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APPENDIX F

HUMAN HEALTH RISK ASSESSMENT SUPPORTING DOCUMENTATION Human Health Risk Assessment APPENDIX F Human Health Risk Assessment

Appendix F.1 Copper and Lead Screening/CLP Comparison Appendix F.2 • CT Remediation Standard Regulations Appendix F.3 • Background Concentrations Appendix F.4 ­ Comparison to Connecticut Quality Standards Appendix F.5 ­ Sample Subsets Appendix F.6 ­ Statistics and Exposure Point Concentrations Appendix F.7 ­ Toxicity Profiles Appendix F.8 ­ Sample Calculations Appendix F.9 ­ Human Health Risk Assessments Spreadsheets ­ Area D Appendix F.10 Human Health Risk Assessment Spreadsheets ­ Area E Appendix F.11 ­ Results of Lead Models Appendix F.12 - Congener Data Quantitation Appendix F.1

Correlation of Copper and Lead Field Screening Data vs. Fixed Lab Data Appendix F-1 Field Screening - CLP Data Correlation

EPA directed Brown and Root Environmental to determine the correlation between data analyzed by field screening and CLP methodologies at the Raymark - Ferry Creek site. A strong correlation would allow for the use of field screening data in quantifying risk at the site. Two statistical procedures were used to determine the correlation between data analyzed by field screening and CLP methodologies: linear regression, which evaluates the correlation on a point-by-point basis; and a nonparametric t-test, which compares the means of two data sets for each method. Paired data selected for the correlation determination were collected at the same location and same depth.

For the first statistical analysis, a scatter plot of paired data was generated for each chemical with the field screening results plotted along the x-axis and the CLP results plotted along the y-axis. A linear regression was then performed on the scatter plot and a correlation coefficient was generated. For data that are strongly correlated, the scatter plot will exhibit a linear relationship with a correlation coefficient (r) of slightly less than 1. The copper and lead data had relatively high correlation coefficients of 0.87 and 0.86, respectively. The PCB data had extremely low correlation coefficients. The PCB scatter plots show that some correlation exists at low concentrations (< 1 ppm), but that this correlation weakens as concentrations increase. This may be due to the narrower calibration ranges of the field screening techniques.

For the second statistical analysis, the field screening data was grouped into one population and the CLP data was grouped into a second population. The Wilcoxon Rank-Sum (WRS) test, a distribution-free or nonparametric t-test, was performed on the two populations to determine whether their means were statistically equivalent. The copper and lead data had statistically equivalent means; the PCB data did not.

Based on the results of the two statistical analyses, the use of field screening data to quantify risk at the site is acceptable for copper and lead, but not for PCBs f"

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U O Copper Correlation Data

nsample para dp res jclp result dp qual dp units scr res iscr result Iscr qual dp res scr res SP-SO-MW110D-1820 COPPER 77 MG/KG 25iND |u 7 25 MF-SO-MW1 01 D-4850-D COPPER 7.9I7.9 MG/KG 25|ND III 7.9 25 MF-SO-MW101D-4850 COPPER 8.7 1 8.7 MG/KG 25 ND U 87 25 SP-SO-MW112B-2628 COPPER 10.6 10.6 MG/KG 25 ND U 10.6, 25 MF-SO-MW104D-6062 COPPER 11.9 11.9 MG/KG 25 ND U 11.91 25 MF-SO-MW101D-2830 COPPER 1 2.4 1 12.4 MG/KG I 25:ND U 12.4 25 MF-SO-SB5-1416 COPPER 13.8 138 MG/KG 8 8 13.8, 8 MF-SO-MW104D-1618 COPPER 15.2152 ~^~ MG/KG 25 ND 'U 15.2 25 MF-SO-MW 102-7880 COPPER 172,172 MG/KG 25iND .U 17.2, 25 MF-SO-MW104D-3234 COPPER 172117.2 MG/KG 25 ND U 17.2! 25 SP-SO-SB9-0608 COPPER 174 17.4 J MG/KG 25 ND JU 17.41 25 MF-SO-MW102-2224 COPPER I 18.5 18.5 MG/KG 25iND lU 18.5 25 MF-SO-TP3-0405 COPPER 22.1 22.1 MG/KG i 53 1 53 U 22.1 53 BC-SO-SB8A-0810 COPPER 22.9 22.9 J MG/KG 25IND ,U 22.9 25 MF-SO-MW102-4244 COPPER 23 4 23.4 MG/KG 25|ND 'U 23.4 i 25 MF-SO-MW104D-4648 COPPER 28.9 28.9 MG/KG 25 ND jU 28.9 25 SP-SO-SB1-0406B COPPER 32.9 32.9 J MG/KG 21 21 i 32.9 21 SP-SO-MW113B-0810 COPPER 33.8 33.8 J MG/KG | 25|ND 'U 33.8 25 MF-SO-MW103-1416 COPPER 34.4 34.4 MG/KG 5900 5900 | 34.4 . 5900 MF-SO-SB1-0810 COPPER 35.8 35.8 MG/KG 26 26 j 35.8 26 BC-SO-SB9-0608 COPPER 37.4 37 4 J MG/KG 25 ND III 37.4 25 MF-SO-MW104D-0002 COPPER 40.3 1 40.3 J MG/KG 25 ND 'U 40.3 25 SP-SO-SB5-1214 COPPER 63.5 63.5 MG/KG 25 ND |U 63.5 1 25 SP-SO-SB9-0810 COPPER 73.373.3 J MG/KG 250)250 ,J 73.3 250 SP-SO-SB7-0204 COPPER 73.5 73.5 J MG/KG 25IND IU 73.5 25 BC-SO-SB2-1214 COPPER 85.4 85.4 J MG/KG 25 ND iu ; 85.4 25 SP-SO-MW111D-1012 COPPER 91.8191.8 J MG/KG 25 ND U ! 91.8 25 SP-SO-MW110D-0406 COPPER 1021102 MG/KG 25 ND jU 1021 25 MF-SO-MW 1 01 D-0608 COPPER 106 106 J MG/KG 70 70 I 1061 70 BC-SO-MW 120-0406 COPPER i 108 108 IMG/KG 110 110 J 108! 110 MF-SO-SB2-1416 'COPPER 110 110 MG/KG 51 51 110 51 BC-SO-SB8A-1012 I COPPER 129 129 J IMG/KG 25IND U 1291 25 SP-SO-MW110D-1012 COPPER 160 160 MG/KG 110 110 J 160 110 SP-SO-MW111D-0810 COPPER 222 222 |J MG/KG 1501150 |J 222 1 50 BC-SO-SB9-0204B I COPPER 234 234 J MG/KG 1701170 J ; 234 1 70 MF-SO-SB8-0608 COPPER 287 '287 J MG/KG 410 i4io ; 287 410 MF-SO-SB3-0810 COPPER 352 1 352 J MG/KG 95 1 95 I 352 95 SP-SO-SB6-0608A COPPER | 400 400 MG/KG 300 1 300 400 300 SP-SO-SB3-1416 iCOPPER 559(559 J MG/KG 220 1 220 559 1 220 MF-SO-SB2-0608 ICOPPER 742 742 MG/KG 410|410 ' | 742 1 410 MF-SO-MW103-1618 COPPER 762762 MG/KG 1400 1400 762 1400 SP-SO-MW11 3B-0406 COPPER 885 1 885 J i MG/KG 530J 530 885 530 SP-SO-MW113B-0204B COPPER 997 1 997 J MG/KG 9101910 i 997 910 SP-SO-SB8-0002 COPPER 1230 1 1230 J MG/KG 1300J1300 1230' 1300 BC-SO-SB6-0810 COPPER 145011450 MG/KG 5500 5500 ' 14501 5500 MF-SO-TP2-0506 COPPER 2270 2270 MG/KG 420 420 ; 22701 420 MF-SO-SB7-1416 COPPER 2370 2370 J MG/KG 3600 1 3600 23701 3600 SP-SO-MW112B-0810A COPPER , 2830 j 2830 IMG/KG 1400 1400 2830 1 1400 BC-SO-SB5-0002B JCOPPER 3770 1 3770 MG/KG 1000 1000 3770' 1000 MF-SO-SB7-0406 [COPPER , 4000I4000 J MG/KG 1300H300 4000 1300 MF-SO-SB4-1214 COPPER 6260'6260 |MG/KG 6700 6700 6260' 6700 MF-SO-SB6-0204 COPPER 6390 6390 MG/KG ' 14000 '14000 6390 14000 SP-SO-MW112B-0608 COPPER 78507850 IMG/KG 2800 2800 7850' 2800 MF-SO-MW 102-0406 COPPER 11300 11300 J .MG/KG 4300 4300 11300 4300 SP-SO-SB4-0406 COPPER 12800| 12800 |J IMG/KG | 12000 12000 12800 12000 MF-SO-SB4-0406 COPPER 13900113900 J 'MG/KG 150 150 13900 150 BC-SO-SB3-0204A COPPER 15200 '15200 J 'MG/KG 7700 7700 1 5200 7700 BC-SO-SB 1-0608 COPPER 17500 17500 J , MG/KG 5900 5900 17500 5900 SP-SO-SB2-0204B COPPER 25200 25200 i MG/KG 21000 21000 25200 21000 BC-SO-SB4-0204 COPPER 26300 i 26300 MG/KG 20000 20000 26300 ' 20000 BC-SO-SB1-0406 .COPPER 33200:33200 J MG/KG 17000 17000 33200 1 7000 MF-SO-MW1 03-0810 COPPER 34600 1 34600 ' | MG/KG 19000 19000 ! 34600' 19000 BC-SO-SB8-0204A COPPER 49900 49900 J .MG/KG 30000 30000 49900' 30000

Page 1 Copper Correlation Data

BC-SO-SB1-0204B COPPER 52300 52300 J MG/KG 3900 3900 j 52300 3900 MF-SO-MW1 03-0608 ,COPPER 97900 97900 MG/KG 40000 40000 | 97900 40000

Page 2 Lead Correlation Data nsample sample no location jpara clp_res ' scr_res clp_qual scr qual i units SP-SO-MW112B-2628 MAES96 SP-SO-MW112B-2628 LEAD 2.1 1 0|J U iMG/KG MF-SO-MW104D-3234 IMAES95 MF-SO-MW104D-3234 LEAD 2.2! o j 'u IMG/KG MF-SO-MW101D-4850 MAES80 MF-SO-MW101D-4850 JLEAD 2.3, 0 UJ U MG/KG MF-SO-MW101D-4850-D MAES81 MF-SO-MW101D-4850 LEAD 2.3 i O.UJ 'U , MG/KG MF-SO-MW104D-6062 MAET04 MF-SO-MW104D-6062 LEAD 2.5, 30'J 'J IMG/KG SP-SO-MW110D-1820 MAET10 SP-SO-MW110D-1820 JLEAD 3 0|J U MG/KG MF-SO-MW101D-2830 MAES78 MF-SO-MW101D-2830 LEAD 3.1 O'UJ U MG/KG MF-SO-SB5-1416 MAEG35 MF-SO-SB5-1416 LEAD 3.3 9i U MG/KG MF-SO-MW102-4244 MAES94 MF-SO-MW 102-4244 LEAD 3.8 Ojj ;u MG/KG MF-SO-MW104D-4648 'MAET03 MF-SO-MW 1 04D-4648 LEAD 5 6 0 J U MG/KG MF-SO-SB1-0810 MAEG32 MF-SO-SB1-0810 LEAD 6 10' U MG/KG MF-SO-MW102-7880 JMAET02 MF-SO-MW 102-7880 LEAD 6.5 0>J U MG/KG MF-SO-MW102-2224 IMAES79 MF-SO-MW 102-2224 LEAD 6.7 O'J U MG/KG MF-SO-MW104D-1618 MAES91 MF-SO-MW104D-1618 LEAD 7.3 0 J U MG/KG BC-SO-SB8A-0810 MAET39 BC-SO-SB8A-0810 LEAD 12.3 0LU 'U MG/KG MF-SO-MW103-1416 MAES98 MF-SO-MW1 03-141 6 LEAD 18.2 2900 'J MG/KG BC-SO-SB9-0608 MAET35 BC-SO-SB9-0608 HEAD 20.8 39! 'J MG/KG SP-SO-SB1-0406B MAES73 SP-SO-SB1-0406B LEAD 26.6 16U MG/KG MF-SO-MW104D-0002 MAES87 MF-SO-MW104D-0002 LEAD 26.8 OU U MG/KG SP-SO-SB9-0608 MAET37 SP-SO-SB9-0608 LEAD 32 oi ,u IMG/KG SP-SO-MW113B-0810 MAET25 SP-SO-MW113B-0810 LEAD 40.1 Oi iU MG/KG SP-SO-SB5-1214 MAES83 SP-SO-SB5-1214 LEAD 52.7 0|J U | MG/KG BC-SO-MW 120-0406 MAES77 BC-SO-MW 120-0406 LEAD 55.3 61|J J MG/KG MF-SO-TP3-0405 MAEH50 MF-SO-TP3-0405 LEAD 59.8 173 MG/KG MF-SO-SB2-1416 MAEG34 MF-SO-SB2-1416 LEAD 72.5i 31 MG/KG BC-SO-SB2-1214 IMAEF93 BC-SO-SB2-1214 LEAD ! 75.9 O'J U MG/KG SP-SO-SB7-0204 MAET06 SP-SO-SB7-0204 LEAD 89.9 53 MG/KG BC-SO-SB8A-1012 JMAET40 BC-SO-SB8A-1012 LEAD 94 1 49 J MG/KG SP-SO-SB9-0810 MAET38 SP-SO-SB9-0810 LEAD 101 280 ' MG/KG SP-SO-MW1 1 1 D-081 0-D MAET22 SP-SO-MW1 11 D-081 0 LEAD 122 140' MG/KG MF-SO-MW101D-0608 MAEH58 MF-SO-MW101D-0608 LEAD 130 71 J MG/KG BC-SO-SB9-0204B IMAET34 BC-SO-SB9-0204B LEAD 137 140 MG/KG SP-SO-MW113B-0204B MAET24 SP-SO-MW113B-0204B LEAD 157 1201 MG/KG SP-SO-MW113B-0406 MAET29 SP-SO-MW113B-0406 LEAD 182 170! MG/KG SP-SO-MW111D-1012 MAET23 SP-SO-MW111D-1012 LEAD 183 130 MG/KG MF-SO-SB3-0810 MAEH53 MF-SO-SB3-0810 LEAD ^ 189 18 J MG/KG SP-SO-MW113B-0608 MAET26 SP-SO-MW113B-0608 LEAD 215 210 MG/KG MF-SO-SB3-0810-D |MAEH54 MF-SO-SB3-0810 LEAD 227 59 J MG/KG SP-SO-SB6-0608A |MAES84 SP-SO-SB6-0608A LEAD 273 270 J MG/KG MF-SO-MW103-1618 JMAETOO MF-SO-MW103-1618 LEAD 275 500 1 J MG/KG SP-SO-MW110D-0406 MAET08 SP-SO-MW110D-0406 LEAD 305 160iJ MG/KG MF-SO-SB8-0608 MAET18 MF-SO-SB8-0608 LEAD 310 530 ! i MG/KG SP-SO-MW111D-0810 MAET21 SP-SO-MW111D-0810 LEAD 354 130 'MG/KG SP-SO-MW110D-1012 IMAET13 SP-SO-MW110D-1012 LEAD 363 160 J MG/KG SP-SO-SB3-1416 MAES85 SP-SO-SB3-1416 LEAD ' 459 180 J MG/KG MF-SO-SB2-0608 MAEG33 !MF-SO-SB2-0608 LEAD 678 290 MG/KG 3C-SO-SB6-0810 MAES76 BC-SO-SBc-CSIO LEAD 946 3200 J MG/KG MF-SO-TP2-0506 MAEH49 MF-SO-TP2-0506 LEAD 1290 270 MG/KG SP-SO-SB8-OCC2 MAET33 SP-SO-SB5-0002 LEAD 1480 1100 MG/KG MF-SO-SB7-0406 MAET17 MF-SO-SB7-0406 LEAD , 1690 670 MG/KG SP-SO-MW1 12B-0810A MAES93 SP-SO-MW112B-0810A LEAD 1870 630 J 'MG/KG BC-SO-SB5-0002B MAES75 BC-SO-SB5-0002B LEAD 2460 660 J MG/KG MF-SO-SB4-1214 MAEH55 IMF-SO-SB4-1214 LEAD , 3220 200 MG/KG MF-SO-SB7-1416 MAET16 IMF-SO-SB7-1416 LEAD 3980 3000 MG/KG

Page 1 Lead Correlation Data

SP-SO-MW112B-0608 MAES92 SP-SO-MW1 12B-0608 LEAD 5390 1200 J ,MG/KG MF-SO-MW 102-0406 MAES71 MF-SO-MW 102-0406 LEAD 7400 2300 J iMG/KG MF-SO-MW102-0406-D MAES72 MF-SO-MW 102-0406 LEAD 7450 2700 J ! MG/KG MF-SO-SB6-0204 MAEH48 MF-SO-SB6-0204 LEAD 9600 6600 MG/KG SP-SO-SB4-0406 MAES86 SP-SO-SB4-0406 LEAD 11500 8200 J IMG/KG BC-SO-SB1-0608 MAES89 BC-SO-SB 1-0608 LEAD 11500 4800 J MG/KG MF-SO-SB4-0406 MAES88 MF-SO-SB4-0406 LEAD 11600 310 J IMG/KG BC-SO-SB3-0204A MAEH57 BC-SO-SB3-0204A LEAD 12000 5800 J i MG/KG SP-SO-SB2-0204B MAES82 SP-SO-SB2-0204B LEAD 13600 9100 J I MG/KG MF-SO-MW103-0810 MAES99 MF-SO-MW103-0810 LEAD 14900 6300 J IMG/KG MF-SO-MW 103-0608 MAET01 MF-SO-MW1 03-0608 LEAD 25600 7200 J ; MG/KG BC-SO-SB8-0204A MAET27 BC-SO-SB8-0204A LEAD 32400 18000 iMG/KG BC-SO-SB4-0204 MAES74 BC-SO-SB4-0204 LEAD 32900 11000 J ! MG/KG BC-SO-SB1-0204B _j MAEF91 BC-SO-SB1-0204B LEAD 32900 2100 J 'MG/KG BC-SO-SB 1-0406 MAEF92 BC-SO-SB 1-0406 LEAD 38700 16000 J IMG/KG

Page 2 Aroclor 1262 Correlation Data nsample sample no location para clp res scr res 'qual units scr qua! MF-SO-MW104D-6062 SAA687 | MF-SO-MW 104D-6062 AROCLOR-1262 18.5 100jU UG/KG U MF-SO-MW 102-2224 SAA663 MF-SO-MW 1 02-2224 AROCLOR-1262 185 100 U UG/KG U MF-SO-MW 102-7880 SAA685 MF-SO-MW 102-7880 AROCLOR-1262 "~ 19 100 U UG/KG ,U MF-SO-SB5-1416 JSA4046 MF-SO-SB5-1416 AROCLOR-1262 19 100 U UG/KG U SP-SO-MW110D-1820 ^SAA694 SP-SO-MW110D-1820 AROCLOR-1262 195 100 UJ UG/KGlU MF-SO-SB1-0810 SA4043 MF-SO-SB1-0810 AROCLOR-1262 20 100 U UG/KG 'U MF-SO-MW104D-0002 SAA671 JMF-SO-MW104D-0002 AROCLOR-1262 20 100,U UG/KG U MF-SO-MW 104D-3234 SAA678 MF-SO-MW 104D-3234 AROCLOR-1262 20' 100 U UG/KG U MF-SO-MW 1 01 D-4850 SAA664 MF-SO-MW 101 D-4850 AROCLOR-1262 20 100 U UG/KG U MF-SO-MW101D-4850-D SAA665 MF-SO-MW 101 D-4850 AROCLOR-1262 20 1 100 U UG/KG U MF-SO-MW101D-2830 SAA662 MF-SO-MW101D-2830 AROCLOR-1262 20.5 100 U UG/KG U SP-SO-MW112B-2628 SAA679 SP-SO-MW112B-2628 AROCLOR-1262 20.5 100iU iUG/KG U MF-SO-MW 102-4244 SAA677 MF-SO-MW 102-4244 'AROCLOR-1262 225 100 U UG/KG U MF-SO-MW 104D-4648 SAA686 MF-SO-MW 104D-4648 AROCLOR-1262 23.5 100,U jUG/KG U SP-SO-SB1-0406B SAA651 |SP-SO-SB1-0406B AROCLOR-1262 26 1 100|J UG/KG IU BC-SO-SB9-0608 SA9041 BC-SO-SB9-0608 AROCLOR-1262 29 100 J UG/KG U MF-SO-MW104D-1618 SAA674 MF-SO-MW104D-1618 AROCLOR-1262 31.5 100 U UG/KG U MF-SO-MW 1 03-141 6 SAA681 MF-SO-MW103-1416 AROCLOR-1262 385 100 U UG/KG U SP-SO-SB5-1214 SAA667 SP-SO-SB5-1214 AROCLOR-1262 51 100 J UG/KG U SP-SO-MW113B-0810 SA2742 SP-SO-MW113B-0810 AROCLOR-1262 58 100iJ UG/KG U BC-SO-SB8A-0810 SA2773 BC-SO-SB8A-0810 AROCLOR-1262 : eg i 100iJ IUG/KG U SP-SO-MW1 13B-0204B SA2741 SP-SO-MW11 3B-0204B AROCLOR-1262 72! 100iJ UG/KG JJ MF-SO-SB2-1416 SA4045 1MF-SO-SB2-1416 AROCLOR-1262 76' 100 J UG/KG U MF-SO-TP3-0405 SAA640 MF-SO-TP3-0405 AROCLOR-1262 79' 100 UG/KG U SP-SO-SB7-0204 SA2748 SP-SO-SB7-0204 AROCLOR-1262 90' 100J UG/KG U SP-SO-MW113B-0406 SA2746 SP-SO-MW113B-0406 AROCLOR-1262 99' 100J UG/KG U SP-SO-MW110D-0002 SAA696 JSP-SO-MW110D-0002 AROCLOR-1262 140! 100 J UG/KG U BC-SO-SB9-0204B SAA656 BC-SO-SB9-0204B i AROCLOR-1262 180 100 J UG/KG U SP-SO-SB9-0810 ,SA9043 SP-SO-SB9-0810 AROCLOR-1262 230 360 J UG/KG MF-SO-SB3-0810 ISAA652 MF-SO-SB3-0810 AROCLOR-1262 230 100 J UG/KG U SP-SO-MW110D-0406 !SAA692 ISP-SO-MW110D-0406 AROCLOR-1262 240 100 J UG/KG U SP-SO-SB6-0608A SAA668 SP-SO-SB6-0608A AROCLOR-1262 260 100 J UG/KG U MF-SO-SB4-1214 SAA654 MF-SO-SB4-1214 AROCLOR-1262 280 1 100 UG/KG U BC-SO-SB2-1214 SAA645 BC-SO-SB2-1214 AROCLOR-1262 280' 220 UG/KG MF-SO-SB3-0810-D SAA653 MF-SO-SB3-0810 AROCLOR-1262 320 100 J UG/KG U BC-SO-SB8A-1012 SA2774 BC-SO-SB8A-1012 AROCLOR-1262 330' 100 J UG/KG U SP-SO-MW11 iD-081 0-D SA273~9 SP-SO-MW1"11D-0810 " AROCLOR-1262 340 100 J UG/KG U MF-SO-SB8-0608 SA2734 MF-SO-SB8-0608 AROCLOR-1262 340 100 J UG/KG U BC-SO-MW 120-0406 |SAA661 BC-SO-MW 120-0406 AROCLOR-1262 380 100 UG/KG U SP-SO-MW111D-0810 SA2738 SP-SO-MW111D-0810 AROCLOR-1262 500 100 J UG/KG U MF-SO-MW101D-0608 SAA648 MF-SO-MW 1 01 D-0608 AROCLOR-1262 540 100 UG/KG U MF-SO-TP2-0506 SA4048 MF-SO-TP2-0506 AROCLOR-1262 550 100 UG/KG U SP-SO-SB9-0608 SA9042 SP-SO-SB9-0608 AROCLOR-1262 580 100 J UG/KG U MF-SO-SB7-0406 SA2733 | MF-SO-SB7-0406 AROCLOR-1262 650 100 J UG/KG U SP-SO-SB4-0406 |SAA670 SP-SO-SB4-0406 ' AROCLOR-1262 1100 9100 UG/KG MF-SO-SB2-0608 SA4044 MF-SO-SB2-0608 AROCLOR-1262 1500 2800 J UG/KG BC-SO-SB5-0002B SAA659 BC-SO-SB5-0002B AROCLOR-1262 2100 410 J UG/KG MF-SO-MW102-0406-D SAA650 MF-SO-MW 102-0406 AROCLOR-1262 2600" 200 UG/KG SP-SO-SB3-1416 SAA669 SP-SO-SB3-1416 AROCLOR-1262 2800 100 J "" UG/KG U MF-SO-MW 102-0406 SAA649 MF-SO-MW1 02-0406 AROCLOR-1262 2900 100 UG/KG U SP-SO-MW112B-0608 SAA675 SP-SO-MW112B-0608 AROCLOR-1262 3600 1700 J UG/KG SP-SO-SB8-0002 SAA655 SP-SO-SB8-0002 AROCLOR-1262 7700 1 1800 J UG/KG BC-SO-SB1-0204B SAA643 BC-SO-SB1-0204B AROCLOR-1262 17000 240 UG/KG MF-SO-MW 103-08 10 SAA682 MF-SO-MW103-0810 AROCLOR-1262 21000 1900 UG/KG BC-SO-SB6-0810 SAA660 BC-SO-SB6-0810 AROCLOR-1262 23000 400 UG/KG MF-SO-SB7-1416 SAA690 MF-SO-SB7-1416 AROCLOR-1262 36000 100 J* UG/KG U

Page 1 Aroclor 1262 Correlation Data

MF-SO-SB6-0204 SA4047 MF-SO-SB6-0204 AROCLOR-1262 48000 780 UG/KG BC-SO-SB3-0204A SAA647 BC-SO-SB3-0204A AROCLOR-1262 70000 1100 UG/KG BC-SO-SB4-0204 SAA658 BC-SO-SB4-0204 AROCLOR-1262 79000 2300 UG/KG BC-SO-SB1-0406 SAA644 BC-SO-SB1-0406 AROCLOR-1262 81000J 2100 JUG/KG SP-SO-SB2-0204B SAA666 SP-SO-SB2-0204B AROCLOR-1262 97000 1 12000 UG/KG ]_ BC-SO-SB8-0204A SA2744 BC-SO-SB8-0204A AROCLOR-1 262 1 230000 1 2900 J UG/KG

Page 2 Aroclor 1268 Correlation Data nsample sample no location {para >clp res'scr res clp qual scr qual 'units MF-SO-MW 102-2224 SAA663 MF-SO-MW1 02-2224 I AROCLOR-1268, 3| 200 U III lUG/KG MF-SO-MW1 02-7880 SAA685 MF-SO-MW102-7880 AROCLOR-1268 1 35i 200 U |U UG/KG MF-SO-TP3-0405 SAA640 MF-SO-TP3-0405 AROCLOR-1268 19 200 J 'U UG/KG SP-SO-SB1-0406B SAA651 SP-SO-SB1-0406B JAROCLOR-1268i 32 200 1 J |U UG/KG BC-SO-SB9-0608 SA9041 JBC-SO-SB9-0608 AROCLOR-1268! 33, 200, J ,U UG/KG MF-SO-MW103-1416 SAA681 MF-SO-MW103-1416 AROCLOR-1268 34 ! 200 'J U UG/KG MF-SO-MW104D-6062 SAA687 MF-SO-MW104D-6062 AROCLOR-1268 1 37 200 |U iU UG/KG MF-SO-SB5-1416 SA4046 MF-SO-SB5-1416 AROCLOR-12681 38 200 lU iU UG/KG SP-SO-MW110D-1820 SAA694 SP-SO-MW110D-1820 AROCLOR-1268i 39 200 |UJ U UG/KG MF-SO-SB1-0810 SA4043 MF-SO-SB1-0810 AROCLOR-1268, 40, 200 1 U U UG/KG MF-SO-MW 104D-0002 SAA671 MF-SO-MW 104D-0002 AROCLOR-1268 40 200 U U UG/KG MF-SO-MW 104D-3234 SAA678 j MF-SO-MW 104D-3234 AROCLOR-1268, 40' 200 'U 'U UG/KG MF-SO-MW101D-4850 SAA664 IMF-SO-MW101D-4850 AROCLOR-1268 40! 200 1 U U UG/KG MF-SO-MW 1 01 D-4850-D SAA665 I MF-SO-MW 1 01 D-4850 AROCLOR-1268 40 200 'U U UG/KG MF-SO-MW 1 01 D-2830 SAA662 MF-SO-MW101 D-2830 AROCLOR-1268 41 200 |U ,U UG/KG SP-SO-MW112B-2628 SAA679 SP-SO-MW112B-2628 AROCLOR-1268. 41 ' 200 iU U UG/KG MF-SO-MW 102-4244 SAA677 MF-SO-MW1 02-4244 AROCLOR-12681 45 200 IU |U UG/KG MF-SO-MW 104D-4648 SAA686 MF-SO-MW 104D-4648 AROCLOR-1268 47 200 U ,U I UG/KG SP-SO-SB6-0608A SAA668 SP-SO-SB6-0608A AROCLOR-12681 51 200 J JU UG/KG MF-SO-MW104D-1618 SAA674 MF-SO-MW104D-1618 AROCLOR-1268 63 200 |U U LUG/KG SP-SO-MW113B-0204B SA2741 SP-SO-MW1 13B-0204B AROCLOR-1268 1 65 1 200 |J JU UG/KG SP-SO-MW113B-0810 SA2742 SP-SO-MW113B-0810 AROCLOR-1268J 78 200 1 J 'U UG/KG BC-SO-SB8A-0810 SA2773 BC-SO-SB8A-0810 AROCLOR-1268 1 82 200 |j |U UG/KG SP-SO-SB5-1214 SAA667 SP-SO-SB5-1214 AROCLOR-1268 84 200 1 ,U UG/KG MF-SO-SB2-1416 SA4045 MF-SO-SB2-1416 [AROCLOR-1268 1 92 200 |U UG/KG BC-SO-MW1 20-0406 SAA661 BC-SO-MW1 20-0406 AROCLOR-12681 120i 200 J U UG/KG SP-SO-SB7-0204 SA2748 SP-SO-SB7-0204 AROCLOR-1268 130 200 U U UG/KG BC-SO-SB9-0204B 'SAA656 BC-SO-SB9-0204B AROCLOR-1268 130 200 J U UG/KG SP-SO-MW113B-0406 SA2746 SP-SO-MW113B-0406 iAROCLOR-1268 150 200 J U UG/KG SP-SO-MW110D-0002 SAA696 SP-SO-MW110D-0002 lAROCLOR-1268 200 210 J UG/KG MF-SO-SB3-0810 SAA652 MF-SO-SB3-0810 AROCLOR-1268 250 200 J U UG/KG SP-SO-SB9-0608 SA9042 SP-SO-SB9-0608 AROCLOR-12681 260 1 200 J 'U UG/KG MF-SO-SB4-1214 SAA654 MF-SO-SB4-1214 AROCLOR-1268 260 200 U UG/KG SP-SO-MW110D-0406 SAA692 SP-SO-MW110D-0406 AROCLOR-1268 270 200 U JU UG/KG MF-SO-SB7-0406 SA2733 MF-SO-SB7-0406 AROCLOR-1268 340 200 J U UG/KG BC-SO-SB2-1214 ;SAA645 BC-SO-SB2-1214 AROCLOR-1268 340 200 ,U UG/KG MF-SO-SB3-0810-D ISAA653 IMF-SO-SB3-0810 lAROCLOR-1268 350 200 J U UG/KG SP-SO-SB9-0810 SA9043 SP-SO-SB9-0810 AROCLOR-1268 400 380 J UG/KG SP-SO-MW111D-0810 SA2738 SP-SO-MW111D-0810 AROCLOR-1268 420 200 J U UG/KG BC-SO-SB8A-1012 ISA2774 BC-SO-SB8A-1012 AROCLOR-1268 490 200 J UG/KG MF-SO-SB8-0608 SA2734 |MF-SO-SB8-0608 AROCLOR-1268 490 200 J U UG/KG MF-SO-TP2-0506 SA4048 |M F-SO-TP2-0506 AROCLOR-1268 500 200 U UG/KG MF-SO-MW101D-0608 1SAA648 MF-SO-MW101D-0608 AROCLOR-1268 620 200 U UG/KG SP-SO-MW111D-0810-D |SA2739 SP-SO-MW111D-0810 AROCLOR-1268 760 200 J U UG/KG MF-SO-SB2-0608 SA4044 MF-SO-SB2-0608 AROCLOR-1268 1200 1600 UG/KG SP-SO-SB4-0406 SAA670 SP-SO-SB4-0406 ' AROCLOR-1268 1600 3600 UG/KG MF-SO-MW 102-0406-D SAA650 MF-SO-MW1 02-0406 AROCLOR-1268 1600 200 U UG/KG MF-SO-MW 102-0406 SAA649 I MF-SO-MW 102-0406 AROCLOR-1268 1800 200 U UG/KG SP-SO-SB3-1416 SAA669 SP-SO-SB3-1416 AROCLOR-1268 2400 200 U UG/KG SP-SO-MW112B-0608 SAA675 'SP-SO-MW1 12B-0608 AROCLOR-1268 2400 780 UG/KG BC-SO-SB5-0002B SAA659 'BC-SO-SB5-0002B ' AROCLOR-1268 3800 290 UG/KG MF-SO-MW1 03-0810 SAA682 MF-SO-MW1 03-0810 AROCLOR-1268 9300 640 UG/KG SP-SO-SB8-0002 SAA655 SP-SO-SB8-0002 i AROCLOR-1268 11000 1700 J UG/KG BC-SO-SB1-0204B SAA643 BC-SO-SB1-0204B AROCLOR-1268 20000 200 U UG/KG BC-SO-SB6-0810 SAA660 BC-SO-SB6-0810 AROCLOR-1268 41000 1000 UG/KG BC-SO-SB3-0204A SAA647 BC-SO-SB3-0204A AROCLOR-1268 44000 340 UG/KG MF-SO-SB6-0204 SA4047 MF-SO-SB6-0204 AROCLOR-1268 49000 580 UG/KG MF-SO-SB7-1416 SAA690 MF-SO-SB7-1416 AROCLOR-1268 50000 200 J * U UG/KG

Page 1 Aroclor 1268 Correlation Data

SP-SO-SB2-0204B SAA666 SP-SO-SB2-0204B | AROCLOR- 1268 57000 2200 1 UG/KG BC-SO-SB4-0204 SAA658 BC-SO-SB4-0204 AROCLOR-1268 93000 1800 1 UG/KG BC-SO-SB1-0406 SAA644 BC-SO-SB 1-0406 AROCLOR-1268 100000 18001 UG/KG BC-SO-SB8-0204A SA2744 BC-SO-SB8-0204A AROCLOR-1268! 300000 1 1500^J i UG/KG

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Variable 1 Variable 2 Mean 6700.495385 3549.830769 Variance 261525929.3 59073767.02 Observations 65 65 Pooled Variance 160299848.2 Hypothesized Mean Difference 0 df 128 tStat 1.418656658 P(T<=t) one-tail 0.079214719 t Critical one-tail 1.656844688 P(T<=t) two-tail 0.158429439 t Critical two-tail 1.978669388 Lead t-Test Output t-Test: Two-Sample Assuming Equal Variances

Variable 1 Variable 2 Mean 4199.56087 1714.043478 Variance 79076275.86 13087412.01 Observations 69 69 Pooled Variance 46081843.94 Hypothesized Mean Difference 0 df 136 tStat 2.150608854 P(T<=t) one-tail 0.016637564 t Critical one-tail 1.656135282 P(T<=t) two-tail 0.033275128 t Critical two-tail 1.977559805

Page 1 Appendix F.2

Summary of RSRs Developed by B&RE for New London (1998) Brown & Root Environmental

C-49-12-7-188

December 23. 1997

Brown & Root Environmental Project Number 7237

Mr. Mark Lewis Connecticut Department of Environmental Protection Water Management Bureau 3ermitting, Enforcement, and Remediation Division -ederal Remediation Program T9 Elm Street Hartford. Connecticut 06106-5127

Reference: CLEAN Contract No. N62472-90-D-1298 Contract Task Order No. 0260

Subject: Calculated CTDEP Remediation Standards Lower Subase Remedial Investigation Naval Submarine Base - New London, Groton, Connecticut

Dear Mr. Lewis:

:n preparation of the Lower Subase Remedial Investigation (Rl) Report. Brown & Root Environmental has calculated Remediation Standards following the State of Connecticut Remediation Standard Regulations of January 1996. Stanaaras were developed for ail cnemicals that were analyzed for during the Rl sampling and analysis program that did not have previously established CTDEP standards. The intent of this memo is to identify the sources of the standards to be used in the Rl Report and to identify those values which have been developed by B&R Environmental using the State guidance.

Background information and the calculated Remediation Stanaaras are provided in Table " and Table 2. respectively, which are enclosed. Table 1 summanzes the basis for the chemicai­ specific remediation standards (i.e., promulgated, calculated, or calculated using a surrogated to be included in the Rl. The calculatea soil Direct Exposure and Pollutant Mobility standards. as well as the Grounawater Stanaard. are provided in Table 2.

;t should be noted that pollutant mobility and groundwater stanaards for GA classified grounawater are proviaed in Table 2 for completeness. The groundwater at the Lower Subase is classifies as G3. therefore standaras applicable to GB classified grounawater will be empnasizea in the Lower Subase Rl Report. Mr. Mark Lewis Connecticut Department of Environmental Protection December 23, 1997 - Page 2

B&R Environmental intends on using these critena. as well as Region III RBCs. as part of the human health risk assessment for the Lower Subase Rl to screen for chemicals of potential concern. Therefore. B&R Environmental, on the behalf of the United States Navy, requests that the CTDEP review and approve the standards in Table 2. It is hoped that pnor approval of the criteria will alleviate unnecessary revisions to the Rl Report in the future and expeaite any additional nsk-related work required by the State (i.e., application for use of alternative critena).

Due to the current time constraints for prepanng the Lower Subase Rl, it is requested that the CTDEP complete their review by no later than January 16, 1997. If you have any questions regarding the information provided in the tables or the schedule for the review please contact Mr. Mark Evans at (610) 595-0567 (ext. 162) or me at (412) 921-8244.

Very truly yours.

^ Rich; P.E. Project Manager

Endosure(s) c: Mr. Mark Evans, NORTHDIV Mr. Richard Conant, NSB-NLON Environmental Ms. Karen Smecker, B&R Environmental File: CTO 0260 TABLE 1

SOURCE OF CONNECTICUT REMEDIATION STANDARDS CTO 260 LOWER SUBASE Rl NEW LONDON. GROTON, CONNECTICUT PAGE 1 OF 4

Basis of V alue to be Used in Rl Report | Chemical CAS Chemical Promulgated Calculated Surrogate 1 12 Number Fraction Value' ' Value ' Calculated [ Value"1 I Acenaohthene 33329 SVOC X I Acenaphthylene 208968 SVOC X I Anthracene 120127 SVOC X 1 Acetone 67641 voc X 1 Aldrin 309002 PEST X («) i«> Aluminum 7429905 INORG (*) Antimony 7440360 INORG X _ Arsenic 7440382 INORG X \ Barium 7440393 INORG X \ Benzene 71432 VOC X \ Benzia (anthracene 56553 SVOC X 1 Benzo(b)fluoranthene 205992 SVOC X I Benzol k)fluoranthene 207089 SVOC X I Benzo(g,h,i)perylene 191242 SVOC X (naphthalene) Benzota)pyrene 50328 SVOC X 1 Beryllium 744O417 INORG X BCH (alpha-) 319846 PEST X BCH (beta-) 319857 PEST X BCH (delta-) 319868 PEST X (alpha-BHC) BCH (gamma-: lindane) 58899 PEST X Bis(2-chloroethoxy)methane 111911 SVOC til |5) (5) Bis(2-chloroethyl)ether 111444 SVOC X Bis(2-ethylhexyl)phthalate 117817 SVOC X Bromocnloromethane 74975 VOC (chloromethane* ) Bromooichloromethane 75274 voc X Bromoform 75252 VOC X Bromomethane 74839 VOC X 4-Bromophenyl-phenylether 101553 SVOC X 2-Butanone 78933 VOC X Butylbenzylphthalate 85687 SVOC X Cadmium 744O439 INORG X Calcium 7440702 INORG (6) '.6> ,6, Carbazole 86748 SVOC X Carbon disulfide 75150 VOC x Carbon tetrachtoride 56235 VOC X 1 Chloraane (alpha-) 57749 PEST X1" Chlordane (gamma-) 57749 PEST X1" 4-Chloroaniline 106478 SVOC X 1 Chlorobenzene 108907 VOC X Chloroaibromomethane 124481 VOC X 1 Chloroethane 75003 VOC x 1 Chloroform 67663 VOC x 1 Chloromethane 74873 voc x 1 TABLE 1

SOURCE OF COHNECT1CUT REMEDIATION STANDARDS CTO 260 LOWER SUBASE Rl NEW LONDON, GROTON, CONNECTICUT PAGE 2 OF 4

Basis of Value to be Used in Rl Report Chemical CAS Chemical Promulgated Calculated Surrogate 12 Number Fraction alue<" Value ' Calculated Value'31 4-Chloro-3-methylphenol 59507 SVOC X (3-methylphenot) 2-Chloronaohthalene 91587 SVOC X 2-Chlorophenol 95578 SVOC X 4-Chlorophenyl-phenyletrter 7005723 SVOC X (4-Bromophenyl­ phenylether) Chromium (total) INORG X"" Chrvsene 218019 I SVOC X Cobalt 7440484 I INORG X Cooper 7440508 I INORG (.*) I*) («) 4,4'-ODD 72548 | PEST X 4,4'-DDE 72559 PEST X 4,4'-DDT 50293 PEST X Dibenzofuran 132649 SVOC X Oibenzia.h)anthrac8ne 53703 SVOC X 1 ,2-Dibromo-3-chloropropanc 96128 VOC X 1 ,2-Oibromoethane 106934 VOC X 1 ,2-Dichlorobenzene 95501 voc/svoc X 1 ,3-Dichlorobenzene 541731 voc/svoc X 1 ,4-Oichlorobenzene 106467 voc/svoc X 3.3'-Oichlorobenzidine 91941 SVOC X 1,1-Oichloroethane 75343 VOC X 1 ,2-Oichloroethane 107062 VOC X 1,1-Dichlorocthene 75354 VOC X 1 .2-Oichloroethcne (cis-1 1 56592 VOC X 1 .2-Dichloroethene (trans-) 156605 VOC X 1 1 ,2-Oichloroethene (total) 1 56605 VOC X 2.4-Oichlorophenol 120832 SVOC X 1 .2-Dichloropropane 78875 VOC X 1 ,3-Oichloropropene (cis-) 542756 VOC X 1 ,3-Oichloroprooene (trans-) 542756 VOC X Oieldnn 60571 PEST X Diethyl pnthalate 34662 SVOC X 2,4-Oimelhylphenol 105679 SVOC X Dimetrwlphthalate 131113 I SVOC X Di-n-butylphthalate 84742 SVOC X D'wi-octylphthalate 117840 SVOC X I 4,6-Dinitro-2-metriylpnenol 534521 SVOC X 2.4-Dinitroohenol 51285 SVOC X 2,4-Dinitrotoluene 121142 SVOC X 2,6-Oinitrotoluene 606202 SVOC X Endosulfan 1 115297 PEST X'9' Endosulfan II 115297 PEST X(i) Endosulfan sulfate 1031078 PEST X (endosuifan) TABLE 1

SOURCE OF CONNECTICUT REMEDIATION STANDARDS CTO 260 LOWER SUBASE Rl NEW LONDON, GROTON, CONNECTICUT PAGE 3 OF 4

Basis of Value to be Used in RTRtoan [ Chemical CAS Chemical Promulgated Calculated Surrogate Number 1 121 Fraction Value' ' Value Calculated 31 bndnn ~ Value' 775nn rta 1 X • Endnn aldehyde 7421363 PEST X (endrirO Endnn ketone 53494705 PEST Ethylbenzene (endrin) 100414 voc X Muoranthene 206440 I SVOC X I Fluorene 86737 X Heptacnlor r~ svoc 76448 1 PEST X Heptacnior epoxiae 1024573 1 PEST X •—• Hexacniorobenzene 118741 ! svoc X Hexacnlorobutaaiene 87683 1 SVOC X Hexacniorocyctopentadiene 77474 ! SVOC X Hexacnloroetnane 67721 svoc X ——————. 2-Hexanone" voc X lndeno< 1 ,2.3-cd)pyrene •—• — • 193395 svoc X Iron 7438896 INORG («) 1*) i*5 ' Isophorone SVOC X Lead | 7439291 INORG X Magnesium 7439954 INORG (6) 10) 7439965 INORG X Mercury 7439976 INORG X Methoxvcftlor ~ " I 72435 PEST X Methylene cnionae 75092 VOC x 91576 SVOC x 4-Methvl-2-pemanone 108101 VOC 1 2-Methvipnenoi 95487 106445 svoc 91203 SVOC | 7440020 INORG 88744 SVOC 99092 svoc 1 x 1 svoc 98953 SVOC | 2-Nitrophenol 88755 svoc X (4-nitrophenoO 100027 SVOC 1 [ x N-Nitrosooiphenviamme N-Nitrosoai-n-prppylamme 621647 svoc 1 2.2'-Oxvbis(1-chloroDropane) 108601 | svoc i lS( x i_ Phenantnrene 85018 svoc X (naphthalene) Phenol 108952 I SVOC | X | | Potassium 7440097) INORG | "" ^6) " | 1 TABLE 1

SOURCE OF CONNECTICUT REMEDIATION STANDARDS CTO 260 LOWER SUBASE Rl NEW LONDON, GROTON, CONNECTICUT PAGE 4 OF 4

Basis of V alue to be Used m Rl Report i Chemical CAS Chemical Promulgated Calculated Surrogate 11 121 Number Fraction Value ' Value Calculated Value131 Selenium 7782492 INORG X Silver 7440224 INORG X 16) Sodium 7440235 INORG ..) Styrene 100425 VOC X 1 ,1 ,2.2-Tetracnloroethane 79345 VOC X Tetracnloroethylene 127184 VOC X Thallium 6533739 INORG X Toluene 108883 VOC X Toxaphene 8001352 PEST X 1 2,4-Tnchlorobenzene 120821 svoc X 1.1.1 -Tnchloroethane 71556 VOC X 1 .1 ,2-Tncnloroethane 79005 VOC X Tnchioroetnylene L 79016 VOC X 2,4.5-Tnctilorophenol 95954 svoc X 2.4,6-Tnchlorophenol 88062 svoc X Vanadium 7440622 INORG X Vinyl chlonde 75014 VOC X Xylene (total) 1330207 VOC X Zinc 744O666 INORG X

INORG Inorganic PEST Pesticide SVOC Semrvolatile organic compound VOC Volatile organic compound

1 State of Connecticut Remediation Standard Regulations. Section 22a-133k (January 19961 2 Published toxicity cntena is available Toxicity criteria from the current USEPA Region ill Risk-Based Concentration Table (October 22. 1997) will be used to calculate a value using the methodology presented in the State guidance (January 1996). 3 No toxicity cntena is available. Toxicity cntena for a similarly structured chemical (noted in parentheses) will be used to calculate a value. 4 Region I does not advocate a quantitative evaluation of this chemical. Exposure to this chemical will be addressed in a qualitative fashion 5 No promulgated value or published toxiaty cntena are available. A similarly structured chemical with published toxicity cntena could not be identified. Exposure to this chemical will be aodressed in a qualitative fashion 6 Chemical is an essential nutnent 7 Value for chlordane is used. 8 Value for hexavalent chromium is used for conservative purposes. 9 Value for endosuifan is used. TABLE 1

SOURCE OF CONNECTICUT REMEDIATION STANDARDS CTO 260 LOWER SUBASE Rl NEW LONDON, GROTON, CONNECTICUT PAGE 1 OF 4

Basis of V alue to be Used in Rl Report Chemical CAS Chemical Promulgated Calculated Surrogate 1 21 Number Fraction Value " Value' Calculated Value1" Acenaohthene 83329 svoc X Acenaorithylene 208968 svoc X Anthracene 120127 svoc X Acetone 67641 voc X Aldnn 309002 PEST X t*> Aluminum 7429905 INORG t«l i<) Antimony 7440360 INORG X Arsenic 7440382 INORG X Banum 7440393 INORG X Benzene 71432 VOC X Benzia)anthracene 56553 SVOC X i Benzol b)fluorantnene 205992 SVOC X ! Benzol lOfluoranthene 207089 SVOC X Benzo(g,n,i)peryiene 191242 SVOC X fpvrene) Benzola tpyrene 50328 SVOC X Beryllium 7440417 INORG X BCH (aloha-) 319846 PEST X BCH fbeta-1 319857 PEST X BCH (delta-) 319868 PEST X (alcha-SHCi BCH (gamma- Lindane) 58899 PEST X Bis(2-chloroethoxv)methane 111911 SVOC (5) (5) |S) Bis(2-chloroethv1)ether 111444 svoc X Bis<2-ethvlhexvODhtrialate 117817 svoc X Bromocnloromethane 74975 voc X (bromoaichloro­ methanei Sromoaichloromethane 75274 voc X Bromoform 75252 voc X Bromomethane 74839 voc X 4-Bromoonenvi-ohenviether 101553 svoc X 2-Butanone 78933 voc X ButvlbenzvlDhthalate 85687 svoc X Cadmium 7440439 INORG X |S) IS) in Calcium 7440702 INORG Carbazoie 86748 SVOC X Carbon aisulfide 75150 voc X Carbon tetrachlonae 56235 voc X Chloraane i aloha-) 57749 PEST x,7> Chloraane loamma-i 57749 PEST x,7) 4-Chloroaniline 106478 SVOC X Chlorooenzene 108907 voc X Chloroaibromo methane 124481 voc X Chloroethane 75003 voc X Chloroform 67663 voc X Chloromethane 74873 voc X 4-Chloro-3-methvlohenoi £9507 svoc '-' 5) 'SI

Revrsion 1 - 3/20/98 TABLE 1

SOURCE OF CONNECTICUT REMEDIATION STANDARDS CTO 260 LOWER SUBASE Rl NEW LONDON, GROTON, CONNECTICUT PAGE 2 OF 4

Basis of Value to be Used in Rl Report Chemical CAS Chemical Promulgated Calculated Surrogate Number . Fraction Value111 Value'2' Calculated Value'31 2-Chloronaphthalene 91587 svoc X 2-Chloroofienol 95578 svoc X 4-Chloropfienyl-pnenyiether 7005723 svoc X (4-Bromophenyt­ phenyl ether) Chromium (total) INORG X" Chrysene 218019 SVOC X Cobalt 7440484 INORG X Copper 7440508 INORG I*) t«) i«) 4,4'-ODD 72548 PEST X 4.4'-DDE 72559 PEST X 4.4'-DDT 50293 PEST X Dibenzofuran 132649 SVOC X Dibenzia.hlanthracene 53703 svoc X 1 ,2-Cibromo-3-chloroDrooane 96128 voc X 1 ,2-Dibromoethane 106934 voc X 1 ,2-Dichlorobenzene 95501 voc/svoc X 1 ,3-Oichlorobenzene 541731 voc/svoc X 1 1 .4-Oichlorobenzene 106467 voc/svoc X 3,3'-Dichlorobenrioine 91941 svoc X 1,1-Dichloroethane 75343 voc X 1,2-Dichloroethane 107062 voc X 1 , 1 -Dichloroetnene 75354 voc X 1.2-Dichloroethenc (cis-1 1 56592 voc X 1.2-Dichloroetnene (trans-) 1 56605 voc X 1.2-Dichloroethene (total! 1 56605 voc X 2.4-DicnioroDnenoi 120832 svoc X 1 .2-Dichloroorooane 78875 voc X 1.3-OichlorooroDene icis-) 542756 voc X 1.3-Dichloroprooene itrans-i 542756 voc X Dieldnn 60571 PEST X Diethvl phthalate 84662 svoc X 2.4-Dimethylphenol 105679 svoc X Dimethylphthalate 131113 svoc X Oi-n-butylphthalate 84742 svoc X Di-n-octvlDhthalate 117840 svoc X 4 6-Oinrtro-2-metnviphenoi 534521 svoc X 2.4-Dinitrophenol 51285 svoc X 2.4-Dinrtrotoluene 121142 svoc X 2.6-Dinrtrotoluene 606202 svoc X Endosulfan 1 115297 PEST x« Endosurfan II 115297 PEST X131 Endosurfan surfate 1031078 PEST X (endosulfan) Enann 72208 PEST X Enann aiaefiyae 7421363 PEST X (endnn) Enarm Ketone 53494705 PEST X (endnn)

Revision 1 - 3/20/ TABLE 1

SOURCE OF CONNECTICUT REMEDIATION STANDARDS CTO 260 LOWER SUBASE Rl NEW LONDON, GROTON, CONNECTICUT PAGE 3 OF 4

Basis of Value to be Used in Rl Reoort Chemical CAS Chemical Promulgated Calculated Surrogate 111 121 Number Fraction Value Value Calculated Value'3' 100414 VOC X Fluoraruhene 206440 SVOC X 36737 SVOC X 76448 PEST X Heotachlor epoxioe 1024573 PEST X Hexachlorobenzene 118741 SVOC X 87683 SVOC X 77474 SVOC x 67721 SVOC X 73663715 VOC X IndenoM 2.3-cd)Dyrene 193395 SVOC X 7439896 INORG i«> 78591 SVOC X Lead 7439291 INORG X Maanesium 7439954 INORG IS) <«) (S> 7439965 INORG X Mercurv 7439976 INORG X 72435 PEST X Methviene cnionde 75092 VOC X 2-MethvlnaDhthalene 91576 SVOC X 108101 VOC X 2-Methvtohenol 95487 SVOC X 4-MethvlDhenol 106445 SVOC X 91203 SVOC X Nickel 7440020 INORG X 38744 SVOC X 99092 SVOC x --Nrtroaninne 100016 SVOC X Nrtrooenzene 98953 SVOC X 2-Nitrooneno! 88755 SVOC X (4-nrtroDhenoO 4-NrtroDnenol 1 00027 SVOC 1 X 86306 SVOC X N-Nrtrosoai-n-DroDviamine 621647 SVOC X 2.2 -Oxvcisd-chlcroDrooane) 108601 SVOC i5) IS) Fentacnloroohenol 87865 SVOC X SVOC I X Phenoi 10895? 9VOr X 16) Potassium 7440097 INORG 16] (15) Pvrene | 129000 SVOC I X

Silver | 7440224 INORG X I Sodium 7440235 INORG .6) (6) ;6) Styrene 100425 VOC x 7 1.1 2.2-Tetracnioroethane 9345 VOC X i etracnioroethviene 127184 I VOC X i hallium 5533739 iNORG I X oiuene | '08883 ,CC ' oxaonene 8001352 =£ST I .',

Revision 1 - 3/20/S8 TABLE 1

SOURCE OF CONNECTICUT REMEDIATION STANDARDS CTO 260 LOWER SUBASE RI NEW LONDON, GROTON, CONNECTICUT PAGE 4 OF 4

Basis of Value to be Used in RI Report Chemical CAS Chemical Promulgated Calculated Sur -gate 2 Number Fraction Value111 Value' ' Calc.tated Vaiue13' 1 ,2.4-Tnchlorobenzene 120821 svoc X 1,1,1 -Tnchloroethane 71556 voc X 1 , 1 ,2-Tnchloroethane 79005 voc X Tnchloroethyjene 79016 voc X 2,4, 5-Tnchlorophenoi 95954 svoc X 2,4,6-Tnchloroohenol 68062 svoc X Vanaaium 7440622 INORG X Vmyt chlonde 75014 VOC X Xytene (total) 1330207 voc X Zinc 7440666 INORG X

INORG Inorganic PEST Pesticide SVOC Semivolatile organic compound VOC Volatile organic compound

1 State of Connecticut Remediation Standard Regulations, Section 22a-133k (January 1996) 2 Published toxicrty cntena is available. Toxicrty criteria from the current USEPA Region III Risk-Based Concentration Table (October 22, 1997) will be used to calculate a value using the methodology presented in the State guidance (January 1996). 3 No toxicrty cntena is available. Toxicrty cmena for a similarly structured chemical (noted in parentheses) will be used to calculate a value. 4 Region I does not advocate a quantitative evaluation of this chemical. Exposure to this chemical will be addressed in a qualitative fashion 5 No promulgated value or published toxicrty cntena are available. A similarly structured chemical with published toxicrty cntena could not be identified Exposure to this chemical will be addressed in a qualitative fashion. 6 Chemical is an essential nutrient. 7 Value for chlordane is used. 8 Value for hexavalent chromium is used for conservative purposes 9 Value for endosulfan is used.

Revision 1 - 3,20/9 £ 1

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A Division ol Halliburton NUS Corooranon C-49-03-8-156

March 20, 1998

Brown & Root Environmental Project Number 7237

Mr. Mark Lewis Connecticut Department of Environmental Protection Water Management Bureau Permitting, Enforcement, and Remediation Division " -~ Federal Remediation Program 79 Elm Street Hartford, Connecticut 06106-5127

Reference: CLEAN Contract No. N62472-90-D-1298 Contract Task Order No. 0260

Subject: Responses to CTDEP's Comments on Calculated Remediation Standards Lower Subase Remedial Investigation Naval Submarine Base - New London, Groton, Connecticut

Dear Mr. Lewis:

Brown & Root (B&R) Environmental and the Navy received your February 27, 1998 comment letter regarding the Remediation Standards that were calculated for use in the Lower Subase Remedial Investigation. Responses to CTDEP's comments have been prepared and the appropnate revisions have been made to Tables 1 and 2, which were previously enclosed in B&R Environmental^ Decemoer 23. 1997 letter. B&R Environmental, on the behalf of the United States Navy, Northern Division Facilities Engmeenng Command and Naval Submarine Base - New London, has enclosed the Navys responses to CTDEP's comments and the revised tables for your review and approval.

If you have any questions regarding the responses or the information provided in the revised tables, please contact Mr. Mark Evans at (610) 595-0567 (ext. 162) or me at (412) 921-8244 It is anticipated that any remaining issues can be resolved during a conference call.

Very truly yours. //

Project Manager

Enclosure(s) c: Mr. Roger Boucher, NORTHDIV (letter only) Mr. Mark Evans, NORTHDIV Mr. Andy Stackpole, NSB-NLON Environmental Mr. John Trepanowski, B&R Environmental Mr. Daryl Hutson, B&R Environmental (letter only) Ms. Karen Smecker, B&R Environmental File: CTO 0260 RESPONSES TO CTDEP'S COMMENTS (2/27/98) ON THE CALCULATED CTDEP REMEDIATION STANDARDS (12/23/97) CTO 260 - LOWER SUBASE REMEDIAL INVESTIGATION NAVAL SUBMARINE BASE-NEW LONDON, GROTON, CONNECTICUT MARCH 20, 1998

I. SURROGATE CHEMICALS USED TO SUPPLY TOXICITY VALUES

Comment;

1. Th e Navy has used naphthalene as a surrogate to represent the toxicity of benzo(g,h,l)perylene. As noted in Dr. Ginsberg's memorandum, pyrene (RfD 0.03 mg/kg/d) is a more appropriate surrogate. The RfD for naphthalene has been withdrawn from IRIS. Please recalculate the direct exposure, pollutant mobility, and ground water protection criteria for benzo(g,h,i)perylene using this approach. This approach is appropriate for a screening level risk assessment. However, the uncertainties involved with this approach should be acknowledged if these two chemicals are found to be major risk drivers at the site.

Response:

The direct exposure, pollutant mobility, and groundwater protection criteria for benzo(g,h,i)perylene will be recalculated using pyrene as a surrogate. Benzo(g,h,i)perylene was detected in soil and groundwater at the Lower Subase but was not found to be a major risk driver at any of the zones that were evaluated in the risk assessment. Benzo(g,h,i)perylene was only identified as a COC in groundwater at Zone 4 where it was detected in one sample at a concentration exceeding the State's Ambient Water Quality Criteria (AWQC) for the protection of human health. Consequently, this does not have any impact on the human health nsk assessment.

Comment:

2. It is unclear why the Navy calculated criteria for phenanthrene since the regulations list direct exposure, pollutant mobility, and groundwater protection criteria for this compound. Please use the criteria listed in the Regulations for this compound. The Navy should either withdraw their request for approval of criteria for phenanthrene, or, if the Navy is requesting approval of alternative criteria for this compound under the Regulations, the Navy should so state.

Response

The Navy retracts its request for approval of cntena for phenanthrene. The promulgated criteria for phenanthrene were used m the selection of COCs in the human health risk assessment Consequently, this does not have any impact on the human health risk assessment.

1 of 4 Comment;

3. Bromodichloromethane should be used as a surrogate for bromochlorom*"hane Please use the criteria calculated for bromodichloromethane in place of those • -ul using chloromethane as a surrogate.

Response:

Bromodichloromethane will be used as a surrogate for mochloromethane. Bromodichloromethane was not detected in soil and groundwater samples. ;r any of the zones evaluated in the human health risk assessment, consequently this does not have any impact on the analysis.

Comment:

4. The Navy's proposal to use 3-methylphenol as a surrogate for 4-chloro-3-methylphenol is not appropriate, due to structural differences between the two compounds. The use of a qualitative risk assessment would be acceptable assuming that concentrations of this chemical do not exceed the low part-per-billion range. Please see Dr. Ginsberg's comments for additional details.

Response:

No criteria will be developed for 4-chloro-3-methylphenol. Instead, as suggested, 4-chloro-3­ methylphenol will be evaluated qualitatively. 4-Chloro-3-methylphenol was only detected in one soil sample at the Lower Subase and at a low concentration (34 ppb), consequently, this does not have any impact on the human health risk assessment.

II. INCORRECT OR UNSUPPORTED POTENCY VALUES

Comment:

5. Several of the CSFs or RfDs used by the Navy appeared to be incorrect, based on a comparison to the values listed in the EPA Region III Risk Based Concentrations table, IRIS, or HEAST. Please recalculate the direct exposure, pollutant mobility, and ground water protection criteria using correct values for total 1,2-dichloroethene. Please assume that this value pertains to the mixture of c/s and trans isomers. The RfD for the mixture should be 9E-3 mg/kg/d.

Response:

The direct exposure, pollutant mobility, and groundwater protection criteria for total 1.2­ dichloroethene will be recalculated using an oral reference dose of 9E-3 mg/kg/day. This revision does not impact the human health risk assessment since all detected concentrations of total 1.2-dichloroethene are less than the recalculated criteria.

2 of 4 Comment:

6. The Department was unable to verify the potency factors listed by the Navy for several chemicals. Please either provide references to support the listed potency factors, or derive criteria using acceptable surrogates for the following compounds: chloroethane, 4,6-dinrtro-2-methylphenol, 2-hexanone, and 2-methylnaphthalene. Please note that naphthalene is not an appropriate surrogate for 2-methylnaphthalene as the RfD for naphthalene has been withdrawn from IRIS. Please refer to Dr. Ginsberg's memo for additional guidance.

Response: The toxictty criteria for chloroethane, 4,6-dinitro-2-methylphenoi, 2-hexanone,. and 2­ methylnaphthalene were obtained from the current U.S. EPA Region III Risk-based Concentration (RBC) Table dated October 22, 1997. The RBC table crtes EPA's National Center for Environmental Assessment (NCEA) as the source for the values for chloroethane, 4,6-dinitro­ 2-methylphenol, and 2-methylnaphthalene. Although not cited in the RBC table, EPA Region III stated in telephone call on March 12, 1998, that NCEA is also the source for the toxicity crrtena for 2-hexanone. Therefore, there are no changes necessary to the proposed values.

Comment:

7. The Department was unable to verify the RfD listed by the Navy for 4-nitrophenol (8.00E-3 mg/kg/d). Please either provide a reference for the listed value, or use the default RfD currently listed in the RBC tables (6.2E-2 mg/kg/d).

Response:

The current RBC table lists 8.00E-3 mg/kg/day as the oral RfD for 4-nitrophenol and cites EPA's NCEA as the source for the value. The value of 6.2E-2 mg/kg/day was listed in the previous, outdated version of the RBC table. Therefore, there are no changes necessary to the proposed cntena.

III. POLLUTANT MOBILITY CRITERIA FOR METALS

Comment:

8. The ground water protection criterion for cobalt was calculated correctly by the Navy. However, the approach used by the Navy in calculating pollutant mobility criteria for cobalt is unacceptable. Rather than using the calculated ground water protection criterion (420 ^g/l) to establish a pollutant mobility criterion for cobalt, the Navy used the EPA Region III Risk Based Criteria for tap water (2,200 ^g/L) as the GAA/GA pollutant mobility criterion. This approach is less conservative than using the calculated ground water protection criterion. The correct pollutant mobility criteria for cobalt, based on the groundwater protection criteria calculated by the Navy, are 420 ng/L for a GAA/GA area, and 4,200 ng/L for a GB area (measurement by TCLP or SPLP).

3 Of 4 Response:

The pollutant mobility criteria for cobatt will be changed to 420 ^g/L for a GAA/GA area and 4,200 (AQ/L for a GB area. This revision has no impact on the human health risk assessment because of the following reasons: (1) none of the histoncal soil samples that were analyzed by TCLP had leachates that were analyzed for cobalt, and (2) only the soil samples from Zone 6 had SPLP leachates that were analyzed for cobalt and all of the results were nondetects.

Comment:

9. Th eground water protection criterion for manganese was calculated correctly by the Navy. Rather than using the calculated ground water protection criterion (160 u.g/1) to establish a pollutant mobility criterion for manganese, the Navy used the EPA Secondary MCL for drinking water (50 ^g/L) as the GAA/GA pollutant mobility criterion. This approach is acceptable as it is more conservative than using the calculated ground water protection criterion.

Response:

No response required.

IV. GB POLLUTANT MOBILITY CRITERIA FOR DIMETHYLPHTHALATE

Comment:

10. The GB pollutant mobility criteria listed for dimethylphthalate (1,400 mg/kg) in the Navy's Table 2 appears to be a typo. The correct value should be listed as 14,000 mg/kg.

Response:

The GB pollutant mobility criteria for dimethylphthalate will be corrected to 14,000 mg/kg. "his revision has no impact on the analysis since dimethylphthalate was not detected in soil samples in any of the zones that were evaluated in the human health risk assessment.

V. BIS(2-CHLOROETHOXY)METHANE

Comment:

11. Th eNavy proposes a qualitative risk assessment for this compound. This approach is acceptable provided that the compound is not present at concentrations above the low part-per-billion range. As noted by Dr. Ginsberg, if it is present above this range, a more quantitative risk assessment may be required.

Response:

Bis(2-chloroethoxy)methane was not detected in soil or groundwater samples for any of the zones evaluated in the human health risk assessment, consequently this does not have any impact on the analysis.

4 of 4 Appendix F.3

Background Concentrations in 10

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IETHYLBENZENE ICO 3 3 3 3 3

IMETHYLENE CHLORIDE 100 in IN 3 3 UJ UJ I Z CO a a 3 3 ITETRACHLOROETHENE 3 3 3 [TOLUENE «. CO 3 c* 3 a 3

[TRANS- ,3-DICHLOROPROPEN1 E 100 a 3 N 3 3

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Sample Number 0

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[4-METHYLPHENOL 1§ 3 8 3 3 3 — 8 |

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Notes: All Locations Considered Approximate Plan Not to be Used For Design Coordinates Obtained from EPA Region I GIS Coordinates for THN Second Hill Lane School and SH Tree House Nursery Not Available

SOIL BACKGROUND LOCATIONS DRAFT REMEDIAL INVESTIGATION REPORT - AREA RAYMARK - FERRY CREEK - OU3 TETRA TECH NUS, INC. STRATFORD, CONNECTICUT

Drawn By: D.A. Chisholm I Date: February 27, 11999 55 JONSPIN ROAD WILMINGTON, MA 01887 Scale: As Shown |Fj|e: .. .\RaYmark\OU3FIGS.APR__. (978)658-7899 Appendix F.4

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1 Z O o O DC § Volatile s Pesticides/PCB s COBAL T Semivolatile s CADMIU M AROCLOR-125 4 SODIU M ALPHA-CHLORDA N POTASSIU M N [ACETON E [STYREN E |BIS(2-ETHYLHEXY L [ALPHA-BH C | [AROCLOR-126 8 iQAMMA-CHLORD A IHEPTACHLO R [ALUMINU M [ARSENI C IBARIU M ICALCIU M ICHROMIU M | [COPPE R IMAGNESIU M [MANGANES E [NICKE L | [SILVE R [VANADIU M Appendix F.5

Sample Subsets TABLE F-5.1 SAMPLE LIST AREA D CURRENT/FUTURE COMMERCIAL WORKERS

AOC 1 RECEPTOR [ MATRIX | BORING

._.D „ _ dscm SOIL BPM A+09 dscm "iSOIL*" TBPMA+IOO" D dscm """SOIL iBPMA+140 D 'dscm !SOIL BPM A+250 D dscm SOIL BPM A+300 D ,dscm :SOIL !BPM A+350 D idscm SOIL 'BPMA+50 D idscm 'SOIL BPM B+00 D idscm SOIL :BPM B+100 D 'dscm -SOIL 'BPMB+150 D dscm 'SOIL BPM B+200 D " dscm SOJL •lPM~B+247/17E D dscm SOIL BPM B+350 D dscm SOIL 'BPM B+400 D •dscm SOIL JBPMB+425 b~ ^dscm SOIL" "BPM'C+OO D dscm SOIL BPMC+165 D dscm SOIL 'BPMC+200 b" dscm SOIL "" BPMC+265 D dscm SOIL BPM C+50 D dscm SOIL BPM C+95 D dscm SOIL BPMG3 D" dscm "SOIL BP~MG4 " " b dscm SOIL ."BPMB+50~ b dscm SOIL BPMG2 D •dscm SOIL .BPRA+00 D dscm SOIL BPR B+00 b dscm SOH. BP'R c+do D dscm SOIL D-SB01 D dscm SOIL D-SB02 D dscm SOIL D-SB03 TABLE F-5.2 SAMPLE LIST AREA D FUTURE COMMERCIAL WORKERS | AOC | RECEPTOR MATRIX j BORING D dscn SOIL BPM A+09 D dscn SOIL BPM A+100 HTCO DE+860 D dsfr SOIL THTCO E+865 TABLE F-5.4 SAMPLE LIST AREA D CURRENT/FUTURE WETLAND/MARSH RECEPTORS

1 AOC I RECEPTOR |_ MATRIX | BORING D dswmr SEDIMENT iBN01 D dswmr (SEDIMENT BN02 D dswmr SEDIMENT tBN04 !D dswmr SEDIMENT 3S01

D dswmr SEDIMENT _JBS02 ( D dswmr 'SEDIMENT BS07 D dswmr SEDIMENT D-SD03R D dswmr SEDIMENT D-SD04 D dswmr SEDIMENT D-SD05 D dswmr SEDIMENT D-SD08 D dswmr SEDIMENT D-SD09 D dswmr SEDIMENT D-SD10 D dswmr SEDIMENT THTCOCD+715(W) D dswmr SOIL D-SS03 D dswmr SOIL THTCO C+525 D dswmr WETLAND BN03 D dswmr WETLAND BN05 D dswmr WETLAND BN06 D dswmr WETLAND BN07 D dswmr WETLAND BPMG1 D dswmr WETLAND BPRA+100 D dswmr WETLAND BPRB+100 D dswmr WETLAND BPR B+200 D dswmr WETLAND BPRC+100 D dswmr WETLAND BPR C+200 D dswmr WETLAND BR A+100 D dswmr WETLAND BR A+150 D dswmr WETLAND BR A+200 D dswmr WETLAND BR A+250 D dswmr WETLAND BR C+00 D dswmr WETLAND BR E+00 D dswmr WETLAND BRG07 D dswmr WETLAND BRG09 D dswmr WETLAND BRD+00 D dswmr WETLAND BS03 D dswmr WETLAND BS04 D dswmr WETLAND BS05 D dswmr WETLAND BS06 D dswmr WETLAND D-SD01 D dswmr WETLAND D-SD02 D dswmr WETLAND D-SD06 D dswmr WETLAND D-SD07 D dswmr WETLAND THTCO AB+600 D dswmr WETLAND THTCO AB+650 (W) D dswmr WETLAND THTCO C+625 (W) D dswmr WETLAND THTCO CD+605 TABLE F-5.4 SAMPLE LIST AREA D CURRENT/FUTURE WETLAND/MARSH RECEPTORS

| AOC | RECEPTORJ ^ MATRIX | BORING | ,D ''dswmr ^WETLAND JTHTCO CD+700 1 "b" """ dswmr "1 WETLAND "IjHfco D+790 """"_j D 'dswmr ""WETLAND !THTCOD+910(W) ; ;D _j dswmr WETLAND 1-THTCODC+810(W) ! rD ! dswmr "WETLAND ,THTCO"""DE+966 !D _|dswmr sw JBN01 i ID" dswmr "•SW "~1BN02 " ~ ; D dswmr !SW BN03 D dswmr sw BN04 !°. dswmr - 'SgW BS01 'D dswmr w " "BS02' TABLE F-5.5 SAMPLE LIST AREA E CURRENT/FUTURE WETLAND/MARSH RECEPTOR

AOC I RECEPTOR MATRIX | BORING E eswmr SOIL •ES1100A-002 "E leswmr WETLAND "" Zl^^iZ^JLJiriZL, "E eswmr 'WETLAND ~*E-SD02 E i eswmr WETLAND IE-SD03 "E eswmr WETLAND TESOI E i eswmr ^ZETLAND _JES02 jLL-_ 1 eswmr WETLAND TES03 "" leswmr WETLAND SES06 1 ™~~ leswmr WETLAND 1ES07 E s ewwmr SW SES01 E " ewwmr SW 1ES02 E ewwmr sw ""!ES03 " E ewwmr SW jEsoe E~ ewwmr SW ""ESO? Appendix F.6

Sample Calculations for UCL Statistics TETRA TECH NUS, INC. CALCULATION WORKSHEET PAGE .OF,

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Toxicity Profiles TABLE OF CONTENTS

SECTION PAGE

F.7.1 ANTIMONY F.7-1 F.7.1.1 Pharmacokinetics F.7-1 F.7.1.2 Noncancer Toxicity F.7-1 F.7.1.3 Carcinogenicity F.7-2

F.7.2 ARSENIC F.7-2 F.7.2.1 Pharmacokinetics F.7-2 F.7.2.2 Noncancer Toxicity F.7-3 F.7.2.3 Carcinogenicity F.7-3

F.7.3 BARIUM F.7-4 F.7.3.1 Noncancer Toxicity F.7-4 F.7.3.2 Carcinogenicity F.7-4

F.7.4 CADMIUM F.7-5 F.7.4.1 Pharmacokinetics F.7-5 F.7.4.2 Noncancer Toxicity F.7-5 F.7.4.3 Carcinogenicity F.7-6

F.7.5 CHROMIUM F.7-6 F.7.5.1 Noncancer Toxicity F.7-6 F.7.5.2 Carcinogenicity F.7-7

F.7.6 COPPER F.7-7 F.7.6.1 Noncancer Toxicity F.7-7 F.7.6.2 Carcinogenicity F.7-8

F.7.7 LEAD F.7-8 F.7.7.1 Pharmacokinetics F.7-8 F.7.7.2 Noncancer Toxicity F.7-9 F.7.7.3 Carcinogenicity F.7-10

F.7.8 MANGANESE F.7-11 F.7.8.1 Noncancer Toxicity F.7-11 F.7.8.2 Carcinogenicity F.7-11

F.7.9 MERCURY F.7-12 F.7.9.1 Pharmacokinetics F.7-12 F.7.9.2 Noncancer Toxicity F.7-13 F.7.9.3 Carcinogenicity F.7-13

F.7.10 NICKEL F.7-14 F.7.10.1 Noncancer Toxicity F.7-14 F.7.10.2 Carcinogenicity F.7-14 TABLE OF CONTENTS (Continued)

SECTION PAGE

F.7.11 THALLIUM F.7-15 F.7.11.1 Noncancer Toxicity F.7-15 F.7.11.2 Carcinogenicity F.7-15

F.7.12 VANADIUM F.7-15 F.7.12.1 Noncancer Toxicity F.7-15 F.7.12.2 Carcinogenicity F.7-16

F.7.13 ZINC F.7-16 F.7.13.1 Pharmacokinetics F.7-16 F.7.13.2 Noncancer Toxicity F.7-16 F.7.13.3 Carcinogenicity F.7-17

F.7.14 POLYAROMATIC HYDROCARBONS F.7-17 F.7.14.1 Pharmacokinetics F.7-17 F.7.14.2 Noncancer Toxicity F.7-18 F.7.14.3 Carcinogenicity F.7-18

F.7.15 BENZO[A]ANTHRACENE F.7-20 F.7.15.1 Noncancer Toxicity F.7-20 F.7.15.2 Carcinogenicity F.7-20

F.7.16 BENZO(B)FLUORANTHENE F.7-21 F.7.16.1 Noncancer Toxicity F.7-21 F.7.16.2 Carcinogenicity F.7-21

F.7.17 BENZO[A]PYRENE (BAP) F.7-21 F.7.17.1 Pharmacokinetics F.7-21 F.7.17.2 Noncancer Toxicity F.7-22 F.7.17.3 Carcinogenicity F.7-22

F.7.18 DIBENZO[A,H]ANTHRACENE F.7-24 F.7.18.1 Noncancer Toxicity F.7-24 F.7.18.2 Carcinogenicity F.7-24

F.7.19 INDENO(1,2,3-CD)PYRENE F.7-25 F.7.19.1 Noncancer Toxicity F.7-25 F.7.19.2 Carcinogenicity F.7-25

F.7.20 ALDRIN/DIELDRIN (CLEMENT 1985) F.7-26 F.7.20.1 Pharmacokinetics F.7-25 F.7.20.2 Non-Carcinogenic Toxicity F.7-26 F.7.20.3 Carcinogenicity F.7-26 TABLE OF CONTENTS (Continued)

SECTION PAGE

F.7.21 CHLORDANE F.7-26 F.7.21.1 Pharmacokinetics F.7-26 F.7.21.2 Non-Carcinogenic Toxicity F.7-27 F.7.21.3 Carcinogenicity F.7-27 F.7.22 DIELDRIN F.7-28 F.7.22.1 Noncancer Toxicity F.7-28 P.7.22.2 Carcinogenicity F.7-28

F.7.23 HEPTACHLOR EPOXIDE (CLEMENT, 1985) F.7-29 F.7.23.1 Health Effects F.7-29

F.7.24 POLYCHLORINATED BIPHENYLS F.7-30 F.7.24.1 Noncancer Toxicity F.7-30 F.7.24.2 Carcinogenicity F.7-31

F.7.25 DIOXINS F.7-31 F.7.25.1 Noncancer Toxicity F.7-31 F.7.26.2 Carcinogenicity F.7-32

F.7.26 ASBESTOS F.7-33 F.7.26.1 Noncancer Toxicity F.7-33 F.7.26.2 Carcinogenicity F.7-33

REFERENCES F.7.1 Antimony

F.7.1.1 Pharmacokinetics

Ingested antimony is absorbed slowly and incompletely from the gastrointestinal (Gl) tract (Iffland 1988). Within a few days of acute exposure, highest tissue concentrations are found in the liver, kidney, and thyroid. Organs of storage include skin, bone, and teeth. Highest concentrations in deceased smelter workers (inhalation exposure) occurred in the lungs and skeleton. Excretion is largely via the urine or feces, although some is incorporated into the hair.

F.7.1.2 Noncancer Toxicity

Acute intoxication from ingestion of large doses of antimony induces Gl disturbances, dehydration, and cardiac effects in humans (Iffland 1988). Chronic effects from occupational exposure include irritation of the respiratory tract, pneumoconiosis, pustular eruptions of the skin called "antimony spots," allergic contact dermatitis, and cardiac effects, including abnormalities of the electrocardiograph (ECG) and myocardial changes. Cardiac effects were also observed in rats and rabbits exposed by inhalation for six weeks and in animals (dogs, and possibly other species) treated by intravenous injection (Blinder and Friberg 1986).

Chronic oral exposure studies in laboratory animals include two briefly reported lifetime drinking water studies in rats and mice (Kanisawa and Schroeder 1969; Schroeder et al. 1970). The only dose tested, 5 ppm potassium antimony tartrate, resulted in reduced longevity in both species and in reduced mean heart weight in the rats. The EPA (2000) verifies a RfD of 0.0004 mg/kg/day for chronic oral exposure to antimony from the LOAEL of 5 ppm potassium antimony tartrate (0.35 mg antimony/kg body weight-day) in the lifetime study in rats (Schroeder et al. 1970). An uncertainty factor of 1000 was applied; factors of 10 each for inter- and intraspecies variation and to estimate an NOAEL from an LOAEL. The heart is considered a likely target organ for chronic oral exposure of humans.

F.7-1 F.7.1.3 Carcinogenicity

Data were not located regarding the carcinogenicity of antimony to humans. Antimony fed to rats did not produce an excess of tumors (Goyer 1991), but a high frequency of lung tumors was observed in rats exposed by inhalation to antimony trioxide for one year (Elinder and Friberg 1986). Antimony is classified in EPA cancer weight-of-evidence Group D (not classifiable as to carcinogenicity to humans) (EPA 1997).

F.7.2 Arsenic

F.7.2.1 Pharmacokinetics

Several studies confirm that soluble inorganic arsenic compounds and organic arsenic compounds are almost completely (>90 percent) absorbed from the Gl tract in both animals and humans (Ishinishi et al. 1986). The absorption efficiency of insoluble inorganic arsenic compounds depends on particle size and stomach pH. Initial distribution of absorbed arsenic is to the liver, kidneys, and lungs, flowed by redistribution to hair, nails, teeth, bone, and skin, which are considered tissues of accumulation. Arsenic has a long half-life in the blood of rats, compared with other animals and humans, because of firm binding to the hemoglobin in erythrocytes.

Metabolism of inorganic arsenic includes reversible oxidation-reduction so that both arsenite (valence of 3) and arsenate (valence of 5) are present in the urine of animals treated with arsenic of either valence (Ishinishi et al. 1986). Arsenite is subsequently oxidized and methylated by a saturable mechanism to form mono- or dimethylarsenate; the latter is the predominant metabolite in the urine of animals or humans. Organic arsenic compounds (arsenilic acid, cacodylic acid) are not readily converted to inorganic arsenic. Excretion of organic or inorganic arsenic is largely via the urine, but considerable species variation exists. Continuously exposed humans appear to excrete 60 to 70 percent of their daily intake of arsenate or arsenite via the urine.

F.7-2 F.7.2.2 Noncancer Toxicity

A lethal dose of arsenic trioxide in humans is 70 to 180 mg. (approximately 50 to 140 mg arsenic; Ishinishi et al. 1986). Acute oral exposure of humans to high doses of arsenic produces liver swelling, skin lesions, disturbed heart function, and neurological effects. The only noncancer effects in humans clearly attributable to chronic oral exposure to arsenic are dermal hyperpigmentation and keratosis, as revealed by studies of several hundred Chinese exposed to naturally occurring arsenic in well water (Tseng 1977; Tseng et al. 1968; EPA 2000). Similar effects were observed in persons exposed to high levels of arsenic in water in Utah and the northern part of Mexico (Cebrian et al. 1983; Southwick et al. 1983). Occupational (predominantly inhalation) exposure is also associated with neurological deficits, anemia, and cardiovascular effects (Ishinishi et al. 1986), but concomitant exposure to other chemicals cannot be ruled out. The EPA (2000) derived a RfD of 0.3 ug/kg/day for chronic oral exposure, based on an NOAEL of 0.8 ug/kg/day for skin lesions from Chinese data. The principal target organ for arsenic appears to be the skin. The nervous system and cardiovascular systems appear to be less significant target organs. Inorganic arsenic may be an essential nutrient, exerting beneficial effects on growth, health, and feed conversion efficiency (Underwood 1977).

F.7.2.3 Carcinogenicity

Inorganic arsenic is clearly a carcinogen in humans. Inhalation exposure is associated with increased risk of lung cancer in persons employed as smelter workers, in arsenical pesticide applicators, and in a population residing near a pesticide manufacturing plant (EPA 2000). Oral exposure to high levels in well water is associated with increased risk of skin cancer (Tseng 1977; EPA 2000). Extensive animal testing with various forms of arsenic given by many routes of exposure to several species, however, has not demonstrated the carcinogenicity of arsenic (International Agency for Research on Cancer [IARC] 1980). The EPA (2000) classifies inorganic arsenic in cancer weight-of-evidence Group A (human carcinogen), and recommends an oral unit risk of 0.00005 ug/L in drinking water, based on the incidence of skin cancer in the Tseng (1977) study. The EPA presents a chronic oral slope factor of 1.5 per mg/kg/day based on the same information. The EPA (2000) notes that the uncertainties associated with the oral unit risk are considerably less than those for most

F.7-3 carcinogens, so that the unit risk might be reduced in order of magnitude. An inhalation unit risk of 0.0043 per ug/m3 was derived for inorganic arsenic from the incidence of lung cancer in occupationally exposed men (EPA 2000). An inhalation cancer slope factor, equivalent to 15.1 per mg/kg/day, was derived from the same data assuming an inhalation rate of 20 m3/day and a body weight of 70 kg for humans.

F.7.3 Barium

F.7.3.1 Noncancer Toxicity

Barium is a naturally occurring alkaline earth metal that comprises approximately 0.04 percent of the earth's crust (Reeves 1986). Acute oral toxicity was manifested by Gl upset, altered cardiac performance, and transient hypertension, convulsions, and muscular paralysis. Repeated oral exposures were associated with hypertension. Occupational exposure to insoluble barium sulfate induced benign pneumoconiosis (ACGIH 1991). The EPA (2000) presents a verified chronic oral RfD of 0.07 mg/kg/day, based on an NOAEL of 0.21 mg/kg/day in a ten-week study in humans exposed to barium in drinking water and an uncertainty factor of 3. The EPA (1997) presented the same value as a provisional RfD for subchronic oral exposure. A provisional chronic inhalation RfC of 0.0005 mg/m3 and a provisional subchronic inhalation RfC of 0.005 mg/m3 were based on a NOEL for fetotoxicity in a four-month intermittent-exposure inhalation study in rats (EPA 1997). Uncertainty factors of 1000 and 100 were used for the chronic and subchronic RfC values, respectively. The chronic and subchronic inhalation RfC values are equivalent to 0.0001 and 0.001 mg/kg/day, assuming a human inhalation rate of 20 m3/day and body weight of 70 kg. Barium is principally a muscle toxin. Its targets are the Gl system, skeletal muscle, the cardiovascular system, and the fetus.

F.7.3.2 Carcinogenicity

The EPA (2000) classifies barium as a cancer weight-of-evidence Group D substance (not classifiable as to carcinogenicity in humans). Cancer risk is not estimated for Group D substances.

F.7-4 F.7.4 Cadmium

F.7.4.1 Pharmacokinetics

Estimates of cadmium uptake by the respiratory tract range from 10 to 50 percent; uptake is greatest for fumes and small particles and least for large dust particles (Friberg et al., 1986; Goyer, 1991). Gl absorption of ingested cadmium is ordinarily 5 to 8 percent, but may reach 20 percent in cases of serious dietary ion deficiency. Highest tissue levels are normally found in the kidneys followed by the liver, although levels in the liver may exceed those in the kidneys of persons suffering from cadmium-induced renal dysfunction. The half-life of cadmium in the kidneys and liver may be as long as 10-30 years. Fecal and urinary excretion of cadmium are approximately equivalent to normal humans exposed to small amounts. Urinary excretion increases markedly in humans with cadmium-induced renal disease.

F.7.4.2 Noncancer Toxicity

Acute inhalation exposure to fumes or particles of cadmium induces respiratory symptoms, general weakness, and, in severe cases, respiratory insufficiency, shock, and death (Friberg et al., 1986). Acute oral exposure induces Gl disturbances. Chronic inhalation exposure induces pulmonary emphysema, and chronic exposure by either route consistently produces renal tubular disease in humans and laboratory animals. Proteinuria is a reliable early indicator of cadmium-induced kidney disease. The combination of pulmonary emphysema and renal tubular disease, if severe, may result in early mortality. Painful osteomalacia and osteoporosis may arise from altered metabolism of bone minerals secondary to renal damage. The combination of renal and skeletal damage is called itai-itai disease in Japan. Cadmium exposure ahs been associated with liver damage, but the liver appears to be less sensitive than the kidney. The kidney is the primary target organ of cadmium toxicity. The EPA (2000) derived chronic oral RfD values of 0.5 ug/kg/day for cadmium ingested in water and 1 ug/kg/day for cadmium ingested in food, based on a toxicokinetic model that predicted NOAELs from renal cortical concentration of cadmium. The different RfD values reflect assumed differences in Gl absorption of cadmium from water (5 percent) and food (2.5 percent).

F.7-5 F.7.4.3 Carcinogenicity

Carcinogenicity data in humans consist of several occupational studies that associate cadmium exposure with lung cancer, but concomitant exposure to other carcinogenic chemicals and smoking were not adequately controlled. Other occupational studies reported significantly increased risk of prostatic cancer, but this effect was not observed in the largest occupational study of workers exposed to high levels (Thun et al., 1985). The animal data consist of an inhalation study in rats that showed a significant increase in lung tumors, and several parenteral injection studies that produced injection site tumors. No evidence of Carcinogenicity, however, was observed in seven oral studies in rats and mice. The EPA (2000) classifies cadmium a cancer weight-of-evidence Group B1 substance for inhalation exposure on the basis of limited evidence of Carcinogenicity in humans and sufficient evidence in animals. The data were insufficient to classify cadmium as carcinogenic to humans exposed by the oral route. An inhalation unit risk of 0.0018 ug/m3, equivalent to 6.3 per mg/kg/day, was derived from the occupational exposure study by Thun et al. (1985) assuming an inhalation rate of 20 m3/day and a body weight of 70 kg for humans.

F.7.5 Chromium

F.7.5.1 Noncancer Toxicity

In , chromium (III) predominates over chromium (VI) (Langard and Norseth, 1986). Little chromium (VI) exists in biological materials, except shortly after exposure, because reduction to chromium (III) occurs rapidly. Chromium (III) is considered a nutritionally essential trace element and is considerably less toxic than chromium (VI). No effects were observed in rats consuming 5% chromium (lll)/kg/day in the diet for over two years (EPA, 1997). The NOEL of 5% Cr2O3 was the basis for a verified chronic oral RfD of 1.5 mg/kg/day (EPA, 1997). The same NOEL and an uncertainty factor of 1000 were the basis for a provisional subchronic oral RfD of 1 mg/kg/day (EPA, 1997).

Acute oral exposure of humans to high doses of chromium (VI) induced neurological effects, Gl hemorrhage and fluid loss, and kidney and liver effects. Parenteral dosing of animals with chromium (VI) is selectively toxic to the kidney tubules. An NOAEL of 2.4 mg chromium (VI)

F.7-6 /kg/day in a one-year drinking water study in rats and an uncertainty factor of 500 was the basis of a verified RfD of 0.003 mg/kg/day for chronic oral exposure (EPA, 2000). The same NOAEL and an uncertainty factor of 100 were the basis of a provisional subchronic oral RfD of 0.02 mg/kg/day (EPA, 1997).

Occupational (inhalation and dermal) exposure to chromium (III) compounds induced dermatitis (ACGIH, 1991). Similar exposure to chromium (VI) induced ulcerative and allergic contact dermatitis, irritation of the upper respiratory tract including ulceration of the mucosa and perforation of the nasal septum, and possibly kidney effects. An inhalation RfC values was not located for chromium (III), however, EPA (2000) presents an inhalation RfD of 0.03 ug/kg/day for chromium (VI).

A target organ was not identified for chromium (III). The kidney appears to be the principal target organ for repeated oral dosing with chromium (VI). Additional target organs for dermal and inhalation exposure include the skin and respiratory tract.

F.7.5.2 Carcinogenicity

Data were not located regarding the carcinogenicity of chromium (III). The EPA (2000) classifies chromium (VI) in cancer weight-of-evidence Group A (human carcinogen), based on the consistent observation of increased risk of lung cancer in occupational studies of workers in chromate production or the chrome pigment industry. Parenteral dosing of animals with chromium (VI) compounds consistently induced injection-site tumors. There is no evidence that oral exposure to chromium (VI) induces cancer. An inhalation unit risk of 0.012 per ug/m3, equivalent to 41 per mg/kg/day, assuming humans inhale 20 m3/day and weigh 70 kg, was based on increased risk of lung cancer deaths in chromate production workers (EPA, 2000).

F.7.6 Copper

F.7.6.1 Noncancer Toxicity

Copper is a nutritionally essential element that functions as a cofactor in several enzyme systems (Aaseth and Norseth 1986). Acute exposure to large oral doses of copper salts was

F.7-7 associated with Gl disturbances, hemolysis, and liver and kidney lesions. Chronic oral toxicity in humans has not been reported. Chronic oral exposure of animals was associated with an iron-deficiency type of anemia, hemolysis, and lesions in the liver and kidneys. Occupational exposure may induce metal fume fever, and, in cases of chronic exposure to high levels, hemolysis and anemia (ACGIH 1991). Neither oral nor inhalation RfD or RfC values were located for copper. The target organs for copper are the erythrocyte, liver, and kidney, and, for inhalation exposure, the lung. An oral RfD of 0.04 mg/kg/day was presented for copper (EPA, 1997). A RfC value was not located for copper.

F.7.6.2 Carcinogenicity

Copper is classified in cancer weight-of-evidence Group D (not classifiable as to carcinogenicity to humans) (EPA 1997). Quantitative risk estimates are not derived for Group D chemicals.

F.7.7 Lead

F.7.7.1 Pharmacokinetics

Studies in humans indicate that an average of 10 percent of ingested lead is absorbed, but estimates as high as 40 percent were obtained in some individuals (Tsuchiya, 1986). Nutritional factors have a profound effect on Gl absorption efficiency. Children absorb ingested lead more efficiently than adults; absorption efficiencies up to 53 percent were recorded for children three months to eight years of age. Similar results were obtained for laboratory animals; absorption efficiencies of 5 to 10 percent were obtained for adults and > 50 percent were obtained for young animals. The deposition rate of inhaled lead averages approximately 30 to 50 percent, depending on particle size, with as much as 60 percent deposition of very small particles (0.03 mm) near highways. All lead deposited in the lungs is eventually absorbed.

Approximately 95 percent of the lead in the blood is located in the erythrocytes (EPA, 2000). Lead in the plasma exchanges with several body compartments, including the internal organs, bone, and several excretory pathways. In humans, lead concentrations in bone increase with

F.7-8 age (Tsuchiya, 1986). About 90 percent of the body burden of lead is located in the skeleton. Neonatal blood concentrations are about 85 percent of maternal concentrations (EPA, 2000). Excretion of absorbed lead is principally through the urine, although Gl secretion, biliary excretion, and loss through hair, nails, and sweat are also significant.

F.7.7.2 Noncancer Toxicity

The noncancer toxicity of lead to humans has been well characterized through decades of medical observation and scientific research (EPA, 2000). The principal effects of acute oral exposure are colic with diffuse paroxysmal abdominal pain (probably due to vagal irritation), anemia, and, in severe cases, acute encephalopathy, particularly in children (Tsuchiya, 1986). The primary effects of long-term exposure are neurological and hematological. Limited occupational data indicate that long-term exposure to lead may induce kidney damage. The principal target organs of lead toxicity are the erythrocyte and the nervous system. Some of the effects on the blood, particularly changes in levels of certain blood enzymes, and subtle neurobehavioral changes in children, appear to occur at levels so low as to be considered nonthreshold effects.

The USEPA (1986b and 1990a) determined that it is inappropriate to derive a RfD for oral exposure to lead for several reasons. First, the use of a RfD assumes that a threshold for toxicity exists, below which adverse effects are not expected to occur. However, the most sensitive effects of lead exposure, impaired neurobehavioral development in children and altered blood enzyme levels associated with anemia, may occur at blood lead concentrations so low as to be considered practically nonthreshold in nature. Second, RfD values are specific for the route of exposure for which they are derived. Lead, however, is ubiquitous, so that exposure occurs from virtually all media and by all pathways simultaneously, making it practically impossible to quantify the contribution to blood lead from any one route of exposure. Finally, the dose-response relationships common to many toxicants, and upon which derivation of a RfD is based, do not hold true for lead. This is because the fate of lead within the body depends, in part, on the amount and rate of previous exposures, the age of the recipient, and the rate of exposure. There is, however, a reasonably good correlation between blood lead concentration and effect. Therefore, blood lead concentration is the appropriate parameter on which to base the regulation of lead.

F.7-9 USEPA (1997) presented no inhalation RfC for lead, but referred to the National Ambient Air Quality Standard (NAAQS) for lead, which could be used in lieu of an inhalation RfC. The NAAQSs are based solely on human health considerations and are designed to protect the most sensitive subgroup of the human population. The NAAQS for lead is 1.5 mg/m3, averaged quarterly.

F.7.7.3 Carcinogenicity

USEPA (2000) classifies lead in cancer weight-of-evidence Group B2 (probable human carcinogen), based on inadequate evidence of cancer in humans and sufficient animal evidence. The human data consist of several epidemiologic occupational studies that yielded confusing results. All of the studies lacked quantitative exposure data and failed to control for smoking and concomitant exposure to other possibly carcinogenic metals. Rat and mouse bioassays showed statistically significant increases in renal tumors following dietary and subcutaneous exposure to several soluble lead salts. Various lead compounds were observed to induce chromosomal alterations in vivo and in vitro, sister chromatic exchange in exposed workers, and cell transformation in Syrian hamster embryo cells; to enhance simian adenovirus induction; and to alter molecular processes that regulate gene expression. USEPA (1997) declined to estimate risk for oral exposure to lead because many factors (e.g., age, general health, nutritional status, existing body burden and duration of exposure) influence the bioavailability of ingested lead, introducing a great deal of uncertainty into any estimate of risk.

The USEPA IEUBK lead model is an iterated set of equations that estimate blood lead concentration in children aged 0 to 7 years (USEPA, 1994a). The biokinetic part of the model describes the movement of lead between the plasma and several body compartments and estimates the resultant blood lead concentration. The rate of the movement of lead between the plasma and each compartment is a function of the transition or residence time (i.e., the mean time for lead to leave the plasma and enter a given compartment, or the mean residence time for lead in that compartment). Compartments modeled include the erythrocytes, liver, kidneys, all the other soft tissue of the body, cortical bone, and trabecular bone. Excretory pathways and their rates are also modeled. These include the mean time for excretion from the plasma to the urine, from the liver to the bile, and from the other soft tissues to the hair, skin, sweat, etc. The model permits the user to adjust the transition and residence times.

F.7-10 USEPA guidance (USEPA, 1994b) recommends using 400 mg/kg as a screening level for lead in soil for residential scenarios at CERCLA sties and at RCRA Corrective Action sites. Residential areas with soil lead below 400 mg/kg generally require no further action. However, in some special situations, further study is warranted below the screening level (e.g., wetlands, agricultural areas).

F.7.8 Manganese

F.7.8.1 Noncancer Toxicity

Manganese is nutritionally required in humans for normal growth and health (EPA, 2000). Humans exposed to approximately 0.8 mg manganese/kg/day in drinking water exhibited lethargy, mental disturbances (1/16 committed suicide), and other neurologic effects. The elderly appeared to be more sensitive than children. Oral treatment of laboratory rodents induced biochemical changes in the brain, but rodents did not exhibit the neurological signs exhibited by humans. Occupational exposure to high concentrations in air induced a generally typical spectrum of neurological effects and an increased incidence of pneumonia (ACGIH, 1986).

EPA presented the oral RfD for manganese of 0.02 mg/kg/day (EPA, 2000) based on drinking water and an oral RfD of 0.14 mg/kg/day based on food. The EPA (2000) presented a verified chronic inhalation RfC based on a LOAEL for impairment of neurobehaviorial function in occupationally exposed humans. The inhalation RfC is equivalent to 0.0143 ug/kg/day, assuming humans inhale 20 m3 of air/day and weigh 70 kg. The CNS and respiratory tract are target organs of inhalation exposure to manganese.

F.7.8.2 Carcinogenicity

The EPA (2000) classifies manganese in cancer weight-of-evidence Group D (not classifiable as to carcinogenicity to humans). Quantitative cancer risk estimates are not derived from Group D chemicals.

F.7-11 F.7.9 Mercury

Mercury occurs in three forms: elemental, organic, and inorganic. Although the toxicity of all forms is mediated by the mercury cation, the extent of absorption and pattern of distribution within the body, which determines the effects observed, depends on the form to which the organism is exposed (Goyer, 1991). Bacterial activity in the environment converts inorganic mercury to methyl mercury (Berlin, 1986). It is likely that either inorganic mercury or methyl mercury may be taken up by plants and enter the food chain, and this discussion will focus on inorganic and methyl mercury. Exposure to elemental mercury, which is more likely to occur in an occupational setting, is not discussed herein.

F.7.9.1 Pharmacokinetics

The Gl absorption of inorganic mercury salts is about 2 to 10 percent in humans, and slightly higher in experimental animals (Berlin, 1986; Goyer, 1991). Inorganic mercury in the blood is roughly equally divided between the plasma and erythrocytes. Distribution is preferentially to the kidney, with somewhat lower concentrations found in the liver, and even lower levels found in the skin, spleen, testes, and brain (Berlin, 1986). Inorganic mercury is excreted principally through the feces and urine, with minor pathways including the secretions of exocrine glands and exhalation of elemental mercury vapor.

Methyl mercury is nearly completely (90 to 95 percent) absorbed from the Gl tract (Berlin, 1986). The concentration of methyl mercury in the erythrocytes is about 10 times that in the plasma. Methyl mercury leaves the blood slowly, showing particular affinity for the brain, particularly in primates. In rats, 1 percent of the body burden of methyl mercury is found in the brain, but in humans, 10 percent of the body burden is found in the brain. Somewhat lower levels are found in the liver and kidney. During pregnancy, methyl mercury accumulates in the fetal brain, often at levels higher than in the maternal brain. Most tissues except the brain transform methyl mercury to inorganic mercury. Excretion of methyl mercury is principally via the bile, with a half-life of 70 days in humans not suffering from toxicity. Following exposure to methyl mercury, some of the mercury in the bile exists as methyl mercury and some as the inorganic form. The inorganic form is largely passed in the feces, but the methyl mercury is

F.7-12 subject to enterohepatic recirculation. Another important excretory pathway for methyl mercury is lactation.

F.7.9.2 Noncancer Toxicity

Target organs for inorganic or methyl mercury include the kidney, nervous system, fetus, and neonate. Acute oral exposure to high doses of inorganic mercury causes severe damage to the Gl mucosa because of the corrosive nature of mercury salts, which may lead to bloody diarrhea, shock, circulatory collapse, and death (Berlin, 1986; Goyer, 1991). Acute sublethal poisoning induces severe kidney damage. Chronic exposure induces an autoimmune glomerular disease and renal tubular injury. The U.S. EPA (1997) presented a verified RfD of 0.3 ug/mg-day for chronic oral exposure to inorganic mercury, based on kidney effects in rats.

Acute or chronic exposure to methyl mercury leads to neurologic dysfunction (Berlin, 1986; Goyer, 1991). The region of the nervous system affected is species-dependent. Methyl mercury poisoning in rats induces peripheral nerve damage and kidney effects. In humans, the sensory cortex appears to be the most sensitive. The brain of the fetus and the neonate may be unusually sensitive to methyl mercury; retarded neurologic development was observed in prenatally exposed children whose mothers showed no clinical signs of poisoning. The U.S. EPA (1997) derived a RfD of 0.1 ug/kg/day for chronic oral exposure to methyl mercury based on developmental neurological abnormalities in human infants. An inhalation RfC of 0.0003 mg/m3 (uncertainty factor of 30) has been established for inorganic mercury based on neurotoxic effects in humans. This translates into a chronic RfD of 0.000086 mg/kg/day (U.S. EPA, 2000).

F.7.9.3 Carcinogenicity

The U.S. EPA (2000) classifies inorganic mercury in cancer weight-of-evidence Group D (not classifiable as to carcinogenicity to humans), based on no data regarding cancer in humans, and inadequate animal and supporting data. In an intraperitoneal injection study with metallic mercury in rats, sarcomas developed only in those tissues in direct contact with the test material (ATSDR, 1992c). A two-year dietary study in rats with mercuric acetate (inorganic mercury) yielded no evidence of carcinogenicity (ATSDR, 1992c). In mice, however, dietary

F.7-13 exposure to high doses of mercury chloride for up to 78 weeks induced renal adenomas and adenocarcinomas (ATSDR, 1992c). The U.S. EPA has not yet evaluated the carcinogenicity of organic mercury. No carcinogenic effect, however, was observed in a two-year feeding study with phenylmercuric acetate in rats (ATSDR, 1992c).

F.7.10 Nickel

F.7.10.1 Noncancer Toxicity

In a subchronic gavage study with nickel chloride in water, clinical signs of toxicity in rats included lethargy, ataxia, irregular breathing, reduced body temperature, salivation, and discolored extremities (EPA 2000). Inhalation exposure was associated with asthma and pulmonary fibrosis in welders using nickel alloys (ACGIH 1986). Lung effects were observed in laboratory animals exposed by inhalation. The EPA (2000) presented a verified RfD of 0.02 for chronic oral exposure to nickel, based on an NOAEL for decreased organ and body weights in a two-year dietary study with nickel sulfate in rats and an uncertainty factor of 300. The EPA (1997) presented the same value as a provisional subchronic oral RfD. The CNS appears to be the target organ for the oral toxicity of nickel. The lung is clearly the target organ for inhalation exposure.

F.7.10.2 Carcinogenicity

Occupational exposure to nickel was associated with increased risk of nasal, laryngeal and lung cancer (ATSDR 1995). Inhalation exposure of rats to nickel subsulfide increased the incidence of lung tumors. The EPA (2000) presents a cancer weight-of-evidence Group A classification (human carcinogen) for nickel, and presents an inhalation unit risk of 0.00024 per mg/m3 for nickel refinery dust. The unit risk is equivalent to 0.84 per ug/kg/day, assuming humans inhale 20 m3 of air/day and weigh 70 kg. The quantitative estimate was derived from the human occupational studies.

F.7-14 F.7.11 Thallium

F. 7.11.1 Noncancer Toxicity

Thallium is highly toxic; acute ingestion by humans or laboratory animals induced gastroenteritis, neurological dysfunction, and renal and liver damage (Kazantzis, 1986). Chronic ingestion of more moderate doses characteristically caused alopecia. Thallium was used medicinally to induce alopecia in cases of ringworm of the scalp, sometimes with disastrous results. In industrial (inhalation, oral, dermal) exposure, neurologic signs preceded alopecia, suggesting that the nervous system is more sensitive than the hair follicle. The EPA (2000) presented verified chronic oral RfD values for several thallium compounds (thallium acetate, thallium acetate, thallium carbonate, thallium chloride, thallium nitrate, thallium sulfate, and thallic oxide) based on increased incidence of alopecia and increased serum levels of liver enzymes indicative of hepatocellular damage in rats treated with thallium sulfate for 90 days. EPA (2000) presented a chronic oral RfD for thallium of 0.07 ug/kg/day.

F.7.11.2 Carcinogenicity

Thallium was classified as a cancer weight-of-evidence Group D substance (not classifiable as to carcinogenicity to humans) (EPA, 2000).

F.7.12 Vanadium

F.7.12.1 NONCANCER TOXICITY

The oral toxicity of vanadium compounds to humans is very low (Lagerkvist et al. 1986), probably because little vanadium is absorbed from the Gl tract. Effects in humans exposed by inhalation include upper and lower respiratory tract irritation. A provisional subchronic and chronic oral RfD of 0.007 mg/kg/day was derived from an NOEL in rats in a lifetime drinking water study with vanadyl sulfate and an uncertainty factor of 100 (USEPA, 1997). A target organ could not be identified for oral exposure. The respiratory tract is the target organ for inhalation exposure.

F.7-15 F.7.12.2 Carcinogenicity

No information was located regarding the carcinogenicity of vanadium.

F.7.13 Zinc

F.7.13.1 Pharmacokinetics

Zinc is a nutritionally required trace element. Estimates of the efficiency of Gl absorption of zinc in animals range from <10 to 90 percent (Elinder 1986). Estimates in normal humans range from approximately 20 to 77 percent (Elinder 1986; Goyer 1991). The net absorption of zinc appears to be homeostatically controlled, but it is unclear whether Gl absorption, intestinal secretion, or both are regulated. Distribution of absorbed zinc is primarily to the liver (Goyer 1991), with subsequent redistribution to bone, muscle, and kidney (Elinder 1986). Highest tissue concentrations are found in the prostate. Excretion appears to be principally through the feces, in part from biliary secretion, but the relative importance of fecal and urinary excretion is species-dependent. The half-life of zinc absorbed from the Gl tracts of humans in normal zinc homeostasis is approximately 162 to 500 days.

F.7.13.2 Noncancer Toxicity

Humans exposed to high concentrations of aerosols of zinc compounds may experience severe pulmonary damage and death (Elinder 1986). The usual occupational exposure is to freshly formed fumes of zinc, which can induce a reversible syndrome known as metal fume fever. Orally, zinc exhibits a low order of acute toxicity. Animals dosed with 100 times dietary requirement showed no evidence of toxicity (Goyer 1991). In humans, acute poisoning from foods or beverages prepared in galvanized containers is characterized by Gl upset (Elinder 1986). Chronic oral toxicity in animals is associated with poor growth, Gl inflammation, arthritis, lameness, and a microcytic, hypochromic anemia (Elinder 1986), possibly secondary to copper deficiency (Underwood 1977). The EPA (1997) presented a verified RfD of 0.3 mg/kg/day for chronic oral exposure to zinc, based on anemia in humans.

F.7-16 F.7.13.3 Carcinogenicity

The EPA (2000) classifies zinc in cancer weight-of-evidence Group D (not classifiable as to carcinogenicity to humans) based on inadequate evidence for carcinogenicity in humans and animals. The human data consist largely of occupational exposure studies not designed to detect a carcinogenic response, and of reports that prostatic zinc concentrations were lower in cancerous than in noncancerous tissue. The animal data consist of several dietary, drinking water, and zinc injection studies, none of which provided convincing data for a carcinogenic response.

F.7.14 Polyaromatic Hydrocarbons

PAHs are a large class of ubiquitous natural and anthropogenic chemicals, all with similar chemical structures (ATSDR 1990).

F.7.14.1 Pharmacokinetics

Although quantitative absorption data for the PAHs were not located, benzo(a)pyrene was readily absorbed across the Gl (Rees et al. 1971) and respiratory epithelia (Kotin et al. 1969; Vainich et al. 1976). The high lipophilicity of other compounds in this class suggests that other PAHs also would be readily absorbed across Gl and respiratory epithelia.

Benzo(a)pyrene was distributed widely in the tissues of treated rats and mice, but primarily to tissues high in fat, such as adipose tissue and mammary gland (Kotin et al. 1969; Schlede et al. 1970a). Patterns of tissue distribution of other PAHs would be expected to be similar because of the high lipophilicity of the members of this class.

Studies of the metabolism of benzo(a)pyrene provide information relevant to other PAHs because of the structural similarities of all members of the class. Metabolism involves microsomal mixed function oxidase hydroxylation of one or more of the phenyl rings with the formation of phenols and dihydrodiols, probably via formation of arene oxide intermediates (EPA 1979a). The dihydrodiols may be further oxidized to diol epoxides, which, for certain members of the class, are known to be the ultimate carcinogens (LaVoie et al. 1982).

F.7-17 Conjugation with glutathione or glucuronic acid, and reduction to tetrahydrotetrols are important detoxification pathways. Metabolism of naphthalene resulted in the formation of 1,2­ naphthoquinone, which induced cataract formation and retinal damage in rats and rabbits.

Excretion of benzo(a)pyrene or dibenzo(a,h)anthracene residues was reported to be rapid, although quantitative data were not located (EPA 1979b). Excretion occurred mainly via the feces, probably largely due to biliary secretion (Schlede et al. 1970a, 1970b). The EPA (1980) concluded that accumulation in the body tissues of PAHs from chronic low level exposure would be unlikely.

F.7.14.2 Noncancer Toxicity

Oral noncancer toxicity data are available for acenaphthene, anthracene, fluoranthene, fluorene, and naphthalene. Newborn infants, children, and adults exposed to naphthalene by ingestion, inhalation, or possibly by skin contact developed hemolytic anemia with associated jaundice and occasionally renal disease (EPA 1979c). In a 13-week gavage study in rats, treatment with 50 mg naphthalene/kg, 5 days/week for 13 weeks (35.7 mg/kg/day) induced no effects; higher doses presumably reduced the growth rate (National Toxicology Program (NTP) 1980). Application of an uncertainty factor of 1000 yielded a provisional RfD for chronic oral exposure of 0.04 mg/kg/day (EPA 1997). The very mild effect (decreased growth rate) apparently observed at higher doses suggests that the RfD is very conservatively protective.

F.7.14.3 Carcinogenicity

The PAHs are ubiquitous, being released to the environment from anthropogenic as well as from natural sources (ATSDR 1992a). Benzo(a)pyrene is the most extensively studied member of the class, inducing tumors in multiple tissues of virtually all laboratory species tested by all routes of exposure. Although epidemiology studies suggested that complex mixtures that contain PAHs (coal tar, soots, coke oven emissions, cigarette smoke) are carcinogenic to humans (EPA 1984), the carcinogenicity cannot be attributed to PAHs alone because of the presence of other potentially carcinogenic substances in these mixtures (ATSDR 1992a). In addition, recent investigations showed that the PAH fraction of roofing tar, cigarette smoke, and coke oven emissions accounted for only 0.1 to 8 percent of the total

F.7-18 mutagenic activity of the unfractionated complex mixture in Salmonella (Lewtas 1988). Aromatic amines, nitrogen heterocyclic compounds, highly oxygenated quinones, diones, and nitrooxygenated compounds, none of which would be expected to arise from in vivo metabolism of PAHs, probably accounted for the majority of the mutagenicity of coke oven emissions and cigarette smoke. Furthermore, coal tar, which contains a mixture of many PAHs, has a long history of use in the clinical treatment of a variety of skin disorders in humans (ATSDR 1990).

Because of the lack of human cancer data, assignment of individual PAHs to EPA cancer weight-of-evidence groups was based largely on the results of animal studies with large doses of purified compound (EPA 1984). Frequently, unnatural routes of exposure, including implants of the test chemical in beeswax and trioctanoin in the lungs of female Osborne- Mendel rats, intratracheal instillation, and subcutaneous or intraperitoneal injection, were used. Benzo(a)anthracene, benzo(a)pyrene, dibenz(a,h)anthracene, and indeno(1,2,3-cd)pyrene were classified in Group B2 (probable human carcinogens).

The EPA (2000) verifies a slope factor for oral exposure to benzo(a)pyrene of 7.3 per mg/kg/day, based on several dietary studies in mice and rats. Neither verified nor provisional quantitative risk estimates were available for the other PAHs in Group B2. The EPA (1980) promulgated an ambient water quality criterion for "total carcinogenic PAHs," based on an oral slope factor derived from a study with benzo(a)pyrene, as being sufficiently protective for the class. Largely because of this precedent, the quantitative risk estimates for benzo(a)pyrene were adopted for the other carcinogenic PAHs when quantitative estimates were needed.

Recent reevaluations of the carcinogenity and mutagenicity of the Group B2 PAHs suggest that there are large differences between individual PAHs in cancer potency (Krewski et al., 1989). Based on the available cancer and mutagenicity data, and assuming that there is a constant relative potency between different carcinogens across different bioassay systems and that the PAHs under consideration have similar dose-response curves, Thorslund and Charnley (1988) derived relative potency values for several PAHs. A more recent Relative Potency Factor (RPF) scheme for the Group B2 PAHs was based only on the induction of lung epidermoid carcinomas in female Osborne-Mendel rats in the lung-implantation experiments (Clement International 1990).

F.7-19 F.7.15 BenzofAIAnthracene

F.7.15.1 Noncancer Toxicity

The oral and inhalation RfD and RfC are not available at this time (EPA 2000).

F.7.15.2 Carcinogenicity

Benzo[a]anthracene has a weight of evidence classification of B2, a probable human carcinogen. The classification was based on sufficient data from animal bioassays. Benzo[a]anthracene produced tumors in mice exposed by gavage; intraperitoneal, subcutaneous or intramuscular injection; and topical application. Benzo[a]anthracene produced mutations in bacteria and in mammalian cells, and transformed mammalian cells in culture.

Although there are no human data that specifically link exposure to benzo[a]anthracene to human cancers, benzo[a]anthracene is a component of mixtures that have been associated with human cancer. These include coal tar, soot, coke oven emissions and cigarette smoke (U.S. EPA, 1984, 1990; IARC, 1984; Lee et al., 1976; Brockhaus and Tomingas, 1976).

Benzo[a]anthracene administration caused an increase in the incidence of tumors by gavage (Klein, 1963); dermal application (IARC, 1973); and both subcutaneous injection (Steiner and Faulk, 1951; Steiner and Edgecomb, 1952) and intraperitoneal injection (Wislocki et al., 1986) assays. A group of male mice was exposed to gavage solutions containing 3% benzo[a]anthracene for 5 weeks. There was an increased incidence of pulmonary adenomas and hepatomas.

Supporting data for carcinogenicity include genetic mutations in five different strains of Salmonella typhimurium. Benzo[a]anthracene produced positive results in an assay for mutations in Drosophila melonqaster (Fahmy and Fahmy, 1973).

The currently used Oral Slope Factor (CSF) for Benzofajanthracene is 7.3E-01 per (mg/kg)/day which is extrapolated from the CSF for Benzo[a]pyrene (BaP), i.e., 0.1 x 7.3 (BaP)

F.7-20 = 7.3E-01 per (mg/kg)/day (USEPA Region III Risk-Based Concentration Table, 10/1/99). The inhalation CSF is not available.

F.7.16 Benzo(B)Fluoranthene

F.7.16.1 Noncancer Toxicity

Little information is available on benzo(b)fluoranthene. However based on the similarities of chemical structures, most properties should be similar to benzo(a)pyrene.

F.7.16.2 Carcinogenicity

A Toxicity Equivalency Factor (TEF) has been developed (EPA, 1993) for benzo(b)fluoranthene which allows the estimation of an oral CSF of 0.73 mg/g/day. The EPA (2000) has classified benzo(b)fluoranthene in cancer weight-of-evidence Group B2 (Probable Human Carcinogen, sufficient evidence of carcinogenicity in animals with inadequate or lack of evidence in humans) based on lung tumors in mice.

F.7.17 BenzoFAIPyrene (BAP)

F.7.17.1 Pharmacokinetics

Benzo(a)pyrene was readily absorbed across the Gl (Rees et al. 1971) and respiratory epithelia (Kotin et al. 1969; Vainich et al. 1976). Benzo(a)pyrene was distributed widely in the tissues of treated rats and mice, but primarily to tissues high in fat, such as adipose tissue and mammary gland (Kotin et al. 1969; Schlede et al. 1970a).

Studies of the metabolism of benzo(a)pyrene provide information relevant to other PAHs because of the structural similarities of all members of the class. Metabolism involves microsomal mixed function oxidase hydroxylation of one or more of the phenyl rings with the formation of phenols and dihydrodiols, probably via formation of arene oxide intermediates (EPA 1979a). The dihydrodiols may be further oxidized to diol epoxides, which, for certain members of the class, are known to be the ultimate carcinogens (LaVoie et al. 1982).

F.7-21 Conjugation with glutathione or glucuronic acid, and reduction to tetrahydrotetrols are important detoxification pathways.

Excretion of benzo(a)pyrene residue was reported to be rapid, although quantitative data were not located (EPA 1979b). Excretion occurred mainly via the feces, probably largely due to biliary secretion (Schlede et al. 1970a, 1970b). The EPA (1980) concluded that accumulation in the body tissues of PAHs from chronic low level exposure would be unlikely.

F.7.17.2 Noncancer Toxicity

The oral RfD and inhalation RfC are not available at this time.

F.7.17.3 Carcinogenicity

The PAHs are ubiquitous, being released to the environment from anthropogenic as well as from natural sources (ATSDR 1992a). Benzo (a)pyrene is the most extensively studied member of the class, inducing tumors in multiple tissues of virtually all laboratory species tested by all routes of exposure. Although epidemiology studies suggested that complex mixtures that contain PAHs (coal tar, soots, coke oven emissions, cigarette smoke) are carcinogenic to humans (EPA 1984), the carcinogenicity cannot be attributed to PAHs alone because of the presence of other potentially carcinogenic substances in these mixtures (ATSDR 1990). In addition, recent investigations showed that the PAH fraction of roofing tar, cigarette smoke, and coke oven emissions accounted for only 0.1 to 8 percent of the total mutagenic activity of the unfractionated complex mixture in Salmonella (Lewtas 1988). Aromatic amines, nitrogen heterocyclic compounds, highly oxygenated quinones, diones, and nitrooxygenated compounds, none of which would be expected to arise from in vivo metabolism of PAHs, probably accounted for the majority of the mutagenicity of coke oven emissions and cigarette smoke. Coal tar, which contains a mixture of many PAHs, has a long history of use in the clinical treatment of a variety of skin disorders in humans (ATSDR 1990).

Because of the lack of human cancer data, assignment of individual PAHs to EPA cancer weight-of-evidence groups was based largely on the results of animal studies with large doses of purified compound (EPA 1984). Frequently, unnatural routes of exposure, including implants of the test chemical in beeswax and trioctanoin in the lungs of female Osborne-Mendel rats,

F.7-22 intratracheal instillation, and subcutaneous or intraperitoneal injection, were used. Benzo (a)anthracene, benzo(a)pyrene, benzo(b)fluoranthene, benzo(k)fluoranthene, chrysene, dibenzo(a,h)anthracene, and indeno(1,2,3-cd)pyrene were classified in Group B2 (probable human carcinogens).

The EPA (2000) verifies a slope factor for oral exposure to benzo(a)pyrene of 7.3 per mg/kg/day, based on several dietary studies in mice and rats. Neither verified nor provisional quantitative risk estimates were available for the other PAHs in Group B2. The EPA (1980) promulgated an ambient water quality criterion for "total carcinogenic PAHs," based on an oral slope factor derived from a study with benzo(a)pyrene, as being sufficiently protective for the class. Largely because of this precedent, the quantitative risk estimates for benzo(a)pyrene were adopted for the other carcinogenic PAHs when quantitative estimates were needed.

Human data specifically linking benzo[a]pyrene (BAP) to a carcinogenic effect are lacking. There are, however, multiple animal studies in many species demonstrating BAP to be carcinogenic following administration by numerous routes. In addition, BAP has produced positive results in numerous genotoxicity assays.

The data for animal carcinogenicity was sufficient. The animal data consist of dietary, gavage, inhalation, intratracheal instillation, dermal and subcutaneous studies in numerous strains of at least four species of rodents and several primates. Repeated BAP administration has been associated with increased incidences of total tumors and of tumors at the site of exposure. The tumor types in mice from oral diet studies include forestomach, squamous cell papillomas and carcinomas (Neal and Rigdon 1967).

Benzo [a]pyrene has been shown to cause genotoxic effects in a broad range of prokaryotic and mammalian cell assay systems (EPA 1990).

The oral slope factor presented in the Region III Risk-Based Concentration Table is 7.3E+0 per mg/kg/day. The cancer slope factor for inhalation is not available.

F.7-23 F.7.18 DibenzofA.HIAnthracene

F.7.18.1 Noncancer Toxicity

The oral RfD and inhalation RfC are not available.

F.7.18.2 Carcinogenicity

Classification -- B2; probable human carcinogen

The EPA (1997) has classified dibenzo(a,h)anthracene in cancer weight-of-evidence group B2 (Probable Human Carcinogen, sufficient evidence of carcinogenicity in animals). Based on carcinomas in mice following oral or dermal exposure and injection site tumors in several species following subcutaneous or intramuscular administration. Dibenzo[a,h]anthracene has induced DNA damage and gene mutations in bacteria as well as gene mutations and transformation in several types of mammalian cell cultures.

Although there are no human data that specifically link exposure to dibenzo[a,h]anthracene with human cancers, dibenzo[a]anthracene is a component of mixtures that have been associated with human cancer. These include coal tar, soot, coke oven emissions and cigarette smoke (EPA, 1984, 1990; IARC, 1984).

Dibenzo[a,h]anthracene has been shown to be carcinogenic when administered to mice by the oral route (Snell and Stewart, 1962, 1963) in a water-olive oil emulsion. Mice developed pulmonary adenomas, pulmonary carcinomas, and mammary carcinomas.

Dibenzo[a,h]anthracene has produced positive results in bacterial DNA damage and mutagenicity assays and in mammalian cell DNA damage, mutagenicity and cell transformation assays.

The currently used Oral Slope Factor (CSF) for Dibenzo[a,h]anthracene is 7.3E+00 per (mg/kg)/day which is extrapolated from the CSF for Benzo[a]pyrene i.e., 1.0 x 7.3 (BaP) = 7.3 per (mg/kg)/day) (USEPA Region III Risk-Based Concentration Table, 10/1/99).

F.7-24 The inhalation Cancer Slope Factor for dibenzo(a,h)anthracene is not available.

F.7.19 IndenoM .2.3-CcOPvrene

F.7.19.1 Noncancer Toxicity

Little information was found on the toxicity of indeno(1,2,3-cd)pyrene. Because of its structural similarity its properties should resemble benzo(a)pyrene.

F.7.19.2 Carcinogenicity

A Toxicity Equivalency Factor (TEF) has been developed for indeno(1,2,3-cd)pyrene (EPA 1993). This allows the estimation of an oral CSF of 0.73 mg/kg/day. The EPA (2000) has classified indeno(1,2,3-cd)pyrene in cancer weight-of-evidence Group B2 (Probable Human Carcinogen, sufficient evidence of carcinogenicity in animals with inadequate or lack of evidence in humans) based on tumors in mice following lung implants.

F.7.20 Aldrin/Dieldrin (Clement 1985)

F.7.20.1 Pharmacokinetics

Both aldrin and dieldrin are carcinogens, causing increases in a variety of tumors in rats at low but not at high doses and producing a higher incidence of liver tumors in mice. The reason for this reversed dose-response relationship is unclear. Neither appears to be mutagenic when tested in a number of systems. Aldrin and dieldrin are both toxic to the reproductive system and teratogenic. Reproductive effects include decreased fertility, increased fetal death, and effects on gestation; while teratogenic effects include cleft palate, webbed foot, and skeletal anomalies. Chronic effects attributed to aldrin and dieldrin include liver toxicity and central

nervous system abnormalities. Both chemicals are acutely toxic; the oral LD50 is around 50

mg/kg, and the dermal LD5o is about 100 mg/kg.

F.7-25 F.7.20.,f Non-Carcinogenic Toxicity

Chronic feeding with aldrin induced evidence of degeneration of the liver in rats. (EPA 1997). The EPA (1997) presented a verified chronic oral RfD of 0.03 ug/kg/day based on a LOAEL for liver effects in rats and an uncertainty factor of 1000. The principal target organ of aldrin is the liver.

F.7.20.2 Carcinogenicity

The EPA (1997) classifies aldrin in cancer weight-of-evidence Group B2 (probable human carcinogen), based on inadequate human data and sufficient animal data. The human data consist of epidemiologic studies that had results that were statistically insignificant. Animal studies associated treatment with liver tumors in male and female mice. The EPA (1997) presented a verified oral slope factor of 17 per mg/kg/day, based on the increased incidence of liver tumors in mice treated in the diet. An inhalation risk estimate was not derived.

F.7.21 Chlordane

Technical chlordane is a mixture of at least 50 related compounds (ATSDR 1992b). The principal components of the mixture are cis- and trans-chlordane, heptachlor, cis- and trans-nonachlor, and alpha-, beta- and gamma-chlordane. Each component has its own environmental fate and transport kinetics, so it is unlikely that the chlordane identified at the site would have the same chemical composition as technical chlordane. It is unclear which chlordane component(s) were found at the site.

F.7.21.1 Pharmacokinetics

Kinetic studies in rats, in which the area under the curve was compared following intravenous and oral dosing, indicate that approximately 80 percent of an oral dose of trans-chlordane is absorbed from the Gl tract (Ohno et al. 1986). In animals, absorbed chlordane is distributed most rapidly to the liver and kidneys, probably because of the extensive vascularity of these organs (Ohno etal. 1986), followed by redistribution to adipose tissue (Barnett and Dorough 1974). In humans, levels of chlordane residues in adipose tissue increase with increasing

F.7-26 duration of exposure (ATSDR 1992b). Metabolism involves principally oxidation, dechlorination, and conjugation, yielding lipophilic products that accumulate in adipose tissue, as well as more polar products that are excreted. Chlordane residues are excreted principally through the bile, although considerable species differences occur. Lactation is an important mechanism of excretion of chlordane residues retained in body fat.

F.7.21.2 Non-Carcinogenic Toxicity

An acute oral lethal dose of chlordane in humans is estimated to be 25 to 50 mg/kg (ATSDR 1992b). Symptoms of acute oral or inhalation intoxication in humans consistently include Gl disturbances such as vomiting, cramps, and diarrhea, and neurological effects including headache, irritability, dizziness, incoordination, convulsions, and coma. Data were not located regarding symptoms or effects in humans chronically exposed by the oral route, and no noncancer effects were observed in several studies of occupationally exposed humans. Mild liver lesions were observed in chronic oral studies in rats and mice. Prenatal or early postnatal exposure of mice to chlordane damages the developing immune system and nervous system. Target organs of chlordane include the liver, nervous system, and the fetus and neonate.

The EPA (1997) derived an RfD of 0.06 mg/kg/day for chronic oral exposure to chlordane, based on an NOEL of 0.055 mg/kg/day for liver effects in a 30-month dietary study in rats (Velsicol Chemical Company 1983). An uncertainty factor of 1,000 was applied; factors of 10 each for inter- and intraspecies variation, and to reflect deficiencies in the database.

F.7.21.3 Carcinogenicity

The EPA (2000) classifies chlordane in cancer weight-of-evidence Group B2, based on inadequate evidence in humans and sufficient evidence in animals. The human data consist of several epidemiologic studies of chlordane manufacturing workers and pesticide applicators. The only indication of a carcinogenic effect was a borderline significantly increased incidence of bladder cancer in one study of pesticide applicators, but chlordane exposure was not quantified and the workers were concomitantly exposed to other carcinogenic pesticides. The animal data consist of several studies in which oral exposure induced a dose-related increase in the incidence of liver tumors. The evidence for carcinogenicity in rats is equivocal. The

F.7-27 EPA (1997) derived an oral slope factor of 1.3 per mg/kg/day and an inhalation unit risk of 0.00037 per ug/m3 based on liver tumor incidence in two dietary studies in mice. The unit risk is equivalent to an inhalation reference dose of 1.29 per mg/kg/day (EPA 1997), assuming humans inhale 20m3 of air/day and weigh 70 kg.

F.7.22 Dieldrin

F.7.22.1 Noncancer Toxicity

The EPA (2000) derived a RfD of 5 x 10~5 mg/kg/day for chronic oral exposure based on a NOAEL of 0.005 mg/kg/day for liver lesions in a two-year rat feeding study (Walker et al., 1969) with an uncertainty factor of 100. The LOAEL was identified as 0.05 mg/kg/day.

At the end of two years the rats had increased liver weights and histopathological examinations revealed liver parenchymal cell changes. These hepatic lesions were considered to be characteristic of exposure to an organochlorine insecticide.

The chronic inhalation RfC is not available at this time.

F.7.22.2 Carcinogenicity

EPA (2000) classifies dieldrin in cancer weight-of-evidence B2. Dieldrin is carcinogenic in seven strains of mice when administered orally. Dieldrin is structurally related to compounds (aldrin, chlordane, heptachlor, heptachlor epoxide, and chlorendic acid) which produce tumors in rodents.

Human carcinogenicity data is considered inadequate. Two studies of workers exposed to aldrin and to dieldrin reported no increased incidence of cancer. Both studies were limited in their ability to detect an excess of cancer deaths.

Animal carcinogenicity data was sufficient. Dieldrin has been shown to be carcinogenic in various strains of mice of both sexes. At different dose levels the effects range from benign liver tumors, to hepatocarcinomas with transplantation confirmation, to pulmonary metastases.

F.7-28 Supporting data for carcinogenicty include genotoxicity tests. Dieldrin causes chromosomal aberrations in mouse cells (Markaryan, 1966; Majumdar et al., 1976) and in human lymphoblastoid cells (Trepanier et al., 1977), mutation in Chinese hamster cells (Ahmed et al., 1977), and unscheduled DNA synthesis in rat (Probst et al., 1981) and human cells (Rocchi et al., 1980).

EPA (2000) reports an Oral Slope Factor of 16 per (mg/kg)/day based on a diet study in mice that produced liver carcinomas.

This inhalation cancer slope factor of 16 per mg/kg/day was calculated from the oral slope factor.

F.7.23 Heptachlor Epoxide (Clement. 1985)

F.7.23.1 Health Effects

Heptachlor epoxide is a liver carcinogen when administered orally to mice. Results from mutagenicity bioassays suggest that this compound also may have genotoxic activity. Reproductive and teratogenic effects in rats include decreased litter size, shortened life span of suckling rats, and development of cataracts in offspring.

Tests with laboratory animals, primarily rodents, demonstrate acute and chronic toxic effects due to heptachlor exposure. Although heptachlor epoxide is absorbed most readily through the gastrointestinal tract, inhalation and skin contact are also potential routes of exposure. Acute exposure by various routes can cause development of hepatic vein thrombi and can effect the central nervous system and cause death. Chronic exposure induces liver changes, affects hepatic microsomal enzyme activity, and causes increased mortality in offspring. The

oral LD50 for heptachlor epoxide in the rat is 47 mg/kg.

Although there are reports of acute and chronic toxicity in humans, with symptoms including tremors, convulsions, kidney damage, respiratory collapse, and death, details of such episodes are not well documented. Heptachlor epoxide has been found in a high percentage of human adipose tissue samples, and also in human milk samples and biomagnification of heptachlor

F.7-29 epoxide occurs. This compound also has been found in the tissues of stillborn infants, suggesting an ability to cross the placenta and bioaccumulate in the fetus.

The oral RfD for heptachlor epoxide is 1.30E-05 mg/kg-day based on increased liver to weight ratios in male and female dogs. Heptachlor epoxide is classified as a B2 carcinogen oral CSF for heptachlor epoxide is 9.1 per mg/kg-day based on an increased incidence of liver carcinomas. The inhalation CSF for heptachlor epoxide is 9.1 per mg/kg-day.

F.7.24 Polychlorinated Biphenyls

F.7.24.1 Noncancer Toxicity

Epidemiologic studies of women in the United States associated oral PCB exposure with low birth weight or retarded musculoskeletal or neurobehavioral development of their infants (ATSDR 1992d). Oral studies in animals established the liver as the target organ in all species, and the thyroid as an additional target organ in the rat. Effects observed in monkeys included gastritis, anemia, chloracne-like dermatitis, and immunosuppression. Oral treatment of animals induced developmental effects, including retarded neurobehavioral and learning development in monkeys. Oral RfD values of 0.02 ug/kg/day for Aroclor-1254 and 0.07 ug/kg/day for Aroclor-1016 were located.

Occupational exposure to PCBs was associated with upper respiratory tract and ocular irritation, loss of appetite, liver enlargement, increased serum concentrations of liver enzymes, skin irritation, rashes and chloracne, and, in heavily exposed female workers, decreased birth weight of their infants (ATSDR 1992d). Concurrent exposure to other chemicals confounded the interpretation of the occupational exposure studies. Laboratory animals exposed by inhalation to Aroclor-1254 vapors exhibited moderate liver degeneration, decreased body weight gain and slight renal tubular degeneration. Neither subchronic nor chronic inhalation RfC values were available.

Target organs for PCBs include the skin, liver, fetus, and neonate.

F.7-30 F.7.24.2 Carcinogenicity

The EPA (2000) classifies the PCBs as EPA cancer weight-of-evidence Group B2 substances (probable human carcinogens), based on inadequate data in humans and sufficient data in animals. The human data consist of several epidemiologic occupational and accidental oral exposure studies with serious limitations, including poorly quantified concentrations of PCBs and durations of exposure, and probable exposures to other potential carcinogens.

The animal data consist of several oral studies in rats and mice with various aroclors, kanechlors, or clophens (commercial PCB mixtures manufactured in the United States, Japan and Germany, respectively) that reported increased incidence of liver tumors in both species (EPA 2000).

The EPA (2000) presents a verified oral slope factor and an inhalation slope factor of 2.0 per mg/kg/day for PCBs based on liver tumors in rats treated with Aroclor-1260.

F.7.25 Dioxins

Specific congeners and homologues of these classes of interest at this site include 1,2,3,4,6,7,8-heptachlorodibenzofuran and -heptachlorodibenzo-p-dioxin; 1,2,3,4,7,8,9­ heptachlorodibenzofuran and -heptachlorodibenzo-p-dioxin; 1,2,3,4,7,8-hexachloro­ dibenzofuran and -hexachlorodibenzo-p-dioxin; 1,2,3,6,7,8- and 2,3,4,6,7,8-hexachloro­ dibenzofuran; 1,2,3,7,8,9-hexachlorodibenzofuran and -hexachlorodibenzo-p-dioxin; 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin; unspecified hexachlorodibenzofurans and dibenzo-p­ dioxins; 1,2,3,7,8- and 2,3,4,7,8-pentachlorodibenzofuran; unspecified pentachlorodibenzo­ furans; 2,3,7,8-tetrachlorodibenzofuran; and unspecified tetrachloro-dibenzofurans.

F.7.25.1 Noncancer Toxicity

Of the members of these classes, the toxicity of 2,3,7,8-TCDD has been studied most extensively. The only effect in humans clearly attributable to 2,3,7,8-TCDD was chloracne (ATSDR 1999). The data, however, also associated exposure to 2,3,7,8-TCDD with hepatotoxicity and neurotoxicity in humans. In animals, toxicity of 2,3,7,8-TCDD is most

F.7-31 commonly manifested as a wasting syndrome with thymic atrophy, terminating in death, with a large number of organ systems showing nonspecific effects. Chronic treatment of animals with 2,3,7,8-TCDD or a mixture of two isomers of hexachlorodibenzo-p-dioxin resulted in liver damage. Immunologic effects may be among the more sensitive endpoints of exposure to the PCDDs in animals. In animals 2,3,7,8-TCDD is a developmental and reproductive toxicant. No verified or provisional noncancer toxicity values were located for any of the chemicals of interest in these classes (EPA 1999, 2000). />~­ F.7.25.? Carcinogenicity

Data regarding the carcinogenicity of 2,3,7,8-TCDD to humans, obtained from epidemiologic studies of workers exposed to pesticides or to other chlorinated chemicals known to be contaminated with 2,3,7,8-TCDD, are conflicting (ATSDR 1999). The interpretation of these studies is not clear because exposure to 2,3,7,8-TCDD was not quantified, multiple routes of exposure (dermal, inhalation, oral) were involved, and the workers were exposed to other potentially carcinogenic compounds. In animals, however, 2,3,7,8-TCDD is clearly carcinogenic, inducing thyroid, lung, and liver tumors in orally treated rats and mice (EPA 1985). Similarly, oral treatment with a mixture of two hexachlorodibenzo-p-dioxin isomers induced liver tumors in rats and mice. On the basis of the animal data, 2,3,7,8-TCDD and the hexachlorodibenzo-p-dioxins were assigned to EPA cancer weight-of-evidence Group 82 (probable human carcinogen). Although the other PCDDs and PCDFs were not formally classified as to carcinogenicity to humans, for regulatory purposes they are treated as probable human carcinogens.

The EPA (1997) presents provisional oral and inhalation slope factors for 2,3,7,8-TCDD of 150,000 per mg/kg/day, based on the incidence of liver and lung tumors in an oral study in rats.

Much less is known about the toxicity of other cdd and cdf congeners. Based on available toxicity data, epa has developed a method for expressing toxicities of these compounds in terms of equivalent amounts of 2,3,7,8-tcdd. "Toxicity equivalency factors", or tefs, are used to convert the concentration of a given cdd/cdf into an equivalent concentration of 2,3,7,8-tcdd.

F.7-32 F.7.26 Asbestos

F.7.26.1 Noncancer Toxicity

Data not available at this time.

F.7.26.2 Carcinogenicity

This section provides information on three aspects of the carcinogenic assessment for the substance in question; the weight-of-evidence judgment of the likelihood that the substance is a human carcinogen, and quantitative estimates of risk from oral exposure and from inhalation exposure. 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 rationale and methods used to develop the carcinogenicity information in IRIS are described in The Risk Assessment Guidelines of 1986 (EPA/600/8-87/045) and in the IRIS Background Document. IRIS summaries developed since the publication of EPA's more recent Proposed Guidelines for Carcinogen Risk Assessment also utilize those Guidelines where indicated (Federal Register 61 (79): 17960-18011, April 23, 1996). Users are referred to the following sections for information on long-term toxic effects other than carcinogenicity.

Weight-Of-Evidence Classification

Classification - A; human carcinogen

Basis - Observation of increased mortality and incidence of lung cancer, mesotheliomas and gastrointestinal cancer in occupationally exposed workers are consistent across investigators and study populations. Animal studies by inhalation in two strains of rats showed similar findings for lung cancer and mesotheliomas. Animal evidence for carcinogenicity via ingestion is limited (male rats fed intermediate-range chrysotile fibers; i.e., >10 um length, developed benign polyps), and epidemiologic data in this regard are inadequate.

F.7-33 Human Carcinogenicitv Data

Sufficient. Numerous epidemiologic studies have reported an increased incidence of deaths due to cancer, primarily lung cancer and mesotheliomas associated with exposure to inhaled asbestos. Among 170 asbestos insulation workers in North Ireland followed for up to 26 years, an increased incidence of death was seen due to all cancers (SMR=390), cancers of the lower respiratory tract and pleura (SMR=1760) (Elmes and Simpson, 1971) and mesothelioma (7 cases). Exposure was not quantified.

Selikoff (1976) reported 59 cases of lung cancer and 31 cases of mesothelioma among 1249 asbestos insulation workers followed prospectively for 11 years. Exposure was not quantified. A retrospective cohort mortality study (Selikoff et al., 1979) of 17,800 U.S. and Canadian asbestos insulation workers for a 10-year period using best available information (autopsy, surgical, clinical) reported an increased incidence of cancer at all sites (319.7 expected vs. 995 observed, SMR=311) and cancer of the lung (105.6 expected vs. 486 observed, SMR=460). A modest increase in deaths from gastrointestinal cancer was reported along with 175 deaths from mesothelioma (none expected). Years of exposure ranged from less than 10 to greater than or equal to 45. Levels of exposure were not quantified. In other pidemiologic studies, the increase for lung and pleural cancers has ranged from a low of 1.9 times the expected rate, in asbestos factory workers in England (Peto et al., 1977), to a high of 28 times the expected rate, in female asbestos textile workers in England (Newhouse et al., 1972). Other occupational studies have demonstrated asbestos exposure-related increases in lung cancer and mesothelioma in several industries including textile manufacturing, friction products manufacture, asbestos cement products, and in the mining and milling of asbestos. The studies used for the inhalation quantitative estimate of risk are listed in the table in Section II.C.2.

A case-control study (Newhouse and Thompson, 1965) of 83 patients with mesothelioma reported 52.6% had occupational exposure to asbestos or lived with asbestos workers compared with 11.8% of the controls. Of the remaining subjects, 30.6% of the mesothelioma cases lived within one-half mile of an asbestos factory compared with 7.6% of the controls.

F.7-34 The occurrence of pleural mesothelioma has been associated with the presence of asbestos fibers in water, fields and streets in a region of Turkey with very high environmental levels of naturally-occurring asbestos (Baris et al., 1979).

Kanarek et al. (1980) conducted an ecologic study of cancer deaths in 722 census tracts in the San Francisco Bay area, using cancer incidence data from the period of 1969-1971. Chrysotile asbestos concentrations in drinking water ranged from nondetectable to 3.6E+7 fibers/L. Statistically significant dose-related trends were reported for lung and peritoneal cancer in white males and for gall bladder, pancreatic and peritoneal cancer in white females. Weaker correlations were reported between asbestos levels and female esophageal, pleural and kidney cancer, and stomach cancer in both sexes. In an extension of this study, Conforti et al. (1981) included cancer incidence data from the period of 1969-1974. Statistically significant positive associations were found between asbestos concentration and cancer of the digestive organs in white females, cancers of the digestive tract in white males and esophageal, pancreatic and stomach cancer in both sexes. These associations appeared to be independent of socioeconomic status and occupational exposure to asbestos.

Marsh (1983) reviewed eight independent ecologic studies of asbestos in drinking water carried out in five geographic areas. It was concluded that even though one or more studies found an association between asbestos in water and cancer mortality (or incidence) due to neoplasms of various organs, no individual study or aggregation of studies exists that would establish risk levels from ingested asbestos. Factors confounding the results of these studies include the possible underestimates of occupational exposure to asbestos and the possible misclassification of peritioneal mesothelioma as Gl cancer.

Polissar et al. (1984) carried out a case-control study which included better control for confounding variables at the individual level. The authors concluded that there was no convincing evidence for increased cancer risk from asbestos ingestion. At the present time, an important limitation of both the case-control and the ecologic studies is the short follow-up time relative to the long latent period for the appearance of tumors from asbestos exposure.

F.7-35 Animal Carcinoqenicitv Data

Sufficient. There have been about 20 animal bioassays of asbestos. Gross et al. (1967) exposed 61 white male rats (strain not reported) to 86 mg chrysotile asbestos dust/cu.m for 30 hours/week for 16 months. Of the 41 animals that survived the exposure period, 10 had lung cancer. No lung cancer was observed in 25 controls.

Reeves (1976) exposed 60-77 rats/group for 4 hours/day, 4 days/week for 2 years to doses of 48.7-50.2 mg/cu.m crocidolite, 48.2-48.6 mg/cu.m amosite and 47.4-47.9 mg/cu.m chrysotile. A 5-14% incidence of lung cancer was observed among concentration groups and was concentration-dependent.

Wagner et al. (1974) exposed CD Wistar rats (19-52/group) to 9.7-14.7 mg/cu.m of several types of asbestos for 1 day to 24 months for 7 hours/day, 5 days/week. A duration-dependent increased incidence of lung carcinomas and mesotheliomas was seen for all types of asbestos after 3 months of exposure compared with controls.

F344 rats (88-250/group) were exposed to intermediate range chrysotile asbestos (1291E+8 f/g) in drinking water by gavage to dams during lactation and then in diet throughout their lifetime (NTP, 1985). A statistically significant increase in incidence of benign epithelial neoplasms (adenomatous polyps in the large intestine) was observed in male rats compared with pooled controls of all NTP oral lifetime studies (3/524). In the same study, rats exposed to short range chrysotile asbestos (6081E+9 f/g) showed no significant increase in tumor incidence.

Ward et al. (1980) administered 10 mg UICC amosite asbestos 3 times/week for 10 weeks by gavage to 50 male F344 rats. The animals were observed for an additional 78-79 weeks post- treatment. A total of 17 colon carcinomas were observed. This result was statistically significant compared with historical controls; no concurrent controls were maintained.

Syrian golden hamsters (126-253/group) were exposed to short and intermediate range chrysotile asbestos at a concentration of 1% in the diet for the lifetime of the animals (NTP, 1983). An increased incidence of neoplasia of the adrenal cortex was observed in both males

F.7-36 and females exposed to intermediate range fibers and in males exposed to short range fibers. This increase was statistically significant by comparison to pooledcontrols but not by comparison to concurrent controls. NTP suggested that the biologic importance of adrenal tumors in the absence of target organ (Gl tract) neoplasia was questionable.

Quantitative Estimate Of Carcinogenic Risk From Oral Exposure

Not available.

Quantitative Estimate Of Carcinogenic Risk From Inhalation Exposure

SUMMARY OF RISK ESTIMATES

Inhalation Unit Risk - 2.3E-1 per (f/mL)

Extrapolation Method — Additive risk of lung cancer and mesothelioma, using relative risk model for lung cancer and absolute risk model for mesothelioma.

Air Concentrations at Specified Risk Levels:

Risk Level Concentration

E-4 (1 in 10,000) 4E-4 f/mL E-5 (1 in 100,000) 4E-5 f/mL E-6 (1 in 1,000,000) 4E-6 f/mL

Additional Comments (Carcinogenicitv. Inhalation Exposure)

Risks have been calculated for males and females according to smoking habits for a variety of exposure scenarios (U.S. EPA, 1986). The unit risk value is calculated for the additive combined risk of lung cancer and mesothelioma, and is calculated as a composite value for males and females. The epidemiological data show that cigarette smoking and asbestos exposure interact synergistically for production of lung cancer and do not interact with regard

F.7-37 to mesothelioma. The unit risk value is based on risks calculated using U.S. general population cancer rates and mortality patterns without consideration of smoking habits. The risks associated with occupational exposure were adjusted to continuous exposure by applying a factor of 140 cu.m/50 cu.m based on the assumption of 20 cu.m/day for total ventilation and 10 cu.m/8-hour workday in the occupational setting.

The unit risk is based on fiber counts made by phase contrast microscopy (PCM) and should not be applied directly to measurements made by other analytical techniques. The unit risk uses PCM fibers because the measurements made in the occupational environment use this method. Many environmental monitoring measurements are reported in terms of fiber counts or mass as determined by transmission electron microscopy (TEM). PCM detects only fibers longer than 5 um and >0.4 um in diameter, while TEM can detect much smaller fibers. TEM mass units are derived from TEM fiber counts. The correlation between PCM fiber counts and TEM mass measurements is very poor. Six data sets which include both measurements show a conversion between TEM mass and PCM fiber count that range from 5-150 (ug/cu.m)/(f/ml_). The geometric mean of these results, 30 (ug/cu.m)/(f/ml_), was adopted as a conversion factor (U.S. EPA, 1986), but it should be realized that this value is highly uncertain. Likewise, the correlation between PCM fiber counts and TEM fiber counts is very uncertain and no generally applicable conversion factor exists for these two measurements.

In some cases TEM results are reported as numbers of fibers <5 um long and of fibers longer than 5 um. Comparison of PCM fiber counts and TEM counts of fibers >5 um show that the fraction of fibers detected by TEM that are also >0.4 um in diameter (and detectable by PCM) varies from 22-53% (U.S. EPA, 1986).

It should be understood that while TEM can be specific for asbestos, PCM is a nonspecific technique and will measure any fibrous material. Measurements by PCM which are made in conditions where other types of fibers may be present may not be reliable.

In addition to the studies cited above, there were three studies of asbestos workers in mining and milling which showed an increase in lung cancer (McDonald et al., 1980, Nicholson et al., 1979; Rubino et al., 1979). The slope factor calculated from these studies was lower than the other studies, possibly because of a substantially different fiber size distribution, and they were

F.7-38 not included in the calculation. The slope factor was calculated by life table methods for lung cancer using a relative risk model, and for mesothelioma using a absolute risk model. The final slope factor for lung cancer was calculated as the weighted geometric mean of estimates from the 11 studies cited in section II.C.2. The final slope factor for mesothelioma is based on the calculated values from the studies of Selikoff et al. (1979), Peto et al. (1982), Seidman et al. (1979), Peto (1980) and Finkelstein (1983) adjusted for the mesothelioma incidence from several additional studies cited previously.

There is some evidence which suggests that the different types of asbestos fibers vary in carcinogenic potency relative to one another and site specificity. It appears, for example, that the risk of mesothelioma is greater with exposure to crocidolite than with amosite or chrysotile exposure alone. This evidence is limited by the lack of information on fiber exposure by mineral type. Other data indicates that differences in fiber size distribution and other process differences may contribute at least as much to the observed variation in risk as does the fiber type itself.

The unit risk should not be used if the air concentration exceeds 4E-2 fibers/ml, since above this concentration the slope factor may differ from that stated.

Discussion Of Confidence (Carcinogenicity. Inhalation Exposure)

A large number of studies of occupationally-exposed workers have conclusively demonstrated the relationship between asbestos exposure and lung cancer or mesothelioma. These results have been corroborated by animal studies using adequate numbers of animals. The quantitative estimate is limited by uncertainty in the exposure estimates, which results from a lack of data on early exposure in the occupational studies and the uncertainty of conversions between various analytical measurements for asbestos.

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R-6 Ohno, Y., T. Kawanishi, and A. Takahashi, 1986, "Comparisons of the Toxicokinetic Parameters in Rats Determined for Low and High Dose of Gamma-chlordane," Journal of Toxicological Science. Vol. 11, pp. 111-124.

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Peto, J., R. Doll, S.V. Howard, L.J. Kinlen and H.C. Lewinsohn. 1977. "A mortality study among workers in an English asbestos factory." Br. J. Ind. Med. 34: 169-172.

Peto, J., H. Siedman and I.J. Selikoff. 1982. "Mesothelioma mortality in asbestos workers: Implications for models of carcinogenesis and risk assessment." Br. J. Cancer. 45: 124-135.

Polissar, L., R.K. Severson and E.S. Boatman. 1984. "A case-control study of asbestos in drinking water and cancer risk." Am. J. Epidemiol. 119(3): 456-471.

Probst, G.S., R.E. McMahon, L.W. Hill, D.Z. Thompson, J.K. Epp and S.B. Neal. 1981. "Chemically induced unscheduled DNA synthesis in primary rat hepatocyte cultures: A comparison with bacterial mutagenicity using 218 chemicals." Environ. Mutagen. 3: 11-32.

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Reeves, A. L., 1986, "Barium," Handbook on the Toxicology of Metals. Friberg, L., G. F. Nordberg, and V. B. Vouk, eds., Vol. II, Elsevier Science Publishers B. V., New York, pp. 84­ 94.

R-7 Rocchi, P., P. Perocco, W. Alberghini, A. Fini and G. Prodi. 1980. "Effect of pesticides on scheduled and unscheduled DMA synthesis of rat thymocytes and human lymphocytes." Arch. Toxicol. 45: 101-108.

Rubino, G.F., G. Piolatto, M.L Newhouse, G. Scansetti, G.A. Aresini and R. Murrary. 1979. "Mortality of chrysotile asbestos workers at the Balangeromine, Northern Italy." Br. J. Ind. Med. 36: 187-194.

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Schroeder, H. A., M. Mitchner, and A. P. Nasor, 1970. "Zirconium, Niobium, Antimony, Vanadium, and Lead in Rats: Life Term Studies," Journal of Nutrition, Vol. 100, pp. 59-66.

Seidman, H., I.J. Selikoff and E.G. Hammond. 1979. "Short-term asbestos work exposure and long-term observation." Ann. N.Y. Acad. Sci. 330:61-89.

Selikoff, I.J. 1976. "Lung cancer and mesothelioma during prospective surveillance of 1249 asbestos insulation workers, 1963-1974." Ann. N.Y. Acad. Sci. 271:448-456.

Selikoff, I.J., E.G. Hammond and H. Siedman. 1979. "Mortality experience of insulation workers in the United States and Canada, 1943-1976." Ann. N.Y. Acad. Sci. 330: 91-116.

Snell, K.C. and H.L. Stewart. 1962. "Pulmonary adenomatosis induced in DBA/2 mice by oral administration of dibenz[a,h]anthracene." J. Natl. Cancer Inst. 28(5): 1043-1049.

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LEAD MODEL Version 0 99d

AIR CONCENTRATION 0 100 ug Pb/m3 DEFAULT Indoor AIR Pb Cone 30 0 percent of outdoor Other AIR Parameters Age Time Outdoors (hr) Vent Rate (m3/day) Lung Abs (%) 0-1 2 0 32 0 1-2 3 32 0 2-3 3 0 32 0 3-4 4 0 32 0 4-5 32 0 5-6 32 0 6 7 4 0 32 0

DIET DEFAULT

DRINKING WATER Cone 4 00 ug Pb/L DEFAULT WATER Consumption DEFAULT

SOIL & DUST Soil constant cone Dust constant cone

Age Soil (ug Pb/g) House Dust (ug Pb/g) 0-1 266 200 0 1-2 266 200 0 2-3 266 0 200 0 3-4 266 0 200 0 4-5 266 0 200 0 5-6 266 0 200 0 6-7 266 0 200 3

Additional Dust Sources None DEFAULT

PAINT Intake 0 00 ug Pb/day DEFAULT

MATERNAL CONTRIBUTION Infant Model Maternal Blood Cone 2 50 ug Pb/dL

CALCULATED BLOOD Pb and Pb UPTAKES

Blood Level Total Uptake Soil+Dust Uptake YEAR (ug/dL) (ug/day) (ug/day)

D 5-1 4 4 8 23 5 33 1-2 4 9 11 91 8 38 2-3 4 6 12 44 8 48 3-4 4 4 12 52 8 59 4-5 3 7 10 45 6 51 5-6 3 2 10 12 5 91 6 7 2 9 10 17 5 60

Diet Uptake Water Uptake Paint Uptake Air Uptake YEAR (ug/day) (ug/day) (ug/day) (ug/day)

0 5-1 2 52 0 36 0 00 0 02 1-2 60 0 90 0 00 0 03 2 3 96 0 95 0 00 0 06 3-4 88 98 0 00 0 07 4-5 84 04 0 00 0 07 5-6 02 10 0 00 0 09 6-7 3 35 13 0 00 0 09 IEUBK MODEL - EXPOSURE TO LEAD SITE NAME: AREA D: BEACON POINT LOCATION: FERRY CREEK, STRATFORD. CONNECTICUT RECEPTOR: FREQUENT RECREATIONAL USER DATE: MARCH 16, 2000

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AOC MATRIX BORING SAMPLE NAME PARAMETER RESULT QUAL UNITS D SOIL BPM A+09 BPM A+09 Lead 5170 MG/KG D SOIL BPM A+50 BPM A+50 Lead 1670 MG/KG D SOIL BPMB+50 BPMB+50 JLead 1750 ^MG/KG D SOIL I BPMB+50 BPMB+50 JLead 1490 MG/KG D SOIL D-SB02 OU3-D-SB02-0002 Lead 14000 MG/KG Avg =4816 TABLE F-11 2 LEAD HOTSPOT SAMPLES FUTURE COMMERCIAL WORKERS ALL SOIL (0-15 FEET BGS) AREAD

AOC MATRIX BORING SAMPLE NAME PARAMETER RESULT QUAL ' UNITS D SOIL BPM A+09 BPM A+09 Lead 5170 MG/KG D SOIL BPM A+50 1 BPM A+50 Lead 1670 MG/KG D SOIL BPMB+50 BPMB+50 Lead 1750 MG/KG D SOIL BPMB+50 BPMB+50 Lead 1490 MG/KG D SOIL D-SB02 OU3-D-SB02-1214 Lead 340 MG/KG D SOIL D-SB02 OU3-D-SB02-0002 [Lead 14000 MG/KG D SOIL D-SB02 OU3-D-SB02-0204 Lead 49000 MG/KG D SOIL D-SB02 OU3-D-SB02-0204 Lead 32000 MG/KG D SOIL D-SB02 OU3-D-SB02-0406 Lead 30000 MG/KG D SOIL D-SB02 OU3-D-SB02-0608 Lead 20000 MG/KG D SOIL D-SB02 OU3-D-SB02-0810 Lead 8200 MG/KG D SOIL D-SB02 OU3-D-SB02-1416 Lead 18 J MG/KG D SOIL D-SB02 OU3-D-SB02-1416 Lead 100 U MG/KG D SOIL D-SB02 OU3-D-SB02-1012 Lead 260 MG/KG Avg =11,711 TABLE F-11.3 LEAD HOTSPOT SAMPLES CURRENT/FUTURE FREQUENT RECREATIONAL USERS SURFACE SOILS/SEDIMENTS (0-2 FEET BGS) AREAD

AOCl MATRIX BORING SAMPLE NAME PARAMETER RESULT QUAL UNITS D WETLAND BN03 " RM-SD-BN03-02 Lead 17400 MG/KG D WETLAND 'BRE+00 BR E+00 Lead 770 MG/KG D WETLAND "D-SD06 OU3-D-SD06-0002 Lead 3310 MG/KG D WETLAND THTCO DE+960 THTCO DE+960 (0 00-0 25) Lead 2400 MG/KG Avg.=59>6 | in CD 0 o CN o LO o> CM n CN LO CD CN S a CD 0 0 CD o o CN CO 1 § . CD 75.26 %

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Adul t Q) FERR Y FREQUEN T Interi m Approac h Methodoloq v UATION S Probabilit y tha t Site-specifi c ARE A concentratio n Typica l bloo d lea concentratio n Intak e materna l Lea d Estimat e Exposur e frequenc y (days/year ) C absenc e Constan t hav e i n a CL Absolut e gastrointestina l absorptio n fractio Calculate d centra l estimat e child-bearin g Centra l estimat e Calculate d 95t h percentil e bloo lea concen t wome n 0 | iBiokineti c | (Averagin g | | LU = i 0 « a lii or LU 1- £ « S I 6 aj O 5 0 = LL o S O 0 L_ Ift C T3 CO 5 fl flj f~i co rv LL° LL" F or a. O — Q m ro z a 2 co° Q. - UJ •* £ LU lii LU LU .a CD co 1 m o: CD UJ O o 0. CD t— LU £ O or" f o UJ m LU 0. o en O^ O or ^ in 0 0 in CN o m en 0 pa d CN 0 in co CN

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3 Adul t exposur e I FREQUEN T RECREATIONA L USE R Intak e FERR Y Interi m Approac h Methodoloq v Probabilit y tha t Site-specifi c Exposur e frequenc y (days/year ) Estimat e materna l bloo d lea concentratio n Lea d i n a ARE A concentratio n Typica l Absolut e gastrointestina l absorptio n Constan t Centra l hav e Calculate d 95t h percentil e bloo lea concentrat i absenc e Calculate d centra l estimat e child-bearin g -5 wome n o [Biokineti c [Averagin g | LU LU QL LU o S E i! O 5 O > 3 « LL aj 1 CD o co trt 1 ra 1­ H in c CO of LL" LL o: z Q. O LU < Q" CD LU £ j CL 1 J CO 5 til LU LU M m V „ £ LU o O —l X m J LU £. Q. O K. XI 0. 0. g LU m LU Q. 55 £ Q O ce IEUBK MODEL - EXPOSURE TO LEAD SITE NAME AREA D BEACON POINT LOCATION FERRY CREEK STRATFORE CONNECTICUT RECEPTOR FREQUENT RECREATIONA^ USER DATE APRIL 7 2000

LEAD MODEL Version 0 99d

AIR CONCENTRATION ICO ug Pb/rru DEFAULT Indoor AIR Pb Cone 30 0 percent of outdoor Other AIR Parameters Age Time Outdoors (hr) Vent Rate (m3/day) Lung Abs 0-1 1 0 32 0 1-2 2 0 32 0 2-3 3 0 32 0 3-4 4 0 32 0 4-5 4 0 32 0 5-6 4 0 7 0 32 0 6-7 4 0 7 0 32 0

DIET DEFAULT

DRINKING WATER Cone 4 00 ug Pb/L DEFAULT WATER Consumption DEFAULT

SOIL & DUST Soil constant cone Dust constant cone

Age Soil (ug Pb/g) ]House Dust (ug Pb/g) 0-1 1436 0 200 0 1-2 1436 0 200 0 2-3 1436 0 230 0 3-4 1436 0 230 0 4-5 1436 0 200 0 5-6 1436 0 200 0 6-7 1436 0 200 0

Additional Dust Sources None DEFAULT

PAINT Intake 0 00 ug Pb/day DEFAULT

MATERNAL CONTRIBUTION Infant Model Maternal Blood Cone 2 50 ug Pb/dL

CALCULATED BLOOD Pb and Pb UPTAKES

Blood Level Total Ijptake Soil+Dust Uptake YEAR (ug/dL) (ug/day) (ug/day)

0 5-1 9 6 IS 17 15 59 1-2 11 0 27 C6 23 98 2-3 10 3 28 20 24 68 3-4 9 9 28 90 25 37 4 5 8 3 23 C7 19 90 5-6 7 C 22 *B 18 30 6 7 6 3 21 fc2 17 48

Diet Uptake Water Uptake Paint Uptake Air Uptake YEAR (ug/day) lug/cay) (ug/day) (ug/day)

0 5-1 2 24 0 3^ 0 00 0 02 1-2 2 26 0 76 0 00 0 03 2-3 2 62 0 84 0 00 0 C6 3-4 2 58 C 8S 0 00 C C~ 4-5 2 64 C 96 0 00 C 07 5-6 2 84 1 04 0 00 0 09 6-7 3 17 1 07 0 00 0 09 IEUBK MODEL - EXPOSURE TO LEAD SITE NAME: AREA D: BEACON POINT LOCATION: FERRY CREEK, STRATFORD CONNECTICUT RECEPTOR: FREQUENT RECREATIONAL USER DATE: APRIL 7, 2000

Cutoff: 10.8 ug/dL X Above: 36.05 X. Below: 63.95 G. Mean: 8.8

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