v>EPA
United States
Environmental Protection
Agency
Office of Water
Regulations and Standards (WH-553)
Washington DC 20460
March 1 982
EPA-440/4-85-007
Water
An Exposure
and Risk Assessment
for Chlorinated Phenols
-------
DISCLAIMER
This is a contractor's final report, which has been reviewed by the Monitoring and Data Support
Division, U.S. EPA. The contents do not necessarily reflect the views and policies of the U.S.
Environmental Protection Agency, nor does mention of trade names or commercial products
constitute endorsement or recommendation for use.
-------
30272-101
REPORT DOCUMENTATION «• REPORT "°- «•
PAGE EPA-440/4-85-007
4. Title end Subtitle
An Exposure and Risk Assessment for Chlorinated Phenols
2-Chlorophenol 2,4-Dichlorophenol 2,4,6-Trichlorophenol
7. Author^) Scow, K. ; Goyer, M. ; Perwak, J. ; Woodruff, C.;
Saterson, K. ; Payne, E. ; and Wood, M.
9. Performing Organization Nam* and Address
Arthur D. Little, Inc.
20 Acorn Park
Cambridge, MA 02140
12. Sponsoring Organization Name and AddrMi
Monitoring and Data Support Division
Office of Water Regulations and Standards
U.S. Environmental Protection Agency
Washington, D.C. 20460
3. Recipient's Ace**alon No.
5. Report Data
Final Revision— March 198;
6.
8. Performing Organization Rapt. No.
10. Projeet/Taak/Work Unit No.
11. Contract(O or Grant(Q) No.
(0 C-68-01-3857
C-68-01-5949
(G)
13. Type of Report & P*riod Covered
Final
14.
13. Supplementary Note*
Extensive Bibliographies
1*. Abstract (Limit: 200 words)
This report assesses the risk of exposure to 2-chlorophenol, 2-4-dichlorophenol, and
2,4,6-trichlorophenol. This study is part of a program to identify the sources of and
evaluate exposure to 129 priority pollutants. The analysis is based on available
information from government, industry, and technical publications assembled in June of
1981.
The assessment includes an identification of releases to the environment during
production, use, or disposal of the substance. In addition, the fate of chlorophenols
in the environment is considered; ambient levels to which various populations of
humans and aquatic life are exposed are reported. Exposure levels are estimated and
available data on toxicity are presented and interpreted. Information concerning all
of these topics is combined in an assessment of the risks of exposure to chlorophenols
for various subpopulations.
17. Document Analyst* a. Descriptor*
Exposure
Risk
Water Pollution
Air Pollution
b. Identlfiers/Open-Ended Terms
Pollutant Pathways
. Risk Assessment
e. COSATI Field/Group
Effluents
Waste Disposal
Food Contamination
Toxic Diseases
Chlorinated Phenols
2-Chlorophenol
2 , 4-Dichlorophenol
2,4, 6-Trichlorophenol
iori Agancy
FJOOC
I. Availability Statement
Release to Public
19. Security Class (This Report)
Unclassified
20. Security Class (This Page)
IIncl?kssif ied
21. No. of Pag**
118
22. Price
$13.00
«eANSI-Z39.18)
See Instruction* en Reverse
OPTIONAL FORM 272 (4-77)
(Formerly NTIS-35)
Department of Commerce
-------
EPA-440/4-85-007
June 1981
(Revised March 1982)
AN EXPOSURE AND RISK ASSESSMENT
FOR CHLORINATED PHENOLS
2-Chlorophenol
2,4-Dichlorophenol
2,4,6-Trichlorophenol
by
Kate Scow
Muriel Goyer, Joanne Perwak, Caren Woodruff,
Kathy Saterson, Edmund Payne, and Melba Wood
Arthur D. Little, Inc.
Michael Slimak and Stephen Kroner
Project Managers
U.S. Environmental Protection Agency
U.S. EPA Contract 68-01-3857
68-01-5949
Monitoring and Data Support Division (WH-553)
Office of Water Regulations and Standards
Washington, D.C. 20460
OFFICE OF WATER REGULATIONS AND STANDARDS
OFFICE OF WATER AND WASTE MANAGEMENT
U.S. ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON, D.C. 20460
-------
FOREWORD
Effective regulatory action for toxic chemicals requires an
understanding of the human and environmental risks associated with the
manufacture, use, and disposal of the chemical. Assessment of risk
requires a scientific judgment about the probability of harm to the
environment resulting from known or potential environmental concentra-
tions. The risk assessment process integrates health effects data
(e.g., carcinogenicity, teratogenicity) with information on exposure.
The components of exposure include an evaluation of the sources of the
chemical, exposure pathways, ambient levels, and an identification of
exposed populations including humans and aquatic life.
This assessment was performed as part of a program to determine
the environmental risks associated with current use and disposal
patterns for 65 chemicals and classes of chemicals (expanded to 129
"priority pollutants") named in the 1977 Clean Water Act. It includes
an assessment of risk for humans and aquatic life and is intended to
serve as a technical basis for developing the most appropriate and
effective strategy for mitigating these risks.
This document is a contractors' final report. It has been
extensively reviewed by the individual contractors ?nd by the EPA at
several stages of completion. Each chapter of the draft was reviewed
by members of the authoring contractor's senior technical staff (e.g.,
toxicologists, environmental scientists) who had not previously been
directly involved in the work. These individuals were selected by
management to be the technical peers of the chapter authors. The
chapters were comprehensively checked for uniformity in quality and
content by the contractor's editorial team, which also was responsible
for the production of the final report. The contractor's senior
project management subsequently reviewed the final report in its
entirety.
At EPA a senior staff member was responsible for guiding the
contractors, reviewing the manuscripts, and soliciting comments, where
appropriate, from related programs within EPA (e.g., Office of Toxic
Substances, Research and Development, Air Programs, Solid and
Hazardous Waste, etc.). A complete draft was summarized by the
assigned EPA staff member and reviewed for technical and policy
implications with the Office Director (formerly the Deputy Assistant
Administrator) of Water Regulations and Standards. Subsequent revi-
sions were included in the final report.
Michael W. Slimak, Chief
Exposure Assessment Section
Monitoring & Data Support Division (WH-553)
Office of Water Regulations and Standards
ii
-------
TABLE OF CONTENTS
List of Figures vi
List of Tables vii
Acknowledgments ix
1.0 TECHNICAL SUMMARY
1.1 Introduction 1-1
1.2 Risks to Humans and Aquatic Biota 1-1
1.3 Human Exposure and Effects 1-2
1.4 Aquatic Biota Exposure and Effects 1-3
1.5 Environmental Fate 1-4
1.6, Materials Balance 2-1
2.0 INTRODUCTION
3.0 MATERIALS BALANCE
3.1 Introduction 3-1
3.2 Materials Balance 3-1
3.3 Production 3-1
3.3.1 Direct Chlorination of Phenol 3-4
3.3.2 Hydrolysis of Chlorobenzenes 3-7
3.3.3 Emissions From Production 3-9
3.3.4 Emissions From Transport and Storage 3-9
3.3.5 Miscellaneous Emissions 3-9
3.3.6 Emissions From POTWs 3-10
3.4 Uses 3-10
3.4.1 Emissions From Uses 3-13
3.4.2 Emissions From Transport and Storage 3-13
3.5 Future Projections 3.13
3.6 Summary 3-16
References 3-17
4.0 FATE AND DISTRIBUTION OF CHLOROPHENOLS IN THE
ENVIRONMENT
4.1 Introduction 4-1
4.2 Physical and Chemical Properties 4-2
4.3 Environmental Pathways 4-2
4.3.1 Introduction 4-2
4.3.2 Pathway 1—Discharges to Surface Water 4.5
iii
-------
TABLE OF CONTENTS (Continued)
4.3.2.1 Oxidation 4-5
4.3.2.2 Photolysis 4-6
4.3.2.3 Hydrolysis 4-6
4.3.2.4 Volatilization 4-6
4.3.2.5 Biodegradation in Water 4-7
4.3.2.6 Bioaccumulation 4-10
4.3.3 Pathway 2—Emissions to Air 4-12
4.3.3.1 Free Radical Oxidation 4-13
4.3.3.2 Atmospheric Photolysis 4-13
4.3.4 Pathway 3—Land Disposal 4-14
4.3.4.1 Sorption . 4-14
4.3.4.2 Biodegradation in Soil 4-15
4.3.4.3 Terrestrial Plants 4-15
4.3.4.4 Field Studies 4-16
4.3.5 Pathway 4—Behavior of Chlorophenols in
Wastewater Treatment 4-16
4.4 Monitoring Data 4-17
4.4.1 Method of Analysis 4-17
4.4.2 Water 4_18
4.4.2.1 STORET Data Base 4-18
4.4.2.2 Other Water Monitoring Data 4-20
References 4-24
5.0 EFFECTS AND EXPOSURE—HUMANS
5.1 Summary 5-1
5.2 Human Toxicity 5-2
5 2.1 Introduction 5-2
5.2.2 Metabolism and Bioaccumulation 5^2
5.2.3 Animal Studies 5-3
5.2.3.1 Carcinogenesis 5<-3
5.2.3.2 Mutagenesis 5r-5
5.2.3.3 Adverse Reproductive Effects 5r-8
5.2.3.4 Other Toxicological Effects 5-8
5.2.4 Human Studies 5-11
5.3 Human Exposure 5-12
5.3.1 Introduction 5-12
5.3.2 Ingestion . 5-12
5.3.2.1 Drinking Water 5-12
5.3.2.2 Food 5-13
5.3.3 Inhalation 5-14
5.3.4 Dermal Absorption 5-14
References 5-16
iv
-------
TABLE OF CONTENTS (Continued)
Page
6.0 EFFECTS AND EXPOSURE—AQUATIC BIOTA 6-1
6.1 Summary /• ,
6.2 Effects on Aquatic Biota g i
6.2.1 Introduction g_j_
6.2.2 Freshwater Organisms 6-2
6.2.2.1 Chronic and Sublethal Effects 6-2
6.2.2.2 Acute Effects 6-2
6.2.2.3 Effects on Plants 6-3
6.2.3 Marine Organisms 6-3
6.2.4 Factors Affecting the Toxicity of 6-3
Chlorinated Phenols 6-5
6.2.5 Water Quality Criteria 6-5
6.3 Exposure to Aquatic Biota 6-5
6.3.1 Introduction 6-5
6.3.2 Monitoring Data 6-5
6.3.3 Exposure to Industrial Effluents 6-6
6.3.4 Fish Kill Data ' 6-6
References g_g
7.0 RISK CONSIDERATIONS
7.1 Introduction j_±
7.2 Humans • 71
7.2.1 Statement of Risk 7_!
7.2.2 Effects and Exposure Levels for
Chlorophenols 7_1
7.2.3 Risk of Exposure to 2,4,6-Trichlorophenol 7-3
7.2.3.1 Carcinogenicity of
2,4,6-Trichlorophenol 7-3
7.2.3.2 Discussion of Available Data 7-7
7.2.3.3 Calculations of Human Equivalent
Doses 7_9
7.2.3.4 Estimation of Human Risk 7-9
7.2.3.5 Conclusions 7-14
7.2.4 Margins of Safety for Exposure to
2-Chlorophenol and 2,4-Dichlorophenol 7-L6
7.2.5 Recommendations 7-18
7.3 Aquatic Biota 7 1Q
References jlffi
APPENDIX A: PRODUCTION AND EMISSION ESTIMATES A-l
-------
LIST OF FIGURES
Figure
No- Page
3-1 Commercial Flow of Three Chlorophenols—1977 3-3
3-2 General Process Flow Diagram for Chlorophenol
Producion Via Direct Chlorination. 3-6
3-3 Production Schematic For 2,4,5-Trichlorophenol
Production by Hydrolysis of 1,2,4,5-
Tetrachlorobenzene 3^8
4-1 Possible Cycling of Chlorophenols in the Environment 4-4
4-2 Disappearance of 2,4-Dichlorophenol in an Aerated
and Buffered Lake Water. 4-9
vi
-------
LIST OF TABLES
Table
No. Page
3-1 Supply Consumption and Emissions of Three
Chlorophenols (1977) 3-2
3-2 U.S. Producers of Chlorophenols (1977) 3-5
3-3 Uses of 2-Chlorophenol, 2,4-Dichlorophenol, and
2,4,6-Trichlorophenol 3-11
3-4 Manufacturers of 2,4-Dichlorophenoxyacetic Acid
and its Esters and Salts 3-12
3-5 Estimated Discharges of 2,4-Dichlorophenol and
2,4,6-Trichlorophenol From Selected Industries 3-14
3-6 Estimated Supply and Demand for Pentachlorophenol 3-15
4-1 Physical and Chemical Properties of 2-Chlorophenol,
2,4-Dichlorophenol, and 2,4,6-Trichlorophenol 4-3
4-2 Henry's Law Constants for 2-Chlorophenol, 2,4-
Dichlorophenol, and 2,4,6-Trichlorophenol 4-7
4-3 Degradation of 2,4-Dichlorophenol in Aerated and
Buffered Lake Waters 4_8
4-4 Degradation of 2,4-Dichlorophenol in Unaerated and
Unbuffered Lake Waters 4-U
4-5 Chlorinated Phenols in Ambient Waters—STORET
Data (1977-1979) 4_19
4-6 Reported Concentrations of Chlorinated Phenols
in the Environment 4-23
4-7 Chlorophenols in River Water—Northern Europe 4-24
5-1 Incidence of Neoplasms in F344 Rats Fed 2,4,6-
Trichlorophenol in the Diet for Two Years 5-4
5-2 Incidence of Neoplasms in B6C3F1 Mice Fed 2,4,6-
Trichlorophenol in the Diet for Two Years 5-6
5-3 Incidence of Tumors in Sutter Mice Initiated with
0.3% Dimethybenzanthracene and Treated with Various 5-7
Substituted Phenols.
vii
-------
LIST OF TABLES (continued)
Table
Ji2j— Page
5-4 Acute Lethal Values for Chlorophenols in Mammalian
Species 5.9
6-1 Acute Toxicity (LC50) of Chlorinated Phenols
to Aquatic Animals g_4
6-2 Data on Fish Kills Attributed to Chlorinated
Phenols (1971-1974) 6_7
7-1 Human Exposure to Chlorinated Phenols Through
Ingestion 7_2
7-2 Adverse Effects of 2-Chlorophenol in Mammals 7-4
7-3 Adverse Effects of 2,4-Dichlorophenol in Mammals 7-5
7-4 Adverse Effects of 2,4,6-Trichlorophenol in Mammals 7-6
7-5 Carcinogenic Response in Rats and Mice Fed 2,4,6-
Trichlorophenol in the Diet 7-8
7-6 Estimated Lifetime Probability of Cancer to Humans
Due to Ingestion of 2,4,6-Trichlorophenol at
Various Exposure Levels Based on Three Extrapolation
Models. 7-12
7-7 U.S. EPA Interim Target Risk Levels and Corresponding
Water Quality Criteria for 2,4,6-Trichlorophenol—
Protection of Human Health 7-13
7-8 Estimates of Carcinogenic Risk for Various Waterborne
Routes of Exposure to 2,4,6-Trichlorophenol 7-15
7-9 Margins of Safety For Human Exposure to
2-Chlorophenol and 2,4-Dichlorophenol 7-17
viii
-------
ACKNOWLEDGMENTS
The Arthur D. Little, Inc., Task Manager for this study was
Kate Scow. Major contributors were Muriel Goyer (human effects),
Joanne Perwak (human exposure), Caren Woodruff (fate), Kathy Saterson
(aquatic effects), Melba Wood (monitoring), and Edmund Payne (monitoring)
Other contributors included Anne Littlefield and Judith Harris.
Pearl Hughes was responsible for organization and typing of the final
draft report. The EPA Task Manager for this study was Michael Slimak.
Additional review was provided by Steve Kroner.
The materials balance for chlorophenols (Chapter 3.0) was adapted
from a draft report by Versar, Inc., produced under Contract 68-01-3852
to the Monitoring and Data Support Division, Office of Water Regulations
and Standards, U.S. EPA.
ix
-------
1.0. TECHNICAL SUMMARY
1.1 INTRODUCTION
The Monitoring and Data Support Division, Office of Water Regulations
and Standards, U.S. Environmental Protection Agency is conducting an ongoing
program to identify the sources of and evaluate the exposure to 129 priority
pollutants. This report assesses the environmental exposure and
risk associated with 2-chlorophenol '(2-CP) , 2,4-dichlorophenol
(2,4-DCP), and 2,4,6-trichlorophenol (2,4,6-TCP). Most environ-
mental releases of these chlorophenols are aquatic discharges from
chemical production plants and from the use of derivative products.
Chlorophenols are used primarily as intermediates in the synthesis of
pesticides, dyes, pigments, and phenolic resins and have only limited
direct use.
1.2 RISKS TO HUMANS AND AQUATIC BIOTA
Exposure levels to individuals have been estimated for different
exposure conditions. Dose-response extrapolations based on three models
have been applied to these exposure levels for 2,4,6-trichlorophenol
using data from a study with B6C3F1 mice in which hepatocellular car-
cinomas and adenomas were induced by ingestion of this compound. Risk
estimates of excess individual lifetime tumor incidence associated with
2 4,6-trichlorophenol intakes due to continuous lifetime consumption of
drinking water contaminated at average observed levels of 2,4.6-tri-
chlorophenol are in the <10~10 to 10~7 range. At maximum 2,4,6-TCP
concentrations observed in drinking water, estimated excess individual
lifetime cancer risk levels range from 10~6 to 2 x 10~5. Estimated
excess individual lifetime cancer risk associated with 2,4,6-TCP intakes
from ingestion of contaminated fish range from 3 x 10"7 to 1 x 10~5.
The U.S. EPA Water Quality Criterion for protection of human health
specifies criterion levels of 0.12 ug/1, 1.2 ug/1 and 12 yg/1 2,4,6-TCP
for target risk levels of 10~7, 10~6 and 1Q-5, respectively.
There is considerable controversy over the most appropriate model
for performing such extrapolations. Moreover additional uncertainty
is introduced into the risk estimates by the choice of a particular set
of laboratory data, by the conversion techniques used to estimate human
equivalent doses, and by possible differences in susceptibility between
humans and rats and mice. Due to the use of a number of conservative
assumptions in the risk calculations, the estimated risks most likely
over-estimate the actual risk to humans.
A quantitative estimation of the risks to humans associated with
exposure to 2-chlorophenol or 2,4-dichlorophenol could not be adequately
made due to the lack of available toxicological data on these compounds,
particularly with respect to long-term effects. However, margins of
safety (lowest effects level divided by exposure level) were estimated
for these two compounds. These calculations provide a rough indication
of the relative safety of typical exposure situations. Margins of
1-1
-------
safety for 2-chlorophenol were estimated to be 2 x lO4 for maximum
exposure for fish-eaters, and 2 x 105 for a more typical exposure for
fish-eaters, and 1 x 10 7 for ingestion of drinking water alone. For
2,4-dichlorophenol, the margins of safety are estimated to be 2 x 101*
for the maximum exposure (including ingestion of food and drinking water)
and 2 x 10 for a more typical exposure through drinking water only.
It must be emphasized that these margins are based on very limited
short-term effects data and limited exposure data. Chronic data for
2-CP and 2,4-DCP, which are not available at this time, would likely
result in the determination of lower effects levels which would be
reflected in a decreased margin of safety.
The risk of adverse environmental exposure of aquatic communities
to chlorophenols appears to be low. Assuming 10 yg/1 as a typical
mean concentration for any of the chlorophenols in U.S. surface waters
(probably an overestimate), the lowest chronic effects level exceeds this
concentration by over one order of magnitude while acute LC- 's exceed it
by over two orders of magnitude. There is a possibility, due to the lim-
ited number of species which have been tested, that more sensitive species
do exist but have not been identified at this time.
1.3 HUMAN EXPOSURE AND EFFECTS
Daily exposure to chlorophenols in drinking water was estimated to
be 0.4 yg/day as an average level and 100 yg/day as a maximum. These
estimates are based on concentrations reported for 2,4-dichlorophenol
in drinking water; no equivalent data were available for other chloro-
phenols. The frequency of occurrence of high chlorophenol concentrations
in water is unknown.
Sources of chlorophenols to surface and drinking water include
direct industrial wastewater discharges from organic chemicals, pesticide
manufacturers, and plastics producers, timber and pulp/paper plants, and
foundries. Chlorination of phenols during industrial, POTW, and drink-
ing water treatment processes is a potential source of chlorophenols.
Another source is from the degradation of complex chlorinated organics
(i.e., the herbicide 2,4-D or pentachlorophenol) into lower chlorinated
phenols.
Ingestion of contaminated food results in the highest known exposure
levels of chlorophenols for humans. Maximum exposure through consumption
of fish was estimated to be 137 yg/day for 2-chlorophenol, 26 yg/day for
2,4-dichlorophenol, and 95 yg/day for 2,4,6-trichlorophenol. These
numbers are based on theoretical bioconcentration factors assuming fish
are exposed to concentrations of 30-50 yg/1 (highest ambient water con-
centrations reported in STORET), which may result in an overestimation.
Due to a paucity of monitoring data, it is not possible to determine
how common an occurrence fish contamination by chlorophenols is. Human
consumption of contaminated kidney from cattle fed 2,4-D-treated fodder
has an associated maximum exposure of 280 yg/day of 2,4-dichlorophenol.
There is a potential for contamination of edible crops with chlorophenols
present as impurities or breakdown products in agricultural herbicides,
but no reported measurements of residue levels were available.
1-2
-------
Limited data are available concerning the effects of chlorophenols
on humans or laboratory animals. In general, the compounds appear to
be readily metabolized and excreted in urine. Acute median lethal doses
range from 100 to 900 mg/kg for 2-chlorophenol and 2,4,6-trichlorophenol,
and from 400 to 4,000 mg/kg for 2,4-dichlorophenol. No chronic studies
were available on 2-chlorophenol to estimate the effects of long-term
human exposure to low concentrations. An acceptable daily intake level
of 7 mg 2,4-dichlorophenol/day has been estimated for humans, based on
a long-term feeding study in rats. The compound 2,4,6-trichlorophenol
was determined by NCI to be carcinogenic in both rats and mice, indicated
by increased incidences of leukemia and heptatocellular carcinoma in
rats and mice, respectively, at concentrations on the order of 5,000
mg/kg diet. Based on limited studies, the other two chlorophenols do
not appear to be carcinogenic.
1.4 AQUATIC BIOTA EXPOSURE AND EFFECTS
The small monitoring data base for chlorophenol concentrations in
surface water limits the assessment of environmental exposure of aquatic
organisms. Concentrations for all three compounds were usually reported
at less than 10 yg/1 and at a maximum of 100 ug/1 according to the STORET
data base (1977-1979). Most of the observations were remarked as equal
to or below the level of detection so the data base overestimates ambient
environmental concentrations.
Higher concentrations than those reported in STORET are likely to
be associated with certain industries using or producing chlorophenols;
however, the limited data can provide only examples of the levels to
which aquatic organisms may be exposed. Higher than ambient concentra-
tions may be found in the vicinity of chemical producers, pesticide
manufacturers, pulp and paper mills, wood processers, textile manufac-
turers, leather tanners, and sewage treatment plants. The compound 2-
chlorophenol tends to be nondetectable or detected at lower concentrations
than the other two chlorophenols. Effluent concentrations on the order
of 1 to 100 mg/1 have been reported for various industries; however, on
dilution in the receiving waters, these concentrations are expected to
be considerably reduced by factors such as biodegradation, volatilization
and adsorption.
Fish kills attributed to chlorophenols in general (possibly includ-
ing pentachlorophenol) were reported following discharge from cooling
towers and wood preservative storage tanks. The leakage of 2,4-dichloro-
phenol from a break in a holding dike was specifically responsible for
another large fish kill.
The limited information on the effects of chlorophenols on aquatic
organisms indicates acute toxicity for fish at concentrations on the
order of 0.1-10 mg/1. Reported LC50's for bluegill were 6.6, 2.02,
and 0.32 mg/1, respectively, for 2-chlorophenol, 2,4-dichlorophenol,'
1-3
-------
and 2,4,6 trichlorophenol. Daphnia were affected at concentrations
ranging from 2 to 11 mg/1. Chronic values for fathead minnows were
reported >3.9 mg/1, 0.37 mg/1, and 0.72 mg/1 for 2-chlorophenol, 2,4-
dichlorophenol, and 2,4,6-trichlorophenol, respectively. Toxicity
tended to increase with the degree of chlorination. Water hardness,
the only variable tested for its effect on chlorophenol toxicity, had
no influence on the toxicity of 2-chlorophenol.
1.5 ENVIRONMENTAL FATE
The majority of chlorophenols entering the environment is discharged
to water primarily by chemical producers. Following release, adsorption,
volatilization, and biodegradation are expected to be the major processes
responsible for removal of chlorophenols from the water column. Adsorp-
tion onto organic matter appears to be more significant than adsorption
onto clay material, and, based on their octanol/water partition coef-
ficients, trichlorophenol is more likely to be sorbed than the lower
chlorinated phenols. Volatilization to the atmosphere of the soluble
fraction of chlorophenols is likely based on the compounds' high vapor
pressures, especially the mono- and dichlorophenols. No actual measure-
ments of volatilization from water were available to confirm its signifi-
cance as a transport process for chlorophenols. Biodegradation is an
important transformation process, especially for the lower chlorophenols.
Acclimated microbial cultures can reduce mono- and dichlorophenol con-
centrations to negligible levels in about one week under laboratory
conditions. Aquatic species may bioaccumuluate all three chlorophenols
to levels 100 to 400 times above concentrations in water.
Dichlorophenol is released to soil through the application of the
herbicide 2,4-D and an unknown amount of all the chlorophenols enter
the soils as impurities or breakdown products of 2,4-D, 2,4,5-T, silvex,
and other pesticides. The movement of chlorophenols is controlled by
adsorption onto organic matter and, apparently less importantly, sorption
onto bentonite and other clays. The sorption bond is hypothesized to be
weak and lower chlorophenols are easily desorbed by water based on similar
observations on acidic pesticides. As in water, biodegradation is an
important removal process for chlorophenol in soil. Soil populations
can significantly reduce chlorophenol concentrations in about two to
three weeks and in even less time following acclimation. In porous soils
and conditions unfavorable to biodegradation, there is a potential for
migration of chlorophenols into groundwater. In agricultural areas,
runoff and sediment transport are likely to transfer chlorophenols from
soil to surface water, especially immediately after their application
to land.
Very little is known about the atmospheric fate of chlorophenols
following emission. However, the total amount of chlorophenols released
to air each year is small compared to other better characterized environ-
mental compartments. There were no monitoring data available for any of
the chlorophenols to indicate their presence in ambient air. Based on
1-4
-------
their physical and chemical properties, the chlorophenols are estimated
to have an atmospheric half-life of roughly three weeks controlled by
free radical oxidation. This estimate, however, has not been validated
in the laboratory or under field conditions. Little is known about
other atmospheric fate processes.
Secondary treatment is very effective at removing chlorophenols
from wastewater, especially if well acclimated microbial populations
are present. Inhibitory levels in activated sludge for 2,4-dichlorophenol
and 2,4,6-trichlorophenol have been reported at 200 mg/1. Other commonly
employed treatment techniques, such as those used in primary treatment,
do not appear to be very effective at chlorophenol removal.
Monitoring data on chlorophenol concentrations in environmental
media are very few and limited to surface water. According to the
STORE! data base, the total of 300 ambient samples for chlorophenols
were all at or below the detection limit (usually 10 ug/1, occasionally
100 ug/1). Concentrations in an effluent from a chemical plant ranged
from 3 mg/1 to 73 mg/1 for the three chlorophenols. No measurements
of chlorophenols in air or soil were available.
1.6 MATERIALS BALANCE
The majority (85%) of the known (600 kkg) environmental releases
of the three chlorophenols are to surface water. Releases to air and
through generation of solid waste are expected to be negligible. A
small amount of 2,4-dichlorophenol is released to land in the use of
the herbicide 2,4-D, and some of this may eventually enter water through
agricultural runoff.
Over 90% of the known discharges of chlorophenols to water are made
during the production of 2-chlorophenol and 2,4-dichlorophenol; releases
associated with production of 2,4,6-trichlorophenol are unknown. Moni-
toring data of chlorophenol concentrations in various industrial effluents
indicate that 37% of the positive samples were found in organic chemical
and plastics producers. Chlorophenols are also reported in effluents
from timber and pesticide-related industries and from foundries. The
occurrence in foundry effluents is, at this point, unexplained.
1-5
-------
2.0. INTRODUCTION
The Monitoring and Data Support Division, Office of Water Regulations
and Standards, U.S. Environmental Protection Agency is conducting a pro-
gram to evaluate the exposure to and risk of 129 priority pollutants in
the nation's environment. The risks to be evaluated include potential
harm to human beings and deleterious effects on fish and other biota.
The goal of the tasks under which this report has been prepared is to
integrate information on cultural and environmental flows of specific
priority pollutants and estimate the risk based on receptor exposure to
these substances. The results are intended to serve as a basis for
developing suitable regulatory strategy for reducing the risk, if such
action is indicated.
This report is intended to provide a brief, but comprehensive sum-
mary of the manufacture, use, distribution, fate, effects, and potential
exposure and risk in regard to 2-chlorophenol, 2,4-dichlorophenol, and
2,4,6-trichlorophenol. In order to make effective use of this report
and to understand the uncertainties and qualifications of the data
presented herein, several problems must be identified.
The three chlorophenols are produced primarily for use as
intermediates in the manufacture of other chlorinated phenols and many
organic chemicals. The compound 2,4,6-trichlorophenol is used directly
to a lesser degree as a disinfectant in assorted products. The produc-
tion and use emissions data for all chlorophenols are very limited.
A source of chlorophenols to waterways which is of unknown but
potentially high significance is inadvertent synthesis during chlorination
ol phenols or lower chlorinated phenols. Production may occur in POTWs
drinking water treatment, and in certain industrial treatments. These
sources should be accounted for as best as possible in a materials
balance; however, in this case it was not possible to quantify these
releases.
Environmental fate and monitoring data regarding the chlorophenols
are few. It is difficult, therefore, to predict and confirm their per-
sistence in the environment. In order to estimate the chlorophenols1
environmental behavior, extrapolations from similar substances (such as
derivative products) and based on the compounds' physical and chemical
properties were made. The estimates of exposure to chlorophenols are
associated with some uncertainty due to these inadequacies.
This report is organized as follows:
• Chapter 3.0 contains information on the production,
consumption, discharge, and disposal of chloro-
phenols.
2-1
-------
• Chapter 4.0 describes the environmental 'fate of chloro-
phenols in four pathways originating from the point of
release and presents available monitoring data on levels
in environmental media.
• Chapter 5.0 presents reported effect levels in humans
and laboratory animals and exposure pathways for humans.
• Chapter 6.0 discusses reported effects levels and exposure
pathways for aquatic organisms.
• Chapter 7.0 discusses risk of exposure to chlorophenols
for the general population of humans and aquatic
organisms.
• Appendix A provides details concerning the production and
emission estimates in Chapter 3.0.
-------
3.0 MATERIALS BALANCE
3.1 INTRODUCTION
In this chapter, data on the sources of chlorophenols and their
pathways of entry into the environment are presented. A materials
balance checklist was used to help locate the potential sources of the
compounds. Current and past EPA reports, other readily available litera-
ture and personal contacts with EPA provided the basis for this chapter,
which was prepared by Versar, Inc.
Appendix A presents the methodology employed to derive estimates
of production, use, and emissions. The environmental compartments (air,
land, water, etc.) initially receiving and transmitting the compounds
are identified in this chapter whenever possible, as are the locations
at which the environmental loadings occur. There are many uncertainties
in this analysis; current releases have not been identified from all
sources, past releases are not well documented, and future releases
are difficult to predict. Nevertheless, sufficient information is avail-
able to indicate in general terms the nature, magnitude, location, and
time dependence of pollutant loading of the environment with chlorophenols.
3.2 MATERIALS BALANCE
This section presents a materials balance for three chlorophenols:
2-chlorophenol, 2,4-dichlorophenol, and 2,4,6-trichlorophenol for the
year 1977. A total of 22,000 to 38,000 kkg of all compounds were pro-
duced in 1977. There were no reported imports or exports of any of the
chlorophenols. Because of the lack of information specific to the
chlorophenols, production quantities, use statistics, and emissions have
been estimated based on data for related compounds: pentachlorophenol,
phenol, and 2,4-dichlorophenoxyacetic acid.
The majority of the supply of these compounds is used to produce salts,
esters, or other chlorophenol derivatives. These derivatives are used
as herbicides, insecticides, germicides, or in related applications.
Small quantities of chlorophenols may have a highly specialized use, but
the extent of their use in these applications is unknown. The most
significant known source of environmental emissions of these compounds
is the discharge from production operations or from derivatives in the
biosphere. Total known environmental emissions for all 3 chlorophenols
are estimated to be about 600 kkg, with the majority released to aquatic
systems. Solid wastes and discharge to POTWs are believed to be negligible.
Summaries of production, use, and emissions are presented in Table 3-1 and
Figure 3-1. An estimated 1 to 70 kkg of 2,4-dichlorophenol is released to
land each year as a contaminant in 2,4-D herbicide applications.
3.3 PRODUCTION
There are thirteen isomers of chlorophenols which are produced in
the United States. Recent production data on all but one of these
3-1
-------
TABLE 3-1. SUPPLY, CONSUMPTION, AND EMISSIONS OF THREE CHLOROPHENOLS (1977)'
OJ
1
NJ
PRODUCTION AND EMISSIONS
2-chlorophenol
2 , 4-dichlorophenol
2,4,6-trichlorophenol
USES AND EMISSIONS
2-chlorophenol
Production of other
Supply
(kkg)
8,150
14,000
0-16,000
Airborne
Consumption Emissions
(kkg) (kkg)
b 9
14
Aquatic Discharge
Discharge to POTW
(kkg) (kkg)
170
294
Discharge to
Land
(kkg)
Negligible
Negligible
chlorophenols
Miscellaneous
2,4-dichlorophenol
Production of 2,4-di-
chlorophenoxyacetic acid
Miscellaneous
2,4,6-trichlorophenol
Insecticide and
related products
Production of higher
chlorophenols
TOTAL
a
b
8,060
81
81'
14,000
2.1
42
22,150-
38,150
22,150
25.1
587
Negligible
Negligible
1-70
70
is based on material presented in Appendix A.
Blanks denote information not available.
Receiving medium either surface water or POTWs.
-------
2 Chlorophenol
Production 8150*
2,4 Dichlorophenol
Production 14,000
6069
Unknown
00 _ ,, ^ Production nf 7 4-ni<-hlnrnnhBnnvu:u-ati<-
nl
acid
14,000
fc Miscellaneous
Unknown
5.000 _ . ....^ Prnrlurtinn <>f other chloronhfinols
Unknown
Air Water POTW Land
^- 9 170 Negligible
^ mb
— i» a i
14 294 Negligible
»• 1-70
Negligible
^-
2,4,6-Trichlorophenol
Production 0-16,000
Unknown
Emissions from storage and transportation, if any, are unknown.
a. All units in metric tons.
b. Receiving medium either surface water or POTWs.
Source: Versar, Inc., estimates.
FIGURE 3-1 COMMERCIAL FLOW OF THREE CHLOROPHENOLS - 1977
-------
compounds is proprietary and unpublished. The production of the three
isomers addressed in this report, 2-chlorophenol, 2,4-dichlorophenol,
and 2,4,6-trichlorophenol has been estimated for 1977 as follows:
Compound
2-chlorophenol
2,4-dichlorophenol
2,4,6-trichlorophenol 0-16,049
The basis for these estimates is presented in Appendix A.
The production of these compounds is interrelated because they have
little commercial importance separately and thus only small amounts of
these compounds are isolated. The balance is used directly in mixed
batches for the production of other chlorophenols (JRB Associates 1980).
A total of four chemical plants produced the three chlorophenols
in 1977. The names of the producers and their locations are listed in
Table 3-2 as well as other plants which produce other isomers of the
same compounds.
Chlorophenols are manufactured by two processes using different
feedstock. One process uses phenol as precursor feedstock, and the
other uses the analogous chlorobenzene.
3.3.1 Direct Chlorination of Phenol
A flowsheet for the direct chlorination of phenol is presented in
Figure 3-2. Phenol, chlorine, and catalyst are charged to a reactor
ar.d the product is separated and purified by crystallization. The tem-
perature and stoichiometric quantities of reactants are controlled in
order to optimize the production of the desired isomer, but a mixture
of isomers invariably results. The chemistry of phenol, discussed in
Appendix A, dictates which isomers result from the direct chlorination
of phenol.
Because of the strong ortho-para directing of the hydroxyl group,
successive substitution on the aromatic ring results in the following
isomers by ring nomenclature:
3-4
-------
TABLE 3-2. U.S. PRODUCERS OF CHLOROPHENOLS (1977)
OJ
I
Ui
Monochloro- Dichloro'-
phenol phenol
o
Company Location "fl
o
n)
«s
PH
flJ CO ^ in vO st iA
0) CN| CM es csj ro ro
Trichloro-
phenol
vO »A
-------
VENT
LO
I
DUST & PARTICULATE
TARS TO
INCINERATION
WATER
EXCESS
WASTEWATER
TO TREATMENT
PRINCIPAL PROCESSING ROUTE
FOR ALTERNATIVE PRODUCT-TYPE
Source: Tracor-Jitco (1978a).
PRODUCT
(CRYSTAL-
LIZES)
FIGURE 3-2 GENERAL PROCESS FLOW DIAGRAM FOR CHLOROPHENOL PRODUCTION
VIA DIRECT CHLORINATION
-------
Phenol nomenclature:
Ortbo substitution - positions 2 or 6
Para substitution - position 4
Meta substitution - positions 3 or 5
Isomers Produced by Direct Chlorination
2 chlorophenol
4 chlorcphenol
2,4-dichlorcphenol
2,6-dichlorcphenol
2,4,6-trichloroohenol
2,3,4,6-tetrachlorcphenol
Pentachlorcphenol
Most of the above products are manufactured via the chlorination of
phenol, although small amounts of the ortho and para monochlorophenol
are produced by the hydrolysis of the appropriate dichlorobenzene.
3.3.2 Hydrolysis of Chlorobenzenes
The hydrolysis of chlorobenzene is carried out in aqueous alkali
solutions at high temperatures and pressure. This reaction is feedstock
specific with the substitution of a hydroxyl group for a chlorine on the
aromatic ring. A generalized flow diagram for this process is presented
in Figure 3-3. Although the process can be used to manufacture the
isomers discussed in Section 3.3.1, it is not recommended because of the
formation of chlorinated dibenzo-p-dioxins which detracts from the reac-
tion yield. The hydrolysis route is used to produce the following
isomers using the appropriate chlorobenzene:
3-chlorophenol
2,3-dichlorophenol
2,5-dichlorophenol
3,4-dichlorophenol
3,5-dichlorophenol
2,4,5-trichlorophenol
3-7
-------
SOLVENT
HCI
OJ
I
00
1,2.4.5 TETRACHLOROBENZENE
METHANOL
SODIUM HYDROXIDE
COIL REACTOR
EXTRACTOR
ACIDIFIER
2.4.&TRICHLOROANISOLE
z
o
2.4.5-TRICHLORO
^ PHENOL
Source: Tracor-Jitco (1978b).
FIGURE 3-3 PRODUCTION SCHEMATIC FOR 2.4.5-TRICHLOROPHENOL PRODUCTION
BY HYDROLYSIS OF 1.2.4.5-TETRACHLOROBENZENE
-------
3.3.3 Emissions From Production
The emissions of chlorophenols summarized in Table 3-1 were extracted
or. based on data from a JRB Associates (1980) materials balance for
chlorophenol. These estimates are uncertain and should be used with
caution. Production sources of airborne emissions include the reactor
vent, the dryer vent, and distillation vents. Aquatic discharges may
occur from spills of scrubber liquors or from purification steps.
Reportedly, solid wastes from column and reactor tars are negligible.
The total identified annual airborne emissions are estimated at 23 kkg.
The total identified annual aquatic discharges from the production
process are estimated at 464 kkg. Appendix A presents the assumptions
and calculations for these estimates.
3.3.4 Emissions from Transport and Storage
There is no information available to estimate emissions from the
transport and storage of chlorophenols. Only a small fraction of the
total amount produced of any of these compounds is isolated for direct
use; the majority is used within the plant where it was produced in the
production of chlorophenol derivatives. Consequently, chlorophenol
emissions due to transportation or storage at these sources are believed
to be minimal.
3.3.5 Miscellaneous Emissions
Sources of chlorophenols to the environment other than from direct
industrial releases have been reported. Chlorophenols are apparently
intermediate products resulting from the biodegradation of chlorinated
benzenes and certain pesticides (Ballschmitter et_ al_. 1977, Engst et al.
1977.). This subject is discussed in greater detail in Chapter 4.0.
Chlorophenols may also be produced in POTWs, drinking water, and
through industrial wastewater treatment due to chlorination (JRB Associ-
ates 1980). Phenol is one of the most reactive aromatic compounds under
conditions of dilute aqueous chlorination (Aly 1968, Barnhart and Campbell
1972, Carlson and Caple 1976; Carlson_et_al. 1975). The most commonly
formed products of phenol chlorination are thought to be ortho- and para-
chlorophenol, 2,4- and 2,6-dichlorophenol, and 2,4,6-trichlorophenol'(MCA 1972)
In our study, the synthesis of 2-chlorophenol resulted from the reaction
of 10 mg/1 phenol and 20 mg/1 chlorine, concentrations which are likely
to be encountered in treatment processes (Barnhart and Campbell 1972) /
Monochlorophenols were detected in lakes receiving a chlorinated effluent
from a coal-fired electric plant (Jolley_et_al. 1978). In another labora-
tory chlorination experiment (Burttschell _et al. 1959), reaction of 20 mg
phenol/ml with 40 mg/1 chlorine resulted in a mixture of 1-2% phenol,
2-5% 2-chlorophenol, 20% 2,4-dichlorophenol, 40-50% 2,4,6-trichlorophenol,
and other chlorinated phenol isomers. Trichlorophenols, but no dichloro-
phenols, were detected in municipal wastewaters which were superchlori-
nated during treatment (Glaze _e_t _al. 1978).
3-9
-------
nho« ?Ve; W1 SUCh Str°nS evidence supporting the generation of chloro-
phenols during water treatment processes, it was not possible to estimate
Ctribtl0 °f thlS lndireCt S0urce to th* envir
f C£tributl0? °f tlS lndireCt S0urce to th* environmental
chlorophenols. Most of the data available are laboratory-
and theoretical. Comparison of influent and effluent Ieve2 of
synthesis during wastewater treatment.
raT.,, 3re n°-toown natural sources of chlorophenols. Due to the
rarity of naturally occurring chlorine-containing compounds, chloro-
phenols are expected to be anthropogenic in origin.
3.3.6 Emissions From POTWs
In
« P°'ential source of chlorophenols to surface water is from POTWs
avanabie ind?cLLS) c?nce;t»tlon«- Therefore, since ^limited data
available indicated a low frequency of detectable chlorophenol roncen-
"•
3.4 USES
nrnH ^ ^ ^ J-chlorophenol produced is used as feedstock for the
production of higher chlorophenols with only about 1% (=81 kkg) isolated
for uses other than as an intermediate in the production of other phtnols
(JRB Associates 1980) . Other uses are in the production of specialized
phenolic resins, as a specialty solvent in the rubber industry
r-
, as-
3-10
-------
TABLE 3-3. USES OF 2-CHLOROPHENOL, 2,^-DICHLOROPHENOL,
AND 2,4,6-TRICHLOROPHENOL
Compound
2-Chlorophenol
Use
Feedstock for production of:
a) higher chlorinated phenols used
as fungicides, slimicides, bacteria-
cides, antiseptics, deodorants,
wood and glue preservatives.
b) phenolic resins
In sulfur- and nitrogen-extracting
processes from coal.
2,4-Dichlorophenol
Feedstock for production of:
a) 2,4-dichlorophenoxyacetic acid (2,4-D)
b) 2,4-D derivatives used as germicides,
soil sterilants, and in other
applications
c) various methyl compounds used as
antiseptics, as seed disinfectants,
and in moth-proofing
d) pentachlorophenol
e) miticides (by reacting with benzene
sulfonyl chloride)
2,4,6-Trichlorophenol
Used directly as germicide, as bacteriacide,
as glue and wood preservative, and in antir-
mildew treatment.
Feedstock for production of:
a) 2,3,4,6-tetrachlorophenol used
as a germicide, as a bacteriacide,
as a glue and wood preservative, and
anti-mildew treatment.
b) pentachlorophenol.
Source: U.S. EPA (1980a), U.S. EPA (1980b), U.S. EPA (1980c)
3-11
-------
TABLE 3-4. MANUFACTURERS OF 2,4-DICHLOROPHENOXYACETIC ACID
AND ITS ESTERS AND SALTS
Company
Dow Chemical Co., U.S.A.
Imperial, Inc.
North American Philips Corp.
Thompson-Hayward Chem. Co., Subsidiary
PBI-Gordon Corp.
Rhodia Inc.
Agricultural Division
Riverdale Chem. Co.
Rorer-Amchem
Amchem Products, Inc. Division
Vertac, Inc.
Transvaal, Inc., subsidiary
Location
Midland, MI
Shenandoah, IA
Kansas City, KS
Kansas City, KS
Portland, OR
St. Joseph, MO
Chicago Heights, IL
Ambler, PA
Fremont, CA
St. Joseph, MO
Jacksonville, AR
Source: Versar, Inc. (1980).
3-12
-------
The compound 2,4-DCP is-present as an impurity in 2,4-D at concen-
trations ranging from 70 to 4,500 mg/kg (Aly and Faust 1964). An
estimated 16 x 103 kkg of 2,4-D were used for agricultural purposes in
1971 (USDA 1974). Therefore, in 1971, approximately 1 to 70 kkg of 2,4-
DCP was applied to soil in conjunction with 2,4-D application.
The compound 2,4-6 trichlorophenol has numerous potential uses,
but the majority produced is used as feedstock for the manufacture of
higher chlorophenols. The amount used directly is unknown. Trichloro-
phenol and its derivatives may be used as a wood preservative, glue
preservative, ingredient in insecticide and bactericide, and as an anti-
mildew treatment for textiles (JRB Associates 1980, U.S. EPA 1975).
Small quantities of all three of the compounds may have other
• highly specialized unknown uses.
3.4.1 Emissions From Uses
Relatively minor amounts of these compounds have direct end-use
applications such as pesticide use, and these derivatives are known to
degrade in the environment (JRB Associates 1980). Assessing environ-
mental emissions of these compounds based on their production and use
is virtually impossible since their production is only estimated and
their use pattern, in terms of quantities, is poorly defined.
However, limited sampling data indicate that two of these compounds
(2,4-DCP and 2,4,6 TCP) have been detected in effluents from other types
of industrial operations (U.S. EPA 1980d). In most cases the estimated
annual discharge is less than 1 kkg at each plant. A summary of these
industries and the estimated discharge is presented in Table 3-5. For
other than pesticide manufacturers, the presence of the chlorophenol
compounds is presumably due to their use by these industries in anti-
mildew treatment, wood preserving, disinfection, and bacteriacidal
treatment.
3.5 FUTURE PROJECTIONS
Trends in the production of the three chlorophenols addressed in
this report are not readily discernible bacause actual production
values are not reported. Since the major use of these compounds is in
the production of higher chlorophenols, there may be a correlation between
the production of these compounds and the production of pentachlorophenol.
Pentachlorophenol production from 1960 to 1981 is presented in Table 3-6;
production is expected to exhibit a 4% annual growth in the next few years.
3-13
-------
TABLE 3-5. ESTIMATED DISCHARGES OF 2,4-DICHLOROPHENOL
AND 2,4,6-TRICHLOROPHENOL FROM SELECTED
INDUSTRIES
Industry
Pulp & Paper
Alkaline Market
Alkaline BCT
Alkaline Fine
Alkaline Unbleached
Sulfite dissolving
Sulfite Paperbark
Timber
Wood preserving steaming
Barking
Finishing
Veneer, Plywood
Leather Tanning
Steam Electric
Textiles
Woven Fabric
Stock & Yarn
Paint & Ink
Autos & Other Laundries
Industrial
Power
Pesticides Mfg.
Number of
Plants
Sampled
2
2
3
1
1
5
2
2
3
3
16
20
3
7
2,4-Dichloro-
phenol (average
cone, yg/1)
3
4
ND
ND
1
21
Trace
3,200
233
84,000
1,100
ND
ND
ND
2,4,6-Trichloro-
phenol (average
cone, ug/1)
4.5
1
ND
ND
5
42
ND
3,000
64
ND
8
19
11
22
13
3
27
ND
Trace
10
ND
2,400
ND
ND
526
a
2-chlorophenol was not detected in any of the plants sampled,
ND - Not Detected.
Source: U.S. EPA (1980d).
3-14
-------
TABLE 3-6. ESTIMATED SUPPLY AND DEMAND FOR PENTACHLOROPHENOL
(kkg)
1960 1965 1970 1973 1974 1975 1976 1977 1978
CapacJty NE 25,400
NE
Production 17,800 19,800 21,400 21,100 23,700 17,900 19,900 20,400 21,300
1979
35,400 31,300 33,100 33,100 33,100 27,700 27,700
Demand
1981
NE
NE
17,800 19,800 21,400 21,100 23,700 17,900 20,000 21,300 21,300 21,300 21,300
CO
I
NE - Not Estimated.
Source: JRB Associates (1980).
-------
Through association, the production trends of the- lower chlorophenols
may_be expected to parallel those of pentachlorophenol. These extrapo-
lations are subject to an unknown amount of error, however, because
production trends for pentachlorophenol may not be reflective of future
trends for other chlorophenol-derivative compounds.
3.6 SUMMARY
Although production data on the three chlorophenols are not within
the_realm of published information, reasonable production quantities can
be inferred based on the production of related compounds. These compounds
and their derivatives are produced in relatively small quantities
Apparently, their derivatives have significant end-use applications
but only small amounts of the compounds themselves are isolated for'
consumption.
Intentional discharges are the major source of these compounds
2r2Sne^iSnment bSCaUSe theV are n0t naturallv occurrine. Dis-
persion of these compounds in the biosphere is probably due to the
degradation of derivatives and of other organic compounds in the environ-
ment. The rate of degradation of these substances would be variable and
has not been adequately studied to estimate loadings of chlorophenols
to the environment from most of these sources.
3-16
-------
REFERENCES
Aly, O.M. Separation of phenols in waters by thin layer chromatography.
Water Res., 2:587; 1968. (As cited in U.S. EPA 1980b)
Aly, O.M.; Faust, S.D. Herbicides in surface waters: studies on the
fate of 2,4-D and ester derivatives in natural surface waters. J.
Agricult. Food Chem. 12(6): 541-546; 1964.
Ballschmitter, K.; Unglert, C.; Heinzmann, P. Formation of chlorophenols
by microbial transformations of chlorobenzenes. Angew Chem. Int. Ed.
Engl. 16:645; 1977.
Barnhart, E.L.; Campbell, G.R. The effect of chlorination on selected
organic chemicals. Water Pollut. Control Res. Ser. 12020 Exg. 03/72.
Washington, D.C. U.S. Environmental Protection Agency; 1972. (As
cited in U.S. EPA 1980b)
Burttschell, R.H., et al. Chlorine derivatives of phenol causing odor
and taste. J. Am. Water Works Assoc. 51:205; 1959. (As cited by U.S.
EPA 1980b)
Carlson, R.M.; Caple, R. Organo-chemical implications of water
chlorination. Jolly, R.L. ed. The environmental impact of water
chlorination. Proceedings of the conference on the environmental impact
of water chlorination; October 22-24. Oak Ridge, TN: Oak Ridge National
Laboratory; 1976. (As cited in Scow_et_al. 1981)
Carlson, R.E.; Carlson. R.M.; Kopperman, H.L.; Caple, R. Facile incorpora-
tion of chlorine into aromatic systems during aqueous chlorination pro-
cess. Environ. Sci. Technol. 9:674-675; 1975. (As cited in Scow et
al. 1981) —'
Engst, R.; Macholz; Kujawa, M. Recent state of lindane metabolism.
Residue Rev. 68:59-101; 1977.
Feiler, H. Fate of priority pollutants in Publically Owned Treatment
Works (POTWs). Interim report. Washington, D.C..Effluent Guidelines
Division, U.S. Environmental Protection Agency; 1980.
Glaze, W.H., ej: al^. Analysis of new chlorinated organic compounds
formed by chlorination of municipal wastewater. Jolly, R.L. ed.
Water chlorination-environmental impact and health effects. Ann Arbor,
MI: Ann Arbor Science Publishers; 1978-
JRB Associates. Level I materials balance - chlorophenols - Final
report. Contract #68-01-5793, Washington, D.C. U.S. Environmental
Protection Agency; 1980.
3-17
-------
Jolley, R.L.; Jones, G.; Pitts. W.W.; Thompson, J.E. Chlorination of
organics in cooling waters and process effluents. Jolley, R.L., ed.
Water Chlorination: environmental impact and health effects. Ann
Arbor, MI: Ann Arbor Science Publishers; 1978. pp 105-138.
Kozak, V.P.; Simsiman, G.V.; Chesters, G.; Stensby, D.; Harkin, J.
Reviews of environmental effects of pollutants: XI. Chlorphenols.
EPA 600/1-79-012. Cincinnati, OH: Office of Research and Development,
U.S. Environemtnal Protection Agency; 1979.
Manufacturing Chemists Association (MCA). The effect of Chlorination
on selected organic chemicals. Washington, DC: U.S. Environmental
Protection Agency; 1972. (As cited in Scow et al. 1981)
Scow, K.; Goyer, M.; Perwak, J; Payne, E.; Thomas, R.; Wallace, D.;
Wood, M. Exposure and risk assessment; 1981.
Stanford Research Institute (SRI). Directory of chemical producers-
United States. Menlo Park, CA. Stanford Research Institute; 1978.
Tracor-Jitco. Production and use of 2,4-dichlorophenol. Chapter V~
draft report. Washington, DC: Tracor-Jitco; 1978a.
Tracor-Jitco. Production and use of 2-chlorophenol. Chapter V—draft
report. Washington, DC: Tracor-Jitco; 1978b.
U.S. Department of Agriculture (USDA). Farmers use of pesticides
in 1971—quantities. Agricult. Econ. Rep. No. 252. Econ Res. Serv.
Washington, DC: U.S. Department of Agriculture; 1974.
U.S. Environmental Protection Agency (U.S. EPA). Preliminary environmental
hazard assessment of chlorinated naphthalenes, silicones, fluorocarbons,
benzenepolycarboxylates, and chlorophenols. EPA-560/2-74-001. Washing-
ton, DC: U.S. Environmental Protection Agency; 1973.
U.S. Environmental Protection Agency (U.S. EPA). Production, distri-
bution, use and environmental impact potential of selected pesti-
cides. EPA-540/1-74-001. Washington, DC: U.S. Environmental Protection
Agency; 1975.
U.S. Environmental Protection Agency (U.S. EPA). Ambient water quality
criteria for 2-chlorophenol. EPA-400/5-80-034. Washington, DC: Office
of Water Regulations and Standards, U.S. Environmental Protection Agency
1980a.
U.S. Environmental Protection Agency (U.S. EPA). Ambient water quality
criteria for 2,4-dichlorophenol. EPA-400/5-80-042. Washington, DC:
Office of Water Regulations and Standards, U.S. Environmental Protection
Agency; 1980b.
3-18
-------
U.S. Environmental Protection Agency (U.S. EPA). Ambient water quality
criteria for chlorinated phenols. EPA-400/3-80-032. Washington, DC:
Office of Water Regulations and Standards, U.S. Environmental Protection
Agency; 1980c.
U.S. Environmental Protection Agency (U.S. EPA). Priority pollutant
data base. Washington, DC: Monitoring and Data Support Division,
Water Quality Analysis Branch, U.S. Environmental Protection Agency
1980d. 5 y
Versar, Inc. Environmental material balance for phenol. Draft report.
Contract No. 68-01-3852. Washington, DC: U.S. Environmental Protection
Agency; 1980.
Versar, Inc. Sampling and analysis of the aquatic environment in POTWs
and their vicinity. Contract No. 68-01-4679. Washington, DC: U.S.
Environmental Protection Agency; 1979.
3-19
-------
4.0. FATE AND DISTRIBUTION OF CHLOROPHENOLS IN THE ENVIRONMENT
4.1 SUMMARY
This chapter describes the fate pathways and ultimate distribution of
2-chlorophenol (2-CP), 2,4-dichlorophenol (2,4-DCP), and 2,4,6-trichloro-
phenol (2,4t6-TCP) in environmental media following the intentional dis-
charge or accidental release of these compounds to water, air, and soil.
Laboratory and field data on the chlorophenols, when available, were used
in this analysis. However, because of the limited available data base,
estimates of environmental behavior were also made on the basis of the
compounds' physical and chemical properties and extrapolations from
structurally similar compounds. Monitoring data are presented from
STORET and other surveys to provide indications of concentrations
actually detected in environmental media.
The majority of chlorophenol entering the environment is discharged
to water, primarily by chemical producers. Following release, adsorption,
volatilization, and biodegradation are expected to be primarily responsible
for removal of chlorophenols from the water column. Adsorption onto organic
matter appears to be more significant than adsorption onto clay material,
and, based on their octanol/water partition coefficients, trichlorophenol
is more likely to be sorbed than are the lower chlorinated phenols. Volatili-
zation to the atmosphere of the soluble fraction of chlorophenols is likely
based on the compounds' high vapor pressures, especially the mono- and
dichlorophenols. No actual measurements of volatilization from water
were available to confirm its significance as a transport process for
chlorophenols. Biodegradation is an important transformation process,
especially for the lower chlorophenols. Acclimated microbial cultures
can reduce mono- and dichlorophenol concentrations to negligible levels
on the order of one week under laboratory conditions. Aquatic species
may bioaccumulate all three chlorophenols to levels 100 to 400 times
above concentrations.
Dichlorophenol is released to soil through the application of the
herbicide 2,4-D and an unknown amount of all the chlorophenols enters
the soil as impurities or breakdown products of 2,4-D, 2,4,5-T, silvex,
and other pesticides. The movement of chlorophenols is controlled by
adsorption onto organic matter and, apparently less importantly, sorption
onto bentonite and other clays. The sorption bond is hypothesized to be
weak and the lower chlorophenols to be easily desorbed by water,based on
observations of acidic pesticides. Biodegradation is an important removal
process for chlorophenol in soil, as it is in water. Soil populations can
significantly reduce chlorophenol concentrations on the order of weeks and
in even less time following acclimation. In porous soils and conditions
unfavorable to biodegradation, there is a potential for migration of
chlorophenols into groundwater. In agricultural areas, runoff and sedi-
ment transport are likely to transfer chlorophenols from soil to surface
water, especially immediately after their application to land.
4-1
-------
• Very little is known about the atmospheric fate of chlorophenols
following emission. The total amount of chlorophenols released to air
each year is small, however, compared to other better characterized
environmental compartments. There were no monitoring data available for
any of the chlorophenols to indicate their presence in ambient air.
Based on their physical and chemical properties, the chlorophenols are
estimated to have an atmospheric half-life of roughly three weeks con-
trolled by free radical oxidation. This estimate, however, has not been
validated in the laboratory or under field conditions. Little is known
about other atmospheric fate processes.
Secondary treatment is very effective at removing chlorophenols
from wastewater, especially if well acclimated microbial populations
2r& TTP?^' I?hibitory levels in e^h activated sludge for 2,4-DCP and
ll ; + I beSn reported at 20° m§/l- Other commonly employed treat-
ment techniques, such as in primary treatment, do not appear to be very
effective at chlorophenol removal.
Monitoring data °n chlorophenol concentrations in environmental
f d Umited t0 SUrface Water' According to the STORET
t nr K T*1 °f 3°° amMent Samples for chlorophenLs were all
cLlln, ? the.detect*°n li«it (usually 10 yg/1, occasionally 100 yg/1) .
Concentrations in an effluent from a chemical plant ranged from 3 mg/1
°* chlorophlols
4-2 PHYSICAL AND CHEMICAL PROPERTIES
2 4 ,T^e.e^ironmental fate of 2-chlorophenol, 2,4-dichlorophenol, and
2,4,6-trichlorophenol is dependent upon the compounds' physical and
chloronLPr?PerKler Table/-1 lists some basic properties of the
chlorophenols which are used in the subsequent analysis. In general
the chlorophenols can be charactered as weak acids with a relatively
low solubility decreasing with chlorination and a high volatility at
ambient temperatures (Kozak et al. 1979) .
4-3 ENVIRONMENTAL PATHWAYS
4.3.1 Introduction
Figure 4-1 depicts the potential environmental pathwavs for chloro-
phenols from release into soil and water, and up to the point of exposure
of receptors. Only the major pathways are considered in this chapter,
with empnasis on the initial behavior of the pollutants in the vicinity
of the point of release. Transfers between environmental compartments
are only briefly considered.
Releases to water make up the most significant fraction of environ-
mental releases as estimated in Chapter 3.0. This pathway is described
in Section 4.3.2, Discharges to Surface Water. The atmosphere and land
comoined receive an estimated 15% of the environmental releases of chloro-
4-2
-------
TABLE 4-1. PHYSICAL AND CHEMICAL PROPERTIES OF 2-CHLOROPHENOL,
2,4-DICHLOROPHENOL, AND 2.4,6-TRICHLOROPHENOL
Properties
Molecular Weight (gms)
Melting Point (°C)
Boiling Point at 760 mm Hg (PC)
Vapor Pressure at 20°C (mm Hg)
(atm)
Solubility in Water (mg/1)
Log Octanol/Water Partition
Coefficient
pKa
2-Chlorpphenol
128.56
8.7
175.6
2.2
0.0029
28,500 at 20°C
2.17
8.49
Saturated Vapor Concentration at 20°C,
mg/m3 16,600
"'8/1 3,100
2,4-DIchlorophenol
163.01
45
206
0.11
0.00014
4,600 at 20°C
2.75
7.4
1,060
156
A ^6-TrIchlorophenol
197.46
68
244.5
0.027
0.000036
800 at 25°C
3.69
310
38
Source: Callahan et al. (1979), Kozak et al, (1979),
-------
Industrial Waste,
Spillage (5%)
I
Pathway 2
.-MUA ^^
Degradation
Direct
Application, Spillage,
Industrial
Waste, Sewage,
Pesticide Contaminant
(10%)
Precipitation
Fallout
rptton pesorp,jon _Decay
Industrial Waste,
Spillage, Sewage,
Water Treatment
(85%)
Degiadation
Source: Kozak et al. (1979)
Degradation
FIGURE 4-1 POSSIBLE CYCLING OF CHLOROPHENOLS IN THE ENVIRONMENT
-------
phenols and are described in Emissions to Air (Section 4.3.3) and Land
Disposal (Section 4.3.4). Additionally, in Pathway 4, a brief description
of- the wastewater treatment of cholrophenols is presented
(Section 4.3.5).
4.3.2 Pathway 1: Discharges to Surface Water
The majority (85%) of known environmental emissions of all chloro-
phenols is released to surface water, primarily from production processes
of the compounds themselves and their derivatives. Runoff from agricul-
tural areas may also contribute to the total releases. Following release
the chlorophenols may be present in solution or adsorbed onto suspended
and settled sediment. Since the chlorophenols are weak acids, the
soluble fraction would tend to ionize, with dissociation increasing as
the pH increases above pH 5 (Cserjesi 1972). The degree of dissociation
would be expected to control adsorption onto colloids (Kozak et al. 1979).
In primary treatment processes, chlorophenols are sorbed poorlV To par-
ticulate matter (Kozak et al. 1979). Aluminum and ferric sulfate
flocculents are especially ineffective at removing 2,4-dichlorophenol
from water (Aly and Faust 1964). Through inference, a similarly low
affinity for suspended particulates is also probable in natural aquatic
systems.
The persistence of cholorophenols in surface water is dependent on cer-
tain fate processes resulting in transfer of the compounds to other media
(i.e., volatilization) or transformation within water (i.e., biodegradation).
This section describes the relative importance of various fate
processes potentially influencing the aquatic concentrations and persis-
tence of chlorophenols.
4.3.2.1 Oxidation
There is no information specific to chlorinated phenols in water
regarding oxidation. Highly chlorinated organic compounds are known to
be resistant to oxidation, even at extremely high temperatures in excess
of typical environmental temperatures (Morrison and Boyd 1973) There-
fore, it seems probable that at least 2,4,6-trichlorophenol will not
undergo oxidation in surface waters.
Mono- and dichlorophenols may oxidize in water at a slow rate
Calculations from experimental data show a half-life for phenol the
parent compound, undergoing free radical oxidation by R02 to be nearly
20 hours. Since no specific information is available on 2-CP and 2 4-
may be aSSUmed as a conservative estimate that these compounds
in water at a similar rate, with a half-life of a dav or more
4-5
-------
4.3
-------
The Henry's law constant can be estimated using the following
equation:
H « P /S
vp
where Pvp is the vapor pressure at 20°C in atmospheres and S is the
solubility in water at 20"C in moles/m3. Referring to Section 4.2 on
the physical properties of chlorinated phenols, the Henry's law constant
for 2-chlorophenols, 2,4-dichlorophenols, and 2,4,6-trichlorophenols
can be calculated. The results are shown in Table 4-2.
TABLE 4-2. HENRY'S LAW CONSTANTS FOR 2-CHLOROPHENOL,
2,4-DICHLOROPHENOL, and 2,4,6-TRICHLOROPHENOL
Solubility
Compound Vapor Pressure (atm) (M/m3) H (atm-m3/M)
2-Chlorophenol 0.0029 222 1.3 x 10~3
2,4-Dichlorophenol 0.00014 28.2 5.0 x 10~6
2,4,6-Trichlorophenol 0.000036. - 4.05 8.9 x 10~6
A compound whose Henry's law constant is less» than 3 x 107"7 atm-m3/M
is classified as volatile, 3 x 10- atm-m3/M is classified as moderately
volatile, and H>10~3 atm-m3/M is classified as highly volatile (Mackay'
1979) Mackay and Yuen 1979). Examination of the calculated values for
H for 2-chlorophenol, 2,4-dichlorophenol, and 2,4,6-trichlorophenol
reveals that all three compounds would be classified as moderately vola-
tile. An implication of this for river systems might be that these com-
pounds volatilize out of water before a significant amount is transported
downstream
4.3.2.5 Biodegradation in Water
Aly and Faust (1964) investigated the biodegradation of 2,4-dichloro-
phenol in an aquatic system. To measure this process, solutions of 2,4-
dichlorophenol in concentrations of 100 yg to 1,000 yg per liter were'
prepared using buffered natural lake waters and incubated under aerated
conditions. As shown in Table 4-3, the 2,4-dichlorophenol was totally
degraded within 9 days when the concentration was 100 yg/1. After 9 days
66% of the 500-yg/l solution was oxidized by microorganisms, while only
54^ was degraded in the 1,000-yg/l solution. Near complete degradation
(97.5%) of the 500-yg/l and 1,000-yg/l solutions took place after 30
d<™S' MS sl\ownAin Figure 4-2, the overall biodegradation rate of the
500-yg/l and 1,000-yg/l solutions were equivalent; both decomposed
50% in six days.
4^7
-------
Table 4-3. DEGRADATION OF 2,4-DICHLOROPHENOL IN
AERATED AND BUFFERED LAKE WATERS
Concentrations
Time (Days)
0
2
9
16
23
30
100 yg/liter
£H Concn % Degd.
7.4
7.3
7.3
6.9
100
64
0
0.0
36.0
100.0
100.0
7.1
7.5
7.3
92
32
13
500 ug/liter
£H Concn % Degd.
7.4 500
7.6 390
7.6 170
0.0
22.0
66.0
81.6
93.6
97.5
1,000 ug/liter
pH Concn % Degd,
7.4 1,000 0.0
7.6 760 24.0
7.4 460 54.0
7.2 165 83.5
7.5 78 92.2
7.3 25 97.5
Source: Adapted from Aly and Faust (1964)
4-8
-------
1,000
500
o>
01
'c
'a
€
CM
100
50
500 ng/\ System
10
20
Time (Days)
30
40
Source: Aly and Faust (1964)
FIGURE 4-2 DISAPPEARANCE OF 2.4-DICHLORO-
PHENOL IN AN AERATED AND BUFF-
ERED LAKE WATER
4-9
-------
To model the effect of decaying organic matter on the degradation
rate, 2,4-dichlorophenol was added to unbuffered and unaerated lake
water in the same concentrations outlined above. As shown in Table 4-4,
2,4-dichlorophenol never completely degraded, even at the lowest concen-
tration. For the 100-yg/l solution, it took roughly two weeks for the
concentrations to decompose by 50%. The same level of degradation was
reached for the 500-yg/liter and 1,000-yg/liter solutions at roughly 18
and 44 days, respectively. Anaerobic, unbuffered conditions lengthened
the degradation rate by a factor of three to eight.
In a comparison of the biodegradation of 1,000 ug/1 2-chlorophenol in
polluted river water and in domestic sewage, the compound was found to
degrade in 15 to 23 days in the river water culture, compared to little
degradation in 30 days in the sewage culture (Ettinger and Ruchhoft 1950) .
The difference in degradation rate was attributed to the presence of an
acclimated microflora in the polluted river.
In a static flask study with wastewater treatment microbial popu-
lations, 2-chlorophenol, 2,4-dichlorophenol and 2,4,6-trichlorophenol
were reported to degrade 86%, 100%, and 100%, respectively, in 7 days in
unacclimated cultures (Tabak et_aL. 1980). In acclimated cultures, all
three compounds degraded >98% within 7 days. Therefore, there was little
difference in the biodegradability of the three compounds. Acclimation
did not appear to be an important factor under the simple laboratory
conditions of the experiment. Only primary degradation was measured, so
the identification and persistence of the intermediate metabolites is
unknown.
Aquatic bacteria isolated from activated sludge systems have been
shown to degrade chlorophenols as their sole carbon source or in the
presence of other substances. The particular species which have been
identified are described in Section 4.3.5 under wastewater treatment.
4.3.2.6 Bioaccumulation
Only limited data were available on the uptake and bioaccumulation
of 2-CP, 2,4-DCP, and 2,4,6-TCP by fish and other aquatic organisms.
Uptake of chlorophenols may occur through the gills, the gastrointestinal
tract, or directly through the body surfaces. The factors which control
rate and extent of uptake by aquatic organisms have not been determined
(Kozak et_ al_. 1979) .
Flavor-impairment studies have shown that a variety of fish species
experience tainting of the flesh at 2,4-DCP concentrations of 0.4 yg/1 to
140 yg/1 (U.S. EPA 1980a). Therefore, flavor impairment of fish appears
to occur at lower concentrations than do toxic effects (see Chapter 6);
concentrations of chlorophenols well below toxic effects levels in surface
water may result in the contamination of sport fisheries based solely on
organoleptic criteria although these criteria have no demonstrated adverse
human health effects.
4-10
-------
Time (Days)
0
3
7
14
17
24
43
TABLE 4-4. DEGRADATION OF 2,4-DlCHLOROPHENOL IN
UNAERATED AND UNBUFFERED LAKE WATERS
Concentrations
7.9
40
40
20
100 us/liter
pH Concn % Degd.
7.3 100 0.0
6.2 80 20.0
6.1 70 30.0
60.0
60.0
80.0
6.5 253
192
192
500 us/liter
Concn % Degd.
7.3 500 0.0
5.1 390 22.0
6.1 380 24.0
49.4
61.6
61.6
1.000 ug/liter
pH Concn % Degd.
7.3 1,000
4.1
6.0
6.1
6.3
780
770
620
560
540
506
0.0
22.0
23.0
38.0
44.0
46.0
49.4
Source: Adapted from Aly and Faust (1964)
4-11
-------
An actual laboratory-derived measure of bioaccumulation resulting
from a long-term controlled study is available only for 2-chlorophenol.
Bluegill (Lepomis macrochirus) exposed for one month to 9.2 ug/1 of 2-
chlorophenol had a measured bioconcentration factor (BCF) of 214 (U.S.
EPA 1980b) which would give a body burden of 2 mg/kg. Theoretically
derived estimations of the BCF, based on the properties relationship to
the octanol/water partition coefficient, were calculated for the other
two chlorophenols (U.S. EPA 1980a, U.S. EPA 1980c). For 2,4-dichloro-
phenol the BCF was estimated to be 130, and for 2,4,6-trichlorophenol,
380.
In a second lab study, 2,4-dichlorophenol levels of 18 mg/kg were
detected in the muscle of a European trout, Salmo trutta. after 24
hours exposure to 1.7 mg/1 ( Hattula et al. 1981). The concentration
also resulted in mortality to 50% of the test population. The calculated
BCF was 10, an order of magnitude below the estimated level; however,
this difference may have been due to the short period of exposure..
In a field study, concentrations of 2,4,6-trichlorophenol were
measured in the liver and body fat of rainbow trout exposed to diluted
Is raft pulp bleachery effluents following effluent pretreatment (Landner
et al. 1977). Concentrations ranged from 2 mg/kg to 45 mg/kg in the
liver after exposure for 2 to 11 weeks. The range was dependent on the
pretreatment techniques. Muscle levels measured less than 1 mg/kg after
11 weeks exposure, Perch and northern pike caught in the vicinity of
the same pulp mill had 2,4,6-trichlorophenol concentrations in the liver
fat of 2.7 mg/kg and 0.4^0.5 mg/kg, respectively (Landner et al. 1977).
The compound 2-chlorophenol has a rapid depuration rate with a half-
life of less than one day (U.S. EPA 1980b) presumably due to rapid metabo-
lism. The observed rate of clearance for 2,4,6-trichlorophenol in rainr
bow trout suggests a tentative biological half-life in the liver of less
than 10 days (Landner et al. 1977). No information was available on the
clearance rate for 2,4-dichlorophenol,
The available data do not provide any evidence of differences in
bioaccumulation at lower versus higher trophic levels. It is not known
whether biomagnification occurs with 2-chlorophenol, 2,4-dichlorophenol,
or 2,4,6-trichlorophenol (Kozak et al. 1979).-
4,3.3 Pathway 2; Emissions to Air
Only a small fraction, approximately 5%, of all known environmental
releases of chlorophenols is emitted to the atmosphere. These releases are
primarily in vapor form from production processes. Since very little
is known about the atmospheric fate of chlorophenols (Kozak et al. 1979),
the estimates presented in this section cannot be validated ~at This time
and should be used with caution.
4-12
-------
A.3,3.1 Free Radical Oxidation
No experimental evidence was found regarding the reaction of
chlorinated phenols with free radicals in the atmosphere. Nevertheless,
estimations of the relative reactivity of chlorinated phenols with free
radicals can be made based on compounds, such as phenol, close in struc-
ture to chlorinated phenols. Phenol has a low value for the hydroxyl
radical reaction rate constant, koH> such that-
kOH <5 X 10l° cm3 (Hendry and Kenley 1979)
mole sec
Combing this rate constant with the average value of the concentration
°f °H ^fl^6 aVnosPhere estimated by Neely and Planka (1978) (i.e.,
8 x 10- M/cm3), the rate of oxidation due to hydroxyl radical attack
can be estimated to be:
5 x 1010 x 8 x 10-18 - 4 x 10-7 sec-1
The total rate of oxidation is the sum of the rate of oxidations
due to hydroxyl radicals and to ozone. Values for the ozone reaction
rate constant for phenol or for any of the chlorinated phenols addressed
in this report are not presently available. However, for many aromatic
hydrocarbons the reaction rate due to ozone is much smaller than the
reaction rate due to hydroxyl radicals (Hendry and Kenley 1979) such
that the ozone reaction rate constant, K03, multiplied by the average
ground level ozone concentration (1.6 x 1CT12 M/cm3) is much less than
the oxidation reaction rate due to hydroxyl radicals.
Assuming this to be true for the phenols as well, the rate of
oxidation is governed by the rate of oxidation due to hydroxyl radical
attack. Therefore, the half-life of these compounds in the atmosphere
undergoing oxidation is estimated to be:
-S20 days
where k = 4 x 10"7 sec"1
OX
Assuming that the hydroxyl radical reaction rate constant for chlorinated
phenols is equivalent to that for phenol, chlorinated phenols emitted
into the atmosphere have a half-life of roughly three weeks.
4.3.3.2 Atmospheric Photolysis
All of the information found concerning the photolysis of 2-chloro-
phenol, 2,4-dichlorophenol, and 2, 4, 6-trichlorophenol pertained to photo-
lysis in aqueous solution rather than to atmospheric photolysis. As
discussed in Section 4.3.2.2, in aqueous solution the chlorinated phenols
photolyze under wavelengths of light slightly below the minimum wave-
4-13
-------
length of natural sunlight. Based on these very limited data, atmospheric
photolysis does not appear to be a significant fate process since the
chlorophenols do not absorb UV light in the >290-nm wavelength region
characteristic of solar radiation.
4.3.4 Pathway 3; Land Disposal
Direct releases of chlorophenols to soil in disposal of solid waste
are expected to be minimal relative to aquatic discharges. Waste dis-
posal of chlorophenols combined with 2,4-dichlorophenol releases associ-
ated with the application of the herbicide 2,4-D are estimated to comprise
approximately 10% of the total annual environmental discharges of
chlorophenols. In this section, the influence of biodegradation,
sorption, and bioaccumulation on the concentrations of chlorinated
phenols in the soil will be discussed.
4-3.4.1 Sorption
The ability of a soil to sorb chemical compounds is dependent upon
the clay and organic content of the soil. Aly and Faust (1964) investi-
gated the capability of clay to adsorb 2,4-dichlorophenol using three
different clay types: bentonite, kaolinite, and illite. All clay
sorbed 2,4-dichlorophenol to a small degree and the amount sorbed
was directly related to the surface area of the clay material.
Kaolinite and illite are non-expanding lattice materials low
in surface area and thus limited in their ability to sorb dichloro-
phenol. Bentonite, an expanding lattice material, has a greater surface
area and a consequent ability to sorb dichlorophenol.
The adsorptive capacity of a soil is also dependent upon the soil's
organic content and the compound's hydrophobic tendency as indicated by
its octanol/water partition coefficient. If the log octanol/water par-
tition coefficient is greater than unity, the compound will preferentially
partition into the soil organic matter. Although this is not a completely
reliable correlation it may be used as a rough guide, The compounds
2-chlorophenol, 2,4-dichlorophenol, and 2,4,6-trichlorophenol have log
octanol/water partition coefficients greater than 2, which shows that
the ratio of the affinity of these compounds to bind to organics versus
water^is greater than 100 to 1. If the chlorinated phenols are present
in soils that are high in organic content, it may be suspected that they
will bind to the soil particles. Mineral soils, low in organic matter,
would not be expected to significantly sorb chlorinated phenols.
Although some soils may adsorb chlorinated phenols, the fact that
2,4-dichlorophenol has been found in groundwater in areas near large
deposits of 2,4-dichlorophenol waste and the fact that large quantities
of clay were required to sorb even small amounts of 2,4-dichlorophenol
in the experiments by Aly and Faust (1964) imply that large quantities
of this compound may exceed the sorption capability of some soil types.
leading to the possibility of groundwater contaminations. Consequently,
although small amounts of chlorinated phenols deposited on soil may satis-
factorily be sorbed by the soil, larger quantities associated with waste
disposal or application of derivative pesticides may result in seepage
through the soil column into the • groundwater table.
4-14
-------
4.3.4.2 Biodegradation in Soil
As described in Section 4.3.2.5, microbial degradation of chloro-
phenols in aquatic systems is a significant transformation process.
Several studies have also investigated biodegradation specifically in
soil systems.
Walker (1954) compared the rate of degradation of 2-chlorophenol to
investigate the influence of population acclimation on the rate of degra-
dation. Approximately two-thirds of an initial dosage of 1.0 gram 2-
chlorophenol disappeared within 10 days of application to a light clay
soil (pH 6.8). Subsequent applications, however, required only 5 days
to disappear, a significant increase in the rate of degradation. Walker
concluded that rapid dissipation of 2-chlorophenol was the result of an
acclimated bacterial population. Acclimated microorganisms were also
shown to be highly effective in the removal of both 2-chlorophenol and
2,4-dichlorophenol by Alexander and Aleem (1961).
Several investigations have identified specific microorganisms
capable of biodegrading chlorophenols. Spokes and Walker (1974) showed
that phenol-grown Nocardia sp., Pseudomonas sp., Mycobacterium coelicium.
and Bacillus sp. oxidized 2-chlorophenol, resulting in the formation of
3-catechol. Evans et_ al. (1971) showed that Pseudomonas sp. also degraded
2,4-dichlorophenol. This was elucidated by studying the biodegradation
pathway of the pesticide 2,4-D, a pathway consisting of cleavage
of the ether bond, forming 2,4-dichlorophenol, 3,5-dichlorocatechol,
and a-chloromuconate, which are further metabolized to release Cl~ and
other unidentified metabolites (Evans e± al. 1971). The compound 2-
chlorophenol was hypothesized to be formed via a nonoxidative elimination
of chlorine from 2,4-dichlorophenol or directly from 2,4-D. Ring ortho-
hydroxylation via oxidation by microorganisms transformed 2-chlorophenol
to 3-chlorocatechol which in turn degraded to a-chloromuconate. Bollag
and coworkers (1968) examined a strain of Arthobacter sp. capable of
converting 2,4-dichlorophenol to 3,5-dichlorocatechol through enzymatic
hydroxylation in the presence of NADPH and oxygen.
Fungi have also been found to be capable of degrading chlorophenol.
Lyr (1962) explained the ability of basidiomycetes to degrade chloro-
phenols by the presence of phenol oxidase. He found that the wood-rotting
fungus. Tramates vericolor was able to degrade chlorophenols via secre-
tions of laccase, tyorosinase, and peroxidase. Walker also isolated
fungi capable of degrading chlorophenols. The fungus isolated
Rhodoturula glutinis, was able to use phenol as the sole carbon source,
but required the presence of other substances.
4-3.4.3 Terrestrial Plants
There are no known intentional applications of any of the chloro-
phenols to terrestrial plants. Potential indirect sources to plants
include the metabolism of derivative herbicides and irrigation by con-
taminated water.
Very limited information is available concerning direct uptake of
chlorophenols by terrestrial plants. Oats and soybean roots rapidly
absorbed 2,4-DCP from nutrient solution and soil and minimal transloca-
tion to the edible grain was observed in soybeans (Kozak et al. 1979).
-------
Oats bioconcentrated 2,4-DCP to levels 9 times .greater than the 0.2-ug/l
concentration in the nutrient solution. Bioconcentration factors were
less than one in the oats grown in soil and in the soybeans grown in
solutions and soil (Kozak et al. 1979). No information was available
regarding plant uptake of 2-chlorophenol or 2,4,6-trichlorophenol.
Residues of 2,4-dichlorophenol may appear in plants treated with
the herbicide 2,4-D. Studies on rice, kidney beans, soybeans, peas,
barley, timothy, and various grasses indicated metabolism of 2,4-D to
dichlorophenol following shortly after herbicide application (Kozak et
al. 1979, Steen et al. 1974). Plant levels are usually one to two orTers of
magnitude below the inital 2,4-D concentrations (Steen et al. 1974). In the
rice plants, most of the dichlorophenol disappeared over the course of
the growing season (Kozak et al. 1979). No information was available
on the persistence of 2,4-DCP in other plant species. There is a
possibility that 2-chlorophenol residues in plants may also accumulate
from degradation of the herbicide 2,4-D (U.S. EPA 1980b). Potential
sources of 2,4,6-trichlorophenol include lindane and possibly 2,4-5-1.
Based on the available data, contamination of food crops by chloro-
phenols does not appear likely to occur (Kozak et. al. 1979; U.S. EPA
1980a, 1980b, 1980c).
4.3.4.4 Field Studies
There is evidence for the presence and persistence of chlorophenols
in soxl and groundwater. Swenson (1962) reported an incident occurring
in California in 1945 where a chemical company manufacturing 2,4-D
released 2,4-dichlorophenol into the city sewage system. The chemical
ended up infiltrating downstream shallow wells within 3 weeks and odors
and tastes persisted for 3 years. Walker (1961) reported on groundwater
contamination resulting from the lagoon disposal of 2,4-D wastes at the
Rocky Mountain Arsenal in Colorado. Crop damage was caused by use of
irrigation water from a well downslope from the dumping sites at the
arsenal. The compound was estimated to migrate 5,6 km in 7 to 8 years
and to affect an area of 16.8 km2. Direct contamination of soil is also
likely due to the direct application of the herbicide 2,4-D on cropland,
rangeland bush control, and right-of-ways. A Russian forest was aerially
sprayed with 3 kg of 2,4-D and the soil was monitored for the metabolite
2,4-dichlorophenol. Detectable concentrations were found to persist for
60 to 90 days, staying in the top 50 cm of the soil (Motuzinskii 1975).
4-3.5' Pathway 4; Behavior of Chlorophenols in Wastewater Treatment
Chlorophenols are readily removed from water during secondary waste-
water treatment, especially in well acclimated biological treatment systems.
Haller (1978) found that a wastewater sludge supernatant completely removed
a concentration of 16 mg/1 of 2-CP over a period of 14 to 25 days. Sidwell
(1971) studied the disappearance of 2,4-DCP from an aerated lagoon effluent.
4-16
-------
The initial concentration of 2,4-DCP in the effluent, 64 mg/1, was non-
detectable within five days.
The effect of pH, temperature, and chlorophenol concentrations on
the biodegradability of these compounds in wastewater treatment was
studied by Ingols and coworkers (1966). The optimal temperature for 2-CP
degradation was found to be between 25°C and 27°C and the optimum pH
between 6.5 and 8.0. Concentrations of 2,4-DCP and 2,4,6-TCP greater
than 200 mg/1 inhibited degradation significantly. Several studies have
identified Pseudomonas sp. and Nocardia sp. as the aquatic microorganisms
capable of degrading chlorinated phenols in wastewater treatment
(Nachtigall and Butler 1974).
Primary treatment may not always be effective at removing chloro-
phenols because of their poor sorption by particulates and the apparent
ineffectiveness of flocculants (i.e., aluminum or ferric sulfate) under
certain wastewater treatment conditions (Kozak et al. 1979).
Little information was available concerning the effectiveness of
other treatment methods. Activated carbon adsorption and strongly basic
anion-exchange resin techniques appear to effectively reduce 2,4-dichloro-
phenol concentrations in water (Kozak et al. 1979), Chemical oxidation
is also practiced at some plants to remove chlorophenol tastes and odors.
Lower chlorophenols are chlorinated to higher chlorinated products such
as 2,4,6-trichlorophenol,which subsequently undergoes ring oxidation to
form carboxylic acids and other products (Kozak et al. 1979).
4.4 MONITORING DATA
With the exception of pentachlorophenol, comprehensive monitoring
data on the chlorophenols are scarce for water and practically non-exis-
tent for air, soil, and biota. In addition to a lack of adequate studies,
a number of those completed to date have aggregated (or failed to disaggre-
gate) the data under the more general categories of total phenols or
chlorophenols. The most frequently observed compound of the three is
2,4-dichlorophenol, most likely due to its occurrence in the pesticide
2,4-D. There are no monitoring data available for any of these compounds
in the atmosphere; conjecture would indicate potential sources of atmos-
pheric pollution as chemical manufacturing plants incineration of trash
containing these products, and volatilization from water and soil. There
is a similar lack of data for biota in the literature and also within the
STORET data base (U.S. EPA 1979). All available data for biota are dis-
cussed under Pathways 1 and 2.
4.4.1 Methods of Analysis
Until 2-chlorophenol, 2,4-dichlorophenol, and 2,4,6-trichlorophenol
were identified as priority pollutants, the method most commonly used for
4-17
-------
identification of these compounds was measurement of total phenols or at
iaSa tvni^f chlor°Ph*nols- T*e 4-aminoantipyrine colorimetric method (4-AAP
la a typical non-specific method which estimates the total concentration of
chlorophenols (Buikema et al. 1979, Kozak et al. 1979). RecentlyThowever
there has been an effort to distinguish beFw'eSn" different phenols using
electron-capture gas-liquid chromatography. This change in focus means
that historical and recent monitoring data are not comparable which
prevents analysis of long-term trends in environmental concentrations.
Additionally it means that the monitoring data base, being relatively new
is very limited for each of the chlorophenol compounds.
4.4.2 Water
4.4.2.1 STORET Data Base
and J«S * 5 ^ited t0 draW conclusions on the distribution
and magnitude of concentrations of chlorinated phenols in U.S. ambient
waters (U.S. EPA 1979); sampling of chlorophenols has occurred S only
seven major river basins since 1977. Because of this, it is more bene-
ficial _ to examine water quality conditions on a local level for the
following water regions: Ohio River, Upper Mississippi River, Lake
Michigan Missouri River, Lower Mississippi River, Western Gulf, and
nh^C N°rthwef (seeJable 4-5> - Concentrations for the three chloro-
phenols were undetectable in the Western Gulf region.
Virtually all of the observations (roughly one hundred for each
chlorophenol) are remarked data. It should be noted that the distri-
afdeoA fSeT^°n?
-------
Ohio Ulvcr
ll|i|)i-r Missl ss I |i|i I Klver
Missouri River
l.owc-r Ml H:; Iss i|>|>! Klver
I'nrlfJc- Nnrihwcst
IINlri'll STATICS
TABI.K 4-5. CHLORINATED PHENOLS IN AMBIENT WATKRS-STOIIKT DATA (1977-1979)
(HR/1)
2,4,6-Tri.-liloio|)licnol
Number ot
Observations
6
5
6
27. l"
5
51
100,l"
Percentage of
Observations
0.1-1 1.1-10 10.1-100
100
100
50 50
96 4
100
29 71
3 57 40
Number of
Observations
6
5
12
28
5
51
107
Percentage of
Observ.'it Ions
0.1-1 1.1-10 10.1-100
100
too
75 25
96 4
100
29 71
8 54 37
Number of
Observat ions
6
5
12
27.1"
5
51
106, l"
I'eiventane of
OliKerv.il Ions
0.1-1 I.I-IO 10. 1- 100
100
100
50 25 2r>
96
100
ft n
6 57 37
tl.ll.l.
Soiin-e: U.S. El'A (1979).
-------
100 yg/1. As with 2-chlorophenol, 71% of the observations in the Pacific
Northwest region for 2,4-dichlorophenol fall between 10.1 to 100 yg/1,
with the remainder between- 1.1 to 10 ug/1. To combine all observations
for 2,4-dichlorophenol, the distribution results are 8% of the observa-
tions between 0.1 to 1 yg/1, 54% between 1.1 to 10 yg/1, and 37% between
10.1 to 100 yg/1. From 1977 to 1979, the mean values of the regions
reporting ranged from 0.0 to 30 yg/1 and centered around 10 yg/1.
For 2,4,6-trichlorophenol, 50% of the observations appear between
0.1 to 1 yg/1; the remaining percentage is divided equally between the
ranges of 1.1 to 10 yg/1 and 10.1 to 100 yg/1. The distribution of
observations for other basin regions is identical to those for both 2-
chlorophenol and 2,4-dichlorophenol. An aggregation of the observations
for 2,4,6-trichlorophenol results in a distribution of 6% in the range
of 0.1 to 1 yg/1, 57% between 1.1 to 10 yg/1, 37% between 10.1 to 100
yg/1. The mean values of 2,4,6-trichlorophenol for the seven basins
ranged from 0.0 to 30 yg/1 and centered around 10 yg/1.
4.4.2.2 Other Water Monitoring Data
Jungclaus and coworkers (1978) studied the wastewater and receiving
water and sediments at a specialty chemicals manufacturing plant pro-
ducing a broad range of chemicals for use in other industries. In the
plant wastewater levels ranging from 10 to 20 yg/1 of chlorophenol were
reported. A non-quantifiable amount was present in the river water but
was not detected in the sediment. In addition, dichlorophenol was
detected in wastewater and river water, but was not quantified.
In a study of the wastes from the manufacture of herbicide, par-
ticularly 2,4-D and 2,4,5-T in a Jacksonville, Arkansas plant, Sidwell
(1971) reported levels of 2.88, 73.16, and 2.78 mg/1 for 2-chlorophenol,
2,4-dichlorophenol, and 2,4,6-trichlorophenol, respectively. Kawahara
(1971) reported detectable levels of 2,4r-dichlorophenol in the Ohio
River and at a dam in West Virginia, and a level of 6.6 yg/1 at an in-
take for the Cincinnati water supply. The median concentration of 2,4-
dichlorophenol for drinking water supplies for all cities examined in
the National Organic Monitoring Survey was 0.02 to 0.05 yg/1. The mean
was 0.18 yg/1 for 80% of the cities detecting this compound (U.S.
EPA 1975).
In a Swedish study of chlorophenols in the spent bleach liquors
produced at several kraft pulp mills, Lindstrom and Nordin (1976") found
detectable but non-quantifiable levels of dichlorophenol. For 2,4,6-
trichlorophenol reports of 25 yg/1 in the chlorination stage and 1,150
yg/1 in the extraction stage were made. In the pulp, 0.9 yg/ton in the
chlorination stage and 1.8 g/ton in the extraction stage were reported.
(These results are for one of three mills; results from the three were
in close agreement).
4-20
-------
The Rhine River and ot>er Dutch surface waters were sampled for
chlorophenol content in a two-year monitoring study (January 1976 through
December 1977) reported by Wegman and Hafstee (1979). A total of 206
samples were taken at 6 sampling sites. For the Rhine, levels of the
three compounds decreased in both frequency and concentration over the
sampling period; this trend also applied to the Meuse River. However,
the Boven Merwede and the Ijssel Rivers both showed slight increases in
the levels of 2,4,6-trichlorophenol in 1977. An earlier study encompassing
many of the same water bodies was reported by Piet and De Grunt (1975)
and showed significantly higher levels for these three compounds. From
these results it appears that increasingly stringent regulations have
contributed to an appreciable decrease in chlorophenol pollution in the
Netherlands.
Summaries of concentrations of chlorophenols reported in the liter-
ature are presented in Tables 4-6 and 4-7.
4-21
-------
TABLE 4-6. REPORTED CONCENTRATIONS OF CHLORINATED PHENOLS IN THE ENVIRONMENT
JN
I
K)
K)
Compound
Chlorophenol
Chlorophenol
Dichlorophenol
Dichlorophenol
2-Chlorophenol
2,4,6--Trichlorophenol
2-Chlorophenol
2,4-Dichlorophenol
2,4,6-Trichlorophenol
2,4-Dichlorophenol
Concentration (mg/1)
D3
0.01-0.02
D
D
0.0017
D
2.88
73.16
2.78
0.00018
Comment
river
wastewater from chemical
producer
river
wastewater from chemical
producer
secondary sewage effluent
pulp mill effluent (Sweden)
herbicide production waste
herbicide production waste
herbicide production waste
urban drinking water
Reference
Jungclaus £t al. (1978)
Jungclaus ejt al. (1978)
Jungclaus e£ al. (1978)
Jungclaus £lt al. (1978)
Jolley et_ al.. (1975)
Landner et^ al. (1977)
Sidwell (1971)
Sidwell (1971)
Sidwell (1971)
U.S. EPA (1980a)
D = detected but non-quantifiable
-------
I
NJ
TABLE 4-7. CHLOROPHENOLS IN RIVER WATER (ug/l) NORTHERN EUROPE
1974'
1976
1977
Mean
2-Clilorophenol
Rhine 3-20
Meuse (at Eijsden) 2-20
2 , 4-Dichlorophenol
Rhine 0.03-1.5
Meuse (at Eijsden) 0.01-0.04
2,4, 6-Tr ichlorophenol
Rhine 0.07-0.1
Meuse (at Eijsden) 0.003-0.02
Boven Merwede
Ijssel
Meuse (at Lith)
Frequency of
Detection (%)C Max.
2
0
47
0
94
30
92
92
27
2.3
ND
0.59
ND
2.5
0.05
0.27
0,35
0.12
Frequency of
Med. Detection (%) Max.
ND
ND
ND
ND
0.19
ND
0,12
0.18
ND
0
0
48
0
87
23
92
92
31
ND
ND
0.35
ND
0.51
0.05
0.37
0.37
0.04
Med.
ND
ND
ND
ND
0.18
ND
0.15
0.16
ND
aljiet and DC Grunt (1975).
Wegman and Hafstee (1979),
Out of a total of 206 grab samples .
ND = Not detected.
-------
REFERENCES
Alexander M. ; Aleem, M.I. Herbicide structure and stability, effect
° °
fat! ofM25/nUSt; S'D< *erbicides in ^rface waters: studies on the
fate of 2 4-D and ester derivatives in natural surface waters. J. of
Agricul. Food Chem. 12(6) :54l-546; 1964.
.' C'S;; Alexander> M' 2, 4-D metabolism, enzymatic
Chl°rinated Phenols' J' of Agricul. Food Chem. 16(5):
Buikema, A.L.; McGinnis, M.J.; Cairns, J. Phenolics in aquatic eco-
2:87-T8l; 1979 "^ °f ""^ literature- Marine Environ. Res.
aeofl2Q'n';- Slimak'N-W-; Gabe1' N'W. Water-related environmental
US Envir * *tl P°llutants - EPA-440/4-79^029. Washington, DC:
U.S. Environmental Protection Agency; 1979.
hin t'J> T^ adaptation of fungi ^ pentachlorophenol and its.
biodegradation. Can. J. Microbiol. 13(9) : 1243-1249: 1972 (As cited
in Kozak et_ al^. 1979) .
Ettinger, M.B.; Ruchhoft, C.C. Persistence of monochlorophenols in
III iQv r^vfr/ater and sewage dilutions. Cincinnati, OH: Environ-
e
i
Kozak ee| 1979)?^ U'S' PUbUC Health Service; 1950' ^ cltd in
™ZInJfi?' °'i o^?; J'S'W>; Fernley» H-N- Davies, J.I. Bacterial
metabolism of 2, 4-dichlorophenoxyacetate. Biochem. J. 122(4): 543-551-
1971. (As cited in Kozak et al. 1979) . '
Haller, H.D. Degradation of mono-substituted benzoates and phenols by
wastewater. J. Water Poll. Cont. Fed. 2771^-2777; 1978.
Hattula, ML.; Wasenius, V.M. ; Reunanen, H.; Arstila, A. U. Acute
toxicity of some chlorinated phenols, catchehols, and cresols to trout
Bull. Environm. Contam. Toxicol. 26:295-298; 1981.
Hendry, D.Y.; Kenley, R.A. Atmospheric reaction products of organic
compounds. Draft report. EPA 68-015-123. Washington, DC: U.S Environ-
mental "Protection Agency; 1979. environ.
Ingols, R S.; Gaffrey, P.E.; Stevenson, P.C. Biological activity of
halophenols. J. Water Poll. Fed. 38(4) : 629-635; 1966.
4-24
-------
Jolley, R.L.; Jones G.; Pitt, W.W.; Thompson, J.E. Chlorination of
organics in cooling waters and process effluents. Jolley, R.L. ed.
Proceedings of the conference on the environmental impact of water
Chlorination; 1975. October 22-24, Oak Ridge, TN: 1975. pp. 115-152.
Jungclaus, G.; Lopez-Avila, V.; Kites, R. A. Organic compounds in an
industrial wastewater: a case study of their environmental impact.
Environ. Sci. Technol. 12(1):88-96; 1978.
Kawahara, F.K. Gas chromatographic analysis of mercaptans, phenols,
and organic acids in surface waters with use of pentafluorbenzyl deriva-
tives. Environ. Sci. Technol. 5(3):235-239; 1971. (As cited in
Callahan et_ al. 1979).
Kozak, V.P.; Simsiman, G.V.; Chesters, G.; Stensby, D.; Harkin, J.
Reviews of the environmental effects of pollutants: XI. Chlorophenols.
ORNL/EIS-128, Oak Ridge, TNj Oak Ridge National Laboratory; 1979.
Landner, L.; Lindstrom, K.; Karlson, M.; Nordin, J.; Sorenson, L.
Bioaccumulation in fish of chlorinated phenols from kraft pulp mill
bleachery effluents. Bull. Environm. Contain. Toxicol. 18(6); 1977.
Lindstrom, K.; Nordin, J. Gas chromatography-mass spectrometry of
chlorophenols in spent bleach liquors. J. Chromatogr. 128:13-26; 1976.
(As cited in Buikema et_ al. 1979) .
Lyr, H. Detoxification of heartwood toxins and chlorophenols by higher
fungi. Nature 195:289-290; 1962. (As cited in Kozak et al. 1979).
MacKay, D. Finding fugacity feasible. Environ. Sci. Technol. 13:1218-
1223; 1979.
MacKay, D.; Yuen, T.K. Volatilization of organic contaminants from
rivers. Proc. 14th Canadian Syrap.; 1979. Water Pollut. Res. Can;
undated.
Morrison, R.J. ; Boyd, R.N. Organic chemistry. Boston, MA: AUyn and
Bacon; 1973.
Motuzinskii, N.F. Migration and decomposition of 2,4-D derivatives in
forest soils. Mekh. Deistiviya Gerbits. Sint. Regul. Rosta Rast. Ikh "'
Sud'ba Biosfere. Mater, Mezhdunar. Simp. Stran-Chlenov SEV. 10th, 2:52-
55. (.USSR;.' 1975. As referenced in Agrochemicals, Vol. 88, 1978.
Nachtigall, M.H.; Butler, R.G. Metabolism of phenols and chlorophenols
by activated sludge microorganisms (abstract). Abstr. Annu. Meet. Am.
Soc. Microbiol; 1974. p. 184.
Neely, W.B.; Planka, J.H. Estimation of time averaged hydroxyl
radical concentrations in the troposphere. Environ. Sci. Technol.
12(3):317; 1978.
4-25
-------
man and his environment by persistent pesticides and organo-halogenated
iTUIt:92EU1975ean
-------
Walker, N. Preliminary observations onthe decomposition of chlorophenols
in soils. Plant soil. 5(2):194-204; 1954.
Wegman, R.C.; Hafstee, A.W. Chlorophenols in surface waters of the
Netherlands (1976-1977). Water Research 13:651-657; 1979.
Yasuhura, A.; Otsuki, A.; Fuma, K. Photodecomposition of odorous chloro-
phenols in water. Chemosphere 6(10):1659-1664; 1977,
4-2!
-------
5.0. EFFECTS AND EXPOSURE—HUMAHS
5.1 SUMMARY
The available data on the toxicity of 2-chlorophenol (2-CP), 2,4-
dlchlorophenol (2,4-DCP), and 2,4,6-trichlorophenol (2,4,6-TCP) are limited.
As a group, these compounds appear to be readily metabolized and excreted in
urine as glucuronide and sulfate conjugates; supporting data, however, are
scanty. Acute median lethal doses of 2-CP and 2,4,6-TCP are in the 100 to
900 mg/kg range; 2,4-DCP is somewhat less toxic. Subacute studies are few,
but alteration of liver function appears to be the principal finding. All
three compounds have been shown to inhibit oxidative phosphorylation in
rat liver mitochondria in vitro.
Dietary administration of 2,4,6-TCP is carcinogenic in male F344
rats, inducing lymphomas or leukemias. This compound is also carcinogenic
in both sexes of B6C3F1 mice, inducing hepatocellular carcinomas or adenomas.
The carcinogenicity of 2,4-DCP and 2-CP has not been examined by the oral '
route, although both compounds do possess tumor-promoting activity in mice.
The trichlorinated 2,4,6-TCP is inactive in this respect.
Chromosomal damage in mammalian somatic tissues was induced by 2-CP
treatment; available data on 2,4-DCP and 2,4,6-TCP are insufficient to
evaluate the mutagenicity of these compounds. There is no information
available on the effects of 2-CP, 2,4-DCP, or 2,4,6-TCP on the develop-
ing embryo.
An estimation of the risk to man associated with exposure to 2-CP
and 2,4-DCP cannot be adequately made due to the lack of available toxi-
cological data on these compounds, particularly with respect to long-
term effects in experimental animals and/or human exposure.
The limited information available suggests that human exposure to
chlorinated phenols is low. The most common route of exposure appears
to be in drinking water, with 2,4-dichlorophenol detected at low levels in
numerous drinking water samples. Maximum exposures of 60~-100 ug/day were
estimated for the three compounds considered, based on concentrations in
unfinished drinking water, with a more typical exposure of 0.4 yg/day for
2,4-DCP. Typical exposures for 2-chlorophenol and 2,4,6-TCP are unknown,
but may be lower than that for 2,4-DCP due to the lower likelihood of
their entering the environemnt.
Exposure of humans through seafood has a potential on the order of
1 mg/day, but this estimate is highly speculative, and few actual residues
have been reported in fish. In fact, metabolic data for fish indicate a
rapid excretion of at least chloro- and dichlorophenols. The use of
other products (2,4-D, 2,4,5-T) may result in exposure to the chloro-
phenols, however, such exposure cannot be quantified due to a lack of
information on use patterns, exposure concentrations, and other
parameters.
5-1
-------
to chlorinated phenols is unknown, but based
on the limited information available, it is probably less significant
than other routes of exposure.
5.2 HUMAN TOXICITY
5.2.1 Introduction
w ^Ch^°rl?afd Phenols are commercially important intermediates in the
synthesis of dyes, pigments, phenolic resins, pesticides, herbicides
Jow^vprTh 6XP°SUre is therefore predominately occupational in nature.
as wln'^ S^ USe aS antisePtic*> disinfectants, and fungicides,
as well as their presence in drinking water, can result in exposure of
the population at large. This section of the report will examine the
somewhat limited data available on the toxicity of 2,chloroPhenol,
2,4-dichlorophenol, and 2 4,6-trichlorophenol to mammalian species.
5-2.2 Metabolism and Bioaccumulation
na<- ,Li"le 7information is available on the metabolic pathways of chlori-
nated phenols in experimental animals or in man. The lipophilic naturT
atld I™ degree °f i°nization at physiological pH of 2-CP, 2,4-DCP, and
^,b-TCP suggest facile absorption of these compounds by all routes of
hUS' vPenftra^ion °f 2'4-DCP and 2,4,6-TCP through intact, excised
!ral!^a:Lb!en demonstrated in vitro (Roberts et al. 1977) . however.
0*r> me^abolism of thfise compounds are also sparse, but, in
general chlorinated phenols appear to be handled in a manner similar
to phenol (i.e. conjugation with glucuronic acid and/or conjugation
-
.
and Thomas 1943, Dodgson et al. 1950). Korte and coworkers Q9 8) reposed
rapid clearance of 2,4,6-TCP in rats fed 1 mg 2,4,6-TCP/kg diet for 3 days
Elimination occurred predominately in urine (82% of the administered
dose) with a smaller amount in feces (22% of the administered dose).
?Jve1iv ^ Ji ^' ^"^ W3S dSteCted ln liV6r' lun«. or fat
rive days after the last dose'.
Exposure to other chemicals can also result in exposure to chloro-
worr^ HQT^'f Ol^od/e8rdati0n °f the parent co^P^nd. Kohli and co-
workers (1976) found 2,4,6-TCP to be a major urinary metabolite of
rabbits exposed to 1, 3, 5-trichlorobenzene. Kurihara (1975) noted 2 4-
DCP and its conjugates in the urine of mice given gamma- or beta- ben-
zene hexachloride. In sheep and cattle fed the herbicide 2,4-dichloro-
Phenoxyacetic acid (2.4-D) 2,4-DCP was found to be a major Metabolite
aiark et_ al. 1975) . Lindsay-Smith and coworkers (1972) reported 2-CP
5-2
-------
in the urine of rabbits given chlorobenzene, while Selander and coworkers
(1975) noted the in vitro conversion of chlorobenzene to 2-CP by perfused
rat livers. The above examples serve to demonstrate that exposure to
chlorophenols can occur in mammals indirectly as a metabolite of other
compounds, but these indirect routes do not appear to be a major route
of exposure.
While highly lipophilic compounds, such as the chlorinated phenols
generally accumulate in adipose tissue, there are no data available
to suggest that bioaccumulation occurs. As stated earlier, Korte and
coworkers (1978) found no radiolabelled 2,4,6-TCP in liver, lung, or
fat of rats five days after oral exposure to 2,4,6-TCP, and Clark and
associates (1975) detected less than 0.05 mg 2,4-DCP/kg tissue in both
fat and muscle of sheep and cattle fed the herbicide 2,4-D (2,000 mg/kg
diet) for 28 days. Tissue residues of 2,4-DCP in sheep liver and kidney
were slightly higher (0.16 and 0.26 mg/kg tissue, respectively) but
dropped to 0.15 and 0.07 mg/kg tissue, respectively, seven days after
withdrawal of the herbicide from the diet.
5.2.3 Animal Studies
5.2.3.1 Carcinogenesis
Little information is available on the carcinogenicity of the three
chlorinated phenols under evaluation. Only the trichlorinated 2,4,6-TCP
has been tested by the oral route (Innes £t al. 1969,NCI 1979).
Innes and coworkers (1969) administered 100 mg 2,4,6-TCP/kg by
gavage to two strains of hybrid mice (C57BL/6 x C3H/Anf and C57BL/6 x
AKR) for three weeks beginning when the mice were seven days old,
followed by 260 mg/kg diet for 18 months. This resulted in an estimated
exposure of 20-25 mg/kg of 2,4,6-TCP. Elevated incidences of reticulum-
cell sarcomas and hepatomas were reported" but data were not provided.
The National Cancer Institute (1979) has recently completed an
assessment of the carcinogenicity of 2,4,6-TCP in F344 rats and B6C3F1
mice. In rats, groups of 50 animals of each sex were given 5,000 or
10,000 mg 2,4,6-TCP/kg diet for 106 to 107 weeks; 20 rats of each sex
served as controls. Dose-related reductions in mean body weights of
treated males and females compared to controls were noted throughout
the study. Statistically significant dose-related incidences of lymphomas
or leukemias were noted in male rats (See Table 5-1). Treated female rats
did not exhibit lymphomas or monocytic leukemia at a significant incidence.
Leukocytosis and monocytosis of peripheral blood and hyperplasia of the
bone marrow were present, however, in treated female rats and male rats
not exhibiting lymphoma or leukemia.
In a separate experiment with B6C3F1 mice, 50 male mice were given
5,000 or 10,000 mg 2,4,6-TCP/kg diet for 38 weeks. The dietary concen-
tration was subsequently reduced to 2,500 and 5,000 mg/kg diet respectively,
due to excessively low body weights in females. This reduced dietary
5-3
-------
TABLE 5-1. INCIDENCE OF NEOPLASMS IN F344 RATS FED 2 4 6 -
TRICHLOROPHENOL IN THE DIET FOR TWO YEARS* ' '
Treatment
Group
(mg/kg diet)
Males:
0
5,000
10,000
Malignant
Lymphoma
Leukemia
Bone Marrow
Hyperplasia
1/20 (5%) 3/20 (15%) 0/20 (0%)
2/50 (4%) 23/50 (46%) 26/50 (52%)
0/50 (0%) 29/50 (58%) 15/50 (30%)
Leukocytosis
0/20 (0%)
13/50 (26%)
11/50 (22%)
Females:
0
5,000
10,000
0/20 (0%) 3/20 (15%) 0/20 (0%) 0/20 (0%)
0/50 (0%) 11/50 (22%) 16/50 (32%) 6/50 (12%)
2/50 (4%) 11/50 (22%) 2/50 (4%) 3/50 (6%)
Source: Adapted from NCI (1979)
5-4
-------
concentration was maintained for the remaining 67 weeks of the study.
The time-weighted average doses were 5,214 and 10,428 mg/kg diet, respec-
tively. Statistically significant incidences (p <0.001) of hepatocellu-
lar carcinomas or adenomas were recorded in all groups of mice treated
with 2,4,6-TCP (see Table 5-2).
No data are available on the potential carcinogenicity of 2-CP or
2,4-DCP by the oral route. However, both of these compounds, as well
as 2,4,6-TCP, have been evaluated for their tumor-promoting activity in
a series of experiments by Boutwell and Bosch (1959). Female Sutter
mice were initiated with a single dermal application of 0.3% dimethyl-
benzanthracene (in benzene) to the back, followed by repetitive, twice-
weekly applications of ^25 ul of a 20% solution of either 2-CP, 2,4-DCP,
or 2,4,6-TCP to the same area for 15 weeks. The results of these experi-
ments are presented in Table 5-3; related promoter experiments with
phenol are included for comparative purposes. The promoting activities
of 2-CP and 2,4-DCP appear comparable to phenol; however, no statistical
evaluation or dose-response data were presented. The trisubstituted
2,4,6-TCP was inactive. As with phenol, the promoting activities of
2-CP and 2,4-DCP are probably associated with their irritancy and sub-
sequent skin hyperplasia and are thus not appropriate for assessment of
human risk by ingestion.
In a separate experiment, Boutwell and Bosch (1959) treated female
Sutter mice with 20% 2-CP in dioxane twice weekly for 12 weeks without
prior initiation. Forty-six percent of the survivors at 12 weeks had
developed papillomas but no epithelial carcinomas were found.
In summation, dietary administration of 2,4,6-TCP is carcinogenic
in male F344 rats, inducing lymphomas or leukemias. This compound is
also carcinogenic in both sexes of B6C3F1 mice, inducing hepatocellular
carcinomas or adenomas. The carcinogenic potentials of 2-CP and 2,4-
DCP have not been tested by the oral route, but both compounds do appear
to possess tumor-promoting activities in mice, probably a result of an
irritant response. The trisubstituted 2,4,6-TCP is inactive in this
respect.
5.2.3.2 Mutagenesis
Chung (1978) noted a fivefold increase in chromatid deletions (12%
vs. 2% in controls) in bone marrow cells of Sprague-Dawley rats orally
administered 130 mg/kg 2-CP every other day for one week. Complete
inhibition of mitosis was noted in bone marrow cells taken from similarly
treated rats after exposures of two to three weeks.
Fahrig and associates (1978) reported a weak but significant increase
(p <0.02) in forward mutations in the yeast, Saccharomyces cerevisiae
MP-1 following exposure to 400 mg/1 2,4,6-TCP for 3.5 hours. Mutants
numbered 10.29 colonies in 2,4,6-TCP-treated cells compared to 5.63
colonies for control cultures. No positive control agents were tested,
making evaluation of the significance of the results with 2,4,6-TC?
difficult to adequately assess.
5-5
-------
TABLE 5-2. INCIDENCE OF NEOPLASMS IN B6C3F1 MICE FED 2,4,6, -
. TRICHLOROPHENOL IN THE DIET FOR TWO YEARS
Treatment
Group
(mg/kg diet)
Hepatocellular
Carcinoma
Hepatocellular
Adenoma
Hepatocellular
Males:
0
5,000
10,000
1/20 (5%)
10/49 (20%)
7/47 (15%)
3/20 (15%)
22/49 (45%)
32/47 (68%)
2/20 (10%)
12/49 (24%)
6/47 (13%)
Females:
0
5,214a
10,428a
0/20 (0%)
0/50 (0%)
7/48 (14%)
1/20 (5%)
12/50 (24%)
17/48 (35%)
1/20 (5%)
1/50 (2%)
6/48 (13%)
Time-weighted average dose.
Source: Adapted from NCI (1979)
5-6
-------
TABLE 5-3. INCIDENCE OF TUMORS IN SUTTER MICE INITIATED WITH 0.3% DIMETHYLBENZANTHRACENE
AND TREATED WITH VARIOUS SUBSTITUTED PHENOLS
Promoter
(applied two times
per week)
(20% soln. in benzene)
Duration of Treatment
(week)
Incidence of Papillomas
(% of survivors)
Incidence of
Epithelial
Carcinoma (%)
None
2 - Chlorophenol
2,4 - Dichlorophenol
2,4,6 - Trichlorophenol
Phenol
15
15
15
15
12
1/15 (7%)
19/31 (16%)
13/27 (48%)
0/26 (0%)
14/22 (64%)
10%
11%
0%
0%
Benzene (control)
2,4 - Dichlorophenol
Phenol
24
24
24
3/27 (11%)
12/16 (75%)
18/20 (90%)
0%
6%
15%
Source: Adapted from Boutwell and Bosch (1959)
-------
ami 7ZA A*?™6* "I?*5'l Rasanen and coworkers (1977) tested both 2,4-DCP
of 0 5 ?" sn ^ Jh^Ames .Salmonella microsomal test at concentrations
uo, D, au, and 500 yg/plate. Both compounds were evaluated in the
^TJ,:^^^^CS^ sj^^^i^^ «-
52:«>^lSrBB?1IalZESas^=- Soine "^^ "^evident ?
Antimitotic and antimeiotic effects (e.g., chromosome stickiness
lagging chromosomes fragmentation) have also been noted in vetch" ("c
faba) exposed to 2,4-DCP (Amer and Ali 1974) and in pea plants
cnangJs toXauI«tio!!r?ery and,flson, 196« • Tl>« relationship of th«e
established "an^lian cells, however, has not been
bt^ „ f ^TT^' there^ore' 2-CP exhibits mutagenic activity in mice
anv alni! , ^ °? 2'4"DCP and 2'4'6-TCP are insufficient to draw
any conclusions on the mutagenic potential of these chlorinated phenols.
5-2.3.3 Adverse Reproductive Effects
There are no data available on the effects of 2-rPl -> L nr-o
2,4,6-TCP on the developing embryo or thf repro^uctiv? proems ' "
5-2.3.4 Other Toxicologjcal Effects
with phenol. The median acute lethal dose of 2-CP or 2 4
£ji^^nr^js^^~
dose for phenol falls into the 180-to-600-mg/kg range regardless of
species or route of administration (RTECS 1978) . regardless of
nhP f1? SJSnJ °f aCUte toxicity for chlorinated phenols are similar to
of excit^ T S ** miCe' FollowinS - ^thal dose, a brief peJiod
of excitation and increased respiratory rate occurs, followed by clonic
finSv10dLth /0n-?ft0r WeakneSS (h^otoni*>' dyspnea, coma, and?
of each'of ?h , ?lfferences in the ^set of symptoms following doses
of each of the chlorinated phenols have been attributed to the number
of chlorine substituents. Increasing the number of chlorine substituents
also appears to reduce convulsant activity (Farquharson et al. 1958)
"** ^ ^bsorptio^an^ distribu-
hv FJh\C°nVUlSaf activity of various chlorinated phenols was described
by Farquharson and coworkers (1958). At sublethal doses, convulsions
occur in rats within one minute after intraperitoneal injection and are
5-8
-------
TABLE 5-4. ACUTE LETHAL VALUES FOR CHLOROPHENOLS
IN MAMMALIAN SPECIES
Compound
2-Chlorophenol
2,4-Dichloro-
phenol
2,4,6-Trichloro-
phenol
Route Species
Oral Rat
Mouse
Subcutaneous Rat
Rabbit
Guinea Pig
Intraperi- Rat
toneal
Intravenous Rabbit
Oral Rat
Mouse
Subcutaneous Rat
Intraperi- Rat
toneal
Oral Rat
Human
Intraperi- Rat
LD50 (mg/1
670
670
950
950 LDLo3
800 LDLo
230
120 LDLo
4,000
2,330
580
1,630
1,600
l,730b
430
820
500 LDLo
276
RTECS (1978)
RTECS (19/8)
RTECS (1978)
RTECS (1978)
RTECS (1978)
Farquharson
et al.. (1958)
RTECS (1978)
Kobayashi et al.
(1972)
Vernot et al.
(1977)
RTECS (1978)
Vernot et al.
(1977)
Kobayashi et al.
(1972)
RTECS (1978)
Farquharson
et al. (1958)
RTECS (1978)
RTECS (1978)
Farquharson
et al. (1958)
Lowest reported lethal dose.
Fuel oil was used as the vehicle in this experiment and may have
enhanced rapid uptake of 2.4-dichlorophenol.
5-9
-------
characterized by the appearance of generalized tremors, sometimes
starting in the neck and forepaws, and increasing in severity to inter-
mittent convulsions and loss of righting reflex. Hypotonia was also
observed, progressing to the point of complete prostration. With 2,4-
DCP, auditory or mechanical stimuli elicited muscle twitches during'
hypotonia (Farquharson et al. 1958). Angel and Rogers (1972) described
similar manifestations in mice with 2-chlorophenol.
Farquharson and associates (1958) noted acute exposure to chloro-
phenols with pk values of 7.85 or less appear to be associated with
marked hypotonia, increase in body temperature, and early onset of
rigor mortis following death—effects not uncommon to oxidative un-
couplers. Limited in vitro studies indicate that 2-CP, 2,4-DCP, and
2,4,6-TCP do indeed inhibit oxidative phosphorylation (i.e., inhibit
production of ATP) in rat liver mitochondria (Farquharson et al. 1958
Mitsuda £t aJL. 1963). Mitsuda and coworkers (1963) reported that the'
150 (the concentration at which ATP production is approximately halved)
decreased in the order of phenol (5000 uM), 2-CP (520 yM), 2,4-DCP (42
UM), and 2,4,6-TCP (18 yM).
Relatively few long-term studies are available on 2-CP, 2,4-DCP,
and 2,4,6-TCP. Chung (1978) treated rats orally every other day for
three weeks with 65 or 130 mg/kg of 2-chlorophenol dissolved in olive
oil. Weight gain was significantly reduced in both treatment groups,
and,notably, liver weight was increased in treated animals. Hemoglobin
levels and hematocrit values were significantly depressed by the third week.
but there were no significant effects on total serum protein or serum
albumin. Serum alkaline phosphatase (Alk. Phos.) and serum lactic
dehydrogenase (LDH) activities were initially increased after one week,
but by three weeks Alk. Phos. had dropped below baseline, while LDH had
returned to control values. Serum glutamate-oxaloacetate transaminase
(GOT) activity was significanlty elevated after one week of treatment.
Liver function was also signficantly altered by 2-chlorophenol. Mito-
chondrial respiration in vivo and in vitro was depressed; microsomal
cytochrome P-450 was depressed as were liver LDH and GOT activities.
Histologically, liver tissue was degenerated with congestion, atrophy,
swelling, vacuolation, dilation of rough endoplasmic reticulum and
mitochondrial swelling and destruction of mitochondrial cristae.
Kobayashi and coworkers (1972) studied the effects of 2,4-dichloro-
phenol in mice fed the compound in the diet for six months. Based on
food consumption data, the dosages in the 4 treatment groups were approxi-
mately 17, 45, 100, and 230 mg/kg/day. Growth rate was slightly depressed
at the 45- and 100-mg/kg levels and significantly depressed in the 230-
mg/kg group, particularly early in the study (3 to 13 weeks). Food con-
sumption of the treatment groups compared with the control group was
essentially unaffected. Liver-and kidney-to-body-weight ratios were
somewhat depressed in treated mice compared to those in the controls,
but a dose-effect relationship was not clearly evident. Erythrocyte and
leucocyte counts were similar in all groups as were serum glutamicoxal-
acetic transaminase (GOT) and glutamic-pyruvic transaminase (GPT) levels.
5-10
-------
The histological appearance of heart and kidneys was also similar. A
slight increase in incidence of histologic abnormalities of the liver,
such as "small round-cell infiltration", "swelling of hepatic cells",
and "unequal size of hepatic cells", was noted in the highest treatment
group when compared to controls.
In another study, Miura and coworkers (1978) examined the ability
of orally administered 2,4-DCP to induce hepatic porphyria in rats. In
one experiment, the dosage of 2,4-DCP was 250 mg/kg/day the first week,
340 mg/kg/day the second week, 1,000 mg/kg/day for the first 4 days of
the third week, and finally 550 mg/kg/day for the first three days of
the fourth week. Urinary excretion of Y aminolaevulinic acid and copro-
porphyrin was slightly deceased by the treatment with 2,4-DCP, but
urinary porphobilinogen and fecal porphyrin showed no significant in-
crease compared to controls. Accumulation of porphyrins in the liver
and kidneys was normal. In a second experiment, rats were given 30
to 70 mg/kg/day of 2,4-DCP in the diet for 17 weeks. As in the first
experiment, there were no significant changes in excretion of porphyrins
and related compounds. A slightly reduced growth rate and slight histo-
logic changes in the liver were noted in the treated rats compared to
controls. The livers of 3/5 treated rats showed vacuolar degeneration,
5/5 had intralobular leucocytic infiltration, and 3/5 displayed leucocytic
infiltration of the perivascular fibrous capsule.
No adverse effects were noted in either F344 rats fed up to 14,700
mg 2,4,6-TCP/kg diet or B6C3F1 mice given up to 21,000 mg/kg diet for
7 weeks. Reduced survival was observed in male rats fed 21,500 mg/kg
diet and in female rats and both sexes of mice at a dietary exposure of
31,500 mg/kg diet. Histopathological changes were noted only in rats
fed the 46,000 mg TCP/kg diet. These changes consisted of moderate to
marked increase in splenic hematopoiesis in both males and females and
midzonal vacuolation of hepatocytes in 2/5 males. No abnormal histo-
pathology was seen in mice fed 31,500 mg TCP/kg diet for 7 weeks (NCI
1979).
5.2.4 Human Studies
Aside from a single report of an oral lethal dose of 500 mg/kg for
2,4,6-TCP (RTECS 1978), there are no data on the effects of 2-CP, 2,4-
DCP, or 2,4-6-TCP in humans. The acute toxicity of chlorophenols to
humans on a mg/kg basis, however, would appear to be comparable to that
in animals.
It is difficult to estimate subchronic and chronic toxicity of 2-CP,
2,4-DCP, and 2,4,6-TCP in humans since there is no available information
on human exposure and the experimental data in animals for these com-
pounds are minimal or non-existent.
Hardell (1979) notes an apparent association between human exposure
to phenoxyacetic acid or chlorophenols and malignant lymphoma of the
histiocytic type. The correlation to chlorophenols is uncertain and
5-11
-------
one must also take into consideration the effect of exposure to impuri-
ties such as dibenzodioxins and dibenzofurans that contaminate commercial
chlorophenol preparations.
5.3 HUMAN EXPOSURE
5.3.1 Introduction
It is apparent that data on chlorophenols is lacking in many areas,
including monitoring, fate,and toxicity. Thus, there is little basis
for estimating exposure of human receptors to these compounds. However,
the releases of 2-chlorophenol, 2,4-dichlorophenol, and 2,4,6-trichloro-
phenol to the environment are limited, thus reducing the potential for
exposure. Recent reviews of the subject by the EPA (1980a, 1980b, 1980c)
and Kozak and coworkers (1979) concluded that there was little likelihood
of widespread human exposure to these compounds.
This section will examine the limited data available in an attempt
to define exposure further. It should be noted that limited data make
such estimates quite tentative and that it is difficult to associate
subpopulations with exposures.
5.3.2 Ingestion
5.3.2.1 Drinking Water
Sources of chlorophenols to ambient waters and potentially to drink-
ing water supplies include chemical manufacturers' discharges, waste-
water chlorination, and agricultural runoff. Land application of the
herbicide 2,4-D could potentially result in the contamination of ground-
water wells used for drinking water. There is also a potential for
formation of chlorophenols in the chlorination of drinking water supplies
(see Chapter 3.0).
The only information available on chlorophenol levels in finished
drinking water is for 2.4-dichlorophenol. The compound was detected in
56 out of 108 samples at a mean level of 0.18 yg/1 (for positive values)
(U.S. EPA 1978). Assuming a two-liter daily consumption of drinking
water, a daily exposure level of approximately 0.4 yg of 2,4-dichloro-
phenol can be estimated.
According to ambient surface water data for all three chlorophenols,
also a limited data base, concentrations are usually less than 50.0 \
A maximum daily amount of 60 to 100 yg can be estimated for exposure
through drinking untreated water contaminated with any of the chloro-
phenols. This estimate should be considered an upper limit and is
probably applicable to a very small subpopulation. An exposure of 0.4
yg/day may be more common, at least for 2,4-DCP.
The majority of these data are remarked as either at or below the
reported level, which is a detection limit, therefore the actual con-
centrations present are overestimated.
5-12
-------
Spills can result in localized contamination of surface or ground -
1 water, as described in Chapter 4.0. These types of incidents have the
potential for resulting in higher exposures than those discussed above.
However, based on the conclusions of Chapter 4.0, the chlorophenols,
especially the mono- and dichlorophenols, are readily biodegradable in
surface waters following an initial period of microbial population
acclimation. Therefore for chloro- and dichlorphenol spills in aerated,
biologically active surface waters, high concentrations are likely to
be short term. Spills of trichlorophenol and of all three chlorophenols
under reduced conditions (i.e., into groundwater) may be more persistent
and present a long-term potential for exposure.
A characteristic of phenols in general which would tend to
decrease the likelihood of human exposure to high concentrations is
the compounds' low odor thresholds in water. The two EPA Water Quality
Criteria proposed for some chlorophenol compounds reflect this (U.S.
EPA 1980a,b,c). The human health criterion based on odor characteristics
is four orders of magnitude below the criterion based on available
toxicity data for 2,4-dichlorophenol.
5.3.2.2 Food
Ingestion of chlorinated phenols in food has not been documented
(Kozak et_ al_. 1978, U.S. EPA 1979). However, as was discussed in
Chapter 4.0, their presence in food is possible, especially 2,4-dichloro-
phenol. This compound has been reported in plants as a result of application
of the herbicide 2,4-D. The presence of 2,4-DCP in plants may be a result
of plant metabolism of 2,4-D or uptake of the herbicide from soil.
Although the possibility of these residues persisting to consumption
exists, the exposures can not be approximated without residue data for
food crops.
Chapter 4,0 also reports tissue residue levels and bioconcentration
factors (BCFs) in fish for the three compounds. Based on U.S. EPA esti-
mated BCFs for the chlorophenols in the edible portion of fish, tissue
levels are 4.0 mg/kg, 1.2 mg/kg, and 4.5 mg/kg for 2-CP, 2,4-DCP, and
2,4,6-TCP, respectively assuming ambient water levels of 10 ug/1 (U.S.
EPA 1980a, 1980b, 1980c). Assuming an average fish consumption of 21 g/
day (USDA 1979), intakes of 27, 9 and 32 ug/day can be estimated for the
respective chlorophenols. Maximum intakes, based on water concentrations
of 60 ug/1 for 2-CP and 30 ug/1 for 2,4-DCP and 2,4,6-TCP, are estimated
to be 137, 26 and 95 ug/day, respectively. However, actual residues of
these compounds in aquatic organisms are limited to reports of 2 mg/kg
(bluegill) and 18 mg/kg (trout) for 2-CP and 2,4-DCP, respectively. These
limited data suggest that the theoretically derived bioconcentration pro-
vides an upper limit measure of uptake, although more data are required
to confirm this. Metabolic data indicate that fish may rapidly metabolize
and excrete the chlorophenols so that significant levels of accumulation
are not achieved.
5-13
-------
The contamination of livestock by 2,4-DCP through the ingestion of
crops treated with herbicides was estimated by the U.S. EPA (1980b). A
worst case estimate was made assuming a dosing of 2,4-DCP of 7 mg/kg body
weight for cattle. The levels of 2,4-DCP accumulating in liver and kidney
were estimated at 0.11 yg/g and 0.56 ug/g, respectively. Assuming inges-
tion of 0.5 kg of kidney daily for humans, an exposure of 280 ug/g of
2,4-DCP was estimated. This level is a worst case example because it
assumes a constant diet for cattle of 2,4-D sprayed foliage only and no
metabolism of the substance.
Dairy cattle dosed with high levels of 2,4-DCP were not found to ac-
cumulate the compound in their milk (U.S. EPA 1980b). Therefore, inges-
tion of milk is not considered to be a significant exposure route for
2,4-DCP.
5.3.3 Inhalation
There is a potential for exposure of humans to airborne levels of
chlorophenols, most significantly during the use of products containing
these compounds. In addition, di- and trichlorophenols were identified
in the gas condensates from municipal incinerators (Olie et_ al_. 1977);
unfortunately, however, levels were not quantified. There was no infor-
mation on ambient atmospheric levels of any of the chlorophenols. All
three compounds are fairly volatile but little is known about their
persistence or ultimate fate in the troposhere (Chapter 4.0).
The only air monitoring data available for any of the chlorophenols
reported 2-chlorophenol concentrations in the immediate vicinity of a
train derailment spill of the compound (APHA 1979). Concentrations on
the day of the spill measured 0.02 mg/m3 to 0.7 mg/m3 (0.004-0.19 ppm) .
Eighteen days following the spill, air levels were reduced to <2 yg/m3
(<0.0005 ppm). Urine levels in the clean-up workers measured 1.98 mg/1
approximately 2 months following the spill; however the pathways, dura-
tion, and time of exposure were not given, so the exposure levels cannot
be estimated. The urine levels were not detectable (detection limit
0.25 mg/1) by the following month. People living within 40-200 feet of
the spill area who were expected to be exposed solely via inhalation
had no detectable levels in their urine 3 months after the spill. No
earlier sampling was done for acute exposure levels.
A small subpopulation may be exposed to 2,4,6-trichlorophenol
through the use of derivative products such as fungicides used for pre-
serving wood, leather, and glue. This exposure is expected to be pri-
marily occupational during the process of chemical treatment. Exposure
levels could not be quantified since the chemical composition and appli-
cation rates of these compounds are unknown. There may be exposure to
volatilization of 2,4-dichlorophenol during application of the widely
used herbicide 2,4-D; however, no specific information regarding this
exposure was available.
5.3.4 Dermal Absorption
Due to their lipid-solubility and low degree of ionization at typical
biological pH, the chlorophenols are theoretically expected to be absorbed
through intact skin (Farquharson _et_ a.1. 1958) . The only information
5-14
-------
available on absorption of chlorophenols indicated that 2,4,6-trichloro-
phenol in a 0.09% solution permeated a human epidermal membrane In vitro
without causing harm (Roberts et al. 1977). No other data were provided.
Dermal absorption of chlorophenols from either surface of municipal water
supplies is expected to be minimal due to the low concentrations (<50 ug/D
usually detected (see Section 5.3.2.1). Exposure to higher concentrations
would be expected in occupational settings such as at chemical production
plants, textile and leather process plants, and in certain wood preserving
operations.
5-15
-------
REFERENCES
Ataer, S.M.; All, E.M. Cytological effects pesticides. V. Effect of
U?S? EP?1979)eS °n^£^f^a. Cytologia 33,633; 1974. (As cited in
Angel, A.; Rogers, K.J. An analysis of the convulsant activity of sub-
stituted benzenes in the mouse. Toxicol. and Appl. Pharmac. 21:214-229;
tell^T PpbUC Hf^^/ssociation (APHA) . Report received from Lois L.
Gerchman, Poison Lab, Enbionics; 1979. (As cited in U.S. EPA 1979)
Boutvell, R.K.; Bosch, D.K. The tumor-promoting action of phenol and
related compounds for mouse skin. Cancer Res. 19:413-424; 1959.
Hoe *>
J-S>; Radeleff> R'D-J Crookshank, H.R.; Farr, F.M.
in tl«u« nf hl°rOPheT7 aCld herbicides and ^eir phenolic metabolites
in tissues of sheep and cattle. J. Agric. Food Chem. 23(3) :573-578; 1975
(As cited
Dodgson K.S.; Smith, J.N.; Williams, R.T. Biochem. J. 46:
(As cited in Williams 1959) °.
Hardell, L. Malignant lymphoma of histiocytic type and exposure to
phenoxyacetic acids or chlorophenols . Lancet 1, ISS 8106, 55-56; 1979.
artRpn L.; Fishbein, L. ;
MitcheU I till*' ^J';.BateS' R;R'; FSlk' H'L-; Gart' J'J' Klein, M.;
for tSi;^:f- I ' • Bl°assay of P^ticides and industrial chemicals
' Preliminar^ note' J' ^t. Cancer Inst.
5-16
-------
Karpow, G. On the antiseptic action of three isomeric chlorophenols
and their salicylate esters and their fate in the metabolism. Arch.
Sci. Biol. St. Petersburg 2:304; 1893. (As cited in U.S. EPA 1979)
Kobayashi, S.; Toida, S.; Kawamura, H.; Chang, H.S.; Fukuda, T.;
Kawaguchi, K. Chronic toxicity of 2,4-dichlorophenol in mice a simple
design for the toxicity of residual metabolites of pesticides. J. Med.
Soc. Toho, Japan 19(3-4):356-362; 1972.
Kohli, J. et_ al. The metabolism of higher chlorinated benzene isomers.
Can. Jour. Biochem. 54:203; 1976. (As cited in U.S. EPA 1979)
Korte, F. et_ al_. Ecotoxicologic profile analysis, a concept for establish-
ing ecotoxicologic priority list for chemicals. Chemosphere 7:79; 1978. (As
cited in U.S. EPA 1979)
Kozak, V.P.; Simsiman, G.V.; Chesters, G.; Stensby, D.; Harkin, J.
Reviews of the environmental effects of pollutant: XI. Chlorophenols.
Washington, DC: Office of Research and Development, U.S. Environmental
Protection Agency; 1979.
Kurihara, N. Urinary metabolites from y " B-BHC in the mouse: chloroi-
phenolic conjugates. Environ. Qual. Saf. 4:56; 1975. (As cited in U.S.
EPA 1979)
Lindsay-Smith, J.R.; Shaw, B.A.; Foulkes, D.M. Mechanisms of mammalian
hydroxylation: some novel metabolites of chlorobenzene. Xenobiotica
2(3):215-226; 1972.
Mitsuda, H.; Murakami,K.; Kawai, F. Effect of chlorophenol analogues
on the oxidative phosphorylation in rat liver mitochondria. Agr. Biol.
Chem. 27(5):366-372; 1963.
Miura, H.; Ohmori, S.; Yamakawa, M. Are chlorinated phenols capable to
induce hepatic porphyria? Jap. J. Ind. Health 20:162-173; 1978.
National Cancer Institute (NCI). Bioassay of 2,4,6-trichlorophenol for
possible carcinogenicity. NCI Tech. Rep. Ser. 155:1-115; 1979.
Nethery, A.A.; Wilson, G.B. Classification of the cytological activity
of phenols and aromatic organophosphates. Cytologia 31:270-275; 1966.
Olie, K. _et. _al^ Chlorodibenzo-p-dioxins and chlorodibenzo-furans are
trace components of fly ash and flue gas of some municipal incinerators
in the Netherlands. Chemosphere 8:445; 1977. (As cited in U.S. EPA
1980c)
Rasanen, L.; Hattula, M.L.; Arstila, A.U. The mutagenicity of MCPA and
it soil metabolites, chlorinated phenols, catechols and some widely used
slimicides in Finland. Bull. Environ. Contain. Toxicol. 18(5):565-571;
1977.
5-17
-------
Registry of Toxic Effects of Chemical Substances (RTECS). Washington,
DC: U.S. Department of Health, Education and Welfare; 1978.
Roberts, M.A.; Anderson, R. A.; Swarbrick, J. Permeability of human
epidermis to phenolic compounds. J. Pharm. Pharmacol. 29(11) 5677^-683;
JL7 / / •
Selander, H.G.; Jerina, D.M.; Daly, J. W. Metabolism of chlorobenzene
with hepatic microsomes and solubilized cytochrome Pr-450 systems. Arch.
of Biochem. and Biophysics 168:309-321; 1975.
Spencer, B.; Williams, R.T. Biochem. J. 47:279; 1950. (As cited in
Williams 1959)
U.S. Department of Agriculture (USDA). Food consumption, prices,
expenditures, economics, statistics, and cooperatives service. Supple-
ment for 1976 to Agricultural Economic Report No. 138. Washington, DC:
U.S. Department of Agriculture; 1979.
U.S. Environmental Protection Agency (U.S. EPA). National Organics
Monitoring Survey (NOMS). Washignton, DC: Office of Water Supoly,
U.S. Environmental Protection Agency; 1978.
U.S. Environmental Protection Agency (U.S. EPA). Proposed ambient water
quality criteria—2-chlorophenol; 2,4-dichlorophenol; chlorinated phenols.
Draft. Washington, DC: Criteria and Standards Division, Office of Water
Planning and Standards; 1979.
U.S. Environmental Protection Agency (U.S. EPA). Ambient water quality
criteria for 2-chlorophenol. EPA 400/5-80-034. Washington, DC: Office
of Water Regulations and Standards, U.S. Environmental Protection Agency;
1980a.
U.S. Environmental Protection Agency (U.S. EPA). Ambient water quality
criteria for 2,4-chlorophenol. EPA 400/5*-80-042. Washington, DC:
Office of Water Regulations and Standards; U.S. Environmental Protection
Agency; 1980b.
U.S. Environmental Protection Agency (U.S. EPA). Ambient water quality
criteria for chlorinated phenols. EPA-400/5r80-032. Washington, DC:
Office of Water Regulations and Standards, U.S. Environmental Protection
Agency; 1980c.
Vernot, E.H.; MacEwen, J.D.; Haun, C.C.; Kinkead, E.R. Acute toxicity
and skin corrosion data for some organic and inorganic compounds and
aqueous solutions. Toxicol. and Appl. Pharmacol. 42:417-423; 1977.
Williams, R.T. Detoxification mechanisms, 2nd ed. J. Wiley & Sons Inc
New York, NY; 297-302. 1959. "'
5-18
-------
6.0. EFFECTS AND EXPOSURE—AQUATIC BIOTA
6.1 SUMMARY
The lowest concentration of 2-chlorophenol (2-CP) at which toxic
effects have been reported in a freshwater organism was 2.58 mg/1, a
48-hour LCsgfor Daphnia magna (water flea). The lowest reported LC50
for a vertebrate to 2-CP was 6.6 mg/1 for the bluegill. The compound
2,4-dichlorophenol (2,4-DCP) appears somewhat more toxic to the bluegill,
with the only LCsg reported at 2.02 mg/1. For the compound 2,4,6-tri-
chlorophenol (2,4,6-TCP) the LC5o for bluegill was substantially lower,
0.32 mg/1. LCso values for Daphnia magna did not vary significantly
among the three compounds. Chronic levels for Pimephales promelas
(fathead minnow) were reported at >3,9 mg/1, 0.37 mg/1, and 0,72 mg/1
for 2-CP, 2,4-DCP and 2,4,6-TCP, respectively.
The alga Chlorella pyrenoidosa was apparently much more sensitive
than either fish or daphnids to variations in the degree of chlorination
in the phenol with successive increases in phenol chlorine content. The
duckweed was approximately ten times as sensitive to 2,4,6-TCP as to
2,4-DCP. Since toxicity values for pentachlorophenol are generally in
the 0.01 to 1.0 mg/1 range, it appears that toxicity generally increased
for all aquatic species with increasing chlorination of phenol.
One study found that water hardness had no effect on the toxicity
of 2-CP to fathead minnows, but other species and the other chlorinated
phenols remain to be tested. It has been hypothesized that the toxicity
of a substituted phenol increases as the pH of the solution approaches
the pKa (dissociation constant) value of the phenolic compound. However,
this parameter has not been tested using any of the three chlorinated
phenols.
Very limited information was available concerning the exposure of
aquatic life to chlorophenols in the environment. The monitoring data
for all three chlorophenols in ambient surface waters are, for the most
part, at or below analytical detection limits, usually less than 0.01 mg/1.
A few observations were between 0.01 and 0.1 mg/1. At least three fish
kills have been attributed to chlorophenols accidently released from
chemical plants and a cooling tower. Therefore, occasionally aquatic
life are exposed to much higher concentrations than the monitoring data
indicate.
6.2 EFFECTS ON AQUATIC BIOTA
6.2.1 Introduction
This section provides laboratory information about the levels of
2-CP, 2,4-DCP, and 2,4,6-TCP at which the normal behavior and metabolic
processes of aquatic organisms are disrupted. Limited data were avail-
able representing only a few aquatic species.
6-1
-------
Most of the available data were derived from, static bioassays,
which are usually less reliable than continuous-flow experiments because
there is less control of toxicant concentrations. This is especially
important for the relatively volatile chlorophenols which undergo a
decrease in concentration due to volatilization over the course of a
toxicity experiment.
No information on the toxicity of chlorinated phenols to terrestrial
organisms was available.
6.2.2 Freshwater Organisms
6.2.2.1 Chronic and Sublethal Effects
Low levels of toxicants which remain for extended periods are
generally considered to represent "normally" polluted conditions in
natural waterways. Under these circumstances, aquatic biota may become
acclimated to the pollutant, or they may exhibit certain behavioral or
physiological symptoms. Prolonged exposure even to low concentrations
of chlorinated phenols could ultimately result in mortality. Even if
fish are not killed by long-term exposure to these toxicants, the
survival of local populations may be endangered.
The chronic values for fathead minnows (Pimephales promelas) for
2-CP, 2,4-DCP, 2,4,6-TCP, as determined by U.S. EPA (1980a,1980b,1980c)
are >3.9 mg/1, 0.37 mg/1, and 0.72 mg/1, respectively. In eight-day
chronic bioassays with fathead minnows, Phipps et al. (manuscript)
determined LC50 values of 6.34 mg/1 and 6.5 mg/1 for 2-CP and 2,4-DCP,
respectively. In static bioassays conducted by Applegate et al. (1957),
bluegill sunfish (Lepomis macrochirus) and sea lamprey larvae (Petromyzon
marinus) were exposed to 5.0 mg/1 2,4-DCP. Both species became '"ill,"
in 0.5 hour and 1 hour, respectively.
Telford (1974) reported increased glucose levels in the blood of
three species of crayfish (Oronectes propinquus. (). immunis, and Cambarus
robustus) after 10 days of exposure to 1.0 mg/1 2,4-DCP. A 14% mortality
was also observed during this period.
6.2.2.2 Acute Effects
Acute toxicity is defined as toxicant-induced mortality over a short
period of time, generally within 96 hours, Although fish in natural
waterways are more likely to be exposed to lower concentrations which
may produce chronic or sublethal effects, industrial discharges and
spills can temporarily result in levels high enough to cause fish kills
(see Section 6.3.3 of this chapter).
6-2
-------
A summary of reported LCso values in short-term toxicity tests with
the three chlorinated phenols is given in Table 6-1. The lowest LCso
derived for 2,4,6- TCP (0.32 mg/1) is considerably lox
-------
TABLE 6-1. ACUTE TOXICITY (LC50) OF CHLORINATED
PHENOLS TO AQUATIC ANIMALS
Range of
Concentrations
Ong/1)
6.6-10.0
11.6-14.5
12.3
20.2
58. Oa
2.02
8.23
0.32
0.6-9.04
Species
Fish
Bluegill (Lepomis macrochirus)
Fathead minnow (Pimephales promelas)
Goldfish (Carassius auratus)
Guppy (Poecilia reticulatus)
"Minnows"
Bluegill (Lepomis macrochirus)
Fathead minnow (Pimephales promelas)
Bluegill (Lepomis macrochirus)
Fathead minnow (Pimephales promelas)
Compound
2-Chlorophenol
2-Chlorophenol
2-Chlorophenol
2-Chlorophenol
2-Chlorophenol
2,4-Dichlorophenol
2,4-Dichlorophenol
2,4,6-Trichlorophenol
2,4,6-Trichlorophenol
Invertebrates
2.58-7.43
2.60-11.Ol
6.04
Daphnia magna
Daphnia magna
Daphnia magna
2-Chlorophenol
2,4-Dichlorophenol
2,4,6-Trichlorophenol
Ingols and Gaffney (1966).
Bringmann and Kuhn (1977).
Source: Data compiled from EPA (1980a, 1980b, 1980c), unless otherwise
noted.
6-4
-------
the three chlorinated phenols. Pickering aind Henderson (1966) exposed
fathead minnows to 2-CP in 24-hour, 48-hour, and 96-hour acute tests in
either soft water (20 mg/1 hardness) or hard water (360 mg/1 hardness).
The resultant LC5QS revealed no significant differences in sensitivity
to the two test solutions.
Blackman _ejt al. (1955) have hypothesized that the toxicity of a sub-
stituted phenol increases as the pH of the solution approaches the pKa
value of the phenolic compound. If this were true, the toxicity of 2-CP,
2,4-DCP, and 2,4,6-TCP would be greatest at pHs of 8.4, 7.4, and 6.0, respec-
tively. However, this is a theoretical conclusion, and remains to be corrob-
orated by experimentation with specific compounds over a selected pH range.
6.2.5 Water Quality Criteria
The U.S. Environmental Protection Agency's Division of Water Quality
Criteria and Standards has not proposed specific criteria for any of the
chlorinated phenols for the protection of aquatic life due to lack of
sufficient data (U.S. EPA 1980a, U.S. EPA 1980b, U.S. EPA 1980c). The
lowest effects levels reported in the support document are the same as
those described in the preceeding section.
6.3 EXPOSURE TO AQUATIC BIOTA
6.3.1 Introduction
Information on the levels of chlorophenols in the aquatic environ-
ment is extremely limited. The monitoring data from most regions in
the United States are so scarce that any generalizations would be
unreliable. There are a few instances of fish kills caused by the
release of chlorophenols into natural water bodies, indicating that
chlorophenols do occasionally appear at levels harmful to aquatic life.
No data on terrestrial exposure were available; however, some exposure
would be expected to be associated with the 2,4-dichlorophenol present
as an impurity and degradation product of the widely used herbicide 2,4-D.
6.3.2 Monitoring Data
The data provided by STORET (U.S. EPA 1979a) on chlorophenol levels
in ambient waters of major U.S. river basins during 1977-1979 amount to
barely 300 observations, indicating that these chemicals are monitored
infrequently (see Section!4.4). The only regions in which more than ten
measurements for any of the phenols were reported were Lake Michigan,
the Missouri River basin, and the Pacific Northwest. For 2-CP, 2,4-DCP,
and 2,4,6-TCP, the Pacific Northwest appears to have the highest concen-
trations, with 108 (71%) of the 153 observations in the 10.1-100 yg/1
category. For the United States excluding the Pacific Northwest, a
large majority of the measurements are between 1.1 yg/1 and 10.0 ug/1 for
the three phenolics, while only 4-8% are between 10.1 yg/1 and 100 yg/1.
It should be noted that virtually all available data are either at or
below the level of detection, indicating that the concentration distribution
6-5
-------
represented tends to overestimate the concentrations actually present
in the samples.
6.3.3 Exposure to Industrial Effluents
Concentrations of chlorophenols in industrial effluents have been
reported in excess of ambient levels (see Tables 3-5 and 4-6). Indusr-
tries with relatively high average effluent concentrations of 2,4-di-
chlorophenol include timber finishing plants (84 mg/1), timber barking
plants (3.2 mg/1), leather tanners (1.1 mg/1) and pesticide producers
(73.2 mg/1 in wastewater). High concentrations of 2,4,6-trichlorophenol
are discharged by the timber industry (up to 3 mg/1), paint and ink
plants (2.4 ug/1) and pesticide producers (up to 2.8 mg/1 in wastewater).
Information on 2-dichlorophenol is much more limited; one pesticide
plant had a concentration of 2.8 mg/1 in wastewater.
These data suggest that aquatic life in the vicinity of effluent
pipes may be exposed to chlorophenol concentrations significantly higher
than those reported in STORET. As reviewed in Chapter 4.0, the available
concentration would be reduced by dilution in the receiving waters,
adsorption onto sediment and volatilization to the atmosphere, especially
in aerated waters. Biodegradation may reduce concentrations of 2-chloro-
phenol and 2,4-dichlorophenol significantly within one to two weeks in
the presence of acclimated active microbial populations.
6.3.4 Fish Kill Data
Table 6-2 provides information on the location of and activities
associated with fish kills attributed to chlorophenols between 1971 and
1974. Unfortunately, no data on aqueous concentrations were given in
the reports nor were other toxic substances present in the spill (e.g.
pentachlorophenol) always identified. It is impossible to speculate
upon the most frequent sources of chlorophenol emissions on the basis
of such_limited evidence. However, since chlorophenols are used primarily
by chemical plants, it is likely that spills and discharges will occur
more frequently in areas which are densely industrialized than in rural
areas. In addition, spills associated with releases from chlorophenol-
treated industrial cooling waters would have a similar national distri-
bution.
6-6
-------
TABLE 6-2. DATA ON FISH KILLS ATTRIBUTED TO CHLORINATED PHENOLS
(1971-1974)
Year
1971
1973
1974
Water Body
Allen Creek
Anderson Creek
Fourmile Creek
and tributaries
Location
Rochester, NY
Anderson, CA
Model City, NY
Duration
2 days
34 days
3 days
Number Killed
2,000
700
Severe
Cause
Possibly chlorinated phenols
from air cond. system
in cooling tower.
Wood preserv. storage
tanks discharge of "poly-
chlorinated phenols and
phenates" to sawmill waste
collection system, then to
Anderson Creek
Break in 2,4-DCP holding
dike
Source: U.S. EPA (1979b).
-------
REFERENCES
Applegate, V.C., Howell, J.H.; Hall, A.E.; Smith, M.A. Toxicity of
4,346 chemicals to larval lampreys and fishes. U.S. Fish Wildlife Serv.,
Spec. Sci. Kept. - Fish., No. 207; 1957. (As cited in Becker and
Thatcher 1973).
Batte, E.G.; Swanson, L.E. Laboratory evaluation of organic compounds
as mulluscacides and ovocides. II. Four. Parasitol. 38:65; 1952. (As
cited in U.S. EPA 1980c)
Becker, C.C.; Thatcher, T.O. Toxicity of power plant chemicals to
aquatic life. WASH-1249. Washington, DC: U.S. Atomic Energy Commission;
i? / J •
Blackman, G.E.; Parke, M.H.; Carton, C. The physiological activity of sub-
stituted phenols, II. Relationships betveen physical properties and
physiological activity. Arch. Biochem. Biophys., 54:55-71; 1955. (As
cited in Buikema .et .al. 1979) .
Bringmann, G.; Kuhn, R. Befunde der Schadwirkung wasser gefahrdender
Stoffe gegen Daphnia magna. Z. fur wasser und Abwasser forschung
10(5): 151-166; 1977. (As cited in Buikema _et _al. 1979)
Buikema, A.L., McGuiness, M.J.; Cairns, J. Phenolics in aquatic eco-
systems: A selected review of recent literature. Mar. Environ. Res.
2:87-181; 1979.
Gersdorff, W.A.; Smith, L.E. Effect of introduction of the halogens
into the phenol molecule on toxicity to goldfish. I. Monochlorophenols.
Am. J. Pharmacol. 112:197; 1940. (As cited in U.S. EPA 1980a)
Hiatt, R.W., _et_al. Effects of chemicals on a schooling fish. Biol
Bull. 104:28; 1953. (As cited in U.S. EPA 1980b).
Huang, J.; Gloyna, E.F. Effect of organic compounds on photosynthetic
oxygenation. I. Chlorophyll destruction and suppression of photosyn-
thetic oxygen production. Water Research 2:347-366; 1968.
Ingols, R.S.; Gaffrey, P.E.; Stevenson, P.C. Biological activity of
halophenols. J. Water Pollut. Fed. 38(4):629-635; 1966.
Phipps, G.L, et.al. The acute toxicity of phenol and substituted phenols
to the fathead minnow. (Manuscript). (As cited in U.S. EPA 1980a).
Pickering, Q.H.; Henderson, C. Acute toxicity of some important petro-
chemicals to fish. J. Water Pollut. Control Fed. 38(9): 1419-1426;
1966.
Telford, M. Blood glucose in crayfish. II. Variations induced by
artificial stress. Comp. Biochem. Physiol., 48A:555-560- 1974 (\s
cited in Buikema et al. 1979).
.6-8
-------
U.S. Environmental Protection Agency (U.S. EPA). STORET. Washington,
D.C.: Monitoring and Data Support Division, U.S. Environmental Protection
Agency; 1979a.
U.S. Environmental Protection Agency (U.S. EPA). Fish kill data.
Washington, D.C.: Monitoring and Data Support Division, U.S. Environ-
mental Protection Agency; 197-9b.
U.S. Environmental Protection Agency (U.S. EPA). Ambient water quality
criteria for 2-chlorophenol. EPA 400/5-80-034, Washington, D.C.: Office
of Water Regulations and Standards, U.S. Environmental Protection Agency;
1980a.
U.S. Environmental Protection Agency (U.S. EPA). Ambient water quality
criteria for 2,4-dichlorophenol. EPA 400/5-80-042, Washington, D.C.:
Office of Water Regulations and Standards, U.S. Environmental Protection
Agency; 1980b.
U.S. Environmental Protection Agency (U.S. EPA). Ambient water quality
criteria for chlorinated phenols. EPA 400/5-8CW332, Washington, D.C.:
Office of Water Regulations and Standards, U.S. Environmental Protection
Agency; 1980c.
6-9
-------
7.0 RISK CONSIDERATIONS
7.1 INTRODUCTION
The purpose of this chapter is to evaluate the potential risks to
humans and aquatic biota resulting from exposure to environmental con-
centrations of chlorophenols. The analysis of risk is reduced by a
limited data base regarding the health effects of mono- and dichloro-
phenol and environmental monitoring data for all three chlorophenols
which permit no more than very general estimates of exposure levels.
In this chapter the two lesser chlorinated phenols are discussed sepa-
rately from 2,4,6-trichlorophenol because the lack of dose-response data
for the two compounds necessitates different treatment in the estimation
of risk.
7.2 HUMANS
7.2.1 Statement of Risk
A quantitative estimate of human risk resulting from chronic environ-
mental exposure to chlorophenols can only be made for 2,4,6-trichlorophenol
(2,4,6-TCP). The limited availability of toxicological data for 2-chloro-
phenol (2-CP) and 2,4-dichlorophenol (2,4-DCP) prevents an equivalent
analysis for these compounds. Lifetime feeding of male mice with 2,4,6-
trichlorophenol at -\-600 mg/kg/day (5,000 ppm in diet) resulted in an
increased incidence of hepatocellular carcinoma or adenoma above controls.
Based on the results of several extrapolations of the animal data to esti-
mate human dose-response, the predicted excess lifetime risk to humans of
developing cancer from exposure to 10 yg/day, 100 yg/day, or 1,000 yg/day
of 2,4,6-trichlorophenol is 0.1 to 3 x 1Q-6, 0.4 to 3 x 10~5, and 2 to
3 x 10-\ respectively. Daily exposure to 2,4,6-trichlorophenol
through drinking water only was estimated to range from 0.4 yg/day as a
typical exposure level to 60 yg/day as a maximum which would be associ-
ated with a per capita risk of 1 x lO'10 to 2 x 1(T5. Fisheaters were
estimated to be exposed to a maximum of 155 yg/day with a per capita
risk between 1 x 10~5 and 5 x 10~5.
Humans are rarely exposed to concentrations of 2-chlorophenol and
2,4-dichlorophenol in environmental media that are high enough to cause
adverse effects. This is based on a very limited data base regarding
both exposure and toxicological effects levels. The lowest effects level
for 2,4-dichlorophenol is 7,000 mg/day, estimated for long-term exposure*
through ingestion. The maximum exposure level for humans drinking con-
taminated water and ingesting beef kidneys is four orders of magnitude
below the effects level. No long-term feeding studies are available for
2-chlorophenol. Exposure levels, however, are significantly below acute
and subacute effects levels.
7'2'2 Effects and Exposure Levels for Chlorophenols
ri. Tab=SrJ~l summarizes the exposure estimates described previously in
Chapter 5.0. It is apparent that fish consumption presents the gresfest
fSf eXp°SUr? t0 ^lorinated phenols; no information regarding actual
chlorophenols in fish were available. Beef kidney consumption may
-------
TABLE 7-1. HUMAN EXPOSURE TO CHLORINATED PHENOLS THROUGH 1NGESTION
(ng/day)
Drinking water
2-Chlorophenql 2,A-Dichlorophenol
100 60
0.4C
O.A
2,4 ,6-Trlchlorophcnol
60
0.4a
Comments
Maximum ambient concen-
tration of 30 Mg/1.
Consumption of 2 I/day.
Mean concentration
reported in drinking water
(of positive values).
Consumption of 2 I/day.
Food
Fish
137
26
95
I
NJ
27
32
Beef kidney - 280
a
No information was available on typical levels of these substances in drinking water.
were assumed to be equivalent to those reported for 2,4-dichlorophenol.
Source: Chapter 5.0.
Maximum of all mean major
river basin concentrations
reported in ambient water
approximately 30 pg/1 for
2,4-DCP and 2,4,6-TCP;
50 pg/1 for 2-CP.
Respective BCF of 130,
40.7, and 150. Fish
consumption of 21 g/day.
Mean of all major river
basin concentrations
approximately 10 Mg/1.
Same assumptions as above.
Maximum concentration
reported in beef kidney
(560 ug/kg). Kidney
consumption of 0.5 day.
Concentrations
-------
also be a significant exposure route for 2,4-dichlorophenol: however,
due to rapid metabolism and clearance of the substance in mammals , this
estimate represents a worst case. Consumption of contaminated drinking
water is the only known exposure route for humans.
Tables 7-2, 7-3, and 7-4 describe lowest reported effect levels and
no-effect levels, if available, for 2-CP, 2,4-DCP, and 2,4,6-rCP,
respectively.
It has been shown that ingested 2,4,6-TCP is carcinogenic in male
rats and both sexes of mice. No chronic feeding studies are avail-
able for the other two chlorinated phenols considered here;however,
they both have been shown to possess tumors-promoting activity when'
applied dermally to mice, probably a result of an irritant response and
of no relevance to ingestion exposures. Chromatid deletions have been
reported in bone marrow cells of mice given 130 mg/kg 2-chlorophenol every
other day for one week; data on the mutagenic activity of the other two
compounds are inadequate. There is also no information available on the
effects of these 3 chlorinated phenols on reproduction. Lethal oral doses for
2-CP and 2,4,6-TCP are in the 100 mg/kg to 900 mg/kg range, while 2,4-DCP is
somewhat less toxic. An acceptable daily intake level of 7 ms/day has been
proposed for human consumption of 2,4-dichlorophenol by the U.S. EPA (1980a).
Section 7.2.3 discusses the risk of adverse human exposure to 2,4,
6-trichlorophenol and Section 7.2.4 addresses the risks associated with
exposure to 2-chlorophenol or 2,4-dichlorophenol.
7•2•3 Risk of Exposure to 2.4.6-Trichlorophenol
7-2-3.1 Carcinogenicity of 2,4,6-Trichlorophenol
In this section, the potential carcinogenic risk to human? due to
2,4,6-trichlorophenol ingestion is estimated. Ideally, this problem
would be dealt with in two ways: FrODj.em
• Various extrapolation models would be applied to occupa-
tional vs. ambient human exposure data (from retrospec-
tive studies) in order to obtain an approximate dose-.
response relationship.
• These same models would be applied to data from rontrolled
experiments on laboratory animals, and i_V^• aninm dose-
response relationship would bS converted to an astimated
human dose-response.
In the first approach, the overriding uncertainty i- ± ..^ d
selves; usually the exposure levels, lengths of expose, and even "~
response rates (responses per number exposed) are "besc estimates " *nH
furthermore unknown factors (background effects, etc?' may^as the '
data. In the second approach, the data are usually -.ore accurate bin-
the relationship between animal and human response'rates must be '
7-3
-------
TABLE 7-2. ADVERSE EFFECTS OF 2-CHLOROPHENOL IN MAMMALS
Adverse Effect Species
Carcinogenic!ty
ingestion
promotion DMBA- Mouse
induced tumors
Chromatid Mouse
deletions
Altered liver Rat
function/pathology
Teratogenesis
Oral LD50 Mouse
Lowest Reported
Effect Level
No data available
25 uI/mouse two times
per week, 20% soln.,
15 weeks
130 mg/kg every other
day for one week
(bone marrow cells)
65 mg/kg every
other day for 3 weeks
No data available
670 mg/kg
No Apparent
Effect Level
Source: Section 5.1.
7-4
-------
TABLE 7-3. ADVERSE EFFECTS OF 2,4-DICHLOROPHENOL IN MAMMALS
Adverse Effect Species
Carcinogenicity
ingestion
promotion DMBA- Mouse
induced tumors
Liver abnormalities Mouse
Teratogenesis
Oral
No effect level
Mouse
Humans
Lowest Reported
Effect Level
No data available
25 uI/mouse two times
per week 20% soln.,
15 weeks
"230 mg/kg/day for 6 mo.
No data available
1,600 mg/kg
No Apparent
Effect Level
'100 mg/kg/day
for 6 mo.
Acceptable Daily
Intake (ADI)a is
7 mg/day.
As reported by U.S. EPA (1980a).
Source: Section 5.1.
7-5
-------
TABLE 7-4. ADVERSE EFFECTS OF 2,4,6-TRICHLOROPHENOL IN MAMMALS
Adverse
Effect
Species
Hepatocellular Mouse
Carcinoma
Lowest Reported
Effect Level
5,000 mg/kg diet for
2 years3
No Apparent
Effect Level
Lymphoma/
Leukemia
Rat
5,000 mg/kg diet for
2 yearsb
Reticulum-cell Mouse
Sarcoma
260 mg/kg for 18 months
Promotion DMBA- Mouse
Induced Tumors
25 yl/mouse 2 times per
week, 20% soln.,
15 weeks
Teratogenesis
No data available
Oral LDLo
Man
500 mg/kg
Approximately 600 mg/kg for humans assuming a 25-gram mouse eats 3 grams
of feed daily.
Approximately 250 mg/kg for humans assuming a 180-gram rat eats 9 grams
of feed daily.
Source: Section 5.1.
7-6
-------
questioned. At present there is no universally accepted solution to
this problem. In short, in the former case relevant data are of ques-
tionable validity; in the latter case valid data are of questionable
relevance. If it is possible to perform both analyses and the results
corroborate each other, confidence is gained in these results. If, on
the other hand, data are not available for one of the two analyses and
some result is assumed to be better than no result, the analysis must
be performed based upon the available data.
Further complicating the issue, at present, is that there is no
basis for judging the relative merits of the various extrapolation
models. It is impossible to say which, if any, of them is correct.
However, the models applied here are believed to be conservative (i.e.,
tend to overestimate the true risk).
7.2.3.2 Discussion of Available Data
The available data concerning human and other mammalian effects
were discussed in Section 5.1.2. For 2,4,6-trichlorophenol, the best
quantitative carcinogenicity data currently available are from a National
Cancer 'Institute study (NCI 1979) with male and female F344 rats and B6C3F1
mice. The data indicate increased incidence of lymphoma or leukemia in
male rats and of hepatocellular carcinoma or adenoma in both sexes of
mice fed 2,4,6-trichlorophenol in the diet. The dose-response data
from the study are listed in Table 7-5.
To deal with the uncertainties inherent in extrapolation, three
commonly used dose-response models have been applied to the data in the
table to establish a range of potential human risk. The assessment of
potential human risk based on these models is subject to a number of
important qualifications and assumptions:
• In view of possible species differences in susceptibility,
pharmacokinetics, and repair mechanisms, the carcinogeni-
city of 2,4,6-trichlorophenol to humans is far from
certain.
• Assuming that the positive findings indeed provide a
basis for extrapolation to humans, the estimation of
equivalent human doses involves considerable uncer-
tainty. Scaling factors may be based on a number of
variables, including relative body weights, body
surface areas, and life spans.
• The large difference between the typically high experir-
mental doses and the actual human exposure levels intro-
duces uncertainty into the extrapolation from animals
to humans. Due to inadequate understanding of the
mechanisms of carcinogenesis, there is no scientific
basis for selecting among several alternate dose-
response models, which yield differing results.
7-7
-------
TABLE 7-5. CARCINOGENIC RESPONSE IN RATS AND MICE
FED 2,4,6-TRICHLOROPHENOL IN THE DIET
I
oo
Concentration in
Animals' Food
Equivalent Human
Dosea
Percent Excess
Male Ratsb
Male Mice0
Female Mice
Human dose =
(mg/day)
bp, .
10,000
5,000
0
10,000
5,000
0
10,428
5,214
0
Concentration in Pood
(mg/kg) x
5,400
2,700
0
5,600
2,800
0
5,840
2,920
0
Animal Food
Intake (mg/day)
29/50
25/50
4/20
39/47
32/49
4/20
24/48
12/50
1/20
/Human
I Animal
58
50
20
83
65
20
50
24
5
weight \ 2/3
weight/ *
38
30
—
63
45
^
45
19
/Exposure Duration! ,„-*;
Total Animal 1* 1U .,
I Lifetime 1 »ier m8/k8
Exposure beginning at age 6 weeks} ending with sacrifice of rats after 106 weeks of exposure
J07 weeks for controls. * '
-Exposure beginning at age 6 weeksj ending with sacrifice of mice after 105 weeks of exposure.
for67week nMm r ' (1" diet) for 38 weeka fo11™^ W 5,000 mg/kg
for 67 weeks for time-weighted average of 10,428 mg/kg for 105 weeks, low dose group at 10,000 mg/kg for
38 weeks, 2,500 mg/kg for 67 weeks, average of .5,214 mg/kg for 105 weeks.
Source: NCI (1979).
-------
7.2.3.3 Calculations of Human Equivalent Doses
Obtaining a quantitative human risk estimate based on animal data
requires first determining the human dose equivalent to a given animal
dose. The approach used has been recommended by the EPA (Arthur D.
Little, Inc. 1980) and normalizes the dose rate according to body sur-
face area. This approach is relatively conservative in that it results
in a lower equivalent human dose than would be obtained from simple
multiplication of animal dose rate (mg/kg/day) by human body weight.
Whether the surface area or body weight ratio is the more appropriate
normalization factor is still open to debate. Neither ratio is ulti-
mately correct, however, since differing metabolisms and other factors
are ignored in either case. Since for mice the weight ratio is roughly
14 times the surface area ratio and for rats the weight ratio is roughly
6 times the surface area ratio, the choice of a conversion method intro-
duces an uncertainty of an order of magnitude at least.
The rats were exposed to 2,4,6-trichlorophenol in their diet begin-
ning at age 6 weeks and concluding with sacrifice of the rats after 106
weeks of exposure (107 weeks for controls), for a total rat lifetime of
112 weeks (113 weeks for controls). Male mice were exposed beginning
at age 6 weeks for 105 weeks, giving a total lifetime of 111 weeks. Female
mice were exposed at age 6 weeks. Females in the high^dose group were
exposed to 20,000 mg/kg in the diet for 38 weeks, followed by 5,000 mg/
kg for 67 weeks, for a weighted average dose of 10,428 mg/kg for 105
weeks. Females in the low-dose group were exposed to 10,000 mg/kg in
the diet for 38 weeks, followed by 2,500 rag/kg for 67 weeks, for a
weighted average dose of 5,214 mg/kg for 105 weeks. Total lifetime for
all females was 111 weeks.
From this information, assumed body weights of 70 kg, 0,3 kg, and
0.025 kg for humans, rats, and mice, respectively, and assumed daily in-
takes of 3 g/day for mice and 15 g/day for rats, a human equivalent
daily dose were estimated using the following equation-
Human Concentration Animal /Human \2^ /Exposure1"
Dose » in Food x Food Intake x 10~6 per / Weight) / Duration
(mg/day) (mg/kg) (mg/day) mg/kg I Animalf Total
\ Weight/ \ Animal
\Lifetimey
From this, a concentration in food of I mg/kg for mice is calculated to
be equivalent to a dose of roughly 0.56 mg/day for humans. Similarly,
1 ing/kg for rats is calculated to be equivalent to a dose of roughly
0.54 mg/day for humans.
7.2.3.4 Estimation of Human Risk
The three dose-response models used to extrapolate human risk were
the linear "one-hit" model, the log-probit model, and the multistage
model. The latter is actually a generalization of the one-hit model in
7-9
-------
which the hazard rate is taken to be a quadratic rather than a linear
function of dose. All of these models are well described in the
literature, and a thoretical discussion may be found in Arthur D.
Little, Inc. (1980). The one-hit and multistage models assume that the
probability of a carcinogenic response is described by
P (response at dose X) - 1 -
where h(x) is the "hazard rate" function. The logrprobit model assumes
that human response varies with dose according to a logo-normal distri-r
bution. Due to their differing assumptions, these dose-response models
usually give widely differing results when effects data are extrapolated
from relatively high doses to the low doses typical of environmental
exposure .
Since carcinogenic response in male mice was significantly higher
than that in female mice and rats at roughly the same exposure level
(see Table 7-5) , only the data relating to male mice were used for dose-
response extrapolation.
For the linear one-hit model, the equation
P(x) =1 -e~Bx,
where P(x) is the probability of response to dose x, is solved for the
parameter B. It may be shown that
R - I i A -
B " ln
x l - P(x)
\ ;
where P(o) is the average control group response and P(x) is the response
of the test group subjected to dose x. It is assumed that the "true"
B value is given by
B = (B • B B
X2 ........ ' ' xn
the geometric mean of the BXi from experimental data. From the data
obtained from the study on male mice, B is calculated to be approximately
3 x 10"4 per mg/day.
For the log-probit extrapolation, the "probit" intercept A results
from the following equation:
Pg(x) » is the cumulative normal distribution function, and Pe(x) is the
excess probability of response, Pe(x) = p (x) T P(o) ,
This equation makes the usual assumption that the log-probit dose-
response curve has unit slope with respect to the log-dose. From tables
7-10
-------
of the standard normal distribution, A (the geometric mea^ of the in-
dividually determined A^), is found to be approximately equal to -3.5.
This value was used to determine the probability of a response at various
concentrations according to the above equation.
The multistage model with a quadratic hazard rate function,
h(x) - ax + bx + c,
was also fit to the data. For estimating the parameters a, b, and c,
a maximum likelihood method was used, aided by a computer program that
performed a heuristic search for the best fit. It was found that a ~
1 x 10~10, b =. 3 x lO"4, and c =. 2 x 10"1. The probability of response
attributable to dose x is then given by
P(x) =l-e-(ax2'
Note that since the value of the parameter a is vastly less than the
value of b, P(x) varies linearly with dose for all doses below 1,000 mg/
day. In this case (mainly by coincidence), the multistage and linear
one-hit predictions are roughly identical. Normally, the multistage
model predicts lower risk than the linear model.
Table 7-6 summarizes the risk estimates obtained from these three
models. No attempt was made to determine statistical confidence bounds
for the results. The uncertainties inherent in choosing a dose-response
model and in determining a human equivalent dose make suspect any further
purely statistical analyses of the data.
The estimates in Table 7-6 represent probable upper bounds on the
true risk, since both the dose^response models and the estimation of
human equivalent dose are believed to be conservative. Note, however,
that the gap between the estimates is large in the low-dose region,
so there is substantial range of uncertainty concerning the actual
carcinogenic effects of 2,4,6-trichlorophenol. This points
to the general lack of understanding of the mechanisms of car-
cinogenicity.
EPA's Cancer Assessment Group (CAG) has not specified 2,4,6-trichloro-
phenol as a potential human carcinogen. The EPA Water Quality Standard
Division, however, calculated the risk associated with human exposure to
ambient levels of 2,4,6-trichlorophenol in water. The same NCI study
described previously was used and the CAG linear model was implemented
for the extrapolation of risk. Table 7-7 presents the criteria for pro-
tection of humans from exposure to 2,4,6-trichlorophenol concentrations
in surface water and the associated risk levels. Since the supporting
calculations were not presented in the criterion document for chlorinated
phenols, it was not possibly to compare the results of the four models.
7-11
-------
TABLE 7-6. ESTIMATED LIFETIME EXCESS PROBABILITY OF
CANCER TO HUMANS DUE TO INGESTION OF
2, 4, 6-TRICHLOROPHENOL AT VARIOUS EXPOSURE
LEVELS BASED ON THREE EXTRAPOLATION MODELS
I
Estimated Lifetime J2xcg_ssj^robabmt^jofj^
Extrapolation Exposure
___M°deL__ JNgvejLjmg/dayh Ojn OJ, 1 JQ 1QQ j_fooo
Linear Model 3 x 10"6 3 x ID'S 3 x 10~4 3 x 1Q_3 3 x 10_2 3 x 1Q-i
Log-Probit Model
-------
TABLE 7-7. U.S. EPA INTERIM TARGET RISK LEVELS AND CORRESPONDING
WATER QUALITY CRITERIA FOR 2,4,6-TRICHLOROPHENOL—
PROTECTION OF HUMAN HEALTH
Risk Levels and
Exposure Assumptions Corresponding Criteria (yg/1)
(per day)
10"7 IQ"6 10~5
2 liters of drinking water 0.12 1.2 12
and consumption of 6.5 grams
fish and shellfish
Consumption of fish and 0.36 3.6 36
shellfish only.
Source: U.S. EPA (1980b) , p. C-75.
7-13
-------
7.2.3.5 Conclusions
_ Daily exposure through drinking water to 2,4,6-trichlorophenol was
estimated to be 60 yg/day for a maximum exposure with an average level
around 0.4 yg/day (see Table 7-1). Fish-eaters are estimated to be
exposed to a maximum of 155 ug/day and an average level of 32 yg/day
assuming maximum and average drinking water exposure concurrently. The
only known exposure routes for the compound are through ingestion of
drinking water and contaminated fish. The average exposure through
f.1™5 water is based on ch*
-------
TABLE 7-8. ESTIMATES OF CARCINOGENIC RISK FOR
VARIOUS WATER-BORNE ROUTES OF
EXPOSURE TO 2,4,6-TRICHLOROPHENOL
Estimated Lifetime Excess Probability of Cancer^
Drinking Water Only Fish-Eaters
Model
average maximum average maximum
(0.4 ug/day) (60 us/day) 32 ug/day) (155 ug/day)
Linear and
multistage
1 x 10~7
2 x 10
,-5
9 x 10~6
5 x 10~5
Log-probit
x 10
~10
1 x KT6
3 x 10~7
1 x 10~5
A range of probability is given, based on several different dose-
response extrapolation models. The lifetime excess probability of
cancer represents the increase in probability of cancer over the
normal background incidence, assuming that an individual is
continuously exposed to 2,4,6-trichlorophenol at the indicated
daily intake over their lifetime. There is considerable variation
in the estimated risk due to uncertainty introduced by the use of
laboratory rodent data, by the conversion to equivalent human
dosage, and by the application of hypothetical dose-response
curves. In view of several conservative assumptions that were
utilized it is likely that these predictions overestimate the
actual risk to humans.
7-15
-------
7'2'4 !a!gJ:nS °f Sa!etY f°r E*P°«"~ • to 2-Chloroph^-, ,^
2 , 4-Dichlorophenol -- K -
7'1 Can be comPared with the
=-~^=£
tnis time are likely to result in the determination of lower effects
levels which would be reflected in a decreased margin of safety
Similarly, although the effects study for 2,4,dichlorophenJl is'a
longer-term study, it was not possible to evaluate the
eXposurerdaJa ^ * ^ ^^ °f uncertai^y associated with the
exposure data. Monitoring data were extremely limited with actual
sUar chsȣT " T 3re esti"a"s ^Sed on extrapolations fr
^ r^^-f^^^^^^^
£«--^
routes of exposure (inhalation, dermal absorption) due to lack of data!
7-16
-------
TABLE 7-9. MARGINS OF SAFETY FOR HUMAN EXPOSURE
TO 2-CHLOROPHENOL AND 2,4-DICHLOROPHENOL
2-Chlorophenol
• drinking water
Exposure
(pg/kg/day)'
Typical Maximum
0.006
fish consumption 0.4
TOTAL 0.4
1.4
2.0
3.4
Lowest Effects Margin of Safety
Level (ug/kg/day) Typical Maximum"
Altered liver
function:
65,OOQC
(orally every
other day for
3 weeks)
1 x 107
2 x 105
2 x 105
5 x 10 ^
3 x 10"
2 x 1U1*
2,4-Dichlorophenol
• drinking water 0.006
• fish consumption 0.1
• kidney
consumption
TOTAL
0.1
0.9
0.4
4.0
5.3
6 mo. no
effects level
a 100,000d
2 x 107 1 x 105
1 x 106 3 x 105
3 x lQk
1 x 105 2 x
Calculated for a 70-kg human.
^Effects level
Exposure level.
cResults of a single study (Chung 1978) with rats. The future availability of
chronic studies may substantially lower the lowest effects level.
d
Results of a single study (Kobayashi et al. 1972) on mice. The future
availability of chronic studies may substantially lower the lowest
effects level.
-------
Taking into account the large amount of uncertainty inherent in the
calculated margins of safety, it can be concluded that humans are rarely
exposed through ingestion to concentrations of 2-chlorophenol and 2,4-
dichlorophenol in environmental media that are high enough to cause
adverse effects. Exposure through dermal absorption is not expected to
be significant due to the low concentrations of chlorophenol in ambient
and drinking water. Human exposure through inhalation was not possible
to evaluate due to a lack of data. The highest inhalation^related exr-
posure would probably be through herbicide use, through occupational
exposure,and in subpopulations living in the vicinity of chemical pro-
duction plants. Atmospheric releases of chlorophenols are minimal on a
national level, so ambient air concentrations to which the majority of
the U.S. population are exposed are likely to be negligible. These
speculations require monitoring data for validation.
7.2.5 Recommendations
There are numerous areas in which additional work could strengthen
this exposure and risk assessment. While it is obvious that more moni-
toring and toxicological data are needed, other specific areas in which
further work is needed are:
• Investigations into the formation of chlorinated phenols
in soil and food items resulting from the use of
compounds such as 2,4-D and 2,4,6-T.
• More detailed descriptions of the uses of 2-CP, 2,4-DCP,
and 2,4,6-TCP and products containing them. Although
the compounds are largely used as intermediates,
significant exposure routes may result from other,
currently undefined uses of these compounds.
7.3 AQUATIC BIOTA
The monitoring data provided by STORET (U.S. EPA 1979) were in-
sufficient to allow estimation of chlorinated phenol exposure levels
to aquatic organisms on a national scale. Observations in major river
basins consisted of remarked data, all below 100 yg/1; a large majority
of the observations in the United States (excluding the Pacific North-
west) were between 1.1 Ug/l and 10.0 pg/1. In the Pacific Northwest
S6r^ !KSreat^t nUmber °f Sampl6S Was taken> 71% of the measurements
for the three chlorinated phenols fell between 10.1 yg/l and 100 0 us/1
This may indicate that less sensitive detection techniques were used in'
the analysis of samples from this basin rather than that there were
higher actual concentrations of chlorophenols. Monitoring for these
compounds should be conducted more frequently in all basins if an
accurate nationwide assessment of risk is to be made. The effects of
such aqueous parameters as pH, hardness, and temperature on the toxicitv
ot chlorinated phenols have not been studied adequately, therefore
their significance with regard to a geographical'analysis of risk is
7-18
-------
According to the toxicity data surveyed in the previous chapter,
the lowest level of any chlorinated phenol which produced toxic effects
in laboratory studies was 320 yg/1 for 2,4,6-TCP (an LC50 for bluegill).
None of the environmental concentrations reported in STORE! (1979-1979)
exceeded 100 ug/1 for any of the three compounds, which suggests that
aquatic biota are probably not at serious risk with respect to long-term
exposure to chlorinated phenols.
There is a possibility that chronic sublethal effects could appear
in aquatic organisms at concentrations well below 320 yg/1. Very few
species, and perhaps not the most susceptible ones, have been bioassayed
for their reactions to the chlorinated phenols, so the available data
may not accurately reflect the potential sensitivity of aquatic species
or ecosystems. There are indications that fish can fairly rapidly metabo-
lize and excrete low levels of chlorophenols, so the potential for long-
term sublethal effects may be reduced through this mechanism.
Several fish kills have been attributed to chlorophenols released
from wood-preserving and chemical production plants and from a cooling
tower discharge. The presence of other substances in the effluent
especially from the wood-preserving plant, may have contributed to the
adverse effects on the aquatic communities exposed. However, the inci-
dents suggest that there is a risk for aquatic species to -be acutely
exposed to adverse levels of chlorophenols. Chemical production plants,
wood-preserving facilities, and textile plants are expected to be the
most likely to spill chlorophenols at high enough concentrations to
result in deleterious effects on aquatic ecosystems.
7-19
-------
REFERENCES
Arthur D. Little, Inc. Methodology for exposure and risk assessment.
Mathematic appendix. Washington, DC: Office of Water Regulations and
Standards, U.S. Environmental Protection Agency; 1980.
Chung, Y. Studies on cytochemical toxicities of chlorophenols to rats.
Yakhak Hoe Chi 22(4): 175-192; 1978.
Kobayashi, S.; Tolda, S.; Kawamura, H.; Chang, H.S.; Fukuda, T.;
Kawaguchi, K. Chronic toxicity of 2,4-dichlorophenol in mice: a
simple design for the toxicity of residual metabolites of pesticides.
J. Med. Soc. Toho, Japan. 49:(304):355-362; 1972.
National Cancer Institute (NCI). Bioassay of 2,4,6-trichlorophenol
possible carcinogenicity. NCI-CG-TR-155. Washington, DC: National
Cancer Institute; 1979. (As cited in U.S. EPA 1980b).
U.S. Environmental Protection Agency (U.S. EPA). STORE!. Washington,
DC: Minitoring and Data Support Division, U.S. Environmental Protection
Agency; 1979.
U.S. Environmental Protection Agency (U.S. EPA), Ambient water quality
criteria for 2,4-dichlorophenol. EPA-400/5-80^-042, Washington, DC:
Office of Water Regulations and Standards, U.S. Environmental Protection
Agency; 1980a.
U.S. Environmental Protection Agency (U.S. EPA). Ambient water quality
criteria for chlorinated phenols. EPA-400/5-80-032. Washington, DC:
Office of Water Regulations and Standards, U.S. Environmental Protection
Agency; 1980b.
7-20
-------
APPENDIX A: PRODUCTION AND EMISSION ESTIMATES
1. PRODUCTION ESTIMATES
There are thirteen isomers of chlorophenols commercially available.
Production data on these compounds (except for 2,4-chlorophenol and
pentachlorophenol) are proprietary in order to protect each producer's
market position. Some producers only produce one of the isomers,
probably in very small quantities. Production estimates for the three
isomers addressed in this report are based on previously reported esti-
mates, the known production numbers on two of the isomers, and the
estimated amount of phenol used to manufacture these compounds. The
year 1977 has been chosen as the basis year.
AMOUNT OF PHENOL USED FOR CHLOROPHENOL PRODUCTION
Using data published by Monsanto Company, Versar, Inc. (1980) estimated
the amount of phenol used in chlorophenol manufacture as follows:
Product
2,4-dichlorophenoxyacetic acid1
Pentachlorophenol
All other chlorophenols
Amount of Phenol
(kkg)
10,36^6
5,183
15,550
31,099
All of the isomers can be produced via the direct chlorination of
phenol or the hydrolysis of the appropriate chlorobenzene.
The hydroxyl group in phenol is an extremely powerful ortho-para
director. Halogenation of phenol results almost exclusively in substi-
tution at the 2,4, or 6 positions on the aromatic ring (Morrison and
Boyd 1973).
ORTHO
ORTHO
If phenol is used as the raw material for production of chlorophenols,
the phenol chemistry dictates the following product distribution upon
successive substitution:
la derivative of 2,4-dichlorophenol.
A-l
-------
•0,
Z - CHtOHOf H6«0t 4 -
Z. 4.1 TBICHlOROFHiNOl_ Z. J. 4. I TETHACHlOHOrHgNOl
2. * OICHIOIWHCJIOt I 4
PfNTACHUOROPMENOl
hvdrovsi f ^ y thSt the remainin§ is«ers are produced via the
hydrolysis of the appropriate chlorobenzene . Although any of the isomers
liklv Va te "^i- of • chlorobenzene, it is not
likely to be the preferred route since hydrolysis can give rise to the
unwanted formation of chlorinated dibenzo-p-dioxins.
ESTIMATED PRODUCTION OF 2.4-DICHLOROPHENOL
C° estimate the Production in 1977 of 2,4-dichloro-
Method 1:
Year
1978
1977
Production (kkg)
12,009a
1977 Production = (1978 Production)
(12,009 kkg)
13,472 kkg
,593 kkg
USITC (1979) .
'USITC (1978) .
Sales (kkg)
3,593a
4,031b
A-2
-------
Method 2; - a
The compound 2,4-dichlorophenol is the precursor for the production
of 2,4-dichlorophenoxyacetic acid (2,4-D). Versar, Inc. (1980) estimates
that about 10,366 kkg of phenol were used for the production of 2,4-D
via the 2,4-DCP route. The yield of the reacion is about 80% (Morrison
and Boyd 1973).
1977 Production = (Amount of phenol used for 2,4-D)
/molecular wt of 2,4-DCP\
^molecular wt of phenol /
= (yield) /.,,\
(10,366 kkg) M—1 (0.80)
\ /
= 14,534 kkg
The second method has assumed that virtually all of the 2,4-dichloro-
phenol production is via the chlorination of phenol. This is a reasonable
assumption because two producers (Dow and Monsanto) produce ortho and
para monosubstituted chlorophenol and Dow produces 2,4,6 and pentachloro-
phenols, which is consistent with phenol chemistry. According to JRB
Associates (1980), the other two producers of 2,4-dichlorophenol did not
produce the compound in 1977 and one of these producers makes the 2,4,5
trisubstituted product, which would be consistent with the hydrolysis
route. Additionally, Tracor-Jitco (1978) estimated the annual produc-
tion of 2,4-dichlorophenol to be about 14,000 kkg. These three estimates
are independent of each other and within 5% of each other. Therefore,
the estimated production in 1977 of 2,4-dichlorophenols is 14,000 kkg.
ESTIMATED PRODUCTION OF OTHER CHLOROPHENOLS
The estimated production of 2 and 4 monochlorophenols, 2,4,6-
trichlorophenol, 2,3,4,6-tetrachlorophenol, and pentachlorophenol is
not as well defined as is that for 2,4-dichlorophenols because the lower
chlorophenols are used to produce the higher chlorophenols.
Production of pentachlorophenol in 1977 was 20,345 kkg (USITC 1978).
Reportedly, pentachlorophenol is only made by the direct chlorination of
phenol at about an 85% yield on a phenol basis (Morrison and Boyd 1973) .
(molecular wt of phenol \
molecular wt of penta- J
chlorophenol /
(yield)
*
= (20,345 kkg) / 93 \ j (0.85)
I 260
6,185 kkg X
A-3
-------
-
production of the isomers via the chlorination of phenol.
JRB Associates (1980) estimates that about 2,000 kkg of the ortho
fe
. They further estimate that about
n§ ^ thS Phen01 «"*~l«f uLcountedlor are used
duction of ^ °£ uheSe tW° iS°merS at 80% ?ield sho^ for the pro-
duction of monochlorophenol via direct chlorination:
/molecular wt of chlorophenol \
Amount » (Amount of phenol) ^ molecular wt of phenol - ) (yield)
= (12,427 kkg) /128\ (0.80)
I 93 ;
- 13,683 kkg
!hoT!s/^the non-sPecificity of the reaction, the ortho-to-para ratio is
about 45/55, respectively (Morrison and Boyd 1973). Therefore:
ortho product = (13,683 kkg) (0.45) = 6,157 kkg
para product = (13,683 kkg) (0.55) = 7,526 kkg
Total ortho production = 6,157 kkg + 2,000 kkg = 8,157 kkg » 8,150 kk*
Total para production = 7,526 kkg + 1,300 kkg = 8,826 kkg §
The amount of monochlorophenol used to produce the 2,4,6- and 2 3 4
6-chlorophenols via direct chlorination is: ^»J^>
Amount = (8,157 kkg) (1-0.01)+ (8,826 kkg) (1-0.13)
= 15,754 kkg
Assuming an 80% yield upon chlorination of the monochlorophenol to the
r the umt °f
r,,^^ -i . , , /molecular wt of phenol
Phenol equivalents = (Amount of monochlorophenol I m^IIZulaT~wt of chloro
phenol
(0.80)
9,157 kkg
A-4
-------
Assuming only 2,4,6 is produced:
Amount produced » (9,157 kkg) /163\= 16,048 kkg max.
(-»)
Assuming only 2,3,4,6 is produced:
Amount produced » (9,157 kkg) / 198\ = 19,495 kkg max.
\-93J
It is likely that both are produced and therefore that the production
of each is less than the maximum quantity derived above. Production
quantities of these two compounds are interdependent.
2. EMISSION ESTIMATES
1
2-Chlorophenol
Emission factors from production:
Water: 2.1 x 10~2 kkg/kkg product
Air: 57, of aquatic discharges
Land: negligible
Water discharges = (2.1 x 10"2 kkg/kkg) (8,150 kkg)
a 170 kkg
Air discharges = (0.5) (170 kkg)
«8.6 kkg
Emission factors for uses:
Phenolic resin production = 0.005 of production
Solvent usage = 0.005 of production
Total emissions from use = (2) (0.005) (8,150)
2-4 Dichlorophenol
Emission factors for production:
Water: 2.1 x KT2 kkg/kkg product
Air: 1 x 10~3 kkg/kkg product
Land: negligible
Air emissions = (14,000 kkg) (1 x 10~3 kkg/kkg)
= 14 kkg
Aquatic discharges =(14,000 kkg)(2.1 x 10~2 kkg/kkg)
«294 kkg
iData extracted from JRB Associates (1980).
A-5
-------
REFERENCES
JRB Associates. Level I materials balance—chlorophenols— final
68"-
Boston, MA: Allyn and
dr!fTnintC0' wpr??uction and use of 2,4-dichlorophenol. Chapter V-^
draft paper. Washington, DC: Tracor-Jitco; 1978.
U.S. International Trade Commission (USI-TC) . Synthetic organic chemicals
S^ LtS^^T^ ^ S3leS 1977' USISC 833' Washington? ^
U.S. International Trade Commission; 1978.
U.S. International Trade Commission (USITC) . Synthetic organic chemicals
United States production and sales 1977. USITC 833. Washington? S:
U.S. International Trade Commission; 1977. 'S<-on,
Versar, Inc. Environmental material balance for phenol. Draft report
""- Washi^t0n' DC: U^ Environmental Protection
A-6
------- |