MP& M EEBA Part III: Benefits Chapter 12: Benefit Overview INTRODUCTION Part III of the EEBA assesses the benefits to society from the reduced effluent discharges that will result from the MP& M industry regulations. EPA expects that benefits will accrue to society in several broad categories, including reduced health risks, enhanced environmental quality, and increased productivity in economic activities that are adversely affected by MP& M industry discharges.

This chapter provides a discussion of the pollutants of concern ( POCs) , their effect on human health, their environmental effects, a framework for understanding the benefits likely to be achieved by the MP & M regulation, and a qualitative discussion of those benefits. The following chapters quantify and estimate the economic value of these benefit categories. Appendices I and H provide further information on environmental effects of MP& M pollutants and water quality models used to assess these effects. Chapter 12: Benefit Overview CHAPTER CONTENTS 12.1 ................. ........ 12 2 12.1.1 teristics of MP& M Pollutants ..... 12 2 12.1.2 ects of MP& M Pollutants on Human Health ................. .............. 12 3 12.1.3 ental Effects of MP& M Pollutants ................. ........... 12 7 12.1.4 ects of MP& M Pollutants on Economic Productivity ................. ......... 12 8 12.2 to Beneficial Outcomes . . 12 9 12.3 ive and Quantitative Benefits Assessment 12 11 12.3.1 ........ 12 11 12.3.2 n Health Benefits .............. 12 13 12.3.3 ................. 12 13 12.3.4 c Productivity Benefits ........ 12 14 12.3.5 or Valuing Benefit Events .... 12 14 Glossary ................. ................. .. 12 16 Acronyms ................. ................. . 12 19 References ................. ................. 12 20 MP& M Pollutants Charac Eff Environm Eff Linking the Regulation Qualitat Overview of Benefit Categories Huma Ecological Benefits Economi Methods f EPA estimated national benefits expected to accrue from the regulation on the basis of sample facility data. The Agency extrapolated findings from the sample facility analyses to the national level using two alternative extrapolation methods: ( 1)

traditional extrapolation and ( 2) post stratification extrapolation. The traditional extrapolation approach relies on sample facility weights that were developed based on information about the economic and technical characteristics of the regulated community. This extrapolation approach does not incorporate information that could significantly affect the occurrence and distribution of regulatory benefits, such as characteristics of the receiving water body and the size of the population that may benefit from reduced pollutant discharges. EPA recognizes that using a traditional extrapolation method to estimate national level benefits may lead to a large degree of uncertainty in benefits estimates. Thus, EPA also used an alternative set of sampling weights, based on a post sampling stratification method, to calculate alternative national estimates of benefits. EPA adjusted the original sample weights using two variables that are likely to affect the occurrence and size of benefits associated with reduced discharges from sample MP& M facilities: receiving water body type and size, and the size of the population residing in the vicinity of the sample facility. The following chapters present two sets of estimates of benefits expected to accrue from the MP& M regulation based on both traditional and post stratification extrapolation approaches. Appendix G of this report provides detailed information on extrapolation methods.

In addition, the Agency used the Ohio case study results to develop a third estimate of the monetary value of national benefits. 1 EPA extrapolated the Ohio case study results to the national level based on three key factors that affect the occurrence and magnitude of benefits: ( 1) the estimated change in the MP& M pollutant loadings, ( 2) the level of recreational activities on the reaches affected by MP& M discharges, and ( 3) state level income. The Agency recognizes that this method is not rigorous for extrapolation to the national level. Therefore, EPA used this method only as a sensitivity analysis ( see Appendix G of this report for detail).

EPA notes that effluent limitations guidelines for the MP& M industry are technology based. EPA is not required to demonstrate environmental benefits of its technology based rules. It is well established that EPA is not required to consider receiving water quality in setting technology based effluent limitations guidelines and standards. Weyerhaeuser v. Costle,

590 F. 2nd 1011, 1043 ( D. C. Cir. 1978) (" The Senate Committee declared that '[ t] he use of any river, lake, stream or ocean as a waste treatment system is unacceptable' regardless of the measurable impact of the waste on the body of water in question.

Legislative History at 1425 ( Senate Report). The Conference Report states that the Act ' specifically bans pollution dilution as 1 See Chapter 21 for a detailed discussion the Ohio case study.

12 1 MP& M EEBA Part III: Benefits Chapter 12: Benefit Overview an alternative to treatment.' " Id. at 284). In establishing effluent limitations and standards, EPA considers benefits as one of the factors that the Agency evaluates.

12.1 MP& M POLLUTANTS EPA defines three general categories of pollutants: priority or toxic pollutants; nonconventional pollutants; and conventional pollutants. Priority pollutants ( PPs) are defined as any of 126 named pollutants. 2 Conventional pollutants include biological oxygen demand ( BOD) , total suspended solids ( TSS) , oil and grease ( O& G) , pH, and anything else the Administrator defines as a conventional pollutant. Nonconventionals are a catch all category that includes everything that is not in the two previously described categories. The naming system is somewhat confusing in that some nonconventional pollutants may be as " toxic" as, or more " toxic" than some of the PPs.

MP& M effluents contain a variety of priority, nonconventional, and conventional pollutants. The release of these pollutants to our nation's surface water degrades aquatic environments, alters aquatic habitats, and affects the diversity and abundance of aquatic life. It also increases the health risks to humans who ingest contaminated surface waters or eat contaminated fish and shellfish ( U. S. EPA, 1997). A number of the pollutants commonly found in MP& M effluents also inhibit biological wastewater treatment systems or accumulate in sewage sludge or sediment.

Metals are a particular concern because of their prevalence in MP& M effluents. Metals are inorganic compounds, generally non volatile ( with the notable exception of mercury), and cannot be broken down by biodegradation processes. Metals can accumulate in biological tissues, sequester into sewage sludge in publicly owned treatment works ( POTWs), and contaminate soils and sediments when released to the environment. Sediments contaminated with metals become resuspended by dredging, boat propellers, water currents or wave action, and storm events, releasing metals back into the water column.

Metals can also become biologically available and enter terrestrial food chains once the sludge is applied on land. Sludges with high concentrations of metals are therefore unsuitable for land application. Some metals are quite toxic even when present at relatively low levels.

Some of the inorganic POCs found in MP& M effluents are also natural constituents of water, including potassium, calcium,

magnesium, iron, chlorine, fluoride, sulfate, phosphates, silica, and a number of trace metals such as copper and zinc.

Human and ecological exposure and risk from environmental releases of MP& M pollutants depend on chemical specific properties, the mechanism and medium of release, and site specific environmental conditions. Chemical specific properties include toxicological effects on living organisms, hydrophobicity/ lipophilicity, reactivity and persisistence. These properties are described in sections 12.1.1 through 12.1.4.

12.1.1 Characteristics of MP& M Pollutants EPA sampled MP& M facilities nationwide to assess the concentrations of pollutants in MP& M effluents. The Agency collected samples of raw wastewater from MP& M facilities and applied standard water analysis protocols to identify and quantify the pollutant levels in each sample. EPA used these analytical data, along with selection criteria, to identify 132 contaminants of potential concern. 3 EPA then evaluated the potential environmental fate and transport of these pollutants and their toxicity to humans and aquatic receptors. Fate of the MP& M pollutants was estimated based on the propensity of those pollutants to volatilize, adsorb onto sediments, bioconcentrate, and biodegrade. Table I. 1 in Appendix I lists MP& M pollutants and provides data on human health concerns, and fate and effects.

EPA used various data sources to evaluate pollutant specific fate and toxicity. To evaluate potential human health effects, the Agency relied on reference doses ( RfDs) and cancer potency slope factors ( SFs), human health based water 2 The Agency originally had 129 PPs, but 3 have been dropped from the list bringing the number of PPs to 126.

3 EPA originally identified 150 MP& M POCs. Of these 150 POCs, the Agency estimated loadings for 132 pollutants for the phase 2 proposal and NODA. The benefits analysis presented in this chapter and the following chapters was based on 132 pollutants for which loadings are available. The final regulation covers only the Oily Wastes subcategory and benefit reductions were estimated for 122 pollutants.

12 2 MP& M EEBA Part III: Benefits Chapter 12: Benefit Overview quality criteria ( WQC) , maximum contaminant levels ( MCLs) for drinking water protection and other drinking water related criteria, and hazardous air pollutant ( HAP) and PP lists. Appendix I. 1.2 provides short descriptions and definitions for each of these measures of human health effects.

To evaluate potential fate and effects in aquatic environments, the Agency relied on measures of acute and chronic toxicity to aquatic species, bioconcentration factors for aquatic species, Henry's Law constants ( to estimate volatility),

adsorption coefficients ( Koc) ( to estimate association with bottom sediments), and biodegradation half lives ( to estimate the removal of chemicals via microbial metabolism).

The data sources used in the assessment include EPA ambient water quality criteria ( AWQC) documents and updates,

EPA's ASsessment Tools for the Evaluation of Risk ( ASTER) , the AQUatic Information REtrieval System ( AQUIRE) , and the Environmental Research Laboratory Duluth fathead minnow database, EPA's Integrated Risk Information System ( IRIS ), EPA's Health Effects Assessment Summary Tables ( HEAST) , EPA's 1991 and 1993 Superfund Chemical Data Matrix ( SCDM) , Syracuse Research Corporation's CHEMFATE and BIODEG databases, EPA and other government reports, scientific literature, and other primary and secondary data sources.

To ensure that the assessment is as comprehensive as possible, EPA also obtained data on chemicals for which physical chemical properties and/ or toxicity data were not available from the sources listed above. To the extent possible,

EPA estimated values for the chemicals using the quantitative structure activity relationship ( QSAR) model incorporated in ASTER, and for some physical chemical properties, used published linear regression correlation equations.

12.1.2 Effects of MP& M Pollutants on Human Health Individuals are potentially exposed to MP& M pollutants released to the aquatic environment via consumption of contaminated fish. Populations served by drinking water utilities located downstream of effluent discharges from MP& M facilities are also exposed to M P& M pollutants via contaminated drinking water. Many of these pollutants may increase risks to human health.

Based on the available human health toxicity data for the 132 POCs presented in Table I. 1 ( Appendix I), EPA found that: 4   76 pollutants are human system ic toxicants;

  13 pollutants with published SFs are classified as known, probable, or possible human carcinogens when ingested via drinking water or food. Lead is also classified as a possible human carcinogen in IRIS but EPA has not developed a SF for it ( U. S. EPA, 1998/ 99d);

  36 pollutants have drinking water criteria ( 27 with enforceable health based MCLs, 7 with secondary MCLs for taste or aesthetics, and 2 with action levels for treatment);

  35 pollutants are designated as HAP s in wastewater;

  43 pollutants are identified as PPs; and   76 pollutants have human health based water quality criteria ( WQC) to protect against the ingestion of water and organisms or organisms only ( see Chapter 13, Table 13.3).

The carcinogens identified by EPA in MP& M effluent samples include known ( A), probable ( B1 and B2) and possible ( C)

human carcinogens. These pollutants are associated with the development of cancers in the spleen, liver, kidney, lung,

bladder, and skin, among others. These pollutants and target organs are shown in Table 12.1.

4 Facilities in the Oily Wastes subcategory discharge: 75 of the 76 systemic toxicants; all 13 human carcinogens; all 36 pollutants with drinking water criteria; all 35 pollutants designated as HAPs; 41 of the 43 priority pollutants; and 75 of the 76 pollutants that have human health based water quality criteria. Of the 132 POCs evaluated, facilities in the Oily Wastes subcategory do not discharge the following 10 pollutants: amenable cyanide, boron, cadmium, cyanide, phosphate, sodium, sulfide, total dissolved solids, weak acid dissociable cyanide,

and ziram/ cymate.

12 3 MP& M EEBA Part III: Benefits Chapter 12: Benefit Overview Table 12.1: Human Carcinogens Evaluated, Weight of Evidence Classifications, and Target Organs CAS Number Carcinogen Weight of Evidence Classification Target Organs 62533 Aniline B2 Spleen 7440382 Arsenic A Liver, kidneys, lungs, bladder,

117817 Bis( 2 ethylhexyl) phthalate B2 Liver 75003 Chloroethane a 75092 Dichloromethane B2 Liver, lungs 75354 Dichloroethene, 1,1 C Inconclusive b 123911 Dioxane, 1,4 B2 Liver, nasal cavity, gall bladder 78591 Isophorone C Preputial gland 62759 Nitrosodimethylamine, N B2 Liver, lungs, skin, seminal vesicle,

lymphatic/ hematopoetic system 86306 Nitrosodiphenylamine, N B2 Bladder tumors, reticulum cell sarcomas 127184 Tetrachloroethene B2 Liver 79016 Trichloroethene a 67663 Trichloromethane B2 Kidneys skin A = Human Carcinogen B1 = Probable Human Carcinogen ( limited human data)

B2 = Probable Human Carcinogen ( animal data only)

C = Possible Human Carcinogen a Pollutant has been withdrawn from the IRIS database for additional study.

b There is equivocal evidence for the oral route of exposure. This chemical is likely a systemic carcinogen via inhalation.

Target organs include: kidney, pancreas, skin, mammary gland, and blood forming elements ( lymphoma and leukemia).

Source: U. S. Environmental Protection Agency verified ( IRIS) or provisional ( HEAST) ( U. S. EPA ( 1998/ 99d), U. S. EPA ( 1997)).

Non carcinogenic hazards associated with pollutants in MP& M effluent include systemic effects ( e. g., impairment or loss of neurological, respiratory, reproductive, circulatory, or immunological functions), organ specific toxicity ( e. g., kidney, small intestines, blood, testes, liver, stomach, thyroid), fetal effects ( e. g., increased fetal mortality, decreased birth weight), other effects ( e. g., lethargy, cataracts, weight loss, hyperactivity), and mortality. These effects are listed by pollutant in Table 12.2.

12 4 MP& M EEBA Part III: Benefits Chapter 12: Benefit Overview Table 12.2: MP& M Pollutants Exhibiting Systemic and Other Non Cancer Human Health Effectsa CAS Number Toxicant RfD Target Organ and Effects 83329 Acenaphthene Liver, hepatotoxicity 67641 Acetone Increased liver and kidney weights, nephrotoxicity 98862 Acetophenone General toxicity 107028 Acrolein Cardiovascular toxicityc 7429905 Aluminum Renal failure, intestinal contraction interference, adverse neurological effectsd 120127 Anthracene General toxicity 7440360 Antimony Longevity, blood glucose, cholesterol 7440382 Arsenic Hyperpigmentation, keratosis and possible vascular complications 7440393 Barium Increased kidney weight 65850 Benzoic acid General toxicity 100516 Benzyl alcohol Forestomach, epithelial hyperplasia 7440417 Beryllium Small intestinal lesions 92524 Biphenyl Kidney damage 117817 Bis( 2 et hylhexy l )

phthalate Increased relative liver weight 7440428 Boron Testicular atrophy, spermatogenic arrest 85687 Butyl benzyl phthalate Significantly increased liver to body and liver to brain weight 7440439 Cadmium Significant proteinuria ( protein in urine)

75150 Carbon disulfide Fetal toxicity, malformations 108907 Chlorobenzene Histopathologic changes in liver 75003 Chloroethane General toxicity 7440473 Chromium Renal tubular necrosis ( kidney tissue decay) d 18540299 Chromium hexavalent Reduced water consumption 7440484 Cobalt Heart effectsd 7440508 Copper Gastrointestinal effects, liver necrosisd 95487 Cresol, o Decreased body weight and neurotoxicity 106445 Cresol, p Central nervous system hypoactivity and respiratory system distress 57125 Cyanide Weight loss, thyroid effects and myelin degeneration 75354 Dichloroethene, 1,1 Toxic effects on kidneys, spleen, lungsd; hepatic lesions 75092 Dichloromethane Liver toxicity 68122 Dimethylformamide,

N, N Liver and gastrointestinal system effects 105679 Dimethylphenol, 2,4 Clinical signs ( lethargy, prostration, and ataxia) and hematological changes 84742 Di n butyl phthalate Increased mortality 51285 Dinitrophenol, 2,4 Cataract formation 606202 Dinitrotoluene, 2,6 Mortality, central nervous system neurotoxicity, blood heinz bodies and methemoglobinemia, bile duct hyperplasia, kidney histopathology 117840 Di n octyl phthalate Kidney and liver increased weights, increased liver enzymes 122394 Diphenylamine Decreased body weight, and increased liver and kidney weights 100414 Ethylbenzene Liver and kidney toxicity 206440 Fluoranthene Nephropathy, increased liver weights, hematological alterations, clinical effects 86737 Fluorene Decreased red blood cell count, packed cell volume and hemoglobin 16984488 Fluoride Objectionable dental fluorosis ( soft, mottled teeth)

591786 Hexanone, 2 Hepatotoxicity and nephrotoxcity c 12 5 MP& M EEBA Part III: Benefits Chapter 12: Benefit Overview Table 12.2: MP& M Pollutants Exhibiting Systemic and Other Non Cancer Human Health Effectsa CAS Number Toxicant RfD Target Organ and Effects 7439896 Iron Liver pathology, diabetes mellitus, endocrine disturbance, and cardiovascular effects c 78831 Isobutyl alcohol Hypoactivity and ataxia 78591 Isophorone Kidney pathology 7439965 Manganese Central nervous system effects 78933 Methyl ethyl ketone Decreased fetal birth weight 108101 Methyl isobutyl ketone Lethargy, increased liver and kidney weights and urinary protein 80626 Methyl methacrylate Increased kidney to body weight ratio 91576 Methylnaphthalene, 2

7439987 Molybdenum Increased uric acid 91203 Naphthalene Decreased body weight 7440020 Nickel Decreased body and organ weights 100027 Nitrophenol, 4

59507 Parachlorometacresol 108952 Phenol Reduced fetal body weight 129000 Pyrene Kidney effects ( renal tubular pathology, decreased kidney weights)

110861 Pyridine Increased liver weight 7782492 Selenium Clinical selenosis ( hair or nail loss)

7440224 Silver Argyria ( skin discoloration)

100425 Styrene Red blood cell and liver effects 127184 Tetrachloroethene Liver toxicity, weight gain 7440280 Thallium Liver toxicity, gastroenteritis, degeneration of peripheral and central nervous systemc 7440315 Tin Kidney and liver lesions 7440326 Titanium Considered to be physiologically inertc 108883 Toluene Changes in liver and kidney weights 79016 Trichloroethene Bone marrow, central nervous system, liver, kidneys 4 75694 Trichlorofluoromethane Histopathology and mortality 67663 Trichloromethane Fatty cyst formation in liver 7440622 Vanadium Kidney and central nervous system effectsb 108383 Xylene, m Central nervous system hyperactivity, decreased body weight 179601231 Xylene, m & p ( c)

95476 Xylene, o Central nervous system hyperactivity, decreased body weight 136777612 Xylene, o & p ( c)

7440666 Zinc 47% decrease in erythrocyte superoxide dismutase ( ESOD) concentration in adult human females after 10 weeks of zinc exposure 137304 Ziram \ Cymate a Chemicals with EPA verified ( IRIS) or provisional ( HEAST, or other Agency document)) human health based RfDs, referred to as   systemic toxicants  ( U. S. EPA ( 1998/ 99d), U. S. EPA ( 1997)).

b RfD based on a no observed adverse effect level ( NOAEL). Health effects summarized from Amdur, M. O., Doul, J., and Klaassen, C. D.,

eds. Cassarett and Doul s Toxicology, 4th edition, 1991.

c Target organ and effects summarized from Amdur, M. O., Doul, J., and Klaassen, C. D., eds. Cassarett and Doul s Toxicology, 5th edition,

1996.

d Target organ and effects summarized from Wexler, P., ed. Encyclopedia of Toxicology, Volumes 1 3, 1998.

Source: U. S. EPA analysis.

12 6 MP& M EEBA Part III: Benefits Chapter 12: Benefit Overview 12.1.3 Environmental Effects of MP& M Pollutants Ecological impacts of MP& M pollutants include acute and chronic toxicity to aquatic receptors by dozens of pollutants present in MP& M effluents, uptake of certain pollutants into aquatic food webs, sub lethal effects on metabolic and reproductive functions, habitat degradation from turbidity, eutrophication, dissolved oxygen depletion, and loss of prey organisms. Metals are of particular concern to this regulation because they ( 1) do not volatilize, ( 2) do not biodegrade, ( 3)

can be toxic to plants, invertebrates and fish, ( 4) adsorb to sediments and ( 5) bioconcentrate in biological tissues.

EPA obtained the environmental fate and toxicity information for the 132 MP& M POCs. Table I. 1 in Appendix I shows the environmental fate and toxicity of each MP& M pollutant. 5 EPA found that:

  56 pollutants are not volatile or are only slightly volatile ( all metals were assumed to be non volatile except for mercury);

  57 pollutants have moderate to high adsorption potentials ( all metals were assumed to have high adsorption potential except for nickel);

  42 pollutants have moderate to high bioconcentration factors;

  62 pollutants biodegrade slowly or are resistant to biodegradation altogether ( all metals were assumed to be resistant to biodegradation);

  For freshwater environments, 32 pollutants have acute toxicities to aquatic life that range from moderate to high, and 33 pollutants have chronic toxicities that range from moderate to high;

  For saltwater environments, 20 pollutants have acute toxicities to aquatic life that range from moderate to high, and 23 pollutants have chronic toxicities that range from moderate to high.

The available information shows that dozens of the MP& M POCs have the potential to pose significant hazards to the aquatic environment when released to receiving waters. A number of pollutants are of particular concern because of their combined toxicity and fate. These include several polyaromatic hydrocarbons ( acenaphthene, anthracene, 3,6 dimethyl phenanthrene,

fluoranthene, phenanthrene, and pyrene), several metals ( aluminum, cadmium, copper, mercury, and selenium) and several phthalates ( di n octyl phthalate, butyl benzyl phthalate, and di n butyl phthalate). Other pollutants are of concern chiefly because of their toxicity ( arsenic, cyanide, chromium, lead, nickel, silver, and zinc) or their fate ( bis( 2 ethylhexyl) phthalate,

bromo 2 chlorobenzene, bromo 3 chlorobenzene, dibenzofuran, dibenzothiophene, diphenylamine, long chained petroleum hydrocarbons, 1 methylfluorene, N nitrosodiphenylamine, and several metals).

The available fate and toxicity data indicate that many MP& M pollutants tend ( 1) to be " toxic", ( 2) to not readily volatilize from the water column, ( 3) to adsorb to sediments, ( 4) to bioconcentrate in aquatic organisms, and ( 5) do not biodegrade.

Such pollutants accumulate in sediments and reach concentrations which can impair benthic communities. Pollutants that have accumulated in sediments can be released back into the water column because sediments act as long term sinks. The pollutants can also enter soils and reach high levels over time if present in sewage sludge that is applied to land. The tendency of these pollutants to resist biodegradation and to bioconcentrate in biological tissue also causes them to be taken up into aquatic food chains where they can affect predators or humans who consume fish and shellfish ( U. S. EPA, 1998).

The toxicity data also indicate that a sizable number of the POCs in MP& M effluents have toxicities that result in lethal or sub lethal responses in aquatic receptors, including algae, vascular plants, invertebrates, fish, and amphibians. Responses include death, which may occur within a matter of hours to days, or longer term sub lethal responses ( such as reproductive failure or growth impairment) that manifest themselves over weeks, months, or even years. The effects of toxic chemicals are not shared equally among exposed species: sensitive species are typically more affected than species that are more resistant.

Hence, toxic conditions could selectively remove sensitive species from receiving waters. Such a pattern is of particular concern to threatened and endangered ( T& E) species, which may already be close to extinction. Aquatic receptors are exposed to many different toxicants at the same time, which may have additive effects. The EPA assessment is based on a 5 Note that EPA was unable to obtain fate or toxicity data for a substantial number of POCs.

12 7 MP& M EEBA Part III: Benefits Chapter 12: Benefit Overview chemical by chemical approach and therefore does not consider additive effects. This approach may understate the benefits of the rule.

EPA also did not evaluate the potential fate and effects of the four conventional pollutants ( BOD, pH, O& G, TSS) and several other pollutants, including Total Petroleum Hydrocarbon ( TPH), Total Kjeldahl Nitrogen ( TKN), phosphorus, and chemical oxygen demand ( COD) , which may nonetheless adversely affect aquatic environments. 6,7 Effluents with high levels of BOD or COD consume large amounts of dissolved oxygen in a short time, causing surface waters to become oxygen depleted, thereby killing or excluding aquatic life ( U. S. EPA, 1986). At current discharge levels, MP& M facilities discharge 1.1 million pounds of BOD per year.

Low pH ( high acidity) water can be lethal to aquatic organisms; sensitive species of fish and invertebrates are eliminated from surface waters at pH's between 6.0 and 6.5 ( U. S. EPA, 1999).

O& G and TPH can have lethal effects on fish by coating gill surfaces and causing asphyxia, depleting dissolved oxygen levels due to excessive BOD, and impairing stream re aeration due to the presence of surface films. Compounds present in O& G or TPH can also be detrimental to waterfowl by affecting the buoyancy and insulating capacity of their feathers ( U. S. EPA,

1998). At current discharge levels, MP& M facilities discharge 553,481 pounds per year of O& G, including 67,427 pounds a year of TPH.

TSS increases the turbidity of surface water and impairs underwater visibility and transparency, thereby inhibiting photosynthesis by diminishing the amount of sunlight that reaches algae or submerged aquatic plants. TSS also causes a general degradation of aquatic habitats by increasing the rate of sedimentation, which smothers eggs, covers aquatic plants,

and affects benthic invertebrates ( U. S. EPA, 1998).

High input of nitrogen in estuarine and marine systems or phosphorus in freshwater systems can increase primary productivity and result in eutrophication. Such a process overloads surface waters with algae and reduces the transparency of the water column. The excess algae sink to the bottom and decompose at the end of their life cycle. This process consumes large amounts of dissolved oxygen and can turn surface waters anoxic ( U. S. EPA, 1998; U. S. EPA, 1995).

12.1.4 Effects of MP& M Pollutants on Economic Productivity Most MP& M pollutants associated with adverse health effects are subject to drinking water criteria. Thus, MP& M discharges to surface water can increase the cost of municipal water treatment by requiring investment in chemical treatment and filtration. Public water treatment systems must comply with drinking water criteria MCLs and secondary standards.

Compliance may require treatment to reduce the levels of regulated pollutants below their MCLs. Capital investment and operating and maintenance ( O& M ) costs associated with treatment technologies can be substantial. To the extent that the MP& M regulation reduces the concentration of MP& M pollutants in source waters to values that are below pollutant specific drinking water criteria, public drinking water systems will accrue benefits in the form of reduced water treatment costs.

Releases of MP& M pollutants to surface waters may also increase treatment costs of irrigation water and industrial water.

Releases of large quantities or high concentrations of toxic pollutants in MP& M effluents may interfere with POTW processes ( e. g., inhibiting microbial degradation), reduce the treatment efficiency or capacity of POTW s, and reduce disposal options for the sludge. In addition, toxic pollutants present in the effluent discharges may pass through a POTW and adversely affect receiving water quality, or may contaminate sludges generated during primary or secondary wastewater treatment. EPA expects no changes in the current status of POTW processes or disposal options for the sludge at POTWs receiving effluent discharges from MP& M facilities associated with the MP& M rule since all indirect dischargers have been excluded from the final option. EPA, however, analyzed changes in interferences of POTW operations and contamination of sewage sludge at 6 TKN is defined as the total of organic and ammonia nitrogen. It is determined in the same manner as organic nitrogen, except that the ammonia is not driven off before the digestion step.

7 EPA, however, considered environmental effects of TKN in the Ohio case study. EPA evaluated the impact of in stream TKN concentrations on recreational value of fishing, boating, swimming, and wildlife viewing sites. For detail see Chapter 21 of this report.

12 8 MP& M EEBA Part III: Benefits Chapter 12: Benefit Overview POTWs receiving effluent discharges from MP& M facilities for the alternative regulatory options which include indirect dischargers.

12.2 LINKING THE REGULATION TO BENEFICIAL OUTCOMES This section describes the linkages between promulgation of a regulation and the expected benefits to society. As indicated in Figure 12.1, the benefits of the MP& M regulation occur from a chain of events. These events include: ( 1) Agency publication of the regulation, ( 2) industry changes in production processes and/ or treatment systems, ( 3) reductions in pollutant discharges, ( 4) changes in water quality, ( 5) changes in ecosystem attributes and sewage sludge quality, ( 6) changes in human responses, and ( 7) changes in human health and ecological risk. The first two events reflect the institutional and technical aspects of the regulation. The benefit analysis begins with the third event, the changes in the pollutant content of effluent discharges.

12 9               MP& M EEBA Part III: Benefits Chapter 12: Benefit Overview Figure 12.1: Chain of Events in a Benefits Analysis 1. EPA Publication of Regulation 2. ges in Production Processes and/ or Treatment Chan 3. ctions in Pollutant Discharges Redu 4. ges in Ambient Water Quality ( Pollutant Concentrations &

Aquatic Habitat) Chan 5. ge in Aquatic Ecosystem ( e. g., Increased Fish Populations &

Diversity & Reduced Bioaccumulation) Chan 6.

Demand & Value of Fishery ( e. g., Recreational &

Other Benefit Categories) Change in Level of 7. tial Change in Health Risk ( e. g., from Consumption of Fish Caught) Poten Source: U. S. EPA analysis.

In event four, changes in pollutant discharges translate into improvements in water and sludge quality. In event five, these improvements in turn affect in stream and near stream biota ( e. g., increased diversity of aquatic species and size of species populations) and sludge disposal options. Finally, human effects and the related valuation of benefits occur in events six and seven. For example, improvements to recreational fisheries and enhanced enjoyment by recreational anglers is connected to 12 10 MP& M EEBA Part III: Benefits Chapter 12: Benefit Overview improved water quality and the value of reduced risk to human health. These linkages are the basis of the benefits analysis presented in this and the following chapters.

12.3 QUALITATIVE AND QUANTITATIVE BENEFITS ASSESSMENT A benefit assessment defines and quantifies the types of improvements to human health and ecological receptors that can be expected from reducing the amount of MP& M pollutants released to the environment. The following sections provide an overview of the concepts and analytic approaches involved in the benefits assessment. The first section describes the general categories of benefits expected to result from the regulation and the level of analysis undertaken for them. The following three sections review, within the broad categories of benefits likely to be achieved by the MP& M regulation, the specific benefits that are evaluated in this analysis. Finally, Section 12.3.5 summarizes methods for attaching values to some of the benefit measures. Chapters 13 through 16 present the quantitative assessment of benefits.

12.3.1 Overview of Benefit Categories The benefits of reduced MP & M discharges may be classified in three broad categories: human health, ecological, and economic productivity benefits. Table 12.3 summarizes the different types of benefits that fall in each of these categories.

Each category is comprised of a number of more narrowly defined benefit categories. EPA expects that the MP& M regulation will provide benefits to society in all of these categories. EPA was not able to bring the same depth of analysis to all of these categories, however, because of imperfect understanding of the link between discharge reductions and benefit categories, and how society values some of the benefit events. EPA was able to quantify and monetize some benefits,

quantify but not monetize other benefits, and assess still other benefits only qualitatively.

In addition to the national level benefits analysis, the Agency conducted a case study in the state of Ohio to provide in depth analysis of the regulation's expected benefits. The Ohio case study improves on the national analysis in two ways. First, the analysis uses improved data and methods to address co occurrence of M P& M facility benefits and other source contributions of MP& M pollutants in the same locations. Second, the analysis of recreational benefits is based on original travel cost models of resource valuation in a random utility framework. The analysis values changes in the value of water resources for four recreational activities  fishing, boating, swimming, and near water recreation. Due to data limitations, only three of these four activities were valued at the national level benefits analysis.

To provide perspective on the extent to which this regulatory impact assessment was able to comprehensively analyze the benefits, Table 12.3 summarizes the specific benefits within each of the three broad benefit categories that are expected to accrue from the MP& M regulation and the level of analysis applied to each category. As shown in Table 12.3, only a few of the relevant benefit categories can be both quantified and monetized.

12 11 MP& M EEBA Part III: Benefits Chapter 12: Benefit Overview Table 12.3: Level of Analysis Performed for Specific Benefit Categories Benefit Category Quantified and Monetized Quantified but Not Monetized Qualitative Human Health Benefits Reduced cancer risk due to ingestion of chemically contaminated fish and unregulated pollutants in drinking water X Reduced non cancer adverse health effects ( e. g.

immunological, neurological, circulatory, or respiratory toxicity)

due to ingestion of chemically contaminated fish and unregulated pollutants in drinking water X Reduced non cancer adverse health effects from exposure to lead from consumption of chemically contaminated fish X Reduced cancer risk and non cancer adverse health effects from exposure to unregulated pollutants in chemically contaminated sewage sludgea X Reduced health hazards from exposure to contaminants in waters used recreationally ( e. g., swimming) X Ecological Benefits Reduced risk to aquatic life X Enhanced water based recreation including fishing, boating, and near water ( wildlife viewing) activities X Other enhanced water based recreation such as swimming,

waterskiing, and white water rafting X Increased aesthetic benefits such as enhancement of adjoining site amenities ( e. g. , working, traveling, and owning property near the water) X Nonuser value ( i. e., existence, option, and bequest value) X Reduced contamination of sediments X Reduced non point source nitrogen contamination of water if sewage sludge is used as a substitute for chemical fertilizer on agricultural landa X Satisfaction of a public preference for beneficial use of sewage sludgea X Economic Productivity Benefits Reduced sewage sludge disposal costsa X Reduced management practice and record keeping costs of sewage sludge that meets exceptional quality criteriaa X Reduced interference with POTW operations a X Benefits to tourism industries from increased participation in water

based recreation X Improved commercial fisheries yields X Improved crop yield ( the organic matter in land applied sewage sludge increases soil s water retention) a X Avoidance of costly siting processes for more controversial sewage sludge disposal methods ( e. g., incinerators) because of greater use of land applicationa X Reduced water treatment costs for municipal drinking water,

irrigation water, and industrial process and cooling water X reproductive,

residing a These benefit categories are not applicable to the final rule since all indirect dischargers have been excluded from the selected option. EPA, however, analyzed these benefit categories for the alternative regulatory options which include indirect dischargers.

Source: U. S. EPA analysis.

Each category of benefits and the level of analysis applied to this category are discussed in greater detail below.

12 12 MP& M EEBA Part III: Benefits Chapter 12: Benefit Overview 12.3.2 Human Health Benefits Reduced pollutant discharges to the nation s waterways will generate human health benefits by several mechanisms. The most important and readily analyzed benefits stem from reduced risk of illness associated with the consumption of water, fish,

shellfish, and other aquatic organisms that is taken from waterways affected by MP& M discharges. Human health benefits are typically analyzed by estimating the change in the expected number of adverse human health events in the exposed population resulting from a reduction in effluent discharges. While some health effects such as cancer are relatively well understood and thus may be quantified in a benefits analysis, others are less well characterized and cannot be assessed with the same rigor or at all.

EPA analyzed the following direct measures of change in risk to human health: incidence of cancer from fish and water consumption; reduced risk of non cancer toxic effects from fish and water consumption; and lead related health effects to children and adults. EPA was able to monetize only two of the three measures ( cancer related and lead related health risks).

Incidence of cancer was translated into an expected number of avoided mortality events and, on that basis, monetized. Lead impacts to children were evaluated in terms of potential intellectual impairment as measured by estimated changes in IQ.

Changes in adverse health effects to adults from lead exposure were measured in terms of reduced risk of hypertension, non

fatal coronary heart disease, non fatal strokes, and mortality.

EPA also quantified but did not monetize the expected reduction of pollutant concentrations in excess of health based AWQC limits. This benefit measure was obtained by comparing in waterway pollutant concentrations to toxic effect levels.

In concept, the value of these health effects to society is the monetary value that society is willing to pay to avoid the health effects, or the amount that society would need to be compensated to accept increases in the number of adverse health events.

  Willingness to pay  ( WTP) values are generally considered to provide a fairly comprehensive measure of society s valuation of the human and financial costs of illness associated with the costs of health care, losses in income, and pain and suffering of affected individuals and of their family and friends.

In some cases, available economic research provides little empirical data for society's WTP to avoid certain health effects.

One component of the cost of an illness estimates the direct medical costs of treating a health condition ( e. g., hypertension),

and can be used to value changes in health risk from reduced exposure to toxic pollutants such as lead. These estimates represent only one component of society's WT P to avoid adverse health effects and therefore produce a partial measure of the value of reduced exposure to MP& M pollutants. Employed alone, these monetized effects will significantly underestimate society's WTP.

12.3.3 Ecological Benefits EPA expects that the ecological benefits from the regulation will include protection of fresh and saltwater plants,

invertebrates, fish, and amphibians, as well as terrestrial wildlife and birds that prey on aquatic organisms exposed to MP& M pollutants. The regulation will reduce the presence and discharge of various pollutants and will enhance or protect aquatic ecosystems currently under stress. The drop in pollutant loading is expected to reestablish productive ecosystems in damaged waterways and to protect resident species, including T& E species. EPA also expects that the regulation will enhance the general health of fish and invertebrate populations, increase their propagation to waters currently impaired, and expand fisheries for both commercial and recreational purposes. Improvements in water quality will also favor increased recreational activities such as swimming, boating, fishing, and water skiing. Finally, the Agency expects that the regulation will augment nonuse values ( e. g., option, existence, and bequest values) of the affected water resources.

It is frequently difficult to quantify and attach economic values to ecological benefits. The difficulty results from imperfect understanding of the relationship between changes in effluent discharges and the specific ecological changes, lack of water quality monitoring data for most locations, and time lags between water quality changes and changes in species population and composition. In addition, it is difficult to attach monetary values to these ecological changes because they often do not occur in markets in which prices or costs are readily observed. As such, ecological benefits may be loosely classified as nonmarket benefits. This classification can be further divided into nonmarket use benefits and nonmarket nonuse benefits.

Nonmarket use benefits stem from improvements in ecosystems and habitats, which in turn lead to enhanced human use and enjoyment of these areas. For example, reduced discharges may lead to increased recreational use and enjoyment of affected waterways in such activities as fishing, swimming, boating, hunting or near water activities such as bird watching. In some 12 13 MP& M EEBA Part III: Benefits Chapter 12: Benefit Overview cases, it may be possible to quantify and attach partial economic values to ecological benefits using market values ( e. g., an increase in tourism or boat rentals associated with improved recreational fishing opportunities); in this case, these benefit events might better be classified as economic productivity related events, which are discussed below. Economic markets,

however, do not provide enough information to fully capture the value of these benefits. Such markets capture only related expenditures made by recreationists ( e. g., food and lodging) and do not capture the value placed on the experience itself. A variety of nonmarket valuation techniques can be used to capture the value placed on the resource in question. These techniques include hedonic valuation ( wage risk studies) and travel cost methods ( TCM), stated preferences methods ( i. e.,

contingent valuation ( CV) , contingent rating ( CR) , contingent activity ( CA) , benefits transfer, and averting behavior models.

Nonmarket nonuse benefits are not associated with current use of the affected ecosystem or habitat, but rather arise from ( 1)

the realization of the improvement in the affected ecosystem or habitat resulting from reduced effluent discharges and ( 2) the value that individuals place on the potential for use sometime in the future. Nonmarket nonuse benefits may also be manifested by other valuation mechanisms, such as cultural valuation, philanthropy, and bequest valuation. It is often extremely difficult to quantify the relationship between changes in discharges and the improvements in societal well being associated with such valuation mechanisms. That these valuation mechanisms exist, however, is indisputable, as evidenced,

for example, by society s willingness to contribute to organizations whose mission is to purchase and preserve lands or habitats to avert development.

12.3.4 Economic Productivity Benefits Reduced pollutant discharges may also benefit economic productivity. First, economic productivity benefits may accrue from reduced treatment costs of drinking water, irrigation water, and industrial use water. Reduced pollutant concentrations in public water systems source water to levels at or below MCLs or secondary standards could reduce ongoing treatment costs and avoid the need to invest in treatment technologies in the future. Reduced pollutant discharges may also reduce sediment dredging costs. Contaminated sediments may contribute substantially to contamination of aquatic biota and to human exposure of human health toxicants. Controlling point source discharges of toxic pollutants can prevent sediment contamination and eliminate the need for future remediation ( i. e., dredging) of contaminated sediments.

Other economic productivity gains may result from improved tourism opportunities in areas affected by MP& M discharges.

Improved aquatic species survival may contribute to increased commercial fishing yield. When such economic productivity effects can be identified and quantified, they are generally straightforward to value because they involve market commodities for which prices or unit costs are readily available.

Economic productivity gains may also occur through reduced costs to public sewage systems ( POTWs) for managing and disposing of the sludge ( i. e., biosolids) from treating effluent discharges. For example, higher quality sludge may be applied to agricultural land or otherwise beneficially used rather than being incinerated or disposed of in landfills. POTWs may also incur lower costs because of lower record keeping requirements. Under the final regulatory option, EPA expects no POTW productivity gains since all indirect dischargers have been excluded from the final regulatory option.

12.3.5 Methods for Valuing Benefit Events Some of the benefits expected from the MP& M regulation will manifest themselves in economic markets through changes in price, cost, or quantity of market valued activities. For benefits endpoints traded in markets, such as increased yields from commercial fisheries, benefits can be measured by market prices or market based factor pricing. Competitive prices can be used also to measure avoided cost type of benefits. For example, reduced pollutant loadings to public water supplies may lower costs of drinking treatment. Market prices can be used also to value direct medical costs of illnesses associated with exposure to pollutants. For this analysis, EPA used medical costs associated with treating hypertension, coronary heart disease, and stroke to estimate benefits from reduced exposure to lead ( see Chapter 14). The estimated values can be used as minimum measures of the benefits associated with reduced cases of these illnesses.

In other cases, benefits involve activities or sources of value that either do not involve economic markets or involve them only indirectly. Methods used to value such benefits are described briefly below:

12 14 MP& M EEBA Part III: Benefits Chapter 12: Benefit Overview a. Wage risk approach.

The wage risk approach uses regression estimates of the wage premium associated with greater risks of death on the job to estimate the amount that persons are willing to pay to avoid death. Benefit values based on this approach are used as part of the basis for valuing reduced cancer cases due to fish consumption in Chapter 13.

b. Travel cost method The T CM uses information on costs incurred by people in traveling to a site and in using the site to estimate a demand curve for that site. The demand curve is then used to estimate the   consumer surplus  associated with the use of the site, that is, the value that consumers receive from the site over and above the costs that they incur in using it. Consumer surplus is an estimate of the net benefits of the resource to the people using that resource. For example, if the resource is a recreational fishing site, the TCM can be used to value the recreational fishing experience. The Agency used an original travel cost study to value benefits from enhanced water based recreation in Ohio ( see Part V: Chapter 21). The analysis of recreational benefits in Chapter 15 uses a meta analysis of water based recreation studies ( including TCM studies) to derive the baseline and post compliance values of water based recreation activities ( including fishing, boating, and wildlife viewing) and to estimate benefits to consumers of water based recreation from improved water quality resulting from reduced MP& M dischargers.

c. Contingent valuation In the CV method, surveys are conducted to elicit individuals  WTP for a particular good, such as a fishery, or clean water.

CV is more broadly applicable than TCM. Like TCM, CV can be used to estimate the consumer surplus associated with recreational fisheries. CV can also be used to estimate less tangible values, such as how much people care about a clean environment. Values from both the CV approach and the wage risk approach support the estimated value of avoided death that is used to monetize reduced cancer cases from consumption of contaminated fish ( Chapter 13). Similarly to the TCM studies, CV studies are used in a meta analysis to derive the baseline and post compliance values of water based recreation activities ( including fishing, boating, and wildlife viewing) and to estimate benefits from improved opportunities for water

based recreation from reduced MP& M dischargers ( Chapter 15).

d. Benefits transfer When time and resource constraints preclude primary research, benefit assessment based on benefits transfer from existing studies is used. This approach involves extrapolating benefit findings for one analytic situation to another. The relevant study situations are defined by type of environmental resource ( e. g., fishery), policy variable( s), and the characteristics of user populations. The benefits transfer approach is used to monetize several benefit categories, including changes in the incidence of cancer cases ( Chapter 13) and the national level benefits from enhanced water based recreation ( Chapter 15).

The techniques described above form the basis of the benefits methodologies described in Chapters 13,14, and 15.

12 15 MP& M EEBA Part III: Benefits Chapter 12: Benefit Overview GLOSSARY acute toxicity: the ability of a substance to cause severe biological harm or death soon after a single exposure or dose.

Also, any poisonous effect resulting from a single short term exposure to a toxic substance. ( See: chronic toxicity, toxicity.)

( http:// www. epa. gov/ OCEPAterms/ aterms. html)

adsorption coefficients ( Koc): represents the ratio of the target chemical absorbed per unit weight of organic carbon in the soil or sediment to the concentration of that same chemical in solution at equilibrium.

ambient water quality criteria ( AWQC): AWQC present scientific data and guidance of the environmental effects of pollutants which can be useful to derive regulatory requirements based on considerations of water quality impacts; these criteria are not rules and do not have regulatory impact ( U. S. EPA. 1986. Quality Criteria for Water 1986. U. S.

Environmental Protection Agency, Office of Water Regulations and Standards, Washington, DC. EPA 440/ 5 86 001).

AQUatic Information REtrieval System ( AQUIRE): a web based ecotoxicity database maintained by EPA's Mid Continent Ecology Division ( MED) which summarizes ecotoxicity data retrieved from the literature.

( http:// www. epa. gov/ med/ databases/ databases. html# aquire) ( U. S. EPA, 1998/ 99b)

ASsessment Tools for the Evaluation of Risk ( ASTER): an ecological risk assessment tool developed by EPA's Mid Continent Ecology Division ( MED); ASTER integrates information from the AQUIRE toxic effects database and the QSAR system ( a structure activity based expert system) to estimate ecotoxicity, chemical properties, biodegradation and environmental partitioning. ( http:// www. epa. gov/ med/ databases/ aster. html) ( U. S. EPA, 1998/ 99c)

avoided cost: costs that are likely to be incurred in the future if current conditions still prevail at the time, but which will be avoided if particular actions are taken now to change the status quo.

benthic: relating to the bottom of a body of water; living on, or near, the bottom of a water body.

BIODEG: a web based biodegradation database developed by Syracuse Research Corporation.

( http:// esc. syrres. com/ efdb/ BIODGSUM . HTM) ( Syracuse Research Corporation, 1999)

biodegradation half lives: represents the number of days a compound takes to be degraded to half of its starting concentration under prescribed laboratory conditions.

biological oxygen demand ( BOD): the amount of dissolved oxygen consumed by microorganisms as they decompose organic material in an aquatic environment.

cancer potency slope factor ( SF): a plausible upper bound estimate of the probability of a response per unit intake of a chemical over a lifetime. The slope factor is used to estimate an upper bound probability of an individual developing cancer as a result of a lifetime of exposure to a particular level of a potential carcinogen.

CHEMFATE: a web based chemical fate database developed by Syracuse Research Corporation.

( http:// esc. syrres. com/ efdb/ Chemfate. htm) ( Syracuse Research Corporation, 1999)

chemical oxygen demand ( COD): a measure of the oxygen required to oxidize all compounds, both organic and inorganic, in water. ( http:// www. epa. gov/ OCEPAterms/ cterms. html)

chronic toxicity: the capacity of a substance to cause long term poisonous health effects in humans, animals, fish, and other organisms. ( http:// www. epa. gov/ OCEPAterms/ cterms. html)

contingent activity: one of the stated preference methods ( see: contingent valuation and contingent activity). Survey respondents are asked how their behavior would change in response to a proposed change in one or more attributes of an activity ( e. g., cost of the activity, site accessibility, or site attractiveness). Given responses to this type of question, and given information about incremental travel costs and value of time, a revealed preference method can be used to estimate the value of change.

12 16 MP& M EEBA Part III: Benefits Chapter 12: Benefit Overview contingent rating: one of the stated preference methods ( see: contingent valuation and contingent activity). Survey respondents are asked to rate several alternatives on an ad hoc utility scale ( e. g., 1 to 10). The choice set of alternatives usually includes the environmental effect to be valued, substitutes for the effect, and a good with a monetary price to act as a threshold. Based on the respondent's rating of the environmental effect and the threshold good, and the monetary price of the threshold good, the value of the environmental effect can be determined.

contingent valuation ( CV): a method used to determine a value for a particular event, where people are asked what they are willing to pay for a benefit and/ or are willing to receive in compensation for tolerating a cost. Personal valuations for increases or decreases in the quantity of some good are obtained contingent upon a hypothetical market. The aim is to elicit valuations or bids that are close to what would be revealed if an actual market existed.

( http:// www. damagevaluation. com/ glossary. htm)

Environmental Research Laboratory Duluth fathead minnow database: a database developed by EPA's Mid Continent Ecology Division ( MED) which provides data on the acute toxicity of hundreds of industrial organic compounds to the fathead minnow. ( http:// www. eoa. gov/ med/ databases/ fathead_ minnow. html) ( U. S. EPA, 1998/ 99a)

hazardous air pollutant ( HAP): compounds that EPA believes may represent an unacceptable risk to human health if present in the air.

Health Effects Assessment Summary Tables ( HEAST): a comprehensive listing of provisional human health risk assessment data relative to oral and inhalation routes for chemicals of interest to EPA. Unlike data in IRIS, HEAST entries have received insufficient review to be recognized as high quality, Agency wide consensus information. ( U. S. EPA. 1997.

Health Effects Assessment Table; FY 1997 Update. EPA 540 R 97 036)

Henry's Law constant: a numeric value which relates the equilibrium partial pressure of a gaseous substance in the atmosphere above a liquid solution to the concentration of the same substance in the liquid solution.

human health based water quality criteria ( WQC): human health based criteria are based on specific levels of pollutants that would make the water harmful if used for drinking, swimming, farming, fish production, or industrial processes ( see ambient water quality criteria ( AWQC)). ( http:// www. epa. gov/ OCEPAterms/ wterms. html).

hydrophobicity: having a strong aversion to water. ( http:// www. epa. gov/ OCEPAterms/ hterms. html)

Integrated Risk Information System ( IRIS): IRIS is an electronic database with information on human health effects of various chemicals. IRIS provides consistent information on chemical substances for use in risk assessments, decision making and regulatory activities.

lipophilicity: having a strong attraction to oils maximum contaminant levels ( MCLs): the maximum permissible level of a contaminant in water delivered to any user of a public system. MCLs are enforceable standards.

( http:// www. epa. gov/ OCEPAterms/ mterms. html)

metals: inorganic compounds, generally non volatile, and which cannot be broken down by biodegradation processes. They are a particular concern because of their prevalence in MP& M effluents. Metals can accumulate in biological tissues,

sequester into sewage sludge in POTWs, and contaminate soils and sediments when released to the environment. Some metals are quite toxic even when present at relatively low levels.

microbial metabolism: biochemical reactions occurring in living microorganisms such as bacteria, algae, diatoms,

plankton, and fungi. POTWs make use of bacterial metabolism for wastewater treatment purposes. This process is inhibited by the presence of toxins such as metals and cyanide because these pollutants kill bacteria.

oil and grease ( O& G): organic substances that may include hydrocarbons, fats, oils, waxes, and high molecular fatty acids. Oil and grease may produce sludge solids that are difficult to process. ( http:// www. epa. gov/ owmitnet/ reg. htm)

pH: an expression of the intensity of the basic or acid condition of a liquid; natural waters usually have a pH between 6.5 and 8.5. ( http:// www. epa. gov/ OCEPAterms/ pterms. html)

12 17 MP& M EEBA Part III: Benefits Chapter 12: Benefit Overview pollutants of concern ( POCs): are the 150 contaminants identified by EPA as being of potential concern for this rule and which are currently being discharged by MP& M facilities.

priority pollutant ( PP): 126 individual chemicals that EPA routinely analyzes when assessing contaminated surface water,

sediment, groundwater, or soil samples.

publicly owned treatment works ( POTWs): a treatment works, as defined by section 212 of the Act, that is owned by a State or municipality. This definition includes any devices or systems used in the storage, treatment, recycling, and reclamation of municipal sewage or industrial wastes of a liquid nature. It also includes sewers, pipes, or other conveyances only if they convey wastewater to a POTW Treatment Plant. ( http:// www. epa. gov/ owm/ permits/ pretreat/ final99. pdf)

quantitative structure activity relationship ( QSAR) model: an expert system which uses a large database of measured physicochemical properties such as melting point, vapor pressure, and water solubility to estimate the fate and effect of a specific chemical based on its molecular structure. ( http:// www. epa. gov/ med/ databases/ aster. html) ( U. S. EPA,

1998/ 99)

reference doses ( RfDs): chemical concentrations expressed in mg of pollutant/ kg body weight/ day, that, if not exceeded,

are expected to protect an exposed population, including sensitive groups such as young children or pregnant women.

secondary MCLs: human health based drinking water criteria to assess the health hazards associated with the presence of certain toxic chemicals in drinking water. SMCLs are established for taste or aesthetic effects.

Superfund Chemical Data Matrix ( SCDM): a source for factor values and benchmark values applied when evaluating potential National Priorities List ( NPL) sites using the Hazard Ranking System ( HRS).

( http:// www. epa. gov/ superfund/ resources/ scdm/ index. htm).

suspended solids: small particles of solid pollutants that float on the surface of, or are suspended in, water bodies.

( http:// www. epa. gov/ OCEPAterms/ sterms. html)

systemic toxicants: chemicals that EPA believes can cause significant non carcinogenic health effects when present in the human body above chemical specific toxicity thresholds.

threatened and endangered ( T& E): animals, birds, fish, plants, or other living organisms threatened with extinction by anthropogenic ( man caused) or other natural changes in their environment. Requirements for declaring a species endangered are contained in the Endangered Species Act.

Total Petroleum Hydrocarbon ( TPH): a general measure of the amount of crude oil or petroleum product present in an environmental media ( e. g., soil, water, or sediments). While it provides a measure of the overall concentration of petroleum hydrocarbons present, TPH does not distinguish between different types of petroleum hydrocarbons.

Total Kjeldahl Nitrogen ( TKN): the total of organic and ammonia nitrogen. TKN is determined in the same manner as organic nitrogen, except that the ammonia is not driven off before the digestion step.

total suspended solids ( TSS): a measure of the suspended solids in wastewater, effluent, or water bodies, determined by tests for " total suspended non filterable solids." ( See: suspended solids.)

( http:// www. epa. gov/ OCEPAterms/ tterms. html)

travel cost method ( TCM): method to determine the value of an event by evaluating expenditures of recreators. Travel costs are used as a proxy for price in deriving demand curves for the recreation site.

( http:// www. damagevaluation. com/ glossary. htm)

uptake: the movement of one or more chemicals into an organism via ingestion, inhalation, and/ or through the skin.

vascular plants: plants that are composed of, or provided with, vessels or ducts that convey fluids. ( www. infoplease. com)

willingness to pay ( WTP): maximum amount of money one would give up to buy some good.

( http:// www. damagevaluation. com/ glossary. htm)

12 18 MP& M EEBA Part III: Benefits Chapter 12: Benefit Overview ACRONYMS AQUIRE: AQUatic Information REtrieval System ASTER: ASsessment Tools for the Evaluation of Risk AWQC: ambient water quality criteria BIODEG: biodegradation BOD: biological oxygen demand CA: contingent activity CHEMFATE: chemical fate CR: contingent rating CV: contingent valuation COD: chemical oxygen demand HAP: hazardous air pollutant HEAST: Health Effects Assessment Summary Tables IRIS: Integrated Risk Information System Koc: adsorption coefficient MCL: maximum contaminant level O& G: oil and grease POC: pollutant of concern POTW: publicly owned treatment work PP: priority pollutant QSAR: quantitative structure activity relationship RfD: reference dose SCDM: Superfund Chemical Data Matrix SF: cancer potency slope factor T& E: threatened and endangered TCM: travel cost method TKN: Total Kjeldahl Nitrogen TPH: Total Petroleum Hydrocarbon TSS: total suspended solids WQC: human health based water quality criteria WTP: willingness to pay 12 19 MP& M EEBA Part III: Benefits Chapter 12: Benefit Overview REFERENCES Amdur, M. O., J. Doul, and C. D. Klaassen, eds. 1991. Cassarett and Doul's: Toxicology, the Basic Science of Poisons. 4th ed. New York, NY: McGraw Hill Inc.

Amdur, M. O., J. Doul, and C. D. Klaassen, eds. 1996. Cassarett and Doul's: Toxicology, the Basic Science of Poisons. 5th ed. New York, NY: McGraw Hill Inc.

Syracuse Research Corporation ( BIODEG, CHEMFATE). 1999. Syracuse Research Corporation's Environmental Fate Databases. Syracuse, NY: Syracuse Research Corporation. http:// esc. syrres. com/ efdb/ BIODGSUM. HTM and http:// esc. syrres. com/ efdb/ Chemfate. htm.

U. S. Environmental Protection Agency. ( U. S. EPA). 1980. Ambient water quality criteria documents. Washington, DC:

Office of Water, U. S. EPA. EPA 440/ 5 80 Series. Also refers to any update of criteria documents ( EPA 440/ 5 85 and EPA 440/ 5 87 Series) or any Federal Register notices of proposed criteria or criteria corrections, and EPA 822 Z 99 001. The most recent National Recommended Water Quality Criteria used in this report were published in the Federal Register on December 10, 1998.

U. S. Environmental Protection Agency. ( U. S. EPA). 1986. Ambient Water Quality Criteria for Dissolved Oxygen. EPA 440/ 5 86 003.

U. S. Environmental Protection Agency. ( U. S. EPA). 1995. Proceedings of the First Gulf of Mexico Hypoxia Management Conference. EPA 55 R 97 001.

U. S. Environmental Protection Agency. ( U. S. EPA). 1997. Health Effects Assessment Summary Tables ( HEAST).

Washington, DC: Office of Research and Development and Office of Emergency and Remedial Response, U. S. EPA.

U. S. Environmental Protection Agency. ( U. S. EPA). 1998. National Water Quality Inventory. 1996 Report to Congress.

EPA 841 R 97 008.

U. S. Environmental Protection Agency. ( U. S. EPA). 1998/ 99a. QSAR. Duluth, MN: Environmental Research Laboratory,

U. S. EPA.

U. S. Environmental Protection Agency. ( U. S. EPA). 1998/ 99b. Aquatic Toxicity Information Retrieval ( AQUIRE)

Database. Mid Continent Ecology Division ( MED), Duluth, MN. U. S. Environmental Protection Agency. Database retrieval @ http:// www. epa. gov/ ecotox/.

U. S. Environmental Protection Agency. ( U. S. EPA). 1998/ 99c. Assessment Tools for Evaluation of Risk ( ASTER)

Database. Duluth, MN: Environmental Research Laboratory, U. S. EPA. 1998 Database retrieval.

U. S. Environmental Protection Agency. ( U. S. EPA). 1998/ 99d. Integrated Risk Information System ( IRIS). Washington,

DC: U. S. EPA. 1998 Database retrieval @ http:// www. epa. gov/ iris/.

U. S. Environmental Protection Agency. ( U. S. EPA). 1999. Progress Report on the EPA Acid Rain Program. U. S. EPA Office of Air and Radiation. EPA 430 R 99 011.

Wexler, P., ed. 1998. Encyclopedia of Toxicology, Volumes 1 3.

12 20 MP& M EEBA Part III: Benefits Chapter 13: Human Health Benefits INTRODUCTION EPA expects that the final MP& M regulation will yield a range of human health benefits by reducing effluent discharges to waterways used for fishing or drinking water.

This chapter analyzes four categories of expected human health benefits. The first two categories involve reductions in cancer cases from two exposure pathways: consumption of contaminated fish tissue and ingestion of contaminated drinking water for the exposed population. EPA evaluated the expected annual reduction in cancer cases in the exposed population and the associated monetary value of avoiding those cancer cases.

EPA quantified, but did not monetize, two additional measures of human health related benefits. The first is the changes in fish consumption and drinking water exposures to non cancer causing pollutants measured against non cancer health effect reference doses ( RfDs), an indicator of non

cancer health risk. The second benefit measure is the change in occurrence of pollutant concentrations that are estimated to exceed human health based ambient water quality criteria ( AWQC).

EPA also quantified and monetized changes in health risk to adults and children from reduced exposure to lead. This analysis is presented in Chapter 14.

The health related measures were estimated for the baseline and for the final option for all of the benefit categories analyzed. In addition, EPA estimated health benefits for alternative options which EPA considered for the MP& M regulation.

The reduction in the health related measures ( i. e., number of annual cancer cases) from baseline to the post compliance case is the estimated benefit of the MP& M regulation. As discussed in Chapter 12, EPA estimated national benefits for the regulation based on sample facility data. The Agency extrapolated findings from the sample facility analyses to the national level using two alternative extrapolation methods: ( 1) traditional extrapolation and ( 2) post stratification extrapolation.

Appendix G provides detailed information on the extrapolation approaches used in this analysis. Chapter 13: Human Health Benefits CHAPTER CONTENTS 13.1 ............... 13 2 13.1.1 from Fish Consumption ........ 13 2 13.1.2 from Drinking Water Consumption 13 8 13.1.3 s above Non cancer Health Thresholds ................. ........ 13 10 13.1.4 .............. 13 14 13.2 ................. ............... 13 17 13.2.1 ption Cancer Results ..... 13 17 13.2.2 Water Consumption Cancer Results ................. ........... 13 19 13.2.3 er Health Threshold Results . . 13 19 13.2.4 n Health AWQC Results ........ 13 21 13.3 .............. 13 22 13.3.1 e Design & Analysis of Benefits by Location of Occurrence ............... 13 22 13.3.2 Pollutants ................. ......... 13 23 13.3.3 fects of Pollutants ............ 13 23 13.3.4 s of MP& M Pollutants ................. ......... 13 23 13.3.5 ream Effects ................ 13 24 13.3.6 ishing Population .......... 13 24 13.3.7 Treatment of Cancer Latency .......... 13 25 13.3.8 Treatment of Cessation Lag ........... 13 25 13.3.9 Use of Mean Individual Exposure Parameters ................. ........ 13 26 13.3.10 Cancer Potency Factors ............. 13 26 Glossary ................. ................. . 13 27 Acronyms ................. ................. 13 28 References ................. ................ 13 29 Methodology & Data Sources Cancer Cancer Exposure Human Health AWQC Results Fish Consum Drinking Non canc Huma Limitations and Uncertainties Sampl In Waterway Concentrations of MP& M Joint Ef Background Concentration Downst Exposed F EPA estimated that, for combined recreational and subsistence angler populations, the final option would lead to a marginal reduction in cancer cases. The total monetized human health benefits from reduced cancer cases from both the fish consumption and drinking water pathways are essentially negligible ( i. e., $ 90 per year based on the traditional extrapolation and $ 134 per year based on the post stratification extrapolation ( 2001$)).

Benefits will also be realized in the form of reductions in non cancer human health effects ( e. g., systemic effects, reproductive toxicity, and developmental toxicity) from reduced contamination of fish tissue and drinking water sources. For this analysis,

EPA estimates the numbers of individuals in the exposed populations who might be expected to realize reduced risk of non cancer health effects in the post compliance scenario. To evaluate the potential benefits of reducing the in stream concentrations of 76 pollutants that cause non cancer health effects, EPA estimated target organ specific hazard indices ( HI)

for drinking water and fish ingestion exposures in both the baseline and post compliance scenarios. HI values below one are generally considered to suggest that exposures are not likely to result in appreciable risk of adverse health effects during a lifetime, and values above one are generally cause for concern, although an HI greater than one does not necessarily suggest a likelihood of adverse effects.

13 1 MP& M EEBA Part III: Benefits Chapter 13: Human Health Benefits The results of EPA's analysis suggest that the incremental risk of non cancer effects from pollutants discharged by MP& M facilities alone is quite low. This analysis found that HIs for the entire population associated with sample facilities is less than one in the baseline. The results of EPA s analysis of the post compliance scenario indicate that hazard indices for individuals in the exposed population may decrease after facilities comply with the MP& M regulation. Increases in the percentage of exposed populations that would be exposed to no risk of non cancer adverse human health effects due to the MP& M discharges occur in both the fish and drinking water analyses. Whether the incremental shifts in HIs are significant in reducing absolute risks of non cancer adverse human health effects is uncertain and will depend on the magnitude of contaminant exposures for a given population from risk sources not accounted for in this analysis.

Finally, EPA analyzed the effect of the final regulation on occurrence of pollutant concentrations resulting from MP& M discharges that exceed human health based AWQC. EPA estimated that, as the result of baseline MP& M pollutant discharges, in stream concentrations exceed human health based AWQC in 78 and 112 receiving reaches nationwide based on the traditional extrapolation and post stratification extrapolation, respectively. EPA estimated that none of these exceedances will be eliminated under the final option.

13.1 METHODOLOGY & DATA SOURCES Individuals are potentially exposed to pollutants from MP& M facilities via consumption of contaminated fish tissue and drinking water. Potential human health effects include cancer and non cancer health effects. Risks such as skin, lung, liver,

kidney, and bladder cancer and leukemia are associated with exposure to 13 MP& M pollutants ( see Table 13.1). Non cancer health effects are associated with exposure to 76 MP& M pollutants. These effects include increased blood pressure,

gastrointestinal effects, liver and kidney toxicity, cardiovascular and central nervous system effects, and decreased birth weight ( see Table 13.2).

This section summarizes the methodology for estimating national benefits for three benefit categories:

1. reduced incidence of cancer from consumption of fish taken from waterways affected by MP& M industry discharges,

2. reduced incidence of cancer from ingestion of water taken from waterways affected by MP& M industry discharges,

and 3. reduced occurrence of pollutant concentrations resulting from MP& M discharges that exceed human health based AWQC.

This analysis does not include all possible human health benefits and does not provide a comprehensive estimate of the total human health benefits associated with the final MP& M rule. Analyses of health benefits are not possible for a significant number of the pollutants whose discharges will be reduced under the post compliance scenario due to the lack of data on a quantitative relationship between ingestion rate and the potential health effects associated with these chemicals.

Beyond these important limitations, the methodologies used to assess the human health benefits involve significant simplifications and uncertainties. Elements of the analysis involving significant simplifications and uncertainties include the following: sample design and analysis of benefits by location of occurrence; estimation of in waterway concentrations of MP& M pollutants; consideration of the joint effects of pollutants; consideration of background concentrations of MP& M pollutants; consideration of downstream effects; and estimation of the exposed fishing population. Section 13.3 provides more detail on limitations and uncertainties associated with the human health benefits analyses. Whether these simplifications and uncertainties, taken together, are likely to lead to an understatement or overstatement of the estimated economic values for the human health benefits that were analyzed is not known.

13.1.1 Cancer from Fish Consumption The analysis of reduced annual occurrence of cancer in exposed populations via the fish consumption pathway involves three analytic steps:

  estimating the reduced annual risk of incurring cancer per exposed individual;

  estimating the population that would be expected to benefit from reduced contamination of fish; and 13 2 MP& M EEBA Part III: Benefits Chapter 13: Human Health Benefits   calculating the c hange in the nu mbe r of can cer ev ents in the expo sed p opu lation.

Each step is discussed in detail below.

a. g change in individual cancer risk The estimated increm ental risk to an individual of de veloping ca ncer is based on four factors: 1   the quantity of carcinoge nic chemica ls that MP & M facilities discharge to waterways,

  the rate at which the discharged chemicals accumulate in fish tissue,

  the cancer effect of the chemicals, and   the rate of personal consumption of contaminated fish.

For each sample M P& M facility and the waterway to which it discharges, EPA calculated the incremental cancer risk to four population classes with different fish consumption rates: children in families that participate in recreational angling, children in families tha t particip ate in sub sistence angling, adults in families that particip ate in rec reational ang ling, and adults in families that participate in subsistence angling. sk values for baseline ( i. e., before regula tion) p ollutant d ischarg es and for po st com plianc e disch arges base d on the po licy options co nsidered in th e final rule analysis. iscussion summ arizes the increme ntal cancer risk calculations.

EPA calculated the in waterway pollutant concentrations for each reach receiving discharges from an M P& M facility using a simplified dilution model for all chemicals for which a quantitative relationship between ingestion rate and the annual probability of developing cancer has been estimated. reach  is a specific length of river, lake shoreline, or marine coastline, and an   MP& M reach  is one to which a n M P& M facility discharges. 2 This analysis considered only the discharge reach and did not estimate concentrations below the initial MP& M reach. T he water quality model used for calculating in

waterway po llutant concentrations acc ounts for the dilution chara cteristics of different water body types ( i. e., streams,

estuaries, and lakes). It does not account for other fate processes, such as chemical degradation or photolysis. The estimated pollutant concentrations reflect the average pollutant concentrations in the reach to which a facility discharges. For additional details on the calculation of waterway concentrations, see Appendix I.

The incremental cancer risk associated with each pollutant was calculated based on the estimated concentration of the pollutant in the affected waterway, the assumed uptake of the pollutant into fish flesh, the daily rate of fish ingestion, and the cancer risk factor for each pollutant. a for calculating the risk to an individual from consumption of a given chemical is as follows:

( 13.1)

where:

Risk = incremental risk of incurring cancer from fish consumption ( change in probability);

C = pollutant concentrations in surface water (   g/ l);

CF1 = conversion factor, micrograms to milligrams ( 0.001 mg/   g);

BCF = bioconcentration factor of pollutant in fish ( l/ kg);

CR = human consumption rate of fish ( kg/ day);

EF = exposure frequency ( 365 days/ year);

ED = exposure duration ( years);

BW = human body weight ( 70 kg for adults and 30 kg for children under 18); Estimatin EPA calculated the incremental cancer ri The following d A

The formul 1 The risk value is referred to as the incremental risk because it is the incremental lifetime probability that an individual will develop cancer above and beyond the baseline probability posed by all other extant factors that contribute to a risk of developing cancer.

2 A reach is a length of river, shoreline, or coastline with relatively uniform water flow characteristics. Thus, it is reasonable to assume that pollutant dischargers have a relatively uniform effect on concentrations within a reach.

13 3 MP& M EEBA Part III: Benefits Chapter 13: Human Health Benefits LT = human lifetime ( years);

CF2 = conversion factor, years to days ( 365 days/ year); and SF = pollutant cancer potency factor ( mg/ kg/ day) 1 .

The pollutants analyzed and their cancer potency factors are presented in Table 13.1. EPA used the relationship outlined above to estimate lifetime risk values for individuals in subsistence and recreational fishing households. The risks to recreational and subsistence households are estimated over two lifetime segments. Specifically, children living in recreational fishing households are assumed to consume 7.27 grams per day ( 0.007 kg/ day) of freshwater/ estuarine fish over an 18 year period ( ages 0 to 18). Adults are assumed to consume 17.5 grams per day ( 0.018 kg/ day) of freshwater/ estuarine fish over a 52 year period ( ages 18 to 70). Risks for individuals living in recreational and subsistence fishing households differ in the assumed consumption rates. Children living in subsistence fishing households are assumed to consume 60.58 grams per day ( 0.061 kg/ day) of freshwater/ estuarine fish over an 18 year period ( ages 0 18). Adults in subsistence households are assumed to consume 142.4 grams per day ( 0.142 kg/ day) of freshwater/ estuarine fish over a 52 year period ( ages 18 to 70). The total lifetime incremental risk for these households is calculated by summing the risks for both lifetime segments.

Fish consumption rates for adults are taken from the Methodology for Deriving Ambient Water Quality Criteria for the Protection of Human Health ( EPA, 2000a). Both these rates, 142.4 g/ day for adult subsistence anglers and 17.5g/ day for adult recreational anglers, are used for the specific sub population that they represent. EPA was not able to break the data supporting these rates down by gender or age group for use in this analysis.

EPA has determined that the fish consumption rate of 142.4 g/ day for adult subsistence anglers falls within the range of the arithmetic mean of adult subsistence angler studies representative of the United States ( EPA, 1998). The value represents the average consumption rate for this population of anglers. It represents uncooked, fresh and estuarine finfish and shellfish.

This rate is reported on an uncooked basis because pollutant concentration data is reported on an uncooked weight basis.

Similarly, the fish consumption rate of 17.5 g/ day falls within the average consumption rate for adult recreational anglers.

This rate also represents uncooked, fresh and estuarine finfish and shellfish. 3 Fish consumption rates for children in recreational angling households are based on W est et al. ( 1989) in the Exposure Factors Handbook ( EPA 1997c). This study has the most specific data for this population group and cites an intake of 7.27 grams/ day of freshwater and estuarine fish for children in recreational angling households. For children in subsistence angling households, the consumption rate was extrapolated from the 7.27 grams/ day rate for children in recreational angling households using the proportional relationship between consumption rates for adult subsistence and recreational anglers ( 142.4 grams/ day divided by 17.5 grams/ day). The consumption rate for children in subsistence angling households is calculated to be 60.58 grams/ day.

Currently, data on marine fish consumption rates for recreational anglers and subsistence anglers are not readily available.

Given that there are few marine reaches affected by the MP& M effluent guideline, EPA decided to use the fresh and estuarine fish consumption rates in lieu of marine fish consumption rates. This may result in underestimation of benefits,

however, it may also be argued that few subsistence fishers eat fresh/ estuarine fish and marine fish at the same rate.

3 For detail see memorandum Fish Consumption Rates by Lynn Zipf ( EPA, 2002).

13 4 MP& M EEBA Part III: Benefits Chapter 13: Human Health Benefits Table 13.1: Cancer Potency Factors for MP& M Pollutants CAS Number Regulated Pollutant Cancer Potency Factor ( mg/ kg/ day) a Drinking Water Criterion?

62533 Aniline 0.0057 62759 Nitrosodimethylamine, N 51 67663 Trichloromethane 0.0061 Yes 75003 Chloroethane 0.0029 75092 Dichloromethane 0.0075 Yes 75354 Dichloroethene, 1,1 0.6 Yes 78591 Isophorone 0.00095 79016 Trichloroethene 0.011 Yes 86306 Nitrosodiphenylamine, N 0.0049 117817 Bis( 2 ethylhexyl) phthalate 0.014 Yes 123911 Dioxane, 1,4 0.011 127184 Tetrachloroethene 0.052 Yes 7440382 Arsenic 1.5 Yes a The cancer potency factor is the incremental probability of developing cancer over a lifetime resulting from ingestion of the indicated chemical at the rate of one milligram per day per kilogram of body mass. For the incremental rates of exposure in this analysis and assuming reasonable background chemical exposures, the potency factor may be reasonably assumed to be a linear constant.

Source: U. S. EPA ( 1998/ 99); U. S. EPA ( 1997a).

The pollutant specific risks to recreational and subsistence anglers from MP& M facility discharges were then summed across pollutants for each type of angler, to obtain incremental risks for each population group from each facility s discharge. EPA developed separate estimates of cancer risk for each combination of angler type and facility discharging at least one pollutant with a cancer risk factor. The total change in probability of developing cancer from exposure to more than one MP& M pollutant is assumed to be the sum of the incremental risk effects from each pollutant: that is, the effects of the individual pollutants are assumed to be linearly additive. 4 The annual increased risk of cancer was estimated by dividing the increased lifetime risk values by 70 ( an estimate of lifetime).

b. Estimating the affected population The population exposed to contaminated fish and thus expected to benefit from reduced discharges includes recreational and subsistence anglers who fish the affected reaches, as well as members of such anglers' households. The geographic area from which anglers would travel to fish a reach is assumed to include only those counties that abut a given reach. 5 This assumption is based on the finding in the 1991 National Survey of Fishing, Hunting, and Wildlife Associated Recreation that 65 percent of anglers travel less than 50 miles to fish ( U. S. Department of the Interior, 1993). The average diameter of the counties abutting the reaches receiving discharges from the sample MP& M facilities is approximately 20 miles. Given that counties may have different shapes and that the road distance to the fishing site is likely to be greater than a straight line, the MP& M approach is likely to account for the majority of anglers that are likely to fish the affected reach. It is, however, likely to 4 Note that the assumption of linear additivity of cancer risk effects applies not only to the combination of pollutants from a single facility but also to the combined effects of multiple facility discharges. When more than one MP& M facility discharges to the same affected waterway a circumstance found to occur with some frequency in the sample facility data the combination of the multiple facility discharges may be accounted for by simply analyzing the effects of each facility independently. The cancer effects from multiple facilities can be aggregated to estimate cancer cases in the exposed population.

5 The exposed, and thus potentially benefiting, population would also include a category of   all other individuals  who consume freshwater and estuarine fish. Although these individuals are expected to have a much lower average daily consumption rate than anglers in the adjacent counties, they nevertheless would likely receive some benefit from reduced exposure to pollutants through fish consumption. This analysis omits this consumption category and the associated benefit estimate.

13 5 MP& M EEBA Part III: Benefits Chapter 13: Human Health Benefits introduce a downward bias into the estimate of the affected population. Given that anglers tend to travel farther to visit sites of very good or exceptional quality, the magnitude of this bias will depend on the fishing quality of the affected sites.

Estimating the number of persons fishing a reach involved the following steps:

  estimating the licensed fishing population in counties abutting MP& M reaches;

  estimating the population of subsistence fishermen in counties abutting MP& M reaches;

  estimating the fraction of the total fishing population in counties abutting an MP& M reach that fish the MP& M reach and, from that fraction, the size of population expected to fish each MP& M reach;

  adjusting the calculated fishing populations for the presence of fish advisories; and   including family members in the exposed population estimates.

  Estimating the licensed fishing population in counties abutting MP& M reaches The number of fishing licenses sold in counties abutting MP& M reaches is assumed to approximate the number of anglers residing in the abutting counties. EPA excluded the nonresident, one day, and three day license categories from the total number of licenses used in this analysis. Data on fishing licenses are not available for every state in which MP& M facilities are located. EPA used state level data to estimate the number of fishing licenses per county for those states for which county

level data were not assembled. Total state licenses were apportioned to counties based on the ratio of total population in the county abutting a discharge reach to total state population. Where an M P& M reach spans more than one county, fishing licenses were summed across all counties abutting the discharge reach. Where a reach lies in more than one state, EPA separately calculated the number of licenses for the abutting county( ies) based on the fishing license and county population data for the respective states.

EPA s analysis does not account for recreational anglers who do not purchase licenses as required by law. This may result in a significant underestimate of the fishing population at risk from exposure to MP& M pollutants. For example, the 1996 National Survey of Fishing, Hunting, and Wildlife Associated Recreation found that 34 percent of the anglers ( 16 years of age and older) did not have licenses ( U. S. Department of the Interior, 1996).

  Estimating the population of subsistence fishermen in counties abutting MP& M reaches Although fishing licenses may be sold to subsistence fishermen, many of these individuals do not purchase fishing licenses.

The extent of subsistence fishing in the U. S. or in individual states is not generally known. For this analysis, EPA assumed that the number of subsistence fishermen would be an additional 5 percent of the licensed fishing population. 6 That is, after estimating the licensed fishing population in counties abutting MP& M reaches, EPA added 5 percent to this value as the estimated number of subsistence fishermen. 7   Estimating the population fishing an MP& M reach EPA assumed that fishing activity among anglers residing within counties abutting a discharge reach is distributed evenly among all reach miles within those counties. Thus, the number of anglers who fish an MP& M reach was estimated by computing the length of the reach as a percentage of total reach miles within corresponding counties and multiplying the estimated ratio by the total fishing population in counties abutting the reach.

  Adjusting for fish advisories For MP& M reaches where fish advisories are in place ( typically due to non MP& M regulated pollutants such as dioxin and mercury), EPA assumed that some proportion of anglers would adhere to the advisory and not fish those reaches ( U. S. EPA,

1999a). Past studies suggest that anglers have a high, although not complete, level of awareness of fish advisories. These studies further suggest that while anglers may change their behavior in response to fish consumption advisories, they do not necessarily refrain from fishing in these reaches or consuming fish taken from reaches under an advisory. For example,

6 It is important to estimate recreational and subsistence populations separately because fish consumption rates for subsistence anglers are considerably higher than those for recreational anglers.

7 The environmental justice analysis presented in Chapter 17 of this report shows that the percent of residents living below the poverty level in the counties affected by MP& M discharges ranges from 7.4 to 25.2. Thus, the assumption that subsistence anglers are an additional 5% of the licensed fishing population is likely to provide a reasonable estimate of the subsistence anglers population.

13 6 MP& M EEBA Part III: Benefits Chapter 13: Human Health Benefits studies conducted by Belton et al ( 1986), Knuth and Velicer ( 1990), Silverman ( 1990), W est et al. ( 1989), Connelly, Knuth,

and Biso gni ( 19 92), and C onne lly and K nuth ( 1 993 ) indica te that 50 to 87 percent of an glers surveyed were a ware of state fish advisories on water bodies where they fish.

These studies also indicate that only 10 to 34 percent of anglers who were aware of advisories modified their fishing behavior in response by no longe r fishing a p articular locatio n, chan ging the locatio n in whic h they fish, o r taking fe wer fishing trips.

Ho wever, 13 to 68 p ercen t of anglers who were a ware of advisories changed their consumption or preparation h abits in response to advisories. udy by Knuth and Velicer ( 1990) also found some confusion among anglers regarding which waters were under advisory: 37 percent of fishermen actually fishing in waters under advisory reported that they were fishing in uncontam inated waters.

On the basis of these data, EPA assumed that recreational fishing activity would be 20 percent less on reaches subject to an advisory than wo uld otherwise b e estimated. A also assum ed that fish advisories do not affect fishing participation by subsistence anglers; thus, no adjustment was made to the estimates of the subsistence fishing population based on the presence of fish advisories.

The assumed 20 pe rcent decrease in recreationa l fishing could lead to either an o verestimate or un derestimate o f the risk assoc iated with consump tion of contam inated fish. ne thing, anglers who c hange loca tions may simp ly be switching to other locatio ns where advisories are in p lace and therefore maintain or increase their current risk. lso, those who continue to fish contaminated w aters may chang e their consum ption and prepa ration habits to minimize the risks. Data on the sp ecific fish advisories was pulled from EP A s on line Listing of Fish and Wildlife Advisories ( U. S. EPA , 1999a).

  Including family mem bers in the exposed population estimates EPA assumed that, in addition to anglers themselves, families of anglers would also consume fish taken from waters affected by MP & M facility discharges. Therefore, for each MP& M reach, EP A multiplied the estimated numbers of recreational and subsistence anglers fishing the affected reaches by 2.65, the size of the average U. S. household in 1996 based on C urrent Population Reports, ( U. S. Bureau of the Census, 1997). These calculations yielded the household populations of recreational and subsistence anglers who are estimated to consume fish from the reach to which the MP& M facility discharges, either directly or indirectly through a POT W . EPA expe cts that family members will benefit from reduced M P& M industry discharges by consuming fish that has lower levels of pollutant contamination.

c.

EPA calculated the number of cancer cases associated with the pollutant discharges ( baseline and post compliance) from each facility by multiplying the incremental cancer risk value for the two population classes times the estimated sizes of the population classes living near the facility. of the incremental risk value and the population size yields the number of annual can cer ev ents in the given p opu lation cla ss estima ted to result from consump tion of fish ta ken fro m wa terways affected by MP& M pollutant discharges. the values for the recreational and subsistence fishing household classes yields the total number of cancer cases associated with the sample facility discharges. Because the number of cancer cases apply to sample facilities, EP A extrapo lated the samp le results to the total M P& M pop ulation b y multiplying the resu lt obta ined fo r each samp le facility by its sam ple we ight and summ ing the sa mple  weighte d facility resu lts. formu la follows:

( 13.2)

where:

TCCf c = total national estimate of annual cancer cases associated with consumption of contaminated fish tissue ( baseline or post compliance);

Wti = facility samp le weigh t i ( i = 1 to N facilities, where N is the number of facilities in the sample);

POPi, sprt = exposed pop ulation in recreational fishing househo lds for the reac h to which facility i discha rges ( with adjustments as indicated for the presence of fish consumption advisories);

POPi, sbst = exposed pop ulation in subsistence fishing households for the reac h to which facility i discharges; The st EP For o A Calculating the change in the number of cancer events in the exposed population The product Summing The 13 7 MP& M EEBA Part III: Benefits Chapter 13: Human Health Benefits Riski, sprt = incremental cancer risk from fish consumption in the recreational fishing household population assoc iated with MP& M pollutant discharges from facility i; and Riski sbst = incremental cancer risk from fish consumption in the subsistence fishing household population assoc iated with MP& M pollutant discharges from facility i.

These values were calculated for the baseline and post compliance discharge cases. difference is the number of cancer cases estimated to be avoided annually through the fish consumption pathway as a result of the final regulation.

13.1.2 Cancer from Drinking Water Consumption Th e analysis of red uced cancer incid ence via the d rinking w ater pathway involve s three analytical step s that are largely parallel to those performed for the fish co nsumption pathw ay:

  estimating cancer risk to an exposed individual from consumption of contaminated drinking water,

  estimating the population that would benefit, and   calculating the change in the number of cancer events in the exposed population.

The majo r differences in the analysis for the drinking water pathway involve the identification of the exposed po pulation and the analysis of pollutant discharge effects in both the reach to which a facility discharges and reaches downstream of the discharge p oint.

a. water consumption Estimating cancer risk from consumption of drinking water affected by MP& M discharges requires calculating in waterway pollutant concentrations in locatio ns whe re drin king wa ter treatm ent system s draw water fo r pub lic con sump tion. his analysis involves three eleme nts:

  estimating in waterway pollutant concentrations for each pollutant in the reach to which a facility directly or indirec tly discharges. he me thod and fo rmulas for this calculation are ide ntical to tho se describe d for the analysis of cancer effec ts for the fish consumptio n pathway.

  estimating the pollutant concentrations over a distance of 500 kilometers downstream from each facility s discharge reach, using an exponential decay model in which pollution concentrations diminish below the initial point of discharge ( e. g., dilution, adso rption, partitioning, vola tilization, an d hydrolysis). ethod s used to calculate downstream pollutant concentrations are described in more detail in Appendix H.

  identifying the location of any drinking water intakes in the initial and downstream reaches where pollutant concentrations were calculated and assigning pollutant concentration values to each relevant intake point. The EPA's Safe Drinking Water Information System ( SDWIS) file in the Risk Screening Environmental Indicator ( RS EI) model provided information on drinking water intakes ( U. S. EPA , 1999b).

Estimated pollutant concentrations at each drinking water intake determines cancer risk. nking water treatment systems will reduce concentrations to below adverse effect thresholds for all chemicals for which EPA has pub lished a drinking water criterion . refore , pollutants exam ined in the M P& M drinkin g water analysis inc lude o nly six carcinogens for which current drinking water criteria are not available. See Table 13.1 for a list of the pollutants, their cancer potency factors, and drinking water criteria.

The formula for calculating the incremental risk to an individual resulting from the discharge of a given pollutant from a given facility at reaches with a known pu blic drinking water intake is as follows:

( 13.3)

where:

Risk = incremental risk of incurring cancer from drinking water consumption ( change in probability), calculated at each drinkin g water intake w ithin 50 0 km of the initial d ischarg e po int; The Estimating cancer risk from drinking T T M EPA assumed dri The 13 8 MP& M EEBA Part III: Benefits Chapter 13: Human Health Benefits C = pollutant concentration in surface water in the reach with an intake (   g/ l);

CF1 = conversion factor, micrograms to milligrams ( 0.001 mg/   g);

CR = human consumption rate of water ( 1.24 l/ day);

EF = exposure frequency ( 350 days/ year);

ED = exposure duration ( 70 years);

BW = human body weight ( 70 kg);

LT = human lifetime ( 70 years);

CF2 = conversion factor ( 365 days/ year); and SF = pollutant can cer p otenc y factor ( m g/ kg/ day) 1 .

The consumption rate of 1.24 liters per day used in this analysis to represent the average daily consumption of drinking water by a person in the United States is taken from Estimated Per Capita Water Ingestion in the United States ( EPA, 2000b).

reco mmended in the Exp osure Facto rs Ha ndb ook ( 1997c ), EP A use s an exposure freq uenc y of 35 0 da ys per ye ar to es timate the increased risk of cancer from consuming drinking water supplied by drinking water systems with intakes on local surface water b odie s.

The incremental individual risk from each facility s pollutants are then summed over pollutants at each drinking water intake to calculate the incremental risk at each intake resulting from pollutant discharges by each upstream facility. The findings carried forward to the next step include the incremental cancer risk for each combination of facility and associated drinking water intake( s).

To estimate the annual increa sed risk of cance r in consume rs served by d rinking water intakes affected b y MP & M discharges,

the lifetime risk values were then divided by 70 years ( an estimate of lifetime). These values were calculated for both the baseline and post com pliance discha rge cases.

b.

The exposed population for each combination of discharging facility and drinking water intake is the general population served by the drinking water system for which the drinking water intake was identified. fe Drinking Water Information System ( SDW IS) file in the Risk Screening Environmental Indicator ( RSEI) model provided information on drinking water intakes.

c.

EPA calculated the number of cancer cases for baseline and post compliance pollutant discharges for each combination of facility and affected drinking water intake by multiplying the incremental cancer risk value times the population served by the water system drawing water at the drinking water intake.

The total number of cancer cases associated with the facility discharges is the sum of cancer cases over all drinking water intakes. PA extrap olated the sam ple results to the to tal M P& M pop ulation b y multiplying the resu lt for eac h sam ple fac ility by its sample weight and summing the sample weighted facility results. Because incremental cancer effects are assumed to be linearly ad ditive, ca ncer risk effects are aggre gated over facilities and drinkin g water intakes b y simple add ition of the effects calculated sep arately for each co mbination o f facility and drinking wa ter intake. ula follows:

( 13.4)

where:

TCCdw = total national estimate of cancer cases associated with consumption of chemically contaminated drinking water ( baseline or post compliance);

Wti = facility samp le weigh t i ( i = 1 to N facilities);

POPi, j = population exposed to discharges by facility i at drinking water intake j ( j = 1 to M water supply intakes); and Riski, j = increm ental ca ncer risk for d ischarg es by fac ility i at drinking water intake j.

EPA calculated these values for the baseline and post compliance discharge cases. ference in the values is the number of drinking water asso ciated canc er cases estimated to be avo ided ann ually by reduced MP & M industry discharges. As Estimating the benefiting population Sa Calculating the changes in the number of cancer events E The form The dif 13 9 MP& M EEBA Part III: Benefits Chapter 13: Human Health Benefits 13.1.3 Exposures above Non cancer Health Thresholds Exposed populations are also at risk of developing non cancer health problems ( including systemic, reproductive,

immunological, neurological, or circulatory problems) from fish ingestion and water consumption. The common approach for assessing the risk of non cancer health effects from the ingestion of a pollutant is to calculate a hazard quotient by dividing an individual's oral exposure to the pollutant, expressed as a pollutant dose in milligrams per kilogram body weight per day ( mg/ kg/ day), by the pollutant's oral reference dose ( RfD). An RfD is defined as an estimate ( with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure that likely would not result in the occurrence of adverse health effects in humans, including sensitive individuals, during a lifetime. Toxicologists typically establish an RfD by applying uncertainty factors to the lowest or no observed adverse effect level ( NOAEL) for the critical toxic effect of a pollutant. A hazard quotient less than one means that the pollutant dose to which an individual is exposed is less than the RfD, and, therefore,

presumed to be without appreciable risk of adverse human health effects. A hazard quotient greater than one means that the pollutant dose is greater than the RfD. RfDs are available for 77 of the 132 MP& M pollutants of concern. The pollutants analyzed and their RfDs are listed in Table 13.2.

Table 13.2: RfDs for MP& M Pollutants CAS Number Regulated Pollutant RfD ( mg/ kg/ day) Drinking Water Criterion? a Target Organ and Effects 83329 Acenaphthene 0.060 No Liver toxicity 67641 Acetone 0.100 No Increased liver and kidney weights; nephrotoxicity 98862 Acetophenone 0.100 No General toxicity 107028 Acrolein 0.020 No Cardiovascular toxicityb 7429905 Aluminum 1.000 Yes Renal failure, intestinal contraction interference, adverse neurological effectsc 120127 Anthracene 0.300 No 7440360 Antimony 0.000 Yes Longevity, blood glucose, cholesterol 7440382 Arsenic 0.000 Yes Hyperpigmentation, keratosis and possible vascular complications 7440393 Barium 0.070 Yes Increased kidney weight 65850 Benzoic acid 4.000 No 100516 Benzyl alcohol 0.300 No Forestomach, epithelial hyperplasia 7440417 Beryllium 0.002 Yes Small intestinal lesions 92524 Biphenyl 0.050 No Kidney damage 117817 Bis( 2 ethylhexyl)

phthalate 0.020 Yes Increased relative liver weight 7440428 Boron 0.090 No Testicular atrophy, spermatogenic arrest 85687 Butyl benzyl phthalate 0.200 No Significantly increased liver to body weight and liver to brain weight ratios 7440439 Cadmium 0.001 Yes Significant proteinuria ( protein in urine)

75150 Carbon disulfide 0.100 No Fetal toxicity, malformations 108907 Chlorobenzene 0.020 No Histopathologic changes in liver 75003 Chloroethane 0.400 No 7440473 Chromium 1.500 Yes Renal tubular necrosis ( kidney tissue decay) c 18540299 Chromium hexavalent 0.003 Yes Reduced water consumption 7440484 Cobalt 0.060 No Heart effectsc 7440508 Copper 0.040 Yes Gastrointestinal effects, liver necrosisc 95487 Cresol, o 0.050 No Decreased body weights and neurotoxicity.

13 10 MP& M EEBA Part III: Benefits Chapter 13: Human Health Benefits Table 13.2: RfDs for MP& M Pollutants CAS Number Regulated Pollutant RfD ( mg/ kg/ day) Drinking Water Criterion? a Target Organ and Effects 106445 Cresol, p 0.005 No Central nervous system hypoactivity and respiratory system distress 57125 Cyanide 0.020 Yes Weight loss, thyroid effects and myelin degeneration 75354 Dichloroethene, 1,1 0.009 Yes Toxic effects on kidneys, spleen, lungsc; hepatic lesions 75092 Dichloromethane 0.060 Yes Liver toxicity 60297 Diethyl ether 0.200 No Depressed body weights 68122 Dimethylformamide, N, N 0.100 No Liver and gastrointestinal system effects 105679 Dimethylphenol, 2,4 0.020 No Clinical signs ( lethargy, prostration, and ataxia) and hematological changes 84742 Di n butyl phthalate 0.100 No Increased mortality 51285 Dinitrophenol, 2,4 0.002 No Cataract formation 606202 Dinitrotoluene, 2,6 0.001 No Mortality, central nervous system neurotoxicity, blood heinz bodies and methemoglobinemia, bile duct hyperplasia, kidney histopathology 117840 Di n octyl phthalate 0.020 No Kidney and liver increased weights, liver increased SGOT and SGPT activity 122394 Diphenylamine 0.025 No Decreased body weight, and increased liver and kidney weights 100414 Ethylbenzene 0.100 Yes Liver and kidney toxicity 206440 Fluoranthene 0.040 No Nephropathy, increased liver weights, hematological alterations, clinical effects 86737 Fluorene 0.040 No Decreased red blood cell count, packed cell volume and hemoglobin 16984488 Fluoride 0.060 Yes Objectionable dental fluorosis ( soft, mottled teeth)

591786 Hexanone, 2 0.040 No Hypatotoxicity and nephrotoxcity d 7439896 Iron 0.300 Yes Liver, diabetes mellitus, endocrine disturbance, and cardiovascular effectsd 78831 Isobutyl alcohol 0.300 No Hypoactivity and ataxia 78591 Isophorone 0.200 No Kidney pathology 7439965 Manganese 0.140 Yes Central nervous system effects 78933 Methyl ethyl ketone 0.600 No Decreased fetal birth weight 108101 Methyl isobutyl ketone 0.080 No Lethargy, increased liver and kidney weights and urinary protein 80626 Methyl methacrylate 1.400 No Increased kidney to body weight ratio 91576 Methylnaphthalene, 2 0.020 No 7439987 Molybdenum 0.005 No Increased uric acid 91203 Naphthalene 0.020 No Decreased body weight 7440020 Nickel 0.020 Yes Decreased body and organ weights 100027 Nitrophenol, 4 0.008 No 59507 Parachlorometacresol 2.000 No 108952 Phenol 0.600 No Reduced fetal body weight in rats 7723140 Phosphorus ( elemental) 0.000 No Parturition mortality; forelimb hair loss 13 11 MP& M EEBA Part III: Benefits Chapter 13: Human Health Benefits Table 13.2: RfDs for MP& M Pollutants CAS Number Regulated Pollutant RfD ( mg/ kg/ day) Drinking Water Criterion? a Target Organ and Effects 129000 Pyrene 0.030 No Kidney effects ( renal tubular pathology, decreased kidney weights)

110861 Pyridine 0.001 No Increased liver weight 7782492 Selenium 0.005 Yes Clinical selenosis ( hair or nail loss)

7440224 Silver 0.005 Yes Argyria ( skin discoloration)

100425 Styrene 0.200 Yes Red blood cell and liver effects 127184 Tetrachloroethene 0.010 Yes Liver toxicity, weight gain 7440280 Thallium 0.000 Yes Liver toxicity, gastroenteritis, degeneration of peripheral and central nervous systemb 7440315 Tin 0.600 No Kidney and liver lesions 7440326 Titanium 4.000 No 108883 Toluene 0.200 Yes Changes in liver and kidney weights 79016 Trichloroethene 0.006 Yes Bone marrow, central nervous system, liver, kidneys d 75694 Trichlorofluoromethane 0.300 No Survival and histopathology 67663 Trichloromethane 0.010 Yes Fatty cyst formation in liver 7440622 Vanadium 0.007 No Kidney and central nervous system effects b 108383 Xylene, m 2.000 Yes Central nervous system hyperactivity, decreased body weight 179601231 Xylene, m& p* 2.000 Yes 95476 Xylene, o 2.000 Yes Central nervous system hyperactivity, decreased body weight 136777612 Xylene, o& p* 2.000 Yes 7440666 Zinc 0.300 Yes 47% decrease in erythrocyte superoxide dismutase ( ESOD)

concentration in adult human females after 10 weeks of zinc exposure 137304 Ziram \ Cymate 0.020 No a   Yes = there is a published drinking water criterion for a given chemical.

b Reference dose based on a no observed adverse effect level ( NOAEL). Health effects summarized from Amdur, M. O.; Doul, J.; and Klaassen, C. D., eds. 1991. Cassarett and Doul s Toxicology, 4th edition. Target organ and effects summarized from Wexler, P., ed. 1998. Encyclopedia of Toxicology, Volumes 1 3.

d Target organ and effects summarized from Amdur, M. O.; Doul, J.; and Klaassen, C. D., eds. 1996. Cassarett and Doul s Toxicology,

5th edition.

Source: U. S. EPA ( 1998/ 99); U. S. EPA ( 1997a).

EPA guidance for assessing exposures to mixtures of pollutants recommends calculating a hazard index ( HI) by summing the individual hazard quotients for those pollutants in the mixture that affect the same target organ or system ( e. g., the kidneys,

the respiratory system). For example, for three liver toxicants discharged from an MP & M facility ( pollutant A with a hazard index of 0.10, pollutant B with a hazard index of 0.05, and pollutant C with a hazard index of 0.15), the combined hazard index is 0.30. HI values are interpreted similarly to hazard quotients; values below one are generally considered to suggest that exposures are not likely to result in appreciable risk of adverse health effects during a lifetime, and values above one are generally cause for concern, although an HI greater than one does not necessarily suggest a likelihood of adverse effects.

To evaluate the potential benefits of reducing the in stream concentrations of 76 pollutants that cause non cancer health effects, EPA estimated target organ specific HIs for drinking water and fish ingestion exposures in both the baseline and post compliance scenarios. HI is calculated for each discharge reach associated with one or more MP& M sample facilities by dividing the estimated ingestion rate of each pollutant by the RfD value for the pollutant. The formula follows:

13 12 c MP& M EEBA Part III: Benefits Chapter 13: Human Health Benefits ( 13.5)

where:

HI = haza rd ind ex for the po llutants disc harge d from a facility and ingested by a specific co nsumption pathw ay;

DCRk = estimated d aily consump tion rate per kilogram of bo dy ma ss for pollutant k via a specific consumption pathway ( mg/ kg/ day);

RfD k = reference d ose fo r pollutant k ( mg/ kg/ day); and K = number of pollutants affecting a given organ or system.

Daily consumption rate ( DCR) per kilogram of body mass for pollutant k is estimated as follows:

( 13.6)

where:

DCRk = estimated daily consump tion rate per kilogram of bo dy ma ss for pollutant k via a specific consumption pathway ( mg/ kg/ day);

C = pollutant concentration in surface water in the MP& M reach (   g/ l);

CF1 = conversion factor, micrograms to milligrams ( 0.001 mg/   g);

CR = human consumption rate of water ( mg/ day);

BCF = bioc oncentratio n factor for po llutant k;

B W = human body weight ( kg).

These HIs are calculated separately for the fish and water consumption pathways. The fish consumption pathway was further divided into recreational and subsistence fish consumption rates. s and formulas for estimating the in waterway concentrations and ingestion of pollutants by exposed pop ulations are the same as those used for the fish consumption and drinking water cancer analyses. s that the analysis of non cancer health pathways was performed for the discharge reach only and not for reac hes downstream , due to time and reso urce c onstraints. sult, this analysis unde restimates populatio ns exp osed to non  cance r risks via d rinking w ater pathways EP A then com bined estimate s of the nu mbe rs of ind ividua ls in the exp osed pop ulations with the H Is for the pop ulations to determine how many individuals might be expected to realize reduced risk of non cancer health effects in the post compliance scenario. The basis for identifying exposed populations is the same as that described for the analysis of reduced incidence of cancer via the fish con sumption a nd drinking w ater consum ption pathw ays. 8 The shift in populations from a higher to a lower HI value fro m the b aseline to po st com plianc e case s is the qu antitative m easure of benefits fro m this an alysis. T his analysis was limited in two primary w ays:

  First, haz ard ind ices estim ated in this analysis m ay und erstate the actual p otentia l for ad verse health e ffects be cause this analysis consid ers co ntributio ns to no n canc er risk resulting on ly from M P& M facility discharges, and d oes not take into account other sources of exposure to MP& M p ollutants or other chemicals that may contribute to an aggregate non

cancer risk. result is that the analysis understates the numerical value estimated for HIs, but the incremental change in HIs between the baseline and the final option would remain the same. EPA therefore evaluated potential incremental changes in non cancer health risks over the entire range of hazard indices, including hazard indices below one.

  Sec ond , EPA used me an individual expo sure param eters and not the distribution o f expo sure param eters to estimate hazard ind ices for the pop ulations affected by M P& M discharges.

Th e results fro m the non cancer health risk analysis ap ply to sample discha rge loc ations o nly. Analytic tractability issues prevented this analysis from being cond ucted on a sample we ighted national ba sis. EPA d id not mo netize these bene fits. The procedure The only exception i As a re The net 8 The exposed populations for the drinking water consumption pathway are those associated with drinking water intakes only in a facility s discharge reach.

13 13 MP& M EEBA Part III: Benefits Chapter 13: Human Health Benefits 13.1.4 Human Health AWQC EPA used another approach to quantify reductions in health risk from the final MP& M regulation, based on the extent to which reduced MP& M discharges would decrease the occurrence of pollutant concentrations in affected waterways that exceed human health based AWQC. This analysis provides a measure of the change in cancer and non cancer health risk by comparing the number of discharge reaches exceeding health based AWQC for regulated pollutants due to MP& M activities in the baseline to the number exceeding AWQC under the final option.

AWQC are set at levels to protect human health through ingestion of aquatic organisms and ingestion of water and aquatic organisms. Accordingly, reducing the frequency at which human health based AWQC are exceeded should translate into reduced risk to human health. This measure should be viewed as an indirect indicator of reduced risk to human health,

9 because it does not reflect the size of the exposed population and is not tied to changes in human health risk per se.

EPA estimated the baseline concentrations of all MP& M pollutants for each reach to which one or more MP& M facilities discharge. The calculation of concentrations used the same in waterway dilution and mixing model described in the analysis of cancer risk for the fish consumption pathway. The baseline concentrations were compared with human health based AWQC values. ( See Table 13.3 for a list of MP& M pollutants with AWQC values.) Reaches in which concentrations of one or more pollutants were estimated to exceed an AWQC value were identified as exceeding AWQC limits in the baseline.

This analysis was repeated using the post compliance discharge values for the final option. Reaches estimated to have concentrations in excess of AWQC in the baseline but not in the post compliance case were assessed as having substantial water quality improvements relative to human health based criteria as a result of regulation. EPA deems such water quality improvements to be indicative of reduced risk to human health. Although not explicitly accounted for in this analysis, human health risk reductions are also likely to occur wherever in waterway concentrations are reduced, regardless of whether or not they are reduced to levels below AWQC.

Table 13.3: MP& M Pollutants with Human Health Based AWQC CAS Number Pollutant Human Health Based AWQC ( ug/ l) Target Organ and Effectsa Organisms Only Water &

Organisms 83329 Acenaphthene 2700 1200 Liver, hepatotoxicity 67641 Acetone 2800000 3500 Increased liver and kidney weights; nephrotoxicity 98862 Acetophenone 98000 3400 General toxicity 107028 Acrolein 1000 410 Cardiovascular toxicityc 7429905 Aluminum 47000 20000 Renal failure, intestinal contraction interference, adverse neurological effectsd 62533 Aniline 95 5.8 Spleen and body cavity 120127 Anthracene 6800 4100 No observed effects 7440360 Antimony 4300 14 Longevity, blood glucose, cholesterol 7440382 Arsenic 0.16 0.02 Liver, kidneys, lungs, bladder, and skin 7440393 Barium 1000 Increased kidney weight 65850 Benzoic acid 2900000 130000 No observed adverse effects 100516 Benzyl alcohol 810000 10000 Forestomach, epithelial hyperplasia 7440417 Beryllium 1100 66 Small intestinal lesions 92524 Biphenyl 1200 720 Kidney damage 9 The following chapter uses this same information in part as a direct indicator of improved water quality.

13 14 MP& M EEBA Part III: Benefits Chapter 13: Human Health Benefits Table 13.3: MP& M Pollutants with Human Health Based AWQC CAS Number Pollutant Human Health Based AWQC ( ug/ l) Target Organ and Effectsa Organisms Only Water &

Organisms 117817 Bis( 2 ethylhexyl)

phthalate 5.9 1.8 Liver 85687 Butyl benzyl phthalate 5200 3000 Significantly increased liver to body weight and liver to brain weight ratios 7440439 Cadmium 84 14 Significant proteinuria ( protein in urine)

75150 Carbon disulfide 94000 3400 Fetal toxicity, malformations 108907 Chlorobenzene 21000 680 Histopathologic changes in liver 75003 Chloroethane 520 12 1854029 9 Chromium hexavalent 2000 100 Reduced water consumption 7440473 Chromium 1000000 50000 Renal tubular necrosis ( kidney tissue decay) d 7440508 Copper 1200 650 Gastrointestinal effects, liver necrosisd 106445 Cresol, p 3100 170 Central nervous system hypoactivity and respiratory system distress 95487 Cresol, o 30000 1700 Decreased body weights and neurotoxicity.

57125 Cyanide 220000 700 Weight loss, thyroid effects and myelin degeneration 117840 Di n octyl phthalate 39 37 Kidney and liver increased weights, liver increased SGOT and SGPT activity 84742 Di n butyl phthalate 12000 2700 Increased mortality 75354 Dichloroethene, 1,1 3.2 0.057 Inconclusive 75092 Dichloromethane 1600 4.7 Liver, lungs 60297 Diethyl ether 770000 6900 Depressed body weights 131113 Dimethyl phthalate 2900000 310000 68122 Dimethylformamide, N, N 220000000 3500 Liver and gastrointestinal system effects 105679 Dimethylphenol, 2,4 2300 540 Clinical signs ( lethargy, prostration, and ataxia) and hematological changes 51285 Dinitrophenol, 2,4 14000 70 Cataract formation 606202 Dinitrotoluene, 2,6 900 34 Mortality, central nervous system neurotoxicity, blood heinz bodies and methemoglobinemia, bile duct hyperplasia, kidney histopathology 123911 Dioxane, 1,4 2400 3.2 Liver, nasal cavity, gall bladder 122394 Diphenylamine 1000 470 Decreased body weight gain, and increased liver and kidney weights 100414 Ethylbenzene 29000 3100 Liver and kidney toxicity 206440 Fluoranthene 370 300 Nephropathy, increased liver weights, hematological alterations, clinical effects 86737 Fluorene 14000 1300 Decreased red blood cell count, packed cell volume and hemoglobin 591786 Hexanone, 2 65000 1400 Hypatotoxicity and nephrotoxcity b 7439896 Iron 300 Liver, diabetes mellitus, endocrine disturbance, and cardiovascular effectsc 13 15 MP& M EEBA Part III: Benefits Chapter 13: Human Health Benefits Table 13.3: MP& M Pollutants with Human Health Based AWQC CAS Number Pollutant Human Health Based AWQC ( ug/ l) Target Organ and Effectsa Organisms Only Water &

Organisms 78831 Isobutyl alcohol 1500000 10000 Hypoactivity and ataxia 78591 Isophorone 2600 36 Preputial gland 7439965 Manganese 100 50 Central nervous system effects 7439976 Mercury 0.051 0.05 80626 Methyl methacrylate 2300000 48000 Increased kidney to body weight ratio 78933 Methyl ethyl ketone 6500000 21000 Decreased fetal birth weight 108101 Methyl isobutyl ketone 360000 2800 Lethargy, increased liver and kidney weights and urinary protein 91576 Methylnaphthalene, 2 84 75 91203 Naphthalene 21000 680 Decreased body weight 7440020 Nickel 4600 610 Decreased body and organ weights 100027 Nitrophenol, 4 1100 220 62759 Nitrosodimethylamine,

N 8.1 0.00069 Tumors observed at multiple sites 86306 Nitrosodiphenylamine,