United States       Region 2    EPA/902/R 93-001 h
Environmental Protection    902     January 1993
Agency
Staten Island/New Jersey
Urban Air Toxics
Assessment Project
Report

Volume VI
Part B	

Appendices

-------
                         ACKNOWLEDGEMENTS
     This report is a collaborative effort of the staffs of the
Region II Office of the U.S. Environmental Protection Agency
 (EPA), the New Jersey Department of Environmental Protection and
Energy, the New York State Department of Environmental
Conservation, the New York State Department of Health, the
University of Medicine and Dentistry of New Jersey and the
College of Staten Island.  The project was undertaken at the
request of elected officials and other representatives of Staten
Island concerned that emissions from neighboring industrial
sources might be responsible for suspected excess cancer
incidences in the area.

     Other EPA offices that provided assistance included the
Office of Air Quality Planning and Standards, which provided
contract support and advice; and particularly the Atmospheric
Research and Exposure Assessment Laboratory, which provided
contract support, quality assurance materials, and sampling and
analysis guidance, and participated in the quality assurance
testing that provided a common basis of comparison for the
volatile organic compound analyses.  The Region II Office of
Policy and Management and its counterparts in the States of New
York and New Jersey processed the many grants and procurements,
and assisted in routing funding to the project where it was
needed.

     The project was conceived and directed by Conrad Simon,
Director of the Air and Waste Management Division, who organized
and obtained the necessary federal funding.

     Oversight of the overall project was provided by a
Management Steering Committee and oversight of specific
activities, by a Project Work Group.  The members of these groups
are listed in Volume II of the report.  The Project Coordinators
for EPA, Robert Kelly, Rudolph K. Kapichak, and Carol Bellizzi,
were responsible for the final preparation of this document and
for editing the materials provided by the project subcommittee
chairs.  William Baker facilitated the coordinators' work.

     Drs. Edward Ferrand and, later, Dr. Theo. J. Kneip, working
under contract for EPA, wrote several sections, coordinated
others, and provided a technical review of the work.

     The project was made possible by the strong commitment it
received from its inception by Christopher Daggett as Regional
Administrator (RA) for EPA Region II, and by the continuing
support it received from William Muszynski as Acting RA and as
Deputy RA, and from Constantine Sidamon-Eristoff, the current RA.
The project has received considerable support from the other

-------
project organizations via the Management Steering Committee,
whose members are listed in Volume II.
                               ii

-------
 PREFACE - DESCRIPTION OF THE STATEN ISLAND/NEW JERSEY URBAN AIR
                 TOXICS  ASSESSMENT  PROJECT REPORT


     This report describes a project undertaken by the States of
New York and New Jersey and the United States Environmental
Protection Agency with the assistance of the College of Staten
Island, the University of Medicine and Dentistry of New Jersey
and, as a contractor, the New Jersey Institute of Technology.

     Volume I contains the historical basis for the project and a
summary of Volumes II, III, IV, and V of the project report.

     Volume II of the report lists the objectives necessary for
achieving the overall purpose of the project, the organizational
structure of the project, and the tasks and responsibilities
assigned to the participants.

     Volume III of the report presents the results and discussion
of each portion of the project for ambient air.  It includes
monitoring data, the emission inventory, the results of the
source identification analyses, and comparisons of the monitoring
results with the results of other studies.   Volume III is divided
into Part A for volatile organic compounds,  and Part B for
metals, benzo[a]pyrene  (BaP), and formaldehyde.  Part B includes
the quality assurance (QA) reports for the metals, BaP, and
formaldehyde.

     Volume IV presents the results and discussion for the indoor
air study performed in this project.  It contains the QA reports
for the indoor air study, and a paper on the method for sampling
formaldehyde.

     Volume V presents the results of the detailed statistical
analysis of the VOCs data, and the exposure and health risk
analyses for the project.

     Volume VI, in two parts, consists of information on air
quality in the project area prior to the SI/NJ UATAP; quality
assurance (QA) reports that supplement the QA information in
Volume III,  Parts A and B; the detailed workplans and QA plans of
each of the technical subcommittees; the QA reports prepared by
the organizations that analyzed the VOC samples; descriptions of
the sampling sites; assessment of the meteorological sites; and a
paper on emissions inventory development for publicly-owned
treatment works.

     The AIRS database is the resource for recovery of the daily
data for the project.  The quarterly summary reports from the
sampling organizations are available on a computer diskette from
the National Technical Information Service.
                               iii

-------
                     STATEN ISLAND/NEW JERSEY
               URBAN AIR TOXICS ASSESSMENT PROJECT
VOLUME VI.  APPENDICES
                                        PART A, EPA/902/R-93-001g
                                        PART B, EPA/902/R-93-001h
                        TABLE OF CONTENTS
PART A
     1. DESCRIPTION OF APPENDICES 	 1-1
     2. AIR QUALITY HISTORY IN THE PROJECT AREA	2-1
     3. AIR QUALITY MONITORING PRIOR TO THE INITIATION
          OF THE PROJECT	3-1
     4. SUBCOMMITTEE WORKPLANS AND QUALITY ASSURANCE PLANS    4-1
     5. MEMORANDUM ON FIELD TRIP TO METEOROLOGICAL SITES  .  . 5-1
     6. SAMPLING SITE DESCRIPTION REPORTS 	 6-1
     7. QUALITY ASSURANCE SUBCOMMITTEE REPORTS  	 7-1

PART B
     8. NYSDEC VOCS QUALITY ASSURANCE REPORT  	 8-1
     9. CSI VOCS QUALITY ASSURANCE REPORT	9-1
    10. NJIT VOCS QUALITY ASSURANCE REPORT  .	10-1
    11. PAPER ON EMISSIONS INVENTORY DEVELOPMENT
          FOR PUBLICLY-OWNED TREATMENT WORKS  	   11-1
    12. SUPPORT DOCUMENTS FOR REFERENCE CONCENTRATIONS AND
          INHALATION UNIT RISK FACTORS FROM THE INTEGRATED
          RISK INFORMATION SYSTEM 	   12-1
    13. SUPPORT DOCUMENTS FOR REFERENCE CONCENTRATIONS
          FROM THE NEW YORK STATE DEPARTMENT OF HEALTH  .  .   13-1
    14. MEMORANDUM ON THE REFERENCE CONCENTRATION
          FOR CHROMIUM	14-1
    15. MEMORANDUM ON THE REFERENCE CONCENTRATION
          FOR XYLENE	15-1
    16. MEMORANDUM ON WEIGHT-OF-EVIDENCE CLASSIFICATIONS
          OF TETRACHLOROETHYLENE AND TRICHLOROETHYLENE  .  .   16-1
    17. TOXICOLOGICAL SUMMARIES FOR CHEMICALS  NOT INCLUDED
          IN THE QUANTITATIVE RISK ASSESSMENT  FOR THE
          SI/NJ UATAP	17-1
                               iv

-------
8.  NYSDEC VOCS QUALITY ASSURANCE REPORT
               8-

-------
 New York State Department of
   Environmental Conservation
    Division of Air Resources
    Staten  Island Toxics Study
         1987  -  1989

   Quality  Assurance Summary
          Prepared by
   Bureau of Toxic  Air Sampling
Bureau of Air Quality  Surveillance
   Bureau of Technical  Services

          April  1990
               8- 2

-------
                          Table of Content

Introduction

Map of Sampling Network

Chapter I.   Blanks (Page 5)

Chapter 2.   Duplicate Samples (page 9)
             a. Tabulation of data by quarter
             b. Bar graphs of precision data by
             quarter

Chapter 3.   Distributed volume tables (Page 38)

Chapter 4.   Tenax vs. Cansiter (Page 45)

Chapter 5,   Minimum analytical Detection Limits (Page 51)
             Summary Table

Chapter 6.   Accuracy Assessment (Page 53)
             a. 1988 Gas Chromatograph Performance
                Audit
             b. 1988 1st Quarter Gas Chroraatograph
                Performance Audit
             c. 1988 3rd Quarter Gas Chromatograph
                Performance Audit

Chapter 7.   Chronological Log (Page 63)
             Narrative Summaries by Quarter

Chapter 8.   Assessment of Variability of Data  (Page 72)
             Narrative by Quarter

Chapter 9.   Miscellaneous  /page 82)
             a. Summary of Data Availability
             b. Permeation Tube Calibration System
                Flow Audits and Calibrations
             c. Quality Assurance Laboratory
                Certification Procedures
             d. Flow Performance Audits
             e. Report on Effectiveness of Gravity
                Valve in Prevention of Passive
                Sampling of Sorbent Tubes
             f. Standard Operating Procedure for
                Envirochem Thermal Desorbtion Hewlett
                Packard Analytical System
             g. Staten Island/Northern New Jersey Urban
                Air Toxics Assessment Project Quality
                Assurance Subcommittee Audit Report
                               8-

-------
                              -2-
Appendix A:  Results of 1989 Gas Chromatograph (Page 127)
             Performance Audits

         B:  A Sample of a Field Flow Performance (Page 132)
             Audit

         C.  Sample Precision Analysis Data (Page 173)

         O.  Sample Tabulation and Calculations for (Page 203)
             Distributed Volumes

-------
                          INTRODUCTION
                    STATEN ISLAND TOXICS STUDY

     The goal of the Staten Island Toxics Study was to provide an
assessment  of  the  magnitude  and  distribution  of  toxic  air
pollutants on Staten Island and nearby New Jersey counties and to
develop the  methodology  to  accomplish this task.   This project,
begun in 1987, was a cooperative effort involving various State and
Federal  agencies as  well  as academia,  EPA,   NYSDEC and  NJDEP
provided  the funding  for this  project.    EPA provided  project
coordination.

     An  integral element of  this  project  has been  the  quality
control/quality  assurance procedures that were  established from
project inception.   These procedures were performed for both sample
collection and sample analysis.  The  Quality Assurance Section, in
addition,  performed  independent  flow  audits on  the  sampling
equipment and arranged, with assistance from EPA, to perform audits
on the gas chromatograph used to analyze the samples collected.

     The  Staten Island  Project  allowed DEC  to  develop  a  VOC
monitoring network that will be used throughout the State.

     The developmental work completed during  the  2  year project
progressed  from manual  equipment  and  a  basic plan to  a  fully
automated laboratory analytical system and fully operational field
sampling program.
                              8-

-------
     The  data obtained is  generally  very good with  the  first 2
quarters  (4th *87 and  1st  X88) being the weakest as we progressed
on the  learning  curve.   The 17 analytes monitored have proved to
be an effective  choice for  statewide monitoring.

     The  only portion of  our voc plan  that did not develop as
planned was  the realtime  automated  gas  chromatograph  station.
Staff transfers and shortages ended any possibility of testing and
developing a  system for deployment in  this project.  Review of one
year of auto GC data revealed  it to be invalid because  of valve and
software malfunctions.

     The  NYSDEC  VOC  monitoring  network by the  end  of  1989
encompasses 3 Bureaus  and  Region 2 for field sampling, analysis,
calibration and  quality assurance of  the systems.   General VOC
accuracy is +/~  30% with some analytes better and some worse.  A
realistic goal of +/" 20%  is possible as we correct individual
analyte problems.   A major accomplishment was the use  of three
sample  tubes  (2 hi,  1  lo flow)  for each sample run.  Comparison of
the hi  flow duplicates  allows us to determine the 95% confidence
limits  of the measurement precision which ranged from 20% to 80%.
Graphical presentation of the precision information is  in the text.

     Precision and accuracy numbers which range as high as +/- 50%
may seem large while actually being very respectable for this low
level ambient  toxic air monitoring program.   In  many  cases these

-------
percentages reflect data differences of only  fractions  of a part
per billion.

     Following  is  a  summary of  the essential  elements  of  the
Quality Assurance,  sample analysis and monitoring effort.

90-3-16
                             8-   7

-------
    1
          p
        Elizabeth
                                   New/York  4
*Lft
*&
ITTTl
/
       ~/
         i'.-l
                  TORT ELIZABETH  / <

                          .  CJ
                      /' ^  -A
                   •/   _J /Wfi!^
                   ^,T^j - !T*n" N_/-4''y'*Iffr''
                                          .rf^o1
                                           1*- -
                      ..*  |L»
                    Port Richmond r..
                       7097-03
                                                          ,: «'8|t
    ".  t.
                      : b-r
                                    "•» 1
                                          < wwJ
                                  ;--?>jOcSiw
                                 •Si:. g^»ftJ.-
                                                            '.f.K
                        •~*---£/;i
   Und<
      Staten Island Mall
    ^'   7097-08
         "5k^7r/
                            ^,'5.
                  \« -v
                  \Vf*»l«ri«i
                  ... i Ccmn
                   I
                asssrtf
               «T
                 .Tt!
                                         Susan Wagner HS
                                             7097-01     !v
                                                  4, ^*-
     PS 26
   7097-02
                        >,..
            I
       .Carteret"
                       ViK'
                        »  *»!)•

                    ' STATED
                     /  /.
      •Vx/^'.lV  ''v/^

 Port fitiomg
         ••c»i.,in
             ^i
               .c*>.
              &i
           \\ RICH-
           Vi MONO

           ISLANI
                 •,
                      .*^»r.«»a
                fl
                    ufu*no<
                        «
                       t^
th
\r
«P..
^
.JMi
    fc YT.n.
        ^
                 ^r^CMJ
/
          Tottenville
           7097-05
                                    Great Kills
                                    7097-06
                                           Staten Island
                                       Toxics Survey Project

-------
         Chapter 1




Summary of Field Blank Data
     8-

-------
                 N.Y.S. DEC STATEN ISLAND PROJECT
                    SUMMARY OF FIELD  BLANK DATA

     Table 1-1 is a listing of the average blank values obtained
during the S.I.N.J. monitoring project.  The 2 analytical methods
are separate as the adsorption tubes and desorbtion systems
were very different.
     During the 2nd quarter of 1986 the average of the last
5 blanks were subtracted from the sample prior to the calculations
of the ppb concentration value.  This process was then used
for the duration of the project.
     The ENV data shows a gradual increase in the benzene and
toluene blanks.  This is probably due to the aging of the tenax
in the adsorbtion tubes used during the first year.  The Envirochem
System tubes were made of glass and during the study the tenax
portion of the tubes became noticeably more brown with repeated
cleaning and use.
     The changeover to the ATD (Automatic Thermal Desportion)
system brought brand new tubes and a  storage system that was
not as effective as the Envirochem1s.
     The 0-ring sealed caps supplied  by the manufacturer did
not seal the samples as well or the teflon capped vials used
by Envirochem.
                           8-  10

-------
OTR & OO   Dli:H-ORCMEThflMF.


190? OnTRCJS)         HF


                      NF


                      NF


                      NF
1ST OTR 88
2ND DTK 88 ENU<15>
3RD OTR 88 EHVJ'.F)


    OTR 88 EMK13)
               IH


ill TPICtCOPlltTHHrC


         HF





         NF


         HF


         HF
                                                           IF
                                                                                          dev>
(KHZE'IE.  JCLUIiNE  ETHVlBElgENC    M.P-XYLEI€  Q-XVLENE 13 DtCHl.fJBEriZ


[»i=.l(lt.> 12-91'1O) [2U(17>           NF       [21(2)      NF


[l>41f!8) 1161(6)  [71«.4>             NF          NF       IIP


[411(16) [191.; 3)  IS]>.4>          [171(14)       if    [21(1)


iniKMID 1231(8)  141(2)          [33(5)         NF    I2K.2)


(•I21f;»3) [261(10) [51(2)             NF          NF    (31(1)
	88 RTO<19)    (181(14)


1ST OTR 89 BTD(24).    [71(6>


2NQ OTR 89 fiTO_«i_24_)    1161 (24)


3M1 OTR 89 flTO
                                        [211<20>
                                        C51<5>
(J4KU)  [631(49) [51(3)


I231C7)  [721(61> [41(3)


[311111) [761(40)


         [421«47>
                                                                                        C151C8>


                                                                                        1121(11)


                                                                                        £141(9)


                                                                                        [61(9)
                                                                                                     C41C2)
                                                                      141(3)


                                                                      121(4)
                                                        [4K5>


                                                        [6J-.4)


                                                        CI5K5)


                                                        [91(12)
oo
I

-------
    Chapter 2




Duplicate Samples
       8-   12

-------
                                                                            10




                      SAMPLE PRECISION ANALYSIS
     Duplicate samples were analyzed on the gas chromatograph routinely




to evaluate sample analysis precision.








     Every sampling event was done in triplicate.  Two adsorption




tubes at normal sample volume and one at a low sample volume for




distributed volume statistics.








     In reviewing the following data the following should be noted:








     1.  Even though the 95% confidence limits appear wide, the




         means are generally very low and the data will be used




         based upon computed annual averages.








     2.  These 95% confidence limits appear wide, the means are




         generally very low and the data will be used based upon




         computed annual averages.








     3.  Even errors of 50% represent fractions of a part per billion




         at the concentrations being measured.








     Following is a summary of these precision results by quarter




both in tabular and graphical form.  Appendix C contains the details




of this sample precision analysis.
                          8-   13

-------
                                                                  11
                 Staten Island  Toxics Study
                       4th Quarter 1987
                  Sample Precision Analysis
                          Envirochem
Compound
Dichloromethane
Chloroform
1,2 Dichloroethane
1,1,1 Trichloroethane
Benzene
Carbon Tetrachloride
Tzichloroethylene
1,1,2 TrIchloroethane
Toluene
Tetrachloroethylene
Chlorobenzene
Ethylbenzene
M,P-Xylene
0-Xylene
1,3 Oichlorobenzene
1,4 Dichlorobenzene
1,2 Dichlorobenzene
* Insufficient data pairs to evaluate statistically
Mo.
15
3*
2*
22
23
0*
4
0*
21
20
0*
21
23
23
10
•0
*0
Mean
5.4


2.0
3.4

8.3

1.1
0.4

-0.2
3.0
2.6
13.2


Std.
Dev.
24.4


16.7
27.5

15.3

19.1
18.2

23.0
17.2
16.4
15.3


Lover
Limit
-42


-31
-51

-22

-36
-35

-45
-31
-30
-17


Upper
Limit
4-53


+35
+57

+ 38

+39
+36

+ 45
+37
+35
+43


                          8-  14

-------
                                                                  13
                 Staten Island  Toxics Study
                       2nd Quarter 1988
                  Sample Precision Analysis
                          Bnvirochem
Compound
Dichloronethane
Chloroform
1,2 Dichloroethane
1,1/1 Trichloroethane
Benzene
Carbon Tetrachloride
Trichloroethylene
1/1,2 Trichloroethane
Toluene
Tetrachloroethylene
Chlorobenzene
Ethylbenzene
M/P-Xylene
0-Xylene
1,3 Dichlorobenzene
1,4 Dichlorobenzene
1,2 Dichlorobenzene
* Insufficient data pairs
Mo.
16
14
4
35
24
14
17
0*
34
28
5
28
36
33
19
.•*
B*
Mean
-2.7
-4.7
-0.5
1.7
2.5
10.5
-6.4

-2.0
1.5
-10.2
-0.2
4.9
1.0
0.5


Std.
Dev.
13.9
13.5
11.7
13.2
27.2
24.7
20.9

11.7
5.6
14.1
10.5
30.9
6.0
7.5


Lover
Limit
-30
-31
-24
-24
-51
-38
-47

- -25
-9
-38
-21
-56
-11
-14


Upper
Limit
4-24
+22
+23
+28
+ 56
+59
+ 35

+ 21
+12
+17
+20
+65
+13
+15


to evaluate statistically
                          8-  15

-------
                                                                  15
                 Staten Island  Toxics Study
                       3rd Quarter 1988
                  Sample Precision Analysis
                             ATO
Compound                  No.    Mean   Std.   Lover  Upper
                                        Oev.   Limit  Limit
Dichloromethane           6      13.7   18.8   -23    +51
Chloroform                6      2.7    38.1   -72    +77
1/2 Dichloroethane        1*
1,1,1 Trichloroethane     6      12.2   38.0   -63    +87
Benzene                   8      -9.5   47.7   -103   +84
Carbon Tetrachloride      8*
Trichloroethylene         4      12.5   59.9   -105   +130
1,1,2 Trichloroethane     0*
Toluene                   9      11.1   20.0   -28    +50
Tetrachloroethylene       9      6.8    10.5   -14    +27
Chlorobenzene             0*
Ethylbenzene              9      10.6   19.3   -27    +48
M,P-Xylene                9      7.4    14.5   -21    +35
0-Xylene                  9      8.4    17.1   -25    +42
1,3 Dichlorobenzene       0*
1,4 Dichlorobenzene       5      22.5   16.4   -10    +55
1,2 Dichlorobenzene       2*
* Insufficient data pairs to evaluate statistically
                          8-  16

-------
                                                                 17
                 Staten Island  Toxics Study
                       4th Quarter 1938
                  Sample Precision Analysis
                              &TD
Compound                  Mo.    Mean   Std.   Lover  Upper
                                        Oev.   Limit  Limit
Dlchloromethane           33     1.4    18.3   -34    +37
Chlorofora                27     -4.3   21.3   -46    +37
1,2 Dichloroethane        1*
1,1,1 Trichloroethane     44     -8.4   42.0   -91    +74
Benzene                   48     -0.8   36.8   -73    +71
Carbon Tetrachloride      9      -3.0   31.2   -64    +58
Trichloroethylene         31     1.5    36.7   -71    +73
1,1,2 Trichlotoethane     f*
Toluene                   52     1.9    23.8   -45    +49
Tetrachloroethylene       46     1.1    13.6   -26    +28
Chlorobenzene             4*
Ethylbenzene              58     -0.7   11.7   -24    +22
M,P-Xylene                52     2.4    16.0   -29    +34
0-Xylene                  37     0.3    10.8   -21    +21
1,3 Dichlorobenzene       15     -3.8   22.3   -47    +40
1,4 Dichlorobenzene       5      -29    41.0   -108   +51
1,2 Dichlorobenzene       0*
* Insufficient data pairs to evaluate statistically
                        8-  17

-------
                                                                  19
                 Staten Island  Toxics Study
                       2nd Quarter 1989
                  Sample Precision Analysis
                              ATD
Compound                  No.    Mean   Std.   Lover  Upper
                                        Dev.   Limit  Limit
Dichloromethane           36     -1.5   29.3   -59    +56
Chloroform                23     4.8    13.8   -23    +31
1,2 Dichloroethane        12     0.5    25.5   -51    +50
1,1,1 Trichloroethane     68     -1.0   25.3   -51    +48
Benzene                   64     7.5    22.9   -37    +52
Carbon Tetrachloride      24     6.2    27.4   -47    +60
Trichloroethylene         60     -7.0   36.6   -79    +65
1,1,2 Trichloroethane     0*
Toluene                   73     5.8    33.3   -60    +71
Tetrachloroethylene       62     0.9    14.2   -27    +29
Chlorobenzene             8      301    21.4   -39    +45
Ethylbenzene              71     5.7    23.9   -41    +53
M,P-Xylene                73     -1.6   21.2   -43    +40
0-Xylene                  73     2.2    13.4   -24    +28
1,3 Dichlorobenzene       39     -5.8   33.3   -71    +60
1,4 Dichlorobenzene       0*
1,2 Dichlorobenzene       0*
* Insufficient data pairs to evaluate statistically
                          8-  18

-------
                                                          21
                 1987 -1989
         STATEN ISLAND TOXICS STUDY
         SAMPLE PRECISION ANALYSIS
            DICHLOROMETHANE
400-
•0-
TO-
CO*
50-
£ 40-
bJ
0 30-
bJ
O. 20
»
bJ 40'
_i O-
Ul
0 -(0
bJ
0 -20-
§ -SO
« -*o
S -W
-SO-
-TO
•80
-»0
•400
1













;--*-|
x
_y
^r
x
^x
x^
X
^^
x
x
X
x
X
X
X
X
X
X
x
x!
X
X
x
x
i^-tf















4ttiOtr.
087




i









^
x
x
x
x
x
x
x
x
x
[x
X
x
x
x
x
x^
X
X
X
^















1st Otr.







— .
"-"^
X
x
x
X
X
x
X
X







2nd Otr.
• «







X
x
X
X
X
x
X
Ld
•^•™






—







3rd Otr.






•^••i
X
x
x
X
X
X
X
__






—






4ttiOU.















—









••^•i















4dOtr.















••^••i



























X

NtfC
198
)tr.














MMM








•••I















BftfOtr.





















SAMPLING METHOD

     EHVIROCHEM
     ATD
                     8-   19

-------
                                                              23
                   1987 - t989
            STATEN ISLAND TOXICS STUDY
            SAMPLE PRECISION ANALYSIS
                     BENZENE
100
»0
•0
70
60-
50'
£ 40-
la
0 50
AiJ
* 20
£ <0
u


UJ
0 HO-
lu
9 -20'

§ -SO
o
0 -40-
8 -90-
-60-
-TO-
-BO-
•90-
-400-




















P""
X
X
X
X
X
X
X
X
X
X
_^


X

X

X
X
X


X
x
x
^
s*
-S
_x^
^
s^
x
x
x
__J



















J«t fM*




















»—
X
X
X
X
_^
^
X
X
X
X
^
s^
X
X
,x
yT

!x
x
X
j^^
_^
^^
.s
^
x1
/
x
x
x
-d




















n.^ rw.








X
X
X
X


*^
X
X
X
X




























J
H03
m.^ A*.




X
X
^
^
^
x


I^x
K
Cx
Lx"
X
X
p



—




















^*^ *kA.




















••M































•*- - 4hM._


















1
"•












•i^H



















M . ^ -




















iHHB













— ^^













































1»87  H-
                  19SS
SAMPLING METHOD

     ENVffiOCHEM

     ATO
                      8-  20

-------
                                                     25
           1987 - 1989
    STATEN ISLAND TOXICS STUDY
    SAMPLE PRECISION ANALYSIS
            TOLUENE
100
90
to
TO
CO
SO-
ti; 40-
UJ
0 50-
UJ
a 20-
UJ 40-
-J 0-
w
0 -40-
0 -»•
0 -SO-
u
e -40-
g -50-
-60-
.70-
•80-
•90<
-<00-






PT3






^~
x
X
x
x
.X
X
X
?*•
X
X
X
X
X
^x
x^
X
^












4ffiOtr.
1987













•MM
x
x
x
x
x
X
x
X
X
X
x
^^
S^^
^






K-J





1H Oir.



























j;
X
k\\\\\l








2nd





















Oir.
*l






F5
Ex
^
^
X
x
x
1^
—













9*4
188-









k




H^IH







^_










__
































i











^^H



























Otr. 4fhOtr. IflOtr. 1

^1
196
















^^m































Mr. MOtr.

   METHOD
ENVHOCHEM
              8-  21

-------
                                                             27
                  1987-1989
          STATEN ISLAND TOXICS STUDY
          SAMPLE PRECISION ANALYSIS
400'
•0-
•0-
TO
«0-
50
£ 40-
kl
g 90
£ 20
g .0-
_l 0-
kJ
0 -20
5 -»o
*s *40
m -90
•TO
•to
•90
' "°°










4


^
^
X
X
£
<^











1M7















^~
X
/
x
X
/
X
x
x
X
X
X
X
X
x
X
X
x
xj
X
X*
X
x
^ .
X
X
•M













•««tOtr.















x
x
x
x
x
x
^
x^
x
^
^
x
x
x
X
x
x
x
x
X
X
X
X
X
^x
x^
X
X
X














ludOir.
AM
!• 	 — ^






^
^
^
^
x
^•M










— 1






V









^
^
i^


















•







































•^






































^™






H^M












IQtr. -««0tr. -tefOtr. ft




MC
IM





















I^^H






























Kr Irt Off.

SAMPLING MTTHOO

      CWVROCHEM

      ATO
                       8-  22

-------
                                                              29
                  1987 -1989
           STATEN ISLAND TOXICS STUDY
           SAMPLE PRECISION ANALYSIS
             1.2 DICHLOROBEN2ENE
100-
•0-
•0-
TO-
CO-
SO-
£ 40-
UJ
§ "•
Q.^ 20-
-J
UJ 40-
UJ
-J 0-
UJ
o - «w
-70-
-•0-
-to-
-100-








ENV
*






4ft Otr.
MI7 1








ENV















ENV
-K-















ENV ATD















ENV «TD
^^ ^^»
^^ ^^»






^vtll wtF.















^Otr.








ATO



















—



MM

























        DATA NURS TO EVNUOUTC ST^HTCALLY


SAMPLING METHOD
I    I ATD
                    8-   23

-------
                                                                31
                       1987 -1969
                STATEN ISLAND TOXICS STUDY
                SAMPLE PRECISION ANALYSIS
                 1,1,1 TRICHLOROETHANE
UJ
^
UJ
o.

>
UJ
^
UJ
o
\L.
I
400 <
80 <
TO-
60<
SO-
40-

SO-
20-
HO-
•20-
-SO-
-40-
-50-
•60-
-ro-
-80-
HOC-






^n
s
\x\\\\\
'•
L\\\\\\\









4thOtr.
4fl«7 I











?
S
^^
\\x\\\x
NXXXXXXXN
Ld










1st Olr.
u










k\\\\\\i
^







—— «»






^
^
|OOA\\Y
^
S














J








pn
s
^
\\\\\\>
\\\\\\\Y
*-
l^























41k On.














^^m






















u 	 '. —












^••^






mtmf
























—








SfriOtr.
















     SAMPLING METHOD
     I   »  *TO
                          8-  24

-------
                                                              33
                   1987 - 1989
            STATEN ISLAND TOXICS STUDY
            SAMPLE PRECISION ANALYSIS
            1,i,2  TRICHLOROETHANE
100-
•0-
to-
70
•0'
SO-
, PERCENT
l» W *
000
lit
mi
Ui 40-
UJ
UJ
u .40 •
Ut
9 -20-
S -SO-
U
ff> -50'
-60-
•70-
-80-
•to-
HOC-







ENV
•)f








4ttiO»r.
MIT 1







ENV
^








1H Qtr.
1






ENV
7>








2nd On.







ENV ATO
* «*









1






ENV ATO
* *








*»»».
1






ATO
*
















ATO
*
















ATD


























'MSUFFOENT OCTA nuts TO EWU.UATE STATOTCAU.Y

 SAMPLING MTTHOD
      ATD
                       8-  25

-------
                                                            35
                   1987 - 1989
           STATEN ISLAND TOXICS STUDY
           SAMPLE PRECISION ANALYSIS

                 ETHYLBENZENE
100
to
ao
TO
€0
50
£ 40-
bJ
^ SO
UJ
B^ 20
«T
U 40-
U)
-I O-
u
0 .10
8 .*>.
§ -30
o
. *40'
£ -5O-
-TO-
•to-
•to-
-WO •


















r—
X
j^
^^
^^
r
X
X
X
X
x
X
X
X
x
X
X
X
x
~ ^
^
^
^^
J^
x
^
















4«iQtr.



















>•"
X
X
X
__^
jr
X
^^
jr
s*
x
X
^
^
_^*
^
X
x
x
x
x
x
x
x
x
*^
x
x
MM


















let Otr.






















2n
1»87 H 	










r?i
x^
x
x
X
x





























dOtr.






^


^
X
X
X
X
X
x
x
X
x








u







MOtr.









^.^
[x
^x
p'
i





























^MOtr.
If88 	



























^"*






UtOtr.

















•^^











HHH

















2i«0tr

















•••





























5f«0tr.























SAMPLING MFTMOP

     ENVIROCHEM
LH3
                     8-  26

-------
                                                              37
                  1987 - 1989
           STATEN ISLAND TOXICS STUDY
           SAMPLE PRECISION ANALYSIS

             1,4 DICH LORD BENZENE
100-
90*
§0-
TO-
eo-
SO-
, PERCENT
Ml**
000
III
UJ 40-
bJ
^ -«0-
bJ
9 -20-
5 -so-
u
jj «
S -W-
-SO-
.TO-
•to-
-',"'







ENV






4ttiOtr.
«*»7







ENV






«« Oir.







ENV
*






tndOtr.
_— 11







ENV
^





—





MOtr.
•e-







ENV






-4lti(
^








«oe
^»»















i^








•HtOtr.







ATD






Si^Otr.







ATD






MOtr.















        0«TA WUW TO CVM.UATE !T*rSTeAU.V


SAMPLIMS METHOD

      ENVMOCHEM
      ATO
                         8-  27

-------
                                                      38
     Chapter 3




Distributive Volumes
       8-  28

-------
          OKHNIZRT1OH: NEH YORK SIHIt
                                   QURRTER OF OCTOOCR TO DECEMBER ,  1967

                                             DISTRIBUTED VOLUMES
COMPOUND
« PR IRS
RUN
RUERRGE
DIFFERENCE
(PPB)
STO. OEV.
RUG. OIFF.
 0.05

-------
                                     QUARTER OF JULY TO SEPTEMBER,  1968

                                               DISTRIBUTED VOLUMES
            COMPOUND
           TOLUENE
           BENZENE
           M.P XVLENE
            1,1,1  TRICHLOROETHRNE
           TETRfiCHLOROETHYLENE
           DICHLOROMETHflNE
           CflRBON TETRRCHLORIDE
           ETHYLBENZENE
           CHLOROFORM
           0 XYLENE

           NOTES  HTTfCHED (Y/N):
PRIRS
RUN
  16
  13
  15
  16
  14
  15
  RUERRGE
DIFFERENCE
           
            LL       UL
     NO DflTR RWILRBLE
  16      -0.02
  11       0.02
  16       0.00
0.13
0.13
0.05
0.02
O.OO
O.OS
0.01
0.02
0.01
-0.15
-0.04
-0.04
-0.03
O.OO
0.02
-0.05
-0.02
-0.03
0.41
0.52
0.20
0.07
0.02
0.24
0.01
0.06
0.03
T > 0705
 
                                 N
                                 N
                                 N
                                 N
                                 V
                                 V

                                 N
                                 N
                                 N
oa
OURRTER OF OCTOBER TO DECEMBER, 1999
DISTRIBUTED VOLUMES
COMPOUND



TOLUENE
BENZENE
N/P XYLENE
1.1,1 TRICHLOROETHRNE
TETRRCHLOROETHYLENE
OICHLOROMETHRNE
CARBON TETPRCHLORIDE
ETHYLBENZENE
CHLOROFORM
0 XYLENE
• PRIRS RUERRGC
RUN


35
33
32
32
32
32
DIFFERENCE


0.04
0.00
0.05
0.01
0.00
0.06
STD. OEV.
RUG. DIFF.
(PPB)

0.05
0.07
0.02
0.02
0.00
0.02
95% CL

1NTERURL

LL
-0.07
-0.14
0.01
-0.03
-0.01
0.01

UL
0.15
0.14
0.09
0.05
0.01
0.11
T > 0.05



N
N
Y
N
N
Y
NO DflTR AURILRBLE
34
22
32
0.00
0.00
0.00
0.02
0.01
0.01
-0.04
-0.01
-0.01
0.04
0.01
0.01
N
N
N
           NOTES ATTRCHEO :

-------
                    ton; nc.* ICNUS
                                    QUARTER OF JANUARY TO MRRCH, 1989

                                              DISTRIBUTED VOLUMES
COMPOUND



TOLUENE
BENZENE
M,P XYLENE
1,1.1 TRICHLOPOETHRNE
OTRACHLOROETHYLENE
OICHLOROMETHRNE
CflRBON TETRRCHLORIOE
ETHYLBENZENE
CHLOROFORM
0 XYLENE
• PRIRS
RUN


74
73
74
71
68
66
68
72
58
74
AVERAGE
DIFFERENCE
(PPB)

0.39
-0.06
0.07
0.02
0.01
-0.02
0.00
0.02
-0.01
0.02
STO. OEM.
BVG. OIFF.
(PPB)

0.10
0.04
0.03
0.02
0.01
0.05
0.00
0.01
0.01
0.01
95X CL

INTERMRL
(PPB)
LL
0.19
-0.14
0.01
-0.02
-0.01
-0.11
-0.01
0.00
-0.03
0.00

UL
0.59
0.02
0.13
0.06
0.03
0.07
0.01
0.04
0.01
0.04
T > 0.05
(Y/N>


V
N
Y
N
N
N
N
Y
N
Y
           NOTES RrnCHED CY/N):
oo
I
QUARTER OF RPRIL TO JUNE, 1989

          DISTRIBUTED VOLUMES
COMPOUND
• PAIRS
RUN
AVERAGE
DIFFERENCE
(PPB)
STD. OEV.
AVG. DIFF.
(PPB)
95X CL
INTERVAL
(PPB)
LL UL
T > 0.05
(Y/N)
           TOLUENE
           BENZENE
           h/P XYLENE
           1,1,1 TRICHLOROETHANE
           TETRACHLOROETHYLENE
           DICHLOROMETHANE
           CflRBON TETRACHLORIDE
           ETHYLBENZENE
           CMLOROFORH
           0 XYLENE
68
65
70
67
67
53
59
70
45
TO
0.10
-0.04
-0.01
0.01
0.08
0.02
0.01
0.03
0.01
0.00
0.15
0.04
0.04
0.02
0.04
0.07
0.00
0.02
0.00
0.01
-0.21
-0.11
-0.09
-0.03
0.00
-0.12
0.00
0.00
0.00
-0.03
0.41
0.03
0.07
0.05
0.16
0.16
0.02
0.06
0.02
0.03
                                                           N
                                                           N
                                                           N
                                                           N
                                                           Y
                                                           N
                                                           Y
                                                           N
                                                           Y
                                                           N
           NOTES ATTACHED (Y/N):

-------
                                                        45
        Chapter 4




Sorbent Tube vs.  Canister
            8-   32

-------
        ORGflMlZRTIGN:  NEW YORK STATE ENCON                                 SORBEHT: ENUI&OCHEH

                                    OURRTER OF APRIL TO JUNE. 1988
                                     SORBENT TUBE VS. CANISTER
COMPOUND


• PAIRS
RUN

AVERAGE
DIFFERENCE
(PPB)
STO. DEV.
AVG. DIFF.
(PPB)

95XCL



T > 6105
INTERVAL 

(PPB)
LL
TOLUENE
BENZENE
M.P XYLENE
0 XYLENE
1.1.1 TRICHLOROETHANE
TETRACHLOROETHYLENE
OICHLOROHETHANE
CARBON TETRACHLORIDE
11
9
11
B
5
6
5

-0.03
0.32
-0.32
-0.30
-0.16
-0.31
-0.13
NO
0.24
0.27
0.21
0.12
0.19
0.22
0.15
DATA PAIRS
-0.
-0.
-0.
-0.
-0.
-0.
-0.

,56
,30
,78
.58
,68
.88
,54





AVERAGE X
DIFFERENCE

UL
0
0
0
-0
0
0
0

.
.
.
•
.
•
.

50
94
14
02
36
26
28

N
N
N
N
N
N
N

29.5
-17.6
41.1
137.5
B5.9
184.3
80.2

00
'       NOTES ATTACHED (Y/N):
u>

-------
    ORGANIZATION: NEH YORK STRTE ENCON
                                       SORBENT: HTO
                             OURR'ItU OF OCTOBER TO DECEMBER, 1988

                                 SORBENT TUBE VS. CANISTER
    COMPOUND
    TOLUENE
    BENZENE
    M,P XYLENE
    0 XYLENE
    1.1.1 TRICHLDROETHANE
    TETRACHLOROETHYLENE
    DICHLOROHETHANE
    CARBON TETRACHLORIDE
• PAIRS    AVERAGE
  RUN    DIFFERENCE
            
            LL       UL
0.71
0
0.1S
-0.05
-0.16
-0.05
-0.11

Q.24
0.06
0.07
0.05
0.13
0.03
0.11
NO PATA PAIRS
           0.20
          -0.12
           0.00
          -0.15
          -0.46
          -0.13
          -0.34
1.22
0.12
0.30
0.05
0.14
0.03
0.12
        T > 0705
         
-------
     (RGANIZRTION:  NEW YORK STATE ENCON                                SORBENT: flTO


                             OURRTER OF JULY TO SEPTEMBER, 1989

                                  SORBENT TUBE VS. CANISTER

    COMPOUND                    i~PfllRS    ROERRGESTO. DEV.95X CLT > 0.05RVERRGE X
                                  RUN    DIFFERENCE    RUG. DIFF.   INTERVflL                DIFFERENCE
                                                   (PPB>        CPPB)
                                                                   LL       UL

    TOLUENE                         42       O.S9       0.15      0.30      O.BB        Y             -14
    BENZENE                         42      -0.40       O.O4     -O.48     -0.32        N              14
    H.P XYLENE                      42      -0.39       0. IB     -0.75     -O.03        N              30
    0 XYLENE                        41      -O.BO       0.23     -1.26     -0.34        N             227
     1.1.1 TRICH.OROETHHNE           39      -0.24       0.03     -O*30     -0.18        N             109
     TETQflCHLOROETHYLENE             14      -0.16       0.08     -0.33      0.01        N              62
     DICHLOeOMETHflNE                 42      -0.25       O.O3     -0.31     -0.19        N             101
     CRRBON TETRRCHLORIDE             2      -0.12       0.02     -0.23     -0.01        N              17
     NOTES nrrmcHEO :	
09
LJ
Ol
                                                                                                                      U>
                                                                                                                      O

-------
                                                           51
             Chapter 5




Minimum Analytical Detection  Limits
          8-  36

-------
                                                                               52
                  MINIMUM ANALYTICAL DETECTION LIMITS
Chemical

Dichloromethane
Chloroform
1,2 Dichloroethane
1,1,1 Trichloroethane
Benzene
Carbon Tetra Chloride
Trichloroethylene
1,1,2 Trichloroethylene
Toluene
Tetra Chloroethylene
Chlorobenzene
Ethylbenzene
M,P xylene
0-xylene
Dichlorobenzenes
D.L. (NG)

   10
    3
    3
    3
   10
    6
    2
    4
    6
    5
    2
    3
    3
    3
    2
PPBU5 L. Samples)

    .2
    .04
    .04
    .06
    .2
    .06
    .02
    .04
    .1
    .04
    .02
    .04
    .04
    .04
    .02
Samples in the range from 1-3 times the detection limit are not as precise
as values above these limits.  A 50% variation is expected in the
range close to the detection limit.
                               8-   37

-------
                                                      53
     Chapter 6




Instrument Accuracy
      8-   38

-------
                                                                               54
              1988 GAS CHROMATOGRAPH PERFORMANCE AUDITS


During the first full year of this study (19883, blank sample  tubes

were provided to EPA which spike then with various organic compounds

of interest to this study.  These sample tubes were then routinely

analyzed on the gas chromatograph and the results reported to  EPA

who then reported back on the audit results.   The actual results

of the audits can be found in Appendix D.  Following is  a summary

of these results for both audits.
Compound

Chloroform
1,1,1-Trichloroethane
Carbon Tetrachloride
Benzene
1,2-Dichloroethane
Triehloroethylene
Toulene
Tetrachloroethylene
Chlorobenzene
Ethylbenzene
0-xylene
f Spiked
'ubes
22
22
22
22
22
20
22
22
22
22
22

Mean
2.1
-34.3
-27.0
26.9
0.0
-35.6
11. 8
-19.5
-5.3
-6.4
-3.0

Std Dev.
19.2
61.6
31.0
17.4
14.4
10.7
22.8
21.5
15.3
11.8
25.1
UL
LL
Percent
41
89
35
62
29
-14
+35
24
25
17
47
-36
-158
-89
-8
-29
-57
-11
-63
-36
-30
-53
                  UL - Upper 95% confidence level
                  LL - Lower 95% confidence level
                               8-   39

-------
                                                                               55
       1989  PARTICIPATION IN EPA GC PERFORMANCE AUDITS
     Twice during the term of this study, in the 1st quarter and




3rd quarter 1989, an audit of the gas chromatograph used to analyze




the ATD-50 and Envirochem samples was performed.








     The audit gas utilized was loaned to as by Research Triangle




Institute, Center for Environmental Measurements.  This gas was




used to spike 4 sample tubes which were then analyzed on the gas




chromatograph and reported to RTI.  The audit results were then




reported back to us.  The actual results of the audits can be found




in Appendix A.  The following is a statistical summary of the results.
                               8-  40

-------
    Summary of Independent Hazardous Organic Gases Audit Results
                                                                          56
Compound                   n

Chloroform                 3
Carbon  Tetrachloride       3
Methylene Chloride         3
1,2 Dichloroethane         3
Trichloroethylene          2
Benzene                   3
Tetrachloroethytene        3
1,1,1-Trichloroethane      3
Toluene                   3
Chlorobenzene              3
Ethylbenzene               3
Ortho-Xylene               3
UL
                                                            LL
+13.3
-10.3
38.7
3.0
34.5
-3.0
-2.7
-17.7
10.3
-0.7
15.0
-9.0
3.4
9.0
7.0
2.8
1.5
5.4
18.9
11.8
16.0
3.1
2.8
8.5
20.1
7.7
53
8.6
37.5
7.8
35.1
5.9
42.3
5.5
20.6
8.0
6.5
-28.3
25
-2.6
31.5
-13.8
-40.5
-41.3
-21.7
-6.9
9.4
-26.0
                        n-  Number  of samples
                        u-  Mean value
                        ^*-  standard deviation
                        UL- Upper  95% confidence  limit
                        LL- Lower  95% confidence  limit
                              8-  41

-------
                                                      57

    I
50
45
40
3*
30-
25
20
15
10
,
^ 5
<0 0
£.,
-10'
•15-
•20-
•25-
-30-
•35-
-40'
-45-
-50-























1 !
1 ^
v
s
7
X













•C
Carbon Tefroc









!••
/
/
' 'A
^
/
^
x
^









m»
X
/
/
X
/
/
^

/
/
'/
/
<^


I
1
i
^>
<

/, 2 Dichloroe
7
/
j
f.





*B














r
/
\
/
/
^
^
^
^
^
/
^
L^






1
1


Benzene














p-
X
'i
*
',
'
-A



















l^b
r^^
^
7
/

/
/
/
/
/
/
/
/
^
X
^
^
^
^
/
^
/
^
^
i
«
/, / - Trichtoroei
*^











'T
/
^
^
/
^
/
^
/
^
•d







r
X
/
^
X
/
'
j
',
/
^
'/.
O

k
X*
£
1
A
'hlorobenzene
\\\\\^ Fthvi

n /
y *
'
U /
LJ








- 1
•Se
$
\
I
6
IT
^
f
f
1
'
',
/
^





Hazardous Organic Gases Audit Results
       95% Confidence Limits
8-  42

-------
                                                                                  58
                 UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
 \                  ENVIRONMENTAL MONITORING SYSTEMS LABORATORY
„/                           RESEARCH TRIANGLE PARK

-------
                                                                                     59
                                                                                 ^

                         UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
          ,
          5                  iNVIRONMENTAL MONITORING SYSTEMS LABORATORY
         J                           RESEARCH TRIANGLE PARK
    '«. me*<-                             NORTH CAROLINA 2771 1
MEMORAfJDUM

DATE:  SepTember 1, 1988

SUBJ:  Audft ResulTs for Staten  Island Project
FROM:  Howard L. Crist
       PEB/QAD/EMSL (MD-77B)

  TO:  Paul Brown
       Air and Water Section (2ES-MM)
       Reg I on II


     The results of the audit sample analyses from the New York State Depart
ment of Environmental Conservation for the Staten Island Project are  in the
enclosed tables.

     If you have any questions, please call me at FTS 629-2723.

Enclosures

cc:  Garry Boynton, NYS/DEC
     Dick Means. NSI
                                    8-  44

-------
                                                                                    61
                   Table 3.  Percent Bias of  Audit Results
                                    (NYS/DEC)
Bias

chloroform
1,1, 1-tr i ch 1 oroethane
carbon tetrach 1 or ide
benzene
1,2-dlch 1 oroethane
tr i ch 1 oroethy 1 ene
toluene
tetrach 1 oroethy 1 ene
chlorobenzene
ethy 1 benzene
o-xylene


chloroform
1,1, 1-tr i ch 1 oroethane
carbon tetrach lor ide
benzene
1 ,2-d i ch 1 oroethane
tr 1 ch 1 oroethy.lane
toluene
tetrach 1 oroethy lene
chlorobenzene
ethy 1 benzene
o-xylene
T-1
-16
-12
-39
38
11
-28
3.2
-39
-9.1
-20
-20

A002
19
-99
-50
51
10
-41
7.7
-24
-4.6
-5.1
-8.3
T-2
-22
-23
-41
14
-15
-32
-14
-33
-20
-18
-22

A006
11
-99
-46
43
-7.1
-49
76
-26
-11
-9.9
-14
T-3
-15
-8.2
-24
6.0
-9.1
-29
-6.1
-26
-20
-6.9
-7.0

A009
4.2
-98
-55
40
-12
-53
6.8
-29
-13
-12
-16
T-4
-20
-13
-38
28
-0.7
-27
-16
-36
-11
-13
-23

A013
31
-98
-66
57
11
-45
43
-22
-2.9
-3.2
-6.7
T-5
-24
-13
-33
-3.1
-8.2
-27
-5.8
-29
-15
-18
-21
Bias,
A015
10
-98
-53
42
-3.3
-39
42
-24
25
-9.0
-12
T-6
-8.3
-4.9
-15
12
-1.1
-26
-0.2
-28
-7.8
-9.8
-13
%
A021
-4.6
-98
-38
2.6
-19
-39
5.6
-28
-10
-9.5
-12
T-7
-11
-23
-27
36
-19
-21
4.1
-29
-8.7
-3.2
-10

A028
24
-98
-64
45
5.8
-45
43
-25
-8.3
-8.9
-12
T-8
-24
-18
-32
19
-16
-28
-0.3
-35
-20
-11
-14

A043
17
-98
-46
39
-3.3
-42
14
-29
-9.9
-11
-13
T-9
-7.4
-2.1
-16
26
-0.4
-50
0.9
-30
-18
-3.5
-5.4

A046
-15
-98
-35
36
-13
-49
-4.1
-34
-18
-20
-23
         reported - spiked
  Bias « ————  x  100
             spiked
No corrections made for blank background
                                    8-  45

-------
                                                                      63
                    Chapter 7




           Narrative Reports by Quarter




Gas Chromotography Operation and Sample Collection




                   Prepared by




           Bureau of Toxic Air Sampling
                     8-   46

-------
                                                                       64
                            DATA REPORT
                        4th Quarter - 1987

     Envirochem System is running satisfactorily.  The performance
evaluation and shoot out samples indicated problem areas that
allowed us to fine tune the system.

     This quarter's data has several sampling days missing as
logistics and analysis deadlines are being firmed up.

     Data prior to the shoot out is not included, as integration
parameters were changed significantly to increase reliability
and accuracy.

     The analysis time has been shortened to allow all three
sites to be analyzed in one day.  The room must be kept cool
to decrease oven cooling time and integration and data transfer
speeded up.

     This was accomplished by the end of the year, so in 1988
each day's samples will be analyzed in one day.
                           8-  47

-------
                                                                       66
                            DATA REPORT
                        2nd Quarter - 1988

     Data completeness is increasing.

     A variation between the lower volume and higher volume
samples was noted prior to March.  The first stage absorption
time was increased by 257. to insure complete desorbtion of all
samples.  Data variability decreased markedly.  This shows that
breakthrough during sampling is not the problem, but rather,
incomplete desorbtion.  Our gradient tube with tenax, ambersorb
and carbon will help increase our minimum detection level by
increasing sample volume, but we must insure that the sample
is completely desorbed.

     The AID system is being prepared for the July shoot out.
Third quarter data will be compared so a complete changeover
can occur this fall.  The AID system allows for overnight automatic
analysis.
                               8-  48

-------
                                                                       68
                            DATA REPORT
                        4th Quarter - 1988

     Comparison of the colocated samplers at Port Richmond show
• good correlation between the ATD and Envirochem systems.
The conversion to all ATD tubes will be completed for the January
1989 sampling runs.

     The data completeness for this quarter was excellent.
Workload was reduced with the loss of the Texas and UMDNJ contract
cites.  The 6 sites for ATD sampling and the new field log forms
created by Mike Steiniger have helped immensely in decreasing
sampling errors and decreasing sample turnaround time.

     In December, we changed the calibration level for toluene.
Our calibration range now extends from 0 to 7 ppb.  This level
will encompass the vast majority of samples, yet not interfere
with the surrounding peaks because of peak size.
                               8-  49

-------
                                                                       70
                            DATA  REPORT
                        2nd Quarter - 1989

     Mailing problems cropped up again.   The April 22 and June 2
sample runs was lest in the mail.  Discussions with the postal
service have prompted us to change to first class mail only.
Business rate mail is easily lost with no way to trace.  At
$1200 per sample run, we can not afford  to lose 20 AID tubes
at a time.  We will be using next day mail to Staten Island
and certified on the return.  This has worked successfully since
we began this method of shipping.

     Field sampling errors eliminated samples on 4/28 at sites
1 and 6 and 6/9 at site 3.
                                8-  50

-------
                                                            72
            Chapter 8




Assessment of Variability of  Data
              8-  51

-------
                                                                      73
                           CHAPTER VTII
                         PROJECT SUMMARY
     The SI/NJ Toxics Air Monitoring Program was a major success.
Toxic  air monitoring  developed  from 2  or 3  day  studies with
analysis contracted out,  to capabilities for a 12 Station Statewide
network on a 6 day schedule with GC/MS, rapid turnaround, in house
analysis.  The QA procedures work, and accuracy and precision for
most chemicals exceeds EPA Contract Laboratory Program protocols.
The development stage has been completed and routine monitoring is
now a capability.

     The   following  narrative   collects  the  most  pertinent
observations for the Staten Island Project in one chapter.  It is
done in a bulletin form to be concise.

1)  The 4th quarter 87  data while acceptable is the least accurate
of the  study.   The desorbtion  system was  modified.  The data
quantification program was modified extensively prior to 1988 and
sample analysis was spread out  over  2  days.  Analysis times were
trimmed to allow  a  days'  samples to be analyzed in  a single MSD
run.  This reduced the probability of  instrument sensitivity drift.

2)  MDL's were  determined by the method  listed in the  EPA audit
report.   These  values  are conservative and for a  few chemicals,
levels below MDL's were routinely reported.  These values are not

                                8- 52

-------
                                                                     74
as precise or accurate as values 3 times the detection limit.  They
are reported because it was our  feeling that the data  represents
real detects.   All the  data  handling  was  done by computer  and
scanned by staff for obvious irregularities.

3)  Initial calibration procedures included weighing the permeation
tubes  each  quarter to  verify  the certified  permeation  rate.
Humidity,  static  and other  unknown problems  prevented us  from
continuing this verification method.   Tubes  were checked twice a
year to insure enough  chemical  to permeate.   We  now use  the
certified  rate  and replace tubes when  they reach 3/4  empty as
permeation rates begin to change significantly at this  point.

4)  The  Dichloromethane values for 1989 are biased approximately
25% high.  The permeation tube was not replaced on time and both
data and QA  checks  for 1989 indicated  a positive bias.   The data
has not been corrected for measurement bias.

5)  The  trichloroethylene  values for the 3rd quarter  89 are NOT
VALID.   Calibration problems existed throughout the year resulting
in  a +25%  bias for the  first quarter  89  and +50% bias for the
second quarter 89.   The data has  not been corrected for this bias.

6)  Blank  data usage changed  in  early  1988  from subtracting that
sampling days' blank from the samples averaging the last 5 blanks
and subtracting the average from the samples.   The latter worked

                             8-  53

-------
                                                                     75
very well  at smoothing the blank subtraction, and  allowed us to
watch sorbent tube aging throughout the study.

7)   The sample  tubes storage caps  were  changed during  the 2nd
quarter of 89.  The o-ring sealed storage caps were replaced with
swagelock caps using teflon ferrules.  These sealed much better and
our  blank valves  were immediately  reduced as passive  sampling
during storage and transport was halted.

8)  Special  ball valves were used at the  inlet end  of the sample
tube through the  majority  of the  study  to  reduce  the  passive
sampling  occurring prior to sampling and after sampling before
staff could  collect and ship the samples for analysis.  A special
study was conducted to prove the value of using the ball valves in
our network.  The  conclusion was that valves  reduced the passive
sampling  by  sample tubes  but were  not as  effective as capped
blanks.  Extended  passive sampling times up to 140  hours yielded
a  slight  but measurable  difference  from  0  to  10%  from capped
blanks.   Our methods  of  capping with  ball valves  continued  as
planned and  the pickup of weekend samples  were delayed  until the
next regular workday.

     All other voc data from NYS  DEC can be used  at a  +/~ 30%
accuracy level and precision of  +/-  40 to 50%.  Averaging the 3
samples (two hi  and one low flow) per  site allows us much more
confidence  in the values.    The  use  of true  duplicates  and
distributed volume sample insures our ability to track  precision

                              8-  54

-------
                                                                     76
and guard  against breakthrough or  desorption  problems in an  on
going program.  We will continue to use the 3 sample system for the
Statewide network.

90-3-17
                             8-  55

-------
      —  ORGANIZATION: NEW YORK STATE EHCON
COMPOUND: CHLOROFORM
                                             DATA VARIABILITY FOR STUDY
METHOD » SRMPLES HERN
SRMPLE
CONCENTRRTION
PPB
ENVIROCHEM < 10/1/87 - 12/31/87) 3
ENVIROCHEM C 1/1/88 - 12/31/88) 51
flTD-50 (6/1/96 - 9/30/89) 199
NOTES ATTACHED (Y/N>:
09
' ORGANIZATION: HEM YORK STATE ENCON
in
Ok
DATA VARIABILITY
METHOD • SAMPLES MEAN
SRMPLE
CONCENTRATION
PP8
ENVIROCHEH < 10/1/87 - 12/31/87) 28
ENVIROCHEH 11/1/88 - 12/31/883 97
RTD-50 (6/1/89 - 9/30/89) 237
HERN DIFFERENCE
BETWEEN pfllREO
SAMPLES (PPB)
0.01
-0.04
0.00

COMPOUND:
FOR STUDY
MEAN DIFFERENCE
BETWEEN PRIREO
SAMPLES CPPB)
0.09
0.05
0,05
STANDARD DEVIATION
OP THE HERN
DIFFERENCE BETWEEN
PAIRED SRMPLES (PPB)
0.02
0.04
0.01

DICHLOROMETHRNE

STANDARD DEVIATION
OF THE HERN
DIFFERENCE BETWEEN
PRIRED SRHPLES (PPB)
0.06
0.02
0.04
NOTES ATTACHED (Y/N):

-------
             ORGMIZttTIOH: MEH YORK STRTE ENCOH
COMHXJHO: H,P XYLENE
                                                 DflTR VARIABILITY FOR STUDY
Ul
METHOD
ENVIROCHEM (10/1/87 - 12/31/87)
ENVIROCHEH (1/1/88 - 12/31/88)
ATD-50 (6/1/88 - 9/30/89)
NOTES ATTACHED (Y/N):
ORGANIZATION: NEH YORK

METHOD
ENVIROCHEH (10/1/87 - 12/31/87)
ENVIROCHEH (1/1/88 - 12/31/89)
ATD-5D (6/1/88 - 9/30/89)
• SAMPLES MEAN MEAN DIFFERENCE
SAMPLE BETHEEN PAIRED
CONCENTRATION SAMPLES (PPB)
PPB
33 0.49
119 0.08
281 -0.07

STATE ENCON COMPOUND:
DATA VARIABILITY FOR STUDY
t SAMPLES MEAN MEAN DIFFERENCE
SAMPLE BETHEEN PAIRED
CONCENTRATION SAMPLES (PPB)
PPB
29 0.02
120 -0.01
282 0.03

STANDARD DEVIATION
OF THE MEAN
DIFFERENCE BETHEEN
PAIRED SAMPLES (PPB)
0.13
0.03
0.02

ETHYLBENZENE


STANDARD DEVIATION
OF THE MEAN
DIFFERENCE HblHEhN
PAIRED SAMPLES (PPB)
0.03
0.01
0.01
   NOTES ATTACHED (Y/N):
                                                                                                                     -j
                                                                                                                     «o

-------
             OCGANIZRTION:  NEW YORK STflTE ENCON
                                    COMPOUND: 1,1,1 TR1CHLOROETHANE
                                                 DRTR MRRIRBILITY FOR STUDY
    METHOD




    ENVIRDCHEH (10/1/87 - 12/31/87)

    EWIROCHEH u/t/ea - 12/31/99)

    RTD-50 (6/1/BB - 9/30/89)
* SRHPLES
    HERN
   SAMPLE
CONCENTRRTION
    PPB
      32

     121

     264
MERN DIFFERENCE
BETHEEN PRIREO
 SflMPLES 
                      0.05

                      0.01

                      0.00
STRNDRRD DEVIfiTION
   OF THE HERN
DIFFERENCE BETWEEN
PRICED SRMPLES (PPB)

    0.03

    0.02

    0.01
    NOTES flTTHCHED 

                      0.04

                      0.01

                      0.01
    NOTES RTTRCHED (Y/N):

-------
                                                          82
         Chapter 9a



       Miscellaneous



Summary of Data Availability
           8-   59

-------
                                                                               83
                     STATEN ISLAND TOXICS STUDY




                      DATA AVAILABILITY SUMMARY






                         % Data Availability




Quarter                Envirochem Samplers               ATD  Samplers




4th 1987                       75                              *




1st 1988                       91                              *




2nd 1988                       85                              *




3rd 1988                       34                              *




4th 1988                       82                              93




1st 1989                       *                               84




2nd 1989                       *                               82




3rd 1989                       *                              100




•Not in operation during this  quarter.




Overall study data availability - 81%
                                  8-   60

-------
                                                             84
            Chapter 9b



          Miscellaneous




Permeation Tube Calibration System




   Flow Audits and Calibration
                8-  61

-------
                                                                                           85
                  New York State Department of Environmental Conservation

                                  MEMORANDUM

TO:        G. Boynton
FROM:      G. Froehlich
SUBJECT:    BTAS Permeation Tube  Calibration System
DAT*      February 17, 1989


           On February 2, 1989 I certified the BTAS Permeation Tube Calibration
           System at the Hemlock Street facility.  Due to back pressure problems
           1 didn't use the Hastings Mass Flow Controller, instead I used
           our NBS Standard bubble meter.  The Hastings Mass Flow Controllers
           in the Permeation Tube Calibration System were calibrated as per
           their respective instruction manual procedures.

           The results are listed below:

                                   Tube Flow Controllers

                                        B.O.M.                        Setpoint
           Range               Set at   Measured at   Adj. to   ,%d   Measured at

           #!•  0-500 seem     4.90V    493.6         Not adj.  +0.7     252.3

           12   0-500 seem     4.90V    587.1         488.0     -0.4     251.9

           «3   0-500 seem     4.90     587.7         498.1     +1.7     254.9

           «4   0-500 seem     4.90     606.7         488.3     -1.4     246.5

           •transducer #1 replaced with new transducer before calibration/certification.

                                 Dilution Flow Controllers

           II  Blank

           12  Not done by request

           13  0-5 SLPM        2.00V    2047.3         Not Adj.  +2.4

           14  0-10 SLPM       4.75V    4931.1         4813.3    +1.3

           This  certification is valid from 2/2/89 to the week of 8/7/89.
           Please  notify me at least two weeks  in advance so Z can schedule
           the  recertification.   If you have any questions, please don't hesitate
           to call.
           cc:   Mr.  Webster
                Mr.  Coon
           GF/bc                           8-   62

-------
                                                                                         86
 15 CJ-75)
TO:
FROM:
SUBJECT:

DATE:
      New York State Department of Environmental Conservation

                          MEMORANDUM
                   .1
Garry Boynton     vStS
George Froehlich^ftrf"
Sorbent Tube Calibration System
October 31, 1989
           On August 15,  1969 Quality Assurance Standard's Lab staff audited
           and re-calibrated for  certification the Bastings mass flow controllers
           in the BTA5 Sorbent Tube  Calibration System at the Hemlock Street
           facility.

           The Bastings mass flow controller audits were conducted with the
           Standard's Lab NBS traceable Bubble-meter (Hastings Model HBM-1,
           SN-64) and the flows were corrected for temperature and pressure.
           The results were  as follows:

           Dilution Flows:
           Unit «2 (500  seem  total  flow)

           Audit

           Set 250 seem
           B.O.H.  289.9  seem   (+16.5%)


           Unit 13 (5  SLP.M  Total Flow)

           Audit

           Set 2000 seem
           B.O.M.  2059.6 seem  (+3.0%)


           Unit «4 10  SLPK  Total Flow)

           Audit

           Set 4750.0  seem
           B.O.M.  4781.1 seem  (+0.9%)
                                             Calibration
                                         Before            After
                                       zero: 0.005         +0.00
                                       span: 5750          4900
                                  Set point: 2500          2505
                                            Calibration
                                        Before            After
                                       zero: 0.07         +0.00
                                       span: 5270         4940
                                  Set point: 2500         2510
                                            Calibration
                                       Before            After
                                       sero: 0.06         +0.00
                                       spam 10425.4       9867
                                  Set point: 4750         4624
                                     8-   63
                                                                  H
                                                              NOV-2B89
                                                         '*'
                                                         OF TOXIC
                                                    AIRSAMPtlNR

-------
                                                                                87
                               -2-
 Tube  Flews;

 Unit  tl  (500  seem  Total Flow)

 Audit

 Set 250.0 scon
 B.O.M. 254.7  seen   (4-2.01)


 Unit  12  (500  seem  Total Flow

 Audit

 Set 250  seem
 B.O.M. 246.0  scon   (-1.6%)


 Unit  «3  (500  seem  Total Flow)


 Audit

 Set 250  seem
 B.O.M. 2S5.fi  seem   (+2.41)


 Unit  14  (500  scan  Total Flow)

 Audit
Set 250 seem
B.O.M. 245.6 scan
(-1.6%)
                          Calibration
                     Before            After
                      zero:  0.01       4-0.00
                      span:  487         493
                  Set point: 250         253
                          Calibration
                     Before            After
                     zero: 0.03         10.00
                     •pant 481           492
                Set point: 250           251.5
                          Calibration
                     Before            After
                     zero: 0.06         40.00
                     span: 499.2         492.0
                Set point: 250           251.0
          Calibration
     Before            After
     zero: 0.05         sO.OO
     span: 486.0         490.0
Set point: 250           251.5
The sorbent tube calibration system is due for a flow controller
audit the week of January 15, 1990, and a new certification the
week of August 13, 1990.  If you have any questions, please don't
hesitate to let me know.

cc:  Randy Coon

GF/bc
                                8-   64

-------
                                                          88
         Chapter 9c



       Miscellaneous




Quality Assurance laboratory




  Certification Procedures
             8-   65

-------
                                                                                       89
A. VOTS Flow Channel and Flow Measuring Module Certification Procedures

     To assure flow accuracy in the VOTS monitoring instrumentation, the following
procedures were adopted for flow channel and measuring module certification.

     1. VOTS flow channel certification procedure.

        a. Each flow channel was built, adjusted and locked to a preset flow.

        b. Each flow channel was tested, at constant vacuum (20"Hg) on at least
           10 different days and until it showed no more than i.3 cc/min. variation
           over 5 days.  Flow graphs are kept for each channel to monitor its
           stability.  Unstable flow channels were reset if possible or eliminated.

        c. Each flow channel was marked with a brass identification tag to
           assure proper record keeping both in the laboratory and in the field.

        d. Each flow channel was used until a field flow audit indicated its
           certified value had changed more than ±10% at 20" Hg vacuum at which
           time it was returned to the laboratory for recertification.

     2. VOTS flow measurement module certification procedure.

        a. Each flow measurement module was built, adjusted to 8 cc/min nominal
           flow and locked in position.

        b. Each flow measurement module was run at the following nominal flows
           8, 15, 22, 29 and 36 cc/min with the total manometer deflection
           recorded at each flow.

        c. A linear regression was then calculated by entering deflection as
           the X value and the corresponding flows as the y value.

        d. The correlation factor, slope and intercept was then recorded on
           the modules certification sheet as well as on the module itself.

        e. Each flow measurement module was used until a field flow audit indicated
           its certified value had changed at which time it was returned to
           the laboratory for recertification.

B. VOTS Audit Flow Box Certification Procedure.

         a. Several VOTS audit devices were built and maintained in the laboratory.
            These audit devices have a 0-50 cc/min range and are internally
            heated and insulated to assure stable operation.

         b. Each VOTS audit device is certified at six month intervals.

         c. The following checks are made prior to certification.

            i.    visual inspection performed.
            ii.   electrical and safety inspection performed.
            iii.  heater circuitry checked


                                       8-   66

-------
                                                                                       90
             iiii. mass  flow meter  calibrated  following manufacturers procedure.
             iiiii certification  sheet  and  lab documentation  completed.

C.  Canister  Sampler  Modifications  and  Certification  Procedures

          a.  Modifications  performed  prior  to  operation

             i.   Leak check performed  and  internal plumbing  leaks eliminated.
             ii.  New pumps procured  from manufacturer and interchanged with
                 existing  leaky  pumps.
             iii. Formaldehyde  inlet  removed from  rear of instrument and teed
                 into the  stainless  steel  sampling manifold  as per EPA recommendation.

          b.  Flow Certification

             i.   Internal  plumbing leak checked under pressure before installing
                 evacuated cylinder.

             ii.  Visual, electrical  and safety inspection performed.

             iii. Canister  mass flow  controller is calibrated with bubble-0-
                 meter  following manufacturers procedure.

             iiii.Certification sheet and lab  documentation completed.

 p.  VOTS Monitoring Shelter Modifications

          a.  Installation  of mud-dauber fittings  on  the vacuum reflief valves
              to eliminate  the  plugging of  the orifice by insects and airborne
              debris.

          b.  A 12" extension of  the  above  vacuum  relief valve to facilitate
              checking,  cleaning  and  replacement when necessary.

          c.  Purchase and  certification of 4" vacuum test gauges for each site.
              This insures  on a weekly basis that  the manifold vacuum is 20"
              Hg i 1.5"  Hg.
                                        8-  67

-------
                                                        91
      Chapter 9d




     Miscellaneous




Flow Performance Audits
          8-   68

-------
                                                                               92
                       PERFORMANCE FLOW AUDITS
     Routine performance flow audits were performed by the operations




group.  In the fall of 1988, the Quality Assurance Section of the




Bureau of Technical Services assumed responsibility for biannual




oversight performance flow audits in addition to the routine operational




audits.  These Quality Assurance audits were performed in the fall



of 1988, spring and fall of 1989.  The summary statistics that




follow represent the combined results of both operational and Quality




Assurance Section audits.  Appendix B is a sample of the flow performance




audits performed during the 3rd quarter 1989.
                                  8-  69

-------
                                                  93
   Summary Statistics
Flow Performance Audits
U u a UL LL
Poropak 17 3-02 8.2 19.4 -13.4
Envirochem 19 2.2 4.9 12.0 -7.6
N.J. Tenax 13 -0.7 8.4 16.1 -17.5
ATD-50 66 3.1 7.2 17.5 -11
Trace Metal 6 0.7 1.2 3.1 -1
Hi-vols
Wedding 6 8.0 3.2 14.4 1
PM-10
.3
.7

.6

n- Number of samplers UL- Upper 95% confidence limit
u- Mean value LL- Lower 95% confidence limit
f- Standard deviation

Poropak Envirochem IN. J. Tenax ATD-50 Trace Wedding
20

15
10
_ 5'
£
w 0'
a
-5-
-to-
-15-
•20-
Metals PM-10









S~
/-^
/
^
/^
s^
K:
/^

Hi-x/nk


^/
/
•"^
s^
/^
^



s .,
/,
s'

-------
           Chapter 9e




          Miscellaneous




            Report on




 Effectiveness of Gravity Valve




In Prevention of Passive Sampling




        of Sorbent Tubes
              8-   71

-------
                                                                           95
Effectiveness of Gravity Valve in Prevention of Passive
               Sampling of Sorbent Tubes

                       May 1989

     Garry Boynton,  Dr. William Webster, Brian  Lay
          N.Y.S.  D.E.C. Div.  of Air Resources
                            8-   72

-------
                                                                                      96
     This short study was set up to show the effectiveness of a gravity
ball valve in reducing passive sampling by sorbent tubes before and after
the active sampling period.  This capability would reduce the overtime
and scheduling problems of a sorbent tube network run on a 6 day schedule
by allowing the field staff to work normal hours as degradation of samples
would not occur over a weekend.

     The study consisted of 11 sampling events from Feb. to April 1989.
Two tubes were left capped with the standard storage caps from the time
they were cleaned until they were analyzed.  Two tubes were placed 1n
an unplugged sampler with the gravity valves attached.  Parallel to these
two were two more tubes attached to the sampler and their ends left open.

     These tubes were analyzed with the routine samples taken on the
six day schedule for the Staten Island/New Jersey Monitoring project.

     Bar charts for Oichloromethane, 111 Trichloroethane, Benzene, and
Toluene are attached as well as the raw data.  The first 5 columns in
the raw data are sample information from the analytical system.  The
fourth column is the key to the sample.  The AT#     refers to the capped
blanks, the PASOPE  refers to a passive test with open end and PASVAL,
refers to a passive test with a valved end.  The fifth column 1s the
number of hours the tubes were exposed.

      A rough comparison was performed.  Each passive test was compared
to the average of the 2 blanks for that day.  The results are tabulated
1n two groups, less than the Avg. blank or greater than.  These results
Mere then used In the Binomial Test (same as used for breakthrough).
Failing this test means that passive sampling occurred enough to show
                                                                 8—   73
a statistical difference from the average blank values.

-------
                                            98
   DICHLOROMETHANE
BLANK
            VALVE
                        OPEN
        TOLUENE
200 -r
190 -
160 -
170 -
ISO -
?150 -

1*0 -

C 130 -
C1JO

tJiio-

£ 100 -
: 90 -
> 80 -
O 70 -
60 —

SO -
40 -

jO "
2O —
10 -




































j





Y
D
D
P
T
rj
'X*
I
















j]

sQ
* '



f
^
I
j — '










•i
•i

N
>
/ \

S \

/ «



-* 1
f
T
















[
t





•*
_/


1







t


t

f

S i<
s.
T


s '
j 1
1 -1










. ,


1

1
!
'
<
J "^
i^ S /
j -;

> ../
^ s /
t /
f S /
L—t



n
- /
i, i/

s /


' * '
? ( ;
. *
' H '
- '
^ J -
,• j 4** .
r- s < ^ S/ « 1 /
f , . - S^ . w
r> « ' - -• »•' r' ^ ^
C . - . - JJ S/ S^
- J J X , i k J
. i ! x p- 5
<• s t * / ', ' s *• \ ,-
! jlli :i :l ;i
*J J i 	 ; u





^ '
•

r '

i /
< ^ ^
/ x
• * t
/ /
/ -
/ /
/
* / p
•n ' '



V >' J $ P
> / NC "• < ' .'
S / S ' '• ' V • •*
f t < 1 f
.,, J, s - •, ,. y
JdJud.iLQJudJCdi
_i 1 	 1 i 	 1

















n
2
q
T1

s;

u-














.
;
,
;
;

r"



_!
                                       8-  74
BLANK
VALVE
                         OPEN

-------
      tft.
 tmr-n,
 7IM? M>
 7H97-M.
 7U97-Ob
 71197-ni
 7IH7-H*-.
 7U47-IU
 7U47-03
                                           - kt
            il.* -<:r- l*l>r« MLllttiH | (,H
            O.* -.:,- • i-WN HillftiiridN
                                       » M .Mm V.!
                                       »-flMMtHI
                                                     II.IKKI  , .\^:»> tM.
                                                    -tii.iifm  |..-»i.' Mi.
n.vri.'iTi  wflNi
O.V2I/II9  Ulim
OM-Oft- I'lirCiN. 11 Win OH

IJJ Oil- l-tWllUrilHI 1144
                                       nr.:uii
                                       r-MSWiU 1/3
                                       » rt'..»»MI V-l
             •HI.IM4I  12.2i* IN.
             •yi.rn.il  I.-..VI IH.
             '  fl.iV.rt  4.Ml IH'
                                                                                   I.:. mi IHI
                                                                                   1.'. .1 ; IH.
            (i^TrT/iri  01 liHls          in i-iu I
                                                                  IN.
                                                   I11.IHNI  'i.l.-HI IH.
                                       f-Hi.01 Lll I   in.mi.1
                                            r.t n  mi
                                            III. 01  IN.
                                            U.-Mf  IH>
                                                                                                            if
                                                                                                         I,*. Hi

                                                                                                         VJiV
                                       PHSKHLMS
            O:i  10- II^SCIILIfiRHridN   Ifl-.VMt VO
            oj- in- is I'N-iiuHKHrinN   f-HSOPiMS
            n i- in - isH'iC'ii II.RHIIHH
            3V5/r:-i—TI nin:  —a-
            -VS/U9     in HM»:
            n i -;-ci- i-iii-n IH iHRRfldH
            0 J- .''I!- t'JH*«l III IdRiiridH   PHUCM U.-
            o i-.-o- riH^iiLiiiRnnoN   f-HSOftiio
            «)"»-.-ii- t'jii'iMrt. i tiRnri dN   i-nM>H( VIL
            3/II/'l»T
'Anna i
 ftnuin
                                        . .-.^-.  --.y^  ••••
                                         (l.iwm  I.'.ill  IN'.
                                         n.i'Miii  -i.ubii  IN.
                                       121.(HI"  D.II-I  Hi.
                                       I2I.IHMI  I..IU-;  IN.
                                       I2I.IHMI  |J. |l.  IH.
                                      JZI.miii  "I. Irt'i  Hi-
                                         O.iWi  2ri.'U'  Mf.

                                       HsliHill  Ss!?.*  IN.
                                       MS.cum  ,'i.t-i  IN,
                                       M'..lMiH  .II. 'Ill  HI.
                                      _MV.i««i  .:.-. I-I  m.
                                         il.UliH  17.m  W.
                                            |-|.|M'III.
                                            1 >.»*.!  W,
                                            »..'.>:>  IH.
                                            lll.bi  Ml,
                                            H.iVH  IHi
                                            I.MI  IH.
                                                                                                         .U.K.
                                                                                                         HI. 11
                                                                                                         HI. 1:1
                                                                                                         •4-1. Ill
                                                                                                         ri.-jn

                                                                                                         311. Ul:
                                                                                                         '•I I. Ml
                                                                                                         •41.05
                                                                                                         II.'..-
                                                                                                        ".••.'.bl
                                                                        .••IHI
                                                                        .I-UIJ
                                                                         IHi
                                                                         IH,
                                                                         im~
                                                                         IN,
                                                                        ..'ml
                                                                         IN,
                                                                         IN.
                                                                         IHI
                                                                        Tur-
                                                                         in;
                                                                         IHi
                                                                        . Mill
                                                                         III.
                                                                         III.
                                                                        TBT-
                                                                         in;
                                                                         IN.
                                                                         Ml.
                                                                         Mi.
                                                                         IH.	
                                                                        TO—
                                                                                                                                   13.100
                                                                                                                    11?.9 KG
                                                                                                                   _|2I.9 IHi
                                                                                                                   "7-t.H? Ht!
                                                                                                                    91.113 NG
                                                                                                                    8J.13 HG
                                                                                                                    01.53 Hb
                                                                                                                    71.1,- INi
                                                                                                                                I50.7
                                                                                                                               •trnr
                                                                                                                                81.22 lib
                                                                                                                                I23.b »«•
                                                                                                                                   si.r.oo
                                                                                                                                111.3 MO
                                                                                                                     K-
TTTmiiT
 u..:ii HI,
 21.22 IN.
 II.MO Ml.
 21..-i iir.
            m nur
i/ii/e-i    HI.IIH»:
0:1-27- riasi iH.KiRnnoH
            03-2,--
                           IHRIirlOH
    ?- m
 7U97-UJ
 7M97-OI
                                                     U.IHH)  IT.5II Ml.
                                                   I7U.I.NHI     l.'.i'lHI
                                                   I7U.OIIU     I.-.MH)
                                                   1/n.OtM)  Jf .3!. IN.
                                                   iro.i««i      ,-.-1110
            I) 1-31-fJA'CIM.IIiRnriCiN
            o i- j i- i9«si. id imnr i (IN
            o i-11 - i-iaw ic i MUM- i UN
            HlOI-HMfrrilLli
            3/23/B'J   DI.
            3/23/8-j
            ni-07-MasriiLimnriMi
            O-I-07- I
f-HGCM Vi
PflSOI-tlO
>-MWHtlO
HI32O1
ft(.1211       O.UI«> Not la.M.1
PHUOPEIt    72.UHI      ll.ilfl
m-MTUi    72.(«MI Hot I.KJT.J
PH-jt/MII    72.(4M1 H->l I.Hjr»i
f'H'JWjl t2    7.-.IIHII M.,1 l.,u.>l
RT310I       O.I'Kii'l H..I l'<.ui«J

PHSOPCU
"in.Lii HI;

 li.sir. mi
 •9.,'J(l INi
 21.7S IHi
      i-.MIi)
                                                                  2U.MI
                                                                  11. «5
                                                                  ?»..i)l
                                                                  TI.-I5
                                                                  *Jl..t>J
                                                                                                   Mb
                                                                                                   IHi
                                                                                                   INi
                                                                                                   IN',
                                                                                                    Hi
                                                                                  s.oj.i iir.
                                                                                  7.1.10 iw
                                                                                  M.,1'1 lift
                                                                                  2-1. iT. IHi
                                                                                  !•!.(> 1 IMi
                                                                                  J I.Ui: IH.
                                                    ti.ono NO
                                                   -rs.m-i N.>I  r««i«j
srnrtH ISLWIII MKO
  SUE •     SHHPL
               ofin:
7017-01   0-I/01/M9
                                                           HOI
7II97-01
70-J7-(K.
7017-01
7H-J7-OJ
                                   MMNK mm sccww mi:
                          SOMflt    WMLVSIS •   „     ,
                            rvpc                   H»v<(5
                       nmtt:          nrrMoi       u.otm 3.;.?," HI.
           oi/01/MY  WHHK          nriiii.       a.oiiQ i.-iti. IK,
                                                   tt.,inm ll.7*i 1*.
                                                   9C.IWMI II. 411 IM.
                                                   90. W 41 II. (US IV.
                                                   *,-fniO -J. ;7 1 Ih.
           Ol 2
           0-l-^-nA^IM.IMUiriON    HH.VMI5
            . I ii/0*l
            / 1O/ !)•<
                       BL
                       UI.HN*:
                                            I I.MI IH,
                                            u.,".. IH:
                                                H.'fM
                                                i,.'. in
                                                i:..i,'ti
                                            IS. 71 IH3

                                            I.I.I

                                            11.11*.. mi
                                            8.i*i3 IH.
                                            21. J,- IHi
                                            t\.f.t INi
                                            2I.T* INi
                                            III '*.' III.
                                                                                                 ntt
                                                                                             !(•..(. In,
                                                                                             2(1.11 INi
                                                                                                ir. imi
                                                                                             2f.. J'l INi
                                                                                             jii.ir. iw
                                                                                             .MI. -ti IH;
                                                                                             2ii.ni IN.
                                                                                             .-::. ri mi
                                                                                             3.r.5!. IHi
                                                                                             2*j.r*j IH;
                                                                                             22.81 Mi
                                                                                             2*..5i" IHi

                                                                                              UtNTUU

                                                                                             21. n IN;
                                                                                             M.u;- in;
                                                                                             3«l.(l'i IHi
                                                                                             3(1.7*1 IN.
                                                                                             31-U'< IN,
                                                                                             •:V-(HI IH.	
                                                                                                                       n*
           itiiMrTOg
                            KHflbH
             ll.lMMl »..1-|.' IH.

            9s!otMj riiisi IN!
            97..(KM) b.MH IK.
            9S.MNI S.IW.I IK.
       1B_  3'..-iJi«* 'i.tri IH.
                                                                      •ri-'ji IN;
                                                                      3b.-*% INi
                                                                      •Ti.ll.i IHi
                                                                      77.«1 IHi
                                                                      I.'.IIS IHi
                                                                      «•!•;• \K
                                                                      17.SO Ihi
                                                                      in.so iNi
                                                                      31. JI IHi
                                                                   II..UII IN.
                                                                   III. Ml Mli
                                                                  2;'.ir. !«•
                                                                  2J.3"J INi
                                                                      It.. MM
                                                                  2 1. iir IN.
                                                                                                                               81.73 Mb
                                                                                                                                ini.r, no
                                                                                                                               95.12 MG
                                                                                                                                190.2 MG
                                                                                                                                HH.*J HG
                                                                                                                               101.2 NG
                                                                                                                               115.2 NC
                                                                                                                                  S2.bOO
                                                                                                                               105.5 NG
                                                                                        43h»-
                                                                                         19.67  NG
                                                                                         69.05  HG
                                                                                         90.51  HG
                                                                                         611.30  HG
                                                                                                                   IIS. 9 NG
                                                                                                                   • 1.96 HG
                                                                                                                      SO. 700
                                                                                                                   6U.11 NG
                                                                                                                   137.9 HG

                                                                                                                    rOLUCHC

                                                                                                                   102.7 HO
                                                                                                                   78.35 HG
                                                                                                                   lbS.9 HG
                                                                                                                   17S.1 NG
                                                                                                                   IS1.0 INi
                                                                                                                   !!.>». lift
                                                                                                                   67.27 INi
                                                                                                                   11.11 HG
                                                                                                                       56.600
                                                                                                                       79.700
                                                                                                                       7 I. 200
                                                                                                                       39.100
                       BUHN:
           0*.. -U-t-
           OV-.UI. IH.



                                                  •^•"ij{ i"-v* T-'
                                                    O.UfMl I. .HI i III.*
                                                    ii.mm 1,.,-en IH.
                                 22    7.1. Oml     n.nm
                          »-H1>UHL2l    7I.IIIMJ H.j« lau..i
                                       7J.UIO     1.1 m
                                                                                      «.. i in
                                                                   JS.n IMi
                                                                  21.9(1 IHi
                                                                  3'l.lt. IH.
                                                                  T'l.lHi INi
                                                                  21. Hi' IHi
                                                                  2*i. U: IN.
                                                                                                                   fl.U» Mi
                                                                                                                   73.01 Hti
                                                                                                                   151.6 HG
                                                                                                                       S1.UOO
                                                                                                                       17.300
                                                                                                                       'K-.'.'W
7IISir-OJ
           o-.i-i;--
           «,- K- -
       oo  u*.  i;--
                      M HH»:
                                                                                  !•».::(:  IHi
                                                                                  2J.'4I  IH.
                                                                                      lli.-HNI
                                                                                  ri.M.  IH.
                                                                                         '.ou
                                                                  17. 0(. Ml.
                                                                  i;i. o~j IH.
                                                                      J;-.MMI
                                                                      i.-. urn
                                                                  ttl.lM. IH.
                                                                      31. .110
                                                                                                                                IIU.8 HG
                                                                                                                                   60. <.OO
                                                                                                                                tOt. I INi
                                                                                                                                   10.500
                                                                                                                                   27.WO
       Ul
                                                                                                                                                                           O
                                                                                                                                                                           o

-------
                                                           102
            Chapter  9f




          Miscellaneous




 Standard  Operating  Procedure for




Envirochem Thermal Desorbtion




Hewlett Packard 5970 6C/MS




Volatile Organic Analytical System
          8-   76

-------
                                                            103
 STANDARD OPERATING PROCEDURE  FOR
  ENYIROCHEM THERMAL DESORBTION
    HEWLETT PACKARD 5970 6C/MS
VOLATILE ORGANIC ANALYTICAL SYSTEM
              11/88
             NYS DEC
     DIVISION OF AIR RESOURCES
   BUREAU OF TOXIC AIR SAMPLING
  AMBIENT TOXICS INVESTIGATIONS
         6ARRY A.  BOYNTON
              8-   77

-------
                                                                            104
1. CLEAN UP
   A. ENVIROCHEH (TENAX, AMBERSORB, CARBON)
   Tubes 1n storage longest are chosen for cleaning and logged
on a shipping 11st.  Tube cleaner 1s preset for temperature.
(290-C) and purge Flow (50-70cc/m1n. (UPC NZ)).  Time cycle
Is programed Into Gralab electric timer - N£ purge 20 m1n.
                                          Heat cycle 10 m1n.
After cleaning cycle, tubes are Immediately placed 1n teflon
capped glass storage tubes and placed In foam lined shipping
container.

2. SHIPPING
   The foam lined container 1s sealed 1n a cardboard box for
Parcel Post.
Extra foam 1s placed over the glass sample tubes to hold them
1n place.  Business return mall placard Is used to eliminate
need for postage from field.

3. SAMPLING
   See Toxics QA Manual Section 30 Sorbent Tube Vapor Collection

4. RETURN SHIPPING
   All tubes from sampling event are shipped same method as
to the field.

5. LOG IN
   Once samples are received by ATIS staff they are logged  Into
                                                                     8-   78
a computer to calculate flows and Initiate the analysis process.
The loo 1n also creates a unique analyses number for future

-------
                                                                            106
tubes are cleaned up the same way as sample tubes.  Calibration
tubes are then generated at  200 ng per analyte  and cycled  the
same as the Internal ref. 1n the sample tubes.

7. ANALYSIS                   See Appendix for Parameters List
   A. Timer controlled flush cycle - Timer to start Envlrochem
system should be at 5:15 AM to allow 3 cycles to flush the  Internal
traps prior to an analysis run.

   B. Turn MSO from standby to on and turn heater on  evening
before analysis run.

   C. Turn timer controller off and unplug unit  to prevent  continued
cycling and allow traps to cool below 50*C.  Turn on  both  transfer
lines, power and bring helium flow up to 4 (top  of ball on  rotameter)
switch rear transfer valve to H.P. to allow carrier gas flow
to equilibrate.  Turn desorber control from off  to auto.

   D. Autotune - dally full autotune with P.F.T.B.A.  as prescribed
by Hewlett Packard - no modifications from standard H.P. method.

   E. Turn on IBM PC and call up HP transfer program.  This
program accepts the final report transmitted by  RS 232 from
the chemstatlon and stores 1t In lotus compatible files for
validation and printout,  (see appendix for basic program)

   F. Specify and load method (Auto.N or Callb.M) appropriate
for analysis.  Calibration 1s first analysis of day then blank
                             8-   79

-------
                      108
  SIM   ACQUISITION     lONovSS   9:12 aa

 aolvent delaV  6.01-    efl volte    6 relative       resulting voltage 140C'

        Croup     |234S6769tt
    I of Ions     1?    20   26    If'    26    20    21'    26    20    20
   start Tiae   8.00 11.60 14.60 19.60			
 low am Resolution  NO                            eyelet per second 6.9

 ion 1123456789     16
   a/Z  47.80  49.60 61.00 62.66  63.69  64.60  83.60  84.66  85.00  86.66
 Dwl)     75757575757575757575

 ion I     11     12    13
   a/Z  67.80  97.80 99.00
 Dwtll     75     75    75

    nUkber  of plot traces  1        initially ON         lie* Window 25.0

  Plot t 1  •i/Z TOTAL    aCale 1GOOGCO



  Sin  ACQUISITION     16 Nov 88   9:13 aa  DATft:TrERK>l.A

 eolvent delaY  8.00    efl volts     0 relative       resulting voltage 1400

        Group     1     |     3     4     5     f     7     8     9    10
    • of )on»     13     2C-    2D    10    20    20    20    26    20    20
   itaM Tin*   8.00 11.60  14.0P 19.00	
 low MS* Resolution   NO                            cycle* per tecond 6.6

 ion 1123456769     10
   a/Z  49.00  60.00  61.00  62.00  63.PC'  64.PC'  77.80  78.86  63.80  65.00
 Dwell     75757!-     7575757!-     757575

 ion S     11      12     13     14     15     16     17     16     19     20
  a/Z  95.00  96.00  97.00  99.00 117.00 119.60 121.60 138.60 132.00 134.60
 Dwell      75     75     75     75     75     7!-     75     75     75     75

    nltater  of plot trac«f 1        initially ON         liae Window 25.P

 Plot t  1  a/Z TOTAL   aCale 1600008


 SIN   ACQUISITION     16Nov68   9:13 u  WTA:TrC961.A

solvent dtltY  6.88    eft volts     8 ralAtive      raw!ting voltage 1460

       Group      121456789    16
   I of lout     13    28    20   -16   28    28   28   tB   »    28
  start Titt   8.80 11.80 14.86 19.80	-		
low BUS Resolution    NO                           cycles  par  second 8.6

ionS123456789)E>
  e/Z  61.60  77.60  83.80  65.90 91.80 92.00  95.08  96.88  97.00  99.80
Dwell     75     757575757575757575

•cot     11      12      13     14    15    16    17     18     19    20
  e/Z 105.60 106.60  112.60 114.98 129.60 131.06 133.66 164.* 166.80 168.60
          75757575757575757575

   nUaber of plot trace* 1        initially ON        tiet Window 25.8
8-   80

-------
                                                                                                       110


REPORT  GENERATOR                            R«v M. J  31-lhf-K
  Integration
 Reultb Flit:
  Report Type: ESTD         Fomit :  Sonar y
              Ctl File MM :  DATA: CALEXSTD.fi
  Definition: __
              OestTTl* nu* : WTA:GORPT.«SC

     Sequence
   Macro File: DATfeAUTDRFT

CALIBRATION                                     Rev 3.1.1 3t-fer-6C

 Integration RewJt* Fili: WTfijCDRf'T.l

   Ulibration Table File: DATAzCftLEKTD.O
             Lut Update:   4 Nc.v 83  10: OS u

       Calibrate &;.•; Area         Level Minber:   1

      Lfrvel nutter exists, recthbration of (hit  level utuwd

   ---------------- C*]ibratiwi Table Header  Jnfore*tion — •

 Tttlt: THERtttl DESORBT10N CAI1BRAT1W «1TH
  nultipljer:  l.DOO       Sample flaount: 6.GDO      Unca) Peak  RT: &.«<'
              Signal Correlation Window. 6.63010    kin

                     Re»on:tipn Window!-,  a» Percent ef Rl
       Reference Peaks: 5.0C-0              Nofl-Ref er ence Pea>.»:  5.6«'
                                              8-   81

-------
                                                                                                           112
                            ••« CTRKW-TETRftC •««

   Peak     Int    Ret       Si mil         Coeptund
 Mum  Type Type    Tine     Deteription        Nate        (tea     Amount
  6        IBB   1C. 159  117.&0- 119.00 uu CflRBON-TETRR  13865*  12.44 NG

                       ••« He Additional Qualifiers •••

                   Counts • Response Factor • Corrected tat
                          130O.3 « 9S.07e-6 • 12.44
                             ••• TRJDLETHENE •«•

   Peak     Int    Ret       Signal        Compound
 ton  Type  Type   TIM     Description        Nate        ATM     fount
  ?        IBBfl   12.949  130.00- 134.00 MI TRlCHLETrOC  132854  5.985 NG

                       •** No Additional (kialifiers ••*

                   Ceunt* « Response Factw •  Corrected tat
                          1326S4 « 45.05e-C •  5.9S5
                            •««  112TT?JO€THflH •••

  Peak     Int    Ret       Signal         Compound
 Nii».   Type Ty;*   Tim*     Description        Nam        flrea     taount
  8        j    	   oj,^^,.   99^ „„ ii2TR]CHETHFt   «•« Not  Found «••
                               — TOLUENE •••

  Peak     Int    Rel       Sipn&l         Coop
-------
                                                                                                         114
                   Counts • Response factor • Corrected (kt
                                • 28.Pfce-f • 11.73
                             •«« 14-D1CHLKMZ ••«

   Peak     Int    Ret       Signal         Coepound
 NUB  Type Type   Tiw     Description        Nut        ATM     Aeount
 1$       i    	  M6>e&. t48>ee ^ i4.rjiCH.8EKZ   ••• Nc>l Found «•«
                             ••»  12-DlOtBDC •••

   Pe»k     Int    Ret       Si^t)         &wpovnd
 Mua  Type Type   TIM     Dmcription        UBM       ATM     feeunt
 17       1B6   21.565  14C.PO-  14S.90 uu 12-DlDtBOG  129^3$  1.623 NG
                              ••• ftutlifiws •••
        Channel Description   Exp ftesp    Tolertnct   Actual Reap
        74.K-  7S.OO IHJ      Jt'.eC'     • 50/-15X    «•« Nut Found •••

        Nut    111.00 IKU      2S-.Df-     < SO/- 101    ••• Mot Found •••

                   Counts * Respcflk*  Fictrr • Corrected  Ait
                                •  27.97»-6 • J.K.*
   Peak     Int    Ret       Signal         Co*p»und
 Nu»  T/p« Type   Tit*     De&criptic>n        Nthe        Area
 16 *      1BV   22.^74   Hase   222.06 aw FlC*'-2JDOG-B 778^036  S03.9

                              ••• Qualifiers •*•
         Channel 0«*cr ipt ion   Exf. Resp    Toletanc*    Actual Re*p
         7«. W-  7S.Ot- anu      39.«»    •• «/-!»      39. S7
         Has:    9S.OC •«      2&.DO    « 4S/-1U      47.30

                   Counts • Ke&ponb* Factor • Corrected Akt
                          7786038 •  M.72e-6 • 50i.9
     Calibration Pe*k t^'s Qualifiers were not Htisfied.
Error : Could not find Calibration Peak
                                              8-   83

-------
                                                                  115
                Chapter 9g




               Miscellaneous




Staten Island/Northern New Jersey Urban Air




Toxic Assessment Project Quality Assurance




Subcommittee Audit Report
                  8-  84

-------
                                                                       116
                  STATEN*ISLAND/NORTH£RN NSW JERSEY

                 URBAN AIR TOXICS ASSESSMENT PROJECT

                    QUALITY ASSURANCE SUBCOMMITTEE

                             AUDIT REPORT

                               OF THE

       NEW YORK STATE DEPARTMENT OF ENVIRONMENTAL CONSERVATION
Auditors:
	
Avraham Teitz        ?=
Monitoring Management  Branch, USEPA - Region II
Josep  Soroka, Ph.D
Technical Support Branch, USEPA - Region II
Paul-Brown.
Monitoring'Management Branch, USEPA - Region II
Approved by:
      _^L_
Marcus Kantz, QA Subeonunittee Chairman
Monitoring Management. Branch, USEPA -Region II

                                      8-  85

-------
                                                                        117
                              BACKGROUND
 This Audit report contains information on the performance of the New
 York  State  Department  of  Environmental Conservation  (NYSDEC),  in
 carrying  out  their  duties  and  responsibilities  for  the  Staten
 Island/New Jersey Urban Air  Toxics Assessment Project  (SI/NJ UATAP).
 Specific  areas  evaluated  vere  the  implementation  of  field  and
 laboratory procedures used by NYSDEC.  The findings reported are the
 result of  data  submitted  by NYSDEC,  conversations and meetings with
 NYSDEC  researchers  and   an  onsite  audit.  Conclusions  and
 recommendations are reported at the end of this  document. This report
 has  been  prepared  by  the  United  States  Environmental  Protection
 Agency - Region XI  for the Quality Assurance  Subcommittee  of the
 SI/NJ UATAP.

 Agency audited:  New York State
                 Department of Environmental  Conservation
                 Air Resources
                 50 Wolf Road
                 Albany,  New York 12233-3527
                 (518)  457-7454

 On site portion of Audit:  September 15,  1988

 Personnel present at audit:
                 Joseph Soroka,  Ph.D
                 Paul Brown
                 Avraham Teitz
                 Garry Boynton
                 Brian Lay
          - USEPA - Region II
          - USEPA - Region II
          - USEPA - Region II
          - NYSDEC
          - NYSDEC
 Organization responsibilities for the SI/NJ UATAP:

                 1.  Collect samples of Tenax, sorbent traps,canisters
                    formaldehyde,  and metals at appropriate sites.

                 2.  Prepare and analyze  sorbent traps from NYSDEC
                    sites  in Staten Island.

                 3.  Maintain all samplers used  in the study.
Project  Director:
Monitoring  Network Manager:
Quality  Assurance  Officer:
Don Gower
Will Smith
Ray McDermot
 Field  Operations  Supervisor: Mike Steineger
Laboratory  Supervisor:
.Data Management Supervisor:
Garry A. Boynton
Brian Lay
                                  8-  86

-------
                                                                        119
 points  of  each  method  are  demonstrated.   Thi§  includes  special
 handling  to avoid  contamination and hand*  on experience. Training
 culminates with the trainee demonstrating proficiency with the use of
 the   equipment  while  being  monitored  by   the  Field   Operations
 Supervisor.

 4. The samplers for all sorbent trap media, and the high volume metal
 samplers, function  on the  same principles, and are  calibrated in the
 same  fashion.  The  principle  of operation is a  vacuum drawing air
 through a critical orifice.  After every sampling  run,  a manometer is
 used to measure the pressure drop  across the  orifice.  This number is
 recorded, and using the calibration equation  for  the  orifice  and the
 time that the sampler was run,  the volume of  air sampled is computed.
 The critical  orifice is  audited quarterly by the Field  Operations
 Supervisor  using  a  mass  flow  controller   whose  calibration  is
 traceable to  a primary  standard.    Audits  are conducted by NYSDEC
 Quality  Assurance  personnel  to  monitor field performance  of  the
 samplers.  The criterion for acceptable  performance of any sampler is
 ±_10% of the actual level.

 The formaldehyde  and canister  samplers used by  NYSDEC  are housed
 together, but use  different  sampling  lines. Flows  for  both  are
 regulated by mass flow controllers.  The flow rates were  measured at
 the  start  of  the  study,  but  QA/QC  measures  have  not  yet  been
 implemented  for   insuring  the  calibration  of  the   mass  flow
 controllers.   This is  more  important  with  formaldehyde  samples
 because  canister  performance can  be judged  by  the final pressure
 after sampling. Also,  measurements of  flow  rate  are not needed to
 determine concentrations of pollutants  in  a  canister sample, as the
 wh?J*-    "nP1«d is contained in the canister; this is not the cas*
 with  formaldehyde  samples.

 5.  gravel  blanks  for  Tenax,  Envirochem,  and ATD-50 samples  are
 handled as follows.  Samples are received by the field office in bulk,
 with  generally 10-30  tubes per  shipment.   One sealed tube of each
 type  is taken to  a  site where that  particular tube will  be  sampled
 that  day.   After  sampling, the  sealed  travel blank  is sent to the
 appropriate  laboratory  together  with all  the  sorbent  tubes  of the
 same  type that were  run  that  day.  In  the  case that  not enough
 sampling tubes are available, travel  blanks can not be sent, although
 this has been  the  exception rather  than  the rule.

 Travel  blanks  for the Poropak samples are handled differently.  Upon
•receipt of  a  shipment of  Poropak  tubes, two  tubes are selected as
 travel  blanks.  These blanks are  taken to a site  and left sealed on
 •its  for  four to  five days.  After this time  they are sent to the
 laboratory for analysis. Poropak  tubes from regular sampling runs are
 not accompanied by a travel blank  on the return trip from the field
 to  the  laboratory.    Travel blanks  are. not  used  for canister and
 formaldehyde samples.  Duplicate samples  for  sorbent media are taken
 at each sampling run as  follows:  Two tubes are run at different flow
^•ates,  as are all sorbent  tubes  throughout  the  studyJ and a third
 tube  is run at the  higher  of the two  flow  rates. Formaldehyde and
 canister samples are not duplicated.
                                   8-  87

-------
                                                                        121
 •orbent cleaning and the packing of sorbent into the tubes  is carried
 out by a contractor to the state.  When new tubes are received by the
 NYSDEC, they  twice undergo the  standard  cleaning procedure used to
 clean sampled tubes.

 After  tubes have  been sampled  and analyzed,  they are  cleaned by
 heating them  for  10 minutes  at 290C  and are  then  purged  for 10
 minutes with an nitrogen.  Six  tubes are cleaned at one time and 10%
 of all cleaned tubes are  treated as oven blanks.  This cleaning has
 been  found  by NYSDEC to  be  sufficient,  vith  background  levels of
 cleaned blanks having <  60  ng of  benzene and <  12-20  ng toluene.
 Tubes are replaced when background  levels  of organic compounds begin
 to rise in  the oven blanks.  This has not been observed to date, and
 this has been attributed to the  fact  that each  tube  has only been
 recycled 15-16 times.

 3. Analysis of all  sorbent  tubes is by  GC/XS.   Compounds  used as
 standards are obtained as KBS  certified liquid permeation tubes and
 placed in permeation ovens.   Calibration  of the tubes is taken per
 the  manufacturers  specifications.   Direct weighing  of  permeation
 tubes,  to  give   direct   gravimetric determinations  of  permeation
 efficiency  was  attempted, but fluctuations  in  the  weight  of  the
 tube,  due  to heating  effects,   static   electricity  and  humidity
 rendered this approach impractical.
                 •
 4. The  KYSDEC calibration system  is set  up  as follows: Permeation
 tubes  are  first   grouped according to   the   temperature  that  is
 specified in their calibration. Each group  of tubes is then placed in
 an oven set at the appropriate temperature. Currently there are four
 Ketronix ovens in  18 tubes in use.  All the ovens outputs are ganged
 together by copper tubing that was cleaned with hexane and methanol
 and air then dried.   A pump is  in constant  operation which sucks zero
 air through  the permeation ovens.  Zero air  is obtained by cooling air
 to a dew point of  -100C and then passing it through two canisters of
 carbon,  one  canister of molecular sieve,  and  one  canister  of
 Drierite.  Air flow  through 'the system  is  controlled with mass flow
 controllers.  This zero air is checked daily through the calibration
 process.  When a tube is  to be calibrated, it is connected to a 1/4"
 Swagelok  fitting and the  output of the permeation ovens are diverted
 through the  tube.  The calibration system is set-up in  such a manner
 that  the  output  of any of  the   four   permeation  ovens  in  any
 combination  may be diverted through the tube to be calibrated.  Up to
 four  sorbent tubes may be spiked at one time.   Spike  concentration
 is  a function of  the time that the oven  outputs flow  through  the
 sorbent tube and the  quantity of dilution air.

Minimum detection  limits  (MDL)  are determined as follows. Injections
 of  25  ng  of  each  compound  are made  into the GC/MS system. Then data
 are  examined  from previous  runs where  lower  levels  (0-20 ng)  of
 compounds were observed.    These  two sets  of data  were compared  for
their  relationship and consistency  and determinations of  MDL made.
§ystem  linearity has also been checked  and found to hold for levels
up  to  300  ng for the Envirochem  tubes and at least 200  ng with the
ATD-50 tubes.


                                 8-  88

-------
                                                                       123
samples. Oven blanks  arc  examined to insure that their levels do not
exceed criteria  that  were established during a cleaning study at the
beginning of the project. Contamination of tubes is determined at the
discretion of the laboratory supervisor.

9. Laboratory equipment is maintained by Carry  Boynton.   Repairs of
equipment is done by the appropriate manufacturer although no service
contracts are  in place.   Criteria  for column .replacement  are that
peak shapes and retention times differ from the norm.  Parameters for
repair of the US are evident from the  results of the  daily autotune
procedure. To date, no columns  have  been replaced and  neither source
has yet had to be cleaned.

10. Documentation  of samples received  by the laboratory  includes  a
unique sample number and the field data sheet.  Logbooks are kept for
most  laboratory  instruments.   Data  transfer  from  the GC/MS  to  a
personal  computer  for  data  manipulation is done automatically.  Raw
data is stored on a Hewlett  Packard  minicomputer for a period of two
years and is then archived on tape.
                                   8-  89

-------
     Site

01
S. Uagner M.S.
a
P.S. *26
Trawla
•4
Mr* Station
Creat Kllla
•oat Oflie*
Port Ulchaond
  17
  Pup Station
  S.I. Hall
  •9
  fir* Station
fletttnvlUe
8/23/88
88-3-U1
                    Poftoafc


                     «/83





                     */85





                     N.A.





                     N.A.
                   M.A.
                   •.A.
«_-».,*- , 3
NTS Oijar tauit af Envf mortal Conservation '"»
£
ttartcn lalanl i2
fade Air Nonf tarlnt Statua *
ZTUbe
T«"M
10/87
(ttt/UMDNJ)
^ - —
• • »*"«•
3/Z7/68
((MM)

N.A.



10/87
toW*
Tnaa AM)
N.A.


S/zr/88
(6M/
Crad.
7/87
(Envtroctw)

7/87
(EnvlrodiM)

8V88
8TMT 8/31
(ATP-SO)

7/87
(Eiwlrodway
ATD-30)
9/88
BTMT 9/30
ATO-M
7/88
STMT
EPA Auto HI-
CM. CC'j Vol |
«/27/S8 3-Oper Ongoing
(Every 7/87-7/88 (Trace
A days) CMX.D) Metal*)
8/88 N.A. Ongoing
(Every (Trace
18 day*) Metals)
8/88 N.A. N.A.
•Every
18 days)

a/88 mte TSP only
(Every
6 -ay)
9/88 NOLO N.A.
(Every
18 d".)
4/88 N.A. N.A.
(Every
tllirJ Spd Met. 0«ta Sorbet* Tifct Trace Netala Poro-
tarM(e)eltv<% Wind Plr Keoortlna Oata Reporting nk Data Reuortlna
7/88 Ongoing Throuoh 7/88 10/87 7/88
•71/88-EPA Foraat Alt Oita
2nd Otr. 1988
N.A. N.A. N.A. 10/87 7/88 *»
8/1/88-EPA ForMt All Data ••'
2nd Otr. 1988 • . «
N.A. K.A. N.A. 18/1/88 EPA ranatt N.A. f
3rd Otr. 1988
""
»
7/88 Optional Optional 10/87 N.A.
4/1/88 EPA roTMt
' >
N.A. 9/30/88 9/30/8* 10/1/88 EPA forMt I.A. j
3rd Otr. 1908

N.A. 4/27/88 Tttrou* 7/88 18/1/88 fPA ForMt N.A.
(alto N.N.) 3rd Otr. 1908
                                                                                                                                                                    10
                                                                                                                                                                    Ul

-------
                                                           127
          APPENDIX A




          RESULTS OP




GAS CHROMATOGRAPB FIELD AUDITS
              8-  91

-------
                                                                                    128
         PPB  FIELD AUDIT REPORT             AUDIT f 312 page 1

PART A - To be  filled out by organization supplying audit cylinders

1.  Individual requesting Audit, organization, and phone number:
    Ray McDermolt, NY State Dept. of Env. Consevatlon

2.  Audit supervisor, organization, and phone number:
    Dr. R.K.M. Jayanty, Research Triangle Institute (919) 541-6483

3.  Shipping Instructions:
    Ray McDermolt
    NY State Dept. of Env. Conservation
    QA Section
    50 Wolf Road
    Albany, NY 12233-3253
4.  Cylinder shipping date: 1-24-1989
5.  Expected arrival date:  2-1-1989

6.  Audit cylinder status:
    a. Cylinder  ID:         AAL 19655
    b. Pressure, pslg:      1120
    c. Construction:        aluminum
    d. Balance gas:         nitrogen

7.  Organic chemical manufacturing process:
    none

8.  Name of Individual or organization being audited:
    1n house

9.  Location of audit:
    Albany, NY

10. Use of audit material:
    Ascertain accuracy of adsorption tube sampling and GC/FID analysis
    procedures used at Staten Island toxic ambient air monitoring study.
    a. Sampling method:        adsorption tube (charcoal)
    b. Analytical method:      GC/FID
    c. Accuracy assessment of:

           VOST method prior to RCRA trial  burn
           bag method prior to RCRA trial burn
           VOST method during actual  RCRA trial burn
           bag method during actual RCRA trial  burn
XX
           measurement method used for routine ambient air measurements
           measurement method used at hazardous waste landfill
           other (explain): _
cc: Darryl von Lehmden, EPA/EHSL, RTP
    Robert Lampe, EPA/EMSL, RTP
    Gary Boynton, Bureau of Toxic A1r Sampling,  NY


                                     8-  92

-------
                                                                                   130
        PPB FIELD AUDIT REPORT              AUDIT I  370  page  1

PART A - To be filled out by organization supplying  audit  cylinders

1. Individual requesting Audit, organization,  and phone  number:
   Ray McDermolt, NY State Dept. of Env.  Conservation

2. Audit supervisor, organization, and phone number:
   Dr. R.K.M. Jayanty, Research Triangle  Institute (919) 541-6483

3. Shipping Instructions:
   Ray McDermolt
   NY State Dept. of Env. Conservation
   QA Section
   50 Wolf Road
   Albany, NY 12233-3253
4. Cylinder shipping date: 08/8/89
5. Expected arrival date:  08/8/89

6. Audit cylinder status:
   a. Cylinder ID:         370
   b. Pressure, pslg:      1300
   c. Construction:        aluminum
   d. Balance gas:         nitrogen

7. Organic chemical manufacturing process:
   none

8. Name of Individual or organization being audited:
   no contractor

9. Location of audit:
   NY State Lab

10.Use of audit material:
   Ascertain accuracy of charcoal tube sampling and GC/FID analysis
   procedures prior to ambient air sampling at Staten Island
   a. Sampling method:        Adsorption  Tube(charcoal)
   b. Analytical method:      GC/FID
   c. Accuracy assessment of:

           VOST method prior to RCRA trial burn
           bag method prior to RCRA trial bum
           VOST method during actual RCRA trial burn
           bag method during actual RCRA trial burn
           measurement method used for routine ambient air measurements
           measurement method used at hazardous waste landfill
           other (explain):	.
XX
cc: Darryl von Lehmden, EPA/AREAL, RTP
    Robert Lampe, EPA/AREAL, RTP
                                      8-  93

-------
                                                        132
      APPENDIX B




 A  Sample of a Field




Flow Performance Audit




   3rd Quarter 1989
       8-   94

-------
                                                                       133
  27-S»p-B9
                               TABLE 1
            NEW YORK STATE DEPT. OF ENVIRONMENTAL CONSERVATION
        DIVISION OF AIR RESOURCES   BUREAU OF TECHNICIAL SERVICES
                        QUALITY ASSURANCE SECTION
                          ATD-50 AUDIT RESULTS
                            3rd QUARTER 1989
Sit*
            Sampler  Flow     C»rt.Flow/VOTS  Calc.Flow/VOTS  Comment*
            Type     Moduli*        %d              '/.d
S. WAGNER
7097-01
            ATD-30
                     L010
                     LOBS
                     L023
  6.7
 -8.2
 -3.*
•9.7
-0.2
•3.9
Changed
vacuum
relief
valve
PUMP STA.
7097-08
            ATD-50
                     L0103
                     L0107
                     L0033
 -S.9
 •8.8
  2.3
 0.2
 2.*
GREAT KILLS ATD-50
7097-06
                     L070
                     L015
                     LOS*
                                   -1J.1
                                   -7.6
                                   -3.7
                  *.8
                  0.9
                  3.5
TOTTENVILLE ATD-50   L0057
7097-05              LOO**
                     L00*l
                                   -11.*
                                   -10.6
                                   -6.6
                                                    -1.7
                                                    •1.0
                                                    -2.0
P.S. 26
7097-02
            ATD-50
                     L0036
                     L0022
                     L0003
-13.6
 -8.6
 -1.5
•3.9
•2.9
-3.*
P. RICHMOND ATD-50
7093-07
                     L010
                     LOO*0
                     L0002
                                   -8.2
                                   •17.6
                                   -6.0
                                                    •1.6
                                                    •3.2
                              8-  95

-------
                                                                       134
 2B-Sep-B9
               TABLE 2
           NEW YORK STATE DEPT. OF ENVIRONMENTAL CONSERVATION
        DIVISION OF AIR RESOURCES   BUREAU OF TECHNICIAL SERVICES
                         QUALITY ASSURANCE SECTION
           CANISTER, HI-VOL, AND PM-10 SAMPLER AUDIT RESULTS
                             3rd QUARTER 1989
Site
Sampler
Type
Audit Device
    Flow
Sampler Flow
•/.d
S. WAGNER
7097-01
CANISTER

WEDDING

TRACE
METALS
  8.95 cc/min

  36.08 CFM

  40.43 CFM
   N/A

  40.92 CFM

  40.99 CFM
 N/A

13.4

 1.4
PUMP STA.
7097-08

GREAT KILLS
7097-06

TOTTENVILLE
7097-05

P.S. 86
7097-OS
P. RICHMOND
7097-03
CANISTER


CANISTER


CANISTER


CANISTER

WEDDING

TRACE
METALS


CANISTER

WEDDING

TRACE
METALS
  8.66 cc/min


  8.31 cc/min


  9.63 cc/min


  8.59 cc/min

  38.12 CFM

  40.81 CFM



  8.91 cc/min

  36.91 CFM

  38.52 CFM
   N/A


   N/A


   N/A


   N/A

  40.21 CFM

  40.39 CFM



   N/A

  40.31 CFM

  39.17 CFM
 N/A


 N/A


 N/A


 N/A

 5.5

•1.0



 N/A

 9.2

 1.7
                                  8-  96

-------
                                                                       135
   New  York  State  Department of Environmental Conservation
                        Division of Air
                 Bureau of Technical  Services
                   Quality Assurance Section
           Volatile Organic Sampler Performance Audit
          <
Date.
Site
Type  of Sampler.^5_7jJ_.55L	Performed by.//D
VOTS  Box  No..^__ Cert.  Date *J/&£lL Vac. Test Gauge No. QC£{
Meas. nod.
Temp. i/ijL_*F  jl2-2_*C  Vacuum Relief Valve Vac.  ,z?/:Ji_-"H9'
Atmospheric  Pressure	£_£.'_ _jL-"MQ'  —•Z.^A-— mm H9 •
Correction Factors:
                      Ai
                         LT * S73J  L29'9d
    T« Actual  Temperature *C   P« Actual Pressure "Hg
Flo** Module  Number  1
Module No. 4^_/j2__  Cert.  Date 5^-§K??Cert. Flow JL'^/.
VOTS Flow  Box  J>_J	cc/min  Percent d (Cert./VOTS)".tfL'-Z	y-
Manometer  Reading R £/.2fl L ^I'.Z.€"TO*»1 J-2-,
Calc. Flow i?-^	cc/min X (Corr. Fact. A>- JL'J_ZL	cc/min
                              Percent d • JjliHi.?*
Manometer  Reading R 2.^1 L .rjj^ Total .f^'Jc
C«lc.  Flow  ^2.*_2	cc/min X (Corr. Fact. A)»_x?,f^^cc/min
                             Percent d (Calc./VOTS)- ~~£'3** y.
                             Page 1          8-  97
                            06/16/69

-------
                                                                      137

                            r» .

                             Percent  d  < Calc./ VOTS )

Flow Module Number  2

Module No. tP-C~-  Cert. Date I2jj£j§& Cert. Flow j

VOTS Flow Box ^l.2._.CC/min  Percent  d  < Cert./ VOTS )*J^/

Manometer Reading R J^i'-L  L -^i~ Tetal J-~.

Calc.  Flow ^2l^.Z__cc/min X (Corr.  Fact. A>«_

                            Percent d (Calc./ VOTS

                                       8-   98

                            Page 1
                           06/16/89

-------
                                                                      139
   New York State Department of Environmental
                       Division of Air
                                                  >*
                 Bureau of Technical Service*            •
                  Duality Assurance Section         •$ *(.["
          Volatile Organic Sampler Performance Audit
Site Name_J_Uj^i\_Wa^•_.......*

Manometer Reading R ..... L ..... Total .....

Calc.  Flow .........cc/min X (Corr. Fact. A)•..._.____«/«»in

                            Percent d (Calc./VOTS)-         •/.
                            Pag.  1        8"
                           06/16/B9

-------
                                                                       14.1
    NEW YORK STATE DEPARTMENT OF ENVIRONMENTAL CONSERVATION
                        DIVISION OF AIR

                  BUREAU OF TECHNICAL SERVICES
                   OUALITY ASSURANCE SECTION

                 PARTICULATE SAMPLER FLOW AUDIT
 DATE	.IJj&iilJXL	   AUDITOR __#*

 SITE NAME _Sj^&A^^\yOcXQ^^X.   SITE NUMBER J

 TEMP. £>L£_*F _27.«i_*C   ATM. PRES. «?9j?J."HGr7&5'..«» Hg
 SAMPLER TYPE i  TSP _____ TRACE METALS _____  PM10-WEDDING__*£t_

 COLLOCATED ____ LEAD ____ PM10- DICOT _______ PMIO-ANDERSEN

                                            SLOPE
               Q(FLOU CPM)» INTERCEPT X IA H ) _
                                                     CHK .  INT
 AUDIT  DEVICE DATA;                                    USED
 ID«         PR I.  CAL.         SLOPE _   __ INT. _______ *0*F_.
                                                       60 fF___
 LEFT  _____ " RIGHT _____ "  TOTAL _____ " Q ________ CFM

                                                     CHK . I NT .
 SAMPLER  DATA;           •                              USED
 ID«         PRI.  CAL.         SLOPE ______ INT..     .  <.0*F
                                                       60»F ___
 LEFT _____ "  RIGHT _____ "  TOTAL _____ "  Q ________ CFM

                                   PERCENT DIFF.  ____________ V.

 DICOT ONLY;      ROTOMETER         ORIFICE DEVICE       PERCENT
 -    COB     LP«      SN       H     LPM     DIFF.
TOTAL FLOWi

COARSE FLOUs
AUDITOR CHECKS  (INDICATE EQUIPMENT  CONDITION)!

SHELTER            __J2j£s.__  BASKET         .    __J0j£_
HOTOR              __.__  TIftER

ORIFICE            _^lA ___  ELECTRICAL WIRING

MANOMETER & TUBING ..OjC ___  CHECK  ORIFICE  NO. .J^f/ft ____
COMMENTS:
                                         8- 100
                            Pag*  1
                           06/16/89

-------
                                                                      143
   NEW YORK STATE DEPARTMENT OF ENVIRONMENTAL CONSERVATION
                       DIVISION OF AIR

                 BUREAU OF TECHNICAL SERVICES
                  DUALITY ASSURANCE SECTION

                PARTICULATE SAMPLER FLOW AUDIT
9f_Z_ql8_9_
                           AUDITOR .

SITE NAME ,kiS&^S*-J^MAfiA.  SITE NUMBER .

TEMP. _SL4— *P  -5-IL-rL'c   ATM. PRES. 5SL'?£HHS_7S£.^m Hg
SAMPLER TYPE* TSP.J^ TRACE METALS_JfelI  PM10-WEDDINB	

COLLOCATED	LEAD	PM10- DICOT	P« 10-ANDERSEN.
                                           SLOPE
              0-  INTERCEPT  X  (AH) 	
                                                     UMK. .  INI
AUDIT DEVICE DATA;                                    USED
           PRI. CAL.         SLOPE   L
                     r~ — T                              , — tf ^^f

LEFT Jjft." RIGHT^.J^," TOTALS.^." 0_flO>}p.CFM

                                                     CHK .  I NT .
SflnPLER DflTfl;                                         USED
ID« 5.0137 PRI.

LEFT J;4.."

                                  PERCENT  DIFF.  .. ____

DICOT ONLY;     ROTOMETER         ORIFICE DEVICE       PERCENT
-    COB     LPM     SN      H      LPM     DIFF.
TOTAL FLOW:

COARSE FLOW>
AUDITOR CHECKS  (INDICATE EQUIPMENT  CONDITION)!

SHELTER            ___ $£=__  BASKET
WOTOR              __     ___  TWER

ORIFICE            _.t^!k ___  ELECTRICAL  HIRING ..C^ ____

MANOMETER L TUBING .JPjCc ___  CHECK ORIFICE NO. __

COMMENTS:
                            P.Q. 1      "- 101
                            O6/16/B9

-------
                                                                       145
   N»*  York  State Department of Environmental Conservation
                        Division of Air

                  Bureau of Technical Services
                   Quality Assurance Section

           Volatile Organic Sampler Performance Audit
Site H***aj&lfi4L4l- ___ Site Number

Type of  S..pi.r_AnL£?- ____ ^formed ty

VOTS Box  No.^2._ Cert.  Date U^Jfi Vac. Test Gauge Ho. /{£'£•?

Mea*.  Mod.  No.5^..Slope^L7_Inter^£^7.Cert. Date.i^/St.'/

Temp.  ?££__• F  5t^._*C  Vacuum Relief Valve Vac. J?/-J?__"Hg.


Atmospheric Pressure 3&±?3. ___ "H0 •  ___ -Z6.S ____ mn» HQ •

Correction  Factors:

                                  x   P
    T« Actual Temperature  *C   P« Actual  Pressure "Hg

Flow Module  Number  1

Module No. t?PJjL$-  Cert. Date CCiLil- Cert.  Flow £i~_£
              ~Q  7                                      XT 6
VOTS Flow Box Pjjl	cc/min  Percent d (Cert./VOTS)«_r.-J_'— *'•

                      II      1 /•)          -9  /
Manometer Reading R .ILL-  L JL~- Total  ..fill
             rt r-fl                              d  ,-«.r£l

Flow Module  Number  8

Module No. rJ?/~7-  Cert. Date 2/3-li. C»rt.  Flow

VOTS Flow Box /Oi.f	cc/min  Percent d (Cert./VOTS)'	

                     ^ 3     >9 n        Z/ <""
Manometer Reading R _C.lJi  L «s-~ Total  «Z'--_
             • p 5».r.CljL.-*

                                        8- 102

                             Page  1
                            06/16/B9

-------
    New York State Department of Environmental  Conservation
                        Division of Air
                  Bureau of Technical  Services                .__
                   Ouality Assurance Section
           Volatile Organic Sampler Performance Audit

 Date. _____ ^WJ?1_

 Site H*™Jl^.liMft5$!M&L __ Site

 Type of B.mpl.r.^au.ft&C. _____ Performed by6mi?i.%//} /

 VOTS Box NO. ____ Cert.  Date __ ..... Vac.  Test  Gauge No.  _. __

 Mea*. nod. No. ______ Slope ______ Inter _______ Cert.  Date _______

 Temp. ./jJife/F  J?4'.3i.*C  Vacuum Relief Valve Vac.  _______ "Hg

 Atmospheric Pressure __ ^L'£3.."*V •  ___ ~2&J2 ____  «m HQ •

 Correction Factors:
                        « r  gpe  i x r  P n «
                         LT  *  S7^J  [S9.9SJ
    T«  Actual  Temperature  *C    P-  Actual  Pressure  "Hg

Flow  Module  Number  1

Module  No. -------  Cert. Date  _______  Cert.  Flo** ______ cc/min

VOTS  Flow Box  _______ cc/min Percent d (Cert ,/VOTS>» ________ */.

Manometer Reading R „„„_„  L __„.__  Total ___

Calc. Flow --------- cc/min X (Corr. Fact. A)«  _________ cc/min

                             Percent d < Calc./ VOTS >».....„..«

FIOM  nodule  Number  2

Module No. -------  cert. Date  ..^ ____  Cert.  Flow ______ cc/min

VOTS  Flow Box  .......cc/min Percent d ( Cert. /VOTS >•........*

nanometer Reading R .....  L .....  Total .....

Calc.  Flow  --------- cc/min X  (Corr. Fact. A>«_ ________ cc/min

                            Percent d  (Calc./VOTS>» _________ •/.


                                       8- 103
                            Page 1
                            06/16/89

-------
                                                                       149
    New  York  State Department of Environment*! Conservation
                        Division of Air

                  Bureau of Technical Services
                   Quality Assurance Section

           Volatile Organic Sampler Performance Audit
Site Name_^r£^jr__£///S ________ Site Number___7<22.7_"#£

Type of  Sampler _/£ .LiJ.T-5?^ _____ Performed

VOTS Box No.jJL_ Cert.  Date &£$$. Vac.  Test Gauge N

flea*. Mod. No.5^/Z..Slopet1l/2ilnt»r?t.Z.'"/5l.Cert. DateX/26/fJ'

Temp. _/<[ ___ *F 2jT'j5__*c  Vacuum  Relief Valve Vac.
Atmospheric Pressure ._Il£_."Hg .   „».„„„„ __ .. ""»•

Correction Factors:
                         T
     T* Actual Temperature *C   P» Actual Pressure  "Hg

 Flow Module Number 1

 Module No./L.Oj^L. Cert. Date d/f§L^'cert. Flo« .

 VOTS Flow Bex 5^^ __ ce/min  Percent d (Cer t . /VOTS >»_7//: .._*/•

 Manometer Reading R ^.'A- L _^1-- Total JjJ2,

 Calc.  Flow .jL'-^jZ __ cc/min X (Corr. Fact. A>»

                              Percent d «_~ /j; ^   y.

Manometer  Reading R _/^_ L j^_3_ Total J?1^T

Calc.  Flow .l^lJL^l.cc/ffiin X (Corr. Fact. A)*_./..'A51_«/min

                             Percent d (Calc . /VOTS)


                                        8-  104
                             Page  1
                           06/16/69
                                                            n

-------

   New York State Department of Environmental Conservation
                       Division of Air          ^              ^j
                                                $e*  CG.n*J»<-4i i*
                 Bureau of Technical Services
                  Duality Assurance Section

          Volatile Organic Sampler Performance Audit
Site Name____V_£_j£jJJ5;	Site Number__7__)__Z--_-l.
                /°    -f                      M(l\
Type of Sampler^Sjj.iiJ/.C.	..Performed byj______/>t

VOTS Box No.	 Cert. Date	 Vac. Test Gauge No. 	

Meas. Mod. No.	Slope	_..Inter___.._.Cert. Dat»__	

Temp. 3Zi	*P J_5_i*C  Vacuum Relief Valve Vac. 	"Hg.

Atmospheric Pressure	_______"Kg.	_____!—. mm  H0-

Correction Factors:


                         IT *  573)  [s9• 9d


    T- Actual Temperature *C   P« Actual Pressure "Hg

Flow Module Number  1

Module No.	Cert. Date	Cert. Flow	cc/min

VOTS Flow Box	cc/min   Percent d  (Cert./VOTS)»	*/.

Manometer Reading R	 L ..... Total

Calc. Flow	cc/min X  (Corr. Fact. A)"	cc/min

                              Percent d  (Calc./VOTS)»	1C

Plow Module Number  2

Module No.	Cert. Date	 Cert. Flow	cc/min

VOTS Flow Box	cc/min   Percent d  (Cert./VOTS>-___.„___*

Manometer Reading R _____ L _____ Total

Calc.  Flow	__cc/min X (Corr. Fact. A)»_->p_-_-__cc/mi n

                            Percent d (Calc./VOTS)-	.	V.


                                       8- 105
                            Page 1
                           06/1./B9

-------
                                                                       153
    New York State Department of Environmental Conservation
                        Division of Air

                  Bureau of Technical Service*
                   Quality Assurance Section

           Volatile Organic Sampler Performance Audit
 Site Name__££jOlC^J.£jX.	Site Number.

 Type of Sampler.j^t,£yil/_<^^._<.->-(_<1.Performed by

 VOTS Box No._2^._ Cert. Date J^^L-Ll Vac. Te»t Gauge No.
 Meat.  Mod. N

 Temp./(.A	*F i^_^:_cC  Vacuum Relief Valve Vac. 2/-..JL	"H9-
                        s\G C /           "7/ I
 Atmospheric Pr«»»ur« _^Li'_i.—"^9 •  .-t.&X.-__--_ mm H0 •

 Correction Factor*:
                         r  g9B ixr  P >  ^
                         IT * 273J  [S9.92J
     T*  Actual  Temperature *C   P» Actual Pre«»ure "Hg

    « Module Number i

Module  No. h@Q5,Z. Cert.  Date ly3xJ[L- Cert. Flow J^'J^	cc/min

VOTS Plow  Box  _
-------
                                                                       155
   New  York  State Department  of  Environmental  Conservation
                        Division  of  Air            ^               -a.
                                                   }.*»C.   £ Cj^ >»V i: ^
                 Bureau of  Technical  Services
                  Quality Assurance Section

          Volatile  Organic  Sampler  Performance Audit
Si t» Name 7Vtt?n ? ' " €           Si te  Number. 79 SZl^-f
         ^••••••••aMBk—V^ V< •»••>•»••> ^^^•^•WiOVaV'MeJ^           ••»*• ^» ^ ^"J" ^ ^^-«" ^m^

Type of  SamplerJ^jj./pjffCI _______ Performed  byJu^l^^O

VDTS Box No. ____  Cert. Date ....... Vac.  T»«t Gauge  No. . ___

Meas.  Mod.  No. ______ Slope ______ Inter... ___ ..Cert. Date ___ ....
Temp. _J.2_.'F _J*fc.-Jt-*C  Vacuum Relief Valve Vac.	"Hg.

Atmospheric Pressure ..?__*-_r--"Hfl •  —_ZA_—— mfn H5-

Correction Factors:

                         "     " x r  p
                          liaaJ
                            *  B73J
    T« Actual Temperature  *C    P*  Actual  Pressure "Hg

Flow Module  Number  1

Module No.	Cert. Date .......  Cert.  Flo** .	cc/min

VDTS Flow Box	cc/min   Percent d «	•/.

Manometer Reading R _____  L .....  Total  .....

Calc. Flow	cc/min X  (Corr. Fact. A)- ....	..cc/min

                              Percent d (Calc./VOTS)-	X

Flow Module  Number  2

Module No. .......  C«rt. Date/ .......  Cert.  Flow ......cc/mln

VOTS Flo*- Box	_,	..ceymin   Percent d (Cert./VOTS>".._.....%

Manometer Reading R .....  L .....  Total  .....

Calc.  Flow  ._.__..._cc/min X (Corr. Fact. A)»_________«/mJn

                            Percent d  (Cale./VOTS>«	y.


                                         8- 107
                            Pag* 1
                           06/16/89

-------
                                                                        157
    New York State Department of Environmental  Conservation
                        Division of  Air

                  Bureau of Technical Service*
                   Quality Assurance Section

           Volatile Organic Sampler  Performance Audit
 Site Name__i_5.__2^ ____________ Site Number. __

 Type of,Sampler._Ar/L<6!2L _____ Performed t

 VOTS Box No._2^_ Cert. !>•*• *l/&liuL Vac. Test Gauge  No.
 Me««. Mod. No

 Temp. l'j?;j^_*F /L2-1.*C  Vacuum Relief Valve Vac.

 Atmospheric Pressure __2±iT.^l_.."Hg .  «__Z£j£>_____  ">n»

 Correction Factors:
                              87
     T«  Actual  Temperature *C   P* Actual Pressure  MHg

    * Module Number 1

Module  No. £-££3.0, Cert.  Date 4^1tZ. Cert. Flo«

VOTS Flew Box  _L'_3_	cc/min  Percent d (Cert./VOTS>-_7/

Manometer  Reading  R _/'_£.- L --J-- Total £^j^

Calc. Flow _£•_££.	cc/min X (Corr. Fact. A)-

                              Percent d tCalc./VOTS)-."^'.!.	X

Flow Module  Number £

Module No. A<2i!^_ Cert.  Date &Z.HiLi.L C«rt. Flow 2j^^£cc/«in

VOTS Flow  Box  y^j^.	cc/min  Percent d I Cert. /VOTS >».r^L.-—y«
                      O 1     1 ^         _-Ji: L jclC. Total „_£_£
             1-5 ^                              77 7"7
Calc.  Flow  jL/^.l._.cc/min X (Corr. Fact. A>»_/ii/j^^cc/mi n

                             Percent d (Calc./VOTS)- ~ P-?   y.
                                      8- 108
                             Page 1
                            OA/1A/S9

-------
                                               is fa-
                                                                      159
New York State Department of Environmental Conservation
                    Division of Air           c                -i
                                              J f c  C. Ot » m < » i I 5
              Bureau of Technical Service*
               Quality Assurance Section

       Volatile Organic Sampler Performance Audit
                                                          tf/rv.
                                                         tl«	V.

Manometer Reading R	 L  ..... Total 	..

Calc. Flow 	..cc/min X CCorr. Fact. A)«  ._.	....cc/min

                             Percent d (Calc./VOTS>«	V.

Flow nodule Number S

nodule No.	Cert.  Date	.	Cert. Flow	cc/min

VOTS Flow Box	cc/«in  Percent d (Cert./VOTS>•......._*.

nanometer Reading R ..... L  ..... Total .....

Calc.  Flow .	cc/min  X 
-------
                                                                       161
NEW YORK STATE DEPARTMENT OF ENVIRONMENTAL CONSERVATION
                    DIVISION OF AIR

              BUREAU OF TECHNICAL SERVICES
               QUALITY ASSURANCE SECTION

             PARTICULATE SAMPLER FLOW AUDIT


  .4/Zfi/ft2 ______
 DATE .            ______   AUDITOR

 SITE NAME .JcLS;_2te _____________  SITE NUMBER .

 TEMP. _924_*F 33:3. »C   «TH. ™ES- 35>J,SL"HBj?J!L ____

MANOMETER & TUBING __£>tt» ___  CHECK ORIFICE  NO. ..

COMMENTS :
                            Pag* 1

-------
                                                                      163
   NEW YORK STATE DEPARTMENT OF ENVIRONMENTAL CONSERVATION
                       DIVISION OF AIR

                 BUREAU OF TECHNICAL SERVICES
                  QUALITY ASSURANCE SECTION
                P ARTICULATE SAMPLER FLOW AUDIT
DATE	ZI/Z§±»:1	   AUDITOR JJ.

SITE NAME	Jl*^iJ2Cft	  SITE NUMBER ___jLS£


TEMP. H^JJI.'F jZ3jjL_*C   ATM. PRES.



SAMPLER TYPE: TSP__*^TRACE METALS__fe£^PM10-HEDDING	

COLLOCATED	LEAD	PM10- CICOT	PM10-ANDERSEN.
                                           SLOPE
              0-  INTERCEPT  K   -7      **.™          60-F]^
LEFT Ll-sL." R1BHTJ^_" TOTAL«4.LL_'
                                  PERCENT  DIFF.
DICDT ONLV;     ROTOMETER         ORIFICE  DEVICE      PERCENT
	    COB     LPM     SN      H     LPM     DIFF.
TOTAL FLOWs

COARSE FLOW:
AUDITOR CHECKS  (INDICATE EQUIPMENT  CONDITION>s
SHELTER            ..J?JrL-.  SASKET


MOTOR              ..J5J4.	  TXflER


ORIFICE            ..^SftfeK*ELECTRICAL WIRING


MANOMETER i TUBING .J2&	  CHECK ORIFICE NO. J

COMMENTS * 	

                                    8- Hi


                            P«g» 1
                            ^A /14./00

-------
                                                                        165
    New York State Department of  Environmental  Conservation

                         Division  of  Air


                  Bureau of Technical  Service*

                   Duality Assurance Section


           Volatile Organic Sampler  Performance Audit
 Site Name_£j£££__^_K_h22.20j2'_	...Sit* Number


 Type of Sampler_/rJ_/J_j5cJ	...Performed b

              s\              Lll-i^lM
 VOTS Box No.-_'^*C  Vacuum Relief Valve Vac.


 Atmospheric Pressure	sJl'jlT	"H0-  — J_rLS..__- mm  HQ •


 Correction Factors:
                            39B  "I

                          T * 273]
,59.92]
     T« Actual  Temperature *C   P« Actual Pressure  "Hg


 Flow Module Number 1
                                 O

 Module No./^CO/^ Cert.  D*te __ S ____ Cert. Flo**
VOTS  Flow Box  j'_  ___ cc/min  Percent d .'J2. _*/.


Manometer  Reading  R _/'.£_ L -dl^L Total J^O


Calc. Flow ,O_'_X ____ cc/min X (Corr. Fact. A)« J&Ji/S ___ cc/min


                              Percent d tCalc


Flow Module Number 8


Module No.Z££V<2_ Cert.  Date ___,*._„ C»rt. Flow
VOTS Flow Box _ui£— cc/min  Percent d ( Cer t . / VOTS > » J


nanometer Reading R _/;./„-  L _/!/_ Total ^i2..


Calc.  Flow _Jj^?_ __ ec/min X (Corr. Fact. A


                             Percent d 
-------
                               r
                               J O i
                                                                       167
    New York  State Department of Environmental Conservation

                        Division of Air
                  Bureau of Technical Services              -I

                   Quality Assurance Section             J«V (<£lv



           Volatile Organic Sampler Performance Audit



 Date	.JZ/JlLj.l  _..__.„.



 Site Name-j^)i£j^_j^2i"^1*'^ £...  Sit*. Numb»r.^j[Js L£.Tr'-5—-

                 /"*   •  "T*                      /M^/l     "///I  ( 'T~
 Type of Sampler C^jt;/^!^^"	Performed by^[(.J^ci- ________ •/.


Manometer Reading R _____ L _____ Total



Calc. Flow ________ .cc/min X (Corr. Fact. A)» ___ __ ....cc/min



                              Percent d (Calc ./VOTE)- ________ X


Flow Module  Number  8



Module  No. _.__._..  Cert.  Date „_«____ C»rt. Flew ......cc/iiiin



VOTS Flow Box  _______ cc/min  Percent d 
-------
                                                                       169
    NEW YORK STATE DEPARTMENT OF ENVIRONMENTAL CONSERVATION
                        DIVISION OP AIR

                  BUREAU OF TECHNICAL SERVICES
                   DUALITY ASSURANCE SECTION

                 PARTICULATE SAMPLER FLOW AUDIT
                            AUDITOR

 SITE NAME -eiatoart^L...  SITE NUMBER ...l

     . .3.6...* F 2j5i£L*C   ATM. PRES. ^3l8£"HG.7£6..^"< Hg
 SAMPLER TYPE* TSP _____ TRACE METALS ____  PM10-WEDDIN6..

 COLLOCATED ____ LEAD ____ PM10- DICOT _______ PM10-ANDERSEN _____

                                            SLOPE
 _ Q(FLDU) CFM>» INTERCEPT X (AH)
                                                     CHK.  INT.
 AUDIT DEVICE DATA;                                    USED
=====                                     30.p
 ID* ______ PRI.  CAL.    ... SLOPE ___    INT.         <*0*F
                                                       60 rF
 LEFT _____ " RIGHT _____ " TOTAL _____ " Q ________ CFM

                                                     CHK.  INT.
 SAMPLEP DATA;                                        USED
                                                       30CF
 ID* ______ PRI.  CAL. ________ SLOPE _______ JNT. ________ «0*F ___
                                                       60»F~ __
 LEFT _____ " RIGHT  ___ " TOTAL _____ " Q        CFM
                                   PERCENT DIFF.
                 ROTOMETER         ORIFICE DEVICE      PERCENT
                COB      LPM     SN       H     LPM     DIFF.
TOTAL FLOW*

COARSE FLOWt
AUDITOR CHECKS  (INDICATE  EQUIPMENT CONDITION)!
SHELTER               CSl—  GASKET               _fl/C.
                   ^^^^^^^»^^»                     ^••••ib A*^^^v^«»^

MOTOR              ..J?K	  TWER             	Q|C.	

ORIFICE            «^iL6	  ELECTRICAL  WIRING _

MANOMETER I TUBING ..OJ^.	  CHECK ORIFICE NO. ...A

COMMENTS*
                                       8- 114
                            Pag*  1
                           06/16/89

-------
                                                                      1.71
   NEW YORK STATE DEPARTMENT OF ENVIRONMENTAL CONSERVATION
                       DIVISION OF AIR

                 BUREAU OF TECHNICAL SERVICES
                  DUALITY ASSURANCE SECTION

                PART1CULATE SAMPLER FLOU AUDIT
DATE	^£feyJ2ZL_   AUDITOR ..(.{.(
SITE NAME _J?Oji_.^l^i^OJ3ct.  SITE NUMBER _J?fi£7r_C3
TEMP. .IZ£L.*F j?Si51cc   ATM. pREs.«?ij2jL"HG..7!5Eb.«« HQ
SAMPLER TYPEt TSP..    TRACE METALS.jtl   PM10-WEDDJNB	

COLLOCATED	LEAD	PM10- DICOT_	. PM10-ANDERSEN_
                                           SLOPE
              0(FLOW CFM)« INTERCEPT X (AH)
                                                    CMK . INT
AUDIT DEVICE DATAt                                   USED
LEFT
                                                    CHK. INT.
SAMPLER DATA;                                        USED
                                  PERCENT DIFF. ....'j. _____ */.
 1COT ONLY:     ROTOMETER        ORIFICE DEVICE      PERCENT
               COB     LPM     SN       H     LPM     DIFF.
TOTAL FLOW:  	

COARSE FLOWI
AUDITOR CHECKS (INDICATE EQUIPMENT CONDITION)!

SHELTER            ___££•—-  BASKET            .

MOTOR              ..£11	  TlflER

ORIFICE            _J2.£._  ELECTRICAL WIRING	Off

MANOMETER & TUBING __£>.f=t.  CHECK ORIFICE NO.

COMMENTS:
                                     8- 115
                            Pag* 1
                           06/16/89

-------
                                                             173
           APPENDIX C




SAMPLE PRECISION ANALYSIS RESULTS
              8- 116

-------
                                                                                            174
 ECISION ANALYSIS
 UTRH QUARTER 19 87

 ALYTE:  DICHLOROMETHANE
 HBER OF FAIRS:   15
 ERAGE % DIFFERENCE:     5.35
 ANDARD DEVIATION OF % DIFFERENCE:    24.38
 VER 95% CONFIDENCE LIMIT:   -42.44
 PER 95% CONFIDENCE LIMIT:    53.15


 ALYTE:  CHLOROFORM
 HBER OF PAIRS:   3
 T ENOUGH PAIRS  TO EVALUATE STATISTICS


 ALYTE:  1.2DICHLOROETHANE
 HBER OF PAIRS:   2
 T ENOUGH PAIRS  TO EVALUATE STATISTICS


 ALYTE:  1.1.1TRICHLOROETHANE
 HBER OF PAIRS:   22
 ERACE % DIFFERENCE:     1.95
 ANDARD DEVIATION OF % DIFFERENCE:    16.70
 WER 95% CONFIDENCE LIMIT:   -30.78
 PER 95% CONFIDENCE LIMIT:    34.68


 ALYTE:  BENZENE
 MBER OF PAIRS:   23
 ERAGE % DIFFERENCE:     3.36
 •ANDARD DEVIATION OF % DIFFERENCE:    27.49
 >UER 95% CONFIDENCE LIMIT:   -50.52
 •PER 95% CONFIDENCE LIMIT:    57.23


 IALYTE:  CARBON TETRACHLORIDE
 MBER OF PAIRS:   0
 )T ENOUGH PAIRS  TO EVALUATE STATISTICS


 JALYTE:  TRICHLOROETHYLENE
 IMBER OF PAIRS:   4
 /ERAGE % DIFFERENCE:     8.28
 ANDARD  DEVIATION OF % DIFFERENCE:    15.30
 JWER 95% CONFIDENCE LIMIT:   -21.70
 ?PER 95% CONFIDENCE LIMIT:    38.27


 IALYTE:  1,1,2TRICHLOROETHANE
 MBER OF PAIRS:   0
 )T ENOUGH PAIRS  TO EVALUATE STATISTICS
JALYTE:  TOLUENE
JMBER OF PAIRS:   21
                                               8-  117

-------
                                                                                              176
  .ECISION ANALYSIS
  kST QUARTER 19 88

  ALYTE: DICHLOROMETHANE
  USER OF PAIRS:  21
  •ERACE % DIFFERENCE:    0.73
  •ANDARO DEVIATION OF % DIFFERENCE:   22.99
  iWER 95% CONFIDENCE LIMIT:  -44.34
  'PER 95% CONFIDENCE LIMIT:   45.80


  IALYTE: CHLOROFORM
  MBER OF PAIRS:  13
  TRACE % DIFFERENCE:   -6.72
  :ANDARD DEVIATION OF % DIFFERENCE:   26.18
  JUER 95% CONFIDENCE LIMIT:  -58.03
  'PER 95% CONFIDENCE LIMIT:   44.59


  IALYTE: 1.2DICHLOROETHANE
  MBER OF PAIRS:  3
  )T ENOUGH PAIRS TO EVALUATE STATISTICS


  4ALYTE: 1.1.1TRICHLOROETHANE
  JMBER OF PAIRS:  25
  /ERAGE % DIFFERENCE:    1.02
  IANDARD DEVIATION OF % DIFFERENCE:   20.70
  DWER 95% CONFIDENCE LIMIT:  -39.56
  PPER 95% CONFIDENCE LIMIT:   41.60


 NALYTE: BENZENE
 UMBER OF PAIRS:  25
 VERAGE % DIFFERENCE:   -0.18
 TANDARD DEVIATION OF % DIFFERENCE:   23.83
 OUER 95% CONFIDENCE LIMIT:  -46.89
 PPER 95% CONFIDENCE LIMIT:   46.52


 NALYTE: CARBON TETRACHLORIDE
 UMBER OF PAIRS:  2
 '01 ENOUGH PAIRS TO EVALUATE STATISTICS


 •NALYTE: TRICHLOROETHYLENE
 UMBER OF PAIRS:  19
 vVERAGE % DIFFERENCE:   -1.52
 STANDARD DEVIATION OF % DIFFERENCE:   22.11
 jOVER 95% CONFIDENCE LIMIT:  -44.85
JFPER 95% CONFIDENCE LIMIT:   41.81


\NALYTE: 1.1.2TRICHLOROETHANE
DUMBER OF PAIRS:  0
WT ENOUGH PAIRS TO EVALUATE STATISTICS
                                                 8- 118

-------
                                                                                            178
NALYTE:  1.4DICHLOROBENZENE
UMBER OF PAIRS:   0
OT ENOUGH PAIRS  TO EVALUATE STATISTICS


NALYTE:  1.2DICHLOROBENZENE
OKBER OF PAIRS:   2
DT ENOUGH PAIRS  TO EVALUATE STATISTICS
                                             8-  119

-------
                                                                                             180
 M.YTE: 1,1,2TRICHLOROETHANE
 ffiER OF PAIRS:  0
 I ENOUGH PAIRS TO EVALUATE STATISTICS
 ALYTE: TOLUENE
 MBER OF PAIRS:  34
 ERAGE I DIFFERENCE:   -1.96
 AKDARD DEVIATION OF % DIFFERENCE:    11.74
 3ER 95% CONFIDENCE LIMIT:  -24.96
 PER 951 CONFIDENCE LIMIT:   21.05
 ALYTE:  TETRACHLOROEHTYLENE
 .1BER OF PAIRS:  28
 ERAGE % DIFFERENCE:    1.53
 ANDARD DEVIATION OF % DIFFERENCE:     5.58
 3ER 95% CONFIDENCE LIMIT:   -9.41
 PER 95% CONFIDENCE LIMIT:   12.46
 ALYTE: CHLOROBENZENE
 MBER OF PAIRS:  5
 ERAGE % DIFFERENCE:   -10.16
 ANDARD DEVIATION OF % DIFFERENCE:    14.09
 WER 95% CONFIDENCE LIMIT:   -37.78
 PER 95% CONFIDENCE LIMIT:    17.46
 ALYTE:  ETHYLBENZENE
 MBER OF PAIRS:   28
 ERAGE % DIFFERENCE:   -0.22
 ANDARD DEVIATION OF % DIFFERENCE:    10.48
 UER 95% CONFIDENCE LIMIT:   -20.76
 PER 95% CONFIDENCE LIMIT:    20.33
ALYTE:  M.P-XYLENE
MBER OF PAIRS:   36
TRACE t DIFFERENCE:     4.90
•ANDARD DEVIATION OF  %  DIFFERENCE:    30.89
iWER 95% CONFIDENCE LIMIT:   -55.66
'PER 95% CONFIDENCE LIMIT:    65.45
IALYTE:  0-XYLENE
MBER OF PAIRS:   33
rERACE  % DIFFERENCE:     0.97
:ANDARD DEVIATION OF %  DIFFERENCE:     5.95
WER 95% CONFIDENCE  LIMIT:   -10.69
'PER 95% CONFIDENCE  LIMIT:    12.64
IALYTE:  1.3DICHLOROBENZENE
JMBER OF PAIRS:   19
                                                8- 120

-------
                                                                                           182
 iCISION ANALYSIS    ENVIROCHEM  SYSTEM
 [RD QUARTER 19  88

 VLYTE:  DICHLOROMETHANE
 1BER OF PAIRS:  12
 SRAGE % DIFFERENCE:     1.30
 \NDARD DEVIATION OF %  DIFFERENCE:   13.47
 JER 95% CONFIDENCE  LIMIT:  -25.09
 ?ER 95% CONFIDENCE  LIMIT:    27.69


 VLYTE:  CHLOROFORM
 IBER OF PAIRS:  13
 JRAGE % DIFFERENCE:    -4.13
 \NDARD DEVIATION OF %  DIFFERENCE:   12.89
 JER 95% CONFIDENCE  LIMIT:  -29.40
 PER 95% CONFIDENCE  LIMIT:    21.14


 \LYTE:  1.2DICHLOROETHANE
 iBER OF PAIRS:  2
 T ENOUGH PAIRS  TO EVALUATE STATISTICS


 U.YTE:  l.l.lTRICHLOROETHANE
 IBER OF FAIRS:  15
 ERAGE % DIFFERENCE:     5.04
 ANDARD DEVIATION OF %  DIFFERENCE:   16.40
 •JER 95% CONFIDENCE  LIMIT:  -27.10
 PER 95% CONFIDENCE  LIMIT:    37.18


 ALYTE:  BENZENE
 tfBER OF PAIRS:  12
 ERAGE % DIFFERENCE:    -2.78
 ANDARD DEVIATION OF %  DIFFERENCE:   15.00
 UER 95% CONFIDENCE  LIMIT:  -32.17
 PER 95% CONFIDENCE  LIMIT:    26.61


 ALYTE:  CARBON TETRACHLORIDE
 KBER OF PAIRS:  3
 t ENOUGH PAIRS  TO EVALUATE STATISTICS


 ALYTE:  TRICHLOROETHYLENE
 HBER OF PAIRS:  8
 ERASE % DIFFERENCE:    -3.57
        DEVIATION OF %  DIFFERENCE:   10.10
     95% CONFIDENCE  LIMIT:  -23.37
'PER 95% CONFIDENCE  LIMIT:    16.23


1/aYTE:  1,1,2TRICHLOROETHANE
      OF PAIRS:  0
   ENOUGH PAIRS  TO EVALUATE STATISTICS


                                           8- 121

-------
                                                                                          184
LYTE:  1.2DICHLOROBENZENE
BER OF PAIRS:   1
 ENOUGH PAIRS  TO  EVALUATE  STATISTICS
                                         8-  122

-------
                                                                                            186
 U.YTE: TOLUENE
 ttER OF PAIRS:  9
 •SAGE % DIFFERENCE:   11.10
 \JJDARD DEVIATION OF % DIFFERENCE:   19.96
 ffR 95% CONFIDENCE LIMIT:  -28.01
 PER 95% CONFIDENCE LIMIT:   50.22
 U.YTE: TETRACHLOROEHTYLENE
 1BER OF PAIRS:  9
 SRAGE % DIFFERENCE:    6.80
 \NDARD DEVIATION OF % DIFFERENCE:   10.52
 JER 95% CONFIDENCE LIMIT:  -13.81
 ?ER 95% CONFIDENCE LIMIT:   27.42
 \LYTE: CHLOROBENZENE
 tfER OF PAIRS:  0
 r ENOUGH PAIRS TO EVALUATE STATISTICS
 U.YTE: ETHYLBENZENE
 «ER OF PAIRS:  9
 TRACE % DIFFERENCE:    10.62
 \NDARD DEVIATION OF  %  DIFFERENCE:   19.27
 JER 95% CONFIDENCE LIMIT:   -27.14
 PER 95% CONFIDENCE LIMIT:   48.38
 U.YTE: M.P-XYLENE
 1BER OF PAIRS:   9
 ERACE % DIFFERENCE:    7.42
 4NDARD DEVIATION OF  % DIFFERENCE:   14.46
 JER 95% CONFIDENCE LIMIT:  -20.92
 PER 95% CONFIDENCE LIMIT:   35.76
ALYTE: 0-XYLENE
MBER OF PAIRS:  9
ERAGE % DIFFERENCE:    8.38
ANDARD DEVIATION OF  % DIFFERENCE:    17.09
UER 95% CONFIDENCE LIMIT:  -25.13
PER 95% CONFIDENCE LIMIT:   41.88
ALYTE: 1.3DICHLOROBENZENE
MBER OF PAIRS:  0
1 ENOUGH PAIRS TO EVALUATE  STATISTICS
ALYTE: 1.4DICHLOROBENZENE
HBER OF PAIRS:  5
•£RAGE % DIFFERENCE:   22.53
•ANDARD DEVIATION OF  % DIFFERENCE:    16.43
,y£R 95% CONFIDENCE LIMIT:    -9.67
•PER 95% CONFIDENCE LIMIT:    54.73
                                                 8-  123

-------
                                                                                             188
 SCISION ANALYSIS  ENVIROCHEM SYSTEM
 JTRH QUARTER 19 88

 »JLYTE: DICHLOROMETHANE
 1BER OF PAIRS:   29
 31AGE % DIFFERENCE:    -2.36
 VNDARD DEVIATION OF % DIFFERENCE:    17.18
 JER 95% CONFIDENCE LIMIT:   -36.03
 PER 95% CONFIDENCE LIMIT:    31.31


 ILYTE: CHLOROFORM
 iflER OF PAIRS:   17
 iBACE % DIFFERENCE:    -8.24
 \NDARD DEVIATION OF % DIFFERENCE:    29.84
 JER 95% CONFIDENCE LIMIT:   -66.73
 PER 95% CONFIDENCE LIMIT:    50.25


 U.YTE: 1.2DICHLOROETHANE
 1BER OF PAIRS:   1
 F  ENOUGH PAIRS  TO EVALUATE STATISTICS


 U.YTE: 1,1,1TRICHLOROETHANE
 1BER OF PAIRS:   34
 ERAGE % DIFFERENCE:    -4.90
 ANDARD DEVIATION OF % DIFFERENCE:    23.75
 •JER 95% CONFIDENCE LIMIT:   -51.46
 PER 95% CONFIDENCE LIMIT:    41.65


 ALYTE: BENZENE
 -BER OF PAIRS:   34
 ERAGE % DIFFERENCE:    10.21
 ANDARD DEVIATION OF % DIFFERENCE:    29.30
 tfER 95% CONFIDENCE LIMIT:   -47.23
 PER 95% CONFIDENCE LIMIT:    67.64


 ALYTE: CARBON TETRACHLORIDE
 KBER OF PAIRS:   7
 ERAGE I DIFFERENCE:    -6.51
 ANDARD DEVIATION OF % DIFFERENCE:     B.34
 UER 95% CONFIDENCE LIMIT:   -22.86
 PER 95% CONFIDENCE LIMIT:     9.84


 ALYTE:  TRICHLOROETHYLENE
 MBER OF PAIRS:   22
 ERACE % DIFFERENCE:    -7.58
 ANDARD DEVIATION OF  % DIFFERENCE:    23.64
VER 95% CONFIDENCE LIMIT:   -53.92
•PER 951 CONFIDENCE LIMIT:    38,76


        1.1.2TRICHLOROETHANE

                                               8- 124

-------
                                                                                           190
ȣR 95% CONFIDENCE LIMIT:    34.16
     :  1.4DICHLOROBENZENE
1BER  OF PAIRS:  0
f ENOUGH PAIRS TO EVALUATE  STATISTICS
U.YTE:  1.2DICHLOROBENZENE
1BER  OF PAIRS:   2
[ ENOUGH PAIRS  TO  EVALUATE STATISTICS
                                             8- 125

-------
                                                                                            192
 HBER OF FAIRS:  0
 T ENOUGH PAIRS TO EVALUATE STATISTICS
 ALYTE: TOLUENE
 HBER OF PAIRS:  52
 ERACE % DIFFERENCE:    1.90
 ANDARD DEVIATION OF % DIFFERENCE:   23.82
 PER 95% CONFIDENCE LIMIT:  -44.79
 PER 951 CONFIDENCE LIMIT:   48.58
 ALYTE: TETRACHLOROEHTYLENE
 HBER OF PAIRS:  46
 ERACE % DIFFERENCE:    1.06
 ANDARD DEVIATION OF % DIFFERENCE:   13.57
 tf£R 95% CONFIDENCE LIMIT:  -25.54
 PER 95% CONFIDENCE LIMIT:   27.65
 ALYTE: CHLOROBENZENE
 HBER OF PAIRS:   4
 ERAGE % DIFFERENCE:     0.00
 ANDARD DEVIATION OF % DIFFERENCE:     0.00
 WER 95% CONFIDENCE LIMIT:     0.00
 PER 95% CONFIDENCE LIMIT:     0.00
 ALYTE:  ETHYLBENZENE
 MBER OF PAIRS:   50
 ERAGE % DIFFERENCE:   -0.66
 ANDARD DEVIATION OF % DIFFERENCE:    11.70
 VER 95% CONFIDENCE LIMIT:   -23.60
 'PER 95% CONFIDENCE LIMIT:    22.28
1ALYTE:  M.P-XYLENE
MBER OF PAIRS:   52
TRACE % DIFFERENCE:     2.35
•ANDARD DEVIATION OF  % DIFFERENCE:    16.04
JWER 95% CONFIDENCE LIMIT:   -29.09
'PER 95% CONFIDENCE LIMIT:    33.79
IALYTE:  0-XYLENE
JHBER OF PAIRS:   37
'ERACE % DIFFERENCE:     0.29
TANDARD DEVIATION OF  %  DIFFERENCE:    10.80
WER 95% CONFIDENCE LIMIT:   -20.87
'PER 95% CONFIDENCE LIMIT:    21.45
IALYTE:  1.3DICHLOROBENZENE
JHBER OF PAIRS:   15
7ERAGE  % DIFFERENCE:    -3.79
TANDARD DEVIATION OF  %  DIFFERENCE:    22.28
WER 95% CONFIDENCE LIMIT:   -47.46
                                                8-  126

-------
                                                                                           194
iCISION ANALYSIS  frTt>
1ST QUARTER 19 89

U.YTE: DICHLOROMETHANE
1B2R OF PAIRS:  48
SRACE % DIFFERENCE:   -A.04
\NDARD DEVIATION OF % DIFFERENCE:   25.86
JER 95% CONFIDENCE LIMIT:  -54.74
?ER 95% CONFIDENCE LIMIT:   46.65


U.YTE: CHLOROFORM
1BER OF PAIRS:  34
2RAGE % DIFFERENCE:   -1.54
UJDARD DEVIATION OF % DIFFERENCE:   20.27
JER 95% CONFIDENCE LIMIT:  -41.26
PER 95% CONFIDENCE LIMIT:   38.18


\LVTE: 1.2DICHLOROETHANE
iBER OF PAIRS:  2
I ENOUGH PAIRS TO EVALUATE STATISTICS


U.YTE: 1.1.1TRICHLOROETHANE
iBER OF PAIRS:  74
ERAGE % DIFFERENCE:   -2.44
tfJDARD DEVIATION OF % DIFFERENCE:   33.12
J£R 95% CONFIDENCE LIMIT:  -67.35
PER 95% CONFIDENCE LIMIT:   62.47


ALYTE: BENZENE
HBER OF PAIRS:  72
ERAGE % DIFFERENCE:   -4.23
ANDARD DEVIATION OF % DIFFERENCE:   21.38
UER 95% CONFIDENCE LIMIT:  -46.13
PER 95% CONFIDENCE LIMIT:   37.67


ALYTE: CARBON TETRACHLORIDE
MflER OF PAIRS:  33
ERAGE % DIFFERENCE:   -0.19
•ANDARD DEVIATION OF % DIFFERENCE:   17.99
,WER 95* CONFIDENCE LIMIT:  -35.46
•PER 95% CONFIDENCE LIMIT:   35.07


IALVTE: TRICHLOROETHYLENE
MBER OF PAIRS:  62
rrRAGE * DIFFERENCE:   -5.54
•ANDARD DEVIATION OF % DIFFERENCE:   21.96
)VER 95% CONFIDENCE LIMIT:  -48.58
•PER 95% CONFIDENCE LIMIT:   37.50


J/O.YTE: 1.1.2TRICHLOROETHANE

                                               8- 127

-------
                                                                                            196
3. 95% CONFIDENCE LIMIT:   59.72


YTE: 1.4DICHLOROBENZENE
ER OF FAIRS:  7
ACE % DIFFERENCE:    5.51
DARD DEVIATION OF I DIFFERENCE:   18.31
R 951 CONFIDENCE LIMIT:  -30.39
R 95% CONFIDENCE LIMIT:   41.40


YTE: 1.2DICHLOROBENZENE
ER OF PAIRS:  5
:.CE % DIFFERENCE:   -0.82
DARD DEVIATION OF % DIFFERENCE:    1.83
R 95% CONFIDENCE LIMIT:   -4.39
R 95% CONFIDENCE LIMIT:    2.76
                                     8- 128

-------
                                                                                           198
ALYTE: 1.1.2TRICHLOROETHANE
KBER OF FAIRS:  0
T  ENOUGH PAIRS TO EVALUATE STATISTICS
ALYTE: TOLUENE
HBER OF PAIRS:  73
ERACE % DIFFERENCE:     5.77
ANDARD DEVIATION OF  % DIFFERENCE:    33.3A
tfER 95% CONFIDENCE LIMIT:  -59.59
PER 951 CONFIDENCE LIMIT:    71.12
 ALYTE: TETRACHLOROEHTYLENE
 HBER OF  PAIRS:   62
 BRACE %  DIFFERENCE:     0.93
 ANDARD DEVIATION OF  %  DIFFERENCE:    U.17
 UER 95%  CONFIDENCE LIMIT:   -26.64
 PER 95%  CONFIDENCE LIMIT:    28.70
 ALYTE:  CHLOROBENZENE
 HBER OF PAIRS:   8
 •ERAGE % DIFFERENCE:     3.07
 ANDARD DEVIATION OF  %  DIFFERENCE:    21.37
 ,tfER 95% CONFIDENCE LIMIT:   -38.83
 •PER 95% CONFIDENCE LIMIT:    44.96
'ALYTE:  ETHYLBENZENE
TIBER OF PAIRS:   71
•ERACE % DIFFERENCE:     5.72
•ANDARD DEVIATION OF % DIFFERENCE:    23.93
tWER 95% CONFIDENCE LIMIT:   -41.18
•PER 95% CONFIDENCE LIMIT:    52.62
        M.P-XYLENE
JMBER OF PAIRS:   73
FERAGE % DIFFERENCE:    -1.62
•ANDARD DEVIATION OF % DIFFERENCE:    21.23
,VER 95% CONFIDENCE LIMIT:   -43.23
>PER 95% CONFIDENCE LIMIT:    40.00
JALYTE:  0-XYLENE
jKBER OF PAIRS:   73
/TRACE % DIFFERENCE:     2.15
PANDARD DEVIATION OF % DIFFERENCE:   13.39
)VEB. 95% CONFIDENCE LIMIT:   -24.10
?PER 95* CONFIDENCE LIMIT:    28.40
4ALYTE: 1.3DI CHLOROBENZENE
      OF PAIRS:   39
                                              8-  129

-------
                                                                                            200

 VISION ANALYSIS  ATO
 JU> QUARTER 19 89

 XYTE: DICHLOROMETHANE
 IBER OF PAIRS:  38
 IRAGE % DIFFERENCE:    0.41
 JIDARD DEVIATION OF % DIFFERENCE:   21.74
 /ER 95% CONFIDENCE LIMIT:  -42.19
 'ER 95% CONFIDENCE LIMIT:   43.01


 J.YTE: CHLOROFORM
 ffiER OF PAIRS:  41
 :RAGE % DIFFERENCE-.    6.86
 >NDARD DEVIATION OF % DIFFERENCE:   20.57
 JER 95% CONFIDENCE LIMIT:  -33.47
 'ER 95% CONFIDENCE LIMIT:   47.18


 O.YTE: 1.2DICHLOROETHANE
 IBER OF PAIRS:  3
 : ENOUGH PAIRS TO EVALUATE STATISTICS


 O.YTE: l.l.lTRICHLOROETHANE
 IBER OF PAIRS:  82
 RAGE % DIFFERENCE:    4.60
 \NDARD DEVIATION OF % DIFFERENCE:   13.52
 JER 95% CONFIDENCE LIMIT:  -21.91
 PER 95% CONFIDENCE LIMIT:   31.10


 U.YTE: BENZENE
 IBER OF PAIRS:  82
 2RAGE % DIFFERENCE:   -0.46
 ANDARD DEVIATION OF % DIFFERENCE:   26.24
 JER 95% CONFIDENCE LIMIT:  -51.89
 PER 95% CONFIDENCE LIMIT:   50.97


 &LYTE: CARBON TETRACHLORIDE
 MBER OF PAIRS:  35
 ERAGE % DIFFERENCE:    0.55
 ANDARD DEVIATION OF % DIFFERENCE:   17.97
 WER 95% CONFIDENCE LIMIT:  -34.68
 PER 95% CONFIDENCE LIMIT:   35.77


 ALYTE: TRICHLOROETHYLENE
 MBER OF PAIRS:  78
 ERAGE % DIFFERENCE:    0.82
 ANDARD DEVIATION OF % DIFFERENCE:   33.67
 WER 95% CONFIDENCE LIMIT:  -65.18
 PER 95% CONFIDENCE LIMIT:   66.81


iALYTE: 1,1,2TRICHLOROETHANE

                                              8-  130

-------
                                                                                           202


•ER 95% CONFIDENCE LIMIT:   41.14


J.YTE: 1.4DICHLOROBENZENE
BER OF PAIRS:  0
• ENOUGH PAIRS TO EVALUATE STATISTICS
      1.2DICHLOROBENZENE
BER OF PAIRS:  6
SAGE % DIFFERENCE:    -3.06
JJDARD DEVIATION OF %  DIFFERENCE:   16.63
ItS. 95% CONFIDENCE LIMIT:  -35.65
'ER 951 CONFIDENCE LIMIT:   29.53
                                              8- 131

-------
                                                              203
            APPENDIX D




Sample Tabulation and Calculations




      for Distributed Volumes
             8- 132

-------
                                                                                           204
                           Sample Distributed Volume Calculations
                           4th Quarter 1987     Benzene Envirochem
                 Diff.                      Oiff.                    Diff.
 High    Low     High-Low    High   Low    High-Low   High   Low    High-Low
1.16
1.79
1.20
1.11
0.98
0.91
1.22
1.04
1.07
0.81
0.55
0.87
3.07
1.09
2.15
1.45
1.44
1.83
1.03
1.77
1.58
1.05
1.27
1.27
1.91
-0.70
0.95
0.34
0.46
0.92
-0.19
0.73
0.51
0.24
0.96
0.40
0.66
1.02
0.66
1.90
0.64
0.96
0.83
1.06
1.09
1.00
1.22
1.01
1.50
1.35
1.46
1.96
1.06
1.47
1.52
1.96
2.49
2.96
A. 22
1.78
0.84
0.33
0.80
0.06
0.42
0.51
0.69
0.90
1.40
1.96
3.00
0.77
1.30
1.90
1.37
0.86
1.85
3.91
1.16
0.90




2.83
2.61
2.16
1.14
2.26
5.10
2.24
1.62




1.53
0.71
0.79
0.28
0.41
1.19
1.08
0.72




n - 32
Mean -0.78
Std. dev. •









 n » no.  of sample
 p * mean
0- m std. deviation
                  t (calc) - mean/std dev. - 0.78 - 1.16
                                             0.67

                  t (table) n-i,o.05 " t (table) 3i,0.05 " 2.042

                  t > 0.05, No

                  95% Confidence Interval
                                                      )(tn -i.«-)
                                 /IT                      fTT

                       0.78 - (0.67) (2. 042) <. U <. 0.78 + (0.67) (2.042)


                       0.78 - 0.24 <. " £ 0.78 + 0.24

                         0.54 £ JT <. 1.02
                                                                                           0.67
                                            8- 133

-------
9. CSI VOCS QUALITY ASSURANCE REPORT
            9-   1

-------
Staten Island/New Jersey Urban Air Toxics Assessment Program
                  QUALITY ASSURANCE REPORT

                             for

              CENTER FOR ENVIRONMENTAL SCIENCE
                THE COLLEGE OF STATEN ISLAND
               THE CITY UNIVERSITY OF NEW YORK
                        50 Bay Street
                Staten Island, New York 10301

                 John R. Oppenheimer, Ph. D.
                          Director

                      for the period of
                 July 1987 to September 1989
                        Submitted to
      U. S. Environmental Protection Agency, Region II
                  Quality Assurance Branch
                     Edison, New Jersey
                     Draft  20 July 1990
                   Final  10 November 1990

                          9-   2

-------
      STATEN ISLAND/NEW JERSEY
URBAN AIR TOXICS ASSESSMENT PROGRAM
     QUALITY ASSURANCE REPORT
               for
 CENTER FOR ENVIRONMENTAL SCIENCE
   THE COLLEGE OF STATEN ISLAND
  THE CITY UNIVERSITY OF NEW YORK
           50 Bay Street
   Staten Island, New York 10301

    John R. Oppenheimer, Ph. D.
             Director

         for the period of
    July 1987 to September 1989
             9-

-------
                  Submitted to
U. S. Environmental Protection Agency, Region II
            Quality Assurance Branch
               Edison, New Jersey
               Draft  20 July 1990
             Final  10 November 1990
                    9-

-------
                QUALITY ASSURANCE REPORT FOR THE

                     COLLEGE OF STATEN ISLAND
                      INTRODUCTORY  COMMENTS
      Since the guidance document  for  preparation  of this report
included extensive  analysis  by use of the  paired-sample t-test,
it  is  important   to   understand   its  interpretation  and  its
limitations.
     The underlying hypothesis of the paired-sample t-test is  that
"meanl - mean2 » 0".  If the two means are different, the t-  value
will be large and this  will be indicated  by a "Yes" in the  tables
as   formatted  by   the  instructions   given.     However,   the
paired-sample   t-test   is   extremely  sensitive   to  consistent
difference  or bias.   This   will be seen  in the  figures  in the
various chapters  that  show  data  in relation to  time on  the X--
axis, where data for a quarter are significantly different if one
set of  values  (such as tenax values)  are consistently  above or
consistently below the other  (such as canister values).  Data for
a quarter are not different,  if during the quarter, the values of
one  set vary above  and below those of  the other set.    Thus  a
quarter's data, where one set of values is consistently 0.001 ppb
above the other set, will  be different even though the means are
very similar, whereas if the  data pair differ by 10  ppb, but  shift
back and forth, in  terms of  which  one  is higher,  the means  will
be statistically the same,  even though quantitatively  different.
Because of  this, little comment will   be made  about  the results
of the paired-sample t test, but the results will be  given in the
tables.  More emphasis will  be given to  whether  there is visual
agreement between the two  sets of  measurements  as   seen in these
figures and as looked at below.
     The real question  in terms of quality assurance is whether the
two sets of data are in agreement with  one another.  This  will be
addressed below in  terms  of  regression analysis  and   figures
showing a scattergram with  either one or  more regression  lines or
a  45  degree  lines  plotted  through the data  points.   If   the
regression  line runs through the origin  and its slope (beta)   is
equal to 1,  then the values of the two data  sets  are equal; if  the
slope is <  1, the values on  the  x-axis are larger  than those  on
the y-axis  and vice versa.   This  analysis will be  done for the
entire time span of  the study, as opposed  to quarterly.   Quarterly
analysis would  be more helpful,  but the time required   to carry
this out is currently  not  available because of deadlines  which
need to be met.  A further step, which may be attempted at a later
date   would be to  plot a  95% confidence  belt parallel  to   the
regression line.  For now note will simply be made of data  points
which are clear outliers.

     Means  will be  reported  with plus or minus (±)  one standard
deviation  (S).   Unless  otherwise  indicated, the  95% confidence
                            9-

-------
limits  reported  in  the  tables  are  the  limits  for  the  mean
difference, i.e.,  that  there is a 95% probability  that the true
mean lies within the stated limits.

     ACKNOWLEDGMENTS.   I wish  to  thank  Qingmei  Zha,  Susmita
Biswas, and Donna Daly for their assistance in the preparation of
this report, and particularly Wa King  Chan for doing much of the
data processing and sniffing out of errors.   An earlier draft of
this document  was  reviewed  by Avraham  Teitz of the Monitoring
Management Branch, USEPA, and by Clifford P.  Weisel,  formerly at
CSI, but now at UMDNJ.  Their comments were greatly appreciated.
                                 -6

-------
                             CHAPTER I

                             BLANKS

                         PROJECT SUMMARY


     The  following method  was  used in  this  report to  assess
contamination of  blanks and consequently  of samples.   The mean
monthly concentration  for an individual compound  was determined
for ambient samples.  If the blank trap had a concentration which
was greater  than 30%  of  the monthly mean level,  the blank was
considered contaminated.  However, what was recorded when  this  was
done was the number of samples that were consequently  determined
to represent contamination values.   Thus in the  following table
the information is  reported  as % of samples   contaminated (# of
contaminated sample traps/# of sample traps  processed).

     However, for duration of the study,  the working procedure  was
to take a rolling average of the blank  value and ambient  values
over 5 days; if the mean  blank value exceeded 50%  of the  of the
mean ambient value, contamination was assumed to have  occurred (C.
P. Weisel,  pers.  com., 5 November  1990).  Five day   mean blank
values were subtracted from ambient sample values.

     The average percent contamination of samples (or blanks) was
3.4% over  the whole study  for all  compounds (Table 1.1).   six
compounds  had  more   than  5%  of  their  samples   and  blanks
contaminated:   methylene   chloride    (8%),   chloroform   (6%),
ethylbenzene  (7%),  m/p  xylene  (7%),   o-xylene  (6%),   and  p-
dichlorobenzene  (17%).    Without  these   six compounds,  the  %
contamination was 1.5 + 1.3.   The average % contamination for the
eight compounds that were usually at or below their  MDLs was 4.3
± 5.4, with  methylene  chloride  and  p-dichlorobenzene having the
highest contamination levels of more than 7%.

     Over the quarters,  the % contamination ranged from 1.4  in  4th
quarter  '88   to  7.5  in  2nd quarter  '89.   The high levels  of
contamination in 2nd quarter  '89 were probably due to the  extended
use of the tenax absorbent in the traps.   This was  corrected in
July when newly cleaned tenax was loaded into the traps.  The high
levels   of   contamination   with    1,1-dichloroethane       and
trichloroethene in 3rd quarter '89 were probably due to  the  new
tenax,  as the levels of these  compounds dropped after the  traps
had been used a couple of times.

     The lowest number of compounds contaminating the traps was
in 3rd quarter  '89,  after new tenax had been  cleaned by soxlet
extraction with  cyclohexane,  acetone,  and methanol  each  for 48
hours.    The stainless  steel  traps  were  also cleaned with full
strength chromic sulfuric acid; this had not been done before.
                            9-

-------
                             CHAPTER II

                        DUPLICATE SAMPLES

      Duplicate sampling for low and high flows started at the end
of July  1988  and continued until the end of  the study.  This was
done by using a  second  set of  flowmeters in the field (C-low and
D-high).   The  second of  each pair  of duplicates  (C  &  D)  was
processed along with the first  (A & B)  in terms of GC/MS  analysis,
but the  data did  not go  through  blank value   substraction and
temperature-pressure correction. Consequently  only data from the
A and B samples  were included  in the  data set  sent to the USEPA
and  thus appear in  the  report  this  is appended   to.  During
preparation of this report, it seemed unnecessary to  do this for
the second of each pair, since data uncorrected for  blank values
and uncorrected for temperature-pressure already  existed for both,
and the  differences between them would have  remained  the same.
However, some compounds appear to have values  above their MDLs in
this presentation because subtraction  of  blank values  was not
done, when in fact they were at or below  their MDL (see below).

     Duplicate low  flows  (A & C) and duplicate high flows  (B & D)
were similar over the entire study, i.e., no paired-t values were
significant  (Tables  2.1 and 2.2).

     There  were minor  differences in  precision by  compound  in
terms  of  %  difference,  and this tended to  be greatest  for those
compounds which  were measurable only on a third or  fewer of the
days.  Methylene chloride was  the  most  volatile of the compounds
looked  at and  is held  weakly by  tenax,  the absorbent;  it had
measurable  levels on 22.1% of  the days,  and for low flow had a
6.19% difference.  1,1-Dichloroethane was the second most  volatile
compound looked  at  and had measurable levels on only  6.6% of the
days;  it had the greatest %  difference for low  (46%)   and high
(269%)  flows; however,  the  sample sizes  were small  and   the
concentrations   were only  4   times  greater  than  the  MDL.
Chlorobenzene  was  seen  on  only  31%   of  the  days,  but  more
frequently on the high flow traps and only slightly above its  MDL;
thus at  low flow it had a 12.8% difference.  Bromoform  occurred
on  only 6 of 180 days (3.3%)  at  only  one of the three   sites.
Meta-dichlorobenzene occurred above  its  MDL on  2  of 180   days
(1.1%) and  only  at  one of  the three sites; thus what  is  measured
here is variation in trap contamination  levels.   The   same  is true
for o-  and  p-dichlorobenzene,  though  they were  seen  above their
MDLs  on    28  (15.6%)  and 23  (12.3%)   of  180  sampling   days,
respectively.  1,1,2-trichloroethane was never seen above   its MDL
in the 180 days for which measurement  was attempted; thus   the low
% difference  for both low  and high flow rates.

     Hereafter  attention will  only be  given to those  compounds
which were  measurable, and the  low and high flows will be  treated
separately.
                              9-   8

-------
LOW flOWS

     With  the  above  eight  compounds  omitted,  the  average  %
difference was 2.97 +  2.69.   There were only four compounds with
%    differences    above    5%:    hexane,    1,2-dichloroethane,
trichloroethene and o-xylerie  (Table 2.1).   With the exclusion of
these four compounds,  the  average  % difference for the remaining
nine compounds was 1.45 + 1.31.

     In terms of regression analysis,  the variation in the second
of each pair (C) of the low flow set was almost totally accounted
for by variation in the value of the first of each pair (A) (mean
RA2 - 0.93 +  0.05; Table 2.3).  The  regression coefficient fell
below   0.92   for  only  three  of  the   measurable  compounds:
trichloroethene,  styrene  and  o-xylene.    For  many  compounds
(benzene,    trichloroethene,    toluene,     tetrachloroethene,
ethylbenzene,   styrene,  and  o-xylene)  the deviation  from  the
regression line was greatest at the higher concentration values.

High flows

     With the compounds which occurred infrequently at measurable
levels   omitted,  the average  %  difference was 3.15 +  2.64 (N -
13).  Again  there were  only four  compounds with  a % difference
above 5%,   but they were  different compounds  from  those  at low
flow: chloroform,  1,1,1-trichloroethane,  1,2-dichloroethane,  and
benzene  (Table 2.2).   Without these four compounds the average %
difference for the remaining nine compounds was 1.68 + 1.18.

     In terms of regression analysis,  the variation in the second
of each pair  (D)  of the high flow set was  again  almost totally
accounted for by variation in the value of the first of each pair
(B)  (mean RA2  -  0.93 ±  0.07; Table    2.3).   The  regression
coefficient  fell  below  0.93  for  only  two  of  the  thirteen
measurable compounds:  chloroform and 1,1,1-trichloroethane.  For
most  compounds  (hexane, 1,2-dichloroethane, carbon  tetrachloride,
toluene, and ethylbenzene)  the deviation from the  regression line
was greatest at the higher concentration values.

    The most deviant data pair for most compounds (Figures 2.1 to
2.26) had a low value for the first high flow sample (it occurred
at Eltingville  on 7 September 1989)(see  benzene,  mid-point);  it
represents  a  total  desorption failure  on the  cold  trap  as
confirmed by both internal  standards.  The first internal  standard
for  sample  B  was  only 38% of the  first internal standard   for
sample D, and the 2nd internal standard  for sample B was only  29%
of that for sample  D.  This  represents  the type of  sample that
should  be and  normally is  removed from the  overall  data  set for
failing QA standards.  (See quarterly treatment below.)
                             9-

-------
                        DUPLICATE SAMPLES

                        QUARTERLY REPORTS

     Attention  will be  focused on  the  13  compounds  which had
measurable concentrations most  of the time (Tables 2.4 to 2.13).
 At  lov  flow five  had significantly different  values  in one
quarter each: one in 4th quarter '88 (1,2-Dichloroethane) and  four
in  3rd  quarter  '89  (ethylbenzene,  m/p-xylene,  o-xylene  and
styrene).     At  high  flow,  two   measurable   compounds   had
significantly different values in one quarter each: styrene in 4th
quarter '88,  and  chloroform  in  1st quarter '89.   With the  small
number of samples per compound per quarter, it is to be  expected
that occasionally the values for the first of each pair  would be
slightly, but consistently above or below that of the  other.

     The  average   %  difference   for  the  thirteen  frequently
measurable compounds varied across quarters: low flow varied from
5.69% in  3rd quarter '88 to 47.73% in  2nd quarter '89, and high
flow varied  from 4.48% in 1st quarter  '89 to 8.30% in 3rd quarter
•89 (Tables  2.4 to 2.13).
 Mean average % difference by quarter for 13 frequent compounds


                   1988                   1989
              3rd Q    4th Q    1st Q    2nd Q    3rd Q    Mean
Low flow
Mean
S
High flow
Mean
S

5.69
4.76

6.85
5.94

9.45
6.43

4.70
3.19

8.09
3.09

4.48
3.37

47.73
39.47

7.04
7.10

11.98
9.96

8.30
13.02

2.97
2.69

3.15
2.64
                             	—- -— ••• ^^ w *•* ««• W^ W*« «••• WB^V^ ^^ p ^^ •»••  ^ v •^••v
the  cold trap  as  seen  in  the  quantification  of the  internal
standards that  were placed  on the  traps in the laboratory  just
prior to analysis on the GC/MS.   For instance, in 2nd quarter '89
there were  4 days with duplicate low  flow values; two  of these
days had already been eliminated from the data  base  because,  in
the "A" sample of each A:C pair,  there was a failure of  desorption
of the  second internal  standard relative to the first   (2nd/lst
should have been 46%,  but it  was < 27%) .    The remaining  two daily
pairs were  entered into the database,   but  one of them  had  a
failure  in  the  opposite direction, i.e., the second   internal
standard was larger than it should have been (66%  instead of 46%);
however, both failed  for another reason.  The  "C" sample, which
was not included in the data base,  had an 83%  greater desorption
of the 1st  internal standard  as compared to that  in the "A" sample
                              9-  10

-------
of each pair, and the  2nd  internal   standard had more than a 54%
greater desorption.  During 2nd   quarter '89 there  were similar
problems with the high flow   duplicates,  but to a lesser extent.
Third quarter '89 had  similar desorption problems.  Consequently,
the data for these   two quarters show larger average differences
and larger  standard   deviations than in previous  quarters (see
table on page 10).
                              9-  11

-------
                           CHAPTER III

                       DISTRIBUTED VOLUMES

     Of the 21 compounds where quantification was attempted, only
thirteen occurred above their minimum detection limits (MDLs)  most
or all of the time, and will be called "measurable.1*  Eight  other
compounds were measurable at one  or more sites on less than  31%
of the days: chlorobenzene (30.5%),  methylene chloride  (22.1%),
o-dichlorobenzene     (15.6%),     p-dichlorobenzene    (12.8%),
1,1-dichloroethane     (6.6%),    bromoform    (3.3%),    and    m-
dichlorobenzene  (1.1%);  and one  compound was  apparently  always
below its MDL - 1,1,2-trichloroethane (0%).  These compounds will
be called "unmeasurable."


Analysis based on paired-sample t tests

          Measurable  compounds.    Since  data  for the  thirteen
measurable  compounds  were obtained  for different  numbers  of
quarters, some for  9  and others for only 8 or 7,  the easiest way
to summarize is on the basis of the % of "compound-quarters"  where
the paired-sample t  tests were insignificant (see table on  next
page).  There were 107 compound-quarters,  and  in 38% of  these the
low and high flows were the same.   There  appeared to  be a strong
seasonal effect,  with 62%  agreement  (no  significant   difference)
in 2nd quarter and only 22% agreement in 3rd quarter.
           Percent agreement by "compound-quarters"
       Year    1st Q    2nd Q    3rd Q    4th Q Combined
1987
1988
1989
_
38
38
^
54
69
17
8
38
56
15
—
40
29
49
       Combined 38       62       22       32      38
     In terms of measurable compounds,  the best agreement was for
tetrachloroethene (75% of the quarters),  and for m/p  xylene (71%
of the quarters) (Table 3.1).  The worst agreement  was for 1,1,1-
trichloroethane  (0%)  and  carbon tetrachloride  (0%).  However,  a
                                8
                             9-   12

-------
further pattern can be seen.  The first seven measurable  compounds
had a higher percentage difference (mean » 78.9% ±  15.6) than did
the last six  (mean - 41.2 ± 12.2)(two sample t  test - 4.78, df -
11, p < 0.001).  [The compounds are listed in  terms of increasing
retention time, or decreasing volatility.]

     Upm,ea^ujrable compounds.  The eight unmeasurable compounds had
significantly different means for low and high flow rates 72%  of
the time  (Table 3.1).   Since 70 to 100% of the values for  these
compounds  were  recorded  at   one-half  their  minimum  detection
limits, and the low flow mdl was twice the high flow mdl, this is
reasonable. In those  few  quarters where the all the values for a
compound were one-half the MDLs, the standard error of the  average
difference was zero and the t-value was  insignificant.
Table 3.1.  Comparison of low and high flow values on basis of

            paired sample t test
Measurable most of time
Compound
1
Hexane
Chloroform
111-Trichloroethane
12-Dichloroethane
Benzene
Carbon tetrachloride
Trichloroethene
Toluene
Tetr achl or oethene
Ethylbenzene
m/p Xylene
Styrene
o Xylene
Quarters
f % diff*
9
9
9
9
9
9
8
8
8
7
7
7
7
78
67
100
78
67
100
62
50
25
57
29
43
43
Measurable < 33% of time
Compound Quarters
1 % diff*
Methylene chloride 8
1 , 1-Dichloroethane 7
112-Trichloroethane 4
Chlorobenzene 9
Bromoform 4
m Dichlorobenzene 3
o Oichlorobenzene 4
p Dichlorobenzene 4





75
71
75
100
25
33
100
100





                              -  13

-------
Mean % quarters different  61.5                           72.4



S                          23.8                           29.5



* difference based paired t test
                            9-  14

-------
Analysis based on means and ratios of low to high flow rates


     The ratios of  low  flow values  to high flow values show that
there were three groups of compounds (Table 3.2):  Al) measurable
compounds with large standard deviations (0.11 to 0.32), A2)  those
with small standard deviations  (0.04 to 0.07), and B)  unmeasurable
compounds with low  flow values almost twice as high  as high flow
values (1.73 to 1.98).

     Al)  These seven measurable  compounds were the more volatile
ones with retention times  ranging from 9.7 minutes for hexane to
 13.9 minutes for  trichloroethene.   Their low flow values on the
average were  16% higher than the high flow values (Table 3.2).
This difference had a strong seasonal component,  which  was what
was shown  in  the  paired-sample t test above.   Low and high flow
values were similar in  the cold months of October to March (4th
and 1st quarters),  but  in the warm months of April to June (2nd
quarter)  low flow values were 15 to 19% higher than were high  flow
values, and in the  hot months of July to September  (3rd  quarter)
were 42%  higher (Figure  3.1) . [Temperature data  currently are only
partially complete for the months  of April  1988 to  March  1989 (see
Fig.3.1), and are  not yet  available for  prior or following time
periods.]  Consequently, low flow values   would appear to be the
most accurate measure of ambient  air  concentrations in the second
and third quarters of each  year for  these compounds, or they could
be used for all quarters.

     Comments  on  compounds.   1,1,1-Trichloroethane (RT  « 11.6
minutes)  and carbon tetrachloride (RT -12.4 minutes) both showed
breakthrough  in  all quarters,  though it was greatest in the hot
quarter as  above.    For both compounds  the deviation between low
and high values increased  with increasing  ambient concentrations.
 Low  flow values   are  probably  the best estimates  of ambient
concentrations of these two compounds.

     1,2-Dichloroethane  (RT  « 11.7  minutes)  followed the above
group pattern,  but its  mean ratio across  all quarters was close
to  1.0 because it  also had  quarters where  the  average  low flow
value  fell  14 to  25% below that of the  high  flow value (1Q88,
4Q88, and  1Q89).   This  occurred  because there was a large number
of  days  in  these  quarters  when the ambient  air concentration
occurred  close  to  the  low flow  MDL (0.02) and was reported by
convention to be  at 1/2 the MDL  (0.01).   However,  the high flow
values for  these days  ranged  from  0.005   (1/2 the  MDL)  to to as
high  as   0.05.    All  other values   above the  MDL  showed  good
agreement in these  quarters.

     Benzene had a retention time of   12.3 minutes, which would
suggest a potential problem with  breakthrough, but  its mean ratio
across quarters was close to 1.0.    Because it  is  an  aromatic
compound,  it  is held more strongly  by  Tenax GC  (C.  P. Weisel,

                                13


                             9-   15

-------
pers. com. 11 September 1990).  It none-the-less did have low flow
values 17 to 21% higher than high flow values in the hot quarter.
The  reason  for the mean ratio  close to 1.0 was because  in one
quarter  (1Q89) almost  all  high  flow values were higher  than low
flow at all concentrations  (see trichloroethene  below).


     Trichloroethene  (RT  - 13.9 minutes)  showed what appears to
be breakthrough in 3rd quarter 1988, but not in  3rd quarter 1989.
 In addition,  in  4th  quarter 1987  its low flow values were lower
than the  high flow values.   In both quarters  where  there was a
difference between  low and high flow values,  it occurred at all
concentrations;  this  does  not  appear to  fit  the breakthrough
pattern.   Without  these two  deviant  quarters, trichloroethene
would have been included with the group A2 compounds.

     A2) These six measurable compounds had lower volatility with
retention times  of  17.0 minutes for toluene  to 23.2  minutes for
ortho xylene.  Their low and high flow values were essentially  the
same in all seasons (Table 3.2,  Fig. 3.1).

     Comments on compounds: Toluene, the xylenes, and ethylbenzene
are  aromatics and should  be held  tightly to  Tenax  GC   (C.  P.
Weisel, pers. com.  11 September 1990).  However, in 3rd  and 4th
quarters of 1988 toluene's low flow values  were 9-10%  higher than
the  high  flow values.   This difference increased  progressively
with increasing ambient concentrations.  In other  quarters the low
and  high flow values  were the  same.   The  xylenes   (ortho  and
meta/para) and ethylbenzene, showed the same  phenomenon in these
two quarters.

     Tetrachloroethene  values were almost  the same for  low  and
high  flow,  with  low  flow  slightly lower.   For most quarters,
values under  1 ppb  were the same for low  and high  flow, whereas
values  above  1  ppb  tended to  be  higher  for high  flow.    An
exception was first quarter 1989 when intermediate values (0.4 to
0.8 ppb) were  30  to 50% higher  for high flow,  and high values (>
1.4 ppb) were up  to 21% lower for high flow; this might be  related
to the shape of the calibration curves.


     B) The  unmeasurable  compounds showed  little variation with
season (Table 3.2, Fig. 3.1), but did have low flow values almost
twice  as  high   as   high  flow  values   because  most  of  the
concentrations were below the MDLs,  and low flow MDLs were twice
as high as high flow MDLs.

     Some of  this problem is eliminated for these   compounds if
only those days,  which had low  and high flow  values  at or above
their MDLs,  are  used  (Table  3.3).   As indicated at  the  start,
1,1,2-trichloroethane  (RT -18.0 min)  had ambient concentrations
which apparently were below the  low and high flow MDLs.

                                14


                           9-  16

-------
     The  difference  was  eliminated  for  five  compounds:  1,1-
dichloroethane,   chlorobenzene,   bromoform,   and   m-  and   o-
dichlorobenzene.  1,1-Dichloroethane had good agreement, with  half
of the values at the low flow MDL (0.02).  The slight  difference
for bromoform is  an artifact;  on 5 of the 6 days  the  high flow
value was above the high flow MDL of 0.01, but below  the low flow
MDL of 0.02.  Thus the low flow values were reported  at one-half
their MDL or at 0.01.  This resulted in the high flow  values being
higher by 10%.

     However,  the  high flow  means  were  still  lower  for  two
compounds:   methylene   chloride   (RT   -   7.5   min),  and   p-
dichlorobenzene  (RT -  28.2  min).  For methylene  chloride,  this
probably represents  breakthrough,  as this was the most volatile
of the compounds and Tenax was known to hold this  compound  poorly.
One suspects that the low flow  values for methylene  chloride also
suffered from  breakthrough,  but to  a lesser extent.    (This is
confirmed  by  comparison with  canister values   for   methylene
chloride - Chapter  IV.)  It  is not clear why p-   dichlorobenzene
should show a difference between low and high  flow values, as it
had next to the lowest volatility of the  compounds looked at and
it is an aromatic,  which should  be held  tightly by  Tenax (C. P.
Weisel, pers.  com,  1  Sept.  1990).   0-  dichlorobenzene,  which
follows it by 0.1 minutes showed similar  values for low and high
flows based on the variability in the  data.
                                15


                             9-   17

-------
Table 3.3.  Means of lo-hi values > MDL for 7 compounds seen on <
           31% of days
Compound (N-)
      Flow
Low     High   Diff   % Diff  t-value
Methyl ene chloride
58*
1 , 1-Dichloroethane
10
Chlorobenzene
112
Bromoform
6
m-Dichlorobenzene
1
o-Dichlorobenzene
20
p-Dichlorobenzene
14
Mean
S
Mean
S
Mean
S
Mean
S
Mean
S
Mean
S
Mean
S
1.
0.
1.
0.
0.
0.
0.
0.
0.
0.
0.
0.
40
032
874
036
033
022
029
100
037
032
592
183
0
0
1
0
0
0
0
0
0
0
0
0
.77
.032
.874
.032
.026
.024
.025
.140
.031
.033
.292
.086
0.
0.
0.
0.
0.
0.
0.
0.
63
000
005
004
0025
040
006
300
81.
0.
13.
10.
28.
19.
102.
8
0
1
3
6
4
7
6.43
0.00





  values through December 1988
                         9-  18

-------
                   DISTRIBUTED VOLUMES
                    QUARTERLY REPORTS


 The quarterly tables are attached (Tables 3.4 to 3.12).  See
A ff%y* s**rMnniAT*4» a
above for comments.
                            18
                        9-  19

-------
                           CHAPTER IV

                       TENAX vs. CANISTER

     Matching tenax and   canister   data were obtained for eleven
compounds  during  the study.    Eight  compounds had  regression
coefficients (RA2) that  ranged  from  0.1 (N - 43) to 0.9 (N - 26)
with all  data  points included, and  0.4 (N - 40) to 0.9  (N - 3)
with outlier  points removed  from  the  regression analysis.   The
slopes of the regression lines for these eight compounds differed
significantly  from zero at  p < 0.001  (Table 4.1; Figs.  4.1 to
4.10).  Two compounds,  carbon tetrachloride and trichloroethene,
had  five  or fewer data  points, with all  values at or  near the
canister MDL; the variability of the complete set of tenax values
for these two compounds had no relation to variability in  canister
values (RA2 - 0.07 and 0.27, p > 0.05).  One compound,   methylene
chloride (dichloromethane),  had fifty-one pairs, but only in seven
of these was the tenax value above its MDL.

     One  additional  compound,  chloroform,   was  reported  for
canisters only in the  last quarter.  This was because the  canister
MDL was higher than the  ambient chloroform  concentrations as seen
with tenax throughout the study.

     Data on  the paired  t  test are given in Table 4.2  for the
study as a whole.  The individual compounds will be treated below
in  the  order of  their  retention  times,   and  consequently their
volatility.


     Methylene chloride (RT  - 7.5 min):  Fifty-one .data pairs  were
obtained, with a  mean canister value of 1.51 ±3.37 and  a  mean
tenax value of  0.26 ± 0.17.   However,  only eight  of the   tenax
values were above the tenax  MDL.    Since all values at  or  below
the MDL are reported as  one-half the  MDL there was an even  larger
difference due to this.   It  was known  at the start of  the  study
that nethylene chloride  would be poorly held by tenax,  and  that
the values reported for  our  three  sites would be well below  the
actual ambient concentrations.

     The RA2 - 0.01 as most tenax values were reported at the MDL
and thus did not track the canister values.


     Hexane (RT » 9.7 min):   Forty-five data pairs were obtained.
The mean canister value  was 9.61 ppb ± 25.35  and the mean tenax
value was 0.86 ppb +  0.62.   However,  during 1st quarter '88 the
canister values  ranged  from 8  to  120  ppb   (tenax values  for 1st
quarter ranged from 0.4  to  3.5  ppb), whereas canister values for
the rest of the study ranged from 0.1 to 1.9 ppb (Fig.  4.la).  It
is assumed that  these high  canister values were due to  an error
in laboratory analysis and/or reporting.

                                19


                             9-  20

-------
     Without 1st  quarter '88 (37 data pairs),  the  mean canister
value was  0.87  ppb  + 0.71  and the mean tenax value  was  0.81 +
0.50.   However,  removal  of one additional  data  pair  (C:T  -
4.84:0.49) seems  warranted,  as  it appears to  be  a typographical
error,  i.e.,  it  probably should have been  0.48  (the canister
values preceding and following ranged from 0.4 to 0.9 with a mean
of 0.67, N *  5).  Thus with 36 data pairs  (Fig.  4.1b), the means
for canisters and tenax were the  same (C: mean - 0.820 + 0.32; T:
mean -  0.827  + 0.50); the paired-t for these 36 data pairs was
0.8023, which was not significant.
     If 1st quarter  88  is used  (45 data pairs),  RA2 - 0.11, and
the slope  was  significant at p - 0.05.  Without  1st quarter '88
and the additional data  set  (36 data  pairs),  RA2  - 0.52, and the
slope  (1.12)  was  significant  at 0.001.   Figures  including and
excluding  1st quarter  '88  follow.  It may  be that removal of one
or more additional  data points, such  as  0.6:1.7  would further
improve  the  relationship,  but  at   this  point  there  is  no
information available for excluding them as above.


     Chloroform (RT  * 10.5 min):   This compound was reported for
canisters  only  in  3rd  quarter  1989,  when  tenax  showed  the
concentrations as below  its MDL of 0.015 ppb.  During  the earlier
quarters tenax showed chloroform at values up to 0.1 ppb, but  this
was below  the canister MDL of 0.2 ppb.  The five canister  values
in 3rd  quarter  89  ranged between 0.3  and 0.5 ppb (mean -  0.39 ±
0.09), whereas tenax showed  it  below  its MDL of 0.015 ppb;  this
may indicate  a  problem with tenax data during 3rd quarter   '89.
(With tenax, breakthrough occurred, at least at high flow,  in 2nd
and 3rd quarters  of  both years  - Chapter III.)
     1,1,1-Trichloroethane  (RT  - 11.6 min):   Canister values on
the  average were  higher than  tenax  values  (C:  mean -  0.764 +
0.511; T: mean - 0.417 + 0.314).  However, one canister value  for
3rd  quarter '89 was higher than any of the other values reported
in the study  (C -  2.7, T - 0.23) and probably was a typographical
error  (Fig.  4.2).    Without this data  pair,  the mean difference
decreased from 152% to  130%   (C: mean * 0.719 ± 0.390; T: mean •
0.421  + 0.359),  but was  still significantly  different  at  p <
0.001.   (With tenax, breakthrough caused high  flow  values to be
24%  lower than  low flow values  - Chapter III.   Thus if low flow
values were used  instead of means,  the difference with canisters
would be reduced  to about 6%, which could be  due to error or to
slight breakthrough at low flow.)

     There  were 43 data pairs with an RA2 -  0.308 and the slope
of the regression line was  significantly greater than zero.   With
the  above data pair omitted  (N  - 42),  RA2 - 0.57, and the  slope
of  the regression  line  increased  from  0.34  to 0.57 and more

                                20


                              9-  21

-------
closely fit the rest of the data points.  The low slope indicates
that canister values were higher than tenax  (see above comments).


     Benzene  (RT  » 12.3  min):  Canister values were the same as
tenax values  (C:  mean  -  1.288 + 0.592; T:  mean - 1.246 + 0.879;
paired-t - 0.555, p > 0.5).

     With  65  data  pairs RA2  -  0.529  and  the  slope  of  the
regression line - 1.08, which was significantly greater than 0 at
p < 0.001 (Fig. 4.3).


     Carbon tetrachloride  (RT » 12.35 min):  There were only five
data pairs*  for this  compound,  but  the  means for  canister and
tenax were similar  (C: mean » 0.28 + 0.09; T: mean - 0.29 ± 0.23;
paired-t » 0.144,  p >  0.5).   *[The  low number of data pairs was
due  to  the  high  canister   MDL  of  0.2   ppb relative  to  the
concentration in the air, which was mostly below 0.16 ppb, except
for 1st quarter '89 when it rose to 0.25 ppb.]

     Three of  the canister values were at  or below the canister
MDL of  0.20  (tenax MDL * 0.03).  On three  days the tenax values
were above  the canister  MDL,  but the  canister  saw only  two of
them.   Consequently, RA2  « 0.07 and  the slope of the regression
line did not differ from zero (Fig. 4.4).


     Trichloroethene (RT » 13.9):  There were only  four data  pairs
for this compound, but the means were the same (C: mean «  0.29 ±
0.05; T: mean » 0.23 ± 0.20;  paired-t - 0.736, p > 0.5).

     The MDL  for  canisters was  0.2 ppb and  for tenax  was 0.01.
On  two  of  the days  tenax and  canister  values  were  above  the
canister MDL. On one day the tenax value was 0.1 and the canister
value was reported as the MDL.  On the fourth day the tenax value
was 0.01 (the tenax MDL)  and  the  canister was 0.3,  0.1 above its
MDL.    Because  of this  RA2  -  0.266 and  the  slope  was  not
significantly  different   from  zero.   With this  one  data  pair
omitted  (N  »  3),  RA2  -  0.994  and  the slope was  significantly
greater than  zero  (Fig.  4.5).    A  larger  sample size would be
needed to determine the actual level of agreement between  canister
and tenax.
     Toluene   (RT -  16.97):   There were  66 data pairs  and the
means were similar  (C: mean - 3.18 + 2.05;  T: mean - 3.51 +  1.97;
paired-t - 1.517, p > 0.1).

     For 66 data pairs RA2 » 0.36 with a slope of 0.58, which was
significantly different from zero at p < 0.001.  One data pair  was

                                21
                             9-  22

-------
an extreme  outlier and  pulled the regression  line down  (C:T  -
13.0:3.6);  with  this data  pair  removed,  RA2 -  0.59  with  a
regression line that   went more closely through the  data points
(Fig.  4.6).    Removal  of  two  other outliers (1.926:7.47  and
6.42:1.64, N  - 63) further  improves the  regression  coefficient
(RA2 - 0.78, df - 61,  slope - 1.08, t - 14.9, p < 0.001).


     Tetrachloroethene (RT -  18.84):  There were 26 data pairs  and
the means were similar (C: mean  -  0.71 ± 0.64;  T: mean  -0.76  +
0.76; paired-t - 1.092, p > 0.2).  The RA2  -  0.91 with a slope  of
1.134, which was significant at p < 0.001  (Figure 4.7).


     Ethylbenzene (RT - 21.06):  There were 41 data pairs and the
means were significantly different because most tenax values were
close to but slightly higher than canister values (C:  mean -0.49
± 0.23; T: mean - 0.69 +  0.51; paired-t - 2.950, p < 0.01).

     For 41 data  pairs,  RA2  - 0.242 with  a  slope of  1.09, which
differed significantly from zero  at p < 0.002. However, the first
two data pairs, which were taken in January 1988, have  problems;
the canister values were  higher (above 1.0  ppb)  than for the rest
of the study  (less  than  0.9  ppb),  and the first  tenax value was
more than twice  as high  (3.16 ppb) as the highest   tenax values
reported later  (1.46  ppb)(this appears to  be a   problem with the
calibration  curve,  which  was  changed  at   the    beginning  of
February).  With these two data pairs removed  (N - 39), RA2 -0.44
with a slope of 1.24  (Fig. 4.8).
     Meta/para-Xylene  (RT  -  21.4):   There  were  61  data pairs and
the means were  significantly different because  most tenax values
were close to but slightly higher than canister values (C: mean »
1.42 ± 0.85; T:  mean - 1.78 ± 1.06; paired-t - 3.034, p <   0.005).


     For  61  data pairs  RA2  - 0.28 with a slope of  0.66, which
differed significantly from  zero at p < 0.001.  However, one data
pair from 1st quarter 88  is a clear outlier (C:T  - 5.3:0.89),  with
the canister  value twice as high  as  the highest canister  value
reported later in the study  and more than  five  times higher  than
other canister values for 1st quarter '88.  With this data  pair
removed,  RA2  -  0.68 with  a  slope of  1.39,  which  differed
significantly from  zero  at p < 0.001  (Fig. 4.9).


     Ortho-Zylene  (RT *  22.42):  There were 48  data pairs  and the
means  were  significantly  different  because  the canister values
were  almost  twice as  high as  the  tenax  values  (C:  mean - 0.62 +
0.28; T: mean » 0.39 ±   0.24;  paired-t - 9.029, p < 0.001).

     For  48  data pairs RA2  -  0.613 with a slope of 0.680, which
differed significantly from zero at p  < 0.001  (Fig.  4.10).  During

                                22
                              9-  23

-------
1st quarter '88 and the first sampling day for 2nd quarter   '88 the
canister MDL was 0.5 ppb and two of the sampling days had  values
at the MDL; tenax values  on these two days and on two  others were
below this level.  Removal  of  the  two  days  with  canister values
at the MDL gave an RA2  - 0.624, and consequently   only a slight
improvement.  The  canister  MDL for most of  the  study thereafter
was 0.2 ppb and tenax was 0.075 ppb.

     To summarize,  four  compounds  had  similar  means  on canister
and tenax  (mean tenax/mean canister:   hexane  - 1.01,  benzene  -
0.97,   toluene -  1.10,  and tetrachloroethene  -  1.07),  and  had
regression coefficients ranging  from 0.52 to 0.91 with slopes of
1.08 to 1.13.  Two compounds (mt/mc: 1,1,1-trichloroethane  - 0.59,
o-xylene - 0.63) had higher values  on canisters, but the  canister
and tenax  values changed together  over time (RA2's -   0.57  and
0.61)  with slopes  less than one  (0.57  and 0.68).   Two  compounds
(mt/mc: ethylbenzene  -  1.41,  and  m/p  xylene - 1.25) had  lower
values on  canisters, but again the values changed together  over
time (RA2's - 0.44 and 0.68) with  slopes greater than one  (1.24
and 1.39).

     So to answer the  questions  posed,  the difference  between
canister and tenax values did differ among the various compounds.
 The reasons for this may be clear to others.  However,  one would
need  to look at  whether  there was  any  consistency  in these
differences across the different laboratories; if so, the problem
would  be  with  the canister values.    If   other  labs  showed  no
difference, then the problem(s) is  (are) here. If other labs show
a different pattern of differences, perhaps a meeting would be in
order.

     To partially  assess  laboratory  bias,  we can  look  at  the
results of the  proficiency tests  done for the  New York State
Department of Health's Environmental Laboratory Approval  Program
(Table 4.3).   These tests  were done once every 6  months; a mean
was taken  for each concentration  of  each  compound for  all  the
values reported by the participating laboratories  and the 95  and
99% confidence limits were calculated  (for additional details see
Chapter VI).  Table 4.3 shows  our  reported  values divided by the
mean value.  For sixteen compounds with two to eight values each,
our mean was 1.095 ± 0.099, or 9.5% greater.  For comparison with
the eight  compounds" where we  had  canister  and tenax matches  as
reported above see the list below:
                                23


                              9-  24

-------
                        Tenax/Canister            ELAP    (N-)
Hexane
Benzene
Toluene
Tetrachloroethene
Ethylbenzene
vm/p-Xylene
1.01
0.97
1.10
1.07
1.41
1.25
-
1.04
1.14
1.12
1.11
1.12
(0)
(2)
(6)
(4)
(6)
(8)
    1,1,1-Trichloroethane     0.59                  -      (0)

    o-Xylene                  0.63                  -      (0)
     Based on this  comparison,  it would seen that  for the first
four  compounds  where canister and tenax values  agree,  that the
values  are close to the ambient concentrations.  For ethylbenzene
and  m/p-xylene,  it  would appear that the canister values were low.
For  1,1,1-trichloroethane  and o-xylene,  additional  points  of
reference  are  needed, perhaps from the other  two  laboratories.
However, for 1,1,1-trichloroethane breakthrough did occur on high
flow tenax (Chapter III).

     In conclusion,  at least for the compounds where  there were
matches for tenax and canisters,  it seems that the tenax values
were close to ambient, with a tendency to be 10% above.
                                24


                              9-  25

-------
                       TENAX VS. CANISTER

                        QUARTERLY REPORTS

     Quarterly data  are  presented for the paired  t test (Tables
4.4 to  4.10).   Data  are  also provided for  each compound across
quarters (Figures 4.11 to 4.20).

Methylene chloride

     Tenax and canister  values differed in  all  quarters, except
the 1st quarter  of  1988,  when the tenax  MDL was  highest.   The
large  percent difference  in  1st  quarter was due to  a single
canister value  of  24,  which  was  way above all  other canister
values.
Hexane
         with the exclusion of 1st quarter '88, canister and tenax
values were the same in all quarters (Figs. 4.11a and b)


Chloroform

     The only  comparison  data for this compound  occurred in 3rd
quarter '89.  See above for details.


1,1,i-Trichloroethane

     The canister and  tenax values were similar  in  the 1st, and
4th quarters of 1988, and 2nd quarter of '89, but differed in 2nd
and 3rd quarter  '88  and in  the 3rd quarter of '89 Fig.  4.12). In
1st quarter '88 all four canister values  were  at  its MDL  (0.5
ppb), whereas one tenax value was above this and three were  below.
In the remaining quarters the canister MDL was 0.2  ppb  and all
canister values  were reported above this  level.   The   greatest
differences  occurred in  2nd  and  3rd  quarters of  '88  and   3rd
quarter of  '89 when ambient concentrations were at their  lowest,
close to the canister MDL.  (It was also in these three  quarters
when the highest levels of breakthrough were seen in the  high flow
tenax traps - Chapter III).


Benzene

     The canister and tenax values were similar in the first  three
quarters of  '88,  but differed thereafter  (Fig.  4.13).      Tenax
values were usually slightly higher than canister in 4th  quarter
•88 and 1st quarter  '89; however, canister values were  higher in
2nd and 3rd  quarters of  '89.   This same phenomenon   occurred in
latter half of 2nd quarter and early half of 3rd quarter '88.  The

                                25

                              9-   26

-------
second and third  quarters of both years had the   lowest ambient
concentrations of benzene as seen on tenax.


Carbon tetrachloride

     Ambient concentrations  tended to be below the canister MDL,
so little comparison can be made (Fig. 4.14).


Trichloroethene

     Same as for carbon tetrachloride (Fig. 4.15).
Toluene

     Tenax /was  slightly but  consistently  higher in  1st  and 3rd
quarters of  '88 and thus significantly  different from canister,
but the means were similar (C  - 2.82 and 3.62, T - 3.39 and  4.86).
 In all other quarters,  tenax  values tended to be  slightly higher,
but there  were  some days when  canister values   were the higher
ones, and thus there were no significant  differences (Fig. 4.16).


Tetrachloroethene

     During 1st quarter '88 the canister MDL was  0.5 ppb and most
values  fell  below that,  but one  data pair  was  obtained  with
similar values  (C  » 0.66, T * 0.62).  Thereafter -the canister MDL
was 0.2 ppb and there  was good  agreement in all quarters, except
3rd quarter '88 when tenax values were slightly, but consistently
higher  (C - 0.59,  T - 0.82) (Fig. 4.17).


Ethylbenzene

     The  agreement in  1st quarter  '88 should be  ignored  (see
above).   In  the  2nd to  4th  quarters  of  '88  tenax  values  were
slightly  and  consistently higher  than  canister.   In  the  three
quarters of '89 there was no  significant difference between tenax
and canister; however,  the tenax mean was  higher in 1st quarter
(0.53:0.73),  the same in 2nd quarter (0.29:0.30), and lower in  3rd
quarter (0.40:0.27) (Fig. 4.18).


m/p-Xylene

     Tenax  and  canister  means  were  the   same in  1st and  2nd
quarters  of  '88,  but  differed  thereafter  (Fig.  4.19).   In 3rd
quarter  '88  through 2nd  quarter  '89 tenax  values  were slightly

                                26
                              9-  27

-------
                           CHAPTER V

                   MINIMUM ANALYTICAL DETECTION

            (Written in consultation with Dr. Weisel.)


     Minimum detection  limits (HDL) were  determined for twenty-
one compounds.  These compounds  fell  into two groups: those that
had consistent measurable blank values and those that did not.

     There were seven compounds with consistently measurable  blank
values:  methylene   chloride,  benzene,   toluene,  ethyIbenzene,
m/p-xylene,  o-xylene,  and  p-dichlorobenzene.   Since the  blank
values  for  these  compounds were much higher  than the instrument
detection limits,  "method detection limits'* were determined.   This
was done by taking twice the average  oven blank value  for  the
compound for the month.

     For the remaining  14  compounds,  which  did not have  blank
problems,   a   series    of   standard  samples  with   different
concentrations was analyzed.  A  concentration that could just be
detected by  the instrument was the  suspected  limit of detection.
 Five  replicates  were   run  close  to  the   suspected  limit  of
detection,   and  the  standard deviation  was calculated.    The
standard deviation was  multiplied by the Student  t-value at the
99% confidence limit at 4 degrees of freedom to determine the MDL.


     The values of the detection limits were  determined relative
to the instrumental response in nL of gas  .  These MDL values were
divided by the nominal volumes expected for 8  and 16 cc/min for a
24 hour period, or 12 and 24 liters, to convert to ppb.

     The following tables show the  monthly  "ppb11 values  for each
compound as determined above  (Table 5.la  and  b), and "ng" values
as converted from  the ppb  table  for this report (Table  5.2a and
b).

     For most  compounds, precision  seemed
                          9-  28

-------
higher than canister,  and in 3rd quarter  '89 they  were slightly
lower.  The biggest differences occurred in 3rd quarter  '88  and
2nd quarter '89.

o-Xylene

     Tenax and canister  values differed  in  all quarters,  with
canister values slightly higher  on all but two days in 1st  quarter
'89 (Fig. 4.20).
     To  summarize  the  quarterly  data,  the  absolute  percent
difference between the tenax and canister values were calculated.
 This was done by dividing the compound's mean tenax value for the
quarter by  the mean  canister  value  (Table  4.11),  and then  the
absolute  difference  was  determined  (Table  4.12).   The  largest
differences occurred  in  2nd and 3rd quarters of  '88,  and  in  the
3rd quarter  of '89,   periods of high temperatures.   Differences
tended to be greatest for benzene when its ambient concentrations
were low, but this did not hold  for toluene,  tetrachloroethene,
or  ethylbenzene.    Further tenax  values were  lower in  these
quarters  for  benzene,  but higher for toluene and ethylbenzene.
In 3rd quarter '88 tenax values tended to be higher than canister,
whereas in 3rd quarter '89 they tended to be lower.
                                27


                              9-  29

-------
- - rm" •—**-•
Quarter

* handling blanks run
Hethylene chloride
1, 1 -O i chl or oe thane
Hexane
Chloroform
1,1, 1— Trich lor oe thane
1 , 2-O i chl or oe thane
Benzene
Carbon tetrachloride
Tr i chl oroethene
Toluene
1,1, 2— Tr ichloroethane
Te trach 1 oroethene
Ch 1 rvi-thttt-t-r&rtf*
O*i O» OCJi. f LZ.UI WJ
^L i 	 vi 	 __
c. tncj i Dcnzerwr
•/p-Xylene
Broaofor*
Styrene
o-Xylene

p— O i eh 1 or obenzene
o-Oichlorobenzene
Hean
S
or *«
3087

87


2.7
22.0
8.2
O.O
14.3
O.5
O.O
10.4

0.0
4Q
. 7





19.2



7.5
7.7
•pie*
4Q87

86
13.3

0.2
O.4
l.O
O.4
O.O
0.0
O.O
0.0

O.O
On
• u





1.8



1.4
3.6
juooea
1Q88

97
11.6
O.O
0.8
0.8
0.0
O.O
O.O
0.0
O.O
0.0

O.O
Oo
* *J
30
• o
5.9

O.O
3.8



1.7
3.1
conc-ai
2088

85
11.6
O.O
1.4
O.O
O.2
O.2
O.6
O.O
O.2
1.6

l.O
10
. o
6*>
. «£
9.6

2.2
6.8



2.7
3.6
MirMil-V
3Q8CI

68
9.2!
O.CI
O.2
2.4
O.*i
0.2!
O.CI
O.CI
O.CI
0.7'

0.2'
Oe:
• ^'
1 O *"l
l&.LI
12.7
O.CI
O.Si
8.7



2.S<
4.4
a oase
4QG8

74
5.O
O.O
0.0
O.O
0.2
O.O
O.O
O.O
O.O
0.2
a.o
0.0
On
• u
if
* 1
1.1
O.O
0.6
O.9
1->
. r
15.4
3.2
1.4
3.4
a on D
1089

87
2.9
0.0
O.4
2.2
0.7
0.0
O.2
O.O
0.2
0.7
O.O
a.o
On
. u
2f\
. U
2.4
0.0
2.4
1.5
O^
. ^
17.5
0.4
1.6
3.7
A«nK «
2089

7
10.7
a.o
O.O
14.3
o.a
a.a
3.6
0.0
3.6
10.7
O.O
a.a
in 7
1U. f
'|>ft-. r%
25. O
14.3
O.O
10.7
10.7
71
. A
25.O
1O.7
7.5
7.7
wet
3089

20
0.0
19.5
O.O
7.3
O.O
O.O
O.O
O.O
12.2
O.O
0.0
0.0
1-3
,£.
On
.O
a.o
O.O
2.4
O.O
On
. u
8.5
a.o
2.4
5.1


Hean

8.O
2.8
0.6
5.5
1.3
0.1
2.1
O.I
1.8
2.7
O.O
0.1
20
mf.
7«
. 1
6.6
0.0
2.8
5.9
20
. a
16.6
3.6
3.4
3.8


S

4.5
6.8
O.9
7.3
2.5
0.1
4.5
O.2
3.8
4.2
O.O
0.3
3,4
. 4
8»^
.2
5.3
O.O
3.4
5.9
2Q
. *y
5.9
4.3
2.2


-------
Table 2.1
Organization: College oF Staten Island
                                                           Sorbent: Tenax
                                   SUHMRRY REPORT  CJULY 88 TO SEPTEMBER 89>




                                           DUPLICRTE  LOW  FLOM
CMpound na»e * Pairs


to
1

u*
M

















rfrtnylene Chloride
1,1 Dichloroethane
ttxane
CiloroFor*
1,1,1 Triehloroe thane
1.2 Dichloroethane
-~
utn^cene
Carbon Tetrachloride
Tr i ch 1 or oe thene
Tvluene
1.1,2 Triehloroe thane
Tttrach 1 or oe thene

Eihyl Benzene
•rfp Xylene
BroaoForM
SJyrene
o Xylene



o Dichlorobenzene
run
25
6
27
2O
27
15
27
27
26
27
2
26

26
26
O
26
26

22
3

Low
Flow 1
0.211
O. 146
O.987
0.050
O.464
0.069
1.354
0. 1O9
0.069
3.777
O.O4B
0.524

O.641
2.3O7

O.O86
O.459

O. 176
0.023
fiver age
Low
Flow 2
O.224
O.079
0.937
O.O5O
0.453
0.065
1.345
0. 1O7
0.065
3.727
0.04B
O.548
Oni.4
0.637
2.282

O.O85
O.421

0.172
O.O21
Overage
DiFF.

-O.O13
0.067
0.050
.OOO
O.O11
O.OO4
O.O09
O.OO2
0.004
O.OSO
.000
-O.O23

0.004
O.O26

O.OO1
O.O37

O.OO4
O.002
y.
DiFF.

6. 19X
45.91X
5.09X
O.O5X
2.33X
5.91X
O.64X
1.7SX
6.42X
1.33X
O.76X
4.45X
i ~y fvyv
0.58X
1.12X

0.78X
B. 16X

2.36X
6.81X
Std. Err. 95X d_
Hvg- OiF. interval

0.016
0.036
O.O35
0.002
O.O14
O.OO4
O.052
O.O04
O.OO4
0.111
0.001
O.O36

O.O24
O.O76

O.OO5
O.025

O.O2S
O.OO4

O. 159 >
0.122 >
O.OO5 >
O.O4O >
O.O13 >
O. 116 >
O.O1O >
0.014 >
0.279 >
0.008 >
O.O52 >
OOO4 1
O.O52 >
O. 182 >

0.011 >
O.OB9 >

0.055 >
O.O11 >
T Test

O.8O2
1.857
1.435
0.010
0.768
O.999
O. 167
O.5O3
O.991
O.45O
O.532
0.641
O 757
0.158
0.339

0.132
1.492

O. 166
O.385
T > O.n

N
N
N
N
N
N
N
N
N
N
N
N
N
N
N

N
N

N
N

-------
 T»bl« 2.2
Organization: Col1
of Stat*n Island
Sorbent: Tenax
                                     SUMMRRY REPORT (JULY 88 TO SEPTEMBER B9>




                                               DUPLICflTE  HIGH  FLOH
compound namo * Pairs
run
n>thylene Chloride
I 1,1 Dichloroethane
Htxarte
£ Chi or of or*
1,1,1 Trichloroe thane
1,2 Dichloroethane
B*nzene
C*i-bor» Tetrachloride
Trichloroethene
Toluene
1,1,2 Trichloroe thane
T» tr ach. 1 or pethene
Ch 1 or obenzene
Ethyl Benzene
*'p Xylene
BroMoForM
Siyrene
o Xylene
• DicHl or obenzene
p Dichl or obenzene
o Oich lor obenzene
24
4
25
23
25
24
25
25
25
25
2
24
13
24
24
0
23
24
0
2O
9
Average
High
Flow 1
0.123
O.012
O.663
O.O38
O.354
O.O5O
1.190
0.095
O.O64
3.098
O.O47
O.S32
O.OO9
O.546
1.9O9

O.O79
O.383

0.121
O.O1O
fiver age
High
Flow 2
O.12O
O.O46
O.675
0.036
O.322
0.048
1.122
0.094
O.O62
3.128
Q.047
0.515
0.009
0.555
1.924

C.O81
0.385

0.140
0.012
Rverage
DiFF.

O.OO2
-O.O33
-0.012
O.OO2
O.O32
O.OO3
O.068
.OOO
O.O02
-O.O3O
.OOO
O.017
.OOO
-O.O10
-O.O15

-O.OO1
-O.OO2

-o.oie
-O.OO2
•x.
DiFF.

1.75X
269. 38X
1.81X
6.O9X
8.98X
S.O4X
5.72X
0.47X
3.84X
O.95X
0.63X
3. 16X
2.32X
1.76X
O.81X

1.87X
0.47X

15.19X
16.68X
Std. Err. 95X CL
Hvg. OiF. interval
 Cppb)
O.OO9
O.O21
0.022
O.OQ3
0.027
O.OO2
O.O38
0.003
0.004
O.O74
O.OO1
0.017
0.001
O.O19
0.059

O.OO3
O.O11

O.O2O
O.OO1
<-O.O17 -
<-O.O84 -
<-O.O58 -
<-O.OO3 -
C-O.O24 -
(-O.OO2 -
<-O.OO9 -
<-O.OO7 -
<-O.OOS -
<-O. 182 -
<-O.003 -
<-O.O18 -
<-O.OOl -
C-O.O49 -
< -0.136 -

C-O.OO7 -
C-O.Q24 -

C-O.059 -
<-O.OO4 -
0.021 )
0.017 3
0.034 3
o.ooa :
O.O87 3
O.OO7 1
O. 146 :
o.ooa :
o.oio :
o. 122 :
o.ooa :
0.052 :
0.002 :
0.030 :
o. IDS :

o.oo4 :
0.020 :

0.022 :
.000 :
T Test
i O.23O
> 1.613
> 0.539
) O.841
• 1.173
1 1.205
I 1.801
> 0.130
> 0.646
> 0.398
1 O. 3O3
> O.992
> O.318
> O. 497
> O.26S

> O.588
> 0.166

> -O.929
> 1.806
T > O.tl

N
N
N
N
N
N
N
N
N
N
N
N
N
N
N

N
N

N
N

-------
     Table  2.3
     Organization:  Coll
                       of Staten Island
Sorbent:
              Regress i on
«0
I
                          r-y for-  July 19GB to September- 19B9

                           Lou Flow duplicate Samples
                                                                        High Flow Duplicate Samples
     Compound name
                       dF
Mcthylene Chloride    23
1,1 Oichloroethane     4
Hexane                 25
Chlor-oForM             18
1,1,1 TrichloroetHane 25
1.2 Dichloroethane    13
Benzene                25
Carbon Teti-achloride  25
Tr i eh 1 oroe thene       24
Toluene                25
1,1.2 Trichloroethane
Tetrachloroethene     24
Chlorobenzene          5
Ethyl Benzene         24
m/p Xijlene             24
BrOMoForm
Slyrene                24
o Xylene               24
• Dichlor-obenzene
p Oichlor-obenzene     2O
o Dichlor-obenzene      1
egress—
on coe—
Ficient
O.81
O.83
O.97
O.93
O.95
O.99
O.95
O.95
O.89
O.95
O.96
O.6O
O.92
O.94
O.86
O.83
O.46
O.98
Slope

0.84
O.42
0.89
O.84
0.99
O.B9
O.91
O.91
O.85
O.93
1.1O
1.01
O.94
0.96
0.90
o.as
O.67
1.28
t-Test
on
slope
9.82
4.35
29.21
15.25
21.14
29.39
21.1O
21.87
14.18
20.79
25.45
2.72
16.79
18. BO
12.27
1O.65
4.16
6.28
SigniFi—
R
dF i

«g* *-i>±i
on coe—
Slope
cance FFicient
P <
P •
P «
P «
P '
P •
P «
P •
P '
P «
P •
P «
P «
P «
P «
P «
P «
P :
c O.OS
c O.OS
c O.OS
c O.OS
c 0.05
c O.OS
c 0.05
c O.OS
c O.OS
c O.OS
c O.OS
c O.OS
c O.OS
i: O.OS
c O.OS
e O.OS
: O.OS
- O.OS
22
2
23
21
23
22
23
23
23
23
22
11
22
22
21
.Z2
18
7
0.82
O.67
O.96
O.81
O.76
l.OO
O.98
O.95
O.92
O.97
l.OO
0.67
0.93
O.95
O.96
O.96
0.71
O.96
O. 84
11. OO
O.99
0.71
O.75
O.9O
0.95
1.04
O. 87
O.99
0.91
O.64
0.99
0.96
O.98
O. 95
1.47
1.15
t-Test
on
slope
9.96
1.99
24.83
9.51
8.62
74.75
3Q.58
21.18
16.38
25.38
76.17
4.77
17.28
20.87
23. 4O
23.65
6.61
13.24
SigniFi—
a
P
P
P
P
P
P
P
P
P
P
P
P
P
P
P
P
P
P
mt
<
>
<
<
<
<
<
<
<
<
<
<
<
<
<
<
<
<
:e
O.OS
0.05
0.05
O.OS
o.as
O.OS
O.OS
0.05
O.OS
O.OS
0.05
O.OS
O.OS
O.OS
O.OS
O.OS
O.OS
0.05

-------
0
     Table 2.4
    Organization:  Callvg* of Staten Island
Sorbent: Tervax
                                       Quartet- of   July    to  September ,  1988





                                                 DUPLICATE  LOW  FLOW
compound name * Pairs
run
Methylene Chloride
1.1 O i ch 1 or oe thane
Hexane
ChloroFot-M
1,1,1 Tr ich lor oe thane
1,2 Dichloroe thane
Benzene
Carbon Tetrachlor ide
Tr i ch 1 oroethene
Toluene
1 , 1.2 Tr i chl or oe thane
Tetrachl oroethene
Ch 1 or obenzene
Ethyl Benzene
m/p Xy 1 ene
BromoForiB
Styrene
o Xylene
f Dichlorobenzene
1^ Dichlorobenzene
o Dichlorobenzene
3
O
5
3
5
3
5
5
5
5
O
5
O
5
5
O
5
5
1
O
O
Overage
Low
Flow 1
O.281

1.013
0.102
0.532
O.221
1.239
O.O93
O. 131
4.727

0.459

O.969
3.547

0.093
O.474
O.38O


Rverage
Low
Flow 2
O.337

O.921
O.O94
O.454
0.198
1.2O2
0.092
O. 124
4.65O

0.450

O.947
3.484

O.O6O
O.484
O.421


flverage
DiFF.

-O.O57

O.O93
.o.ooa
O.O78
0.022
O.O37
O.OO1
O.OO8
0.078

O.OO8

0.022
O.062

0.012
-0.010
-0.041


y.
DiFF.

20.22X

9-17X
7.59X
14.65X
1O. 15X
2.99X
O.92X
5.84X
1.64X

1.8OX

2.29X
1.76X

13.07X
2.O6X
1O.81X


Std. Err. 95X CL
Hvq. OiF. interval
 
0.112

O.O51
O.OO9
O.O43
O.O17
0.073
O.O11
o.ooa
0.184

O.O17

O.O56
O. 151

O.O12
O.021



< -0.539 -
.
C-O.O49 -
C-O.O33 -
C-0.042 -
C-O.O52 -
<-O. 165 -
C-O.029 -
C-O.O14 -
C-O.434 -

C-O.O4O -

<-0. 132 -
C-O.357 -

C-O.021 -
<-O.O67 -



O.425 >

0.234 >
O.O48 >
O. 198 >
O.O97 >
O.239 >
O.O3O >
O.O29 >
O.589 >

O.OS6 >

O. 177 )
O.482 )

O.O45 >
O.O47 >



T Test
O.5O6

1.822
0.826
1.798
1.294
0.509
O.O81
O.988
O.421

O.477

O.399
0.413

1.026
O.476



T > O.O
CY/N>
N

N
N
N
N
N
N
N
N

N

N
N

N
N




-------
     Table 2.5
    Organization:  College  of Staten Island
!>orbent:  Tenax
(O
I
u
uu«*ri,(?f^ or «_»u u«ju*?r i-«j u
DUPL1CHTE LOW F
compound name S Pairs
run
Methylene Chloride
1,1 Oichloroe thane
Hexane
Chloroform
1,1,1 Tr i chl or oe thane
1,2 Dichloroethane
Benzene
Carbon Tetrachlor ide
Tr i ch 1 or oe thene
Toluene
1,1,2 Trichloroe thane
Te trach 1 or oe thene
Ch 1 or obenzene
Ethyl Benzene
m/p Xylene
BromoForm
Styrene
o Xylene
f Dich lor obenzene
M» Dich lor obenzene
o Dich lor obenzene
a
O
8
4
a
2
a
a
7
a
i
a
o
a
a
o
a
a
a
o
i
fiver age
Low
Flow 1
O.299

O.856
0.025
O.4O1
O.O57
1.599
0.126
O.O53
3.358
0.085
O.695

0.579
2.228

O.O8S
O.446
O.244

O.O13
Hverage
Low
Flow 2
0.346

O.B86
O.O31
O.432
O.O48
1.677
O.131
0.054
3.582
O.O86
O.8O5

O.630
2.412

O.O9S
O.481
O.215

O.OOS
Hverage
DiFF.

-0.047

-O.O31
-O.OO6
-0.031
O.O1O
-O.O78
-O.OOS
-O.OO1
-O. 224
-O.OO1
-O. 1 1O

-0.051
-0. 184

-O.O1O
-O.O34
O.O29

O.OOS
DiFF.

15.60X

3.61X
25.O3X
7.78X
16.79X
4.9OX
3.66X
2.34X
6.67X
1.22X
15.89X

B.77X
8.25X

1 1 . 46X
7.67X
1 1 . 78X

62.96X
me ci. mnjtft
LOW
9 A 7OCJ

Std. Err. 955* CL
Rvg. OiF. interval
 
0.028

O.O37
0.003
O.O15
.OOO
0.082
O.OOS
O.OO4
0.171

O.O89

0.038
0.124

O.OOS
O.023
O.O55


(-0.112 -

<-O. 118 -
<-0.017 -
<-O.O66 -
< O.OOS -
< -0.273 -
<-O.O17 -
C-0.010 -
C -0.628 -

<-O.322 -

<-O. 140 -
<-0.477 -

C-O.O22 -
<-O.O89 -
C-0. 1O2 -


O.O19 >

0.056 >
O.OOS >
O.OO4 >
O.O11 >
O. 116 >
O.OOS >
O.OO8 >
O.18O >

O.1O1 >

O.O38 >
0.109 >

O.OO3 >
O.O21 >
O. 16O )



T Test T
1.682

O.844
1.773
2.098
68.615
0.953
O.865
O.329
1.310

1.234

1.349
1.485

1.856
1.466
0.520



> O.O!

N

N
N
N
Y
N
N
N
N

N

N
N

N
N
N



-------
 Table 2.6
Organization: Co1109* of Staten Island
Sorbent: Tenax
                                  Quarter- of January   to    March   ,  1989




                                            DUPLICRTE  LOW  FLOW
compound na«e • Pairs
ron
W> MetHtjlene Chloride
1 1,1 DichloroetHane
Hexane
Ul
Ot Chloroform
1,1,1 Trichloroethane
1,2 Dichloroethane
Benzene
Carbon Te trichloride?
Tr i ch 1 oroethene
Toluene
1,1,2 Trichloroethane
Tetrachl oroethene
Ch 1 orobenzene
Ethyl Benzene
m/p Xy 1 ene
Bromofcx-m
5t«jrene
o Xy,lerte
fk Oichlorobenzene
* Oichlorobenzene
o Oichlorobenzene
5
O
5
4
5
1
5
5
5
5
O
4
0
4
4
O
4
4
4
O
O
Average
Low
Flow 1
Q.294

O.779
O.O39
O.549
O.O55
1.788
O. 187
O.O55
3.913

O.4O7

0.778
2.730

0.122
0.632
O. 19O


fiver age
Low
Flow 2
O.2S9

O.6B9
O.O36
0.535
O.O59
1.S47
0. 176
O.O52
3.532

O. 369

O.699
2.466

O. 115
O.S74
0.198


Hverage
Diff,

O. 036

O.O9O
a. 003
O.O14
-O.OO4
O.241
a. on
O.OO2
a. sal

O.O38

O.O79
O.264

O.OO7
o.osa
-o.ooe


7.
Oiff.

12.O8X

11. sax
6.57X
2.53X
7. 19X
13.46X
5.75X
4.1BX
9.75X

9.38X

1O. I9X
9. sax

S.G4X
9.21X
4-OSX


Std. Err. 952 CL
Rvg. Oif. interval
(ppb> Cppb>
0.018

O.059
O.OO3
O.O36

O. 156
o.ooa
O.O04
0.302

O.O29

O.O74
0.222

O.O14
O.O56
0.019


(-O.O14

C-O.O74
(-0.006
<-O.O87

C-0.191
C-O.O11
C-O.O1O
C-O.457

(-O.O54

<-O. 157
<-O.441

<-O.O37
t-O. 121
C-O.068


- O.O85 >

- O.255 >
- 0.011 >
- 0. 115 >

- 0.673 >
- O.O32 )
- 0.014 )
- 1.220 >

- 0.130 >

- 0.315 >
- 0.97O >

- 0.051 >
- O.238 >
- O.O53 )


T Test T > 0. 1
1.986

1.52O
O.926
0.382

1.546
1.388
O.53O
1.262

1.317

1.O7O
1.192

O.496
1.D31
O.4O4


N

N
N
N

N
N
N
N

N

N
N

N
N
N



-------
 Table 2.7
Organization: College of Statcn I*land
Sorbent: Tenax
                                   Quarter- oF  flpril    to     June    ,  1989





                                             DUPLICATE  LOW  R.OM
compound name * Pairs

Methyl one Chloride
1, 1 Dichloroethan*
1 Hexane
Chl or of or*
U 1.1.1 Tr i chl or oe thane
^ 1.2 O i chl or oe thane
Benzene
Carbon Tetrachloride
Tr i ch 1 oroe t hene
Toluene
1,1,2 Tri chl oroe thane
Te trach 1 or oethene
Ch 1 or obenzene
Ethyl Benzene
mSf> Xylene
Or o~o form
Styrene
o Xylene
f Oi chl or obenzene
pi Oi chl or obenzene

run
2
1
2
2
' 2
2
2
2
2
2
O
2
2
2
2
0
2
2
2
0
I
flverage
Lou
Flow 1
O.O77
0.007
O.489
O. 100
O.425
O.OO9
0.349
O. 115
O.O39
2.252

O.421
O.016
0.519
1.309

0.044
0.637
0.069

n n4A
Overage
Lou
Flow 2
O.O86
0.018
O.589
0.103
O.421
O.O17
O.766
O.O93
0.063
3.017

0.617
O.O23
0.686
1.81O

O.O9O
O.443
0.240

n r«i
fiver-age X
OiFF. DiFF.
Cppb)
-O.OO9
-0.011
-0.100
-O.OO3
O.OO4
-0.009
-0.417
0.023
-0.025
-0.764

-O. 196
-O.OO7
-0. 167
-0.501

-0.047
O.194
-0.171

— n CM-XT

11.89%
143.96%
2O. 51%
2.83%
O.94%
104.98%
119.33%
19.70%
63.73%
33.94%

46.64%
46.01%
32.29%
38.27%

1O6.77%
30.50%
247.66%

• * 0f^->
Std. Err. 95% CL
Rvg. OiF. interval
Cppb>
O.O16

O.287
O.O11
O.O41
O.OO4
0.255
O.O13
0.011
O.289

O. 139
O.OO5
0.071
O. 189

0.023
0.290
O.O21



(-O.216 -

C-3.750 -
(-0. 143 -
C-O.512 -
(-O.O6O -
(-3.66O -
< -0.143 -
<-0. 169 -
C-4.436 -

C-1.958 -
< -0.072 -
<-1.069 -
C-2.902 -

C-O.338 -
C-3.494 -
<-O.438 -



0.198 >

3.55O >
0.137 >
0.52O >
0.043 >
2.827 >
0.188 >
0. 12O >
2.907 >

1.565 >
O.O58 >
0.734 >
1.900 >

0.245 >
3.882 )
0.097 >


T Test

O.564

O.349
O.257
O.O99
2.209
1.632
1.747
2.173
2.646

1.417
1.431
2.361
2.652

2.029
O.670
8.113


T > 0.0
tV/N>
N

N
N
N
N
N
N
N
N

N
N
N
N

N
N
Y



-------
  Table 2.8
Organization: College of Stat«n Island
Sorbent: Tenax
                                  Quarter of   July     to  September ,  1969





                                            DUPLICATE   LOW  FLOW
compound name 1* Pairs
run

«O
1
W
09















Methylene Chloride
1,1 Dichloroe thane
Hexane
Chloroform
1,1.1 Tr i chl or oe thane
1.2 Dichloroe thane
Benzene
Carbon Tetrach 1 or i de
Tr i ch 1 or oethene
Toluene
1,1.2 Trichloroethane
Tetrachl or oethene
Chl or obenzene
Ethyl Benzene
mXp Xy 1 ene
Br-omoform
Styrene
o Xylene
f Di chl or obenzene
»•> Di chl or obenzene
o Di chl or obenzene
7
5
7
7
7
7
7
7
7
7
1
7
5
7
7
0
7
7
7
O
1
Rverage
Low
Flow 1
O.O59
O. 173
1.4O9
O.O33
O.436
O.027
1.134
O.O42
a. 0&0
3.915
O.O10
O.473
O.O11
O. 433
1.556

O.074
O.311
O.O91

O.OO9
fiver age
Low
Flow 2
O.O51
0.091
1.282
O.O34
0.426
O.O28
1.091
O.O44
O.043
3.575
O.O1O
0.4O5
0.01O
O.375
1.303

O.059
0.214
0.052

O.OO7
Rverage
Diff.

O.OO8
0.082
0.127
.OOO
0.011
.OOO
O.O44
-O.O02
0.018
0.340
.OOO
O.O68
O.OO1
O.O58
0.253

0.014
O.O96
0.039

O.OO2
%
Oiff.
 
O.OO9
0.04O
O.O9O
O.OO5
O.O23
O.OO1
0.05O
O.OO8
O.O13
0.179

O.O62
O.OO1
0.018
O.O82

O.OO6
0.029
0.028


<-O.O15
C-O.O28
C-O.094
C-0.012
C-O.O46
<-O.OO4
<-O.079
C-O.O23
C-O.O15
C-O.O98

<-O.O83
C-O.OO3
< O.O13
C O.O54

< .OOO
C O.025
(-O.O29


- 0.031 >
- O.193 >
- 0.348 >
- O.O11 >
- 0.068 >
- O.OO3 >
- 0.167 >
- O.O18 >
- O.O5O >
- O.779 >

- 0.219 >
- O.OO5 >
- 0. 1O3 >
- 0.453 >

- O.029 )
- 0.168 >
- O. 1O8 )


T Test
o.eai
2.069
1.4O9
0.083
O.455
O.312
0.872
0.256
1.329
1.899

1.10O
O.511
3.178
3. 1O4

2.394
3. 3O7
1.4O1


T > o.o:
CY/N>
N
N
N
N
N
N
N
N
N
N

N
N
Y
Y

Y
Y
N



-------
Table 2.9
Organization:  College of States Island
fvarbent: Tenax
                                   Quarter of   July    to  September- , 1988




                                             DUPLICRTE  HIGH  FLOW
compound name II Pairs
run


to
1

(*>
U>















Met.hylene Chloride
1,1 Dichloroefchane
Hexane
ChloroForm
1,1,1 Trichl oroethane
1,2 O i ch 1 oroefchane
Benzene
Carbon Tetrachlor ide
Tr i ch 1 or oethene
Toluene
1,1,2 Trichl oroethane
Te trach 1 oroe thene
Ch 1 or obenzene
E thy 1 Benzene
mv/p Xy 1 ene
BromoForm
Styrene
o Xylene
0 Oichlorobenzene
\H Oichlorobenzene
o Oichlorobenzene
4
O
5
3
5
4
5
5
5
5
O
5
3
5
5
O
5
5
1
O
O
Average
High
Flow 1
O. 179

0.769
0.066
0.369
O. 177
O.9O2
o.osa
O. 112
4.293

O.5O9
O.O1O
0.782
2.781

O.OBO
O.397
O.293


Average
High
Flow 2
0.213

0.708
O.O71
0.275
0.163
O.863
O.O57
0. 1O4
4.162

0.478
O.010
0.831
2.881

0.083
0.413
O.456


Rverage
DiFF.
Cppb)
-O.O33

O.O61
-O.OO5
O.O94
O.O14
O.O38
O.OOl
o.ooa
O. 131

O.O31
.000
-o.nso
-o. 100

-0.003
-O.O15
-O. 163


DiFF.
1B.64X

7.93X
7.84X
25.43X
7.75X
4.24X
1.71X
7.O1X
3.05X

6. 15X
3.O4X
6.37X
3.602

4.O4X
3.88X
55. 48X


Std. Err. 95X CL
RVg. DiF. interval

O.O4O

0.063
0.015
0.137
O.012
O.O8O
O.OO4
O.OO7
O. 174

O.O18
O.OOl
O.O78
O.245

O.OO3
O.O24



(-0.161

(-0.113
(-0.069
(-O.296
(-O.O24
(-O. 183
(-O.O11
(-O.O12
(-O.353

(-O.O19
(-O.O04
(-0.267
(-0.779

(-0.012
(-O.O82



- O.O95 >

- 0.235 >
- O.O59 >
- O.474 >
- O.O51 >
- O.259 >
- O.O13 >
- O.O28 >
- 0.615 >

- O.O82 >
- O.OO4 >
- O. 167 >
- O.579 >

- O.OO6 >
- O.OS1 >



T Test
0.831

O.972
O.35O
O.685
1.171
0.481
O.227
1.O72
0.751

1.712
O.342
0.637
O.4O9

0.963
0.64S



T > O.fl
(Y/N)
N

N
N
N
N
N
N
N
N

N
N
N
N

N
N




-------
u>
    Table  2.10
   Organization:  College of St«t«n Island
Sorbent: Tenax
                                      Quarter of October   to   December  ,  19B8




                                                DUPLICATE  HIGH  FLOW
compound name * Pairs
run
Methyl ene Chloride
1,1 Dichloroethane
Mexarte
Chloroform
1,1.1 Trichloroe thane
1,2 O i chl or oe thane
Benzene
Carbon Tetrachlor ide
Trichloroethene
Toluene
1.1.2 Trichloroethane
Te tr ach 1 or oe thene
Ch 1 or obenzene
Ethyl Benzene
mXp Xylene
Bromoform
Styrene
o Xylene
f Oichlorobenzene
- fl I * llllHIll lflf~ft f iM lift
o Oi chl or obenzene
a
O
a
a
8
a
a
a
a
a
2
O
1
a
a
o
7
a
a

3
Rverage
High
Flow 1
O. 147

0.839
O.O21
O.324
O.O29
1.577
O.098
O.055
2.955
0.047
0.697
0.014
O.493
1.84O

0.087
O.366
0. 1O9

O.OO2
Fiver age
High
Flow 2
0.132

O.899
O.O24
O.3O5
O.O28
1.486
O.O93
O.O56
2.968
0.047
0.663
0.012
O.5O6
1.882

0.094
0.378
0.1O5

O.OO2
OiFf.
O.O15

-0.061
-0.003
O.O19
O.OOl
O.O91
O.OO5
-O.OOl
-0.012
.OOO
O.O34
0.002
-0.013
-O.O42

-0.006
-0.012
O.O05

.OOO
X
Diff.

1O.48X

7.22X
12.39X
S.78X
2.15%
5.77X
5. 19X
1.61X
0.42X
O.63X
4.88X
13.96X
2.67X
2.30X

7.42X
3.26X
4.222

14.96X
Std. Err. 95X CL
flvg. Oif . interval
(ppb> (ppb)
O.O1B

O.O34
O.OO3
O.013
O.OOl
0.071
O.O03
0.002
O.O55
O.OOl
0.038

O.O1O
0.029

O.OO2
O.006
0.012

O.OOl
<-O.O27

<-O. 142
(-O.OO9
<-O.Oll
(-O.OO2
(-O.O77
(-O.OO3
(-0.005
(-O. 143
(-0.013
(-0.056

(-0.036
(-0.112

(-O.O12
(-O.O26
(-O.O24

(-O.OO3
- O.O58 >

- O.O21 >
- O.OO4 )
- O.O49 >
- O.OO3 >
- O.26O >
- 0.013 >
- O.OO3 >
- 0. 118 >
- O.O12 >
- 0.124 )

- O.OO9 >
- O.O27 )

	 O,OO1 >
- Q. 002 )
- O.O33 )

- O.OO2 )
TT^t
O.851

1.759
0.943
1.468
O. 599
1.279
1.461
O.491
O.227
O.3O3
O.898

1.381
1.444

2.9O3
1.955
O.3S1

O.41B
T > 0
(Y/N
N

N
N
H
N
N
N
N
N
N
N

N
N

Y
N
N

N

-------
  Table 2.11
Organization:  College of Staten
                             Sen-bent: Tenax








Quarter- of Januar-y    to    r Larch   ,  1989





           DUPLICHTE   HIGH  fl_OH
*• ompiMMtrt name It Pairs

Methylene Chloride
1,1 Dichloroethane
. .
»? Chloroform
I
1,1,1 Tr ichl or oe thane
^, 1,2 Dichloroethane
*•* Benzene
Car lion Tetrachlor ide
Tr- i ch 1 or oe thene
Toloene
1,1,2 Tr i chl or oe thane
Tetr ach 1 or oe thene
Chl or obenzene
Ethyl Benzene
m/p Xylene
BroMofor*
Sfcyrene
o Xylene
f Dichlorooenzene
H Dichlorooenzene
o D ichl or obenzene
run
5
O

5

5
5
5
5
5
5
O
4
2
4
4
O
4
4
4
O
2
fiver age
High
Flow 1
O. 162

r» •yrMa
U. r cO
O.O38

O.494
O.O36
2.022
O. 167
0.058
3.535

O.411
O.OOS
O.7OO
2.501

0.124
0.629
0.139

O.007
Rverage
High
Flow 2
O.145

n '7^if%
0.033

O.488
0.036
1.867
0.175
O.O59
3.661

O. 391
0.006
O.686
2.399

0.115
0.593
0.147

O.OO8
Rverage
DifF.

O.017

Oo^o
• ^ ~g j
O.OOS

O.OO6
.OOO
O. 155
-o.ooa
.000
-0. 127

0.020
-O.OO1
O.O14
0. 1O2
1
0.009
O.O35
-o.ooa

-0.001
X
DifF.

10.65X

9 W*»V
12.97X

1.172
0.93X
7.652
4.7O2
O.74Z
3. 58X

4.84X
10.97X
1.99X
4.O8X

6.9OX
5.63X
5.91X

7.88X
Std. Err. 95X CL
ftvg. DiF. interval

O.OO3

Oni7
• U A r
O.OO2

O.O1O
O.OO1
0.128
O.OOS
0.002
0.154

O.Oil
O.OO1
O.O14
O.O52

O.OOS
O.O19
0.012

.OOO
T Test
Cppb)
< 0.009

/'—fl fflO*S
< .000

C-O.021
<-O.O03
<-O. 199
C-O.O33
<-0.005
< -0.556

C-O.O14
<-O.O19
C-O.O3O
C-O.O63

C-O.O07
C-O.O24
<-O.O47

<-O.O03
- O.O26 >

— n n7i %
U.Ur A ^
- O.O1O >

- O.O32 >
- O.OO2 >
- O.5O9 >
- O.O17 >
- 0.004 >
- 0.302 >

- O.O54 >
- o.oie >
- O.O58 >
- 0.267 5

- O.O24 >
- O.O94 >
- 0.030 )

- 0.001 >
5.574

Io-ai
. jj A
2.612

O.601
O.41O
1.212
0.901
O.258
O.82O

1.841
O.4O3
1.005
1.961

1.793
1.906
O.679

3.686.
T > O.O!

Y


Y

N
N
N
N
N
N

N
N
N
N

N
N
N

N

-------
  Tabla 2.12
Organization: College of Stat*n Island
Sorbent: Tenax
                                  Quartet- of   flpril     to     June   , 1989




                                            DUPLICATE  HIGH  FLOM
compound name * F
Mtthylene Chloride
1,1 Dichloroethane
H*xane
^ ChloroForM
1 1,1,1 Triehloroethane
1,2 Dichloroethane
J^ Benzene
Carbon Tetrachloride
Tr i ch 1 oroe therte
Toluene
1,1,2 Triehloroethane
T* t r ach 1 or oethene
Ch 1 or obenzene
Ethyl Benzene
«/p Xylene
Bro«oFor«
Slyrene
o Xylene
f Oichlorobenzene
^ Oichlorobenzene
o Oichlorobenzene
•airs
run
4
2
4
4
4
4
4
4
4
4
O
4
4
4
4
O
4
4
4
O
3
fiver age
High
Flou 1
0.04O
O.O11
O.312
0.070
0.346
O.O14
O.34S
O. 1O1
O.045
1.9O1

0.246
0.012
0.402
1.O76

0.037
O.261
O. 144

0.023
fiver age
High
Flou 2
O.O45
O.O15
O.369
O.O53
O.321
0.014
0.351
O.O94
O.O40
1.907

0.272
O.O11
O.381
1.04O

0.036
O.252
0.214

0.027
Rverage
DiFF.
-O.005
-O.OO4
-O.O56
O.O16
O.O25
.OOO
-O.OO6
O.007
O.OO4
-O.OO5

-O.O26
b.ooi
O.O2O
O.036

.OOO
O.OO9
-O.O70

-O.OO4
OiFF.
Cppbi
12.46X
39.76X
17.93X
23.5SX
7.29X
O.08X
1.63X
7.2SX
9.91X
O.29X

1O.76X
7. SIX
5.08X
3.39X

0.73X
3.59X
4B.41X

18.62X
Std. Er
Rvg. Di

O.O12
O.OO1
O.082
o.ooa
O.O49
O.OO3
O.058
O.O17
O.012
0.289

0.032
0.002
O.068
O.184

O.OO9
O.O51
0.088

0.002
r. 95X
F. intei
Cppb
<-O.O42
C-O.O23
<-O.318
C-O.OO8
C-O. 13O
C-O. 010
C-O. 189
C-O.O46
(-0.033
C-O. 926

C-O. 129
C-O.O05
C-O. 196
C-O.55O

C-O.O28
C-O. 153
C-O. 351

C-O.O14
CL
rval
>
- O.O32
- O.O14
- O.2O6
- O.O41
- O. 181
- 0.010
- O.178
- 0.061
- O.O42
- O.915

- O.O76
- O.007
- O.237
- 0.623

- O.028
- O.172
- O.211

- 0.006

>
>
>
>
>
>
)
>
>
>

>
>
>
>

>
>
>

>
T Test
0.433
2.896
0.681
2.113
O.515
O.OO3
O.O98
O.436
0.377
0.019

O.824
O.5O3
O.3OO
O. 198

O.O30
O. 183
0.791

1.880
T > o.o;
CY/N)
N
N
N
N
N
N
N
N
N
N

N
N
N
N

N
N
N

N

-------
 Table 2.13
Organization: College of Statvrt Island
Sot-bent:  Tertax
                                     Ooar-ter- of   July     to  September , 1989





                                                DUPLICATE  HIGH  FLOW
compound name * Pairs

Methylene Chloride
1.1 Oichloroethane
10 Hexane
1 ChloroForai
1.1,1 Tr ichloroethane
£j 1.2 Oichloroethane
Benzene
Carbon Tetrachloride
Tr i ch 1 or oethene
Toluene
1,1.2 Tr ichloroethane
Tetrachl oroethene
Ch 1 or obenzene
Ethyl Benzene
«/p Xylene
BroAoFor*
Sturerte
o Xylene
f Dichlorobenzene
A Oich lor obenzene
o Dichlorobenzene
run
3
• 2
3
3
3
3.
3
3
3
3
0
3
3
3
3
O
3
3
3
O
1
Average
High
Flow 1
O.O26
O.O14
0.293
0.013
0.190
O.O13
0.377
O.O16
O.O45
2.357

0.673
O.O05
O.281
O.959

O.O57
0.239
0.043

O.OO3
Hverage Rverage
High OiFF.
Flow 2 
0.027
O.O76
0.296
O.O13
0.174
O.O12
O.366
O.O24
O.O4O
2.569

0. 673
0.006
0.285
0.988

0.059
O.255
0.020

O.OO4
-O.OO1
-O.O62
-O.OO3
.OOO
0.016
O.OO1
O.011
-o.ooa
o.oos
-O.213

.000
-O.OO1
-0.004
-0.029

-0.003
-O.O17
0.023

-0.001
y.
DiFF.

5.322
444. 75X
1.17X
2.21X
8.29X
7.392
2.862
50. 17X
10.552
9.O32

O.O12
18.O92
1.59X
3.OOX

4.652
6.932
53. 732

17. SOX
Std. Err. 95S£ CL
Rvg. OiF. interval
Cppb)
0.010
O.O29
0.028
0.004
O.O2O
0.001
0.027
O.OO6
O.O3O
0.357

0.087
0.001
0.034
0.129

o.oia
0.036
O.O28


T Test

<-O.O43
C-O.436
<-O.122
C-0.017
C-O.O69
C-O.004
C-0. 1O5
<-O.O34
<-0. 125
<- 1.747

< -0.374
<-O.OO7
<-0.150
<-O.583

<-O.O57
<-O. 171
<-0.098


- O.O4O >
- O.312 >
- O. 115 >
- O.O16 >
- 0.100 >
- O.OO6 >
- O. 127 >
- O.O18 >
- O. 135 >
- 1.322 >

- O.374 >
- O.OOS >
- O.141 >
- 0.526 >

- O.O51 5
- 0.138 >
- 0.144 )


0.145
2.118
0.125
0.072
O. 800
0.758
O.4O1
1.354
O. 157
O.596

O.OO1
O.66O
0.132
O.223

0.210
O.461
0.823


T > o.o:

N
N
N
N
N
N
N
N
N
N

N
N
N
N

N
N
H



-------
Table 3.1.  Comparison of low and high flow values on basic of
            paired sample t test
Measurable most of time Measurable < 33X of time
Compound Quarters Compound Quarters
* X diff* * % diff*
Hexane
Chloroform
1 1 1-Trichloroethane
1 2-0 i ch 1 oroethane
Benzene
Carbon tetrachloride
Trichloroethene
Toluene
Tetrachloroethene
Ethyl benzene
m/p Xylene
Styrene
o Xylene
9
9
9
9
9
9
8
8
8
7
7
7
7
Mean x quarters different
S

78 Methylene chloride 8
07 1 , 1 -D1 ch 1 oroethane 7
100 112-Trichl oroethane 4
78 Chlorobenzene 9
67 Bromoform 4
100 m Dichlorobenzene 3
62 o Dichlorobenzene 4
50 p Dichlorobenzene 4
25
57
29
43
43
61.5
23.8
75
71
75
100
25
33
100
100





72.4
29.5
 *  difference  based paired t test
                           9-  44

-------
Table 3.2.  Distributed Volume Comparison:  Quarterly mean  low  flow
            divided by quarterly mean high  flow for each compound
Compound
4Q87 1Q88 2Q88 3Q88 4Q88 1Q89 2Q89 3Q89  Mean 8
A. Measurable most of the
Hexane
Chloroform
1 1 1-Trichloroethane
1 ,2-Dichloroethane
Benzene
Carbon Tetrachloride
Trichloroethene
Toluene
Tetrach 1 oroethene
Ethyl benzene
m/p Xylenes
Styrene
o Xylene
Mean for all 13
S
Mean for first 7
S
Mean for last 6
S
0.96
1.02
1.20
0.95
0.98
1.19
0.89
0.99
0.96



0.96
1.01
0.10
1.03
0.11
0.97
0.01
time
0.
0.
1 .
0.
1.
1.
0.
1.
0.
1.
1.
0.
1.
1.
0.
1.
0.
1.
0.
99
96
23
75
03
16
90
03
98
09
02
98
06
01
11
00
15
03
04
1.14
1.34
1.32
0.94
1.02
1.29
1.03
1.02
0.90
1.00
1.02
0.92
0.92
1.07
0.15
1.15
0.15
0.96
0.05
1.43
.83
.60
.30
.17
.43
.28
.09
0.91
.05
.09
.00
.05
1.25
0.25
1.43
0.21
1.03
0.06
1.02
1.19
1.31
0.86
0.94
1.27
0.96
1.10
0.97
1.07
1.09
1.01
1.07
1.07
0.12
1.08
0.16
1.05
0.05
0.94
1.01
1.19
0.75
0.86
1.12
0.93
1.02
0.97
0.99
1.01
0.97
0.98
0.98
0.10
0.97
0.14
0.99
0.02
1.04
1.47
1.26
1.16
1.00
1.40
1.00
1.01
0.91
1.01
0.94
0.91
0.94
1.08
0.18
1.19
0.18
0.95
0.04
1.31
1.75
1.48
1.56
1.21
1.61
0.95
0.99
1.02
1.10
1.07
1.14
0.95
1.24
0.26
1.41
0.25
1.05
0.06
1.10
1.32
1.32
1.03
1.03
1.31
0.99
1.03
0.95
1.04
1.03
0.99
0.99
1.09
0.13
1.16
0.14
1.01
0.03
0.17
0.32
0.14
0.27
0.11
0.15
0.12
0.04
0.04
0.04
0.05
0.07
0.06
0.10

0.17

0.04


B. Measurable less than 31%
Methylene chloride
1 , 1-Dichloroethane
1 1 2-Tr 1 ch 1 oroethane
Chlorobenzene
Bromoform
m 01 Chlorobenzene
p D1 Chlorobenzene
o Oichlorobenzene
Mean
S
Mean of columm means
S
2.15


1.38




1.77
0.39


1.
1.

1.




Of
78
78

30




1.62
0.23




the
2.11
1.99

1.19




1.76
0.41


time*
1.87
2.00

1.41
2.00



1.82
0.24



2.02
1.73
1.99
1.57
1.85
1.92
1.93
1.68
1.84
0.15



1.93
1.74
1.99
1.39
2.00
1.63
2.02
1.54
1.78
0.23



2.00
1.60
1.94
1.59
2.00
2.00
1.97
2.07
1.90
0.18



2.00
1.28
2.00
1.61
1.98
2.00
1.97
1.96
1.85
0.25



1.98
1.73
1.98
1.43
1.97
1.89
1.97
1.81
1.79

1.85
0.18

0.11
0.23
0.02
0.14
0.06
0.15
0.03
0.21
0.08



* most or all values at or below MOL
                               9-  45

-------
Table 3.3.  Means of lo-hl values >  MDL for  7  compounds seen on <
            3IX of days
Compound (N=)
Methyl ene chloride
58*
1 , 1-D1chloroethane
10
Chlorobenzene
112
Bromoform
6
m-D1 Chlorobenzene
1
o-D1 ch 1 orobenzene
20
p-Di Chlorobenzene
14
Flow
Low High
Mean
S
Mean
S
Mean
S
Mean
S
Mean
S
Mean
S
Mean
S
1.40
0.032
1.874
0.036
0.033
0.022
0.029
0.100
0.037
0.032
0.592
0.183
0.77
0.032
1.874
0.032
0.020
0.024
0.025
0.140
0.031
0.033
0.292
0.086
D1ff
0.63
0.000
0.005
0.004
0.0025
0.040
0.006
0.300
X 01 ff t- value
81.8 6.43
0.0 0.00
13.1
10.3
28.6
19.4
102.7
* values through December 1988
                         9-   46

-------
 Table 3.4


Organization: College of Staten  Island                 Sorbent:  Tenax


                                 er of   July  to     Septeeiier ,  1987

                                        DISTRIBUTED UOLUMES
compound na*e
1,1 Dichloroethane-
1,1,1 Triehlot-oethane
1,2 Dichloroethane
1,1,2 Trichloroethane
Benzene
Broeofore,
Chiorofore
Ch 1 orobenzen
Carbon Tetrachloride
Ethyl Benzene
Hexane
Methylene Chloride
M Dichlorobenzene
mSp Xylene
o Dichlorobenzene
o Xyl
p Dichl
Styrene
Toluene
Tetraehloroethene
Trichloroe thene
* Pairs
run
ane B9
91
ane
86
78
79
de 91
91
Rverage
Low
Flow
O.467
O.O65
1.381
O.O31
O.O32
0.117
0.907
Overage
MDL
Studj
O.O41
O.O2O
0.130
O.O21
0.1320
O.O4O
o. too
___
Diff.
Cppb)
0.170
O.O12
0.414
O.O12
0.010
0.045
0.310
Std. Err. 95X CL
Bvg. Dif. interval
Cppb) 
O.O25
O.OO7
*
O.O46
0.002
O.OO2
O.OO6
O.O37
< 0.121
< -0.001
€ 0.323
< O.OOB
C 0.007
< 0.033
€ 0.237
- 0.219
- O.O26
- 0.505
- O.O16
- O.014
- O.057
- O.383
)
>
>
>
>
>
>
T-Test T > O.OS

6.839
1.813
9.020
6.003
5.255
7.397
8.415
Y
N
Y
Y
Y
Y
Y
             K =  = 1X2 MDLCUM FLOH>

-------
     Table 3.5
    Organization: College of Stater* Island
     Sorbent: T
                                Quarter- of Octcfcer
to
December  » 1987
                                            DISTRIBUTED VOLUMES
00
compound nannr *
re
1 , 1 D i chl or oe thane
1,1.1 Trichloroethane
1,2 D i chl or oe thane
1,1,2 Trichloroethane
Benzene
BroAoforat
Chl or of ore.
Chlorobenzene
Carbon Tetrachloride
Ethyl Benzene
Hexane
rtethylene Chloride
M Oichlorobenzene
eyp Xylene
o Oichlorobenzene
o Xylene
p Oichlorobenzene
Styrene
Toluene
T J * • • a_

Tr ichloroethene
Pairs
m

243
244

244

244
249
244

244
244



243


245
g»*W"
«£-^n
245
flverage F
Low t
Flow £

O.456
O.O55

1.848

O.055
O.013 M
O. 131

1.122
O.759**



O.567


5. ISO
rt ^oo
"• ^*t*>
O.O72
tverjtge
OL
;tudi|

0.041
O.H2O

0.1. 3O

O.U21
O.CI2O
O.O4O

0.1.00
I.AOO



0.1.39


O.'tOO
ft tf tfTlfc
U« IK^U
O.CI25
flverage
Oiff.


0.07B
-O.OO3

-0.023

O.001
0.004
O.022

-O.O37
O.4O6



-O.O16


-O.OO5
_f^ n« tf
^^»« U15
-O.OOB
Std. Err
Rvg. Oil


O.OO8
O.OO2

O.O22

O.OO1
.000
O.OO2

O.O17
O.O21



O.OO5


O.05B

.OO9
O.OO2
95%
". inte


- 0.093 >
- O.OO2 >

- 0.020 >

- 0.004 >
- O.OO4 >
- O.O25 >

	 0.003 >
- 0.448 >



	 0.006 >


-0.108 >

— O.OO2 >
	 O.OO5 >
T-Te*t 1
<

1O.241
1.16O

1.O35

O.949
12.946
12.150

2.12O
18.936



3.O94


0.094

. 6BB
5.198
r > o.os
CY/N>

Y
N

N

N
Y
Y

Y
Y



Y


N


Y
                 M »  = 1X2 HDLCLOM FLOM)

-------
10*
    Table 3.6
    Organization: College of Staten Island
                                      Sorbent:  T
                               Quarter  of January   to     March   , 1988

                                            DISTRIBUTED VOLUMES
compound name «
Pairs
run
1..1 Dichloroe thane
1*1.1 Trichloroethane
I.;2 Dichloroethane
M.2 Trichloroethane
Qfenxene

BroMoFore.
Cftlorofore.
Ck lorobenzene
Carbon Tetrachloride
FJhyl Benzene
MtMane
Mithylene Chloride
orfp Xylene
o Dichlorobertzene
o Xylene
p Oich lorobenzene
Sfcjrene
Taluene
Ti tr ach 1 or oethene
Y " j • 4-**

112
184
184

185

183
185
184
183
180
181
1O1

184

183
184
165
184

Lou 1
Average
«L
Flow Study
O.O1O *
O.493
O.O26

1.843

O.O4S
0.014 M
0.112
1.23O
1.OB4
0.700**
1.995

O.42O

O. 1O9
4.917
O.419
O.O76
O.O2O
O.O41
O.O2O

O. 13O

O.O21
O.O2O
O.O4O
0.223
0.100
1 - 1 00
O.417

0.139

O.O31
O.40O
O.O50
O.O25
DiFF.
Cppb)
O.OO4
O.O94
-0.009

O.O64

-O.OO2
0.003
O.O16
0.104
-O.OO5
0.308
0.045

O.O27

-0.001
0.164
-0.004
-o.ooa
Std. Err. 9S3£ CL
Rvg. DiF. interval
Cppb>
.OOO
O.OO8
O.OO1

O.O28

O.OO1
.OOO
O.OO2
0.017
O.022
0.024
0.040

O.OO7

0.002
0.059
0.007
O.OO1
T-Test
T > O.O5
 CY/tO
€ O.004
< O.078
< -O.O1O

< O.OO9

< -O.004
< 0.003
< 0.012
< O.O71
< -0.047
< O.26O
C -O.O34

< O.014

< -O.O05
< O.O49
< -0.018
< -43.O1O
- O.O05 >
- 0. 1O9 >
	 O.O07 >

- O. 119 >

- .OOO >
- O.OO4 >
- O.020 >
- O. 137 >
— O.O3B >
- 0.355 >
- 0.124 >

- O.040 >

- O.OO2 >
- O.278 >
- 0.009 >
	 0.006 >
18.741
11.786
9.134

2.292

1.697
10.056
8.691
6.144
0.212
12.701
1.137

4.O95

0.771
2.793
0.636
7.009
Y
Y
Y

Y

N
Y
Y
Y
N
Y
N

Y

N
Y
N
Y
    MUXHIGH FLOM>

-------
 Table 3.7
Organization: College of Stated  Island
                                       Sorbent: Tenax
                            Quarter- of    Rpi-il     to     June   ,  1988

                                        DISTRIBUTED VOLUMES
compound name *
Pairs
run
1,1 O i chl or oe thane
1,1,1 Trichloroethane
1,2 Dichloroethane
1,1,2 Trichloroethane
*0 Benzene
Broaofor*
m Chlorofora
° Oilorobenzene
Carbon Tetrachloride
Ethyl Benzene
Hexane
Methyl ene Chloride
•/p Xylene
o Xyleoe
Styrene
Toluene


251
250
251

243
251
221
248
216
248
251
216
218
218
224
226
245
Rverage F
Lou t

O.OO5 0.083 -O.OOl O.O20 O.OO6 O.OO2 O.O22 O.OOl O.O7O 0.163 O.O44 -O.O20 -O.OO5 O.O61 -O-O32 O.OO3 Std. Err. Rvg. Dif. .OOO o.ooa O.OOl O.O22 O.OOl .000 O.OO2 O.OO8 O.O13 O.O16 0.026 O.O15 O.OOl O.O31 o.ooa O.OO2 953C CL interval T-Te*t T > O. O5 C c c c c c c c c c c c O.OOS O.O68 -0.003 -0.023 O.004 0.001 o.oia -0.015 O.O44 0.131 -0.007 -O.O49 -0.007 -O.OOl -O.O48 -O.OOl - o.oos : - O.O98 J - O.OOl 3 - O.O63 : - O.O07 3 - 0.003 : - O.O26 : - O.O17 3 - O.O96 3 - O. 196 3 - O.O94 : - 0.009 : O.OO2 3 - O. 123 : O.O16 3 - O.OO7 3 » 347.OO8 > 10.826 > O.9O7 > O.9O5 > 6.821 > 6.3O1 > 1O.7O3 > 0.152 > 5.255 > 9.961 > 1.682 » 1.366 > 4.097 > 1.942 > 3.870 » 1.293 Y Y N N Y Y Y N Y Y N N Y N Y N HDL(HIGH FLOM> =

-------
      Table 3.8
     Organization:  College of Staten Island
                                      Sorbent: T
                                  Quarter- of  July    to    Septeeber .  1988

                                              DISTRIBUTED VOLUMES
     compound na«e
            fiver-age  Average  Rverage  Std. Er-§-.
    » Pairs Low       MDL      DiFF.    Rvg. DiF.
    run     Flow      Studj        
 95X CL
interval

                                                                                              T-Test  T > O.O5
                                                                                                      
- O. 179 >
- o.ooa >

- O.241 >
- 0.005 >
- 0.020 >
- O.OO4 >
- 0.027 >
- O.O59 >
- 0.24O >
- 0. 124 >

- 0.262 >

- 0.031 >

- 0.004 >
- O.432 >
- -O.O22 >
- O.O2O >
O.OOO
8.879
3.883

5.060
0.000
1O.727
11.980
9.853
2.681
14.303
12.502

4.806

2.611

O. 142
7.708
4.631
10.349
N
Y
Y

Y
N
Y
Y
Y
Y
Y
Y

Y

Y

N
Y
Y
Y
     HDLCHIGH FLOH> =
    MDL
1X2 HDLCLOM FUDU>

-------
    Table 3.9
    Orc|anization: College of Staten Island
                                       Sot-bent: Tenax
                                 Quarter of Octot»»r   to    December  » 1988

                                              DISTRIBUTED VOLUMES
    coifipound name
        Rverage
« Pairs Lou
        Flow
                          run
Rverago
HDL
Study
Rverage
Oiff .

Std. Err.
Hvg. Dif.

                                                         95X CL
                                                        interval
                                                          O.O5
         
    1.
 I
JJ   Chloroform
    Chi orobenzene
    C«M^
    Ell-.
    He>-_
    Met-hyle
    m Dichl
    «/P Xyl
    o Dichloi
    o Xjylene
    p Oitchloi
    Styprene
    Toluene
oethane 227
i lor oethane 22O
oethane 228
i lor oethane 231
228
21O
228
ne 21O
achloride 228
ne 21O
228
Ihloride 228
tenzene 2O9
210
lenzene 21O
210
ienzene 2O9
209
228
Athene 228
lien* 227
O.O11
0.491
0.022
O.O2O
1.7O9
O.O1O
O.O39
O.O11
0.127
0.653
O.969
0.327
0.011
2.357
0.012
0.479
0.236
O.1O3
3.855
0.352
O.O74
M 0.0213
O.O41
O.O2I3
M 0. 0413
0.1313
M O.O2I3
O.O21
M 0.0213
0.04(3
0.223
O. 1OO
M O.611
M O.O2I3
O.417
M O.O2I3
O. 13-3
M O.403
0.031
0.403
O.O5I3
O.O2I5
O.OOS
O. 117
-O.O04
O.O1O
-O.O94
O.OO4
O.OO6
O.OO4
O.O27
O.O44
O.O25
0.166
O.OOS
O. 198
O.OOS
0.034
O. 114
O.OO1
O.358
-O.O1O
-O.OOS
.OOO
O.O11
O.O01
.OOO
O.021
.000
O.001
.000
0.002
O.009
O.O11
O.O16
.000
O.O24
.OOO
0.005
0.008
a.aO2
O.O3O
O.OO6
O.O01
< O. OO4 -
< O.O96 -
< -O.OOS -
< O.O1O -
< -O. 135 -
< O.OO4 -
< 0.004 -
< O.OO4 -
C O.O24 -
< O.O27 -
< 0.004 -
< O. 135 -
< O.OOS -
< 0. 151 -
< O.OO4 -
< O.023 -
< O.099 -
< -0.003 -
< O.3OO -
C -0.021 -
C -0.005 -
O.OOS >
0.138 >
-O.OO2 >
O.O1O >
-O.OS2 )
0.005 >
0.009 >
O.OOS >
O.O30 >
0.061 >
O.047 >
0.196 >
O.O06 >
O.244 >
0.005 >
0.044 >
O.129 >
O.006 >
0.416 >
0.001 >
-0.001 >
34.515
10.989
5.8O8
226S.86O
4.444
34.38O
5.4O3
17.060
16.062
5.06O
2.306
10.603
14.118
8.340
16.272
6.448
14.688
O.523
12.028
1.723
2.84O
Y
Y
Y
Y
Y
Y
Y
Y
Y
Y
Y
Y
Y
Y
Y
Y
Y
N
Y
N
Y
                 M  B
    MOLCHIGH FLOW)
•*= MDL
1X2 HOLCLOH FLOW)

-------
 Table  3.10
Organization: College  oF Staten Island
                                     Sorbenfc:  Tenax
                            Quarter- of  January   to     March   , 1989

                                        DISTRIBUTED VOLUMES
compound name It
ru
1,1 Dichloroethane
1,1,1 TricKloroethane
1,2 Dichloroethane
1 1,1,2 Trichloroe thane
Benzene
{* BroMFot-M
ChloroFor*
Ch 1 or obenzerte
Carbon Tetrachloride
EUvjl Benzene
Hexane
HetHylene Chloride
m DicHlorotoenzene
«n/p Xtjlono
o Dichlorobenzene
o Xylene
n ~ L i i-h
SlyrerJ^
Toluene
Tfrtrachloroethene
Tr ich t or oe t hene
Pairs
n
228
228
228
228
225
225
227
222
225
219
228
228
219
219
217
217
217
217
225
223
226
HVerage 1
Low 1
Flow «
O.O1O M
0.490
0.027
Q.O2O M
1.S98
O.O1O *
0.039
0.012 »«
0.178
O. 587
O.78O
O.326 M
O.O1O H
2.O28
O.O11 M
O.4S1
O213 M
O.O91
3.004
O.416
0.077
Iverck^e
10L
>tuckj
O.O2O
O.O41
o.a?o
O.O4O
o. 1:30
O.O2O
O.O21
O.O20
O.O40
O.223
0.100
O.&ll
O.O.JO
0.417
0.0.20
O.i:39
O^nri
0.0:11
O.4OO
O. OSO
O.O25
Overage
OiFF.

0.004
O.OSO
-O.OO9
O.O1O
-0.259
O.OOS
.OOO
O.OO3
O.O2O
-O.OO4
-O.O43
O. 158
O.OOS
0.021
O.OO4
-o.ooa
01 01
-0.003
O.071
-O.OO9
-O.OQS
Std. Err
Rvg. Dif
tppb>
.000
O.OO7
0.00 1
.OOO
O.O21

O.OO1
.OOO
0.002
O.OOS
O.O1O
O.OOS

o.oia
.000
O.OOS
OFVI4
0.001
O.O33
O.OO6
O.OOl
ssx a.
irrterv<
Cppb>
t 0.004 -
< 0. 067 -
C -O.O11 -
< 0.010 -
< -0.301 -
C nil at
C -O.OQ2 -
< O.OO3 -
C O.O15 -
< -O.O15 -
< -O.O63 -
< 0.141 -
< nil *t
< -0.013 -
< 0. 003 -
< -O.O18 -
t o n
0.094 >
-O.OO7 >
O.O1O >
-0.217 >
NDL >
O.OO2 >
O.OO4 >
0.025 >
O.O06 >
-O.O23 >
0.175 >
HDL J
O.056 J
O.OOS >
O.OO2 >
O1OQ >
.OOO >
0.136 >
O.OO4 >
-0.003 >
T-Test 1
<
23.132
11.489
9.339
227. OOO
12. 140

0.384
9.4O7
8.322
0.800
4.269
17.991

1.2O5
10.526
1.595
28 332
2.322
2.14O
1.397
5.242
r > o.os
;YXN>
Y
Y
Y
Y
Y

N
Y
Y
N
Y
Y

M
Y
N
y
Y
Y
N
Y
HDLCH16H FLOM> =
<= MOL
1X2 MOL
-------
 Table 3.11
OrganizationI College of  Staten
Sorbent: Tenax
                            Quartet- of  flpril    to      June   , 1989

                                         DISTRIBUTED VOLUMES



Pairs
run





«0
1















1,1 O i chl or oe thane
1,1,1 Triehloroethane
1,2 O i chl or oe thane
1,1.2 Triehloroethane
Benzene
BroMoFore,
Ch 1 or of ore.

Carbon Tetrachloride
Ethyl Benzene
Hexane
Hethylene Chloride
• Dichlorobenzene
aVp Xylene
o Oichlorobenzene
o Xylene


Sturene
Toluene
Te tr ach 1 oroe thene
Triehloroethene
14
14
14
14
13
14
14
m
14
14
14
14
14
14
14
14
14
14
14
14
14
Average Average
Low MDL
Flow Study
O.O15 M
O.445
O.012 M
0. 020 M
0.725
O.O1O M
O.O43
O O15 x
0.123
O.295
O.519
O.2OO **
O.O1O M
1.O1O
O.O11 M
O. 230
O.219 M
O. 037
2.330
0.267
O. 037
O.O2O
O.O41
O.O2O
O.O4O
O. 13O
O.O2O
O.O21
O.O2O
O.O4O
0.223
O. 1OO
0.611
O.O2O
0.417
O.O2O
O. 139
0.4OO
O.O31
O.400
0.05O
O.025
Average
Diff.
Cppb>
O.O06
O.O93
O.OO2
O.O1O
O.O06
O.OOS
O.O14
O OO6
O.O35
O.O04
O.O22
O. 100
O.OOS
-O.O57
O.OO6
-O.O14
o. loa
-O.O03
0.039
-O.O24
.OOO
Std. Err.
Hvg. Oif.

0.001
O.O28
O.OO1
.OOO
O.O72
0.000
O.OO4
O OO1
O.OO4
O.O23
O.O53
O.OOO
O.OOO
O.O74
.OOO
O.O16
0.007
O.OO4
O. 1O9
O.O18
O.OO2
9SX CL
interval

C
C
<
<
<
C
<
{
C
<
(
<
<
<
C
<
C
C
<
C
<
O.OO3
O.O33
.OOO
O.OO9
-0.150
O.OOS
0.006
O OO3
O.O26
-O.O45
-O.O92
O. 1OO
O.OOS
-0.216
O.OOS
-O.O48
O.O93
-0.012
-0.197
-O.O62
-O.004
- O.OO9 >
- O. 153 >
- O.OO3 >
- O.O1O >
- 0. 162 >
- O.OOS >
- O.O22 >
— O OO9 >
- O.045 >
- O.053 >
- 0. 136 >
- 0. 1OO >
- O.OOS >
- O. 1O2 >
- O.OO7 >
- O.O20 >
- 0.123 >
- O.OOS >
- O.275 >
- O.O15 >
- O.OO4 >
T-Te»t T > O.OS

4.277
3.350
2.350
31.534
O.O82
O.OOO
3.787
3 oca
8.097
O. 158
O. 422
0.000
O.OOO
O.768
12.071
0.885
15.474
O.898
0.357
1.3O8
0.055
Y
Y
Y
Y
N
N
Y

Y
N
W
N
N
N
Y
N
Y
N
N
N
N
              M = 
-------
     Table 3.12
    Organization:  Colltrg* of Statvn Island
                                      Sot-bent: T«nax
                                 Quarter of  July     to    September , 1989

                                             DISTRIBUTED VOLUMES
                                  Rverage
    compound
    • Pain
    run
                                  Fit
Rvwage
MOL
Study
Std. En-.
Rvg. Dif.
Cpnb>
 95X d_
int«rval

T-T»st  T > O.O5
        €AI^0

Hethylene Chloride

•ft/p Xylene


o Di chlorobenzene
a Xylene
p Oichlorob*
Styrene
Toluene
Tetrachloroe
Trichloroeth

'ffUDtfflV


thene
(•nv
39
39
39
39
32
39
41
39
39
39
35
39
39
^9^
39
39
39
39
39
39
4O
39
O.011 M
0.254
O.O18 M
O.O2O *•
O.844
O.OIO M
O.O13 M
O.O11 M
O.O3O M
0.337
O.782
O.2OO M
OO1O M
• ^JaVU ^*
1.175
O.OIO M
O.227
0.200 M
O.O96
2.835
O.378
O.O23 M
O.O20
O.O41
O.02O
O.D40
O. 13O
O.O2O
O.O21
O.O2O
O.O4O
O.223
O. 1OO
O.iSll
O tT^fl
O.417
O.Q2O
O. 139
0.400
O.Q31
O.40O
O.O5O
O.IJ25
0.002
0.083
O.OO7
O.OIO
O. 148
O.OO5
O.O06
O.OO4
O.O12
0.031
O. 188
0. 10O
OntTS
. l^W*J
0.085
O.OO5
-O.012
O.O99
O.O07
-O.O26
O.OIO
-O.OO1
O.OO2
0.011
O.OO1
O.OOO
0.029
.OOO
O.001
.OOO
O.OO1
0.013
O.O35
.OOO
rwi
. IMMJ
0.043
.000
O.O14
0.001
O.OO3
0.086
O.O28
O.OO3
<
<
<
<
<
<
<
<
<
<
(
<
'f
%
<
€
<
<
C
c
<
<
-O.OO1
O.O6O
O.OO5
O.OIO
O.O89
O.OO5
O.OO4
O.OO3
O.OO9
O.OO4
O. 118
0.100
OOO5
• ^FU^f
-O.OO2
O.OO5
-O.O4O
O.O97
O.OO2
-O.2OQ
-0.046
-0.007
- O.OO6 >
- O. 105 >
- 0.008 >
- O.OIO >
- 0.206 >
- O.OO5 >
- O.007 >
- 0.005 >
- O.O14 >
- o.osa >
- O.258 >
- O. 100 >
— O DOS >
^fm *^P*%* f
- 0.172 >
I
- o.oos! >
- O.016 >
- O. 101 >
- O.O12 >
- 0.147 >
- 0.067 >
- O.OO5 >
1.3O7
7.55O
1O.4O5
0.000
s.oao
122.024
8.392
14.21O
. 8.429
2.350
5.443
.OOO
nan
* MMJ
1.978
1O1.O25
0.854
88.625
2.612
O.307
0.373
O.357
M
Y
Y
JK
Y
Y
Y
Y
Y
Y
Y
N

N
Y
N
Y
Y
N
N
N
    MDL

-------
 Table 4.1
Organization: College of Stater*  Island
                                                    Sorbent: Tervax
Ol
A
         Regression summary For January 1998 to September 1989

                           TENHX vs. CHNISTER
Compound
                             Regress—       t-Test  SigniFi-
                         dF  ion coe— Slope   on
                             FFicient       slope   cance
                                                                Regress-       t-Test  SigniFi-
                                                            dF  ion coe- Slope   on
                                                                FFicient       slope   cance
Metnylene chloride   49
ChloroForot            O
111-Trichloroethane  41
Carbon Tetrachloride  3
Benzene              63
Triehloroethene       2
Tetrachloroethene    24
Ethylbenzene         39
m/p Xylenes          59
o Xylene             46
He'xane               43
Toluene              64
I O.O11
O.3O8
1 O.O73
1 0.529
! 0.266
I 0.9O9
1 O.242
1 0.281
. O.613
\ 0.109
\ 0.363
O. 005
O.341
O.677
1.O8O
2. 13O
1.134
1.O90
O.66O
O.68O
O.OO8
O.578
O.714
4.272
O.486
8.425
O.851
15.501
3.531
4.8OO
8.527
2.292
6.O48
P -
P "
P :
P "
P :
P <
P "
P "
P "
P "
P "
» 0.2
C O.O01
» O.5
£ O.OO1
» 0.5
C O.OO1
C O.OO2
C O.OO1
C 0.001
C O.O5O
C 0.001

4O


1

37
58

34
63

0. 570 I


O.994

O.436
O.681

0.516
O.588 i
                                                                   O.570 O.570  7.280  p < O.OO1
                                                                   O.994 3.008 12.873  p < O.OO1

                                                                   O.436 1.236  5.347  p < O.OO1
                                                                   O.681 1.387 11.138  p < O.OO1

                                                                   O.516 1.118  6.O15  p < O.OO1
                                                                   O.588 0.939  9.SO1  p < O.OO1

-------
 Table 4.2




Organization: Col leg* of Staten Island                 Sorbent: Tenax


                              of January 19138 to September 1989

                                   TENRX VS.. CRNISTER


1
m
vj


fT O^fKM ITHJ r%Aflk9

Methylene chloride
Ch 1 or of or •
1 1 1-trichloroethane
Carbon Tetrachloride
Benzene
Te trach 1 or oetnene
•Xp Xylenes
o Xylene
Toluene
« Pairs
run
51
5
43
5
65
26
41
61
48
45
66
fiver age

1.251
O.381
0.347
-O.O14
O.O42
O O67
-O.O52
-O.204
-O.366
O.23O
8 747
-0.335
Difference

552.4
3814. O
152.3
1OI.4
36.1
77O 8
10.1
0.5
-1.7
115.6
10,32 2
O.3
Std. Err.
Rvg. Oif.
Cppb>
O.47O C
O.O39 <
0.065 <
O. 1OO C
O.O75 <
Onqt f
0.048 C
O.O69 <
O. 121 <
O.O25 <
3 75O <
O.221 <
9SX CL
interval

0.301 -
O.274 -
O.216 -
-O.292 -
-0.108 -
-0.151 -
-O.345 -
-0.607 -
O.178 -
1 169 —
-0.776 -


2.201 >
O.488 >
O.479 >
0.263 >
O. 192 >
Ooco \
0.046 >
-O.O64 >
-0.125 >
O.281 >
16.326 >
0.107 >
t Test

2.662
9.896
5.35O
O. 144
0.555
Oyafe
1.O92
2.950
3.034
9.O29
2.333
1.517
                                                                                                      > o.o
                                                                                                      

                                                                                                        Y
                                                                                                        Y
                                                                                                        Y
                                                                                                        N
                                                                                                        N
                                                                                                        N
                                                                                                        N
                                                                                                        Y
                                                                                                        Y

                                                                                                        Y
                                                                                                        N

-------
Table 4.3
       New York State DOH ELAP Proficiency Test Results for CSI-CES
                     (reported value/mean for compound)

1 , 2-Dichlorobenzene
1 , 3-Dichlorobenzene
1 i 4-Dichlorobenzene
1 i 1-Dichloroethane
1 , 2-Dichloroethane
Benzene
Bromoforn
Carbon Tetrachloride
Chlorobenzene
Chloroform
Ethyl benzene
Hethylene Chloride
•/p-Xylene
Tetrachloroethene
Toluene
Trichloroethene
Cone. Jan 88 Jul 88
low
high
low
high
low
high
low 1.325 * 0.987
high 1.169 1.004
low 1.025 1.381
high 0.809 1.034
low
high
low
high
low
high
low 1.018 1.012
high 0.975 0.919
low
high
low 1.243 1.062
high 1.094 1.032
low
high
low 1.155 1.124
high 1.018 1.079
low 1.227 1.120
high 1.059 1.063
low
high
low
high
Jan 89 Jul 89 Jan 90
1.161
1.057
1.136 1.153
0.996 0.981
1.278 * 1.150
1.071 0.992


1.041
1.038
1.258 1.145
1.028 1.024
1.098
1.182

1.023
1.033
1.102
1.097
0.885
1.048
1.285 * 1.170
1.164 0.992

1.336 ** 1.160 1.153
1.162 0.972 1.067
1.337 * 1.374 *
1.145 1.269 *
  between 2 and 3 S from mean     ** beyond 3 S


                                9-   58

-------
  Table 4.4









Organization: College of Stafc*n Island                  So«-b«nt: Twvax







                      Quarter oF January   to  March  „  1988




                                   TENRX US.  CRNISTER
compound naa*
Hvthylen* chlorid*
Ch loroforaj
0 1 1 l-tr ichloroatnan*
Carbon T»trachlorid*
UiBwnz*n*
*° Tr ichloro»th*rMr
Te trachl oro»th*n»
Et hy 1 bwnz«o»
mSp Xylvnex
o Xyl*n»
ttoxanv
Toluvn*
Rv*rag» D
» Pair*
run
6
O
4
O
9
O
1
2
8
4
8
9

4.275

0.055

-0.26O

0.040
-0.535
O.325
O.49O
48.690
-1.133
* £f^m-**m-.^

1124.7

25.5

-15.1

6.5
215.7
53.1
267.9
5563.3
-28.1
Std. Err.
Avg. Oif.

3.88

O. 10

0.13


1.64
O.67
0.14
14.82
0.33
C

C

C


C
<
€
C
C
95% CL
interval

-5.688

-0.254

-0.561


-21.3O9
-1.262
0.044
13.644
-1.898
- 14.238 >

- O.364 >

- O.O41 >


- 20. 239 >
- 1.911 >
- O.936 >
- 83.737 >
	 O.367 >
t T**t T > O.O

1.1O3

0.566

1.995


0.327
0.484
3.499.
3.286 .
3.412
N

N

N


N
N
Y
Y
Y

-------
    Table 4.5
   Organization: Colleg* of  Staten  Island
                                                        Sorbent: Tenax
                        Quarter of April      to June       ,  1968

                                      TENflX US. CRNISTEP
o»
o
   Compound name
Httnylene chloride
Chlorofor«
111 - tt- i oh 1 oroethane
Carbon Tetraehloride
Benzene
Trichloroethene
Tetr ach 1 oroethene
Ethyl benzene
m/p Xyl
o Xyl
Hex
Tol
» Pair*
run
1O
O
>e 6
de 2
12
O
4
3
11
7
6
12
Rverage Difference

1.12O

O.388
O. 143
0.356

-O.O38
-O.268
-O.159
0.227
O.729
-O.214
<*>
554.6

217.1
276.9
94.8

-0.8
-39.1
3.4
173.5
188.5
15.O
Std. Err. 9SX CL
Rvg. Oif . interval t Test

O.474

0.159
0.027
O.268

O.O58
0.025
O. 148
O.Q75
0.757
O.643
 2.363

- O.797
- O.486
- O.945

- O. 145
	 0.160
- O.I TO
- 0.411
- 2.676
2.438
5.296
1.328

0.663
1O.658
1.078
3.O22
O.962
- 1.2O2 > O.332
                                                                                                    T > O.O5
                                                                                                      
N
Y
N

N
Y
N
Y
N
N

-------
 Table  4.6
Organization: Collvg*  of Stafcen Island
Sor-bwnt:
                     Quarter- of July      to SvptMbcr .1988




                                   TENRX US.  CANISTER
vo
1
Ot







Compound na*,»
Hethylcn* chlorid*
ChloroforM
1 1 1-tr ichlorowfchan*
Carbon T»tf-achlorid»
BenzBn*
Trichlorovthen*
Tetrachloro*th«n»
EthylbOTizOTMr
fl»/p Xyl«m«E
HexarM»
Toluerw


* Pairs
run
10
O
8
1
13
1
8
11
12
12
6
13

O.794
0.231
O.122
O.219
-O.O41
-O.230
-O.392
-1.192
O. 195
-O.010
-1.242
rTtfv~0ncv
<*>
516.2
151. 7
42.1
6O.O
-11.7
-31.0
-44.9
-43.5
46.8
11.4
—26. 3
Std. Err. 95X CL
flvg- Dif. interval
 (ppb>
O. 140
0.071
O. 148

O.037
O.O51
O. 116
O.O37
0.123
O. 146
< O.477
< O.062
< -O. 1O4

< -O.318
< -O.506
< -1.447
< 0.114
< -O.327
< -1.561
- 1.111 >
- 0.400 >
- O.S42 >

	 0.142 >
	 0.279 >
	 0.937 >
- 0.276 >
- 0.306 >
	 0.924 >
t T»st
5.671
3.236
1.479

6.193
7.714
1O.274
5.290
O.083
8.498
T > O.O5

-------
    Table 4.7
   Organization: Colleger  oF Staten Island
                                                        Sorbent: Tenax
                         Quarter of October-   to December  ,1968

                                      TENRX VS. CRNISTER
to
I
Ok
K>
   Compound na«e
Methtjlene chloride
Chlorofora
1 1 1-tr ichloroethane
Carbon Te trichloride
Benzene
Trichloroethene
Tetrachloroethene
Ethylberueene
m/p Xyl
o Xyl
   Tol
Rverage Di
* Pairs
run
« 6
O
ne 3
ide O
1O
O
7
6
1O
6
6
10

O.415

0.190

-O.291

-0.059
-O. 242
-0.473
0.225
-O.26O
-O.244
Fference-

254.6

33.7

-14.O

2.5
-25. O
-18.3
102.1
-22.2
-9.9
Std. Err. 9SX CL
Hvg. Oif. interval

< O. 189

< -O.27O

< -0.517

C -0.288
< -O.465
< -O.8O4
< 0.099
< -O.539
< -0.581

- 0.641 >

- O.650 >

	 0.065 >

- 0.171 >
	 O.O19 >
	 0.142 >
- 0.351 >
- O.O19 >
- O.O93 >
t Text T > O.OS

4.716

1.777

2.913

0.625
2.786
3.235
4.582
2.395
1.637

Y

N

Y

N
Y
Y
Y
N
N

-------
   Table 4.B




   Organization:  Col leg* of Stat*n Island                  Sorbent: T*nax


                        Quarter of January   to  March     , 1989
                                     Rverag* Difference      Std. Err.      95X CL
   Compound na*e         « Pairs   	Bvg. Dif.     interval          t Test    T > O.O!
                            run                      (ppb)                                  
   Methylene chloride        9        O.591       191.4       O.254   C   O.OO5  -  1.177 >   2.327        V
   Chloroform                 O
 I  lU-trichloroethane      11        8.367        62.8       O.O84   <   0.179  -  8.555 >   4.352        Y
   Carbon Tetrachloride      2       -8.24O       -44.4       8.128   C  -1.765  -  1.285 >   2.O88        N
Q  Benzene                   11       -8.293        -9.8       8.128   <  -8.578	8.887 >   2.286        V
   Trichloroethene           2        8.885        47.S       8.115   <  -1.456  -  1.466 >   8.843        N
   T*trachloro»then*         2        8.835        13.4       8.865   <  -O.791  -  0.861 >   O.538        N
   Eihylb«nz»n*              8       -8.172       -23.6       8.886   <  -8.377  -  O.O32 >   2.080        N
   «/p Xylvn^s               9       -8.621       -21.5       8.269   <  -1.242  -   .OO8 >   2.387        V
   o Xylwn*                  9        8.129        26.6       8.853   C   8.8DB  -  8.258 >   2.451        V
   BVxan*                     9        8.838         7.8       8.877   <  -8.148  -  8.216 >   8.493        N
   Toluen*                   1O       -8.487        -1.8       8.386   <  -1.288  -  8.466 >   1.854        N

-------
 Table 4.9
Organization: Collvg* of Statcn I*land
Quarter of Rpr-il     to  Jun*




             TENRX VS. CANISTER
                                    Sortwnt:  T
                                                         .1989
compound naa*
Methylen* chlorid*
Ch 1 or ofor •
1 1 11— trichloroetharxr
Carbon T*trachlor-id*
1 r i en 1 or*O9 tFivn^
T*t«-achloro»tn*rw
Ethylbenzenv
mtSp Xyl*n*x
o Xylvn*
H*xan»
Toluan*
• Pairs
run
4
O
4
O
4
O
O
4
4
3
3
4

O.775

O.O96
0.270

-O.OO8
-O.158
O.11O
-O. 167
-0.181



516.7

33.0
45.1

-3.2
-13.5
44.0
9.5
-8.5
Std. Err. 95X CL
. Hvg. Dif. interval
 (ppb>
O.4O5

0.027
O.O37

O.O2O
0.012
O.O29
O.239
0.159
C -0.514

< 0.010
< O.1S3

C -O.O71
< -0. 196
C -0.015
< -1.196
< -O.686
- 2.064 >

- 0.182 >
- O.387 >

- O.O54 >
	 O.121 >
- O.23S >
- 0.862 >
- 0.324 >
t T*st
1.914

3.555
7.348

O.419
13.448
3.793
0.697
1.141
T > 0.0

N

Y
Y

N
Y
Y
N
N

-------
 Table 4.10
Organization: Coll«g» of Statmi Island
Sorbmnt: T*nax
                     Quarter- of July      to  September  .1969

                                  TENRX VS. CANISTER
1
ot
en






Compound rvaa*
Hvtnylvn* chloride
Ch 1 oroForM
lll-trichloroethan*
C*rbon Tetrachloride
B*nz™.
• r i en 1 oroethene
T* traeh 1 or o*th*ne
Ethyl benzene
«/p Xylenes
o Xylene
Htxane
Toluene
* Pairs
run
6
5
7
O
5
1
4
7
7
7
7
7
Rv-rag. Oif F-rene.

1.350
O.361
0.793
O.436
0.30O
0.233
O. 129
O.299
0.328
0.217
1.976
<30
9OO.O
3614.0
429.4
1O1.6
3000.0
115.6
81.9
62.6
245.2
111.1
61.1
Std. Err. 95X CL
flvg. Dif. interval
 Cppb>
0.771
O.039
£.285
O.lll
O.182
O.O39
O.081
O.O32
0.100
1.317
< -0.632 -
< O.274 -
< O.O95 -
< O. 126 -
< -0.345 -
< O.O32 —
< O. 1OO -
< O.249 -
< -0.027 -
< -1.246 -
3.332 >
0.488 >
1.491 >
O.744 >
0.811 >
0.225 >
O.497 >
0.408 >
0.461 >
5.199, >
t T*st T :
1.751
9.896
2.78O
3.926
1.284
3.268
3.685
10. 106
2.172
1.500
                                                                                                        N
                                                                                                        Y
                                                                                                        Y
                                                                                                        N
                                                                                                        Y
                                                                                                        Y
                                                                                                        Y
                                                                                                        N
                                                                                                        N

-------
Table 4.11
Tenax quarterly mean divided by canister quarterly mean
Compound
1988
1st Q
Hexane
1,1, 1-Trichloroethane
Benzene
Carbon tetrachloride
Trichloroethene
Toluene
Tetrachloroethene
Ethylbenzene
m/p-Xylene
o-Xylene
Mean
0.02
0.90
1.22


1.20
0.94
1.46
0.81
0.46
0.88
2nd Q
0.47
0.39
0.71
0.31

1.08
1.12
1.56
1.15
0.51
0.81
3rd Q
1.01
0.58
0.84
0.70
1.13
1.34
1.39
1.82
1.76
0.70
1.13
4th Q
1
0
1


1
1
1
1
0
1
.34
.78
.22


.08
.07
.49
.29
.66
.12
1st Q
0.96
0.64
1.19
1.87
0.98
1.11
0.95
1.37
1.35
0.81
1.12
1989
2nd Q
1
0
0


1

1
1
0
0
.23
.76
.69


.09

.03
.16
.69
.95
Mean
3rd Q
0.
0.
0.

0.
0.
0.
0.
0.
0.
0.
70
20
60

03
54
78
68
76
38
52
0.09
0.55
0.97
1.05
0.77
1.11
1.07
1.42
1.26
0.63
0.89
                           9-  66

-------
 Table  4.12


Absolute percent difference between mean tenax and canister values


                              19881989
Compound             —_____«___________ _______________     Mean
                     1st Q 2nd Q 3rd Q 4th Q 1st Q 2nd Q 3rd Q

Hexane0.530.010.340.040.230.306724
1,1,1-Trlchloroethane 0.10  0.61  0.42  0.22  0.36  0.24  0.80     0.39
Benzene               0.22  0.29  0.16  0.22  0.19  0.31  0.40     0.26
Carbon tetrachlorlde        0.69  0.30        0.87                 0.62
THchloroethene                   0.13        0.02        0.97     0.37
Toluene               0.20  0.08  0.34  0.08  0.11  0.09  0.46     0.20
Tetrachloroethene     0.06  0.12  0.39  0.07  0.05        0.22     0.15
Ethyl benzene          0.46  0.56  0.82  0.49  0.37  0.03  0.32     0.44
m/p-Xylene            0.19  0.15  0.76  0.29  0.35  0.16  0.24     0.31
0-Xylene              0.54  0.49  0.30  0.34  0.19  0.31  0.62     0.40

Mean                  0.25  0.39  0.36  0.26  0.25  oTTi  0748     oTsT
                          9-  67

-------
Table 5.la
A|eacj:  College of SUten Itltid
Ttble  :  lioiiui Detection Lilit (ppb)
     1DCI
1TCI
2DCB
2T«
1
CT
I/T  IF    IF    IF   IF   LF    IF    LF  IF   LF   IF   IF   IF   LF  IF    LF    IF   LF   IF    LF   IF  IF   IF    I/T
JOIST g.oi o.04 o.o: o.oi
11617 0.04 0.02 0.02 O.OI
SUIT 0.04 0.02 0.02 0.01
OCTIT 0.04 0.02 0.02 0.01
WIT 0.04 0.02 0.02 0.01
DKIT 0.04 0.02 0.02 0.01
JIMS 0.02 0.01 0.04 0.02 0.02 0.01
FIBtl 0.04 0.02 0.02 0.01
I1US 0.02 0.01 0.04 0.02 0.02 0.01
1FUI 0.02 0.01 0.04 0.02 0.02 0.01
liTSI 0.02 0.01 0.04 0.02 0.02 0.01
JHii 0.02 0.01 0.04 0.02 0.02 0.01
JULII 0.04 0.02 0.02 0.01
10611 0.02 0.01 0.04 0.02 0.02 0.01 (
SEPI1 0.04 0.02 0.02 0.01 (
OCTII 0.02 0.01 0.04 0.02 0.02 0.01 0.04 0.02 1
MTU 0.02 0.01 0.04 0.02 0.02 0.01 0.04 0.02 (
DBCIJ 0.02 0.01 0.04 0.02 0.02 0.01 0.04 0.02 (
am 0.02 o.oi 0.04 .02 0.02 o.oi 0.04 0.02 (
FUI9 0.02 0.01 0.04 .02 0.02 0.01 0.04 0.02 (
111!) 0.02 0.01 0.04 .02 0.02 0.01 0.04 0.02 (
1PU) 0.02 0.01 0.04 .02 0.02 0.01 0.04 0.02 (
I1TI1 0.02 0.01 0.04 .02 0.02 0.01 0.04 0.02 (
JOIN
JOIN
10GI) 0.02 0.01 0.04 0.02 0,02 0.01 0.04 0.02 0
SIPB9 0.02 0.01 0.04 0.02 0.02 0.01 0.04 0.02 (
OCTI)
1071) 0.02 0.01 0.04 0.02 0.02 0.01 0.04 0.02 (
DICt) 0.02 0.01 0.04 0.02 0.02 0.01 0.04 0.02 C
JUDO 0.02 0.01 0.04 0.02 0,02 0.01 0.04 0.02 0
FIDO 0.02 0.01 0.04 0.02 0.02 0.01 0.04 0.02 C
I1UO 0.02 0.01 0.04 0.02 0.02 0.01 0.04 0.02 C
I/T IOCS 1TCI 2DCt 2TCK 1
.1)
.13
.11
.11
.11
.1)
.11
.11
.11
.11
.11
.11
.11
.11
1.11
.11
1.11
.11
.11
.01
.01
.Of
.Of
.Of
.Of
.Of
.06
.01
.01-
.Of
.Oi
.0« 0.02 O.OI
.Oi 0.02 0.01
.Oi 0.02 0.01
.01 0.02 0.01
.Oi 0.02 0.01
.Oi 0.02 0.01
.Of 0.02 0.01
.13 O.OI 0.02 0.01
.11 O.Oi 0.02 0.01
.11 O.Oi 0.02 0.01
.11 O.OI 0.02 0.01
.02 0.01
.02 0.01
.02 0.01
.02 (.01
.04 0.02
.02 0.01
.02 0.01
.02 0.01
.02 0.01
.02 (.01
.04 (.02
.02 0.01
.02 0.01
.02 0.01
.02 0.01
.02 0.01
.02 (.01
.02 0.01
.02 (.01
.02 (.01
.02 (.01
.02 (.(1
.02 (.(I


.11 O.Oi 0.02 0.01 0.02 0.01
.11 O.Oi 0.02 0.01 0.02 0.01

.11 O.Oi 0.02 0.01 0.02 0.01
.11 0.06 0.02 0.01 0.02 0.01
.11 O.Of 0.02 0.01 0.02 0.01
.11 O.Oi 0.02 0.01 0.02 0.01
.11 O.Oi 0.02 0.01 0.02 0.01
.(2 1.01
.(2 (.(1
.(4 (.02
.02 l.d
.(2 (.(1
.02 0.01
.(2 (.(1
.(2 (.(1
.(2 (.(1
.02 0.01
.(2 (.(1
.(2 0.01
.02 (.(1
.(2 (.01
.02 (.01
.(2 (.01
.02 0.01
.02 (.(1
.(2 (.01
.02 (.01
.02 (.(1
.(2 (.(1
.(2 (.01
.(4
.(4
.(2
.(4
.(4
.(4
.(4
.(4
.(4
.(4
.(4
.(4
.(4
.(4
.(4
.(4
.(4
.(4
.04
.(4
.(4
.(4
.(4


.02 (.(1 (.04
.02 (.(1 (.04

.(2 0.01 (.(4
.02 0.01 0.04
.02 0.01 1.04
.02 (.01 (.04
.02 0.01 (.04
.(2 (.
.02 0.
.01 0.
.02 , (.
.(2 (.
.(2
.(2
.(2
.(2
.(2
.(2
.(2
.(2
.(2
.02
.02
.(2
.02
.02
.02
.02
.(2
.02


.02
.(2

.(2
.(2
.02
.(2
.02
•
•
•






o!
(.
0.
(.
(.

*
.
•


,
•

t
•
.
•
•
(.
0.
(.
0.
(.
n
(.
o.
0.
o.
J.
o,
0.
0.
(.
(.
0.






















(.1


0.1
(.1

(.1
1.1
(.1
(.1
(.1
.0! miT
.05 106IT
.05 KPfT
.($ OCTIT
.05 writ
.05 DKIT
.05 Jllll
.05 mil
.05 mil
.IS1PUI
.IS Mill
.15 JDIII
.05 mil
.05 10611
.os mil
.0$ OCTII
.is iom
.(5 DKII
.05 Jllll
.0$ FIJI)
.15 III!)
.IS IPIII
.is mil
JOII)
JOUI
.IS 10611
.05 IIPI!
OCTII
.OS Mill
.1$ DKII
.« Jllll
.IS FUII.
.IS HIM
BF C Cl CT n 1 I/T '
IF IF LF IF LF IF LF HF LF EF LF IF LF HF LF IF LF IF LF IF IF IF
                                          9-    68

-------
 Table 5.1b
     j:  Collcfe of SUtet liline



 Tiblt :  liBini Dctcctiot Liiit (ppb|
      1C
IDCB
IFI
OOCI
01
PDC1
J
T4CI
                                                                                                      TCI
1/T   it   IF    LP    HP   11    V    LF   HP   IF    If   LP   EF    LP    IF   LP    IF    IF   IF    IF    IF   I/T
TOUT
ADGIT
SIP!?
OCTIT
IOTIT
DICI?
am
Fill!
Hill
mil
I1TII
JPIII
JDL3I
men
SIPII
OCTIt
novas
DICII
aii9
nm
tiiiJ
mil
mil
JDIIf
JOIM
4D6II
SIPII
OCTIJ
wrii
1ICII
ano
PIBJO
I1I90























'






t


1
0,4
0.4
0.4
0.4
0.4
0.02 0.01 0.4
0.4
0.4















.02 0.01 0.
.02 0.01 0.
.02 0.01 0.
.02 0.01 0.
.02 0.01 0.
.w2 v.ul i.
.02 0.01 0.
.02 0.01 0.4

0.
0.
0.
0.
0.02 9.01 0.
0.
.
0.02 9.01 .
0.02 0.01 .
0.0! 0.01 .
0.0! 0.01 .
0.02 Ml .
v.02 5.51 .
0.0! 1.01 .
0.02 O.OI 0.


.02 0.01 0.4 0.2 0,01 0.01 0,
.01 0.01 0.4 0.1 0,0! 0.01 0.

.01 O.OI 0.4 0.! 0.0! .01 0,
.02 0.01 0.4 0.1 0.02 .01 0,








0
0
0
0




.t
.1
.1
.1
.1
.1
.1
.1
05
OS
OS
05
.1
.1
.1
.1 0.4 0.
O.OS
O.OS
0,05
0,05
8,05
0,05
0.05


O.OS
0.05

O.OS
0.05
0.02 0.01 0.4 0.2 0.02 .01 0.1 0.05
0.0! 0.01 0.4 0.1 0,0! .01 0.1 O.OS
9.0! 0.01 0.4 0.2 0.0! .01 0.1 0.05
.4 0.
.4 0.
.4 0.
.4 0.
.i i.
.1 t.
.4 0.


.4 0.
.4 0.

.4 0.
.4 0.
.4 0.
.4 0.
.4 0.


















.0! 0.015
.0! 0.015
.03 O.OIS
.01 0.015
.0! 0.015
.01 0.015
.01 O.'O!
.01 0.015
.01 0.11$
.0! 0.01$
.03 0.01$
.03 0.515
.01
.0)
.03
.0!
.01


.01
.01

.01
.01
.01
.01
.0!
.915
.015
.ii$
.915
.115


.115
.11$

.015
.015
.015
.015
.015
.4
.4



4


,
.4
.4
.4
,
,
,
t
f
i
f

,
•
i


i
•

«
•

«
i

































.OS 0.01 0.0! 0.01 J011T
.05 0.0! 0.04 O.OtUGIT
,05 0.0! 0.04 0.02UPIT
.OS 0.03 0.04 0.02 OCTIT
.os o.o) 0.04 o.o! mm
.05 0.0) 0.04 1.0! OUIT
.05 o.oi o.o! o.oi am
.05 0.01 0.04 0.0! PIBM
.05 0.01 0.04 0.0! Illtl
.05 0.11 0.0! 0.01 1PUI
.05 0.01 0.0! O.OI UT1I
.os o.oi o.oi t.oi inn
.os o.oi o.oi o.oi ma
.05 0.03 O.Oi 0.01 10GII
.05 0.01 0.0! 0.01 SIPII
.05 0.01 0.0! Ml OCTIJ
.05 0.01 0.0! 0.01 MYM
.05 0.03 0.0! O.Ot DICII
.OS 0.03 0.0! 0.01 ail!
.05 0.0) 0.0! 0.01 FUlf
.(5 i.ii u.ti 9.9i mii
.05 0.01 0.0! 0.01 mil
.05 0.01 0.0! 0.01 IMJ
J01II
mil
.os o.oi o.o! o.oi iron
.05 0.01 0.01 0.01 Sttlt
OCTIJ
.01 0.01 0.0! O.OI MHJ
.05 1.01 0.01 O.Ot OKU
.os 0.01 o.o! o.ot ano
.OS 0.0) 0.0! 0.01 FtllO
.05 0,0! 0.01 O.OI IUII
     1C         IDCB       IPI         ODC1       01         POCB        S          T          T4CI        TCI




I/T  IP    IF   LP   EP    LP   BP    LP    IP    LP    IF    LP   IP    LP    BP   IF    IP    LP   IF    LP    IF   I/T
                                           9-    69

-------
Table  5.2a

Ifeicj: Collefe of Sttten Iihnd

Table : liiiiui Deteetiet Liiit (nj)
       ( Converted froi ppb I
I/T 1DCI
JGLJr
10617
SIPI7
OCTI7

Dttll
Jilll 0.17
FIBII
UUI .17
tPtlt .17
UTII .17
JOIII .97
m»
tOGll .97
SEP88
OCTII .97
BOTH .11
llCti .17
ami .97
mil .97
UMS .!?
mil .97
MTU .97
JDX19
mil
1DG1! 0.97
SEP89 0.97
OCTt!
MVM .17
OEC89 .97
JU10 .11
FH10 .97
IAE90 .97
I/T IOCS
LF IF
1TCB -
.25
.13
.(3
.63
.13
.13
.(3
.13
.63
.M
.13
.63
.63
.63
.63
.63
.63
.13
2.63
2.63
••!«
2.13
2.63


2.13
2. 83

2.63
2.63
2.63
2.63
2.63
1TCS
LF IF
2DCE
0,97
0.97
0.97
0.97
0.97
0.91
0.97
0.97
0.97
0.97
0.97
0.97
0.97
0.9?
0.97
0.97
0.97
0.97
0.97
0.97
A At
0.9?
0.97


0.97
0.97

0.9?
0.97
0.9?
0.9?
0.9?
2DCE
LF IF
2TCE I















.99
.99
.99
.99
.99
.99
.99
.99
.99
.19
.99
.99
.99
.99
.99
2.63 4.99
2.63 4.99
2.63 4.99
2.6) 4.99
2.63 4.99
!.« '..5!
2.63 4.99
2.61 4.99


2.63 .99
2.63 .99

.63 .99
.63 .99
.63 .99
.63 4.99
.(3 4.99
mi 8
IF IF LF IF
BF












.49
.49
.49
.4)
.49
.41
.49
.49
!.'!
2.49
2.49


.49
.49

.41
.4!
.41
.41
.41
BF
LF IF
C CB CT
1.15
1.15
1.15
1.15
2.21
1.15
1.15
1.15
1.15
1.15
2.21
1.15
1.15
1.15
1.15
1.15
1.15
1.15
1.15
1.15
!.!£
1.15
1.15


1.15
1.15

1.15
1.15
1.15
1.15
1.15
.11
.11
.21
.11
.11
.11
.11
.11
.11
.11
.11
.11
.11
.11
.11
.11
.11
.11
.11
.11
.!!
.11
.11


.11
.11

.11
.11
.11
.11
.11
.02
.02
.51
.02
.02
.02
.02
.02
.02
.02
.02
.02
.02
.02
.02
.02
.02
.02
.02
.02
.0!
.02
.02


.02
.02

.02
.02
.0!
.02
.02
C CB CT
LF IF LF IF LF IF
n





20.11
20.11
20.11
10.44
10.44
10.44
10.44
10.44
10.44
10.44
10.44
10.44
10.44
10.44
10.44
!5.!!
11.44
10.44


10.44
10.44

10.44
10.41
11.44
11.44
10.44
KB
LF
1
4.24
4.24
4.24
4.24
4.24
4.24
4.24
4.24
4.24
4.21
4.24
4.24
4.24
4.24
4.24
4.21
4.24
4.24
4.24
4.24
1.J!
4.24
4.24


4.24
4.24

1.24
4.24
4.24
4.24
4.24
1
IF LF IF
I/T
mil
iOtftt
mil
OCTIf
tvvtf
8 Kit
Jilll
mil
uui
mil
mil
JOlll
;oui
iUSU
SIPII
ocni
wnt
DKII
jiiii
mil
Sill!
4PIII
I1TII
JOlll
juui
AD6II
HPlI
OCTII
HTII
PICII
Jilll
run
UIM
••*•••**
I/T

0
                                               9-    70

-------
Table  5.2b
l(ticr  C«lle(t of Stitei Iiltid

Tttlt :  liiim Dttcctioi Liilt (i||
        ( Coiverttd fni >pb )
I/T
«UT
10SIT
SIF1T
OCTIT
wm
DECI7
JU1I
rust
I1UI
1PUI
urn
JDIII
mil
ant
SIPI8
ocrsi
IOTII
DICH
Jill)
FEBIJ
UMI
1PU)
I1T1I
JON)
JDLH
iDGS!
SIPti
OCTti
ion)
OKI!
J1I10
FIDO
111)0

I/T
1C 1



14.21
54.2)
54.2)
54.2)
41.71
41.7S
25.01
{4.2)
ll.TO
II. TO
if.ro
11.70
ll.TO
11.70
11.70
15.70
15.70
M.W
15.70
15.70


15.70
15.70

15.70
15.70
15.70
15.70
15.70
1C 1
IF EF L
)CI












.45


.45
.45
.45
.45
.45
.4!
.45
.45


.45
.45

.45
.45
.45
.45
1.45
DC!
F IF
IFI 01







20.81
20.SI
20.11
20.1)
20.11
20.11 1
20.11
20.31
20.11
20.11
41.78
20.11
20.11
!«.!•
20.18
20.11


20.81
20.11

20.11
20.11
20.11
20.11
20.11
IP! 0
LF BF I
1C)












.45


.45
.45
.45
.45
.45
.'.5
.ii
.45


.45
.45

.45
.45
.45
.45
.45
1C8
P IF
OX
10.44
10.44
10.44
10.44
10.44
10.44
10.44
10.44
5.22
5.22
5.22
5.22
10.44
10.44
10.44
10.44
.22
.22
.22
.22
.1!
in
.21


.22
.22

.22
.22
.22
.22
.22
01
LF IF
nu















21.94
21.14
21.14
21.14
21.14
!!.!<
21.14
21.14


21. M
21.14

21.)4
21.14
21. )4
21.14
21.14
PDCB
IF
S






1.54
1.54
1.54
1.54
1.54
1.54
1.07
1.54
1.54
1.54
l.!4
1.54
1.54
1.54
S.5J
1.54
1.54


1.54
1.54

1.54
1.54
1.54
1.54
1.54
S
IF If IF
t T4
11.14 4
11.14 4
11.14
11.14
11.14
11.14
11.14
11.14
11.14
11.14
11.14
11.14
11.14
11.14
11.14
11.14
11.14
11.14
11.14
11.14
!!.!(
11.14
11.14


11.14
11.14

11.14
11.14
11.14
11.14
11.14
T t
LF IF I
Cl Tt
.01
.01
.01
.01
.01
.01
.01
.01
.01
.01
.01
.01
.01
.01
.01
.01
.01
.01
.01
.01
.::
.01
.01


.01
.01

.01
.01
.01
.01
.01
(CI T
F IF L
1
.»
.SI
.SI
.u
.51
.51
.2)
.51
.SI
.21
.2)
.2)
.2)
.2)
.2)
.2)
.21
.21
.21
.21
.::
.21
.2)


.21
.21

.2)
.2)
.2!
.21
.2)
BE
F IF

JOU7
1DCI7
SIPI7
OCTI7
mm
HCI7
;uii
run
lilt!
iPUl
urn
JDIII
mil
1DGI1
mit
OCTII
NTH
DIM!
juu
FIJI)
MM!
1FUI
1171!
HID
mil
10011
juii
OCTII
MVI!
OKI)
JUU
FIDO
111)0

I/T
                                           9-   71

-------
Table  6.1
Tut ItMlti f«r Cfl/CSI    (riMrtM1
                                                    nl« fir
TNttff
Tut evil
MMMt

frMfftn

-)
CMC.
IN

IN
kllk
ftrkM TttfflM
cklriM
Ckttrt-
kMZIM
Cklmfiri
kiok
IN
klfk
IN
kl|k
mi
1.04
l.ll


.11
.11
.11
.71
.M
.JO
EMI EU*
Mr 07 JM U
1
1
1
1
1
1
1
1
t
1
.It
11
.11
.It
.M
.11
.N LI!
.71 LIT
.U
.11
t.Hlckbra-lN
kNIMI (0)
kiok



t.MltklwHN
kNItMll)
kiik



1,4-licktcrHN
k»UM« ( I)
kiok



t,l-l EniruMKUl Kwitorim SriUN Ukcritonr, M. EnirwMtttl *r*t*ct
-------
              Table  6,2a
                       tli»»t»iA •«»ult» »«r- C99VC92 O»l«*lv» «• V*lm O»r-r*»« fc» OU»r»
                               	~	oci'of	Jui'oo'i	
                     Fmt.
                                        F1«M M   ^1    22      25     20      27     »
                                  •_•«.>• J   •—^^.—.^.^^-i » MM^" • 1.  J. J J    Jl -U-J.  A"J—I— • " J.' J	  — J. 	  A J~A~ ' • A. V»X  — 1.1.1." ' • ' U mAB '  ' J A.^ '" 1 ".I...    '  ""  '
                                   DEC  IflM         O.BBB O.9B4    a.ZDO  O.BB7  0.KZ3  O.O4B  B.^W  O.ZW  D. mm3    Q.rar   A.BMI  l.^B^
                                        Mfh        O.OTO O.OM                                                   '            0.721  O.1S7    O.**7
                                   tinr !«•  1.9*t  2.M7 1.40O    O.O52          0.9*0  O.97O  O.O90  O.90O  O.647    2.179   I.U9  O.792
                                        Mgh 1.7U  2. DM 1.24D                                                               l.Cft*  O.9W
                                   CON ;                             O.OSO  1.1O9  O.4K  O.997  O.M5  O.1T4  O.2OO    O.Uf   O.992  O.9W
                                   MV  IMH  0.*4>  1.000          O.S91  0.00*                                              O.O42  O.1O4    O.OO5
                                             1.107. 1.979                                                                     1.940  O.299
                       	                         2.714  O.M7  0.000  1.000                                 1.2*5  O.O2O
                        0.049        0.229                                                               O.194  O.O*1
                                   OHM                              0.109  0.100 0.200  O.999                                O.2O»  O.1OS
                                   •rr  I«H                                                                                                    0.204
                       	      OK  I«M         O.lll                  0.910         0.977 O.444  O.417  O.I1O    O.27O   O.49O  O.291
                       IMUMM*         M«t.        0.1**                                                                      0.1*9   .000    1.102
                                   WJ17 I«H                0.091                          0.2*5 9.000  9.OOO  9.OOO    9.OOO   9.9O9  2.2OO
                                   CHN                                     0.477         O.315 O.9OO  O.2OO  O.O71    O.149   O.2O4  O.W2
                                   OHM                                     0.729         0.977                                0.999  O.1TO
                                   «rr  IM   o.ioo o.tco                                                                      0.227  O.OM    1.749
                                        M«h  0.221 O.S05                  4.9OO                                              1.7O2  1.O49
                     •Uiyl         DEC  I*M                         2.971  5.429  4.IOO  9.977                                9.41*  O.O4*
                       fcinama         M«h                                                                                                   S.14O
                                   CM                              0.709  2.097  1.941  2.7*9                                1.7*9  O.T34
                                   OMB                              0.709  1.0*5  1.709  2.929                                l.fc**  0.9*5
                                   war  IM                                                                                                    1.010
                                        MoH                        1.000  1.412                                              1-200  O.2O*

-------
Table  e.2b
                                                        «CSt
oct or
**•*• j_ i
c*^p4u»4 n«M 2O 21-22
r«tr«cMarw- OKC lw 1.1*7 1.323
•UMM MO* 1.O90 1.290
MAT law 9.900 4.**7 1.O91
M«h 4.1*7 1.000 1.000
am
•*•
«rr tm
T*l«Mm OEC I«M 1.M9 l.*2*
MO*» i.m i.os*
NJir iMi 9.911 9.924 2.129
IdOh 4.37S 4.KB 2.917
COM
OMi
•IF l«i I.49T l.*M
M«ti 1.73* 1.991
llirricMar* DEC I«M 9.7*4 O.7*«
•tiMM Mo* O.*20 0.**7
MJCT I«M 1.9X4 4.O97 9.2O*
M«H O.79O 1.1O7 O.*29
CMt
om
RtP I«M 9^*4 •.**•
M«fc O.9O9 9.7*1
frlcMvra- OR I«M
NJIT I«M
•IF 1«M

**
2.OOO
1.2*7
1.190
1.110
1.043
2.C70
1.9*7
1.409
1.240
1.320
O.099
0.010
0.999
O.429
0.447
2.00O
0.9*7
O.099
O.200
Jut 00 *
24 2?
1.93* 1.309
0.944
1.429 0.904
1.99O O.OSO
0.747
1.2*4 1.K47
0.92O 1.009
1.O99 1.0**
1.10* 1.0*2
1.092
1.O99 1.O40
O.T9*
0.99* 0.97*
9.9O3 O.924
0.310
l.**T 2.000
O.90O
9.999 0.100
O.9OO

29 1
2.13* O.10O
1.4*9 0.1 tT
2.399 O.299
l.*CO

l.*91 0.971
...9,
1. 1T7 0.*OO
1.241

0.094 9.121
0.719 0.441
O.92O 9.1O7
0.7T4

2.333
1.1*7
9.999
9^,09 tt
13 M -29 HMM
1.000 I.19O 1.293 I.33O
1.170
0.477 14.290 3.O74
0.3*9 0.921 3.O9O 1.997
1.299
0.0*9
O.942 0.9*1 0.711 1.319
1.029
" ~3.9*«"
O.9O9 O.779 O.92* O.94O
1.102
1.993
1.903
0.143 0.143 0.390 O.*2T
O.*43
9.2M O.431 l.OOO 1.439
0.027
O.O7I 0.104 0.194 O.441
O.*91
O.OI7
O.499
2.290
O.77O
0.403
*
0.091
O.OOO
9.713
1.493
1.111
0.303
0.140
O.kTO
O.034
19.201
O.7S1
O.2O1
0.073
olssi
0.34*
O.OX3
i:S
O.349
0.1*1
O.999
9.149
9.27*
0.209
0.339
0.190
t *
1.9*4



9.O79
"3.312



9.001
0.703



o;oir
1.090

9.0*3

-------
                        f ,'2e-
                                                                          ftttrg     OS
                  "*
                                  law
                                                            t-MT
                                                                                           0.-*?»  O.S3»-   0.«*



                                                                         I.«?0  I.2T*  1.IOO O.M9       '  *T.3OO
                                                            t.«M t.SM  1-6*5  l.*O O.1HC O.9V4  O.MS    O.T«O   1.K2* 0.9


                                                            l.OOO l.*U»  I.Tll  l.ir*   ;                          1.HS •.
                             ore  >•«
                                              ».«M
                                                                                       ;*•  O.STS  o.ior   O.MS
                                                                                                                       o.«o
                                                                                                                                i.
     t.san  I.M*  a.sx
                             aw
                                                             .<*« •.««  o.M

                                                             .f99 o.*«t  O.MS •-•rr
                                                                                                                 i.ui o.ois

                                                                                                                 O.SM o.»i
                                                            O.»W O.-WS
(n
tM  l.«0  O.OU
M«li O.FM  O.OSV

B^.' i.Uf  I.M
c    i.««r  I.OM  O.TWI   0.0*2 O.OM  a.ra* o.ow
                                                                                            t.oM  ».ti»
                                                                                             f«r

-------
 Table  6.3a
   Shootout KM* Vilutt for CES/CS1  Rilitivi to films »»port«d hf Othiri
                             Oet IT           Jil II      S4» 1)1    Ovirtlll              HUM
 tat                    Lot Hi    cortfnd    Cortfm*   Cortind    Co* into1
   CMpowd         Mow NM»  S    MM  S    Mu  I    Ma S     MM  I    KC  WIT  Ul   »   IIP

             DEC  1m   0.47  0.01  0.10        T«       M?Oil       Oil
                  high  0.71  fl.1l       0.10       1.12       0.21        l.tt

             WIT  1m   I.I)  0.51  1.71       O.It       0.00       1.21            Ut
                  high  1.07  0.32       0.47       0.10       0.14        0.07

             CAM                             0.7]       0.11       8.51                 O.H
                                                   1.27       0.20        0.31
             RTF  1m   0.17  0.03  1.10       0.71                 1.01                            1.01
                  high  1.34  0.23       0.25       0.10                  0.31
Ctrften Titrt- DEC
ehloridi
UIT

6K«

RTP


Chlorofori DEC

UIT

«Nt

m

1m
high
1m
high


1m
high

1m
high
1m
high


1m
high


1.13
0.40


0.71
0.72


O.IT
0.13
0.13






0
0


0
0


0
0
0






.3!
.14


.02
.OS


.41
.OS
.01




t.»

0.10 0.41
0.44
0.40

1.75
0.05 0.41

0.17 0.25
0.41
0.13 0.51
0.07
0.21




0.13

0.30

0.25


0.00

0.12

0.00

0.10


1.30

0.70

0.40

0.11


0.31

0.31

0.21



1.10
0.11
0.70
0.45
0.40
0.25
0.11
0.14

o.ii
0.14
0.11
0.22
0.21
0.10


Dichloro-    DEC   1m    0.31  0.00  0.25       0.75       0.11       0.41       0.41
  MthiM          high   0.11  0.00       0.01       0.21        0.13       0.25
            WIT  1m    0.03  0.00  0.03       0.27       5.00       1.31             3.30
  chloridl)         high                   0.00       0.00        0.00       2.20

            CAN                              0.40       0.21       0.21                  0.21
                                                  0.01        0.11       0.11
            fid*                              0.55                  0.55                       0.55
                                                  0.11                  0.10
            RTP   1m    0.23  0.04  0.31       4.30                  1.11                            l.tt
                  high   0.40  0.10        0.11                            1.10
                                          9-   76

-------
Table  6.3b
  Shootout Nun Viluu for CES/CSI RiUtiv« to Vilini fcportd by OtlMri

Tut
'CMpOM
EUyl
bMIMI








J
DEC

Ul

OK

RTP

Oetl7
Lo | Ni CoBbind
Flm Mu S Nun S
low
ki(h




1m
high
M II J*p IM
Cortiwd CoibiNd
Mu 1 HUB S
1.42
I.SS
1.71
0.71
1.70
O.S7
1.21
0.21
OviriHI Dun
CnbiMd
Km I KC UIT CM
1.42 1.42
o.ss
1.7! 1.7!
0.71
1.70
0.57
1.21
0.21


m IT?




1.70

1.21

Titrtchloro-  DEC   lov    1.24  O.M  1.21        1.12        O.II       1.30       I.JO
  ithlRl           hijh   1.17  0.01       0.0!       0.11       0.41        O.St

             UIT  1m    3.75  1.11  2.SO        1.24        0.12       LSI             1.11
                   hi|h   2.01  1.4S       1.!t       0.22       0.15        1.77

             CAN                                1.47        1.11       1.40                  1.40
                                                     O.S4       1.47        1.11
             «*                                1.25                   1.2S                        US
                                                     0.10                   0.10
             RTP   1m                          O.M                   0.90                             O.M
                                                     0.1S                   0.15-
ToluiM      DEC   1m    1.77  0.14  1.10        t.lt        0.10       1.40       1.40
                   hi;!:   !.!2  !.i!       Ml       S.J2       3.S7        S.::

             UIT  1m    1.72  1.27  S.14        1.11        0.14       3.3!             1.11
                   hijh   3.17  0.7S       2.74       0.21       0.1S        2.»

             CAN                                1.11        0.70       0.14                  0.14
                                                     0.14       0.11        0.21
             00                                1.11                   1.11                        t.ll
                                                     0.07                   0.07
             RTP   1m    I.SS  0.07  1.11                              1.S2                             1.5!
                   ii|k   1.11  0.01       O.tS  1.11                         0.27
                                                     0.14
MITriehlore  DEC   Im    0.77  0.00  0.70        O.SI        0.21       0.11       0.63
  ithini           high   0.14  0.02       0.01       0.0!       0.10        0.12

             UIT  1m    3.32  1.24  2.07        0.71        0.17       1.12             1.12
                   •ilk   O.M  0.20       LSI       0.04       0.0!        1.11

             CAN                                (.71        0.12       0.44                  0.44
                                                     O.tl       O.OS        0,14
             SK«                                0.13                   0.11                        0.11
                                                     0.11                   0.11
             RTP   Im    0.12  O.OS  0.11        0.11                   0.54                             O.S4
                   high   O.It  0.11        0.0!       0.07                   0.14
                                             9-    77

-------
Table  6.3c
   Skootont dun »iIw for CES/CSI  ftilitm to Vilm KiporUtf ky Ottert
TMt
coqoud
Irirtloro-
•ttaM






•/HriM*









Oct 17 Jll It
U t Hi Cnoigtd COMfMd
Flo* Nun S Nun S Nui 1
DEC

UIT

an*

ITP

DEC

UIT

CAN

SN*

RTF

)M
kill
tw
kj|k


In
bi|h
lev
hi[lt
Iw
hijh




In
higk
2.21
1.21
0.71
0.21
0.40
0.31
o.»
o.ts
l.il
0.21
2.01
0.11
I.5S
0.31
1.12
0.42

l.il
M» III Ownlll nut
CMtJJMd CaAiMtf
Nui 1 Nut
2.21

0.71

0.40



O.S7 1.27
0.07
0.04 ).5i
O.tl
O.S1 1.01
0.11
1.12

1.31

1 ICC
2.21
0.20

0.21

0.13

0.11
1.27
0.72

0.11

O.M

1.42

1.10
uir out ON ITT


0.71

0.40

0.31



1.SS

1.01

1.12

t.ll

                                                  MS
0-IfltW      DEC   I«    0.74  0.1S  0.7(       1.07       0.40       0.74       0.74
                  hi«h   0.74  0.10       O.IJ       0.07       0.01       0.21

             UIT  In    2.11  2.01  2.21       1.14       0.1!       I.U            1.10
                  high   1.12  0.11       1.01       0.24       0.17       1.47

             CAN                              O.S7       0.10       0.37                 0.17
                                                  0.01       0.13       0.22
             Ot                              MS                 O.lf                      O.U
                                                  0.11                 O.ti
             RTF   Iw    O.IS  0.10  0.72       O.S7                 0.17                            0.07
                  Hit*   0.71  O.OT       O.U       0.14                 0.11


                  Klin              1.5t       1.14       0.71       1.11       1.21  1.ft  0.71 O.M  l.tt
                  S                      1.17       O.U       1.12       1.22  I.U  O.S5  O.U t.SI  O.Jt

*  CSI dmdrt by grind MIR of ill nporttd viiuu far July It ihwtwrt
I  UIT vilmi for Z5  Siptubir IMS oiittid it obvioot outliir du* to diiorption fiilin
                                       9-    78

-------
Table 6.4.  Comparison of mean winter (4th and  1st  quarters)
            values over the two years of the study  *
Aroma tics Chlorinated
NJIT DEC CSI NJIT
Benzene
m/p-xylene
o-Xylene
Toluene
Carbon tetrachlorlde
Trlchloroethylene
1,1, 1-trichloroethane
Tetrachloroethylene
Chloroform
Mean
S
0.55 1.57 1.09
0.46 1.29 1.19
0.59 1.26 1.21
0.46 0.90 1.38
1
2
0
1
1
0.52 1.25 1.22 1
0.06 0.24 0.10 0


.20
.00
.18
.53
.00
.18
.60
DEC


0
0
1
1
0
1
0


.50
.90
.42
.75
.75
.06
.46
HCs
Mean
CSI


0
1
1
1
1
1
0


.81
.01
.03
.26
.35
.09
.19
1,
0
1
0
0
1
0
1
1
1
0
.07
.98
.02
.91
.83
.30
.88
.52
.03
.06
.21
* (4Q87 + 1Q88)/(4Q88 + 1Q89)
                        9-  79

-------
    Table 7.la
   Chronology of Maintenance for RTD5O,  GC arid HS        3rd Quarter 1987
   Date  Heliue. HTDSO Cold   RTD    Tune  Mass Film- Leaks Coaaants
                      trap   progX       spec Merits
                             •ethod
    Uul                    5X1               broke
    3Jul              replace     auto       switch
    9Jul new tank
    14Jul   M                6X1                           ^increase Me pressure to increase Flow rate
                                              change      open coluan to tighten liquid nitrogen line
                                           »«              Mhigh air background, tighten fitting*
,0  20Jul                                              M   Mstill high background, replace seal between
I                                                          GC & HS, pump down over night
   2IJul                    6/1    auto
g  23Jul              prob. 6/2    auto
   24Jul system down     «                                Mreplaced cold trap, resolder wires in heat sink,
    to 26th                                                apply new silicone heat sink coapound to plates
   29Jul                    6X2    auto
    4Rug                    6X2    auto
    19flug              *    &X2            M              «failed to reach m*x teap.
                                                          Mshut oFF 22 »in into sasple
   20Bug   »«          replace                            xreplace aoisture, O2, and MC traps on He line
   21 Rug   M                                              **water still high, replace charcoal in trap on
                                                           heliUM line
   24Bug                           auto
   2(Sep                                   M              MabnorMl termination in 2nd, 4th t Sth traps
   22Sep                    3X2
   23Sep new tank           6X2

-------
     Table 7.1b
   Chronology etf Maintenance far RTO5O. GC and HS
                              4th Quarter 1987
   Date  Heliue. HTD5O Cold  RTD   Tun*  Nax»  Fi la-
                       trap  progX       •P*6
                             •efchod
«O
I
09
 lOct
 2Oct
 9Oct
130ct
14Oct
Ifioct
19Oct
210ct
 2Nov
25Nov

27Nov
                             6X2
                             7X2
7HX2
7X2
7X2
7X2
7X2
                             3X1
                             8X2
      twice
                                                           EM at 2200V
                                                           EM »t 2OOOU
                                                                     uir-«« in CT
pooar F»ilur»
                                                                           lovt
1*.
blown
                              M«witch tn» H» tank and *tar-t at  15OO p«i
                              EM at 18OO *V
                              EM at 19OO »U, ion focu» hi^h >4O
   23O«c
   300
-------
       Table 7.1c


  Chronology of  «aint*nanc* for HTDSO , GC and H!»        1st and 2nd Quart**- 1988
  D*t»  H*Iiu« HTDSO Cold  ttTD   Tun*  Mass Filw- Leaks Co«a*nts
                      trap  prog/       *p*c «»*nfcs
                            aethod
  1st Q 1988
   bJan n*u tank
   BJan                                                   out of  liq.  Nit.  and us* dry  io*
  22 Jan                                       *1  iiurn
  2SJan                                                   MS turn»d off du* to mxc»m» pr«**ur*.  H* flow
                                                           rat* too hiojh
  2bJan                                 **     *2 liurn     *«op«n MS
                                              rvpl.ace
«O
I 2Man                                 **                 »*air leak, open *y*t*a, and adjust O-ring around
  29Jan                     S/2
»  IF*b               r*plac*                             split systa* to rapair liq. Nit.  valv*
  10F«b                     8X2
   tHar                     BX1
   3Mar                     8X1               *1 tujrn
   ttlar                     8X2               us* *2
  22Har                     8X1
  23Mar                     8X2

  2nd Q 1988
   2f|pr-                                 *•                 Mrough  pu^>  aaking no is*
   SBpr n^rf tank                        ••                 **rough  puap  r*plac*d
   (flpr                                                   r*plac* Si s*als on hot box and catnri
  2SH»y                                                   r*sold*r wir*s in cold tr.
  >Uun                                                   tighten clips on RTO5O tr-.

-------
   Table  7.Id
                                                      3rd Quarter 1988
Chronology of maintenance for RTO5O, GC and I1S

Date  Heliu* flTDSO Cold  flTD   Tun*  Mass Film- Leaks CoMents
                   trap  prog/       spec «ents
3rd Q 1S88
 BJul oew tank
13Jul   «

19Jul
 9Hug
ISHug new tank
17Rug
                   repl
 9S«p rww tank
14S«p n»w tank
change Oxygen trap
Mr-eadjust aao gain and oFFset, ant  lens,  ion Fi
 and EM at 22OO.  * He Flow rate adjusted
change Si seal on hot box
put 2nd Moisture trap on He line
reaove 2nd Moisture trap , reset purge
 Flow to SO cc/a.. 28 pks fc 9OO ct on Btune. drop
 pressure to 34.5-35 psi and tank at 272O psi.
tank at 262O psi, lower purge to SO ccXain
      ce oxygen trap on line
                                                                                               MS shut OFF
                                                                                               coluan, no
MS high water peek, put on new He tank
 - excessive pressure separated,
 voltage in MS, replaced Filaaent. cl
        Floppy disk drive

-------
 Table 7.1e
Cnronology of Maintenance for- RTO5O. GC and) MS
            4th Quarter 1988
Date  HeliuM RTD50 Cold  RTO   Tun*  Mass File- Leak* CoMeents
                   trap  prog/       spec »ents
                         •ethod
 eoct
 7Oct
lOOct
14Oct
ieoct          M
26Oct          M
280ct          M
 4Nov

lONov new tank
llNov          M
                                          burn
                    icing up
                          BX2
                                                            air background,  leak in
                                                       replace Si  O—ring on  hot box
            "replace fuc** in flTDSO
            MRTDSO hot box not functioning
            xreplace fuse
            Mair background started high . and then drooped dur
              day
            •tart tank at 28OO pci
            Mhot box fuse blown and replaced
            Mchange Si O-ring on hot box
            cryogenic valve ••Icing noi«e
                    replace
                    tighten
                    replace
repl
            repl
                                                               cryogenic valve and
ZSOec

27Dec
                                               •1
                                               •2
            column broke at MS end, reinsert,
             rough P"""P doe» not start
            got rough piirap started by waving rotor, repl4
             •oisture trap

-------
      Table l.lf
Chronology of Maintenance for HTOSO,  GC and MS
                                                           1st Quarter- 1989
         Heliu* HTDSO Cold  RTD   Tun*  Mass Fila- Leaks CoMents
                       trap  prog/       spec ments
    23Jan
    3tJan
     IFeb
    2IFeb
     2Mar
                         8/2
«0
I
0>
Ul
 Mar

IDMar
lIMar
ISMar

ITMar
22Mar
              tank
     l*ak at inl*t of trap — rvplac* Si O-ring, cold
 trap not reaching —3D C, rtrplac* n»at sink ctM»fto»mtd
 top plat*
**CT not reaching high fr«ap,  reaov* resistance 

HF9
HF9
replace Si O—ring on RTO5O oven
HF9, caused by aetal flange  on heated valve,
 should rotate in about  1 ««cond
change transfer line between RTD5O and GC
replace rough puep, install  ion gauge
connect transfer line and coluMn with new union
 f roe, J fc M
                                                                                      present, raised GC
                                                                                        C for several Minutes
                                                       tune shows other
                                                         teeperature to 22O

-------
   Table 7.1g
Chr-onolooy of «Mjintanano» far- RTOSO.  GC  and US

        HiTitji~~fiT555~CoT3~
                                                                       2nd.  3r-d
2nd Q  1989
 SRpr-
15flp«-
                 8X2
19Hau.
29M4MJ
28Jur>

30Jun
     Q  1909
 HJul
 to 3Oth
ZOJul
  TBug
                                                                       background  mtr count,  vwr^j hign Firo* oolu«n bl»«»d.
                                                                         urtttbl*  to  run,  hutmtott ooluniri  Fcjc- ••v*«~«l
                                                                         225  C.  «od ov*r  night «t ISO  C
                                                                       9Mll column bl««9itivitu too low
                                                                       Or-. Ztta  tat<»*  ovor-
                                                                       r-oplAco  GC  coluan. ion •our-c*  ol»«r>«d
                                                                       r-o tent ion ti»«» shifted,  «nd thu* oo«put«r- pi IKJ •<•
                                                                       For-  ind^nt-ifuing  compounds  Ke» to b*
                                                                         RTDSO blowing fus*»  whm^ CT ft
                                             H20


                                               ••naitivitu ?or-
                                                 »UJp*ot dir-tu
                                                                                           to 279 C to
                                                                                 down du» to  lo«« oF
                                                                         wor-l<*t«tion  2. v»r-»ion 3.1
                                                                       cold tr«p  «nd ff>mc*r nut*
                                                                         highvr- mmmmmm lost,  •utotuo* f»il
                                                                       EM volt
                                                                                      oh^^god from 22OO  to  18OO.
                                                                                    thr-*»hold  fr-o-. SO to TOO
                                                        M

                                                        ch
                                                                       **fi 1
                                                                       EH
18Ruo.
20nug
  to 5S*p
18S<^>
  to SOot

     O 1989
             bade  to  22OO


HS shut down. 3 circuit

MnTDSO ahut  down with
                                                                                                                r-*pl«e«d in ns
  7Oot
                                                                                                          »i
                                                                                   f ix«d bu (-•placing *1O  r-»l«u
                                                                       Mtr«n*f*r-  lino cr-ACt<«d>  rvpl*o»d
                                                                       Mfix l»mt<  in hot  box
                                                                          •r-    o «n* UK*  •>                      ^»»

-------
Table 7.2
     Number and data or nama of calibration curvaa by  quartar*
      Welael  ~>
      3087   4Q87
    1Q68   2Q88   3Q88  4088
     !  Zha  —>
1069   2089   3069
70387
71087
72187
73087
80487
80787
81087
81487
82187
82187
82487
82887
90487
90887
91587
91787
91887
92787
100287
100587
101287
101387
102187
103087
110487
112487
112587
120287
120487
121187
121887
122387




11868 4 588
12888 MAY
20288
2 388
2 588
2 688
21088











70888 101188
70988 111288
90288 111588
NOV
NOVEX
DECEX
122886











11769 62869
20289
20389
30289
31689
32069
3ava89











81189
91289
















         18
14
           1
     •Reduction related to shift from autotune to manual tune
                            9-   87

-------
Table 7.3a
Tune parameters and mass spectrometer condition (ATune file)
3rd and 4th Quarters, 1987


Date  Multl- Amu  Amu  Ion Ent Repel- X-ray Mass Mass   Air-  Three*
       pller gain off- fo- lens Isr         gain offset H20   hold
                  set  cus                              count
30Jun
3Jul
7Jul
14JU1
16Jul
17JU1
21Jul
23Ju1
29Jul
4Aug
7Aug
10Aug
21Aug
24Aug
27Aug
31Aug
04Sep
ISSep
ATune
10ctA
20ctA
50ctA
90ctA
130ctA
25NovA
27NovB
30NovA
2DecB
400CB
80ecB
23DecB
1800



1800
2000
2000






2000




(auto)
2000


2200
2000
1800
1600
1800
1400
2200
2000

154
151

152
155
152
151

152
150
151
152

149
154


151

151
149
156
155

158
157
158
150

151

09



67
68

67
68
67
68
67

67
66



BTune
66






69
72
73
71
72
0





. 4
0


4

8
4
0



50
55


45

55
50
60
50
60

70
75
60

55
45
(manual
0
4
0
16
4
0
52
0
20
25
22
0
45
70

60
65
50
55
50
50


62
10.2 64
90
80
76
88
68
88
76
92
80
88
80




72
84
tune with BFB
10.2 84
68
76

72

8.8 52

10.2 48

8.4 60
10.2
-2


-4
117
-9
-4
-7
-4
4
-6
-6
-1
2
-1


2
to
2
4
-8
-1
2
31
44
31
46

38

16



15
16




17

16




17
USEPA
17
16
17
16
17
16
15
16
16

15

1064
377
764
304
1916
4652
675
563
369
681
305
596
2015
15188
1275
2307
783
813
conditions)
787
2857
406
22424
585
259
19480
323
13301
1002
602
168
5







8

7

5






5







5



                            9-   88

-------
 Table 7.3b


Tune parameter* and mass spectrometer  condition (BAA Tunes)
1st, 2nd, 3rd, and 4th Quarters,  1988


Date  Multl- Amu  Amu  Ion Ent Repel-  X-ray Mass Mass   Air-  Thres-
       pHer gain off- fo- lens ler         gain offset H20   hold
                  set  cue                             count
IIJanB
HJanB
18JanB
3FebB
9FebB
22FebA
IMarA
3MarB
TMarA
1 TMarA
ISMarA
22MarA
3 IMarA
6AprA
12AprA
12AprB
ISAprA
25AprA
29AprA
SMayB
11 May A
UulB
13JU1A
14JU1B
OSepB
19SepB
60ctB
290ecB
2000
2200
2000

2200
2000
1800
2000


1800
1600
2000
2000


1800

2000

1800
2000
2200



2200

151
158
151

102
159
158
151
158




155
158
151
158


151
157
151
154
155


155

72
68
72

68
66
68
72
66

68


68

72
68


72
68
72
88


69
69

0
4
0

4
8
12
0



48
16
16
0

16
12

0
8
?
16
24


24

62 10.2
55 10
62 10.2

50
55
50
62
55
50
45
60
45
45 10.2

62
50

45
62
45
? 10.2
48 10.2
47


47 10.2

60
84
60

80
72
60


76
60
56
88
76
60


58
60

80
?
88


68
68

38
-4
38

-3
0
7
38
-3
-1
-4
-6
2
-1
0
38
-7
-6
-4
38
-6
?
-12



-12

15
16
18
16
16

16
15
16
16
17

16
16

15
18
17
16
15
18
?
18


16
16

677
543
195
333
633
18208
151
168
17672
288
12088
16251
162
180
275
275
257
182
294
169
156
132
167
914
488
650
1038
378
6












5










20
20
20

                             9-   89

-------
 Table 7.3c


Tun* parameters and mass spectrometer condition (B i A Tunes)
1st, 2nd, and 3rd Quarters, 1989


Date  Mulfl- Amu  Amu  Ion Ent Repel- X-ray Mass Mass   Air-  Thres-
       pHer gain off- fo- lens ler         gain offset H2O   hold
                  set  cue                              count
13JanB
19JanB
23JanB
29HarB
2200


2200
155
162

152
69


69
24


24
47


47
10.2


10.2
68


68
-12


-12
16


16
399
291
291
304
20

5
5
 lAprB  2200  152   69  24  47   10.2    68  -12     16   304      6
27Hay   system shut down, source needs cleaning

New HP Software -Installed (Increase sensitivity lOOx)
 2AugB  2200  148   70   8  65   10.2    88   20     15  1278     20
 9AugB        145       22  55          104   -3          637    500
19AugB        150       28  65           64  -11          462    750
23AugB  2400             0  50          112 -465     11   850
24AugB        152   71                      -696     12   339
25AugB  2200                                              600
26AugB        159   68  10  55           88 -175     11   239
29AugB  2400  150   70   4  45           84 -327     12   500
SOAugB                                      -236          373
 ISspB                                      -580          352
 OSepB        210   68      48          112   47      6   481
 SSepB  2600                                  53      4   460

SOOctB  2400  204   71   0  65   10.2    88   16     -5   670
UNovB        212   68      55                18    -19   411
15NovB        210   70      47                40    -17   318
16NovB        203   71      37           84   61    -23   236
 1DecB  2000  196   68      40           92    3    -12   374
                           9-   90

-------
Table 7.3d
Tune parameters and mass spectrometer condition  (B  * A Tunes)
Summary of quarterly means from 3rd quarter 87 to 4th quarter 89


Date  Hultl- Amu  Amu  Ion Ent Repel- X-ray Mass Mass   Air-  Thres-
       pHer gain off- fo- lens ler         gain offset H20   hold  '
                  set  cue                             count
3q87
4q87
1q88
2q88
3q88
4q88
1q89
2q89
3q89
4q89
1920
1889
1960
1900
2100
2200
2200
2200
2360
2200
152
154
156
155
153
155
153
152
159
205
67
71
69
70
76
69
69
69
69
70
3
12
10
9
20
24
24
24
12
0
56
56
54
52
48
47
47
47
55
49
10
10
10
10
10
10
10
10
5
10
80
66
70
67
78
68
68
68
93
88
6
19
9
7
-12
-12
-12
-12
-216
28
18
16
16
16
17
16
16
16
10
-15
1919
5183
5175
224
470
708
321
304
546
402
e
5
5
5
20
20
10
5
318

                            9-  91

-------
Table 7.4
       Mean  value  for  -internal standards for a subset of samples
         from each  quarter
Quarter
3q87«
4q87
1q88
2a88
3q88
4q88
1q89
2q89
3q89
N Stat.
10 Mean
S
10 Mean
S
19 Mean
S
23 Mean
S
24 Mean
S
32 Mean
S
20 Mean
S
1 6 Mean
5
28 Mean
S
Internal
1st*
214.8
34.3
237.5
42.5
263.1
48.7
204.3
37.7
232.0
70.6
206.9
39.2
197.8
37.2
192.3
50.5
164.8
42.8
standards
2nd*
111.9
61.4
141.1
39.1
90.6
32.1
74.4
37.9
41.6
16.7
31.1
5.3
41.7
9.2
102.4
42. G
85.9
49.9
2nd/ 1st
0.52
0.59
0.34
0.36
0.18
0.15
0.21
0.53
0.52
8/Mean
1st
0.16
0.18
0.18
0.18
0.30
0.19
0.19
0.26
0.26
2nd
0.73
0.28
0.36
0.61
0.40
0.17
0.22
0.41
0.68
       * 4q87 to 1q89 adjusted to fit ratio of 1st to 2nd of 1:0.46
       t without split!ess valve, which was Installed at start of
           next quarter
                         9-  92

-------
Table 8.1
       Organization: College of Staten Island
Sorbent:  Tenax
                 Regression summary for January to March 1989
                      DISTRIBUTED VOLUME (Low-High Flow)
Compound name
Methylene chloride
1 , 1-Dichloroethane
Hexane
Chloroform
1 1 1-Trichloroethane
1 ,2-Dichloroethane
Benzene
Carbon Tetrachloride
Trichloroethene
Toluene
112-Trichloroethane
Tetrachloroethene
Chlorobenzene
Ethyl benzene
m/p Xylenes
Bromoform
Styrene
o Xylene
m Di Chlorobenzene
p Dichlorobenzene
o Dichlorobenzene
Regress-
df ion coe-
fficient
226 *
226 »
226
225
226
226
223
223
224
223
226 »
221
220 *
217
217
223 *
215
215
217 «
215 *
215 *
0
0
0
0
0
0
0
0
0
0
1
0
0
0
0
1
0
0
0
0
0
.788
.241
.927
.626
.909
.472
.941
.951
.934
.968
.00
.951
.541
.963
.968
.00
.946
.952
.294
.127
.118
Slope
0
0
0
0
0
0
1
0
1
1
•
•
•
•
•
•
•
t
•
•
558
989
906
549
727
451
071
853
006
039
all
0
0
0
1
•
•
•
•
896
823
952
013
all
1
1
0
0
0
•
•
•
.
•
019
043
323
054
318
t-Test
on
slope
29
8
56
19
48
14
63
71
59
86
at
68
16
79
84
at
63
69
9
6
5
.368
.526
.625
.607
.467
.548
.000
.083
.176
.583
MDL
.923
.137
.333
.417
MDL
.688
.533
.500
.000
.390
Signifi-
cance
P <
P <
P <
P <
P <
P <
P <
P <
P <
P <

P <
P <
P '
P <

P <
P <
P <
n <
P <
: o
; o
: o
: o
: o
C 0
C 0
: o
C 0
C 0

C 0
C 0
C 0
C 0

C 0
( 0
C 0
f n
C 0
.001
.001
.001
.001
.001
.001
.001
.001
.001
.001

.001
.001
.001
.001

.001
.001
.001
.nni
.001
       * most or all  values at or below MDL
                           9-  93

-------
Table 8.2
                            Table 6.2
                     Regression summary for study
                     COMPARISON ACROSS CATEGORIES
Duplicate
Compound name Low
df R*2
Methylene chloride *
1 ,1-Dichloroethane *
Hexane
Chloroform
111 -Tri chl oroethane
1 ,2-Dichloroethane
Benzene
Carbon Tetrachloride
Trichloroethene
Toluene
1 12-Trichloroethane *
Tet rach 1 oroethene
Chlorobenzene *
Ethyl benzene
m/p Xylenes
Bromoform *
Styrene
o Xylene
m Dlchlorobenzene *
p Oichlorobenzsne *
o Dichlorobenzene *
All compounds
Mean 20
25
6
27
20
27
15
27
27
26
27
2
26
7
26
26

26
26

22
3

.6
S 6.8
For measurable compounds
Mean 23
S 6
only
.4
.8
0.81
0.83
0.97
0.93
0.95
0.99
0.95
0.95
0.89
0.95

0.96
0.60
0.92
0.94

0.86
0.83

0.46
0.98

0.88
0.14

0.93
0.04
Duplicate
High
df
24
4
25
23
25
24
25
25
25
25
4
27
13
24
24

23
24

20
9

20.7
7.1

23.1
5.4
R*2
0.81
0.67
0.96
0.81
0.76
1.00
0.98
0.95
0.92
0.97
1.00
1.00
0.67
0.93
0.95

0.96
0.96

0.71
0.96

0.89
0.11

0.94
0.07
1st Q 1989
Low-High
df
226
226
226
225
226
226
223
223
224
223
226
221
220
217
217
223
215
215
215
217
215

221.4
4.3

221.9
4.0
R*2
0.79
0.24
0.93
0.63
0.91
0.47
0.94
0.95
0.93
0.97

0.95
0.54
0.96
0.97

0.95
0.95
0.13
0.29
0.12

0.72
0.31

0.89
0.15
Canister
- Tenax
df


34

40

63
3
1
63

24

37
58


46




37
21

37
21
R-2


0.52

0.57

0.63
0.07
0.99
0.59

0.91

0.44
0.68


0.61




0.59
0.24

0.59
0.24
* most or all values at or below MOL
                         9-  94

-------
   Table  8.3
          Comparison of results From Blind Samples and Shootouts  
to
I
to
01
Compound Blind samples
retention time) ELfiP
Methylene chloride O.97
Chloroform 1.O3
111 Tr i ch 1 or oe thane
Benzene
Carbon Tetrachlor-ide
Tr i ch 1 or oet hene
Toluene
Te tr ach 1 oroe thene
Ethyl benzene
m/p— Xy 1 ene
o-Xylene
.04
.14
.28
.14
.12
.10
.12
EMSL
1.34
O.99
O.91
0.02
O.94
1.115
1.1-1
1.31
0.77
Shootouts CSI-PEI
DEC
0.41
O.39
O.63
O.96
1.30
2.25
1.40
1.30
3.42
1.27
0.74
NJIT
3.38
0.31
1.32
1.21
0.7O
O.78
3.39
1.98
1.55
1.60
CRN
O.28
O.44
O.53


0.94
1.40
1.79
1.03
0.37
CRN

0.59
O.97
1.04
O.79
1.1O
1.07
1.41
1.25
O.63
Mean
1.26
O.77
0.79
O.94
1.00
1.21
1.52
1.33
1.B1
1.24
O.82

-------
                          DUPLICATE LOW FLOW
                                     HEXANE
                                                                  X D
                                                  D
to
I
(0
    UJ
_J
a
n
a
    0
    a
    UJ
    en
          2.5 -
           2 ~
      1.5 -
           1 -
          0.5 ~
           0
             0
                      1



                     a
                                      a
    I      i

    2


FIRST DUPLICATE
\

4
                             pair
     Figure 2.1

-------
Id
-l
D.
2
o
a
u
Ll
     0.13
0
                       DUPLICATE-LOW FLOW

                                 CHLOROFORM
0.02
0.04




pair
  O.Q6     0.0(3


F1R5T DUFUCATE
                                                           0.12
0.14
Figure 2.2

-------
u>
I
UJ
H

a
_i
Q.

a

a
z:
•:"i
a
tii
            o.i
                           DUPLICATE-LOW FLOW

                                  1,1,1-TRICHLOROETHANE:
                  0.3
                           D
0,5        0.7       0.9


     FIRST DUPLICATE
1.1
1.3
                               par
     Figure 2.3

-------
         0,4
                           DUPLICATE-LOW FLOW
                                   1,2-D 1C HLORO ETHANE
        0,35 -
                                                                  ..--t
10
   it)
   3
   a
   z
   O
   O
   111
   en
         0.3 ~
        0.25 -
         0.2 -
0.15 -
         0,1 -
        O.O5 -
          0
                               D
                            O.I
                                   0.2


                            FIRST DUPLICATE
0.3
                              par
0.4
    Figure 2.4

-------
*-*  Q.
s  =•
0  a
   O
   Q
   id
   n
        4.5 -




         4 ~



        3.5 -
2.5 ~
        1.5 -



          1 -



        0.5 -
         O
           0
                         DUPLICATE-LOW FLOW
                                    BENZENE
                           2           3


                         FIRST DUPLICATE
                            pair
    Figure 2.5

-------
to
i
o
H
a
y

"a
i
a
     C
     a
     u
     u
           O
             0
                           DUPLICATE LOW FLOW

                                       Tetrashloride
                         PAIR
                                    First Duplicate

                                       - —  REGRESSION
     Figure 2.6

-------
O
(O
                        DUPLICATE-LOW FLOW
                                TRICHLOROETHENE




UJ
s
n.
u
a
a
0
u
UJ
in




'-•'.O
0.28 ~
0.26 -
0.24 -
0.22 ~
0.2 ~
0.19 -
0.16 -

0.14 -
0.12 -
0.1 -
0.08 ~
0.06 ~
0.04 ~
0.02 -
0 -
(
D
..--"
.,-*"
/
D ..--""'
a ,,-'-'"'
/"'
^*-r~
^-^
^
D s*
D jS"^
a Jf*° D
r^^ °
n
1 1 1 I 1 1 1 I 1 1 1 I I 1 1
? 0.04 O.O5 0.12 0.16 0.2 0.24 0.25 0.:
                                 PIE5T DUFUCATE
                           pair
     Figure 2.7

-------
          10
                          DUPLICATE LOW FLOW
                                                           D
                                                                   n
(0
I
    a
    u

    a

    a

    TJ

    0
    u
    u
           4 -
           n
           a
                         a  FAIR
First. Duplicate

   	 REGRESSION
    Figure 2.8

-------
                     DUPLICATE-LOW FLOW
UJ
a.
n
a
U
UJ

Ll
                             •ETRACHLORDETHENE
                              FIRST DUFLJCATE
                         pair
 Figure 2.9

-------
10
I
O
tfl
                         DUPLICATE LOW FLOW
                                   Ethyl Scnzcnc









liJ
H
3
D
D
a
i—
t/1
It
"-









i .0 —
1.7 ^
1.6 -
1.5 -

1.4 -
1.3 -

1.2 -


1.1 ~
1 -

0.9 -

0.5 -

0.7 -
0.6 ~
0.5 -
0.4 ~
0.3 ~

0.2 -

.1
O

^•"'
j.**
f.s*~' n

.X
a ^,'

_•»•
>- D
n ^
a ,X^
j^
s
a a >^ p

'*1i
/"
S'"''
j^ a
a >^° P
,X°
v^ri °
Q^^^
D
1 1 1 1 1 1 1 1 I 1 1 1 1 1 1 1
0.1 0.3 0.5 0.7 0.9 1.1 1.3 1,5 1.7
                                 SECOND OU FLIC ATE

                            PAIR       	  REGRESSION
   Figure 2.10

-------
                      DUPLICATE-LOW FLOW
                            KCTA OR FAKA
        6 ~
hi

a
_i
D.
01 S
  Q
  UJ
        4 -
              X-,U  °
             cK a
                            a
          0
                        2               4


                             RR5T DUPUCATE
                                                        T

                                                        6
                         par
  Figure 2.11

-------
u>
I
o
Nl
UJ
I
J
a.
n
a
a
-r
O
fj
UJ
in
0.32
 0.3
0.26
0.26
0.24
0.22
 0.2
o.ie
0.16
0.14
0.12
 0.1
o.oe
0.06
0.04
0.02
  0
                             DUPLICATE-LOW FLOW
                                          5TTKEHE
                     0.04
                          —I	
                           0.08

                             pcrir
                                        T
T
T
0.12      0.16
FIRST DUPLICATE
                                                 0.2
                      0,24
                          0.20
    Figure 2;12

-------
t-*
o
CD
   u
o


O
U
Ul
LI
1.3 -T



1.2 -



1.1



  \ -



0.9 -



o.e -



0.7 -



0.6 -



0.5 -



0.4 ~



0.3 -



0.2 -



0.1 -



  0
             0
                           DUPLICATE-LOW FLOW
                                      ORTOO OTLENE
                                      a
                                D
                                     T
                                            T
                   0.2
                       0.4
                               pair
     0.6        0.9


PIR5T DUPLICATE
                                                                       D
T	1	T~

 !         1.2
    Figure 2.13

-------
M

O
u


i
_j
D.
3
a

a

0
a
ui
en
        3.5 -
        2.5 i
        1.5 -
        0.5 -
                         DUPLICATE HIGH FLOW
                                    HEXANE
                                 FIRST PUPUCATE
                           pair
   Figure 2.14

-------
UJ
a
n
a

a

O
u
UJ
in
     0.09
     0.00 -
     0.07 ~
     0.06 -
     0.05 ~
0.04 -
     0.03 -
     0.02 -
     0.01 '
        0
                         DUPLICATE HIGH FLOW
                                    CHLOROFORM
                                   D
                                                D
                                   a
                     0.02
                           0.04        0.06


                              FIRST DUPLICATE
0.09
0.1
                            pair
                                       rog rcssion
 Figure 2.15

-------
   tu

   \
'
   5
l_  ID

P  a


   O
   'J
   u
   m
         1,2 -
         1.1 -
0.9



o.e



M ~7




0.6




0.5



0.4




0.3



0.2



0.1 n



 O
                            DUPLICATE HIGH FLOW

                                   1,1,1-TRI CHLOKOETHANE
                                  D
                             D
                         n
                              D

                                                                ...-f-"
                      0.2
                                0.4
                                      I
                                           I
                                                I
     0.6        o.e


F1R5T DUPLICATE
                                                                1.2
             par
    Figure 2.16

-------
          0.4
                            DUPLICATE HIGH FLOW
                                    1 ,2 DICHLOROETnANE
          0.3 -
                                                                      "D
vo
*
    UJ
    h
    a
    CL
    Zl
    a

    a
0,25 ~
                                  D
    a
    u
    an
0.15 -
          0.1 -
         0,05 "
           0
                         a-''
T-    ~r
      0.4
             0
                  0.1
                           n
0.3
                                      FIRST DUPUCATE
                               pair
     Figure  2.17

-------
   UJ

   §

f  3
   a
   a
   UJ
   tfl
         4 -
                  a
                         DUPLICATE HIGH FLOW
                                    BENZENE
                            D
                                  I

                                  2


                                 FIR5T DUPLICATE
                           pair
   Figure 2*18

-------
.  d
I  -J
   Q.
H  a

£  a
   a

   c\
   G
   UJ
         0.4
0.35 -






 0.3 ~






0.25






 0.2






0.15






 0.1
        0.05 -





           0





       -0.05
                            DUPLICATE HIGH FLOW

                                  CARBON TETRACHLORIPE
                      ~T	


                       0.1





                       pair
                                                   D
                                                 0.2
                                     FIRST DUPLICATE
                                                                            D
T~


0,3
    Figure 2.19

-------
I

H
H
Ul
IU

I
a
a
a
    o
    UJ
    in
         0.28
9.26 -


O.24 -


0.22 -


 0.2 -


0.16 -


0.16 -


0.14 ~


0.12 -


 0.1 -


0.06 ~


O.06 -


0.04 -


O.02 ~


  0
                              DUPLICATE HIGH FLOW
                                       TRICHLOROETHENE
                                                       D
                     O.C'4
                       T	1	T

                          O.OB
                                                    T
0,12      0,16

  FIRST DUPLICATE
—T~

 0.2
                                                       0,24
0.20
0.32
                             D
                                 pair
    Figure 2.20

-------
      11



      10
                      DUPLICATE HIGH FLOW

                                 TOLUENE
111
a.
n
a

a


6
a
UJ
9




7




6




5




4




3




2




I




0
                D
                                 D
                      I

                      2




                     Q
D
                                         I

                                         6
                         par
                        FIRST DUPLICATE

                           	 regression
 Figure 2.21

-------
      3.5
                        DUPLICATE HIGH FLOW

                               TfiTRA CHLOROETHYLENE
U
to
•   5:

M  a
**  a
   2
   o
   a
   ui
   ci
      2.5 -
       2 -
      1.5 ~
       1  •*
      0.5 -
                                 T        r

                                         2



                                 FIRST DUPLICATE
                                                             i

                                                             3
                           pair
Figure 2.22

-------
f
09
   iu
   §
a
a
f
0
a
1.5

1.4 -

1.3 -

1.2 -

1.1 -I

  1 -

0.9 -

0.9 -

0.7 -

0.6 -

0.5 -

0.4 -

0.3 ~

0.2 -

0.1 -

  0
                            DUPLICATE HIGH FLOW
                                      ETHYLBENZENE
                      D
                                                 D
                  I     I     I     I
              1        0.3        0.5
                                   i     I     I
                                  0.7        0.9
                                                             1.1
1.3
                                      F1K5T DUPLICATE
                           D
                               pair
   Figure  2.23

-------
   ui
.
to  a
   a


   O
   a
   Id
   in
          4 -
          3 ~
          2 -*
          0
                          DUPLICATE HIGH FLOW

                                 META OR PARA XYLENE
                                          a
                 a
                                                   a a
                                 T     I
                                             r

                                             3
i

4
                         a
                                   FIRST DUPLICATE
                            pair
f

5
   Figure 2*24

-------
to
I
to
o
tu


|

_j
D.

a

a


O
O
UJ
in
         0.26
0.24 -



0.22 ~




 0.2 ~




0.10 -



0.16 -




0.14 ~



0.12 -




 0.1 -



0.09 ~




0.06 -



0.04 -




0,02 -



   0
             0.02
                             DUPLICATE HIGH FLOW
                     D a
                I     I

                    0.06
                                          5TYRENE
                                                                          TT
 1      I     I


0.1         0.14



    FJR5T DUPLICATE
                                                0.10
0.22
0.26
                            o
                                par
    Figure 2.25

-------
u>
i
   til
   g
   a
   z
   O
   a
   Hi
   LI
                           DUPLICATE HIGH FLOW
                                    ORTHD XYLEME
                     0.2
    0.6


RR5T DUPLICATE
 I

0.8
1.2
                         D
                             pair
   Figure 2.26

-------
to
I
tv>
IO
     o
I
\

o
u.

o
2.3

2.2

2.1

 2

1.9

1.8

1.7

1.6

1.5

1.4

1.3

1.2

1.1

 1

0.9
                          Change in lo/hi ratio by quarter
                                         (see Table 3.2)
                                               TEMP/32
                                                                 B. NON-MEASURABLE
                                                                            T 6
          4Q87    1088    2Q88    3088   4088

                               QUARTERS
                                                          1Q89
                                                             2089
3Q89
      Figure 3.1

-------
\o
i
10
   a
   a
   ••—'

   c
   a
c
u
u

a
u

K
a

u
               Canisier-Tenax Comparison for 1988-09
        0.5
                                   HEXANE
                            Canister concentration (ppb)

                          pair       	  regression
                                                        100
                                                               120
   Figure 4.la

-------
JJ
a
a.
c
a
u
u

a
u

K
a
c
u
       0.4
            Canister-Tenax Comparison for 1968-69
                               HEXANE
0.6
O.B
                       par
    1


ion (ppb)

regression
1.2
1.4
Figure 4.1b

-------
  JJ

  a
  a
vo -g
s j

  a
  u

  K
  a

  u
        1,6
               Canister-Tenax Comparison for 1966-69

                               11} -Trk
          0.2
0.6
 pair




Figure
             •*•   regression (n=39)
 1



Canister
                                                                2.6
                            o  nsgrcwfon (n»40)
        4.2

-------
                Canister-Tenax Comparison for 1988-89

                                     Bcnzwic
         4.5
          4 -

         3.5 -
u>
I
10
ov
   -D
   a
   a
ti
u

D
u

X
0
c
11
         2.5 -
         1.5 -
          I -
         0.5 -
                                                a
                                  D
                           a
                                              a
           0.2
                  0.6
1
1.4
1.0
                               Canister concentration (ppb)
                             par
2.2
2.6
    Figure 4.3

-------
        0.6
                Canister-Tenax Comparison for 1988-09

                                      Tetm;hl
-------
to
I
to
09
    JO
    a
    a
    c
    Q
U
u
c
a
u

x
a
c
u
         0.45
 0,4 -





0.35 -





 0.3 -





0.25 -





 0.2 -





0.15 -





 0,1 ~





0.05 -





   0
            o.ie
    Figure 4.5
                 Canisfer-Tenax Comparison for 1988-4J9
                  0.2
                     0.22
0.24
0.26
0,26
 a

T~

0.3
                                 Canister concentration (ppb)

                               par        	  regression
0.32

-------
 to
 I
   J]
   a.
   a
a
*  P
io
   u
   u

   a
   u

   x
   a
   c
   u
     10




      9




      a




      7
      5




      4




      3 -




      2 -




      1 -
               Canister-Tenax Comparison for 1966-69
                                  TOLUENE
                              D
                        a
                     a
a
                      a
                   ~r

                   2
                        T

                        4
                            Canister
                       a
                          par
  	r

      e


  (ppb)
regression
                                   T~

                                   10
12
    Figure 4.6

-------
vo
i
u
a
XJ
a
a
••_'

c
a
    u
    u
    c
    a
    u

    x
    a

    u
                Canister-Tena K Comparison for 1988-89
         3.5 -
          •5 ~
         2.5 -
          2 -
      1.5 -
         0.5 -
            0.2
                  1

                 0.6
 I

1.4
1.0
2.2
                               Canister concentration (ppb)

                             pair       	 regression
 I

2,6
    figure 4.7

-------
  J3
  a
  a
  ••_-*

  c
  a
vo '+>

•  e
  u

  a
  u

  x
  a

  u
  H
          0.2
               Canister-Tenax Comparison for 1988-69

                                  ETHYLBENZENE
                                        D
                                  a



                                  D
    ~T~

    0.6
                  D
                      pair
~~F~

0.6
Canister conccntratkn (ppb)

  	regression (n=39)
                                                                     1.2
   Figure 4.8

-------
            Canister-Tenax Comparison for 1988-89

                           META OR PARA XYLENE
                             a
_D
a.
a
5
£
U
c
a
u

K
D
C
U
I-
                                a
4 -
2 ~
      1  -
                        a  a
         D
               Jn
                 D
                        a
                   n  a
     D:TO DB°D
     a/a Q    n
          a
                                             i

                                             4
                         Canisstcr concentration (ppb)
                       par
Figure 4.9

-------
   a
   a.
  ••_••'
to

1   E
  u
  u
  c
  a
  Q
       1.2
         0,2
             Canister-Tenax Comparison for 1968-69
                             ORTHO-XYLZNE
   Figure 4.10

-------
I

M
LJ
                 Canister-Tenax for Jan "86 to Sep P89
                                  HEXANE tcrt.nl
130 -
120 -
no -
1 00 -
.- -.
90 -
a
c
a
| 70 -
u 60 •
u
c
o fin _
a
40 -
30 -
20 ~
10 -
o -
T
I




1
\
\

,
\
C^J C-

5 7 91113 2nd? 579
57911 4th3 579 1st3 579 2nd5
                            canbter
57
                                                                    M
    Figure 4.11a

-------
VD
I
    U

    D
r
n
P

E
<->
c

u

D
Q
                   Canisler-Teniix for Jan '86 to Sep "89
                                      HEXANE partial
4.5 -




 4 -




3.5 -




 3 -




2.5 -




 2 ~~




1.5 -




 1  -




0.5 -
           o


           M 111 11 111 11 U I 111 I 11 I H 11 11 111 111 11 111 M I 11 111 11 11 M 11 H I M 111 111 11 111 11 111 111 111 I

             5 7 91113  2nd? 57911 .?rd3 57911  4thi3 579 1^13 579 2nd3 3rd3 57    M
                               cantetcr
                                           y quarter
                                                  tenax
    Figure 4.lib

-------
CJ
CT,
   H
   D.
   CL
c
D
i5
*j
L
    E
    G
         2,6 -


         2.4 H
1.6 -


1.4


1,2 -


 1 -


0.0 ~


0.6 -j


0.4 '


0.2 ~


 0
                   Canister-Ten.ax for Jan P88 to Sep '89
                                   1,1,1-1
                                                                          •
              i M 1111
       5 7 91113 2nrf3 57911
                                       m ill 111 i 1111 11 111 i 11 11 11 11 11111 i 11 11 11 1111 11 11 I
                                   57911 4th3 579 1st3 579 2nd3 3rt3 57
                                        ^5 b'
                                                                          M
    Figure 4.12

-------
  a
  a.
  DL
'  5
  §
                 Canister-Ten.ax for Jan "68  to Sep "89
        4,5
         4 -
        .3.5 -
2.5 ~
         i —
        1.5 -
        0.5 -
                                     BENZENE
            11111 n 111 M 11 n 11 M 1111111111 n 11 ii 11111 n n 111111111111 M 1111 M n in 1111111 n 11111

              5 7  91113 2nd? 57911  3n*3 57911  4th3 579 Ist3 579 2ncE 3rd3 5 7   M
                                     «T5 b
                     canbter
                                                  tenax
   Figure 4.13

-------
to
I
09
   J3
   a
   a
   c
   a
   u
   u

   D
   a
                Canister-Tena* Comparison for 1968-69

                                 Carbon Tetn*;nlaride
         0.6
         0.5 -
         U.4 -
         0.3 -
         0.2 -
         0.1 -
     a
                                   A
             M 111111111 in 111111111111' 11111111111111111111111111111111firmTrTTTTTTTTIT

              35791113151 357911131  357911131  3579135791 3 51 357   X
tcnax
                                        by Quarter

                                          ^   can mdl
ten mdl
   Figure 4.14

-------
vo
I
VO
   _n
   a.
   a
c
a
   c
   u
   u

   0
   Q
               Canister-Tenax Comparison for 1966-69
0.4 -
0.35 ~
0.3 ~

0.25 -
0.2 -
0.15 -
0.1 -
0.05 -
o -

4-
a c


0 *




D
1

1 O



A AA 4
1 1 M 1 M 1 1 1 1 II 1 1 M 1 II 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 II 1 1 1 1 1 1 Ml 1 1 1 1
111 HIM 111 iiirmrrrn



i






1357 9 111315 1357 9 1113 1 3 5 7 9 1 113 1 3 5 7 9 1 3 5 79 1 3 51 3 5 7 X
                      tenax
                                   ty Quarter

                                     
-------
-D
a
a.
c
a
11
u

n
U
               Canister-Ten ax for Jan '88 to Sep '89
14



13



12



11


10



 9


 g


 j



 6



 g



 4
       -7 -
       1 -
       0
                                    TOLUENE
           IT I I

          *t3 5 7 91113 2nd? 57911  ^rxJ3 57911 4th3 579 Ist3 579  2no3 3rd3 5 7   M
                                5ampl<55 try quarter
                                                  tcnax
 Figure 4.16

-------
   -D

   D
   ..
Ifl
M  E
   u

   a
   • .
                  Canister-Tenax for Jan P88 to Sep '89
                                 TETRACHLOROETHENE
         3.5 -
          -» 	
2.5 -
1,5 ~
          1 -
        0.5 -
                                            >

                                  '3
             IN111 11 111 11M I 111 111 11 111 11 111 I I I 11 111 111 11 111 11 111 111 111 11 111 111 III11 11 11II11 I

              3 5 7 91113 2nd3 57911 3rt3 57911 4th3 579 Ist3 579 2nrf3 3rrJ3 5 7   M
   Figure 4.17

-------
              Canister-Ten ax for Jan '88 to Sep '89
                                ETHYLBENZENE






D
a
D.
c
D
E
Concent



.1. ^
.1 -
2.0
2.6 -
2.4
2.2 ~

2 -

1.0 -

1.6 -
1.4
1.2 -
1
O.R ~
0.6 -
0.4
0.2 -
— ,
.
•











n1














t \^l f II «
Iv 1 1 / \ ; •**• i J ft

Jl'k ' pfte ^''jr33 1\1\ S ^' n
n 1 1 1 1 1 1 1 1 M 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 M 1 1 1 1 1 1 1 1 1 1 1 1 1 M i f 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 M 1 1 1
            5 7 91113 2nd? 57911  CinJ.3 57311 4th3 579 Ist3 579 2nd3 3nJ3 57   M
                          canister
                                   «^5 t»>- q
tcnax
Figure 4.18

-------
a
a
a
c
a
u
u
c
a
O
               Canisler-Teivax for Jan '88 to Sep '89

                                 m/p XYLENE
       4 -
       g -
           0|
                                                                   -I-



                                                                   IH
II           Ml


 0 5 7 91 11."5 2nd? 5 7 911  3nd3 57911  4th3 579



                         5 ty quarter

            a  canbter            +
579  2nrf3 5nd3 5 7
                                                                   M
 Fiaure 4.19

-------
   a
   L.
   D
H
   u

   o
                  Canister-Tenax for Jan '88 to Sep '89
                                         SffLEME
1.4 -

1.3 -

1.2 -

1.1 -\



0.9

O.R

0.7

0.6

0.5

0.4

0.3

0.2

0.1

  0
nf



                            J/

                          1
                           f,1 *
             11111111111 n i n 111111 n 111111 n 1111111111111111 H 111111 H i n 1111111 u 11111 n 1111111
                5 7 91113 2nd? 57911  ."intf 57911  4th3 579 l^W 579  2nd3 3rt3 5 7   M

                                   5ampl«T5 by
    Figure 4.20

-------
cn
    c
    D
    U
    II
    £
c
a
    ii
    a
      1,5
      1.0
      1.7
      1.6
      1.5
      1.4
      1,3
      1.2
      1.1
       1
      0.9
      0.0
      0.7
      0.6
      0,5
      0.4
      0.3
      0.2
      0,1
       0
        a
Figure 7.1
                       Quantification of Internal Standards
                                     ly mean:? far sub^set of
                     _.V---"
                       \
                            \
                     4q57
                    internal
                        1q00
                                                      Iq03
                                                   2nd internal
2qB9

-------
                Comparison of 1st kiternal standard
                          with H5 electron multiplier setting






u
T
•-
c
a
u
e
E
E
i+-
c
g
a
u
a






£
1.9 -
1.0 ~
1.7 ~
1.6 -
1.5 -

1.4 -
1.3 -

1.2 ~

1.1 -
1 -
0.9 ~
0.8 ~
0.7 ~
0.6 -
0.5 -
0.4 ~
0.3 -
0,2 ~
0.1 -










-•EL
__--~" "•-.,
--~~~~ '"•••. j)
a """-,, .--Q-_. r. 	 -- ^w~~
"'-•, _.--""" _.--^ 	 """^"-B—
,v 	 — •*— — — 1---"""" " B — ~-a-.^
"^-H







1 1 1 1 1 1 1 1
   4q87    Iq88


internal staid
3q88    4q88

Quarters
 1q09    2q89


MS ev multiplier
                                                                3q89
Figure 7.2

-------
10. NJIT VOCS QUALITY ASSURANCE REPORT
                  10-

-------
            New Jersey Institute of Technology

            Air Pollution Research Laboratory
           Final Quality Assurance Report


Staten Island/Northern New Jersey Air Toxics Project
                      April 1990
                   Dr. B. Kebbekus
                 Professor of Chemistry
      Department of Chemical Engineering, Chemistry
                        and
                 Environmental Sciences
              10-

-------
                                    Chapter 1

                                     Blanks
Tenax:
      Blanks are done on each batch of Tenax traps before they are used for sampling.
These blank data are not kept or reported, since they are simply used to determine that the
set of traps on the manifold has been properly cleaned. The blanks which accompany each
day's set of samples are the blanks which are reported here, and which are used for the cor-
rection of data. The data show that the average quantity of individual target compounds
varied considerably over the course of the project However, the levels were usually below
1 ng/trap, with benzene, toluene and xylene occasionally rising as high as 5 ng. These
amounts are usually much less than 10% of the amount found in samples, and have not
posed a problem.
Canisters:
      The canisters are each blanked before being sent to the field. No measurable con-
atminaton is expected in the canisters, and they are not used if there is any measurable
amount of the target compounds. The only major problem which arose with blanks in the
canister system was the problem with methylene chloride contamination in one of the bel-
lows pumps. This contamination was impossible to remove, although extensive purging and
mild wanning of the pump was tried. Finally, a considerable amount of data for this com-
pound at the Carteret site was lost because of the contamination of the pump. Since the
daily blanks for the canisters could not show problems with the sampling system and pumps
on site, the problem continued over a major period of time before it was detected and its
source determined.
Blank Data:
                                 10-

-------
      The data on the Tenax blanks is shown in Tables 1-1 to 1-9. These tables show the
average quantity in nanograms for each compound over each quarter of sampling. The
standard deviation of each group of data is given and the limits of the range of blanks at
the 95% confidence level is also calculated. Figures 1-1 to 1-4 show the blanks for several
compound plotted against time, showing that elevated blanks tend to come in sequential
groups. This is an indication that the techniques which lead to high quality analyses by this
method are sometimes quite subtle, and the causes of deviations are not always obvious.
Remediation of these problems takes time and careful checking.
      In the smaller volume samples, those taken at the lower flow on Tenax, a 1 ppb
sample contains approximately 20 ng of the compound, so it can be seen that the blanks
were not excessive.

-------
                         Table  l-l
Organization:  NJIT
                                     Sorbent:   Tenax
QUARTER OF
Jul . TO
BLANKS
Sep. ,
1987
95% CL


l.MeCL
2.DCM
3.C6
4 . CFor
5.111
6.BZ
7 . CC14
8. Trie
9.Tol
10 . Perc .
ll.pmX
12. oX
f Blanks
Run
12
12
12
12
12
12
12
12
12
12
12
12
Avg.
(ng)
0.30
0.00
0.69
0.00
0.56
1.84
0.00
0.00
1.18
0.09
0.70
1.02
Std.Dev
(ng)
0.62
0.00
1.13
0.00
0.79
1.72
0.00
0.00
0.82
0.17
0.90
0.61
Interval

-0.09
0.00
-0.02
0.00
0.06
0.76
0.00
0.00
0.66
-0.02
0.13
0.64
(ng)
0.69
0.00
1.40
0.00
1.06
2.92
0.00
0.00
1.70
0.20
1.27
1.40
                       Table 1-2



Organization:  NJIT                  Sorbent:  Tenax
QUARTER OF

I

l.MeCL
2.DCM
3.C6
4 . CFor
5.111
6.BZ
7.CC14
8. Trie
9.Tol
10. Perc.
ll.pmX
12. OX

I Blanks
Run
12
12
12
12
12
12
12
12
12
12
12
12

Avg.
(ng)
0.08
0.00
0.24
0.00
0.00
0.62
0.00
0.00
0.17
0.00
0.15
0.16
Oct . TO
BLANKS

Std . Dev
(ng)
0.23
0.00
0.73
0.00
0.00
1.36
0.00
0.00
0.33
0.00
0.36
0.44
Dec. , 1987
95% CL
Interval
(ng)
-0.06 0.22
0.00 0.00
-0.22 0.70
0.00 0.00
0.00 0.00
-0.24 1.48
0.00 0.00
0.00 0.00
-0.04 0.38
0.00 0.00
-0.08 0.38
-0.12 0.44
                             10-

-------
                           Table 1-3
Organization:  NJIT
Sorbent:   Tenax
QUARTER OF



l.MeCL
2.DCM
3.C6
4 . CFor
5.111
e.bz
7.CC14
8 . Trie
9.T01
lO.Perc.
ll.pmX
12. oX

# Blanks
Run
15
15
15
15
15
15
15
15
15
15
15
15

Avg.
(ng)
0.02
0.00
0.27
0.00
0.14
0.86
0.00
0.00
0.27
0.00
0.09
0.30
Jan. TO
BLANKS

Std.Dev
(ng)
0.08
0.00
0.38
0.00
0.42
1.22
0.00
0.00
0.47
0.00
0.26
0.63
Mar. , 1988
95% CL
Interval
(ng)
-0.02 0.06
0.00 0.00
0.06 0.48
0.00 0.00
-0.09 0.37
0.19 1.53
0.00 0.00
0.00 0.00
0.01 0.53
0.00 0.00
-0.05 0.23
-0.05 0.65
                          Table 1-4
Organization:  NJIT
Sorbent:  Tenax
QUARTER OF



1 . MeCL
2.DCM
3.C6
4 . CFor
5.111
6.BZ
7.CC14
8. Trie
9.Tol
lO.Perc.
ll.pmX
12. oX

* Blanks
Run
14
14
14
14
14
14
14
14
14
14
14
14

Avg.
(ng)
0.14
0.00
0.10
0.00
0.15
1.44
0.00
0.00
0.72
0.00
0.70
0.70
Apr. TO
BLANKS

Std . Dev
(ng)
0.38
0.00
0.19
0.00
0.54
1.64
0.00
0.00
0.86
0.00
1.06
0.90
Jun. , 1988
95% CL
Interval
(ng)
-0.08 0.36
0.00 0.00
-0.01 0.21
o.oo o.oo
-0.16 0.46
0.50 2.38
o.oo o.oo
o.oo o.oo
0.22 1-21
o.oo o.oo
0.09 1-31
0.18 1.21
                           10-

-------
                           Table 1-5
Organization:  NJIT                  Sorbent:   Tenax




l.MeCL
2.DCM
3.C6
4 . CFor
5.111
6.BZ
7.CC14
8. Trie
9.Tol
lO.Perc.
ll.pmX
12. OX
QUARTER

f Blanks
Run
15
15
15
15
15
15
15
15
15
15
15
15
OF

Avg.
(ng)
1.81
0.00
2.50
0.00
0.07
3.63
0.00
0.00
1.04
0.00
0.55
0.18
Jul . TO
BLANKS

Std.Dev
(ng)
1.08
0.00
1.10
0.00
0.18
1.48
0.00
0.00
0.49
0.00
0.46
0.34
Sep. ,
9
In

1.22
0.00
1.90
0.00
-0.03
2.82
0.00
0.00
0.77
0.00
0.30
-0.01
1988
5% CL
terval
(ng)
2.40
0.00
3.10
0.00
0.17
4.44
0.00
0.00
1.31
0.00
0.80
0.37
                          Table  1-6
Organization:  NJIT                  Sorbent:  Tenax
QUARTER OF Oct. TO
BLANKS
Dec. ,
1988
95% CL
1

l.MeCL
2.DCM
3.C6
4 . CFor
5.111
6.BZ
7.CC14
8. Trie
9.Tol
lO.Perc.
ll.pmX
12. oX
Blanks
Run
15
15
15
15
15
15
15
15
15
15
15
15
Avg.
(ng)
2.50
0.00
0.00
0.00
0.00
4.18
0.00
0.00
1.32
0.00
0.66
0.24
Std.Dev
(ng)
1.01
0.00
0.00
0.00
0.00
1.05
0.00
0.00
0.78
0.00
0.56
0.59
Interval

1.95
0.00
0.00
0.00
0.00
3.61
0.00
0.00
0.89
0.00
0.35
-0.08
(ng)
3.05
0.00
0.00
0.00
0.00
4.75
0.00
0.00
1.75
0.00
0.97
0.56
                            10-

-------
                          Table 1-7
Organization:  NJIT
Sorbent:  Tenax
QUARTER OF



l.MeCL
2.DCM
3.C6
4 . CFor
5.111
6.BZ
7 . CC14
8. Trie
9.Tol
lO.Perc.
ll.pmX
12. oX

# Blanks
Run
14
14
14
14
14
14
14
14
14
14
14
14

Avg.
(ng)
1.42
0.00
0.45
0.00
0.00
3.69
0.00
0.00
0.98
0.00
1.13
0.00
Jan. TO
BLANKS

Std.Dev
(ng)
0.95
0.00
0.83
0.00
0.00
2.49
0.00
0.00
0.78
0.00
1.00
0.00
Mar. , 1989
95% CL
Interval
(ng)
0.88 1.96
0.00 0.00
-0.02 0.93
0.00 0.00
0.00 0.00
2.26 5.11
0.00 0.00
0.00 0.00
0.53 1.42
0.00 0.00
0.56 1.70
0.00 0.00
                          Table 1-8
Jrganizat
ion: NJIT
Sorbent: Tenax
QUARTER OF




l.HeCL
2.DCM
3.C6
4 . CFor
5.111
6.BZ
7.CC14
8 . Trie
9.T01
lO.Perc.
ll.pmx
12. oX


# Blanks
Run
15
15
15
15
15
15
15
15
15
15
15
15


Avg.
(ng)
0.92
0.00
1.80
0.00
0.42
3.08
0.00
0.00
1.29
0.00
1.00
0.70
Apr. TO
BLANKS

Std.Dev
(ng)
1.29
0.00
2.15
0.00
1.46
1.71
0.00
0.00
1.81
0.00
1.13
0.76
Jun. , 1989

95% CL
Interval
(ng)
0.20 1.63
0.00 0.00
0.62 2.98
0.00 0.00
-0.39 1.22
2.14 4.01
0.00 0.00
0.00 0.00
0.30 2.29
0.00 0.00
0.37 1.62
0.28 1.12
                           10-    8

-------
                          Table 1-9




Organization:  NJIT                  Sorbent:  Tenax



               QUARTER OF   Jul.  TO  Sep. ,  1989



                               BLANKS
*

l.MeCL
2.DCM
3.C6
4 . CFor
5.111
6.BZ
7.CC14
8. Trie
9.T01
lO.Perc.
ll.pmX
12. oX
Blanks
Run
13
13
13
13
13
13
13
13
13
13
13
13
Avg.
(ng)
4.43
0.00
2.61
0.00
1.73
4.82
0.67
0.09
4.72
0.24
0.89
0.63
Std.Dev
(ng)
5.87
0.00
3.05
0.00
2.39
4.46
0.81
0.33
5.30
0.60
1.11
0.63
951
Inte
<
0.92
0.00
0.78
0.00
0.30
2.15
0.18
-0.10
1.55
-0.12
0.23
0.25
; CL
srval
>g)
7.95
0.00
4.44
0.00
3.16
7.49
1.15
0.29
7.90
0.60
1.56
1.01
                             10-

-------
         Fig. 1-1
              Tenax Blank, 1989


            Carbon Tetrachlorid
        201~
Q)
c
10
        0
        01/04
               03/05
             O.V04
                    07/0.5
09/01

-------
  Hg. 1-
      Tenox  Blank,  1989
            Benzene
01/04
       03/05
05/04
               DAII:
       07/03
09/01

-------
  Fig. 1-3
20
15
       enox Blank,  1989
            Toluene
01/04
       03/05

-------
         Fig. 1-4
               enax Blank,  1989
en
c
        20
10
         01/04
                p  &  m-Xylene
                03/05
05/04
                        D.Afll
                     07/03
                            09/01

-------
                                    Chapter 2

                                Replicate Samples
      Tenax: Because samples were being taken at two flows, and canister samples were
being taken at the same sites every sampling day, duplicate Tenax samples were not done.
      Canister Samples: As each canister contained sufficient sample for several injections
into the gas chromatograph, routine analytical procedure was developed in which each
canister was analyzed three times and the results averaged. These averages were reported
in the data tables. The three replicates were not entered into the computer spreadsheets of
record, and so are not readily available for study. However, two periods were studied to ob-
tain the reproducibility data for the canister samples. These periods from April to Decem-
ber, 1988 and from January to September 1989 cover early and later samples. The data
tables (Tables 2-1 and 2-2) show  that the avarages of three replicate analyses showed aver-
age standard deviations on the order of 10%. It is also obvious there was some improve-
ment  in the analytical technique between the early and later samples. The number of com-
pounds for which the relative standard deviation of the mean exceeded 10% dropped from
7 to only 3, and those were compounds which are detected at levels very close to the detec-
tion limit
      While these replicates are solely replications of the analytical procedure, and not of
the sampling system, the possible error sources in the sampling system are many fewer than
those  found when sample flows and the constancy of these flows are critical, as in absorbent
sampling. Flow rate into the canister has no bearing on the concentration found, as long as
the total amount of sample is kept within the limits imposed by the pressure rating of the
canister and the minimum volume of sample required  for analysis. Therefore it appears
that the analytical system contains the  major sources of variability in this system, and the
                                  10-   14

-------
replicates of the analysis are a good estimate of the overall error level of this analysis.
                                      10-   15

-------
                    Table 2-1




Organization:  NJIT           Sampling:   Canister
COVERING FROM Apr. TO Dec. , 1988
DUPLICATE SAMPLES



1 . MeCL
2.DCM
3.C6
4 . CFor
5.111
6.Bz
7.CC14
8 . Trie
9.T01
lO.Perc.
ll.pmX
12. OX

1 Run
(each 3 dup.)
19
19
19
19
19
19
19
19
19
19
19
19
SD Of
MEAN
(ppb)
0.00
0.00
0.07
0.01
0.08
0.06
0.03
0.02
0.14
0.04
0.07
0.03
SD Of
MEAN
(%)
-
-
7.71
18.48
10.07
4.63
13.42
15.89
5.01
15.28
10.71
12.78
                    Table 2-2




Organization:  NJIT           Sampling:   canister
COVERING FROM Jan. TO Sep. , 1989
DUPLICATE SAMPLES



1 . MeCL
2.DCM
3.C6
4 . CFor
5.111
6.BZ
7.CC14
8. Trie
9.T01
lO.Perc.
ll.pmX
12. oX

f Run
(each 3 dup. )
20
20
20
20
20
20
20
20
20
20
20
20
SD of
MEAN
(PPb)
0.13
0.00
0.05
0.01
0.08
0.08
0.02
0.01
0.14
0.01
0.10
0.05
SD of
MEAN
(%)
9.54
—
5.67
15.30
6.75
5.36
12.50
10.63
5.96
6.39
8.81
9.17
                              10-  16

-------
                                    Chapter 3

                               Distributed Volumes
      Tenax: To assure samples which were free of the influence of sample breakthrough,
samples were taken at two flows, 5 and 10 ml/min. This resulted in total sample volumes
over 24 hours of approximately 7 and 14 liters. If substantial and regular breakthrough is
occurring for any particular compound, the concentration determined for the lower flow
trap will exceed that determined for the higher flow sample. The statistics for the high and
low flow traps are shown for each quarter in Tables 3-1 to 3-9. Evidence of breakthrough is
most readily seen graphically. Figures 3-1 to 3-3 show the levels found for typical com-
pounds, benzene, hexane, and tetrachloroethylene, with the concentrations determined on
the two traps plotted against each other. The amount of difference between traps is indi-
cated by the distance of each point from the straight line with a slope of 1. Points below the
line are those where the high flow traps showed evidence of breakthrough.
       It can be seen that for many of the compounds, the majority of the samples fall be-
low the 1:1 line, but in most cases the deviation is within an acceptable limit, and in some
cases does not appear to be concentration dependant. For  example, in the case of benzene,
the points lie mostly along a line below, but parallel to the 1:1 line, while in the case of
tetrachloroethylene, the least squares line and the 1:1 line  diverge as concentrations in-
 crease.
       This would argue for separate causes of the differences. If sample is breaking
 through due to migration of the sample front through the tube, the amount lost should be
 proportional to the the concentration. The case of deviations which are constant, rather
 than proportional to the concentration may be related to problems with the blank.
       The t-test is used to determine if there is a significant difference between the results
 for samples done at the different flows. It appears that breakthrough is more of a problem

                                    10-   17

-------
later in the project than it was in the first few quarters. Actually, the small difference due to
breakthrough is more apparent in the later samples when the precision of the measurement
has improved. The larger amount of scatter in the earlier measurements masked the effect
of breakthrough. The apparantly significant differences in some quarters for the higher
boiling compounds are not due to breakthrough, but rather due to occasional cold spot
problems in the analytical system. A constant loss from two samples which contain masses
of material, differing by a factor of two will lead to apparent concentration differences.
                                  10-   is

-------
                          Table 3-1
Organization:  NJIT                  Sorbent:   Tenax
QUARTER OF Jul. TO
Sep. , 1987
DISTRIBUTED VOLUMES
*

l.MeCL
2.DCM
3.C6
4 . CFor
5.111
6.B2
7.CC14
8. Trie
9.T01
lO.Perc.
ll.pmX
12. OX
Pairs
Run
9
4
9
8
9
9
9
9
9
9
9
9
Avg.
Dif.
(PPb)
0.14
0.00
0.11
-0.01
-0.03
0.18
0.01
0.01
0.21
-0.03
0.17
0.04
Std.Dev
Avg. Dif
(PPb)
0.11
0.00
0.22
0.01
0.16
0.21
0.03
0.03
0.89
0.03
0.43
0.16
95* CL
Interval
T Test
(PPb)
-0.11
0.00
-0.40
-0.02
-0.39
-0.30
-0.06
-0.06
-1.80
-0.10
-0.81
-0.32
0.38
0.00
0.61
0.01
0.34
0.66
0.07
0.08
2.21
0.04
1.14
0.40
1.30
-
0.48
-0.83
-0.17
0.83
0.19
0.26
0.23
-0.90
0.39
0.25
T> 0.05
(Y/N)
N
-
N
N
N
N
N
N
N
N
N
N
                           Table 3-2
               QUARTER OF   Oct.  TO  Dec. ,  1987
DISTRIBUTED VOLUMES



l.MeCL
2.DCM
3.C6
4 . CFor
5.111
6.BZ
7.CC14
8. Trie
9.T01
lO.Perc.
ll.pmX
12. oX

# Pairs
Run
9
4
10
10
11
11
11
11
11
11
11
11
Avg.
Dif.
(PPb)
0.00
0.00
-0.42
0.00
-0.14
-0.24
0.01
0.01
-0.50
0.00
-0.30
-0.10
Std.Dev
Avg. Dif
(PPb)
0.06
0.00
0.42
0.00
0.12
0.48
0.02
0.03
1.42
0.03
0.41
0.14
95% CL
Interval
(PPb)
-0.14 0.13
0.00 0.00
-1.35 0.51
0.00 0.00
-0.40 0.12
-1.30 0.82
-0.03 0.04
-0.06 0.07
-3.62 2.61
-0.06 0.07
-1.20 0.60
-0.41 0.21

T Test

-0.03
_
-1.01

-1.20
-0.50
0.31
0.27
-0.36
0.14
-0.73
-0.73

T> 0.05
(Y/N)
N

N
N
N
N
N
N
N
N
N
N
                               10-  19

-------
                           Table 3-3


Organization:  NJIT                   Sorbent:  Tenax
              ^^memmmmm*                           ^^^^^a

               QUARTER OF   Jan.   TO  Mar.  ,   1988


                         DISTRIBUTED  VOLUMES
I

l.MeCL
2.DCM
3.C6
4 . CFor
5.111
6.BZ
7.CC14
8. Trie
9.Tol
lO.Perc.
ll.pmX
12. oX
Pairs
Run
12
12
12
12
12
11
12
12
10
12
12
12
Avg.
Dif.
(ppb)
0.06
0.00
0.17
-0.01
0.17
0.36
0.05
0.02
-0.04
0.06
0.13
0.14
Std.Dev
Avg. Dif
(Ppb)
0.02
0.00
0.11
0.01
0.05
0.22
0.02
0.01
0.27
0.02
0.09
0.07
95=
Int<
(PI
0.02
0.00
-0.08
-0.02
0.05
-0.13
0.00
0.00
-0.65
0.01
-0.08
-0.02
k CL
srval
?b)
0.11
0.00
0.41
0.01
0.28
0.85
0.09
0.04
0.57
0.11
0.33
0.30
T Test

2.95
-
1.50
-1.07
3.11
1.63
2.40
1.95
-0.14
2.47
1.34
1.91
T> 0.05
(Y/N)
Y
-
N
N
Y
N
Y
N
N
Y
N
N
                            Table 3-4
               QUARTER OF   Apr.  TO  Jun.  ,  1988
DISTRIBUTED
*

l.MeCL
2.DCM
3.C6
4 . CFor
5.111
6.BZ
7.CC14
8. Trie
9.Tol
lO.Perc.
ll.pmX
12. OX
f Pairs
Run
13
13
13
11
13
13
13
13
13
13
13
13
Avg.
Dif.
(ppb)
0.05
0.00
0.10
0.00
0.21
0.20
0.05
0.01
0.41
0.07
0.12
0.04
Std.Dev
Avg. Dif
(ppb)
0.05
0.00
0.27
0.03
0.12
0.25
0.04
0.02
1.00
0.05
0.27
0.09
VOLUMES

95% CL
Interval

T Test
(PPb)
-0.06
0.00
-0.49
-0.06
-0.05
-0.33
-0.04
-0.04
-1.76
-0.03
-0.47
-0.15
0.15
0.00
0.69
0.05
0.48
0.73
0.14
0.05
2.57
0.17
0.71
0.23
0.97
-
0.37
-0.20
1.72
0.83
1.29
0.40
0.41
1.53
0.44
0.46

T> 0.05
(Y/N)
N
-
N
N
N
N
N
N
N
N
N
N
                                  10-   20

-------
                          Table 3-5



Organization:  NJIT                  Sorbent:  Tenax
QUARTER OF
Jul . TO
DISTRIBUTED


l.HeCL
2.DCM
3.C6
4 . CFor
5.111
6.BZ
7.CC14
8. Trie
9.Tol
lO.Perc.
ll.pmX
12. oX

f Pairs
Run
27
27
27
27
28
27
27
24
27
27
27
26

Avg.
Dif .
(PPb)
0.14
0.00
0.34
0.00
0.19
0.30
0.03
0.01
0.44
0.02
0.09
0.03

QUARTER OF
Std.Dev
Avg. Dif
(PPb)
0.03
0.00
0.28
0.01
0.14
0.19
0.03
0.02
0.72
0.05
0.26
0.08
Table 3-6
Oct. TO
DISTRIBUTED



l.MeCL
2.DCH
3.C6
4 . CFor
5.111
6.Bz
7.CC14
8. Trie
9.Tol
lO.Perc.
ll.pmX
12. oX

# Pairs
Run
29
29
29
29
29
29
29
29
. 29
29
29
29
Avg.
Dif.
(PPb)
0.20
0.00
0.08
0.00
0.08
0.17
0.01
0.01
0.42
0.02
0.16
0.05
Std.Dev
Avg. Dif
(ppb)
0.03
0.00
0.03
0.00
0.02
0.06
0.00
0.00
0.15
0.00
0.08
0.03
Sep. ,
VOLUMES
1988

95% CL
Interval

0.09
0.00
-0.24
-0.02
-0.10
-0.10
-0.03
-0.03
-1.04
-0.08
-0.44
-0.14

Dec. ,
VOLUMES

(PPb)
0.19
0.00
0.91
0.02
0.48
0.70
0.09
0.04
1.92
0.12
0.61
0.20

1988

95% CL
Interval

0.14
0.00
0.03
0.00
0.05
0.05
0.00
0.00
0.12
(PPb)
0.25
0.00
0.14
0.00
0.12
0.29
0.02
0.02
0.73
0.01 0.03
-0.01
0.00
0.33
0.10


T Test

5.43
-
1.20
0.35
1.36
1.54
0.93
0.33
0.61
0.36
0.34
0.38




T Test

7.78
-
3.23
-
4.66
2.84
3.48
1.57
2.81
4.31
1.98
1.99


T> 0.05
(Y/N)
Y
N
N
N
N
N
N
N
N
N
N
N




T> 0.05
(VN)
Y
_
Y
_
Y
Y
Y
N
Y
Y
N
N
                                 10-  21

-------
                           Table 3-7
Organization:  NJIT                  Sorbent:   Tenax
QUARTER OF Jan. TO
DISTRIBUTED
*
l.MeCL
2.DCM
3.C6
4 . CFor
5.111
6.BZ
7.CC14
8. Trie
9.Tol
lO.Perc.
ll.pmX
12. oX
Pairs
Run
31
31
28
29
28
30
28
30
29
30
31
Avg.
Dif.
(PPb)
0.00
0.09
0.00
0.05
0.20
0.01
0.00
0.35
0.03
0.22
0.12
Std.Dev
Avg. Dif
(PPb)
0.00
0.06
0.00
0.03
0.08
0.01
0.00
0.16
0.01
0.10
0.05
Mar. , 1989
VOLUMES
95% CL
Interval
(PPb)
0.00
-0.03
0.00
-0.01
0.04
0.00
0.00
0.02
0.01
0.01
0.01
0.00
0.21
0.00
0.11
0.36
0.02
0.01
0.68
0.05
0.43
0.23
T Test
-
1.57
-
1.58
2.52
1.37
0.79
2.18
4.04
2.11
2.30
T> 0.05
(Y/N)
—
N
-
N
Y
N
N
Y
Y
Y
Y
            Table 3-8
QUARTER OF   Apr.  TO  Jun.
                                              1989
DISTRIBUTED
*
l.MeCL
2.DCM
3.C6
4 . CFor
5.111
6.BZ
7.CC14
8. Trie
9.Tol
lO.Perc.
ll.proX
12. oX
\ Pairs
Run
50
48
51
50
49
51
51
48
51
48
48
Avg.
Dif.
(PPb)
0.00
0.24
0.00
0.08
0.18
0.02
0.00
0.11
0.01
0.04
0.07
Std . Dev
Avg. Dif
(PPb)
0.00
0.07
0.00
0.02
0.05
0.01
0.00
0.12
0.01
0.04
0.02
VOLUMES

95% CL
Interval
(PPb)
0.00
0.09
0.00
0.04
0.08
0.01
0.00
-0.14
-0.01
-0.04
0.02
0.00
0.39
0.01
0.12
0.28
0.03
0.01
0.36
0.03
0.12
0.12

T Test
_
3.33
1.07
4.04
3.60
2.86
0.95
0.90
0.89
1.07
3.03

T> 0.05
(Y/N)
_
Y
N
Y
Y
Y
N
N
N
N
Y
                                 10-  22

-------
                          Table 3-9
Organization:  NJIT                  Sorbent:   Tenax
QUARTER OF
Jul.
TO
Sep
. , 1989
DISTRIBUTED VOLUMES

l.MeCL
2.DCM
3.C6
4.CFor
5.111
6.BZ
7.CC14
8. Trie
9.Tol
lO.Perc.
ll.pmX
12. oX
1 Pairs
Run
47
47
47
47
47
47
47
47
47
47
47
47
Avg.
Dif .
(PPb)
0.93
0.00
0.17
0.01
0.22
0.30
0.07
0.02
0.51
0.07
0.21
0.12
Std.Dev
Avg. Dif
(PPb)
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
42
00
09
01
07
08
03
01
31
05
12
06
0
0
-0
-0
0
0
0
-0
-0
-0
-0
-0
95% CL
Interval
(PPb)
.09
.00
.01
.01
.07
.14
.00
.01
.12
.03
.04
.01
1.77
0.00
0.35
0.04
0.36
0.46
0.13
0.04
1.13
0.17
0.45
0.25
T Test
2.
-
1.
1.
3.
3.
1.
1.
1.
1.
1.
1.
21

91
19
02
74
89
48
63
46
70
81
T> 0.05
(Y/N)
Y
-
N
N
Y
Y
N
N
N
N
N
N











                                  10-  23

-------
V »
2

I
m
CL
CL
  o
  10
      6
            Fig. 3-1

            Comparison of Low and  High  Flowrate
                            (Benzene, 1—6/89)
      5 -
      A- -
2 -
                          ~T
                          2
                                       T
                                       4
                                                       -50%
6
                            PPB (Low Rowrate)

-------
2

I
<<^f


CD
  o
  J
  01
           Fig. 3-2



            Comparison  of Low  and High Flowrate

                             (Hexanc 1-6/89)
                            PPB (Low Flowrute)

-------
2

I
L_

§
I
«^>

m

ft
 o
 I
           Fig. 3-3


           Comparison of  Low  and High  Flowrate

                             (Pcrc,1-6/B9)
        0
                           PPB (Low Flowrate)

-------
                                    Chapter 4

                            Tenax vs. Canister Analyses
      At the two sites, Elizabeth and Carteret, canister samples were taken each sampling
day, along with the Tenax samples. Tables 4.1 to 4.9 show the differences in the data ob-
tained by the two methods over the course of the project. While the differences between
the two methods were greater than the differences between the two Tenax tubes, and also
greater than the differences between the replicate canister analyses, the differences aver-
aged below 1 ppb for most compounds and for most quarters. There are no easily discern-
ible patterns of higher concentrations of certain compounds by one or the other method.
      In the first quarter of the project only three compounds were reported by the
canister method. These appear to show significantly higher levels on the canister analyses,
but the numbers of analyses are small, and the canister method was not optimized, and was
showing poor separation. In the second quarter only one compound, carbon tetrachloride
showed a significant difference between the methods, which can be attributed to the fact
that the canister method was being done with quantitation on the FID detector, while
Tenax samples were being quantitated using the ECD, which was less prone to interference
by the nearby benzene peak. The  first two quarters of 1988 show significantly larger con-
centrations in the  canister samples, which are probably the more accurate, as several cold
spots had developed in the Tenax system, leading to small losses of the heavier boiling
compounds.
      Early in 1989, a group of compounds which gave significant differences between the
two methods began to be evident. These were principally the chlorinated compounds,
which gave low results on the Tenax system for several months due to a loss of sensitivity in
the ECD detector. This can be seen graphically for 1,1,1-trichloroethane and


                                   10-   27

-------
tetrachloroethylene, in Figures 4-1 and 4-2. Other statistically significant differences scat-
tered over the length of the project occur mostly in the  compounds which are present in
the air at very low levels, just above the detection limits. The low levels of these samples
makes the occurrence of subtle biases, of unknown origin, in the two systems more likely.
This probably accounts for the fact that there appear to be significant differences in these
compounds from time to time. The average differences, even those which are statistically
significant, infrequently exceed 1 ppb, except during the period before April 1988, when the
canister analysis system was being refined.
       The variations between the two systems can be seen graphically for three typical
compounds, benzene, toluene and tetrachloroethylene in Figures 4-3 to 4-5. Toluene was
subject to some losses due to the recurring cold spot in  the Tenax system in the early part
of 1988.
       The two analytical systems were calibrated with  the same standard gas mixture, to
prevent any bias due to calibration from occurring. Since all analytical biases which  have
been discovered have been negative, usually due to losses of analyte at some point in the
system (cold spots, breakthrough, low detector sensitivity), when the two methods disagree,
and there is sufficient difference between the results to require a choice to be made, the
higher value is more likely to be closer to the actual level.
                                     10-   28

-------
                          Table 4-1
Organization:  NJIT                  Sorbent:  Tenax

               QUARTER OF   Jul.  TO  Sep. ,  1987

                         TENAX vs. CANISTER
 l.MeCL
 2.DCM
 3.C6
 4.CFor
 5.111
 e.Bz
 7.CC14
 8.Trie
 9.Tol
 lO.Perc.
 ll.pmX
 12. oX
           I Pairs
             Run
10
       Avg.
       Dif.
      (ppb)
-0.51
 7
 8
 •1.46
 •1.10
        Std.Dev
        Avg.Dif
         (PPb)
0.22
0.40
0.11
             95% CL
            Interval
             (PPb)
-1.00
 •2.41
 •1.35
                                 -0.02
-0.52
-0.85
                  T Test  T> 0.05
                           (Y/N)
         -2.32
 -3.67
•10.35
Y
Y
                           Table 4-2

               QUARTER OF   Oct.  TO  Dec.  ,   1987
TENAX VS. CANISTER



l.MeCL
2.DCM
3.C6
4 . CFor
5.111
6.BZ
7.CC14
8. Trie
9.Tol
lO.Perc.
ll.pmX
12. oX

# Pairs
Run
-
-
13
—
-
13
13
— ' '
13
13
13
13
Avg.
Dif.
(PPb)
.
-
-0.11
-
-
0.19
-0.07
-
-1.35
-0.02
-0.12
-0.03
Std
Avg
.Dev
.Dif


95% CL

Interval
(PPb)


0


0
0

1
0
0
0
_
Wk
.26
_
_
.35
.02
.
.01
.03
.31
.12


-0


-0
-0

-3
-0
-0
-0
w
•»
.68
_
_
.57
.12
_
.53
.09
.79
.29
(PPb)
_
^
0.
^—
—
0.
-0.
^
0.
0.
0.
0.

T Test

T> 0.

05
(Y/N)


46


95
02

83
05
54
24

^
-0.43

_
0.53
-3.06

-1.33
-0.63
-0.40
-0.24

_
N


N
Y

N
N
N
N












                                  10-  29

-------
                          Table 4-3
Organization:  NJIT                  Sorbent:   Tenax
QUARTER OF Jan. TO
Mar. ,
1988


TENAX vs. CANISTER
1 Pairs
Run
l.MeCL
2.DCM
3.C6
4 . CFor
5.111
6.BZ
7.CC14
8. Trie
9.Tol
lO.Perc.
ll.proX
12. oX
-
15
-
-
15
15
-
14
15
14
15
Avg.
Dif .
(ppb)
-
-0.31
-
-
-0.05
0.07
—
-3.85
0.09
-2.11
-0.50
Std.Dev
Avg. Dif
(PPb)
-
0.25
-
-
0.29
0.02
-
0.77
0.03
0.46
0.16
95% CL
Interval
(PPb)
-
-0.85
-
-
-0.68
0.03
-
-5.50
0.03
-3.09
-0.83
-
0.24
-
-
0.58
0.11
-
-2.19
0.14
-1.12
-0.16
T Test
-
-1.20
—
-
-0.16
3.54
-
-4.99
3.06
-4.58
-3.19
T> 0.05
(Y/N)
-
N
—
-
N
Y
-
Y
Y
Y
Y
                             Table 4-4
               QUARTER OF   Apr.   TO  Jun.  ,   1988
TENAX VS. CANISTER



l.MeCL
2.DCM
3.C6
4 . CFor
5.111
6.BZ
7.CC14
8. Trie
g.Toi
lO.Perc.
ll.pmX
12. oX

1 Pairs
Run
14
14
14
12
14
14
14
14
14
14
14
14
Avg.
Dif.
(PPb)
0.02
0.00
-0.20
0.04
-0.24
-0.24
0.00
0.03
-0.69
0.10
-1.60
-0.55
Std.Dev
Avg. Dif
(PPb)
0.04
0.00
0.30
0.02
0.14
0.24
0.03
0.02
0.85
0.03
.0.32
0.12
95% CL
Interval
(PPb)
-0.07 0.11
0.00 0.00
-0.84 0.45
0.00 0.07
-0.54 0.06
-0.75 0.27
-0.08 0.07
0.00 0.06
-2.52 1.14
0.03 0.17
-2.29 -0.90
-0.81 -0.29

T Test

0.40
•
-0.65
1.95
-1.73
-1.02
-0.06
1.98
-0.81
3.08
-4.91
-4.49

T> 0.05
(Y/N)
N
-
N
N
N
N
N
N
N
Y
Y
Y
                                10-  30

-------
                          Table 4-5
Organization:  NJIT                  Sorbent:   Tenax
QUARTER OP Jul. TO Sep. , 1988
TENAX vs. CANISTER



l.MeCL
2.DCM
3.C6
4.CFor
5.111
6.Bz
7.CC14
8. Trie
9.Tol
lO.Perc.
ll.pmX
12. oX

f Pairs
Run
27
27
27
27
27
27
27
27
27
27
27
27
Avg.
Dif.
(Ppb)
0.09
0.00
-0.73
0.00
-0.30
-0.09
0.00
0.00
-0.15
0.15
0.37
0.10
Std.Dev
Avg. Dif
(ppb)
0.06
0.00
0.57
0.01
0.15
0.20
0.03
0.01
0.74
0.04
0.22
0.08
95% CL
Interval
(PPb)
-0.04 0.22
0.00 0.00
-1.89 0.44
-0.02 0.02
-0.62 0.01
-0.50 0.31
-0.06 0.06
-0.03 0.03
-1.67 1.36
0.06 0.23
-0.08 0.83
-0.06 0.25

T Test

1.42
—
-1.28
0.23
-2.01
-0.46
0.00
-0.20
-0.21
3.61
1.67
1.25

T> 0.05
(Y/N)
N
N
N
N
N
N
N
N
N
Y
N
N
                           Table  4-6
               QUARTER OF   Oct.  TO  Dec. ,   1988
TENAX vs. CANISTER



l.MeCL
2.DCM
3.C6
4.CFor
5.111
6.Bz
7.CC14
8. Trie
9.T01
lO.Perc.
ll.pmX
12. oX

# Pairs
Run
29
27
29
29
29
29
?.9
29
29
29
29
29
Avg.
Dif.
(PPb)
0.16
0.00
0.22
-0.03
-0.24
0.50
-0.06
-0.03
1.90
0.01
0.94
0.31
Std . Dev
Avg. Dif
(PPb)
0.10
0.00
0.16
0.01
0.17
0.18
0.02
0.02
0.55
0.03
0.17
0.06
95% CL
Interval
(PPb)
-0.04 0.36
0.00 0.00
-0.11 0.55
-0.04 -0.02
-0.60 0.11
0.13 0.88
-0.10 -0.02
-0.06 0.00
0.78 3.01
-0.05 0.06
0.58 1.29
0.19 0.42

T Test

1.61
_
1.35
-4.74
-1.40
2.76
-3.19
-1.86
3.47
0.21
5.41
5.47

T> 0.05
(Y/N)
N
N
N
Y
N
Y
Y
N
Y
N
Y
Y
                                 10-  31

-------
                           Table 4-7
Organization:  NJIT                  Sorbent:   Tenax
QUARTER OF Jan. TO
Mar. ,
1989


TENAX vs. CANISTER
*
l.MeCL
2.DCM
3.C6
4 . CFor
5.111
6.BZ
7.CC14
8. Trie
9.Tol
lO.Perc.
ll.pmX
12. oX
Pairs
Run
22
22
23
24
24
24
24
24
24
23
23
Avg.
Dif.
(PPb)
0.00
0.17
-0.02
-0.36
0.40
-0.12
-0.05
1.28
-0.11
0.21
0.11
Std . Dev
Avg. Dif
(PPb)
0.00
0.18
0.00
0.11
0.20
0.02
0.01
0.63
0.03
0.34
0.10
95% CL
Interval
(PPb)
0.00
-0.20
-0.03
-0.58
0.00
-0.16
-0.07
0.02
-0.17
-0.49
-0.09
0.00
0.54
-0.02
-0.14
0.80
-0.08
-0.03
2.55
-0.04
0.90
0.31
T Test
-
0.91
-7.50
-3.39
2.00
-5.90
-4.87
2.05
-3.43
0.62
1.13
T> 0.05
(Y/N)
-
N
Y
Y
N
Y
Y
Y
Y
N
N
                            Table 4-8
               QUARTER OF   Apr.   TO  Jun.  ,   1989
TENAX VS. CANISTER



l.MeCL
2.DCM
3.C6
4 . CFor
5.111
6.Bz
7 . CC14
8. Trie
9.Tol
lO.Perc.
ll.pmX
12. oX

# Pairs
Run
_
27
27
27
27
27
27
26
27
27
28
27
Avg.
Dif.
(Ppb)
_
0.00
0.21
-0.02
-0.60
-0.02
-0.05
-0.03
0.06
0.07
-0.69
-0.26
Std. Dev
Avg. Dif
(PPb)
_
0.00
0.12
0.01
0.13
0.13
0.02
0.01
0.33
0.03
0.18
0.09
95% CL
Interval
(PPb)
_ _
0.00 0.00
-0.02 0.45
-0.04 -0.01
-0.86 -0.34
-0.28 0.24
-0.08 -0.02
-0.04 -0.01
-0.60 0.71
0.01 0.12
-1.05 -0.33
-0.43 -0.08

T Test

—
mm
1.81
-3.88
-4.80
-0.13
-3.19
-3.10
0.18
2.31
-3.92
-2.92

T> 0.05
(Y/N)
—
-
N
N
Y
N
Y
Y
N
Y
Y
Y
                                10-  32

-------
                         Table 4-9
Organization:  NJIT                  Sorbent:  Tenax
               QUARTER OF   Jul.   TO  Sep. ,   1989
                         TENAX VS. CANISTER
f

l.MeCL
2.DCM
3.C6
4.CFor
5.111
6.BZ
7.CC14
8. Trie
g.Tol
lO.Perc.
ll.pmX
12. oX
Pairs
Run
28
28
28
28
28
28
28
28
28
28
28
28
Avg.
Dif.
(PPb)
-0.02
-0.01
-0.05
-0.03
-0.65
-0.78
-0.05
-0.01
-0.39
0.17
-0.19
-0.05
Std.Dev
Avg. Dif
(PPb)
0.44
0.00
0.17
0.01
0.25
0.27
0.03
0.02
0.85
0.05
0.18
0.06
95
Inb
(p:
-0.92
-0.01
-0.40
-0.05
-1.15
-1.32
-0.11
-0.06
-2.13
0.06
-0.55
-0.18
% CL
erval
pb)
0.89
0.00
0.30
-0.01
-0.15
-0.23
0.01
0.04
1.35
0.28
0.18
0.08
T Test

-0.03
-5.29
-0.30
-2.85
-2.65
-2.90
-1.66
-0.45
-0.46
3.30
-1.05
-0.77
T> 0.05
(Y/N)
N
Y
N
Y
Y
Y
N
N
N
Y
N
N
                                   10-   33

-------
         Fig. 4-1
             1,1,1—Trichloroethane
                 Carferet,  1989
   o
   I
_

8:
         4
2
         0
         01/04
                02/15
                        Days
                     Ob/10
                                            Canister
                                    "lena-:

-------
         Pig. 4-2
  o
  I
  u
  U)
.O
Q
Q
             Te'trachloroethylene

                Carteret, 1989
        01/04
               02/15
05/10
              Taia<

-------
                Fig. 4-3
                      Benzene
                  Elizabeth,  1988
   o
   I
   o\
.£)
Q.
D
         0
          06/14
                                               Can isle'
                                 Teriax
      08/25        11 /05
07/20        09/30


           Days
                                      12/11

-------
                    Fig. 4-3 (cent)
                                     n / p n p
                                     > I I jL. V.' I  I V..*
                           """ 1 •     1     II      -1
                             i/'ohoth    i
                           .=«-. I I JL. . V.'l K..>' V.*' I I  I 4   U v
    o
    I
    U
    •si
.
Q
f)
              6
              4
              2
              0
               01/04
                          02/15
0.5/29
           Ob/10
0( >'v!

-------
                Fig. 4-4
Toluene
                 Carteret,  1988
 o
 I
 u
 09
.O
8
         0
          01/04
                 02/15
  03/28
         05/09
                                        Ll
                                               i ;j
                                              'I c* K ix
06/20

-------
             Fig. 4-4 (cont)
Toluene
                 Carteret,  1988
o
I
LJ
                                               L'i
                                               mnx
         07/02          09/24
                08/1,5
         11 /05
                12/17

-------
                 Pig. 4-5
                         exone
                  Elizabeth, 1988
Q.
Q
  o
  I
          06/14        08/25         11 ,/05

               07/20        09/JO        12/11


                          Days
                                                Carlisle'
                                                 ..! Kl v

-------
               Fig. 4-5(cont)
                       Hexone
                  Elizabeth,  1989
  H
  O
  I
_
o.
a.
                                      i\\\\
                                      rHJ v\i
                                    *: I   U
          01/04
                  02/15
0,5/29
                           Days
        05/10

-------
                                     Chapter 5

                                  Detection Limits
      Detection limits for all the target compounds are listed in Table 5-1. These were
constant over the span of the project. The higher detection limit for carbon tetrachloride is
due to its relatively difficult separation, as it elutes just after the much bigger benzene
peak. Compounds not detected in each analytical run were listed in the reported data as
being one half of the detection limit. The absolute quantitation for compounds whose usual
ambient concentration falls at or near the detection limit cannot be considered accurate.
Sub part-per-billion concentrations may show 100 to 200 percent errors, when the absolute
error is of the order of 0.1 ppb.
      Therefore, when a compound's level hovers around the detection limit, the results
can only be discussed in terms of orders of magnitude. However, the assurance that the
compound is not present at a substantially higher level than the detection limit is reliable.
This is sufficient for risk assessment purposes^.
                                   10-   42

-------
                   Table 5-1

           Minimum Detectable Levels
                     (ppb)

Chloromethane                             0.01
Dichloromethane                           0.01
Chloroform                                 0.01
1,1,1-Trichloroethane                        0.01
Carbon Tetrachloride                        0.05
Trichloroethylene                           0.01
Tetrachloroethylene                         0.01
Benzene                                   0.01
Toluene                                   0.01
Hexane                                    0.01
o-Xylene                                    0.01
m- and p-Xylene                             0.01
                    10-   43

-------
                                    Chapter 6

                         Performance Evaluation Samples
      The EMSL Tenax and canister spikes from August 1987, November 1987 and June
1988 are shown in Table 6-1 to 6-3.The first data set showed wide variations in the data.
The Telcmar desorber was exhibiting symptoms of a cold spot in the transfer system when
these traps were being analyzed, so that most of the compounds were hanging up badly,
and being carried over to subsequent samples. This was especially obvious in the
trichloroethylene, perchloroethylene and toluene analyses. The results alternate from high
to low, as sample material was lost from one sample and added to the next. Also, the losses
due to a hot spot at the end of the oven had not yet been detected.
   It should also be noted that the EPA was not informed, due to our oversight, of the
proper end to load the tube. This may have led to some tubes being desorbed from the op-
posite end from that in which they were loaded. Finally, the blank trap was found to be
contaminated, when it was analyzed, although all traps were clean when sent The fact that
the glass tube in which it was shipped was broken in transit may have contributed to the
contamination. More seriously, the blank was subjected to the same sample carryover as
the other samples.
      The samples from the EPA filled canisters contained more moisture than we had
encountered in the samples we had taken up to that time. Therefore, the on-column
cryogenic trap plugged before the entire sample had been transferred to the column. This
allowed only a portion of the sample to be focussed, while  most of it passed onto the
column without being focussed, after the separation had begun. The problem was eventual-
ly resolved by changing the carrier gas from pressure control to flow control, so that plug-
ging was eliminated. With the flow controller, a plugged column is immediately obvious,
                                   10-  44

-------
since the pressure would rise dramatically. Actually, this pressure rise seems sufficient to
keep the trap open. The problem of slow release of components from the focussing trap
was relieved by heating the trap momentarily before allowing it to return to the column
temperature. This evaporates the water, and frees the organic compounds. Heating this
trap sharpened the peaks, and improved the recoveries. Further, the liquid argon trap for
concentration'the sample was still in use at this time.
      The second set of samples done in November, 1987, showed much more consistency,
but were still low. This was finally attributed to the premature desorption taking place at
the bottom of the oven. The canister samples were not much improved, since the major
change, substitution of the -110 degree trap for the liquid argon trap had not yet been
made.
      The canisters sent to PEI for confirmatory analyses likewise showed improved
agreement over the course of the project The  early samples analyzed at PEI were done
with such high detection limits that few compounds were detected at all.  PEI split canister
data is shown in Table 6-4.
                                  10-  45

-------
                                                                (August, 1987)
Compound
Table 6-1   Results of EPA Spiked Samples

               Tenax spiked  tubes, ng/tube

        Spike  Reported      %Diff.          Spike  Reported
                     HDiff
Chloroform

11 itrlchloroethane

Carbon Tet.

Benzene

Trichloroethylene

Toluene

Perchloroethylene

o-Xylene

Overall average * difference
108
292
233
384
320
441
354
384
37,48
201,180
9, trace
357,282
288.213
268,80
122,26
28,10
                            -60

                            -35




                            -16

                            -21

                            -60

                            -79

                            -96

                            62%
64    trace

146   467,286,333     +147

116   126,118,tr       -30

192   238,26,273       -7

160   358,286.235     +83

221   450,294,386     +70

177   195,116,203     +3

192   13,3,100        -80

                       60*
     The Tekmar desorber was exhibiting symptoms of a  cold spot in the transfer sys-
tem when these traps  were being  analyzed, so that most of the compounds were  hang-
ing up badly, and being carried over to subsequent samples. This is especially obvious
in the trichloroethylene, perchloroethylene and toluene analyses. The results alternate
from high to low,  as sample material is  lost from one sample and  added to the next.
     It should also be noted that the EPA was not Informed, due  to our oversight,  of
the proper end to load the tube. This may have led to some tubes being desorbed from
the opposite end from  that in which they were loaded. Finally, the blank trap was
found to be contaminated, when it was analyzed, although all traps were clean when
sent.  The fact that the glass tube in which it was shipped was broken in transit may
have  contributed to the contamination.  More  seriously, the blank was  subjected to the
same  sample carryover as  the other samples.
Tenax Blank:

Chloroform
11 Itrichloroethane
Carbon Tet.
Benzene
trichloroethylene
toluene
perchloroethylene
o-xylene
        ng/trap  reported
        205
        115
        5
        190
        100
        10
        6
                                       10-  46

-------
                                 Table 6—1 (cont)

                                   Canister spikes
                         (August,  1987)
Compound


Chloroform

11 Itrichloroethane

Carbon Tet.

Benzene

trichloroethylene

toluene

perchloroethylene

o-xylene
Spike

^^^••M

3.9


2.8


3.2


4.2


3.8


2.8


3.2


2.9
  Reported
             H Difference
             A	B_
4.6

0.8

2.7

0.7

2.2

1.7

0.5

0.3
0.6
0.7

0.6

0.5

0.5

0.6
18

-71

-16

-83

-42

-39

-84

-90
-79
-83

-84

-82

-84

-83
     The  samples from the EPA filled canisters contained more moisture than we had
encountered in the samples we had taken all winter. Therefore, the on-column
cryogenic trap plugged before  the  entire sample had  been transferred to the column.
This allowed only a portion of the sample to be focussed. while most of it passed  onto
the column without being  focussed, after  the separation  had begun. The problem has
been resolved by changing the carrier gas from pressure control to flow control, so
that plugging has been eliminated. With the  flow controller, a plugged column is im-
mediately obvious, since the pressure would  rise dramatically. Actually, this pressure
rise seems sufficient to keep the trap open.  The problem of slow release of com-
ponents from  the focussing trap has been relieved by heating the trap momentarily
before allowing  it to return to the column temperature. This evaporates the water, and
frees the organic compounds. Heating this trap has sharpened the peaks, and improved
the recoveries.
                                       10-  47

-------
              Table 6-2   Results of EPA Spiked  Sanples
                          Tenax QA Samples for Staten  Island
                          VOC Methods Comparison  (NJIT)
                                                          (November,  1987)
Spiked, nq
Con pound
chloroform
1 , 1,1-trichloroethane
car bon tetrach 1 or i de
benzene
t , 2-d i ch 1 or oethane
trichloroethy lene
1,2-dichloropropane
to I uene
tetrach lor oethy lene
ch t orobenzene
ethy 1 benzene
o-xylene
bromoform
120
54
121
145
192
137
213
84
220
177
241
157
192
210
122
108
243
291
384
275
426
168
441
354
483
315
384
420
Reported, ng
120
15
51
52
69
NR
49
NR
50
37
NR
NR
68
NR
122
45
112
129
157
NR
159
NR
137
119
NR
NR
122
NR
Difference, %
120
-72
-58
-64
-64
—
-77
—
-77
-79
—
—
-65
—
122
-58
-54
-56
-59
—
-63
~
-69
-66
~
—
-68
—
NR - not reported

Tenax blank - o-xylene 5 ng (results uncorrected)
                                 10-  48

-------
                              Table  6-2  (cont)

                        Results  of EPA  Spiked  Samples
                       Oni?t*»r QA Samples for Staten Island
                       VOC Methods Comparison INJIT)
                                                          (November,  1987)
Compound
vinyl chloride
bromomethane
tr i ch lorof 1 uoromethane
chloroform
carbon tetrachloride
i ,2-d i ch 1 oroethane
1,1, 1-tr i ch 1 oroethane
tr i ch 1 oroethy 1 ene
1 , 2-d i ch 1 or opropane
benzene - dg
1 ,2-d i bromoethane
tetrach 1 oroethy 1 ene
toluene - dg
chlorobenzene
ethy 1 benzene
styrene
o-xylene
Spiked, ppb
A and 8
2.5
5.9
4.2
5.2
4.2
3.4
3.7
5.1
3.1
5.5
1.7
4.2
3.7
3.9
3.0
3.4
3.9
Reported,
A
NR
NR
NR
0.1
3.9
NR
2.6
3.5
NR
3.0
NR
3.8
2.5
NR
NR
NR
3.7
PPb
B
NR
NR
NR
5.0
5.8
NR
2.9
3.6
NR
3.7
NR
4.0
3.3
NR
NR
NR
5.5
Difference, %
A B
—
—
—
-98 -3.8
-7.1 38
—
-30 -22
-31 -29
__
-45 -33
—
-9.5 -4.8
-32 -11
— —
—
—
-5.1 41
*4R - not reported
                                    10-  49

-------
             Table  6-3  Audit Sample Results for Staten Island  Study
                                 (Tenax Tubes and Canisters)
                                                                      June 1988
Compound
chloroform
1,1,1 -tr i ch t oroethane
carbon tetrachloride
benzene
trlchloroethylene
toluene
tetroch 1 oroethy 1 ene
o-xylene
methyl ene chloride
m,p-xylene
Spiked, vtq
T-103
72
97
116
128
142
147
118
128
...
_..
T-109
72
97
116
128
142
147
118
128
__ _
M«
T-110
108
146
174
192
213
220
177
192
—
ww
ppb
Canister
4.8
4.7
4.6
4.3
5.6
4.8
4.9
4.9
4.6
— ~**
Reported,
T-103
79
97
163
155
175
233
155
118
...
•— -
T-109
85
103
167
155
176
234
162
118
——
••••
no
T-110
134
146
246
226
256
341
230
177
—
• *••»
ppb
Canister
4.1
6.6
4.4
4.0
5.4
5.3
4.9
2.4
3.4
0.1
Tenax-118 (Tenax blank):   benzene 2 ng, toluene 2  ng, o-xyl«ne 3 ng
                                Percent Bias of Audit Results
Compound
chloroform
1 1 1 1 1-tr i ch 1 oroethane
carbon tetrachlorlde
benzene
tr ichl oroethy 1 ene
toluene
tetrach 1 oroethy 1 ene
o-xy 1 ene
methyl ene chloride
T-103
9.7
0
40
21
23
58
31
-7.8
--
Dlas, *
T-109 T-110
18
6.2
44
21
24
59
37
-7.8
—
24
0
41
18
20
55
30
-7.8
~
Can i ster
-15
40
-4.3
-7.0
-3.6
10
0
-51
-26
                                     10-

-------
    Table 6-4
            Comparison of PEI and NJIT for Canister

Date
01/16/88
03/22/88
06/20/88
09/06/88
12/23/88
01/22/89
03/11/89
04/16/89
06/27/89
07/15/89
08/26/89
AVG.
SO

Date
01/16/88
03/22/88
06/20/88
09/06/88
12/23/88
01/22/89
03/11/89
04/16/89
06/27/89
07/15/89
08/26/89
AVG.
SD

PEI
ND
ND
ND
ND
ND
ND
ND
ND
ND
ND
ND
0.00
0.00

PEI
1.80
ND
ND
ND
1.20
1.30
ND
1.50
ND
1.00
2.20
1.50
0.80
MECL
NJIT
ND
ND
ND
ND
ND
ND
ND
ND
ND
ND
ND
0.00
0.00
C6
NJIT
2.00
0.15
1.47
1.59
1.51
1.83
1.28
1.52
0.70
1.11
1.33
1.32
0.49

BIAS
_
-
-
-
-
-
•
-
-
-
-
0.00
0.00

BIAS
-11.11
_
-
-
-25.83
-40.77
-
-1.33
-
-11.00
39.55
-8.42
18.85

PEI
ND
1.40
1.20
2.50
0.85
0.40
ND
260.00
1400.00
570.00
1.30
248.63
415.31

PEI
ND
ND
ND
ND
ND
ND
ND
ND
ND
ND
ND
0.00
0.00
DCM
NJIT
ND
UD
ND
ND
ND
ND
ND
ND
ND
ND
ND
0.00
0.00
CFOR
NJIT
ND
ND
0.08
0.02
0.04
0.04
0.04
0.04
0.07
0.04
0.02
0.04
0.02

BIAS
_
-
-
-
-
-
-
•
-
—
-
0.00
0.00

BIAS
^m
_
_
_
_
_
_
_
_
.
-
0.00
0.00
BIAS= (PEI-NJIT)/PEI*100
                               10-  51

-------
       Table 6-4  (cont)



             Comparison of PEI and NJIT for Canister

Date
01/16/88
03/22/88
06/20/88
09/06/88
12/23/88
01/22/89
03/11/89
04/16/89
06/27/89
07/15/89
08/26/89
AVG.
SD

Date
01/16/88
03/22/88
06/20/88
09/06/88
12/23/88
01/22/89
03/11/89
04/16/89
06/27/89
07/15/89
08/26/89
AVG.
SD



0

0
0
0

0
0
0
1
0
0







0



0

0
0

PEI
ND
.75
ND
.60
.90
.80
ND
.70
.60
.50
.20
.76
.38

PEI
ND
ND
ND
ND
ND
.20
ND
ND
ND
.30
ND
.25
.10




0
0
0
0
0
1
0
0
1
0
0


0
0
0
0
0
0
0
0
0
0
0
0
0
1,1,]
NJIT
ND
ND
.89
.55
.95
.95
.95
.26
.74
.65
.67
.96
.47
CC14
NJIT
.20
.03
.30
.10
.29
.33
.26
.24
.12
.52
.20
.24
.13
L




8
-5
-18

-80
-23
-30
-39
-26
24







-65



-73

-69
26

BIAS
_
-
-
.33
.56
.75
-
.00
.33
.00
.17
.92
.50

BIAS
_
-
-
-
-
.00
-
-
-
.33
—
.17
.74



0
1
1
2
1

3
0
1
2
1
0


0










0
0

PEI
ND
.85
.00
.80
.05
.70
ND
.10
.90
.00
.10
.61
.89

PEI
.50
ND
ND
ND
ND
ND
ND
ND
ND
ND
ND
.50
.14
BZ
NJIT
2.49
0.19
1.70
2.40
2.47
2.19
2.01
3.26
0.86
1.07
2.61
1.93
0.86
TRIG
NJIT
ND
ND
ND
0.08
0.07
0.09
0.08
0.09
0.05
0.06
0.09
0.08
0.04



77
-70
-33
-20
-28

-5
4
-7
-24
-11
34













0
0

BIAS
-
.65
.00
.33
.49
.82
-
.16
.44
.00
.29
.89
.29

BIAS
_
—
-
-
-
-
-
-
-
-
—
.00
.00
BIAS- (PEI-NJIT)/PEI*100
                              10-  52

-------
            Table 6-4(cont)

            Comparison of PEI and NJIT for Canister

Date
01/16/88
03/22/88
06/20/88
09/06/88
12/23/88
01/22/89
03/11/89
04/16/89
06/27/89
07/15/89
08/26/89
AVG.
SD

Date
01/16/88
03/22/88
06/20/88
09/06/88
12/23/88
01/22/89
03/11/89
04/16/89
06/27/89
07/15/89
08/26/89
AVG.
SD

PEI
3.10
3.15
5.10
5.30
3.40
3.10
ND
6.80
1.90
2.30
5.60
3.98
1.85

PEI
0.60
1.75
2.30
1.40
0.80
0.70
ND
3.20
0.70
0.90
2.10
1.45
0.89
TOL
NJIT BIAS
11.90 -283.87 *
3.30 -4.76
7.20 -41.18
8.30 -56.60
3.30 2.94
3.80 -22.58
7.90
5.70 16.18
1.50 21.05
1.90 17.39
4.60 17.86
5.40 -5.52
3.01 25.53
PMX
NJIT BIAS
3.80 -533.33 *
6.43 -267.43 *
3.07 -33.48
1.37 2.14
0.64 20.00
0.65 7.14
2.38
2.23 30.31
0.77 -10.00
0.57 36.67
1.43 31.90
2.12 10.59
1.71 21.50

PEI
ND
ND
ND
ND
0.20
ND
ND
0.20
0.20
ND
0.20
0.20
0.10

PEI
ND
0.60
0.90
0.50
0.30
0.30
ND
1.20
0.30
0.40
0.90
0.60
0.36
PERC
NJIT
0.10
ND
0.09
0.09
0.18
0.12
0.43
0.15
0.06
0.05
0.10
0.14
0.11
OX
NJIT
0.87
1.50
1.01
0.37
0.17
0.18
0.56
0.83
0.28
0.21
0.59
0.60
0.40

BIAS
-
-
-
-
10.00
-
-
25.00
70.00
-
50.00
38.75
23.24

BIAS
_
-150.00*
-12.22
26.00
43.33
40.00
-
30.83
6.67
47.50
34.44
27.07
19.81
BIAS- (PEI-NJIT)/PEI*100
*:Deleted in Avg.  and SD.
                                 10-  53

-------
                                    Chapter 7

                         Changes in Analytical Methodology
      The results of the QA samples done during the year showed that there were prob-
lems with the Tenax desorption system. It was determined that there was serious carryover
between one sample and the next. This was attributed to a cold spot in the desorber, which
was corrected by applying some insulation, to keep the tubing from being chilled when the
cryo trap was cooled. The second set of traps loaded for us by EMSL indicated that our
analysis was much more precise, but still had a significant bias on the low side. This was
finally traced to the desorption oven, which was still hot at its lower end, when the
temperature readout indicated that it was cool. This caused the sample at the end of the
tube to begin to desorb much before the first cryotrap was cooled to collect the sample.
This was addressed by removing the Tenax from the lower inch of the trap, so that the
warmed end would contain no sample. The third set of traps from EMSL, analyzed after
these improvements were made showed good sample recovery and quantitation.
      It was determined late in the first year that there was some interference with some
of the halogenated compounds, especially  carbon tetrachloride, which was giving much
higher values than were being obtained by other groups. The electron capture detector is
not subject to this interference, so the system was modified to obtain areas for the ECD
peaks as well as the FID. This change was made on the Tenax analyses in midsummer, and
on the canister system in early November.
      Finally, when the canister analysis system was first set up, the peaks were poorly
resolved at the beginning of the chromatogram. This was thought to be due to water con-
densing in the second cryotrap and  interfering with the rapid injection of the volatiles onto
the column. A Permapure drier containing a semipermeable membrane to remove water
                                    10-  54

-------
from the sample before the first trap was tried. This proved not to be successful. Further
study showed that the problem with water was not the main cause of the poor resolution. If
water did not enter the trap at a very rapid rate, it tended to freeze on the walls, allowing
the gas flow to pass through the tube center. If the trap was not plugged, there was no sig-
nificant effect on the resolution. However, the presence of carbon dioxide in the sample
was the major cause of the peak broadening. The gaseous carbon dioxide, which occupies a
volume of nearly half a milliter, in the average sample, expands rapidly from the solid state
in the focussing trap, and spreads the previously concentrated sample band. The problem
was addressed by raising the temperature of the first trap to -110°C, thus preventing the
trapping of carbon dioxide. This change was made in April, 1988. The data from canister
samples done prior to that time were removed from the database, except for a few late-
eluting compounds which  could be reasonably well measured.
      A summary of the improvements made in the VOC analysis, with the dates the
changes were implemented is shown in Table 7-1.
                                    10-   55

-------
July 1987

August/Sept
                 Table 7.1

Summary of Changes in Analytical Methodology

               Tenax Samples

Testing, no samples reported.

Late eluting compounds were not reported because a cold spot in the
Tekmar desorber caused carryover between samples for these less
volatile compounds.
Oct/March '88      All compounds reported, cold spot eliminated.

April '88           The length of Tenax in the traps was reduced to keep the adsorbent
                   bed out of the hot spot at the bottom of the desorber oven. Data from
                   previous analyses was not deleted, since the impact of this hot spot
                   was felt to affect the loaded performance evaluation samples much
                   more seriously than the actual samples.

Jan-June '89        Slightly lower values were reported for the chlorinated compounds
                   due to a somewhat diminished detector sensitivity. No data was
                   eliminated, as the results were not seriously different from the
                   canister results.
                                    10-   56

-------
                                Canister Samples
Sept 1987
Early compounds were not well separated. Only 3 compounds were
reported, and only FID detection was used.
Oct/March '88
Separation still poor, but ECD was installed for identification of
chlorinateds, so additional compounds are reported.
April/June
Major improvement in the canister analysis is accomplished by raising
the temperature of the concentrating trap, to avoid the trapping of
carbon dioxide. Some chlorinated compounds were still subject to in-
terference, and the ECD was not calibrated for quantitation at this
time.
July'88
All compounds were being determined, and the method was working
well.
                                       10-   57

-------
                                    Chapter 8

                  Assessment of the Data for Each Target Compound

                                     Chloromethane
      The variability of chloromethane was constant over the project time. While the
results appear to agree reasonably well from both analytical systems, experiments in our
laboratory show that both methods show substantially low results for this compound, due to
the fact that it breaks through on Tenax, and is not completely trapped if the temperature
of the concentrating trap in the canister system is not rigidly controlled at -110°C. Since this
temperature was controlled by a manually placed cold bath for much of the project, losses
invariably occurred. The data for this compound should only be used as "minimum levels
present".

Method      Time period        Number      Mean       MeanDiff.   SD of Mean
                               Samples      Cone       Between     Diff. of
                               Run         (ppb)       Pairs        Pairs (ppb)
Tenax       7/87-10/89        146         0.47         0.22         0.21
                                                        Pooled SD for 3
                                                        Replicates
Canister     7/87-10/89         98          0.61         0.07

                                 Dichloromethane
A substantial number of data points for this compound were lost because of a contamina-
tion in one of the bellows sampling pumps used in the canister system. The variability did
not change substantially over the course of the project. Most of the data points were very
near to the detection limits and therefore can only be considered as order of magnitude
measurements.
                                   10-   58

-------
Method

Tenax
Time period

7/87-10/89
Number
Samples
Run
217
Mean
Cone
(ppb)
0.01
Mean Diff.
Between
Pairs
0.0
SD of Mean
Diff. of
Pairs (ppb)
0.0
Pooled SD for 3




Replicates

Canister     7/87-10/89
                  145
           0.01
                                    Hexane
            Hexane showed good agreement between and within methods, and
laboratory experiments as well as performance evaluation samples showed acceptable
recovery for hexane.

Method     Time period

Tenax      7/87-10/89
Canister     7/87-10/89
Number
Samples
Run
225
Mean
Cone
(ppb)
0.87
Mean Diff.
Between
Pairs
SD of Mean
Diff. of
Pairs (ppb)
0.10 0.08
Pooled SD for 3
Replicates
                  185
            1.17
            0.06
                                   Chloroform
             Chloroform levels throughout the project were very near to the detection
limits and therefore the data must be be considered as order of magnitude measurements.
 Method      Time period
                  Number
                  Samples
                  Run
            Mean       Mean Diff.   SD of Mean
            Cone       Between     Diff. of
            (ppb)       Pairs        Pairs (ppb)
Tenax
7/87-10/89
223
 Canister     7/87-10/89
                  146
0.02
            0.04
0.0
0.01
                                                       Pooled SD for 3
                                                       Replicates
            0.01
                                     10-  59

-------
                              1,1,1-TrichIoroethylene
            The reliability of the analysis for this compound was improved several times
during the project, by substitution of the BCD detector for the FID in each system, and by a
change in the concentrating trap temperature to improve resolution.
            However, the Tenax method gave consistently lower results for this com-
pound than did the canister method. In the various performance evaluation and Shootout
samples, the Tenax method showed better agreement than did the canister. While we have
no evidence that there was an interference in the canister analysis which was not a problem
with the Tenax analysis, the PE samples and Shootout results lead us to have more con-
fidence in the Tenax results, where the two results differ.
Method
Tenax
Tenax
Time period
7/87-3/88
4/88-10/89
Number
Samples
Run
32
196
Mean
Cone
(ppb)
0.51
0.56
Mean Diff.
Between
Pairs
0.0
0.10
SD of Mean
Diff. of
Pairs (ppb)
0.04
0.04
Canister     7/87-3/88
Canister     4/88-10/89
0
149
1.06
Pooled SD for 3
Replicates
0.08
                                     Benzene
             Benzene showed good agreement between and within methods, and
laboratory experiments as well as performance evaluation samples showed acceptable
recovery for benzene.
                                   10-   60

-------
Method
Tenax
Time period
7/87-10/89
Number
Samples
Run
224
Mean
Cone
(ppb)
1.23
Mean Diff.
Between
Pairs
0.18
SD of Mean
Diff. of
Pairs (ppb)
0.08
Pooled SD for 3




Replicates

Canister     7/87-10/89
                  177
1.41
0.07
                               Carbon Tetrachloride
             The reliability of the analysis for this compound was improved several times
during the project, by substitution of the ECD detector for the FID in each system, and by a
change in the concentrating trap temperature to improve resolution.

Method      Time period
Tenax
Tenax
7/87-3/88
4/88-10/89
Number
Samples
Run
32
197
0
149
Mean
Cone
(ppb)
0.14
0.13
0.18
Mean Diff.
Between
Pairs
SD of Mean
Diff. of
Pairs (ppb)
0.02 0.0
0.03 0.01
Pooled SD for 3
Replicates
0.03
0.02

 Canister     7/87-3/88
 Canister     4/88-10/89
                                 Trichloroethylene
             The reliability of the analysis for this compound was improved several times
 during the project, by substitution of the ECD detector for the FID in each system, and by a
 change in the concentrating trap temperature to improve resolution.
                                   10-   61

-------
Tenax
Tenax
Canister     7/87-3/88
Canister     4/88-10/89
Time period
7/87-3/88
4/88-10/89
Number
Samples
Run
32
192
Mean
Cone
(ppb)
0.12
0.05
Mean Diff.
Between
Pairs
0.01
0.01
SD of Mean
Diff. of
Pairs (ppb)
0.01
0.0
0
148
0.06
Pooled SD for 3
Replicates


0.01
                                     Toluene

             Changes in the concentrating trap temperatures for the canister system and

the detection and elimination of the cold spot problems in the Tenax desorption system al-

lowed improvements in the quantitation of this compound.
Method
Tenax
Tenax
Canister
Canister
Time period
7/87-6/88
7/88-10/89
7/87-3/88
4/88-10/89
Number
Samples
Run
43
181
27
149
Mean
Cone
(ppb)
2.47
3.92
4.83
3.6
Mean Diff. SD of Mean
Between Diff. of
Pairs Pairs (ppb)
0.02 0.43
0.37 0.17
Pooled SD for 3
Replicates
0.14
0.14
                                Tetrachloroethylene

             Remediation of the cold spot problems in the desorption system and substitu-

tion of the ECD in the analytical systems improved the analysis of this compound.
                                    10-   62

-------
Method
Tenax
Tenax
Time period
7/87-6/88
7/88-10/89
Number
Samples
Run
45
183
Mean
Cone
(ppb)
0.18
0.20
Mean Diff.
Between
Pairs
0.03
0.03
SD of Mean
Diff. of
Pairs (ppb)
0.01
0.02
                                                       Pooled SD for 3
                                                       Replicates
Canister
Canister
7/87-3/88
4/88-10/89
28
149
0.11
0.14
0.04
0.01
                                  m & p-Xylene
            The cold spot problems in the Tenax analysis system caused low values for
this compound in the early stages of the project. The samples done before 7/88 should be
considered low.
Method
Tenax
Tenax
Time period
7/87-6/88
7/88-10/89
Number
Samples
Run
45
181
Mean
Cone
(Ppb)
0.77
1.12
Mean Diff.
Between
Pairs
0.03
0.14
SD of Mean
Diff. of
Pairs (ppb)
0.12
0.06
Pooled SD for 3
Replicates
Canister     7/87-10/89         183          1.63         0.09

                                     o-Xylene
             The cold spot problems in the Tenax analysis system caused low values for
this compound in the early stages of the project. The samples done before 7/88 should be
considered low.
                                    10-   63

-------
Method
Tenax
Tenax
Time period
7/87-6/88
7/88-10/89
Number
Samples
Run
45
181
Mean
Cone
(ppb)
034
037
Mean Diff.
Between
Pairs
0.03
0.08
SD of Mean
Diff. of
Pairs (ppb)
O.C3
0.02
                                                        Pooled SD for 3
                                                        Replicates
Canister     7/87-10/89         184         0.72         0.04
                                  10-  64

-------
11. PAPER ON EMISSIONS INVENTORY DEVELOPMENT FOR
       PUBLICLY-OWNED TREATMENT WORKS
                      11-1

-------
                             (HI ealaatona Inventory Development
                         tor Volatile Organic Compounds Iron
                        Publicly Owned Treatment Mark* In the
                  H*tt fork and N«v Jersey Otoat Nor»tt«lnment Areas
                                   Koch C. neemantfe
                                        M*rtlno*lch
 I
ro
Air and M**t* Management Division
 Environmental Protect loo Aoency
            lUglon ||
         if Federal riaaa
     M*« fork. Ne« Tork 10310

           October IttJ
                                          541
                                                                                                    •EPOHT CM EMISSIONS INVENTOM DEVELOPMENT Po* VOLATILE
                                                                                                    ORGANIC COMPOUNDS IHOH PUBLICLY OWNED TREATMENT WORKS
                                                                                                   IM THE HEN YORK MID NEW JtXSEI OZONE
Publicly Owned Treatw-nt Works IPoiWal . *ora ccuMnly knovn
•s savage treatment pluiti, ar« Increasingly 9alnin9
Mttonal attention •• twlng inrqe MUt«r« of wclattl*
organic compounds tVOCat «nd aJrbarne toiclci.  Ttm
EnvironiMiitBl Ptotectlan *}OKr |K>M MV! tlw Btttea do not
nov regulate voc mi.alon. fro. rortM. He h«««  in
anticipation ot poat-l*l7 SiP pluming . cwvSuctea a
pretlainary atuoy or tlw POTVs in the otona nonatl«ln>ent
area* of New Tort  and Hew
Jersey (the entire State 1. nonattaliwentl .  Ualng data
obtained froai pretraatMnt report* on volatile organica in
the Influent atreaM to the POTWa Blong with the percent
reaorals of tlMee organic* at each plant ana eetluted
volatilization percentage* or each pollutant (obtained fro»
the Becoxl tO CQMreaa OH UtS nlBchargg d Haiaraoim
tfl PjlIOlcUt OMlfia TreatMnt UQtkal. «• have
                                                                                                «w result, are «l9nlttcaj)t.  KWM» In our area appear to
                                                                                                emit aore than 10,000 tone of VQCa per year.  T»lil«
                                                                                                roughly «qu»l to the enlsalon raductlona projected to be
                                                                                                achievable through the Implementation of Individual
                                                                                                •extraordinary a*a3ures* aoch aa the control of VOC« from
                                                                                                •uto reflniahing oper*tloiH or architectural surface
                                                                                                coatinga.  Thi» report mttlinea the ctepa used in developing
                                                                                                the eatiuted eailaalona Inventory of VOCs fro> rorwa and
                                                                                                further coopares the retulta to the extraordinary aaaaurea
                                                                                                under atudy in Region u.  The result* strongly auagest that
                                                                                                a BMil number of pOTHa In the Deglon may be Major source*
                                                                                                or voca. each emitting greater than 100 tona pet rear.
                                                                                                "hlJe no air aonttorln? atudlaa were done to support these
                                                                                                eiflBAtea, aoeie air data la available and these aseia to
                                                                                                support our conclusions.  The results also suggest that EPA
                                                                                                and the atatea mat consider POTWa in a comprehensive post-
                                                                                                l«7 planning effort to attain the national aatolent air
                                                                                                quality standard for oxone.
                                                                                                   349

-------
 Our estimates of the percent of the organlcs that volatilize
 from the  amount removed were also based upon the assumption
 that each system was not acclimated.  We used Table «.• in
 TJU IftBOJCt  to Cunqreaa. which also lists the average
 fractions released  lue chose the •Unacclimated Median
 Release"  values).   Nhen this assumption Is Bade,
 volatilization becomes the dominant mechanism for the
 removal of  volatile organic* tin an acclimated system,
 blodegradatIon plays a much larger role). 141  Ths values
 listed In this table are based upon each Individual
 chemical's  Henry's  Constant and solubility, among other
 factors.

 There are better methods to estimate the percent subject to
 volatilisation at a specific POTW. but these imply
 knowledge of detailed information at the PO1M. Including
 wlndspeeds  and volumes of aeration tanks.  However, our
 Intention was to attempt to simplify these calculations
 because we  didn't have such information available at the
 time this paper was written.  For alternate methods, see
 Namkung and Rlttman. "Estimating Volatile Organic Compound
 (VOC1 Emissions from Publicly Owned Treatment Works (fonts).
 JWPCr. St.  »70. 1»«7; and Coral. Chang. Schroeder and Olu.
 •Emissions of Volatile and Potentially Toxic Organic
 Compounds from Hun I cl pal Wastewater Treatment Plants" APCA
 meeting.  Mew fork. Nr.  a7-»S.7.  June 1»«7.

 With this Information,  we simply multiplied the  influent
 concentration by the percent removal  to give the amount of
 the influent removed.   Multiplying this product  by the
 percent that volatilises gave us the  air emissions Cthe
 percent that volatilises of  the  percent removed).   This
 value  represents the estimated air emissions (In ug/l)  of
 priority pollutant*. TO get our low  estimate of total
 emissions  at the POTH.  we assumed a 50 percent non-priority
 contribution.  Our nigh estimate,  based upon conversations
 with staff of the New Jersey Department of Environmental
 Protection 191 and staff  from an environmental consulting
 fir*. Science Applications International Corporation -  the
 authors of TJu Bepjm tfl Congress,  U>,  reflects  a non-
 priority contribution of »O  percent.

This value Is then scaled to tons/year  via the following
conversion!
Air Emissions lug/1) x flow at POTH (Millions of Cal/dayl  x
 (101tters/2.t4gal> x 3(S days/year x 10exp-9 Kg/ug x
2.20llb/kg x 1 ton/20001b.

Flow at each POM Is available in each pretreatment report.
Our data was provided by the Water Management Division of
EPA, Region  II.  (?)
                              352
ft sample calculation'Is shown in Table  3  for the Middlesex
County POTH.  Table 4 presents a summary of our results.  It
Is Important  to note that our low  and high estimates do not
Include photochemically unreactlve VOCa (methylene chloride.
1,1,1-trlchIoroethane.  and chlorinated  fluorocarbona).
However, their emissions tend to be quite slcable.  The "Low
Total* column includes  these emissions.   While not Important
for their contribution  to osone formation, these emissions
may be subject to air toxics. NESHAPS or  HSPS regulations.
As Table 4 shows, the low estimate of photochemically
reactive VOCa in Hew Tork Is relatively low  (460.14
tons/year).  But the low estimate  including non-reactive
VOCs is over  twice as high 11135.tf tons/year).

Once we established emissions estimates for POTHs for which
there was sufficient data, further estimations had to be
made to include those facilities for which no data was
available. This was done by calculating  the emissions per
unit flow at  each POTW  (with data) in a state and then
taking the average of these quotients.  We then multiplied
this by the total flow  (for all POTHs requiring
pretreatment) in the state.   Note  that  there is a high and a
low estimate  that reflects the estimates  made for individual
facilities.  In New fork, the range of  emissions per unit
flow was from O.21 to l.o* tons VOC/yr/HGO. which gives a
range of total emissions of  4*0.14 to 2100.71 tons VOC/year.
In New Jersey, because  of the uniqueness  of  the Middlesex
county POTW (see figure 1).   we based the total for the rest
of the state  on the range of emissions  per unit flow that we
calculated without including this  facility.  The emissions
from the Middlesex County facility were then added to this
total to get  the total  estimates for the entire State.  In
New Jersey, the range of emissions per  unit  flov wss from
4.(2 to 23.12 tons VOC/yr/NGD. This translated to a range
of emission*  (including Middlesex  County I of S3H.52 to
2(912.42 tons VOC/yesr.   Our estimated emissions for the
region Is SMC.67 to 29233.14 tons VOC/year.  It is not
surprising that the majority of VOC emissions are estimated
to come from New Jersey POTHs. The mean industrial
discharge to  POTHs In New Jersey  is almost  five times as
great as that in Hew Tork, with a  much  larger number of
organics manufacturers  located in  New Jersey.  (I)

We did not have the resources to verify our  estimates
through an air monitoring program. However, we obtained
dat» from a monitoring program conducted by the New Jersey
Department of Environmental Protection  at the Middlesex
                                                                                                                  553

-------
ar« of the  same magnitude •• those projected through the
•extraordinary measures."  considering the numbers of
sources needed for  full compliance of the "extraordinary
measure*" (gasoline mt.mt.ionm, dry cleaners, etc.). POTWs Bay
b* one of the most  feasible and more easily achievable
categories  for reduction* regaining.

in this study, we nave not explored tlte actual Methods for
reducing VOC emissions from POiws.  some plant* now have odor
controls, of which  we any be able to taka advantage in
designing controls  for voca.  We nope to explore this issue
In the future.  If  our estlaiataa are correct, it appears
that these  control* will be eaaential in a comprehensive
post-1917 effort to attain the national ambient air quality
etandard for ocona.
1. Baamonde,  Kaplchak and Trnchan, "An Evaluation of the
Program* to Attain the Osone and Carbon Monoxide Standards
in Mew Jeraey and New fork*. USEPA Air Programs Branch
Region II, Hew York, MT, presented at AFCA convention, June
2. USEPA. Office of Water Regulations and standards. 'Report
to Congress on the Discharge of Hazardous Haste* to Publicly
Owned Treatment Work**, Washington, O.C., February 19*t.

I. CFH Incorporated BnvirorsMntal Engineering Services,
•Report Upon Investigation of Organic Priority Pollutants  in
the Influent to the Passaic Valley Sewerage Conatlss loners
Treatment Plant, Wilppany, Hew Jersey, May !••«.

4. Report to Congress. Table 4.«.

S. J. Bel ley. New Jersey Department of Environmental
Protection, Trenton, Mew Jersey, private communication,
!*•».

». A. Jones, Science Applications International Corporation.
McLean Virginia, private communication, IMt.

7. Gallup and Prorok. USEPA. Office of Hater Enforcement and
Permits, "Pretreatment Prograsi Approval Status List"
Haahington. D.C. . March 19lt.

•. Ibid.
                              556
9. Harkov, Jenke, and Rugger!,  "Volatile Organic Compounds
in the Ambient Air Near a Large.  Regional Sewage Plant  In
New Jersey", Mew Jersey Department of Environmental
Protection, Trenton, New Jersey,   presented at APCA
convention June, 19(7.

10. creenberg and Pause, CRT Inc. "Ambient Air Monitoring
and Wastewater and Sludge Monitoring for VOCs and Trace
Metals at the fields Point POTN.  Providence Rhode Island".
Department of Environmental Management, State of Rhode
Island, Providence, Rhode Island, March 19*7.

It. Regulatory Integration Dlviaion, Office of Policy
Planning and Evaluation, USEPA. "Draft final Report  of  the
Philadelphia Integrated Environmental Management Project",
Washington. D.C., June Hit.

12. CFH Incorporated. "Report Upon Investigation of  Organic
Priority Pollutant* in the Influent to the Passaic Valley
Sewerage Commissioner'* Treatment Plant*, Whippany,  New
Jeraey. May 1911.

Pretreatment Reports Uiedt

1. Stony Brook Regional Sewerage Authority, "Pretreatment
Program Submission*. Princeton. New Jersey. April  1913.

2. Malcolm Pirnle. Inc.. "Industrial Pretreatment  Program
Phase One - The Pequannock, Lincoln Park and fairfleld
Sewerage Authority* Paramus, New Jeraey, September 19*1.

3. BCH. Inc., "final Draft Report, Hamilton Township,
Municipal-Industrial Pretreatment Program* Plymouth Meeting,
PA March 19S3.

4. Elson T. K11lam Associate*. Inc. "Rahway Valley Sewerage
Authority Industrial Pretreatment Program Part I*   Mllburn,
New Jersey, August 19S2.

5. Metcalf l Eddy. Inc., •Somerset Raritan Valley Sewerage
Authority Industrial Pi01reatment Program Phase 1,  Part 2
Technical Report, Hew fork, April 19(4.

(. Buck. Slefert * Jost, Inc.  "Swing-Lawrence Sewerage
Authority Industrial Pretreatment Program*. Englewood
Cliffs, New Jersey, April  1913.

Middlesex County Data Obtained from t7:

7. USEPK, "fate of Priority Pollutants In publicly Owned
Treatment Works", Volumes  I and  II. Washington,  D.C.,
September 1912.
                              557

-------
              TMUt
Priority PoMutMita
             560
                                                                                                                           TABLB  1
                                                                                      CMtai IMnrtitaMi
                                                                                      I.MHrtiluiuiU.il
                                                                                      1.1.1 Til
                                                                                      ItlcM
IN
III
«U
I
J
1
1
II
<•
1ST
in
•
i.
w.
1
Ml.
•MS
tw
IS.
M.
«
II*
H.
m
ttn
n

MII
•
u
•0
w.
»
Ml
II.
HI.
1?
ft.
»
Ml
S*
Mr
«.
Ml.
•»
Ml.
1
S
»
M.
Ml.
n.
it.

•


























m a
MI n
IK4M
J0>
• w
• •
• w
in
IN >
in M
IM.M
5t.ll
I W
1.31
*.M
NM.U
MHH
IMM
II.1S
•.II
•.II
U.M
,,JJ"
tn»
sm.ii
11.11
StST.SJ
                                                                                                                  MU.U
                                                                                                                     II
                                                                                                                  Nil.II
                                                                                                             561

-------
                       rieou 1
    Emissions/Flow at New Jersey POTWs
 Brook
Two BrtdjM MlddloMx L- L«w«nt» Mammon
          POTW
                                          fUtiw»y   S-fUrt
                     riaa*i
POTW Emissions v Extraordinary Measures

26 -
3O -
34 -
33 -
30 -
ta -
to -
w -
12 -
JO -
a -
0 -
4 -
3 -
0 -






~
•
/
/
'
/
/

— —
\
\
s
\
s
s
\
'*'
J/>
2
^
,'
2








r-

-1
,•
/
1
v
S
"v
s
s
v
S
v
s
V
s
s
v-
v
s
S

s
^
!
i





3
/
/
/
/•
/

^
\
\
•
-
1
'


1 1







V
\
k








;:


















<
v
1








1








s








1

Stop*// SSftfCt C/C 8*rg* H«rVV«* A/to








/
/
/
/
/
X
/
/
\
\^
\
s
s
V
K
h-
"
[
:


1
1 1







\ ,
:•'

















—









i







- ,

















-^
s
s
\
k-,
-







; .
:•.
''


J





E
sx
\^
\^
x^
1
1
1
t
V«*i ///U ^are POTW-/^OTW-(
              11-6

-------
12.   SUPPORT DOCUMENTS FOR REFERENCE CONCENTRATIONS AND
     INHALATION UNIT RISK FACTORS FROM THE INTEGRATED RISK
     INFORMATION SYSTEM (IRIS)
                               12-1

-------
                       Description of Carcinogenicity Section

The Carcinogeniclty Assessment Section provides information on three aspects of
the carcinogenic risk assessment for the agent in question; the U.S. EPA
classification, and quantitative estimates of risk from oral exposure and from
inhalation exposure.  The classification reflects a weight-of-evidence judgment
of the likelihood that the agent is a human carcinogen.  The quantitative risk
estimates are presented in three ways.  The slope factor is the result of
application of a low-dose extrapolation procedure and is presented as the risk
per mg/kg/day-  The unit risk is the quantitative estimate in terms of either
risk per ug/L drinking water or risk per ug/cu.m air breathed.   The third form
in which risk is presented is a drinking water or air concentration providing
cancer risks of 1 in 10,000, 1 in 100,000 or 1 in 1,000,000.  The Carcinogen
Assessment Background Document provides details on the rationale and methods
used to derive the carcinogenicity values found in IRIS.  Users are referred to
the Oral RfD and Inhalation RfC Sections for information on long-term toxic
effects other than carcinogenicity.


Note: Under Review indicates that the chemical is currently being review by the
      Carcinogen Risk Assessment Verification Endeavor.
                                       12-2

-------
                                      Xylenes

               CARCINOGENICITY ASSESSMENT FOR LIFETIME EXPOSURE
 Substance Name:  Xylenes
 CASRN:           1330-20-7
            EVIDENCE FOR CLASSIFICATION AS TO HUMAN CARCINOGENICITY
WEIGHT-OF-EVIDENCE CLASSIFICATION

Classification:  D; not classifiable as to human carcinogenicity

BASIS

Orally administered technical xylene mixtures did not result in significant
increases in  incidences in tumor responses in rats or mice of both sexes.

HUMAN CARCINOGENICITY DATA

None.

ANIMAL CARCINOGENICITY DATA

Inadequate.   In an NTP (1986) study, 50 male and 50 female F344/N rats were
treated by gavage with mixed xylenes in corn oil (60X m-xylene, 14% p-xylene,
9X o-xylene and 17X ethylbenzene) at dosages of 0, 250 or 500 mg/kg/day, 5
days/week for 103 weeks.  Similarly, 50 male and 50 female B6C3F1 mice were
treated with  the same xylene mixture at dosages of 0, 500 or 1000 mg/kg/day.
Animals were killed and examined histologically when moribund or after 104-105
weeks.  An apparent dose-related increased mortality was observed in male rats,
but this difference was statistically significant for the high dose group,
only.  No other differences in survival between dosage groups of either sex
were observed.  Interstitial cell tumors of the testes could not be attributed
to administration of the test compound observed in male rats (43/50 control,
38/50 low-dose and 41/49 high-dose).  NTP (1986) reported that there were no
significant changes in the incidence of neoplastic or nonneoplastic lesions in
either the rats or mice that could be considered related to the mixed xylene
treatment, and concluded that under the conditions of these 2-year gavage
studies, there was "no evidence of carcinogenicity" of xylene (mixed) for rats
or mice of either sex at any dosage tested.

Maltoni et al. (1985), in a limited study, reported higher incidences (compared
with controls) of malignant tumors in male and female Sprague-Dawley rats
treated by gavage with xylene in olive oil at 500 mg/kg/day, 4 or 5 days/week
for 104 weeks.  This study did not report survival rates or specific tumor
types; therefore,  the results cannot be interpreted.

Berenblum (1941) reported that "undiluted" xylene applied at weekly intervals
produced one tumor-bearing animal out of 40 after 25 weeks in skin-painting
experiments in mice.   No control groups were described.  Pound (1970) reported
negative results in initiation-promotion experiments with xylene as the

                                        12-3

-------
 initiator and croton oil as the promoter.


 SUPPORTING DATA FOR CARCINOGENICITY

 The frequency of sister chromatid exchanges and chromosomal aberrations were
 nearly identical between a group of 17 paint industry workers exposed to xylene
 and their respective referents (Haglund et al., 1980).  In vitro, xylene caused
 no increase in the number of sister chromatid  exchanges in human lymphocytes
 (Gemer-Smidt and Friedrich, 1978).  Studies indicate that xylene isomers,
 technical grade xylene or mixed xylene are not ntutagenic in tests with
 Salmonella typhimurium (Florin et al., 1980; NTP, 1986; Bos et al., 1981) nor
 in mutant reversion assays with Escherichia coli (McCarroll et al., 1981).
 Technical grade xylene, but not o- and m-xylene, was weakly mutagenic in
 Drosophila recessive lethal tests.  Chromosomal aberrations were not increased
 in bone marrow cells of rats exposed to xylenes by inhalation (Donner et al.,
 1980).

   	 QUANTITATIVE ESTIMATE OF CARCINOGENIC RISK FROM ORAL EXPOSURE 	

 No Data Available

   — QUANTITATIVE ESTIMATE OF CARCINOGENIC RISK FROM INHALATION EXPOSURE —

 No Data Available
                         EPA DOCUMENTATION AND REVIEW
Source Document:  U.S. EPA.  1987.  Drinking Water Criteria Document for
Xylene.  Prepared by the Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office, Cincinnati, OH for the Office of
Drinking Water, Washington, DC.  Final.

The Drinking Water Criteria Document for Xylene has received Agency and
external review.

Agency Work Group Review:  12/02/87

Verification Date:  12/02/87

   	 EPA CONTACTS (CARCINOGENICITY ASSESSMENT) 	
Bruce Mintz / OST -- (202)260-9569

W. Bruce Peirano / OHEA -- (513)569-7540

   	 BIBLIOGRAPHY
Berenblum, I.  1941.  The cocarcinogenie action of croton resin.  Cancer Res.
1: 44-48.
                                        12-4

-------
Bos, R.P., R.M.E. Brouns, R. Van Doom, J.L.G. Theuws and P.Th. Henderson.
1981.  Non-mutagenicity of  toluene, o-, m- and p-xylene, o-methylbenzylalcohol
and o-methylbenzylsulfate in the Ames assay.  Mutat. Res.  88: 273-280.

Donner, M., J. Maki-Paakkanen, H. Norppa, M. Sorsa and H. Vainio.  1980.
Genetic toxicology of xylenes.  Mutat. Res.  74: 171-172.

Florin, I., L. Rutberg, M.  Curvall and C.R. Enzell.  1980.  Screening of
tobacco smoke constituents  for mutagenicity using the Ames' test.  Toxicology.
15: 219-232.

Gemer-Smidt, P. and U. Friedrich.  1978.  The mutagenic effect of benzene,
toluene and xylene studied  by the SCE technique.  Mutat. Res.  58: 313-316.

Haglund, U., I. Lundberg and L. Zech.  1980.  Chromosome aberrations and sister
chromatid  exchanges in Swedish paint industry workers.  Scand. J. Work Environ.
Health.  6: 291-298.

Maltoni, C., B. Conti, G. Cotti and F. Belpoggi.  1985.  Experimental studies
on benzene carcinogenicity  at the Bologna Institute of Oncology: Current
results and ongoing research.  Am. J. Ind. Med.  7: 415-446.

McCarroll, N.E., C.E. Piper and B.H. Keech.  1981.  An E. coli microsuspension
assay for  the detection of  DNA damage induced by direct-acting and promutagens.
 Environ. Mutagen.  3: 429-444.

NTP (National Toxicology Program).  1986.  Toxicology and carcinogenesis
studies of xylenes (nixed)  in F344/N rats and B6C3F1 mice.  (Gavage studies).
NTP TR 327.  NIH PB No. 86-2583.

Pound, A.W.  1970.  Induced cell proliferation and the initiation of skin tumor
formation in mice by ultraviolet light.   Pathology.  2: 269-275.

U.S. EPA.  1987.  Drinking Water Criteria Document for Xylene.  Prepared by the
Office of Health and Environmental Assessment,  Environmental Criteria and
Assessment Office, Cincinnati,  OH for the Office of Drinking Water, Washington,
DC.  ECAO-CIN-416.  Final.
                                       12-5

-------
                                    Ethvlbenzene

                CARCINOGENICITY ASSESSMENT FOR LIFETIME EXPOSURE
 Substance Name:   Ethylbenzene
 CASRN:            100-41-4
             EVIDENCE FOR CLASSIFICATION AS TO HUMAN CARCINOCENICITY
 WEIGHT-OF-EVIDENCE CLASSIFICATION

 Classification:   D;  not classifiable  as  to human carcinogenicity

 BASIS

 nonclassifiable  due to lack of animal bioassays  and human  studies.

 HUMAN CARCINOGENICITY DATA

 None.

 ANIMAL CARCINOGENICITY DATA

 None.   NTP  has plans to initiate  bioassay.  Metabolism and excretion  studies at
 3.5,  35 and 350  mg/kg are  to be conducted as well.

 SUPPORTING  DATA  FOR CARCINOGENICITY

 The metabolic pathways  for  humans and rodents are different  (Engstrom et al.,
 1984).   Major metabolites  in humans,  mandelic acid and phenylglyoxylic acid,
 are minor metabolites  in rats  and rabbits (Kiese and Lenk, 1974).  The major
 animal  metabolites were  not detected  in  the urine of exposed workers  (Engstrom
 et al.,  1984).

 Ethylbenzene at  0.4  mg/plate was not  mutagenic for Salmonella strains TA98,
 TA1535,  TA1537 and TA1538 with or without Aroclor 1254 induced rat liver
 homogenates  (S9)  (Nestmann  et al., 1980).  Ethylbenzene was shown to  increase
 the mean number  of sister chromatid exchanges in human whole blood lymphocyte
 culture  at  the highest dose examined  without any metabolic activation system
 (Norppa  and Vainio,  1983).

 Dean et  al.  (1985) used  a battery of  short-term tests including bacterial
mutation assays,  mitotic gene conversion in Saccharomyces cerevisiae JD1 in the
presence and absence of  S9 and chromosomal damage in a cultured rat liver cell
 line.   Ethylbenzene was  not mutagenic in the range of concentrations  tested
 (0.2,  2, 20, 50 and  200  ug/plate) for S.  typhimurium TA98, TA100, TA1535,
TA1537 and TA1538 or for Escherichia  coli WP2 and WP2uvrA.  Ethylbenzene also
showed no response in the S. cerevisiae JD1 gene conversion assay.  In
contrast, ethylbenzene hydroperoxide  showed positive responses with E. coli WP2
at 200 ug/plate in the presence of S9 and an equally significant response with
the gene conversion system of yeast.
                                        12-6

-------
    	 QUANTITATIVE  ESTIMATE OF CARCINOGENIC RISK FROM ORAL EXPOSURE 	

 No Data Available

    — QUANTITATIVE  ESTIMATE OF CARCINOGENIC RISK FROM INHALATION EXPOSURE —

 No Data Available

    	  EPA DOCUMENTATION AND REVIEW 	

 Source  Document:  U.S. EPA.  1980.  Ambient Water Quality Criteria Document for
 Ethylbenzene.   Prepared by the Office of Health and Environmental Assessment,
 Environmental  Criteria and Assessment Office, Cincinnati, OH for the Office of
 Water Regulations and  Standards, Washington, DC.  EPA  440/5-80-048.  NTIS PB
 81-117590.

 U.S.  EPA.   1984.  Health  Effects Assessment for Ethylbenzene.  Prepared by the
 Office  of Health and Environmental Assessment, Environmental Criteria and
 Assessment  Office,  Cincinnati, OH for the Office of Emergency and Remedial
 Response, Washington,  DC.  EPA/540/1-86/008.

 U.S.  EPA.   1987.  Drinking Water Criteria Document for Ethylbenzene.  Prepared
 by the  Office  of Health and Environmental Assessment, Environmental Criteria
 and Assessment Office, Cincinnati, OH for the Office of Drinking Water,
 Washington, DC.

 The Ambient Water Quality Criteria Document and the Health Assessment Document
 have  received  Agency and  external review.  The Drinking Water Criteria Document
 has been extensively reviewed.

 Agency  Work Group Review:  10/07/87

 Verification Date:  10/07/87

    	  EPA CONTACTS (CARCINOGENICITY ASSESSMENT) 	
Arthur Chiu / OHEA -- (202)260-6764

Linda Papa / OHEA -- (513)569-7587

   	—	 BIBLIOGRAPHY
Dean, B.J., T.M. Brooks, G. Hodson-Walker and D.H. Hutson.  1985.  Genetic
toxicology testing of 41 industrial chemicals.  Mutat. Res.  153: 57-77.

Engstrom, K.,  V. Riihimaki and A. Laine.  1984.  Urinary disposition of
ethylbenzene and m-xylene in man following separate and combined exposure.
Int. Arch. Occup. Environ. Health.  54: 355-363.

Kiese, M. and W. Lenk.  1974.  Hydroxyacetophenones: Urinary metabolites of
ethylbenzene and acetophenone in the rabbit.  Xenobiotica.  4(6): 337-343.
                                        12-7

-------
Nestmann, E.R., E.G-H. Lee, T.I. Macula, G.R. Douglas and J.C. Mueller.  1980.
Mutagenicity of constituents identified in pulp and paper mill effluent using
the Salmonella/mammalian-raicrosome assay.  Mutat. Res.  79: 203-212.

Norppa, H. and H. Vainio.  1983.  Induction of sister-chromatid exchanges by
styrene analogues in cultured human lymphocytes.  Mutat. Res.  116: 379-387.

U.S. EPA.  1980.  Ambient Water Quality Criteria Document for Ethylbenzene.
Prepared by the Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH for the Office of Water
Regulations and Standards, Washington, DC.  EPA 440/5-80-048.  NTIS PB
81-117590.

U.S. EPA.  1984.  Health Effects Assessment for Ethylbenzene.  Prepared by the
Office of Health and Environmental Assessment, Environmental Criteria and
Assessment Office, Cincinnati,  OH for the Office of Emergency and Remedial
Response, Washington, DC.

U.S. EPA.  1987.  Drinking Water Criteria Document for Ethylbenzene.  Prepared
by the Office of Health and Environmental Assessment,  Environmental Criteria
and Assessment Office,  Cincinnati,  OH for the Office of Drinking Water,
Washington,  DC.   (Final report)
                                       12-8

-------
                                  Dichloromethane

               CARCINOGENICITY ASSESSMENT FOR LIFETIME EXPOSURE
 Substance Name:  Dichloromethane
 CASRN:           75-09-2
 Primary Synonym: Methylene Chloride
            EVIDENCE FOR CLASSIFICATION AS TO HUMAN CARCINOGENICITY
WEIGHT-OF-EVIDENCE CLASSIFICATION
Classification:  B2; probable human carcinogen

BASIS

Based on inadequate human data and sufficient evidence of carcinogenicity in
animals; increased incidence of hepatocellular neoplasms and
alveolar/bronchiolar neoplasms in male and female mice, and increased incidence
of benign mammary tumors in both sexes of rats, salivary gland sarcomas in male
rats and leukemia in female rats.  This classification is supported by some
positive genotoxicity data, although results in mammalian systems are generally
negative.

HUMAN CARCINOGENICITY DATA

Inadequate.  Neither of two studies of chemical factory workers exposed to
dichloromethane showed an excess of cancers (Ott et al., 1983; Friedlander et
al., 1978; Hearne and Friedlander, 1981).  The Ott et al. (1983) study was
designed to examine cardiovascular effects, and consequently the study period
was too short to allow for latency of site-specific cancers.  In the
Friedlander et al. (1978) study, exposures were low, but the data provided some
suggestion of an increased incidence of pancreatic tumors.  This study was
recently updated to include a larger cohort, followed through 1984, and an
investigation of possible confounding factors (Hearne et al., 1986, 1987).  A
nonsignificant excess in pancreatic cancer deaths was observed, which was
interpreted by EPA (1987a) as neither clear evidence of carcinogenicity in
humans, nor evidence of noncarcinogenicity.  An update of the Ott et al.
(1983) study, based on longer follow-up, indicated possible elevation of liver
and biliary tract cancers (TSCA section 8(e) submission no. 8eHQ-0198-0772 FLWP
et seq., 1989).

ANIMAL CARCINOGENICITY DATA

Sufficient.  Dichloromethane administered in the drinking water induced a
significant increase in combined hepatocellular carcinoma and neoplastic
nodules in female F344 rats and a nonsignificant increase in combined
hepatocellular carcinoma and neoplastic nodules in male B6C3F1 mice (NCA, 1982,
1983).  Two inhalation studies with dichloromethane have shown an increased
incidence of benign mammary tumors in both sexes of Sprague-Dawley (Burek et
al., 1984) and F344 (NTP, 1986) rats.  Male Sprague-Dawley rats had increased
salivary gland sarcoma (Burek et al., 1984) and female F344 rats had increased
                                        12-9

-------
 leukemia incidence (NTP, 1986).  Both sexes of B6C3F1 mice developed liver and
 lung tumors after dichloromethane treatment (NTP, 1986).

 In a 2-year study by the National Coffee Association (1982, 1983), groups of 85
 F344 rats/sex/dose received 5, 50, 125, or 250 (mg/kg)/day of dichloromethane
 in the drinking water.  Control groups consisted of 135 rats/sex.  In female
 rats the incidence of combined hepatocellular carcinoma and neoplastic nodules
 was statistically significantly increased in the 50 and 250 mg/kg dose groups
 when compared with matched controls (0/134, 1/85, 4/83, 1/85,  and 6/85 in the
 five dose groups 0, 5, 50,  125, and 250 (mg/kg)/day,  respectively).   The
 incidence of hepatocellular carcinoma alone was not significantly increased
 (0/134, 0/85, 2/83, 0/85,  2/85).   The combined incidence of hepatocellular
 carinoma and neoplastic nodules in controls and the 4 dose groups (472 rats:  4
 with carcinoma and 8 with neoplastic nodules)  was similar to that for
 historical controls (419 rats; 5  with carcinoma,  19 with neoplastic  nodules).
 Male rats showed no increase in liver tumors.

 In the same National Coffee Association study  (1982,  1983), B6C3F1 mice
 received 0, 60,  125,  185,  or 250  (mg/kg)/day of dichloromethane in drinking
 water.   Treatment groups consisted of 50 female mice  and 200,  100, 100, and 125
 male mice (low to high dose).   One hundred females and 125 males served as
 controls.   Male  mice had an increased incidence of combined neoplastic nodules
 and hepatocellular carcinoma (24/125,  51/200,  30/100,  31/99,  35/125).   The
 increase was not dose-related, but the pairwise comparisons for the  two
 mid-dose groups  were reported to  be statistically significant  (U.S.  EPA,
 1985a).   The hepatocellular carcinoma incidence alone  for male mice  (which was
 about 55 to 65Z  of the total)  was not significantly elevated.   Female mice did
 not have increased liver tumor incidence.   The  EPA (1985b) regarded  this  study
 as suggestive but not conclusive  evidence  for  carcinogenicity  of
 dichloromethane.

 A  gavage bioassay of dichloromethane  conducted  by NTP  (1982) has not been
 published because of high mortality,  much  of which was  attributed to gavage
 accidents.

 Inhalation  exposure  of 107  to  109  Syrian hamsters/sex/dose to  0,  500,  1500, or
 3500  ppm of dichloromethane  for 6  hours/day, 5  days/week for 2 years did  not
 induce neoplasia  (Burek et  al., 1984).   Sprague-Dawley  rats (129/sex/ dose)
 were  exposed under the  same  conditions.  Female rats administered the  highest
 dose  experienced  significantly reduced survival from 18-24 months.   Female rats
 showed a dose-related increase in  the  average number of benign mammary tumors
 per rat  (1.7,  2.3, 2.6,  3.0),  although the  numbers  of rats with tumors were not
 significantly  increased.  A  similar response was  observed in male rats, but to
 a  lesser degree.   In  the male  rats  there was a  statistically significant
 positive trend in the  incidence of  sarcomas  of  the  salivary gland (1/93,  0/94,
 5/91, 11/88);  the  incidence was significantly elevated  at the  high dose.   There
 is a question  as  to whether  these  doses  reached the MTD,  particularly  in  the
hamsters and the  male rats.  In another  study (Dow  Chemical Co.,  1982), 90
 Sprague-Dawley rats/sex were exposed by  inhalation  to 0,  50, 200, or 500  ppm
 dichloromethane for 20 months  (male) or  24 months  (female).  No  salivary  tumors
were observed, but there was an exposure-related  increase  in the  total number


                                       12-10

-------
 of benign  mammary  tumors  in  female rats, although the increase was not
 statistically  significant in any  individual exposure group.

 Groups  of  50 each  male  and female F344/N rats and B6C3F1 mice were exposed to
 dichloromethane by inhalation,  6  hours/day, 5 days/week for 2 years  (NTF,
 1986).   Exposure concentrations were 0, 1000, 2000, or 4000 ppm for  rats and 0,
 2000, or 4000  ppm  for mice.   Survival of male rats was low; however, this
 apparently was not treatment-related.  Survival was decreased in a
 treatment-related  fashion for male and female mice and female rats.  Mammary
 adenomas and fibroadenomas were significantly increased in male and  female rats
 after survival adjustment, as were mononuclear cell leukemias in female rats.
 Among treated  mice of both sexes  there were significantly increased  incidences
 of hepatocellular  adenomas and  carcinomas, and of alveolarbronchiolar adenomas
 and carcinomas, by life table tests.  Adenomas and carcinomas were
 significantly  increased alone as  well as in combination.  In addition, there
 were significant dose-related increases in the number of lung tumors per animal
 multiplicity in both sexes of mice.

 Two inhalation assays using  dogs, rabbits, guinea pigs, and rats showed no
 tumors,  but were not conducted  for the lifetime of the animals (Heppel et al.,
 1944; MacEwen  et al., 1972).  Theiss et al., (1977) injected  Strain A male
 mice intraperitoneally  with  0,  160, 400, or 800 mg/kg of dichloromethane 16 to
 17 times,  over 5 to 6 weeks.  Survival of the animals was poor.  The animals
 remaining  24 weeks after  the  first treatment were killed and examined for lung
 tumors;  pulmonary  adenomas were found.

 SUPPORTING DATA FOR CARCINOGENICITY

 Dichloromethane was mutagenic for Salmonella typhimurium with or without the
 addition of hepatic enzymes  (Green, 1983) and produced mitotic recombination in
 yeast (Callen  et al., 1980).  Results in cultured mammalian cells have
 generally  been negative,  but  dichloromethane has been shown to transform rat
 embryo  cells and to enhance viral transformation of Syrian hamster embryo cells
 (Price  et  al., 1978; Hatch et al., 1983).  Although chlorinated solvents have
 often been suspected of acting  through a nongenotoxic mechanism of cell
 proliferation, Lefevre  and Ashby  (1989) found methylene chloride to  be unable
 to  induce  hepatocellular  division in mice.

   — QUANTITATIVE ESTIMATE OF  CARCINOGENIC RISK FROM INHALATION EXPOSURE —

Unit Risk:              4.7E-7 per (ug/cu.m)
 Extrapolation Method:   Linearized multistage procedure, extra risk

Air Concentrations  at Specified Risk Levels:

   Risk Level               Concentration
   E-4  (1  in 10,000)        2E+2  per (ug/cu.m)
   E-5  (1  in 100,000)       2E+1  per (ug/cu.m)
   E-6  (1  in 1,000,000)     2E+0  per (ug/cu.m)
                                       12-11

-------
            DOSE-RESPONSE DATA (CARCINOGENICITY,  INHALATION EXPOSURE)
 Tumor Type:              combined adenomas  and carcinomas
 Test Animals:            mouse/B6C3Fl,  female
 Route:                   inhalat ion

                                  Dose
                                                                   Tumor
 Tumor Type         (ppm)           (mg/kg)/day       (mg/kg)/day      Incidence
Administered
(ppm)
0
2000
4000
0
2000
4000
Transformed
Animal
(mg/kg)/day
0
1582
3162
0
1582
3162
Human
Equivalent
(mg/kg)/day
0
356
712
0
356
712
   Liver               000              3/45
                                                                      16/46
                                                                      40/46

   Lung               000              3/45
                                                                      30/46
                                                                      41/46
          ADDITIONAL COMMENTS  (CARCINOGENICITY, INHALATION EXPOSURE)
The unit  risk of 4.7E-7 per  (ug/cu.m), which incorporates information on
pharmacokinetics and metabolism of dichloromethane, is approximately nine-fold
lower  than  the previous applied dose estimate  (U.S. EPA, 1987a,b).  Internal
dose estimates were based on the metabolism of dichloromethane by the
glutathione-s-transferase pathway, as estimated by the model developed by
Andersen  et al. (1987).  The internal dose was corrected for interspecies
differences in sensitivity by using the surface area correction factor.

Calculation of a slope factor from the unit risk is inappropriate when
pharmacokinetic models are used.  (When dose-response relationships are figured
on the basis of internal or  metabolized dose, a slope factor in terms of per
(mg/kg)/day represents a back calculation using different absorption
assumptions than the pharmacokinetic models.  This introduces possible
contradictions.)

The unit  risk should not be  used if the air concentration exceeds 2E+4 ug/cu.m,
since above this concentration the unit risk may differ from that stated.
Since the unit risk is based on a pharmacokinetic model, the risk may change
with alterations in exposure patterns.  Thus, the unit risk presented here may
not be applicable to acute,  high exposures.

   	 DISCUSSION OF CONFIDENCE (CARCINOGENICITY, INHALATION EXPOSURE) 	

Adequate numbers of animals were observed and tumor incidences were
significantly increased in a dose-dependent fashion.  Analysis excluding
animals that died before observation of the first tumors produced similar risk
estimates, as did time-to-tumor analysis.   The use of animal and human
metabolism and pharmacokinetic data reduces some of the uncertainty typically
associated with dose-risk extrapolation.  A great deal of uncertainty still


                                       12-12

-------
exists, however,  in the estimates of  internal dose generated by the model of
Andersen et al.  (1987).   Important uncertainties remain regarding the
pharmacokinetics, pharmacodynamics, and mechanisms of carcinogenicity for
dichloromethane.
                         EPA DOCUMENTATION AND REVIEW
Source Document:  U.S. EPA.  1985a.  Health Assessment Document for
Dichloromethane  (Methylene Chloride).  Final Report.  Office of Health and
Environmental Assessment, Washington, D.C.  EPA/600/8-82/004F,

U.S.  EPA.  1985b.  Addendum to the Health Assessment Document for
Dichloromethane  (methylene chloride).  Updated carcinogenicity assessment.
Prepared by the  Carcinogen Assessment Group, OHEA, Washington, DC.
EPA/600/8-82/004FF.

U.S.  EPA.  1987a.  Update to the Health Assessment Document and Addendum for
Dichloromethane  (Methylene Chloride):  Pharmacokinetics, Mechanism of Action
and Epidemiology.  Review Draft.  Office of Health and Environmental
Assessment, Washington, DC.  EPA/600/8-87/030A.

U.S.  EPA.  1987b.  Technical Analysis of New Methods and Data Regarding
Dichloromethane  Hazard Assessments.  Review Draft.  Office of Health and
Environmental Assessment, Washington, DC.  EPA/600/8-87/029A.

The Addendum to  the Health Assessment Document, the Update to the Health
Assessment Document and Addendum, and the Technical Analysis of New Methods and
Data for dichloromethane have received Agency and external review, including a
review by the Science Advisory Board (SAB).  Although the last two documents
are not yet finalized and the SAB comments are not yet incorporated, these do
not alter this document's analyses or conclusions.

Agency Work Group Review:  11/12/86, 12/04/86, 04/06/89

Verification Date:  04/06/89

   	 EPA CONTACTS (CARCINOGENICITY ASSESSMENT) 	
Lorenz Rhomberg / OHEA  --  (202)260-5723

Dharm Singh / OHEA  -- (202)260-5958

   	.	 BIBLIOGRAPHY
Andersen, M.E., H.J. Clewell, III, M.L. Gargas, F.A. Smith and R.H.  Reitz.
1987.  Physiologically based pharmacokinetics and the risk assessment process
for methylene chloride.  Toxicol. Appl. Pharmacol.  87: 185-205.

Burek, J D   K D. Nitschke, T.J. Bell, et al.  1984.  Methylene chloride: A two
year inhalation toxicity and oncogenicity study in rats and hamsters.  Fund.
Appl. Toxicol.  4: 30-47.


                                       12-13

-------
 Callen,  D.F.,  C.R.  Wolf  and R.M.  Philpot.   1980.  Cytochrome P-450 mediated
 genetic  activity  and  cytotoxicity  of  seven halogenated aliphatic hydrocarbons
 in Saccharomyces  cerevisiae.  Mutat.  Res.  77:  55-63.

 Dow Chemical Company.   1982.  Methylene chloride:  A two-year inhalation and
 oncogenicity study  in rats.  Toxicology Research Laboratory, Health and
 Environmental  Sciences, Dow Chemical  Company, Midland, MI.

 Friedlander, B.R.,  F.T.   Hearne andS.  Hall.  1978.  Epidemiologic
 investigation  of  employees chronically exposed to methylene chloride.  J.
 Occup. Med.  20(10):  657-666.

 Green, T.  1983.  The metabolic activation of dichloromethane and
 chlorofluoromethane in a  bacterial mutation  assay using Salmonella typhimurium.
 Mutat.  Res.   118(4):  277-288.

 Hatch, G.G., P.O. Mamay,  M.L. Ayer, B.C. Casto and S. Nesnow.  1983.  Chemical
 enhancement of viral  transformation in Syrian hamster embryo cells by gaseous
 and volatile chlorinated  methanes and ethanes.  Cancer Res.  43: 1945-1950.

 Hearne,  F.T. and  B.R.  Friedlander.  1981.  Follow-up of methylene chloride
 study.   J. Occup. Med.  23: 660.

 Hearne,  F.T.,  F.  Grose, J.W. Pifer and B.R.  Friedlander.  1986.  Methylene
 chloride mortality  study  update.  Eastman Kodak Company, Rochester, NY.  June
 16.

 Hearne,  F.T.,  F Grose,  J.W. Pifer, B.R. Friedlander and R.L. Raleigh.  1987.
 Methylene Chloride  mortality study: dose-response characterization and animal
 model comparison.   J.  Occup. Med.  29 (3): 217-228.

 Heppel,  L.A.,  P.A.  Neal,  T.L. Perrin, M.L. Orr and V.T. Porterfield.  1944.
 Toxicology of  dichloromethane (methylene chloride).  I. Studies on effects of
 daily inhalation.   J.  Ind. Hyg. Toxicol.  26(1): 8-21.

 Lefevre, P.A.  and J. Ashby.  1989.  Evaluation of dichloromethane as an inducer
 of  DNA synthesis  in B6C3F1  mouse liver.  Carcinogenesis.  10(6): 1067-1072.

 MacEwen, J.D., E.H.  Vernot and C.C. Haun.   1972.   Continuous animal exposure
 to  dichloromethane.  AMRL-TR-72-28, Systems  Corporation Report No. W-71005.
 Wright Patterson Air  Force Base, Ohio, Aerospace Medical Research.  AD746295.

 NCA  (National  Coffee Association).  1982.  Twenty-four-month chronic toxicity
 and oncogenicity study  of methylene chloride in rats.  Final Report.  Prepared
by Hazleton Laboratories,  America, Inc., Vienna, VA.  Unpublished.

NCA  (National  Coffee Association).  1983.  Twenty-four month oncogenicity study
of methylene chloride in mice.  Final Report.  Prepared by Hazleton
Laboratories,  America,  Inc., Vienna, VA.

NTP  (National Toxicology Program).  1982.  Draft technical report on the
Carcinogenesis bioassay of dichloromethane (methylene chloride) (CAS No.

                                       12-14

-------
75-09-2)  in F344/N rats and B6C3F1 mice (gavage study).  Research Triangle
Park, NC  and Bethesda, MD.  Unpublished.  NTP-82-061.

NTP  (National Toxicology Program).  1986.  Toxicology and carcinogenesis
studies of dtchloromethane (methylene chloride) (CAS No. 75-09-2) in F344/N
rats and  B6C3F1 mice (inhalaltion studies).  NTP-TRS-306.

Ott, M.G., L.K.  Skory, B.B.  Holder, J.M.  Bronson and P.R. Williams.  1983.
Health evaluation of employees occupationally exposed to methylene chloride:
Mortality.  Scand. J. Work Environ. Health.  9(Suppl. 1): 8-16.

Price,  P.J., C.M.  Hassett and J.I.  Mansfield.  1978.  Transforming
activities of trichloroethylene and proposed industrial alternatives.  In
Vitro.  14(3): 290-293.

Thiess, J.C., G.D.  Stoner, M.B.  Shimkin and E.K.  Weisburger.  1977.  Test
for carcinogenicity of organic contaminants of United States drinking waters by
pulmonary tumor response in strain A mice.  Cancer Res.  37: 2717-2720.

Toxic Substances Control Act.  1989.  Section 8(e) submission no.
8eHQ-0198-0772 FLWP et seq.

U.S.  EPA.  1985a.  Health Assessment Document for Dichloromethane (Methylene
Chloride).  Final Report.  Office of Health and Environmental Assessment,
Washington, D.C.  EPA/600/8-82/004F.

U.S.  EPA.  1985b.  Addendum to the Health Assessment Document for
Dichloromethane (methylene chloride).  Updated carcinogenicity assessment.
Prepared by the Carcinogen Assessment Group, OHEA, Washington, DC.
EPA/600/8-82/004FF.

U.S.  EPA.  1987a.  Update to the Health Assessment Document and Addendum for
Dichloromethane (Methylene Chloride):  Pharmacokinetics, Mechanism of Action
and Epidemiology.  Review Draft.  Office of Health and Environmental
Assessment, Washington, DC.  EPA/600/8-87/03OA.

U.S.  EPA.  1987b.  Technical Analysis of New Methods and Data Regarding
Dichloromethane Hazard Assessments.  Review Draft.  Office of Health and
Environmental Assessment, Washington, DC.  EPA/600/8- 87/029A.
                                       12-15

-------
                                       Benzene

                CARCINOGENICITY ASSESSMENT  FOR  LIFETIME EXPOSURE
 Substance  Name:   Benzene
 CASRN:            71-43-2
             EVIDENCE  FOR  CLASSIFICATION AS TO HUMAN CARCINOGENICITY
 WEIGHT-OF-EVIDENCE  CLASSIFICATION

 Classification:  A; human  carcinogen

 BASIS

 Several  studies  of  increased  incidence of nonlymphocytic leukemia from
 occupational  exposure,  increased incidence of neoplasia in rats and mice
 exposed  by  inhalation and  gavage,  and some supporting data form the basis  for
 this classification.

 HUMAN CARCINOGENICITY DATA

 Aksoy et al.  (1974) reported  effects of benzene exposure among 28,500 Turkish
 workers  employed in the shoe  industry.  Mean duration of employment was 9.7
 years  (1-15 year range) and mean age was 34.2 years.  Peak exposure was
 reported to be 210-650 ppm.   Twenty-six cases of leukemia and a total of 34
 leukemias or  preleukemias  were observed, corresponding to an incidence of
 13/100,000  (by comparison  to  6/100,000 for the general population).  A
 follow-up paper  (Aksoy, 1980) reported eight additional cases of leukemia  as
 well as  evidence suggestive of increases in other malignancies.

 In a retrospective  cohort  mortality study Infante et al. (1977a,b) examined
 leukemogenic  effects of benzene exposure in 748 white males exposed while
 employed in the  manufacturing of rubber products.  Exposure occurred from
 1940-1949, and vital statistics were obtained through 1975.  A statistically
 significant increase (p less  than  or equal to 0.002) of leukemias was found by
 comparison to the general  U.S. population.  There was no evidence of solvent
 exposure other than benzene.  Air  concentrations were generally found to be
 below the recommended limits  in effect during the study period.

 In a subsequent  retrospective cohort mortality study Rinsky et al. (1981)
 observed seven deaths from leukemia among 748 workers exposed to benzene and
 followed for at  least 24 years (17,020 person-years).  This increased incidence
was statistically significant; standard mortality ratio (SMR) was 560.  For the
 five leukemia deaths that  occurred among workers with more than 5 years
exposure, the SMR was 2100.   Exposures (which ranged front 10-100 ppm 8-hour
TWA) were described as less than the recommended standards for the time period
of 1941-1969.

In an updated version of the Rinsky et al. (1981) study, the authors followed
the same cohort  to 12/31/81 (Rinsky et al., 1987).  An in his earlier study,
cumulative exposure was derived from historic air-sampling data or interpolated

                                       12-16

-------
 estimates based  on  exisitng  data.  Standardized mortality rates ranged from 109
 at  cumulative benzene exposures under 40 ppm-years and increased montonically
 to  6637  (6  cases) at 400 ppm-years or more.  The authors found significantly
 elevated risks of leukemia at cumulative exposures less than the equivalent
 current  standard for occupational exposure which is 10 ppm over a 40-year
 working  lifetime.

 Ott et al.  (1978) observed three deaths from leukemia among 594 workers
 followed for at  least 23 years in a retrospective cohort mortality study, but
 the increase was not statistically significant.  Exposures ranged from <2 to
 >25 ppm  8-hour TWA.

 Wong et  al. (1983)  reported  on the mortality of male chemical workers who had
 been exposed to  benzene for  at least 6 months during the years 1946-1975.  The
 study population of 4062 persons was drawn from seven chemical plants, and jobs
 were categorized as to peak  exposure.  Those with at least 3 days/week exposure
 (3036 subjects)  were further categorizeed on the basis of an 8-hour TWA.  The
 control  subjects held jobs at the same plants for at least 6 months but were
 never subject to benzene exposure.  Dose-dependent increases were seen in
 leukemia and lymphatic and hematopoietic cancer.  The incidence of leukemia was
 responsible for  the majority of the increase.  It was noted that the
 significance of  the increase is due largely to a less than expected incidence
 of  neoplasia in  the unexposed subjects.

 Numerous other epidemiologic and case studies have reported an increased
 incidence or a causal relationship between leukemia and exposure to benzene
 (IARC, 1982).

 ANIMAL CARCINOGENICITY DATA

 Both gavage and  inhalation exposure of rodents to benzene have resulted in
 development of neoplasia.  Maltoni and Scarnato (1979) and Maltoni et al.
 (1983) administered benzene  by gavage at dose levels of 0, 50, 250, and 500
 mgAg bw to 30-40 Sprague-Dawley rats/sex for life.  Dose-related increased
 incidences of mammary tumors were seen in females and of Zymbal gland
 carcinomas, oral cavity carcinomas and leukemias/lymphomas in both sexes.

 In  an NTP (1986) study, benzene was administered by gavage doses of 0, 50, 100,
 or  200 mgAg bw  to  50 F344/N rats/sex or 0, 25, 50, or 100 mgAg bw to 50
 B6C3F1 mice/sex.  Treatment  was 5 times/week for 103 weeks.  Significantly
 increased incidences (p<0.05) of various neoplasic growths were seen in both
 sexes of both species.   Both male and female rats and mice had increased
 incidence of carcinomas of the Zymbal gland.  Male and female rats had oral
 cavity tumors,  and males showed increased incidences of skin tumors.  Mice of
both  sexes had increased incidence of lymphomas and lung tumors.  Males were
observed to have harderian and preputial gland tumors and females had tumors of
mammary gland and ovary.  In general, the increased incidence was dose-related.

Slightly increased  incidences of hematopoietic neoplasms were reported for male
C57B1 mice exposed by inhalation to 300 ppm benzene 6 hours/day, 5 days/ week
for 488 days.   There was no  increase in tumor incidence in male AKR or CD-I
mice similarly exposed to 100 ppm or 100 or 300 ppm benzene, respectively.

                                       12-17

-------
 Likewise male Sprague-Dawley rats exposed by inhalation to 300 ppm benzene were
 not observed to have increased incidence of neoplasia (Snyder et al.,  1981).
 Maltoni et al.  (1983)  treated male and female Sprague-Dawley rats in the
 following manner.   Starting at 13 weeks of age rats were exposed to 200 ppm
 benzene 4 hours/day, 5 days/week for 7 weeks; 200 ppm 7 hours/day,  5 days/week
 for 12 weeks;  300  ppm 7 hours/day, 5 days/week for 85 weeks.   An 8-hour/day TWA
 for 5 days/week was calculated to be 241 ppm.  A statistically significant
 increase was noted in hepatomas and carcinomas of the Zymbal gland.

 SUPPORTING DATA FOR CARCINOGENICITY

 Numerous investigators have found significant increases in chromosomal
 aberrations of bone marrow cells and peripheral lymphocytes from workers with
 exposure to benzene (IARC,  1982).   Benzene also induced chromosomal aberrations
 in bone marrow cells from rabbits (Kissling and Speck,  1973),  mice  (Meyne and
 Legator,  1980)  and rats (Anderson and Richardson,  1979).   Several investigators
 have reported positive results for benzene in mouse micronucleus assays (Meyne
 and Legator,  1980).   Benzene was not mutagenic in several bacterial and yeast
 systems,  in the sex-linked recessive lethal mutation assay with Drosophila
 melanogaster or in mouse lymphoma cell forward mutation assay.

    — QUANTITATIVE ESTIMATE OF CARCINOGENIC RISK FROM INHALATION EXPOSURE —

 Unit Risk:              8.3E-6 per (ug/cu.m)
 Extrapolation Method:   One-hit (pooled data)

 Air Concentrations at  Specified Risk Levels:

    Risk Level                Concentration
    E-4 (1  in  10,000)         1E+1 per (ug/cu.m)
    E-5 (1  in  100,000)        1E+0 per (ug/cu.m)
    E-6 (1  in  1,000,000)      1E-1 per (ug/cu.m)
           DOSE-RESPONSE DATA  (CARCINOGENICITY, INHALATION  EXPOSURE)
Tumor Type:             leukemia
Test Animals:           human
Route:                  inhalation, occupational exposure

No additional data.

          ADDITIONAL COMMENTS (CARCINOGENICITY, INHALATION EXPOSURE)
The unit risk estimate is the geometric mean of four ML point estimates using
pooled data from the Rinsky et al. (1981) and Ott et al.  (1978) studies, which
was then adjusted for the results of the Wong et al. (1983) study.  The Rinsky
data used were from an updated tape which reports one more case of leukemia
than was published in 1981.  Equal weight was given to cumulative dose and
weighted cumulative dose exposure categories as well as to relative and
absolute risk model forms.  The results of the Wong et al. (1983) study were
incorporated by assuming that the ratio of the Rinsky-Ott-Wong studies to the
Rinsky-Ott studies for the relative risk cumulative dose model was the same as

                                       12-18

-------
 for  other  model-exposure  category  combinations and multiplying this ratio by
 the  Rinsky-Ott  geometric  mean.  The  age-specific U.S. death rates for 1978  (the
 most current year  available) were  used for background leukemia and total death
 rates.   It should  be noted  that a  recently published paper (Rinsky et al.,
 1987)  reported yet another  case of leukemia from the study population.

  The unit  risk  should  not be used  if the  air concentration exceeds 100 ug/cu.m,
 since above this concentration the unit risk may not be appropriate.
         DISCUSSION  OF  CONFIDENCE  (CARCINOGENICITY, INHALATION EXPOSURE)
 The  pooled cohorts were  sufficiently  large and were followed for an ade quate
 time period.  The increases  in  leukemias were statistically significant and
 dose-related  in  one  of the studies.   Vong et al.  (1983) disagrees that
 exposures  reported in Rinsky et al. (1981) were within the recommended
 standards.  For  the  five leukemia deaths in persons with 5 or more years
 exposure,  the author notes that mean  exposure levels  (range 15-70 ppm) exceeded
 the  recommended  standard (25 ppm) in  75X of the work  locations sampled.  The
 risk estimate above  based on reconsideration of the Rinsky et al. (1981) and
 Ott  et  al.  (1978) studies is very similar to that of  2.4E-2/ppm  (cited in U.S.
 EPA,  1980)  based on  Infante  et  al.  (1977a,b), Ott et  al. (1978) and Aksoy et
 al.  (1974).   It  was  felt by  the authors of U.S. EPA (1985) that the exposure
 assessment provided  by Aksoy was too  imprecise to warrant inclusion in the
 current risk  estimate.   A total of  21 unit risk estimates were prepared using 6
 models  and various combinations of  the epidemiologic  data.  These range over
 slightly more than one order of magnitude.  A geometric mean of these estimates
 is 2.7E-2/ppm.   Regression models give an estimate similar to the geometric
 mean.
                         EPA DOCUMENTATION AND REVIEW
Source Document:  U.S. EPA.  1980.  Ambient Water Quality Criteria Document  for
Benzene.  Prepared by the Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office  (Cincinnati, OH) and Carcinogen
Assessment Group  (Washington, DC), and the Environmental Research Labs
(Corvalis, OR; Duluth, MN; Gulf Breeze, FL) for the Office of Water Regulations
and Standards, Washington, DC.  EPA 440/5-80-018.

U.S. EPA.  1985.  Interim Quantitative Cancer Unit Risk Estimates Due to
Inhalation of Benzene.  Prepared by the Office of Health and Environmental
Assessment, Carcinogen Assessment Group, Washington, DC for the Office of Air
Quality Planning and Standards, Washington, DC.

U.S. EPA.  1987.  Memorandum from J. Orme, HEB, CSD/ODW to C. Vogt, Criteria
and Standards Division, ODW, June, 1987.

The 1985 Interim Evaluation was reviewed by the Carcinogen Assessment Group.

The 1987 memorandum is an internal document.

Agency Work Group Review:  03/05/87, 10/09/87


                                       12-19

-------
Verification Date:   10/09/87

   	 EPA  CONTACTS  (CARCINOGENICITY ASSESSMENT)

David Bayliss / OHEA --  (202)260-5726

Robert McGaughy / OHEA  --  (202)260-5898

   	 BIBLIOGRAPHY 	
Aksoy, M., S. Erdem and G. Dincol.  1974.  Leukemia in shoeworkers exposed
chronically  to benzene.  Blood.  44(6): 837-841,

Aksoy, M.  1980.  Different types of malignancies due to occupational exposure
to benzene:  A review of recent observations in Turkey.  Environ. Res.  23: 181.

Anderson, D. and C.R. Richardson.  1979.  Chromosome gaps are associated with
chemical mutagenesis (abstract No. Ec-9).  Environ. Mutat.  1: 179.

IARC  (International Agency for Research on Cancer).  1982.  Benzene. In: Some
industrial chemicals and dyestuffs. IARC Monographs on the evaluation of
carcinogenic risk of chemicals to humans.  IARC, WHO, Lyon, France.  29:
93-148.

Infante, P.P., R.A. Rinsky, J.K. Wagoner and R.J. Young.  1977a.  Benzene and
Leukemia.  The Lancet.  2(8043): 867-869.

Infante, P.F., R.A. Rinsky, J.K. Wagoner and R.J. Young.  1977b.  Leukemia in
benzene workers.  Lancet.  19: 76-78.

Kissling, H. and B. Speck.  1973.  Chromosome aberrations in experimental
benzene intoxication.  HELV. Med. Acta.  36: 59-66.

Maltoni, C.  and C. Scamato.  1979.  First experimental demonstration of the
carcinogenic effects of benzene. Long-term bioassays on Sprague-Dawley Rats by
oral administration.  Med. Lav.  70: 352-357.

Maltoni, C., B. Conti and G. Cotti.  1983.  Benzene: A multipotential
carcinogen.  Results of long-term bioassays performed at the Bologna Institute
of Oncology.  Am. J. Ind. Med.  4: 589-630.

Meyne, J. and M.S. Legator.  1980.  Sex-related differences in cytogenetic
effects of benzene in the bone marrow of Swiss mice.  Environ. Mutat.  2:
43-50.

NTP (National Toxicology Program).  1986.  Toxicology and carcinogenesis
studies of benzene (CAS No. 71-43-2) in F344/N rats and B6C3F mice (gavage
studies).  NTP Technical Report Series No. 289.  NIH Publication No. 86-2545.

Ott,  M.G., J.C.  Townsend, W.A. Fishbeck and R.A. Langner.   1978.  Mortality
among individuals occupationally exposed to benzene.  Arch. Environ. Health.
33:  3-10.

                                       12-20

-------
Rinsky. R.A., R.J. Young and A.B. Smith.  1981.  Leukemia in benzene workers.
Am. J. Ind. Med.  2: 217-245.

Rinsky, R.A., A.B. Smith, R. Hornung, et al.  1987.  Benzene and Leukemia.  New
England J. Med.  316(17): 1044-1050.

Snyder, C.A., M.N. Erlichman, S. Laskin, B.D. Goldstein, and R.E. Albert.
1981.  The pharmacokinetics of repetitive benzene exposure at 300 and 100 ppm
in AKR mice and Sprague-Dawley rats.  Toxicol. Appl. Pharmacol.  57: 164-171.

U.S. EPA.  1980.  Ambient Water Quality Criteria Document for Benzene.
Prepared by the Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office (Cincinnati, OH) and Carcinogen Assessment Group
(Washington, DC), and the Environmental Research Labs (Corvalis, OR; Duluth,
MN; Gulf Breeze, FL) for the Office of Water Regulations and Standards,
Washington, DC.  EPA 440/5-80-018.

U.S. EPA.  1985.  Interim Quantitative Cancer Unit Risk Estimates Due to
Inhalation of Benzene.  Prepared by the Office of Health and Environmental
Assessment, Carcinogen Assessment Group, Washington, DC for the Office of Air
Quality Planning and Standards, Washington, DC.

U.S. EPA.  1987.  Memorandum from J. Orme, HEB, CSD/ODW to C. Vogt, Criteria
and Standards Divisibn, ODW, June 1987.

Wong, 0., R.W. Morgan and M.D. Whorton.  1983.  Comments on the NIOSH study of
leukemia in benzene workers.  Technical report submitted to Gulf Canada, Ltd.,
by Environmental Health Associates.
                                       12-21

-------
                                       Toluene

                CARCINOGENICITY ASSESSMENT FOR LIFETIME  EXPOSURE
 Substance Name:   Toluene
 CASRN:            108-88-3
             EVIDENCE FOR CLASSIFICATION AS  TO HUMAN CARCINOGENICITY
 WEIGHT-OF-EVIDENCE CLASSIFICATION

 Classification:   D;  not classifiable  as  to human  carcinogenic!ty

 BASIS

 No human data and inadequate  animal data.  Toluene did not produce positive
 results  in the majority of genotoxic  assays.

 HUMAN CARCINOGENICITY DATA

 None.

 ANIMAL CARCINOGENICITY DATA

 A chronic (106-week)  bioassay of  toluene in F344  rats of both sexes reported no
 carcinogenic  responses (CUT, 1980).  A total of  960 rats were exposed by
 inhalation for 6  hours/day, 5 days/week to toluene at 0, 30, 100, or  300 ppra.
 Groups of 20/sex/dose were sacrificed at 18 months.  Gross and microscopic
 examination of tissues and organs identified no increase in neoplastic tissue
 or tumor masses among treated rats when compared  with controls.  The  study is
 considered inadequate because the highest dose administered was well  below the
 MTD for  toluene and because of the high incidence of lesions and pathological
 changes  in the control animals.

 Several  studies have  examined the carcinogenicity of toluene following repeated
 dermal applications.   Toluene (dose not reported) applied to shaved
 interscapular  skin of 54 male mice (strains A/He, C3HeB, SWR) throughout their
 lifetime  (3 times weekly)  produced no carcinogenic response (Poel, 1963).  One
 drop of  toluene (about 6 mL)  applied  to the dorsal skin of 20 random-bred
 albino mice twice weekly for  50 weeks caused no skin papillomas or carcinomas
 after a  1-year latency period was allowed (Coombs et al., 1973).  No  increase
 in  the incidence of skin or systemic  tumors was demonstrated in male  or female
mice of  three strains  (CF, C3H, or CBaH) when toluene was applied to  the back
of  25 mice of each sex  of  each strain at 0.05-0.1 raL/mouse, twice weekly for 56
weeks  (Doak et al., 1976).  One skin papilloma and a single skin carcinoma were
reported among a group  of  30  mice treated dermally with one drop of 0.22 (w/v)
solution toluene twice weekly, administered from  droppers delivering  16-20 uL
per drop for 72 weeks  (Lijinsky and Garcia, 1972).  It is not reported whether
evaporation of toluene  from the skin was prevented during these studies.
                                       12-22

-------
 SUPPORTING DATA FOR CARCINOGENICITY

 Toluene was found to be  nonmutagenic  in reverse mutation assays with S.
 typhimurium (Mortelraans  and Riccio, 1980; Nestmann et al., 1980; Bos et al.,
 1981;  Litton Bionetics,  Inc.,  1981; Snow et al., 1981) and E. coli  (Mortelmans
 and Riccio,  1980),  with  and without metabolic activation.  Toluene  did not
 induce mitotic  gene conversion (Litton Bionetics, Inc., 1981; Mortelmans and
 Riccio, 1980) or mitotic crossing over (Mortelmans and Riccio, 1980) in S.
 cerevisiae.   Although Litton Bionetics, Inc. (1981) reported that toluene did
 not cause  increased chromosomal aberrations in bone marrow cells, several
 Russian studies (Dobrokhotov,  1972; Lyapkalo, 1973) report toluene  as effective
 in causing chromosal damage in bone marrow cells of rats.  There was no
 evidence of chromosomal  aberrations in blood lymphocytes of workers exposed to
 toluene only (Maki-Paakkanen et al.,  1980; Forni et al., 1971), although a
 slight increase was noted in workers  exposed to toluene and benzene (Forni et
 al.,  1971;  Funes-Craviota et al., 1977).  This finding is supported by studies
 of cultured human lymphocytes  exposed to toluene in vitro; no elevation of
 chromosomal aberrations  or sister chromatid exchanges was observed
 (Gerner-Smidt and Friedrich, 1978).

    — QUANTITATIVE ESTIMATE OF CARCINOGENIC RISK FROM INHALATION EXPOSURE —

 No Data Available

    	 EPA DOCUMENTATION AND REVIEW 	

 Source Document:   U.S. EPA.  1987.  Drinking Water Criteria Document for
 Toluene.   Prepared by the Office of Health and Environmental Assessment,
 Environmental Criteria and Assessment Office, Cincinnati, OH for the Office of
 Drinking Water,  Washington,  DC.

 The values  in the 1987 Drinking Water Criteria Document for Toluene have
 received peer and administrative review.

 Agency Work  Group Review:   09/15/87

 Verification Date:   09/15/87

   	  EPA CONTACTS (CARCINOGENICITY ASSESSMENT) 	
Dharra Singh / OHEA --  (202)260-5958

Robert McGaughy / OHEA -- (202)260-5898

   	 BIBLIOGRAPHY
Bos, R.P., R.M.E. Brouns, R. van Doom, J.L.G. Theuws and P.Th. Henderson.
1981.  Non-mutagenicity of toluene, o-, m- andp-xylene, o-methylbenzylalcohol
and o-methylbenzylsulfate in the Ames assay.  Mutat. Res.  88(3): 273-279.

CUT (Chemical Industry Institute of Toxicology).  1980.  A twenty-four-month
inhalation toxicology study in Fischer-344 rats exposed to atmospheric toluene.
                                       12-23

-------
 Executive Summary and Data Tables,  October 15.    CUT,  Research Triangle Park,
 NC.

 Coombs,  M.M.,  T.S.  Bhatt and C.J.  Croft.   1973.   Correlation between
 carcinogenicity and chemical structure in cyclopenta(a)phenanthrenes.   Cancer
 Res.   33(4):  832-837.

 Doak,  S.M.A.,  B.J.E.  Simpson,  P.P.  Hunt and D.E.  Stevenson.   1976.   The
 carcinogenic  response  in mice  to the topical application of  propane  sultone to
 the  skin.  Toxicology.   6:  139-154.

 Dobrokhotov,  V.B.   1972.   The  mutagenic influence of benzene and toluene under
 experimental  conditions.   Gig.  Sanit.   37:  36-39.   (Rus.)  (Evaluation based on
 an English translation provided by  the U.S.  EPA.)

 Forni, A.,  E.  Pacifico  and A.  Limonta.   1971.  Chromosome  studies  in workers
 exposed  to benzene  or  toluene  or both.   Arch. Environ.  Health.   22(3):  373-378.

 Funes-Craviota,  F., B.  Kolmodin-hedman,  J.  Lindsten,  et al.   1977.   Chromosome
 aberrations and sister-chroraatid exchange in workers  in chemical laboratories
 and  a  rotoprinting  factory and in children of women laboratory  workers.
 Lancet.   2: 322-325.

 Gerner-Smidt,  P.  and U.  Friedrich.   1978.   The mutagenic effect of benzene,
 toluene  and xylene  studied by  the SCE  technique.   Mutat. Res.   58(2-3):
 313-316.

 Lijinsky, W. and H. Garcia.  1972.   Skin  carcinogenesis tests of hydrogenated
 derivatives of anthanthrene and other  polynuclear  hydrocarbons.   Z.
 Krebsforsch. Klin. Onkol.   77:  226-230.

 Litton Bionetics, Inc.   1981.   Mutagenicity  Evaluation  of  Toluene Mouse
 Dominant  Lethal  Assay.   Final Report.   Submitted  to the American Petroleum
 Institute, Washington,  DC  in January,  1981.  LBI  Project No.  21141-05.   Litton
 Bionetics,  Inc., Kansington, MD.  p. 58.

 Lyapkalo, A.A.   1973.   Genetic  activity of benzene  and  toluene.  Gig. Tr. Prof.
 Zabol.  17(3): 24-28.   (Rus.)   (Evaluation based on an  English  translation
 provided by the U.S. EPA.)

 Maki-Paakkanen, J., K. Husgafvel-Pursiainen, P.L. Kalliomaki, J. Tuominen and
 M. Sorsa.  1980.  Toluene-exposed workers and chromosome aberrations.   J.
 Toxicol.  Environ. Health.   6: 775-781.

 Mortelmans, K.E. and E.S. Riccio.  1980.  In vitro  microbiological genotoxicity
 assays of toluene.  Prepared by  SRI  International,  Menlo Park,  CA, under
 Contract No. 68-02-2947 for  the U.S. EPA, Research  Triangle  Park, NC.   p. 25.

Nestmann, E.R., E.G.H. Lee, T.I. Matula, G.R. Douglas and J.C. Mueller.   1980.
Mutagenicity of constituents identified in pulp and paper mill  effluents  using
 the Salmonella/mammalian-microsome assay.  Mutat. Res.   79:  203-212.
                                       12-24

-------
Poel, W.E.  1963.  Skin as a test site for the bioassay of carcinogens and
carcinogen precursors.  Natl. Cancer Inst. Honogr.  10: 611-625.

Snow, L.,  F. MacNair and B.C. Casto.  1981.  Mutagenesis testing of toluene in
Salmonella strains TA100 and TA98.  Report prepared for the U.S. EPA by
Northrup Services, Inc., Research Triangle park, NC.

U.S. EPA.   1987.  Drinking Water Criteria Document for Toluene.  Prepared by
the Office of Health and Environmental Assessment, Environmental Criteria and
Assessment Office, Cincinnati, OH for the Office of Drinking Water, Washington,
DC.
                                       12-25

-------
                                 Arsenic.  inorganic

                CARCINOGENICITY ASSESSMENT FOR LIFETIME  EXPOSURE
 Substance Name:   Arsenic,  inorganic
 CASRN:            7440-38-2

 Note:  Important*'** Page  down to  see  oral  quantitative  estimate message.

    	 EVIDENCE FOR CLASSIFICATION AS TO HUMAN CARCINOGENICITY 	
 WEIGHT-OF-EVIDENCE CLASSIFICATION

 Classification:   A; human carcinogen

 BASIS

 based  on observation  of  increased  lung cancer mortality  in populations exposed
 primarily through inhalation  and on increased skin cancer incidence in several
 populations  consuming drinking water with high arsenic concentrations.

 HUMAN  CARCINOGENICITY DATA

 Studies  of smelter worker populations (Tacoma, WA; Magma, UT; Anaconda, MT;
 Ronnskar,  Sweden;  Saganoseki-Machii, Japan) have all found an association
 between  occupational  arsenic  exposure and lung cancer mortality  (Enterline and
 Marsh, 1982; Lee-Feldstein, 1983; Axelson et al., 1978;  Tokudome and Kuratsune,
 1976;  Rencher et  al.,  1977).  Both proportionate mortality and cohort studies
 of pesticide manufacturing workers have shown an excess  of lung cancer deaths
 among  exposed persons  (Ott et al., 1974; Mabuchi et al., 1979).  One study of a
 population residing near  a pesticide manufacturing plant revealed that these
 residents  were also at an excess risk of lung cancer (Matanoski et al., 1981).
 Case reports of arsenical pesticide applicators have also demonstrated an
 association between arsenic exposure and lung cancer (Roth, 1958).

 A cross-sectional  study of 40,000 Taiwanese exposed to arsenic in drinking
 water  found significant excess skin cancer prevalence by comparison to 7500
 residents  of Taiwan and Matsu who consumed relatively arsenic-free water (Tseng
 et al.,  1968).  This  study design limited its usefulness in risk estimation.
 Arsenic-induced skin  cancer has also been attributed to  water supplies in
 Chile, Argentina and Mexico (Borgono and Greiber, 1972;  Bergoglio, 1964;
 Cebrian  et al., 1983).  No excess skin cancer incidence  has been observed in
 U.S. residents consuming  relatively high levels of arsenic in drinking water
 (Morton  et al., 1976;  Southwick et al.,  1981).  The results of these U.S.
 studies,  however, are not necessarily inconsistent with  the existing findings
 from the foreign populations.   The statistical powers of the U.S. studies are
 considered to be inadequate because of the small sample  size.

A follow-up study  (Tseng,  1977) of the population living in the same area of
Taiwan, where arsenic contamination of the water supply was endemic, found
 significantly elevated standard mortality ratios for cancer of the bladder,
 lung, liver,  kidney, skin and colon.   This study of bladder, liver and lung

                                       12-26

-------
cancer cases in the endemic area found a significant association with arsenic
exposure that was dose-related.  The association of arsenic ingestion and
cancer of various internal organs has also been cited in a number of case
reports (Chen et al., 1985, 1986).  Persons treated with arsenic-containing
medicinals have also been shown to be at a risk of skin cancer (Sommers and
McManus, 1953).

ANIMAL CARCINOGENICITY DATA

None.  There has not been consistent demonstration of arsenic carcinogenicity
in test animals for various chemical forms administered by different routes to
several species (IARC, 1980).  There are some data to indicate that arsenic may
produce animal tumors if retention time in the lung can be increased (Pershagen
et al., 1982, 1984).

SUPPORTING DATA FOR CARCINOGENICITY

Sodium arsenate has been shown to transform Syrian hamster embryo cells
(Dipaolo and Casto, 1979) and to produce sister-chromatid-exchange in DON
cells, CHO cells and human peripheral lymphocytes exposed in vitro (Wan et al.,
1982; Ohno et al., 1982; Larramendy et al., 1981; Andersen, 1983; Crossen,
1983).  While arsenic compounds have not been shown to mutate bacterial
strains, it produces preferential killing of repair deficient strains (Rossman,
1981).

   — QUANTITATIVE ESTIMATE OF CARCINOGENIC RISK FROM INHALATION EXPOSURE —

Unit Risk:             4.3E-3 per (ug/cu.m)
Extrapolation Method:  absolute-risk linear model

Air Concentrations at Specified Risk Levels:

   Risk Level               Concentration
   E-4 (1 in 10,000)        2E-2 per (ug/cu.m)
   E-5 (1 in 100,000)       2E-3 per (ug/cu.m)
   E-6 (1 in 1,000,000)     2E-4 per (ug/cu.m)
                                       12-27

-------
            DOSE-RESPONSE DATA (CARCINOGENICITY,  INHALATION EXPOSURE)
 Tumor Type:              lung cancer
 Test Animals:           human, male
 Route:                  inhalation, occupational exposure

                          Ambient Unit Risk Estimates
Exposure
Source
Anaconda
smelter
Study
Brown and Chu,
1983a,b,c
Unit
Risk
1.25 E-3
Geometric Mean
Unit Risk

Final Estimates
Unit Risk

            Lee-Feldstein,  1983   2.80 E-3     2.56  E-3
            Higgins,  1982;         4.90 E-3                       4.29  E-3
            Higgins et al.,  1982;
            Welch et al.,  1982

 ASARCO     Enterline and         6.81 E-3     7.19  E-3
 smelter    Marsh,  1982           7.60 E-3
           ADDITIONAL COMMENTS  (CARCINOGENICITY,  INHALATION  EXPOSURE)
 A geometric  mean was  obtained for  data  sets obtained within  distinct  exposed
 populations  (U.S.  EPA,  1984).   The final  estimate  is the  geometric mean  of
 those  two values.   It was  assumed  that  the increase in  age-specific mortality
 rate of lung cancer was a  function only of cumulative exposures.

 The unit risk should  not be used if the air concentration exceeds 2 ug/cu.m,
 since  above  this concentration the unit risk may not be appropriate.

   	 DISCUSSION OF CONFIDENCE (CARCINOGENICITY. INHALATION EXPOSURE)  	
Overall a  large study population was observed.  Exposure assessments  included
air measurements for the Anaconda smelter and both air measurements and  urinary
arsenic for the ASARCO smelter.  Observed lung cancer incidence was
significantly increased over expected values.  The range of  the estimates
derived from data from two different exposure areas was within a  factor  of  6.
                         EPA DOCUMENTATION AND REVIEW
Source Document:  U.S. EPA.  1984.  Health Assessment Document for Inorganic
Arsenic.  Environmental Criteria and Assessment Office, Research Triangle Park,
NC.  EPA 600/8-83-021F.

The 1984 Health Assessment Document for Inorganic Arsenic received Agency and
external review including a review by SAB.

Agency Work Group Review:  01/13/88

Verification Date:  01/13/88
                                       12-28

-------
                   EPA CONTACTS  (CARCINOGENICITY ASSESSMENT)
Herman Gibb / OHEA  --  (202)260-5898

Chao Chen / OHEA  --  (202)260-5719

   	 BIBLIOGRAPHY
Anderson, 0.  1983.  Effects of coal combustion products and metal compounds on
sister chromatid exchange  (SCE) in a raacrophage cell line.  Environ. Health
Perspect.  47:  239-253.

Axelson, 0., E. Dahlgren,  C.D. Jansson and S.O. Rehnlund.  1978.  Arsenic
exposure and mortality: A  case referent study front a Swedish copper smelter.
Br. J. Ind. Med.   35: 8-15.

Bergoglio, R.M.  1964.  Mortality from cancer in regions of arsenical waters of
the province of Cordoba Argentine Republic.  Prensa Med. Argent.  51: 994-998.

Borgono, J.M. and  R. Greiber.  1972.  Epidemiological study of arsenicism in
the city of Antofagasta. In: Trace Substances in Environmental Health-V.
Proceed. 5th Annual Conference, University of Missouri, Columbia, MO, June
29-July 1, 1971. D.C. Hemphill, Ed., University of Missouri, Columbia, MO.  p.
13-24.

Brown, C.C. and K.C. Chu.  1983a.  Approaches to epidemiologic analysis of
prospective and retrospective studies: Example of lung cancer and exposure  to
arsenic.  In: Risk Assessment Proc. SIMS Conf. on Environ. Epidemiol. June
28-July 2, 1982, Alta, VT.  SIAM Publication.

Brown, C.C. and K.C. Chu.  1983b.  Implications of the multistage theory of
carcinogenesis  applied to  occupational arsenic exposure.  J. Natl. Cancer Inst.
 70: 455-463.

Brown, C.C. and K.C. Chu.  1983c.  A new method for the analysis of cohort
studies, implications of the multistage theory of carcinogenesis applied to
occupational arsenic exposure.  Environ. Health Perspect.  50: 293-308.

Cebrian, M.E.,  A.  Albores, M. Aguilar and E. Blakely.  1983.  Chronic arsenic
poisoning in the north of Mexico.  Human Toxicol.  2: 121-133.

Crossen, P.E.   1983.  Arsenic and SCE in human lymphocytes.  Mutat. Res.  119:
415-419.

DiPaolo, J. and B.  Casto.  1979.  Quantitative studies of in vitro
morphological transformation of Syrian hamster cells by inorganic metal salts.
Cancer Res.  39: 1008-1013.

Higgins, I.  1982.   Arsenic and respiratory cancer amony a sample of Anaconda
smelter workers.   Report submitted to the Occupational Safety and Health
Administration  in  the comments of the Kennecott Minerals Company on the
inorganic arsenic  rulemaking.  (Exhibit 203-5)

                                       12-29

-------
Higgins, I., K. Welch and C. Burchfield.  1982.  Mortality of Anaconda smelter
workers in relation to arsenic and other exposures.  University of Michigan,
Dept. Epidemiology, Ann Arbor, MI.

IARC  (International Agency for Research on Cancer).  1980.  IARC Monographs on
the Evaluation of Carcinogenic Risk of Chemicals to Man, Vol. 23.  Some Metals
and Metallic Compounds.  World Health Organization, Lyon, France.

Larramendy, M.L., N.C. Popescu and J. DiPaolo.  1981.  Induction by inorganic
metal salts of sister chromatid exchanges and chromosome aberrations in human
and Syrian hamster strains.  Environ. Mutagen.  3: 597-606.

Lee-Feldstein, A.  1983.  Arsenic and respiratory cancer in man: Follow-up of
an occupational study.  In: Arsenic: Industrial, Biomedical, and Environmental
Perspectives, W. Lederer and R. Fensterheim, Ed.  Van Nostrand Reinhold, New
York.

Mabuchi, K., A. Lilienfeld and L. Snell.  1979.  Lung cancer among pesticide
workers exposed to inorganic arsenicals.  Arch. Environ. Health.  34: 312-319.

Matanoski, G., E. Landau, J. Tonascia, C. Lazar, E. Elliot, W. McEnroe and K.
King.  1981.  Cancer mortality in an industrial area of Baltimore.  Environ.
Res.  25: 8-28.

Morton, W., G. Starr, D. Pohl, J. Stoner, S. Wagner and P. Weswig.  1976. Skin
cancer and water arsenic in Lane County, Oregon.  Cancer.  37: 2523-2532.

Ohno, H., F. Hanaoka and M. Yamada.  1982.  Inductibility of sister chromatid
exchanges by heavy-metal ions.  Mutat. Res.  104: 141-145.

Ott, M.G., B.B.Holder and H.I. Gordon.  1974.  Respiratory cancer and
occupational exposure to arsenicals.  Arch. Environ. Health.  29: 250-255.

Pershagen, G., B. Lind and N.E. Bjorkund.  1982.  Lung retention and toxicity
of some inorganic arsenic compounds.  Environ. Res.  29: 425-434.

Pershagen, G., G. Nordberg and N.E. Bjorklund.  1984.  Carcinomas of the
respiratory tract in hamsters given arsenic trioxide and/or benzo(a)pyrene by
the pulmonary route.  Environ. Res.  34: 227-241.

Rencher, A.C., M.W. Carter and D.W. McKee.  1978.  A retrospective
epidemiological study of mortality at a large western copper smelter.  J.
Occup. Med.   19: 754-758.

Rossman, T.G.  1981.  Enhancement of UV-mutagenesis by low concentrations of
arsenite in E. Coll.  Mutat. Res.  91: 207-211.

Roth, F.  1958.  Uber den Bronchialkrebs Arsengeschodigter Winzer.  Virchows
Arch.  331:  119-137.
                                       12-30

-------
Somners, S.C. and R.G. McManus.   1953.   Multible arsenical cancers of the skin
and internal organs.  Cancer.   6: 347-359.

Southwick, J., A. Western, M.  Beck, T.  Whitley,  R.  Isaacs, J.  Petajan and C.
Hansen.  1981.  Community health associated with arsenic in drinking water in
Millard County, Utah.  Health Effects Research Laboratory, Cincinnati, OH,
EPA-600/1-81-064.

Tokudome, S. and M. Kuratsune.  1976.  A cohort study on mortality from cancer
and other causes among workers at a metal refinery.  Int. J. Cancer.  17:
310-317.

Tseng, W.P.  1977.  Effects and dose response relationships of skin cancer and
blackfoot disease with arsenic.   Environ. Health Perspect.  19: 109-119.

U.S. EPA.  1984.  Health Assessment Document for Inorganic Arsenic.  Prepared
by Environmental Criteria and Assessment Office, Research Triangle Park, NC.
EPA/600/8-83/021F.

Wan, B., R.T. Christian and S.W. Sookup.  1982.   Studies of cytogenetic effects
of sodium arsenicals on mammalian cells in vitro.  Environ. Mutag.  4: 493-498.

Welch, K., I. Higgins, M. Oh and C. Burchfield.   1982.  Arsenic exposure,
smoking, and respiratory cancer in copper smelter workers.  Arch. Environ.
Health.  37: 325-335.
                                       12-31

-------
                                      Cadmium

               CARCINOGENICITY ASSESSMENT FOR LIFETIME EXPOSURE
Substance Name:  Cadmium
CASRN:           7440-43-9
            EVIDENCE FOR CLASSIFICATION AS TO HUMAN CARCINOGENICITY
WEIGHT-OF-EVIDENCE CLASSIFICATION

Classification:  Bl; probable human carcinogen

BASIS

Limited evidence from occupational epidemiologic studies of cadmium is
consistent across investigators and study populations.  There is sufficient
evidence of careinogenieity in rats and mice by inhalation and intramuscular
and subcutaneous injection.  Seven studies in rats and mice wherein cadmium
salts (acetate, sulfate, chloride) were administered orally have shown no
evidence of carcinogenic response.

HUMAN CARCINOGENICITY DATA

Limited.  A 2-fold excess risk of lung cancer was observed in cadmium smelter
workers.  The cohort consisted of 602 white males who had been employed in
production work a minimum of 6 months during the years 1940-1969.  The
population was followed to the end of 1978.  Urine cadmium data available for
261 workers employed after 1960 suggested a highly exposed population.  The
authors were able to ascertain that the increased lung cancer risk was probably
not due to the presence of arsenic or to smoking (Thun et al., 1985).  An
evaluation by the Carcinogen Assessment Group of these possible confounding
factors has indicated that the assumptions and methods used in accounting for
them appear to be valid.  As the SMRs observed were low and there is a lack of
clear cut evidence of a causal relationship of the cadmium exposure only, this
study is considered to supply limited evidence of human carcinogenicity.

An excess lung cancer risk was also observed in three other studies which were,
however, compromised by the presence of other carcinogens (arsenic, smoking) in
the exposure or by a small population (Varner, 1983; Sorahan and Waterhouse,
1983;  Armstrong and Kazantzis, 1983).

Four studies of workers exposed to cadmium dust or fumes provided evidence of a
statistically significant positive association with prostate cancer (Kipling
and Waterhouse, 1967; Lemen et al., 1976; Holden, 1980; Sorahan and Waterhouse,
1983),  but the total number of cases was small in each study.  The Thun et al.
(1985)  study is an update of an earlier study (Lemen et al., 1976) and does not
show excess prostate cancer risk in these workers.  Studies of human ingestion
of cadmium are inadequate to assess carcinogenicity.
                                       12-32

-------
ANIMAL CARCINOGENICITY DATA

Exposure of Wistar rats by inhalation to cadmium as cadmium chloride at
concentrations of 12.5, 25 and 50 ug/cu.m for 18 months, with an additional
13-month observation period, resulted in significant increases in lung tumors
(Takenaka et al., 1983).  Intratracheal instillation of cadmium oxide did not
produce lung tumors in Fischer 344 rats but rather mammary tumors in males and
tumors at multiple sites in males (Sanders and Mahaffey, 1984).  Injection site
tumors and distant site tumors (for example, testicular) have been reported by
a number of authors as a consequence of intramuscular or subcutaneous
administration of cadmium metal and chloride, sulfate, oxide and sulfide
compounds of cadmium to rats and mice (U.S. EPA, 1985).  Seven studies in rats
and mice where cadmium salts (acetate, sulfate, chloride) were administered
orally have shown no evidence of a carcinogenic response.

SUPPORTING DATA FOR CARCINOGENICITY

Results of mutagenicity tests in bacteria and yeast have been inconclusive.
Positive responses have been obtained in mutation assays in Chinese hamster
cells (Dom and V79 lines) and in mouse lymphoma cells (Casto, 1976; Ochi and
Ohsawa, 1983; Oberly et al., 1982).

Conflicting results have been obtained in assays of chromosomal aberrations in
human lymphocytes treated in vitro or obtained from exposed workers.  Cadmium
treatment in vivo or in vitro appears to interfere with spindle formation and
to result in aneuploidy in germ cells of mice and hamsters (Shimada et al.,
1976; Watanabe et al., 1979; Gilliavod and Leonard, 1975).
           DOSE-RESPONSE DATA (CARCINOGENICITY, INHALATION EXPOSURE)
Tumor Type:             lung, trachea, bronchus cancer deaths
Test Animals:           human/white male
Route:                  inhalation, occupational exposure

                                            No. of Expected     Observed No.
                                           Lung, Trachea and     of Deaths
 Cumulative                    24 hour/    Bronchus Cancers    (lung, trachea,
  Exposure        Median       ug/cu.m        Assuming No        bronchus
(mg/day/cu.m)   Observation   Equivalent    Cadmium Effect       cancers)


less than or
equal to 584        280           168            3.77               2

   585-2920        1210           727            4.61               7

greater than
or equal to
2921               4200          2522            2.50               7

The 24-hour equivalent - median observation x 1E+3 x 8/24 x 1/365 x 240/365.


                                       12-33

-------
           ADDITIONAL COMMENTS (CARCINOGENICITY, INHALATION EXPOSURE)
 The unit risk should not be used if the air concentration exceeds 6 ug/cu.m,
 since above this concentration the unit risk nay not be appropriate.

    	 DISCUSSION OF CONFIDENCE (CARCINOGENICITY, INHALATION EXPOSURE) 	
 The data were derived from a relatively large cohort.  Effects of arsenic and
 smoking were accounted for in the quantitative analysis for cadmium effects.

 An inhalation unit risk for cadmium based on the Takenaka et al. (1983)
 analysis is 9.2E-2 per (ug/cu.m).  While this estimate is higher than that
 derived from human data [1.8E-3 per (ug/cu.m)] and thus more conservative, it
 was felt that the use of available human data was more reliable because of
 species variations in response and the type of exposure (cadmium salt vs.
 cadmium fume and cadmium oxide).
                          EPA DOCUMENTATION AND REVIEW
 Source Document:   U.S.  EPA.   1985.   Updated Mutagenicity and Carcinogenicity
 Assessment of Cadmium:  Addendum to  the Health Assessment Document for Cadmium
 (May 1981,  EPA 600/B-B1-023).   EPA  600/B-83-025F.

 The Addendum to the Cadmium Health  Assessment has  received both Agency and
 external  review.

 Agency Work Group  Review:  11/12/86
 Verification Date:   11/12/86
                    EPA CONTACTS  (CARCINOGENICITY ASSESSMENT)
William  Pepelko  / OHEA  --  (202)260-5904

David Bayliss /  OHEA  --  (202)260-5726

   	 BIBLIOGRAPHY
Armstrong, B.C. and G. Kazantzis.   1983.  The mortality of cadmium workers.
Lancet.  June 25, 1983: 1425-1427.

Casto, B.  1976.  Letter to Richard Troast, U.S. EPA. Enclosing mutagenicity
data on cadmium chloride and cadmium acetate.

Gilliavod, N. and A. Leonard.  1975.  Mutagenicity tests with cadmium  in the
mouse.  Toxicology.  5: 43-47.

Holden, H.  1980.  Further mortality studies on workers exposed to cadmium
fumes.  Presented at Seminar on Occupational Exposure to Cadmium, March 20,
1980, London, England.

Kipling,  M.D. and J.A.H.  Waterhouse.  1967.  Cadmium and prostatic carcinoma.
Lancet.  1: 730.

                                       12-34

-------
Lemen, R.A., J.S. Lee, J.K. Wagoner andH.P. Blejer.  1976.  Cancer mortality
among cadmium production workers.  Ann. N.Y. Acad. Sci.  271: 273.

Oberly, T., C.E. Piper and D.S. McDonald.  1982.  Mutagenicty of metal salts in
the L5178 Y mouse lymphoma assay.  J. Toxicol. Environ. Health.  9: 367-376.

Ochi, T. and M. Ohsawa.  1983.  Induction of 6-thioguanine-resistant mutants
and single-strand scission DNA by cadmium chloride in cultured Chinese hamster
cells.  Mutat. Res.  Ill: 69-78.

Sanders, C.L. and J.A. Mahaffey.  1984.  Carcinogenicity of single and multiple
intratracheal instillations of cadmium oxide in the rat.  Environ. Res.  33:
227-233.

Shimada, T., T. Watanabe and A. Endo.  1976.  Potential mutagenicity of cadmium
in mammalian oocytes.  Mutat. Res.  40: 389-396.

Sorahan, T. and J.A.H. Waterhouse.  1983.  Mortality study of nickel-cadmium
battery workers by the method of regression models in life tables.  Br. J. Ind.
Med.  40: 293-300.

Takenaka, S., H. Oldiges, H. Konig, D. Hochrainer and G. Oberdoerster.  1983.
Carcinogenicity of cadmium aerosols in Vistar rats.  J. Natl. Cancer Inst.  70:
367-373.

Thun, M.J., T.M. Schnorr, A.B. Smith and W.E. Halperin.  1985.  Mortality among
a cohort of U.S. cadmium production workers: An update.  J. Natl. Cancer Inst.
74(2): 325-333.

U.S. EPA.  1985.  Updated Mutagenicity and Carcinogenicity Assessment of
Cadmium.  Addendum to the Health Assessment Document for Cadmium (EPA
600/B-B1-023). EPA 600/B-83-025F.

Varner, M.O.  1983.  Updated epidemiologic study of cadmium smelter workers.
Presented at the Fourth International Cadmium Conference. Unpublished.

Watanabe, T., T. Shimada and A. Endo.  1979.  Mutagenic effects of cadmium on
mammalian oocyte chromosomes.  Mutat. Res. 67: 349-356.
                                       12-35

-------
                                    Chromium(VI)

               CARCINOGENICITY ASSESSMENT FOR LIFETIME EXPOSURE
Substance Name:  Chromlum(VI)
CASRN:           18540-29-9
            EVIDENCE FOR CLASSIFICATION AS TO HUMAN CARCINOGENICITY
WEIGHT-OF-EVIDENCE CLASSIFICATION

Classification:  A; human carcinogen

BASIS

Results of occupational epidemiologic studies of chromium-exposed workers are
consistent across investigators and study populations.  Dose-response
relationships have been established for chromium exposure and lung cancer.
Chromium-exposed workers are exposed to both chromium III and chromium VI
compounds.  Because only chromium VI has been found to be carcinogenic in
animal studies, however, it was concluded that only chromium VI should be
classified as a human carcinogen.

HUMAN CARCINOGENICITY DATA

Sufficient.  Epidemiologic studies of chromate production facilities in the
United States (Machle and Gregorius, 1948; Brinton et al., 1952; Mancuso and
Hueper, 1951, Mancuso, 1975; Baetjer, 1950; Taylor, 1966; Enterline, 1974;
Hayes et al., 1979; Hill and Ferguson, 1979), Great Britain (Bidstrup, 1951;
Bidstrup and Case, 1956; Alderson et al., 1981), Japan (Vatanabe and Fukuchi,
1975; Ohsaki et al., 1978; Sano and Mitohara, 1978; Satoh et al., 1981) and
West Germany (Korallus et al., 1982; Bittersohl, 1971) have established an
association between chromium (Cr) exposure and lung cancer.  Most of these
studies did not attempt to determine whether Cr III or Cr VI compounds were the
etiologic agents.

Three studies of the chrome pigment industry, one in Norway (Langard and
Norseth, 1975), one in England (Davies, 1978, 1979), and the third in the
Netherlands and Germany (Frentzel-Beyme, 1983) also found an association
between occupational chromium exposure (predominantly to Cr VI) and lung
cancer.

Results of two studies of the chromium plating industry (Royle, 1975;
Silverstein et al., 1981) were inconclusive, while the findings of a Japanese
study of chrome platers were negative (Okubo and Tsuchiya, 1979).  The results
of studies of ferrochromium workers (Pokrovskaya and Shabynina, 1973; Langard
et al., 1980; Axelsson et al., 1980) were inconclusive as to lung cancer risk.

ANIMAL CARCINOGENICITY DATA

Sufficient.  Hexavalent chromium compounds were carcinogenic in animal assays
producing the following tumor types:  intramuscular injection site tumors in

                                       12-36

-------
Fischer 344 and Bethesda Black rats and in C57BL mice (Furst et al.,  1976;
Maltoni, 1974, 1976; Payne, 1960; Heuper and Payne,  1959);  intraplural implant
site tumors for various chromium VI compounds in Sprague-Dawley and Bethesda
Black rats (Payne, 1960; Heuper 1961; Heuper and Payne,  1962);  intrabronchial
implantation site tumors for various Cr VI compounds in Wistar rats (Levy and
Martin, 1983; Laskin et al., 1970; Levy as quoted in NIOSH, 1975);  and
subcutaneous injection site sarcomas in Sprague-Dawley rats (Maltoni,  1974,
1976).

SUPPORTING DATA FOR CARCINOGENICITY

A large number of chromium compounds have been assayed in in vitro genetic
toxicology assays.  In general, hexavalent chromium is mutagenic in bacterial
assays whereas trivalent chromium is not (Lofroth, 1978; Petrellie and Flora,
1977, 1978).  Likewise Cr VI but not Cr III was mutagenic in yeasts (Bonatti et
al., 1976) and in V79 cells (Newbold et al., 1979).   Chromium  III and VI
compounds decrease the fidelity of DNA synthesis in vitro (Loeb et al., 1977),
while Cr VI compounds inhibit replicative DNA synthesis in mammalian cells
(Levis et al., 1978) and produce unscheduled DNA synthesis, presumably repair
synthesis, as a consequence of DNA damage (Raffetto, 1977).  Chrornate has been
shown to transform both primary cells and cell lines (Fradkin et al., 1975;
Tsuda and Kato, 1977; Casto et al., 1979).  Chromosomal effects produced by
treatment with chromium compounds have been reported by a number of authors;
for example, both Cr VI and Cr III salts were clastogenic for cultured human
leukocytes (Nakamuro et al., 1978).

There are no long-term studies of ingested Cr VI.  There appears to be
significant in vivo conversion of Cr VI to Cr III and III to VI; Cr III is an
essential trace element.
   — QUANTITATIVE ESTIMATE OF CARCINOGENIC RISK FROM INHALATION EXPOSURE —

Unit Risk:             1.2E-2 per (ug/cu.m)
Extrapolation Method:  Multistage, extra risk

Air Concentrations at Specified Risk Levels:

   Risk Level               Concentration
   E-4 (1 in 10,000)        8E-3 per (ug/cu.m)
   E-5 (1 in 100,000)       8E-4 per (ug/cu.m)
   E-6 (1 in 1,000,000)     8E-5 per (ug/cu.m)
                                       12-37

-------
           DOSE-RESPONSE DATA (CARCINOGENICITY, INHALATION EXPOSURE)
Tumor Type:              lung cancer
Test Animals:           human
Route:                  inhalation, occupational exposure
                                       12-38

-------
Midrange
(ug/cu.m)
5.66
25.27
46.83
4.68
20.79
39.08
4.41
21.29
Deaths from
Lung Cancer
3
6
6
4
5
5
2
4
Person
Years
1345
931
299
1063
712
211
401
345
Exposure Level
Subject Age
(years)

   50
   60
   70
          ADDITIONAL COMMENTS (CARCINOGENICITY, INHALATION EXPOSURE)

The cancer mortality in Mancuso (1975) was assumed to be due to Cr VI,  which
was further assumed to be no less than one-seventh of total chromium.  It was
also assumed that the smoking habits of chromate workers were similar to those
of the U.S. white male population.  The unit risks of Langard et al. (1980),
Axelsson et al. (1980), and Fokrovskaya and Shabynina (1973) are 1.3E-1, 3.5E-2
and 9.2E-2 per (ug/cu.m), respectively.

Hexavalent chromium compounds have not produced lung tumors in animals by
inhalation.  Trivalent chromium compounds have not been reported as
carcinogenic by any route of administration.

The unit risk should not be used if the air concentration exceeds 8E-1 ug/cu.m,
since above this concentration the unit risk may not be appropriate.

   	 DISCUSSION OF CONFIDENCE (CARCINOGENICITY, INHALATION EXPOSURE) 	

Results of studies of chromium exposure are consistent across investigators and
countries.  A dose-relationship for lung tumors has been established.  The
assumption that the ratio of Cr III to Cr VI is 6:1 may lead to a 7-fold
underestimation of risk.  The use of 1949 hygiene data, which may underestimate
worker exposure,  may result in an overestimation of risk.  Further
overestimation of risk may be due to the implicit assumption that the smoking
habits of chromate workers were similar to those of the general white male
population, since it is generally accepted that the proportion of smokers is
higher for industrial workers than for the general population.
                         EPA DOCUMENTATION AND REVIEW
Source Document:  U.S. EPA.  1984.  Health Assessment Document for Chromium.
Prepared by the Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH.  EPA 600/8-83-014F.

The quantification of cancer risk in the 1984 Health Assessment Document has
received peer review in public sessions of the Environmental Health Committee
of the U.S. EPA's Science Advisory Board.
                                       12-39

-------
 Agency Work Group Review:   06/26/86

 Verification Date:   06/26/86

    	 EPA CONTACTS (CARCINOGENICITY ASSESSMENT)

 Herman Gibb / OHEA --  (202)260-5898

 Chao Chen / OHEA --  (202)260-5719

    	 BIBLIOGRAPHY 	
 Alderson,  M.R.,  N.S.  Rattan and L.  Bidstrup.   1981.  Health of workmen  in  the
 chromate-producing industry in Britain.  Br. J.  Ind. Hed.  38: 117-124.

 Axelsson,  G., R.  Rylander  and  A.  Schmidt.   1980.  Mortality and  incidence  of
 tumours  among ferrochromium workers.   Br. J. Ind. Med.   37: 121-127.

 Baetjer, A.M.  1950a.   Pulmonary carcinoma  in  chromate workers.   I. A review of
 the  literature and report  of cases.  Arch.  Ind.  Hyg. Occup. Med.  2(5):
 487-504.

 Baetjer, A.M.  1950b.   Pulmonary carcinoma  in  chromate workers.   II. Incidence
 on basis of hospital  records.   Arch. Ind. Hyg. Occup. Med.  2(5): 505-516.

 flidstrup,  P.L.   1951.   Carcinoma of the lung in  chromate workers.  Br, J.  Med.
 8: 302-305.

 Bidstrup,  P.L. and R.A.M.  Case.   1956.  Carcinoma of the lung in workmen in the
 bichromates-producing industry in Great Britain.  Br. J. Ind. Med.  13:
 260-264.

 Bittersohl, G.   1971.   Epidemiological research  of cancer cases  in the  chemical
 industry.  Arch. Geschwulstforschl.  38(3-4):  198-209.

 Bonatti, S., M. Meini  and  A. Abbondandolo.  1976.  Genetic effects of potassium
 dichroraate in Schizosaccharomyces pombe.  Mutat. Res.  38: 147-150.

 Brinton, H.P., E.S. Frasier  and A.L. Koven.  1952.  Morbidity and mortality
 experience among chromate  workers.  Public Health Rep.  67(9): 835-847.

 Casto, B.C., J. Meyers  and J.A. DiPaolo.  1979.  Enhancement of viral
 transformation for  evaluation  of  the carcinogenic or mutagenic potential of
 inorganic metal salts.  Cancer  Res.  39: 193-198.

 Davies, J.M.  1978.  Lung-cancer mortality in workers making chrome pigments.
 Lancet.  1: 384.

 Davies, J.M.  1979.  Lung  cancer mortality of workers in chromate pigment
manufacture: An epidemiological survey.  J. Oil Chem. Assoc.   62: 157-163.
                                       12-40

-------
 Enterline.  F.E.   1974.  Respiratory cancer among chrornate workers.  J. Occup.
 Med.   16:  523-526.

 Pradkin, A., A. Janoff, B.F. Lane and M. Kuschner.  1975.  In vitro
 transformation of BHK21 cells grown in the presence of calcium chromate. Cancer
 Res.   35:  1058-1063.

 Frentzel-Beyme, R.  1983.  Lung cancer mortality of workers employed in
 chromate pigment  factories.  A multicentric European epidemiological study.  J.
 Cancer Res. Clin. Oncol.  105: 183-188.

 Furst, A.,  M. Schlauder and O.F. Sasmore.  1976.  Tumorigenie activity of lead
 chromate.   Cancer Res.  36: 1779-1783.

 Hayes, R.B., A.M. Lillenfeld and L.M. Snell.  1979.  Mortality in chromium
 chemical production workers: A prospective study.  Int. J. Epidemiol.  8(4):
 365-374.

 Hueper, V.C.  1961.  Environmental carcinogenesis and cancers.  Cancer Res  21*
 842-857.

 Hueper, tf.C. and W.W. Payne.  1959.  Experimental cancers in rats produced by
 chromium compounds and their significance to industry and public health.  Ind.
 Hyg.  J. 20: 274-280.

 Heuper, W.C. and W.W. Payne.  -1962.  Experimental studies in metal
 carcinogenesis: Chromium, nickel, iron, and arsenic.  Arch. Environ. Health  5-
 445-462.

 Hill, W.J. and W.S. Ferguson.  1979.  Statistical analysis of epidemiological
 data  from a chromium chemical manufacturing plant.  J. Occup. Med.  21(2):
 103-106.

 Korallus, U., H. Lange, A. Ness, E. Wustefeld and T. Zwingers.  1982.
 Relationships between precautionary measures and bronchial carcinoma mortality
 in the chronate-producing industry.  Arbeitsmedizin, Socialmedizin,
 Preventivmedizin.  17(7): 159-167.   (German - Eng. summary)

 Langard, S. and T. Norseth.  1975.  A cohort study of bronchial carinomas in
workers producing chromate pigments.  Br. J. Ind. Ked.  32: 62-65.

Langard, S., A. Anderson and B. Gylseth.  1980.  Incidence of cancer among
 ferrochromium and ferrosilicon workers.  Br. J. Ind, Med.  37: 114-120.

Laskin, S., M.  Kuschner and R.T. Drew,  1970.  Studies in pulmonary
carcinogenesis. In: M.G.  Hanna, Jr., P. Nettesheim, and J.R. Gilbert, Eds.
Inhalation Carcinogenesis, M.G. Hanna, Jr., P. Nettesheim, and J.R. Gilbert,
Eds.   U.S.  Atomic Energy Comm. Symp. Series.  Sponsored by the National Cancer
Institute and U.S. Atomic Energy Commission.  18: 321-350.
                                       12-41

-------
 Levis,  A.G.,  M.  Buttignol,  V.  Bianchl and G.  Sponza.   1978.   Effects  of
 potassium dichromate on nucleic acid and protein syntheses  and on precursor
 uptake  in BHK fibroblasts.   Cancer Res.   38:  110-116.

 Levy, L.S.  and P.A.  Martin.   1983.   The  effects  of a  range  of
 chromium-containing  materials  on rat lung.   Sponsored by  Dry  Color
 Manufacturers'  Association  and others.   (Unpublished)

 Loeb, L.A., M.A. Sirover and S.S.  Agarwal.   1977.   Infidelity of  DNA  synthesis
 as  related to mutagenesis and  carcinogenesis.  Adv. Exp.  Biol.  Med.   91:
 103-115.

 Lofroth,  G.   1978.   The mutagenicity of  hexavalent chromium is  decreased by
 microsomal metabolism.   Naturvissenschaften.   65:  207-208.

 Machle, U.  and F. Gregorius.   1948.   Cancer  of the respiratory  system in the
 United  States chromate-producing industry.   Public Health Rep.  63(35):
 1114-1127.

 Maltoni,  C.   1974.   Occupational carcinogenesis.   Excerpta  Med. Int.  Congr.
 Ser.  322:  19-26.

 Maltoni,  C.   1976.   Predictive value of  carcinogenesis bioassays.  Ann. NY.
 Acad. Sci.  271: 431-443.

 Mancuso,  T.F.   1975.  Consideration  of Chromium  as an  Industrial  Carcinogen.
 International Conference on  Heavy Metals  in  the  Environment,  Toronto,  Ontario,
 Canada, October  27-31.   p.  343-356.

 Mancuso,  T.F.  and W.C.  Hueper.   1951.  Occupational cancer  and  other  health
 hazards in a  chromate plant: A medical appraisal.   I.  Lung  cancers in chromate
 workers.   Ind. Med.  Surg.   20(8):  358-363.

 Nakamuro, K., K. Yoshikawa,  Y.  Sayato and H. Kurata.   1978.   Comparative
 studies of chromosomal  aberration and mutagenicity of  trivalent and hexavalent
 chromium.  Mutat. Res.   58:  175-181.

 Newbold,  R.F., J. Amos  and J.R.  Connell.  1979.  The cytotoxic, mutagenic and
 clastogenic effects  of  chromium-containing compounds on mammalian cells in
 culture.  Mutat. Res.   67: 55-63.

 NIOSH (National Institute for  Occupational Safety  and Health).  1975.  Criteria
 for a recommended standard occupational exposure to chromium  (VI). U.S.
 Department of Health, Education, and Welfare, Washington, DC.

 Ohsaki,  Y., S. Abe,  K.  Kimura,  Y. Tsuneta, H. Mikami and  M. Murao.  1978. Lung
 cancer in Japanese chromate workers.  Thorax.  33:  372-374.

 Okubo, T. and K. Tsuchiya.   1979.  Epidemiological  study  of chromium  platers in
Japan.  Biologic. Trace  Elem. Res.   1: 35-44.
                                       12-42

-------
Payne, W.W.  1960a.  The role of roasted chromite ore in the production of
cancer.  Arch. Environ. Health.  1: 20-26.

Payne, W.W.  1960b.  Production of cancers in mice and rats by chromium
compounds.  Arch. Ind. Health.  21: 530-535.

Petrilli, F.L. and S. DeFlora.  1977.  Toxicity and mutagencity of hexavalent
chromium on Salmonella typhimurium.  Appl. Environ. Microbiol.  33(4): 805-809.

Petrilli, F.L. and S. DeFlora.  1978.  Oxidation of inactive trivalent chromium
to the mutagenic hexavalent form.  Mutat. Res.  58: 167-178.

Pokrovskaya, L.V. and N.K. Shabynina.  1973.  Carcinogenic hazards in the
production of chromium ferroalloys.  Gig. Tr. Prof. Zabol.  10: 23-26.

Raffetto, G., S. Parodi, C. Parodi, M. DeFerrari, R. Troiano and G. Brambilla.
1977.  Direct interaction with cellular targets as the mechanism for chromium
carcinogenesis.  Tumori.  63: 503-512

Royle, H.  1975.  Toxicity of chromic acid in the chromium plating industry.
Environ. Res.  10: 141-163.

Sano, T. and I. Mitohara.  1978.  Occupational cancer among chromium workers.
Japanese J. Chest Disorders.  37(2): 90-101.

Satoh, K., Y. Fukuda, K. Torii and N. Katsuno.  1981.  Epidemiologic study of
workers engaged in the manufacture of chromium compounds.  J. Occup. Med.
23(12): 835-838.

Silverstein, M., F. Mirer, D. Kotelchuck, B. Silverstein and M. Bennett. 1981.
Mortality among workers in a die-casting and electroplating plant. Scand. J.
Work Environ. Health.  7(Suppl. 4): 156-165.

Taylor, F.H.  1966.  The relationship of mortality and duration of employment
as reflected by a cohort of chromate workers.  Amer. J. Public Health.  56(2):
218-229.

Tsuda, H. and K. Kato.  1977.  Chromosomal aberrations and morphological
transformation in hamster embryonic cells treated with potassium dichromate in
vitro.  Mutat. Res.  46: 87-94.

U.S.  EPA.  1984.  Health Assessment Document for Chromium.  Prepared by the
Office of Health and Environmental Assessment, Environmental Criteria and
Assessment Office, Cincinnati, OH.  EPA 600/8-83-014F.

Watanabe, S. and Y. Fukuchi.  1975.  An epidemiological survey on lung cancer
in workers of a chromate-producing industry in Hokkaido, Japan.  Presented at
International Congress on Occupational Health.
                                       12-43

-------
                                     Copper

                CARCINOGENICITY ASSESSMENT FOR LIFETIME EXPOSURE
 Substance Name:   Copper
 CASRN:            7440-50-8
             EVIDENCE FOR CLASSIFICATION AS TO HUMAN CARCINOGENICITY
 WEIGHT-OF-EVIDENCE CLASSIFICATION

 Classification:   D;  not classifiable  as  to human carcinogenicity

 BASIS

 There are no human data,  inadequate animal data  from  assays of  copper
 compounds,  and equivocal  mutagenicity data.

 HUMAN CARCINOGENICITY DATA

 None.

 ANIMAL CARCINOGENICITY DATA

 Inadequate.   Bionetics Research Labs  (1968) studied the carcinogenicity of a
 copper-containing compound, copper hydroxyquinoline,  in two strains of mice
 (B6C3F1  and  B6AKF1).   Groups of 18 male  and 18 female 7-day-old mice were
 administered 1000 mg copper hydroxyquinoline/kg bw (180.6 mg Cu/kg) suspended
 in 0.5X  gelatin daily until they were  28 days old, after which  they were
 administered 2800 ppm (505.6 ppm Cu)  in  the feed  for  50 additional weeks.  No
 statistically significant increases in tumor incidence were observed in the
 treated  78-week-old  animals.

 In the same  study, Bionetics Research  Labs (1968) administered  a single
 subcutaneous  injection of gelatin (control) or 1000 mg of copper
 hydroxyquinoline/kg  bw (180.6 mg CuAg) suspended in 0.5% gelatin to groups of
 28-day-old mice of both strains.  After 50 days of observation, the male B6C3F1
 had an increased  incidence of reticulum cell sarcomas compared with controls.
 No tumors were observed in the treated male B6AKF1 mice, and a  low incidence of
 reticulum cell sarcomas was observed in the treated female mice of both
 strains.

 Gilman (1962) administered intramuscular injections containing 20 mg of cupric
 oxide (16 rag Cu),   cupric  sulfide (13.3 mg Cu),  and cuprous sulfide (16 mg Cu)
 into the left and  right thighs of 2- to 3-month-old Wistar rats.  After 20 •
months of observations, no injection-site tumors were observed in any animals,
but other tumors were observed at very low incidence in the animals receiving
cupric sulfide (2/30) and cuprous sulfide (1/30).  As the relevance of the
organic copper compound to the observation of sarcoma induction is uncertain
and the incidence  of tumors in rats treated i.m.  with inorganic copper was very
low,  data are considered  inadequate for classification.


                                     12-44

-------
SUPPORTING DATA FOR CARCINOGENICITY

Moriya et al.  (1983) reported no increase in mutations in E. coli and S.
typhimurium strains TA98, TA1535, TA1537 and TA1538 incubated with up to 5 mg
copper quinolinolate/plate and in S. typhimurium TA98 and TA100 incubated with
up to 5 mg copper sulfate/plate.  Deraerec et al. (1951) reported dose-related
mutagenic effects in E. coli with 2 to 10 ppm copper sulfate in a reverse
mutation assay.  Negative results were obtained with copper sulfate or copper
chloride in assays using S. cerevisiae (Singh, 1983) and Bacillus subtilis
(Nishioka, 1975, Hatsui, 1980, Kanematsu et al., 1980).  Errors in DNA
synthesis from poly(c)templates have been induced in viruses incubated with
copper chloride or copper acetate (Sirover and Loeb, 1976).  Chromosomal
aberrations were induced in isolated rat hepatocytes when incubated with copper
sulfate (Sina  et al., 1983).  Casto et al. (1979) showed enhanced cell
transformation in Syrian hamster embryo cells infected with simian adenovirus
with the addition of cuprous sulfide and copper sulfate.  High concentrations
of copper compounds have been reported to induce mitosis in rat ascites cells
and recessive  lethals in Drosophila melanogaster.  Law (1938) reported
increases in the percent lethals observed in Drosophila larvae and eggs when
exposed to copper by microinjection (0.1X copper sulfate) or immersion
(concentrated  aqueous copper sulfate), respectively.


   — QUANTITATIVE ESTIMATE OF CARCINOGENIC RISK FROM INHALATION EXPOSURE —

No Data Available

   	 EPA DOCUMENTATION AND REVIEW 	

Source Document:  U.S. EPA.  1987.  Drinking Water Criteria Document for
Copper.  Prepared by the Office of Health and Environmental Assessment,
Environmental  Criteria and Assessment Office, Cincinnati, OH for the Office of
Drinking Water, Washington, DC.

The values in  the 1987 Drinking Water Criteria Document for Copper have
received peer  and administrative review.

Agency Work Group Review:  09/15/87

Verification Date:  09/15/87

   	 EPA CONTACTS (CARCINOGENICITY ASSESSMENT) 	
David J. Reisman / OHEA -- (513)569-7588

W. Bruce Peirano / OHEA -- (513)569-7540

   	 BIBLIOGRAPHY
Casto, B.C., J. Meyers and J.A. DiPaolo.  1979.  Enhancement of viral
transformation for evaluation of the carcinogenic or mutagenic potential of
inorganic metal salts.  Cancer Res,  39: 193-198.

                                     12-45

-------
 Demerec,  M.,  G.  Bertani and J.  Flint.   1951.   A survey of chemicals  for
 mutagenic action on E.  coli.   Am.  Natur.   85(821):  119-136.

 Gilman, J.P.W.   1962.   Metal carcinogenesis.   II. A study on  the  carcinogenic
 activity  of  cobalt,  copper,  iron and nickel  compounds.   Cancer Res.   22:
 158-166.

 Kanematsu, N., M.  Hara  and T.  Kada.  1980.   Rec assay  and mutagenicity studies
 on metal  compounds.  Mutat.  Res.   77:  109-116.

 Law,  L.W.  1938.   The effects  of chemicals on  the lethal mutation rate in
 drosophilia  melanogaster.   Froc. Natl.  Acad. Sci.,  USA.   24:  546-550.

 Matsui, S.   1980.   Evaluation  of a Bacillus  subtilis rec-assay for the
 detection of mutagens which  may occur  in water environments.  Water  Res.
 14(11): 1613-1619.

 Moriya, M.,  T. Ohta, K.  Watanabe,  T. Miyazawa,  K. Kato  and Y. Shirasu.  1983.
 Further mutagenicity studies on pesticides in  bacterial  reversion assay
 systems.  Hutat. Res.   116(3-4): 185-216.

 NCI (National Cancer Institute).   1968.  Evaluation of  carcinogenic,
 teratogenic  and mutagenic  activities of selected pesticides and industrial
 chemicals.  Vol. I.  NCI-DCCP-CG-1973-1-1.

 Nishioka, H.  1975.  Mutagenic  activities of metal  compounds  in bacteria.
 Mutat. Res.   31: 185-189.

 Sina, J.F., C.L. Bean, G.R. Dysart, V.I. Taylor  and M.O.  Bradley.  1983.
 Evaluation of the alkaline elution/rat  hepatocyte assay  as a  predictor of
 carcinogenic/mutagenic potential.  Mutat. Res.   113(5):  357-391.

 Singh, I.  1983.  Induction of  reverse  mutation  and mitotic gene  conversion by
 some metal compounds in  Saccharomyces cerevisiae.   Mutat. Res.  117(1-2):
 149-152.

 Sirover, M.A. and L.A. Loeb.  1976.  Infidelity  of  DNA synthesis  in  vitro:
 Screening for potential metal mutagens  or carcinogens.   Science.   194:
 1434-1436.

U.S. EPA.   1987.  Drinking Water Criteria Document  for Copper.  Prepared by the
Office of Health and Environmental Assessment,  Environmental  Criteria and
Assessment Office, Cincinnati, OH for the Office of Drinking Water,  Washington,
DC.
                                     12-46

-------
                         Lead and compounds (inorganic)

               CARCINOGENICITY ASSESSMENT FOR LIFETIME EXPOSURE
 Substance Name:  Lead and compounds (inorganic)
 CASRN:           7439-92-1
            EVIDENCE FOR CLASSIFICATION AS TO HUMAN CARCINOGENICITY
WEIGHT-OF-EVIDENCE CLASSIFICATION

Classification:  B2; probable human carcinogen

BASIS

Sufficient animal evidence.  Ten rat bioassays and one mouse assay have shown
statistically significant increases in renal tumors with dietary and
subcutaneous exposure to several soluble lead salts.  Animal assays provide
reproducible results in several laboratories, in multiple rat strains with some
evidence of multiple tumor sites.  Short term studies show that lead affects
gene expression.  Human evidence is inadequate.

HUMAN CARCINOGENICITY DATA

Inadequate.  There are four epidemiologic studies in occupational cohorts
exposed to lead and lead compounds.  Two studies (Dingwall-Fordyce and  Lane
1963, Nelson et al., 1982) did not find any association between exposure to
lead and cancer mortality.  Selevan et al. (1985) in their retrospective cohort
mortality study of primary lead smelter workers found a slight decrease in the
total cancer mortality (SMR-95).  Apparent excesses were observed for
respiratory cancer (SMR-111, obs-41, p>0.05) and kidney cancer (SMR-204, obs-6,
p>0.05).  Cooper and Gaffey (1975) and Cooper (1985 update) in their cohort
mortality study of battery plant workers and lead smelter workers found
statistically significant excesses for total cancer mortality (SMR-113,
obs-344), stomach cancer (SMR-168, obs-34) and lung cancer (SMR-124, obs-109)
in battery plant workers.  Although similar excesses were observed in smelter
workers, they were not statistically significant.  Cooper and Gaffey (1975)
felt it was possible that individual subjects were monitored primarily on the
basis of obvious signs of lead exposure, while others who show no symptoms of
lead poisoning would not be monitored.

All of the available studies lacked quantitative exposure information, as well
as information on the possible contribution of smoking.  All studies also had
exposures to other metals such as arsenic, cadmium and zinc for which no
adjustment was done.  The cancer excesses observed in the lung and stomach were
relatively small (<200).  There was no consistency of site among the various
studies, and no study showed any dose-response relationship.  Thus, the
available human evidence is considered to be inadequate to refute or
demonstrate potential carcinogenicity for humans from lead exposure.

ANIMAL CARCINOGENICITY DATA
                                     12-47

-------
 Sufficient.   The carcinogenic potential of lead salts,  primarily phosphates  and
 acetates,  administered by the oral route,  diet or by injection has  been
 demonstrated in rats  and mice by more  than 10 investigators.   The most
 characteristic cancer response is bilateral renal carcinoma.   Rats  given lead
 acetate or subacetate orally have developed gliomas,  and lead subacetate also
 produced lung adenomas in mice after i.p.  adminstration.   Most of these
 investigations found  a carcinogenic response only at the highest dose.   The
 lead compounds tested in animals are almost all soluble salts.   Metallic lead,
 lead oxide and lead tetralkyls have not been tested adequately.   Studies with
 inhalation exposure have not been located  in the literature.

 Azar et al.  (1973)  administerd 10,  50,  100,  and 500 ppm lead  as lead  acetate in
 dietary concentrations to fifty rats/sex/treatment group for  2 years.   One
 hundred control rats  of each sex received  the basal laboratory diet.   In a
 second 2-year feeding study,  20 rats/group were given diets containing 0, 1000,
 and 2000 ppm lead as  lead acetate.   No  renal tumors were  reported in  the
 control groups or in  treated animals of either sex receiving  10 to  100 ppm.
 Male rats  fed 500,  1000,  and 2000 ppm  lead acetate had  an increased renal tumor
 incidence  of 5/50,  10/20,  and 16/20, while 7/20 females in the 2000 ppm
 developed  renal tumors.

 The Azar et  al.  (1973)  study is limited by the lack of  experimental detail.
 The possibility of  environmental contamination from lead in the air or drinking
 water was  not mentioned.   The strains of rats used were not specified in the
 study,  but the Health Effects Assessment for Lead (U.S.  EPA,  1984)  indicated
 the rats were Wistar  strain.   The weight gain at 1000 and 2000 ppm  was reported
 to  be depressed,  but  details  were not given.

 Kasprzak et  al.  (1985),  in investigating the interaction of dietary calcium  on
 lead carcinogenicity,  fed a diet with IX lead subacetate  (8500 ppm  Pb)  to male
 Sprague-Dawley rats for  79 weeks.   Of the  rats surviving  (29/30)  in this
 treatment  group  beyond 58  weeks,  44.8X  had renal tumors.   Four rats had
 adenocarcinomas;  the  remainaing nine had adenomas.   Bilateral  tumors  were
 noted.   No renal tumors were  noted  among the controls.

 As  part  of a  study  to determine interactions between sodium nitrite,  ethyl urea
 and lead, male Sprague-Dawley rats  were  given lead acetate in  their drinking
 water  for  76  weeks  (Koller et al.,  1986).   The concentration of lead  was 2600
 ppm.  No kidney  tumors were detected among the 10  control rats.   Thirteen of 16
 (SIX)  lead-treated rats had renal tubular  carcinoma,  with three tumors detected
 at  72 weeks and  the remainder detected  at  the termination of  the  study.

Van Esch and  Kroes  (1969)  fed basic  lead acetate  at 0,  0.1X, and  l.OX  in the
 diet  to  25 Swiss mice/sex/treatment group  for 2  years.  No renal  tumors
 developed in  the control group,  but  6/25 male mice  of 0.1X basic  lead acetate
group had renal  tumors  (adenomas  and carcinomas  combined).  In the  l.OX  group,
one  female had a renal tumor.   The  authors  felt  that  the  low incidence  in the
l.OZ group was due to early mortality.

Hamsters given lead subacetate  at 0.5X and  IX  in  the  diet  had no  significant
renal tumor response  (Van  Esch and Kroes,  1969).


                                     12-48

-------
 SUPPORTING  DATA FOR CARCINOGENICITY

 Lead acetate  induces cell  transformation  in  Syrian hamster embryo cells
 (DiPaolo  et al.,  1978)  as  well  as enhances the incidence of simian adenovirus
 induction.  Lead oxide  showed similar enhanced adenovirus induction (Casto et
 al.,  1979).

 Under certain conditions lead compounds are  capable of inducing chromosomal
 aberrations in vivo and in tissue cultures.  Grandjean et al. (1983) showed a
 relationship  between SCE and lead exposure in exposed workers.  Lead has been
 shown,  in a number  of DNA  structure and function assays, to affect the
 molecular processes associated  with the regulation of gene expression (U.S.
 EPA,  1986).

   — QUANTITATIVE  ESTIMATE OF  CARCINOGENIC  RISK FROM INHALATION EXPOSURE —

 No Data Available

   	 EPA DOCUMENTATION AND REVIEW 	

 Source Document:  U.S.  EPA.  1984.  Health Effects Assessment for Lead.
 Prepared  by the Office  of  Health and Environmental Assessment, Environmental
 Criteria  and  Assessment Office, Cincinnati,  OH, for the Office of Emergency and
 Remedial  Response,  Washington,  DC.  EPA/540/1-86/055.  NTIS PB85-163996/AS.

 U.S.  EPA.   1986.  Air Quality Criteria Document for Lead.  Volumes III, IV.
 Prepared  by the Office  of  Health and Environmental Assessment, Environmental
 Criteria  and  Assessment Office, Research  Triangle Park, NC, for the Office of
 Air Quality Planning and Standards.  EPA-600/8-83/028dF.

 U.S.  EPA.   1987.  Preliminary review of the  carcinogenic potential of lead
 associated  with oral exposure.  Prepared  by  the Office of Health and
 Environmental Assessment,  Carcinogenic Assessment Group, Washington DC, for the
 Office  of Drinking  Water,  Office of Solid Waste and the Office of Emergency and
 Remedial  Response (Superfund).  OHEA-C-267.  Internal Review Draft.

 The review  of the carcinogenic  potential  of  lead associated with oral exposure
 has received Agency review.

 The 1986 Air Quality Criteria Document for Lead has received Agency and
 External Review.

Agency Work Group Review:   05/04/88

Verification Date:   05/04/88

   	  EPA  CONTACTS (CARCINOGENICITY ASSESSMENT) 	
William Pepelko / OHEA -- (202)260-5904
Jim Cogliano / OHEA -- (202)260-7338
                                 BIBLIOGRAPHY

                                     12-49

-------
 Anderson,  E.L.,  and CAG (Carcinogenic Assessment Group).   1983.   Quantitative
 approaches in use to assess cancer risk.   Risk Analysis.   3:  277-295.

 Azar,  A.,  H.J.  Trochimowicz and M.E.  Maxfield.   1973.   Review of lead  studies
 in animals carried out at Haskell Laboratory -  Two year feeding  study  and
 response to hemorrhage study.   In:   Barth D.,  A.  Berlin,  R.  Engel,  P.  Recht and
 J.  Smeets, Ed.   Environmental  health aspects of lead:  Proceedings International
 Symposium; October 1972;  Amsterdam,  The Netherlands.    Commission of the
 European Communities,  Luxemberg.   p.  199-208.

 Casto,  B.C.,  J.  Meyers and J.A.  DiPaolo.   1979.   Enhancement of  viral
 transformation for evaluation  of the carcinogenic or mutagenic potential of
 inorganic  metal  salts.   Cancer Res.   39:  193-198.

 Cooper,  W.C.   1985.  Mortality among employees  of lead battery plants  and lead
 producing  plants,  1947-1980.   Scand.  J. Work Environ.   Health.   11:  331-345.

 Cooper,  W.C.  and W.R.  Gaffey.   1975.   Mortality of lead workers.   In:
 Proceedings of the 1974 Conference on Standards  of Occupational  Lead Exposure,
 J.F. Cole, Ed.,  February,  1974.   Washington,  DC.   J. Occup.  Med.   17:  100-107.

 Dingwall-Fordyce,  I. and R.E.  Lane.   1963.  A follow-up study of lead  workers.
 Br. J.  Ind. Med.   20:  313-315.

 DiPaolo, J.A., R.L.  Nelson and B.C.  Casto.   1978.   In  vitro  neoplastic
 transformation of Syrian hamster  cells by lead  acetate and its relevance to
 environmental carcinogenesis.   Br. J.  Cancer.   38:  452-455.

 Grandjean,  P., H.C.  Wulf and E. Niebuhr.   1983.   Sister chromatid exchange  in
 response to variations  in occupational lead exposure.   Environ.  Res.   32:
 199-204.

 Kasprzak,  K.S., K.L. Hoover and L.A.  Poirier.   1985.   Effects of dietary
 calcium acetate on lead subacetate carcinogenicity in  kidneys of male
 Sprague-Dawley rats.  Carcinogenesis.  6(2):  279-282.

 Roller, L.D., N.I. Kerkvliet and J.H.  Exon.   1986.  Neoplasia induced  in male
 rats fed lead acetate,  ethyl urea and sodium nitrate.   Toxicol.  Pathol.   13:
 50-57.

 Nelson, D.J., L. Kiremidjian-Schumacher and G. Stotzky.   1982.   Effects  of
 cadmium, lead, and zinc on macrophage-mediated cytotoxicity  toward  tumor cells.
 Environ. Res.  28:  154-163.

 Selevan, S.G., P.J. Landrigan,  F.B. Stern and J.H. Jones.  1985.  Mortality of
 lead smelter workers.  Am.  J. Epidemiol.  122: 673-683.

Van Esch, G.J. and R. Kroes.  1969.  The  induction of  renal tumors by  feeding
of basic lead acetate to mice and hamsters.  Br. J. Cancer.   23:  265-271.

U.S. EPA.  1984.  Health Effects Assessment for Lead.   Prepared by  the Office
of Health and Environmental Assessment, Environmental  Criteria and Assessment

                                      12-50

-------
Office, Cincinnati, OH, for the Office of Emergency and Remedial Response,
Washington, DC.  EPA/540/1-86/055.  NTIS PB85-163996/AS.

U.S. EPA.  1986.  Air Quality Criteria Document for Lead.  Volumes III, IV.
Prepared by the Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Research Triangle Park, NC, for the Office of
Air Quality Planning and Standards.  EPA-600/8-83/028dF.

U.S. EPA.  1987.  Preliminary review of the carcinogenic potential of lead
associated with oral exposure.  Prepared by the Office of Health and
Environmental Assessment, Carcinogenic Assessment Group, Washington DC, for the
Office of Drinking Water, Office of Solid Waste and the Office of Emergency and
Remedial Response (Superfund).  OHEA-C-267.  Internal Review Draft.
                                     12-51

-------
13.   SUPPORT DOCUMENTS FOR REFERENCE CONCENTRATIONS FROM THE
     NEW YORK STATE DEPARTMENT OF HEALTH
                              13-1

-------
               STATE OF NEW YORK - DEPARTMENT OF HEALTH
                        INTEROFFICE MEMORANDUM
TO:
John K. Hawley, Ph.D., Research Director

Division of Environmental Health Assessment
FROM:     Mary Jo Miller, Research Scientist II

          Bureau of Toxic Substance Assessment



SUBJECT:  Staten Island Project - RfCs
DATE:
 March 26,  1992
1.   Most of the RfC's listed in your 3/23/92 memorandum were derived
     from oral RfDs assuming a 70 kg adult inhales 23 m3/day.  The
     oral RfD, calculated RfC and source of the oral RfD are listed
     below.  Short paragraphs on these chemicals are attached.


     Chemical

     chloroform
(1991)
     carbon tetrachloride
(1991): HEAST (1991)
     tetrachloroethene
(1991)
     benzene
     trichloroethene

2.   The RfC for toluene (2,000 ug/m3)  is  from HEAST (1991).
     (Verified and IRIS input pending.)
Oral RfD RfC
fma/ka/dl fua/m^
1E-2 30

1E-2
7E-4
7.4E-3
7E-4
30
2.1
23
Oral RfD
Source
IRIS (1991); HEAST
2 . 1 IRIS
IRIS (1991); HEAST
US EPA (1986)
US EPA (1987)
                            13-2

-------
 3.    The RfC for chloromethane (826  ug/m3) is equivalent to the
      minimal risk level for inhalation exposure derived by ATSDR
      (1990).  A short toxicological  paragraph  and ATSDR's  risk
      derivation is attached.
 References
 Agency for Toxic Substances  and Disease  Registry (ATSDR).   1990.
 Toxicological Profile for  chloromethane  (TP-90-07).  ATSDR, Atlanta,
 GA.

 Health Effects Assessment  summary  Tables (HEAST).  1991.  Annual  FY-
 1991.   US EPA, Office of Research  and  Development, Washington,  D.C.

 Integrated Risk Information  System (IRIS).   1991.  Online.  US  EPA,
 Environmental Criteria and Assessment  Office,  Cincinnati, OH.

 U.S. Environmental  Protection Agency  (US EPA).   1986.  Volatile
 organic chemicals,  us EPA,  Office of  Drinking Water, Washington,  DC.
 (As cited in Draft  ATSDR Toxicological Profile on  Benzene,  1987.)

 U.S. Environmental  Protection Agency  (US EPA).   1987.  Drinking Water
 Health Advisory for trichloroethene.   US EPA,  Office of Drinking
 Water,  Washington,  DC.
 gfi J. or ome thane

     Chronic inhalation exposure to chloromethane  causes  liver  and
 kidney damage,  nervous system effects, decreased body weight gain,
 and male reproductive system effects.  Male  mice exposed  by
 inhalation to high  concentrations  of chloromethane over their
 lifetimes developed kidney tumors,  but no tumors were observed  in
 female mice and male  and female rats.  It is not known whether
 chloromethane could cause  reproductive effects or  cancer  in humans.

     Based on a NOAEL of 225 ppm (464  mg/m3)  for reduced body weight
 gain in rats and mice (CUT, 1981), the  Agency for Toxic  Substances
 and Disease Registry  derived a  minimum risk  level  of 0.4  ppm  (826
 ug/nr)   (ATSDR, 1990).   This risk level was derived by adjusting the
 NOAEL  for intermittent exposure (6 hr/day, 5 day/week) and  dividing
 by a 100  fold uncertainty  factor.
References
ATSDR.  1990.  Toxicological Profile for Chloromethane  (TP-90-07).
ATSDR, Atlanta, GA.

CUT.  1981.  Final report on a chronic inhalation toxicology  study
in rats and mice exposed to methyl chloride.  Unpublished study: OTS
Submission Document ID 40-8120717.  (As cited in ATSDR, 1990.)
                            13-3

-------
Benzene

     Chronic exposure to benzene causes damage to the blood-forming
system (leukopenia and anemia), immune system and nervous system.
Benzene has also been associated with leukemia in occupational
exposed workers and in experimental animals.  The US EPA proposed an
oral RfD of 0.0007 mg/kg/day using the wolf et al.  (1956) inhalation
study in rats and leukopenia as the adverse health effect of concern
(US EPA,  1986).  A RfC of 2. l ug/m3 was  derived  from the oral RfD
assuming a 70 kg adult inhales 23 m'/day.

References

Wolf, M.A., V.K. Rowe, D.D. McCollister, R.R. Hollingsworth and F.
Oyin.  1956.  Toxicological studies of certain aIkylated benzenes and
benzene.   AHA Arch. Ind. Health. i±:  387-398.

U.S. Environmental Protection Agency (US EPA).  1986.  Volatile
organic chemicals.  US EPA, Office of Drinking water, Washington, DC.
(As cited in Draft ATSDR Toxicological Profile on Benzene, 1987.)
                            13-4

-------
     Chronic exposure to chloroform causes liver and kidney damage
and central nervous system effects.  Chloroform has been associated
with cancer of the liver and kidney in experimental animals.  Based
on a LOAEL of 12.9 mg/kg/d for liver damage  in beagle dogs  (Heywood
et al., 1979), and using a 1,000 fold uncertainty factor, the US EPA
derived an oral RfD of  0.01 mg/kg/day for chloroform  (IRIS, 1991).  A
RfC of 30 ug/m3 was derived from the oral RfD assuming a 70 kg adult
inhales 23 ar/day.

References
Heywood, R., R.J. Sortwell, P.R.B. Noel, et al.  1979.  Safety
evaluation  of toothpaste containing chloroform. III.  Long-term study
in beagle dogs.  J. Environ. Pathol. Toxicol. 1: 835-851.

Integrated  Risk Information System (IRIS).  1991.  Online.  US EPA,
Environmental Criteria and Assessment Office, Cincinnati, OH.

Tetrftchloroethene

     Chronic exposure to tetrachloroethene causes liver and kidney
damage and  central nervous system effects.  Tetrachloroethene has
been associated with cancer of the liver and kidney in experimental
animals.  Based on a NOAEL of 14 mg/kg/day for liver damage in rats
(Buben and  0'Flaherty, 1985) and using a 1,000 fold uncertainty
factor, the US EPA derived an oral RfD of 0.01 mg/kg/day for
tetrachloroethene (IRIS, 1991).  A RfC of 30 ug/m1  was derived from
the oral RfD assuming a 70 kg adult inhales 23 m3/day.

References

Buben, J.A. and E.J. O'Flaherty.  1985.  Delineation of the role of
metabolism  in the hepatotoxicity of trichloroethylene and
perchloroethylene: a dose-effect study.  Tox. Appl. Pharm. 28.: 105-
122.

Integrated Risk Information System (IRIS).  1991.  Online.  US EPA,
Environmental Criteria and Assessment Office, Cincinnati, OH.
                             13-5

-------
Trichloroethene

     Chronic exposure to trichloroethene causes liver and kidney
damage and effects on the nervous system, immune system and blood.
Trichloroethene has been associated with liver cancer in experimental
animals.  The US EPA derived an oral RfD of 0.0074 mg/kg/day based on
an inhalation study in rats by Kimmerle and Eben (1973) and increased
liver weight as the adverse health effect of concerns (US EPA, 1987).
A RfC of 23 ug/m3 was  derived from the oral  RfD assuming a 70 kg
adult inhales 23 m3/day.   The oral RfD for trichloroethene is
currently under review by the US EPA.

References

Kimmerle, 6. and A. Eben.  1973.  Metabolism, excretion and
toxicology of trichloroethylene after inhalation. 1.  Experimental
exposure on rats.  Arch. Toxicol. 30: 115-126.

U.S. Environmental Protection Agency  (US EPA).  1987.  Drinking Water
Health Advisory for Trichloroethene.  US EPA, Office of Drinking
Water, Washington, DC.

Carbon Tetrachloride

     Chronic exposure to carbon tetrachloride causes liver and kidney
damage and central nervous system effects.   Carbon tetrachloride has
been associated with liver cancer in experimental animals.  Based on
a NOAEL of 0.71 mg/kg/day for liver damage in rats (Bruckner et al.,
1986) and sing a 1,000 fold uncertainty factor/ the US EPA derived an
oral RfD of 0.0007 mg/kg/day for carbon tetrachloride (IRIS, 1991).
A RfC of 2.1 ug/m3 was derived from the oral RfD assuming a 70 kg
adult inhales 23 m3/day.

References

Bruckner, J.W.,  W.F. Mackenzie, S. Muralidhara, R. Luthra, G.M. Kyle
and D. Acosta.  1986.   Oral toxicity of carbon tetrachloride: acute,
subacute and subchronic studies in rats.   Fund. Appl. Toxicol. £: 16-
34.

Integrated Risk Information System (IRIS).   1991.  Online.  US EPA,
Environmental Criteria and Assessment Office, Cincinnati, OH.
                             13-6

-------
                           DEPARTMENT or HEALTH
                                                                           v\
                                                                        _r
     AxCLROO.
                                  January  4,  1990
Dear Commissioner Jorllng:

          Enclosed Is the document on formaldehyde  prepared  by  staff of the
Health Department's Bureau of Toxic Substance Assessment.

          Exposure to formaldehyde causes  irritation  of  the  eyes, mucous
membranes of the  upper respiratory tract and skin.   Studies of people exposed
for five hours cr less under controlled conditions provide the best data upon
which to base an  ambient air criterion for Irritant effects.  The most
3en«1tive objective response to Irritation 
-------
                                     -2-
 cancer  risk,  estimate.   One  approach  would  be  to  use  the  carcinogenic data
 to  support  formaldehyde's placement  in  the hlgh-toxicity category which
 would require  Best Available  Control  Technology  control.   In  addition,  the
 non-carcinogenic guidance value  (30  ug/mj) would be  used to evaluate
 short-term emissions; it should be used  as  a short-term ambient concentration
 (e.g. one to four hours).
                                  David Axel rod, M.D.
                                  Commissioner of Health
Enc.

Hon. Thomas Jorlfng
Commissioner
NYS Department of Environmental Conservation
50 Wolf Road
Albany, New York  12233
                              13-8

-------
                                  STATE or New YO«K
                               DEPARTMENT OF HEALTH
                                        ALBANY

    DAVID AXCIMOO, M.O.


                                  April 3, 1990




Dear Commissioner Jorllng:

          Enclosed is the document on cadmium (Cd) exposure prepared by staff of the Health
Department's Bureau of Toxic Substance Assessment.

          Most human exposure to cadmium results from ingestion for which the critical toxic
endpoint Is kidney damage.  Inhalation of cadmium also represents a risk for respiratory tract
cancer at concentrations that also contribute to kidney toxicity.

          Although kidney damage generally occurs when kidney levels exceed 200 ppm Cd,
some individuals are at risk at lower concentrations.  A kidney concentration of 40 ppm Cd,
which corresponds to a daily uptake of 2.9 ug Cd, is a conservative estimate of a 0.1 percent
probability for renal dysfunction. This value has been used for estimating the recommended
ambient air limit of 20 ng Cd/m*.

          There is limited evidence in humans and sufficient evidence in animals to conclude
that cadmium compounds are carcinogenic by Inhalation. An increased risk of respiratory
cancer was observed among cadmium production workers exposed primarily lo cadmium oxide
dusts.  These data have been used in this document to estimate an air concentration expected
to result in an excess human lung cancer risk of 1 x 1&'  after lifetime exposure.  This
quantitative risk estimate which resulted in an air concentration of 0.5 ng/Cd m1, was based on
human data from a well-conducted epidemiology study, with  good exposure estimates, and a
sufficient follow-up period to detect an effect. Because of the quality of these data.
human-based risk estimates rather than animal-based estimates were used. These risk
estimates are applicable to all cadmium compounds.

          Exposures from airborne cadmium emissions which accumulate in the soil and
foodchain were considered in the derivation of the air limit of 20 ng Cd/ma. a maximum
concentration designed to protect against renal effects. Cadmium has not been demonstrated
to be carcinogenic by ingestion exposure alone. If air concentrations are (ess than 20 ng/m*.
the ingestion  pathway is not a  critical pathway and would not be separately considered for
carcinogenic risk.

                                  Sincere!
                                  David Axelrod, M.O.
                                  Commissioner of Health
Attachment
Hon. Thomas C. Jorling
Commissioner
NYS Department of Environmental Conservation
50 Wolf Road
Albany. New York 12233             13_9

-------
0*v«o
                             STATC or New Yc««

                          DEPARTMENT or HEALTH
                                  ALBANY
                                  May  2,  1990
Dear Commissioner Jorllng:

          Enclosed 1s the health risk assessment  of chromium  (Cr) exposure
prepared by staff of the Health Department's  Bureau of Toxic  Substance
Assessment.

          Occupational exposure to chromium compounds causes  allergic
dermatitis, respiratory tract Irritation,  ulceratlons of  the  nasal  septum
and cancer.  In experimental animals. Inhalation  exposure to  chromium
compounds produces pathological changes In the lungs, respiratory
Impairment, 1mmunosuppress1on,  nasal  irritation, kidney damage, liver damage
and cancer.  In general,  hexavalent chromium (CrVI) compounds are more  toxic
than trlvalent chromium (Grill) compounds  due to  their  relatively higher
solubility, greater absorption by body tissues,  and greater reactivity.

          The most sensitive endpolnts on  which to base  a non-carcinogenic
guideline are chromium's effects on the pulmonary system.  The severity of
these effects depends on the amount Inhaled,  the  duration of  the exposure,
and the solubility and valence state of the chromium  compound.  These
factors, along with the likelihood that chromium In ambient air will not be
present In just one form or valence state, were taken Into consideration  1n
calculating an ambient air  limit of 0.1 ug total  Cr/m1  for non-cancer
endpolnts.

          Workers 1n the chromate Industry have an Increased risk of
respiratory cancer.  Host studies of the carcinogenic effects of chromium
compounds  In humans Involved exposures to a combination of metallic,
trlvalent and hexavalent chromium.  Although the relative contributions  of
each of these three forms of chromium to cancer risk 1s unknown, hexavalent
chromium Itself has been Implicated as an etlologlc agent.

          A cohort study of workers  In a chromate production  facility was
chosen  for the quantitative cancer risk assessment as 1t has  a relatively
long follow-up period and adequate exposure data.  The estimate of  the
ambient air concentration of Cr(VI) that corresponds  to an  excess human lung
cancer  risk of 1 x 10-4 after lifetime exposure 1s 0.02 ng  Cr(VI)/a'.  Since
Cr(VI)  1s  Implicated  as  the principal, 1f  not the only carcinogenic agent,
the cancer risk estimate should  only be used  for evaluating  emissions where
Cr(VI)  1s  present.
                                  13-10

-------
                                    -2-
          Ptoplt can be exposed to chromium emissions by  Inhalation or
Ingestlon of foods (vegetables or animal  products).  Increased exposures  fro*
chromium emissions which accumulate In the soil  are expected to be small.
If the suggested guidelines are not exceeded,  'the Ingestlon  pathway 1s  not
critical and normally would not have to  bt evaluated.

                                  Sincerely,
                                        Axtlrod/M.O.
                                  Commissioner of Health
Enclosure

Hon. Thomas C. Jorllng
Commissioner
New York State Department of
    Environmental Conservation
SO Wolf Road
Albany, New York  12233-1010
                              13-11

-------
                             STATE OF NEW YORK
                          DEPARTMENT OF HEALTH
                                   ALBANY
OAVIO AxCLMOO, M. O.
                                 January 4,  1989
    Dear Commissioner Jorling:

              Enclosed Is the document on nickel (N1) prepared by staff
    of the Health Department's  Bureau of Toxic Substance  Assessment.

              Occupational exposure to nickel compounds causes allergic
    dermatitis, nasal and respiratory tract Irritation and  asthmatic
    lung disease.  In experimental  animals, subchronic and  chronic
    Inhalation exposure to nickel  compounds (0.025 to 2 mg/m1) causes
    pathological changes in the lungs, respiratory Impairment,
    1mmunosupprer.sion, hyperglycemfa and fetotoxiclty.  An  ambient air
    limit of 20 ng Nl/m1 1s recommended to  provide the general
    population with a sufficient margin-of-safety over the Inhaled dose
    associated with adverse respiratory effects.

              Nickel subsulfide and refinery dust  created during the
    nickel refining process are associated  with an excess cancer risk
    in humans or animals.  The  data on the  carcinogenic potential  for
    other forms of nickel are  Insufficient  to make definitive
    conclusions about their carcinogenicity by Inhalation.   Some
    evidence, although limited, suggests that nickel  powder,  sulfide,
    oxide, hydroxide, carbonate, acetate and nlckelocene forms may have
    carcinogenic activity.

              From the animal data,  we estimated that the  concentration
    of nickel subsulfide in air associated  with one In one  million
    excess cancer risk is 0.2  ng  Nl/m1.  For those compounds having
    limited evidence of carcinogenicity, the process being  regulated
    should determine whether the  air concentration associated with a
    one In one million excess cancer risk 1s based on either the animal
    nickel subsulfide data (0.2 ng  Nl/m*)  or the human nickel refinery
    dust data (4 ng Ni/m1);  the limited strength of the cancer data
    should also be noted.  Other  nickel compounds  should  be regulated
    on the basis of non-carcinogenic endpoints.
                                  13-12

-------
                                -2-
          Presently, the risk assessments for nickel exposure from
air emissions evaluate both the Inhalation and ingestlon pathways.
Increased Ingestlon exposures and the risks from nickel emissions
which accumulate in the soil are expected to be small.  The
Ingestlon pathway 1s not critical and normally would not have to
be evaluated.
                             Slncer
                             David Axelrod, M.D.
                             Commissioner of Health
Attachment
Hon. Thomas Jorllng
Commissioner
NYS Department of Environmental Conservation
50 Wolf Road
Albany, New York  12233
                           13-13

-------
                                  or New YO«K

                          DEPARTMENT or HEALTH
                                  ALBANY
                                  January  28,  1991
Dear Commissioner Jorllng:

          Enclosed Is the report on vanadium prepared by staff of the Health
Department's Bureau of Toxic Substance  Assessment.

          A wide array of adverse  effects  on the  respiratory  tract,
Including bronchitis, emphysema,  tracheltls,  pulmonary edema  and  bronchial
pneumonia, have been associated with exposure to vanadium compounds 1n  air.
Pulmonary sensltlzatlon has also  been reported.   Although several  studies
have been conducted on factory workers  exposed  to vanadium pentoxlde dust,
these studies have deficiencies which limit their usefulness for developing
an ambient air criterion.   Animal  studies,  though limited with respect to
duration of exposure and/or presentation of study details,  provide
dose-response data on lung effects which were used to  derive  a criterion
of 0.2 ug vanadlum/m1 of air.

          Exposures from airborne  cadmium emissions which accumulate in the
soil and foodchain were considered in the  derivation of the criterion  of
0.2 ug/m1.  The health risk from  ingested  vanadium Is  less than that of
inhaled vanadium.  If air concentrations are less than 0.2 ug/m1,  the
ingestion pathway Is not critical  and would not need  to be considered.


                                  Sincerely,
                                  David
                                  Commissioner of Health
Enclosure
Hon. Thomas C. Jorllng
Commissioner
NYS Department of Environmental Conservation
SO Wolf Road
Albany, New York  12233
                               13-14

-------
                               STATC or New YO«K
                            DEPARTMENT or HEALTH
                                     ALBANY
 OAVIO AxCkHOe, M.O
                                   May 23.  1989
 Dear ConMnLwoner Jorllng:
        In September of 1984  the  Departments of Health  and Environmental
Conservation entered into a memorandum of understanding which formalized the
working relationship between the two agencies for health risk assessments for
chemicals associated with air  emissions from  municipal waste incinerators.  The
Department of Health  agreed  to develop  ambient air guidance for six  heavy
metals, hydrogen chloride, polychlorinated dibcnzodioxins (PCDOs). polychlorinated
dibenzofurans  (PCDFs), polychiorinated hydrocarbons (PAHs),  benzo[alpha)pyrene
(BaP). crysene. formaldehyde,  and  PCBs.  Now PCDDs and PCOFs are In one
document, as  are PAHs. BaP.  and crysene:  three  additional metals arc added to
the list of chemicals.

       Scientific documentation to support  air guidelines arc being finalized for
fourteen compounds or groups of compounds.  These drifts have  undergone
scientific  peer review  by independent scientists outsid« of the Department of
Health.  The drafts have also been reviewed  by  Department of Environmental
Conservation staff.   Responsiveness summaries have been prepared to  address
comments and final revisions to the documents arc expected to be completed soon.
Each  document is being transmitted to the  Department of Environmental
Conservation with recommendations which arc protective of  public health.

       The  zinc  document  is  enclosed, along with the peer  reviewers' comments.
and a  response to the  reviewers' comments.  The fourteen other documents will
be completed  during the  next  few months,  and  transmitted at the rate of two
p«r month.

       Zinc Is an essential  element necessary for normal growth and  many  body
functions.  The respiratory tracts  of  humans  and animals have been adversely
affected by inhalation  of particular*  zinc compounds.   However,  the  respiratory
effects elicited by particulate matter containing zinc  and/or zinc oxide  arc the
same  as  those elicited by particulate matter  which does  not contain  zinc.
Therefore, control of  paniculate*  in  ambient air  should adequately protect the
public  health from exposure to zinc and  zinc oxide.
                                   13-15

-------
                                      •  2 •
        Specific  zinc compounds (I.e.. zinc chloride, zinc sulfatc. and  zinc
 chromate) have  a greater toxic potential than zinc and zinc oxide;  these effects
 arc  primarily attributable to the anionic component of the compound and not zinc
 itself.  Control  of these specific zinc compounds,  when warranted,  should be
 achieved  by compliance with specific, more  stringent,  criteria associated with the
 anions (e.g.. zinc chloride will  be  covered by the  hydrochloric  acid  criterion and
 zinc chromate by the chromium criteria).

        I  recommend that ail the documents, the Health Department's
 recommendations, and control information  from  DEC be taken to public hearings.
 along with proposed ambient  air standards.  Following the  public hearings, ambient
 air standards should be  adopted.  Our staff is available to work with yours on  this
 project.   As further discussions are  warranted,  please  feel free to contact  me.

                                    Sincerely,
                                    Oavid  Axelrod,  M.D.
                                    Commissioner of Health
Enclosures
Hon. Thomas  C.  Jorling
Commissioner
NYS Dept. of  Environmental Conservation
50 Wolf  Road
Albany. New York  12233
                                         13-16

-------
14.   MEMORANDUM ON THE REFERENCE CONCENTRATION FOR CHROMIUM
                               14-1

-------
     1
    „ ?   UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
    '/            OFFICE OF RESEARCH AND DEVELOPMENT
             ENVIRONMENTAL CRITERIA AND ASSESSMENT OFFICE
                          CINCINNATI. OHIO 45268
                          August  26,  1992

 SUBJECT:   RfC  for  Total  Chrom
 FROM:     Joan  S.  Dollarhide -/
          Chemical Mixtures Assessment Branch
          Environmental  Criteria  and  Assessment Office

 TO:       Marian Olsen
          Policy and  Program Integration  Branch
          U.S.  EPA, Region II


     This memo is in response to your request for ECAO's assistance
 in  evaluating  .the appropriateness  of various  RfCs  for  total
 chromium.   As I mentioned during our phone conversation,  I  feel
 that the uncertainties  surrounding the chromium RfC are  so great
 that  your  best approach would be to  postpone a final  decision
 regarding an appropriate RfC until the results of a public meeting
 on the  subject, to be held in December, are  available.   However,
 since your time-frame makes this  impossible,  I  will  summarize the
 information we  currently have.

 Review  of the NYSDOH  RfC for
     The RfC for chromium derived by the New York State Department
of  Health  (NYSDOH)  is not  consistent  with the U.S.  EPA  approach
described  in  Interim  Methods   for   Development  of  Inhalation
Reference Doses (U.S. EPA, 1989;  EPA/600/8-88/066F).  The specific
aspects of the NYSDOH number which  are inconsistent are described
below:

1.  Use of animal data:   The Interim Methods state that human data
are preferred  over  animal data  for deriving an RfC.   The  NYSDOH
uses animal data although adequate  human studies are available.

2.  Selection  of  critical study  and LOAEL:  U.S.  EPA methodology
states that the  study which defines the highest  NOAEL,  or  lowest
LOAEL if a NOAEL is not defined,  and demonstrates a dose-response
relationship should be selected  as  the critical study.   The NOAEL
or LOAEL from the critical  study is then used  to estimate the RfC
by applying the appropriate  uncertainty factors.  The NYSDOH  report
did not  select a  single critical  study, but  rather selected  a
LOAEL, defined as "reasonable",  from a range of LOAELs defined by
several animal studies.

3.  Estimation of animal inhaled dose  and human ADI:   The Interim
Methods state that dosimetric adjustments are to be used to convert
                          14-2                        it& Printed on Recycled Pap

-------
an  animal  LOAEL to a Human  Equivalent Concentration (HEC) LOAEL
[LOAELpjBo] •    For  aerosols  and  particulates,  the  dosimetric
adjustment consists of multiplying the animal LOAEL by the Regional
Deposited Dose Ratio (RDDR) for the region of the respiratory tract
in  which an adverse effect  was  observed to obtain  the I/DAEL^^.
The  RDDR  takes  into  account the  aerodynamic  properties  of the
particles  and the  differences  between  animal  and  human  in the
respiratory tract surface area and architecture.  The LOAELfHEQ is
then divided  by  the appropriate  uncertainty factor to obtain the
RfC  in mg/cu.m.   The  NYSDOH  method of calculating animal  inhaled
dose  (air  concentration  multiplied by animal inhalation rate and
divided by  animal body weight)  does not consider the aerodynamic
properties of the particles.  By using the animal inhaled  dose to
derive the human ADI, NYSDOH does not  account for interspecies
differences in respiratory system surface area  and structure.


p.S. EPA RfC  for Chromium

     As you know,  in  1990  the  RfD/RfC Work Group  reviewed and
subsequently  verified an RfC for total chromium of  2E-6 mg/cu.m.
This RfC was based on a human occupational  study   (Lindberg and
Hedenstierna, 1983) which  identified  nasal  mucosa atrophy as the
critical effect at a LCAKL^^, of  0.000714 mg/cu.m.  An uncertainty
factor of 300 was applied.  The sources of the differences  between
this RfC and the NYSDOH RfC include different critical study (human
vs.  animal),  different critical  effect  (nasal mucosa atrophy vs.
effects on alveolar  macrophages),  different choice of  LOAEL^Ec,
(.000714 mg/cu.ra vs.  .03 mg/kg/day),   and  different  choice of
uncertainty factor  (300  vs.  1000).

     Since this RfC was reviewed,  EPA  has received numerous public
comments which have resulted in the RfC being placed  "under review
and  also withdrawn from the HEAST.    Below is a  summary of the
public comments received.  These  issues will be  considered as part
of the ongoing development process for a chromium RfC.

1.  The proposed RfC  is  below the analytical limits of detection
recommended by EPA and below  naturally occurring levels of  Cr(III)
and Cr(VI)  in much of the United states.

2.   In the critical study,  workers were exposed  to chromic acid
mists,  which  contain almost no  Cr(III).     Therefore,  it  is
inappropriate to  use  this  study to  derive an RfC  for Cr(III).
Furthermore,  separate RfCs   for  Cr(III)  and  Cr(VI)   have  been
suggested as more appropriate than a single RfC.

3.   Since  the physico-chemical  and  toxicological  properties of
chromic acid  appear to  be  different from  those  associated with
environmental chromium,   separate RfCs for mists and particulates
have been suggested.

4.  The critical  effect selected  may be due  to the irritant nature
                           14-3

-------
of the chromic acid mist and not to  any direct effect of chromium.
In other  words,  other types of  chromates which  have  a higher pH
might not have the same effects.

5.  The critical  study  appears  to define a NOAEL of .001 mg/cu.m
that would be more appropriate than  the LOAEL of  .002 mg/cu.m used
by the RfD/RfC Work Group.

6.    The  choice  of  uncertainty  factors  was   questioned.    In
particular/   comments  suggested  that  the  UF  for  absence  of
developmental  studies  and  the  UF  for  extrapolation  from  a
subchronic study were not necessary.
     As you can see, there are significant problems with both the
NYSDOH and EPA RfCs  for  chromium  that make each less than ideal.
Whichever RfC you select, be sure  to include a complete discussion
of all the uncertainties  associated with that RfC.  Also note that,
given the uncertainties  associated with a chromium  RfC,  using a
Hazard Index of 1 as the  threshold for action may be unnecessarily
restrictive.  I have enclosed a summary of the previously reviewed
EPA chromium RfC.  It should give you more information on how the
RfC was  derived,  and  it gives  the  NOAELjHEQ and  LOAELfHEQ using
dosimetric adjustments for several of the animal studies cited in
the NYSDOH report.  If you have additional questions, please call.
                           14-4

-------
15.   MEMORANDUM ON THE REFERENCE CONCENTRATION FOR XYLENE
                               15-1

-------
         UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
                OFFICE OF RESEARCH AND DEVELOPMENT
              ENVIRONMENTAL CRITERIA AND ASSESSMENT OFFICE
                         CINCINNATI. OHIO 45268


                         September 3, 1992
 SUBJECT:   Reference Concentration (RfC) listings for xylene (mixed
           and o-,  m- and p-isomers)  in HEAST

 FROM:      Kenneth  A. Poirier,  Ph.D.
           Environmental Health Scientist
           Chemical Mixtures Assessment Bra

 TO:        Marian Olsen
           U.S.  EPA - Region II
           0PM,  Policy and Program Integration Branch


     This memo  is  a response to your telephone query on September
 1 regarding the Reference Concentration (RfC)  listings for xylene
 (mixed and o-, m- and p-isomers) in HEAST.  As you pointed out, the
 most  recent  update of HEAST  (March 1992), no longer has  these
 values listed.   The reason for this  is as  follows:

     The  HEAST  lists toxicity  values for chemicals  that come from
 a number  of  sources that have  various levels of Agency  review.
 Many times a listing for  a  RfC or Reference Dose  (RfD) is  taken
 from  an Agency  document that  has had some programmatic  review,
 though not necessarily an Agency consensus review as occurs within
 the RfD/RfC Work Group.   It is for  this  reason that  the  user of
 HEAST  carefully  check  the  source  of the toxicity  value  when
 choosing  to use a  value  that is listed on  HEAST.

     For  the RfC  and RfD  toxicity  values,  the  ultimate  Agency
 review occurs when a risk assessment  for a chemical is reviewed and
 verified   by  the  Agency's  RfD/RfC   Work  Group.    When  a  risk
 assessment reaches  verified status, it is  loaded onto the Agency's
 Integrated Risk information System  (IRIS).   When  this occurs  a
 notation of  "IRIS"  is made in HEAST.   Because the  documentation of
 a verified risk assessment is extensive, the HEAST user is strongly
 urged to consult IRIS.  By not  listing the  IRIS value,  the  user is
 forced to use IRIS  and hopefully read the rationale used and limits
 placed on  each  risk assessment.

     In the case of  the  xylenes, the RfC values have been  left
 blank pending loading onto IRIS.  The RfCs  for mixed, o-, m- and p-
 xylene  have reviewed and  verified by the Agency's RfD/RfC  Work
 Group.   These four  inhalation risk assessments have  been found to
have  inadequate  data  on  which  to  establish  a   chronic  risk
 assessment and have been designated as NOT VERIFIABLE.  A statement
                         15-2

-------
to this  effect will soon appear on  IRIS.   At that  time  an IRIS
notation will be placed on HEAST.  Until appropriate data is made
available to reassess the chronic inhalation effects,  a RfC can not
be derived.

cc:  J« Dollarhide
     L. Knauf
     C. Sonich-Mullin
                          15-3

-------
16.  MEMORANDUM ON THE WEIGHT-OF-EVIDENCE CLASSIFICATION OF
     TETRACHLOROETHYLENE AND TRICHLOROETHYLENE
                               16-1

-------
  Memorandum  to M. Olsen concerning  carcinogen characterizations
  for  perchloroethylene and  trichloroethylene.  Cincinnati,  OH:
  Office of Research  and Development,  Environmental  Criteria and
  Assessment  Office,  U.S. Environmental Protection Agency.   1992.
 yqtrachloreerhvlene  fperafrloroethvlena.  PERC1  /CA3RN 127-ia-4l
      The carcinogenicity character! cation hae a long history.  A
 July  1985  Health  AssasBment  Document  for  Tatraehloroethylene
 (Verohloroetnyione} , EPA t 600/8-82/005F,  classified the agent in
 Weight-of-Evidence Group "c - Possible Hunan carcinogen" mentioning
 HJU£ ?ls W0uld be *««valuated because of new information.  The
 1985 document  also  provided upper bound inhalation and oral riek
 e«tinate».   An April  i»g?  Addendum  to  the  Health  Assessment
 Document, EPA# 600/8-82/005FA, propo»«d that the walgnt-of-Evidence
 be upgraded  to "B2  - probable Hunan Carcinogen"   and provided a
 revised  inhalation risk estimate.  A February 1991 document titled
 Response to issues and Data submissions on the Carcinogenicity of
 Tetrachloroethylene,  EPA#  COO/S-91/002A  diecussed  newer  data
 relative to  wsight-of-evidenee  classification.    The  Agency's
 Science Advisory Board has reviewed these documents finding them to
 be technically adequate while offering an opinion that the weight-
   "          ia on C~D2 continuum  (OPoasible Human carcinogen,
                                                               ,
 B2-probable Human Carcinogen) .  At present time, the Agency has not
 adopted a final position on the weight-of-«vidence classification.

     The upper bound risk estimates from the 1985 Health Assessment
 Document  as  amended by updated inhalation values  from  the 1987
 Addendum have not as yet been verified by the IRIS-CRAVE workgroup.
 The a*tim«t«»  are viewed as usaful information in the context of
 the information available in the  1985-1987 period.

 ORAL:  1985 BAD;     Unit risk - l.SB-6 per ug/L

                    Slope Factor - 5.2E-2 p«r rag/kg/ day

 INKALATIOK: 1987  Addendum;    Unit risk -  range form 2.9B-7  to
                             9.!>E-7  with  a   geometric  mean  of
                             5.8E-7 per ug/eu.m

                    Slope factor - 2.flE-3 per mg /kg/day

     Those needing  to  make  a choice about carcinogenicitv have
  i'    8n a"?  TL™ **»»«*• and the 188 end
Science  Advisory  Board  lettara  of  advice  useful  background
information,   when too Agency makes a  decision  about weioht-of-
                                              ''
                       16-2

-------
Triehloroethylene fTCEV fCASRH 79-01-gl


     The current phase of the carcinogenic!ty characterization for
trichloroetfaylene  started  with  a  July  1985  Health  Assessment
Document for Trichloroethylene, EPA# 600/8-82/OQ6F which classified
trichloroethylene in weight-of-Kvidenca Group "B2 - Probable Hunan
carcinogen".  Inhalation and oral upper bound risk estimates were
provided.  This information was verified on IRIS from 3/87 through
7/89.  A Juno i»u/ Addendum to the Health Assessment Document for
Trichloroethylene, EPA/ 6oo/a-82/ooeTA proposed that the w«ight-of-
Evidence finding of "B2" was further supported by newly available
animal bioassay data and offered a minor revision  to the inhalation
upper bound risk estimate.   In 1988 the Agency's Science Advisory
Board offered an opinion that,  the weignt-o£-evidence was on C-B2
continuum   (OPossible  Human   Carcinogen,    B2»Probabl«   Human
Carcinogen).  The Agency withdrew the IRIS carcinoganioity file in
7/89 and has not  adopted  a current  position on the weight-of-
evidence classification.

     The quantitative  risk estimates provided  in the 1985 Health
Assessment Document  and  1987  Addendum have been reviewed  ny the
IRIS-Crave  Workgroup  but  are  not  verified  as  such  pending
resolution of  the weiqht-of-evidence classification.   The upper.
bound risk values in these documents are as followsi

ORAL:  1983 HAD;    Unit Rink - 3.2E-7 per ug/L
                    Slope  Factor - 1.1E-2 per mg/kg/day

INHALATION:  1987 Addendum;   Unit Risk - 1.7E-6 per ug/cu.m.
                              slope Factor = 6.0E-3 per mg/kg/day

     When  the  Agency  adopts  a  current  position  on weight-of-
evidence  classification,  the  trichloroethylene  file  will  be
rcentered on TRTS.
                           16-3

-------
17.  TOXICOLOGICAL SUMMARIES FOR CHEMICALS FOR WHICH
     TOXICOLICAL INFORMATION WAS INSUFFICIENT FOR
     RISK ASSESSMENT IN THE SI/NJ UATAP
          Barium and compounds
          Chlorobenzene
          Cobalt
          Copper
          Dichloroethane, 1,1-
          Selenium
          Styrene
          Trichloroethane,  1,1,1-
          Xylenes
          Zinc
                               17-1

-------
           TOXICOLOGICAL PROFILE FOR
             BARIUM AND COMPOUNDS
                 Prepared by:

       Clement  International Corporation
        Under Contract No. 205-88-0608

                Prepared for:

Agency for Toxic Substances and Disease Registry
          U.S.  Public Health Service
                  July 1992
                                    76*
17-2              --11&3
                                    TP-11J

-------
2.4  RELEVANCE TO PUBLIC HEALTH

     No acute-, intermediate-, or chronic*duration inhalation MRLs were
derived for barium because studies evaluating the effects of barium in humans
and animals following acute, intermediate, and chronic inhalation exposure
were inadequate for establishing the exposure concentrations associated with
edveree health effects.  The human studies (Doig 1976? Bssing et al. 1976)
Seaton et al. 1986; Shankle and Keane 1988) were limited by the small number
of subjects and the lack of quantitative exposure information.  The animal
studies (Ricks et al. 1986; Tarasenko et al. 1977) were limited by inadequate
descriptions of the experimental design.

     No acute-, intermediate-, or chronic-duration oral MRLs were derived for
barium because of limitations of the studies evaluating oral exposure to
barium for such durations.  Case studies of acute exposures in humans did not
provide adequate characterization of the doses associated with adverse health
effects and acute-duration animal studies did not provide sufficient data to
identify a target organ.

     Intermediate-duration oral studies in humans either did not provide
adequate characterization of doeee aeaociated with adverse health effects
(Brenniman and Levy 1985; Brenniman et al. 1979a, 1981) or the number of
subjects examined was too small (Wones et al. 1990) .  The observation of
increased blood pressure in an intermediate-duration oral study in rats  (Perry
et al. 1983, 1985, 1989) was not used to set an MRL because the resulting MRL
would be approximately 1.5-4-fold lower than the estimated daily intake of
barium from air, water, and dietary sources combined.

     No chronic-duration oral MRL was established for barium, despite the
observation of a NOAEL and a LOAxL for blood pressure effects in a chronic rat
study by Ferry et al.  (1983. 1985, 1989), because the resulting MRL would have
been approximately 19-50-fold lower than the estimated daily intake of barium
from air.  water, and dietary sources combined.

     No acute-,, intermediate-, or chronic-duration dermal MRLs were derived
for barium because of the lack of an appropriate methodology for the
development of dermal MRLs.

     Barium is naturally present to some extent in water and food.
Consequently, the general population is exposed normally to barium  through the
ingestion of drinking water or food.  The  general population also is exposed
by inhalation to low levels of barium in ambient air.  Exposure to barium
                              17-3

-------
                                      35

                              2.  HEALTH EFFECTS
 through public drinking water supplies, food, or ambient air generally should
 not pose a significant health risk to humans because of the very low levels of
 barium that would typically be associated with these types of exposures.

      Since barium is a frequent contaminant at hazardous waste sites, humans
 living or working near these sites may potentially become exposed to barium.
 Concentrations of barium in soil or groundwater may be significantly elevated
 over  background levels at hazardous waste sites, thereby posing a potential
 health risk to humans.  Soil contaminated with barium is of concern because
 airborne dusts generated from contaminated surface soil through the action of
 wind  may potentially expose individuals by inhalation.  Airborne barium dusts
 generated from contaminated surface soil could potentially form residues on
 foods that are ingested.  There is also the potential that children may ingest
 barium through hand to mouth contact following playing in contaminated soil.
 Groundwater contaminated wich barium is of concern because of che potential
 for humans to ingest such water.  Contaminated soil and groundwater also are
 of concern because individuals may directly become exposed dentally through
 airborne dusts, through direct contact with contaminated soil from
 construction, excavation, or recreational activities, and/or through direct
 contact by showering with contaminated water.

      There is little quantitative information regarding the extent of barium
 absorption following inhalation, oral, or dermal exposure.  Available evidence
 indicates that barium is absorbed to some extent following inhalation, oral,
 and dermal exposure; however, absorption in some cases is expected to be
 limited.  For example, there is some evidence that gastrointestinal absorption
 of barium in humans is less than 5-302 of the administered dose.  These latter
 data  suggest that although individuals may become exposed orally to high
 levels of barium, adverse health effects may not necessarily develop because
 of the limited gastrointestinal absorption.  Another important factor
 affecting the development of adverse health effects in humans is the
 solubility of the barium compound to which the individual is exposed.  Soluble
 barium compounds would generally be expected to be of greater health concern
 than  insoluble barium compounds because of the greater potential of soluble
.barium compounds to be absorbed by the body.

     The different barium compounds have different solubilities in water and
body fluids and therefore they serve as variable sources of the Ba2* ion.   The
Ba2* ion and the soluble  compounds of  barium (notably chloride,  nitrate,
hydroxide) are toxic to humans.  The insoluble compounds of barium  (notably
sulfate and carbonate) are inefficient sources of Ba2* ion because  of limited
solubility and are therefore generally nontoxic to humans (ILO 1983).  The
insoluble, nontoxic nature of barium sulfate has made it practical to use this
particular barium compound in medical applications such as enema procedures
and in x-ray photography of the gastrointestinal tract.  Barium provides an
opaque contrasting medium when ingested or given by enema prior to x-ray
examination.   Under these routine medical situations, barium sulfate is
generally safe.   However, barium sulfate or other insoluble barium compounds
                                  17-4

-------
                                      36

                              2.   HEALTH  EFFECTS
may potentially be toxic when it is introduced into the  gastrointestinal  tract
under conditions where there is colon cancer (Princenthal et al.  1983)  or
perforations of the gastrointestinal tract and barium is allowed to enter the
blood scream.

     Barium has been associated with a number of adverse health effects in
both humans and experimental animals.  Both human and animal evidence suggests
that the cardiovascular system may be one of the primary targets of barium
toxicity.  In addition to cardiovascular effects, exposure of humans and/or
animals to barium has been associated with respiratory,  gastrointestinal,
hematological, musculoskeletal, hepatic, renal, neurological, developmental,
and reproductive effects.  No data or insufficient data are available to draw
conclusions regarding the immunological, genotoxic, or carcinogenic effects of
barium.  Death has been observed in some individuals following acute oral
exposure to high concentrations of barium.  The following section evaluates
the significance of existing toxicity data on barium with regard to human
health.

     Death.  No studies were available regarding death in humans or animals
after inhalation or dermal exposure to barium.  However, mortality has been
reported to occur in a number of cases where humans have been exposed acutely
to barium through accidental or intentional ingestion (Das and Singh 1970;
Diengott et al. 1964; McNally 1925; Ogen et al. 1967; Talwar and Sharma 1979).
The observations from human case reports are supported by findings from acute
studies with rodents that indicate barium is toxic by the oral route
(Borzelleca et al. 1988; Tardiff et al. 1980).  Reduced lifespan also has been
observed in chronic oral studies with mice (Schroeder and Mitchener 1975b).
The results from human case studies and animal studies suggest that humans who
are exposed orally to high levels of barium may be at increased risk for
mortality.

     One death in an adult female due to acute intravasation of barium
gulfate during a barium enema was found in the literature.  Direct entry of
barium sulfate into the circulatory system apparently resulted in
cardiorespiratory failure (Cove and Snyder 1974).  Acute parenteral
administration of barium compounds to animals has  resulted  in death.  Rate of
administration, total dose, species, and individual differences are all
factors affecting the ability of barium and its compounds to cause death.
Major symptoms leading to death are hypokalemia  (Jalinski et al. 1967; Roza
and Berman 1971; Schott and McArdle 1974), muscle  paralysis  (Roza  and Berman
1971; Schott and McArdle 1974), cardiorespiracory  failure (Cove and Snyder
1974; Roza and Berman 1971), and convulsions  (SegreCi et al. 1979; Welch et
al. 1983).  Parenteral administration is not  a normal route  of barium exposure
in humans and only on the rare occurrence of  intravasation  during  barium enema
would it be expected to be a problem.  However, many of  the  symptoms
experienced are the same as those experienced by humans  and animals  exposed  to
acute doses by inhalation and  ingestion.
                               17-5

-------
                                      37

                              2.   HEALTH EFFECTS
     Systemic Effects

     Respiratory Effects.   Studies evaluating the respiratory effects of
barium following inhalation, oral, and dermal exposure are limited.   Benign
pneumonoconiosis has been observed in workers exposed occupationally by
inhalation to barium (Doig 1976).   However,  no respiratory effects were
observed in another study of workers exposed to barium carbonate dust by
inhalation (Essing et al.  1976).   There are  case reports of individuals who
developed respiratory weakness and paralysis following acute ingestion of
barium (Das and Singh 1970; Gould et al.  1973; Lewi and Bar-Khayim 1964;
Morton 1945; Ogen et al.  1967; Phelan et al. 1984; Wetherill et al.  1981).
Respiratory effects have  not been evaluated  in humans following dermal
exposure.  Accumulation of fluid in the trachea has been noted in acute oral
studies with rats (florzelleca et al. 1988).   The results from human case and
occupational studies and from acute oral studies with rats suggest that humans
who are exposed orally or by inhalation to barium may be at increased risk for
minor respiratory effects.

     Acute intravasation of barium sulfate into the circulatory system of an
adult female patient following a barium enema procedure caused the compound to
be deposited in blood vessels throughout the body, including the lungs, and
resulted in respiratory failure (Cove and Snyder 1974).  Acute parenteral
administration of barium compounds to animals has been shown to result in
paralysis of the respiratory muscles (Roza and Herman 1971).  Similar
respiratory paralysis is  frequently encountered in cases of acute exposure in
humans and animals by ingestion or inhalation.  Incratracheal administration
of barium sulfate into rat lungs produced a mild inflammatory reaction  (Huston
et al. 1952).  Barium sulfate could not be removed by either polymorphonuclear
leukocytes or monocytes.   A tissue reaction followed;  however, no fibrosis
was observed.  Since this mode of entry is similar to inhalation, these
results may be significant for cases of inhalation exposure.

     Cardiovascular Effects.  No reliable information is available regarding
cardiovascular effects in humans or animals  for inhalation or dermal exposure.
However, case reports of humans exposed orally by acute ingestion and results
of acute, intermediate, and chronic oral studies with experimental animals
indicate that barium induces a number of cardiovascular effects.  These
effects include increased blood pressure, changes in heart rhythm, myocardial
damage, and changes in heart physiology and metabolism  (Das and Singh 1970;
Diengott et al. 1964; Gould et al. 1973; Kopp et al. 1985; Lewi and Bar-Khayim
1964; McNally 1925; Perry et al. 1983, 1985, 1989; Talwar and Sharma 1979;
ttetherill et al. 1981).  The results from this study suggest that humans who
are exposed orally to barium may be at increased risk for cardiovascular
effects.

     In addition to cardiovascular effects  following oral exposure,
cardiovascular effects have been observed in humans following intravasation of
barium and in animals following parenteral barium exposure.  During a barium
                                  17-6

-------
                                      38

                              2.   HEALTH  EFFECTS
sulfate enema procedure on an adult female,  the  patient developed
cardiorespiratory failure (Cove and Snyder 1974).   On necropsy,  barium sulfate
was found throughout the circulatory system,  including the  heart.   The authors
attributed the death of the woman to barium intravasation.   In animals,
parenteral administration of barium compounds has  been shown to cause
hypertension and dysrhythmias (Foster et al.  1977;  Mattila  et al.  1986;  Roza
and Berraan 1971).   Although parenteral exposure  is not a common exposure route
for humans,  similar symptoms are observed in cases of acute oral and
inhalation exposure in humans and animals.

     In vitro research in mammalian systems indicated barium induces both
contraction and automaticity in isolated hearts  and heart muscles (Delfino et
al. 1988; Ehara and Inazawa 1980; Hiraoka et al. 1980; Katzung and Morgenstern
1976; Mascher 1973; Munch ec al. 1980; Saeki et  al. 1981; Slavicek 1972; Toda
1970).   Electrical and mechanical effects caused by barium  appear Co be
primarily calcium dependent, although barium could still induce contractions
and pacemaker activity in calcium deficient media (Ebeigbe  and Aloamaka 1987;
Ehara and Inazawa 1980; Hiraoka et al. 1980;  Slavicek 1972; Toda 1970).
Barium has also been shown to cause significant  alterations of most myocyte
components and degeneration of mitochondria and  the contractile apparatus
(Delfino et al. 1988).  Repeated exposures to barium in isolated heart systems
resulted in tachycardia (Ebeigbe and Aloamaka 1987).  These in vitro findings
offer some possible explanations for the heart abnormalities seen in barium
toxicity in humans and animals.

     Gastrointestinal Effects.  Reliable human and animal studies evaluating
the gastrointestinal effects of barium following inhalation and dermal
exposure were not available.  Data from case reports of humans suggest that
gastrointestinal hemorrhage and gastrointestinal disturbances, including
gastric pain, vomiting, and diarrhea, have been associated with acute oral
exposure to barium (Das and Singh 1970; Diengott et al. 1964; Gould et al.
1973; Lewi and Bar-Khayim 1964; McNally 1925; Morton 1945;  Ogen et al. 1967;
Phelan et al. 1984; Talwar and Sharna 1979; Wetherill et al. 1981).
Inflammation of the intestines has been noted in acute oral studies with rats
(Borzelleca et al. 1988).  No data were available from intermediate or chronic
exposure studies.   Results from human case studies and acute studies with rats
suggest that humans exposed orally to barium for acute periods may develop
gastrointestinal effects.

     Two case studies of acute intrusion of barium sulfate into the
peritoneal space during barium enema examination of four men showed barium
sulfate caused an acute inflammatory tissue response  (Kay 1954; Yamamura et
al. 1985), and in one case resulted in formation of a fibrous granuloma  (Kay
1954).   This is an extremely rare mode of entry and not of significant concern
for individuals exposed at a hazardous waste site.  Increased fluid
accumulation in the intestinal lumen of rats was observed after
intraperitoneal injection of barium chloride (Hardcastle et al. 1983b,  1985);
however, this observation is not significant for individuals exposed  at
                               17-7

-------
                                      39

                               2.  HEALTH EFFECTS
 hazardous  waste  sices because of the route of exposure and because  there has
 been no  documentation of  this effect occurring  in humans following  normal
 exposure routes.

      Limited studies have been done in vitro on mammalian gastrointestinal
 systems.   Generally, they indicated that barium induced intestinal  secretion
 by releasing intracellular calcium, which combined with calmodulin  to
 stimulate  the secretory process (Hardcastle et  al. 1983a, 1983b, 1985).
 Barium also  increased gastrointestinal tissue sugar accumulation and decreased
 raucosal  to serosal galactose fluxes.  The two proposed mechanisms for this are
 (1)  activation of the calcium-calmodulin complex or (2) direct action of
 barium on  smooth muscle tone (Alcalde and Ilundain 1988).  The relevance of
 these effects on the gastrointestinal tract is  unknown.

      Hematological Effects.  No reliable studies were available regarding
 hemacological effects in humans or animals following inhalation or  dermal
 exposure to  barium.  There is suggestive evidence from case reports that acute
 inhalation,  oral, and dermal exposure of humans is associated with  lowered
 blood potassium  levels (Diengott et al. 1964; Gould et al. 1973; Lewi and Bar-
 Khayim 1964;  Fhelan et al. 1984; Shankle and Keane 1988; Stewart and Hummel
 1984;  Talwar and Shanna 1979; Wetherill et al.  1981).  These findings suggest
 that humans  exposed to barium by various routes may be at increased risk for
 minor hemacological effects.

      Several studies of animals exposed to barium by parenteral routes
 indicate that barium decreases in serum potassium (Foster et al. 1977;
 Jaklinski  et al. 1967;  Roza and Berman 1971; Schott and McArdle 1974).  In one
 study, dogs  intravenously administered barium chloride demonstrated a decrease
 in serum potassium accompanied by an increase in red blood cell potassium
 concentration (Roza and Berman 1971).  The authors concluded that the observed
 hypokalemia  was  due to a shift of potassium from extracellular to
 intracellular compartments and not to excretion.  Additional intravenous
 studies have  linked the observed hypokaleraia to muscle paralysis in rats
 (Schott and  McArdle 1974) and cardiac arrhythmias in dogs (Foster et al.
 1977).  These experiments in animals strongly support the suggestive human
 case  study evidence indicating hypokalemia is an important effect of acute
 barium toxicity.

     Musculoskeletal Effects.  No studies were  available in humans  or animals
 regarding musculoskeletal effects of barium following dermal exposure.  Case
 reports of humans indicate that acute inhalation and acute oral exposure to
barium has been associated with muscle weakness and paralysis (Das  and Singh
 1970; Diengott et al.  1964;  Gould et al.  1973;  Lewi and Bar-Khayim  1964;
McNally 1925; Morton 1945; Ogen et al.  1967; Phelan et al. 1984; Shankle and
Keane 1988; Wetherill et al.  1981).  Occupational exposure has not, however,
been found to result in radiologically apparent barium deposits in  skeletal
muscle or bone (Essing  et al. 1976).  Very limited animal data are  available
regarding musculoskeletal effects.   No adverse  effects on the musculoskeletal
                                   17-8

-------
                                      40

                              2.  HEALTH EFFECTS
system were reported in an intermediate oral study with rats (Tardiff et al.
1980).   The findings from human case reports suggest that humans having acute
oral or inhalation exposure to barium may develop musculoskeletal effects.

     No data on musculoskeletal involvement in cases of barium exposure by
other than oral or inhalation modes have been reported for humans.  In animals
receiving acute doses of barium compounds parenterally, both muscle twitching
and paralysis have been reported.  Muscle twitching usually occurred within
minutes of injection with flaccid paralysis following (Roza and Herman 1971;
Schott and McArdle 1974).   Parenteral administration is a very rare route of
barium exposure, but once barium has entered the bloodstream and has been
systemically distributed,  it will have the same effects on the same organ.
Similar symptoms are expected to occur in humans acutely exposed to barium via
inhalation and oral routes.

     Barium induced smooth muscle contractions in a variety of in vitro
mammalian systems (Antonio et al. 1973; Breuing et al. 1987; Clement 1981;
Ebeigbe and Aloamaka 1987; Ehara and Inazawa 1980; Karaki et al. 1967; Hishra
et al.  1988; Munch et al.  1980; Saeki et al. 1981; Saito et al. 1972; Slavicek
1972).   Contraction appears to be calcium dependent (Antonio et al. 1973;
Breuing et al. 1987; Clement 1981; Karaki et al. 1967; Saito et al. 1972),
although the exact mechanism is unknown (Breuing et al. 1987; Clement 1981;
Mishra et al. 1988).

     Hepatic Effects.  No reliable human or animal data were available
regarding hepatic effects following inhalation or dermal exposure.
Degeneration of the liver following acute oral exposure to barium has been
noted in one human case report (McNally 1925).  Increased liver/brain weight
ratio and darkened liver were observed in rats following acute oral exposure
to barium (Borzelleca et al. 1988).  Decrease blood urea nitrogen, a potential
sign of altered hepatic activity, was also noted in this study  (Borzelleca et
al. 1988).  The available data are too limited to conclusively determine
whether or not oral exposure to barium is associated with increased risk of
hepatic effects in humans.

     Renal Effects.  No dermal studies evaluating renal effects  in humans or
animals were available.  Renal failure was reported in one case  study of a
human exposed by acute inhalation to barium (Shankle and Keane 1988).   Case
studies of humans developing renal failure, renal insufficiency,  and renal
degeneration following acute oral barium poisoning have been reported  (Gould
et al.  1973; Lewi and Bar-Khayim 1964; McNally 1925; Phelan et al. 1984;
Wetherill et al. 1981).  Increased kidney/body weight ratio has been observed
in rats following acute oral exposure to barium (Borzelleca et al. 1988).
Renal effects have not been observed in intermediate or chronic  oral studies
with rats (Schroeder and Kitchener 1975a; Tardiff et al. 1980).   Together, the
findings from human case reports and animal studies suggest that  individuals
exposed to barium by acute inhalation or ingestion may be at increased  risk  of
developing minor renal effects.
                                17-9

-------
                                      41

                              2.  HEALTH EFFECTS
      One  in vitro study on rat renal tissue horaogenate showed barium weakly
 inhibited the sodium-potassium-adenosine triphosphatase enzyme system (Kramer
 et  al.  1986).  A second study on mouse kidney tubules showed barium chloride
 could depolarize the membrane and inhibit potassium transport (Volkl et al.
 1987).  A similar defect in cell membrane transport in humans could be
 responsible for the renal involvement observed in some cases of acute barium
 poisoning.

      Dermal/Ocular Effects.  Few inhalation or dermal studies evaluating
 dermal/ocular effects in humans or animals are available.  Results of one
 limited study suggested that barium carbonate was a dermal and ocular irritant
 when  applied to the skin and eye of animals; however, it was not clear whether
 or  not  control animals were used (Tarasenko et al. 1977).  In studies with
 Sprague-Dawley rats, both ocular discharge following acute oral exposure
 (Borzelleca et al. 1988) and nonsignificant increases in retinal dystrophy
 following intermediate and chronic oral exposure (McCauley et al. 1985) have
 been  observed.  Although the retinal dystrophy was not statistically
 significant, a dose-related trend was noted in several groups of rats if
 different duration exposure groups were combined.  Both ocular discharge and
 retinal dystrophy are commonly observed in Sprague-Dawley rats; consequently,
 these ocular lesions cannot necessarily be attributed to oral barium exposure.
 Together,  these results from animal studies provide unreliable information to
 draw  firm conclusions about dermal/ocular effects in humans following barium
 exposure.

     Other Systemic Effects.  Other systemic effects have been observed.
 Barium  sulfate was observed to act as an appendocolith in two cases following
 barium  enema procedures (Palder and Dalessandri 1988).  This is a rare
 occurrence and probably not significant in cases of human barium toxicity.
 Intravenous injection of barium sulfate into pigs increased calcitonin
 secretion  from the thyroid (Pento 1979).  This is probably not a significant
 effect  for humans since intravenous exposure is not a common route and the
 dose required was so high (1.7 mg/kg/minute for 20 minutes) it caused
 cardiotoxicity.

     Limited data are available on in vitro effects of barium on the
endocrine system.   Studies done with isolated pancreatic islet cells from mice
show barium is transported across the cell membrane and incorporated into
organelles, especially the mitochondria and secretory granules (Berggren et
al.  1983).  Barium was found to increase cycoplasmic calcium.; consequently,
the insulin-releasing action of barium may be mediated by calcium.  Barium has
also been found capable of stimulating the calcitonin secretion system of the
thyroid in pigs  (Pento 1979).

     Inmunological Effects.   No information was available regarding
immunotoxicity in humans following exposure to barium.  Acute oral exposure of
rats to barium failed to induce changes in thymus weight or gross or
                                 17-10

-------
                                      42

                              2-  HEALTH EFFECTS
microscopic lesions of the thymus (Borzelleca et al.  1988).   Information from
this study is too limited to draw any conclusions regarding relevance to human
health.

     An in vitro immunological study indicated that barium sulfate in low
doses for relatively shore periods posed no serious toxic hazard to phagocytic
cells (Rae 1977).

     Neurological Effects.  No data were available regarding neurological
effects in humans and/or animals following dermal exposure.   One case study of
a human accidentally exposed by acute inhalation to barium noted the absence
of deep tendon reflexes (Shankle and Keane 1988).  Case studies of humans
having acute oral exposure to barium have reported such effects as numbness
and tingling of the mouth and neck,  partial and complete paralysis, and brain
congestion and edema (Das and Singh 1970; Diengott et al. 1964; Gould et al.
1973; Lewi and Bar-Khayim 1964; McNally 1925; Morton 1945; Ogen et al. 1967;
Phelan et al. 1984; Wetherill et al. 1981).  Acute and intermediate oral
exposure of rats to barium has not been associated with changes in brain
weight or with gross or microscopic changes of the brain (Borzelleca et al.
1988; Tardiff et al. 1980).  Based on the limited, but suggestive evidence
from human case studies, there is the potential that individuals exposed by
acute inhalation or acute oral exposure to barium may be at increased risk of
developing neurological effects.

     There are no cases of neurological effects in humans following
parenteral exposure to barium compounds.  In a few animal studies where barium
chloride was injected intracerebroventricularly, insensitivity to pain
occurred within minutes (Welch et al. 1983) followed by fatal convulsions if
the dose was sufficient (Segreti et al. 1979; Welch et al. 1983).  The
significance of these data is difficult to assess since this unusual mode of
entry would not occur in humans, and could be partially responsible for the
rapid and extreme effects.  Intraperitoneal injection of barium sulfate into
mice produced an immediate increase in electroshock sensitivity followed by a
decrease in sensitivity 24 hours later (Peyton and Borowitz 1978).  These
results are also difficult to assess in terns of effects observed in cases of
human exposure, but suggest that barium in sufficient amounts may potentially
influence brain function.

     In most in vitro studies of nerve fibers, barium prolonged the action
potential and caused rhythmic discharges (de No and Feng 1946; Creengard and
Straub 1959).  Barium released catecholamines in the absence of calcium both
after nerve stimulation and in the absence of stimulation (Boullin 1965, 1967;
Douglas and Rubin 1964a; Nakazato and Onoda 1980; Shanbaky et al. 1978).
Barium also inhibited potassium flux in glial cells (Walz et al. 1984).  These
i" vitro effects provide clues to the possible mechanism by which barium
induces toxic effects on the cardiovascular and musculoskeletal systems.
Barium had only a weak effect in blocking activation of spinal cord neurons by
                               17-11

-------
                                      43

                              2.  HEALTH EFFECTS
 excitatory amino acids  (Ault et al. 1980).  Barium was also taken up by
 mitochondria  in bovine  adrenal medulla (Shanbaky et al. 1982).  These
 organelles therefore maybe more susceptible to the toxic effects of barium.

     Developmental Effects.  Little information is available regarding
 developmental effects in humans and/or animals following inhalation, oral, or
 dermal exposure to barium.  One study reported reduced survival,
 underdevelopment, lowered weight, decreased lability of the peripheral nervous
 system, and various blood disorders in offspring of female rats exposed by
 intermediate  inhalation to barium (Tarasenko et al. 1977).  The same study
 also reportedly observed increased mortality, increased leukocyte count,
 disturbances  in liver function, and increased urinary excretion of hippuric
 acid in offspring of female rats treated orally with barium during conception
 and pregnancy (Tarasenko et al. 1977).  These studies are inadequate for
 evaluating the developmental effects of barium because of a number of
 significant study limitations (see Sections 2.2.1.2 and 2.2.2.5).  In view of
 the major study limitations, and until verified by further tests, results from
 these studies should be regarded as providing only preliminary and/or
 suggestive evidence that inhalation and oral exposure to barium is potentially
 associated with adverse developmental effects.

     Reproductive Effects.  No studies were available regarding reproductive
 effects in humans following inhalation, oral, or dermal exposure.
 Disturbances  in spermatogenesis,  shortened estrous cycle, and alterations in
 the morphological structure of the ovaries and testes were reportedly observed
 in intermediate exposure experiments in which rats were treated by inhalation
 with barium carbonate dust (Tarasenko et al. 1977).  However, these
 experiments suffered from a number of major limitations (see Section 2.2.1.2).
 Acute oral exposure of  rats to barium has been associated with decreased
 ovary/brain weight ratio and decreased ovary weight (Borzelleca et al. 1988).
 These latter animal findings suggest that humans exposed orally to barium may
 be at increased risk of reproductive effects.

     Oenotoxic Effects.  No data on in vivo studies of barium genotoxicity
 were available.   In vitro studies were limited and primarily involve
 prokaryotic test systems.   Tests of the fidelity of DNA synthesis using an
 avian myeloblastosis virus (AMV)  DNA polymerase system showed that neither
 barium acetate nor barium chloride affect the accuracy of DNA replication
 (Sirover and Loeb 1976a; Sirover and Loeb 1976b).  Barium chloride produced
negative test results for its ability to inhibit growth in wild and
 recombination deficient strains of Bacillus subtilis.  These results indicate
 that barium chloride is not mutagenic (Nishioka 1975).  However, studies with
 a DNA polymerase I system from Micrococcus luteus. demonstrated that
 concentrations of barium ion less than or equal to 0.1 mM stimulated DNA
polymerase activity while concentrations greater than this inhibited
polymerase activity (Korman et al. 1978).  The significance of the inhibitory
 and stimulatory effects has not been determined.  Results from an experiment
                                 17-12

-------
                                      44

                              2.  HEALTH EFFECTS
designed co test the effect of barium chloride on sporulation frequency,
recombination frequency, and meiotic failures in Saceharomvces cerevisiae
demonstrated a definite inhibition of sporulation.   Effects on recombination
frequency and meiotic failures were ambiguous.  Barium chloride may have
caused a marginal increase in recombination frequency and information of
diploid clones (Sora et al. 1986), but the data are inconclusive.  The data
available to date are insufficient to support a conclusive statement regarding
the genotoxicity of barium and barium compounds.

     Cancer.  No adequate human studies were available that evaluated the
carcinogenic potential of barium.   Two chronic oral studies were available
chat examined the incidence of tumors in rats and mice exposed to barium
acetate in drinking water for lifetime (Schroeder and Kitchener 1975a. 1975b).
Although results of these oral studies were negative for carcinogenicity, they
were inadequate for evaluating carcinogenic effects because insufficient
numbers of animals were used, it was not determined whether or not a maximum
tolerated dose was achieved, a complete histological examination was not
performed,  and only one exposure dose was evaluated.  Precancerous lesions
(dysplasia) were reported in one study in which a woman was treated on the
cervix with a barium chloride solution; however, the relevance of this limited
observation cannot be determined because only one subject was treated and
because the vehicle solution was not specified (Ayre 1966) .  Results of one
skin-painting study with mice suggest that barium hydroxide extract derived
from tobacco leaf acted as a tumor-promoting agent; however, it cannot be
determined whether or not this apparent positive tumorigenic response was due
to barium hydroxide or some other component of the tobacco leaf extract  (Van
Duuren et al.  1968).  Barium has not been evaluated by EPA for human
carcinogenic potential (IRIS 1991).
                                17-13

-------
            TOXICOLOGICAL PROFILE FOR
                  CHLOROBENZENE
                  Prepared by:

               Life Systems, Inc.
              Under  Subcontract to:

            Clement Associates, Inc.
         Under Contract No. 205-88-0608

                  Prepared for:

Agency for Toxic Substances and Disease Registry
           U.S. Public Health Service
                 December 1990
                      17-14

-------
2.4  RELEVANCE TO PUBLIC HEALTH

     Inhalation studies in humans and animals and oral studies in
animals demonstrate that chlorobenzene can affect the central nervous
system, liver, and kidneys.  Chlorobenzene did not affect the developing
fetus, was not genotoxic, and did not affect reproduction.  Data has not
provided clear evidence that chlorobenzene causes cancer in animals.
Existing data are considered inadequate to derive human minimal risk
levels for acute and chronic exposures.

     Death.  No. case studies of human fatalities have been reported
following exposure to chlorobenzene by inhalation, ingestion, or dermal
contact.   Death has been reported in animals at high doses for brief
periods of exposure.  Rabbits died within 2 weeks after removal from
exposure at approximately 537 ppm (Rozenbaun et al. 1947).  The cause of
death has been attributed to central nervous system depression resulting
in respiratory failure.  Animal data suggest that lethality may not be a
concern for humans unless the exposure level is very high.
                                  17-15

-------
                                    28

                            2.   HEALTH  EFFECTS
      Systemic  Effects.  No  studies were  located regarding effects on  the
 respiratory, cardiovascular,  gastrointestinal, hematological,
 musculoskeletal,  or  dermal/ocular systems  in humans or  animals by any
 route of exposure to chlorobenzene.

      Hepatic Effects.  No studies were located demonstrating that
 chlorobenzene  causes hepatic  toxicity in humans by any  route of
 exposure.  Acute  and intermediate exposures in animals  demonstrated that
 chlorobenzene  causes changes  in liver weights and enzyme levels,
 degeneration,  necrosis, and alterations  in microsomal enzymes.  These
 effects  were first evident  during acute  exposure (5 days) at
 1,140 mg/kg/day by gavage (Rimington and Ziegler 1963)  and  intermediate
 exposure (5 days/wk  for 24  weeks) at 75  ppm via inhalation  (Dilley
 1977).   Similar effects were  also observed following ingestion of
 2  250 mg chlorobenzene/kg/day for 91 days.  The precise mechanism for
 liver damage is not  known;  however, direct binding of chlorobenzene
 metabolites to cellular protein may be involved (Reid et al. 1973; Reid
 and Krishna 1973).   There were differential sensitivities in animal
 species  tested which may be due to differences in metabolism.  Based  on
 animal studies, liver toxicity may be an area of concern in humans.

      Renal Effects.   No studies were located demonstrating that
 chlorobenzene  causes renal  effects in humans by any route of exposure.
 Intermediate studies in animals shoved effects on the kidney at doses
 comparable to  those  causing liver effects.  Typical signs included
 tubular  degeneration and necrosis as well as changes in organ weight.
 Changes  In organ weights with accompanying histcpathology occurred at
 2  250 mgAg/flay (90  days) (Kluwe ec al.   1965).   The precise mechanism of
 kidney damage  is not clear.   However, necrosis was associated with
 covalent binding of  substantial amounts  of radiolabeled chlorobenzene to
 kidney protein in intraperitoneal studies (Reid 1973).   This study also
 reported that  autoradiograms revealed that most of the covalently bound
 material was localized within necrotic tubular cells (Reid 1973).   Based
 on animal studies, renal toxicity may be an area of concern in humans.

      Immunological Effects.   Histopathologic evaluations in animals
 suggest that chlorobenzene may be immunotoxic;  however, direct tests of
 immune function have not been performed.   In the absence of functional
 assessment,  the potential for chlorobenzene to affect the immune system
 in humans can not be determined.

     Neurological effects.   Case  reports  of humans  demonstrated that
 chlorobenzene caused disturbances of the central nervous system,  but
 there were no reports of changes  in the  structure of the brain and other
parts of the nervous system.  Effects were observed in humans who
 inhaled vapors  of chlorobenzene in the workplace for up to 2 years
 (Rozenbaum et al.  1947).   Effects included headaches,  dizziness,  and
                               17-16

-------
                                   29

                           2.   HEALTH EFFECTS
sleepiness.  Unconsciousness,  lack of response to skin stimuli,  and
muscle spasms were noted following accidental ingestion.   While  there is
qualitative evidence for central nervous system effects in humans,  a
quantitative assessment can not be made since exposure levels were  not
reported.  Because work practices have changed significantly since  these
studies, it is reasonable to assume that exposure levels in this study
were higher than current permissible federal exposure levels. Acute
studies in animals confirm that chlorobenzene is potentially neurotoxic.
These effects appear to be the result of narcotic effects of
chlorobenzene on the central nervous system.  Acute inhalation exposure
produced narcosis preceded by muscle spasms in rabbits at 1,090  ppm
(Rozenbaum et al. 1947).

     Developmental Effects.  No studies were found regarding the
developmental toxicity of chlorobenzene in humans.  In inhalation and
oral exposure studies, the animals did not demonstrate significant
developmental toxicity when compared with untreated controls.  Negative
responses in two animal species suggest that developmental toxicity may
not be an area of concern for chlorobenzene.

     Reproductive Effects.  No studies were found regarding the
reproductive toxicity of chlorobenzene in humans.  In a two-generation
inhalation study, chlorobenzene did not adversely affect various
reproductive parameters in rats (Nair et al. 1987).  While results of
this study suggest reproductive toxicity may not be an area of concern
to humans, other considerations are warranted before firm conclusions
can be made regarding risk to humans.  The slight increase in the
occurrence of degeneration of the germinal epithelium of the testes
provides some evidence for further consideration.  Also, the study did
not provide histopathological data on other organs related to
reproductive functions (i.e., epididymis, vas deferens, accessory sex
glands, and pituitary).  While the authors reported no treatment-related
impairment of fertility, it should be noted that  fertility assessments
in test animals are limited by their insensitivity as measures of
reproductive injury in humans.

     Genotoxic Effects.  No studies were located  regarding the genotoxic
effects of chlorobenzene in humans.  No in vivo animal assays were
found, except the micronuclear test in mice which was moderately
positive (Mohtashamipur et al. 1987)  (Table 2-3).  Furthermore,  in vitro
tests employing bacterial and yeast assay systems with and without
metabolic activation were negative  (Haworth et al. 1983; NTP 1985;
Prasad 1970).  Chlorobenzene induced transformation  in adult rat liver
epithelial cells but was not genotoxic  to hepatocytes  (Shimada  et  al.
1983).  Since transformations may occur through nongenotoxic mechanisms,
results do not necessarily indicate that chlorobenzene  is  potentially
genotoxic.  Results of in vitro assays  for  chlorobenzene  are presented
                            17-17

-------
                                   31

                           2.  HEALTH EFFECTS
in Table 2-4.  Existing data suggest that genotoxicity may not be an
area of concern for chlorobenzene exposure in humans.

     Cancer.  No studies were found regarding the carcinogen!city of
chlorobenzene in humans.  In a chronic bioassay in animals,
chlorobenzene (up to 120 mg/kg/day) did not produce increased tumor
incidences in mice of both sexes or in female rats (NTP 1985).   It was
noted, however,  that male rats showed a statistically significant
increase in neoplastic nodules at the highest dose level tested.  While
there is strong evidence for neoplastic nodules,  existing data are
inadequate to characterize the potential for chlorobenzene to cause
cancer in humans and animals.
                             17-1 a

-------
            TOXICOLOGICAL PROFILE FOR
                     COBALT
                  Prepared by:

          Syracuse Research  Corporation
              Under  Subcontract  to:

        Clement  International  Corporation
         Under Contract No.  205-88-0608

                 Prepared for:

Agency for Toxic Substances and Disease Registry
           U.S.  Public Health Service
                    July 1992
                 17-19

-------
2.4  RELEVANCE TO PUBLIC HEALTH

     Cobalt has been found to produce adverse effects by the Inhalation,
oral, and dermal routes.  Effects in humans following inhalation exposure to
cobalt included lung effects (respiratory irritation, fibrosis, asthma.
pneumonia, wheezing), cardiovascular effects (cardiomyopathy),  liver and
kidney congestion, ocular effects (congestion of the conjunctiva), and weight
loss.  Effects in humans observed following ingestion of cobalt, as cobalt
sulfate in beer or as coValt chloride as a treatment for anemia, included
cardiomyopathy. gastrointestinal effects, visual disturbances,  and thyroid
effects.   Cobalt dermatitis and sensitization as a result of dermal exposure
to cobalt are well documented.

     Cobalt is essential for the growth and development of ruminants (Becker
and Smith 1951; Keener et al. 1949).  Overexposure of other animals to cobalt
resulted in effects similar to  those in humans following inhalation and dermal
exposure.  After ingestion of cobalt, effects in animals were similar to
effects in humans although some additional effects,  including hypothermia,
neurological effects (effects on reactivity), developmental effects (stunted
fetuses), and reproductive effects (testicular degeneration and atrophy), were
found in animals, but not humans.  In the animal studies, the doses tested
were higher than the levels to  which humans would be expected to be exposed.

     An MRL for inhalation exposure to cobalt was derived for intermediate
duration only.  The intermediate inhalation MRL of 3xlO"5 mg cobalt/m3 was
based on a LOAEL of 0.11 mg cobalt/m3 for metaplasia of  the  larynx in rats
exposed for 13 weeks (6 hours/day, 5 days/week) (NT? 1991).   Similar effects
were reported in mice exposed to the same concentration, but the rats appeared
to be more sensitive.  NOAEL values were not defined for the rats or the mice.
A decrease in lung compliance was reported in pigs exposed to a comparable
level of cobalt for 3 months (0.1 mg cobalt/m3 as  cobalt dust,  6 hours/day,
5 days/week) (Kerfoot 1973).

     The intermediate inhalation MRL was derived by adjusting the LOAEL of
0.11 mg cobalt/m3 for intermittent exposure  (6 hours/24  hours x
5 days/7 days), converting to an equivalent human dose,  and dividing by an
                                17-20

-------
                                      48

                              2.  HEALTH EFFECTS
uncertainty factor of 1,000 (10 for the use of a LOAEL,  10 for human
variability, and 10 for interspecies extrapolation).   An acute inhalation MRL
was not derived because the threshold vas not defined for human effects  and
animal studies reported effects that were serious and occurred at levels above
those reported in the few human studies.  A chronic inhalation MRL vas not
derived because the lowest LOAEL is human sensitization  and ATSDR does not
derive MRLs based on health effects such as sensitization.

     Oral MRL values were not derived for acute, intermediate or chronic
exposure to cobalt.  Acute and intermediate MRLs were not derived because the
reported effects in animals were serious and occurred at levels above those
reported in the few human oral studies.  The intermediate-duration human oral
studies were also insufficient for derivation of MRL values because the
reported effects were serious.  No chronic oral studies  were available for
humans or animals, therefore, a chronic oral MRL was not derived for cobalt.

     Acute-duration, intermediate-duration, and chronic-duration dermal MRLs
were not derived for cobalt due to the lack of appropriate methodology for the
development of dermal MRLs.

     Death.  Lethal cardiomyopathy in humans was reported following repeated
inhalation of airborne cobalt or ingestion of beer that  contained cobalt
(Alexander 1969, 1972; Barborik and Dusek 1972; Morin et al. 1971).
Inhalation exposure levels associated with cardiomyopathy have not been
determined.  In the 1960s, breweries in the United States, Canada, and Europe
added cobalt salts to beer to improve foaming properties at the tap.  Several
deaths occurred among heavy beer drinkers who consumed beer containing
0.04-0.14 mg cobalt/kg/day (8-30 pints of beer daily).  The addition of cobalt
to beer has since been discontinued.  Although the ingestion of cobalt was
identified as a key causative factor in the beer drinkers cardiomyopathy,
other etiologic factors were significant, including heavy alcohol consumption
and related nutritional deficits.  Repeated oral ingestion of 1 mg
cobalt/kg/day to raise the hematocrit of anemic, but otherwise healthy,
patients did not cause cardiac injury (Davis and Fields  1958).

     In animals, deaths from inhalation exposure were related to respiratory
effects and secondary infections (NTP 1991; Palmes et al. 1959).  Deaths in
animals following oral exposure resulted from cardiomyopathy (Mohiuddin et al.
1970) or from multiple lesions (kidney, liver, and heart lesions) (Speijers
et al. 1982).  Acute lethality in animals varies with the .chemical form
administered, with soluble compounds generally being more toxic than insoluble
compounds.  In rats, cobalt fluoride is more toxic than cobalt chloride by a
factor of two (Speijers et al. 1982).  With the exception of tricobalt
cetroxide, the LDJO  values  of the cobalt compounds  for which acute  oral
lethality data are available (Table 2-2), all lie within the same order of
magnitude when expressed in terms of the cobalt ion.  Tricobalt tetroxide
(LD50  >3.672  mg  cobalt/kg)  is insoluble  in water and,  therefore,  is  relatively
nontoxic (FDRL 1984c).
                               17-21

-------
                                       49

                               2.   HEALTH  EFFECTS
      Systemic Effects.   The  primary  target  organ systems for the effects of
 cobalt in humans  are  the respiratory system following inhalation exposure and
 the cardiac  and hematopoietic  systems following oral exposure.

      Respiratory.   Effects on  the respiratory system include irritation,
 fibrosis,  asthma, pneumonia, and wheezing following inhalation exposure
 (Harcung  et  al. 1982; Kusaka et al.  1986b;  Shirakawa et .1. 1988, 1989;
 Sprince et al. 1988).   Individuals can develop a sensitivity to cobalt, and
 inhalation exposure to  airborne cobalt can  precipitate asthmatic attacks in
 sensitized individuals  (Shirakawa et al. 1988, 1989).  Studies in animals
 report similar effects  following inhalation exposure.  Intermediate-duration
 inhalation studies  in rats and mice  reported that the larynx was the part of
 the respiratory tract most sensitive to the effects of cobalt, with the lungs,
 nose,  and  trachea being affected at  higher  exposure levels (NTP 1991).

      Cardiovascular.  In humans, lethal cardiomyopathy resulted from oral and
 inhalation exposure to  cobalt.  Along with  the severe cardiac effects, beer-
 cobalt cardiomyopathy was characterized by  initial effects on the
 gastrointestinal system (vomiting, nausea,  diarrhea), pulmonary rales and
 edema  (resulting from the cardiac failure), liver injury (resulting from
 hepatic ischemia), and  polycythemia  (Alexander 1969, 1972; Morin et al. 1971).
 Beer-cobalt  cardiomyopathy was similar to both alcoholic cardiomyopathy and
 beriberi,  except that beer-cobalt cardiomyopathy had an abrupt onset,
 characterized by left ventricular failure,  cardiogenic shock, polycythemia,
 and acidosis.  Evidence  that ingestion of ethanol was not required for
 development  of cobalt cardiomyopathy  came from studies in animals.  A
 cardiomyopathy similar  to that observed in  humans occurred in guinea pigs
 after repeated exposure  to cobalt (20  mg/kg/day) in foods, with or without
 ethanol consumption (Mohiuddin et al.  1970).

     Gastrointestinal.   Gastrointestinal effects, including nausea, vomiting,
 and diarrhea, were reported  in humans  after ingestion of cobalt-contaminated
 beer  (Morin  et al. 1971) and treatment with cobalt for anemia (Duckham and Lee
 1976; Holly  1955).  No  effects on the  gastrointestinal system, however, were
 reported in  animals after inhalation  or oral exposure (Domingo et al. 1984;
 Holly 1955; NTP 1991).   The data in humans  suggest that therapeutic exposure
 to  cobalt  is likely to  result  in gastrointestinal effects.

     Hematopoietic.  Because cobalt  induces polycythenia in humans following
 oral exposure, it has been used in the treatment of anemia (Davis and Fields
 1958; Duckham and Lee 1976; Taylor et  al. 1977).  Polycythemia was not
 observed in humans following inhalation exposure.  Animal data show increased
hematocrit and hemoglobin levels following both oral and inhalation exposure
                                 17-22

-------
                                      50

                              2.   HEALTH  EFFECTS
(Brewer 1940; Davis and Fields 1958;  Domingo  and Llobet  1984; Domingo et al.
1984; Holly 1955;  Krasovskii and Fridlyand 1971;  Murdock 1959; NTP  1991;
Palmes et al. 1959; Stanley et al.  1947).   The  increase  in hematocrit in both
the humans and animals does not necessarily constitute an adverse effect.

     A possible mechanism of cobalt toxicity  is the irreversible formation of
a cobalt chelate with the sulfhydryl groups of  dihydrolipoic  acid,  resulting
in inhibition of two conversions in the tricarboxylic acid cycle (pyruvate to
acetyl CoA and alpha-ketoglutarate  to succinyl-CoA) (Taylor and Harks 1978).
The resulting inhibition of cellular respiration and oxidative phosphorylation
may lead to decreased oxygen uptake by the tissues, resulting in cardiac
effects.  Tissue hypoxia may in turn stimulate  the release of erythropoietin,
resulting in increased hematocrit and hemoglobin levels  (Taylor and Marks
1978).

     Hepatic.  No conclusive evidence that cobalt is a  direct liver toxicant
in humans has been reported following exposure  to low levels; however,  liver
injury has been associated with cobalt-related  cardiomyopathy following either
inhalation or oral exposure (Alexander 1972;  Barborik and Dusek  1972; Morin
et al. 1971).  Although the mechanism for the liver effects  is not  known,  it
is likely that hepatic ischemia related to cardiovascular impairment is a
significant causative factor.  Liver injury was observed in  animals orally
exposed to near lethal levels of cobalt (Speijers et al. 1982).  Whether this
represents a direct effect of cobalt on the liver or an indirect effect of
cardiac impairment is not known.  A direct effect of cobalt  on the  liver is
plausible since the liver is the major site of accumulation of orally absorbed
cobalt.

     Renal.  No conclusive evidence that cobalt is a kidney toxicant in
humans has been reported.  Congestion of the  kidneys,  however,  has  been
associated with cobalt cardiomyopathy resulting from occupational  exposure to
cobalt  (Barborik and Ousek 1972).  Effects on the proximal tubules  of the
kidneys were observed in animals orally exposed to cobalt (Holly 1955;  Murdock
1959; Speijers et al. 1982).  Adverse effects on the kidneys of both humans
and animals are a possibility because a substantial amount of cobalt absorbed
into the blood is excreted in the urine.

     Dermal/Ocular.  Effects on the human eye have been observed following
occupational exposure (congestion of the conjunctiva)  and oral exposure (optic
atrophy, impaired choroidal perfusion) to cobalt (Barborik and Dusek 1972;
Licht et al. 1972).  Occupational exposure to cobalt also causes dermatitis
(Alomar et al. 1985; Dooms-Goossens et al. 1980; Kanerva et al.  1988).

     Other Systemic Effects.  A decrease in  iodine uptake by the thyroid
resulted from acute oral exposure of humans  to 1 mg cobalt/kg/day or longer-
term exposure to 0.54 mg/kg/day (Paley et al. 1958; Roche and Layrisse 1956).
                               17-23

-------
                                      51

                              2.  HEALTH EFFECTS
     Weight loss was found in workers occupationally exposed  to cobalt.
Similar weight loss was seen in animals; in addition, time- and dose-related
hypothermia was observed in rats given cobalt orally.

     In various species of animals, parenteral administration of cobalt
resulted in cytotoxic effects on the alpha cells of the pancreas (Beskid 1963;
Goldner et al.  1952;  Lacy and Cardeza 1958; Lazarus et al. 1953; Van
Campenhout 1955).   Because this effect has never been reported in humans or
animals following inhalation, oral, or dermal exposure to cobalt, the
relevance of the  effect to humans is not known.

     Inmunological Effects.   Exposure to cobalt  can lead to sensitization.
In its  most serious  form,  cobalt-sensitization can result in  or exacerbate
asthma  (Shirakawa  et  al.  1988,  1989).   Dermal sensitization and related
cobalt-dermatitis  have  also been described.  The mechanism for cobalt
sensitization is not  completely understood.  Antibodies to cobalt have been
detected in individuals  sensitized to cobalt,  suggesting that a humoral immune
response may be a  component of  the sensitization phenomenon (Bencko et al.
1983; Shirakawa et al.  1988,  1989).

     Neurological  Effects.  No  studies were located regarding neurological
effects in humans  following inhalation,  oral,  or dermal exposure to cobalt.
Enhanced behavioral reactivity  to stress,  a slower rate of lever pushing, and
effects on conditioned reflexes  were  observed in rats orally exposed to cobalt
(Bourg  ec al.  1985; Krasovskii  and Fridlyand 1971;  Nation et al.  1983).  The
relevance of these findings to humans  is not known.   In rats,  cobalt applied
directly to the brain has been  found  to  induce epilepsy and has been used
extensively as a model toward a  better understanding of epilepsy in humans
(Bernstein and Keilhoff  1986; Bregman  et al.  1985;  Esclapez and Trottier 1989;
harcman et al. 1974; Hocherman  and Reichenthal 1983;  Lee and Malpeli 1986;
Fayan and Conard 1974; Pitkanen  et al.  1987;  Sugaya et  al.  1988;  Zhao et al.
* - w D ) ,

     Developmental Effects.   No  obvious developmental effects were  observed
ir. nurr.an fetuses from mothers who  were  given cobalt orally to counteract
otcreases in hematocrit  and hemoglobin  levels  that  often occur during
,.*gnancy (Holly 1955).  No studies were located regarding developmental
ho-      ln  Uinans  Allowing inhalation or dermal exposure.   Animal  studies,
»*f.Ver> reP°rted  chat oral exposure to cobalt results  in developmental
«"> "S l1161"'11^  stunted fetuses, a decrease  in the  number of litters and
  -.1,   i-tter weights, and an increase in  the number of dead pups  per litter
 i"-.i.".n8°TJt    1985).  Toxic maternal effects were  also observed in this
,«''!.:   T   relevance of the  effects found  in  animals to possible human
•••'v.s is not known.

     Reproductive  Effects.  No studies were  located  regarding  reproductive
     >* in humans  following inhalation, oral,  or  dermal  exposure  to cobalt.
                                      17-24

-------
                                      52

                              2.   HEALTH EFFECTS
Following both inhalation and oral exposure of animals  to cobalt,  adverse
effects on the testes were observed (degeneration,  atrophy,  decreased weight)
(Corrier et ml. 1985; Domingo et ml.  1985;  Mollenhauer  et ml.  1985;  NTP 1991;
Pedigo et al. 1988).  An increase in the length of the  estrous cycle was also
reported in female mice following inhalation exposure (NTP 1991).   Because  no
effects on the reproductive system were found in patients who  died as a result
of beer-cobalt cardiomyopathy, the significance of the  animal  results to
humans is not clear.

     Genotoxic Effects.  No studies were located regarding genotoxic effects
in humans or animals following inhalation,  oral, or dermal exposure to cobalt.

     Results of genetic testing of cobalt are presented in Table 2-8.
Several different forms of cobalt, including cobalt chloride and cobalt
sulfide, were tested.  No profound differences were found among the various
forms.  Cobalt was found to be generally nonmutagenic in bacteria (Salmonella
tvphimuriuni. Escherichia coin and yeast when compounds with a valence state
of II were tested (Arlauskas et al. 1985; Fukunaga et ml. 1982; Kanematsu
et ml. 1980; Kharab and Singh 1985; Ogawa et ml. 1986;  Singh 1983; Tso and
Fung 1981).  A very weak rautagenic response was found with Bacillus subtilis
(Kanematsu et al. 1980).  A mutagenic response to cobalt was found, however,
when compounds with a valence state of III  were tested in S.tvphimurium and JL.
coll (Schultz et al. 1982).  The authors suggested that this may be due to the
formation of cobalt III complexes that are  inert to ligand substitution,
allowing optimal interaction of cobalt with genetic material (Schultz et al.
1982).  Other studies have shown cobalt to  be a comutagen in combination with
A-substituted pyridines in S. tvnhimurium (Ogawa et al. 1988).  It has been
reported that cobalt acts as an antimutagen in bacterial (S.  tvphimurium.  fi^
subtilis. E. coin and yeast test systems (S. eerevisiae) (Inoue et ml. 1981;
Kada 1982; Kada et ml. 1986; Kuroda and Inoue 1988; Mochizuki and Sora et al.
1986).  A possible explanation was that cobalt acts by correcting the error-
proneness of deoxyribonucleic acid (DNA) replicating enzymes by improving
their performance in DNA synthesis (Inoue et ml. 1981;  Kada et al. 1986;
Kuroda and Inoue 1988; Mochizuki and Kada 1982).  Stable cobalt was genotoxic
in other assay systems:  genetic conversions in S.  cerevisiae (Funkunaga
et ml. 1982; Kharab and Singh 1985; Singh 1983); clastogenic effects in
mammalian cells (Hamilton-Koch et ml. 1986; Painter and Howard 1982);
transformation in hamster cells (Costa et ml. 1982); and sister chromatid
exchanges in human lymphocytes (Andersen 1983).

     Cancer.  Cobalt has not been shown to cause cancer in humans by any
exposure route.  An occupational study reported an increased incidence of
death from lung cancer (SMR-4.66) in workers exposed to cobalt (Mur et ml.
1987), but the difference was not statistically significant; the
characteristic lung diseases commonly found in cobalt workers were not
observed, and the workers were exposed to arsenic and nickel as well as
cobalt.  The induction of tumors (fibrosarcomas) following intramuscular
                                17-25

-------
                                      54

                              2.  HEALTH EFFECTS
injection of cobalt oxide into rats has been shown (Gilaan 1962; Oilman and
Ruckerbauer 1962; Heath 1956, 1960).  No tuners were induced in mice after
intramuscular injection of cobalt (Oilman 1962; Oilman and Ruckerbauer 1962).
Tumors were also induced following subcutaneous (Shabaan et al. 1977) and
intrathoracic injections in rats (Heath and Daniel 1962).  The significance of
these results to humans is not clear because these are not relevant routes of
exposure and no tumors were found in humans with metal-alloy prostheses.  IARC
(1991), however, has classified cobalt and cobalt compounds as group 2B,
possible human carcinogens.
                         17-26

-------
           TOXICOLOGICAL PROFILE FOR
                     COPPER
                  Prepared by:

          Syracuse Research  Corporation
     Under Subcontract No. ATSDR-88-0608-02

                 Prepared for:

Agency for Toxic Substances and Disease Registry
           U.S. Public Health Service
                  December 1990
                    17-27

-------
 2.4  RELEVANCE TO  PUBLIC HEALTH

     Copper  is a metallic element that occurs naturally as the free metal.
 Most copper  compounds occur in +1 (Cu(I)) and +2 (Cu(II)) valence states.
 Although copper is present as numerous chemical species, the biological
 availability and toxicity of copper is probably related to free Cu(II) ion
 activity.  In this section, the term copper refers to Cu(II).

     Copper  is an  essential nutrient that is incorporated into numerous
 enzymes.  These enzymes are involved in hemoglobin formation, carbohydrate
 metabolism,  catecholamine biosynthesis, and cross-linking of collagen,
 elastin, and hair  keratin.  There are numerous copper dependent enzymes,
 some of which are  cytochrome c oxidase, superoxide dismutase, dopamine
 0-hydroxylase, and ascorbic acid oxidase.

     Copper  homeostasis plays an important role in the prevention of copper
 toxicity.  Copper  is readily absorbed from the stomach and small intestine;
 after copper requirements are met, there are several mechanisms that prevent
 copper overload.   Excess copper absorbed into gastrointestinal mucosal cells
 is bound to  metallothionein.  This bound copper is excreted when the cell is
 sloughed off.  Copper that eludes the intestinal barrier can be stored in
 the liver or incorporated into bile and excreted in the feces.  Because of
 the body's efficient means of blocking the absorption of excess copper, the
 most likely  pathway for the entry of toxic amounts of copper would be long-
 term inhalation or possibly through the skin.  Both of these pathways would
 allow copper to pass unimpeded into blood.

     There is little information on copper toxicity in man.   Most reports of
 copper toxicity in humans involve the consumption of water contaminated with
 high levels  of copper or suicide attempts using copper sulfate.  Effects
 observed in humans include gastrointestinal, hepatic,  immunological
 (following dermal exposure), and respiratory effects (following inhalation
 of high concentrations of fine copper metal particles).   Death as a result
 of copper toxicity has also been observed.  Because the taste threshold of
 copper,  2.6 ppm (Cohen et al.  1960),  is much lower than the  levels
 associated with toxicity and the emetic properties of copper, accidental
 poisoning can be prevented.

     The only significant example of copper toxicity in humans is Wilson's
disease  (hepatolenticular degeneration),  an autosomal recessive disorder
 that affects  normal copper homeostasis.  The disease is characterized by
excessive retention of hepatic copper,  decreased concentration of plasma
                             17-28

-------
                                     38

                             2.   HEALTH EFFECTS
ceruloplasmin, Impaired biliary copper excretion, and hypercupruria.  The
systemic manifestations of Wilson's disease are hepatic and renal lesions
and henolytic anemia  (Schroeder et al. 1966).

     The effects observed in humans following exposure to high levels of
copper and in individuals with Wilson's disease are also observed in
animals.  Developmental and reproductive effects are also observed in
animals; these effects have not been reported in humans.

          Death.  There are several reports of humans dying as a result of
copper poisoning.  Most of these involve the intentional ingestion of large
amounts of copper.  Chuttani et al. (1965) attributed these deaths to
extensive hepatic centrilobular necrosis.  Deaths in animals given >250 rag
Cu/k8/day in the diet have also been attributed to extensive hepatic
centrilobular necrosis.

     Systemic Effects.  The primary toxlcological effect of consuming high
levels of copper in humans is gastrointestinal irritation, manifested as
vomiting, nausea, diarrhea, and anorexia.  Centrilobular necrosis of the
liver and necrosis and sloughing of tubular cells in the kidney have been
observed in individuals dying from copper poisoning (Chuttani et al. 1965).

     Gastrointestinal effects (hyperplasia in forestoinach) have been
observed in animals following exposure to large levels of copper in the
drinking water or food.  Centrilobular necrosis and extensive degeneration
of the proximal convoluted tubule epithelium have also been observed in
rats.  These effects are followed by regeneration of the tissue and
development of tolerance to continued dosing.  Tolerance is defined as a
state of decreased responsiveness to a chemical's toxic effect, resulting
from prior exposure to the chemical.  There appears to be an upper limit to
the amount of copper that can be tolerated.  In rats, the limit Is -250 ing
CuAS/d (Havwood 1985).  Tolerance has also been observed in pigs (Suttle
and Mills 1966a,b).

     The mechanisms of tolerance are not known but may involve changes in
the distribution and molecular association of copper.  Tolerance apparently
represents an adjustment of homeostasis: rather than copper being stored in
the liver and excreted in bile,  it is released from the liver and" excreted
into the urine (Haywood et al. 1985b).  It is not known if humans develop a
tolerance to copper.

     Hematological effects have been observed in healthy humans exposed to
high levels of copper and in individuals with Wilson's disease (Forman and
Kumar 1980).  A decrease in hemoglobin and hematocrit values has also been
reported in rats and pigs orally exposed to copper (Kline et al. 1971; Kumar
and Sharma 1987; NTP 1990a,b; Rana and Kumar 1980; Suttle and Mills
I966a,b)-   An increase in hemoglobin levels without a change in hematocrit
levels was also observed (Liu and Medeiros 1986).  The Liu and Medeiros
(1986) study was a longer term study than the studies that observed
                               17-29

-------
                                     39

                             2.  HEALTH EFFECTS
 decreased hemoglobin and hematocrit  levels  (Kline  et  al.  1971;  Kumar and
 Sharma 1987;  NTP 1990a,b;  Rana  and Kumar  1980;  Suttle and Mills 1966a,b).
 The  discrepancy between the  hematological effects  observed in these  shorter
 term studies  and the Liu and Medeiros  (1986)  study may represent a tolerance
 to high copper intake.

      A statistically significant  increase in  systolic blood pressure has
 been observed in rats fed a  diet  containing a moderately  high level  of
 copper.   Because this is the only study that  examined the cardiovascular
 effects associated with increased copper  intake, the  risk of  increased blood
 pressure in humans following exposure  to  high levels  of copper  is not known.

      Immunological Effects.  Dermal  exposure  to copper results  in contact
 allergic dermatitis in some  individuals (Barranco  1972; Saltzer and  Vilson
 1968).   A repor  of a similar dermatitis  in a woman after the insertion  of a
 copper IUD (Barranco 1972) suggests  that  the  dermatitis is mediated  by the
 immune system rather than dermal  irritation.

      Inhalation studies in mice confirm the finding of impaired immune
 function after exposure to copper (Drummond et  al. 1986).   However,  species
 apparently differ in effects of inhaled copper  on  the immune  system.

      Neurological Effects.   Neurological  effects have not been  observed  in
 healthy humans exposed to  high  levels  of  copper in drinking water.
 However,  a clinical manifestation of Wilson's disease is  central  nervous
 system degenerative changes.  Symptoms include  poor coordination,
 psychological impairment,  tremor,  disturbed gait,  and rigidity  (Strickland
 and  Leu 1975).   Increased  copper  levels in  the  brain  have also  been  observed
 in individuals with Wilson's disease (Stokinger 1981).  In a  child who died
 of Wilson's disease,  increased norepinephrine and  decreased dopamine
 concentrations in the basal  ganglia  were  observed  (Nyberg et  al.  1982).

      Although neurotoxicity  has not  been  observed  in  animals  exposed to
 high  levels of copper,  increased  concentration  of  copper  in the brain has
 been  observed in rats  given  high  levels of  copper  orally  or
 intraperitoneally (DeVries et al.  1986; Lai et  al. 1974;  Murthy et al.
 1981).   The effects  of  the ingestion of high  levels of copper on  levels  of
 neurotransmitters  is  equivocal (DeVries et  al.  1986;  Lai  et al. 1974;
 Murthy et  al.  1981).  Because of  the development of tolerance to  copper
 toxicity,  brain copper  levels may  not  reach a level that  would  interfere
 with  the synthesis  or degradation  of neurotransmitters or elicit
 neurological  impairment.

      If humans,  like  rats and pigs,  develop a tolerance to  high levels of
 copper,  then central nervous system  degenerative changes  would  not be  an
 outcome of copper  toxicity.

     Developmental Effects.  Developmental effects have not been  observed in
healthy humans  or  in  the offspring of mothers with Wilson's disease,  whereas
                               17-30

-------
                                      40
                              2.  HEALTH  EFFECTS
 increased fecal mortality and developmental  abnormalities have been
 observed in mice,  mink,  and hamsters  injected with  copper or  fed a diet high
 in copper (Aulerich  et  al.  1982;  DiCarlo  1979,  1980;  Ferm and Hanlon 1974;
 Lecyk 1980;  O'Shea and  Kaufman 1979,  1980).  Developmental  effects have been
 observed in minks  administered doses  50 times lower than those given to mice
 and hamsters.   Increased kit mortality was observed between birth and 4
 weeks due to impaired lactation in females consuming high levels of copper.
 Maternal toxicity  was not observed at this level.

      Developmental effects have not been  reported in humans.  Because of  the
 animal developmental toxicity,  the possibility  that developmental effects
 might occur in humans cannot be ruled out.

      Reproductive  Effects.   Reproductive  effects following  exposure to high
 levels of copper have not been observed in humans.   However,  intrauterine
 devices (lUDs)  have  been used in women as a  method  of birth control.
 Although reproductive performance was not adversely affected  in minks fed a
 diet high in copper  (Aulerich et al.  1982),  the insertion of  copper wires
 into the vas deferens or uterus prior to  conception or at gestational day 3
 resulted in decreased fertility or decreased number of implantation sites in
 monkeys,  rats,  hamsters,  and rabbits  (Chang  and Tatum 1970; Chang et al.
 1970;  Kapur et al. 1984;  Zipper et al. 1969).   No adverse effects were
 observed in control  animals in which  wires of cadmium, cobalt, nickel,
 platinum,  silver,  or zinc were implanted  in  utero (Chang et al. 1970; Zipper
 et al.  1969),  suggesting that the copper, rather than the insertion of an
 exogenous object,  is the contraceptive agent.

      Genotoxicity  Effects.   Several in vitro studies  (Table 2-4) have
 examined genotoxic effects  of copper  in nonhuman systems.   The results of
 Che tests using prokaryotic organisms are equivocal.  However, positive
 results have been  observed in vitro (Table 2-4) and in vivo (Table 2-5) in
 mammalian systems.   At  low levels of  copper  (0.01-0.1 mM Cu as copper
 sulfate),  DNA  strand breaks were  not  observed in rat hepatocytes; however,
 strand breaks  did  occur  at  high concentrations  (0.04 mM Cu  as copper
 sulfate)  (Sina  et al. 1983).   In  vivo studies with  Inbred Swiss mice showed
 that  copper  exposure resulted in  chromosomal aberrations and micronuclei and
 sperm  abnormalities  (Bhunya and Pati  1987).  Copper binds with the
 phosphate  on nucleotides  and nucleic  acids of DNA.   Its mutagenic potential
 fflay be  the  result of this binding (Sharma and Talukder 1987).

     Although  there  is no data  on the mutagenicity  of copper  in humans, in
 vivo  studies and mammalian  system in vitro studies  suggest  that copper is a
 potential human mutagen.

     Cancer.  An elevated incidence of cancer has not been  observed in
humans  or animals exposed to  copper via inhalation,  oral, or dermal routes
 Of  exposure.  Copper  exposure via  intramuscular injection has not been shown
 co  induce cancer in  rats  (Furst 1971;  Gilman 1962).   A slightly increased
 incidence of reticulum cell  sarcoma was observed in mice 18 months after a
                                 17-31

-------
                                    43

                            2.  HEALTH EFFECTS
single subcutaneous injection of copper 8-hydroxyquinoline (BRL 1968).  The
significance of this finding is  difficult to determine because of the
contrary findings of Yamane  et al.  (1984) and because subcutaneous injection
is not a normal route of copper  exposure.
                             17-32

-------
           TOXICOLOGICAL PROFILE FOR
               1,1-DICHLOROETHANE
                 Prepared by:

       Clement International Corporation
         Under Contract No. 205*88-0608

                 Prepared for:

Agency for Toxic  Substances and Disease Registry
           U.S. Public Health Service
                 December 1990
                                    xico105 i Co. »
                               ?fo-Pi
              17-33

-------
                       )    I  .
2.4  RELEVANCE TO PUBLIC HEALTH

     Relatively little information is available on the health effects of
1,1-dichloroethane in humans or animals.  However, the limited data available
in animals indicate that it is less toxic than its isomer, 1,2-dichloroethane,
and most other chlorinated aliphatics (Bruckner 1989).  Chlorinated aliphatics
as a class are known to cause central nervous system depression, and
respiratory tract and dermal irritation when humans are exposed by inhalation
to sufficiently high levels (Parker et al. 1979).

     The available data in animals suggest that inhaled 1,1-dichloroethane may
be nephrotoxic.  However, this finding is limited to one species (cat) and was
not observed in three other species tested under the same conditions.  Another
effect observed in animals but not humans following inhalation exposure to
1,1-dichloroethane exposure is fetotoxicity.  Suggestive, but inconclusive,
evidence of carcinogenicity was obtained in an oral chronic bioassay of
1,1-dichloroethane in rats and mice.

     Death.  No reports of death in humans following exposure to
1,1-dichloroethane were found.  Death has been observed in laboratory animals
following inhalation and oral exposure to 1,1-dichloroethane.  No reliable
LC30 or LD30 data were found,  but lethal doses of 1,1-dichloroethane are
perhaps 5 to 10 times higher than those required to produce death following
exposure to 1,2-dichloroethane or tetrachlorocarbons (EPA 1985; Hofmann et

-------
                                      33

                              2.  HEALTH EFFECTS
al.  1971; Smyth 1956).  Thus, it is likely that 1,1-dichloroethane can be
fatal  to humans, if exposure to high enough levels occurs.

     The cause of death in animals following exposure to 1,1-dichloroethane
has  not been well-defined, but Plaa and Larson (1965) reported that deaths
observed following intraperitoneal injection of this compound appeared to be
due  to fatal central nervous system depression.

     Systemic Effects.  The use of 1,1-dichloroethane as an anesthetic was
discontinued when it was discovered that this compound induced cardiac
arrhythmias in humans at anesthetic doses (approximately 105,000 mg/m3,  or
26,000 ppm).  The mechanism of action for the induction of cardiac arrhythmias
by 1,1-dichloroethane is not known.  However, when the cardiac muscle is
markedly depressed, it is more susceptible to the effects of catecholamines.
Secretion of catecholamines is increased in this situation by compensatory and
other  mechanisms, resulting in exqessive spontaneous contractions of the
heart.  This is an effect common to exposure to other chlorinated aliphatics
at high concentrations (Reinhardt et al. 1971).  Cardiovascular toxicity has
not  been reported in animals following exposure to 1,1-dichloroethane.

     No reports of adverse renal effects in humans following exposure to
1,1-dichloroethane were found.  Nephrotoxicity has been observed in cats
following subchronic inhalation exposure to 1,1-dichloroethane.  However,
rats,  rabbits, and guinea pigs exposed under the same conditions failed to
exhibit any toxic effects on the kidney (Hofmann et al. 1971).  Plaa and
Larson (1965) tested renal function in mice following intraperitoneal
injection of 1,1-dichloroethane, and found that adverse effects on the kidney
were only observed at lethal doses.  These effects included increased glucose
and  protein in the urine and tubular swelling.  Though data obtained following
intraperitoneal injection provides information on potential health effects,
data from oral, inhalation and dermal experiments are more relevant to
possible exposures in humans.  No histopathological changes in the kidney were
noted  after chronic ingestion of 1,1-dichloroethane by rats and mice  (Klaunig
et al. 1986; NCI 1977).  The toxicological significance of the nephrotoxicity
observed in cats and the mice with regard to human health is not known given
the  small number of animals tested (cats), the lack of a nephrotoxic effect in
other  species and in other studies where 1,1-dichloroethane was administered
orally, and the fact that nephrotoxicity is not an effect commonly attributed
to the halogenated hydrocarbons.

     Imntunological Effects.  No studies were located regarding immunologic
effects in humans or animals following exposure to 1,1-dichloroethane, and  it
is not known if 1,1-dichloroethane is immunotoxic in humans.

     Neurological Effects.  Chlorinated aliphatics as a class are known to
cause  central nervous system depression following high-level exposure in
humans and animals.  No reliable dose-response data were found on the central
                              17-35

-------
                                       34

                               2.  HEALTH  EFFECTS
 nervous system depression  induced by  1,1-dichloroethane,  though  1,1-dichloro-
 ethane was  once used  as  an anesthetic agent in humans.  However, Plaa  and
 Larson (1965)  attributed deaths observed  in mice following  intraperitoneal
 injection to fatal  central nervous system depression.  Neurologic effects
 associated  with long-term  exposure to 1,1-dichloroethane  in humans or  animals
 have not been  reported.

      Developmental  Effects.  Adverse developmental effects  in humans
 associated  with exposure to 1,1-dichloroethane have not been reported.  One
 study in rats  indicated  that inhalation exposure to 1,1-dichloroethane
 resulted in retarded  fetal development  (delayed ossification of vertebrae) in
 the  absence of significant maternal toxicity (Schwetz et  al. 1974).  The
 absence of  maternal toxicity implies a direct effect on the fetus, rather than
 effects due to illness in  the dam.  The implications of the findings from one
 study with  regard to  potential developmental effects in humans are not known.

      Reproductive Effects.  No studies were located regarding reproductive
 effects in  humans or  animals following exposure to 1,1-dichloroethane, and it
 is not known if 1,1-dichloroethane has the potential to cause adverse
 reproductive effects  in humans.

      Genotoxic  Effects.  No studies were located regarding  in vivo genotoxic
 effects  in  humans.  The  genotoxic potential of 1,1-dichloroethane has been
 investigated in vitro in Salmonella tvphimurium (Riccio et al. 1983; Simmon et
 al.  1977),  Saccharomvces cerevisiae (Bronzetti et al. 1987; Simmon et
 al.  1977),  and  Syrian hamster embryo cells (Hatch et al.  1983).  In addition
 in vitro and in vivo assays have been conducted using rat and mouse organs
 (Colacci et al. 1985).  Results of these studies are summarized in Table 2-5.
 Results  from three studies conducted in S. tvphimurium tester strains were
 conflicting.  1,1-Dichloroethane was nonmutagenic in yeast cells even in the
 presence of metabolic activation system.  However,  because of insufficient
 reporting of data by Bronzetti et al.  (1987)  and Simmon et al. (1977), no
 assessment of the genotoxic potential of 1,1-dichloroethane in S. cerevisiae
 can be made.  The available data from the remaining studies indicate that,
 although 1,1-dichloroethane did not induce cell transformation in BALB/C-3T3
 cells  (Tu et al. 1985), it increased the frequency of transformations induced
by Simian adenovirus (SA7)  in hamster embryo  cells  (Hatch et al.  1983).

     In the  Ames assay, 1,1-dichloroethane was nonmutagenic in Salmonella
strains TA97,  TA98,  TA100,  and TA102 (Nohmi et al.  1985).   The compound was
tested with  and without metabolic activation.   The  highest dose was toxic to
all strains  of bacteria.   In contrast, 1,1-dichloroethane was mutagenic to
strains TA1537, TA98,  TA100,  and TA1535 exposed to  its vapor in a desiccator
 in the presence and absence of S9 mix (Riccio et al.  1983).  Although the
tests were conducted using three dose levels,  the authors did not report the
actual doses tested, and therefore the presence of  a dose-dependent response
could not be assessed. Simmon et al.  (1977) on the  other hand obtained

-------
                                      36

                              2.   HEALTH  EFFECTS
negative results using the same strains of Salmonella and a similar protocol.
The concentrations of 1,1-dichloroethane tested were not reported.   Because
the reporting of data was insufficient in studies by Riccio et al.  (1983)  and
Siamon et al. (1977), the discrepancies in their reported results cannot be
explained at this time.

     1,1-Dichloroethane was nonnutagenic in yeast strains D3 and D7, even  in
the presence of S9 mix (Bronzetti et al. 1987;  Simmon et al. 1977).  Bronzetti
et al. (1987) conducted an assay using strain D7 of Saccharomvces cerevistae
from the stationary and logarithmic growth phase.  The cells harvested from
the log phase cultures contained cytochrone P-450 and were capable of
metabolizing promutagens to genetically active products.  Both studies lacked
details regarding doses of 1,1-dichloroethane tested, though conflicting
results may also be due to impurities in the chemicals used.

     Tu et al. (1985) exposed BALB/C-3T3 cells to 1,1-dichloroethane in a
sealed chamber for 24 hours.  No cell transformation vas detected.   This lack
of effect may be due to the short period of exposure.  However, 1,1-dichloro-
ethane increased the frequency of transformation induced by SA-7 virus in
Syrian hamster embryo cells (Hatch et al. 1983).  Embryo cell cultures were
exposed in a sealed treatment chamber to volatilized 1,1-dichloroethane for
20 hours and then treated with SA7 virus for 3 hours.  1,1-Dichloroethane
treatment significantly increased the viral transformation frequency in cells
in a dose-dependent manner.  The highest concentration (1,000 /lig/mL) was
cytotoxic.   These results reflect the capacity of 1,1-dichloroethane to
interact with cellular DKA in hamster embryo cells.

     In an in vivo study by Colaeci at al. (1985) 1,1-dichloroethane (98X
purity) was found covalently bound to nucleic acids and proteins from liver,
lung, kidney, and stomach of male rats and nice 22 hours following a single
intraperitoneal injection of approximately 1.2 mgAg-  In vitro binding of
1,1-dichloroethane to nucleic acids and proteins was mediated by liver P-450
dependent aicrosomal mixed function oxidase system.  Glutathione-s-transferase
shifted the equilibrium of the enzymatic reaction and thereby decreased
binding, presumably by reducing the amount of toxic metabolite available for
binding to macromolecules.  On the other hand, phenobarbital increased binding
by increasing cytochrome P-450 activity, thus generating more toxic
metabolites available for binding to macromolecules.  Presumably the
metabolites generated from P-450 enzymatic action on 1,1-dichloroethane bind
to cellular macrooolecules.  Lung microsones wets weakly effective whereas
kidney and stomach microsomal fractions were Ineffective.  Therefore, the
binding to macromolecules of various organs detected in vivo may have been  due
Co a stable hepatic metabolite that was circulated to reach extrahepatic
organs.  Pretreatment with phenobarbital enhanced the binding to DNA,
microsomal RNA and proteins while addition of glutathione-s-transferase (GSH)
to the microsomal systems caused suppression of binding.  Because  only
radioactivity was measured it is difficult to determine whether the ;raole
bound represents 1,1-dichloroethane or its metabolite(s).  However, the fact
                             17-37

-------
                                       37

                               2.   HEALTH  EFFECTS
 that  binding  is  enhanced with  induction  of  P-450  suggests  that  it  represents
 the metabolite(s).   Thus, GSH  appears  to play  a detoxification  role  in  the
 metabolism of 1,1-dichloroethane.  The fact that  1,1-dichloroethane  binds  to
 nucleic  acid  suggests  that it  may have a potential  to produce mutation  in  a
 mammalian  system.

      Cancer.   There  is  inconclusive evidence that 1,1-dichloroethane may be
 carcinogenic  in  humans.  A significant positive dose-related trend was
 observed for  the incidence of  hemangiosarcomas and  mammary adenocarcinomas in
 female rats,  hepatocellular carcinoma  in male mice, and endometrial  stromal
 polyps in  female mice.  However, only  the incidence of endometrial stromal
 polyps in  female mice was significantly  increased over the corresponding
 control  animals.  Limitations  in this study (e.g.,  poor survival in  both
 treated  and control  animals) preclude the consideration of these results as
 conclusive evidence  of  carcinogenicity (NCI 1977).

      Results  of  a recently reported drinking water  bioassay in  mice  indicated
 that  1.1-dichloroethane is not carcinogenic  (Klaunig et al. 1986).   Possible
 differences in the pharmacokinetics of 1,1-dichloroethane between  the NCI
 (1977) and Klaunig et al. (1986) studies because  of the different  methods of
 administration and different vehicle and/or differences in dose levels
 employed may  account for the disparate results.   An in vitro assay of
 carcinogenicity  initiation also yielded negative  results for 1,1-dichloro-
 ethane (Herren-Freund and Pereira 1986).

      The induction of 7-glutamyltranspeptidase (GTP) 'foci, which are putative
 preneoplastic lesions,  in isolated rat liver hepatocytes correlates  well with
 carcinogenicity.  1,1-Dichloroethane failed to induce GTP foci  in  liver
 hepatocytes obtained from rats and mice  treated with 1,1-dichloroethane for
 7 days followed by promotion with phenobarbital (Herren-Freund  and Pereira
 1986).  This suggests that 1,1-dichloroethane is  not carcinogenic, though
 these results are not conclusive.

     There is limited evidence that neither confirms or dispels the
 carcinogenic potential of 1,1-dichloroethane.  Thus, these results are
 inconclusive as to whether it poses a cancer threat for humans.  The EPA has
classified 1,1-dichloroethane as a Class  C chemical which is defined as a
possible human carcinogen (IRIS 1990).
                             17-38

-------
           TOXICOLOGICAL PROFILE FOR
                   SELENIUM
                  Prepared by:

               Clement Associates
         under contract No: 205-88-0608

                  Prepared for:

Agency for Toxic Substances and Disease Registry
           U.S. Public Health Service

              In collaboration with:

      U.S. Environmental Protection Agency
                  December 1989
                    17-39

-------
                                      n
2.3  RELEVANCE TO PUBLIC HEALTH

     Death.  Information regarding death in humans following inhalation or
dermal exposure was not found.  Deaths due to respiratory failure in humans
following ingestion of selenium compounds have been reported, but the amount
of selenium ingested was not quantified.  Concentrations and doses causing
death in animals have been reported for acute inhalation exposures, and for
acute, intermediate, and chronic oral exposures.  The causes of acute
lethality of selenium compounds in animals following either inhalation or oral
exposures appears to be respiratory failure.   The toxic effects of selenium
following oral and inhalation exposure are cumulative.  In guinea pigs, the
LCj0 for  inhalation  exposure  to hydrogen selenide decreases with  increasing
                                     17-40

-------
                                      50

                              2.   HEALTH EFFECTS
duration of exposure:  Che LCSO values are 12.7 mg selenium/m3, 9 mg
selenium/m3,  and 1-4 mg selenium/in3 for durations of 1, 4, and 8 hours
respectively (Dudley and Miller 1941).   Similarly,  sodium selenite
administered to rats at a dose of 0.69  mg selenium/kg/day killed 5 out of
8 male rats between days 28 and 42 (Palmer and Olson 1974),  whereas the same
compound administered at less than half that dose (i.e.,  0.28 mg
selenium/kg/day) killed half of a test  group of male rats after 58 days of
administration (Schroeder and Mitchener 1971a).  Water soluble selenium
compounds are more lethal to animals than elemental selenium by any route.

     Systemic Effects.   Systemic effects in humans and animals following
inhalation and oral exposure to selenium compounds are similar.   One proposed
mechanism of toxicity for selenium compound is that under conditions of excess
body levels of selenium, selenium atoms begin to replace sulfur atoms in
structural and enzymatic proteins (Shamberger 1970), destroying the proteins'
structural and functional integrity.  This mechanism of action is unlikely to
be organ specific and toxic levels of selenium are expected to affect multiple
organ systems.   Differential sensitivities of the various organ systems to
selenium exposure would be expected on  the basis of differential accumulation
or retention of selenium compounds.

     The primary target organ in humans and in animals upon acute exposure by
inhalation or oral routes is the lung,  with cardiovascular,  hepatic, and renal
systems also affected.  Lesser effects  are observed in all other organ systems
but the muscular/skeletal system.  No studies were located regarding effects
in humans or in animals following intermediate or chronic inhalation exposure
to selenium or to selenium compounds.  Following intermediate or chronic oral
exposure to selenium compounds, the primary effects in humans are dermal and
neurological.  Following intermediate and chronic oral exposure to selenium
compounds, the primary effects in livestock exposed to naturally occurring
selenium in range plants are also dermal and neurological.  The primary
effects in laboratory animals exposed to inorganic selenium salts or to
selenium-containing amino acids are cardiovascular, gastrointestinal,
hematological,  hepatic, dermal, immunological, neurological, and reproductive.

     Respiratory Effects.  Following acute inhalation or acute oral exposure
to selenium compounds, the primary sign of selenium toxicity in both humans
and animals is respiratory distress.   Clinical signs in humans have been
reported to include bronchial spasms, severe bronchitis, and bronchial
pneumonia (Buchan 1947; Wilson 1962).  Signs  in animals have included labored
breathing and bronchial pneumonia (Hall et al. 1951).  Death is usually from
respiratory failure associated with pulmonary edema.  Lethal doses of
parenteral sodium selenite (1-4 mgAg)  have also produced moderate pulmonary
edema in pigs (Van Vleet et al. 1974).   Following intermediate and chronic
oral exposure to selenium compounds, however, the lungs do not appear to be a
primary target organ in either humans or animals.
                                  17-41

-------
                                       51

                               2.  HEALTH EFFECTS
      Cardiovascular Effects.  Following acute inhalation or acute oral
 exposure  to  selenium compounds, some cardiovascular signs such as elevated
 pulse rate and  tachycardia have been reported in humans.  In livestock,
 lesions of the  heart have been observed following acute oral exposure to
 seleniferous plants.  Harr et al.  (1967) reported myocardial hyperemia,
 hemorrhage,  and degeneration in old rats following a lifetime administration
 of sodium selenate or sodium selenite in the diet.  In animals,
 intraperitoneal administration of  sodium selenite at 1.0 mg selenium/kg bw has
 produced  ultrastructural abnormalities of mitochondria in myocardial tissue
 but not in liver or kidney tissues (Dini et al. 1981).  The dose was lethal
 for the guinea  pigs, with animals  dying 24 hours or later following the
 intraperitoneal administration.  Pretreatment with pyruvate or methionine
 protected against the mitochondria! changes.  Only one dose was used, however,
 and it is not known whether mitochondria! changes occur at sublethal doses.

      Hepatic Effects.  In animals, the liver is affected following both
 inhalation and  oral exposure to several different selenium compounds.  Liver
 effects were observed in guinea pigs following inhalation exposure to
 elemental selenium dust and hydrogen selenide.  The liver appears to be the
 primary target  organ for the oral toxicity of sodium selenate,  sodium
 selenite, and organic forms of selenium following intermediate and chronic
 exposure, whereas liver cirrhosis or dysfunction has not been a notable
 component of the clinical manifestations of chronic selenosis in humans.
 Selenium  sulfide administration to rats has also produced hepatic effects.

     Renal Effects.   In animals,  the kidney appears not Co be seriously
 affected by  acute inhalation exposure to elemental selenium or hydrogen
 selenide or  acute to chronic oral exposure to sodium selenate,  sodium
 selenite,  or dietary selenium compounds.   Selenium sulfide administration to
mice has produced interstitial nephritis.

     Hematological Effects.   A variety of changes occur in the blood chemistry
of animals after acute oral exposure to sodium selenite (Anderson and Hoxon
1942).  Anemia,  red cell hemolysis, and reduced blood hemoglobin concentration
have been observed in rats following intermediate and chronic oral exposure to
sodium selenite  (Halverson et al.  1966;  Halverson et al. 1970).  Young et al.
 (1981) have  reported a lytic effect for sodium selenite on normal sheep
erythrocytes  in  vitro.

     Dermal/Ocular Effects.   Following chronic oral exposure to organic
selenium compounds found in food,  two principal clinical conditions observed
in humans  are dermal and neurological effects, as described in the
epidemiological  study of endemic  selenosis in the People's Republic of China
(Yang et al.  1983).   The dermal manifestations include loss of hair,
deformation and  loss of  nails,  and discoloration and excessive decay of teeth.
Similar clinical manifestations occur in livestock following intermediate and
chronic exposure to  seleniferous  plants,  including loss of hair and
                                   17-42

-------
                                      52

                              2.   HEALTH EFFECTS
malformation of hooves characteristic of "alkali disease" (Rosenfeld and Beath
1964).

     Other Systemic Effects.  One of the most common effects in animals
following intermediate or chronic oral administration of inorganic and organic
compounds of selenium is reduced growth rate of young animals and loss of
weight in older animals (Halverson et al. 1966; Harr et al.  1967;  Nelson et
al. 1943; Palmer and Olson 1974; Schroeder 1967).  Selenium sulfide
administration has also caused a reduction.in body weight in female mice (NTP
1980c).

     Neurological Effects.  Following chronic oral exposure to selenium
compounds in the diet, neurological manifestations in humans have been
reported to include numbness, paralysis, and occasionally hemiplegia.
Analogous clinical manifestations (i.e., loss of hair, malformation of hooves,
and "blind staggers" in cattle and poliomyelomalacia in swine) occur in
livestock following intermediate and chronic grazing exposure to plants
containing high levels of selenium (see Sections 2.2.2.2 and 2.2.2.4).
Histologically, swine with neurological symptoms also exhibit bilateral
macroscopic lesions of the ventral horn of the spinal cord.

     The neurological symptoms and histopathology observed in livestock
following oral exposure to excess selenium compounds have not been recorded in
laboratory animals.  This suggests that small laboratory mammals might not be
appropriate models for selenium toxicity in humans (e.g., laboratory animals
metabolize and/or excrete selenium compounds more quickly), that some as yet
unidentified organic form of selenium contributes to the neurological
manifestations of chronic selenosis in humans and in livestock, or that
unrecognized confounding factors have contributed to the neurological syndrome
associated with chronic selenosis in field studies of humans and livestock.

     Reproductive/Developmental Effects.  There  is no evidence from
experimental animals administered selenium compounds via the oral route or via
injection that selenium compounds are teratogenic in mammals.  Lee et al.
(1979)  reported reduced fetal weights following  subcutaneous injection of
pregnant mice with sodium selenite (1.6 mg seleniumAg/day) on days  9-12 of
gestation.  The incidence of cleft-palate was not statistically different from
the control group.  Yonemoto et al. (1984) observed a dose-dependent elevation
of maternal death rates and decreases in body weight of offspring of pregnant
nice receiving a single intravenous injection of sodium selenite at  doses
ranging from 1.30 to 2.52 mg selenium/kg/day on  day 12 of gestation.  The
failure to observe teratogenic effects in these  studies is consistent with the
other mammalian studies involving oral administration of potassium selenate
and unspecified selenate salt (Rosenfeld and Beath 1954; Schroeder and
Kitchener 1971b).  In hamsters, Holmberg and Fern (1969) also failed to
produce teratogenic effects with intravenous Injection of sodium selenite at
0.91 mg selenium/kg selenium on day 8 of pregnancy.  The administered dose was
                                 17-43

-------
                                      53

                              2.  HEALTH EFFECTS
just sublethal to the dam, yet caused only six percent resorptions, a
percentage that was comparable with controls.

     Selenium might, however, be a particular hazard to the developing eye.
Ostadalova and Babicky (1980) administered single subcutaneous doses of sodium
selenate, DL-selenomethionine, DL-selenocystine, dimethyl selenide, or
trimethyl selenonium to groups of 10-day-old male rats and observed the
effects on the eye between the ages of 14-16 days (when the eyes opened) to 60
days.  The range of doses administered was adjusted for each compound such
that the lowest dose did not produce cataracts and the highest dose was
lethal.  A dose-related increase in eye cataracts was induced by the
administration of sodium selenate, DL-selenomethionine, and DL-selenocystine;
dimethyl selenide and trimethylselenonium chloride failed to produce
cataracts.

     Daily intraperitoneal injections of male rats with selenium dioxide at
daily doses up to 0.035 mg selenium/kg/day for 90 days produced dose-dependent
histological changes in the testes with significant testicular degeneration
and atrophy at the highest dose tested (Chowdhury and Venkatakrishna-Bhatt
1983).

     The relevance of these reproductive/developmental effects of selenium
exposure in animals to potential reproductive or developmental effects in
humans is not known.

     Carcinogenicity.   The majority of epidemiological studies in humans do
not suggest that excess exposure to selenium is associated with an increased
risk of cancer.   To the contrary,  investigators report an association between
low selenium intake or body levels and an increased risk of developing many
types of cancers (Hocman 1988; Shamberger 1970; Vernie 1984).

     Despite early reports that orally administered selenium produced hepatic
tumors  in rats,  subsequent chronic experimental exposure of rats and mice to
selenium salts and organic forms of selenium in the diet have provided no
further evidence of hepatic carcinogenicity (Harr et al. 1967; Schroeder 1967;
Schroeder and'Mitchener 1972).  Instead,  in the majority of studies conducted
in the  last 15 years,  selenium supplementation has significantly inhibited
spontaneous and chemical-,  viral-,  and UV-induced neoplasia in animals,
although there are a few exceptions (Hocman 1988; Medina 1986; Vernie 1984).
In a review of 39 experiments testing the relationship between selenium
supplementation and tumorigenesis  in animals, Medina (1986) noted that 34 out
of 39 studies demonstrated an inhibitory effect of selenium on tumorigenesis;
in three studies,  selenium administration had no effect on tumorigenicity; and
in two  studies,  selenium enhanced  tumorigenicity.  Thus, selenium appears to
inhibit tumorigenesis  in most, but not all, of the test situations
investigated.
                                  17-44

-------
                                      54

                              2.   HEALTH EFFECTS
     A variety of mechanisms of action have been proposed to explain the
inhibitory effect of selenium on carcinogenesis (Hocman 1988).   Because oxygen
radicals such as 02~' or OH-  may initiate the.process  of carcinogenesis,  one
hypothesis is that adequate or increased activity levels of the selenium-
dependent enzyme glutathione peroxidase (GSH-Px) helps to prevent the
initiation of cancers (Hocman 1988).   Another hypothesis is that selenium
inhibits cell proliferation (Vernie 1984).   It is unlikely, however, that  a
jingle mechanism of action is responsible for selenium1a putative
anticarcinogenic properties.

     Selenium sulfide,  on the other hand, has been demonstrated to be
carcinogenic following oral daily administration by gavage in rats and female
mice (NTP 1980c).

     Genotoxic Effects.   Inorganic selenium compounds have been observed to
have both genotoxic and antigenotoxic effects.  The antigenotoxic effects
generally occur at lower selenium exposure levels than the genotoxic effects.
This discussion will focus on genotoxic effects only.

     In general, sodium selenite and sodium selenate have produced mixed
results in bacterial mutagenicity test systems (Table 2-4).  Sodium selenite
has tested positive for base-pair substitution mutations using the Ames test
in Salmonella tvphiniurium and was also positive in the transformation assay
using Bacillus subtilis (Nakamuro et al. 1976; Noda et al. 1979).  However,
negative results have also been reported for sodium selenite both in the Ames
test in S. tvphimurium and the rec assay using B. subtilis (Lofroth and Ames
1978; Noda et al.  1979).  Sodium selenate on the other hand has tested
positive in the Ames test using S. tvphimurium (base-pair substitution) and  in
the rec assay using B.  subtilis (Lofroth and Ames 1978; Noda et al. 1979), but
has tested negative using the transformation assay in B. subtilis (Nakamuro  et
al. 1976).

     Results with mammalian cell systems are also mixed, although sodium
selenite is more consistently genotoxic in these systems.  Sodium selenite has
been observed to induce unscheduled DNA synthesis (UDS), chromosomal
aberrations, and sister-chromatid exchange in cultured human fibroblasts  (Lo
et al. 1978; Ray et al 1978; Whiting et al. 1980), UDS  in Chinese hamster V79
cells (Sirianni and Huang 1983), and chromosomal aberrations in Chinese
hamster ovary cells (Whiting et al. 1980).  However, sodium selenate induced
chromosomal aberrations in Chinese hamster ovary cells  (Whiting et  al.  1980),
and UDS in Chinese hamster V79 cells (Sirianni and Huang 1983), but did not
induce chromosomal aberrations in human leukocytes or cultured human
fibroblasts (Lo et al. 1978; Nakamuro et al. 1976).

     Addition of glutathione to test mixtures enhances  the genotoxicity of
•odium selenite, sodium selenate, and sodium selenide  in bacterial  test
systems indicating that production of a mutagenic species occurs via a
reductive mechanism following exposure to these compounds  (Whiting  et
                                  17-45

-------
al. 1980).  This mechanism is supported by results in mammalian test systems.
For example, in cultured human leukocytes, sodium selenite induces chromosome
aberrations and sister chromatid exchanges (Nakamuro et al. 1976; Ray et
al. 1978; Ray and Altenburg 1978).  Sister chromatid exchange was not observed
at similar sodium selenite concentrations in a human lymphoblastoid cell line;
however, exchanges were observed when these same cells were incubated with
sodium selenite and red blood cell lysate (Ray and Altenburg 1978).  The
observation that internal constituents of red blood cells may contribute to
the genotoxicity of sodium selenite supports the suggestion that metabolism is
involved in the production of an active species following exposure to sodium
selenite in these test systems.   The active species responsible for the
genotoxic effects is not known.

     At high concentrations,  sodium selenite induces unscheduled DNA synthesis
and chromosome aberrations in cultured human fibroblasts (Lo et al. 1978).
Addition of a metabolic activator (S9 fraction) or glutathione have increased
both the number of aberrations and the toxicity of sodium selenite (Whiting et
al. 1980) and sodium selenate (Lo et al. 1978;  Whiting et al. 1980).

     Sodium selenite has also been studied in vivo in the rat and Chinese
hamster.  An increased number of bone marrow cells with chromosome aberrations
were observed following intraperitoneal injections of sodium selenite.  The
doses at which aberrations were  higher than controls ranged from 3 to 6 mg
selenium/kg of body weight,  a level comparable to reported LDJO values  for
intraperitoneal injection of sodium selenite in rats (Norppa et al. 1980;
Newton and Lilly 1986;  Olson 1986).
                             17-46

-------
                     STYRENE
Synonyms: phenyl cthylcne, vinyl benzene, cinnamene




CAS Registry Number: 100-42-5





Molecular Weight: 104.14





Molecular Formula:
        A«r   toxics
                      17-47

-------
 520     CHEMICAL-SPECIFIC ASSESSMENTS

                              Toxicity Profile


 Carcinogenicity: There is some evidence for an association between styrene ei
 posure in the styrene-butadiene rubber and styrcnc-polystyrcnc manufacturing in
 dustrics and increased risk of lymphatic  and hematopoietic tumors. However, d*
 evidence is insufficient to designate styrene as a human carcinogen on account ot
 limitations in the available studies such as small cohort sizes and concurrent e\p>
 sure to multiple chemicals.
     Jersey et al.7 (cited in NIOSH2) exposed male and female Spraguc-Dawley ni>
 to 0, 600, or 1200 ppm styrene via inhalation for 6 hours per day, 5 days per wed
 for IS.3 (males) or 20.7 (females) months with final sacrifice at 24 months: after."
 months the  highest exposure level was lowered to  1000 ppm because of excessiu
 mortality among the male rats. There was an increased  combined incidence <•'
 leukemia and lymphosarcoma tumor types in female rats in both exposure group*
 which was  statistically significant when data from both exposure groups »err
 combined and for each group compared individually to historical, but not conot
 rent, controls. In addition, there was a higher incidence of alveolar histiocytosis an.1
 increased liver weights in high-dose female rats. There was  no increase in incidetvr
 of tumors attributable to treatment in the male rats; concurrent high mortalit) due t.
 chronic murine pneumonia limits the conclusions that may  be drawn from the nux
 rat data.
     In an NCI bioassay,8 male and female B6C3F, mice and F344 rats received  IS
 or 300 mg/kg/day and 500, 1000, or 2000 mg/kg/day, respectively, by gavapr e
 corn oil 5 days a week for 103 weeks (low-dose rats) or 78 weeks (all other group
 There  was an increased incidence  of lung adenomas in male mice compared »i?
 vehicle,  but not historical, controls. NCI concluded that there was "suggeMnc
 evidence of carcinogenicity in male B6C3F, mice, but the evidence was IKX "o«
 vincing" for either species.
     The possible carcinogenicity of styrene has been investigated in several »fc
 tional  studies that are reviewed in the drinking water criteria document* tni  ft
 NIOSH criteria document.2 Regarding carcinogenicity, NIOSH states  thai "In*
 the experimental animal investigations and from the epidemiological studiev thrr
 seems  to be little basis  to conclude that styrene is carcinogenic."2 li seem* n»*
 reasonable to tentatively place styrene in group C, possible human carcinefff
 under the EPA weight-of-evidence classification.

 Mutagenicity: Positive results are listed in the Gene-Tox database as sumnur-v.'
 in RTECS for the following assays: (1)  micronucleus test—in vitro human S?1
phocytes, (2) Ames assay. (3) Drosophila SLRL test,  (4) 5. cerevisiar genr ««•
version,  and (5) in vivo cytogenetics—human lymphocytes. Negative rrMih» r
listed for the  following assays: (1) cell  transformation—Syrian hamsier emf-
cells by  adenovirus SA7, (2) gene mutation—V79 cell culture, and <3i «> •*"
unscheduled DNA synthesis-human fibroblasts.9 The evidence for genetic *«•«••
of styrene in short-term tests was also recently reviewed by 1ARC.  BaMo <*
               17-48

-------
                                                         STYRENE      521

IARC classification scheme, it is our judgment that the evidence for genetic activity
of styrene in short-term tests is sufficient.

Developmental Toxicity: Although there have been some reports of birth defects11
(cited in NIOSH2) and increased incidence of spontaneous abortions12 (cited in
NIOSH2) in women occupationally exposed to styrene, evidence of developmental
toxicity has not been found in several apparently well-conducted animal studies.
These include a multigeneration study in which  rats were exposed to styrene in
drinking water" and a study in which rabbits were exposed to styrene via inhalation
and rats were exposed via inhalation and gavage.14
   In another study, however, Kankaanpaa et al.15 exposed BMR/T6T6 mice to 0
or 250 ppm styrene for 6 hours per day on gestation days 6 through 16 of gestation
and Chinese hamsters to 0, 300, 500, 750, or 1000 ppm styrene on days 6 through
18 of gestation. Embryotoxicity, in the form of significantly higher incidences of
dead and resorted fetuses, were observed in both species only in the highest ex-
posure group relative to controls. Some degree of maternal toxicity was apparently
observed, but no details were given and the authors did not attribute the embryo-
toxicity to maternal loxicity.

Reproductive Toxicity: No data were found implicating styrene as a reproductive
toxin.
Systemic Toxicity: The best-documented form of systemic toxicity resulting from
styrene exposure involves the central nervous system. Subjectively, this is manifest
as complaints of headache, fatigue, dizziness, confusion, drowsiness, malaise,
difficulty in concentrating, and a feeling of intoxication. Clinical  signs include
altered equilibrium, delayed reaction times,  and abnormal EEGs. Alterations such
as these have been reported in experimental studies at concentrations as low as 100
ppm16-17 (cited in NIOSH2).  Numerous studies, both clinical and  experimental,
documenting the  C.N.S. toxicity of styrene are reviewed in the NIOSH criteria
document.2
    In addition to C.N.S. toxicity,  there is also more limited evidence for other
adverse effects attributable to styrene. These include peripheral neuropathy, abnor-
mal pulmonary function, and  alterations in  liver function. The evidence for these
effects is also reviewed in the criteria document.2
    In a recent review of the toxicity of styrene, Bond et al.16 concluded that many
of the effects of styrene in humans and laboratory animals are similar. Further, it
was noted thai the major metabolic pathway in both humans and animal models
involves oxidation of the vinyl group to styrene oxide with further metabolism to
several products, at least two of which—mandelic and phenylglyoxylic acids—have
been detected in both human and rodent urine subsequent to styrene exposure.

Irritation: The irritancy of styrene to the eyes, nose, skin, and respiratory tract is
*elj documented in both clinical and experimental studies. A  large proportion of
subjects report upper respiratory tract irritation at exposures as low as 100 ppm, and
                        17-49

-------
 522     CHEMICAL-SPECIFIC ASSESSMENTS

 some report eye irritation at concentrations of 20  or SO ppm'6>17>" (cited ui
 NIOSH2). Styrene is reported to have an aromatic odor* and an odor threshold of
 0.32 ppm (geometric mean of reported literature values).20

 Basis for the AALG: Styrene is considered "very slightly" soluble in water and
 has a vapor pressure of 6.1  mm Hg at 2S°C.20 It is  used in the production of
 polystyrene plastics, protective coatings, styrenated polyesters, copolymer itsinv
 and as a chemical intermediate.1 Styrene has been detected in both ambient airinj
 finished drinking water in the United States.21  Based on the lack of data on thr
 environmental fate  and distribution of Styrene  and the expected contribution of
 various media to human exposure, 50% of the contribution to total exposure i«
 allowed from air.
     Given the equivocal nature of the evidence for Styrene carcinogeniciiy. n»»
 AALGs were calculated for Styrene: one based on carcinogenicity and another too!
 on  systemic toxicity.  Also, use of quantitative risk assessment was not deemcv.'
 appropriate on account of the equivocal evidence of carcinogenicity. The AALG iv
 instead  based on the rat LOAEL of 600 ppm from the study of Jersey el al.71 cm'
 in NIOSH2) using an uncertainty  factor approach. The LOAEL was adjusted It*
 continuous exposure (600 ppm x 5/7 x 6/24 x  20.7/24), and the total uncertain^
 factor used was 10,000 (10 for a LOAEL x  10  for interindividual variation * H-
 for interspecies variation  x 10 for the database factor). Use of the database f»ci.»
 was justified based on the severity of the effect and, in addition, data from hum*
 experimental studies22-23 (cited in Amoore and Hautala20). Retention of 60S of the
 exposure dose was assumed. Given the weight-of-evidence ranking for styrenc n.'
 the pending review  of its carcinogenicity by EPA,24 the AALG should be ctwd
 ered provisional.
     An AALG was  also calculated for systemic toxicity, specifically neuiwo»Mt»
 using the NIOSH REL-TWA as a basis. This limit was treated as a human LOAM
 (REL/210; 10 for interindividual variation x  5 for a LOAEL  x  4.2) based on tt*
 review in the criteria document,2 in which it was stated that there were "effect* u».f
 as slower reactions,  subjective complaints related to CNS depression and «bnorm»
EEGs at styrene concentrations  around 50  ppm." This AALG should aK» fc
considered provisional.

AALG:  • carcinogenicity—6.2 ppb (26.3 u,g/m3) annual TWA
         • systemic toxicity—119 ppb (507 u.g/m3) 8-hour TWA
                               References

 1.  ACGIH. 1986. "Documentation of the Threshold Limit Values and Biological Ei»»««-
    Indices." 5:539.
 2.  NIOSH. 1984. "Criteria for a Recommended Standard . . . Occupational
    Styrene." DHHS (NIOSH) 83-119.
 3.  OSHA. 1989. "Air Contaminants; Final Rule." Fed. Keg. 54:2332-2959
               17-50

-------
                                                            STYRENE     523

4. Safe Drinking Water Committee. 1977. Drinking Water and Health. Vol. 1 (Washing-
   ton, DC: National Academy Press).
5. U.S. EPA. 1985. "Drinking Water Criteria Document for Styrene" (draft) (Springfield,
   VA: NTIS), EPA-600/X-84-I95-1, PB86-118056.
6. Ponomarkov, V. I., and L. Tomatis. 1978. "Effects of Long-Term Oral Administration
   of Styrene to Mice and Rats." Scand. J. Work Environ. Health 4(suppl.  2): 127-35.
7. Jersey, G., M. Balmer, J. Quasi, C. N. Park, D. J. Schuetz, J. E. Beyer, K. J. Olson,
   S. B. McCollister, and L. W. Rampy. 1978. "Two-Year Chronic Inhalation Toxicity
   and Carcinogenicity Study on Monomeric Styrene in Rats." Dow Chemical study for
   Manufacturing Chemists Association (12/6).
8. NCI. 1979.  "Bioassay of Styrene for Possible Carcinogenicity." TR-185.
9. NIOSH. 1987. WL3675000. "Styrene." RTECS, on line.
10. 1ARC. 1986. "Styrene." IARC Monog. suppl. 6:498-501.
11. Hemminki,  K., E.  Franssila, and H. Vainio. 1980. "Spontaneous Abortion among
   Female Chemical Workers in Finland." Int. Arch. Occup.  Environ. Health 45:123-26.
12. Holmberg, P. C. 1977. "Central Nervous Defects in Two Children of Mothers Exposed
   to Chemicals in the Reinforced Plastics Industry." Scand. J. Work Environ. Health
   3:212-14.
13. Beliles. R. P., J. H. Butala, C. R. Stack, and S.  Makris. 1985. "Chronic Toxicity and
   Three-Generation Reproduction Study of  Styrene Monomer in the Drinking Water of
   Rats." Fund. Appl.  Tax. 5:855-68.
14. Murray, F.  J.. J. A.  John. M. F. Balmer. and B. A. Schwetz. 1978.  "Teratologic
   Evaluation of Styrene Given to Rats and  Rabbits by Inhalation or by Gavagc." Toxi-
   cology 11:335-43.
13. Kankaanpaa, J. T. J., E. Elovaara, K. Hemminki, and H. Vainio. 1980. "The Effect of
   Maternally Inhaled Styrene on Embryonal and Foetal Development in Mice and Chinese
   Hamsters." Acta Pharm. Tox. 47:127-29.
 16. Hake, C. L.. R. D. Stewart, A. Wu, S. A. Graff. H. V. Forster, W. H.  Keeler, A. J.
   Lebrun, P. E. Newton, and R. J. Solo, (undated).  "Styrene—Development of a Biologic
   Standard for the Industrial Worker by Breath Analysis." NIOSH-MCOW-ENVM-STY-
   77-2. Milwaukee. Medical College of Wisconsin, NIOSH Contract  No. HSM 99-.
   72-84.
 17. Oltramare,  M., E. Desbaumes. C.  Imhoff. and W. Michiels.  1974. "Toxicology of
   Monomeric Styrene—Experimental and Clinical Studies on Man"  (French). Geneva.
   Editions Medicine et Hygiene.
 18. Bond, J. A. 1989.  "Review of the Toxicology of Styrene." CRC Crit. Rev. Tox.
    19:227-49.
 19. Stewart,  R. D.. H. C.  Dodd, E. D. Barctta. and A. W. Schaffer.  1968. "Human
    Exposure to Styrene Vapor." Arch. Environ. Health 16:656-62.
 20  Amoore. J. E.. and E.  Hautala. 1983.  "Odor  as  an Aid to Chemical Safety: Odor
    Thresholds  Compared with  Threshold Limit Values and Volatilities for  214 Industrial
    Chemicals in Air and Water Dilution." J. Appl. Tox. 3:272-90.
 21. IARC.  1979.  "Styrene,  Polystyrene and  Styrene-Butadiene  Copolymers."  IARC
    Monog. 19:231-44.
 - Fiserova-Bergerova, V., and J. Teisinger.  1965.  "Pulmonary Styrene  Vapor Reten-
    tion." Ind.  Med. Surg. 34:620.
 13. Bardodej, Z., and E. Bardodcjova. 1970. "Biotransformation of Ethyl Benzene, Styrene
  ^  and a-Methylstyrene in Man." Am. Ind.  Hyg. Assoc. J. 31:206.
  -4 U.S.  EPA.  1988. "Styrene; CASRN  100-42-5." IRIS (6/30/88).
                            17-51

-------
                      DRAFT

            TOXICOLOGICAL PROFILE FOR
              1,1,1-TRICHLOROETHANE
                  Prepared by:

          Syracuse Research Corporation
              Under Subcontract to:

            Clement Associates, Inc.
         Under Contract No. 205-88-0608

                  Prepared for:

Agency for Toxic Substances and Disease Registry
           U.S. Public Health Service
                 December 1990
                   17-52

-------
           V'
2.4  RELEVANCE TO PUBLIC HEALTH

     Clinical symptoms associated with exposure to 1,1,1-trichloroethane
that have been reported in humans include hypotension,  diarrhea and
vomiting, central nervous system depression and dermal  and ocular
irritation.  Mild hepatic effects may also occur in humans.   Deaths have
been attributed to cardiac arrythmia and respiratory failure secondary to
central nervous system depression.  Effects reported in humans  that also
occur in animals include hypotension, cardiac arrythmia,  mild hepatic
effects, central nervous system depression, and dermal  irritation.    Effects
that have been observed in animals but not investigated in humans include
mild developmental effects.

     Death.  The volatility of 1,1,1-trichloroethane coupled with the rapid
and extensive absorption and elimination of inhaled 1,1,1-trichloroethane
makes acute inhalation (as compared to intermediate and chronic duration)
the most likely lethal exposure scenario in humans.  The acute  lethal air
concentration for humans is unknown; however, simulations of several lethal
exposure scenarios suggest that it may be as low as 6000 ppm.   The results
of animal studies indicate that the acutely lethal exposure concentration
increases substantially with decreasing exposure duration.  Thus, death may
occur at a 3- to 4-fold lower concentration after a 6-7 hour exposure than
after a 15-minute exposure.

     Human deaths from inhalation of 1,1,1-trichloroethane have been
attributed to respiratory failure secondary to central  nervous  system
depression and to cardiac arrythmia.  Based on the results of animal
                           17-53

-------
                                     80

                             2.  HEALTH EFFECTS
 studies,  lethal arrhythmias probably result from sensitization of the heart
 to epinephrine.  Therefore, acutely lethal  exposure levels may be lover in
 individuals exposed during physical exertion.   Physical  exertion nay also
 decrease  the acutely lethal exposure level  by  increasing lung perfusion and
 lung retention of inhaled 1,1,1-trichloroethane.

      Very little is known about  the lethality  of orally  ingested
 1.1,1-trichloroethane  in humans.   In one case  of accidental acute oral
 exposure,  ingestion of 600 mg/kg  of 1,1,1-trichloroethane  did not prove
 lethal.   Based on the  results  of  animal studies,  it is possible that much
 higher acute oral doses can be tolerated.

      Human lethality involving dermal exposure  has  not been reported.
 However,  such an occurrence is extremely unlikely in view  of the high
 volatility of 1,1,1-trichloroethane, which  would limit the absorption of
 1,1,1-trichloroethane  in contact with the skin.   Lethality in animals  has
 been reported only when extremely  high doses (15,800 mg/kg)  are applied to
 the  skin  for prolonged periods (e.g., 24 hours)  under occlusion.

      Systemic Effects.   Systemic effects of 1,1,1-trichloroethane  reported
 in humans  include  hypotension, mild  hepatic effects, diarrhea and vomiting,
 and  dermal and ocular  irritation.  Cardiac  arrhythmias have been implicated
 in cases of death  following inhalation exposure  to high concentrations of
 1,1,1-trichloroethane.

      1,1,1-Trichloroethane  can reduce blood pressure (mild-to-severe
 reduction)  in humans.   However, such effects are  likely only  after exposure
 to high concentrations  of  1,1,1-trichloroethane vapor.  Humans  exposed to
 low  levels  daily for up  to  6 years did not have abnormalities  in blood
 pressure, heart  rate, or electrocardiogram.   Reduced blood pressure
 accompanies  exposure to anesthetic concentrations of 1,1,1-trichloroethane
 vapor  (10,000-26,000 ppm).  The effects are not permanent  and  subside
 shortly after  exposure  ceases.   The mechanism has been studied  in animals
 and appears  to involve  cardiac depression and peripheral vasodilation.

     Human deaths following inhalation of 1,1,1-trichloroethane  are often
 attributed to  cardiac arrhythmia.  Such conclusions are based on animal
 studies in which arrhythmias have been produced during or  immediately
 following acute inhalation exposure to 1,1,1-trtchloroethane.  The mechanism
 for the arrhythmias involves sensitization of the heart to endogenous
 epinephrine.  The level at which cardiac sensitization occurs  in humans  is
not known, but in animals concentrations as  low as 5000 ppm are effective
after only 10 minutes of exposure.  Physical exertion,  stress, or any other
stimulus for the release of epinephrine from the adrenal medulla may render
an individual more vulnerable to 1,1,1-trichloroethane.
                               17-54

-------
                                    81

                            2.  HEALTH EFFECTS
     Nausea, vomiting, and diarrhea have been reported to occur In humans
after acute oral or inhalation exposure to high levels of 1,1,1-trichloro-
ethane.  Vomiting and diarrhea have not been reported in animals, and the
mechanisms for these effects are not known.

     1,1,1-Trichloroethane may be a hepatotoxicant in humans, although the
evidence is not conclusive.  Increased levels of urinary urobilinogen and
serum bilirubin, suggestive of liver injury, have been reported in humans
exposed to 1,1,1-trichloroethane by inhalation or ingestion.  Mild hepatic
changes have also been found at autopsy in people who died following acute
inhalation of high concentrations of 1,1,1-trichloroethane.   Studies in
animals have shown that exposure to relatively high concentrations of
1,1,1-trichloroethane in air (1000 ppm or more) or high oral doses (1334
mg/kg or more) are required to produce liver injury, although some effects
have been observed at 200-500 ppm in air.  Effects observed in animals
include fatty degeneration, slight increases in liver weight, and changes in
liver and serum enzyme levels.  The effects are reversible and subside after
exposure is terminated,

     1,1,1-Trichloroethane is mildly irritating when applied to the skin.
Effects include slight, transient, reversible erythema and edema.  Exposure
to I.1,1-triehloroethane vapor is associated with mild eye irritation in
humans and animals.  Based on these results and the results of direct-
application animal studies, it is likely that 1,1,1-trichloroethatie applied
directly to the eye will produce irritation in humans as well.

     Imaunological Effects.  Inmunological effects of 1,1,1-trichloroethane
have not been reported in humans, and have not been studied extensively in
animals.  Acute inhalation exposure had no effect on survival from a
bacterial pathogen challenge in mice.  Histological evaluation of immune
system tissues from rats and mice (including lymph nodes, thymus, and
spleen) have not revealed any lesions attributable to 1,1,1-trichlcroethane
exposure.  However, more extensive studies of immune function would be
required to adequately evaluate the imraunotoxic potential of
1,1,1-trichloroethane in humans.

     Neurological Effects.  Neurological effects are the preeminent symptoms
of acute inhalation exposure to 1,1,1-trichloroethane in humans.   The
intoxicating effects of inhaled 1,1,1-trichloroethane create a potential  for
abuse of this chemical.   Neurological effects have not been reported
following oral or dermal exposure, and are likely to occur, if at all, only
after exposure to very high levels or doses.  Effects repotted following
acute inhalation in humans increase in severity with increasing exposure
level.   Impaired performance on tests of psychophysiological function have
been reported in subjects exposed to low concentrations (175 ppra or more).
Dizziness, lightheadedness, and loss of coordination are found after
exposure to moderate concentrations (more than 500 ppm).  General anesthesia
occurs  at high levels (10,000 ppm or more).  These effects subside rapidly
                            17-55

-------
                                     82

                             2.  HEALTH EFFECTS
 after exposure is terminated.   Irreversible neurological impairment has not
 been reported in humans.

      Animals appear to provide useful models for examining the neurological
 effects of 1.1,1-trichloroethane.    As in humans,  central nervous  system
 depression is the predominant  effect of inhaled 1,1,1-trichloroethane  in
 animals;  symptoms include  ataxia,  anesthesia,  and death at increasing
 concentrations.   There was no  evidence of gross or histologic  damage found
 in the brains of most  exposed  animals,  but lasting physical changes to the
 brain have been indicated  by reports of increased levels of glial  fibrillary
 acid protein and decreased DNA content in the  brain of gerbils following
 intermediate exposure  to low levels.   Alterations  of brain metabolism  have
 also been found in exposed animals.   Behavioral changes,  including impaired
 performance on behavioral  tests and  increased  motor activity,  have been
 widely reported;  however,  the  sites  of action  and  biochemical  mechanisms of
 neurotoxicity have not been identified.

      Little information was located  regarding  neurological effects in  man
 or animals following oral  or dermal  exposure to 1,1,1-trichloroethane.
 Existing  data indicate that a  single  oral  exposure to  moderate levels  may
 not produce outward signs  of neurotoxicity.  However,  it  is assumed that
 high doses of 1,1,1-trichloroethane  administered orally  or dermally will
 result in neurotoxicity.

      Developmental Effects.  Developmental  effects of  1,1,1-trichloroethane
 in humans have not been reported.   Minor  embryotoxic  effects  were reported
 in rats were  and  rabbits exposed to high concentrations of
 1,1,1-trichloroethane  by inhalation.   Effects  included decreased fetal
 weights,  increased minor soft tissue  and skeletal  anomalies, and delayed
 ossification.  For one  of  these studies, developmental defects may have  been
 associated with the significant maternal toxicity  observed.  Neither an
 inhalation study using  a lower  concentration nor a  drinking water  study
 found  any developmental effects.  Although  there are some  positive reports
 of minor  developmental  effects  in experimental  animals, 1,1,1-trichloro-
 ethane does not appear  to be a potent developmental toxicant in animals.
 However,  only one  study examined potential  effects  on  the  developing
 nervous system.  In view of  the known neurological  effects  of
 1,1,1-trichloroethane in humans and animals, additional developmental
 studies that examine neurological endpoints would be an important  component
 of a complete investigation of the potential for developmental toxicity  of
 1,1,1-trichloroethane in humans.

     Reproductive Effects.   Reproductive effects of 1,1,1-trichloroethane in
humans have not been reported.   Histological evaluation of  reproductive
organs and tissues from male and female rats and mice revealed no  lesions
attributable to 1,1,1-trichloroethane exposure.  More sensitive tests are
 required before a full evaluation of the potential for reproductive effects
 in humans can be made.
                             17-56

-------
                                    83

                            2.  HEALTH EFFECTS
     Genotoxic Effects,  The genotoxic effects of 1,1,1-trichloroethane have
been studied extensively.  The results are summarized in Tables 2-4 through
2-7.  Although most tests of mutagenicity in the Ames Salmonella assay
produced negative results, those conducted in a desiccator, to minimize
evaporation and maximize exposure, were positive.  These results indicate
that 1,1,1-trichloroethane may be mutagenic in Salmonella.  The results were
negative in other tests of genotoxicity in bacteria and yeast.
1,1,1-Trichloroethane is a relatively volatile compound; therefore, a high
evaporation rate could result in lower doses to the microorganisms and thus
affect the outcome of genotoxicity tests.  This explanation could account
for the negative results observed in tests with bacteria and yeast.

     Host assays of genotoxicity in mammalian cells were negative, but
1,1,1-trichloroethane did produce chromosomal aberrations in Chinese hamster
ovary cells in vitro.  In vivo micronucleus tests for chromosomal
aberrations were all negative, however.  Positive or weakly positive results
were reported in assays for degranulation of endoplasmic reticulum, which
measures the ability of a compound to displace polysomes from endoplasmic
reticulum in rat hepatocytes in vitro, and formation of DNA adducts
(binding of the compound to DNA) in mouse liver in vivo.  Tests of  cell
transformation in rat embryo cells, hamster embryo cells, baby hamster
kidney cells, and mouse BALB/c-313 cells were all positive.  It is believed
that cell transformation systems may be similar to the process of neoplastic
transformations.

     Although 1,1,1-trichloroethane was mutagenic in a few assays with
Salmonella, induced chromosomal aberrations in a Chinese hamster ovary cell
assay, and was positive in mammalian cell transformation assays, the
existing genotoxicity data are largely negative.  In addition, there  is  a
possibility that positive results were produced by stabilizers and not
1,1,1-trichloroethane itself.  Therefore, a firm conclusion regarding  the
genotoxic potential of 1,1,1-trichloroethane  in humans is not possible.

     Cancer.  Evidence for or against an association between exposure  to
1,1,1-trichloroethane and cancer  in humans has not been reported.  Among
animals, no effects were  found in a well-designed inhalation study at
exposure levels up to 1500 ppm.  The results  of an oral study indicated  thac
1,1,1-trichloroethane may have produced an increase in the occurrence  of
immunoblastic lymphosarcoma in rats.  However, the biological and
statistical significance of the results of this study are questionable
because of the limitations of the study design.

     There is also limited information on the role of 1,1,1-trichloroethane
metabolites in the toxicity of the compound.  Reactive metabolites are
important in the carcinogenicity  of other chloroethanes.   Binding  to  ONA,
which is correlated with carcinogenicity  in chlorinated ethanes  (Lattanzi
et al. 1988), was weak in both i-n vivo and in vitro tests.  Even weak
binding, however, indicates an ability to interact with DNA.  Cell
biotransformation tests were positive for this chemical.  The results  of
                                 17-57

-------
                                     88

                             2.   HEALTH  EFFECTS
these assays may have been confounded by the presence of stabilizing
agents, however.  Two of the possible stabilizing additives in commercial
formulations of 1,1,1-trichloroethane are 1,2-epoxybutane (butylene oxide),
and 1,4-dioxane (diethylene dioxide).  Both stabilizers have been identified
as potential carcinogens based on animal studies (NTP 1989a).

     At this time, it does not appear that exposure to 1,1,1-trichloroethane
presents a clear cancer risk in animals; however,  as discussed above,
limitations surrounding the studies performed to date prevent a definitive
assessment of- the carcinogenic potential of this compound in humans.
                          17-58

-------
           TOXICOLQGICAL PROFILE FOR
                 TOTAL XYLENES
                  Prepared by:

            Clement Associates, Inc.
         Under Contract No. 205-88-0608
                  Prepared  for:

Agency for Toxic Substances and Disease Registry
           U.S. Public Health Service
                  December 1990
              17-59

-------
2.4  RELEVANCE TO PUBLIC HEALTH

     The concentrations of mixed xylene and xylene itomers used in animal
studies are much higher than the ambient levels encountered in urban and
industrial areas.  However, information about the effects observed at high
concentrations of xylenes is important because potentially high levels may be
present at hazardous waste sites.  In addition, subgroups of the population
may be extremely sensitive and effects seen at high levels in animals may be a
predictor of effects seen in these subgroups when they are exposed at much
lower levels.

     Both human and "animal data suggest that mixed xylene, B-xylene,
2-xylene, and p.-xylene all produce similar effects, although the individual
isomers are not necessarily equal in potency with regard to a given effect.
Human data indicate that both short and long-term xylene exposure result in a
variety of nervous system effects that include headache, mental confusion,
narcosis, alterations in body balance, impaired short-term memory, dizziness,
and tremors.  In animals, xylene also produces nervous system effects.  The
respiratory system may also be affected.   Higher doses of xylene have produced
unconsciousness and death in humans and animals.  The liver and kidney may
also be targets of xylene toxicity in humans,  although more thorough data are
needed to better assess the relationship.
                               17-60

-------
                                      69

                              2.   HEALTH EFFECTS
     Death.   Xylene can be fatal to both humans and animals following
inhalation and oral exposure.  Death has been observed in animals following
dermal exposure to xylene, but no cases have been reported in humans.  Death
in humans and animals appears to be caused by either respiratory failure or
ventricular fibrillation.   The amount of xylene necessary to cause death is
relatively large in both animals and humans, and reports of death in humans
following inhalation of xylene occurred in areas of poor ventilation.
Therefore, it is highly unlikely that inhalation or ingestion of the small
amounts of xylene likely to be present in contaminated water or air would pose
a risk of death.

     Systemic Effects.  In humans, acute inhalation of xylene produced nose
and throat irritation (Goldie 1960; Hake et al. 1981; Klaucke et al. 1982;
Nersesian et al. 1985).  Severe lung congestion with pulmonary hemorrhages and
edema were noted in a worker who died following acute inhalation of paint
fumes containing xylene (Horley et al. 1970).  In addition, chronic
occupational exposure to xylene vapors has been associated with labored
breathing and impaired pulmonary function (Hipolito 1980; Roberts et al.
1988).

     Animal data provide supporting evidence for the respiratory effects
observed in humans following exposure to xylene.  Adverse respiratory effects
noted in rats, mice, and guinea pigs following acute and intermediate
 inhalation exposure to xylene included decreased respiratory rate, labored
breathing, irritation of the respiratory tract, pulmonary edema, and pulmonary
 inflammation (Carpenter et al. 1975; De Ceaurriz et al. 1981; Furnas and Hine
 1958; Smyth and Smyth 1928).

     Chronic occupational exposure of workers to xylene by inhalation has
 been associated with increased heart palpitation and abnormal ECGs  (Hipolito
 1980; Sukhanova et al. 1969).  However, these particular reports provide no
 conclusive evidence that xylene causes cardiovascular effects in humans
 because exposure conditions were not well characterized and workers may have
 been exposed to other chemical agents in addition to xylene.

     Data from animal studies provide limited evidence that humans could be
 •t increased risk of developing cardiovascular effects following exposure  to
 xylene.  Cardiovascular effects observed in rats following acute and
 interaediate inhalation exposure to xylene have included ventricular
 "polarization disturbances, atrial fibrillation, arrhythmias,  occasional
 cardiac arrest, changes in EGG, morphological changes in coronary
 •icrovessels, decreased myocardial blood flow, and increased heart weight
 (Jlorvai et al. 1976, 1987).  However, histopathologic lesions of the heart
      not been obs«™«d in other studies (Carpenter et al. 1975; Hazleton  Labs
        1988b; Jenkins et al. 1970; NTP 1986).
                                 17-61

-------
                                       70

                               2.  HEALTH  EFFECTS
     Symptoms of nausea, vomiting, and  gastric discomfort have been noted  in
workers following inhalation of xylene.  Gastrointestinal effects have not
been reported in animals.  However, there are sufficient human data to
conclude that exposure to xylene could  produce such effects  (e.g., nausea and
vomiting).

     Human and animal data provide no indications of adverse hematological
effects following inhalation of xylene.  In the past, chronic occupational
exposure to xylene by inhalation was thought to be associated with a variety
of hematological effects.  However, exposure in all cases was to solvent
mixtures known or suspected to contain  benzene.  Because benzene is an agent
strongly suspected of causing leukemia  and other blood dyscrasias in humans,
these effects cannot be attributed solely to xylene.

     Hematological effects have not been observed in rats, dogs, or guinea
pigs exposed by inhalation to mixed xylene or a-xylene for an intermediate
period (Carpenter et al. 1975; Jenkins  et al. 1970).  These negative results
from animal studies suggest that humans might not develop hematological
effects from intermediate inhalation of xylene; however, the hematological
effects from chronic inhalation, oral,  and dermal exposure are not known.

     No data were available regarding the musculoskeletal effects of xylene
in humans following inhalation exposure to mixed xylene, Q-,  p.-, or £-xylene.
Animal da   regarding musculoskeletal effects following xylene exposure are
limited.   .icroscopic examination of skeletal muscle of rats exposed for an
intermediate period of time to mixed xylenes, ffl-xylene, or £-xylene revealed
no treatment-related lesions (Carpenter et al. 1975; Hazleton Labs 1988a,
1988b; NTP 1986).  Skeletal anomalies,  delayed ossification,  and extra ribs
have been observed in the fetuses and offspring of pregnant mice and rats
exposed by inhalation to mixed xylene and £-xylene (Mirkova et al. 1983;
Ungvary et al. 1980b).  These latter results suggest that the human fetus
might be at increased risk of such skeletal effects following maternal
exposure to high levels of xylene.  The above studies are not definitive,
however, in terms of possible skeletal  effects.

     Human data regarding the hepatic effects following inhalation of xylene
are limited to several case and occupational studies (Dolara et al. 1982;
Kurppa and Husman 1982; Morley et al. 1970).  However, these studies provide
limited evidence for evaluating the hepatic effects of xylene in humans
because these subjects were concurrently exposed to other chemical agents in
addition to xylene.

     Available animal studies indicate  that mixed xylene and individual
isomers produce a variety of mild hepatic effects, and they provide evidence
that humans might be at increased risk  of developing such effects following
xylene exposure.   Effects seen in animals have included increased hepatic
                               17-62

-------
                                      71

                              2.   HEALTH EFFECTS
cytochrome P-450 and b5 content,  increased hepatic weight, increased liver to
body weight ratios,  decreased hepatic glycogen, ultrastructural changes in
hepatic endoplasnic  reticulum, changes in the distribution of hepatocellular
nuclei, congestion of liver cells, and/or degeneration of the liver (Bowers et
al. 1982; Condie et  al. 1988; Elovaara 1982; Elovaara et al. 1980; Muralidhara
and Krishnakumari 1980; Patel 1979; Pyykko 1980; Smyth and Smyth 1928; Tacrai
and Ungvary 1980; Tatrai et al. 1981; Toftgard and Nilsen 1981, 1982;  Toftgard
et al. 1981;  Ungvary et al. 1980a).  Many of the observed hepatic effects in
animals following inhalation and oral exposure to xylene are likely due to
increased metabolism of the solvent and are not necessarily adverse effects
(EPA 1985a; Tatrai et al. 1981).

     The available human studies that investigate the renal effects following
inhalation of xylene are of limited value because exposure conditions were not
well characterized and subjects were exposed to other solvents in addition to
xylene.  However, they provide suggestive evidence that subjects exposed by
inhalation to solvent mixtures containing xylene may be at an increased risk
of developing renal  dysfunction and/or renal damage (Askergren 1982; Franchini
et al. 1983;  Morley et al. 1970).  Indications of renal effects in humans
exposed to solvent mixtures containing xylene have included increased blood
urea concentrations, decreased urinary clearance of endogenous creatinine,
increased lysozymuria, increased urinary levels of 0-glucuronidase, and
increased urinary excretion of albumin, erythrocytes, and leukocytes
(Askergren 1982; Franchini et al. 1983; Morley et al. 1970).  No human data
were available regarding the renal toxicity of xylene following oral or dermal
exposure.

     Data from ar mal studies provide additional evidence that humans could
be at risk of developing renal effects following inhalation exposure to
xylene.  Effects noted in studies with rats, guinea pigs, dogs, and monkeys
have included increased renal enzyme activity, increased renal cytochrome
p.450 content, increased renal microsomal protein, and increased kidney-to-
body weight ratios (Condie et al. 1988; Elovaara 1982; Toftgard and Nilsen
1982).  In the study by Condie et al. (1988), tubular dilation and atrophy
consistent with early chronic nephropathy were observed, however in studies by
Carpenter et al. (1975) and Jenkins et al. (1970), the biochemical changes
were not associated with any histopathologic lesions of the kidney.

     It has been suggested that xylene induces renal Affects by causing
increased capillary (at the glomerulus) and/or tubular permeability (EPA
1985a).  Increased renal permeability caused by irritant or fluidization
effects could result in physiological and possibly histological effects  (EPA
1985a).  In humans exposed to solvent mixtures containing xylene, the
increased urinary levels of /9-glucuronidase may be due to a faster cellular
turnover in the renal tubular epithelium because of a mild  toxic effect
(Franchini et al. 1983).  The lysozymuria and  increase in urinary excretion of
                              17-63

-------
                                       72

                               2.   HEALTH  EFFECTS
 albumin may be  indicative  of potential damage  to  the  renal  tubules  and  renal
 glomeruli,  respectively  (Askergren  1982; Franchini et al. 1983).  Increased
 urinary excretion of erythrocytes and leukocytes  are  also indicators  of
 potential  toxic  injury to  the kidney (Askergren 1982).

      Dermal exposure of  humans  to xylene causes skin  irritation,  dryness  and
 scaling of the skin, and vasodilation of the skin (Engstrom et  al.  1977;
 Riihimaki  1979).  Exposure of humans to xylene vapors causes ocular irritation
 (Carpenter et al. 1975;  Hake et al. 1981; Klaucke et  al. 1982;  Nelson et
 al. 1943).

      Animal data provide additional evidence that dermal exposure to  xylene
 produces dermal and ocular effects.  These included skin erythema and edema,
 eschar  formation in some animals, and epidermal thickening  (Hine and  Zuidema
 1970).  No studies were  available regarding potential dermal/ocular effects in
 animals following exposure to xylene vapor.

      Immunological Effects.  Very limited human and no animal data  are
 available  to evaluate the  immunological effects of xylene.  Therefore,  the
 relevance  to public health is not known.

      Neurological Effects.  Neurological effects  in humans  following  oral or
 dermal  exposure to xylene have not been studied,  although one case  was
 reported of a man who developed a coma following  ingestion  of xylene  (Recchia
 et al.  1985).  Results of experimental studies with humans  indicate that acute
 inhalation exposure to mixed xylene or jj-xylene causes impaired short-term
 memory, impaired reaction time,  performance decrements in numerical ability,
 and alterations in equilibrium and body balance (Gamberale  et al. 1978;
 Riihimaki  and Savolainen 1980;  Savolainen et al.  1985; Savolainen et  al.
 1979b;  Savolainen and Riihimaki 1981b;  Savolainen and Linnavuo 1979;
 Savolainen  et al. 1984).   Available case and occupational studies together
 provide suggestive evidence that acute and chronic inhalation exposure  to
 xylene  or solvent mixtures containing xylene may be associated with many
 neurological effects and symptoms (Arthur and Curnock 1982;  Goldie  1960;
 Hipolito 1980;  Klaucke et al.  1982;  Morley et al.  1970;  Nersesian et  al. 1985;
 Roberts et al.  1988).   In several case reports, isolated instances of
 unconsciousness, amnesia, brain hemorrhage, and epileptic seizure have been
 associated in a limited number  of individuals with acute inhalation exposure
 to solvent mixtures containing  xylene (Arthur and Curnock 1982; Goldie  1960;
Morley et al.  1970).

     Results of experimental studies with animals provide further evidence
 that mixed xylene and individual isomers are neurotoxicants following
 inhalation exposure.   Signs of  neurotoxicity observed in rats,  mice,  and
 gerbils following acute and intermediate inhalation exposure to the various
                               17-64

-------
                                      73

                              2.  HEALTH EFFECTS
xylene isomers have included narcosis, prostration, incoordination, tremors,
muscular spasms, labored breathing, behavioral changes, hyperactivity,
elevated auditory thresholds, hearing loss, changes in brain enzyme activity
and changes in levels of brain proteins (Andersson et al. 1981; Carpenter et
al. 1975; De Ceaurriz et al. 1983; Furnas and Hine 1958; Ghosh et al.  1987;
Kyrklund et al. 1987; Molnar et al. 1986; NTP 1986; Pryor et al. 1987;  Rank
1985; Rosengren et al. 1986; Savolainen and Seppalainen 1979; Savolainen et
al. 1978; Savolainen et al. 1979a; Wlmolwaccanapun et al. 1987).  No animal
studies evaluating the neurological effects of xylene following chronic
inhalation exposure were available.

     Although a number of mechanisms of action have been proposed, the toxic
mechanism of xylene on the nervous system is not fully understood.  Because
xylene is lipid soluble, it can distribute to the central nervous system.  A
number of investigators have noted the affinity of xylene for nervous system
tissue, such as myelin and axonal membrane, in humans and animals (Oesi et al.
1967; EPA 1985a; Gerarde 1959; Savolainen and Pfaffli 1980).

     Neurological effects, including narcosis and anesthesia, are noted after
acute exposure to high concentration of xylene when high blood and brain
levels of the solvent occur (EPA 1985a).  It has been suggested that xylene
and other alkylbenzenes act simply by being in the nervous system at
sufficiently high concentrations to inhibit normal function (Desi et al. 1967;
EPA 1985a; Gerarde 1959).  A number of experimental studies with humans on CNS
function indicate that the first observable effects of m-xylene are on Che
central vestibular system, which controls equilibrium and body balance
(Riihinaki and Savolainen 1980; Savolainen and Linnavuo 1979; Savolainen et
al. 1979b; Savolainen and Riihimaki 1981b; Savolainen et al. 1984; Savolainen
et al. 1985).

     Also, xylene may directly affect nerve conductivity by altering the
lipid components of the axonal membrane (EPA 1985a; Savolainen and Seppalainen
1979).  Altered lipid components in turn could alter sodium permeability and
decrease action potentials, resulting in signs of intoxication (EPA 1985a).

     Results of experimental studies with rats suggest that mixed xylene and
B-, a-, or p.-xylene can cause alterations in dopamine and/or noradrenaline
levels in the brain (Andersson et al. 1981).  These changes can produce
disturbances in catecholamine neurotransmission, which in turn can potentially
alter brain function, particularly mental, motor, and neuroendocrine control
(Andersson et al. 1981).  Two possible modes of action have been suggested.
Xylene or a metabolite of xylene could act directly on adrenergic receptors in
the brain, causing increased catecholamines and postsynaptic stimulation.  The
second possibility involves alteration of axonal membrane fluidity, which
causes permeability changes and alters neurotransmitter release  (Andersson et
al. 1981; EPA 1985a).
                               17-65

-------
                                       74

                               2.   HEALTH EFFECTS
      Some authors have also suggested that metabolic intermediates, such as
 arene oxides or methylbenzaldehyde,  may be responsible for the toxic effects
 of xylene (Savolainen and Pfaffli 1980).   Oxidation of xylene to these
 intermediates by microsomal enzyme systems may occur within brain cells
 (Savolainen and Pfaffli 1980).

      Developmental Toxicity.   Limited human studies were available regarding
 the developmental or teratogenic  effects  of xylene.   However, because of
 concurrent exposure with chemical agents  in addition to xylene,  they cannot be
 used to assess the relationship between xylene exposure and developmental
 effects in humans.   Findings  in animal studies suggest that adverse effects
 might occur in the unborn and offspring of women exposed to xylene or its
 isomers.   Results of studies  with rats and mice indicate that inhalation
 exposure  to mixed xylene or xylene isomers may induce increased  fetal death,
 decreased fetal weight,  delayed skeletal  development,  skeletal anomalies,
 enzymatic changes in fetal organs, and maternal toxicity (Hudak  and Ungvary
 1978;  Marks et al.  1982;  Hirkova  et  al. 1983;  Ungvary et al.  1980b,  1981).
 Oral exposure to mixed  xylene has  been associated with cleft plate and
 decreased fetal weight  (Marks et  al.  1982).  Dermal  exposure of  rats to xylene
 has been  associated with biochemical  changes in fetal and maternal brain
 tissue (Hirkova et  al.  1979).  However, n-xylene  produced no developmental
 effects,  with maternal  toxicity,  in  rats  (Rosen et al.  1986).  These studies
 were generally limited but, taken  together, suggest  fetotoxic effects,
 although  most of these may have been  secondary to maternal toxicity.

      The  exact mechanism by which  mixed xylene or its  individual  isomers
 produce toxic  effects in fetuses has  not been  fully  investigated.   Based on
 results of  studies with  rats, p.-xylene-induced delayed  fetal  development may
 have been caused by  decreased levels  of progesterone  and estradiol  (Ungvary et
 al.  1981).  The  titers of  these hormones were  apparently lowered  due  to
 xylene's  inductive effect  on metabolism, which caused  increased hormone
 catabolism.

     Reproductive Toxicity.  The relevance to  public health  regarding xylene
 exposure  and adverse reproductive effects  is not  known because of the
 limitations of the human and animal data.   Occupational  exposure  of men  to
xylenes,  in addition to other solvents, was found to increase the potential
for their wives to experience spontaneous abortions, however, this study was
limited by exposure of the men to other solvents  and the  limited  size of the
population studied (Taskinen et al. 1989).  No reproductive effects were found
in rats following inhalation of xylene before mating and during gestation and
lactation (Bio/dynamics 1983).  Histopathological examination following
intermediate and chronic oral bioassays revealed no adverse effects on the
reproductive organs of rats and mice  (Hazleton Labs 1988a, 1988b; NTP 1986).
                            17-66

-------
                                      75

                              2.  HEALTH EFFECTS


No other studies were located regarding reproductive effects in animals
following inhalation or dermal exposure to xylene or its isomers.

     Genotoxicity.  Mixed xylene, as well as each of the individual xylene
isomers, has been tested for genotoxicity in a variety of in vitro and in vivo
assays.  Results of the various assays indicate that mixed xylene and xylene
isomers are nongenotoxic (Tables 2-10 and 2-11).  As summarized in Table 2-10,
the results of the various assays indicate that mixed xylene and xylene
isomers are nongenotoxic following in vitro exposure (Bos et al. 1981; Connor
et al. 1985; Florin et al. 1980; Haworth et al. 1983; Litton Bionetics 1978b:
McCarroll et al. 1981a, 1981b; NTP 1986; Shimizu et al. 1985).

     The induction of genotoxic effects following in vivp exposure to xylene
has been evaluated in the bone marrow chromosomal aberration test with rats
(Litton Bionetics 1978b),  the bone marrow micronucleus test with mice
(Hohtashamipur et al. 1985), and the sperm morphology test with rats
(Washington et al. 1983).   The incidence jf sister-chromatid exchanges and
chromosomal aberrations in the peripheral lymphocytes of workers exposed
occupationally to xylene also has been evaluated (Haglund et al. 1980; Pap and
Varga 1987).  Both human studies involved occupational exposure to other
chemicals in addition to xylene.  As summarized in Table 2-11, the results of
these studies indicate that mixed xylene, m.-, o.-, and £-xylene are
nongenotoxic following in vivo exposure.

     No mutagenic activity was demonstrated for any of the various
metabolites of xylene in bacterial test systems.  S. tvphlmurium strains TA98,
TA100, TA1535, TA1537, and TA1538, with and without S9 metabolic activation,
have been used to test the mutagenic activity of a-xylenol (Epler et al. 1979;
Florin et al. 1980; Hejtmankova et al. 1979; Pool and Lin 1982), ffl-xylenol
(Epler et al. 1979; Florin et al. 1980), and a-methylbenzyl alcohol (Bos et
al. 1981).  2,4-Dimethylphenol has been evaluated in a gene reversion assay
with E. coli strain Sd-4-73 (Szybalski 1958).

     Ethylbenzene, a common component of many technical grades of mixed
xylene, also demonstrated no mutagenic effects in the gene reversion assay
with S. cerevisiae (Nestmann and Lee 1983), the Salmonella/microsome assay
with strains TA98, TA100,  TA1535, TA1537, and TA1538 (Florin et al. 1980;
Nestmann et al. 1980), or in cytogenic assays with cultured Chinese hamster
ovary cells (NTP 1986).  However, in studies with cultured human lymphocytes,
ethylbenzene induced a slight but statistically significant (p<0.01) increase
in the number of the sister-chromatid exchanges (Norppa and Vainio 1983).  The
authors of this latter study suggested that ethylbenzene may be a "weak,
ineffective mutagen."  Ethylbenzene is the subject of a separate toxicological
profile, and the reader should refer to that document for a more detailed
review of its genotoxicity potential.
                              17-67

-------
                                       79

                              2.  HEALTH  EFFECTS
      In summary, genocoxiclcy studies on mixed xylene  and Che  individual
 isomers of xylene have provided consistently negative  results  in a  variety of
 |n vitro and in vivo assays and test systems (bacteria,  yeast,  insects,
 cultured mammalian cells, mice, rats, and humans).  Based on the genotoxicity
 studies conducted to date, there is sufficient evidence  to conclude that mixed
 xylene, n-xylene, o-xylene, and p.-xylene are nonmutagenic.  There is also
 limited evidence from bacterial test systems that suggest that  xylene
 metabolites, specifically ffl-xylenol, p.-xylenol, 2,4-dimethylphenol,  and
 o.-methylbenzyl alcohol, are nonmutagenic as well.

      Cancer.  No data were available regarding the development  of cancer in
 humans following inhalation, oral, or dermal exposure  to mixed  xylene or
 individual isomers.  Animal carcinogenicity data for the xylenes are limited
 to oral studies with mixed xylene (Maltoni et  al. 1983,  1985; NTP 1986)  and
 dermal studies in which the isomeric composition of the  xylene  was  not
 specified, exposures were less than lifetime,  and involved multiple  chemicals
 (fierenblum 1941; Pound 1970; Pound and Withers  1963).  No animal
 carcinogenicity data for the xylenes were available for  inhalation  exposure.
 Because of the limited data, no conclusions can be drawn regarding  the
 relationship between xylene exposure and cancer in humans.

     EPA has classified mixed xylene as a Group D agent  (not classifiable  as
 to human carcinogenicity) (IRIS 1989).   This classification applies  to those
 chemical agents for which there is inadequate  evidence of carcinogenicity  in
 animals.   No cancer potency factor (ql*) or other quantitative  estimate  of
 carcinogenicity has been developed by EPA for mixed xylene, a-xylene,
fi-xylene,  or £-xylene.
                            17-68

-------
           TOXICOLOGICAL PROFILE FOR
                      ZINC
                  Prepared by:

               Clement Associates
         Under Contract No. 205-88-0608

                  Prepared for:

Agency for Toxic Substance* and Disease Registry
           U.S. Public Health Service

             In collaboration with:

      U.S. Environmental Protection Agency
                  December 1989
                  17-69

-------
                              Z/AJC.
2.3  RELEVANCE TO PUBLIC HEALTH

     Death.  Death due to respiratory failure in humans following acute
inhalation of zinc chloride has been reported.   However,  the amount of zinc
exposure was not determined.  Furthermore,  exposure to zinc was concomitant
with exposure to other chemicals.   Hence,  death could not be exclusively
attributed to zinc exposure.

     No information regarding death in animals  following inhalation exposure
was found.  However,  death was reported in ferrets (Straube et al.  1980)  and
mice (Malta et al. 1981) following acute and intermediate oral exposures,
                         17-70

-------
                                      31

                              2.  HEALTH EFFECTS
respectively.  Adverse systemic effects were observed in these animals, but
the specific cause of death could not be determined.

     Systemic Effects.  Effects in humans and animals following acute
inhalation exposure to zinc compounds are primarily limited to the respiratory
tract.  Oral exposure to zinc and its compounds in humans and animals
primarily affects the gastrointestinal system.  Zinc also affects the
hematological and renal systems in both humans and animals following acute,
intermediate or chronic exposures.  Hepatic effects were observed in animals
after acute oral exposure.  No adverse hepatic effects were observed in humans
after intermediate exposure.

     Cardiovascular Effects.  Intermediate duration oral administration of
zinc to humans has resulted in decreased serum HDL-cholesterol levels.
Although this is not a direct effect on the cardiovascular system,  the decline
in HDL levels may be associated with increased risk of coronary artery
disease.

     Gastrointestinal Effects.  The ingestion of  small amounts of zinc is
essential to maintain one's health.  However, evidence shows  that high level
ingestion of zinc presents a potential for gastrointestinal disorders.
Following acute, intermediate or chronic ingestion of zinc, the primary
effects in humans or animals are pancreatic abnormalities  and gastrointestinal
 irritation.  No adverse gastrointestinal effects  were observed after
 inhalation exposure.  Biochemical changes, including  increased serum amylase
 levels and hypocalcemia, found in an individual after drinking a zinc chloride
 solution (unknown amount) are indicative of acute pancreatitis (Chobanian
 1981).  More severe effects are seen in the pancreas  as  exposure levels
 increase in various test animals.  Although morphological  changes,  such as
 pancreatic fibresis and degeneration and necrosis of acinar cells of the
 pancreas, are seen in most animal studies, these  changes occur over a wide
 range of exposure levels  (59 mgAg/day  in  cats  to 3,900  mg/kg/day in mice)
 (Aughey et al. 1977; Drinker et al. 1927d; Maita  et al.  1981).   This
 variability  indicates the existence of  species  differences with  regard to
 gastrointestinal disorders, specifically pancreatic toxicity.  Zinc compounds,
 when ingested at high levels, also cause intestinal bleeding in humans (Moore
 1978) and in animals  (Maita et al. 1981; Straube  et al.  1980).

      Respiratory Effects.  Respiratory  disorders  have been observed in humans
 and animals  following the acute  inhalation exposure to  zinc compounds.  No
 adverse respiratory effects have been observed following ingestion of zinc
 compounds.

      Acute  exposure to high concentrations of airborne  zinc oxide in humans
 causes  metal fume fever.  Zinc oxide penetrates  the alveoli,  damages the lung
 tissue, and transiently impairs pulmonary  function (Brown 1988;  Drinker et al.
 1927b;  Vogelmeier et  al.  1987).  Lung volumes  are decreased as is the carbon
 monoxide diffusion capacity  (Drinker et al.  1972b;  Mueller and Seger 1985;
                                  17-71

-------
                                      31

                              2.  HEALTH EFFECTS
respectively.  Adverse systemic effects were observed  in these  animals, but
the specific cause of death could not be determined.

     Systemic Effects.  Effects in humans end animals  following acute
inhalation exposure to zinc compounds are primarily limited to  the respiratory
tract.   Oral exposure to zinc and its compounds in humans and animals
primarily affects the gastrointestinal system.  Zinc also affects the
hematological and renal systems in both humans and animals following acute,
intermediate or chronic exposures.  Hepatic effects were observed in animals
after acute oral exposure.  No adverse hepatic effects were observed in humans
after intermediate exposure.

     Cardiovascular Effects.  Intermediate duration oral administration of
zinc to humans has resulted in decreased serum HDL-cholesterol  levels.
Although this is not a direct effect on the cardiovascular system, the decline
in HDL levels may be associated with increased risk of coronary artery
disease.

     Gastrointestinal Effects.  The ingestion of small amounts  of zinc is
essential to maintain one's health.  However, evidence shows that high level
ingestion of zinc presents a potential for gastrointestinal disorders.
Following acute, intermediate or chronic ingestion of zinc, the primary
effects in humans or animals are pancreatic abnormalities and gastrointestinal
irritation.  No adverse gastrointestinal effects were observed  after
inhalation exposure.  Biochemical changes, including increased  serum amylase
levels and hypocalcemia,  found in an individual after drinking  a zinc chloride
solution (unknown amount) are indicative of acute pancreatitis  (Chobanian
1981).  More severe effects are seen in the pancreas as exposure levels
increase in various test animals.  Although morphological changes, such as
pancreatic fibrosis and degeneration and necrosis of acinar cells of the
pancreas, are seen in most animal studies, these changes occur  over a wide
range of exposure levels (59 mg/kg/day in cats to 3,900 ag/kg/d&y in mice)
(Aughey et al. 1977; Drinker et al. 1927d; Maita «t al. 1981).  This
variability indicates the existence of species differences with regard to
gastrointestinal disorders, specifically pancreatic toxicity.   Zinc compounds,
when ingested at high levels, also cause intestinal bleeding in humans (Moore
1978) and in animals (Maita et al. 1981; Straube et al. 1980).

     Respiratory Effects.  Respiratory disorders have been observed in humans
and animals following the acute inhalation exposure to zinc compounds.  No
adverse respiratory effects have been observed following ingestion of zinc
compounds.

     Acute exposure to high concentrations of airborne zinc oxide in humans
causes metal fume fever.   Zinc oxide penetrates the alveoli, damages the lung
tissue, and transiently impairs pulmonary function (Brown 1988; Drinker et al.
1927b; Vogelmeier et al.  1987).   Lung volumes are decreased as  is the carbon
monoxide diffusion capacity (Drinker et al. 1972b; Mueller and  Seger 1985;
                                  17-72

-------
                                      32

                              2.   HEALTH  EFFECTS
Sturgis et al.  1927).   Metal fume fever is believed to be the result of an
immune reaction to inhaled metal oxide particles (Mueller and Seger 1985).

     Respiratory tract irritation occurs in both humans and animals (Drinker
and Drinker 1928;  Sturgis et al. 1927) after exposure to zinc oxide.  Most
laboratory animals,  except guinea pigs,  begin to present respiratory
abnormalities (e.g., pulmonary congestion, peribronchial leukocytic
infiltration) at similar exposure levels as humans (Drinker and Drinker 1928).
Cats exhibited more severe effects than other animals, including
bronchopneumonia (Drinker and Drinker 1928).

     In humans, inhalation of zinc chloride causes greater damage to
respiratory tissue than zinc oxide.  Lesions reported were acute pneumonitis,
ulceration of mucous membranes, subpleural hemorrhage, and pulmonary fibrosis.
Exposed individuals may die with respiratory distress syndrome (Evans 1945;
Hjortso et al.  1988; Johnson and Stonehill 1961; Matarese and Matthews 1966;
Milliken et al. 1963; Schenker et al. 1981).

     The studies in humans and animals reveal that inhalation of zinc as
particulate or fume can result in respiratory ailments (Drinker and Drinker
1928; Sturgis et al. 1927).  However, zinc fume or particles are primarily
generated through grinding or welding of zinc-containing metal.  This form of
exposure presents a particular problem for industrial workers.

     Hematological Effects.  Anemia occurs in both humans and animals after
high level acute, intermediate or chronic oral exposure to zinc and its
compounds (Allen et al. 1983; Drinker et al. 1927c; Maita et al. 1981; Moore
1978; Straube et al. 1980).  This effect occurs over a wide range  of doses
(6.47 mgAg/day in humans to 3,900 mg/kg/day in mice), indicating  species
differences regarding the hematological effects of zinc.  The anemia could be
exacerbated by gastrointestinal bleeding that has been associated  with the
ingestion of high levels of zinc.  Inhibition of intestinal absorption of
copper and iron may also be a factor  (Prasad et al. 1978).  Based  on the
reviewed data, humans appear to be susceptible to these effects of zinc.

     Anemia has been observed in patients after they were treated  with renal
dialysis for 2 months using water containing high levels of zinc.   This
suggests that anemia can result from  treatments of intermediate duration.  The
zinc was presumed to have eluted from galvanized hinges in storage containers.
Anemia was reversed after carbon filtration or deionization of the dialysis
water (Gallery et al. 1972; Petrie and Row 1977).

     Hepatic Effects.  Following acute and  intermediate oral exposure to zinc
compounds, hepatic necrosis was reported  in sheep (Allen et al. 1983).
Intermediate oral exposure of rats to zinc compounds at a dose similar to that
administered to sheep resulted  in enzymatic changes  (Kadiiska et al. 1985).
Intermediate oral exposure of humans  to zinc resulted in no adverse hepatic
effects.  No adverse hepatic effects  were reported after inhalation exposure.
                            17-73

-------
                                      33

                              2.  HEALTH EFFECTS
The weight of evidence suggests that the liver is not a primary target organ
in humans or animals for zinc toxicity.

     Renal Effects.  No adverse renal effects have been observed in humans
following inhalation or oral exposure to zinc compounds.  Following
intermediate oral exposure to zinc compounds, renal lesions have been reported
in laboratory animals.  Sheep were the most susceptible to renal toxicity
(Allen et al. 1983).

     Central Nervous. System Effects.  Of additional interest with respect to
neurological symptoms and lethargy observed in human subjects following oral
administration of zinc (Murphy 1970; Potter 1981) are in vitro investigations
of the effects of zinc on neurological tissue.  These studies indicate that
zinc inhibits (competes for) the entry of calcium ions into the nerve
terminals, thereby influencing the release of neurotransmitters (Nishimura
1987).  In addition, zinc (at concentrations that may occur in vivo during
certain pathophysiologic states) has been observed to be toxic to neurons and
glia cells of the central nervous system (Choi et al. 1988; Yokoyama et al.
1986).

     Reproductive and Developmental Effects.  Oral exposure to high doses of
zinc (200-500 mg/kg/day) has resulted in reduced fetal growth and altered
fetal and maternal concentrations of zinc and copper in rats (Cox et al. 1969;
Ketcheson et al.  1969; Schlicker and Cox 1967) and,  in extreme cases,
cessation of reproduction (Sutton and Nelson 1937).

     Congenital malformations such as exencephaly and rib fusions have been
observed in the offspring of pregnant golden hamsters injected intravenously
with a single dose of 2 mg zinc sulfate/kg on the 8th day of gestation (Fern
and Carpenter 1968).  Similarly, zinc chloride injected intraperitoneally in
single doses of 12.5,  20.5,  and 25 mgAg on day 8,  9, 10,  or 11 of gestation
in mice produced skeletal anomalies,  including delayed ossification and ripple
ribs without accompanying soft tissue defects.  Ripple ribs,  an unusual
anomaly, first appeared when zinc salt was given on day 9 of gestation at a
dose of 20.5 rag/kg,  becoming more prevalent when 25  mgAg of the salt was
administered on day 11 of gestation (Chang et al. 1977).   There is no evidence
of similar effects in humans.

     Genotoxic Effects.   Genotoxicity studies conducted in a variety of test
systems have failed to provide evidence for mutagenicity of zinc.   However,
there are indications  of weak clastogenic effects following zinc exposure.
Results of in vitro  studies  are shown in Table 2-3.   Exposure to zinc as zinc
•ulfate or zinc chloride does not increase mutation  frequencies in bacterial
or mammalian cell culture test systems (Amacher and  Paillet 1980;  Marzin and
vo Phi 1985;  Nishioka  1975;  Venitt and Levy 1974).   Treatment of human
lymphocytes in culture with  zinc has,  however, been  observed to result in a
       increase in chromosomal aberrations (Deknudt  and Deminatti 1978).
                                    17-74

-------
                                      35

                              2.   HEALTH  EFFECTS
     Results of in vivo studies are shown in Table 2-4.   A dominant lethal
study in mice was negative,  indicating a lack of a nutagenic effect.   However,
chromosomal aberrations have been observed in bone narrow cells  following
exposure to zinc in vivo both in mice fed 650 mg/kg/day  zinc chloride in diet
(Deknudt 1982) and in mice exposed to zinc oxide by inhalation (Voroshilin  et
al. 1978).  Chromosomal aberrations due to zinc were observed in bone marrow
cells of mice maintained on a low calcium diet (Deknudt  and Gerber 1979).
Calcium may be displaced by zinc in calcium-depleted conditions, thus leading
to chromosome, breaks and/or interfering in the repair process (Deknudt and
Gerber 1979).

     Cancer.  The carcinogenicity of zinc following oral exposure has been
evaluated in a single study with mice (Walters and Roe 1965).  In this study,
mice were administered zinc sulfate at elemental zinc doses of either 0, 170,
or 850 mg/kg/day in drinking water for 1 year.  Relative to controls, no
increase in tumor incidence was observed in treated mice.  The investigation
was not adequate for evaluating the carcinogenicity of zinc because of  several
study limitations.  Teratomas of the testes were observed in fowl given
testicular injections of 2 ml of a 10X zinc sulfate solution (Falin and
Gromzewa 1939).  The relevance of this study to public health is not known.

     No studies were located regarding carcinogenicity In experimental
animals following inhalation or dermal exposure to zinc and  its compounds.
                               17-75

-------