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

-------
                                     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.

-------
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

-------
                                         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

-------
                               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

-------
                            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

-------
                           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

-------
                            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

-------
                            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

-------
                             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

-------
                             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

-------
                             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

-------
                             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

-------
                           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

-------
                            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

-------
                         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.

-------
     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.

-------
     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.

-------
      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.

-------
     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

-------
 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

-------
      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

-------
             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

-------
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

-------
                                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

-------
                               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

-------
     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

-------
                          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

-------
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

-------
      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

-------
      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

-------
      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

-------
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

-------
                    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

-------
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

-------
     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

-------
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

-------
      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

-------
     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

-------
      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

-------
                               REFERENCES
Baird, R.B.; Carmona, L.G.;  Jenkins, R.L.  The direct-injection GLC analysis
of xylenols in industrial wastewaters.  Bull. Environ. Contam. Toxicol.
17:764-767; 1976.  (As cited by Buikema et al. 1979)

Bedard, R.G.  Biodegradability of organic compounds.  Storrs, CT:
University of Connecticut; 1976.  M.S. Thesis.  Available from:  NTIS,
Springfield, VA; PB-264-707.

Bobkov, V.N.  Contamination of snow by phenols in a city with developed
industry.  Gig. Sanit. 11:105; 1974, As cited in Chemical Abstracts 82:
47322q; 1975.  (As cited by Versar 1979b)

Buikema, A.L.; McGinniss, M.J.; Cairns, J.  Phenolics in aquatic ecosystems:
A selected review of recent literature.  In:  Marine Environmental Re-
search.  England:  Applied Science Publishers Ltd.; 1979:87-181.

Burns and Roe, Co.  Unpublished data developed for Effluent Guidelines
Division, U.S. Environmental Protection Agency, Washington, D.C.; 1980.

Carlson, R.M.; Caple, R.  Organo-chemical implications of water chlorina-
tion.  Jolly, R.L. ed.  The environmental impact of water chlorination.
Proceedings of the conference on the environmental impact of water chlorina-
tion; 1975 October 22-24. Oak Ridge National Laboratory, Oak Ridge, TN;
1976: 73.

Carlson, R.E.; Carlson, R.M.; Kopperman, H.L; Caple, R.  Facile incorpora-
tion of chlorine into aromatic systems during aqueous chlorination process.
Environ. Sci. Technol. 9: 674-675; 1975.

Cronin, D.R.; Charleson, R.J.; Knights, R.L.; Crittenden, A.L.; Appel, B.R.
A survey of the molecular nature of primary and secondary components of
particles in urban air by high resolution mass spectrometry.  Atmos.
Environ. 11: 929-937; 1977.

Crosby, D.G.; Wong, A.S.  Photodecomposition of p-Chloro-phenoxyacetic
acid.  J. Agric. Food Chem.  21: 1049-1052; 1973.

Deimel, M.; Gableske, R.  Measurement of several exhaust components in
motor traffic in Cologne.  Staedtehygiene 24: 268-272; 1973.

Delfino, J.J.; Dube, D.J.  Persistent contamination of groundwater by
phenol.  J. Environ. Sci. Health 6:345-355; 1976.

Ellis, B.E.  Degradation of phenolic compounds by fresh water algae.
Plant Sci. Lett. 8:213-216;  1977.
                                   97

-------
 Faust, S.D.; Anderson, P.W.;  Stutz,  H.   Occurrence and distribution of
 phenolic compounds in New Jersey's streams.   American Society of
 Mechanical Engineers joint conference on stream pollution and abate-
 ment; June 1969.

 Fox,  M.E.   Fate of selected organic  compounds in the  discharge of  kraft
 paper mills into  Lake Superior.   Keith,  L.H.  ed.   Identification and
 analysis of organic pollutants  in water.  Ann Arbor,  MI:   Ann Arbor Science
 Publishers, Inc.;  1976:  641-659.   (As cited by Buikema et al.  1979)

 Galan, M.A.;  Smith,  J.M.   Photodecomposition  of  phenol in a  tubular-flow
 reactor.   Chem. Eng.  Sci.  31: 1047-1056;  1976.

 Gould, J.P.;  Weber,  W.J.   Oxidation  of phenols by ozone.   J.  Water Pollut
 Control  Fed.  48:  47-60;  1976.

 Greskovich,  E.J.   Equilibrium data for various compounds  between water
 and mud.   AIChE Journal  20: 1024-1025; 1974.

 Haller,  H.D.  Degradation  of mono-substituted benzoates and phenols  by
 wastewater.   J. Water  Pollut. Control Fed.  2771-2777;  1978.

 Herrington, E.F.G.; Kynaston, W.   The ultraviolet absorbtion spectra and
 dissociation  constants of  certain  phenols in aqueous  solutions.  Trans
 Faraday  Soc.  53: 138-142;  1957.                 -.   .  . .

 Hill, G.A.; Campbell, W.R.  Substrate inhibition kinetics:  phenol degrada-
 tion by Pseudomonas putida.  Biotechnol.  Bioeng. 17:  1599-1615; 1975.

 Jahnig,  C.E.; Bertrand, R.R.  Coal processing:  environmental aspects
 of coal  gasification.  CEP; August 1976.


 Jolley, R.L.;  Jones, G.; Pitt, W.W.; Thompson,  J.E.  Chlorination of
 organics in cooling waters and process effluents.  Jolley, R.L. ed.   The
 environmental impact of water Chlorination.   Proceedings of the conference
 on the environmental impact of water Chlorination; 1975 October 22-24,
 Oak Ridge National Laboratory, Oak Ridge, TN;  1976: 115.

 Joschek, H.I.; Miller, S.I.  Photooxidation of phenol, cresols, and di-
 hydroxybenzenes.  J. Am. Chem. Soc. 88:  3273-3281; 1966.

 Jungclaus, G.A.; Lopez-Avila,  V.; Hites,  R.A.   Organic compounds in an
 industrial wastewater:  A case study of  their  environmental impact.
 Environ.  Sci. Technol. 12: 88-96; 1978.   (As  cited by Buikema et al. 1979).

 Keith, L.H.  GC/MS analyses of organic compounds in treated kraft paper
mill wastewaters.   Keith, L.H. ed.  Identification and analysis of  organic
 pollutants in waters.  Ann Arbor, MI: Ann Arbor Science Publishers  Inc  •
 1976:  671-707.  (As cited by Buikema et  al.  1979)

Kleczkowski, A.S.; Kurdyka, S.;  Stobierski, J.  Influence of a chemical-
plant sewage sedimentation catchpit on ground  waters on the Upper Vistula
 floodplain.  Bull. Acad.  Pol.  Sci., Ser.  Sci.  Terre 19(1): 55-59;  1972.

                                  98

-------
Klemetson, S.L.  Pollution potentials of coal gasification plants.
In:  Proceedings of the 31st industrial waste conference.  Purdue
University, 63-76; 1976.  (As cited by Buikema et al. 1979)

Kobayashi, K.; Akitake, H.  Studies on the metabolism of chlorophenols
in fish.  IV. Absorption and excretion of phenol by goldfish.  Bull. Jap.
Soc. Sci. Fish. 41: 1271-1276; 1975.

Kobayashi, K.; Akitake, H.;  Kimura, S.  Studies of the metabolism of
chlorophenols in fish.  VI.  Turnover of absorbed phenol in goldfish.
•Bull. Jap. Soc. Sci. Fish. 42: 45-50; 1976a.

Kobayashi, K.; Kimura, S.; Shimizu, E.  Studies on the metabolism of
chlorophenols in fish.  VIII. Isolation and identification of phenyl-B-
glucoronide accumulated in bile of goldfish.  Bull. Jap. Soc. Sci. Fish.
42: 1365-1372; 1976b.

Krombach, H.; Barthel, J.  Investigation of a small watercourse accidentally
polluted by phenol compounds.  Adv. Water Pollut. Res. 1: 191-224; 1964.
(As cited by Versar 1979b).

Kurchatova, M.; Mladenova, S.  Composition of rain in Sophia.  Khig.
Zdraveopaz. 18: 174-178; 1975. (As cited in Chemical Abstracts 84: 20593h;
1976. )

Lee, R.F.; Ryan, C.  Microbial degradation of organochlorine compounds in
estuarine waters and sediments.  In:  Microbial degradation of pollutants
in marine environments.  Proceedings of the workshop.  Report No. EPA-
600/9-79-012.  Washington, DC:  U.S. Environmental Protection Agency; 1979.

Liss, P.S.; Slater, P.G.  Flux of gases across the air sea interface.
Nature 247: 181-184; 1974.

Lyman, W.J.; Nelson, L.; Partridge, L.; Kalelkar, H.; Everett, J. ; Allen,
D.; Goodier, L.L.; Pollack,  G. (Arthur D. Little, Inc.).  Survey study
to select a limited number of hazardous materials to define amelioration
requirements.  CG-D-46-75.  U.S. Coast Guard; 1974.

Mackay, D.  Volatilization of pollutants from water.  Hutzinger, E.D.
et al. eds.  Aquatic pollutants:  transformations and biological effects.
Proceedings of the second international symposium on aquatic pollutants;
1977 September 26-28; 1978:  140-148.

Mackay, D.; Yuen, T.K.  Volatilization rates of organic contaminants from
rivers.  In:  Proceedings of the 14th Canadian Symposium, 1979:  Water
pollution research Canada.

Maickel, R.P.; Jondorf, W.R.; Brodie, B.B.  Conjugation and excretion of
foreign phenols by fish and amphibia.  Abstract #1541.  Federation Proc.
17; 1958: 390.
                                    99

-------
 Manufacturing Chemists Association  (MCA).  The  effect  of  chlorination  on
 selected organic chemicals.  U.S. Environmental Protection Agency" 1972

          _R.J.; Boyd, R.N.  Organic chemistry.  Boston, MA:  Allan and
 Mueller, H.  Uptake and metabolism of phenol in food plants.
 1979b)   enernaehr' B°denkd-  4~5: 471-*81; 1975.  (As cited by Versar


 Murphy, K.L.; Zaluom, R. ; Fulford, D.  Effect of chlorination practice on
 soluble organics.  Water Res. 9:389-396; 1975.
 of^eno^ G°"!iChlinS' *'D- Holmes> J.L-; Uiwngat. P.C.  Ozone oxidation
 of phenolic effluents.   In:  Proceedings of the 31st industrial waste
 conference.  Purdue University; 1976: 940-952.   (As cited by Buikema
 o'     T,'   >';        l'  C'T-   Mlxed Culture biooxidation
 of phenol.   Ill  Existence of multiple steady states in continuous culture
 with wall growth.   Biotechnol.  Bioeng.  15:  905-916;  1973.

 Pitt, W.W.  Jr.; Jolley,  R.L. ;  Scott,  C.D.  Determination of trace organics
 in municipal sewage effluents and  natural waters  by  high-resolution ion-
 exchange chromatography.   Environ.  Sci. Technol.  9:  1068-1073;  1975.

                                                      of organic substances

                         "' Campbell> P-G'C-;  ViUeneuve, J.P.   Degradation
                                                   re£inery
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. Environmental Protection
Agency; 1980.

Shetiya, R.S.;  Rao, K.N. ;  Shatnar, J.  OH radical rate constants of phenols
using p-Nitrosodimethylaniline.   Ind. J. Chem. 14A: 575-578: 1976.

Southworth, G.R.  The role of volatilization in removing polycyclic
aromatic hydrocarbons from aquatic environments.   Bull. °Environ. Contam
Toxicol. 21:507-514;  1979.

Swann, R.L.; McCall,  P.J.;  Unger,  S.M.  (Dow Chemical USA,  Midland MI).
Volatility of pesticides from soil surfaces.   Unpublished undated
manuscript received as a personal  communication;  November 16,  1979.
                                  100

-------
 Stanford  Research  Institute.   Estimates  of  physical-chemical  properties
 of  organic  priority  pollutants.   Preliminary  draft.   Washington,  D.C..
 Monitoring  and Data  Support Division, U.S.  Environmental Protection
 Agency; 1980.

 Tabak, H.H.; Quave,  S.A.; Mashni,  C.I.;  Earth, E.F.   Biodegradability
 studies with priority pollutant organic  compounds.   Staff report.   Draft.
 Cincinnati, OH:  Water Research Division; U.S. Environmental  Protection
 Agnecy; 1980.

 Thomas, R.G.  (Arthur D.  Little, Inc.).   Volatilization  from water.
 Lyman, W.J. ed.  Methods  for  estimating  physiochemical  properties  of
 organic compounds  of environmental concern.   Work  in progress.  Frederick,
 MD:   U.S. Army Medical Bioengineering and Development Laboratory;  1980.

 Throp, W.M.  Alternative methods  of phenol wastewater control.  J.  Hazard
 Mat.  1: 319-329; 1975.

 United Nations Food  and Agriculture Organization (UNFAO).   Water quality
 criteria  for European freshwater  fish.   Report on monohydric  phenols and
 inland fisheries.  Water Res.  7:  929-941; 1973.

 U.S.  Environmental Protection  Agency (U.S. EPA).  Ambient  water quality
 criteria.   Phenol.   Washington, DC:  Office of Water  Planning and  Standards;
 1979b. Available from:  NTIS,  Springfield, VA; PB 292 437.

 U.S.  Environmental Protection  Agency (U.S. EPA).  Exposure  Analysis Model-
 ing System  (EXAMS).  Athens, GA:   Environmental Systems Branch, Environ-
 mental Research Laboratory, Office of Research and Development; 1980a.

 U.S.  Environmental Protection  Agency (U.S. EPA).  Preliminary draft of
 data  developed in support of RCRA.  Washington, D.C.:  Office of Solid
 Waste; 1980b.

 U.S.  Environmental Protection  Agency (U.S. EPA).  Preliminary draft material
 on migration of toxic substances  from waste disposal  sites.  Office of Solid
 Waste; 1980c.

U.S. Environmental Protection Agency (U.S.  EPA).   Priority pollutant data
base.   Monitoring and Data Support Division, Water Quality Analysis Branch-
 1980d.

Vela,  G.R.;  Ralston,  J.R.   The effect  of  temperature on phenol degradation
in wastewater.   Can.  J.  Microbiol. 24:1366-1370;  1978.
                                  101

-------
 Versar,  Inc.   Water related environmental fate of  129  priority pollutants,
 Part II.   Halogenated ethers,  monocyclic  aromatics,  phthalate  esters ,
 polycyclic aromatic hydrocarbons,  nitrosamines,  and  miscellaneous  com-
 pounds.   Draft report.   U.S. Environmental Protection  Agency;  1979a.

 Versar,  Inc.   Non-aquatic  fate of  phenol.   Draft report.  Monitoring and
 Data Support  Division,  U.S.  Environmental Protection Agency;  1979b.

 Volesky,  B.;  Czornyi, N. ;  Constantine, T.A. ; Zajic,  J.E.; Yu, K.  Model
 treatability  study  of refinery phenolic wastewater.  In:  Water - 1974:
 I   Industrial waste  treatment AIChE Symposium  Series No. 144.  70- 31-38-
 1974.  (As cited by  Buikema et al. 1979)

 Webb, et_al.  Current practice in GC/MS analysis. of  organics in water
 Environmental Protection Technology Series Report No. EPA-R2-73-222
 US. Environmental Protection Agency; 1973.  (As cited by Buikema et al.
                                                                     •--
White, G.C.  Current chlorination and dechlorination practices in the
treatment of potable water, wastewater, and cooling water.. Jollev, R.L.
ed.  The environmental impact of water chlorination.  Proceedings of the
conference on the environmental impact of water chlorination; 1975
October 22-24, Oak Ridge National Laboratory, Oak Ridge, TN;'l976: 7.

Yang, R.D.; Humphrey, A.E.  Dynamic and steady state studies of phenol
biodegradation in pure and mixed cultures.   Biotechnol.  Bioeng. 17:
    ^      xy ij •
                                   102

-------
                              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%,
                                 103

-------
 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.
                                  104

-------
 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.
                                  105

-------
     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).
                                  106

-------
      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

-------
                       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

-------
 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

-------
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

-------
     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

-------
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

-------
          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

-------
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.
                                 116

-------
              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

-------
     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.
                                  118

-------
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

-------
                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

-------
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

-------
                               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

-------
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-
mental data).  Gig. Tr. Sostoyanie Spetsificheskikh funkts RAB Neftekhm
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-
mental assessment and predictions to 1985 for the lower Mississippi
River and Barataria Bay.  Vol. 1.  Contract No. WQ5AC062; 1975.

National Marine Fisheries Services (NMFS).  Report on the change of
U.S. seafood consumers exceeding the current acceptable daily intake
for mercury and recommended regulatory controls.  NOAA,  Seafood Quality
and Inspection Division, Office of Fisheries Development; 1978.

National Cancer Institute (NCI).   Bioassay of phenol for possible
carcinogenicity.   Draft report.   DHHS Publication No.  (NIH) 80-1759.
National Institutes of Health, U.S.  Department of Health and Human
Services; 1980.
                                  123

-------
 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
 criteria - Phenol.  Washington, D.C.:  Criteria  and Standards Division,
 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

-------
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

-------
                              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

-------
 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

-------
                         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

-------
        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

-------
    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

-------
     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

-------
      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

-------
 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

-------
            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

-------