Nanofiltration with Chloramines ( Ground Water Systems) Source: Stage 1 DBPR RIA ( USEPA 1998a) for Stage 1 technologies; Federal Advisory Committees Act ( FACA) deliberations for Stage 2 technologies ( USEPA 2000p). Economic Analysis for the Stage 2 DBPR Proposal 3 38 July 2003 Exhibit 3.14 Aggregated Treatment Technology Categories for Stage 1 DBPR Used for the Stage 2 DBPR EA Treatment Technology Category Explanation of Technology for Surface Water Plants Explanation of Technology for Ground Water Plants Adjust Primary Disinfectant Dose Reduce primary disinfectant dose ( usually chlorine) NA Enhanced Coagulation/ Enhanced Softening Increased TOC removal through increased coagulant addition to meet Stage 1 DBPR requirements NA Turbo Coagulation Increased TOC removal through increased coagulant addition, but higher than that required by enhanced coagulation NA Moving Point of Disinfection Move point of disinfection downstream to minimize formation of DBPs NA Chlorine Dioxide Chlorine dioxide instead of chlorine for primary disinfection NA Ozone Ozone instead of chlorine for primary disinfection, applied to raw or settled water Ozone instead of chlorine for primary disinfection, applied to raw or settled water MF/ UF Microfiltration or ultrafiltration as the particle removal process NA GAC10 Granular activated carbon with a 10 minute Empty Bed Contact Time ( EBCT) NA GAC10 + Advanced Disinfectants GAC10 + chlorine dioxide ( large and medium systems) GAC10 + UV ( small systems) NA GAC20 Granular activated carbon with a 20 minute EBCT Granular activated carbon with a 20 minute EBCT GAC20 + Advanced Disinfectants GAC20 + UV or ozone NA Membranes Integrated membranes as the particle removal process ( MF/ UF and nanofiltration) Nanofiltration alone as the particle removal process Notes: NA = Not applicable to plant type. Italic font indicates that technology was not considered in estimating costs of rule alternatives.

Source: Technology and Cost Document ( USEPA 2003o); applicability to ground water systems discussed in Chapter 6 and Appendix B of this EA. Economic Analysis for the Stage 2 DBPR Proposal 3 39 July 2003 3.6.2 Treatment Characterization Although cost analyses in Chapter 6 are performed for each of the nine system size categories separately, treatment characterizations are predicted according to the following aggregated categories by population served:

° Small systems ° Serving fewer than 100 people ° Serving 101 to 1,000 people ° Serving 1,001 to 10,000 people ° Medium systems   serving 10,001 to 100,000 people ° Large systems   serving more than 100,000 people Small systems were stratified by the three population categories shown above to reflect differences in the number of systems needing to change technologies and the technology options available to each category. The treatment characterizations presented here and in Chapter 6 show the nine population size categories used for costing, but present one compliance forecast ( as a percentage of the total baseline number of plants) for each of the population size categories listed above.

Exhibits 3.15 and 3.16 summarize the pre Stage 1 DBPR baseline technologies in place for surface and ground water treatment plants, respectively. For plants in large and medium ground water systems, ICR treatment data were used to derive the estimated percent of plants using each technology. For plants in large and medium surface water systems, SWAT predicted results from the " initial plant run" ( USEPA 2001e) are used to characterize the percent of plants using each technology in Exhibit 3.15. SWAT predicted results were used instead of available ICR observed data to allow for consistent comparison of pre Stage 1 data to modeled pre Stage 2 and post Stage 2 data ( if observed data were used for pre Stage 1 technology in place estimates, differences between pre Stage 1 and pre Stage 2 results would reflect potential inconsistencies in observed vs. predicted data, not just the expected change from pre Stage 1 to pre Stage 2).

For all small systems, the only significant use of advanced technologies was reported in the NRWA database for small surface water systems ( approximately 3.6 percent are estimated to be using MF/ UF, as shown in Exhibit 3.16). The percent using each technology is based on evaluation of CWS data; EPA assumed that NTNCWSs use similar technologies for the size categories shown.

Exhibits 3.17 and 3.18 show the predicted technologies in place following the Stage 1 DBPR ( pre Stage 2 DBPR baseline). In most cases, the technologies in place for the pre Stage 2 baseline can be derived by adding the technology selection for the Stage 1 DBPR ( shown in Appendix C) to the technologies in place for the pre Stage 1 baseline ( Exhibits 3.15 and 3.16). This is not true, however, for plants in large and medium surface water systems. SWAT outputs for " technology selection" only reflect those technologies selected for compliance rule and do not account for the corresponding decrease in technologies out of which plants are moving. The SWAT program produces a different type of result Economic Analysis for the Stage 2 DBPR Proposal 3 40 July 2003 NO ADVANCED TECHNOLOGIES 1 WITH ADVANCED TECHNOLOGY CL2 CLM TOTAL Chlorine Dioxide UV Ozone MF/ UF GAC10 GAC10 + AD GAC20 GAC20 + AD Membranes TOTAL A B C = A + B D E F G H I J K L M = SUM( D: L) N £ 100 96.4% 453 0.0% 0 96.4% 453 0 0 3.6% 17 0.0% 0 0.0% 0 0.0% 0 3.6% 17 0% 0 101 500 96.4% 770 0.0% 0 96.4% 770 0.0% 0 0.0% 0 3.6% 29 0.0% 0 0.0% 0 0.0% 0 3.6% 29 0% 0 501 1,000 96.4% 487 0.0% 0 96.4% 487 0.0% 0 0.0% 0 3.6% 18 0.0% 0 0.0% 0 0.0% 0 3.6% 18 0 1,001  3,300 96.4% 1,064 0.0% 0 96.4% 1,064 0.0% 0 0.0% 0 3.6% 40 0.0% 0 0.0% 0 0.0% 0 3.6% 40 0% 0 3,301 10,000 96.4% 1,169 0.0% 0 96.4% 1,169 0.0% 0 0.0% 0 3.6% 44 0.0% 0 0.0% 0 0.0% 0 3.6% 44 0 10,001 50,000 54.0% 695 31.0% 399 85.0% 1,094 8.1% 104 5.1% 66 0.4% 5 1.5% 19 0.0% 0 0.0% 0 0.0% 0 0.0% 0 15.0% 193 35.9% 462 50,001 100,000 54.0% 290 31.0% 167 85.0% 457 8.1% 43 5.1% 28 0.4% 2 1.5% 8 0.0% 0 0.0% 0 0.0% 0 0.0% 0 15.0% 81 35.9% 193 100,001 1 Million 54.0% 309 31.0% 177 85.0% 486 8.1% 46 5.1% 29 0.4% 2 1.5% 8 0.0% 0 0.0% 0 0.0% 0 0.0% 0 15.0% 86 35.9% 206 > 1 Million 54.0% 40 31.0% 23 85.0% 63 8.1% 6 5.1% 4 0.4% 0 1.5% 1 0.0% 0 0.0% 0 0.0% 0 0.0% 0 15.0% 11 35.9% 26 Total %, Plants 80.4% 5,276 11.7% 766 92.1% 6,042 3.0% 199 1.9% 127 2.4% 156 0.6% 36 0.0% 0 0.0% 0 0.0% 0 0.0% 0 7.9% 518 13.5% 887 Note: Detail may not add to totals due to independent rounding. 1" No Adv" includes conventional, non conventional, and softening plants. Source: Surface water systems serving 10,000 people or fewer: National Rural Water Survey ( USEPA, 2001c). Surface water systems serving more than 10,000 people: SWAT initial plant run ( USEPA, 2001e). Percentage using chloramine is taken from the Occurrence Document. TOTAL USING CLM System Size ( Population Served)

NO ADVANCED TECHNOLOGIES 1 WITH ADVANCED TECHNOLOGY CL2 CLM TOTAL Chlorine Dioxide UV Ozone MF/ UF GAC10 GAC10 + AD GAC20 GAC20 + AD Membranes TOTAL A B C = A + B D E F G H I J K L M = SUM( D: L) N £ 100 96.4% 287 0.0% 0 96.4% 287 0 0 3.6% 11 0.0% 0 0.0% 0 0.0% 0 3.6% 11 0% 0 101 500 96.4% 290 0.0% 0 96.4% 290 0.0% 0 0.0% 0 3.6% 11 0.0% 0 0.0% 0 0.0% 0 3.6% 11 0% 0 501 1,000 96.4% 104 0.0% 0 96.4% 104 0.0% 0 0.0% 0 3.6% 4 0.0% 0 0.0% 0 0.0% 0 3.6% 4 0 1,001  3,300 96.4% 69 0.0% 0 96.4% 69 0.0% 0 0.0% 0 3.6% 3 0.0% 0 0.0% 0 0.0% 0 3.6% 3 0% 0 3,301 10,000 96.4% 22 0.0% 0 96.4% 22 0.0% 0 0.0% 0 3.6% 1 0.0% 0 0.0% 0 0.0% 0 3.6% 1 0 10,001 50,000 54.0% 5 31.0% 3 85.0% 8 8.1% 1 5.1% 0 0.4% 0 1.5% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 15.0% 1 35.9% 3 50,001 100,000 54.0% 1 31.0% 0 85.0% 1 8.1% 0 5.1% 0 0.4% 0 1.5% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 15.0% 0 35.9% 0 100,001 1 Million 54.0% 1 31.0% 0 85.0% 1 8.1% 0 5.1% 0 0.4% 0 1.5% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 15.0% 0 35.9% 0 > 1 Million 54.0% 0 31.0% 0 85.0% 0 8.1% 0 5.1% 0 0.4% 0 1.5% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 15.0% 0 35.9% 0 Total %, Plants 95.8% 779 0.4% 3 96.2% 782 0.1% 1 0.1% 1 3.6% 29 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 3.8% 31 0.5% 4 Note: Detail may not add to totals due to independent rounding. 1" No Adv" includes conventional, non conventional, and softening plants. Source: Surface water systems serving 10,000 people or fewer: National Rural Water Survey ( USEPA, 2001c). Surface water systems serving more than 10,000 people: SWAT initial plant run ( USEPA, 2001e). Percentage using chloramine is taken from the Occurrence Document. TOTAL USING CLM System Size ( Population Served) directly, called " ending technologies" that accounts for those plants that already have an advanced technology but must select another to meet the rule alternative.

Exhibit 3.15a Pre Stage 1 DBPR Technologies in Place for CWS Surface Water Plants Exhibit 3.15b Pre Stage 1 DBPR Technologies in Place for NTNCWS Surface Water Plants Economic Analysis for the Stage 2 DBPR Proposal 3 41 July 2003 System Size ( Population Served) No Adv 1 CL2 No Adv 1 CLM UV CL2 UV CLM Ozone CL2 Ozone CLM GAC20 CL2 GAC20 CLM TOTAL USING CLM TOTAL A B C D E F G H I J K = B + D + F + H + J L = SUM( A: J) £ 100 100.0% 7,772 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 100.0% 7,772 101 500 100.0% 15,725 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 100.0% 15,725 501 1,000 100.0% 6,133 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 100.0% 6,133 1,001  3,300 100.0% 7,890 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 100.0% 7,890 3,301 10,000 100.0% 4,975 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 100.0% 4,975 10,001 50,000 92.3% 4,954 5.4% 289 0.8% 41 0.0% 0 0.0% 0 0.0% 0 1.5% 83 0.0% 0 5.4% 289 100.0% 5,367 50,001 100,000 92.3% 682 5.4% 40 0.8% 6 0.0% 0 0.0% 0 0.0% 0 1.5% 11 0.0% 0 5.4% 40 100.0% 738 100,001 1 Million 92.3% 808 5.4% 47 0.8% 7 0.0% 0 0.0% 0 0.0% 0 1.5% 13 0.0% 0 5.4% 47 100.0% 875 > 1 Million 92.3% 17 5.4% 1 0.8% 0 0.0% 0 0.0% 0 0.0% 0 1.5% 0 0.0% 0 5.4% 1 100.0% 18 Total %, Plants 98.9% 48,956 0.8% 377 0.0% 0 0.0% 0 0.1% 54 0.0% 0 0.0% 0 0.0% 0 0.2% 108 0.0% 0 0.8% 377 100.0% 49,495 Note: Detail may not add to totals due to independent rounding 1" No Adv" includes conventional, non conventional, and softening plants. Membranes CLM Membranes CL2 Source: Ground water systems serving 10,000 people or fewer  limited data available. Assumed only cholrine usage and no advanced technologies; Ground water systems serving more than 10,000 people  based on ICR data for 130 large GW plants.

System Size ( Population Served) No Adv 1 CL2 No Adv 1 CLM UV CL2 UV CLM Ozone CL2 Ozone CLM GAC20 CL2 GAC20 CLM TOTAL USING CLM TOTAL A B C D E F G H I J K = B + D + F + H + J L = SUM( A: J) £ 100 100.0% 3,662 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 100.0% 3,662 101 500 100.0% 2,624 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 100.0% 2,624 501 1,000 100.0% 717 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 100.0% 717 1,001  3,300 100.0% 267 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 100.0% 267 3,301 10,000 100.0% 27 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 100.0% 27 10,001 50,000 92.3% 4 5.4% 0 0.8% 0 0.0% 0 0.0% 0 0.0% 0 1.5% 0 0.0% 0 5.4% 0 100.0% 4 50,001 100,000 92.3% 0 5.4% 0 0.8% 0 0.0% 0 0.0% 0 0.0% 0 1.5% 0 0.0% 0 5.4% 0 100.0% 0 100,001 1 Million 92.3% 1 5.4% 0 0.8% 0 0.0% 0 0.0% 0 0.0% 0 1.5% 0 0.0% 0 5.4% 0 100.0% 1 > 1 Million 92.3% 0 5.4% 0 0.8% 0 0.0% 0 0.0% 0 0.0% 0 1.5% 0 0.0% 0 5.4% 0 100.0% 0 Total %, Plants 100.0% 7,303 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 100.0% 7,303 Note: Detail may not add to totals due to independent rounding 1 " No Adv" includes conventional, non conventional, and softening plants. Membranes CLM Membranes CL2 Source: Ground water systems serving 10,000 people or fewer  limited data available. Assumed only cholrine usage and no advanced technologies; Ground water systems serving more than 10,000 people  based on ICR data for 130 large GW plants. Exhibit 3.16a Pre Stage 1 DBPR Technologies in Place for CWS Ground Water Plants Exhibit 3.16b Pre Stage 1 DBPR Technologies in Place for NTNCWS Ground Water Plants Economic Analysis for the Stage 2 DBPR Proposal 3 42 July 2003 NO ADVANCED TECHNOLOGIES 1 WITH ADVANCED TECHNOLOGY CL2 CLM TOTAL Chlorine Dioxide UV Ozone MF/ UF GAC10 GAC10 + AD GAC20 GAC20 + AD Membranes TOTAL A B C = A + B D E F G H I J K L M = SUM( D: L) N £ 100 43.0% 202 30.5% 143 73.4% 345 18.6% 88 3.8% 18 0.0% 0 4.1% 19 26.6% 125 39.6% 186 101 500 35.7% 285 35.6% 284 71.3% 569 2.3% 19 11.9% 95 9.9% 79 2.3% 19 0.9% 7 1.3% 10 28.7% 229 47.5% 379 501 1,000 35.7% 180 35.6% 180 71.3% 360 2.3% 12 11.9% 60 9.9% 50 2.3% 12 0.9% 5 1.3% 6 28.7% 145 47.5% 240 1,001  3,300 33.5% 370 41.5% 457 75.0% 827 5.1% 56 10.1% 111 5.4% 60 2.6% 28 1.1% 12 0.7% 8 25.0% 276 52.8% 582 3,301 10,000 33.5% 406 41.5% 503 75.0% 909 5.1% 62 10.1% 122 5.4% 66 2.6% 31 1.1% 13 0.7% 9 25.0% 303 52.8% 640 10,001 50,000 37.7% 486 36.3% 467 74.0% 952 7.0% 90 12.8% 165 1.8% 24 2.2% 28 1.1% 14 0.4% 5 0.0% 0 0.7% 9 26.0% 335 52.7% 679 50,001 100,000 37.7% 203 36.3% 195 74.0% 398 7.0% 37 12.8% 69 1.8% 10 2.2% 12 1.1% 6 0.4% 2 0.0% 0 0.7% 4 26.0% 140 52.7% 284 100,001 1 Million 37.7% 216 36.3% 208 74.0% 424 7.0% 40 12.8% 73 1.8% 10 2.2% 13 1.1% 6 0.4% 2 0.0% 0 0.7% 4 26.0% 149 52.7% 302 > 1 Million 37.7% 28 36.3% 27 74.0% 54 7.0% 5 12.8% 9 1.8% 1 2.2% 2 1.1% 1 0.4% 0 0.0% 0 0.7% 1 26.0% 19 52.7% 39 Total %, Plants 36.2% 2,376 37.5% 2,463 73.8% 4,839 4.9% 321 10.7% 705 5.9% 388 0.8% 54 0.4% 27 1.8% 117 0.6% 38 1.1% 71 26.2% 1,721 50.8% 3,330 Note: Detail may not add to totals due to independent rounding 1" No Adv" includes conventional, non conventional, and softening plants.

Source: Surface water systems serving 10,000 people or less: Add Technologies in Place for the Pre Stage 1 DBPR Baseline ( Exhibit 3.15) to Stage 1 Technology Selection ( Exhibit C. 1. Surface water systems serving 10,000 people or more: Use ending technologies. System Size ( Population Served) TOTAL USING CLM NO ADVANCED TECHNOLOGIES1 WITH ADVANCED TECHNOLOGY CL2 CLM TOTAL Chlorine Dioxide UV Ozone MF/ UF GAC10 GAC10 + AD GAC20 GAC20 + AD Membranes TOTAL A B C = A + B D E F G H I J K L M = SUM( D: L) N £ 100 43.0% 128 30.5% 91 73.4% 219 18.6% 56 3.8% 11 0.0% 0 4.1% 12 26.6% 79 39.6% 118 101 500 35.7% 108 35.6% 107 71.3% 215 2.3% 7 11.9% 36 9.9% 30 2.3% 7 0.9% 3 1.3% 4 28.7% 86 47.5% 143 501 1,000 35.7% 39 35.6% 38 71.3% 77 2.3% 3 11.9% 13 9.9% 11 2.3% 3 0.9% 1 1.3% 1 28.7% 31 47.5% 51 1,001  3,300 33.5% 24 41.5% 30 75.0% 54 5.1% 4 10.1% 7 5.4% 4 2.6% 2 1.1% 1 0.7% 1 25.0% 18 52.8% 38 3,301 10,000 33.5% 8 41.5% 10 75.0% 17 5.1% 1 10.1% 2 5.4% 1 2.6% 1 1.1% 0 0.7% 0 25.0% 6 52.8% 12 10,001 50,000 37.7% 3 36.3% 3 74.0% 7 7.0% 1 12.8% 1 1.8% 0 2.2% 0 1.1% 0 0.4% 0 0.0% 0 0.7% 0 26.0% 2 52.7% 5 50,001 100,000 37.7% 0 36.3% 0 74.0% 1 7.0% 0 12.8% 0 1.8% 0 2.2% 0 1.1% 0 0.4% 0 0.0% 0 0.7% 0 26.0% 0 52.7% 1 100,001 1 Million 37.7% 0 36.3% 0 74.0% 1 7.0% 0 12.8% 0 1.8% 0 2.2% 0 1.1% 0 0.4% 0 0.0% 0 0.7% 0 26.0% 0 52.7% 1 > 1 Million 37.7% 0 36.3% 0 74.0% 0 7.0% 0 12.8% 0 1.8% 0 2.2% 0 1.1% 0 0.4% 0 0.0% 0 0.7% 0 26.0% 0 52.7% 0 Total %, Plants 38.2% 310 34.4% 280 72.6% 590 1.9% 15 7.3% 60 12.5% 101 0.0% 0 0.0% 0 2.9% 23 0.6% 5 2.3% 18 27.4% 223 45.3% 368 Note: Detail may not add to totals due to independent rounding 1" No Adv" includes conventional, non conventional, and softening plants. Source: Surface water systems serving 10,000 people or less: Add Technologies in Place for the Pre Stage 1 DBPR Baseline ( Exhibit 3.15) to Stage 1 Technology Selection ( Exhibit C. 1. Surface water systems serving 10,000 people or more: Use ending technologies. System Size ( Population Served) TOTAL USING CLM Exhibit 3.17a Pre Stage 2 DBPR Technologies in Place for CWS Surface Water Plants Exhibit 3.17b Pre Stage 2 DBPR Technologies in Place for NTNCWS Surface Water Plants Economic Analysis for the Stage 2 DBPR Proposal 3 43 July 2003 NO ADVANCED TECHNOLOGIES 1 WITH ADVANCED TECHNOLOGIES CL2 CLM TOTAL UV CL2 UV CLM Ozone CL2 Ozone CLM GAC20 CL2 GAC20 CLM TOTAL A B C = A+ B D E F G H I J K L = SUM( D: K) M = B+ E+ G+ I+ K £ 100 95.2% 7,397 2.9% 222 98.0% 7,619 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 1.0% 80 0.4% 31 0.5% 41 2.0% 153 4.4% 343 101 500 95.8% 15,068 2.5% 389 98.3% 15,457 0.0% 0 0.0% 0 0.1% 22 0.4% 67 0.0% 0 0.6% 88 0.1% 18 0.5% 73 1.7% 268 3.9% 617 501 1,000 95.8% 5,877 2.5% 152 98.3% 6,029 0.0% 0 0.0% 0 0.1% 9 0.4% 26 0.0% 0 0.6% 34 0.1% 7 0.5% 28 1.7% 105 3.9% 240 1,001  3,300 96.6% 7,620 2.0% 160 98.6% 7,780 0.0% 0 0.0% 0 0.2% 18 0.7% 55 0.0% 0 0.0% 4 0.0% 3 0.4% 30 1.4% 110 3.1% 248 3,301 10,000 96.6% 4,805 2.0% 101 98.6% 4,906 0.0% 0 0.0% 0 0.2% 12 0.7% 35 0.0% 0 0.0% 2 0.0% 2 0.4% 19 1.4% 70 3.1% 157 10,001 50,000 89.1% 4,783 7.3% 390 96.4% 5,173 0.8% 45 0.8% 42 0.0% 0 0.0% 2 1.7% 89 0.3% 14 3.6% 194 8.4% 449 50,001 100,000 89.1% 658 7.3% 54 96.4% 712 0.8% 6 0.8% 6 0.0% 0 0.0% 0 1.7% 12 0.3% 2 3.6% 27 8.4% 62 100,001 1 Million 89.6% 784 7.0% 61 96.6% 845 0.8% 7 0.7% 6 0.0% 0 0.0% 0 1.6% 14 0.2% 2 3.4% 30 7.9% 69 > 1 Million 89.6% 16 7.0% 1 96.6% 18 0.8% 0 0.7% 0 0.0% 0 0.0% 0 1.6% 0 0.2% 0 3.4% 1 7.9% 1 Total %, Plants 95.0% 47,009 3.1% 1,529 98.1% 48,539 0.0% 0 0.0% 0 0.2% 120 0.5% 238 0.0% 0 0.4% 211 0.4% 178 0.4% 209 1.9% 956 4.4% 2,187 Note: Detail may not add to totals due to independent rounding 1 No advanced technologies includes conventional, non conventional, and softening plants. Source: Add Technologies in Place for the Pre Stage 1 DBPR Baseline ( Exhibit 3.16) to Stage 1 Technology Selection ( Exhibit C. 2) Membranes CL2 Membranes CLM TOTAL USING CLM System Size ( Population Served)

NO ADVANCED TECHNOLOGIES 1 WITH ADVANCED TECHNOLOGIES CL2 CLM TOTAL UV CL2 UV CLM Ozone CL2 Ozone CLM GAC20 CL2 GAC20 CLM TOTAL A B C = A+ B D E F G H I J K L = SUM( D: K) M = B+ E+ G+ I+ K £ 100 95.2% 3,486 2.9% 104 98.0% 3,590 0.0% 0 0.0% 0 0.0% 0 0.0% 0 0.0% 0 1.0% 38 0.4% 15 0.5% 19 2.0% 72 4.4% 162 101 500 95.8% 2,515 2.5% 65 98.3% 2,580 0.0% 0 0.0% 0 0.1% 4 0.4% 11 0.0% 0 0.6% 15 0.1% 3 0.5% 12 1.7% 45 3.9% 103 501 1,000 95.8% 687 2.5% 18 98.3% 704 0.0% 0 0.0% 0 0.1% 1 0.4% 3 0.0% 0 0.6% 4 0.1% 1 0.5% 3 1.7% 12 3.9% 28 1,001  3,300 96.6% 258 2.0% 5 98.6% 263 0.0% 0 0.0% 0 0.2% 1 0.7% 2 0.0% 0 0.0% 0 0.0% 0 0.4% 1 1.4% 4 3.1% 8 3,301 10,000 96.6% 26 2.0% 1 98.6% 27 0.0% 0 0.0% 0 0.2% 0 0.7% 0 0.0% 0 0.0% 0 0.0% 0 0.4% 0 1.4% 0 3.1% 1 10,001 50,000 89.1% 4 7.3% 0 96.4% 4 0.8% 0 0.8% 0 0.0% 0 0.0% 0 1.7% 0 0.3% 0 3.6% 0 8.4% 0 50,001 100,000 89.1% 0 7.3% 0 96.4% 0 0.8% 0 0.8% 0 0.0% 0 0.0% 0 1.7% 0 0.3% 0 3.6% 0 8.4% 0 100,001 1 Million 89.6% 1 7.0% 0 96.6% 1 0.8% 0 0.7% 0 0.0% 0 0.0% 0 1.6% 0 0.2% 0 3.4% 0 7.9% 0 > 1 Million 89.6% 0 7.0% 0 96.6% 0 0.8% 0 0.7% 0 0.0% 0 0.0% 0 1.6% 0 0.2% 0 3.4% 0 7.9% 0 Total %, Plants 95.5% 6,976 2.6% 193 98.2% 7,170 0.0% 0 0.0% 0 0.1% 5 0.2% 16 0.0% 0 0.8% 57 0.3% 19 0.5% 36 1.8% 133 4.1% 302 Note: Detail may not add to totals due to independent rounding 1 No advanced technologies includes conventional, non conventional, and softening plants. Source: Add Technologies in Place for the Pre Stage 1 DBPR Baseline ( Exhibit 3.16) to Stage 1 Technology Selection ( Exhibit C. 2) Membranes CL2 Membranes CLM TOTAL USING CLM System Size ( Population Served) Exhibit 3.18a Pre Stage 2 DBPR Technologies in Place for CWS Ground Water Plants Exhibit 3.18b Pre Stage 2 DBPR Technologies in Place for NTNCWS Ground Water Plants 10 SWAT results are used for both cost and quantified benefits analysis in this EA. SWAT results are used to predict treatment changes and resulting treatment costs ( see Chapter 6) and to predict reductions in average DBP levels. Changes in average DBP levels are the basis for quantifying the reduction in bladder cancer cases attributable to the Stage 2 DBPR ( see Chapter 5).

Economic Analysis for the Stage 2 DBPR Proposal 3 44 July 2003 3.7 DBP Occurrence for the Pre Stage 1 and Pre Stage 2 DBPR Baselines For pre Stage 1 DBPR conditions, observed DBP data is available from the ICR for large systems and from the NRWA survey, WATER:\ STATS, and other data sources for medium and small systems ( see section 3.2 for a summary of data sources). Because the Stage 1 DBPR compliance deadline recently occurred ( January 2002) for large and medium surface water systems and will not occur until January 2004 for all other systems, observed DBP data for pre Stage 2, or post Stage 1 conditions are not available and must be predicted for this EA.

As stated in section 3.3, SWAT was the primary tool used during the M DBP FACA process and in this EA to predict changes in treatment and related reductions in national DBP levels as a result of the Stage 1 and Stage 2 DBPRs. 10 Comparisons of SWAT to ICR data, however, showed large differences between observations and modeled data in some cases ( see Appendix A for plant by plant comparisons of SWAT and ICR data). This is to be expected to some extent   the SWAT predicted DBP concentration is a function of influent water quality, treatment conditions, flows, residence times, and other factors that are incorporated into the model algorithms. In essence, SWAT models a particular " slug" of water from the source through the distribution system. Non uniform flow, mixing, sampling time, and other factors in the field do not allow a perfect correlation between the influent water sample and finished water sample. Also, the distribution system sampling locations for the ICR are similar, but not equivalent to, the conditions modeled by SWAT. For example, the ICR data set uses the average value of the concentrations at four sampling locations: two thought to represent the average residence time in the distribution system, one thought to represent the maximum residence time, and another located elsewhere in the distribution system. The modeled distribution system data are computed using the average residence time in the distribution system, based on the average of the residence times at the four ICR distribution system locations. Appendix A provides the rationale for why SWAT was selected as the primary tool for estimating benefits and costs of the Stage 2 DBPR, along with a summary of uncertainties and biases introduced by its use.

Because of uncertainties in the modeled data, changes in occurrence of peak DBP concentrations are predicted using ICR rather than SWAT data. Section 5.4.1 summarizes the methodology for predicting changes in single peak DBP occurrences using ICR data.

Section 3.7.1 provides background information describing ICR and SWAT DBP data evaluated in this EA. Section 3.7.2 summarizes pre Stage 1 and pre Stage 2 DBP occurrence data for large surface water systems. Pre Stage 1 and pre Stage 2 DBPR occurrence levels for large ground water systems are provided in section 3.7.3. DBP occurrence for medium systems is discussed in section 3.7.4, followed by presentation of small system data in section 3.7.5. Economic Analysis for the Stage 2 DBPR Proposal 3 45 July 2003 3.7.1 Description of ICR and SWAT DBP Data <IP_ADDRESS> ICR DBP Data Analysis of ICR DBP data in this EA is consistent with the methodology used in the Occurrence Document ( USEPA 2003l) and in Chapter 5. A brief description of the data and assumptions used for data analyses are provided below.

Distribution System Sampling Locations Quarterly TTHM and HAA5 data were collected at the following distribution system sampling locations ( note that these locations are each associated with one ICR plant):

° Average 1 ( AVG 1) and Average 2 ( AVG 2)   two sample locations in the distribution system, each representing an approximate average residence time, as designated by the water system.

° Distribution System Maximum ( DS Maximum)   the sample location in the distribution system that has the longest residence time, as designated by the water system.

° Distribution System Equivalent Location ( DSE)   a sample location in the distribution system that has a known residence time, where no additional disinfectant has been added between the plant and sample location, and where there has been no blending with water from other plants.

Sample Collection Period TTHM and HAA5 data were collected quarterly from the period of July 1997 to December 1998 ( 6 quarters). Analyses of TTHM and HAA5 data in this EA were limited to the last 4 quarters of the ICR collection period ( January to December 1998). Only the last 4 quarters were evaluated because they appear to be of higher quality than data collected during the first 6 months of the survey. In addition, using all 18 months of data could skew results ( data from the last 2 quarters of the year would be counted twice).

Plant Source Water Types Plants were required to report source water type for each month from July 1997 to December 1998. The types of sources recorded were surface water, ground water, mixed, or purchased. Most plants reported on one source type for all months, but some plants reported surface water for some months and mixed for others. These plants were considered surface water plants. One ground water plant reported ground water for some months and mixed for others   this plant was considered a ground water. Analyses of all plants includes " blended," " mixed," and " purchased" plant types from the ICR database. These plant types make up a small portion ( less than 10 percent) of the total   most ICR plants are categorized as either surface or ground water plants.

Initial Plant Screening All ICR plants ( there are approximately 500 plants in the ICR database) were screened to ensure that at least 3 of 4 quarters have TTHM and HAA5 data for at least 3 of 4 distribution system locations. Economic Analysis for the Stage 2 DBPR Proposal 3 46 July 2003 Results of the screening process are detailed in Chapter 5 and summarized in Exhibit 5.10. Note that the total number of plants that meet the minimum screening criteria ( 311 plants, of which 213 are surface water plants, 83 are ground water plants, and 15 are either blended, mixed, or purchase plants) represents more than 60 percent of all large plants that participated in the ICR data collection effort.

<IP_ADDRESS> SWAT DBP Data SWAT produces monthly estimates of DBP occurrence for surface water plants at only two distribution system locations:

° Distribution System Average ( DS Average)   theoretical location with average residence time ( calculated by averaging the residence times reported by the water system for the four locations listed above).

° Distribution System Maximum ( DS Maximum)   theoretical location with the maximum residence time ( highest residence time reported for the four locations above).

Data from these locations are compared and summarized in subsequent sections.

3.7.2 Pre Stage 1 and Pre Stage 2 DBP Occurrence for Large Surface Water Plants Exhibit 3.19 summarizes the TTHM, HAA5, bromate, and chlorite occurrence for pre Stage 1 and pre Stage 2 baseline conditions. Pre Stage 1 occurrence is shown for both observed ICR data and SWAT predicted data. Pre Stage 2 data shown in Exhibit 3.19 are predicted by SWAT only. Exhibits 3.20 through 3.23 show the cumulative distributions of the same plant mean and individual observations ( monthly DBP concentrations) for SWAT data. SWAT plant mean data represent plant mean concentrations at the DS Average ( average residence time) location. ICR plant mean data represent the average of four distribution system locations ( AVG1, AVG2, DSE, and DS Maximum). Bromate and chlorite data represent finished water concentrations from both ICR and SWAT data sets, although ICR chlorite data show the maximum finished water concentration at each plant, rather than the plant mean. Statistical calculations of individual observations are for SWAT monthly data and ICR quarterly data.

Pre Stage 1 conditions are modeled by SWAT because, in Chapter 5, predicted pre Stage 2 and post Stage 2 DBP levels are subtracted from pre Stage 1 levels to assess the overall changes in DBP concentrations as a result of the regulations. Pre Stage 1 modeled data were used instead of pre Stage 1 observed ( ICR) data to ensure that the results of the analyses would represent only changes in exposure resulting from different rule requirements and would not reflect inherent differences between observed and modeled data.

As summarized in Exhibit 3.19, SWAT predicts that TTHM plant means will decrease from an average of 49 µ g/ L at pre Stage 1 conditions to 35 µ g/ L at pre Stage 2 conditions. Looking at the average of plant mean data, the HAA5 occurrence decreases by approximately 30 percent, from 36 µ g/ L at pre Stage 1 to 25 µ g/ L at pre Stage 2 conditions. Bromate and chlorite concentrations are predicted to decrease slightly under the Stage 1 DBPR because of the MCLs established for these contaminants. Note, however, that the bromate and chlorite distributions apply only to plants that use ozone and chlorine dioxide, respectively, and that the universe of plants using those technologies may vary from pre Stage 1 Economic Analysis for the Stage 2 DBPR Proposal 3 47 July 2003 to pre Stage 2 ( SWAT predicts that the number of plants using ozone will increase from 15 to 39 from pre Stage 1 to pre Stage 2, while the number using chlorine dioxide will stay constant at 22). Economic Analysis for the Stage 2 DBPR Proposal 3 48 July 2003 Exhibit 3.19 Summary of Pre Stage 1 and Pre Stage 2 DBP Occurrence for Large Surface Water Plants, DS Average Data Parameter Plant Mean Data Individual Observations N Mean Median 90th % ile Range N Mean Median 90th % ile Range TTHM ( µ g/ L)

Pre Stage 1 ( ICR) 213 42 40 70 0 117 3083 42 37 78 0 177 Pre Stage 1 ( SWAT) 273 49 44 90 3 207 2784 49 39 100 0 356 Pre Stage 2 ( SWAT) 273 35 36 57 3 64 2784 36 33 62 0 206 HAA5 ( µ g/ L)

Pre Stage 1 ( ICR) 213 29 24 53 0 116 3083 29 23 55 0 188 Pre Stage 1 ( SWAT) 273 36 29 70 1 146 2784 36 27 77 0 294 Pre Stage 2 ( SWAT) 273 25 25 41 1 48 2784 25 23 44 0 138 Bromate ( µ g/ L) ( Ozone plants only)

Pre Stage 1 ( ICR) 14 2.6 2.2 5.4 0.02 7.2 157 2.6 1.9 6.7 < 0.2 14.6 Pre Stage 1 ( SWAT) 15 6.3 1.8 19.6 0.2 28 156 6.1 1.9 18 0.1 62 Pre Stage 2 ( SWAT) 39 2.2 1.8 4.1 0.04 7.4 409 2.3 1.7 4.7 0.01 17 Chlorite ( µ g/ L) ( Chlorine dioxide plants only)

Pre Stage 1 ( ICR) 18 429 465 701 2.2 1105 192 435 435 830 < 20 1719 Pre Stage 1 ( SWAT) 22 663 708 861 10 1483 177 636 700 1309 42 1680 Pre Stage 2 ( SWAT) 22 417 404 628 140 715 200 402 383 656 14 784 Note: For TTHM and HAA5 data, SWAT data are from the DS Average location and ICR data are the average of four distribution system locations for the last 12 months of the ICR collection period ( January 1998 December 1998). For bromate and chlorite data, finished water data from both SWAT and ICR are used. All SWAT data are based on monthly predicted observations, ICR TTHM and HAA5 data are based on quarterly observations, and ICR chlorite and bromate data are based on monthly observations. For ICR data, only individual observations used to calculate plant means are shown. For ICR data, only plants that have data for 3 of the last 4 quarters were included, and, for ICR TTHM and HAA5 data, only plants with at least 3 of the 4 required distribution system samples each quarter were included.

Sources: SWAT Initial Plant Run and Run 300 ( USEPA 2001e); ICR AUX1 Database ( USEPA 2000h). Economic Analysis for the Stage 2 DBPR Proposal 3 49 July 2003 0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100%

0 50 100 150 200 250 TTHM ( m g/ L) Cumulative Percent Pre Stage 1 Pre Stage 2 0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100%

0 50 100 150 200 250 TTHM ( m g/ L) Cumulative Percent Pre Stage 1 Pre Stage 2 Exhibit 3.20a Cumulative Distributions of TTHM Monthly Data Predicted by SWAT ( DS Average)

Exhibit 3.20b Cumulative Distributions of TTHM Plant Mean Data Predicted by SWAT ( DS Average)

Note: DS Average data from SWAT; for pre Stage 2, SWAT requires all plants to use a technology that results in an annual average less than 64 µ g/ L ( based on the Stage 1 DBPR TTHM MCL of 80 µ g/ L with a 20 percent safety factor).

Source: SWAT Initial Plant Run and Run 300 ( USEPA 2001e). Economic Analysis for the Stage 2 DBPR Proposal 3 50 July 2003 0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100%

0 50 100 150 200 HAA5 ( m g/ L) Cumulative Percent Pre Stage 1 Pre Stage 2 0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100%

0 50 100 150 200 HAA5 ( m g/ L) Cumulative Percent Pre Stage 1 Pre Stage 2 Exhibit 3.21a Cumulative Distributions of HAA5 Monthly Data Predicted by SWAT ( DS Average)

Exhibit 3.21b Cumulative Distributions of HAA5 Plant Mean Data Predicted by SWAT ( DS Average)

Note: DS Average data from SWAT; for pre Stage 2, SWAT requires all plants to use a technology that results in an annual average less than 48 µ g/ L ( based on the Stage I DBPR HAA5 MCL of 60 µ g/ L with a 20 percent safety factor).

Source: SWAT Initial Plant Run and Run 300 ( USEPA 2001e). Economic Analysis for the Stage 2 DBPR Proposal 3 51 July 2003 0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100%

0 5 10 15 20 25 30 35 40 Bromate ( m g/ L) Cumulative Percent Pre Stage 1 Pre Stage 2 0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100%

0 5 10 15 20 25 30 35 40 Bromate ( m g/ L) Cumulative Percent Pre Stage 1 Pre Stage 2 Exhibit 3.22a Cumulative Distributions of Bromate Monthly Data Predicted by SWAT ( Finished Water)

Exhibit 3.22b Cumulative Distributions of Bromate Plant Mean Data Predicted by SWAT ( Finished Water)

Note: Finished water data from SWAT for ozone plants only. Because some plants change technology from pre Stage 1 to pre Stage 2, the number of ozone plants is different for the two data sets ( 15 plants in the pre Stage 1 distribution, and 39 plants in the pre Stage 2 distribution).

Source: SWAT Initial Plant Run and Run 300 ( USEPA 2001e). Economic Analysis for the Stage 2 DBPR Proposal 3 52 July 2003 0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100%

0 200 400 600 800 1000 1200 1400 1600 1800 Chlorite ( m g/ L) Cumulative Percent Pre Stage 1 Pre Stage 2 0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100%

0 200 400 600 800 1000 1200 1400 1600 1800 Chlorite ( m g/ L) Cumulative Percent Pre Stage 1 Pre Stage 2 Exhibit 3.23a Cumulative Distributions of Chlorite Monthly Data Predicted by SWAT ( Finished Water)

Exhibit 3.23b Cumulative Distributions of Chlorite Plant Mean Data Predicted by SWAT ( Finished Water)

Note: Finished water data from SWAT. Includes chlorine dioxide plants only. Both distributions represent 22 plants; however, the plants are not the same because some systems added chlorine dioxide for Stage 1 and some systems changed form chlorine dioxide to a more advance technology for Stage 1 ( resulting a net change of zero in the number of plants).

Source: SWAT Initial Plant Run and Run 300 ( USEPA 2001e). Economic Analysis for the Stage 2 DBPR Proposal 3 53 July 2003 3.7.3 Pre Stage 1 and Pre Stage 2 DBP Occurrence in Large Ground Water Plants ICR data were the only source of pre Stage 1 DBP data for large ground water systems. There are limited or no data on bromate and chlorite, since these DBPs were monitored only by plants using ozone or chlorine dioxide, and only one ground water plant in the ICR used these disinfectants ( USEPA 2001i). TTHM and HAA5 data for these plants are summarized in Exhibit 3.24. DBP levels in ground water are significantly less than in large surface water plants ( see Exhibit 3.19); mean TTHM levels in ground water plants are less than half those in large surface water plants, compared to observed or modeled surface water data. Ground water data are more skewed than surface water data; there is a much bigger difference between the median and the mean values for ground water.

Because a modeling tool similar to SWAT could not be used for large ground water plants, predictions of DBP occurrence for pre Stage 2 DBPR ( post Stage 1) are unavailable. Therefore, average reductions in DBP occurrence were extrapolated from SWAT data, taking into account the percentage of large ground water plants that are predicted to change technologies relative to the percentage of large surface water plants that change. Exhibit 3.24 presents results of the predicted DBP reduction for mean TTHM and HAA5 concentrations. Appendix E ( section E. 3) provides detailed methodology, calculations, and results for predicted pre Stage 2 DBP occurrence for large ground water plants.

Exhibit 3.24 Summary of Pre Stage 1 DBP Occurrence for Large Ground Water Plants, ICR Data Parameter Plant Mean Data Individual Observations N Mean Median 90th % ile Range N Mean Median 90th % ile Range TTHM ( µ g/ L)

Pre Stage 1 96 16.7 7.8 48 0 123 360 16 6.5 47 0 156 Pre Stage 2  16.2

HAA5 ( µ g/ L)

Pre Stage 1 99 8.9 2.7 25 0 71 373 8.8 2.0 28 0 96 Pre Stage 2  8.6

Source: Pre Stage 1 data: AUX1 database ( USEPA 2000h), based on data from January 1998 December 1998. Only plants that had at least 3 distribution system samples in each of at least 3 of the last 4 quarters were included. Pre Stage 2 data: mean DBP concentration derived from percent DBP reduction for surface water plants, adjusted to account for relative change in technologies ( see Appendix E, section E. 3 for derivation). Economic Analysis for the Stage 2 DBPR Proposal 3 54 July 2003 3.7.4 Pre Stage 1 and Pre Stage 2 DBP Occurrence for Medium Surface and Ground Water Plants DBP occurrence data for medium ground water and surface water plants are limited. Plantmean data on TTHM are available from WATER:\ STATS, a database compiled by the American Water Works Association ( AWWA 2000). Graphs of WATER:\ STATS data in Appendix A show that DBP levels and water quality parameter levels are similar in medium and large surface water plants. Graphs for ground water in the Occurrence Document ( USEPA 2003l) also show similarities between medium and large ground water plants. Therefore, EPA assumed that DBP occurrence for medium surface water and ground water plants is roughly equivalent to DBP occurrence for large surface water and ground water plants, respectively.

3.7.5 Pre Stage 1 and Pre Stage 2 DBP Occurrences for Small Surface and Ground Water Plants The small system experts used NRWA survey data and TTHM data submitted to EPA from eight States to assess pre Stage 1 DBP occurrence levels for small surface and ground water plants. Exhibit 3.25 summarizes the TTHM and HAA5 data from these two data sets.

Although Exhibit 3.25 shows that TTHM levels from the State data set are higher than the levels from the NRWA data set, NRWA data are considered more reliable and representative of national pre Stage 1 DBP occurrence than the State surface water data. For further characterization of small surface and ground water plant data sets, refer to Chapter 3 of the Occurrence Document ( USEPA 2003l). Therefore, NRWA observed data were used to describe occurrence for small surface water plants.

A modeling tool similar to SWAT used for large surface water plants was not available to predict pre Stage 2 ( post Stage 1) DBP occurrence for small surface and ground water plants. Reductions in DBP occurrence from pre Stage 1 to pre Stage 2 were extrapolated from SWAT data, taking into account the relative percent of plants that change technologies relative to large surface water plants. Appendix E ( section E. 3) provides detailed methodology, calculations, and results for predicted pre Stage 2 DBP occurrence for small surface and ground water plants. Economic Analysis for the Stage 2 DBPR Proposal 3 55 July 2003 Exhibit 3.25 Summary of Pre Stage 1 DBP Occurrence Data for Small Systems, DS Average Data Parameter ( source) Plant Mean Data Individual Observations N Mean Median 90th % ile Range N Mean Median 90th % ile Range TTHM ( µ g/ L)

Pre Stage 1 ( NRWA survey, SW systems) 96 83 62 168 0 328 192 83 63 162 0 446 Pre Stage 1 ( State data, SW systems) 562 99 66 215 0 687 N/ A N/ A N/ A N/ A N/ A Pre Stage 1 ( State data, GW systems) 233 6 17 3 46 0 655 N/ A N/ A N/ A N/ A N/ A Pre Stage 2 ( SW systems)  35

Pre Stage 2 ( GW systems)  16

HAA5 ( µ g/ L)

Pre Stage 1 ( NRWA survey, SW only) 96 45 35 83 0 262 192 45 34 88 0 381 Pre Stage 2 ( SW systems)  25

Pre Stage 2 ( GW systems)  8

Source: Pre Stage 1 data: NRWA data ( USEPA 2001c) are weighted averages of data at locations with average and maximum residence time in the distribution system. Average residence time data are weighted three times more than maximum residence time data to make data equivalent to DS Averages calculated for ICR TTHM and HAA5. NRWA plant mean data include only those plants that had data for both sampling periods and for both distribution system locations. Only those individual observations that were used to calculate plant mean data are shown here. State data ( USEPA 2001i) are a mixed data set from eight States for surface water and seven States for ground water; N/ A indicates no individual observations were available for this data set. Pre Stage 2 data: mean DBP concentration derived from percent DBP reduction for surface water plants, adjusted to account for relative change in technologies ( see Appendix E for derivation). Economic Analysis for the Stage 2 DBPR Proposal 3 56 July 2003 3.8 Summary of Uncertainties in Development of Stage 2 DBPR Baselines There is uncertainty in this baseline analysis due to measurement error or incomplete information that could result in either an over estimate or under estimate of the costs and/ or benefits as presented in Chapters 5 and 6. Exhibit 3.26 below presents a summary of these issues and an estimate of the effects that each may have on subsequent analyses. Note the effects on benefits and costs is unknown for most of the uncertainties listed in Exhibit 3.26.

Exhibit 3.26 Summary of Uncertainties Affecting Stage 2 DBPR Baseline Estimates Uncertainty Section with Full Discussion of Uncertainty Effect on Benefit Estimate Effect on Cost Estimates Underestimate Overestimate Unknown Impact Underestimate Overestimate Unknown Impact Uncertainty in baseline data inputs ( SDWIS and 1995 CWSS data) 3.4.2 X X Mean value instead of distribution for plants per system and flow per system 3.4.2 3.4.3 X X CWS flow equations for NTNCWSs 3.4.3 X X SWAT prediction of Pre Stage 1 and Pre Stage 2 DBP occurrence 3.7.1 X X Extrapolation of large systems predicted DBP occurrence to medium and small systems for Pre Stage 2 Appendix E X X Uncertainties in NRWA and State data for small systems 3.7.6 X X Economic Analysis for Stage 2 DBPR Proposal July 2003 4 1 4. Consideration of Regulatory Alternatives 4.1 Introduction To address the public health concerns presented in Chapter 2 and discussed in more detail in Chapter 5, the Environmental Protection Agency ( EPA) convened the Microbial Disinfectants/ Disinfection Byproducts ( M DBP) Advisory Committee under the Federal Advisory Committees Act ( FACA) to explore a number of regulatory alternatives for the Stage 2 Disinfectants and Disinfection Byproducts Rule ( DBPR). The M DBP Advisory Committee was composed of representatives from the following groups:

All Indian Pueblo Council, Pueblo Office of Environmental Protection American Water Works Association Association of Metropolitan Water Agencies Association of State Drinking Water Administrators Chlorine Chemistry Council Clean Water Action Conservation Law Foundation Environmental Council of the States International Ozone Association National Association of County and City Health Officials National Association of People with AIDS National Association of Regulatory Utility Commissioners National Association of State Utility Consumer Advocates National Association of Water Companies National Environmental Health Association National League of Cities National Resources Defense Council National Rural Water Association Physicians for Social Responsibility Unfiltered Systems U. S. Environmental Protection Agency Water and Wastewater Equipment Manufacturers Association M DBP deliberations began the Spring of 1999 and culminated in December 2000 and are documented on EPA's website in the form of meeting summaries ( USEPA 2000p).

This chapter describes the process for developing regulatory alternatives, then summarizes the four Stage 2 DBPR regulatory alternatives considered in this Economic Analysis ( EA). Among the four alternatives is the Preferred Alternative, which reflects the recommendation of the M DBP Advisory Committee.

4.2 Process for Development of Regulatory Alternatives The process that led to the development of the Stage 2 DBPR now being proposed began with the initiation of a negotiated rulemaking by EPA in 1992 to address public health concerns related to Economic Analysis for Stage 2 DBPR Proposal July 2003 4 2 disinfectants, disinfection byproducts ( DBPs), and microbial pathogens. The Regulatory Negotiation Committee met from November 1992 through June 1993. The Committee included representatives of State and local public health and regulatory agencies, public water systems, elected officials, consumer groups, and environmental groups. As a result of its deliberations, the Committee recommended the development of three sets of rules:

° A two stage approach for regulations to control risks from DBPs.

° A two stage approach for regulations to control risks from microbial contaminants ( the Interim Enhanced Surface Water Treatment Rule ( IESWTR) and the Long Term Enhanced Surface Water Treatment Rule).

° An information collection rule to support the above.

The Information Collection Rule ( ICR) was promulgated in May 1996. The DBP and microbial regulatory process recommendations of the Committee were subsequently incorporated into the 1996 SDWA Amendments as statutory requirements. The Stage 1 DBPR and the IESWTR were both promulgated by EPA in December 1998.

Results from the 1996 ICR, which were gathered between July 1997 and December 1998, provided the M DBP Advisory Committee and EPA with a wealth of information on large water systems, their treatment processes, and the quality of their source and finished waters. This information was used to develop and run Surface Water Analytical Tool ( SWAT) ( a model that uses a series of algorithms and decision rules to predict treatment changes and DBP occurrence for regulatory alternatives; see Appendix A). The output from SWAT formed much of the basis for estimates of national cost and DBP exposure for the regulatory alternatives under consideration. Additional data were obtained from a survey conducted by the National Rural Water Association ( NRWA) of 120 smaller systems   serving fewer than 10,000 people   as well as from a variety of State data sources.

The M DBP Advisory Committee considered several key questions during the negotiation process, including:

° What health effects will the Stage 2 DBPR address?

° Should disinfectants and DBPs not regulated under the Stage 1 DBPR now be regulated?

° Should standards for disinfectants and DBPs set under the Stage 1 DBPR be amended?

° Should monitoring requirements under the Stage 1 DBPR be amended?

° Should compliance standards be calculated differently than those in the Stage 1 DBPR?

° What are the risk tradeoffs that need to be considered?

EPA used SWAT to develop rough estimates of costs and DBP exposure reductions for over a hundred possible rule alternatives. Of these, the M DBP Advisory Committee focused its attention on those alternatives that would reduce peaks in DBP exposure that may occur throughout the distribution system. Economic Analysis for Stage 2 DBPR Proposal July 2003 4 3 4.3 Regulatory Alternatives Considered There are four Stage 2 DBPR regulatory options considered in this EA. They include what is referred to as the Preferred Alternative, reflecting the recommendation of the M DBP Advisory Committee, and three other alternatives studied by the Committee, but not selected for reasons noted below. Though not selected as a preferred option, the Committee considered each of those other three options as alternatives worth careful consideration; EPA carried them through the full cost and benefit analysis process for comparison with the Preferred Alternative.

The goal of the M DBP Advisory Committee was to increase the stringency of the total trihalomethanes ( TTHM) and haloacetic acids ( HAA5) compliance standards by reducing peak concentrations of DBPs in distribution systems. The Advisory Committee debated three different compliance determination approaches. The first, a running annual average ( RAA), bases compliance on the average of all samples taken over a 12 month period, and allows certain monitoring locations to be exposed to DBP levels higher than the maximum contaminant level ( MCL) as long as the average does not exceed the MCL. The second approach, a locational running annual average ( LRAA), bases compliance on the average of all samples taken at each specific monitoring location over a 12 month period, and requires all monitoring locations to be exposed to average DBP levels lower than the MCL. The third, a single highest ( SH) value, bases compliance on each individual sample meeting the MCL, and requires all monitoring locations never to be exposed to DBP levels higher than the MCL. Compared to RAA compliance options, the options involving LRAA and SH compliance measures focus on reducing peak exposures   and the potential inequalities in exposure resulting from them   to customers served in some parts of distribution systems.

The following discussion provides details of the four main regulatory alternatives considered.

Preferred Alternative The Stage 1 DBPR set MCLs for total TTHM at 80 µ g/ L and HAA5 at 60 µ g/ L, each measured as a RAA based on quarterly averages of all samples taken. The Stage 2 Preferred Alternative retains these MCL values, but modifies how compliance is determined for TTHM and HAA5 under the Stage 1 DBPR. Its components include:

° MCL of 80 µ g/ L TTHM measured as an LRAA ° MCL of 60 µ g/ L HAA5 measured as an LRAA ° MCL of 10 µ g/ L bromate measured as an RAA, based on monthly samples taken at the finished water point ( no change from the Stage 1 DBPR)

Under the Preferred Alternative for the Stage 2 DBPR, systems are required to identify the compliance monitoring sites that most accurately reflect high TTHM and HAA5 levels ( the Initial Distribution System Evaluation ( IDSE)) and to monitor at these locations. The purpose of this alternative is to control the levels of TTHM and HAA5 at locations in the distribution system with the highest levels of these DBPs so that systems are assured of meeting the MCLs throughout the entire distribution system. Economic Analysis for Stage 2 DBPR Proposal July 2003 4 4 Alternative 1 This alternative has the same TTHM and HAA5 requirements as the Preferred Alternative, but has a lower MCL for bromate. Its components include:

° MCL of 80 µ g/ L TTHM measured as an LRAA ° MCL of 60 µ g/ L HAA5 measured as an LRAA ° MCL of 5 µ g/ L bromate measured as an RAA, based on monthly samples taken at the finished water point Members of the M DBP Advisory Committee did not favor this alternative because they were concerned that lowering the bromate level to 5 µ g/ L could have adverse effects on microbial protection. This alternative would probably cause some systems to stop using ozone or not consider ozone for microbial protection   developments that the M DBP Advisory Committee and EPA did not want to encourage because ozone is more effective than chlorine against Cryptosporidium.

Alternative 2 This alternative measures TTHM and HAA5 concentrations as a SH value for the MCL and maintains the MCL for bromate. Its components include:

° MCL of 80 µ g/ L TTHM measured as the SH value for any sample taken ° MCL of 60 µ g/ L HAA5 measured as the SH value for any sample taken ° MCL of 10 µ g/ L bromate measured as an RAA ( no change from the Stage 1 DBPR)

This alternative is more stringent than the Preferred Alternative and Alternative 1. Under Alternative 2, no TTHM or HAA5 sample can exceed the MCL. It is expected that a large portion of the surface water systems covered by the rule would have to switch from their current treatment practice to more expensive advanced technologies to comply with this alternative. The M DBP Advisory Committee did not favor this alternative because it believed that the health effects data are not certain enough to warrant such a potentially expensive regulation.

Alternative 3 This alternative reduces MCLs for TTHM and HAA5 and maintains the MCL for bromate, but does not modify how compliance is measured under the Stage 1 DBPR. Its components include:

° MCL of 40 µ g/ L TTHM measured as an RAA ° MCL of 30 µ g/ L HAA5 measured as an RAA ° MCL of 10 µ g/ L bromate measured as an RAA ( no change from Stage 1 DBPR MCL) Economic Analysis for Stage 2 DBPR Proposal July 2003 4 5 This alternative reduces the average level of TTHM and HAA5 in the distribution system, but does not necessarily reduce peaks in the distribution system as an LRAA compliance strategy is expected to do. As with Alternative 2, a large portion of the surface water systems covered by the rule would have to switch from their current treatment practices to expensive advanced technologies to comply with this alternative. Similarly, the M DBP Advisory Committee did not favor this alternative because it believed that the health effects data are not certain enough to warrant such a potentially expensive regulation.

Exhibit 4.1 shows how compliance would be determined for the Stage 1 DBPR and under each of the regulatory alternatives described above when applied to a hypothetical large surface water system. This hypothetical system has one treatment plant and measures TTHM in the distribution system in four locations per quarter ( the calculations shown would be the same for HAA5). In this example, the system is in compliance with the Stage 1 DBPR, but would be in violation of all four Stage 2 DBPR regulatory options.

In addition to the four regulatory options addressed above, the M DBP Advisory Committee considered other changes in the approach to regulating DBPs worth noting. Both the current Stage 1 DBPR and the Stage 2 DBPR alternatives considered in this analysis use TTHM and HAA5 as the specific DBPs measured for compliance. The M DBP Advisory Committee determined that TTHM and HAA5 are reliable indicators for all halogenated DBPs that exist in chlorinated drinking water, including known DBPs that are unmeasurable and others that have yet to be identified. The Committee considered having EPA modify the group of indicators to include a total of six haloacetic acids ( HAA6), a total of nine haloacetic acids ( HAA9), or other DBPs. They did not, however, recommend this.

The Stage 1 DBPR also set a bromate MCL at 10 µ g/ L measured as an RAA, based on monthly measurements for ozone systems and a chlorite MCL at 100 µ g/ L based on measurements required for chlorine dioxide systems. The M DBP Advisory Committee debated whether the bromate MCL should be lowered ( Regulatory Alternative 1). The Stage 1 DBPR set the MCL for bromate at 10 µ g/ L partly because that was the limit of EPA's measuring capability at that time. New methods now exist to measure lower concentrations of bromate, which would allow a lower limit to be set. However, the Committee was concerned that a lower bromate MCL might discourage systems from switching to ( or continuing to use) ozone to increase microbial protection. Unlike chlorine, ozone is effective in the disinfection of Cryptosporidium   a focus of the Long Term 2 Enhanced Surface Water Treatment Rule ( LT2ESWTR). Therefore, the M DBP Advisory Committee recommended that EPA not change the bromate MCL. The M DBP Advisory Committee did not discuss the chlorite standard, and EPA does not believe it needs to be revised.

Last, it should be noted that reductions in exposure to DBPs could also be achieved through treatment techniques in lieu of or in addition to setting MCLs. For example, reducing organic precursor compounds, measured as Total Organic Carbon ( TOC), by such means as enhanced coagulation has been shown to lower DBP formation. The M DBP Advisory Committee considered regulatory alternatives for reducing precursors and determined that the Stage 1 DBPR reduced TOC to a sufficient degree. Further, removing ever smaller quantities of these compounds will be more difficult, less efficient, and increasingly costly. While analysis of ICR data shows that some systems could improve performance in this way ( and SWAT incorporated that into its decision tree), a regulatory requirement for reducing TOC levels was deemed unnecessary. Economic Analysis for Stage 2 DBPR Proposal July 2003 4 6 Basis of Compliance Violation of MCL Stage 1 DBPR TTHM MCL = 80 µ g/ L measured as an RAA No exceedance of MCL Loc. 1 Loc. 2 Loc. 3 Loc. 4 Qtrly Avg. Q1 100 40 50 50 60 Q2 75 50 40 100 66 Q3 55 45 55 110 66 Q4 60 55 40 75 58 RAA 63 Preferred Stage 2 DBPR Alternative and Alternative 1* TTHM MCL = 80 µ g/ L measured as an LRAA LRAA at Location 4 exceeds MCL Loc. 1 Loc. 2 Loc. 3 Loc. 4 Q1 100 40 50 50 Q2 75 50 40 100 Q3 55 45 55 110 Q4 60 55 40 75 LRAA 73 48 46 84 * The Preferred Alternative and Alternative 1 have the same TTHM MCL; they differ only in regard to the bromate MCL.

Alternative 2 TTHM MCL = 80 µ g/ L measured as a single highest value Three samples at Locations 1 and 4 exceed MCL Loc. 1 Loc. 2 Loc. 3 Loc. 4 Q1 100 40 50 50 Q2 75 50 40 100 Q3 55 45 55 110 Q4 60 55 40 75 Alternative 3 TTHM MCL = 40 µ g/ L measured as an RAA RAA exceeds MCL Loc. 1 Loc. 2 Loc. 3 Loc. 4 Qtrly Avg. Q1 100 40 50 50 60 Q2 75 50 40 100 66 Q3 55 45 55 110 66 Q4 60 55 40 75 58 RAA 63 Exhibit 4.1 Comparison of Compliance Calculations for Regulatory Alternatives Economic Analysis for the Stage 2 DBPR Proposal 5 1 July 2003 5. Benefits Analysis 5.1 Introduction The mission of the Environmental Protection Agency ( EPA) is to protect human health and to safeguard the natural environment ( USEPA 2000m). The specific mandate in the Safe Drinking Water Act ( SDWA) for regulating contaminants provides that the " Administrator shall... publish a maximum contaminant level goal and promulgate a national primary drinking water regulation for a contaminant... if the Administrator determines that  ( i) the contaminant may have an adverse effect on the health of persons; ( ii) the contaminant is known to occur or there is a substantial likelihood that the contaminant will occur in public water systems with a frequency and at levels of public health concern; and ( iii) in the sole judgment of the Administrator, regulation of such contaminant presents a meaningful opportunity for health risk reduction for persons served by public water systems." ( 42 USC § 300g 1( b)( 1)( A))

When carrying out its statutory mandate, EPA must often make regulatory decisions using incomplete or uncertain information. EPA believes it is appropriate and prudent to act to protect public health when there are indications that exposure to a contaminant could present significant risks to the public, rather than take no action until risks are unequivocally proven. Evidence from both human epidemiology and animal toxicology studies indicate that the consumption of drinking water containing disinfection byproducts ( DBPs) may result in adverse health effects. The two main categories of adverse health effects that have been associated with DBPs are reproductive and developmental effects and cancer ( particularly bladder cancer). EPA has concluded that DBPs occur at levels that are of a public health concern in some public water systems ( PWSs) that apply a chemical disinfectant, and that the Stage 2 Disinfectants and Disinfection Byproducts Rule ( DBPR) presents a meaningful opportunity for a reduction in the risk of adverse health effects.

Under Executive Order 12866, EPA must conduct an Economic Analysis ( EA) for rules costing over $ 100 million annually. The benefit analyses presented in this chapter follow the requirements of the executive order and related Office of Management and Budget ( OMB) and EPA guidance, and provide a reasonable basis for estimating potential health benefits using the best available science.

EPA has quantified the benefits associated with expected reductions in the incidence of bladder cancer. The science on the association of reproductive and developmental health effects with DBP exposure, however, is not strong enough to fully quantify these risks of the benefits of reduced DBP exposure. Nevertheless, EPA believes that the reproductive and developmental effects benefits resulting from the Stage 2 DBPR may be substantial. To help inform the assessment of the Stage 2 DBPR benefits, EPA completed an illustrative calculation of potential benefits for one specific reproductive effects endpoint ( fetal loss).

Section 5.1.1 provides an overview of the methodology and key assumptions used to estimate the benefits that may be attributed to the Stage 2 DBPR ( including the illustrative calculations for developmental and reproductive health endpoints). Section 5.1.2 summarizes results.

Section 5.2 presents the problem identification and assessment of potential hazard. Carcinogenic and non carcinogenic ( e. g., reproductive and developmental) risks are presented with both toxicological and epidemiological supporting evidence. Section 5.3 follows with an assessment of exposure. The rule's benefits, including cancer cases avoided and the associated value of those benefits, are addressed in Sections 5.4 through 5.6. Section 5.7 summarizes uncertainties of national benefits estimates. Section 5.8 is a sensitivity analysis looking at the impacts of not considering cessation lag when estimating quantified benefits. Potential benefits from reductions in one reproductive and developmental endpoint   fetal loss   are evaluated through an illustrative calculation in Section 5.9. Economic Analysis for the Stage 2 DBPR Proposal 5 2 July 2003 The following appendices provide additional details in support of this chapter:

° Appendix D shows the schedule for all rule activities ( this information is used as input for the quantified benefits calculation).

° Appendix E provides general background information on population attributable risk ( PAR) and a detailed description of the derivation of PAR values used to quantify benefits associated with reduction in cancer cases. In addition, it supports the discussion of average exposure reduction presented in this chapter. Lastly, Appendix E shows detailed calculations for estimating the number of bladder cancer cases avoided as a result of the Stage 2 DBPR.

° Appendix F describes the valuation of Stage 2 DBPR benefits and presents results for all regulatory alternatives and sensitivity analyses.

° Appendix G provides detailed calculations for the illustrative calculation of reproductive and developmental health impacts.

5.1.1 Overview of Methodology for Quantifying Stage 2 DBPR Benefits There are two categories of benefits that are addressed in this chapter: estimated benefits associated with reductions in the incidence of bladder cancer and estimated benefits associated with reductions in the incidence of adverse reproductive and developmental health effects. The primary benefits analysis in this EA is based on reductions in cancer cases, while potential benefits associated with decreasing adverse developmental and reproductive health effects ( specifically, fetal losses) are presented as an illustrative calculation.

EPA used similar approaches to estimate the number of bladder cancer cases avoided ( the primary benefits analysis) and the avoided incidence of fetal loss ( the illustrative calculation). The major steps in deriving and characterizing cases avoided are:

° Estimate the current and future cases of annual bladder cancer and fetal loss ° Estimate how many cases can be attributed to DBP exposure ° Estimate the reduction in future cases corresponding to anticipated reductions in DBP occurrence and exposure due to the Stage 2 DBPR ( i. e., cases avoided)

For bladder cancer, EPA computed the total national annual monetized benefits of the Stage 2 DBPR by multiplying the estimated number of bladder cases avoided by an estimated monetary value associated with avoiding both fatal and non fatal cases of bladder cancer. The value of statistical life ( VSL) was used for fatal bladder cancers, while two equally valid estimates of willingness to pay to avoid non fatal bladder cancer are used ( one based on avoiding a case of curable lymphoma and the other based on avoiding a case of chronic bronchitis). EPA recognizes that there could be a significant value associated with reducing the number of avoided fetal losses estimated in the illustrative calculation. However, the Agency is unable at this time to develop a specific estimate of the value of avoiding fetal loss or to use a benefit transfer methodology to estimate the value of avoiding fetal loss from existing valuation studies on other endpoints ( see section 5.9 for a full discussion of this issue).

All benefit calculations were performed using the Stage 2 DBPR Benefits Model ( USEPA 2003i). See Appendix L for model documentation and a CD containing benefits model and data files. 1 PAR represents the fraction of occurrence of a particular disease that is attributable to some specified risk factor. Economic Analysis for the Stage 2 DBPR Proposal 5 3 July 2003 To quantify the benefits due to reduction in bladder cancer, EPA begins with an estimated number of new cases per year from all causes of 56,500 ( based on published 2002 American Cancer Society data, available on the web at http:// www. cancer. org/). The estimated percent of bladder cancer cases attributable to DBPs is based on five epidemiological studies conducted in the 1980' s and 1990' s. Analysis of the data from these five studies was used to estimate the PAR of bladder cancer due to DBPs. 1 Results showed that best estimates range from 2 to 17 percent. The total cases of bladder cancer from all causes multiplied by the range of best estimate PAR values results in approximately 1,100 to 9,600 new bladder cancer cases per year that may be attributed to DBPs in chlorinated drinking water. EPA recognizes that the because causality has not yet been established between chlorinated water and bladder cancer, the actual cases attributable to DBPs could be zero.

The baseline cancer incidence and the PAR estimates described above reflect conditions prior to the implementation of not only the Stage 2 DBPR but also the Stage 1 DBPR. To estimate the benefits of the Stage 2 DBPR, EPA first estimated the portion of the 56,500 annual cases expected to be avoided by DBP reductions resulting from the Stage 1 DBPR, and then the additional cases avoided due to the additional reductions in DBP levels predicted for the Stage 2 DBPR. EPA has assumed that reductions in bladder cancer cases avoided is estimated by assuming that reductions in bladder cancer cases attributable to DBP exposure are directly proportional to reductions in the national average DBP levels. Predicted reductions in national average total trihalomethanes ( TTHM) and haloacetic acid ( HAA5) levels obtained from the Surface Water Analytical Tool ( SWAT) models runs were used as indicators of overall DBP reductions. The resulting reductions new in bladder cancer cases are calculated separately for each year over a 25 year time period based on the rule implementation schedule. Adjustments were made to account for the anticipated transition time for individual lifetime risks among those in the exposed population to become more reflective of the post Stage 2 DBP levels rather than pre Stage 2 DBP levels ( referred to as the cessation lag). Also, EPA has estimated that 26% of bladder cancer cases are fatal, while 74% are non fatal ( USEPA, 1999a).

The final step in the benefit calculation is to monetize the estimated reduction in bladder cancer cases by applying economic values for avoided illnesses and deaths. The value of avoiding non fatal bladder cancer cases is based on people's Willingness to Pay ( WTP) for incremental reductions in the risk they face of contracting cancer. The metric of WTP to avoid an increased risk accounts for the desire to avoid treatment costs, pain and discomfort, productivity losses, and any other adverse consequences related to contraction of a non fatal case of bladder cancer.

Because specific estimates of WTP for avoiding non fatal bladder cancer are not available, EPA estimated WTP values from two other non fatal illnesses: chronic bronchitis and curable lymphoma. Both are considered equally valid estimtates of WTP for non fatal cancer.

For fatal bladder cancer cases, the VSL is used to capture the value of benefits. The VSL represents an estimate of the monetary value of reducing risks of premature death from cancer. The VSL, therefore, is not an estimate of the value of saving a particular individual's life. Rather, the value of a " statistical" life represents the sum of the values placed on small individual risk reductions across an exposed population. Other economic factors are taken into consideration when calculating benefits over time, such as income growth and social discount rates.

There are several areas of uncertainty with respect to quantified benefits for bladder cancer. Many are incorporated into the analyses, such as the uncertainty in PAR values reflected by the use of a wide range of " best estimates" of 2 to 17 percent derived from several credible epidemiological studies. Uncertainties in these best estimates of PAR suggest 95 percent confidence interval ranges truncated at 0 percent on the low end and up to 33 percent on the high end ( see Appendix E for details). There is also Economic Analysis for the Stage 2 DBPR Proposal 5 4 July 2003 uncertainty in the valuation of the estimated bladder cancer cases avoided, including the use of two alternatives for valuing non fatal bladder cancer.

As noted previously, EPA expects that a large portion of the total benefits from this rule could come from reduction in developmental and reproductive health effects, although the science on these effects as a result of DBP exposure is not strong enough to fully quantify risk. EPA completed a preliminary quantification of fetal loss risk and rule benefits in an illustrative calculation. Fetal loss was used in the analysis because, while some epidemiology data exist for other reproductive and developmental effects potentially associated with DBP exposure, more data are available on this particular end point. Because approximately one million of the six million pregnancies each year in the United States end in a miscarriage or stillbirth ( Ventura et al. 2000a), even a small risk attributable to DBP exposure that can be avoided by reducing DBP levels may result in a significant number of avoided fetal losses.

EPA estimated the reduction in fetal losses in a similar manner to bladder cancer cases. A range of possible PAR values for relating annual fetal losses to DBP exposure was obtained from available epidemiological studies. Reductions in occurrence of peak DBPs due to the Stage 1 DBPR and the Stage 2 DBPR were estimated. Reductions in exposure to peak DBPs were assumed to be proportional to reductions in peak DBP occurrence. Like the analysis of bladder cancer, there is uncertainty in fetal loss PAR values, reflected in the range of values used in the analysis. There are other important uncertainties in this illustrative calculation, including the assumed proportional relationship between reduction in fetal losses and reduction in exposure to peak levels due to the Stage 2 DBPR.

5.1.2 Summary of National Benefits of the Stage 2 DBPR Exhibit 5.1 summarizes the estimated number of bladder cancer cases avoided as a result of the Stage 2 DBPR and the monetized value of those cases. While causality has not been established, the weight of evidence supports PAR estimates of potential benefits. Although zero is within the range of potential benefits, the evidence indicates that both the number of cases and the value of preventing those cases could be significant. The wide range of total monetized benefits in Exhibit 5.1 primarily reflects the large uncertainty in PAR values for related DBP exposure to bladder cancer. The benefits in Exhibit 5.1 are for the Preferred Regulatory Alternative for the Stage 2 DBPR. Benefits estimates for the other regulatory alternatives were derived using the same methods as for the Preferred Regulatory Alternative and are presented in section 5.6.4.

It is important to note that 26 percent of bladder cancer cases in the US are fatal, and 74 percent are non fatal. The monetized benefits therefore reflect the estimate of avoiding both fatal and non fatal cancers in those proportions.

In addition to bladder cancer cases avoided, EPA provides an illustrative calculation on the potential number of fetal losses that might be avoided per year, ranging from 1,100 to 4,700. Only an illustrative example of potential fetal loss avoided is given because of the much greater uncertainties in quantifying this risk than for bladder cancer. The value of other health benefits, including the potential reduction in other types of cancer such as colon or rectal, could be significant. Also, the value of nonhealth benefits, such as improved taste and odor of water, are expected to be positive. These are discussed further in section 5.5. Economic Analysis for the Stage 2 DBPR Proposal 5 5 July 2003 Exhibit 5.1 Summary of Quantified Benefits for the Stage 2 DBPR PAR Value 1 Average Annual Estimate of Bladder Cancer Cases Avoided Annualized Total Estimated Value of Cases Avoided ( Millions, 2000$) ( 90% Confidence Bounds 2)

Discount Rate WTP for Curable Lymphoma as the Basis for Non Fatal Cases WTP for Chronic Bronchitis as the Basis for Non Fatal Cases 2% 20.9 3 % $ 113.0 ($ 17.9  258.2) $ 54.9 ($ 12.5  119.6)

7 % $ 97.9 ($ 15.6  223.7) $ 47.6 ($ 10.9  103.7)

17 % 182.3 3 % $ 986.2 ($ 156.6  2,252.5) $ 479.3 ($ 109.3  1,043.7)

7 % $ 854.4 ($ 135.8  1,952.3) $ 415.6 ($ 94.9  904.6) Notes: Results are based on analysis of reduction in average TTHM concentrations due to the Stage 2 DBPR. 1. The 2 and 17 percent PAR values used in the bladder cancer risk and benefits analyses reflect the range of best estimates derived from the relevant epidemiological data. EPA recognizes that the lower bound may be as low as zero since causality has not yet been established between exposure to chlorinated water and bladder cancer 2. The 90 % confidence bounds shown in the exhibit reflect uncertainty in the VSL, WTP, and income elasticity adjustment.

Source: Exhibit 5.27.

5.2 Problem Identification and Assessment of Potential Hazard This section provides detailed information from the toxicological and epidemiological literature regarding the key adverse health effects that have been associated with exposure to DBPs. In addition to the specific studies and key reviews presented here, EPA has also addressed reproductive and developmental effects, carcinogenicity, and other adverse health effects at length in several Health Criteria Documents. Specifically, EPA is currently developing external review drafts of Drinking Water Criteria Documents for the following DBPs: brominated trihalomethanes ( USEPA 2003c), brominated haloacetic acids ( USEPA 2003d), cyanogen chloride ( USEPA 2003e), glyoxal and methylglyoxal ( USEPA 2003f), and haloacetonitriles ( USEPA 2003g). EPA is also writing addendums to the Criteria Document for bromate ( IRIS 2001a), chloroform ( IRIS 2001b), chlorine dioxide and chlorite ( IRIS 2001c), and dichloroacetic acid ( IRIS 2002). Similar documents exist for MX ( USEPA 2000r) and chlorohydroxyfurfanones ( USEPA 1999c).

5.2.1 Reproductive and Developmental Health Effects Adverse impacts on reproduction and development that have been hypothesized to be associated with maternal exposure to disinfection byproducts include early term miscarriage ( Waller et al., 1998), stillbirth ( Dodds et al., 1999), low birth weight ( Gallagher et al., 1998), premature birth ( Kallen and Robert, 1999), and some congenital birth defects ( Magnus et al., 1999).

CDC reports that, for the 10 year period between 1986 and 1996, spontaneous fetal losses were estimated to be between 0.8 million and 1.0 million per year. Approximately 15 percent of births are considered very low birth weight ( defined by CDC as below 1.0kg and 2.2kg). Congenital abnormalities are reported to occur in just over 1 percent of all live births per year in the United States. Although research has identified some risk factors for these adverse birth outcomes, including nutritional deficits 2 " Term low birth weight" refers to low weight of infants carried to a full term ( i. e., nine months), as opposed to low birth weight as a general category that includes infants born prematurely.

3 Epidemiology studies often report results as an odds ratio ( OR) or as a relative risk ( RR), usually adjusted to account for confounders, as measures of the strength of the association between a risk factor ( e. g., exposure to some substance) and an adverse health effect. Appendix E provides a detailed discussion of the meaning and derivation of OR and RR values. Economic Analysis for the Stage 2 DBPR Proposal 5 6 July 2003 ( e. g., inadequate folic acid) and fetal exposure to tobacco smoke and alcohol, the causes of many outcomes are unknown.

A variety of research is underway to examine the potential role that maternal exposure to specific air and water pollutants might play in these adverse outcomes. The following sections provide a review of the literature addressing the potential relationship between DBPs and adverse reproductive and developmental outcomes.

<IP_ADDRESS> Epidemiological Evidence of Adverse Reproductive and Developmental Health Effects All published reproductive and developmental epidemiology studies concerning drinking water have been evaluated, including recently published studies of the relationship between exposure to contaminants in chlorinated surface water and potential adverse reproductive and developmental health effects. EPA also considered critical reviews of the epidemiological literature by Reif et al. ( 2000); Bove et al. ( 2002); and Nieuwenhuijsen et al. ( 2000). Dr. John Reif and colleagues at the University of Colorado ( Reif et al. 2000) prepared a report for Health Canada that analyzed and summarized these studies. Similarly, Frank Bove from the Agency for Toxic Substances and Disease Registry ( ATSDR) conducted a qualitative review of 14 reproductive and developmental epidemiology studies on exposure to chlorinated byproducts in the report, " Drinking Water Contaminants and Adverse Pregnancy Outcomes: A Review" ( 2002). In addition, Mark Nieuwenhuijsen and colleagues reviewed toxicological and epidemiological data and evaluated the potential risk of chlorination DBPs on human reproductive health ( 2000).

New epidemiology reports since the Stage 1 DBPR The 1997 Notice of Data Ability ( NODA) ( USEPA 1997f), the 1998 NODA ( USEPA 1998f), the Stage 1 DBPR, and the Stage 1 DBPR companion Regulatory Impact Analysis ( RIA) ( USEPA 1998a) presented EPA's reviews of the reproductive and developmental epidemiological literature published prior to the Stage 1 DBPR concerning DBPs. Eight new epidemiology reports have been published since the 1998 Stage 1 DBPR.

1) Gallagher et al. ( 1998) conducted a retrospective cohort study in Colorado to examine the relationship between TTHM exposure during the third trimester of pregnancy and low birth weight, term low birth weight2, and preterm delivery. Estimates of TTHM concentration at maternal residence were based on routinely collected TTHM data that were adjusted, using a Geographical Information System ( GIS) based modeling technique, to account for spatial variability.

Compared to the reference category used in the study ( # 20 µ g/ L estimated TTHM exposure), women exposed to water containing $ 61 µ g/ L of TTHM had an increased risk for low birth weight ( odds ratio ( OR) = 2.1, 95 percent confidence interval of 1.0 4.8) and for term low birth weight ( OR = 5.9, 95 percent confidence interval 2.0 17.0). 3 Economic Analysis for the Stage 2 DBPR Proposal 5 7 July 2003 The wide confidence intervals for term low birth weight reflect the small sample size ( n= 6 births) in the exposed category.

2) Dodds et al. ( 1999) conducted a retrospective cohort study in Nova Scotia to examine the relationship between the level of TTHMs and low birth weight, term low birth weight, very low birth weight, preterm delivery, small size for gestational age, stillbirth, and congenital anomalies. The study population included 50,755 women residing in an area with municipal surface water who had singleton births ( i. e., birth of one offspring) or pregnancy terminations for major fetal anomalies in Nova Scotia between 1988 and 1995. The authors used linear regression to estimate the concentration of TTHM by month from quarterly sampling data within the distribution system of each public water facility.

The investigators found little association between TTHM level and outcomes related to fetal weight, gestational age, preterm delivery, or congenital defects. They did find an elevated risk for stillbirth among women who experienced average TTHM levels of 100 µ g/ L or greater during pregnancy ( adjusted RR = 1.66; 95 percent confidence interval 1.09 2.52) relative to the referent group of women exposed to levels of 0 49 µ g/ L. ( Because of relatively high TTHM levels in Nova Scotia, the referent group contained women exposed to higher concentrations than were typically used in other studies.) The authors observed an elevated prevalence of chromosomal abnormalities ( adjusted RR = 1.38; 95 percent confidence interval 0.73 2.59 for women exposed to TTHM levels of 100 µ g/ L or greater), but there was no evidence of a dose response relationship.

3) King et al. ( 2000a) used the Dodds et al. ( 1999) Nova Scotia study data to evaluate the relationship between the level of TTHM, as well as specific trihalomethanes ( THMs) in public water supplies, and risk of stillbirth. Individual exposures were assigned by linking mothers' residence location at the time of delivery to the levels of specific THMs observed in public water supplies.

King et al. ( 2000a) found an association between BDCM and stillbirth, comparing exposures $ 20 µ g/ L with exposures < 5 : g/ L ( RR = 1.98; 95 percent confidence interval 1.23 3.49). When analyzed as a continuous variable, BDCM was associated with a 29 percent increase in risk for stillbirth for each 10 : g/ L increase in concentration. King et al. also noted an association between chloroform and an increased risk for stillbirth ( RR = 1.56; 95 percent confidence interval 1.04 2.34).

4) Magnus et al. ( 1999) conducted a " semi individual" ecological study in Norway to examine the relation of water chlorination practice and color ( used as an indicator for the presence of natural organic matter and DBPs) to birth defects. An exposure assessment was performed by linking the national waterworks registry with the national birth registry ( 1993 1995; 141,077 children). The authors reported that DBP concentrations in Norway were generally low ( mean of 9.4 µ g/ L for TTHM and 14.6 µ g/ L for HAAs). In a comparison between exposed ( high color; chlorination) and reference groups ( low color; no chlorination), the adjusted OR was 1.14 ( 95 percent confidence interval 0.99 1.31) for any malformation, 1.26 ( 95 percent confidence interval 0.61 2.62) for neural tube defects and 1.99 ( 95 percent confidence interval 1.10 3.57) for urinary tract defects. Elevated risks were not observed for major cardiac defects, respiratory defects, or oral cleft defects. Economic Analysis for the Stage 2 DBPR Proposal 5 8 July 2003 5) Källén and Robert ( 1999) conducted a cross sectional, population based ecological study in Sweden to examine associations between water disinfection practices and birth defects. The authors compared birth outcomes recorded in the Swedish national registry for women living in municipalities where the water supply was disinfected with chlorine ( sodium hypochlorite) or chlorine dioxide, or was left untreated. Three years of data were analyzed, encompassing approximately 74,300 births in referent areas, 15,400 in areas using chlorine dioxide and 24,700 in areas using sodium hypochlorite. Statistically significant associations with pre term delivery, low birth weight, short body length, and small head circumference were found for chlorination. These associations were not observed in communities which treated water with chlorine dioxide. No data on concentrations of DBPs in Swedish water supplies were provided.

6) Yang et al. ( 2000) conducted a cross sectional, population based ecological study in Taiwan to examine water disinfection practices and birth outcomes. The authors compared birth outcomes in 14 municipalities in which chlorinated water was supplied to over 90 percent of the residents to birth outcomes in 14 non chlorinating municipalities. Two years of singleton data on 18,025 women were analyzed ( 1994 1996). Pre term delivery (< 37 weeks) occurred more often in municipalities that treated water with chlorine ( OR= 1.34; 95 percent confidence interval 1.15 1.56). No statistically significant associations were found for birth weight or the percent term low birth weight. No THM concentration data were provided.

7) Waller et al. ( 2001) published a study that evaluated different exposure assessment methods used to estimate relationships between exposure to chlorinated tap water and the risk of spontaneous abortion by recalculating the total trihalomethane exposures from their original publication ( Waller et al., 1998). The study was co funded by EPA's National Health and Environmental Effects Research Laboratory ( NHEERL) and the California Department of Health Services ( CDHS). The investigators conducted this methods development study as a follow up to a 1998 CDHS study of THMs and miscarriage. The primary purpose was to evaluate improved methods for assessing exposures to DBPs, and to develop and evaluate statistical techniques that might reduce the effects of misclassification. Two methods were compared, the " utility wide" approach and the " closest site" approach, the latter using TTHM levels from the monitoring site closest to the individual's residence. Unweighted, weighted, and subset analyses were performed for both approaches. The researchers concluded that two of the analyses ( called " weighted" and " subset" analyses), when used with the utility wide approach, are relatively simple techniques that may increase the usefulness of utility monitoring records. However, these techniques result in a loss of sample size, which may limit their value in small studies or in areas where TTHM levels vary widely. In conclusion, the results neither strengthen nor weaken the previously reported association between THMs and spontaneous abortions.

8) Hwang et al. ( 2002) conducted a nationwide cross sectional study of birth defects in Norway. The authors reviewed records for 184,676 infants born between 1993 and 1998 to assess the association between chlorination byproducts and specific birth defects. The authors did not measure chlorination by products directly, but rather used six exposure categories based on the presence/ absence of chlorination in combination with low, medium, or high color in raw water as an indicator of natural organic matter ( chlorination by product precursors). To measure risk, the authors used logistic regression to compute odds ratios adjusted for maternal age, previous deliveries, and locality measures. The category of no chlorination and low color was used as the reference category ( adjusted OR = 1.0 for all birth defects). The authors reported that Economic Analysis for the Stage 2 DBPR Proposal 5 9 July 2003 overall, chlorination increases the risk of all birth defects ( adjusted OR= 1.13, 95 percent confidence interval 1.01 1.25 for combined groups of chlorination with medium or high water color). Significant associations were found between chlorination ( medium and high color groups combined) and cardiac defects ( adjusted OR= 1.37, 95 percent confidence interval 1.00 1.89), respiratory system defects ( adjusted OR= 1.89, 95 percent confidence interval 1.00 3.58), and urinary tract birth defects ( adjusted OR= 1.46, 95 percent confidence interval 1.00 2.13). Of the various specific birth defects examined in the study, the risk of ventricular septal defects increased with chlorinated drinking water ( adjusted OR for medium color = 1.63, 95 percent confidence interval 1.02 2.58; adjusted OR for high color = 1.81, 95 percent confidence interval 1.05 3.09). The author's reported that no significant association was observed between chlorination and neural tube defects or oral cleft defects, but did observe that the risk of spina bifida was related to high amounts of organic matter ( i. e., high color) in non chlorinated water.

9) Windham et al., 2003, assessed the relationship between exposure to THMs in drinking water and characteristics of the menstrual cycle among 403 women who provided daily urine samples for an average of 5.6 cycles. Women whose tap water had TTHM levels greater than 0.060 mg/ l had statistically significantly shorter menstrual cycles than women whose tap water had lower TTHMs. On average, the menstrual cycles of women with the higher levels of TTHMs were one day shorter than cycles of women with the lower levels ( adjusted difference:  1.1 days, 95% confidence interval:  1.8 days to  0.4 days). This shortening occurred during the first half of the cycle, before ovulation ( adjusted difference:  0.9 days; 95% confidence interval:  1.6 days to  0.2 days). There were no changes in bleed length or in the regularity of the cycles. Based on their study, Windham et al. suggested that THM exposure may affect ovarian function, but since this is the first study to examine human menstrual cycle variation in relation to THM exposure, more research is needed to confirm the relationship. The public health implication of a small reduction in menstrual cycle length is not clear, but if THMs are related to disturbances in ovarian function, that might provide insight into the observed associations between THMs and a variety of adverse reproductive outcomes.

Critical review of epidemiology literature by Reif et al. ( 2000)

Reif et al. ( 2000) conducted a critical review of the epidemiology literature pertaining to potential reproductive and developmental effects of exposure to DBPs in drinking water. The review included 16 peer reviewed scientific manuscripts and published reports of which 10 were previously discussed in the Stage 1 DBPR. The authors evaluated associations between DBPs and outcomes grouped as effects on ( 1) fetal growth ( birth weight [ as a continuous variable]; low birth weight [ defined as < 2,500 grams]; term low birth weight [ defined as < 2,500 grams]; very low birth weight [ defined as < 1,500 grams]; preterm delivery [ defined as < 37 weeks of gestation] and intrauterine growth retardation [ or decreased rate of growth of the fetus]); ( 2) fetal viability ( spontaneous abortion and stillbirth); and, ( 3) risk of fetal malformations ( all malformations, oral cleft defects, major cardiac defects, neural tube defects, and chromosomal abnormalities).

Reif et al. ( 2000) found mixed evidence in the epidemiological literature they reviewed for associations between DBPs and effects on fetal growth. Studies using TTHM concentrations reached differing conclusions. Some studies found weak but statistically significant associations ( Gallagher et al. 1998; Bove et al. 1992b; Bove et al. 1995), but two found none ( Dodds et al. 1999; and Savitz et al. 1995). Studies with qualitative exposure assessment designs are similarly variable in their findings ( Kanitz et al. 1996; Källén and Robert 1999; and Yang et al. 2000). Economic Analysis for the Stage 2 DBPR Proposal 5 10 July 2003 For effects on fetal viability, the authors reported that some evidence exists for an increased risk of spontaneous abortion and stillbirth. Increased rates of spontaneous abortion associated with TTHM levels of 75 µ g/ L or more were reported by Waller et al. ( 1998). Aschengrau et al. ( 1989) reported a doubling of risk of spontaneous abortion for exposure to surface water compared to ground and mixed water. Although Savitz et al. ( 1995) found an association between high levels of THMs and spontaneous abortion, no relationship with dose or water source was discovered. As discussed previously, an increased risk of stillbirth was found to be associated with THM and BDCM exposure ( Dodds et al. 1999; King et al. 2000a). Aschengrau et al. ( 1993) found an association between stillbirth and the use of chlorinated versus chloraminated water systems. A weak association was found for the use of surface water systems and risk of stillbirth, but these authors found little evidence for an association between TTHM and risk of stillbirth ( Bove et al. 1992a; Bove et al. 1995).

For congenital abnormalities related to DBP exposure, Reif et al. ( 2000) reported that the relatively few studies available in the technical literature provide an inconsistent pattern both in terms of associating exposure with the occurrence of anomalies in general, and with respect to identifying specific anomalies that result from exposure. The authors conceded that an assessment of congenital anomalies is difficult due to the small number of cases available for evaluation and possible selection bias due to elective terminations of pregnancy. In addition, the authors stated that ( 1) categorizing defects may yield etiologically dissimilar aggregations and may dilute the estimated risk, ( 2) at higher DBP concentrations, multiple or lethal defects may be induced and the outcomes may be expressed as spontaneous abortion or stillbirth, or cause unrecognized fetal loss, and ( 3) cases with recognized, single anomalies may represent only a portion of the full range of the potential effects.

Reif et al. provide several possible explanations for the discrepancies and inconsistencies between the epidemiologic studies: ( 1) substantial differences existed between methods of exposure assessment and, in some cases, definition of the outcome, ( 2) referent groups varied across studies, ( 3) the composition of DBP mixtures may have varied across locales and studies, and ( 4) other classes of DBPs may be the causal agents and THMs may or may not be an appropriate exposure indicator for those DBPs. Exposure misclassification in the studies may either hide a true effect or, in rare circumstances, create an artificial effect.

Reif et al. also reviewed the epidemiology literature for dose response relationships. The researchers did not find a dose response pattern of increasing risk with increasing concentration of TTHM, but they did observe a general trend of small increases in risk for concentrations of TTHM greater than 100 : g/ L.

Based on information provided in the literature, Reif et al. ( 2000) estimated PAR for each outcome in each study. A PAR value represents the fraction of disease incidence in a population that is attributable to a specific risk factor. The PAR value, therefore, also reflects the portion of disease in the population that would be eliminated by eliminating the associated risk factor while distributions of other risk factors in the population remain unchanged. Appendix E provides a detailed discussion of the derivation of PAR values from epidemiological studies and their use in risk and benefits assessments.

Reif et al. ( 2000) explored the differential in potential health risk across TTHM thresholds of 80 and 60 µ g/ L. Odds ratios with 95 percent confidence intervals from various studies are compared in Exhibit 5.2 and PAR values with 95 percent confidence intervals ( truncated at zero to reflect biological relevance) from various studies are compared in Exhibit 5.3. The distribution of exposure levels differed among the studies, but when normalized in this way the studies appear to provide some support for establishing a threshold level for TTHM. The PAR value point estimates in Exhibit 5.3 are generally higher when 60 : g/ L is used as the cut point rather than 80 : g/ L. This seems to indicate that an important reduction in disease occurrence may be obtained by eliminating not only TTHM exposure levels above 80 : g/ L, but also levels between 60 : g/ L and 80 : g/ L. The authors note that this conclusion is tentative because many of the 95 percent confidence intervals on the Odds Ratios were very wide and Economic Analysis for the Stage 2 DBPR Proposal 5 11 July 2003 extended to values of one and lower. Moreover, Reif et al. ( 2000) suggest caution when interpreting the PAR values and note that "[ s] ince a number of assumptions regarding attributable fraction do not appear to hold, population attributable risks are unlikely to be useful with the current data set."

The findings for low birth weight are varied and do not strongly support a threshold of 80 or 60 µ g/ L. Reif et al. noted that the higher outcomes in the Gallagher et al. ( 1998) study may result from decreased non differential misclassification by taking spatial variability into account. Also, the DBP mixture may have been different from the mixtures used in other studies. There does not appear to be an increased association between TTHM and intrauterine growth retardation or preterm birth above the thresholds in question, based on the findings presented in Exhibit 5.2. The Waller et al. ( 1998) study presents higher odds ratios for spontaneous abortions than Savitz et al. ( 1995). The odds ratios for spontaneous abortion varied from region to region, possibly due to a difference in concentrations of BDCM and other byproducts ( Waller et al. 1998). The odds ratios for neural tube defects were generally higher than for other defects above both thresholds. There was not strong evidence of increased risk, however, for oral cleft defects or major cardiac defects ( the odds ratios for both defects based on Bove et al. ( 1995) were high). Overall, the odds ratios across 60 and 80 µ g/ L thresholds were similar, but tended to be slightly higher for 80 µ g/ L. Economic Analysis for the Stage 2 DBPR Proposal 5 12 July 2003 Exhibit 5.2 Odds Ratios ( and 95% Confidence Intervals 1) Calculated by Reif et al. ( 2000) for Reproductive and Developmental Health Endpoints at TTHM Levels of > 80 µ g/ L versus < 80 µ g/ L and > 60 µ g/ L versus < 60 µ g/ L Health Endpoint Dodds et al. ( 1999) Bove et al. ( 1995) Klotz and Pyrch ( 1998) Savitz et al. ( 1995) Waller et al. ( 1998) Gallagher et al. ( 1998)

> 80 µ g/ L versus < 80 µ g/ L TTHM Low Birth Weight 1.09 ( 0.99,1.19) 1.20 ( 1.02,1.41) N/ A 1.01 ( 0.69,1.50) N/ A N/ A Intrauterine Growth Retardation 1.05 ( 0.98,1.12) 1.12 ( 1.03,1.22) N/ A N/ A N/ A N/ A Preterm Birth 1.01 ( 0.92,1.10) 1.09 ( 0.99,1.19) N/ A 0.74 ( 0.51,1.07) N/ A N/ A Spontaneous Abortion N/ A N/ A N/ A 1.06 ( 0.63,1.78) 1.29 ( 0.98,1.69) N/ A Stillbirths 1.59 ( 1.21,2.10) 0.65 ( 0.45,0.95) N/ A N/ A N/ A N/ A Neural Tube Defects 1.37 ( 0.88,2.15) 2.12 ( 1.00,4.49) 1.35 ( 0.65,2.79) N/ A N/ A N/ A Oral Cleft Defects 1.01 ( 0.63,1.63) 1.95 ( 0.87,2.90) N/ A N/ A N/ A N/ A Major Cardiac Defects 0.87 ( 0.70,1.08) 1.59 ( 0.87,2.90) N/ A N/ A N/ A N/ A > 60 µ g/ L versus < 60 µ g/ L TTHM Low Birth Weight 1.06 ( 0.98,1.16) 1.07 ( 0.96,1.18) N/ A 1.35 ( 0.90,2.01) N/ A 2.24 ( 1.03,4.88)

Intrauterine Growth Retardation 1.05 ( 0.99,1.12) 1.04 ( 0.99,1.09) N/ A N/ A N/ A N/ A Preterm Birth 0.98 ( 0.91,1.06) 0.96 ( 0.91,1.02) N/ A 1.01 ( 0.71,1.44) N/ A N/ A Spontaneous Abortion N/ A N/ A N/ A 0.97 ( 0.56,1.67) 1.22 ( 0.98,1.53) N/ A Stillbirths 1.56 ( 1.18,2.06) 0.80 ( 0.65,0.97) N/ A N/ A N/ A N/ A Neural Tube Defects 1.01 ( 0.66,1.56) 1.34 ( 0.76,2.38) 1.79 ( 1.08,2.95) N/ A N/ A N/ A Oral Cleft Defects 0.91 ( 0.59,1.40) 1.25 ( 0.78,2.02) N/ A N/ A N/ A N/ A Major Cardiac Defects 0.94 ( 0.78,1.14) 0.93 ( 0.59,1.45) N/ A N/ A N/ A N/ A Notes: N/ A indicates that data for that health endpoint was not presented in the study.

Source: Adapted from Reif et al. ( 2000). Economic Analysis for the Stage 2 DBPR Proposal 5 13 July 2003 Exhibit 5.3 PAR Values ( and 95% Confidence Intervals 1 ) Calculated by Reif et al. ( 2000) for Reproductive and Developmental Health Endpoints at TTHM Levels of > 80 µ g/ L versus < 80 µ g/ L and > 60 µ g/ L versus < 60 µ g/ L ( Values are Percentages)

Health Endpoint Dodds et al. ( 1999) Bove et al. ( 1995) Klotz and Pyrch ( 1998) Savitz et al. ( 1995) Waller et al. ( 1998) Gallagher et al. ( 1998)

> 80 µ g/ L versus < 80 µ g/ L TTHM Low Birth Weight 2.4 ( 0,4.9) 1.5 ( 0.1,2.9) N/ A 0.5 ( 0,13.1) N/ A N/ A Intrauterine Growth Retardation 1.3 ( 0,3.1) 0.9 ( 0.2,1.6) N/ A N/ A N/ A N/ A Preterm Birth 0.2 ( 0,2.2) 0.7 ( 0,1.5) N/ A N/ A N/ A N/ A Spontaneous Abortion N/ A N/ A N/ A 1.9 ( 0,18.2) 4.5 ( 0,9.5) N/ A Stillbirths 14.1 ( 4.6,22.7) N/ A N/ A N/ A N/ A N/ A Neural Tube Defects 9.8 ( 0,23.3) 7.6 ( 0,17.0) 3.0 ( 0,10.2) N/ A N/ A N/ A Oral Cleft Defects 0.4 ( 0,13.1) 6.4 ( 0,13.9) N/ A N/ A N/ A N/ A Major Cardiac Defects N/ A 4.1 ( 0,10.2) N/ A N/ A N/ A N/ A > 60 µ g/ L versus < 60 µ g/ L TTHM Low Birth Weight 3.2 ( 0,7.3) 1.8 ( 0,4.6) N/ A 18.8 ( 0,39.0) N/ A 6.4 ( 0,14.1)

Intrauterine Growth Retardation 2.7 ( 0,5.8) 1.0 ( 0,2.4) N/ A N/ A N/ A N/ A Preterm Birth N/ A N/ A N/ A 0.7 ( 0,20.4) N/ A N/ A Spontaneous Abortion N/ A N/ A N/ A N/ A 6.5 ( 0,13.6) N/ A Stillbirths 22.5 ( 7.7,34.9) N/ A N/ A N/ A N/ A N/ A Neural Tube Defects 0.5 ( 0,20.0) 7.8 ( 0,22.5) 14.1 ( 1,25.5) N/ A N/ A N/ A Oral Cleft Defects N/ A 5.9 ( 0,18.0) N/ A N/ A N/ A N/ A Major Cardiac Defects N/ A N/ A N/ A N/ A N/ A N/ A Notes: 1. Lower confidence limit is truncated at zero N/ A indicates that data for that health endpoint were not presented in the study. Note that Reif et al. ( 2000) did not present PAR values for effects where the OR as shown in Exhibit 5.2 was < 1 ( PAR considered by the authors in those cases as undefined).

Source: Adapted from Reif et al. ( 2000).

Critical review of epidemiology literature by Bove et al. ( 2002)

Bove et al. ( 2002) conducted a qualitative review of 14 reproductive and developmental epidemiology studies on exposure to chlorination byproducts in drinking water ( many studies are the same as those reviewed by Reif et al. [ 2000]). Endpoints reviewed include small size for gestational age, birth defects ( e. g., neural tube defects, cleft defects, and cardiac effects), and spontaneous abortions. Studies that evaluated the end point of " small for gestational age" were limited due to lack of adequate exposure information and low study participation rate. Studies conducted in Denver ( Gallagher et al. 1998), northern New Jersey ( Bove et al. 1995), central North Carolina ( Savitz et al. 1995), and Nova Economic Analysis for the Stage 2 DBPR Proposal 5 14 July 2003 Scotia ( Dodds et al. 1999) based their exposure estimates on tap water samples of THMs taken concurrently with the pregnancy period. However, only one study ( Gallagher et al. 1998) involved modeling the distribution system characteristics and matching the residence with the appropriate sample location; this likely minimized exposure misclassification, and further strengthened the relationship found in the Denver study between TTHM and small for gestational age ( OR = 5.9; no confidence intervals reported).

Bove et al. ( 2002) believed that there was some consistency in the findings for neural tube defects and oral cleft defects, but not for cardiac defects. In the two studies that evaluated neural tube defects and individual THMs, one obtained similar findings for both chloroform and BDCM ( Klotz and Pyrch 1998), while the other study found a much stronger association with BDCM ( Dodds and King 2001). Of the two studies that evaluated oral cleft defects and levels of THMs, one found an association with TTHM ( Bove et al. 1995) and the other found an association with chloroform, but not TTHM ( Dodds and King 2001).

The California prospective cohort study ( Waller et al. 1998) found a correlation between spontaneous abortion and THMs, especially for BDCM. An association was also reported for spontaneous abortion when TTHM levels were evaluated, but this relationship disappeared when water consumption habits were taken into account. Bove et al. ( 1995) noted that this study's low participation rate was a notable weakness. In addition, because the maternal interviews were conducted after the loss had occurred, the potential for recall bias in water consumption habits during pregnancy was introduced. A Massachusetts study ( Aschengrau et al. 1993) found no excess spontaneous abortion correlating with treatment type ( i. e., chlorination vs. chloramination), but an effect was reported correlating with water source ( i. e., surface water vs. ground water).

Bove et al. ( 2002) evaluated three studies on the incidence of fetal deaths and THM levels, that had very different results. The Nova Scotia study ( Dodds and King 2001) found a strong association, especially with BDCM levels. In contrast, the northern New Jersey study ( Bove et al. 1995) could not evaluate the individual THM levels or information on the cause of death. Therefore, its finding of no excess could be the result of misclassification biases due to the failure to evaluate individual THMs and specific causes of death. The Massachusetts study ( Ascehngrau et al. 1993) found an association between stillbirths and chlorinated surface water when compared with chloraminated surface water.

Critical review of epidemiology literature by Nieuwenhuijsen et al. ( 2000)

Nieuwenhuijsen et al. ( 2000) reviewed the toxicological and epidemiological literature and evaluated the potential risk of chlorinated DBPs on human reproductive health. The authors reviewed 10 epidemiological studies according to the type of assessment of exposure used: water source and water treatment as an exposure index, routinely collected measurements of THMs as an index of exposure, and routinely collected THM measurements and estimation of individual THM ingestion as an exposure index. The authors commented that assessment of exposure is one of the weakest aspects of the available epidemiological studies.

The authors concluded that the evidence from a small number of studies suggests a weak association for spontaneous abortions, stillbirths, and birth defects, and the weight of evidence is increasing as more quality studies are completed. Nieuwenhuijsen et al. concluded that, " although studies report small risks that are difficult to interpret, the large number of people exposed to chlorinated water supplies constitutes a public health concern."

EPA's epidemiology research program EPA's epidemiology research program continues to examine the relationship between exposure to DBPs and adverse developmental and reproductive effects. The Agency is supporting several studies using improved study designs to provide better information for characterizing potential risks. Economic Analysis for the Stage 2 DBPR Proposal 5 15 July 2003 <IP_ADDRESS> Toxicological Evidence of Adverse Reproductive and Developmental Health Effects EPA has evaluated all published studies of the potential adverse effects of DBPs on the reproductive and developmental health of laboratory animals. Especially pertinent information comes from reviews of the toxicology literature by Dr. Rochelle Tyl ( 2000): " Review of Animal Studies for Reproductive and Developmental Toxicity Assessment of Drinking Water Contaminants: DBPs" and by the World Health Organization ( 2000): " Environmental Health Criteria 216: Disinfectants and Disinfection Byproducts."

Review of Tyl ( 2000)

Tyl evaluated the literature using the EPA developmental ( USEPA 1991b) and reproductive ( USEPA 1996d) toxicity risk assessment guidelines. Tyl focused her analysis on making determinations regarding hazard identification ( that is, identifying the specific types of adverse effects caused by these substances) and the adequacy of data from the available studies to support the development of doseresponse assessments.

Exhibit 5.4, adapted and updated from Tyl ( 2000), lists the types of reproductive and developmental toxicology studies that have been performed for various disinfectants and specific DBPs. In Exhibit 5.4, the study types are classified as either screening studies or as dose response studies.

Tyl concluded, based upon a weight of evidence approach to the analysis of the available, relevant literature, that " some of the DBPs have the intrinsic capacity to do harm, specifically to the developing conceptus and the male ( and possibly the female) reproductive system." Specific reproductive and developmental hazards that have been identified and associated with exposure to various DBPs are summarized in Exhibit 5.5.

Notwithstanding the evidence supporting the identification of specific developmental and reproductive effects from DBP exposure, Tyl also concluded that the weight of evidence assessment does not support a dose response evaluation based on existing studies. ( Tyl notes as " one possible exception" the 1996 Chemical Manufacturers Association's two generation rat study on chlorite.)

Tyl also noted in her overall summary and conclusions that in a review of animal literature for the purpose of risk assessment, " biological plausibility" is a major concern. Tyl pointed to several aspects of both the in vitro and in vivo studies that support the biological plausibility that DBPs can cause adverse reproductive and developmental effects. In particular, there was an observed temporal relationship between the exposures in toxicological studies and the occurrence of the developmental ( e. g., embryonic neural tube, embryonic heart) or reproductive process ( e. g., spermatogenesis). The observed effects were reproducible in the same or similar study designs. The effects were consistent across study designs. The effects observed in animal toxicological studies were comparable to those observed in some human epidemiological studies ( e. g., embryonic heart and neural tube defects, full litter resorption/ miscarriage, spontaneous abortion, or stillbirth). Economic Analysis for the Stage 2 DBPR Proposal 5 16 July 2003 Exhibit 5.4 Availability of Reproductive and Developmental Toxicology Studies for Specific DBPs Disinfectant or DBP Screens  Hazard Identification Dose Response WEC NTP 35 Day CKA CKA++ Male Repro Seg II Multi GEN DISINFECTANTS Chlorine X Chlorine Dioxide X X Chloramine X TRIHALOMETHANES Chloroform X X X X Bromoform X X X Bromodichloromethane X X X X X Dibromochloromethane X X HALOACETIC ACIDS Monochloroacetic acid X X Dichloroacetic acid X X X Trichloroacetic acid X X X Monobromoacetic acid X X X Dibromoacetic acid X X X X X X Tribromoacetic acid X X Bromochloroacetic acid X X X P Bromodichloroacetic acid X Dibromochloroacetic acid X X HALOACETONITRILES Chloroacetonitrile X Dichloroacetonitrile X X Trichloroacetonitrile X X Bromoacetonitrile X X Dibromoacetonitrile X X Tribromoacetonitrile Bromochloroacetonitrile X X ALDEHYDES Formaldehyde X X X X Acetaldehyde X X Propanal X X MISCELLANEOUS 1,1 Dichloropropanone X Hexachloropropanone X Dichloromethane X Dibromomethane X MX X X Bromate X Chlorite X X X Notes: X = Completed and published in the literature; P = In planning stage; WEC = Whole embryo culture; NTP 35 Day = NTP 35 day reproductive/ developmental toxicity screen; CKA = Chernoff Kavlock Assay; CKA (++) = Chernoff Kavlock Assay ( modified); Male Repro. = Short term adult male reproductive toxicity screen; Seg II = Segment II developmental toxicity study; Multi GEN = Multigeneration reproductive toxicity study.

Source: Adapted and updated from Tyl ( 2000). Economic Analysis for the Stage 2 DBPR Proposal 5 17 July 2003 Exhibit 5.5 Reproductive and Developmental Health Effects Associated with DBPs in Toxicological Studies Type of Effect DBP Developmental defects Trichloroacetic acid ( TCAA), dichloroacetic acid ( DCAA), and monochloroacetic acid ( MCAA)

Whole litter resorption Chloroform, bromoform, bromodichloromethane ( BDCM), dibromochloromethane ( DBCM), DCAA, TCAA, dichloroacetonitrile ( DCAN), and trichloroacetonitrile ( TCAN)

Fetotoxicity ( reduced fetal body weights, increased anomalies like chromosomal defects) Chloroform, BDCM, DBCM, DCAA, TCAA, DCAN, TCAN, dibromoacetonitrile ( DBAN), bromochloroacetonitrile ( BCAN), monochloroacetonitrile ( MCAN) acetaldehyde, formaldehyde Male reproductive defects DCAA, dibromoacetic acid ( DBAA), BDCM, formaldehyde Source: Adapted from Tyl ( 2000).

Review of WHO ( 2000)

The International Programme on Chemical Safety ( IPCS) published an evaluation of Disinfectants and DBPs in its Environmental Health Criteria monograph series ( WHO 2000). In this review of the toxicology data on reproductive and developmental effects from DBP exposure, the World Health Organization ( WHO) concludes that although the data on these effects are not as robust as the cancer database, these effects are of potential health concern. The WHO concludes that reproductive effects in females have been principally embryolethality and fetal resorptions associated with the haloacetonitriles ( HANs) and the dihaloacetates, while DCAA and DBAA have both been associated with adverse effects on male reproduction.

New Toxicology Data Since promulgating the Stage 1 DBPR, EPA has continued to support reproductive and developmental toxicological research on various DBPs through extramural and intramural research programs. Information on EPA's toxicology programs can be found at http:// www. epa. gov/ nheerl/. This research, along with the new published data on several DBPs since the 1998 Stage 1 DBPR, are summarized in the draft updated children's health document " Health Risks to Fetuses, Infants, and Children: A Review" ( USEPA 2002h). Summaries of new studies are provided below.

Christian et al. ( 2001a) conducted a developmental toxicity study with pregnant New Zealand White rabbits exposed to BDCM in drinking water at concentrations of 0, 15, 150, 450, and 900 ppm in drinking water on gestation days 6 29. The NOAEL and LOAEL identified for maternal toxicity in this study were 13.4 mg/ kg day ( 150 ppm) and 35.6 mg/ kg day ( 450 ppm), respectively, based on decreased body weight gain. The developmental NOAEL was 55.3 mg/ kg day ( 900 ppm) based on absence of statistically significant, dose related effects at any tested concentration. Christian et al. ( 2001a) also conducted a developmental study of BDCM in a second species, Sprague Dawley rats. Rats were exposed to BDCM in the drinking water at concentrations of 0, 50, 150, 450, and 900 ppm on gestation days 6 to 21. The concentration based maternal NOAEL and LOAEL for this study were 150 ppm and 450 ppm, respectively, based on statistically significant, persistent reductions in maternal body weight and body weight gains. Based on the mean consumed dosage of bromodichloromethane, these concentrations correspond to doses of 18.4 mg/ kg day and 45.0 mg/ kg day, respectively. The concentration based developmental NOAEL and LOAEL were 450 ppm and 900 ppm, respectively, based on a significantly decreased number of ossification sites per fetus for the forelimb phalanges ( bones Economic Analysis for the Stage 2 DBPR Proposal 5 18 July 2003 of the hand or the foot) and the hindlimb metatarsals and phalanges. These concentrations correspond to mean consumed doses of 45.0 mg/ kg day and 82.0 mg/ kg day, respectively.

Christian et al. ( 2002b) summarized the results of a two generation reproductive toxicity study on bromodichloromethane conducted in Sprague Dawley ( SD) rats. Bromodichloromethane was continuously provided to test animals in the drinking water at concentrations of 0, 50, 150, or 450 ppm. Average daily doses estimated for the 50, 150 and 450 ppm concentrations were reportedly 4.1 to 12.6, 11.6 to 40.2, and 29.5 to 109 mg/ kg day, respectively. The parental NOAEL and LOAEL were 50 and 150 ppm, respectively, based on statistically significant reduced body weight and body weight gain; F1 and F2 generation pup body weights were reduced in the 150 and 450 ppm groups during the lactation period after the pups began to drink the water provided to the dams. Body weight and body weight gain were also reduced in the 150 and 450 ppm F1 generation males and females. A marginal effect on estrous cyclicity was observed in F1 females in the 450 ppm exposure group. Small ( # 6%), but statistically significant, delays in F1 generation sexual maturation occurred at 150 ppm ( males) and 450 ppm ( males and females) as determined by timing of vaginal patency or preputial separation. The study authors considered these effects to be a secondary response associated with reduced body weights cause appears to be dehydration brought about by taste aversion to the compound. The results of this study identify NOAEL and LOAEL values for reproductive effects of 50 ppm ( 4.1 to 12.6 mg/ kg day) and 150 ppm ( 11.6 to 40.2 mg/ kg day), respectively, based on delayed sexual maturation.

Bielmeier et al. ( 2001) conducted a series of experiments to investigate the mode of action in bromodichloromethane induced full litter resorption ( FLR). The study included a strain comparison of F344 and Sprague Dawley ( SD) rats. In the strain comparison experiment, female SD rats ( 13 to 14/ dose group) were dosed with 0, 75, or 100 mg/ kg day by aqueous gavage in 10% Emulphor ® on GD 6 to 10. F344 rats ( 12 to 14/ dose group) were dosed with 0 or 75 mg/ kg day administered in the same vehicle. The incidence of FLR in the bromodichloromethane treated F344 rats was 62%, while the incidence of FLR in SD rats treated with 75 or 100 mg/ kg day of bromodichloromethane was 0%. Both strains of rats showed similar signs of maternal toxicity, and the percent body weight loss after the first day of dosing was comparable for SD rats and the F344 rats that resorbed their litters. The rats were allowed to deliver and pups were examined on postnatal days 1 and 6. Surviving litters appeared normal and no effect on post natal survival, litter size, or pup weight was observed. The series of experiments conducted by Bielmeier et al. ( 2001) identified a LOAEL of 75 mg/ kg day ( the lowest dose tested) based on FLR in F344 rats. A NOAEL was not identified. Mechanistic studies indicate that BDCM induced pregnancy loss is likely to be luteinizing hormone ( LH) mediated ( Bielmeier et al., 2001). It is possible that BDCM alters LH levels by disrupting the hypothalamic pituitary gonadal axis or by altering the responsiveness of the corpora lutea to LH. Since these possible mechanisms are potentially relevant to pregnancy maintenance in humans, EPA believes the finding of BDCM induced pregnancy loss in F344 rats is relevant to risk assessment, and may provide insight into the epidemiological finding of increased risk of spontaneous abortion associated with consumption of BDCM ( Waller et al. 1998, 2001).

Christian et al. ( 2002a) recently completed a two generation drinking water study of DBAA in rats. Male and female Sprague Dawley rats ( 30/ sex/ exposure group) were administered DBAA in drinking water at concentrations of 0, 50, 250, or 650 ppm continuously from initiation of exposure of the parental ( P) generation male and female rats through weaning of the F 2 offspring. Based on testicular histomorphology indicative of abnormal spermatogenesis in P and F 1 males, the parental and reproductive/ developmental toxicity LOAEL and NOAEL are 250 and 50 ppm, respectively.

Previous studies by EPA have reported adverse effects of DBAA, administered via oral gavage, on spermatogenesis that impacted male fertility ( Linder et al. 1994a, 1995, 1997a) at doses comparable to those achieved in the Christian et al. ( 2002a) study. Based on these studies collectively, DBAA is spermatotoxic. Moreover, Veeramachaneni et al. ( 2000) reported in an abstract that sperm from male rabbits exposed to DBA in utero from gestation days 15 and throughout life reduced the fertility of artificially inseminated females as evidenced by reduced conceptions. When published, this study may support the evidence that DBA is a male reproductive system toxicant. Economic Analysis for the Stage 2 DBPR Proposal 5 19 July 2003 In addition, research on DBAA by Klinefelter et al. ( 2001) has demonstrated statistically significant delays in both vaginal opening and preputial separation using the body weight on the day of acquisition ( at postnatal day 45) as the co variant. This was not found by Christian et al ( 2002a) using the body weight at weaning as the statistical covariant. However, the authors analyzed the data for preputial separation and vaginal opening with body weight on the day of weaning as a co variant rather than body weight on the day of acquisition, i. e. the day that the prepuce separates or the day the vagina opens. It is likely that there was an increase in body weight from postnatal day 21 ( weaning) until preputial separation ( day 45) that was independent of the delay in sexual maturation.

Although the Christian et al ( 2002a) study was conducted in accordance with EPA's 1998 testing guidelines, EPA has incorporated newer, more sophisticated measures into recent intramural and extramural studies that have not yet been incorporated into the testing guidelines. Such measures include measuring changes in specific proteins in the sperm membrane proteome and fertility assessments via in utero insemination. EPA believes that additional research is needed, utilizing these newer toxicological measures, to clarify the extent to which DBAA poses human reproductive or developmental risk. The database on male reproductive effects from exposure to DBAA is incomplete and is not suitable for quantitative risk assessment at this time. It does identify reproductive effects as an area of concern.

In addition data compiled in the children's health document, EPA has prepared individual health criteria documents that provide detailed summaries of the relevant new information, as well as an overall characterization of the human health risks from exposure to these DBPs ( USEPA 2003c g). From these new evaluations, EPA has concluded that several new studies on individual byproducts contribute to the weight of evidence for an association between DBP exposure and adverse effects on the developing fetus and reproduction. These effects include fetal loss, cardiovascular effects, and male reproductive effects and are associated with BDCM, DCAA, TCAA, BCAA, and DBAA. The new data from these studies do not change the MCLGs and MRDLGs that were established as a part of the Stage 1 DBPR.

<IP_ADDRESS> Conclusions EPA believes that toxicology and epidemiology data suggests that exposure to chlorinated drinking water has the potential to cause adverse reproductive and developmental effects. Although the science on reproductive and developmental health effects as a result of DBP exposure is not strong enough to include them in the primary Stage 2 DBPR benefits analysis at this time, EPA concludes that the data are sufficient to determine that a concern exists warranting additional regulatory action. The following are the specific key factors used to support EPA's weight of evidence conclusion regarding this conclusion:

° The results of several studies performed by different researchers with different methods at different research sites show similar trends.

° Some health effects observed in animal toxicological studies are comparable to those observed in some human epidemiological studies ( e. g., embryonic heart and neural tube defects, full litter resorption/ miscarriage, spontaneous abortion, or stillbirth) showing similarity of effects between animal toxicity and human epidemiology studies.

° Difficulties in assessing exposure to DBPs, resulting in exposure misclassification, may underestimate reproductive and developmental risks associated with DBPs. It is possible that some of the inconsistencies reported in epidemiological and toxicological study results are due to these misclassifications, and the true effects may be greater than demonstrated. A spurious effect would be produced only in rare cases, and is unlikely as described in Reif et al. ( 2000) and Bove et al. ( 2002). Economic Analysis for the Stage 2 DBPR Proposal 5 20 July 2003 EPA has epidemiology and toxicology research programs that continue to examine the relationship between exposure to DBPs and potential adverse reproductive and developmental health effects. EPA is also supporting several studies using improved study design to provide better information for characterizing potential risks. This research is intended to yield more precise dose response relationships to support a quantitative risk assessment.

5.2.2 Cancer Several DBPs have been identified by EPA as probable or possible human carcinogens. The following sections provide an overview of the epidemiological and toxicological evidence for the carcinogenicity of key DBPs.

<IP_ADDRESS> Epidemiological Evidence of DBP Carcinogenicity New studies published since the Stage 1 DBPR continue to support an association between bladder, colon and rectal cancers and exposure to chlorinated surface water ( Yang et al. 1998; Koivusalo et al. 1998; King et al. 2000b). EPA believes that the available epidemiological studies along with the review of the cancer epidemiology literature in the International Programme on Chemical Safety report on disinfectants and disinfection byproducts ( WHO 2000) provide important information on the potential human health hazards from exposure to chlorinated drinking water.

Bladder Cancer  Studies Supporting EPA's PAR Analysis Bladder cancer and chlorinated DBP exposure has historically been the most strongly supported association of all the possible cancers, based on human evidence. The Stage 1 DBPR RIA ( USEPA 1998a) presents EPA's review of the large body of epidemiology literature for bladder cancer and its association with DBPs in drinking water. From this review, EPA concluded that although causality has not been established, the data support a weak association, which may be a concern. Particular gaps in EPA's understanding include the reason for inconsistent results across subpopulations in the different studies, especially for males versus females and smokers versus nonsmokers.