, formaldehyde, sulfide, phenol, and various
metals. If the influent waste stream concentration of any of these pollutants
violates the concentration limits or variability prescribed as acceptable to
the selected treatment process, Model control programs insert one or more
appropriate treatment technologies upstream as pretreatment. Only after all
parameters satisfy the limits for the treatment technology originally chosen
(activated sludge in this example) will the Model design that treatment
technology unit. Appendix J discusses and lists the design assumptions and
influent quality requirements for each treatment technology.
Using the design assumptions and, as needed, the pollutant-specific
information in the Parameter and Treatment Selection File, these technology
modules size the treatment facilities, calculate the quantities of sludge
generated by the treatment process, and specify the cost and scale variables
necessary for estimating the cost of treatment. Seven of the modules (e.g.,
the activated sludge temperature modification program) merely calculate
numbers that are used by other modules and have no internal cost variables.
TABLE K-3 lists the cost and scale factors of all the modules except those
seven.
C. MODEL LOGIC CONTROL PROGRAMS
The overall model logic control programs were developed to allow maximum
flexibility in manipulating the data files and the treatment technology
program modules. The ten major control programs, their primary functions,
their handling of the permanent files, and user (operator) options are
diagrammed in FIGURE K-l and are discussed next. The Model is not
interactive; the user selects his override options, including raw wasteload
specifications, before the run begins.
The control programs operate sequentially. The Model may be operated in
either of two modes: (1) Model Selection Run Mode, where the Model selects
the unit treatment processes, sequences and sizes a system that will treat the
raw waste load to meet the target limits and estimates the costs of the system
or (2) Specified Unit Process Train mode, where the user selects the major
unit treatment processes, and the Model adds necessary ancillary processes,
sequences and sizes them, and estimates the costs of the system. For both
modes, PARAM, the first program in the control sequence, extracts data from
the Master Process File and the Parameter and Treatment Selection File
necessary to select the major and ancillary treatment units, as appropriate.
The two modes and their routes are described in more detail next.
K-7
-------
TABLE K-3
COST AND SCALE FACTORS FOR EACH UNIT PROCESS
UNIT PROCESS
COST FACTOR
SCALE FACTOR
Equalization
Neutralization
Oil Separation
Dissolved Air Flotation
Coagulation/Flocculation
Clarification
Dual Media Filtration
Activated Sludge
Aeration
Nutrient Addition
Nitrification
Denitrification
Ozonation
Activated Carbon
Adsorption
Activated Carbon
Regeneration
Gravity Thickening
Aerobic Digestion
Vacuum Filtration
Controlled Landfill
Solid and Liquid
Incineration
Solvent Extraction
Ion Exchange
Flow Rate
Flow Rate
Flow Rate
Flow Rate
Flow Rate
Surface Area
Flow Rate
Flow Rate
Installed Horsepower
per Aerator
Nitrogen/Phosphate
Deficiency
Flow Rate
Flow Rate
Ozone Usage Rate and
Flow Rate
Working Bed Volume
Total Hearth Area
Surface Area
Sludge Flow Rate
Filter Media Surface Area
Land Area Requirements
from Sludge
Application Rate
Sludge Moisture
Content
Flow
Working Bed Volume
and Flow
Flow Variability
Chemical Use Rate
Aeration Time
Number of Aerators
Aeration Time
Reaction Time
Number of Beds
Hydraulic Retention Time
Required Heat Release
% Removal Efficiency
Number of Beds
-- = No factor.
K-8
-------
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1. Model Run Modes
a. Model Selection Run Mode
If the Model Selection Run Mode has been input, SELECT develops a
skeletal treatment train by first assessing how much of each pollutant in each
product/process waste stream each in-process control technology can remove.
If removal is sufficient (the precise control percentage varies somewhat
depending on operator input), that technology will be considered by subsequent
programs in the total treatment design. Selection of applicable end-of-pipe
unit processes is then performed similarly.
After the potential treatment technologies for both segregated and
combined waste streams have been identified, they are organized by SEQUENCE
into the sequence which would typically be found in the industry. The Unit
Process Sequence Rules File and information previously extracted from the
Parameter and Treatment Selection File contain the information required for
the sequencing of the technologies. All flow junctions of segregated streams
are identified at this stage. Any redundant treatment unit processes are
eliminated and appropriate ancillary processes (e.g., secondary clarification
after activated sludge) are inserted.
b. Specified Unit Process Train (SUPT) Mode
In the SUPT mode, the user specifies the treatment train to be used,
activating the program HIDNSEQ. Like the SEQUENCE program, HIDNSEQ inserts
appropriate ancillary technologies and tracks merge points (flow junctions) as
streams are comingled. In addition, HIDNSEQ allows the operator to specify
key design parameters for any or all of the technologies included in the
overall design.
2. Subsequent Steps for Both Modes
Once the skeletal treatment train has been developed in either the
Model Selection or SUPT mode, the control program RWLCALC calculates raw waste
loads for segregated and combined waste streams. Where streams are combined,
RWLCALC calculates a dampened combined variability at the merge point from the
variability data for the individual streams.
To this point in a run, the control programs have primarily combined
file data with user input directives to generate a generalized treatment train
that treats the specific pollutants in the waste streams. The next program,
TRTCAT, coordinates the detailed design of the system through the use of the
treatment technology program modules and two auxiliary programs, RESEQUENCE
and COMPARE.
TRTCAT starts the actual design by calling the appropriate treatment
technology module to design the most upstream unit process in the generalized
treatment train. If the constituents in the stream(s) to be treated violate
the acceptable influent quality specifications for that technology, RESEQUENCE
inserts appropriate pretreatment. Once the pollutant concentration and
variability meet the influent quality specifications for the unit process, the
treatment technology program sizes the unit and develops cost and scale
K-ll
-------
factors. Additionally, the program calculates the pollutant reductions
achieved by the unit process. Using the waste load data for the treated
stream, TRTCAT then designs the next downstream unit process.
Iteration continues until all unit processes (and protective
pretreatment, as needed) in the generalized tredtment train have been
designed. If, however, all effluent targets are met before all the unit
processes specified have been designed, the COMPARE program stops adding
further treatment, and TRTCAT transfers all design and cost data files to the
COSTS program. If the user has chosen to design and estimate costs for
appropriate treatment sludge handling p*ocesses, the BYPROD program will be
executed before COSTS. BYPROD is analogous to a combination of the Parameter
and Treatment Selection File and SELECT, SEQUENCE, and TRTCAT, except that it
treats the wastewater treatment sludges rather than the wastewater. The
BYPRODUCT-SUPT program operates on sludges and is analogous to the SUPT mode
for wastewater treatment. Since BYPROD-SUPT was never used during the OCPSF
study, it is not depicted in Figure VIII-1.
COSTS is the control program for estimating the treatment systems
costs. It calculates individual unit process capital costs from their
respective cost and scale factors combined with the Capital Costs File data.
The method for calculating operating costs is contained in the Operating Costs
File. Because entire lime requirements for a treatment system cannot be
determined until the total system is designed, the COSTS program itself
designs a central lime handling facility and calculates its costs. COSTS then
calculates the miscellaneous costs, such as piping, and adds them into the
overall capital cost of the facility.
One final control program is an available option. In OCPSF
facilities, one product line may contribute disproportionately to treatment
costs. The ALLOC program can allocate both effluents loadings and costs back
to the responsible product/processes.
More complete documentation of this Model is in Appendix L of EPA's
November 16, 1981, Contractors Engineering Report - Analysis of Organic
Chemicals and Plastics,/Synthetic Fibers Industries.
U S. Environmental Protection Agency
Region 5, Library (PL-12J)
77 West Jackson Boulevard, IZtti rwoi
Chicago, IL 60604-3590
K-12
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