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
------- |