United States Office of Water October 1981
Environmental Protection Regulations and Standards (WH-553) EPA-440/4-85-013
Agency Washington DC 20460
Water
&EPA An Exposure
and Risk Assessment
for Phenol
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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.
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50372-101
REPORT DOCUMENTATION *• "EPORT NO. 2.
PAGE EPA-440 / 4-8 5-01 3
4. Tttla and Subtltla
An Exposure and Risk Assessment for Phenol
'. Authors) Scow, K. ; Goyer, M. , Payne, E. ; Perwak, J.;
Thomas, R. ; Wallace, D. ; and Wood, M.
*. Performing Organization Nama and Address
Arthur D. Little, Inc.
20 Acorn Park
Cambridge, MA 02140
2. Sponsoring Organization Nama and Addraca
Monitoring and Data Support Division
Office of Water Regulations and Standards
U.S. Environmental Protection Agency
Washington, D.C. 20460
3. Raclplanf s Accession No.
5. Raport Data Final Revision
October 1981
«.
8. Performing Organization Rapt. No.
10. Projact/Taak/Work Unit No.
Task No. 21
11. ContracttQ or Grant(G) No.
(0 68-01-3857
(G)
IX Typa of Raport & Parlod Covarad
Final
14.
5. Supplementary Note*
Extensive Bibliographies
«. Abatract (Limit 200 words) —
This report assesses the risk of exposure to phenol. This study is part of a program
to identify the sources of and evaluate exposure to 129 priority pollutants. The
analysis is based on ax'ailable information from government, industry, and technical
publications assembled in September of 1980.
The assessment includes an identification of releases to the environment during
production, use, or disposal of the substance. In addition, the fate of phenols 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 toxicit3/ are presented and interpreted. Information concerning all
of these topics is combined in an assessment of the risks of exposure to phenols for
various subpopulations.
. Document Analysis a. Descriptor*
Exposure
Risk
Water Pollution
Air Pollution
b. Idantlflan/Open-Emtod Term*
Pollutant Pathways
Risk Assessment
Effluents
Waste Disposal
Food Contamination
Toxic Diseases
Phenol
e. COSATt Field/Group
06F 06T
A Availability Statement
Release to Public
19. Security Ctaaa (This Report)
Unclassified
20. Security Clas* (This Page)
TWIass-if-fprf
21. No. of Pa«e«
199
22. Price
$17.50
Saa /natnicttona on Havana OPTIONAL FORM 272 (4-77>
(Formerly NTIS-35)
Department of Commerce
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EPA-440/4-85-013
September 1980
(Revised October 1981)
AN EXPOSURE AND RISK ASSESSMENT
FOR PHENOL
by
Kate Scow
Muriel Cover, Edmund Payne, Joanne Perwak
Richard Thomas, Douglas Wallace, and Melba Wood
Arthur D. Little, Inc.
Michael Slimak and Mark Mercer
U.S. Environmental Protection Agency
EPA Contract 68-01-3857
Task No. 21
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
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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
c.hemical, 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
11
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TABLE OF CONTENTS
List of Tables
List of Figures
Acknowledgments
I. TECHNICAL SUMMARY 1
II. INTRODUCTION 9
III. MATERIALS BALANCE 11
A. Introduction and Methodology 11
B. Material Balance 11
1. Production 13
2. Releases From Phenol Production 16
3. Sources of Phenol Emissions During Storage,
Loading, and Transport 16
4. Uses of Phenol . 20
a. Consumptive Uses 20
i. Phenolic Resins 20
ii. Bisphenol A 24
iii. Caprolactum 27
'• • ' ' iv. Methylated Phenols 27
v. Plastici2ers 27
vi. Adipic Acid 28
vii. Nonylphenol 28
viii. Salicylic Acid 28
ix. Dodecylphenol 31
x. 2,4-D 31
xi. Pentachlorophenol 31
xii. Other Alkylphenols 35
xiii. Other Chlorophenols 35
b. Non-Consumptive Uses 35
i. Petroleum Refining (Use of Phenol
as a Solvent) 35
ii. Export of Phenol 35
c. User Storage, Loading, and Transport 36
5. Releases from Phenol Utilization 36
6. Miscellaneous Releases 37
a. Industrial Sources 38
b. Fuel Combustion Sources 38
c. POTW's 39
d. Medicinal Products Containing Phenol 39
C. Areas for Further Research 39
D. Summary 41
References 42
iii
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TABLE OF CONTENTS (continued)
IV. FATE PATHWAYS AND ENVIRONMENTAL DISTRIBUTION OF PHENOL 45
A. Introduction 45
B. Chemical and Physical Properties of Phenol 45
c- Pathway #1. Discharges to Surface Water 45
1. Introduction 45
2. Fate Processes 47
a. Hydrolysis 47
b. Photolysis and Photooxidation 47
c. Oxidation 49
d. Volatilization 49
e. Adsorption 51
f. Biodegradation 52
g. Bioaccumulation 53
3. Field Studies 60
4. EXAMS Model Results 64
5. Monitoring Data 68
D. Pathway # 1. Emissions to Air 71
1. Introduction 71
2. Fate Processes and Field Studies 71
3. Monitoring Data 76
E. Pathway/;3. Air to Water/Soil; Rainout
76
Pathway £4. Fate in POTW's and Wastewater Treatment 77
1. Introduction 77
2. Biological Degradation 77
3. Chemical Treatment 78
4. Field Studies 81
Pathway #5. Soil to Groundwater and Surface Water:
Leaching, Runoff 84
1. Introduction 84
2. Fate Processes 84
a. Adsorption 84
b. Volatilization 86
c. Other Processes
3. Field Studies 87
Estimation Methods 88
Monitoring Data 89
H. PATHWAY .>'6. Chlorination of Phenol and Formation
of Chlorophenol 89
I. Summary and Conclusions 94
1. Surface Water 94
2. Fmiq.cions to Air 9
IV
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TABLE OF CONTENTS (continued)
3. Rainout 95
4. Fate in POTW's and Wastewater Treatment 95
5. Soil to Groundwater and Surface Water 96
6. Chlorination of Phenol and Formation of
Chlorophenols 96
References 97
V. HUMAN EFFECTS AND EXPOSURE 103
A. Effects on Humans 103
1. Introduction 103
2. Metabolism and Bioaccumulation 103
3. Animal Studies 105
a. Carcinogenicity 105
b. Mutagenicity 106
c. Adverse Reproductive Effects 110
d. Other Toxicological Effects 111
4. Human Studies 112
B. Exposure of Humans 114
1. Introduction 114
2. Ingestion 114
a. Drinking Water 114
b. Food 116
c. Products Containing Phenol 116
3. Inhalation 118
4. Dermal Absorption 118
5. Exposure Scenario Estimates 119
C. Overview and Conclusions 119
1. Effects 119
2. Exposure 121
References 122
VI. AQUATIC BIOTA EFFECTS AND EXPOSURE 127
A. Effects on Aquatic Biota 127
1. Introduction 127
2. Frestwater Organisms 127
a. Chronic and Sublethal Effects 127
b. Acute Effects 128
3. Marine Organisms 130
4. Factors Affecting the Toxicity of Phenol 133
B. Exposure of Aquatic Biota 134
v
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TABLE OF CONTENTS (continued)
C. Conclusions
1. Effects 136
2. Exposure ^35
References 137
VII. RISK CONSIDERATIONS 141
A. Introduction
B. Humans
1. Statement of Risk
2. Discussion
C. Aquatic Biota 147
1. Statement of Risk 147
2. Discusssion 147
References 156
APPENDIX A: BACKGROUND NOTES ON THE DERIVATION OF
TABLE 2 157
References
APPENDIX B: PHENOL AND PHENOLIC RESIN PRODUCTION 167
Recovery of Phenol From Coal Tar and Petroleum
Streams 167
Phenol From Coal Tar 167
Phenol From Petroleum-Refinery Caustic Wastes 169
Phenol From Cumene Peroxidation 171
Phenol From Benzene Sulfonation 172
Phenol From Toluene Oxidation 174
Phenol Resin Production Process 176
References 184
vi
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LIST OF TABLES
Table
No. Page
1. U.S. Production and Consumption of Phenol 12
2. Environmental Releases of Phenol 14
3. Total U.S. Production of Phenol By Process, 1977 17
and 1978
4. U.S. Phenol Manufacturers 18
5. U.S. Phenol Utilization 21
6. U.S. Bisphenol A Manufacturers 25
7. U.S. Nonylphenol Manufacturers 29
8. U.S. Manufacturers of Technical and Medicinal
Grade Salicylic Acid 30
9. U.S. Dodecylphenol Manufacturers 32
10. U.S. 2,4-DC(2,4-Dichlorophenoxyacetic Acid)
Manufacturers 33
11. U.S. Pentachlorophenol Manufacturers 34
12. Medicinal Products Containing Phenol 40
13. General Physical Properties of Phenol 46
14. Biodegradation Rates For Phenol 54
15. Amount of Phenol Accumulated in Fish 56
16. Distribution of Phenol in the Organs of Fish 58
17. Field Studies of Phenol Discharges to Aquatic Systems 62
18. Rate of Phenol Disappearance From River Water 63
19. Results of EXAMS Simulation 66
20. Estimated Loading Rates of Phenol to Surface Water
For Selected Industrial Plants 67
21. Estimated Industrial Loading Rates of Phenol to
Surface Water 69
22. Ambient Concentrations of Phenol in the United
States, 1970-1979 70
vii
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LIST OF TABLES (continued)
Table
No- Page
23. Effluent Levels of Phenol in Industrial Wastewater 72
24. Concentration of Phenol in Sediment 73
25. Phenol Concentrations in Wastewater Treatment at
Different Stages of Treatment 83
26. . Composition of Soils Used in Phenol Adsorption Study 84
27. Estimated Release Rates of Phenol in Solid Waste
From Waste Disposal Sites 88
28. Chlorine Incorporation in Phenol 89
29. Chlorination of Phenol 90
30. Chlorine Levels in Water Treatment 92
31. Phenol Concentrations in POTW's 93
32. Incidence of Chromosomal Aberrations in
Spermatogonia of Phenol-treated Mice 108
33. Incidences of Chromosomal Aberrations in
Spermatocytes of Phenol-treated Mice 109
34. Exposure Levels Resulting From Ingestion of Phenol
In Food and Water 115
35. Exposure Levels Resulting From Use of Medicinal
Products 117
36. Exposure Scenarios Involving Contact With Phenol 120
37. Chronic and Sublethal Effects on Freshwater Organisms 129
38. Acute Toxicities (LCso) for Freshwater Fish 131
39. Acute Toxicities (LCso) for Freshwater Invertebrates 132
^0. Frequency Distribution of Phenol (Total) Concen-
trations in Ambient Surface Water 135
Vlll
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LIST OF TABLES (continued)
Table
No. Page
41. Adverse Effects of Phenol on Mammals 144
42 Human Exposure to Phenol 145
43 Exposure Levels of Phenol For Various Subpopulations 148
44 Summary of Reported Environmental Concentrations
of Phenol 149
45 Summary of Effects Levels of Phenol on Aquatic
Organisms 150
46. Data on Phenol-Related Fish Kills (1971-1977) 152
47. Exposure Incidents Involving Phenol 153
48. Effects of a Phenol Spill on a River System 155
B-l U.S. Manufacturers of Phenolic Resins 177
IX
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LIST OF FIGURES
Figure
No. Page
1. Materials Balance of Phenol 15
2. Location of U.S. Phenol Manufacturers 19
3. Generalized Flow Pattern For Phenol Use 22
4. Location of U.S. Phenolic Resin and Bisphenol A
Producers 23
5. Bisphenol A Production 26
6. Photooxidation Pathways For Phenol 48
7. Photodecomposition Products of Phenol 50
8. A Schematic View of the Main Excretion Routes for
the Conjugated Phenols in Fish 58
9. Maximum Concentrations and Loads of Phenol
Following Release into River 61
10. Variations in Phenol Content and Stream Flow
During 24-Hour Surveillance 65
11. Phenol, Alkenes, and Ozone Variation During Heavy
Smog Episode 75
12. Oxidation Pathways and Products For Phenol 80
13. Relationship of Ozone Reaction Rate (k) to pH 82
14. Phenol Adsorption Isotherms for Three Types of Clay 85
15. Equilibrium Data for Phenol Between the Soil and
Water at 77°F 85
16. Molar Chlorine Uptake by Test Compounds, Including
Phenol 91
17. Exposure and Acute Effects of Phenol for Humans 143
B-l Segment of Coke Byproduct Recovery Plant 168
x
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LIST OF FIGURES (continued)
B-2 Recovery of Phenol From Petroleum Refinery
Caustic Wastes 170
B-3 Cumene Peroxide Process 173
B-4 Benzene Sulfonate Process 173
B=5 Toluene Oxidation Process 175
B-6 Phenolic Resin Production 182
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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), Richard Thomas (fate), Douglas Wallace
(aquatic effects), Melba Wood (monitoring), and Alfred Wechsler
(technical review). Other contributors included Anne Littlefield,
Warren Lyman, Kenneth Menzies, Edmund Payne, and Katherine Saterson.
Pearl Hughes was responsible for organization and typing of the final
draft report.
The materials balance for phenol (Chapter III) 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.
Xll
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I. TECHNICAL SUMMARY
RISK ASSESSMENT
Environmental exposure of humans to concentrations of phenol at
levels equivalent to those causing effects (as extrapolated from studies
on laboratory animals) appears to be rare. However, one particular
effects study reported chromosomal damage to mice at concentrations
approximately four orders of magnitude lower than other effects levels.
This particular study warrants further exploration due to the variance
of its effects level from other reported effects levels. If the con-
clusions of the chromosomal study are correct, a large fraction of the
human population may be exposed to phenol levels equivalent to the level
which elicited chromosomal damage in mice. In addition, investigation
of the similarities between humans and laboratory mice in regard to
chromosomal damage and the significance of chromosomal damage in human
populations is needed.
Comparison of phenol exposure levels for humans in most subpopula-
tions with effects levels (excluding the chromosomal damage study) shows
a "safety margin" of approximately one order of magnitude or greater.
Exposure levels for other subpopulations (users of medicinal products,
people exposed to multiple sources of phenol) are approximately five
times below effects levels. The size of these other subpopulations is
expected to be very small.
Phenol is rapidly metabolized and excreted from the body. This is
an important factor in reducing possible harm from long-term exposure
to low concentrations. There is no evidence at this time that phenol
is carcinogenic when administered orally to mice or rats; however further
testing has been recommended.
Aquatic organisms only rarely appear to be exposed to concentrations
of phenol in surface water at levels equivalent to concentrations causing
adverse effects in laboratory bioassays. Monitoring of environmental
concentrations of phenol in surface water is limited, however; additional
monitoring is needed to confirm this conclusion. Based on" existing moni-
toring data, sublethal and lethal effects levels for fish and inverte-
brates are higher than exposure levels by approximately one and two
orders of magnitude, respectively. Environmental fate data indicate
that phenol is rapidly degraded by microbial populations which would
reduce the likelihood of long-term persistence in surface water.
HUMAN EFFECTS AND EXPOSURE
Phenol is readily absorbed from all routes of entry, distributed through-
out the body, metabolized and rapidly excreted from the body. The bio-
logical half-life of phenol in man is approximately 3.5 hours.
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Acute lethal values for phenol range from approximately 200 mg/kg
to 700 mg/kg, regardless of the route or species. The cat appears to
be the most sensitive species (oral LDLo 80 mg/kg), probably as a result
of significant metabolic differences in the manner phenol is detoxified
in this species. Slight to moderate kidney damage and slight liver
changes have been reported in rats given 135 daily doses of 100 mg/kg
phenol by gavage. Similar treatment with 50 mg/kg produced slight
damage after 135 doses but not after 20 doses. Rats, however, have been
able to tolerate much larger doses in drinking water (56 mg/rat/day or
^280 mg/kg for a 200-g rat), probably due to its rapid metabolism as
well as the intermittent nature of dosing in contrast to exposure by
gavage.
There are no indications that phenol is carcinogenic by the oral
route. Skin application of phenol, however, is tumorigenic in sensitive
strains of mice but not in standard inbred strains of mice. The tumoro-
genic activity of phenol appears to be associated with its irritancy
and subsequent skin hyperplasia.
Lethal mutations in Drosophila (fruit fly) are induced by exposure
to phenol. In addition a significant increase in the incidence of chromo-
somal defects in a dose-related manner in spermatogonia and spermatocytes
was observed in mice given phenol by gavage at dosage levels as low as
6.4 ug/kg/day. Furthermore, the data from this particular study suggest
incremental increases in the incidence of chromosomal aberrations occur
in consecutively treated generations. However, the treatment schedule
utilized and the lack of data reporting prevent assessment of the sig-
nificance of this finding. No indications of teratogenicity have been
found.
The lowest reported oral lethal dose of phenol in man is one gram,
but the majority of lethal values are in the 5- to 40-gram range. Cen-
tral nervous system disturbances together with peripheral vasodilation
result from an acute lethal dose of phenol leading to sudden collapse
and unconsciousness. Death is due to respiratory arrest. Ingestion of
non-lethal amounts of phenol can result in burning in the mouth, mouth
sores, headache, vomiting, diarrhea, back pain, paresthesia, and pro-
duction of dark urine (probably from oxidation products of phenol).
Recent reports have also linked phenol to the production of cardiac
arrhythmias during chemical face peeling procedures used in clinical
treatments.
Aside from the issue of its mutagenicity, the rapid clearance of
phenol from the body, its relatively high lethal dose, and the fact
that small amounts of phenol are produced endogenously indicate that
man can handle levels normally present in U.S. drinking water with no
untoward effects. Further work needs to be done to validate the single
report of increased chromosomal aberrations in phenol-treated mice and
in particular, to clarify the finding of increased numbers of aberra-
tions in consecutively treated generations of mice.
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Numerous uncertainties are involved in estimates of exposure to
phenol because of a deficiency in monitoring data. The use of phenol-
containing products, especially mouthwash and lozenges, appears to be
the largest consumer exposure in terms of exposure level, although
presumably on a short time scale. Ingestion of contaminated well water
may result in an equivalent exposure level but the duration of this
level is dependent on the persistence of phenol in the groundwater.
Other water supplies appear to contribute to a very small exposure level
through ingestion. Chemical laboratory workers comprise a subpopulation
potentially exposed to levels equivalent to those from use of phenol^
containing mouthwash, however, assumably laboratory exposure occurs
over a long period of time. In both cases the subpopulations are
expected to be small. Ingestion in food and dermal absorption from
cosmetics may contribute to a more continual exposure for a larger sub-
population. Ingestion of fish or smoked meat and inhalation along high-
ways may each represent an exposure of up to 6 mg/day, using worst case
assumptions.
Separate exposure routes were combined into various scenarios to
estimate total exposure. This assumes equal absorption efficiency for
all routes and upper limit exposure levels. The scenarios quantified
include a worst case (combination of all exposures), groundwater con-
tamination, medicinal use, laboratory exposure and the general population.
Associated daily exposure levels with these scenarios were, respectively,
520 mg, 247 mg, 354 mg, 82 mg and 7 mg of phenol.
AQUATIC EFFECTS AND EXPOSURE
The Ambient Water Quality Criteria document for phenol states that
the available data for phenol indicate that acute and chronic toxicity
to freshwater aquatic life occurs at concentrations as low as 10.2 and
2.6 mg/1, respectively. Toxicity may occur at lower concentrations among
species that are more sensitive than those tested.
The lowest concentration of phenol associated with toxic effects
is 0.1 mg/1, in Daphnia magna. The lowest acute level was for a species
of insect (Baetis), a 48-hour LC5g of <1.5 mg/1. The juvenile rainbow
trout was the most sensitive fish tested; LC5Q values were reported at
5.0 mg/1. The grass frog was the only non-piscine vertebrate tested;
lethal toxicosis in embryos was reported at 0.5 mg/1 phenol.
Other toxic effects in addition to mortality have also been
observed such as decreased reproductive rate and fecundity in Daphnia,
loss of balance in pike, lack of pigmentation in developing sturgeon
prolarvae, delayed hatching in bream, and reduced feeding in clams.
Not all effects are obviously detrimental, however; Daphnia pulex grew
faster in a solution of 0.1 mg phenol/1 than under control conditions
and some species had greater hatching success in very low concentrations
of phenol.
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The toxicity of phenol to marine organisms has been only briefly
studied. The effects levels reported are in the same approximate range
as for freshwater species. No community or population studies (labora-
tory or field) are available for both salt and freshwater ecosystems.
The toxicity of phenol to aquatic life is influenced by various environ-
mental factors. Water temperature is the most extensively studied
variable, yet laboratory results present variations between species as
to its general effects. In most cases, the organism is more sensitive
to phenol as temperature increases, although high and low temperature
extremes appear to be detrimental. The anadromous rainbow trout per-
ished at lower phenol concentrations as salinity increased, suggesting
that salmonoid populations might be more sensitive when their migrations
bring them into estuaries. Crucian carp were more sensitive to phenol
at both pH extremes.
Phenol concentrations of significance to aquatic life are few and
short-term, based on the limited available data. Monitoring data
reported 72% unremarked (above detection limit) ambient levels in U.S.
fresh surface water less than 0.01 mg/1. The Tennessee and Ohio River
basins had the highest maximum levels. Few data were available for
estuarine or marine waters.
Industrial and wastewater treatment effluents often have high levels
of phenol. Some of the higher U.S. levels may be for phenolics and not
specifically phenol; therefore, the actual phenol concentration would
be lower than the reported values. According to the results of the
EXAMS model, which simulates the continual discharge of phenol into
selected "average" aquatic systems, typical effluent levels would result
in water column concentrations lower than 50 ug/1, with the majority
less than 10 ug/1. The results are dependent on certain assumptions,
including a high microbial degradation rate, which may not be applicable
to all situations. Therefore, the results are not meant to be predictive.
FATE PATHWAYS AND ENVIRONMENTAL DISTRIBUTION
The fate and distribution of phenol following environmental release
depends on the form of emission, the receiving medium, and various en-
vironmental factors. The critical environmental pathways describing
the behavior of phenol releases include discharges to surface water,
emissions to air, transport from air to water/soil, discharges to POTW's,
releases to soil, and chlorination during water treatment.
Surface Water: Approximately 30% of all known environmental releases
of phenol are made to surface water, primarily by POTWs, petroleum
refiners, phenolic resin and bisphenol A producers, and certain pro-
ducers of phenol itself. The most significant fate process affecting
-------
phenol in surface water is biodegradation. A half-life of 3.5 days was
reported under field conditions in a river. Laboratory studies confirm
a rapid removal rate especially under acclimated conditions and at high
temperatures. Numerous microfloral species have been identified as
capable of degrading phenol. There is some evidence that phenol may
undergo photolysis under environmental conditions. The processes of
hydrolysis, oxidation, adsorption, and volatilization do not appear to
be significant with respect to phenol concentrations in surface water.
Bioaccumulation of phenol has been studied in aquatic organisms.
Absorption is the primary route of intake. Phenol concentrations of
14 to 156 ug/gram of body weight were reported for goldfish exposed to
10-100 mg/1 phenol for 1-5 days. Bioconcentration factors for phenol
were low, ranging from 1.2 to 2.3. Accumulation of phenol occurs
primarily in the gall bladder, liver, and visceral organs. Higher
vertebrates, such as mammals, detoxify phenol by forming conjugation
products with glucuronides and sulfates; fish do not appear to possess
this mechanism, rather bronchial diffusion and biliary excretion are
the mechanisms of decreasing the phenol body burden of these organisms.
Biomagnification of phenol does not appear to be significant because
of its generally low degree of accumulation in tissue.
A monohydric phenols river spill from a benzene sulfonation plant
was monitored and the results showed 93% of the initial 28 mg/1 phenol
concentration was reduced significantly in six days. Associated with
the high rate of phenol degradation was a temporary deficit in oxygen
levels which contributed to the toxic effects resulting from the spill.
Phenol concentrations may show seasonal variation, higher during the
winter than summer due to a decreased rate of microbial degradation at
low temperatures. A river receiving continuous discharges from a petro-
leum refinery and a cumene peroxidation plant had summer phenol levels
approximately one order of magnitude lower than winter levels; however,
some of the variation could have been attributable to differences in
the waste characteristics and discharge levels.
A continous discharge of 3 kg/hr of phenol into a eutrophic lake
and turbid river (1 km length) was simulated by the EXAMS model.
Equilibrium water column concentrations were 1 to 3 ug/1. The self-
purification time for both systems was approximately 3 to 4 hours due
to biodegradation in the eutrophic lake and physical transport out of
the modeled reach in the river system. Sediment concentrations were
approximately 10 ug/kg and 5 x 10-i+ ug/kg (dry weight) in the river
and lake systems, respectively.
Monitoring data in surface water are limited for phenol. The
STORET data base reports a total of approximately 600 observations for
thirteen major river basins between 1978 and 1980. Mean concentrations
ranged from 0.004 to 660 ug/1 with a maximum of 6,794 ug/1. Sediment
levels (348 observations) averaged around 102 mg/kg (unremarked data)
with a maximum value of 454 mg/kg. Concentrations as high as 3,000 mg/1
have been reported in effluents; however, most levels were reported at
less than 1.0 mg/1.
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Emissions to Air; Approximately 64% of phenol releases are to air,
predominately from combustion of wood and automobile exhaust. Phenol
producers, consumers, and the transport and storage of phenol are
responsible for other atmospheric releases. Most releases are presumably
in vapor form or adsorbed onto particulate matter. Phenol is subject to
rainout, photolysis and photooxidation and its estimated atmospheric
lifetime is several days. In urban areas, phenol levels fluctuate
diurnally with higher levels during the day. These levels were attri-
buted to higher traffic volume and industrial activity at that time of
the day. The highest reported phenol concentration in urban air was
289 ug/m3 reported in Frankfurt, Germany. No comparable U.S. levels
were reported. No data were available for atmospheric concentrations
in rural areas.
Rainout; Atmospheric emissions of phenol not photodegraded are sub-
ject to rainout with transfer to land or surface water. Rainwater con-
centrations were estimated initially at 1 to 10 mg/1 in the vicinity of
a source; however the concentrations are expected to be reduced as rain-
fall continued. No monitoring data were available reporting phenol
levels in rain. However, European industrial areas are reported to have
higher rainfall concentrations than do rural areas but the levels were
not quantified.
Fate in POTW's and Wastewater Treatment: Phenol in untreated and
treated waste streams is discharged to POTW's by various industrial
sources. Natural background levels of phenol also contribute some
portion of the total loading. Phenol concentrations in POTW influents
were reported at 0.001 to 0.2 mg/1. Common treatment processes are
successful in removing phenol including activated sludge, trickling
filters, and various chemical treatments. Biodegradation in sludge is
very effective, especially in activated sludge at concentrations less
than 10 mg/1. The decay rate is sometimes inhibited at levels exceeding
this concentration. At approximately 500 mg/1 an activated sludge system
experienced a sharp disruption of tnicrobial activity. The optimum pH
range is 6 to 9.5 and adequate essential nutrient concentrations must be
present.
A number of primarily tertiary treatment methods have been found to
be effective in degrading phenol. These include treatment with chlorine,
hydrogen peroxide, potassium permanganate, ozone, and iron ferrate.
These methods are not expected to be very common at POTW's and variable
in wastewater treatment facilities depending on the industry subcategory.
A high removal efficiency of greater than 90% was reported for
phenol in four POTW plants in a field study evaluating POTW treatment
processes. Efficiencies were not reported for the other three plants
studied.
-------
Soil to Groundwater and Surface Water: A small percentage (approxi-
mately 6%) of the environmental releases of phenol are known to associate
with disposal of wastes on land. Major known sources include sludges
resulting from the synthesis of phenol. Phenol has a relatively low
affinity for adsorption onto soil and a high solubility. Therefore,
some portion of the releases to land may reach either ground or surface
waters unless significantly reduced a priori by biodegradation or other
fate processes.
Biodegradation is expected to be the most important fate process
determining phenol concentrations in biologically active soil. Phenol
volatilization from soil does not appear to be significant. No specific
information describing chemical oxidation nor complexation of phenol was
available. Adsorption onto organic matter and clay is low.
Attenuation and persistence of phenol in soil in the vicinity of
phenol sources were indicated by two field studies. In a peat soil,
the influence of phenol was limited to within 500 m of a catchment pit
which indicated, in contradiction of laboratory results, strong adsorp-
tion onto the highly organic peat. In the second study phenol spilled
onto the soil surface reached groundwater supplies where it persisted
for 19 months. The substratum in the vicinity of the spill was sand,
gravel and undifferentiated dolomite. There was no indication of adsorp-
tion onto the organic fraction of the soil surface layer; however, soil
concentrations were not reported to confirm this.
Chlorination of Phenol and Formation of Chlorophenols: Phenol is
one of the most reactive aromatics during chlorination and synthesis of
chlorophenols is commonly reported during treatment of wastewater and
drinking water. Based on a laboratory experiment conducted under optimal
conditions for chlorination, an upper limit of 1.6 mg of phenol per liter
of water will become chlorinated at typical wastewater treatment chlorine
concentrations. Lower phenol concentrations, however, are probably more
typically subject to reaction with chlorine due to system variability
and stereochemical factors. Any specific conclusions about or quanti-
fication of the chlorination of phenol during POTW treatment of waste-
water cannot be supported by the limited and inconsistent field studies
available.
MATERIALS BALANCE
In 1978, approximately 1,216,100 kkg of phenol were produced in the
U.S. Of this amount, 639,200 kkg (53%) was consumed in the U.S., 103,800
kkg (8%) was exported, and the remaining 473,100 kkg (39%) was assumed
to have been placed in stocks. Phenol is isolated from coal tar and
petroleum streams (1%) and produced synthetically by cumene peroxidation
(90%), benzene sulfonation, and toluene oxidation (together comprising
9%).
-------
_Use of phenol as an intermediate in the synthesis of various organic
chemicals is responsible for 95% of its total consumption. Products
include resins (44%), bisphenol (17%), caprolactam (15%), methylated
phenol (4%), plasticizers, adipic acid, nonylphenol, alicylic acid,
dodecylphenol, 2,^-dichlorophenoxyacetic acid, pentachlorophenol, other
alkylphenols, and other chlorophenols. The remaining 5% of phenol is
used as a solvent in petroleum refining, in medicinal products, or
exoorted.
exported
Production and consumption-related activities are associated with
approximately 19,018 kkg of annual phenol releases ( is discharged to surface water from POTW's. Approximately 1,010
(25%) of the total amount can be related to specific sources
primarily petroleum refiners, phenolic resin and bisphenol A producers
The remainder of the phenol in the discharge originates from other un-'
quantified man-made sources, natural sources such as decaying organic
matter, and possibly as intermediate breakdown products from POTW treat-
ment of more complex organics.
Among the areas requiring further investigation are the POTW dis-
charge estimate, identification of sources to POTW's, the significance
of indirect and natural releases to the overall environmental balance
of phenol and better understanding and quantification of the land dis-
posal practices for phenol wastes.
-------
II. INTRODUCTION
The Office of Water Regulations and Standards, Monitoring and
Data Support Division of the Environmental Protection Agency is
conducting a program 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,
summary of the manufacture, use, distribution, fate, effects, and
potential exposure and risk in regard to phenol. 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.
Phenol is produced for use as an intermediate in the manufacture
of other substances, primarily phenolic resins, bisphenol A,
caprolactam, and many organic chemicals. It is used directly to
a lesser degree as a disinfectant in assorted products and as an
analytical agent. The production and use emissions are widespread
throughout the United States and limited monitoring data suggest that
phenol is ubiquitous in the environment at low concentrations.
Although the physical and chemical properties of phenol are well
understood, environmental fate and monitoring data are few. It is
difficult, therefore, to predict and confirm the persistence of
phenol in the environment. In order to better understand phenol's
environmental behavior, published case studies of spills were
examined and a model simulating various aquatic systems was
implemented to model phenol's fate under conditions of continued
discharge.
An important source of phenol to waterways is inadvertant
discharge from coal and petroleum-using facilities of the "natural"
phenol present in the fuel. In addition there are natural back-
ground levels of phenol found in water. These sources should be
accounted for as best as possible in a materials balance; however,
their releases have not been quantified and any values provided are
rough estimates.
-------
Another problem associated with phenol is its propensity for
chlorination and formation of potentially more toxic and persistent
compounds. Chlorination occurs primarily during wastewater treatment
and drinking water treatment. This exposure assessment does not
consider chlorination products of phenol; however, in a separate
assessment under the same program, the environmental fate of and
exposure to 2-chlorophenol, 2,4-dichlorophenol, and 2,4,6-trichlorophenol
are addressed.
This report is organized as follows:
• Section III contains information on the production,
consumption, discharge, and disposal of phenol.
• Section IV describes the environmental fate of phenol
in five pathways originating from the point of release.
Monitoring data, field studies, and, for surface water, an
environmental fate model, were analyzed to supplement
laboratory studies.
* Section V presents reported effect levels in humans and
laboratory animals and exposure pathways for humans.
• Section VI discusses reported effects levels and exposure
pathways for aquatic organisms.
• Section VII discusses risk of exposure to phenol for the
general population and selected subpopulations of humans
and aquatic organisms.
10
-------
SECTION III.
MATERIALS BALANCE
A. INTRODUCTION AND METHODOLOGY
In this section, a materials balance for phenol is developed
presenting information on production, consumption, and, where available,
disposal of phenol in order to identify pathways of entry to the natural
environment. The section is largely based on a report prepared for the
U.S. EPA in January 1980 (Versar 1980). It is supplemented with infor-
mation from other current and past EPA reports, other available relevant
literature, and personal communications with individuals active in por-
tions of the industry, U. S. EPA staff, and industry experts at Arthur
D. Little, Inc.
For each major source of pollutant release, the environmental
compartments initially receiving and transporting the material (e.g.,
air, land, water, etc.) were studied in order to determine the nature,
location, and quantity of phenol released to the environment. There are
many uncertainties inherent in this analysis: not all current releases
have been identified, past releases have not always been well documented,
and future releases are difficult to predict in terms of type, quantity,
and location. Nevertheless, sufficient information is available to
indicate the nature, scale (temporal and geographical), and general dis-
tribution of the environmental release of phenol.
B. MATERIALS BALANCE
Phenol is an organic chemical which is produced and used domes-
tically. A moderate amount is exported and a small quantity is im-
ported annually. In 1978, approximately 1,216,000 kkg were produced
and 639,200 kkg (53% of total production) were sold domestically (U. S.
International Trade Commission 197£). Of the remainder, 103,800 kkg (8%)
were exported and it is assumed that the difference of 473,100 kkg (39%)
was placed in stocks (U. S. Department of Commerce 1978). Production and
consumption patterns for 1978 are presented in Table 1. Data are reported
for phenol production from coal tar, petroleum streams, and from synthetic
routes (cumene peroxidation, benzene sulfonation, and toluene oxidation).
Amounts of phenol consumed for the synthesis of various derivatives
(e.g., phenolic resins, bisphenol A, caprolactam, methylated phenol,
plasticizers, adipic acid, nonylphenol, salicylic acid, dodecylphenol,
2,4-dichlorophenoxyacetic acid, pentachlorophenol, other alkylphenols,
other chlorophenols) are also presented. These uses account for about 95%
of total phenol usage. Non-consumptive uses (solvents and exports) are
also reported.
11
-------
Total 1,216,266
TABLE 1. U.S. PRODUCTION AND CONSUMPTION OF PHENOL
0y J™6"6 (I,'l08,'850)2
by Toluene Oxidation (107,250)2
by Benzene Sulfonation
Natural Phenol Production
from Coal Tar and
Petroleum Operations 83
Imports g_3
sE^c£s 103>8253
St°CkS 473,0752
Phenolic Resins 2fift 2
Bisphenol A ^88,020
Caprolactam 92'9802
Methylated Phenol ' ;
Plasticizer (Excluding Adipic Acid) ia rnr2
Adipic Acid to Inn2
Nonylphenol ^,40^
Salicylic Acid q ™n2
Dodecyphenol 62002
2,4-D (2,4-Dichlorophenoxyacetic Acid) fi'?nn2
Pentachlorophenol °'^n
Other Alkylphenols TS snn2
Other Chlorophenols q'^nn2
Petroleum Refining I'^nn^
53,'7082
2
1,216,183
* Production data were not readily available for 1978; however, it is
assumed that methylated phenol consumption is included in "Other"
category.
Source: 1. U.S. International Trade Commission 1978.
2. Arthur D. Little, Inc., estimates extrapolated from
Versar 1980.
3. U.S. Department of Commerce 1978.
12
-------
Table 2 presents estimated environmental releases based on 1978
consumption patterns. Approximately 19,018 kkg of phenol were intro-
duced into the environment of the United States in 1978 from numerous
sources including phenol-producing processes, processes in wnich phenol
is used as a feedstock in the manufacture of other products (consumptive
uses), processes in which phenol is used as solvent, storage of phenol
by producers and users, phenol loading and transport operations, and
emissions of phenol from miscellaneous sources: timber products process-
ing, leather tanning, pulp and paper mills, textiles manufacturing and
indirect sources, iron and steel production, steam electric units,
residential wood-burning and hand-stoked coal furnaces, and Publicly
Owned Treatment Works (POTW's).
Of approximately 19,018 kkg of phenol entering the total environ-
ment, about 2,500 kkg (13%) emanated from production processes, 1,850
kkg (10%)resulted from processes that used phenol as-a feedstock, and
about 10,270 kkg (54%) were byproducts from miscellaneous sources.
Of particular note is that residential wood burning and gasoline com-
bustion contributed approximately 9,500 kkg (81%) of the nationwide
phenol air emissions. The remainder of the releases were from POTW's
contributing approximately 4,000 kkg (21%) and releases during storage
of 392 kkg (2%). The total identified emissions (19,018 kkg) were 1.5%
of the total 1978 U.S. production. Figure 1 shows the total annual
phenol flow in the United States based on 1978 data from all recognized
sources from production through disposal in the environment. In future
years, it appears that the amount of phenol released into the environ-
ment will be proportional to its annual production. As the reality of
the nation's energy crisis is more keenly perceived, the popularity of.
wood-burning stoves is likely to increase dramatically causing a con-
concomitant increase in phenol air emissions.
The estimated distribution of phenol releases to the environment in
1978, as shown in Table 2 and Figure 1, is summarized below:
Phenol Releases Percent of
Environmental Compartment (kkg) Total Release (%)
Air 12,121 64%
Water ' 4,658 25%
Land 1,229 6%
POTW's 1,010 5%
It is apparent that air and water are the major recipients of the
various phenol releases.
1. Production
Before 1914, coal tar and petroleum streams (natural phenol) were
the only sources of phenol. Today, synthetic phenol production accounts
for 99% of U.S. phenol production. About 91% is produced by cumene
13
-------
TABLE 2. ENVIRONMENTAL RELEASES OF PHENOL
(Estimated 1978)
Environmental Releases (kkg) to
Source
Production:
by Cumene
by Toluene Oxidation ~|
by Benzene Sulfonation r
Transport
Export
Intermediate Consumption:
Phenol Resins
Bisphenol A
Caprolactam
Methylated Phenol
Plasticizers (Excluding
Adipic Acid)
Adipic Acid
Nonylphenol
Salicylic Acid
Dodecylphenol
2,4-D (2,4-Dichlorophenoxy-
acetic acid)
Pentachlorophenol
Other Alkylphenols
Other Chlorophenols
Petroleum Refining
Other Use Categories
Other Consumption:
Timber Products
Leather Tanning
Textiles
Iron and Steel
Steam Electric
Residential Wood Burning
Hand-Stoked Residential
Coal Furnaces
Pulp and Paper Mills
Automobile Exhaust
POTW
Storage
Other
Total
Air
1.6309
A
196 10
17
77io
748
2710
710
510
310
548
98
2io
210
248
410
188
210
37 10
A
A
A
A
A
7,2248
—
2,280
39211
37
12,121
Direct
Aquatic
20-
A
A
1315
187 16
A
A
A
A
A
A
A
A
A
A
384 17
A
219
620
I21
3 22
1023
:
32*
2^
A
4,658
POTW
18 ^
A
A
—
57215
24716
A
A
-25
A
A
A
A
A
A
A
101 17
A
219
6420
I21
I22
-23
—
4*
A
1,010
Land
83226
39727
_
A
A
A
A
A
A
A
A
A
A
A
A
A
A
A
A
A
A
A
—
A
1,229
currently available
Note: Numbers refer to derivations in Appendix A.
*U.S. EPA, Effluent Guidelines Data 1979, as yet unpublished.
Source: Arthur D. Little, Inc., estimates extrapolated from Versar 1980.
1 A
-------
PRODUCTION
CONSUMPTION
Air
12,121 kkg
ENVIRONMENTAL
COMPARTMENTS
Legend:
POTW
1,010 kkg
Land
1,229 kkg
Land
— Water
... Air
92,980 kkg
:e: Boundaries between receiving media are often undefined and/or changing;
phenol apparently released to one medium may result in another.
irce: Tables 1 and 2.
FIGURE 1 MATERIALS BALANCE OF PHENOL
15
-------
peroxidation, the remaining 9% by benzene sulfonation and toluene
oxidation. The contribution by each process and the total production
of phenol are shown in Table 3. Each process is described in detail
in Appendix B. The names, locations, processes, and capacities of
plants that produce phenol are presented in Table 4 and Figure 2.
The amount of phenol imported in 1978 was 83 kkg (U. S. Department
of Commerce 1978).
2. Releases From Phenol Production
As previously mentioned, about 91% of phenol production is by the
cumene peroxidation process. Known airborne emissions resulting from
this process.amount to between 3% and 17% of total airborne phenol
emissions, that is, between 330 and 1,630 kkg annually in 1978 (see
Table 2). Losses to water amount to 20 kkg, which is small compared
with the total identified phenol aquatic discharges from all sources,
about 4,600 kkg. An estimated 830 kkg were contained in solid waste.
Known discharges to POTW's were estimated to equal 18 kkg.
Releases from phenol production by means of toluene oxidation and
benzene sulfonation are treated collectively in this report; both pro-
cesses together account for only about 9% of total phenol production.
No releases to air, water, or POTW's have been identified, but a solid
waste volume containing approximately 400 kkg was calculated (see Table 2)
Only one company produces phenol by the benzene sulfonation process and'
only one plant uses the toluene oxidation process.
Only about 1% of phenol is recovered from the so-called natural
sources of coal tar and petroleum operations. The quantity of airborne
phenol emissions is unknown but possibly significant. The" amount of
phenol released to aquatic sinks is also unknown, but POTW discharges
from this form of phenol production are considered negligible on a
national scale, as is the volume of phenol-containing solid waste, due
to the small total mass of ohenol produced by this method.
3^ Sources of Phenol Releases During Storage, Loading, and Transport
The estimated releases from storage, loading, and transport associ-
ated with production of phenol are 299 kkg (1978). This estimate is
based on the supposition that 0.161 kg of phenol are lost per 1 kkg
stored and transported (Delaney and Hughes 1979). No process-dependent
discharges are included in this estimate. Phenol, bisphenol,and phenolic
resins are stored and transported according to users' (consumers') needs
in the form of liquids or solids. Frequently metal tanks are used if
the material is stored or transferred in a particularly corrosive chemi-
cal form. Stainless steel tanks are utilized. Train or trunk tank cars
transport the material depending on the quantity involved. Storage is
maintained at both manufacturing points and the site of consumption.
The primary potential for material release is during transfer activities
in which the material passes between manufacturer and storage or transport
16
-------
TABLE 3. TOTAL U.S. PRODUCTION
OF PHENOL BY PROCESS,
1977 and 1978
Process
1977
Phenol Production
(kkg)
1978
Phenol Production
(kkg)
Phenol from cumene
peroxidation
Phenol from toulene
oxidation
Phenol from benzene
sulfonation
966,709
93,500
1,108,850
107,250
Coal tar and petroleum
operations
TOTAL
12,200
1,072,409
83
1,216,183
Source: Arthur D. Little Inc., estimates extrapolated from Versar (1980)
and U.S. International Trade Commission (1978).
17
-------
TABLE 4. U.S. PHENOL MANUFACTURERS
Company
Allied Chemical
Clark Oil
Dow Chemical
Ferro Corp.
Georgia-Pacific
Corp.
Getty Oil
Kalama
Koppers Co. ,
Inc.
Me rich em Co.
Monsanto Co.
Location
Frankford, PA
Blue Island, IL
Oyster Creek, TX
Santa Fe Springs, CA
Plaquemine, LA
El Dorado, KS
Kalama, WA
Follansbee, WV
Houston, TX
Chocolate Bayou, TX
Process
cumene peroxidation
cumene peroxidation
cumene peroxidation
coal tar and petroleum
cumene peroxidation
cumene peroxidation
toluene oxidation
coal tar
petroleum
cumene peroxidation
1977
Annual
Capacity
(103 kkg)
272
40
211
.
120
43
25
_
—
227
Northwest
Petrochemical
Corp.
(Stimson
Lumber Co.)
Reichhold
Chemical
Shell Chem. Co.
Standard Oil Co.
Stimson Lumber
Anacortes, WA
Tuscaloosa, AL
Deer Park, TX
Richmond, CA
petroleum
benzene sulfonation
cumene peroxidation
cumene peroxidation
70
227
25
Union Carbide
Corp.
United States
Steel Corp.
Bound Brook, NJ
Penuelas, PR
Clairton, PA
Haverhill, OH
cumene peroxidation 68
cumene peroxidation 91
coal tar 147
cumene peroxidation
Total 1,566 +
Source: Versar 1980 and U.S. International Trade Commission 1978.
18
-------
A Penuelas, Puerto Rico
Sources: Versar (1980) and U.S. International Trade Commission (1978).
FIGURE 2 LOCATIONS OF U.S. PHENOL MANUFACTURERS
-------
vessel or storage or transport vessel and user. Data are not available
to accurately quantify this release.
Since roughly 0.006% of the total domestic phenol supply was
imported in 197S, releases from unloading of imported phenol and trans-
port to the point of consumption are assumed to be negligible.
4. Uses of Phenol
The utilization of phenol in the United States was 743,000 kkg in
1978 (see Table 1). This can be divided into consumptive and non-con-
sumptive uses. Consumptive uses include processes in which phenol is
chemically converted to another compound. Non-consumptive uses include
exports and processes in which phenol is used as an end-product rather
than as an- intermediate. Table 5 shows the percentage of phenol used
by each end use. Figure 3 presents a generalized pattern of phenol use.
a. Consumptive Uses
It is estimated that 633,000 kkg of phenol were consumptively used
in 1978 (see Table 1). The major use was as a chemical intermediate in
the synthesis of other organic chemicals.
i. Phenolic Resins
The manufacture of phenolic resins consumed 288,020 kkg (24%) of
phenol in 1978 (see Table 1). Phenolic resins are the oldest synthetic
polymers and are produced by reacting phenol, or substituted phenols
with an aldehyde. Almost all resins significant to industry are based
on the.reaction of phenol with formaldehyde. Two types of resins are
produced: resols—a mixture of the two substances with an excess of
formaldehyde—and novalaks—a mixture with a deficiency of formaldehyde.
(Sittig 1975). Both types are manufactured by similar processes
described in greater detail in Appendix B. The locations of manufacturers
of phenol resins are shown in Table B-l and Figure 4.
The major end use for phenolic resins is as an adhesive in ply-
wood. Thus, the demand for these resins is dependent on the housing
industry. To a lesser extent, phenolic resins are used for the hardwood
plywood market to produce waterproof bonds. Phenolic resins contribute
to the weathering properties of low-cost, highly absorptive southern
pine and enable it to be used instead of more expensive northern woods.
Phenolic-bonded wood can be used indoors or outdoors, whereas wood bonded
with protein or urea-formaldehyde adhesives cannot be used outdoors
because the adhesives are not moisture resistant.
The second largest use for phenolic resins is in foundry resins
(e.g., for use in casting automobile parts). These resins are also
used in the comparison molding of plastic parts, laminating, thermal
insulation, and protective coatings.
-------
TABLE 5. U. S. PHENOL UTILIZATION1
Consumptive Uses
Phenolic Resins
Bisphenol A
Caprolactam
Methylated Phenol
Plasticizers
Adipic Acid
Nonylphenol
Salicylic Acid
Dodecylphenol
Other Alkylphenols
2,4-D
Pentachlorophenol
Other Chlorophenols
Percent of Total Phenol Utilization (%)
39
14
13
4
3
2
2
1.5
1
2.5
1
0.5
1.5
Non-Consumptive Uses
Petroleum Refining (solvent application) 1
Exports 14
Total 100
1 Based on annual utilization of 743,000 kkg.
Source: Table 1 in this report.
-------
•" Phanolic flusin
^- Hesols
kf — Molding Compound!
~C
Bonding Resins
E Surface Coatings
Thermosettmg Molding Powder*
Epoxy
Coaling*
Adhesives
PH6NQLH
j— extrusion Compounds for t'uuncJl £ Electronic Components
1— Cj»t Film Form is Eit>ariuii Foti
*— Bjiti ror PhotoijiaphK, Finn
,N',iuii 6 Fi|j«fi ~'-"-i-~ CJiputi
X L- Textiles
^ CjlllQtaciam / I— Tlrei
^v L— Other Industrial
X
I Applications
Nylon 6 Pioincs and Films
Manufacture at Nylon 66 ~ Carpets
^" Ailipic Acid "'" I ' InienneOuie MI Manufacture at Nylon til
h— Manutjctureat Plasnci/e's -Sheets, Tubes, Rods. Films
& Cable Jackets
— Additive to Floor Polishes,
— Additive m Formulation of Specialty Coatings & Adhesives
Phenol-based Plasticners — Flame Retarding Agents
i— Emulsifiers for Toxicants
iNony.onenot -y- Suiiactanis •- I— Metai Cleaners
I— Latex Stabilizers
Intermediate in the Manulacture of Annoxtdants (or the Plastics jnd Rubber Industry
— Oil Additives
— Synthetic Lubricants
, Luoe Oil Additives
Nomomc Surface — Active Agents
Other Alkytphenols
i Phenolic Resins
f— Oil Emuisif'ers
^™" Phosphate Resins
preservative r— Wood Preservative
i Pentachiorophenate -|— Fungicide in Water ba
*— Herbicide and Slimicn
r* P Chtorophenol
Other Chlorophenols —|— O-Chloropnenoi
Sodium
Wood Preservative
iaied Latex Paints
id Slimicide
"2,4-O H
ied Phenols
Synthetic Cresois Jnd Xylenols
Source: Versar 1980-
FIGURE 3 GENERALIZED FLOW PATTERN FOR PHENOL USE
-------
U)
I N OAKOTA~~ \ "Cri _
i \ MINNESOTA
' I
\
S DAKOTA*
v
_ _iMISSOUHI
IOWA
) S~ATA ~T GA. x-
MISS ] i \
I • \
A A j \ N
1 * \ . 1.
LA ) I '
f \ A4 / A ^N
\-A N- «"
X^,. HORIOA '
A Phenolic llcsin
Bjs|ihi.
-------
Significant waterborne wastes emanating from the production of
phenolic resins are water introduced with the raw materials, water
formed as a product of the condensation reaction, caustic solution
used for cleaning the reaction kettles, and blowdown from cooling
towers (Sittig 1975).
ii. Bisphenol A
Bisphenol A is produced by the reaction of phenol with acetone.
Production of bisphenol A consumed an estimated 105,380 kkg (9%) of the
phenol manufactured in 1978 (see Table 1). Four companies produced
bisphenol A in 1977. The names and locations of these plants are given
in Table 6 and Figure 4.
A schematic flow diagram of the production of bisphenol A is shown
in Figure 5. The phenol and acetone are added into the reaction vessel
in a 3 to 1 molar ratio. Small amounts of catalyst promoter (methyl
mercaptan) are added, and then the catalyst, dry hydrogen chloride gas,
is bubbled through the mixture. The temperature is held at 50°C for
8 to 12 hours. A slurry of crystalline bisphenol A is produced.
A number of byproducts are formed in conjunction with the main
reaction. In some plants these impurities are eliminated by batchwise
crystallization. However, in at least one plant, continuous distillation
and extraction crystallization are employed to purify the product. To
produce purified bisphenol A, the slurry is transferred into a still
where it is stripped of excess phenol and water. The overhead is decanted in-
to an organic phase (consisting mainly of phenol which is recycled) and an
aqueous phase. The latter is piped into the hydrogen chloride recovery
unit, and contaminated water is sent to disposal (disposal practices
unknown). Bottoms from the stripper are sent to a series of purification
distillation chambers where excess phenol, isomers, and heavy ends are
removed from the system for either recycle or disposal. Distillate from
the last chamber is sent to the extraction operation, which produces a
slurry of pure crystals. The filtrate from the centrifuge is partially
recycled to the crystallizer, and the remainder is concentrated in an
evaporator to produce liquid bisphenol A.
The major uses for bisphenol A are in epoxy resins and polycarbonate
resins. The epoxy resins are mainly used for coatings and adhesives.
Polycarbonate resins are used in injection molding, as an extrusion com-
pound for electrical and electronic components, as electrical foil in
the cast-film form, and as a basis for photographic film.
The major sources of waterborne wastes are the water separated from
the hydrochloric acid recovery unit, the extracted aqueous phase from
the crystallizer, and the condensate from the final evaporator. The
organic wastes in this water are mainly phenol, bisphenol, and organic
solvent. Organic vapor escaping from the final evaporator may contribute
significant amounts of contaminants (U. S. EPA 1975).
24
-------
TABLE 6. U. S. BISPHENOL A MANUFACTURERS
Company
Location
Annual
Capacity
(103 kkg)
Dow Chemical, U.S.A.
General Electric Company
Plastics Business Division
Engineering Plastics Product Dept.
Shell Chemical Co.
Union Carbide Corporation
Union Carbide Caribe, Inc., subsid.
Total
Freeport, TX
68
Mount Vernon, IN
Deer Park, TX
Penuelas, PR
99
68
32
267
Source: Versar 1980.
25
-------
Himu HC i
r
RECYCIE PlltlWL
AttHltlt
PIIHIIH.
IICL
flEACIOHS
>->
SEP.
IICI
RECOVERY
WASIEWAIER
-»flAKE UISI'IIIIKII
•-LIQUIU BISPIIEHUL
EXCESS PHENOL AND ISOUEHS
MAKE UP WAFEH
Source: U.S. EPA 1975.
FIGURES BISPHENOL A PRODUCTION
-------
ill. Caprolactam
The manufacture of caprolactam consumed 92,980 kkg (8%) of total
phenol produced in 1978 (see Table 1). Allied Chemical Corporation in
Hopewell, Virginia, is the only company in the United States to produce
caprolactam from phenol; this plant has a capacity of 190,000 kkg of
caprolactam. Two other companies that produce this chemical use cyclo-
hexane instead of phenol as their starting material.
Cyclohexanone is the key intermediate in the caprolactam process.
It is derived from phenol by catalyst hydrogenation and from cyclohexane
by an air oxidation process (Lowenheim and Moran 1975). The catalytic
hydrogenation of phenol produces both cyclohexanols and cyclohexanone.
For cyclohexanol, a nickel catalyst is used; for cyclohexanone, palladium
or carbon catalyst is employed. The caprolactam is produced in the
Beckmann process by the addition of hydroxylamine sulfate to the cyclo-
hexanone (Lowenheim and Moran 1975). Small amounts of phenol (estimated
at 27 kkg annually) may be lost to the process water in the catalyst
recovery unit, the wash tower, and the final product purification step
(Lowenheim and Moran 1975).
Over 90% of the caprolactam produced is used to produce Nylon 6
fibers. The largest market for Nylon 6 fibers is carpets. Other uses
are textiles and industrial applications such as tires. Caprolactam is
also used to manufacture Nylon 6 plastics and films. These latter
products are used to make molding compounds for automobile parts and
appliance parts, extrusion compounds for coarse bristle filaments, and
wire and cable jackets.
iv. Methylated Phenols
The production of methylated phenols consumed approximately 41,465
kkg of the phenol produced in 1977 (a 1978 number was not available).
They are made by reacting phenol and methanol.
Methylated phenols are used in turn to produce synthetic cresols
and xylenols. The xylenols are used as antioxidants for gasoline,
lubricating oils, and elastomers. 0-cresol is mainly used in the pro-
duction of agricultural products and plastics and resins.
v. Plasticizers
Approximately 18,600 kkg (2%) of the phenol produced in 1978 were
used to manufacture plasticizers (see Table 1). The most common phenol-
based plasticizer is cresyl diphenyl phosphate. This plasticizer is
used primarily to impart fire retardancy to polyvinyl chloride. Tri-
phenyl phosphate, another phenol-based plasticizer, is used as a flame-
retarding agent and as a plasticizer for cellulose acetate and nitro-
cellulose. Other phenol-derived plasticizers are octyl diphenyl phos-
phate, isodecyl diphenyl phosphate, and dibutyl phenyl phosphate.
27
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vi. Adipic Acid
The manufacture of adipic acid consumed about 12,400 kkg (1%) of
the phenol produced (see Table 1) . Only Allied Chemical Corporation in
Hopewell, Virginia, produces adipic acid using phenol as the raw material;
this plant has a capacity of 13,600 kkg. The other five companies that
produce adipic acid use cyclohexane as the raw material.
Adipic acid from phenol is produced by hydrogenation of phenol in
the presence of nickel catalyst to cyclohexanol, which is then oxidized
with nitric acid to adipic acid (Lowenheim and Moran 1975).
The major use of adipic acid is as an intermediate in the manufacture
of Nylon 66. The carpet market offers the largest outlet for this nylon.
Adipic acid is also used in the manufacture of plasticizers and certain
plastics and as a food acid.
vii. Nonylphenol
About 12,400 kkg (1%) of the phenol consumed is used to manufacture
nonylphenol (see Table 1). The names, locations, and capacities of the
companies that produce nonylphenol are given in Table 7.
Nonylphenol is manufactured by liquid-phase alkylation of phenol
with mixed isomeric nonenes in the presence of an acid catalyst. Pre-
mixed phenol and nonene are fed to an agitated, jacketed tank reactor
where they react, in the presence of catalyst, at 50 to 100°C for a
period of 30 to 120 minutes. In the reaction product, the parasubsti-
tuted derivative predominates, with smaller amounts of ortho and 2,4-
dinonylphenols also present. Vaccum distillation is employed to separate
the par a-nony Iph eno 1 from the dinonylphenols (Lowenheim and Moran 1975).
Most of the nonylphenol produced is consumed in the manufacture of
surfactants. Nonylphenol is converted into detergents either by ethoxyla-
tion or sulfonation. These detergents are used in specialty applications,
such as emulsifiers for toxicants, metal cleaners, and latex stabilizers.
Nonylphenol is also used in the plastics and rubber industry where it is
an intermediate in the manufacture of antioxidants. The reaction of
nonylphenol with formaldehyde produces compounds useful as oil additives
and synthetic lubricants (Lowenheim and Moran 1975).
viii. Salicylic ci
The manufacture of salicylic acid consumed slightly less than 1%
(9,300 kkg) of the phenol produced (see Table 1). Four companies produce
both technical- and medicinal-grade salicylic acid. One additional
company produces only medicinal-grade salicylic acid. The names,
locations, and capacities of these plants are given in Table 8.
28
-------
TABLE 7. U.S. NONYLPHENOL MANUFACTURERS
Company
Location
Borg-Warner Corp.
Exxon Corp.
Ferro Corp.
GAF Corp.
Kalama
Monsanto Co.
Rohm and Haas Co.
Rohm and Haas Texas,' Inc. ,'subsid.
Schenectady Chems., Inc.
Texaco Inc.
Uniroyal Chem.
Total
Annual
Capacity (Id3 kkg)
Morgantown, WV
Bayway, NJ
Sante Fe Springs, CA
Calvert City, KY
Linden, NJ
Kalama, WA
Kearny, NJ
Philadelphia, PA
Deer Park,. TX
Oyster Creek, TX
Rotterdam Junction, NY
Port Neches, TX
Naugatuck, CT
27
13
0.9
2
9
9
18
11
5
23
10
16
5
149
Note: Some capacities also include that for other alkylphenols.
Source: Versar 1980.
29
-------
TABLE 8. U.S. MANUFACTURERS OF TECHNICAL- AND
MEDICINAL-GRADE SALICYLIC ACID
Company
Atomergic Chemetals Corp.1
MUM Chems. Corp., subsid.
Location
Plainview, NY
Annual
Capacity
(103 kkg)
NA
Dow Chem. U.S.A.
Monsanto Co.
Monsanto Chem. Intermediates Co.
Midland, MI
St. Louis, MO
Sterling Drug Inc.
The Hilton-Davis Chem. Co. Div.
Cincinnati, OH
Tenneco Inc.
Tenneco Chems., Inc.
Total
Garfield, NJ
25
Produces only medicinal-grade salicylic acid.
Source: Versar 1980.
30
-------
Salicylic acid is produced by reacting dry, powdered sodium phenate
(made from phenol and sodium hydroxide) with excess carbon dioxide to
produce sodium salicylate solution. This is next acidified with either
hydrochloric acid or sulfuric acid to obtain salicylic acid (Morrison
and Boyd 1970).
Salicylic acid is used primarily in the production of aspirin.
It is also used in the production of salicylate esters and salts, in
resins, as a dyestuff intermediate, and as a prevulcanization inhibitor.
ix. Dodecylphenol
Dodecylphenol is produced from phenol and propylene tetramer. It
consists mainly of a mixture of p-alkylphenols derived from various
isomeric branched-chain dodecylenes. The manufacture of dodecylphenol
consumed about 6,200 kkg (less than 1%) of the phenol produced (see
Table 1). Dodecylphenol is produced by four companies. The names and
locations of the plants are listed in Table 9.
Approximately 95% of the dodecylphenol produced is used in the
production of lube oil additives. The remainder is used in the manu-
facture of nonionic-surface active agents.
x. 2,4-D
The manufacture of 2,4-D (2,4-dichlorophenoxyacetic acid) consumed
about 6,200 kkg (less than 1%) of the phenol produced in 1978 (see
Table 1) . There are nine companies that produce 2,4-D and its esters
and salts. The names and locations of the plants are listed in
Table 10.
The herbicide 2,4-D is manufactured by the reaction of sodium salt
of 2^4-dichlorophenol (made by phenol chlorination) with monochloro
acetic acid. 2,4-D is used as a weed killer and a defoliant. It is
used extensively in the weeding of cereal crops, corn, sorghum, milo,
sugar cane, coffee, pastures, range land, lawns, and unwanted
growth.
xi. Pentachlorophenol
Pentachloropheno! production consumed about 3,100 kkg (less than
0.5%) of the phenol produced (see Table 1). Three companies produce
pentachlorophenol. The names, locations, and capacities of the plants
are listed in Table 11.
Pentachlorophenolis produced by chlorination of phenol or poly-
chlorophenols in a batch operation. Phenol and chlorine are fed to a
reactor where the chlorination is carried out in the absence of a cata-
lyst until trichlorophenol is formed. At that point a metallic chloride
catalyst (e.g., Feds or AlCls) is added to complete the reaction.
31
-------
TABLE 9. U.S. DODECYLPHENOL MANUFACTURERS
Company
Location
Borg-Warner Corp.
Borg-Warner Chems. Div.
Morgantown, WV
GAF Corp.
Chem. Products
Calvert City, KY
Monsanto Co.
Monsanto Indust. Chems. Co.
Kearny, NJ
Schenectady Chems., Inc.
Oyster Creek, TX
Rotterdam Junction, NY
Source: Versar 1980.
32
-------
TABLE 10. U.S. 2,4-D(2,4-DICHLOROPHENOXYACETIC ACID) MANUFACTURERS
Company
Location
Dow Chem. U.S.A.
Fallek-Lankro Corp.
Imperial, Inc.
North American Phillips Corp.
Thompson-Hayward Chem. Co., subsid.
FBI-Gordon Corp.
Rhodia Inc.
Agricultural Div.
Riverdale Chem. Co.
Union Carbide Corp.
Agricultural Products Div.
Amchem Products, Inc., subsid.
Vertac, Inc.
Transvaal, Inc., subsid.
Midland, MI
Tuscaloosa,AL
Shenandoah, IA
Kansas City, KS
Kansas City, KS
Portland, OR
St. Joseph, MO
Chicago Heights, IL
Ambler, PA
Fremont, CA
St. Joseph, MO
Source: Versar 1980.
33
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TABLE 11. U.S. PENTACHLOROPHENOL MANUFACTURERS
Company
1978
Location Capacity (kkg)
Dow Chemical, U.S.A.
Midland, MI
12,000
Reichhold Chemicals, Inc.
Tacoma, WA
8,500
Vuleau Materials Company
Chemicals Division
Wichita, KS
8,500
Total
29,000
Source: U.S. International Trade Commission 1978.
34
-------
The majority of the pentachlorophenol produced is used as a wood
preservative. A small amount is used to produce sodium pentachlorophenate,
which is used as a wood preservative, as a fungicide in water-based latex
paints, and as a herbicide (U. S. EPA 1975). A more detailed considera-
tion of PCP can be found in EPA's Exposure Assessment on Pentachloro-
phenol (Scow, et al. 1980) .
xii. Other Alkylphenols
Approximately 15,500 kkg (1%) of the phenol produced is used to
manufacture alkylphenols other than nonylphenol and dodecylphenol (see
Table 1). One of the most important of these chemicals is para-tert-
butylphenol which is used in the preparation of phenolic resins, in
rubber tackifiers, and in oil demulsifiers. Other important alkylphenols
are the isopropylphenols, which are used in the production of phosphate
esters, which in turn are used in the production of functional fluids
and plasticizers.
xiii. Other Chlorophenols
Approximately 9,300 (less than 1%) of the phenol produced in 1978 was used
in the production of chlorophenols other than 2,4-D and pentachlorophenol
(see Table 1). Included among these chemicals are para-chlorophenol which
is mainly used as an intermediate to produce other materials and ortho-
chlorophenol which is recovered as a byproduct of para-chlorophenol.
Para-chlorophenol is usually chlorinated further to produce higher
chlorophenols.
b. Non-Consumptive Uses
Non-consumptive use is a minor category of phenol use. This cate-
gory totaled 110,000 kkg in 1978, less than 15% of the total for
consumptive use.
i. Petroleum Refining (Use of Phenol as a Solvent)
Approximately 0.5% (6,200 kkg) of the phenol produced in 1978 was
used in petroleum refining (see Table- 1). Phenol is produced at the
refinery through catalytic cracking, crude distillation, and product
finishing operations. In turn, phenol is used in solvent dewaxing
operations where waxes are removed from lubricating oil stocks by pro-
moting crystallization of the wax (U. S. EPA 1979d).
ii. Export of Phenol
Data provided by the Directory of Chemical Producers indicate
103,800 kkg phenol were exported in 1978.
35
-------
c. User Storage, Loading, and Transport
Phenol has a relatively low volatility compared with many liquid
hydrocarbons, but losses do occur during storage, handling, and transport
because of volatilization, leakage, and spillage. The estimated amount
of phenol released to the air because of user handling practices (390 kkg)
is probably too low. Airborne emissions given in Table 2 for the various
use categories probably overlap to some extent with emissions from handling
procedures, but the amount of emissions reported from handling is suffi-
ciently conservative that even with overlap it is unlikely that any
inaccuracy would be significant.
It is known that used phenol drums are recycled into commerce and
that some portion of these drums is available for purchase by the
general public. Drum sellers and recyclers are supposed to flush
phenol drums with sodium hydroxide in order to neutralize the phenol,
and the washings are supposed to be collected in drums and sent to
disposal. The flushing procedure is not always followed, however, and
metallic drums containing up to about 250 g of phenol each are being
purchased and used for various purposes by the general public (J. Warring,
James T. Warring and Sons Barrel Company, personal communication,1979).
The amount of phenol lost to the environment each year is a function of
the number of barrels discarded by phenol handlers and the degree to
which drum recyclers adhere to the proper drum flushing practices.
5. Releases From Phenol Utilization
The single largest aquatic release due to phenol use is the discharge
of about 187 kkg annually associated with the production of bisphenol A.
In fact this is the single largest phenol release to water from production,
use, and miscellaneous emissions, with the exception of POTW and petroleum
refining discharges.
The airborne emission data for the various use categories are dis-
played in Table 2. The atmospheric emission has been derived on the basis
of emission factors associated with generalized phenol-handling practices,
and thus the emission number is proportional to the amount of phenol used
in each use category. No equivalent data were available for those use
categories for which only one airborne emission number is given in Table 2.
Therefore, total airborne emissions due to phenol use (both in the pro-
duction and actual consumer use categories) should actually be larger,
possibly several times larger than shown in Table 2,
36
-------
The specification of an airborne loss resulting from user storage,
loading, and transport is to some extent redundant in that it repeats
the numbers given in Table 2 as airborne emissions in the specific use
categories. However, the emission factor for losses due to handling
has actually been derived on the basis of producer handling losses.
Since there are many more users than producers, and, consequently, since
the number of handling and transfer operations must be much greater for
users than for producers, the reiteration of any airborne emission from
user handling practices seems warranted. In fact, the amount shown in
Table 2 (392 kkg) is actually double the amount calculated on the basis
of the producer-handling emission factor. On the basis of engineering
knowledge, handling losses by users are deemed likely to be several
times greater than 392 kkg, but there is no basis for using a higher
multiplying factor than two in estimating an emissions amount. In fact,
for the whole emission category of airborne emissions, the total emis-
sions from the phenol use categories are certainly on the low side since
the majority of airborne emissions listed are based only on handling
losses and not on process or dissipative losses.
With regard to aquatic discharges from the use categories, few data
were available. A significant amount of phenol is considered to be lost to
water as a result of bisphenol A production; the amount lost (to both sur-
face water and POTW's), is under 1% of the amount of phenol used in bis-
phenol A production. Also, approximately 585 kkg of phenol are lost to
water, primarily to POTW's during the production of phenolic resins. The
use of phenol as solvent in petroleum refining is associated with an
effluent discharge of 485 kkg, of which 101 kkg goes to POTW's (U.S. EPA
1979d) (see also Appendix A No. 17).
Emissions due to export are attributed to transportation plus dock-
side loading. The air emission factor for these operations was based on
the supposition that 0.161 kg of phenol are lost per kkg of material
export (U.S. EPA 1979b). On this basis, the total estimated annual
emissions to air are 6 kkg. No releases to water or land from phenol
export have been identified and it is believed that any would be negligible.
The major discharge to POTW's identified is associated with petroleum
refining, as is mentioned above. POTW emissions from the production of capro-
lactam and adipic acid have been identified as zero. Discharges to POTW's by
other industries such as nonylphenol and chlorophenol producers are unknown.
No solid wastes from phenol uses have been identified, but many
releases to land no doubt exist.
6. Miscellaneous Releases
The category "miscellaneous releases" covers those phenol emissions
that emanate from a wide variety of sources where phenol use or pro-
duction is entirely incidental. The sources can be divided into four
categories: industrial sources, fuel combustion sources, POTW's, and
medicinal products containing phenol.
37
-------
a. Industrial Sources
Information on emissions of phenol from industrial sources is
scanty and primarily deals with phenol in industrial effluents that are
directly discharged to the environment or to POTW's. For the industrial
categories of timber products processing, leather tanning, textile manu-
facturing, and iron and steel production, 12 kkg of phenol were directly
discharged to the environment while 68 kkg were discharged to POTW's
(see Appendix A No. 19-22). In all, the phenol contained in miscel-
laneous industrial effluents accounts for approximately 1% of all the
phenol discharged to the aquatic environment.
b. Fuel Combustion Sources
Data on phenol emissions from fuel combustion are also sparse. Of
note is the fact that emissions from residential wood burning were
estimated to makeup 60% of phenol air emissions nationwide (Versar 1980).
There is some uncertainty in this estimate due to the lack of background
data presented to support it. The type of combustion equipment, for
example, or the kind of wood burned will influence the phenol concentra-
tions emitted from a volume of wood. However, there is some evidence
that a high value may be expected from domestic wood combustion. Phenol
is an incomplete pyrolysis product from organic material (e.g., liquid
fuels, plant material) and its generation is increased under the con-
ditions of low temperature and oxygen typical of home wood-burning units
(J. Allen, Battelle Columbus Laboratories, personal communication, 1980).
More efficient, quick-burning processes (e.g., oil burners, wood-fired
boilers used industrially) would have much lower associated phenol con-
centrations. Due to the increasing use of wood as a home-heating fuel,
several groups are currently investigating wood-combustion emissions
(e.g., Argonne National Laboratories, Monsanto, Battelle) (J. Allen,
Battelle Columbus Laboratories, personal communication, 1980). Steam-
electric units discharged 10 kkg directly to the aquatic environment
trom the ash handling subcategory (Appendix A No. 23).
Phenol is also a combustion product of liquid organic fuels, such
as gasoline and diesel. Phenol emissions from combustion is variable
depending on fuel variables: grade, source, refining technique, and
seasonal variations in composition (PEDCo. 1977). The compound comes
from the breaking of linkages connecting phenol groups, which are con-
stituents of petroleum, and thus relasing them. Approximately 6 mg
phenol were estimated to be released from each kg of exhausted diesel
fuel and slightly greater than 6 mg per kg of gasoline fuel (estimated
by Arthur D. Little, Inc., from information in Barber et_al. 1964 and
Hare and Bradow 1979). This would result in an air emission value on
the same order of magnitude of that resulting from wood combustion,
approximately 2,280 kkg/year. This estimate assumes an average engine
efficiency and fuel composition on a national scale equivalent to those
in the studies on which the estimates are based. It is based on a U.S.
annual gasoline consumption value of 3.8 x 108 kkg (U.S. DOE 1979).
Emissions of phenol to air are also expected from combustion of
other petroleum-based fuels such as aviation fuels, gas turbine fuel oils,
kerosene, and others. It was not possible to estimate what these values
are in this level of effort.
38
-------
c. POTW's
An estimated 4,000 kkg of phenol were discharged directly from
POTW's to the environment (see Appendix A No. 24) based on phenol levels
in POTW effluents and the total U.S. POTW flow rate.
d_. Medicinal Products Containing Phenol
A number of medicinal products, primarily skin lotions and sore
throat remedies, contain phenol at levels of 0.5% to 4.75%. Table 12
lists the names of selected phenol-containing products; however, other
products also exist and this tabulation is not inclusive. There was no
information regarding the total amount of -phenol consumed annually in
production of these products.
C. AREAS FOR FURTHER RESEARCH
As discussed earlier in this section, this report is based on data
from government documents (particularly publications issued by U.S. EPA),
journals, and standard references and texts. In some cases the data are
not associated with a high degree of confidence due to the small sample
sizes supporting them or because they are outdated. Two areas where
future investigations should be focused warrant mention.
Perhaps the weakest portion of the published literature is that
dealing with phenol as an influent or effluent to POTW's. Up until now,
it has only been possible to identify the sources of 1,006 kkg of phenol
influents to POTW's, while an estimated 4,000 kkg of phenol are dis-
charged into the aquatic environment by POTW's. It is expected that
ongoing work under the aegis of U.S. EPA's Office of Water Regulations
and Standards (through both its Effluent Guidelines Division and its
Monitoring and Data Support Division) will identify fully the sources
and amounts of phenol influents to POTW's, as well the sources and
amounts of phenols discharged directly to the environment.
Another area that needs attention is the disposal of phenol as a
solid waste in landfills. This phenomenon is likely to occur when
phenol is adsorbed on a catalyst disposed of with the spent catalyst
or (since phenol is a highly refractory organic compound) when phenol
is disposed of as part of the sludge of industrial and/or wastewater
pre-treatment and treatment plants. It is anticipated that the Back-
ground Documents (being prepared for the Office of Solid Waste both
within and without U.S. EPA) on Processes Generating Hazardous Wastes,
as defined in §250.14(b)(2) of the EPA Proposed Hazardous Waste Regula-
tions under the Resource Conservation and Recovery Act (43 FR 58946,
December 18, 1978), will be very useful as data sources for determining
the fate of phenol in landfills.
39
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TABLE 12. MEDICINAL PRODUCTS CONTAINING PHENOL
Product
Campho Phenique®
Calamine Lotion®
P & S Ointment/liquid®
Panscol Ointment®
Benadex Ointment ®
Kip for Burns Ointment ®
Noxema Medicated Cream®
Tanurol Ointment®
Dri Toxen cream®
Peterson's Ointment®
Cepastat Mouthwash
and Lozenges®
Chloraseptic®
Chloraseptic lozenges®
% Phenol
4.75
1.0
1.0
1.0
1.0
0.5
0.5
0.75
1.0
2.5
1.45
1.45
32.5 mg
total
phenol/
lozenge
Manufacturers
® Glenbrook
® Mallinckrodt Inc., Penich
& Co. (and others)
® Baker Laboratories
® Baker Laboratories
® Fuller
® Young's
® Noxell
® O'Neal, Jones and
Feldman, Inc.
® C. J. Walker, Co.
® Peterson's Ointment Co.
® Merrell-National
Laboratories
® Eaton Laboratories
® Eaton Laboratories
Source: U.S. EPA 1979c.
40
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D. SUMMARY
In 1978, approximately 1,216,100 kkg of phenol were produced in the
U.S. Of the total, 639,200 kkg (53%) was consumed in the U.S., 103,800 kkg
(8%) was exported, and 473,100 kkg (39%) presumably was placed in stocks.
Phenol is produced from coal tar and petroluem streams (1%) and from the
following synthetic routes: cumene peroxidation (90%), benzene sulfona-
tion, and toluene oxidation (together comprising 9%).
The primary use of phenol (95% of total consumption) is as an inter-
mediate in the synthesis of various organic chemicals including phenol
resins (44%), bisphenol A (17%), caprolactam (15%), methylated phenol (4%),
plasticizers, adipic acid, nonylphenol, salicylic acid, dodecylphenol,
2,4-dichlorophenoxyacetic acid, pentachlorophenol, other alkylphenols,
and other chlorpphenols. The remaining 5% of phenol is used as a solvent
in petroleum refining, in medicinal products, or exported.
Approximately 19,018 kkg of phenol (VL.5 of the total amount produced
in 1978) are released to the environment annually by production and con-
sumption-related activities. Of the total amount released, approximately
10% derives from consumption of phenol products, 13% from production,
54% inadvertently from residential wood combustion and gasoline combustion,
21% from POTW discharges, and 2% from transport and export activities.
The estimated environmental distribution of phenol releases is 64%
(12,121 kkg) to air, 30% (5,668 kkg) to water and POTW's, and 6% (1,229
kkg) to land. The most significant discharges to air result from residen-
tial wood burning (7,224 kkg) releasing natural phenols. Aquatic dis-
charges are primarily from petroleum refiners (384 kkg), and bisphenol A
producers (187 kkg) in the form of cooling water blowdown, condensate,
and extracted liquids. Major contributors of phenol to land are the
producers of phenol through disposal of contaminated sludge from column
bottoms and evaporation vessels.
An estimated 4,000 kkg of phenol is discharged to surface water from
POTW's based on reported POTW effluent levels. Only 1,010 kkg (^25%) of the
total amount can be accounted for, primarily from petroleum refiners.
The remainder of the amount discharged originates from other unquantified
intentional sources, natural sources such as decaying organic matter, and
possibly as breakdown products from POTW treatment of more complex organics.
Further investigation is needed regarding the accuracy of the POTW
estimate, identification of sources to POTW's, the significance of indirect
and natural releases to the overall environmental balance of phenol,
and land disposal practices of phenol wastes.
41
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REFERENCES
Barber E.D. ; Sawicki, E. ; McPherson, S.P. Separation and identifica-
tion of phenols in automobile exhaust by paper and gas liquid chroma-
tograpny. Analytical Chemistry. 36 (13) : 2442-2445 ; 1964.
Delaney, J.L. ; Hughes, T.W. (Monsanto Research Corporation). Source
Sl-IoS/f 79 O^^lfT °f aCet°ne and Phen01 from cumene- ^Port No.
EPA 600/2-79-Old. Washington, D.C. : Environmental Protection Agency; 1979.
Eimutls, E.G.; Quill, R.P. ; Rinaldi, G.M. (Monsanto Research Corporation).
Source assessment: Non-criteria pollutant emissions. 1978 Update U S
Hare, C.T. ; Bradow, R.L. Character batron of heavy duty diesel gaseous
-'
Lowenheim, F.D.; Moran, M.K. Faith, Keyes and Clark's industrial
1975:50-55,
MA: Allyn and
Park° NCViruTnpa1' ^^ Atm°Spheric benzene emissions. Research Triangle
029-1977 Environmental Protection Agency. Report No. EPA-450/3-77-
Scow, K.; Gilbert, D.; Goyer, M.; Perwak, J.; Payne, E.; Thomas, R.;
\
-------
U.S. Environmental Protection Agency (U.S. EPA). Development document
for interim final effluent limitations guidelines and new source perfor-
mance standards for the major organic products segments of the organic
chemicals manufacturing point source category. Washington, D.C.:
Effluent Guidelines Division; 1975:156-162.
U.S. Environmental Protection Agency (U.S. EPA). Draft development
document for proposed effluent limitations guidelines for the iron and
steel manufacturing industry point source category. Vol. VII. Pipe and
tube subcategory and cold rolling subcategory. Washington, D.C.:
Effluent Guidelines Division; 1979a.
U.S. Environmental Protection Agency (U.S. EPA). Draft development
document for proposed effluent limitations guidelines and standards
for the iron and steel manufacturing industry point source category.
Vol. II. Byproduct cokemaking subcategory, beehive cokemaking subcate-
gory. Washington, D.C.: Effluent Guidelines Division; 1979b.
U.S. Environmental Protection Agency (U.S. EPA). Ambient water quality
criteria—Phenol. Washington, D.C.: Criteria and Standards Division,
Office of Water Planning and Standards; 1979c.
U.S. Environmental Protection Agency (U.S. EPA). Development document
for effluent limitations guidelines and new source performance standards
for the petroleum refining point source category. Washington, D.C.:
Effluent Guidelines Division. Report No. EPA-440/l-74-014-a; 1979d.
U.S. Environmental Protection Agency (U.S. EPA). Priority pollutant
data base. Monitoring and Data Support Division, Water Quality Analysis
Branch; 1980.
U.S. International Trade Commission. Synthetic organic chemicals. U.S.
production and sales; 1978:47, 48, 78.
Versar, Inc. Materials balance for phenol. Preliminary draft.
Washington, D.C.; Monitoring and Data Support Division, U.S. Environ-
mental Protection Agency; 1980.
43
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SECTION IV.
FATE PATHWAYS AND ENVIRONMENTAL DISTRIBUTION OF PHENOL
A. INTRODUCTION
The following section describes the fate pathways of phenol in the
environment following its intentional discharge or accidental release to
water, air, and soil. Due to the short half-life of phenol under most
environmental conditions, emphasis has been placed on its transformation
and, because of its high reactivity and the potential for conversion to
more harmful compounds, on its reaction products. Intermedia transfers
are discussed in situations where they appeared to occur at a faster
rate than transformation. Due to the limitations of the monitoring
data base which describes phenol concentrations in environmental media,
each major pathway description is followed by a short summary of reported
measured concentrations in the medium considered in each pathway.
The section is organized into the following categories:
Pathway #1 Discharges to Surface Water
Pathway #2 Emissions to Air
Pathway #3 Air to Water/Soil: Rainout
Pathway #4 Fate in POTW's and Wastewater Treatment
Pathway #5 Soil to Groundwater and Surface Water:
Leaching, Runoff
Pathway #6 Chlorination of Phenol and Formation of
Chlorophenol
B. PHYSICAL PROPERTIES OF PHENOL
Table 13 summarizes some of the basic physical properties of
phenol.
C. PATHWAY //I. DISCHARGES TO SURFACE WATER
1. Introduction
Phenol discharges to surface water are responsible for 25% of all
phenol releases to the environment (see Section III). The major known
direct dischargers are petroleum refiners (380 kkg), bisphenol A pro-
ducers (approximately 187 kkg) , and producers of phenol through cumene
peroxidation (20 kkg). Other sources discharge only to POTW's, have
minor aquatic emissions, or there is no information available regarding
their discharges. It should be mentioned that discharges to land
(comprising 6% of all environmental releases) also have a high like-
linucd of movement into groundwater or nearby surface waters,
45
-------
TABLE 13. GENERAL PHYSICAL PROPERTIES OF PHENOL
Molecular weight 94.11 grams
Melting point 4]_oc
Boiling point 182°C
Solubility (g/lOOg H20 at 25°C) 9.3
Acid dissociation constant (Ka) 1.1 x 10~10
Vapor pressure at 20°C (torr) 0.5293
Log octanol/water partition coefficient 1.46
Source: Versar 1979a, Morrison and Boyd 1974.
46
-------
especially at unsupervised landfills or other disposal sites. This
particular pathway is described later (see Pathway ?/5) .
Since release to surface water is such a significant source of phenol
release to the environment, this pathway is considered here in detail.
The section is divided into the following topics:
• Fate processes affecting phenol in surface water
(hydrolysis, photolysis and photooxidation, oxidation,
volatilization, adsorption, biodegradation, and
bioaccumulation);
• Field studies;
• EXAMS model results; and
• Monitoring data.
2. Fate Processes
a. Hydrolysis
Little information appears to exist concerning the hydrolysis of
phenol. By extrapolation of data from similar compounds, however,
phenol is assumed to be relatively resistant to hydrolysis. This is
because the covalent bond of a substituent attached to an aromatic ring
is usually stable due to the high negative-charge density of aromatic
nuclei (Versar 1979a). An OH radical rate constant for hydrolysis of
phenol in aqueous solution is given as k = 8.2-85. x 10-9/mole/cm3/sec
(Shetiya et al. 1976).
b. Photolysis and Photooxidation
Studies of phenol photodecomposition under artificial light indicate
a potential for photolysis (Galan and Svith 1976, Joschek and Miller
1966). It is not known how common this fate process is under natural
light conditions however the process could be employed in tertiary waste
treatment to degrade phenol.
An aqueous solution of phenol with pollutant-level concentrations
was passed through a reactor irradiated at 254 run, not an occurring
wavelength in the atmosphere. Phenol was photolyzed and decomposed.
Final degradation products included CC>2 and H20; intermediates included
benzoquinone, predominately as a transient product, as well as some uniden-
tified stable intermediates. The postulated oxidation sequence is shown
in Figure 6, The initial activation of phenol to produce the phenoxy
radical and the ring opening and conversion of quinones to organic acids
are the slowest steps. No rate constants were calculated in this
experiment.
In another similar experiment (Joschek and Miller 1966) , an aqueous
phenol solution was irradiated with a low-pressure mercury lamp at 253.7
nm, a wavelength outside the spectrum of sunlight. The results are
47
-------
ph
phenoxy
enol — ^ radical — »
intermedi<
complexe
phenoxy
•• radical ^ polyp
ite 1
i
orga
\
henols
i
intermediate
^ complexes
r
nic
ris ^
i
C02 H20
Source: Galan and Smith 1976.
FIGURE 6 PHOTOOXIDATION PATHWAYS FOR PHENOL
48
-------
therefore, not directly applicable to environmental conditions. Certain
compounds were identified as degradation products and are listed in
Figure 7. The products were compatible with the general categories
described in the previous experiment (in Figure 6). No rate constants
were calculated from the results of this experiment.
Phenol was also detected as a photodecomposition product in a
similar experiment on 4-chlorophenoxyacetic acid in which chlorophenol
was an intermediate (Crosby and Wong 1973).
c. Oxidation
Phenol reacts readily with chlorine and bromine in water, forming
halogenated compounds (Versar 1979b). Chlorine or ozone can oxidize
phenol to hydroquinone and other products (Versar 1979b). These pro-
cesses are described in greater detail in Pathway #5. No information
on the significance of these reactions outside of wastewater treatment
was available but it is expected to be low unless the reactants are
immediately available (e.g., in the same effluent).
d. Volatilization
No information was found concerning the rate of volatilization of
phenol from water except that the rate was expected to be slow based on
similar compounds (Versar 1979a) . A volatilization half-life for a repre-
sentative condition can be computed, however, by the following method
(Thomas 1980). The Henry's law constant, which relates the concentra-
tion in air above a solution to the concentration in the solution, can
be found by use of:
H' - P /S
vp
where P = vapor pressure of phenol, 7 x 10 ~ atm
S = solubility of phenol. 988 moles/m3
so that H;is ~7 x 10~7 atm-m3/mole. Based on this value, phenol is
expected to volatilize very slowly, with the rate controlled by slow
diffusion through the air (Mackay 1977, MacKay and Yuen 1979). The
half-life for volatilization can be estimated by using the two-film
theory of volatilization described by Liss and Slater (Liss and Slater
1974) . A phase-exchange coefficient is used to estimate the rate of
transfer across the air or water films adjacent to the interface between
air and water. Using the liquid-phase exchange coefficient, the half-
life is
where K= Hk ki/(Kk + ki) , the overall liquid-
O O
phase exchange coefficient, cm/hr (Liss and
Slater 1974).
-------
OH
Ul
o
4,4 - Dihydroxybiphenyl
OH
16
OH
OH
2,4' - Dihydroxybiphenyl 2,2' - Dihydroxybiphenyl
4 — Hydroxdiphenyl ether
OH
OH
OH
OH
2 — Hydroxydiphenyl ether
Source: Joschek and Miller 1966.
OH
Hydroquinone
Catechol
FIGURE 7 PHOTODECOMPOSITION PRODUCTS OF PHENOL
-------
H /KT = H//0.024 = 2.9 x 10~5 (R is the gas
constant, 8.2 x 10~5atm-m3/mole K and
T is temperature).
k = 1137.5 (V,7ind +Vcurr) (18/M)'5,gas-
& phase exchange coefficient, cm/hr
(Southworth 1979)
V
wind = wind speed, m/sec
V = current speed, m/sec
curr ^
ki = 23.51 (Vcurr >969 /Z'673) (32/M)'5 exp
[. 526 (Vw-^ncj~ * * 9) J, liquid-phase exchange
coefficient, cm/hr (Southworth 1979)
Z = average depth of water body, m
Assuming the following set of conditions; Vwinci = 2 m/sec, Vcurr
=• 1 m/sec, and Z = 1 m, then the computed half-life for volatilization
from a water body having these characteristics is estimated to be -1,550
hours or about two months. An increase in wind speed may reduce the
volatilization rate by a factor of three for a shallower water body,
but as depth increases the estimated half-life increases to a year or
more, even at higher wind speeds.
e. Adsorption
The solid form of phenol is soluble and will sink when spilled and
then dissolve. Solutions of phenol (50% benzo-phenol) will sink when
spilled and may remain at the bottom of the water body in a concentrated
layer in a stratified system. The potential for contact with and sorption
on the sediments will therefore be greatly increased in these situations.
Due to phenol's low log octanol/water partition coefficient (1.46),
however, adsorption onto sediment is theoretically not expected to be a
significant fate process. The relatively low sediment concentrations
reported in monitoring data compared to those for other, for example,
chlorinated compounds support this hypothesis. (See Monitoring Data
section of Pathway #1). The process of adsorption on both organic and
inorganic matter is discussed in greater detail in Pathway #5.
The phenol that sinks to the bottom of a water body is subject to
the turbulence and mixing of the system it is in as well as to its own
rate of diffusion. Therefore, except under conditions of extreme strati-
fication, this phenol would soon be evenly distributed throughout the
water body.
51
-------
f. Biodegradation
Phenol is biodegradable by microorganisms which are prevalent in
the natural soil and water environments. Algae, yeasts, bacteria, other
microorganisms, broadleaf plants, and higher plants are capable of
degrading phenol (Versar 1979a, Versar 1979b, Yang and Humphrey 1975
Vela and Ralston 1978, Throp 1975, Hill and Campbell 1975, Ellis 1977)
and will contribute to the removal of moderate amounts of phenolic com-
pounds from the aqueous environment if concentrations of these compounds
do not reach toxic levels for these species (see Section V-B).
Microorganisms have developed enzymes capable of breaking down phenol
from natural and man-made sources. Nitrogen and phosphate must be avail-
able for quick breakdown (Versar 1979b). In stagnant water phenol will
support organism growth as a sole carbon source (Versar 1979a) . One to
two pounds of oxygen per pound of phenol may be utilized by biodegraders
in metabolizing dissolved phenol in the first few days of degradation at
a rate high enough to deplete local supplies of oxygen (U.S. EPA 1979).
In studies using yeasts as the degrading species, large populations of'
yeast grew on a phenol substrate, oxygen demand was high, and oxygen
transfer rather than phenol concentration became the growth-limiting
factor (Yang and Humphrey 1975). A mixed culture of algae and micro-
organisms degrades phenol faster than only heterotrophs since algae
supply oxygen to the system (Versar 1979b). Streams may therefore be
highly resistant to self-purification below a certain phenol level (Faust
et al. 1969) .
Phenol concentration affects the growth rate of microorganisms, as
well as its own degradation rate. Where phenol is highly diluted, bio-
degradation may become unimportant since microorganisms apparently will
preferentially feed on other material if the phenol concentration is too
low (Versar 1979a). At medium concentrations (1-10 mg/1) phenol is more
likely to be a metabolic stimulant and be degraded rapidly (Versar 1979b).
At higher concentrations, of 100 mg/1 or greater (Yang and Humphrey 1975)',
microorganisms are inhibited or killed so that growth and degradation
cease (Versar 1977, Hill and Campbell 1975). Microorganisms have been
observed to acclimate to high concentrations of phenol, but fluctuations
in phenol concentrations may prevent a constant population level (Versar
1979b). However, phenol can be inhibitory at lower concentrations to
these organisms which use it as a growth substrate (Hill and Campbell
Temperature and pH changes affect the phenol degradation rate
(Versar 1979b, Yang and Humphrey 1975). Higher temperatures may increase
phenol toxicity to microorganisms (Versar 1979b). In studies of temperature
effects on phenol degradation (Vela and Ralston 1978), it was found that the
rate of phenol degradation was not significantly influenced by temperatures
between 10 and 24°C, but that phenol degradation rapidly fell off at
52
-------
temperatures between 2° and 10°C. This decline in degradation was
probably due to a reduction in the numbers and/or activity of the micro-
bial population.
In the biodegradation of phenol, CO?, H20, and biological cells are
end products of the aerobic reactions (Throp 1975). Catechol, CsHit(OH)2,
is a metabolic intermediate in the biooxidation of phenol (Hill and
Campbell 1975). A study of biodegradation of phenol by algae (Ellis
1977) reported that algae metabolized catechol more effectively than
phenol. This pattern was not unexpected since almost all known enzymatic
oxidation reactions capable of aromatic ring fission require at least
two hydroxyl groups on the ring and catechol is therefore able to be
oxidized immediately.
Some degradation "rates" are known, but these have not been described
in sufficient detail to allow them to be applied to environmental situa-
tions in general. Table 14 presents a number of these rates measured
under different conditions. Phenol (dissolved in water) in a microcosm
study degraded at a rate of 2 mg/l/day and in the presence of soil and
plants at 3-5 mg/l/day (U.S. EPA 1979 a). It has been degraded at 30 ug/1/
hr from an initial concentration of 125 ug/1 in river water (Versar 1979a).
At 20°C 1 mg/1 of phenol was assimilated in 1-7 days, and at 4°C the time
was 5-19 days (U.S.EPA 1979a). Under anaerobic conditions degradation
was even slower (U.S. EPA 1979a).
2. Bioaccumulation
There is a limited amount of published information on the bioaccumu-
lation of phenol by aquatic organisms. In this section, data were examined
primarily for fish due to the potential for human exposure through fish con-
sumption. Microcosm, field, or system studies of concentration changes in
biota and media over time or of the biomagnification of phenol in the food
chain were not available. The lack of field observations to reinforce
laboratory findings may be due to problems with field chemical analysis
techniques (UNFAO 1973).
i. ._ Variables Affecting Bioaccumulation
The variables that affect bioaccumulation are likely to be the same
as those that affect toxicity. The toxicity of phenol to rainbow trout
was increased by:
• a decrease in dissolved-oxygen content,
• an increase in water salinity, and
• a decrease in temperature,
but was not affected by changes in pH or water hardness (UNFAO 1973).
Another study noted that the environmental factors affecting the toxicity
53
-------
Table 14. BIODEGRADATION RATES FOR PHENOL
Microcosm study
(Water only)
Microcosm study
(with soil and plants)
River water population
C02 evolution in river
population
Shake flask with river
water population
BOD test with wastewater
population
BOD test with non-
specified population
Static flask with waste-
water population
Rate Constant
or Index
2,000 ug 1 ~l hr'1
3,000-5,000ug l"1 hr'1
30 ug l"1 hr'1
(initial cone, at
125 ug/1)
80 mg COD g'1 hr'1
0.079 day'1
(t1/2 = 9 days)
j
Refractory Index = 0.87'
(classified as highly
degradable)
BOD/COD ratio = 0.81
~100% degradation in
7 days (initial concen-
tration at 5, 10 mg/1)
Reference
U.S. EPA 1979a
U.S. EPA 1979a
U.S. EPA 1979a
Fitter 1976
Lee and Ryan 1979
Bedard 1976
Lyman et al. 1974
Tabak et al. 1980
* Based on BOD/COD ratio.
54
-------
of phenolics include photolytic action, microbial degradation, pH, water
hardness, and temperature (Buikema et al. 1979). These factors are dis-
cussed in greater detail in Section VI-B.
ii. Uptake Rates and Concentrations
Although no information derived from field studies was available,
it is worth noting that soluble phenols derived from leaf litter,
lignan, and humic acids are present in natural surface waters. Total
phenol concentrations ranging from none detected to 0.21 mg/1 have been
detected in rivers in New Jersey and from 0.006 to 12 mg/1 in a reservoir
(Buikema et al. 1979). These background levels in natural waters
suggest that biota are exposed to background levels of phenol as well
as to man-made releases.
Table 15 summarizes the accumulated levels of phenol and bioconcen-
tration factors from two studies using goldfish (Carassius auratus).
The amount of phenol accumulated ("body burden") increased with exposure
to higher phenol concentrations. The maximum accumulation after 5 days,
156 ug/g, was measured in fish exposed to 100 mg/1 phenol. Kobayashi and
Akitake (1975} reported concentrations of phenol in dead goldfish that
ranged from 68 to 85 ug/g following exposure to 40 mg/1 in water.
Phenol concentrations in fish (33 observations) reported in the
STORET data base ranged from non-detectable to as high as 50 mg/kg.
The samples consisted of both remarked (at or below the detection limit)
and unremarked data. The phenol concentrations in the background water
were not available; however no mean major river basin concentration
exceeded 1.0 mg/1 during the years the tissue concentrations were
measured. The reason for such high tissue levels in contrast to the
low levels measured under laboratory conditions is not clear. A possible
explanation is errors due to the analytical techniques used or due to the
way the data were reported in the STORET system. Such high concentrations
are expected to be uncommon based on the rapid metabolism and excretion
of phenol observed under experimental conditions.
iii. Bioconcentration Factors (BCF)
The summary of bioconcentration factors in Table 15 indicates that
phenol is rapidly absorbed by goldfish, showing a concentration factor
of 1.64 after one hour of exposure to 15 mg/1 phenol, but that the in-
crease in phenol in fish then becomes slower. In general, the BCF's
ranged from 1.2 to 2.3. It was assumed that an equilibrium was reached
during the exposure period. The BCF appeared to decrease with increasing
exposure concentrations (Table 15).
The U.S. EPA estimated a weighted-average BCF for phenol in the
edible portions (muscle) of aquatic organisms to be 2.3. This was
calculated from an octanol-water partition coefficient of 31 and an
adjustment factor of 0.2875 and the equation "LOG BCF = 0.76 Log P -
0.23" (U.S. EPA 1979b). This estimation is compatible with the observa-
tions described in Table 15.
55
-------
Ln
TABLE 15. AMOUNT OF PHENOL ACCUMULATED IN FISH
(ug/g body weight)
Phenol
Concentration (ma./1 )
unpolluted river
2-7
(polluted river)
10
15
20
60
100
1 hour
24.7 (1.64)
Exposure Time
1 day
22 (2.2)1
30.3 (2.02)
39 (1.95)
96 (1.6)
138 (1.38)
_^
1977 ND (mean and max)—2 samples
1978 16.7 (mean); 50 (max)—27 samples
1979 16.0 (mean); 16.0 (max)—4 samples
5 days
14 (1.4)
26 (1.3)
92 (1.5)
156 (1.56)
1382 (1.38)
Unspecified
•^0.3 (Roach)
3.2 (Bream
and Barbel)
Goldfish
Reference
UNFAO 1973
UNFAO 1973
Kobayashi and
Akitake 1975
Kobayashi e^t al.
1976a
Kobayashi and
Akitake 1975
Kobayashi and
Akitake 1975
Kobayashi and
Akitake 1975
- - , ...
2Fish found dead in media
3EPA (1980d).
is the ratio of tissue level to water level
-------
iv. Organs Where Phenol is Accumulated
In studies of the distribution of phenol in the organs of five fish
species (carp, bream, trout, brown bullhead, and goldfish), it appears
that a greater concentration of phenol accumulated in the gall bladder,
liver, and other visceral organs than in muscle and gill tissue (see Table 16)
Kobayashi (Kobayashi et al. 1976a) found that in goldfish, except for the
gall bladder, the phenol concentration in each organ reached an equilibrium
after two hours of exposure and rapidly decreased after the fish was trans-
ferred to clean water. Only the concentration in the gall bladder increased
with exposure time, even after transfer to clean water.
v. Metabolic Effects on Bioaccumulation
Many animal species have the ability to detoxify phenol by the
formation of conjugation products with body glucuronides and sulfates
(UNFAO 1973). Maickel (Maickel et al. 1958) found that frogs (Rana
pipiens) excrete 90-95% of absorbed phenols as conjugated compounds 48
hours after parenteral administration. Toads (Bufo marinus) and mammals
also have the ability to conjugate phenols. Lower vertebrates, such as
goldfish, perch,and tadpoles, are considered incapable of forming either
glucuronides or sulfates (Maickel et al. 1958).
However, Kobayashi (Kobayashi et al. 1976b).was able to identify
two conjugates in goldfish: phenyl-B-glucuronide', which accumulates in
the bile, and phenylsulfate,which is excreted directly into surrounding
water (see Figure 8). The biliary excretion of the glucuronide is a
general detoxication mechanism that fish use for phenolic compounds.
The renal excretion of conjugates is considered to be a minor route
compared with branchial and biliary excretion (Kobayashi et al. 1976b).
vi. Depuration
Kobayashi and Akitake (1975) found that phenol absorbed by gold-
fish was so rapidly excreted that the concentration fell to 25% of
the initial level just one hour after transfer of the fish to clean
water. Subsequent decrease was slower. The authors suggested that the
low bioconcentration factors observed reflected a rate of excretion
almost equal to the rate of absorption during the beginning of the
exposure period.
In carp, phenol elimination was also immediate, with the maximum
rate of excretion occurring 10-15 minutes after administration of 200 mg/
kg phenol, either orally or by intraperitoneal injection (Buikema et al.
1979). Seventy-five percent of the phenol was eliminated after one hour
in clean water, and 85-90% was eliminated after three to four hours.
Rainbow trout have a normal urinary excretion rate of 0.7 mg monohydric
phenol/kg/day and about 8 mg total phenols/kg/day. Those rates showed
a graded increase as the exposure level increased from 1.5 to 6 mg/1
(UNFAO 1973). In addition to passive diffusion through the gills and
body surface, the biliary excretion of phenol from the liver is an
57
-------
Table 16. DISTRIBUTION OF PHENOL IN THE ORGANS OF FISH
oo
Species
Rainbow Trout
Bream
Brown Bullhead
Carp
Goldfish
Exposure to Phenol
Time Concentration
10 ing/I
7 days
4 days
3 days
1 day
9 mg/1
5 mg/1
10 mg/1
15 ppm
(- mg/1)
Decreasing Concentration in Organs
higher »lower
Skin, spleen, liver, kidney, gill (11-25 mg/kg)
— ^-muscle (3-2 mg/kg)
Blood & body fluid-
-*-cerebral fluid &
brain
Viscera (10 mg/kg)-
N-muscle (6 mg/kg)
Liver (19 mg/kg) „
test is »• muscle-
-kidney
-intestine (7 mg/kg)
Gall bladder (114. 7 mg/kg) ^liver &
pancreas (41.] mg/kg) »~spleen (33.9 mg/kg)
^testis (26.6 mg/kg) ^dkin (24 mg/kg)
muscle (23.4 mg/kg)—
scales (18.9 mg/kg)
-gills (22 mg/kg)
Reference
UNFAO 1973
Kobayashi ct al,
1976a
-------
Phenol
Absorption
Branchial
Excretion
H03SO
Source: Kobayashi eta/. 1976.
H OH
Phenyl-|3-glucuronide
FIGURE 8 A SCHEMATIC VIEW OF THE MAIN EXCRETION ROUTES
FOR THE CONJUGATED PHENOLS IN FISH
59
-------
important mechanism for the depuration of phenol (Kobayashi et al.
Although the depuration of phenol from tissue is rapid, a phenolic
flavor may persist in fish flesh for several weeks following removal
to uncontaminated water (UNFAO 1973).
vii. Biomagnification in Food Chains
The literature did not provide any direct evidence for, or dis-
cussion of, differences in bioaccumulation between lower-and higher-
trophic level species. However, one study discussed the transfer of
phenol to fish, as indicated by the phenolic flavor in the flesh
through ingesting contaminated .tubifex worms illustrating movement of
phenol up one trophic level in the food chain. In addition, it has been
sow rh I ' on, t as ee
shown that other animals can acquire phenolic flavor bv eatins "tainted
fish (UNFAO 1973) . The low bioconcentration factors observed in biota
and phenol s relatively short biological half-life indicate that bio-
magnification in the food chain is probably minimal. No direct evidence
on biomagnification was available.
viii. Summary Statement
Studies of the bioaccumulation of phenol were only available for
aquatic organisms. Absorption is "the primary route of intake. Phenol
concentrations of 14 to 156 ug/gram of body weight were reported for
goldfish exposed to 10-100 mg/1 phenol for 1-5 days. The bioconcentra-
tion factors of phenol were low, ranging from 1.2 to 2.3 in goldfish
Phenol tends to accumulate in higher concentrations in the gall bladder
liver, and visceral organs than in the muscle and gills of fish. Hi-her
vertebrates (e.g., mammals) have the ability to detoxify phenol by form-
ing conjugation products with glucuronides and sulfates; fish do not
appear to possess this mechanism, excretion of phenol occurs primarily
through bronchial diffusion and biliary excretion. No direct evidence
was obtained for biomagnification of phenol; however, it does not appear
to be significant. ' •
3. Field Studies
Tk. f~n 7P lable " briefly presents the results of each
The following text discusses the conclusions more thoroughlj
studv
study.
n
. holding tan«c at high cone nt a ons 00-lP
10Z (1,10o kg, enterecl a nearby riv
ts the relationship .e^een maxiM
-------
Distance from Site of Discharge
(km)
Sources: Krombach and Barthel, 1964.
FIGURE 9 MAXIMUM CONCENTRATIONS AND LOADS OF PHENOL
FOLLOWING RELEASE INTO RIVER
61
-------
Table 17. FIELD STUDIES OF PHENOL DISCHARGES TO AQUATIC SYSTEMS
Phenol Source
I'henol-producing
factory (benzene
sulfonation)
Aquatic System
River in
Luxembourg
cr.
10
Observations .
A holding dike broke releasing 11,000 kg of phenols (80-^)00 mg/1
in waste). Of this, 90% (9,900 kg) was retained in flooded soil
and 1,100 kg entered the river within 1/2 hour. Samples were
taken in a 36-km stretch. Results were as follows:
Max. Oxygen
Deficit (%)
100
100
94
88
76
41
32
19
20
Distance
Downstream (kin)
1.6
3.8
5.7
9.0
12.7
19.0
24.7
31.5
36.4
Max. Cone, of
Phenols (mg/1)
28
22
18.3
14.0
3.8
2.05
2.0
1.4
1.0
Load of
Phenols
810
532
396
126
80
60
(kfi)
Reference
Krombach and Barlhel 1964
Petroleum refining
complexes and
petrochemical plant
(cumene peroxidation)
St. Lawrence River
1. Based on flow rate and phenols concentration in each
river segment
Background upstream phenols level = 2-10 ug/1 mean (summer
and winter). Downstream phenols level ranged from equivalent
to background up to 100 ug/1. Means fcere as follows:
1'oliaios et al. 1975
Season Distance from Last Source Cone, (ug/1)
Winter 3,000 m downstream
(0.1° C 5,200 m downstream
water) 7,300 m downstream
Summer 3,000 m downstream
(17-21°C 5,800 m downstream
water)
21.2
24.2
17.2
4.0
2.0
Mass
Balance (kg/day)
2,330
2,650
1,940
560
275
Rural and urban
areas
Six river systems
in New Jersey
Phenols samples ranged from not detectable to 210 ug/1
Faust et al. 1969
-------
deficiency, distance from plant, and time since event. At 12.7 km down-
stream and approximately 63 hours (2 1/2 days) following the event, the
phenol concentration began to level off (at approximately 5 mg/1). The
background phenol concentration resulting from normal discharge practices
(preceeding the incident) was 1 mg/1. The maximum phenol level measured
following the incident was 28 mg/1 at 1.6 km downstream and at approxi-
mately 6 hours after the event. The phenols load fell from 810 to 60 kg
in 6 days, a 93% decrease. The accompanying deficit in oxygen levels
was attributed to oxidation of phenols and, initially, other waste
products present (sulfites).
The authors also calculated a decay rate constant for each sampling
point along the river as a function of flow rate. The decay rate (k) at
15°-16°C varied from 0.13 day (at >30 km) to 0.23 day (within 6 km).
The average k was 0.20 day-1which the authors claimed was comparable to
a wastewater treatment plant decay rate for organic constituents. The
rate constant of 0.20 day-1results in a half-life (based on first-order
kinetics) of 3.5 days.
In a Canadian study of the fate of phenols discharged to river water
(Polosios et al. 1975) Polosios found a significant difference (up to one
order of magnitude) between winter and summer mean concentrations of phenols
downstream (see Table 17). Possible explanations offered included
seasonal changes in waste products from the refinery (oil used in winter,
gas in summer), crude oil feedstock differences, and a lower rate of
microbial degradation during the winter. Considering the mass balance
of phenols in the river (mean concentration x stream flow in several
segments), again in the summer a decrease in load was evident further
from the plants while no decrease was present in winter.
The rate of phenol disappearance was estimated from the summer
observations and compared to both laboratory-derived rates and another
field study (see Table 18).
TABLE 18.
RATE OF PHENOL DISAPPEARANCE FROM RIVER WATER1
Mean
Reaction Rate Concentration
(ug I"1 hr"1) (umole I"1 hr"1) Temperature (°C) (ug/1)
Field2 1.3 0.014 17.7-20.7 3.0
Lab 2 0.021 23 15
Field3 0.09-0.17 0.0010-0.0018 15-16 15
Assuming first-order kinetics apply to ug/1 range.
2Polisios et al. 1975; 3Kromach and Barthel 1964.
Source: Arthur D. Little, Inc. estimates
recalculated from Krombach and Barthel 1964
63
-------
In a monitoring survey of phenols in six streams in New Jersey
(Faust et al. 1969), concentrations in industrial, agricultural, urban,
and rural areas were measured. A 24-hour sampling survey was conducted
at one station which receives industrial and municipal wastewaters.
The maximum levels of phenols (66 ug/1) occurred between 8:45 AM and
4:45 PM, dropping to 12 mg/1 (see Figure 10). In addition,
as the stream flow increased so did the phenols concentration until
approximately 2:00 PM; then it dropped significantly. Phenols concen-
trations in a relatively unpolluted river ranged from ^6 ug/1 to 13 ug/1.
In an agricultural area they ranged from 4-10 ug/1. Industrial areas
had considerably higher levels, up to 210 ug/1. The study did not
characterize the types of industries contributing to high phenols con-
centrations nor did it distinguish between industrial and domestic
contributions.
4. EXAMS Model Results
The EXAMS model (U.S. EPA 1980a) was implemented for purposes of
estimating phenol concentrations in water and other aquatic media and to
better understand the significance of fate processes in determining
phenol concentrations. Simulations were conducted using the data base
for phenol estimated by Stanford Research Institute (SRI 1980). The
primary processes determining phenol's persistence were biodegradation
and chemical oxidation. The results of the simulation including phenol
concentrations, total accumulation, and percentage loss by selected means
are presented in Table 19.
According to the data entered, at an equilibrium loading rate of
3 kg/hr a half-life of 10 minutes was predicted in both a eutrophic
lake and a 1-km turbid river segment with resulting maximum water-
column concentrations of 3 ug/1 and 1.3 ug/1, respectively. These
results are consistent with the surface water concentrations (means)
reported in the STORE! monitoring data base (see Section IV-C-4) since
1972; these ranged from 1.0 to 52 ug/1; the variance between the two
sets of numbers was greater than a factor of 40.
To determine how meaningful these comparisons are, the loading
rates of phenol to water in various industrial effluents can be examined.
Presentation of these effluent data must be accompanied by the warning
that the effluent concentrations and flow rates are derived from a
limited number of samples. It is not possible, therefore, to know how
representative the estimated discharge rates are of each industry as a
whole. They serve only as examples of industrial loading rates to
water. Table 20 presents the estimations based on Effluent Guidelines
sampling data presented in Appendix A.
As can be seen in Table 20, most of the estimated loading rates
are less than the 3-kg/hr rate used in the EXAMS analysis. Only the
iron and steel byproduct coking category was higher, None of these
loadings would be significant enough to result in EXAMS-estimated
water-column concentrations greater then 5 ug/1 in the stream and lake
environment.
64
-------
700
600
§ 500
en
u.
« 400
3
O
c
Q
I
300
200
100
i r
1 I ! I I I
P
I 1
70
60
60 |
-------
TABLE 19. RESULTS OF EXAMS SIMULATION
Maximum Phenol Concentration (mg/1)
Turbid
River
3.0 kg hr l
Loading
Eu trophic
Lake
3.0 kg hr l
Loading
Water
Column
(diss.) (Total)
2.97xlO~3 2.97xlO~3
1.33x10" 3 1.33xlO~3
Bottom Plankton
Sediment u8/g
1.99xlO~l* 1.45xlO~2
5. 63xlO~ 7 6.39xlO~3
Benthos
Ug/g
9.68X10"4
2.74xlO~6
I
Total in
Sediment
(dry)
(mg/kg)
1.34X10'1*
5.30xlO~7
Total Steady
State Accum.
(kg)
2.7
1.0
Turbid River
Lost by Processes
% in Water
Column
99.95
100
% in Bottom
Sediment
0.05
0
Chemical
Trans format ion
0.88
0.33
•Bio-
logical
Trans-
formation
1.33
99.63
.
Volati-
lization
0.01
0.00
Other
97.79
0.04
Self-Purification
Time Chrs)
3.34
4.61
Source: U.S. EPA 1980a.
In 12 hrs lost 100% of initial concentration in water; 28.14% of sediment.
In 12 hrs lost 99.99% of initial concentration in water; 99.99% of sediment,
-------
TABLE 20. ESTIMATED LOADING RATES OF PHENOL TO
SURFACE WATER FOR SELECTED INDUSTRIAL PLANTS
Direct Dischargers Discharge Rate (kg/hr)1
Petroleum Refiners 1.1
Hardboard2 S2S 0,2
Insulation - Thermochemical
Pulp & Refining2 0.1
Hair Pulp, Chrome Tan Retan - Wet Finish3 0.4
Hair Save, Chrome Tan Retan3 0.1
No Beamhouse3 0.4
Iron and Steel: Byproduct Coking '• - - • 3.9
Iron and Steel: Cold Rolling 0.9
Steam Electric - Ash Handling 1.61*
Assuming discharge on 250 days/year for 8 hours/day except where noted.
Subcategory of timber products processing industry.
Subcategory of leather tanning industry.
Assuming discharge on 365 days/year.
Source: Based on Effluents Guidelines data presented throughout
Appendix A.
67
-------
In Table 21, loading rates were estimated from materials balance
data (Section III) for two significant aquatic dischargers: phenolic
resin producers and phenol producers by cumene peroxidation. Both of
the rates were higher than the EXAMS-run loading rate of 3 kg hr-1,
especially the rate for phenolic resin producers. Assuming that most of
the phenolics discharged is phenol, and that the EXAMS model still
exhibits a linear relationship between loading rate and resulting water-
column concentration, a phenolic resin producer load would produce con-
centrations of 43 ug/1 and 19 ug/1 in the turbid river and eutrophic
lake systems, respectively. These levels are not significantly higher
than those at the lower loads. Some of the constituents of the phenols
waste, however are probably much more persistent than phenol itself,
so these results cannot be taken as representative of the fate of
phenolic resin waste.
5. Monitoring Data
A limited data base was available describing phenol concentrations
in surface water and industrial effluents. Records of phenol concentra-
tions in surface waters in the STORET water quality system (U.S.EPA 1980d)
entered since 1978 contain less than 600 remarked and unremarked obser-
vations. Records for phenol in sediment and tissue are much lower,
roughly 30 observations each. Of the 18 major river basins in the con-
tinental-United States, phenol concentrations have been reported in
thirteen of them. These basins are located throughout the United States-
Northeast, North Atlantic, Southeast, Tennessee River, Ohio River, Lake
Erie, Lower Mississippi, Colorado River, California, Pacific Northwest,
Great Basin, Lake Huron and Hawaii.
STORET data were far from complete; out of the 555 total observations
reported, 514 were remarked data. This means that, in most cases, the
value reported is a detection limit and the actual concentration may be
below this level. Therefore, remarked and unremarked data were con-
sidered separately. Table 22 presents data for U.S. ambient surface
water for 1978 through 1980.
Given the limited nature of the data, conclusions concerning phenol
levels in the environment should be considered only approximate. The
data indicate that the criterion of 300 ug/1 recommended by the Environ-
mental Protection Agency (U.S. EPA 1980b) to prevent taste and odor
effects has not been violated by major river basin levels since 1978,
with the exception of the Tennessee and Ohio River Basins (unremarked
data). The major values for these two river basins are based on very
limited data, one and nine observations, respectively. Each basin had
only one observation which exceeded the criterion level in the last 3
years.
Although a few studies report monitoring levels for waterwavs, data
on phenol levels in various industrial effluents are available. Jungclaus
examined both the wastewater and receiving water in the vicinity of a
specialty chemicals manufacturing plant and reported finding levels of 0.01
to 0.30 mg/1 of phenol in the wastewater, 0.01 to 0.10 mg/1 in the river
water, and no detectable levels in the sediment. These results have an
68
-------
TABLE 21. ESTIMATED INDUSTRIAL LOADING RATES OF PHENOL TO SURFACE WATER
Discharger
phenolic resin producers
Loading Rate
43 kg hr"1
(of phenols)
Cumene producer
7 kg hr
-1
Assumptions
1. 288,020 kkg produced annually
2. Approximately 100 plants
3. 2,880 kkg produced per plant annually
4. 36,400 kg phenol discharged per plant annually (based
on a release rate of 30 kg phenol/kkg phenolic resins)
5. 350 kg discharged per day (250 days/year)
6. 43 kg discharged per hour (8 hrs/day)
1. 1,108,850 kkg produced annually
2. 6 plants
3. 184,800 kkg produced per plant annually
4. 14,000 kg phenol discharged per plant annually (based
on a release rate of 0.0755 kg phenol lost/ kkg
phenol produced)
5. 56 kg discharged per day (250 days/year)
6. 7 kg discharged per hour (8 hrs/day)
Source: Section III and Appendix A.
-------
Cross Analysis
TABLE 22. PHENOL CONCENTRATIONS (TOTAL; REMARKED AND UNREMARKED) IN
U.S. AMBIENT SURFACE WATER FROM 1978 THKOUCH 1980 (MB/1)
M>jor Uiver basin
Northeast
North Atlantic
Southeast
Tennessee Kiver
Ohio Kiver
Lake llri.-
l.owei Mississippi
Co lorado K 1 ver
Pacific Nortbwes-t
Cal Ifurnla
Creat Uasin
Hawaii
1. ike Huron
No.1
27
36
111
36
77
1
51
19
117
9
11
5
-
Mean
0.07
3.7
194.8
20.8
6.1
50.0
18.4
33.7
11.8
22.8
35.0
42.0
-
Remarked
Median
-"
2.0
10.0
25.0
5.0
50.0
10.0
50.0
10.0
15.0
50.0
50.0
-
Data
852 2
-
5.0
20.0
25.0
10.0
-
10.0
50.0
25.0
50.0
",0.0
50.0
-
Max
1.0
10.0
10000.0
25.0
10.0
50.0
400.0
50.0
25.0
50.0
50.0
50.0
-
S.D.3
0.3
2.2
1334.3
6.8
3.6
-
54.8
19.8
8.2
16.0
17.9
17.9
-
I'nremarkc'd Data
No. Mean Median 85% Max S.D.
9 10.6 1.4 14 65 21.1
3 4.1 0.3 7.0 7.0 3.5
4 54.0 22.0 140.0 140.0 58. /
1 6794.0 6794.0 - 6794.0
9 659.5 1.5 26.0 5900.0 1965.2
-
-
_ -
12 21.4 0.07 1.7 ' 252.0 72.6
-
- - -
_
3 0.004 0.002 0.006 0.006 0.002
514
52.2
10.0
25.0 11)000.(I
'Number ol observations. 285tb percent!le. ^Standard deviation.
Sourt-e: U.S. tPA (1'JdOd)
622.7 41
""No observat ions .
324.6
1.3
26.0
6794.0 1385.1
-------
estimated error of 20%. Faust (Faust et al. 1969) surveyed total
phenols in six New Jersey river basins and found levels ranging from
non-detectable to 0.21 mg/1.
Various other miscellaneous reported concentrations in effluents
include measurements from three monitoring studies of oil refinery
wastewaters with levels ranging from 10 to 100 mg/1. Pitt (Pitt et al.
1975) reported concentrations between 0.006 to 0.012 mg/1 in primary
sewage plant effluents. Table 23 lists phenol concentrations in the
effluents of selected industries.
Concentrations of phenol in sediment have been recorded in major
river basins from 1978 to 1980. With 38 observations, it is impossible
for the data to be aggregated in a meaningful way for national represen-
tation. Average concentrations for the three regions over the three-
year period ranged from none-detected to 454 mg/kg for phenol in sediment.
These figures are presented in Table 24 along with maximum and minimum
values.
D. PATHWAY #2. EMISSIONS TO AIR
1. Introduction
An estimated 64% (12,121 kkg) of all environmental releases of phenol
are to air (see Table 2). Emissions during residential and automobile fuel
combustion contribute approximately 81% (9,500 kkg) of total air releases;
the other significant air source is the phenol producers (by cumene process)
which contribute approximately 14% of air releases. The remaining releases to
air (totalling ^1,000 kkg) can be attributed to numerous consumptive
processes such as production of phenolic resins, bisphenol, and nonyl-
phenol, and losses during transport and storage. Another source which
could not be quantified for this study is the combustion of fossil fuel
by power plants and other fuel consumers.
Losses to the air are associated with two categories; 1) loss of
phenol in steam or vapor from evaporators, coolers, and combustion of
fuel (all usually involving high temperatures); and 2) loss of phenol
during normal handling and transport. No information was available on
handling and transport to determine the amount lost in particulate form
from solid phenol cakes and the amount lost in vapor form from liquid.
2. Fate Processes and Field Studies
Given the major sources of phenol releases to air (see Table 2) it
can be assumed that most of the chemical releases are in vapor form.
In the atmosphere phenol may be adsorbed by airborne particuiates. This
was indicated by its detection in particulate form as a secondary organic
pollutant in an urban atmosphere (Cronin et al. 1977). It is possible,
however, that its presence in this situation was due to a phenol-genera-
ting reaction involving a parent pollutant (e.g., alkene, alkane) already
sorbed on the particulate matter.
71
-------
TABLE 23. EFFLUENT LEVELS OF PHENOL IN INDUSTRIAL WASTEWATER
Industry
Kraft paper mill (A)1
Kraft paper mill (B)1
Paper mill
Petroleum refinery (A)1
Petroleum refinery (B)1
Petroleum refinery
Integrated oil refinery
Petrochemicals
Coal gasification
Specialty chemicals manufacture
Specialty chemicals manufacture
Kraft paper mill
Dye manufacturing plant
Type
Separate plants
2Non-detectable
Source: Buikema et al. 1979
final effluent
final effluent
raw waste
final effluent
final effluent
8-hour lagoon effluent
raw effluent
fire-dry lagoon effluent
processed effluents
wastewater
river water
final effluent
raw effluent
Concentration (ma/1)
ND2
ND
10-2,000
0.88
3036
0.2
120
0.06
<0.2
0.1-0.3
0.01-0.1
0.14-2.4
110-190
Reference
Keith 1976
Keith 1976
Nebel et al. 1976
Baird et al. 1976
Baird ^JL^. 1976
Webb et al. 1973
Volesky et_a_l. 1974
Webb et al. 1973
Klemetson 1976
Jungclaus et al. 1978
Jungclaus et al. 1978
Fox 1976
Buikema et al. 1979
-------
TABLE 24. CONCENTRATION OF PHENOL
IN SEDIMENT (in mg/kg;
1978-1980)
Number of
Observations Mean Median 85% Max. S.D.
Remarked Data
24
14.2 0.05 1.0 143 39.1
Unremarked Data
14
102
0.5 208 454 155
Source: U.S. EPA 1980c.
73
-------
Phenol emissions to the atmosphere are related to combustion of
fossil fuels and are therefore higher in urban areas. During periods
of smog, phenol is detected as a secondary pollutant or originating
from reactions involving primary, directly emitted substances such as
total particulate alkanes and alkenes, alkyl benzenes, naphthalene,
alky piperidenes, and alkyl nitrites, among others (Cronin et al. 1977).
Phenol was one of a group of secondary pollutants characterized by a
low vapor pressure and undergoing condensation to form particulates.
The results of monitoring phenol concentrations over a day are
presented in Figure 11. Phenol levels were plotted against ozone and
total particulate alkene concentrations. Phenol peaks occurred during
the same time periods in which ozone peaks were found as well as during
periods of maximum sunlight intensity. The phenol peak lagged by 7 hours
behind the first alkene peak, suggesting an alkene reaction rate (lead-
ing to phenol) on the order of 7 hours. The phenol level reached a peak
of approximately 0.35 ug/m3 at 4:00 PM and rapidly dropped to its daily
low of about 0.05 ug/m3. Destruction of phenol was not attributed to
any specific process but may have been due to photooxidation or indirect
photolysis (as described later).
In another study of an urban atmosphere conducted in Frankfurt,
Germany, phenol concentrations (in addition to CO and lead concentra-
tions) were reported to be related to traffic flow and volume and
attributed to the combustion of gasoline (presumably due to breakdown
of benzene) by motor vehicles (Deimal and Gableske 1973). Measurements
were made every half hour between 6:00 AM and 8:00 PM. Concentrations
ranged from <0.020 to 0.289 mg/m3. Approximately 50% of all observations
(total = 402) were £ 0.029 mg/m3 and 75% were £ 0.049 mg/m3. The higher
concentrations were associated with periods of inclement weather (pre-
sumably^ inversions) . No supporting data were given to substantiate the
authors' statement of a relationship between phenol levels and traffic
volume. Additionally, no information was given on the possible chemical
reactions responsible for reduction of phenol levels following traffic
slowdown or on the products of these reactions.
The reason that the German atmospheric levels (Deimal and Gableske
1973)^were two to three orders of magnitude higher than the U.S. levels
(Cronin et al. 1977) was not obvious but may have been due to differences
in the total fuel consumption/combustion between the two cities studied,
the distance from sources, or differences in the placement of monitoring
equipment.
The two fate processes influencing phenol concentrations in the
atmosphere are indirect photolysis and photooxidation (Versar 1979a).
Versar estimated, based on interpolations from photodegradation data
for m-xylene and toluene, an atmospheric lifetime of a few days for
phenol due to photolysis and/or photooxidation of the metastable oxygen-
phenol charge transfer complexes.
74
-------
0.4 -
0.3
5
o
-------
Phenol most commonly occurs in the atmosphere in the non-ionic
protonated form, as indicated by its pKa of 10.02 (Versar 1979a) The
spectral absorption curve for non-ionic phenol has had peaks measured
5Wo™ 210/and 26° ™ 290 nm in the atmosphere is thus
not likely to directly photolyze phenol. The anion of phenol has a
higher absorption maximum between 287 and 310 nm which does fall within
the spectral range of natural sunlight; however, this form is expected
to be quite uncommon. Coordination of the phenol oxygen atom with low
valence metal cations (e.g., in soil) may increase the ionization of
the phenolic proton (Versar 1979b).
Indirect photolysis depends on the presence of nitrosyl, hydroxyl
and alkyl peroxyl radicals, which are generated through the photochemical
reactions of nitrogen oxide, water, and organics in the environment
(Versar 1979b).
3. Monitoring Data
The only monitoring data available on phenol concentrations in air
were those observations discussed in the previous section. To summarize,
in two urban areas phenol levels ranged from a low of 0.05 ug/m3 to
VrT / f ' fioctual:i38 on a daily basis (Cronin et al. 1977) and from
<20 ug/m^. to 289-ug/m4 with 50% of all observations less than 30 ug/m3
(Deimal and Gableske 1973).
E. PATHWAY #3. AIR TO WATER/SOIL; RAINOUT
Following the release of phenol to air, the amount not subject to
photodecomposition will be available for transport from the atmosphere
to other media through the process of rainout.
If the concentration of phenol in air is known, the nondimensional
Henry s law constant can be used to provide an estimate of the concen-
tration in rain. The equation
Crain ' Cair/H*
where: c . = concentration in rain
IT a III
cair = concentration in air
H* = nondimensional Henry's law constant
shows this relationship. Using the nondimensional Henry's law constant
or j x iu-3 and assuming phenol concentrations of between 50 and 350
ng/m in air (Cronin et al. 1977), the initial concentration in rain
will be between 0.4 and 3 mg/1.
76
-------
These levels will be the initial amount. As rain keeps falling
it will cleanse the atmosphere in the immediate vicinity and the con-
centration will decline. Phenol has been detected in rainfall, but no
levels have been quantified (Versar 1979a). Detectable phenol levels
in rain can be expected in areas of heavy atmospheric emissions from
autos or industries (Versar 1979a).
Only non-quantified observations reported elevated phenol concen-
trations in industrial-area rain as compared to rural-area rain in
Bulgaria (Kurchatova and Mladenova 1975) and detectable levels in snow
in an industrial region of Russia (Bobkov 1974).
F. PATHWAY #4. FATE IN'POTW'S AND WASTEWATER TREATMENT
1. Introduction
Phenol is frequently detected in the influent of Publicly Owned
Treatment Works (POTW's) at concentrations of 1-200 ug/1 (Burns and
Roe 1980). According to the materials balance_on phenol (Section III),
the only discharges to POTW's that have been quantified (1,010 kkg annually)
originates from phenol resin producers, bisphenol A producers,
cumene production facilities, petroleum refineries, timber products,
leather tanning, textile, and iron and steel industries. For most of
the significant sources of phenol releases to water, no information was
available to discriminate between direct and indirect dischargers. Some
of the influent load may be attributed to leaching or runoff of phenol
into stora sewers, due to the chemical's mobility; however, it is likely
that other industries discharge phenol in their effluents to POTW's.
Quantification of this contribution will require further investigation.
Phenol can be degraded in wastewater treatment plants by numerous
and diverse processes: through biodegradation in activated sludge and
trickling filters (Versar 1979a) and removal by chemical treatment
(Versar 1979a). Observations at POTW's demonstrate the success of
phenol removal by conventional wastewater treatment.
2. Biological Degradation
The biodegradation process for phenol is fast, with a rate on the
order of 0.013-7.6 ug/l/hr (Burns and Roe 1980) measured in several
studies (Versar 1977). Not all organisms existing in biological process
tanks can degrade phenol at the same rate, however. Acclimation is an
important factor in achieving consistently good phenol removal in
biological treatment systems (SCS 1979, Haller 1978). Removal efficiency
is a function of system design. Contact time, flow rate, aeration rate,
etc. are key variables in ultimate removal efficiencies. Also the
importance of the chemicalnakeup and variability of the wastewater can-
not be overlooked.
77
-------
At phenol concentrations of between 1 and 10 mg/1 most of the
phenol will be degraded (Versar 1979a). Oxygen uptake is inhibited by
phenol concentrations of between 10 and 100 mg/1. Microorganisms can
continue to degrade phenol at concentrations of up to 500 mg/1 if the
population is allowed time for acclimation. In completely mixed sus-
pended-growth systems using activated sludge or aerated lagoons with
long hydraulic retention times, inlet concentrations of 200-300 mg/1
were degraded to 0.2-0.5 mg/1 (>99%) in about 24 hours (Throp 1975).
Oxygen was supplied by mechanical agitation and about 2.5 kg 02 were con-
sumed per kg of phenol at 30°C. In wastewater treatment of phenol by
biological methods, pH must be kept between 6 and 9.5; nitrogen and
phosphorous nutrient loadings in the range of BOD5:N:P = 100:5:1 are
optimum for biodegradation. Phosphorous can be added at a concentra-
tion ratio of P:phenol - 1:30 to increase the process efficiency.
A temperature of 18-35°C is desirable. Under these conditions and in
the presence of 0.16 kg phenol per kg of biological solids, biological
oxidation was observed to reduce the phenol level of 100-800 mg/1 to
1 mg/1. Shock loads of phenol must be monitored and kept below 500 mg/1
to prevent a decrease in the efficiency of the system (Throp 1975).
Following these shock loads, different steady states may be achieved in
the activated sludge reactor due to the lag times for recovery from the
shock loads (Pawlowsky et al. 1973 ). Even when acclimated to high
concentrations of phenol, activated sludge may have lag times of from
about 10 hours at an initial concentration of 200 mg/1, to as high as
7 days at an initial concentration of 700 mg/1 before the biodegradation
rate becomes rapid.
A trickling-filter biotreatment process can reduce phenol up to
280 mg/1 with 99.9% efficiency (Throp 1975). To demonstrate the efficacy
of acclimated bacteria on phenol removal, several industrial wastes con-'
taining phenol were treated by adding a freeze-dried PHENOBAC® culture
(acclimated to phenol) to activated sludge/biological filter processes.
Removals were 95%, 99+%, and 99+% for influent phenol concentrations of
86.4, 880, and 332 mg/1, respectively (SCS 1979).
3. Chemical Treatment
Phenol is degraded by a number of chemical treatment methods avail-
able for wastewater treatment. Although many of these methods have only
a limited distribution, some of them are discussed in the following
section. These are chlorination and treatment with hydrogen peroxide,
potassium permanganate, ozone, and iron ferrate.
During normal wastewater treatment and not under the special con-
ditions necessary for chlorine-mediated oxidation, it is very common
for phenols to become chlorinated to form lower chlorinated phenols.
This is discussed separately under Pathway #6.
Chlorine can be used to degrade phenol. At a ratio of 100:1
Cl:phenol, phenol at 123 ug/1 is degraded by 12 mg/1 of chlorine.
Phenol at 13.5 mg/1 completely consumes all applied chlorine up to 16.2
mg/1 within a contact time of one-half hour (MCA 1972).
78
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The reaction progresses rapidly in the first 15 minutes, followed
by a decreasing rate up to 2 hours. With treatment by chlorine at 36 mg/1,
the final pH is above 8.4, outside the pH limits for formation of
chlorophenol (Throp 1975).
The high reactivity of phenol in the formation of chlorophenols is
attributable to the ring-activating electron-releasing properties of the
OH functional group (MCA 1972). The nature of the activating group is
such that halogen substitution in aqueous solution is preferentially
favored in the ortho- and para- positions with respect to the OH group.
2,4,6-trichlorophenol is the final step before ring oxidation. Figure 12
shows the oxidation pathways. The amount of chlorine required for the
complete breakdown is greater than the amount required for the stochio-
metric formation of trichlorophenol. This can be attributed to the
additional chlorine required for direct oxidation.
The presence of ammonia in wastewater treatment facilities inhibits
the chlorination of phenol (Murphy et al. 1975, Jahnig and Bertrand
1976). The presence of inorganic chloramines may degrade phenol, as
suggested by the formation of phenol oxidation products (in wastewater
chlorination). In the decomposition of chloramines free residual
chlorine is released which could in turn react with phenol. Therefore,
decomposition of chloramines would be the rate-controlling step. In a
reaction of chlorine/phenol in the presence of ammonia, the ammonia can
retard the uptake of Cl through the formation of less oxidative chlora-
mines. Given a sufficient contact time, however, phenol can be both
chlorinated and oxidized, even by monochloramines with their weak poten-
tial for oxidation (Murphy et al. 1975).
Other forms of treatment for phenol are also available, and these
processes have varying degrees of efficiency. Hydrogen peroxide, for
example, will degrade phenol. At an initial phenol concentration of
500 mg/1, a temperature of 49°C, and initial pH of 5.5, a 4:1 ratio of
H202 to phenol plus 0.01% of ferrous sulfide will lower the final phenol
concentration to 3 mg in 30 minutes (Throp 1975).
Three kg of potassium permanganate per m3 of waste containing
60-100 mg/1 of phenol at a pH of 8.5-9.5 will destroy 90% of the phenol
in 10 minutes. With 123 mg of phenol and about 10 mg/1 of potassium
permanganate, all phenol will be destroyed in 20 minutes (Throp 1975).
Ozone is used in wastewater treatment and is capable of removing phenol
to almost any low-level concentration (Throp 1975). Ozone can substi-
tute an oxygen atom onto an aromatic ring to form a phenol, but as the
reaction progresses with further additions of oxygen, hydroquinones
and catechol (dihydroxy compounds) will be formed (Gould and Weber
1976). These species appear at the earliest stages of ozonation, with
the concentration peaking about five minutes into the reaction, then
disappearing by ten minutes. There is significant removal of phenol
79
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OH
C1
C1
Phenol
OH
0 - chlorophenol
p — chlorophenol
2,4 - dichlorophenol
2,6 - dichlorophenol
2,4,6 — trichlorophenol
Non-aromatic oxidation products
Source: Manufacturing Chemists Association, 1972.
OH
C1
Ring
Oxidation
FIGURE 12 OXIDATION PATHWAYS AND PRODUCTS FOR PHENOL
80
-------
and aromatic degradation products (as indicated by a 70-80% drop in COD)
after 4-6 moles of ozone per initial mole of phenol have been consumed
(Gould and Weber 1976). 1.24 mg/1 03 applied to 10 mg of phenol at 24°C
will destroy 87% of the phenol in five minutes. More than 1.24 mg/1 of
ozone will remove all of the 110 mg of phenol (Throp 1975).
The kinetics of the ozone reaction can be expressed as (Gould and
Weber 1976):
d[Ph]/dt - -k D [Ph]
where: k » a proportionality constant in the first-order
rate of expression, approximately 0.132 moles
phenol/mole ozone for 0
-------
10
Source: Gould and Weber 1976.
FIGURE 13 RELATIONSHIP OF OZONE REACTION RATE
(K) TO pH
82
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do
TABLE 25. PHENOL CONCENTRATIONS IN WASTEWATER TREATMENT
AT DIFFERENT STAGES OF TREATMENT (ug/1)
Effluent
Final
Sludge
Place
16
25
14
Indianapolis, IN
Belmont WWTP
Lewis ton, ME
Lewis ton-Auburn WWTP
Atlanta, GA
R.M. Clayton WWTP
St. Louis, MO
Coldwater Creek STP
Pottstown, PA
Pottstown Borough STP
Grand Rapids, MI
STP
* ND = Not Detected
Key: 1 Waste Activated Sludge
2 Floatables
3 Digested
4 Heat Treated
5 Heat Treatment Decant
Influent Pre-Clarification Effluent Removal Primary Combined Other
94
< 50
< 300
21
< 50
ND*
ND
93
100
100
100
277
27
882
681, I2
4,297
103 70'
3
2,000
173 1,7174, 9075
Source: Burns and Roe 1980.
-------
PATHWAY #5.
SOIL TO GROUNDWATER AND SURFACE WATER:
RUNOFF
LEACHING,
1. Introduction
Phenol will sorb to some extent onto soils and organic matter and
therefore may be carried away along with the soil by erosion. In soils
onto which phenol does not sorb strongly, its high solubility indicates
that it will leach from the soil (Versar 1979a). Phenol is present in
groundwater due to leaching from strip mines and exposed coal seams and
from water contact in oil and gas fields (Versar 1979a).
2. Fate Processes
a. Adsorption
Phenol exhibits a capacity for adsorption on some soils (Sanks and
Gloyna 1976, Greskovich 1974). It has a log octanol-water partition
coefficient of 1.46, which indicates a low propensity for adsorption,
probably onto the organic matter in soils rather than the clay fraction
(Versar 1979a). In a test with three clays having the properties shown
in Table 26, the isotherms for adsorption of phenol in aqueous solutions
shown in Figure 14 were determined (Sanks and Gloyna 1976). Phenol was
sorbed at about 1-40 x 10~3 mole/kg clay and showed a very low affinity
for any of the clays tested. Very little or no sorption was noted on a
typical Pennsylvania "claey silt" soil, as is shown in Figure 15.
Phenol showed an equal affinity for both the soil and water phases
(Greskovich 1974).
TABLE 26. COMPOSITION OF SOILS USED IN PHENOL
ADSORPTION STUDY
Clay Type Beaumont
Grain Size, 7,
Clay 58
Silt 41
Sand - 1
Clay Mineral, %
Montmorillonite 55
Illite 45
Carbonate content, % 12
Dry Density, lb/ft3 59
Moisture, % 30
Cation Exchange Capacity, 53
me/100 g
Catahoula
38
54
8
Most
1
75
42
56
Eagle Ford
47
41
12
80
20
29
94
26
20
Source: Sanks and Gloyna 1976.
84
-------
100
0.01
0.1 1 10 100
Equilibrium Fluid Concentration (mM/1)
1000
Source: Sanks and Gloyna, 1976
FIGURE 14 PHENOL ADSORPTION ISOTHERMS FOR THREE TYPES OF CLAYS
tO
03
a
a
a.
•a
0 20 40 60 80 100
mg/C in Water Phase
Source: Greskovich 1974.
FIGURE 15 EQUILIBRIUM DATA FOR PHENOL BETWEEN
THE SOIL AND WATER AT 77°F
85
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Phenol is partially present as the phenate ion in soils. The
anionic form present in soils due to reactions with metals has a Amax
?n nhn^6 abs%ptlon JPectrum of natural light and thus may be subjlct
to photolySls (Versar 1979a). Complexes of phenol with metal cations
such as iron III can absorb light strongly at about 600 nm and so are
on^urf^^f -I" P^tol?si* (V^sar 1979a>. Phenol may also photooxidize
on surface films (Versar 1979a); however, due to phenol's mobility in
soil, only a small amount would likely be subject to either process and
for a short duration.
b. Volatilization
Phenol may volatilize slowly from soils (Versar 1979a), but no
rate constant is available. A method will be discussed here from which
a rate constant can be computed. The process of volatilization from
soils is much more difficult to describe than volatilization from water
as it is dependent on many factors; soil water content, soil type, soil
bulk density, soil organic-matter content, sorption properties, depth
to which the chemical is incorporated into the soil, wind speed
temperature, humidity, diffusion coefficient of the chemical, and other
chemical properties such as vapor pressure and solubility. Since phenol
apparently has a low capacity for sorption and has a rather high solu-
bility, it will likely be found in the soil water rather than sorbed
onto soil particles when soil water is present. In very dry soils
however, the low vapor pressure of phenol would tend to cause it to
diffuse slowly in the vapor phase. It would therefore remain loosely
associated with soil particles until water reaches the sorption sites
and is preferentially sorbed, thus displacing the phenol.
_ No accurate methods incorporating all the factors mentioned above
exist for determining a volatilization rate from soil. Some models
have been developed, but do not address the complexities of environ-
mental conditions. Dow (Swann et al. 1979) has tested nine pesticides
for volatilization from soil surfaces and has presented a prediction
method which agrees fairly closely with measurements of their volatili-
zation rates. The rate constant was proportional to Pvp/SKoc, where
PVD is the vapor pressure (0.5293 mm Hg for phenol), S is solubility
(93200 mg/1 for phenol), and KQC is the soil adsorption constant (43
assumed equal to KQW) , so that PVp/SKOc = 1.32 x 10-6. ^^ number is
at the top of the range of values computed for the pesticides and corre-
sponds to a predicted half-life at 0.24 hours (ti/2 = 3.8 x 10-7SKOC/PVD
hours) and a rate constant of 2.4/hr. This is rapid relative to the
other pesticides tested.
Phenol was almost completely lost from oiontmorillonite clay exposed
for one week to an atmosphere of 40% relative humidity (Versar 1979a)
This observation supports the estimation of a short half-life described
previously. Other processes, such as photodegradation, may have also
attributed to the observed loss.
86
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The vapor pressure and solubility of phenol are considerably higher
than those of most pesticides, and the sorption coefficient is much
lower. This may affect the correlation based on pesticide data.
Caution is urged in using this rate since there is little evidence
to verify it.
c. Other Processes
Three other fate processes may affect phenol concentrations in soil:
biodegradation, chemical oxidation, and complexation. No specific infor-
mation on phenol biodegradation in soil was available; however, due to
the susceptibility of the compound in aquatic systems (see Pathway #1)
by biological oxidation, it is assumed that under aerobic conditions
this reaction would also be supported in soil. In aerobic soils con-
taining metals, non-photolytic chemical oxidation of phenol may also
occur (Versar 1979a), although no specific information was available.
It is also probable that phenol forms complexes with metal complexes
(e.g., ferric iron) in soil; however, again no specific information
was found investigating this phenomenon (Versar 1979a).
Bioaccumulation of phenol in terrestrial plants from soil or
irrigation water is not expected due to its short persistence time and
low octanol-water partition coefficient (Versar 1979b). Spinach was
found to absorb less than 1% of phenol applied in solution at concentra-
tions of 2 mg/1 to 200 mg/1 (Mueller 1975).
3. Field Studies
There is a potential for certain soils to retain phenol and prevent
movement into groundwater. In a study in Upper Vistula Floodplain, Poland
(Kleczkowski et al. 1972), soil was monitored in the vicinity of a catch-
pit (sewage sedimentation pit) of a chemical plant in which phenol was
stored with other organics. The surrounding substratum was composed of
peat, sand, and impervious silt. One hundred and twenty analyses from 44
locations (with piezometers and village wells) found the range of phenol
pollution limited to 500 meters from source. This was attributed to attenu-
ation by the peat. No information was given on the concentrations present.
Another study by Delfino and Dube (Delfino and Dube 1976) was of
an accidental phenol spill in Wisconsin. The substance spilled was
carbolic acid (95-100% phenol). The incident, which occurred in June,
was caused by a railroad tanker derailment and the total spill amount-d
to 35,000 liters (out of a total of 80,000 liters). Residues of the
incident persisted for 19 months making well water in the area nonpotable.
Sand and gravel aquifers and undifferentiated dolomite were characteris-
tic of the substratum in the area which resulted in slow groundwater
movement through shallow flow paths and discharge to small streams. The
chemical form of the phenol was liquid (melting point, 4l°C) due to the
summer heat and the residual heat in the chemical itself.
87
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Some of the spill was recovered in solid form following cooling;
the rest percolated into the soil and was mobilized by precipitation
and runoff moving into the aquifer. Well depths in the area were 23-30
meters. Phenol was monitored as far away as 390 meters. Movement was
primarily to the southeast. Control wells beyond the path showed
•phenol-like" concentrations of 0.001-0.10 mg/1 which were natural
phenolics. There were no chlorinated water supplies in the vicinity
of the spill so no chlorophenols formed. The authors of the study
suspected this would have occurred had chlorine been used as part of
local water treatment practices.
4. Estimation Methods
The EPA Office of Solid Waste (U.S. EPA 1980c)evaluated the poten-
tial for and rate of phenol movement from generalized unconfined land-
fills and lagoons into surface water for two waste streams. In both
cases, all phenol present was assumed to be mobilized. Table 27 presents
the estimated release rates.
TABLE 27. ESTIMATED RELEASE RATES OF PHENOL IN
SOLID WASTE FROM WASTE DISPOSAL SITES
Annual Release Rate to Surface Water
Landfills Lagoons
(kg/m2) (kg/m2)
Waste Stream #1 1 10-40 148
Waste Stream #2 19 - 75 280
1Waste streams not identified.
Source: U.S. EPA 1980c.
Two known dischargers of phenol-containing solid waste are producers
using cumene peroxidation and benzene sulfonation (see Section III).
Assuming the discharge rates estimated in Appendix A No. 24, the two largest
producers using these landfill or lagoon methods would annually create
990 kg and 1,260 kg of solid waste, respectively. Assuming a land dis-
posal site of 30 to 125 m2 and 100% mobilization of all phenol present,
the release rate of Waste Stream #1 for landfill could easily be achieved.
A loading rate of phenol to nearby surface water can be estimated for the'
benzene sulfonation process assuming: 1) all of the waste is deposited
at the same location and runoff drains into the same water body, and
2) as a conservative estimate, all phenol present migrates in one half
of a year. The estimated loading rate is approximately 7 kg/day or,
distributing the loading over 24 hours per day, 0.3 kg/hr. This rate
88
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is low compared to other estimated rates (see Tables 20 and 21). Based
on this estimation, the solid waste of phenol, even if 100% mobile,
contributes a lower localized aquatic discharge rate of phenol than
does direct discharge in effluents. However, an industry producing
four times the amount of solid waste produced by the benzene sulfonation
plant (^5,000 kg, benzene sulfonation plant), would have a loading rate
more comparable to some of the direct aquatic waste dischargers (^1.5 kg/
hr). Information on phenol solid waste generation is incomplete and
does not cover all industries so it is not possible to assess whether
a significant solid waste discharger exists.
5. Monitoring Data
No monitoring data were available measuring phenol concentrations
in soil and in groundwater for both natural background levels and in relation
to intentional releases.
H. PATHWAY #6. CHLORINATION OF PHENOL AND FORMATION OF CHLOROPHENOL
Phenol is one of the most reactive of the aromatics under conditions of
dilute aqueous chlorination (Carlson and Caple 1975, Carlson et al. 1976).
Table 28 presents data from a chlorination experiment with pH as a variable.
TABLE 28. CHLORINE1 INCORPORATION IN PHENOL2
% Chlorine remaining
after reaction time*
pH 3 2.2 + 0.1
pH 7 2.4 +0.1
pH 10 2.4 + 0.1
Chlorine at 7.0 x 10"^,
2Phenol at 9.5 + 0.6 x KT^M
320 minutes at 25°C.
Source: Adapted from Carlson and Caple 1975.
Chlorination was independent of pH, indicating the likelihood of chlori-
nation in a wide range of treatment processes using chlorine.
When sufficient chlorine is supplied and enough contact time is
allowed (1 hr), the net chlorine demand by phenols is approximately
8 mmol C12 for each mmol of phenol, or 6.35 mg Cl2/mg phenol. Table 29
and Figure 16 present the results of an experiment measuring this demand
(MCA 1972).
89
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TABLE 29. CHLORINATION OF PHENOL
Net Chlorine Demand
Phenol Applied
Concentration Chlorine
(mg/1) (ma/1)
10 20
10 50
10 100
20 50
20 100
Contact
Time
(hr)
0.25
0.5
1.0
2.0
0.25
0.5
1.0
2.0
0.25
0.5
1.0
2.0
0.25
0.5
1.0
2.0
0.25
0.5
1.0
2.0
Chlorine
Residual
(mg/1)
6.0
1.7
0
0
17.8
8.0
2.8
0
50
44
39
36.5
4.5
0
0
0
12
2.5
0
0
(mg/1)
14
18.3
>20
>20
32.2
42
47.2
>50
50
56
61
63.5
45.5
>50
>50
>50
88
97.5
>100
>100
•• » — .***«• .w^»*4*b*k4V4
(mmol C12)
mmol phenol
1.9
2.4
>2.7
>2.7
4.3
5.6
6.3
6.6
6.6
7.4
8.1
8.4
3.0
>3.3
>3.3
>3.3
5.8
6.5
>6.6
>6.6
Source: MCA 1972.
90
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10
O - Phenol
A — Aniline
O - M-Cresol
D — Hydroquinone
O-
6
14
16
8 10
Chlorine Applied
(MMOL CL2/MMOL Compound)
Source: Manufacturing Chemists Association 1972.
FIGURE 16 MOLAR CHLORINE UPTAKE BY TEST COMPOUNDS, INCLUDING PHENOL
91
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The most commonly formed products of phenol chlorination are chloro-
phenol (o- and p-), 2,4-dichlorophenol, 2,6-dichlorophenol, and 2,4,6-
trichlorophenol (MCA 1972).
Chlorination of phenols can occur during drinking water finishing,
wastewater treatment, and in cooling towers. The concentration of
chlorine available for reaction ranges from 1-50 mg/1, depending on the
the type of treatment (see Table 30). Although not all the chlorine
TABLE 30. CHLORINE LEVELS IN WATER TREATMENT
Drinking Water Treatment
Groundwater Wells
Main Sterilization (in reservoirs, ship tanks)
Wastewater Treatment (secondary effluent)
Cooling Towers
retention time of 24 hours.
Source: White 1975.
present in actual systems will react with phenol due to competition
from other compounds (e.g., benzene, biphenyls), for the purpose of
estimation it is assumed 100% available to phenol based on the results
described in Table 30. In one liter of water in various types of water
treatment, 0.25 to 10 mg of chlorine are present. Assuming the optimum
chlorine demand measured in laboratory studies (Table 29 and Figure
16), then approximately 6.35 mg of Cl2 are consumed by each mg of phenol.
Therefore 0.0 to 1.6 mg of phenol would be chlorinated in each liter of
water during drinking water or typical wastewater treatment in one hour.
This value provides an upper limit on the concentration of phenol that
can undergo chlorination. However, due to variabilities in wastewater
treatment, typically shorter wastewater retention times during treatment,
and the likelihood of formation of more chlorinated phenolic compounds,
the actual concentration of phenol chlorinated during treatment is lower.
Due to the propensity for reaction of phenol with chlorine, it
would be expected that: 1) high phenol levels in wastewater plant
influents would be greatly reduced in the effluent, and 2) chlorinated
phenol levels in the effluent would exceed influent levels. Unfortunately,
92
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little data are available on phenol concentrations at various stages of
wastewater treatment so that the mass of phenol removed by microbial
degradation and other processes can be subtracted from the amount avail-
able for final chlorinaLion. Additionally the same slug of phenol is
seldom followed throughout the entire treatment process so that the
effluent level reported may be for a larger loading than the level
indicated in the influent. In Pathway #3 the behavior of pheno-1 in
wastewater treatment was described and close to 100% efficiencies in removal
were reported (Burns and Roe 1980). Since phenol itself (and not phenols)
was sampled it is possible that some of the amount "removed" was actually
chlorinated and present in the effluent as chlorophenols. If the data
for chlorophenols from the same sampling program is examined, it can be
seen that sometimes effluent levels exceed influent levels but again
the data are erratic. Table 31 presents some concentrations of phenol
and chlorinated phenol reported in sewage treatment influents and
effluents.
TABLE 31. PHENOL CONCENTRATIONS IN POTW'S
Effluent
Influent Levels Levels
Chemical (ug/1) (ug/1) Reference
Phenol 1 - 25 (6 plants) 0 - <50 Burns and Roe 1980
2,4,6-trichlorophenol 0 (2 plants) <2 - <50 Burns and Roe 1980
2,4 dichlorophenol <1 - 1 (2 plants) <1 Burns and Roe 1980
2-chlorophenol <50 (1 plants) <50 Burns and Roe 1980
Chlorinated phenols not given ^0.5 - 1.5 Jolley et al. 1975
Phenol has rarely been detected in drinking water, both raw and
finished (see Section V-B). When detected, levels have been very small,
on the order of 1-5 ug/1.
In conclusion, chlorination of phenol not subject to degradation
appears likely during wastewater treatment. Phenol discharged to POTW's
is first likely to be biodegraded or chemically treated (as described in
Pathway #3) before contact with chlorine. Some phenol reaching the chlori-
nation stage would presumably be chlorinated at the chlorine levels commonly
maintained. Few monitoring data are available to confirm this hypothesis,
especially on phenol concentrations between secondary treatment and
chlorination. The limited data suggest removal of phenol during treat-
ment (whether due to degradation or conversion to chlorinated products).
Some data for chlorophenols indicate formation of chlorophenol during
treatment; other data are not conclusive.
93
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A separate risk assessment on chlorinated phenols (chlorophenol•
^,4-dichlorophenol; and 2,4,6-trichlorophenol) (Scow et al. 1980) considers
the production and use, environmental fate and distribution, effects and
exposure, and risk in regard to these compounds.
I. SUMMARY AND CONCLUSIONS
Following release to the environment, the fate and distribution of
phenol depends on the form of emission, the receiving medium, and various
environmental factors. Five environmental pathways describing the
behavior of phenol releases were identified: emissions to surface water-
emissions to air; transport from air to water/soil; discharges to POTW's'
and releases to soil. A sixth pathway, chlorination during water treat-'
ment, was also considered.
1. Surface Water
Approximately 34% of all known environmental releases of phenol are
made to surface water, primarily by POTW's, bisphenol A producers, petroleum
refiners, and certain producers of phenol itself. The most significant
fate process affecting phenol in surface water is biodegradation. A
half-life of 3.5 days was reported under field conditions in a river
Laboratory studies confirm a rapid removal rate especially under accli-
mated conditions and at high temperatures. Numerous microfloral species
have been identified as capable of degrading phenol. There is some
evidence that phenol may undergo photolysis under environmental condi-
tions. The processes of hydrolysis, oxidation, adsorption, and volatili-
zation do not appear to be significant with respect to phenol concentra-
tions in surface water.
Studies of the bioaccumulation of phenol have been conducted on
aquatic organisms. Absorption is the primary route of intake. Phenol
concentrations of 14 to 156 ug/gram of body weight were reported for
goldfish exposed to 10-100 mg/1 phenol for 1-5 days. The bioconcentration
factors of phenol were low, ranging from 1.2 to 2.3 above the water levels.
Phenol tends to accumulate in greater amounts in the gall bladder liver
a-nd visceral organs. Higher vertebrates (e.g., mammals) have the ability
to detoxify phenol by forming conjugation products with glucuronides and
sulfates; fish do not appear to possess this mechanism, rather, passive
diffusion and biliary excretion are the mechanisms of decreasing the
phenol body burden. No direct evidence was obtained for biomagnification
of phenol; however, it does not appear to be significant because of its
generally low degree of accumulation in tissue.
«,,ifn \ } y ° a monohydric Phenols spill from a benzene
sulfonation plant into a river, 93% of the initial 28 mg/1 phenol con-
phenoltdenradationUCad ** ^ da7S' AsSOCiated with the hijh rate of
win jj v^j-Oiij/ tlCiiClt 111 OXV26TT -Lfi^^S 1S W^tli cln c* on
P^no1ted t0 ChS tOXiC effects on the system resulting from the spill.
Phenol concentrations may be higher during the winter than summer due
to a decreased rate of microbial degradation at low temperatures
94
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The EXAMS model simulation of a continual 3 kg/hr discharge of phenol
into a eutrophic lake and turbid river (1 km length) estimated equilibrium
water column concentrations of 1 ug/1 to 3 ug/1. The self-purification
time for both systems was approximately 3 to 4 hours due to biodegrada-
tion in the eutrophic lake and physical transport in the river system.
Sediment concentrations were approximately 10 ug/kg and 5 x 10"^ ug/kg
(dry weight) in the river and lake systems, respectively.
Monitoring data for phenol in surface water are limited. The STORET
data base reports a total of approximately 600 observations for thirteen
major river basins. Ninety-three percent of all observations were
remarked data, i.e., either at or below the detection limit (M.0-50 ug/1).
Mean concentrations for unremarked data between 1978 and 1980 ranged from
0.004 ug/1 to 660 ug/1 with a maximum of 6,794 ug/1. Mean sediment levels
(38 observations) averaged 102 mg/kg (unremarked data) with a maximum
value of 454 mg/kg. Concentrations as high as 3,000 mg/1 have been
reported in effluents; however, most levels were reported at less than
10 mg/1.
2. Emissions to Air
Approximately 59% of the estimated environmental releases of phenol
are to air, predominately from combustion of wood. Other releases are
from phenol producers, consumers and from transport and storage of phenol.
Most releases are presumably in vapor form, some of which is sorbed onto
particulate matter. Phenol is subject either to rainout or to photolysis
and photooxidation with an estimated atmospheric lifetime of several
days. Phenol levies in urban areas fluctuate on a daily basis with
higher levels during the day, apparently due to higher traffic volume
and industrial activity. The highest reported phenol concentration in urban
air was 289 ug/m3. No data were available for rural areas.
3. Rainout
The amount of atmospheric emission of phenol not photodegraded is
subject to rainout and transfer to land or surface water. Initial con-
centrations in rainwater were estimated at 1 to 10 mg/1 in the vicinity
of a source; however the concentrations would be continually reduced as
rainfall continued. No monitoring data were available reporting phenol
levels in rain; however industrial areas are reported to have qualitatively
higher rainfall concentrations than rural areas.
4. Fate in POTW's and Wastewater Treatment
Phenol is discharged to POTW's both in untreated and treated waste
streams by various industrial sources. In addition, natural background
levels of phenol contribute some portion of the total loading. Typical
POTW influent concentrations measure 1 ug/1 to 200 ug/1. Numerous treat-
ment processes are effective in removing phenol by degradation including
activated sludge, trickling filters and various chemical treatments.
Biodegradation in sludge is very effective, especially in activated sludge
at concentrations less than 10 mg/1. Above this level, the decay rate is
sometimes inhibited. At about 500 mg/1, one activated sludge system experi-
enced a sharp disruption of microbial activity. The optimum pH range is 6
to 9.5 and adequate essential nutrient concentrations must be present.
95
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Chemical removal methods effective in degrading phenol include treat-
ment with chlorine, hydrogen peroxide, potassium permanganate, ozone, and
iron^ferrate. The prevalence of these methods is expected to be small in
POTW s and variable in wastewater treatment facilities dependinp on the
industry subcategory.
A field study investigating the fate of phenol during treatment in seven
POTW s reported a high removal efficiency of greater than 90% for four
plants. Efficiencies were not reported for the other three plants.
5. Soil to Groundwater and Surface Water
Only a small percentage (approximately 7%) of the total environmental
releases of phenol are made to land. Major releases are made in the dis-
posal of sludges resulting from the synthesis of phenol. Due to phenol's
relatively low affinity for adsorption onto soil and its high solubility
some portion of the land releases is expected to reach either ground or surface
waters unless significantly reduced by biodegradation or other fate processes.
The most important fate process determining phenol concentrations in bio-
logically active soil is expected to be biodegradation based on its effective-
ness in degrading phenol in aqua-tic systems. Volatilization from soil does not
appear to be significant. No information specifically regarding chemical
oxidation and complexing of phenol was available.
Two field studies investigating the behavior of phenol in soil indicated
attenuation and persistence of the chemical in the vicinity of the source.
In a peat soil, the range of phenol was limited to within 500 m of a catchment
pit indicating in contradiction of laboratory results, strong adsorption onto
organic matter. In the second study phenol spilled onto the soil surface
reached groundwater supplies and persisted for 19 months. The substratum in
the vicinity of the spill was sand, gravel, and undifferentiated dolomite.
There was no indication of adsorption onto the organic fraction of the soil
surface layer; however, soil concentrations were not reported to confirm this.
6. Chlorination of Phenol and Formation of Chlorophenols
Phenol is one of the most reactive of the aromatics in regard to chlori-
nation. Formation of chlorophenols during treatment of wastewater and drink-
ing water is commonly reported. Based on the results of an experiment con-
ducted under optimum conditions, an upper limit of 1.6 mg of phenol per
liter of water will undergo chlorination at typical wastewater treatment
chlorine concentrations. Lower concentrations, however, are actually
expected to be subject to reaction with chlorine due to system variability
and stereochemical factors. Field studies are too few and inconsistent
to support any specific conclusions about the propensity of chlorination
of phenol during POTW treatment of wastewater.
96
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SECTION V.
HUMAN EFFECTS AND EXPOSURE
A. EFFECTS ON HUMANS
1. Introduction
Phenol was first used as a medicinal disinfectant more than a
century ago and, although largely replaced by other compounds, it is
still found in throat lozenges, mouthwashes, and other medicinal prepa-
rations. Humans also produce phenol endogenously via bacterial action
on 2,-tyrosine in the intestinal tract. This section of the report will
examine the adverse health effects associated with phenol exposure.
2. Metabolism and Bioaccumulation
Phenol is readily absorbed from all routes of entry followed by
rapid generalized distribution in the body and relatively rapid metab-
olism and excretion. In man, inhalation exposure to phenol vapor (via
face mask) resulted in an initial lung retention of 80% of the dose.
This value dropped with time to an average of 70% after 6 to 8 hours
(Piotrowski 1971).
In a similar experiment in which human volunteers were exposed to
phenol vapor in a chamber but allowed to breathe fresh air through a
face mask, Piotrowski(1971) found phenol vapor x^as readily absorbed
through intact skin.
Pullin also reported rapid dermal absorption of phenol (0.05% of
body weight) applied over 35-40% of the total body surface area of
swine for one minute followed by 15 minutes of showering with water.
Peak blood concentrations of phenol occurred 15 to 30 minutes after
application (Pullin et al. 1976).
Phenol's moderate water solubility and lipid/water partition coeffi-
cient favor facile transfer through membranes and biological barriers.
Deichmann reported that within 15 minutes following oral administration
of 500 mg of phenol/kg in the diet to rabbits highest tissue concentrations
were found in liver (637 mg free phenol/kg tissue) followed by heart (530),
lungs (342), kidney (353), blood (308), and muscle (190). Phenol con-
centrations became fairly uniform as time progressed and began to decrease
as metabolism occurred (Deichmann 1944).
A similar distribution scheme was noted in the desert rodent,
Notomys alexis, following intraperitoneal injection of 5, 25, or 100
mg/kg phenol (Wheldrake et al. 1977). Kao reported 84-90% urinary
elimination of 25 mg/kg l^C-phenol within 8 hours in sheep, pigs, and
rats (Kao et al. 1979). Phenyl glucuronide accounted for 49,. 83, and 42%,
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respectively, of the urinary metabolites, while sulfate conjugates
accounted for an additional 32, 1, and 55%, respectively, of the urinary
metabolites in these species. Conjugates of quinol were minor urinary
metabolites (<7%) in all three species. Less than 0.5% of the dose was
excreted in feces, indicating almost complete absorption of phenol had
occurred.
Once absorbed and distributed in the body, phenol undergoes two
main metabolic reactions: (1) conjugation of the hydroxyl group with
glucuronic acid and/or (2) conjugation with sulfuric acid to form
ethereal sulfates. Some species differences are seen with respect to
minor reactions. Hydroxylation to form quinol in rabbits, rats, sheep,
and pigs (Williams 1959, Kao et al. 1979) and methylation of the phenolic
hydroxyl group in rabbits (Williams 1959) have been reported. In the
cat, up to 8% of the dose was excreted as phenyl dihydrogen phosphate
(Capel et al. 1974), while some 12% of the urinary metabolites in sheep
were conjugated with phosphate (Kao et al. 1979). In man, the sulfate
conjugates appear to predominate (Capel et al. 1972).
Glucuronic acid conjugation of phenol generally exceeds that of
sulfate conjugation when the dose of phenol is relatively large. This
appears to be due to the fact that the rate of glucuronic acid conjuga-
tion is proportional to the body level of phenol, whereas the rate of
sulfate conjugation is independent of the phenol level but dependent
on the availability of sulfate (Williams 1959). For example, the ratio
of sulfate to glucuronide metabolites in the desert rodent, Notomys
alexis, decreased with increasing dose of phenol, while the level of
glucuronides showed a contrasting increase with dose. Phenyl sulfate
predominated following intraperitoneal injection of 5 mg/kg phenol
(57% vs. 26% glucuronide) but its proportion decreased as the level of
injected phenol increased (i.e., at 25 and 100 mg/kg, the ratios of
sulfate to glucuronide were 27:32 and 17:36, respectively (Wheldrake
et al. 1978). Similar dose-related excretion patterns have been found
in several species of primates (Mehta et al. 1978).
In mammals, phenol is produced endogenously by the degradative
action of bacteria on tyrosine in the gut. Thus, a large number of
phenolic substances occur both free and in conjugated form in normal
urine (Williams 1959). Between 1.5 and 5 mg of phenol are normally
excreted per liter of human urine per day (Fishbeck et al. 1975).
Phenol levels in normal blood as determined by gas-liquid chromatography
range from 0.04 to 0.56 mg/1 free phenol plus 1.06 to 5.18 mg/1 con-
jugated phenols (Dirmikis and Darbre 1974) and 2-18 mg/1 for total
phenol (VanHaaften and Sie 1965).
The clearance of exogenous phenol from the body is relatively
rapid. The half-life of phenol in man determined after inhalation or
skin absorption is approximately 3.5 hours (Piotrowski 1971). There
are no data to suggest that bioaccumulation occurs.
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3. Animal Studies
a. Carcinogenicity
In one study at NCI, addition of 0.25% or 0.5% phenol by volume for
103 weeks to the drinking water of male and female F344 rats and B6C3F1
mice resulted in an increased incidence of pheochromocytomas and
leukemia or lymphomas in low-dose male rats. This may have been
associated with phenol administration. However, the incidence of these
tumors in high-dose male rats was comparable to control values. Thus, an
association with the administration of phenol was not clearly established.
Under these test conditions, phenol was not considered carcinogenic
for either male or female F344 rats or male and female B6C3F1 mice
(NCI 1980). However, the Data Evaluation/Risk Asssessment subgroup of
NCI's Clearinghouse on Environmental Carcinogens has recommended that
phenol be tested further to clarify the finding of elevated incidences
of the above-named tumors (J. Sontag, Assistant Director for Inter-
agency Affairs, NCI, personal communication, 1980).
The capacity of phenol to elicit epithelial tumors in mice exposed
to a single application of a known carcinogen (i.e., initiation) followed
by repeated skin painting of phenol to the same area (i.e., promotion)
has been demonstrated by a number of investigators (Boutwell and Bosch
1959, Salaman and Glendenning 1957).
Benign tumors developed rapidly and in significant numbers in mice
specially inbred for sensitivity to tumor development following a single
skin application of 75 ug of 9, 10-dimethyl-l,2-benzanthracene (DMBA)
followed one week later by repetitive twice-weekly applications of 2.5
mg phenol (as a 10% solution in benzene) to the same area for 42 weeks.
After 13 weeks, 22 of 23 mice (96%) had papillomas and 73% had developed
carcinomas. Few tumors developed on mice treated either with DMBA alone
(3/21 mice with papillomas at 42 weeks) or with phenol alone (5/14
papillomas at one year). Continuation of skin painting with phenol
alone for an additional 20 weeks resulted in one fibrosarcoma. A few
papillomas were seen in other strains of mice (Holtzman, CAFj C3H)
similarly treated, but at much lower incidences (Boutwell and Bosch
1959).
Salaman and Glendenning reported similar results in "S"-strain
albino mice after initiation with 0.3 mg DMBA followed by repeated
skin application of phenol (Salaman and Glendenning 1957). A twenty
percent solution of phenol plus DMBA induced marked skin trauma and a
tumor incidence of 85% in 13 survivors at 37 weeks (10 weeks after
treatment ceased). Phenol alone at this concentration was mildly
tumorigenic, i.e., 39% tumor incidence (all benign) at 45 weeks. DMBA
plus a five percent phenol solution resulted in a tumor incidence of
28% in 14 survivors at 37 weeks. Two of a total of nine tumors were
malignant. No tumors were seen in mice treated with five percent phenol
alone for 32 weeks.
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As a result of these findings, a comprehensive study of the effects
of dose and purity of phenol was undertaken. The tumor response of
groups of mice exposed to graded amounts of phenol following a single
application of DMBA showed that a maximal response was reached at the
level of 2.5 mg phenol/mouse (10% solution) twice a week. A lesser
response was obtained at 1.25 mg/mouse while 5.0 mg/mouse (20% solution)
caused a number of deaths as a result of systemic toxicity. In addition,
the development of papillomas was partially inhibited by the corrosive
effects on the skin at the 5 mg/mouse level (Boutwell and Bosch 1959).
Since coal tar is a common source of phenol, the possibility of
contamination of phenol with carcinogens was considered. Careful
laboratory purification and subsequent treatment, however, resulted in
no loss of carcinogenic activity (Boutwell and Bosch 1959).
In a series of studies, Van Duuren and others (Van Duuren et al.
1971, 1973; Van Duuren and Goldschmidt 1976) examined the potential
cocarcinogenic activity of phenol with benzo(a)pyrene (BaP) in mice.
Cocarcinogenesis is distinguished from initiation/promotion in that
two or more agents are applied simultaneously or alternatively in
single or repeated doses. No cocarcinogenic activity was found when
reagent-grade phenol (3 mg/mouse, 3 times/week for 52 weeks) was applied
simultaneously with 5 ug BaP to the backs of ICR/Ha Swiss mice. Seven
of 39 survivors (18%) at 52 weeks had tumors compared to 13/42 mice
(31%) receiving BaP alone and 0% in the solvent control group (Van Duuren
et al.1973). In addition, a slight inhibitory effect on tumor formation
was noted, i.e., it took 267 days for the development of the first
papilloma in the phenol-BaP group in contrast to 251 days in mice treated
with BaP alone (Van Duuren and Goldschmidt 1976).
In summary, the addition of 0.5% phenol to drinking water was not
found to be carcinogenic to either rats or mice. Phenol does appear to
have tumor-promoting activity in mice but no cocarcinogenic action.
Skin application of phenol alone does result in carcinogenic activity
in sensitive strains of mice but not in standard inbred mouse strains.
This tumorigenic activity appears to be associated with phenol's irri-
tancy and subsequent skin hyperplasia.
b. Mutagenicity
Several bacterial mutagenicity assays have been conducted with
phenol. Demerec reported that phenol produced back-mutations in
Escherichia coli from streptomycin-resistance to streptomycin-sensi-
tivity, but only at concentrations that were toxic to the bacterium
(survival was only 0.5 to 1.7% at phenol concentrations of 0.2 to 0.1%)
(Demerec et al. 1951). In another study, Dickey and others found phenol
was not mutagenic in Neurospora (Dickey et al. 1949). More recently,
Cotruvo reported phenol was not mutagenic in the bacterium Salmonella
typhimurium or in the yeast Saccharomyces cerevisiae D3 (Cotruvo et al.
1977).
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In Drosophila (fruit fly), exposure of explanted and subsequently
reimplanted larval ovary to phenol (0.01%) for 15-20 minutes produced an
increased frequency of lethal mutations (11.3%) compared to 0% in similarly
treated controls (Hadorn and Niggli 1946).
More recently, Bulsiewicz examined the influence of phenol on
chromosomes in the process of spermatogenesis in Porton-strain mice
for five consecutive generations (Bulsiewicz 1977). Mice in each
generation were given two milliliters of 0, 0.08, 0.8, or 8 mg/1
aqueous solutions of phenol daily by gavage for 30 days or approxi-
mately 0, 6.4, 64, and 640 ug phenol/kg/day, respectively. Six males
and females from each group per generation were then mated; the females
continued to receive phenol during pregnancy and lactation. Testes from
six males per group for each generation were examined for chromosomal
defects in spermatogonia and primary spermatocytes. Aberrations noted
included chromatid and chromosome breaks, ring chromosomes, centric
fusions, acentric fragments, aneuploidy, and polyploidy. A smaller
number of total aberrations was seen in primary spermatocytes (5, 22,
and 24% in the 6.4, 64, and 640 ug/kg groups, respectively) in comparison
to the higher numbers noted in spermatogonia (27, 52, and 81%, respec-
tively). The reasons for this difference are difficult to pinpoint.
Three possible explanations are: (1) gross abnormalities in spermato-
gonia may have been eliminated at that stage of spermatogenesis, (2) some
aberrations were corrected by normal repair processes, and (3) the responses
in spermatogonia and spermatocytes are independent of each other, with the
higher incidence in spermatogonia reflecting the rapidly dividing nature
of these cells.
As can be seen in Tables 32 and 33, dose-related increases in the
incidence of aberrations were found in both spermatogonia and spermato-
cytes. The highest dose, however, was associated with systemic toxicity
and mortality. Apart from dose-related increases in aberrations, an
apparent trend toward increased aberrations in each successive genera-
tion was noted. However, the experimental protocol as well as the
inadequacy of information presented in the paper make interpretation of
this latter point difficult. The issue is complicated by the facts that
(1) both females and males were exposed to phenol prior to mating, and
(2) both sexes of the FI through FS generations were additionally exposed
to phenol in utero. The significance of increased aberrations in subse-
quent generations within a single treatment group is difficult to assess
in that one cannot segregate which of three insults (i.e., to parental
male, to parental female, and to offspring in utero ) or combinations
thereof contributed to the incidence of reported aberrations. Further-
more, although sterility does not appear to have been a problem, the
effect of phenol exposure on other indices of fertility in progeny
could not be assessed because no data on reproductive parameters or
effects of exposure in females were provided.
107
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TABLE 32. INCIDENCE OF CHROMOSOMAL ABERRATIONS IN SPERMATOCONIA OF PHENOL-TREATED MICE
o
oo
Dosage Level
Generation (ug/kg/day)
P 0
6.4
64
640
1' 0
6.4
64
640
I' 0
6.4
64
640
F3 0
6.4
64
640
F4 0
6.4
64
640
F5 0
6.4
64
640
Chromosome
Breaks
0
1.7
5.8
9.2
0
3.3
10.8
12.5
0
9.2
15
19.2
0
5.0
10.8
10*
0
6.7
15.8
20
0
10
17.5
51.3*
Chromatid
Breaks
0.8
3.3
5
7.5
0
10
15
14.2
1.7
8.3
15.8
17.5
0
5.8
14.2
10*
0.8
8.3
20
25
0
6.7
23
37.5*
Aneuploidy
0
1.7
5
10
2.5
11.7
15
17.5
0
9.2
17.5
19.2
0.8
13.3
22.5
36*
0.8
10
20.8
27.5
1.7
13.3
25.8
37.5*
Polyp loidy
0.8
3.3
10.8
13.3
2.5
1.7
15.8
19.2
0.8
5
14.2
22.5
1.7
8.3
15.8
32*
0.8
6.7
23.3
30.8
0
11.7
21.7
56.3*
Associations
0
0.8
2.5
1.7
0
3.3
5.8
7.5
0
5.0'
7.5
5.8
0.1
3.3
9.2
8.0*
0
10
15.8
17.5
0.2
6.7
19.2
25*
*Excludes 3 mice killed in moribund condition. Preparations made from the testes of these mice showed
absence of primary and secondary spermatocytes, spermatids, and spermatozoa.
Source: Arthur D. Little, Inc., adapted from Bulsiewicz 1977.
-------
TABLE 33. INCIDENCE OF CHROMOSOMAL ABERRATIONS IN SPERMATOCYTES OF PHENOL-TREATED MICE
Dosage Level
Generation (ug/kg/day)
P 0
6.4
64
640
Fi °
6.4
64
640
F, 0
6.4
64
640
F 0
6.4
64
640
V 0
6.4
64
640
F 0
6.4
64
640
Chromatid
Breaks
0.3
0.3
1.4
2.5
0.3
0.4
0.9
4.9
0
0
1.6
3.6
0
0.6
0.9
8.7
0
0.8
1.2
6.6
0.2
2.1
1.3
14.2
Aneuploidy
0.1
0.9
2.0
2.5
0
1.7
2.5
1.9
0.3
2.4
8.6
3.8
0
3.0
13.4
7.1
0.1
3.2
12.6
4.7
0.5
2.7
21
14.8
Polyploidy
0.1
1.5
4.4
13.4
0
2.4
5.8
12.1
0.2
3.1
7.2
13.1
0.6
2.4
6.5
14.2
0
4.2
22.9
13.9
0.3
6.8
16.5
26.4
Associations
0.1
1.7
1.9
2.2
0
2.4
2.4
3.0
0.1
1.9
1.8
2.3
0.1
2.4
2.1
1.2
0
2.7
3.6
2.6
0.2
4.2
4.7
3.4
Source: Arthur D. Little, Inc., adapted from Bulsiewicz 1977.
-------
The complications associated with the interpretation of results in
successive generations do not, however, mitigate the marked increase in
chromosomal aberrations seen in the parental and Fj generations. Even
if the effects at the top dose are attributed to cytotoxic effects, the
increased incidences of aberrations in the two lower treatment groups
are noteworthy. Chromosomal breaks in spermatogonia were 1.7% and 5.8%
in the 6.4-and 64-ug/kg parental groups and increased to 3.3% and 10.8%,
respectively, in the Fj generation. There were no chromosomal breaks
in controls. The incidences of chromatid breaks in spermatogonia of
both the parental and 7^ generations were also increased threefold or
more above background. By the spermatocyte stage, the incidence of this
aberration was comparable to controls at the low dose but remained
elevated two to fourfold above background in the 64-ug/kg treatment
group. Similar trends were noted with other chromosomal aberrations
(see Tables 32 and 33).
These findings are cause for concern; even more so, is the apparent
increment in the incidence of aberrations in successive generations.
Further work is needed to clarify the significance of these findings
and their potential implication for humans.
c. Adverse Reproductive Effects
Although not specifically designed as a reproductive study, a study
by Heller and Pursell noted no signficant effects on the reproductive
capabilities of rats administered 5,000 mg phenol/1 in the drinking
water for three generations or 100 mg/1 for five generations (Heller
and Pursell 1938). However, no pathological or biochemical studies
were done and results were based solely on general appearance and body
weights.
Korshunov reported increased incidences of pre-implantation and
early postnatal deaths among offspring of rats exposed by inhalation
to 5 or 0.5 mg/m3 phenol throughout pregnancy (Korshunov 1974).
In another study by Minor and Becker no increase in fetal resorp-
tions or teratogenic effects in offspring of Sprague-Dawley rats injected
intraperitoneally with 20, 63, or 200 mg/kg phenol on either days 9-11
or days 12-14 of gestation was observed (Minor and Becker 1971). Fetal
body weight was reduced at the top dose but only in fetuses from dams
treated on days 12-14 of gestation (4.64 g vs. 5.25 g for controls).
Changes in the sexual cycle of female albino rats (i.e., shortening
of the estrus stage and prolongation of the diestrus stage as well as
disturbances in the functional state of the ovaries) were seen in rats
exposed to 5 or 0.5 mg/m3 phenol for four hours per day for four months
(Kolesnikova 1972). These effects, however, may be related to the
general toxic effects of phenol exposure rather than a selective
response of the reproductive system.
110
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d. Other Toxicological Effects
Regardless of the route of administration, the LD50 values for the
mouse, rat, rabbit, and monkey are within a narrow range (0.18-0.6 g/kg)
(RTECS 1978). The cat is somewhat more sensitive to phenol (oral LDLo
80 mg/kg) due to significant metabolic differences in the manner phenol
is detoxified by this species.
Disturbance of the central nervous system is the predominant toxic
response to phenol regardless of mode of administration. In rats, an
acute lethal dose of phenol produces initial increases in pulse and
respiration which later become slow, irregular, and weak. Blood pressure,
after an initial rise, falls significantly. The pupils constrict in the
early stages but later dilate. Salivation may be evident and dyspnea
is marked. Rats also usually exhibit twitching of isolated bundles of
muscles and uncoordinated movements of the legs until shortly before
death (which can occur within minutes of exposure) usually due to
respiratory arrest (Deichmann and Witherup 1944).
Non-lethal exposure to phenol may result in localized tissue damage.
Ingestion of concentrated phenol solutions causes severe burning of
mucous membranes lining the mouth and esophagus; necrosis and hemorrhage
may follow. Depending on concentration, vehicle, and duration of
exposure, application to the skin may result in inflammation, discolora-
tion, eczema, sloughing, papillomas, necrosis, or gangrene (Deichmann
and Witherup 1944).
Damage to tissues of the lungs, liver, kidneys, heart, and urogeni-
tal system have been reported following prolonged exposure via oral,
subcutaneous, and inhalation routes of administration. In a severe
intoxication the lungs may show hyperemia, infarcts, bronchopneumonia,
purulent bronchitis, and hyperplasia of the peribronchial tissues.
There can be myocardial degeneration and necrosis. The hepatic cells
may be enlarged, pale, and coarsely granular with swollen, fragmented,
and pyknotic nuclei. Prolonged administration of phenol may cause
parenchymatous nephritis, hyperemia of the glomerular and cortical
region, cloudy swelling, edema of the convoluted tubules, and degenera-
tive changes of the glomeruli (Deichmann and Keplinger 1963).
Deichmann and Oesper reported that rats tolerated up to 50 mg
phenol/rat/day (based on actual water consumption data) in their drink-
ing water for up to one year without reduced weight gain (Deichmann and
Oesper 1940). Slightly higher doses, * 55-56 mg/rat/day, did reduce
weight gain and water consumption was significantly reduced from normal.
No histopathological studies were done. Similarly, Heller and Pursell
reported normal growth rate, food consumption, and reproduction in
three generations of rats given phenol in their drinking water at a
concentration of 5 g/1 (Heller and Pursell 1938). At 8 g/1, many
young died, but the animals did reproduce. The daily dosages of'phenol
were not reported nor were water consumption data. No pathological or
111
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biochemical studies were done and the reported findings were based
solely on general appearance and body weights.
In an unpublished study by Dow Chemical Company, rats given 20
daily doses of 0.1 g/kg phenol by gavage were reported to exhibit
"slight liver and kidney effects," while rats which received 20 daily
doses of 0.05 or 0.01 g/kg phenol reportedly demonstrated none of these
effects (Dow Chemical Company 1976). In a subsequent series of tests,
rats received 135 doses of either 0.1 or 0.05 g/kg phenol by gavage
over a six month period. The growth of the rats was reported to be
comparable to that of the controls. "Very slight liver changes and
slight to moderate kidney damage" were reported in rats given 0.1 g/kg
phenol, while administration of 0.05 g/kg of phenol was reported to
result in only "slight" kidney damage.
The earlier studies by Deichmann and Oesper (1940) and Heller and
Pursell (1938) administered phenol in small doses over the course of a
day in drinking water, allowing metabolism and subsequent detoxification
to occur. Thus, dosing regimen as well as lack of histopathological
evaluation in these earlier studies may account for the lack of kidney
and liver pathology in these earlier reports in contrast to the results
of the Dow study.
In another Deichmann study rabbits, guinea pigs, and rats were
exposed to phenol vapor at concentrations ranging from 0.1 to 0.2 mg/1
(= 100-200 mg/m3) for seven hours daily, five days per week (Deichmann
et al. 1944) . Rabbits exhibited no toxic reactions after 63 exposures
over a period of 88 days but examination of the lung showed widespread
confluent lobular pneumonia and organization resembling granulation
tissue. Peribronchial tissue was often hyperplastic and inflamed.
Endothelial hyperplasia occurred in the pulmonary vessels. Upon exami-
nation of the lungs guinea pigs showed similar results but overt signs
of toxicity were apparent in this species after only three to five
exposures. In contrast rats were reported to show no signs of toxicity
or lung damage after 53 days of exposure.
4. Human Studies
As is the case with most experimental animals, an acute lethal dose
of phenol in man causes central nervous system disturbances together
with peripheral dilation of blood vessels, an apparent direct effect
on cardiac contractility and excitability, a failure of the vasomotor
center leading to hypertension, cardiac irregularities, general tremors,
convulsions, and unconsciousness or coma; death results from respira-
tory arrrest (Haddad et al. 1979, Stajduhar-Caric 1968, and Deichmann
and Keplinger 1963). The average lethal dose in man is estimated to be
between 5 and 40 grams for a 70-kilogram man, i.e., 70 to 570 mg/kg.
Deichmann and Keplinger, however, report that a dose as low as one
gram of phenol may be lethal (Deichmann and Keplinger 1963).
112
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Severe chronic poisoning with phenol causes digestive disturbances,
such as excess salivation, vomiting, diarrhea, anorexia, and central
nervous system effects including headache, fainting, and vertigo
(Deichmann and Keplinger 1963).
Chronic human exposure to low levels of phenol was examined by
Baker (Baker et al. 1978) after a large phenol spill contaminated well
water in a town in southern Wisconsin. Most familes continued to drink
well water until an unusual taste or odor was noted. Based on water
testing data for the two months following the spill and data on water
preference histories obtained from impacted individuals interviewed
seven months after the spill, the approximate daily oral dose was esti-
mated to be between 10 and 240 mg. However, since phenol at concentra-
tions of 1 mg/1 imparts an unpleasant taste to water, the above range
may overestimate actual ingestion. This dose range does not take into
consideration skin absorption from bathing in contaminated water.
Urinalyses six months after the spill revealed no significant differences
in excretion of phenol between the exposed population and a control group
(12 ± 12 SD and 12 ± 11 mg/1, respectively). Results of a questionnaire
administered seven months after the spill revealed significant differ-
ences in the incidence of diarrhea, mouth sores, and burning of the
mouth in the exposed population compared to controls.
Recently, Truppman and Ellenby reported the occurence of cardiac
arrhythmias during chemical face peeling with phenol formulations
(Truppman and Ellenby 1979). In 43 consecutive chemical face peels,
electrocardiograms were monitored. Ten patients developed arrhythmias.
The incidence was apparently not related to use of other drugs before
or during the procedure, the use of nasal oxygen flush, the type of
phenol formulation, age, or previous history of arrhythmias. The inci-
dence of arrhythmias, however, did appear to be associated with the size of
the area peeled and the duration of the procedure. The authors suggest
that in patients who had the procedure completed more rapidly, higher
blood levels of phenol were achieved; this postulate was not confirmed
by chemical analyses of blood, however. There was no indication of how
large a dose of phenol the patients actually absorbed, but it can be
presumed that considerable absorption did occur.
Neonatal jaundice has also been recently linked to the use of
phenolic disinfectant detergents in hospital nurseries (Wysowski et al.
1978, Doan et al. 1979). Wysowski evaluated two separate epidemics
of neonatal hyperbilirubinemia. The first epidemic in a New Jersey
hospital coincided with the use of a phenolic detergent at greater than
recommended concentrations for cleaning the nursery and equipment in-
cluding basinets and mattresses. To counteract an increased incidence
of diarrhea believed to be a hospital-acquired infection, the phenolic
detergent was mixed at two to four times recommended strength for a
vigorous cleaning of the nursery. Over the next two days a cluster of
six cases of severe idiopathic hyperbilirubinemia requiring exchange
transfusions occurred. In the second case, an increased incidence of
neonatal hyperbilirubinemia seemed to coincide with normal use of
113
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phenolic detergents in a Wyoming hospital during a period when the
ventilation system was out of order. When the ventilation system was
corrected and use of the phenolic disinfectant detergent was discon-
tinued, the percentage of neonates with bilirubin levels >_ 12 mg/100 ml
fell from an average of 28% to 8-9%, or approximately the percentage
experienced prior to the use of the phenolic detergent.
In another study, blood microbilirubin levels from 3-day-old
infants from two nurseries were analyzed. Analysis of blood indicated
a small but significantly greater microbilirubin level in neonates
maintained in the nursery in which a phenolic detergent was used (Doan
et al. 1979).
B. EXPOSURE OF HUMANS
1. Introduction
Although phenol is widely distributed in the environment, it does
not persist long or at all in the free form. Thus, in addition to the
normal endogenous production of phenol in humans, exposure to phenol
occurs in certain limited situations. The biological half-life of
phenol in humans is short (3-5 hours) following uptake by inhalation or
dermal absorption (see Section V-A). This section will describe known
exposure routes and, when possible, will quantify such exposures.
2. Ingestion
a. Drinking Water;
The drinking water criteria for phenol is proposed to be set below
the threshold level for organoleptic properties of chlorophenols formed
during chlorination (1.0 ug/1) (U.S. EPA 1980). In a survey of 110 raw
water supplies, the National Organic Monitoring Survey reported only
two positive samples of phenol (no concentrations given) and no presence
in finished drinking water (U.S. EPA 1978). Raw water in the lower
Mississippi River averaged around 1.5 ug/1 with a maximum of 7.0 ug/1
of phenol (NCWQ 1975). Surface water concentrations were measured as
high as 10 mg/1 in 1971 but are usually less than 0.1 mg/1 (U.S. EPA
1980), as described in Pathway #1, Monitoring Data (Section IV). Ground-
water levels in southern Wisconsin in the vicinity and beyond the reaches
of a large phenol spill were 0.21-1,130 mg/1 and 0.001-0.1 mg/1,
respectively.
Table 34 presents the reported concentrations of phenol in various
aquatic systems and the resulting human exposure levels, assuming inges-
tion of 2 I/day. The highest exposure levels were associated with the
phenol spill and ingestion of untreated surface water (at 10 mg/1).
The background-level phenol concentrations resulted in exposure levels
similar to those associated with the more typical surface water upper-
limit concentrations. Because virtually no other data were available
on groundwater levels of phenol, it is not possible to know how repre-
sentative the Wisconsin levels are of well concentrations in general.
114
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TABLE 34. EXPOSURE LEVELS RESULTING FROM INGESTION
OF PHENOL IN FOOD AND WATER
Source
Water
• finished drinking water
• raw drinking water
Phenol
Concentration
(mg/1)
ND1
0.007
• unfinished surface water 10(max); 0.1
(more typical)
• well water 1) maximum 1,130
2) initial 0.21 - 3.2
3) calculated
exposure
level from
case study
(Baker et al.
1978) '• '
Daily
Exposure
Level (mg)
negligible
0.0142
20; 0.22
2,2602
0.42 - 6.42
10 - 2402
Food
smoked summer sausage
smoked pork belly
fish
(mg/kg)
7
28.6
50(max); 16(mean)
(mg)
3
0.63
1.1; 0.341"
Non-detectable
"Assuming ingestion of 2 I/day
Assuming ingestion of 20 g/day (USDA 1978)
+Assuming ingestion of 21 g/day (USDA 1978)
115
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Table 34 also presents the more representative exposure levels (taking
into account the fluctuation in phenol levels over time) calculated
for the highest exposure group in a post-spill study of the incident
(Baker et al. 1978). The results of this study are discussed in more
detail in Sections V-A and VII-A.
b. Food
Phenol has occasionally been found in food items, although a com-
prehensive diet analysis has not been conducted. Lustre and Issenberg
found 7 mg/kg phenol in smoked summer sausage and 28.6 mg/kg in smoked
pork belly, the phenol presumably originating from the wood used in
processing the meat (Lustre and Issenberg 1970). In addition, while
only limited data are available, mean concentrations of 16 mg/kg phc-nol
in fish have been reported, while maximum values were 50 mg/kg (see
Section V-B). Table 34 also presents food concentrations and exposure
levels.
The maximum exposure level resulting from ingesting all three food
items (assuming the maximum smoked meat and fish levels) is approxi-
mately 2 mg/day. Assuming the lower flesh concentrations would result
in a combined exposure level of 2.5 mg/day, a maximum consumption of
fish (about 200 g/day—NMFS 1978) would result in a maximum exposure to
phenol at 10 mg/day (for maximum concentration). Likewise, maximum
consumption of smoked meat results in an exposure level of 6 mg/day
(for maximum concentration). Exposures of these magnitudes derived
from ingestion of these particular products are expected to be limited
to small subpopulations; however, monitoring data for phenol in a broad
spectrum of food products are not available. Until monitoring is con-
ducted it is not possible to know the size of the population exposed to
comparable or higher phenol levels in food.
c. Products Containing Phenol
Phenol is used in several consumer products including Cepastst ®
mouthwash and lozenges (1.45% phenol), Chloraseptic® mouthwash (1.4%
phenol), and Chloraseptic® lozenges (32.5 mg/total phenol/lozenge)
(U.S. EPA 1979). Use of the mouthwash (60 ml/day) would result" in the
intake of 870 mg/day, if ingested; however, only a small amount of this
volume would be swallowed and/or absorbed. Assuming a 10% retention of
the mouthwash at a maximum, the actual intake would be 87 mg/day.
Use of the lozenges at the recommended dosage of eight per day would
result in an exposure of 260 mg/day for the duration of use of the
product. Table 35 presents the estimated exposure levels for phenol-
containing products.
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TABLE 35. EXPOSURE LEVELS RESULTING FROM
USE OF MEDICINAL PRODUCTS
Daily Exposure
Source Phenol Concentration1 Level (mg)
Ingestion:
Cepastat® mouthwash 1.45% g-,2
Chloraseptic® mouthwash 1.4%
Cepastat® lozenges 32.5 mg/lozenge 2603
Dermal Absorption:
Noxzema® face cream 0.5% 12.5'
concentrations from U.S. EPA 1979.
2Assuming 60 ml used per day, 10% retention
3Assuming ingestion of eight lozenges per day
^Assuming use of 5 gm/daily and 50% absorption
117
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The number of persons actually using these commonly available
products is unknown. The population associated with these exposures,
therefore, is expected to be large; however, the products are for use
during illness and thus would probably not be used daily for extensive
periods.
Fishbeck examined the urine of a subject ingesting Chloraseptic®
lozenges every two hours for a total of eight doses (Fishbeck et al.
1975). The free phenol level in the urine peaked at 10.0 mg/1 in the
third eight-hour period after starting the doses. The total phenol
content of the urine returned to baseline within 48 hours after inges-
tion of the last lozenge. These results confirm the rapid clearance of
phenol in man.
3. Inhalation
The most significant exposure through inhalation of phenol is
primarily confined to occupational settings. Data found for ambient
air levels of phenol were discussed in Section III. Deimel and Gableski
reported 0.02-0.3 mg/m3 phenol in air along highways in Germany (Deimel
and Gableski 1973). Assuming an inhalation of 20 m3 of air/day, a maxi-
mum exposure of 6 mg phenol/day would result. It is unknown how valid
these exposure levels are for U.S. cities; however, in industrialized
areas with high traffic volume, comparable U.S. levels may exist.
The use of phenol in the laboratory for purposes such as organic
synthesis and plastics formulation would also result in exposure to
humans. Assuming that work was being conducted in a small, poorly
ventilated room in which air saturation by phenol would be reached—a
worst case—an air concentration was estimated. Based on Henry's law,
phenol in a beaker would generate 9.4 mg of phenol/m3 of air. Assuming
an inhalation rate of 7 m3 air in 8 hours, the resulting exposure level
would be 75.2 mg of phenol (Arthur D. Little, Inc., estimate).
4. Dermal Absorption
Phenol is found in various cosmetics and skin care products (U.S.
EPA 1979). Most of these products are used for temporary relief of
skin problems, such as poison ivy or burns; however Noxema Medicated®
(Noxell) and similar products may be used on a daily basis. For pur-
poses of estimation, the use of 5 grams of such a product per day is
assumed and would result in the application to the skin of 0.25 mg
phenol per day. Assuming 50% of this would be washed off, and consider-
ing the rapid dermal absorption of phenol described in Section V-B, then
12.5 mg of phenol is a rough estimation of the amount absorbed per day
(Arthur D. Little, Inc., estimate).
The use of face peels containing phenol has been associated with
an increased incidence of arrhythmias. Although this use apparently
represents a source of human exposure, the dose received cannot be
readily calculated.
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5. Exposure Scenario Estimates
For the purpose of comparing exposure levels from different types
of exposure and total levels resulting from combined exposures, five
exposure scenarios were fabricated (see Table 36). A worst case
scenario (Scenario #1) combining the greatest exposure levels resulted
in a daily exposure of approximately 520 mg of phenol. Three special-
case exposure scenarios for subpopulations exposed to contaminated
groundwater (Scenario #2), treated with phenol-containing medicinal
products (Scenario #3), and working in a laboratory (Scenario #4)
resulted in exposure levels of approximately 250, 350, and 80 mg/day,
respectively. The inclusion of daily use of face cream increased these
levels to 260, 370, and 95 mg/day respectively. Finally a general
population scenario (Scenario #5) had an associated exposure level of
7 mg/day.
G" OVERVIEW AND CONCLUSIONS
This section has discussed the effects on humans of exposure to
phenol and their level of exposure.
1. Effects
Phenol.is readily absorbed from all routes of entry, distributed
throughout the body, and metabolized and excreted from the body in
rather rapid order. The half-life of phenol in man is approximately
3.5 hours. Phenol is also produced endogenously by the degradative
action of bacteria in the gut on tyrosine.
Acute lethal values for phenol are all within an order of magnitude,
regardless of the route or species and, for the most part, are in the
200-700 mg/kg range. The cat appears to be the most sensitive species
(oral LDLo 80 mg/kg), probably as a result of significant metabolic dif-
ferences in the manner phenol is detoxified in this species. Slight to
moderate kidney damage and slight liver changes have been reported in
rats given 135 daily doses of 100 mg/kg phenol by gavage. Similar
treatment with 50 mg/kg produced slight kidney damage after 135 doses
but not after 20 doses. Rats, however, have been able to tolerate much
larger doses in drinking water (56 mg/rat/day or ^ 280 mg/kg for a 200-g
rat), probably due to its rapid metabolism as well as the intermittent
nature of dosing in contrast to exposure by gavage.
There are no indications that phenol is carcinogenic by the oral
route, but it does appear to possess tumor-promoting activity. Skin
application of phenol is tumorigenic in sensitive strains of mice but
not in standard inbred strains of mice. The tumorigenic activity of
phenol appears to be associated with its irritancy and subsequent skin
hyperplasia.
Phenol has been shown to induce lethal mutations in fruit fly
(Drosophila) and to significantly increase the incidence of chromosomal
effects in a dose-related manner in spermatogonia and spermatocytes of
mice given phenol by gavage at dosage levels as low as 6.5 ug/kg/day.
Furthermore, the data suggest incremental increases in the incidence of
119
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TABLE 36. EXPOSURE SCENARIOS INVOLVING
CONTACT WITH PHENOL
Scenario
Scenario #1
Worst Case (very
small subpopulation
affected)
Exposures
Ingestion of contaminated well
Ingestion of contaminated fish
Ingestion of throat lozenges
Use of face cream
Inhalation along highway
Exposure
Level (mg /day)
,'ater
Total
2401
1.1
2601
12.5
63
519.6
Scenario #2
Subpopulation in
area with con-
taminated ground-
water (small sub-
population affected)
Ingestion of contaminated well water 240
Ingestion of contaminated fish _ 1.1
Inhalation along highway 63
Total 247.1
Scenario #3
Subpopulation being
treated with medici-
nal products con-
taining phenol
(small subpopulation
affected)
Ingestion of throat lozenges
Ingestion of mouthwash
Ingestion of raw drinking water
Ingestion of contaminated fish
Inhalation along highway
Total
260 J
871
0.014
354.114
Scenario M
Subpopulation exposed
in laboratory (small
subpopulation
affected)
Inhalation of laboratory air1*
Ingestion of raw drinking water
Ingestion of contaminated fish
Inhalation along highway
Total
75.2
0.014
82.34
Scenario #5
General population
(majority of pop-
ulation affected)
Ingestion of raw drinking water
Ingestion of contaminated fish
Inhalation along highway
Total
0.014
1.1
,3
7.114
^Short-term exposure
2Although inhalation and ingestion are different exposure routes, the levels
have been combined to provide an idea of the overall magnitude of exposure
of each hypothetical subpopulation
3Based on estimate from German study. It is unknown how realistic this is for the U.S.
t^
Assuming daily use of phenol.
Source: Arthur D. Little, Inc., estimates.
120
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chromosomal aberrations occur in consecutively treated generations.
However, the treatment schedule utilized and the lack of data reporting
prevent assessment of the significance of this finding. No indications
of teratogenicity have been found.
The lowest reported oral lethal dose in man is one gram of phenol,
but the majority of lethal values are in the 5- to 40-gram range. An
acute lethal dose of phenol results in central nervous system dis-
turbances together with peripheral vasodilation leading to sudden
collapse and unconsciousness. Death is due to respiratory arrest.
Ingestion of non-lethal amounts of phenol can result in burning in
the mouth, mouth sores, headache, vomiting, diarrhea, back pain,
paresthesia, and production of dark urine (probably from oxidation
products of phenol). Recent reports have also linked phenol to the
production of cardiac arrhythmias during chemical face peeling
procedures.
Aside from the issue of its mutagenicity, the rapid clearance of
phenol from the body, its relatively high lethal dose, and the fact that
small amounts of phenol are produced endogenously indicate that man can
handle levels normally present in U.S. drinking water with no untoward
effects. Further work needs to be done to validate the single report
of increased chromosomal aberrations in phenol-treated mice and, in
particular, to clarify the finding of increased numbers of aberrations
in consecutively treated generations of mice.
2. Exposure
There are numerous uncertainties involved in estimates of exposure
to phenol, primarily due to lack of monitoring data. Based on the
limited information available, the use of phenol-containing products,
especially mouthwash and lozenges, represents the largest consumer
exposure, although presumably on a short time scale. Ingestion of con-
taminated well water may result in an equivalent short-term exposure.
Other water supplies, even untreated surface water, would contribute to
a very small exposure level through ingestion. Laboratory workers are
a subpopulation potentially exposed to levels equivalent to use of
phenol-containing mouthwash; however, it is assumed this exposure would
occur over a longer period of time. Ingestion in food and dermal
absorption from cosmetics may contribute to a more continual exposure
for this subpopulation. Ingestion of fish or smoked meat and inhala-
tion along highways may each represent an exposure of 10 mg/day, using
worst case assumptions.
Special note should be made of the potential conversion of phenol
during chlorination to lower chlorinated phenols. Although phenol is
eliminated during this process, more harmful compounds, including known
carcinogens, may result. A separate exposure assessment considers the
environmental distribution of effects of and exposure to three commonly
detected chlorophenols—2-chlorophenol, 2,4-dichlorophenol, and 2,4,6-
trichlorophenol (Scow et al. 1980).
121
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REFERENCES
Baker, E.L.; Landrigan, P.J.; Bertozzi, P.E.; Field, P.H.; Basteyns, B.J.;
Skinner, H.G. Phenol poisoning due to contaminated drinking water. Arch.
Environ. Health 33:89-94; 1978.
Boutwell, R.K; Bosch, D.K. The tumor-promoting action of phenol and
related compounds for mouse skin. Cancer Res. 19:413-424; 19.59.
Bulsiewicz, H. The influence of phenol on chromosomes of mice Mus
musculus in the process of spermatogenesis. Folia Morphol. (Warsz.)
36(l):13-22; 1977.
Capel, I.D.; Millburn, P.; Williams, R.T. Monophenyl phosphate, a new
conjugate of phenol in the cat. Biochem. Soc. Trans. 2:305-306; 1974.
Cotruvo, J.A.; Simmon, V.F.; Spanggord, R.J. Investigation of mutagenic
effects of products of ozonation reactions in water. Ann. N.Y. Acad
Sci. 298:124-140; 1977.
Deichmann, W.B. Phenol studies. V. The distribution, detoxification,
and excretion of phenol in the mammalian body. Arch. Biochem. 3:345;
1944. (As cited by U.S. EPA 1979)
Deichmann, W.P.; Keplinger, M.L. Phenols and phenolic compounds.
Patty, F.A. ed. Industrial hygiene and toxicology. Vol. II. New York:
Interscience Publishers; 1963:Chapter 33.
Deichmann, W.; Oesper, P. Ingestion of phenol - Effecs on the albino
rat. Ind. Med. 9:296-298; 1940.
Deichmann, W.B.; Witherup, S. The acute and comparative toxicity of
phenol and 0-, m- and p-cresols for experimental animals. J. Pharmacol.
Exp. Ther. 80:233-240; 1944.
Deichmann, W.B.; Kitzmiller, K.V.; Witherup, S. Phenol studies VII.
Chronic phenol poisoning with special reference to the effects upon
experimental animals of the inhalation of phenol vapor. Am. J. Clin.
Pathol. 14:273-277; 1944.
Deimel, M.; Gableske, R. Measurement of several exhaust components in
motor traffic in Cologne. Staed hygiene: 24:268-272; 1973.
Demerec, M., et al. A survey of chemicals for mutagenic action on E.
coli. Am. Natur. 85:119; 1951. (As cited by U.S. EPA 1979.) ~
Dickey, F.H., et. al. The role of organic peroxides in the induction
of mutations. Proc. Natl. Acad. Sci. 35:581; 1949. (As cited by
U.S. EPA 1979)
122
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Doan, McK. H.; Keith, L.; Shennan, A.T. Phenol and neonatal jaundice.
Pediatrics 64:324-325; 1979.
Fishbeck, W.A.; Langner, R=R.; Kociba, R.J. Elevated urinary phenol
levels not related to benzene exposure. Am. Ind. Hyg. Assoc. J.
36(11):820-824; 1975.
Haddad, L.M.; Dimond, K.A.; Schweistris, J.E. Phenol poisoning.
TOXBIB/79/197475. JACEP 8, ISS 7, 267-269; 1979.
Hadorn, E.; Niggli, H. Mutations in Drosophila after chemical treat-
ment of gonads in vitro. Nature 157:162-163; 1946.
Heller, V.G.; Pursell, L. Phenol-contaminated waters and their physio-
logical action. J. Exp. Ther. 63:99-107; 1938.
Kao, J.; Bridges, J.W.; Faulkner, J.K. Metabolism of [lkC] phenol by
sheep, pig and rat. Xenobiotica 9(3):141-147; 1979.
Kolesnikova, T.N. Effect of phenol on the sexual cycle of animals in
chronic inhalation poisoning. Gig Sanit. 37(1):105-106; 1972.
Korshunov, S.F. Early and late emfaryotoxic effects of phenol (Experi-
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Khim. Promsti. 149-153; 1974. (As cited in Chemical Abstracts 87-16735)
Lustre, A.O.; Issenberg, P. Phenolic components of smoked meat products.
J. Food Chem. 18:1056; 1970.
Mehta, R.; Hirom, P.C.; Millburn, P. The influence of dose on the
pattern of conjugation of phenol and 1-naphthol in non-human primates.
Xenobiotica 8:445-452; 1978.
Minor, J.L.; Becker, B.A. A comparison of the teratogenic properties
of sodium salicylate, sodium benzoate, and phenol. Toxicol. Appl.
Pharmacol. 19:373; 1971.
National Commission on Water Quality (NCWQ). Water quality and environ-
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National Marine Fisheries Services (NMFS). Report on the change of
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National Cancer Institute (NCI). Bioassay of phenol for possible
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National Institutes of Health, U.S. Department of Health and Human
Services; 1980.
123
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Piotrowski, J.K. Evaluation of exposure to phenol: absorption of"
phenol vapor in the lungs and through the skin and excretion of phenol
in urine. Br. J. Ind. 28:172-178; 1971.
Pullin, T.G.; Pinkerton, N.M.; Johnston, R.F.; Killian, D.J. Comparison
of decontamination procedures for acute dermal phenol exposures in swine
Toxicol. Appl. Pharmacol. 37:97-98; 1976.
Registry of Toxic Effects of Chemical Substances (RTECS). Cincinnati,
OH: U.S. Department of Health, Education and Welfare, Public Health
Service, Center for Disease Control, National Institute for Occupational
Safety and Health; 1978.
Salaman, M.H.; Glendenning, O.M. Tumor promotion in mouse skin by
sclerosing agents. Br. J. Cancer 11:434-444; 1957.
Scow, K.; Goyer, M.; Payne, E.; Perwak, J.; Saterson, K.; Wood, M.;
Woodruff, C. (Arthur D. Little, Inc.). Exposure assessments of priority
pollutants: Chlorophenol. Contract No. 68-01-3857. Washington, D.C.
Monitoring and Data Support Division, U.S. Envrionmental Protection
Agency; 1980.
Stajduhar-Caric, Z. Acute phenol poisoning - Singular findings in a
lethal case. J. Forensic Med. 15.:41-42; 1968.
Truppman, E.S.; Ellenby, J.D. Major electrocardiographic changes during
chemical face peeling. Plast. Reconstr. Surg. 63:44-48; 1979.
U.S. Department of Agriculture (USDA). Supplement for 1976 to food
consumtpion, price, and expenditures. Agricultural Economic Report
No. 138; 1978. F
U.S. Environmental Protection Agency (U.S. EPA). Ambient water quality
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Office of Water Planning and Standards; 1979.
U.S. Environmental Protection Agency (U.S. EPA). Priority pollutant
data base. Monitoring and Data Support Division, Water Quality Analysis
Branch; 1980.
U.S. Environmental Protection Agency (U.S. EPA). Unpublished data.
National Organics Monitoring Data; 1978.
Van Duuren, L.; Goldschmidt, B.M. Cocarcinogenic and tumor-promoting
agents in tobacco carcinogenesis. J. Natl. Cancer Inst. 56:1237-1242-
1976.
Van Duuren, B.L.; Goldschmidt, B.M.; Katz, C.; Melchionne, S.; Sivak, A.
Cocarcinogenesis studies on mouse skin and inhibition of tumor induction.
J. Natl. Cancer Inst. 46:1039-1044; 1971.
124
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Van Duuren, B.L.; Katz, C.; Goldschmidt, B.M. Cocarcinogenic agents
in tobacco carcinogenesis. J. Natl. Cancer Inst. 51:703-705; 1973.
VanHaaften, A.B.; Sie, S.T. The measurement of phenol in urine by
gaschromatography as a check on benzene exposure. Am. Ind. Hyg. Assoc.
26:52; 1965. (As cited by U.S. EPA 1979)
Wheldrake, J.F.; Baudinette, R.V.; Hewitt, S. The metabolism of phenol
in a desert rodent Notomys alexis. Comp. Biochem. Physiol. 61C:103-107;
1978.
Wysowski, D.K.; Flynt, J.W.; Goldfield, M.; Altman, R.; Davis, A.T.
Epidemic neonatal hyperbilirubinemia and use of a phenolic disinfectant
detergent. Pediatrics 61:165-170; 1978.
125
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SECTION VI.
AQUATIC BIOTA EFFECTS AND EXPOSURE
A. EFFECTS ON AQUATIC BIOTA
1, Introduction
This section provides experimental information on the levels of
phenol at which the normal behavior and metabolic process of aquatic
organisms are disrupted. Although phenol has been studied fairly
extensively for its acute toxic effects, bioassay results are not often
consistent, even for a single species. Tests conducted under static
conditions are normally less reliable than continuous-flow experiments
because there is less control of phenol concentrations. However,
continuous flow conditions may be be suitable for testing certain kinds
of organisms, such as fish larvae and free-floating invertebrates.
In both kinds of bioassays, phenol concentrations are often determined
determined nominally (i.e., by diluting a measured amount of phenol) instead
of by direct periodic measurement during the bioassay. Nominal deter-
mination of concentrations does not account for phenol evaporation,
adsorption onto particles or walls of test tank, or absorption by test
organisms, and so may produce overestimates of lethal and sublethal
levels. In a flow-through experiment where the phenol levels were
monitored (Kristoffersson et al. 1973), the authors twice had to nearly
double the concentration in the influent water to maintain the desired
concentration in the test aquarium. They attributed the loss of phenol
to oxidation by dissolved oxygen or bacterial degradation.
Water temperature has been demonstrated to affect the sensitivity
of aquatic animals to phenol, largely as a result of its influence on
metabolic rate. Other factors such as pH and hardness, which are known
to alter the toxicity of other chemicals, have not yet been studied
extensively for phenol. In addition, the species and the developmental
stage of the test organisms must be considered. Since some species and
stages may be more sensitive to phenol than others, it may not be appro-
priate to compare the data from unrelated studies.
2. Freshwater Organisms
a. Chronic and Sublethal Effects
Low levels of pollutants 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
127
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physiologzcal responses. Prolonged exposure, even to low concentrations
of phenol, could ultimately result in mortality. Even if fish are not
killed by long-term exposure to phenol, the survival of local popula-
tions may be endangered.
A summary of sublethal and chronic effects data for vertebrates
and invertebrates is presented in Table 37. Daphnids were the most
sensitive species tested; however, the increased molting and growth
rate reported for Daphnia pulex cannot necessarily be considered a
detrimental effect. The grass frog (Rana temporaria) is the only non-
piscine vertebrate for which toxicity data were found. According to
the data of Kaufmann (1977), the critical stages for susceptibility
to phenol in frog development are the tail-bud stages and during meta-
morphosis.
The physiological effects in rainbow trout (Salmo gairdneri)
described by Mitrovic and others are more pre-mortality than sublethal
in nature (Mitrovic et al. 1968). In their experiments with freshwater
worms, Alekseev and Uspenskaya observed a general sequence of effects
preceding death from phenol toxicosis (Alekseev and Uspenskaya 1974).
The typical progression was as follows: normal swimming or burrowing
activity, increased locomotor activity, swimming worms sink to floor
of test aquarium, curling of body or tail, and convulsive twitching
followed by a lack of response to mechanical stimulation. The phenol
concentrations producing these effects ranged from approximately 100 to
1,000 mg/1.
Numerous species of algae have been bioassayed for susceptibility
to phenol, with most of the experimentation performed by Kostyaev
(Kostyaev 1973). The lowest concentration at which sublethal effects
have been reported is 8 mg/1, which completely inhibited photosynthesis
in Uroglenopsis divergens. Kostyaev found that green algae generally
were most resistant, while chrysophytes were the most sensitive. In
some cases, low concentrations of phenol stimulated photosynthesis, as
in the case of Chlorella exposed to 10-40 mg/1 (Lukina 1970). Higher
concentrations, however, had the reverse effect, and still higher levels
may inhibit respiration as well. For more details on phenol toxicity
to algae, see Table 13 in Buikema et al. 1979.
b. 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 result in chronic or sublethal effects, industrial discharges
and spills can temporarily result in levels high enough to cause fish
kills (see Section VI-B).
128
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TABLE 37. CHRONIC AND SUBLETHAL EFFECTS ON FRESHWATER ORGANISMS
K)
Concentration
(mg/1)
0.1
0.1
0.5
2.6
3.1
5
6.5, 6.9
25
40
400
Species
Daphnia magna
Daphnia pulex
Grass frog
(Rana temporaria)
Tathjad Minnow
Daphnia magna
Northern Pike
Daphnia longispina
Rainbow trout
(Salmo gairdneri)
Bream (Abramis brama)
Russian sturgeon,
stellate sturgeon
Clams
(Dreissena polymorpha)
(Sphaerium corneum)
Test
Duration
2 weeks
2 weeks
5 hours
2 weeks
7 days
12 days
4-5 days
Effects
Decreased reproductive rate
Increased molting and
growth rate
35% survival of embryos;
survivors undeveloped,
with malformed tails
Chronic value
Chronic value
Loss of balance
Decreased fecundity
Lesions at base of fins,
excessive mucous secretions
on skin and gills, inflamed
and bleeding gills with
damaged lamellae, swollen
spleen, kidney, and liver
Hatching delayed by 1 day
No development of pigmen-
tation in prolarvae
Decreased filtration
(feeding) rate
References
Luferova and Flerov 1974
Luferova and Flerov 1974
Kaufmann 1977
Ilolcombe et. al. , 1980
U.S. EPA 1978
Kristoffersson et al.
1973
Luferova and Flerov 1971
Mitrovic et al. 1968
Volodin et al. 1966
Shmal'gauzen 1974
Smirnova 1973
-------
The acute effects of phenol on freshwater finfish have been studied
for at least thirteen species, resulting in a fairly reliable data base
which has been compiled and condensed in Table 38. It should be noted
that the LC50 values given were derived under a variety of conditions.
Such factors as exposure period (between 24 and 96 hours), age of test
fish, difference in certain water parameters, and bioassay type (static
or flow-through) may account for some of the variation in a given
species' sensitivity. (Factors contributing to variability in phenol
toxicity and fish sensitivity are discussed in greater detail in
Section VI-A4).
Reported LC50 values for phenol range from 5.0 mg/1 for the juvenile
rainbow trout (Salmo gairdneri) to 200 for the goldfish (Carassius auratus).
The data are insufficient to attempt to identify the most sensitive
families; the most frequently tested particular species are likely to
have the widest ranges of reported LC50's. However, it should be noted
that salmonids are normally among the most sensitive of the species
bioassayed.
One study which is occasionally referred to in the literature
reports a very low lethal level of 0.08 mg/1 for a "minnow" species
(Symons and Simpson 1938). The phenol was present, however, in a mixed
waste including other unidentified toxic substances; therefore, this
concentration should not be used to represent phenol's effects (EIFAC
1973).
LC50values for freshwater invertebrates are summarized in Table
39. As a great many species have been tested for sensitivity to
phenol, this list provides only a sample which represents the range
of LC50fs reported. Both the lowest (<1.5 mg/1) and highest (1,840 mg/1
acute values were determined by Alekseev (Alekseev 1973) for aquatic insects,
Baetis species and Mideopsis orbicularis. respectively. Common names
were not found for these invertebrates. Of the eleven species of worms
tested by Alekseev and Uspenskaya (Alekseev and Uspenskaya 1974), ben-
thic worms (habituated to a lack of oxygen) were the most resistant to
phenol. The species which lived in bottom detritus above the silt were
somewhat more sensitive, while those which swam in the water were gener-
ally the most susceptible. For a more complete listing of acute tox-
icity data for freshwater invertebrates see Table 14 in Buikema et al
1979.
3. Marine Organisms
The data base on the toxic effects of phenol on seawater biota is
limited to acute toxicity bioassays on two fish and two mollusc species.
In a 60% (salinity 20^00) seawater solution, rainbow trout (Salmo gairdneri)
exhibited median mortality at 5.2 mg/1 phenol (Brown et al. 1967). Since
resistance decreased as the proportion of seawater increased from 0% to 60%
it could be assumed that the LCso i-s lower in 100% seawater (^30 °/oo) salinity,
Nunogawa and others determined a 96-hour LC50 of 6.0 mg/1 for the mountain
bass (Kuhlia sandvicensis), a species native to Hawaiian waters (Nunogawa
et_ al."l970) .
130
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TABLE 38. ACUTE TOXICITIES (LC50) FOR FRESHWATER FISH
Range of LC50
(mg/1)
5.0-11.6
11.5-60.0
11.7
16.7
19.0
22.0-63.0
24.0-67.5
26.0
31.0-39.19
31.5
33.31-200.0
35.0-129.0
36.3
Species
Rainbow trout (Salmo gairdneri) ; juvenile
Bluegill sunfish (Lepomis macrochirus)
Brook trout (Salvelinus fontinalis)
Channel catfish (Ictalurus punctatus;
Mozambique mouthbrooder (Tilapia mossambica)
Molly (Mollienesia latipinna)
Fathead minnow (Pimephales promelas)
Mosquitofish (Gambusia affinis)
Guppy (Poecilia reticulatus)
Walking catfish (Clarias batrachus)
Goldfish (Carassius auratus)
Golden shiner (Notemigonius chrysoleucas)
Flagfish (Jordanella floridae)
1
Gersdorff 1939
Source: Compiled from Table 1, U.S. EPA 1980, except where noted.
131
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TABLE 39. ACUTE TOXICITIES (LC50) FOR FRESHWATER INVERTEBRATES
Range of LC 5 Q
(mg/1)
7-100
14
15-78
18-93
57
78
94
100
108
122
150
205-300
260-320
341-381
350
351-391
520
780
1,280
Species
Baetis sp.
Daphnia magna
Daphnia longispina
Isopod (Asellus aquaticus)
Daphnia pulex
Cladoceran (Polyphenus pediculus)
Conchostracan (Lynceus brachyurus)
Snail (Physa heterostropha)
Worm (Euplanaria lugubris)
Copepod (Mesocyclops leukarti)
Copepod (Cyclops vernalis)
Worm (Mesostoma ehrenbergii)
Rotifer (Philodina acuticornis)
Snail (Physa fontinalis)
Annelid (Aelosoma headleyi)
Snail (Limnaea stagnalis)
Snail (Nitrocris sp.)
Worm (Lubriculus variegatus)
Clam (Sphaerium corneum)
Worm (Helobdella stagnalis)
Reference
Alekseev 1973
Alekseev and Uspenskaya
1974
Alekseev and Uspenskaya
1974
Alekseev and Uspenskaya
1974
Alekseev and Uspenskaya
1974
1,840 Mideopsis orbicularis Alekseev 1973
Source: Compiled from Table 2 in U.S. EPA 1980, except where noted.
132
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The larvae of the Atlantic oyster (Crassostrea virginica) and the
hardshell clam (Mereenaria mercenaria) have been bioassayed by Davis
and Hidu (1969). The resulting 48-hour LC50 values were 58.3 and 52.6
mg/1, respectively.
4. Factors Affecting the Toxicity of Phenol
Of the many parameters that are controlled in toxicity bioassays,
water temperature is the factor that has been most frequently tested
for its effects on phenol toxicity. In experiments with fathead minnows
(Pimephales promelas), Ruesink and Smith found that the 96-hour LC50
decreased from 36 to 24 mg/1 as the temperatures increased from 15 to
25°C (Ruesink and Smith 1975). Brown and others observed the opposite
effect in rainbow trout (Salmo gairdneri); the 48-hour LCso at 18°C was
almost twice that at 6°C (Brown et al. 1976). However, the response
period of the fish decreased with the rise in temperature so that death
occurred more quickly at the higher temperatures. Moreover, the expected
trend might have reappeared if higher temperatures (>18°C) had been
tested. In a bioassay which allowed brook trout (Salvelinus fontinalis)
a selection of temperatures from 4 to 29°C, fish exposed to phenol con-
sistently chose areas of lower temperature than controls. The difference
in temperature selection was particularly significant in groups exposed
to 7.5 and 10.0 mg/1 phenol (Miller and Ogilvie 1975).
In their bioassays with freshwater worms, Alekseev and Uspenskaya
found that the overall resistance of the worms increased as the water
temperature declined (Alekseev and Uspenskaya 1974). However, the
maximum tolerated concentrations (at which no mortalities occurred)
were lowest at the most extreme temperatures, 2 and 28°C. The results
from all the studies suggest that, to a certain degree, the effects of
variations in temperature are species- or at least group-specific.
In order to determine the effects of salinity variations on the
resistance of a salmonid species, Brown and others exposed rainbow trout
to phenol in water solutions containing from 0 to 60% seawater (0 °/oo to
20 °/oo salinity) (Brown et al. 1967) . At 15°C the 48-hour Unsteadily
decreased from 9.3 mg/1 in fresh water to 5.2 mg/1 in 60% (~20 °/oo)
seawater. Presumably the LCso would have been yet lower in 100% ("33 °/oo)
seawater. The authors pointed out that the greatest hazard to migrating
salmonids with respect to phenol effects would be at the seaward end of
their passage due to increased toxicity at higher salinity. Further
study in this area should consider the ability of salmonid species to
acclimate to saline water in the presence of phenol.
The only information on pH effects on phenol toxicity was from a
study by Flerov and Luk'yanenko (1966). Crucain carp were more sensitive
to phenol at pH extremes, but within an intermediate range, toxicity
levels did not vary. It is likely that pH extremes are harmful to fish
independent of any effects they might have on phenol toxicity.
133
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Acclimation may be an important factor in the ability of fish and
invertebrate populations to survive chronic exposure to phenol. Flerov
found that guppies which had been raised in low concentrations of phenol
for three generations were five times as resistant to phenol as unaccli-
mated stock (Flerov 1971).
B. EXPOSURE OF AQUATIC BIOTA
•
Fish-kill data indicate that phenol containing wastes sometimes
reach concentrations in aquatic systems high enough to have lethal
effects on aquatic organisms. Unfortunately, monitoring data on ambient
phenol levels in surface waters are too limited to support non-speculative
conclusions on the aquatic exposure of biota to phenol. No information
on exposure levels to wildlife in terrestrial systems was available.
Monitoring data for phenol levels in surface waters are quite limited
(see Section IV-Pathway #1). The data provided by STORET on phenol levels
in ambient waters of U.S. river basins during 1978-1980 amount to less
than 600 observations, most of them remarked data, indicating that phenol
is an infrequently monitored chemical. The only major basins with more
than 50 observations were the Southeast, Ohio River, Lower Mississippi,
and Pacific Northwest regions. The river basins with the highest un-
remarked concentrations were the Tennessee and Ohio River basins. The
maximum values were, respectively, 6,794 ug/1 and 5,900 ug/1. In both
basins these maximums were most likely unusual observations and could not
be assumed to be representative of the entire basin due to insufficient
data or a high standard deviation in the available data.
Table 40 summarizes the frequency distribution of phenol concentra-
tions over ranges from O.99 to >1,000 ug/1. In addition to observations
reported in 1978 through 1980, earlier reported ranges are also included
separately. The data were not combined because of the unreliability of
some of the earlier measurements. Unremarked data tended to be reported
at less than 10 ug/1 (72%) and remarked data between 1 ug/1 and 100 ue/1
(89%). S
Ambient surface water concentrations from sources other than STORET
were also few and inconclusive. The highest U.S. phenol concentration
reported (also in STORET) of 142 ug/1 in the Delaware Estuary is actually
for phenolics (Faust eit al. 1975). Therefore, if other concentrations
in the STORET data base also cover other phenols, one would suspect that
phenol itself is present at even lower levels than reported. It is not
possible, however, to check the analytical techniques for each observa-
tion, so it is conservatively assumed that all STORET and other levels
measure only phenol.
Judging by the results of the EXAMS concentration simulations for
a lake and river system (see Section IV-Pathway #1), it appears unlikely
that even raw waste levels are high enough to lead to, under conditions
of continuous discharge, phenol levels of a magnitude greater than that
134
-------
TABLE 40. FREQUENCY DISTRIBUTION OF PHENOL (TOTAL)
Ui
CONCENTRATIONS IN AMBIENT SURFACE WATER
1970-1977
1
Year <0.99
1970
1971
1972 4
1973
1974
1975
1976
1977 3
Cross 7
1
Year <0.99
1978 16
1979 7
1980 38
(.IMS', til
Remarked Data
1 1
1-9.99 10-99.99 100-999.99 >1000 <0.99
21 -
-
1 7
2 8 - -
46 1 -
87 2 -
23 3
10 -
158 17 8-10
1978-1980
Remarked Data
1 1
1-9.99 10-99.99 100-999.99 >1000 <0.99
66 43 - - 7
20 120 - - 8
25 240 322
111 403 3 2 17
Unremarked Data
1-9.99 10-99.99 100-999.99 ^1000
- - J
- - 1
_
6 - -
71
108 6
60 1 -
10 14
255 21-4
i
Unremarked Data
1
1-9.99 10-99.99 100-999.99 HOOO
1
1 - 1
U 6 3 !
14 7 3 2
Numbers .it to|> of column are concentration ranges In units of ug/1. Numbers in body of table are numbers of observations reported within each range
Source: U.S. EPA (1980d).
-------
for typical surface water. However, it was not possible to identify
and/or estimate the quantity of phenol generated by each waste stream
and it is possible that other industries may contribute higher levels.
C. CONCLUSIONS
1. Effects
The lowest concentration of phenol at which toxic effects have
been reported is 0.1 mg/1, in Daphnia magna. The lowest acute level
was for a species of Baetis (insect), a 48-hour LC5o of <1.5 mg/1.
Rainbow trout was the most sensitive fish tested, with LC50 values as
low as 4.2 mg/1. The grass frog was the only non-piscine vertebrate
tested; lethal toxicosis in embryos was reported at 0.5 mg/1 phenol.
Toxicosis was manifested in a number of effects in addition to
mortality. Decreased reproductive rate and fecundity were observed
in Daphnia, loss of balance in pike, lack of pigmentation in developing
sturgeon prolarvae, delayed hatching in bream, and reduced feeding in
clams. Not all effects were detrimental, however; Daphnia pulex grew
more quickly in 0.1 mg phenol/1, and some species had higher hatching
rates in very low concentrations of phenol.
Data on toxicity to marine organisms is extremely limited, although
the toxic levels reported are in the same range as for freshwater species.
No eco-community or population studies in either laboratory or field
conditions were available.
Environmental factors may have an influence on the toxicity of
phenol to aquatic life. Water temperature is the most extensively
studied variable, yet studies present variations between species as to
its general effects. In most cases, the organism becomes more sensitive
as temperature increases, although high and low extremes appear to be
the most detrimental. The anadromous rainbow trout perished at lower
phenol concentrations as salinity increased, suggesting that salmonid
populations are most at risk as their migrations bring them into estu-
aries. Crucian carp were more sensitive to phenol at pH extremes, while
intermediate acidity levels did not affect toxicity concentrations.
2. Exposure
Based on available data, phenol concentrations of any significance
in regard to aquatic life (see Section VI-B) are few and short-term.
Under conditions of continual discharge, most reported effluent levels
appear unlikely to contribute high phenol concentrations in most aquatic
systems. In addition since these loadings are based on raw wastewater
phenol levels, wastewater treatment would reduce them significantly
before release. Examples of situations in which environmentally adverse
phenol concentrations occurred and the effects of these levels on
aquatic populations are discussed in Section VII.
136
-------
REFERENCES
Alekseev, V.A. Toxicological characteristics and symptom complex of
acute phenol intoxication of aquatic insects and arachnids. Tr. Inst.
Biol. Vnutr. Vod. Akad. Nauk SSSR, No. 24(27) -.72-89 (Russ); 1973. (As
cited in Buikema, et al. 1979)
Alekseev, V.A.; Uspenskaya, N.Ye. A toxicological description of acute
phenolic poisoning of certain freshwater worms. Hydrobiol. J. (Engl.
Transl. Gidrobiol Zh.). 10(4):35-41; 1974.
Brown, V.M.; Jordan, D.M.M.; Tiller, B.A. The effect of temperature
on the acute toxicity of phenol to rainbow trout in hard water. Water
Res. 1:587-594; 1967.
Brown, V.M.; Shurber, D.G.; Fawell, J.K. The acute toxicity of phenol
to rainbow trout in saline waters. Water Res. 1:683-685; 1967.
Buikema, A.L., Jr., McGinniss, M.J.; Cairns, J., Jr. Phenolics in
aquatic ecosystems: a selected review of recent literatures. Marine
Envrionmental Research 2:87-181; 1979.
Davis, H.C.; Hidu, H. Effects of pesticides on embryonic development
of clams and oysters and on survival and growth of the larvae. U.S.
UVS. Environmental Protection Agency; 1979.
Faust, S.D.; Clement, W.H.; Hunt, G.T. Significance of phenolic com-
pounds in the Delaware Estuary. National Science Foundation, PB 262
755; 1975.
Flerov, B.A. Problems of hydrobionts' adaptation to a toxic factor.
Abstract: Chem. Abs. 80 78848d, Gidrobiol. Zh., 7(6):61-66 (Russ);
1974. (As cited in Buikema, et al. 1979)
Gersdorff, W.A. Effect of the introduction of the nitro group into the
phenol molecule on toxicity to goldfish. I. •Monochlorophenols. Amer.
J. Pharm. 112:197-204; 1939. (As cited in Buikema, et al. 1979)
Herbert, D.W.M. The toxicity to rainbow trout of spent still liquors
from the distillation of coal. Ann. Appl. Biol. 50:755-777; 1962.
(As cited in UNFAO 1973)
Holcombe, G.W., et al. Effects of phenol 2,4-dimethylphenol, 2,4-dichloro-
phenol, and pentachlorophenol on embryo, larval, and early juvenile fathead
minnows (Pimephales promelas). Manuscript, 1980. (As cited in U.S. EPA 1980)
Kaufmann, Z.S. Effect of phenol on the embryonic and post-embryonic
periods of development of the grass frog. Biol. Vnutr. Vod. Inform
Bull. No. 33, Adak. Nauk SSSR, 61-63; 1977. (As cited in Buikema,
et al. 1979).
Kostyaev, V. Ya. The effect of phenol on the hydrochemical regime,
phytoplankton and plant overgrowth in artificial bodies of water. *Tr.
Ins. Biol. Vnutr. Vod. Acad. Nauk SSSR (Eng. transl.). 24:119-151; 1973.
137
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Kristoffersson, R.; Broberg, S.; Oikari, A. Physiological effects of
a sublethal concentration of phenol in the pike (Esox lucius L.) in
pure brackish water. Ann Zool. Fennici 10(2):392-397; 1973.
Luferova, L.A.; Flerov, B.A. Investigation of phenol poisoning of
Daphnia Biol. Vnutr. Vod., Infor. Buil. No. 10:42-46(Russ); 1971.
(As cited in Buikema et al. 1979)
Lukina, G.A. Action of phenol on the photosynthesis and respiration of
Chlorella. Vop. Vod. Toksikol (Topadrevski, A.V., ed.). 183-185.
"Nauka" Moscow, USSR; 1970. Abstract: Chem. Abs., 74 108291n; 1971.
(As cited in Buikema, et al. 1979)
Flerov, B.A.; Lukyanenko, V.I. Comparative investigation of the resis-
tence to phenol of two different age groups of Salmo iridens. Trudy
Inst. Biol. Vnutrennyh Vod, Akad. Nauk SSSR 10(13):295-299; 1966.
(As cited in Kristoffersson et al. 1973).
Miller, D.L.; Ogilvie, D.M. Temperature selection in brook trout
(Salvelinus fontinalis) following exposure to DDT, PCB, or phenol.
Bull. Environ. Contam. Toxicol. 14(5):545-551; 1975.
Mitrovic, V.V.; Brown, V.M.; Shurben, D.G.; Berryman, M.H. Some patho-
logical effects of subacute. and acute poisoning of rainbow trout by
phenol in hard water. Water Research 2:249-254; 1968.
Nunogawa, J.N. et al. The relative toxicities of selected chemicals to
several species of tropical fish. Adv. Water Poll. Res., Proc. Int.
Conf. 5th; 1970. (As cited in U.S. EPA 1979).
Ruesink, R.G.; Smith, L.L., Jr. The relationship of the 96-hour LC50
to the lethal threshold concentration of hexavalent chromium, phenol
and sodium pentachlorophenate for fathead minnows (Pimephales promelas
rafinesoue). Trans. Am. Fish. Soc. 104(3):567-570; 1975.
Smirnova, N.F. Influence of some factors on freshwater bivalve molluscs.
Tr. Inst. Biol. Vnutr. Vod. Akad. Nauk. SSSR, No. 24(27):90-97 (Russ.);
1973. (As cited in Buikema et al. 1979)
Symons, G.; Simpson, R. Report on fish destruction in the Niagara River
in 1937. Trans. Am. Fish Soc., 68:246-255; 1938. (As cited in UNFAO
1973).
United Nations Food and Agricultural Organization (UNFAO). Water
Quality criteria for European freshwater fish. Report on monohydric
phenol and inland fisheries. Water Res. 7:929-941; 1973.
U.S. Environmental Protection Agency(U.S. EPA). In depth studies on
health and environmental impacts of selected water pollutants. U.S. EPA
Contract No. 68—01-4646; 1978.
138
-------
U.S. Environmental Protection Agency (U.S. EPA). Ambient water quality
criteria - Phenol. Washington, B.C.: Office of Water Planning and
Standards; 1980. Available from EPA 440/5-80^-066.
Volodin, V.M..; Luk'yanenko, V.I.; Flerov, B.A. Comparative characteri-
zation of the resistance of fishes to phenol at early stages of ontogenesis.
1966. Tr. Inst. Biol. Vnutr. Vod., Adad. Nauk. SSSR, No. 24(27):67-71
(Russ). (As cited in Buikema etal. 1979)
139
-------
SECTION VII.
RISK CONSIDERATIONS
A. INTRODUCTION
The purpose of this section is to evaluate the risks of exposure of
humans and aquatic biota to phenol primarily in view of the levels at which
effects have been reported under laboratory conditions. Data are limited for
phenol in the areas of both effects and exposure; however, several field
studies were available on the impact of phenol on human and aquatic
populations exp'osed to environmental concentrations. The following
section addresses, first, risk considerations for man, and then, for
other biota.
B. HUMANS
1. Statement of Risk
Humans are rarely exposed to concentrations of phenol in environ-
mental media at levels high enough to cause adverse effects (as dis-
tinguished from laboratory studies on animals). However, one effects
study reported chromosomal damage to mice at concentrations far below
all other effects levels and at environmental exposure levels that a large
fraction of the human population may encounter. If correct, this study sug-
gests that further investigation of low-level effects of phenol on laboratory
animals is warranted. Other effects in laboratory animals are reported
at concentrations of 50 mg/kg/day and higher. Exposure levels for humans,
even under special phenol-intensive conditions, are generally less than
4 mg/kg/day with few exceptions; users of phenol-containing medicinal
products and people maximally exposed to almost all sources of phenol
simultaneously may be exposed to levels of up to 9 mg/kg/day. Typical
levels of phenol in food, drinking water, and air are far below those
related to adverse effects in laboratory animals (excluding the chromo-
somal study). Caution should be taken, however, in drawing any final
conclusions from comparison of phenol exposure levels for humans and
effects levels for laboratory animals due to species and dosage differ-
ences. As is true for most substances, the significance of toxicity
data obtained under experimental conditions relative to actual conditions
of exposure is not well understood.
2. Discussion
Phenol is readily absorbed from dermal, oral, and inhalation routes,
metabolized, and then rapidly excreted from the body. The half-life of
141
-------
phenol in man is approximately 3.5 hours. Phenol is also endogenously
produced in humans and, in conjugated form, is a normal constituent
of urine.
NCI recently reported that phenol was not carcinogenic in either
rats or mice when administered in drinking water at concentrations of up to
0.5% by volume (NCI 1980). However, further testing has been recommended
(see Section V). Phenol has exhibited some tumor-promoting activity
in skin-painting studies, but the nature of these studies makes them in-
appropriate for the assessment of human risk by ingestion. These and
other data on effects are summarized in Table 41.
Renal damage has been reported in rats at a 50-mg/kg dose of phenol
daily for 4 months. This effect is unlikely to occur in man in that
ingestion exposures are generally distributed throughout the course of
the day and thus allow metabolic processes to rapidly clear phenol from
the body.
Chromosomal aberrations have been observed in mice at very low
doses (6.4 ug/kg/day). These results represent the work of one inves-
tigator (see discussion in Section V) and have not been confirmed.
If these results are valid, and at present there is no reason to dis-
count then on scientific grounds, then, they are cause for concern.
Even given the uncertainties involved in the exposure estimates, and
the fact that the entire dose was administered at once as opposed to
over a 24-hour period, the phenol content of certain foods and phenol-
containing products is sufficiently high to constitute human risk.
Additionally, the study is relevant to humans for several reasons;
similarities in mammalian metabolic processes in regard to phenol, the
fact that the treatment method (exposure of pregnant mothers and their
offspring) represents a reasonable exposure route, and the general
preference of in vivo studies to in vitro studies. The quantification
of such a risk of human genetic impairment from animal data is, at
present, not feasible, and will remain so until a correlation can be
demonstrated between test animals of a rather uniform genetic background
and humans with wide individual variations. In addition, substantiation
of the results of this study is warranted.
Table 42 summarizes exposures described more fully in Section V.
It should be pointed out that these estimates are based on numerous
assumptions and that there is considerable uncertainty involved. In
addition, the size of the subpopulation involved is difficult to quantify.
Nevertheless, it is evident that the use of phenol-containing products
represents the largest single source of exposure other than occupational
exposure.
Figure 17 roughly compares the doses of phenol reported for effects
resulting from various exposures to the frequency of observation. The dia-
gram expresses qualitatively the likelihood of equivalent exposure and
effects levels. It is apparent that single exposures are not high
enough to cause the lowest observed effect. Although the margin
142
-------
Usual
Frequent
_o
*^
CO
£
"o Occasional
u
c
0)
3
£
ul
Rare
0.001
t
Average
Intake
Human
Ingestion
0.01 0.1 1 10
Medicinal Lowest
Lozenges Reported
Lethal Dose
Special
Foods
Dose (gram)
Source: Arthur D. Little, Inc.
FIGURE 17 EXPOSURE AND ACUTE EFFECTS OF PHENOL FOR HUMANS
143
-------
TABLE 41. ADVERSE EFFECTS OF PHENOL ON MAMMALS
Adverse Effect
Carcinogenicity
promotion
DMBA-induced
tumors
skin painting
(alone)
oral route
Chromosomal
damage
Renal damage
Lung damage
(inhalation)
Species
Mouse
Mouse
Mouse
Rat
Mouse
Teratogenicity Rat
Oral LD
50
Rat
Rat
Man
Lowest Reported
Effect Level
2.5 mg/mouse 2 x week
5 mg/mouse 2 x week
(0.025 ml 20% soln.)
6.4 ug/kg/day
(gavage)
50 mg/kg/day for
135 days (gavage)
No Apparent
Effect Level
5 mg/mouse 2 x week
(0.1 ml 5% soln)
0.5% drinking water
for 2 years
200 mg/kg (intra-
peritoneally) days
9-11 or 12-14
50 mg/kg/day for
20 days (gavage)
100-200 mg/m3 7 hrs/
day, 5 days/week, for
53 days
1 gram
No t known.
Source: Section V.
144
-------
TABLE 42. HUMAN EXPOSURE TO PHENOL
Ul
Exposure Route
Ingestion
Drinking Water
Food - fish and
smoked meats
fish
smoked meats
Phenol-containing
mouthwash
Phenol-containing
throat lozenges
Inhalation
Contaminated air
near highways
Dermal
Exposure
(mg/kg/day)
0
0.0002
0.015
0.1667
0.10
1.45
4.33
0.10
Subpopulat ion
large
very small
unknown, may be
large
very small
very small
may be large,
maximum
assumptions
may be large
unknown
Comment
Limited to persons drinking untreated
water from polluted rivers.
Assumes 16 rag/kg in fish and 29 mg/kg
in smoked products; consumption of 20
rag/day of each.
Assumes maximum consumption of fish of
200 mg/day; maximum of 50 mg/kg in fish.
Assumes maximum consumption of smoked
products of 200 mg/day; maximum of
29 mg/kg in smoked foods.
Assumes use of 60 ml/day mouthwash
(1.4% phenol), 10% retention, not
chronic use.
Assumes recommended dosage - 8/day 32.5 ing
total phenol/lozenge, not chronic use.
Maximum concentration of phenol in air
in Germany near highways. 0.3 mg/m3;
inhalation of 20 m^/day.
Face creams
unknown; unknown, may be
probably much less large
than 0.21 mg/kg
Use of 5 grams of face cream per day
containing 0.5% phenol.
Source: Section VI-B.
-------
separating exposure and effects levels is a narrow one, the significance
of this apparent problem is modified by two factors. First, both the
subpopulation size and exposure duration related to the largest exposure,
use of medicinal lozenges, are small. Second, due to the difficulty in
interpreting the study reporting the lowest effects concentration,as
discussed previously, the implications of its results in terms of human
risk are uncertain.
Exposure levels were estimated for several special-case subpopula-
tions as well as for the general population (see Section V-A). All
estimates assumed some exposure to contaminated water, ingestion of some
contaminated food (no total diet study was available), and inhalation of
upper-limit highway levels of phenol. This baseline exposure level
resulted in an exposure level of 0.10 mg/kg daily for the largest fraction
of the population. Any population members using skin creams containing
phenol on a daily basis would increase their exposure approximately by a
factor of 2 to a level of 0.22 mg/kg. Special subpopulations with higher
daily exposure levels were laboratory workers (1.4 mg/kg), people con-
suming phenol medicinal products (5.9 mjz/ka), people exposed via ingestion of
contaminated groundwater (4.1 mg/kg), and a worst-case highly improbable sub-
population exposed to all major pathways for phenol (8.7 mg/kg).
As regards Figure 17, the scenario levels would cause the human
ingestion curve to overlap the effects curve, although still within the
region of the chromosomal damage study. The exposure levels as esti-
mated are approximately 5-10 times less than the other adverse effects
levels reported in Table 41.
The risks due to inhalation exposure are probably limited to a very
small and perhaps nonexistent subpopulation. In addition, these risks
are probably small since effects are observed in animals only at high
concentrations relevant to ambient concentrations.
The use of phenol-containing products resulting in dermal absorption
probably dqes_not represent a risk to the consumer, except perhaps in
the use of face peels, which is a medical procedure. However, phenol's
role as a promoter of carcinogens suggests that the possibility of risk
exists. There are numerous conditions which must be met in order for the
initiation-promotion process to enhance tumor production, and the chances
of these conditions being met are remote.
The one epidemiological study available concerned a phenol spill
into groundwater. The incident is described in greater detail in Section
IV (Pathway #5) and in Section V-B. Sublethal effects, such as diarrhea,
mouth sores, and burning of the mouth, were associated with exposure
levels of 0.11 to 40 mg/kg/day in drinking water (Baker et al. 1978).
The exposure period was several weeks in total for most individuals.
No residual abnormality was noted in exposed individuals after removal "
from contaminated drinking water.
The estimated exposure levels in the above scenarios fall within the
range of exposure levels reported in the preceding field study. Therefore,
it is assumed that sublethal effects similar to those described for this incident
146
-------
would result from all the scenario exposure levels calculated in Table 43.
Presumably, additional effects, such as death or chronic effects,
would not be caused by these levels. The only exception might be
chromosomal damage such as that reported in the Bulsiewicz study
(Bulsiewicz 1977). The effects associated with the epidemiology study
at the reported exposure levels are consistent with the figure. Since
they are sublethal effects rather than lethal (as those in the figure),
they fall within the lower part of the curve, if at all.
•
C. AQUATIC BIOTA
1. Statement of Risk
Based on a limited set of monitoring data, it appears unlikely that
phenol commonly reaches concentrations in surface water which adversely
affect aquatic populations. At least an order of magnitude differ-
ence separated typical ambient surface water levels from the lowest
(primarily sublethal) effects levels and there was at least a two-orders-
of-magnitude difference from the lower lethal effects levels for fish.
Numerous spills or accidental discharges have been documented involving
phenol or phenol-containing waste. However, rapid microbial utilization
of the compound appears to reduce its concentration to harmless levels
in approximately one week (under acclimated environmental conditions).
Therefore, the greatest risk for aquatic organisms is exposure in the
vicinity of spills within a^few days to a week following the incident and
in any area where an active microbial population is not present.
2. Discussion
The lack of adequate monitoring data for phenol levels in surface
waters precludes a detailed assessment of the national risk to
aquatic populations in regard to phenol. A significant fraction of
total environmental releases (30% including POTWs) are to water and,
although phenol is generally rapidly degraded, there are many opportuni-
ties for short-term harm due to the widespread environmental distribution
of phenol. This section discusses the potential risks of aquatic species
by comparison of effects levels to monitoring data, discussion of known
environmental exposure incidents and their resulting effects, and iden-
tification of industrial sources potentially contributing to situations
where harm to aquatic life appears likely.
Table 44 summarizes the phenol concentration ranges described in
Sections IV and VI-B to which aquatic species are likely to be exposed
in the environment. Table 45 presents effects concentration ranges
derived from laboratory data in Section VI-A.
147
-------
TABLE 43. EXPOSURE LEVELS OF PHENOL FOR
VARIOUS SUBPOPULATIONS1
Exposure
Source
Subpopulation
Size
Estimated Exposure
Level2
(ing/kg/day)
Scenario #1
(worst case)
Extremely small,
very unlikely
8.7
Scenario #2
(people exposed
to groundwater
spill)
Very small,
situation
acute
4.1
Scenario #3
(users of phenol
medicinal products)
Very small, acute
situation
5.9
Scenario #4 Very small
(laboratory workers)
Scenario #5
(general
population)
Large
1.4
0.10
0.20 with face cream
All incidents described in greater detail in Section V-A. Note that
different exposure-route concentrations were combined (e.g., inhalation
and ingestion) which may contribute some error to the total level.
^
Calculated for 60-kg human.
148
-------
TABLE 44. SUMMARY OF REPORTED ENVIRONMENTAL
CONCENTRATIONS OF PHENOL
Medium
Concentration
Source
Ambient Surface
Waters
National average
(STORET --unremarked
data)
• mean
• median
• 85 percentile
• maximum
ND - 6.8 mg/1
typically <0.01 mg/1
0.3 mg/1
0.001 mg/1
0.3 mg/1
6.8 mg/1
Tables 22 and 40
Tables 22 and 40
Effluents
Total range
ND - .3,016 mg/1
Table 23
Petroleum refinery1 0.88 -3,016 mg/1
Spills
River
Initially 28 mg/12
reduced to ^1 mg/13
after 1 week
Table 17
ND = not detected.
1Final effluents.
2 Of primarily monohydric phenols
3Typical background concentration for area
149
-------
TABLE 45. SUMMARY OF EFFECTS LEVELS OF PHENOL
ON AQUATIC ORGANISMS
Phenol Concentration
(mg/1) Effect
0>1 ~ 1-° Subacute effects on certain freshwater
invertebrates
1.0 - 10.0 Acute effects on sensitive freshwater
invertebrates and both fresh and saltwater
fish; subacute effects on other fish species,
10.0 - 50.0 Acute effects on all tested freshwater fish
species and saltwater invertebrate1; acute
effects on many freshwater invertebrates.
50.0 - 500 Acute effects on almost all freshwater in-
vertebrates.
on limited marine data
Source: Adapted from Section VI-A.
150
-------
Comparison of the data from the two tables makes it evident that
ambient concentrations are almost entirely below the lowest effects
level of 0.1 mg/1. Some of the effluent levels exceeded the concentra-
tions likely to affect most aquatic species; however, dilution and
degradation would make the likelihood of populations encountering such
high levels very small. Judging by the magnitude of the STORET observa-
tions, which may represent levels measured close to a source, the rare-
ness of high effluent levels contributing to high surface water concen-
trations is apparent.
Table 46 provides information on the location of and activities
associated with United States fish kills attributed either wholly or
partly to phenol between 1971 and 1977. Unfortunately, no data on
phenol concentrations were available in the fish kill reports; moreover,
the presence of other toxic chemicals cannot be ruled out, particularly
when they are not monitored. It is very likely-that, in some cases,
synergy between phenol and other toxicants or oxygen depletion increased
the magnitude of the fish kill beyond the effect of phenol alone. Since
phenol is widely used for synthesizing a variety of aromatic compounds,
the chemical industries themselves and the transport of their products
may continue to be the major sources of serious spills and discharges
of phenol. The fish kills occurred primarily in the northeastern states
in industrial areas, with a few incidents in southern and midwestern
areas.
Most of the more comprehensive field studies of fish kills associ-
ated with measured concentrations of phenol are from Europe and concern
phenols as a group. The proportion of the toxic effects attributable
directly to phenol depends oh the particular waste characteristics.
However, since phenol is rarely present by itself in any waste, for an
approximation of its environmental impact it is useful to examine the
data available on the combined effects of phenols. It should be pointed
out, though, that associated substances, such as chlorophenols, may be
considerably more toxic than phenol so a combined phenol effects level
can be much lower than a phenol effects level.
Table 47 presents brief descriptions of aquatic exposure incidents
caused by phenols. No information was available on the sources of the
wastes; however, accompanying water concentrations were measured and
provide a useful set of data for comparison with U.S. surface water
monitoring data.
Comparison of Table 45 and 47 provides an opportunity to confirm
laboratory-derived concentrations. In the laboratory studies no effects
were observed at lower than 0.1 mg/1 and only subacute effects or lethal
effects on sensitive species were observed between 0.1 and 10 mg/1. In
the field studies, fish kills were usually reported starting at 3 mg/1
(assuming that phenol comprised all the toxic waste present).
151
-------
TABLE 46. DATA ON PHENOL-RELATED FISH KILLS IN U.S. (197L-1977)
l)u t e
Water Body
Location
Number
Killed
Source
Oi
to
5-25-71 Roaring Brook
6-8-71 Casey Fork Cr.
8-6-71 Tunungwant Cr.
8-6-71 Tunugwant Cr.
8-6-71 Allegheny R.
1971 Ohio R.
1971 Milwaukee R.
1972 Severn Run (Branch)
1973 Kingsland Cr.
5-18-74 Hardisty Pond
5-22-74 Banmers Pond
6-18-74 Red Clay Cr.
6-19-74 New Haven Harbor
7-29-74 Black Warrior R.
6-17-76 Black Rock Harbor
6-22-76 Bridgeport Harbor
11-17-76 Treat Miami R.
1976 Bear Cr.
5-10-77 Hebble Cr.
6-1-77 Sanders Branch
8-2-77 Beaverdam Cr.
Glastonbury, CT
Mt. Vernon, IL 6,000
Bradford, PA 53,000
NY, near Bradford, PA 45,000
Irvine Mills, NY 62,000
New Martinsville, WV 5,000
Gratton, WI 1,500
Odenton, MD 100
Lyndhurst, NY 5,000
Southbury, CT 550
Naugatuck, CT 010
Newcastle, DE 2,000
New Haven, CT 20,000
Tuscaloo.sa, AL 10.700
Bridgeport, CT 25,000
Bridgeport, CT 20,000
Ohio 0.848
Fairview, PA 28,000
Greene Co., OH 1,000
Hampton, SC Total
Damascus, VA 150
High phenol, Zn, Cu in fish tissues
No toxics measured Jn water
Wood preservation
Discharge for chemical industry
in area
From Bradford, PA
From Bradford, PA
Phenols from nearby chemical industry
Phenols, oil from storm sewer (?)
Phenols from plastics industry
Phenolic discharge from chemical industry
Mixed solvents, heavy oil,and phenol
Asphalt and phenol
Haveg Industry phenol spill
High phenol, Al, pH, BOD, and collform
17,000-21,500 Ib phenol spill by
Reichhold Chemical
Chemical, textile, metal industries, and
POTW nearby; high phenol, Cu,and Zn
in fish tissues
Discharges from POTW, power plant
Metal and cyanide production
Phenols, cyanides from agric. opt'rat ions
"Government operations"
Railway phenol spill
Discharge by American Cyanamid
Source: MDSD Fish Kill Survey.
-------
TABLE 47. EXPOSURE INCIDENTS INVOLVING PHENOLICS
Concentration of
Phenols
(mg/1)
Effect
Reference
0.02 - 0.3
At 0.02 mg/1 in a river an
abundant and diversified fish
fauna was present. At 0.3
mg/1 no fish were found.
Kalabina 1935
1-10
In a small Luxembourg stream
at 1 mg/1 fish populations
including salmonids were
present. When discharge in-
creased concentrations to 10
mg/1, all fauna within a 9-km
stretch were killed. Dissolved
oxygen levels were 0-10% of air
saturation level. Downstream
at 3-10 mg/1 (D.0.10-50%) only
salmonids were killed. Further
downstream at 3 mg/1, no fish
were killed.
Krombach and
Barthel 1964
0 - 130
3-5
At lower concentrations (up to
3.2 mg/11) in Yugoslavian river,
fish were present. At higher
levels (>3.2 mg/1) all fish were
absent.
Fish kills ascribed to concen-
trations exceeding these levels
UNFAO 1973
Ludemann 1954
Actually presented as 4.4 mg/1 but the lower concentration was assumed
as a conservative estimate.
153
-------
However, one study (Kalabina 1935) reported no fish present at phenol
concentrations of 0.3 mg/1. There was no information available on
oxygen levels or other toxins present which may have influenced the
order of magnitude difference from the other concentrations reported.
Laboratory data (Table 45) suggest, however, that the 3-mg/l lethal
threshhold (on a population scale) is more likely due to the fact that
most species are killed by phenol concentrations of between 1 and 50
mg/1. Therefore these two sets of data, laboratory and field, are com-
patible despite all the potentially interfering factors.
A significant indirect effect of phenol discharge to aquatic systems
is oxygen depletion. As discussed in Section IV, phenol is readily
degradable by microorganisms which can assimilate the chemical as a
sole carbon source. In addition phenol is likely to be discharged in
association with other degradable organics (e.g., sulfites). The
presence of phenol supports the rapid growth of microbial populations
which require oxygen for oxidation processes and auxiliary activities.
This can result in extreme oxygen depletion on a local scale (up to 100%)
which may in turn result in the death through suffocation of invertebrates
and fish. Therefore, the toxic effects of a phenol discharge may be com-
pletely or partially attributable to anaerobic conditions. Table 48
presents phenol concentrations, accompanying degrees of oxygen depletion,
and the effects on an aquatic population from a field study of a phenol
spill (Krombach and Barthel 1964) described in greater detail in Section
IV. The greatest 02 deficiency was associated with the highest phenol
levels and was clearly responsible for some of the toxicity, especially
at a ^100% deficiency.
154
-------
TABLE 48. EFFECTS OF A PHENOL SPILL ON
A RIVER SYSTEM
Distance Phenol Oxygen
From Spill Concentration Deficiency Effect
(km) (mg/1) (%)
0-9 >10 90-100 All aquatic flora and
fauna present destroyed.
Microbial activity on
phenols and sulfites
also present in waste.
9-19 3-10 50-90 Only salmonid population
killed; slight effect on
aquatic flora.
19 - 37 <3 <50 No damage.
Source: Krombach and Barthel 1964.
155
-------
REFERENCES
Baker, E.L.; Landrigan, P.J.; Bertozzi, P.E.; Field, P.H.; Basteyns, B.J.;
Skinner, E.G. Phenol poisoning due to contaminated drinking water.
Arch. Environ. Health. 33:89-94: 1978.
* «
Bulsiewicz, H. The influence of phenol on chromosomes of the Mus
musculus in the process of spermatogenesis. Folia Morphol. (Warsz)
36(1):13-22; 1977.
Kalabina, M.M. Der Phenolzer fall in Fliess - und Staugewassern 2
Fisch. 33:295-317; 1935.
Krombach, H.; Barthel, J. Investigation of a small water-course acci-
dentally polluted by phenol compounds. Adv. Wat. Pollut. Res. 1
191-203; 1964.
Ludemann, D. Die Verunreinigung der Berliner GewSsser und ihre Auswirkung.
Gesundhectsingenieur 75(15/16):260-262; 1954.
National Cancer Institute (NCI). Bioassay of phenol for possible car-
cinogenicity. Draft report. DHHS Publication No. (NIH) 80-1759.
National Institutes of Health, U.S. Department of Health and Human
Services; 1980.
United Nations Food and Agriculture Organization (UNFAO). Water quality
criteria for European freshwater fish. Report on monohydric phenol and
inland fisheries. Water Res. 7:929-941; 1973.
156
-------
APPENDIX A. BACKGROUND NOTES ON THE DERIVATION OF TABLE 2
1. U.S. International Trade Commission 1978.
2. U.S. International Trade Commission 1978 states that 93,500 kkg of
phenol are produced by synthetic processes other than cumene. The
other methods are listed as phenol by toluene oxidation (Kalama
Chemicals, Inc.) and caustic fusion (benzene sulfonation) (Reichhold
Chemicals, Tenneco Oil Co., and Sherwin Williams).
3. D. Beck, U.S. International Trade Commission, personal communica-
tion, January 1980.
4. U.S. Department of Commerce 1978a. Associated handling, storage, and
transport losses are reported under the heading Producer, Storage,
Loading, and Transport.
5. These data were based on the production figures reported in U.S.
International Trade Commission 1978 and on the phenol end-use pattern
reported by percent in Chemical and Engineering News 1978.
6. According to data supplied to U.S. EPA by Monsanto (Eimutls et al. 1978)
there are a number of chemical use categories that are sources of
phenolic emissions:
Source Emission
Residential Wood Combustion* 7,223.5
Acetone and Phenol from Cumene* 233.8
Bisphenol A* 73.9
NonyIphenol* 53.7
Pentachlorophenol and Sodium Salts* 23.6
p-Nitrophenol 22.5
Trichlorophenols* 11.3
Salicyclic Acid* . 9.3
Chlorophenol* 6.4
Polyvinyl Chloride 4.5
Polycarbonate Resins 3.9
Cresyldiphenyl phosphate 3.3
Silvex 1.4
OctyIphenol 0.8
Salicyclates (excluding aspirin) p.6
TOTAL 7,673.0
Appendix based primarily on Versar 1980,
157
-------
The source categories that are marked by an asterisk(*) are listed
in Table 2 in the Airborne Emissions category and are marked in the
table by a note #8. The sum of the emissions from the source cate-
gories not marked by an asterisk is 37 kkg, or about 0.5% of the total
emissions. Since the emissions from these categories are small, and
since no data were accessible on the amounts of or ways that phenol
is used in these categories, they have been combined under the
single heading of "Other Use Category" and the "NA" listed in the
"Consumption" column refers to a small unknown amount of phenol consumed.
7. U.S. Department of Commerce 1978b.
8. These data are taken from EPA information compiled by Monsanto (Eimutls
et al. 1978). Note #6 summarizes the emissions data. Numbers are
rounded to the nearest integer. The Use Category of "Other Chlorophenols"
is actually the sum of "chlorophenols" and "trichlorophenols" as shown
in note #6; i.e., trichlorophenols (11.3 kkg) and chlorophenols (6.4 kkg)
add up to 17.7 kkg, or 18 kkg. Residential wood burning is a signifi-
cant source, accounting for nearly 95% of all phenol emissions listed
in the Monsanto report.
9. Approximately 1,108,850 kkg of phenol were produced by cumene perodixda-
tion (U.S. International Trade Commission 1978). Phenol airborne
emissions from the column vents were estimated to be 1.474 kg/kkg of
phenol produced (Hedley 1975).
Phenol Air Emissions = (1.476 kg/kkg of phenol) (1,108,850 kkg)
^ 1,630 kkg
10. These calculations were based on the supposition that 0.161 kg of
phenol were lost per 1 kkg stored. Emissions factors were taken
from Delaney and Hughes 1979.
Consumption x 0.161 + 1000 = kkg of phenol emission
•The sum of emissions factors:
from product storage and loading (0.51) + transport (0.11) = 0.161 kg/kkg
Fugitive emissions from pressure relief valves, pump seals, equipment
purges, process drains, are not included in this estimate. No process
dependent discharges have been included in the estimate.
Thus, emissions due to the producer handling, loading, and transport
are the product of the above emission factor (0.161 kg/kkg) and the
total phenol production (1,216,100), or 196 kkg. (N.B. Emissions
factors are averages of only two data points.)
11. The 196 kkg of emission listed in note 7/10 as deriving from "Producer
Storage, Loading, and Transport" has been doubled as an estimate of
the emissions resulting from "User Storage, Loading, and Transport".
158
-------
The rationale behind this is that it is likely that since there are
tar more users than producers of phenol, emissions from user handling
procedures probably greatly exceed the handling emissions from pro-
ducers. Therefore the amount of 392 kkg emitted by user handling
practices is probably conservative, if the 196 kkg emission attributed
to producer handling is accurate.
12. Iron and steel production involves the use of a large amount of coal
and coke, so that even though there are no data on the airborne emissions
of phenol from iron and steel production (and the corresponding coal
use), it is possible that the amount of phenol generated during Iron
and steel production is large.
13. No data are available on the phenol airborne emissions from coal-fired
home furnaces, of which there are a large number used in the coal-
producing parts of this country, but since this is a large source of
polycyclic aromatic hydrocarbons (NAS 1972), it seems probable that
phenol is also emitted, but no data could be found from which estimates
of the amount of phenol produced could be made.
14. Approximately 1,108.850 kke of ohenol were produced by cumene peroxida-
tion (U.S. International Trade Commission 1978). Phenol aquatic dis-
charges were estimated to be 0.0755 kg/kkg of phenol produced based on
raw waste levels (Hedley 1975). In a sample of 9 phenol producing
plants, 4 discharge direct to surface water (3 following biological
treatment), 2 to POTW's, 2 to lagoons or deep wells and 1 unknown
(U.S. EPA 1980). Assuming each plant has an equal discharge (9.2 kkg
phenol/plant annually), that the unknown plant discharges in treated
waste to surface water and a 95% efficiency during biological treat-
ment, then aquatic discharges can be estimated as follows.
Phenol Discharge to Surface Water - (9.2 kkg/plant) (3 plants using
biological treatment (0.05 efficiency) + (9.2 kkg/plant) (2 plants
no treatment) = 20 kkg annually.
Phenol Discharge to POTW's = (9.2 kkg/Olant) (2 plants) - 18 kkg
annually.
15. Approximately 87,360 kkg of phenolic resins were produced in 1978 (U S
International Trade Commission 1978; Versar 1980). The manufacture
of phenolic resins produces significant water wastes from the follow-
ing process steps: 1) water introduced with the raw material; 2) water
formed as a product of the condensation reaction; 3) caustic solutions
used for cleaning the reaction kettles; and 4) blow down from cooling
waters (Hedley 1975). The total wastewater quantity was estimated to
contain 30 kg of phenol and phenolic per ton of phenolic resin produced
(Hedley 1975) and calculated as 2,620 kkg annually.
159
-------
In a sample of 29 plants which produce phenolic resins, 17% pretreated
and discharged their waste to POTW's, 10% pretreated and discharged
to surface water, 21% discharged untreated waste to POTW's, 17%
practiced 0 discharge and 35% discharged to lagoons and deep wells.
Assuming a biological treatment efficiency of 95% and equal dis-
charge for all plants, then the annual aquatic discharge can be
estimated.
Phenolics discharge to Surface Water = (10%) (2,620 kkg) (0.05
efficiency) » 13 kkg annually.
Phenolics discharge to POTW's = (17%) (2,620 kkg) (0.05 efficiency)
+ (21%) (2,620 kkg) (0 efficiency) = 572 kkg annually.
The remaining 52% of plants are assumed to discharge 1,362 kkg of
phenolic waste to lagoons, deep wells or recycle the material within
the plant.
16. Approximately 105,380 kkg of bisphenol A were produced in 1978 (U.S.
International Trade Commission 1978) . The phenol aquatic discharge
for this product process was estimated to be 7.1 kg/kkg of bisphenol
A produced (Hedley 1975). The total amount discharged annually is
748 kkg. Based on the sample of phenol producers described in #14
and assuming the same discharge distribution and treatment practices
for bisphenol A producers, then 33% of all plants discharge biologically
treated waste to surface water 22% discharge untreated waste to surface
water, 33% discharge untreated waste to POTW's and the remaining 22%
discharge to .deep wells or lagoons (U.S. EPA 1980). Assuming a 95%
treatment efficiency, then aquatic discharges can be estimated.
Phenol Discharge to Surface Water = (33%) (748 kkg) (0.05 efficiency)
+ (22%) (748 kkg) = 187 kkg annually.
Phenol Discharge to POTW's = (33%) (748 kkg) =247 kkg annually.
17. The average phenol concentration in effluents from 23 plants in the
petroleum refining industry was 670 ug/1 (U.S. EPA 1980. ). The average
flow was 3,325,000 gal/day (U.S. EPA 1980 ). There are 284 refineries -
182 discharge to surface waters, 48 discharge to POTW's, and 54 have
a zero discharge (U.S. EPA 1979a).
Phenol Discharge to Water = (670 ug/1) (3,325,000 gal/day) (3.785
1/gal) (250 days/yr) (10-12 kkg/ug) (182 plants) = 384 kkg
Phenol Discharge to POTW's = (670 ug/1) (3,325,000 gal/day) (3.785
1/gal) (250 day/yr) (10-12 kkg/ug) (43 plants) = 101 kkg
160
-------
18. While no data are available on the aquatic emissions resulting from
"User Storagei Loading, and Transport," it is known that 20-gallon
steel drums that have contained phenol are recycled into commerce, and
that each drum contains approximately a half a pound of phenol. The
number of such drums that are recycled annually is unknown, and the
fate of the phenol is also unknown, but it seems likely that a portion
of the phenol is rinsed out with water which either runs off directly
to aquatic sinks or is flushed into POTW's. The practice that is
supposed to be followed by drum recyclers is neutralization of the
phenol with lye and then collection and landfill disposal of the re-
sultant solution of sodium phenolate, but there is evidence that this
practice is not universally followed (J. Warring, James T. Warring
and Sons Barrel Company, personal communication, November 1979).
19. Phenol was detected in the effluent of the timber products processing
industry during the verification sampling and analysis program (U.S.
EPA 1980 ). Phenol is discharged in significant amounts from three
subcategories - wood steaming, hardboard S2S, and insulation-
thennochemical pulping and refining:
//of Plants # of Plants Avg. Flow Cone. Discharge
Subcategory Direct POTW's (gal/day) (ug/1) (kkg)
Wood Steaming — 13 9,600 15,900 2
S2S 3 — 4,548,170 100 1
Insulation— 4 — 13,803,190 17 1
Thermochemical
Pulping & Refining
TOTAL 4
20. Phenol was detected in the effluents of the leather tanning industry
during the verification sampling and analysis program (U.S. EPA 1980 ).
Phenol is discharged in significant amounts from three subcategories:
Direct Dischargers (U.S. EPA 1980 ; U.S. EPA 1978)
# of Avg. Flow Avg. Cone. Discharge
Subcategory Dischargers (gal/day) (ug/1) (kkg)
Hair Pulp,
Chrome
Tan Retan-Wet
Finish 3 600,000 1,500 3
Hair Save,
Chrome
Tan Retan 3 300,000 920 1
No Beamhouse 3 120.000 6,200 2
TOTAL 6
(Data are an average of one to four plants per Subcategory)
161
-------
Dischargers to POTW's (U.S. EPA 1980 ; U.S. EPA 1978)
# of
Dischargers
Avg. Flow
(gal/day)
Avg. Cone.
(ug/1)
Discharge
(kkg)
71
475,000
1,500
48
Subcategory
Hair Pulp,
Chrome
Tan Retan Wet-
Finish
Hair Save,
Chrome
Tan Retan
No Beamhouse
• ~ y *s^v w , £.\J\J
TOTAL 64
(Data are an average of one to four plants per subcategory)
21. Phenol was detected in significant quantities in two subcategories
of the textiles industry — woven fabric finishing simple, and woven
fabric finishing (U.S. EPA 1980 ).
21
24
300,000
75,000
920
6,200
5
11
Avg.
Cone.
(ug/1)
15
i
9
Total
Flow
Dis-
charges*
(MGD)
15.5
58.3
Phenol
Discharge
to Water
(kkg)
0.2
0.5
Total .
Flow for
Indirect
Discharges
(MGD)
36.5
40
Phenol
Discharge
to POTW's
(kkg)
0.5
0.3
Subcategory
Woven Fabric
Finishing Simple
Woven Fabric
Finishing
Total Discharge to Water - 0.2 kkg + 0.5 kkg - 0.7 kkg « 1 kkg
Total Discharge to POTW's = 0.5 kkg to 0.3 kkg = 0.8 kkg « 1 kkg
*U.S. EPA 1979b.
22. Data were available for 9 of the 15 subcategories in the iron and
steel industry. Phenol was detected in significant quantities from
two subcategories - byproduct coking and cold rolling.
For the byproduct coking subcategory there are 32 direct dischargers
21 indirect dischargers, and 17 zero dischargers (U.S. EPA 1979c). '
The total water usage for the subcategory was 71.1 MGD (U.S. EPA 1979d)
The average phenol concentration from 3 plants was 0.026 mg/1.
162
-------
Phenol Aquatic Discharge g
Byproduct coking = (0.026 mg/1) (71.1 x 10 gal/day)
(3.785 1/gal) (250 days/yr) (10-9 kkg/mg)
- 1.8 kkg
Direct Discharge - (1.8 kkg) —32 plants
32 + 21 plants
= 1 kkg
Discharge to POTW = 1.8 kkg - 1 kkg - 0.8 W 1 kkg
For the cold rolling subcategory, the total flow for the subcategory
is 252.5 MGD. There are 230 direct dischargers, 24 indirect dis-
chargers, and 15 zero discharges (U.S. EPA 1979 d). The average
concentration from three plants is 0.008 mg/1 (U.S. EPA 1979e).
Phenol Aquatic Discharge From Cold Rolling
- (0.008 mg/1) (252. 5 x 10~6 gal/day) (3.785 1/gal) (250 days/yr)
(10-9 kkg/mg)
= 1.9 kkg
3 = 1>7 "* % 2 kkg
Direct Discharge > (1.9 kkg) 23Q+ plants
Discharge to POTW =1.9 kkg - 1.7 kkg = 0.2 kkg a negligible
Thus the total direct discharge for the iron and steel industry =
3.0 kkg while the discharge to POTW' s =1.0 kkg.
23. The average phenol concentration in effluents from 13 plants in the
ash handling subcategory of the steam electric industry was 4 ug/1
(U.S. EPA 198c) . There are 777 plants that discharge ash handling
water to surface waters and the average flow is 2.24 x 10^ gal/day
(U.S. EPA 1980c) .
Phenol Discharge to Water = (4 ug/1) (2. 24 x 10 gal/day) (777 plants)
(365 day/yr)(3.785 1/gal) (10-12 kkg/ug)
= 10 kkg
24. A survey of discharge monitoring reports from 10 sewage treatment
plants indicated that phenol was present in the effluents at a
concentration of 0.128 mg/1 (Versar 1978). The total daily flow
from all POTW's within the United States is estimated
to approximate 22,670 MGD.
Phenol Discharged to Water = (0.128 mg/1) (22, 670 x 10 gal/day)
(365 days/yr) (3. 785 1/gal)
(10-9 kkg/mg = 4,000 kkg/yr
163
-------
25. In these production and use categories there is only one plant. All the
effluent waters are directly discharged after treatment by a waste-
water treatment train. None of the waters are discharged to POTW's
(Maria Irizarry, U.S. Environmental Protection Agency, personal
communication, January 1980).
26. Approximately 1,108,850 kkg of phenol were produced by cumene peroxi-
dation (U.S. International Trade Commission 1978). Phenol solid wastes
from the evaporator residue were estimated to be 0.75 kg/kkg of phenol
produced (Hedley 1975).
Phenol Solid Wastes Discharge = (0.75 kg/kkg of phenol)(1,108,850 kkg)
=832 kkg
27. Approximately 93,500 kkg of phenol are produced by benzene sulfonation
and toluene oxidation (U.S. International Trade Commission 1978).
According to the SRI Directory of Chemical Producers, the maximum
capacity for benzene sulfonation is 70,293 kkg (SRI 1978). Phenol
solid wastes from this production method were estimated to be of
phenol produced (Hedley 1975).
Phenol Solid Waste Discharge = (3.7 kg/kkg of phenol)(107,250 kkg)
= 397
164
-------
REFERENCES
Chemical and Engineering News. Phenol makers face continuing over-
capacity. September 25, 1978:13.
Delaney, J.L.; Hughes, T.W. (Monsanto Research Corporation). Source
assessment: Manufacture of acetone and phenol from cumene. U.S.
Environmental Protection Agency. Report No. EPA 600/2-79-019d; 1979.
Eimutls, E.G.; Quill, R.P.; Rinaldi, G.M. (Monsanto Research Corporation).
Source assessment: Non-criteria pollutant emissions (update). U.S.
Environmental Protection Agency. NTIS PB 291 747; 1978.
Hedley, W.H.; et al. (Monsanto Research Corporation). Potential
pollutants from petrochemicals processes. 111-123; 1975.
National Academy of Science (NAS). Particulate polycyclic organic matter.
Washington, D.C. 1972.
Stanford Research Institute, 1978 Directory of chemical producers:
United States of America. 811; 1978.
U.S. Department of Commerce. U.S. imports for consumption and general
import. Commodity by country of origin. Bureau of Census. 222; 1978a.
U.S. Department of Commerce. U.S. exports schedule B. Commodity by
country. Bureau of Census; 1978b.
U.S. Environmental Protection Agency (U.S. EPA). Draft development document
for petroleum refining industry point source category; 1979a.
U.S. Environmental Protection Agency (U.S. EPA). Draft development document
for proposed effluent guidelines for the iron and steel manufacturing indus-
try point source category; 1979d.
U.S. Environmental Protection Agency (U.S. EPA). Draft development document
for proposed effluent limitations guidelines for the iron and steel manu-
facturing industry point source category. Vol. VII. Pipe and tube
subcategory and cold rolling subcategory- 1979e.
U.S. Environmental Protection Agency (U.S. EPA). Draft document for pro-
posed effluent limitations and guidelines and standards for the iron and steel
manufacturing industry point source category. Vol. II. Byproduct
cokemaking subcategory, beehive cokemaking subcategory; 1979c.
U.S. Environmental Protection Agency (U.S. EPA). MDSD Water Quality Analysis
Branch, Priority pollutant data base; 1980.
165
-------
U.S. Environmental Protection Agency (U.S. EPA). NRDC Consent agreement
industry summary for leather tanning and finishing; 1978.
U.S. Environmental Protection Agency (U.S. EPA). Technical study report
BATEA-NSPS-PSES-PSNS. Textile mills point source category. Contact No.
68-01-3289 and 68-01-3884; 1979b.
U.S. International Trade Commission. Synthetic organic chemicals.
U.S. production and sales;1978. 47, 48, 78.
Versar, Inc. Materials balance for phenol. Preliminary draft.
Washington, DC ; Monitoring and Data Support Division, U.S. Environ-
mental Protection Agency; 1980.
Versar, Inc. Priority pollutant field survey. Vol. 7. Data summary.
251-266, 303-353; 1978.
166
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APPENDIX B: PHENOL AND PHENOLIC RESIN PRODUCTION
This appendix describes in detail the production processes for
synthesizing or extracting phenol and the process for producing phenolic
resins. The processes for synthesizing or extracting phenol described
are: 1) recovery from coal tar and petroleum streams, 2) cumene peroxi-
dation, 3) benzene sulfonation, and 4) toluene oxidation. This infor-
mation can be used to supplement that contained in Section III of this
report (Materials Balance) and to help explicate the potential losses"
of phenol to the environment during production.
RECOVERY OF PHENOL FROM COAL TAR AND PETROLEUM STREAMS
About 12,200 kkg (1%) of the phenol consumed in the United States
is natural phenol derived from coke-oven operations, coal-tar distilla-
tion, and petroleum operations.
Phenol From Coal Tar
Although most coke-oven plants in the United States are equipped
to process tar and light oil, the extent to which an individual plant
produces the various products depends on the size of the plant and its
economic condition (U.S. EPA 1977). Figure B-l presents a segment of
the coke byproduct recovery plant. The processes shown are primary
cooling/reheating, tar decanting, phenol recovery, and the ammonia still.
In the coke-oven process, the hot gases resulting from coke car-
bonization are collected and sprayed with weak ammonia liquor to reduce
the temperature and volume. The tar is condensed and decanted, along
with the unevaporated liquor, into a decanter. The coke-oven gas and
uncondensed vapors are further cooled in a primary cooler. As the gas
cools, tar and ammonia liquor are condensed. This mixture of condensed
liquor flows to the decanter. The gas, with a nominal amount of tar
fog, is sent to an electrostatic precipitator through a steam-driven
centrifugal gas exhauster. The precipitator removes the final traces
of tar, and the gas is reheated and passed through an ammonia scrubber.
The collected tar is added to the decanter.
In the decanter, the tar is separated from the weak ammonia liquor.
Part of this liquor is pumped back to the gas-collecting main sprays,
another part is passed to the cooling coils of the primary cooler, and
the remainder is sent to the ammonia still. The pitch sludges settle to
the bottom of the decanter and are mechanically raked out for disposal,
usually by burning as fuel. Settled crude tar, which contains a large
number of chemical compounds, is sent to a separate plant for secondary
processing by distillation, from which naphthalene is obtained as the
main product.
167
-------
ON
00
I Trimuy (Viol i 1*1
| aiKl l
M<|lil. Oi 1
1 1
llmnol
~*" Heomsry
[l.li|i»>r
....
SodLun
IHajMH 1
Aimmiia I Aiuimtiri
Still | *
i
lo
AmiiHiia
Wisorp-
tion
Phenolate Hticte
Source: U.S. EPA 1977.
FIGURE B-1 SEGMENT OF COKE BYPRODUCT RECOVERY PLANT
-------
Two processes are available to recover phenols: the solvent extrac-
tion process and the vapor recirculation process (U.S. EPA 1977). In
the solvent extraction process, weak ammonia liquor recovered with the
volatile products of coal carbonization is contacted countercurrently in
a scrubber with benzene or light oil to remove phenol. The weak Ammonia
liquor and light oil flow are maintained in the ratio of approximately
1.25 oil to 1.0 liquor.^ The phenol-free liquor flows to a storage tank
for further processing. The phenolized benzene or light oil is washed
with caustic soda in a tower. After a week or two, the caustic in the
light-oil caustic washer is saturated with sodium phenolate, which is
drained into a carbolate concentrator. The sodium carbolate in the con-
centrator is boiled to remove entrained solvent and moisture. It is
then neutralized with carbon dioxide to liberate crude phenols and phenol
compounds (U.S. EPA 1977).
The vapor recirculation method is operated in conjunction with the
ammonia still. This method is only practiced if the weak liquor is not
dephenolized by solvent extraction before being fed to the ammonia still.
The ammonia present in weak liquor is in two forms, classified as "free"
and "fixed." The free ammonia is that which dissociates readily by heat,
such as ammonia carbonates, sulfides, and cyanides. The fixed ammonia
requires the presence of strong alkali to effect displacement of the
ammonia from the compound in which it is present; examples include
ammonia chloride and sulfate (U.S. EPA 1977). In the ammonia still,
free ammonia and acidic gases are removed by passing weak ammonia liquor
down through a column over a series of plates equipped with bubble caps
and overflow pipes. The liquor is heated by steam which vaporizes
ammonia and volatile acidic gases. Ammonia is removed from the weak
liquor in the "free-leg" ammonia still. The liquor leaving the base of
the free-leg is transferred to the dephenolizing unit where phenols are
removed by vaporization with steam followed by extraction with caustic
soda. Phenols are recovered from the sodium phenolate solution. The
dephenolized liquor is transferred to the "fixed leg" of the ammonia
still (U.S. EPA 1977).
Phenol may enter the environment from this process in particulate
matter emitted through leaks in the equipment and from the still, and
in the wastewater generated by the scrubbers and the washers. The water-
borne wastes from this process are usually treated before they are dis-
charged.
PHENOL FROM PETROLEUM-REFINERY CAUSTIC WASTES
Caustic waste from refineries is the feed stream to this process.
This feed stream may contain over 20% phenol along with other tar acids
and thiols. The recovery of phenols from this stream is carried out in
two major operations: acidification and separation. Each operation
encompasses several processing steps. A general flow diagram of both
is shown in Figure B-2.
169
-------
Onisil
fix in
f f Mill-noil in,,
icUwlG I . . 1 Miterial
tttlfinory 1 ""•"•• '«"-•«*» 1
JT~1l
CHul-^.s) 1-ii.Ja
La JiK-iu!L\i( imi LO inciiiDr.il i<>ii
\
or Diaj nail
fioj vent
Mikeiip
^ Creayllc AJ
. ^. piteiifjl
— — »-M,l'-Cresol
ln|Hii i t loa
Lo Turllier I'ro
Source: Radian 1977.
FIGURE B-2 RECOVERY OF PHENOL FROM PETROLEUM REFINING CAUSTIC WASTES
-------
There may be three processing steps involved in acidification:
preparation, springing, and separation.
In the preparation process, the feed stream may be devolatilized
to remove the remaining hydrocarbon gases which may be vented or flared.
In some plants, the mercaptans and thiols are oxidized with air and steam
under alkaline conditions to convert the sulfur compounds to disulfides.
The effluents of this step are sent into a settling tank where the
separation is made by decanting. The disulfide layer is incinerated.
Other plants do not have a preparation step, and the raw feed is sent
to springing instead.
The prepared or raw feed is sent to a packed springing tower in
which the acidification takes place. The feed stream is contacted counter-
currently with C02 in the form of flue gas. Resulting cresylates and
sodium phenates are converted to cresols and phenols.
The acids are decanted from the water in settling tanks. The
phenolic layer enters a fractionation column in which light and heavy
ends are removed and incinerated. The mid-boiling range material is
sent to the solvent extraction unit. The aqueous sodium carbonate layer
contains phenols whose concentrations are reduced by absorption and
stripping. The resultant wastewaters contain phenols and require care-
ful disposal and treatment (Hawley 1977).
Solvent extraction is typically done with aqueous methanol and
naptha. The phenols are concentrated in the methanol layer, while the
naptha removes most of the impurities. The methanol stream is stripped
before the phenolic stream is pumped to a separating tank where water is
removed. The acid stream is then fed to a series of fractional distilla-
tion columns for the separation of phenol, cresols, and xylenols. An
ion-exchange column may be used to remove traces of mercaptans and bases
from the phenolic compounds (Hawley 1977).
The aqueous methanol extraction step generates wastewater contami-
nated with phenolic compounds. There is no available information on the
disposal or treatment of this wastewater.
PHENOL FROM CUMENE PEROXIDATION
The manufacture of phenol by the cumene peroxidation process involves
the liquid-phase air oxidation of cumene to cumene hydroperoxide, which
is then decomposed to phenol and acetone by the addition of acid
(Lowenheim and Moran 1975)
The basic reaction steps are:
1. C6 H5 CH (CH3)2 + 202 +» C6 H5 C (CH3)2 OOH
cumene cumene hydroperoxide
acid
2. C6 H5 C (CH3)2 OOH »» C6 H5 OH + CH3COCH3
phenol acetone
171
-------
Cumene (isopropylbenzene) is produced by liquid- or vapor-phase alkyla-
tion of benzene with propylene.
To produce phenol, cumene is mixed with recycled cumene, purified,
and then charged to the oxidation reactor along with dilute soda ash to
maintain the pH between 6.0 and 8.0. The mixture is oxidized with air
at 110 to 115 °C until 20 to 25% of the cumene is converted to the hydro-
peroxide intermediate. The cumene/hydroperoxide mixture is concentrated
in an evaporator and then fed to a reactor in which the cumene/hydro-
peroxide is cleaved to phenol and acetone in the presence of a small
amount of sulfuric acid. The typical operating temperature of this
reaction is 70 to 80°C, and the resulting mixture consists of acetone,
acetophenone, a-methylstyrene, and cumene.
The products are separated by distillation. In the process shown
in Figure B-3, acetone is removed in the first column and further puri-
fied. The bottoms from the first column are vacuum distilled, and
unreacted cumene and a-methylstyrene are taken overhead. This stream
is further purified by catalytic hydrogenation to convert the a-methyl-
styrene to cumene. In some plants, a-methylstyrene is carefully
fractionated and is available as a byproduct.
The bottoms from the vacuum still are further fractionated to
separate phenol and acetophenone, yielding about 90% phenol (Lowenheim
and Moran 1975).
Estimated total environmental emissions of phenol from this process
are on the order of 2,000 kkg. Airborne emissions are from the sulfuric
acid column vents. Contaminated wastewater comes from the phenol surge
vessel. Solid wastes contaminated with phenol are from the residues in
the evaporation vessels (Hedley 1975).
PHENOL FROM BENZENE SULFONATION
This process involves the reaction of benzene with sulfuric acid
followed by the conversion of the benzene sulfonic acid to phenol.
The benzene sulfonic acid is prepared by reacting concentrated
sulfuric acid with benzene. Water is formed during the reaction and
must be removed to prevent its diluting the sulfuric acid. When the
concentration of sulfuric acid drops below 78%, the sulfonating reaction
stops. This reaction is carried out continuously in vapor phase by pass-
ing benzene vapors up through the reaction zone maintained at 150°C.
The sulfonation proceeds until only a few percent of the sulfuric acid
remains. It is then neutralized. The benzene, water, and acid vapors
are condensed and the benzene recovered.
The sulfonation product is added rapidly to a neutralizing tank
which contains sodium sulfite. The sulfur dioxide formed is boiled off
and piped to the acidifiers. The boiling mixture of sodium benzene
sulfonate and sodium sulfate is filtered. The sodium sulfate precipitates
172
-------
imaurt cum*** »«ve*e
Acttaiw
1
*SSH^-*Lrl
I ff»evei« tcia
T
wastes
Source: Lowenheim and Moran 1975.
FIGURE B-3 CUMENE PEROXIDE PROCESS
Sodium suiht*
Source: Lowenheim and Moran 1975.
FIGURE B-4 BENZENE SULFONATE PROCESS
173
-------
out of the hot liquor and remains on the filter. The sodium benzene
sulfonate is pumped into a fusion pot that contains fused caustic soda
to yield sodium phenate. A ratio of 3 moles of alkali to 1 mole of
sulfonate is used. After the fusion is complete, the pot is emptied,
and the melt is diluted with water. The sodium phenate-sodium hydroxide
sodium sulfate solution is acidified with sulfur dioxide and a small
amount of sulfuric acid. The crude phenol separates as the upper layer
over the aqueous solution of sodium sulfite and sodium sulfate. The
phenolic layer is decanted and distilled under vacuum to produce refined
phenol. The aqueous layer is treated with steam to remove residual
phenol. The distillate is used as makeup water. Part of the sulfide
sludge is used for the neutralization step, and the remainder is crys-
tallized and dried to yield sodium sulfite byproduct. Phenol of UPS
quality is obtained in about 85% by weight yield based on benzene.
The reaction steps for phenol production by benzene sulfonation are
given below. A simplified flow diagram of the process is shown in
Figure B-4.
C6H6 + H2SOt, - »» C5H5S03H + H20
2C5H5S03H + Na2S03 - *• 2C6H5S03Na + S02 + H20 (
C6H5S03Na + 2NaCH - ». C6H5ONa + Na2S03 + H20
H2SOU
2C6Hs ONa + S02 + H20 - ^ 2C6H5OH + Na2S03 ( + Na2SOl+)
Presently only one company uses this method to produce phenol, and
the only identifiable waste stream generated by this process is the
bottoms of the phenol columns containing phenols which is discharged
as solid waste (Hedley 1975).
PHENOL FROM TOLUENE OXIDATION
Less than 2% of the phenol consumed is produced by toluene oxidation.
Toluene is converted to phenol in two successive liquid-phase, air-oxi-
dation steps, as shown in Figure B-5 (Lowenheim and Moran 1975).
In the first step, toluene in the presence of cobalt naphthenate
catalyst is converted to benzoic acid. The reaction conditions are
maintained at 150° to 250°C and at a pressure of 5 to 50 atms (Lowenheim
and Moran 1975).
In the second step, the benzoic acid is melted in biphenyl, mixed
with a small amount of manganese-promoted cupric benzoate, and fed to
a reactor. Air and steam are fed into the reactor where the benzoic
acid is oxidized to phenol. The reactor is maintained at 230°C and 20
to 25 psi. Phenol and benzoic acid are vaporized continuously and passed
to the primary distillation column. Conversion of benzoic acid in the
oxidizer is 70 to 80%; phenol yield is 90% (Lowenheim and Moran 1975).
174
-------
duty* •
*lf 9X4
Hot wanr
Pfttnof wa »4t«f
n
Swsiranr
t
|
5
^
=h«flO
••uri
II
grreic T
Httvy «1OJ
•Phtnol
Source: Lowenheim and Moran 1975.
FIGURE B-5 TOLUENE OXIDATION PROCESS
175
-------
In the primary distillation column, phenol and water vapor pass
overhead and the benzoic acid is removed from the bottom of the column
and returned to the oxidizer. The condensed phenol-water mixture from
the primary column separates into two layers. The lower, phenol-rich
layer is sent to the phenol column where product phenol leaves the
bottom of the column and water is removed from this layer azeotropically.
Phenol is removed from the water layer from the azeotrope by further
fractionation. The main reactions of this process are given below.
2C6H5CH3 + 302 catalyst *" 2C6H5OOOH + 2H20
benzoic acid
2C6H5COOH + 02 catalyst "" 2C6H5OH + 2C02
phenol
Only one plant presently uses the toluene oxidation process. The
economy of it depends on how cheaply toluene can be converted to benzene
(Hedley 1975). Information on discharges from this plant is not avail-
able.
PHENOLIC RESIN PRODUCTION PROCESS
Table B-l lists the manufacturers of phenolic resins and their
locations. There are two major types of phenolic resins produced:
resol and novalaks (Sittig 1975). Resols are a mixture of phenol and
formaldehyde with an excess of formaldehyde. The mole ratio is usually
1-5 moles of formaldehyde to 1 mole of phenol. Sodium hydroxide is
normally used to catalyze the polymerization reaction which takes place
at a pH of 8 to 11 (Sittig 1975).
The reacting mixture contains sufficient formaldehyde to form a
cross-linked thermoset resin. The reaction, however, is stopped short
of completion at an average molecular weight of the polymer appropriate
for the end use of materials (Sittig 1975).
Three classes of products are produced under the general headings
of resols. The first is a water-soluble bonding resin which is either
sold as is or neutralized and partially dehydrated. The second is a
water-insoluble resin which is vacuum dehydrated and dissolved in
solvents to produce laminating resins and varnishes. The third class
of product is similar to the second class but the water is removed and
the reaction is carried further to produce a "one-stage" solid resin
which is then vacuum dehydrated and removed from the reactor for cooling
and solidifying. This type of resin is either made into bonding com-
pounds and surface coatings by adding catalysts and lubricants, or con-
verted into thermosetting molding powders by adding catalysts, lubricants,
pigments, and fillers. The compounding may be performed in the same
facilities or may be shipped to custom compounders (Sittig 1975).
176
-------
TABLE B-l. U.S. MANUFACTURERS OF PHENOLIC RESINS
Company
Allied Products Corp
Acme Chems. Div.
American Cyanamid Co.
Formica Corp., subsid.
American Hoechst Corp.
Indust. Chems. Div.
Ashland Oil, Inc.
Ashland Chem. Co., Div.
Foundry Products Div.
Resins and Plastics Div.
The Bendix Corp.
Friction Materials Div.
Borden, Inc.
Borden Chem. Div.
Adhesives and Chems. Div.
- East
Adhesives and Chems. Div. - West
Brand-S Corp.
Cascade Resins, Inc., Div.
California Resins and Chem. Co., Inc.
The Carborundum Co.
Polymers Venture
Carrier Corp.
Inmont Corp. subsid.
Chagrin Valley Co. Ltd.
Nev mar Corp., subsid.
Location
New Haven, CT
Evandale, OH
Mount Holly, NC
Hammond, IN
Cleveland, OH
Calumet City, IL
Fords, NJ
Pensacola, FL
Troy, NY
Bainbridge, NY
Demopolis, AL
Diboll, TX
Fayetteville, NC
Sheboygan, WI
Fremont, CA
Kent, WA
LaGrande, OR
Missoula, MT
Springfield, OR
Eugene, OR
Vallejo, CA
Niagara Falls, NY
Anaheim, CA
Cincinnati, OH
Detroit, MI
Odenion, MD
177
-------
TABLE B-l. U.S. MANUFACTURERS OF PHENOLIC RESINS
(continued)
Company
Champion International Corp.
U.S. Plywood Div.
Clark Oil & Refining Corp.
Clark Chem. Corp., subsid.
Hercules, Inc.
Haveg Indust., Inc., subsid.
Marshallton Operation
Heresite & Chem. Co.
Inland Steel Co.
Inland Steel Container Co., Div.
International Minerals & Chem. Corp.
Aristo International Corp., subsid.
Foundry Products Div.
The Ironsides Co.
Knoedler, Alphonse & Co.
Knoedler Chem. Co., subsid.
Koppers Co., Inc.
Organic Materials Div.
Kordell Indust.
Lawter Cheras., Inc.
Libbey-Owens-Ford Co.
LOF Plastic Products, subsid.
Masonite Corp.
Alpine Div.
Monagram Indust., Inc.
Spaulding Fibre Co., subsid.
Monsanto Co.
Monsanto Chem. Intermediates Co.
Monsanto Plastics & Resins Co.
Location
Anderson, CA
Blue Island, IL
Wilmington, DE
Manitowoc, WI
Alsip, IL
Detroit, MI
Columbus, OH
Lancaster, PA
Petrolia, PA
Mishawaka, IN
South Kearny, NJ
Auburn, ME
Gulfport, MS
De Kalb, IL
Tonawanda, NY
Addyston, OH
Chocolate Bayou, TX
Eugene, OR
Santa Clara, CA
Springfield, MA
178
-------
TABLE B-l. U.S. MANUFACTURERS OF PHENOLIC RESINS
(continued)
Company
Napko Corp.
Occidental Petroleum Corp.
Hooker Chem. Corp., subsid
Hooker Chems. and Plastics Corp., subsid,
Durez Div.
Onyx Oils & Resins, Inc.
Owens-Corning Fiberglass Corp.
Resins and Coatings Div.
Plastics Engineering Co.
Polymer Applications, Inc.
Polyrez Co., Inc.
Raybestos-Manhattan, Inc.
Adhesives Dept
Rechhold Chems., Inc.
Varcum Chem. Div.
Rogers Corp.
Schenectady Chems., Inc.
Simpson Timber Co.
Chems. Div.
Location
Houston, TX
Kenton, OH
North Tonawanda, NY
Newark, NJ
Barrington, NJ
Kansas City, KS
Newark, OH
Waxahachie, TX
Sheboygan, WI
Tonawanda, NY
Woodbury, NJ
Stratford, CT
Andover, MA
Cartaret, NJ
Detroit, MI
Houston, TX
Kansas City, KS
Moncure, NC
South San Francisco, CA
Tacoma, WA
Tuscaloosa, AL
White City, OR
Niagara Falls, NY
Manchester, CT
Oyster Creek, TX
Rotterdam Junction, NY
Schenectady, NY
Portland, OR
179
-------
TABLE B-l. U.S. MANUFACTURERS OF PHENOLIC RESINS
(continued)
Company
Synres Chem. Corp.
Shanco Plastics & Chems., subsid.
Synthane-Taylor Corp.
Union Carbide Corp.
United-Erie, Inc.
Univar Corp.
Pacific Resins & Chems., Inc., subsid.
Valentine Sugars, Inc.
Valite Div.
West Coast Adhesives Co.
Westinghouse Electric Corp.
Insulating Materials Div.
Weyerhaeuser Co.
Location
Tonawanda , NY
Betzwood, PA
Bound Brook, NJ
Elk Grove, CA
Marietta, OH
Texas City, TX
Erie, PA
Eugene, OR
Newark, OH
Portland, OR
Richmond, CA
Lockport, LA
Portland, OR
West Mifflin, PA
Longview, WA
Marshall, WI
Source: Versar 1980.
180
-------
The resols are only partially polymerized when they are manufactured.
These materials, however, contain sufficient formaldehyde to carry the
reaction to completion. The polymerization is completed when the resin
is heated and set into the final product at the consumer facility (Sittig
xy/j/•
Novalaks are the second category of phenolic resins. These are
formed by reacting a mixture which contains a deficiency of formaldehyde.
The mole ratio is 0.75 to 0.90 moles of formaldehyde to 1.0 mole of
phenol. Polymerization is carried out in an acid medium using a cata-
syst such as sulfuric acid. The pH of the reaction ranges from 0.5 to
1.5. Since the reacting mixture contains a deficiency of formaldehyde,
essentially all of the formaldehyde is consumed during polymerization.
Since no further polymerization can take place, the product is a low-
molecular weight, thermoplastic, stable material. The water which enters
with the formaldehyde and the water of reaction are removed under vacuum,
producing a solid, meltable material (Sittig 1975).
In order to complete the polymerization, the user must add addi-
tional formaldehyde or hexamethylenetetramine. With the latter material,
ammonia is evolved from the reacting mass, leaving the same types of
methylene linkages as can be obtained by using additional formaldehyde
(Sittig 1975). y
The basic resins are sometimes modified by the use of materials
such as drying oils or epoxy compounds in the final stages of polymeri-
zation.
Phenolic resins are produced by batch operations because the plastic
industry calls for a wide variety of polymers. There is rarely a big
enough demand for a single grade of polymer to justify using a con-
tinuous process (Sittig 1975).
A schematic diagram for phenolic resin production is shown in
Figure B-6. The reaction is usually carried out in a jacketed kettle.
In the larger-size kettles, internal cooling coils are used to provide
an adequate surface-to-volume ratio for the removal of the heat generated
during the polymerization. These kettles are agitated and can operate
under pressure or vacuum conditions.
The feed system consists of two weigh tanks, one each for phenol
and formaldehyde solution. Commercial formaldehyde solution at 37% by
weight formaldehyde is usually employed. This solution often contains
about 5% methanol, which acts as a stabilizer. The kettle is equipped
with a water-cooled condenser, which is also joined to a vacuum system.
For resol resin production, the phenol is charged in a molten form
to the kettle, followed by the addition of formaldehyde which washes
the residual phenol out of the lines leading to the kettle. A sodium
hydroxide catalyst solution is next added and the kettle is heated by
181
-------
"•€101.
"3»"«(.B£.HTOe
sr%sou. C30UNO
! , ««rE*
.I»C:JUM
i mrs-a |
"OOUCT »*S;.i
ro cooCiNO
0
Source: Lowenheim and Moran 1975.
FIGURE B-6 PHENOLIC RESIN PRODUCTION
182
-------
steam to bring the mixture to the reaction temperature of 60°C. When
the condensation reaction starts, the reaction becomes highly exothermic.
Thus, the supply of steam is stopped and the coils are supplied with
cooling water. The mixture is held at 60°C for about 3 to 5 hours.
During this period the temperature is controlled by supplying cooling
water through the coils and by using total reflux returning from the
water-cooled condenser on the kettle. When the polymerization reaches
the desired degree, the mixture is cooled to about 35°C and the caustic
solution is neutralized by sulfuric acid to a pH of 7.
The mixture is then heated again by steam to purify the resin by
distillation. The water from this distillation is a concentrated waste
which contains phenol, formaldehyde, and low molecular-weight resin and
is usually segregated for disposal by incineration. The batch is then
dumped. A few resins, such as varnish-type resols, are washed two or
three times, thus generating a considerable amount of wastewater. If a
resin is required to contain a very small quantity of water, a vacuum is
usually applied during the latter part of the dehydration cycle. This
technique is also used to produce anhydrous melt of a single-step resin.
The manufacture of novolak resins is similar to that of resols
except that an acid catalyst is added at the start of the batch and a
vacuum reflux is used to maintain temperatures at 85° to 90°C.
183
-------
REFERENCES
Hawley, G.G. The condensed chemical dictionary. 9th edition. New York:
Van Nostrand Reinhold Company; 1977. (As cited by Versar 1980).
Hedley, W.H. et al. Potential pollutants from petrochemicals processes.
Monsanto Research Corporation; 1975:111-123. (As cited by Versar 1980).
Lowenheim, F.D.; Koran, M.K. Faith, Keyes and Clark's industrial
chemicals. 4th edition. New York: Wiley Interscience; 1975:50-55,
148-153, 201-205, 612-623. (As cited by Versar 1980).
Radian Corporation. Industrial process profiles for environmental uses.
Chapter 5. Basic petrochemicals industry. 1977^102-108. (As cited by
Versar 1980).
Sittig, M. Pollution control in the plastics and rubber industry.
Park Ridge, NJ: Noyes Data Corporation; 1975:43-52. (As cited by
Versar 1980).
U.S. Environmental Protection Agency. Industrial process profiles for
environmental use. Chapter 24. The iron and steel industry. Report No
EPA 600/2-77-0234. 1977:64-66.
Versar, Inc. Materials balance for phenol. Preliminary draft.
Washington, DC: Monitoring and Data Support Division, U.S. Environmental
Protection Agency; 1980.
184
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