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Appendix J: A Tiered Modeling Approach for Assessing the Risks Due to Sources of Hazardous Air Pollutants
Pages 537-582

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From page 537...
... U.S. ENVIRONMENTAL PROTECTION AGENCY Office of Air Quality Planning and Standards Technical Support Division Research Triangle Park, NC 27711 February 1992 537
From page 538...
... 538 SCIENCE AND JUDGMENT IN RISK ASSESSMENT TABLE OF CONTENTS DISCLAIMER 537 FIGURES 539 TABLES 539 1.0 Introduction 540 1.1 Background and Purpose 540 1.2 Risk Assessment in Title III 541 1.3 Overview of Document 544 1.4 General Modeling Requirements 545 2.0 Tier I Analyses 549 2.1 Introduction 549 2.2 Long-term Modeling 549 2.2.1 Maximum Annual Concentration Estimation 550 2.2.2 Cancer Risk Assessment 552 2.2.3 Chronic Noncancer Risk Assessment 553 2.3 Short-term Modeling 554 2.3.1 Maximum Hourly Concentration Estimation 554 2.3.2 Acute Hazard Index Assessment 557 3.0 Tier 2 Analyses 558 3.1 Introduction 558 3.2 Long-term Modeling 558 3.2.1 Maximum Annual Concentration Estimation 558 3.2.2 Cancer Risk Assessment 560 3.2.3 Chronic Noncancer Risk Assessment 561 3.3 Short-term Modeling 562 3.3.1 Maximum Hourly Concentration Estimation 562 3.3.2 Acute Hazard Index Assessment 563 4.0 Tier 3 Analyses 564 4.1 Introduction 564 4.2 Long-term Modeling 564 4.2.1 Maximum Annual Concentration Estimation 565 4.2.2 Cancer Risk Assessment 567 4.2.3 Chronic Noncancer Risk Assessment 568 4.3 Short-term Modeling 569 4.3.1 Maximum Hourly Concentration Estimation 570 4.3.2 Acute Hazard Index Assessment 572 5.0 Additional Detailed Analyses 575 6.0 Summary of Differences Between Modeling Tiers 576 References 577 Appendix A-Electronic Bulletin Board Access Information 579 Appendix B-Regional Meteorologists/Modeling Contacts 580
From page 539...
... 556 Summary of Differences Between Modeling Tiers 576
From page 540...
... The determination of lifetime cancer risk involves the estimation of long-term ambient concentrations of toxic pollutants whereas the determination of noncancer health effects can involve the estimation of long-term and short-term ambient concentrations. Since the measurement of long-term and short-term ambient concentrations for each toxic air pollutant (189 pollutants as listed in §112(b)
From page 541...
... In addition, the procedures may serve as the basis for the residual risk determination processes described above. The guidance addresses the estimation of long-term and short-term ambient concentrations resulting from the atmospheric dispersion of known emissions of hazardous air pollutants, and subsequently addresses the techniques currently used to quantify the cancer risks and noncancer risks associated with the predicted ambient concentrations.
From page 542...
... Based on such an assessment, additional regulation of the source category is deemed necessary if "promulgation of such standards is required in order to provide an ample margin of safety to protect the public health" with respect to noncancer health effects, or if the MACT standards "do not reduce lifetime excess cancer risks to the individual most exposed to emissions from a source in the category or subcategory to less than one in one million" with respect to carcinogens, or if a determination is made "that a more stringent standard is necessary to prevent....an adverse environmental effect." (§112(f)
From page 543...
... For the purposes of this document, cancer risks resulting from exposure to mixtures of multiple carcinogenic pollutants will be assessed by summing the cancer risks due to each individual pollutant, regardless of the type of cancer which may be associated with any particular carcinogen.2 For pollutants causing noncancer health effects from chronic or acute exposure, the levels of concern are chronic and acute concentration thresholds, respectively, which would be derived from health effects data, taking into account scientific uncertainties. For purposes of estimating potential long-term impacts of hazardous air pollutants, EPA has derived for some pollutants (and will derive for others)
From page 544...
... The chronic noncancer hazard index is calculated by dividing the modeled annual concentration of a pollutant by its chronic concentration threshold value. The acute noncancer hazard index is calculated by dividing the modeled 1-hour concentration of a pollutant by its acute concentration threshold value.
From page 545...
... the maximum predicted chronic noncancer hazard index, or (3) the maximum predicted acute hazard index, the analyst may wish to perform a Tier 2 analysis.
From page 546...
... Emission rates may be best estimated from experimental measurements or sampling, where such test methods are available. Alternatively, mass balance calculations or use of emission factors developed for specific types of processes may be used to quantify emission rates.
From page 547...
... In addition, to assess the worst-case impact of a source or group of sources, long-term emission rates used in model simulations should reflect the emissio rates for a plant or process which is operating at full design capacity. In a shortterm impact analysis, the emission rate used for modeling is based on the maximum amount of pollutant emitted over a 1-hour period, during which the source is emitting.
From page 548...
... S~ 4~ 7~- ~ R~ 466~ questions pertain lo Me prickly purposes for which the i-act assessment is being pegged, they me not addressed by this document Instead, this document refers to and provides guidance ~r modeling various scenarios including single-source, mulOple-sou~e, single-pollut~t, and mulOple-pollutant scen~ios. Subsequent EPA documents wH1 address the questions of ~bicb sources and bicb pollutants should be included in an impact analysis far a specific regulatopurpose.
From page 549...
... For carcinogens, the calculation of cancer risk proceeds by multiplying annual concentrations by pollutant-specific cancer potency factors derived from health effects data. The impacts of pollutants with chronic noncancer effects are generally assessed by comparing predicted annual concentrations with chronic threshold concentrations which are again derived from experimental health data.
From page 550...
... 4. Take the appropriate normalized maximum annual concentration for this release height and distance from the table, and multiply by the emission rate
From page 552...
... 2.2.2 Cancer risk assessment Once the maximum annual concentration has been estimated for each release being modeled, upper bound lifetime individual cancer risk may be estimated by mutiplying the maximum annual concentration estimates of each carcinogenic pollutant by the unit cancer risk factor for that pollutant and then summing results. This approach assumes that all cancer risks are additive, regardless of the organ system which may be affected.
From page 553...
... The chronic noncancer hazard index is calculated by summing the maximum annual concentrations for each pollutant divided by the chronic threshold concentration value for that pollutant. if the calculated hazard index is greater than 1.0, the release or releases being simulated may pose a threat to the public, and further modeling may be indicated.
From page 554...
... maximum 1-hour average emission rate of each pollutant from each source included in the simulation (g/s)
From page 555...
... . Multiplying by the emission rate of 0.50g/s results in a maximum hourly concentration estimate for screening purposes equal to 197 ~g/m3.
From page 556...
... 556 V, z o Ed z z o Lie o 1 3 a Pt o ~7 Cal .
From page 557...
... As an example of the acute hazard index approach, consider the same plant being simulated in Section 2.2.2, but this time the maximum 1-hour concentrations are determined using the procedure in Section 2.3.2 to be the following: Source Compound Max. 1-hrimpact Stack 1 Pollutant A 197 ,ug/m3 Stack 2 Pollutant A 257 ,ug/m3 Stack 2 Pollutant B 110 ,ug/m3 Stack 3 Pollutant B 301 ,ug/m3 Stack4 Pollutant B 367 ,ug/m3 Further suppose that pollutants A and B pose health problems from acute exposures with acute threshold concentration values of 200 and 100 ,ug/m3, respectively.
From page 558...
... 3.2 Long-term Modeling Long-te~m Tier 2 modeling utilizes the SCREENS model to estimate 1-hour maximum concentrations, and then utilizes a conservative conversion factor to derive maximum annual concentration values from the SCREEN predictions. i7 These maximum annual concentration estimates are used to assess cancer risk and chronic noncancer risk exactly as in Section 2.2.2 and 2.2.3 of this document.
From page 559...
... Area source emission rates should be converted to glslm2 by dividing the total area of the source.
From page 560...
... 3.2.2 Cancer Risk Assessment Maximum annual concentrations for all releases of carcinogens should be multiplied by the appropriate unit cancer risk factor and summed to estimate the maximum cancer risk. It should be noted that this approach, as in Tier 1, presumes that all worst-case impacts occur at the same location.
From page 561...
... However, the cancer risk level still exceeds 1 x 10-6, indicating that modeling at a higher Tier may be desireable. 3.2.3 Chronic Noncancer Risk Assessment As in Tier 1, maximum annual concentrations are divided by their chronic concentration threshold values and summed to calculate the hazard index values.
From page 562...
... 2. Area source emission rates reflect the total emission rate from divided by the area of the source.
From page 563...
... 3.3.2 Acute Hazard Index Assessment As in Tier 1, maximum 1-hour concentrations are divided by their acute threshold concentration values and summed to calculate the acute hazard index values. Again, this approach conservatively assumes that all worst-case impacts can occur simultaneously at the same location.
From page 564...
... The TOXLT modeling system uses the ISCLT model to calculate these annual concentrations at receptor sites which are specified by the user. A post-processor called RISK subsequently calculates lifetime cancer risks and chronic noncancer hazard index values at each receptor.
From page 565...
... (This doesn't necessarily have to be the case, as long as the product of the emission rate provided as input to ISCLT and the emission rate multiplier provided as input to RISK equals the actual emission rate being modeled for each source.) In the case where more than one pollutant is being emitted from the same source, that source should only be included once in the ISCLT input file, and emission rate multipliers should be provided to the RISK post-processor for each pollutant being emitted from that source.
From page 566...
... The printed ISCLT output will indicate the top 10 impacts for each source group, while the master file inventory will contain all of the annual concentration predictions from each source group at each receptor. Continuing with the examples from Tiers 1 and 2, TOXLT was utilized to perform site-specific ISCLT dispersion modeling for the 4 stacks in the example.
From page 567...
... In general, the Tier 3 maximum concentration values are 25 to 30% as high as the Tier 2 values. 4.2.2 Cancer Risk Assessment Concentrations from the ISCLT master file inventory are used by the RISK post-processor to calculate cancer risks at each receptor site in the ISCLT receptor array.
From page 568...
... 4.2.3 Chronic Noncancer Risk Assessment In this assessment, concentrations from the ISCLT master file inventory are used by the RISK post-processor to calculate chronic noncancer hazard index values for a specific noncancer effect at each receptor site in the ISCLT receptor array. RISK can then provide summaries of the calculated index values according to user specifications.
From page 569...
... Using the chronic noncancer threshold concentration values for pollutants A and B of 20.0 and 5.0 ~g/m3, respectively, the RISK post-processor was exercised for the example facility to obtain a maximum hazard index value of 0.27 located at point Z on Figure 1. This result, which is approximately 30% of the Tier 2 result, would indicate that the facility does not present significant chronic noncancer risk in its current configuration.
From page 570...
... The TOXST modeling system uses "base emission rates" and "emission rate multipliers" to specify the emission rate for each pollutant/source combination. Thus, for a given pollutant and source the emission rate equals the base emission rate (specified in the ISCST input file)
From page 571...
... Alternatively, multiple pollutants from the same source may be modeled as individual sources with actual emission rates in ISCST and unit emission rates in TOXX. This may require more computing time, but may allow direct interpretation of concentration predictions in the ISCST printed output.
From page 572...
... 4.3.2 Acute Hazard Index Exceedance Assessment Concentrations from the ISCST master file inventory are used by the TOXX post-processor to calculate acute hazard index values for each hour of a multipleyear simulation period at each receptor site in the ISCST receptor array. The program then counts the number of times a hazard index value exceeds 1.0 (an exceedance)
From page 573...
... Acute threshold concentration values are provided to TOXX as the health effects thresholds in the TOXX post-processor input file.
From page 574...
... However, resimulation with placement of additional receptors in the ISCST receptor array should be considered as a means of assuring that the simulation is not underestimating the maximum acute hazard index. If the maximum number of hazard index exceedances in the receptor array is greater than the specified value, additional runs of the TOXX post-processor with reduced emissions rate multipliers may be performed to assess the impacts of possible emission control scenarios.
From page 575...
... The determination of an appropriate alternative modeling procedure can Hey be made in a manner consistent with the approach outlined in the "Guideline on Air Quality Models (Revised) ."6 In some cases, the EPA may allow exposure assessments to incorporate available information on actual locations of residences, potential residences, businesses, or population centers for the purpose of establishing the probability of human exposure to the predicted levels of toxic pollution near the source being modeled.
From page 576...
... Within each tier, cancer unit risk estimates, chronic noncancer concentration thresholds, and acute concentration thresholds are required to convert concentration predictions into cancer risks, chronic noncancer nsks, and acute noncancer risks, respectively. Modeling Input Output Major Tier Requirements Parameters Assumptions Tier 1 Tier 3 emission rate, stack height, minimum distance to fenceline emission rate, stack height, minimum distance to fenceline, stack velocity, stack temperature, stack diameter, rural/urban site classification, building dimensions for downwash calculations emission rate, stack height, actual fenceline and release point locations, stack velocity, stack temperature, stack diameter, rural/urban site classification, local meteorological data, receptor locations for concentration predictions, frequency and duration of short-term (intermittent)
From page 577...
... User's Guide to TSCREEN: A Model for Screening Toxic Air Pollutant Concentrations.
From page 578...
... , 1987. Toxic Air Pollutant Source Assessment Manual for California Air Pollution Control District and Applications for Air Pollution Control District Permits, Volumes 1 and 2.
From page 579...
... This network, entitled the OAQPS Technology Transfer Network (TTN) , is comprised of individual bulletin boards that provide information on OAQPS organization, emission measurement methods, regulatory air quality models, emission estimation methods, Clean Air Act Amendments, training courses, and control technology methods.
From page 580...
... 255-7214 E-mail: EPA9663 FAX: FTS 255-2164 Richard L Daye EPA Region VII 726 Minnesota Avenue Kansas City, KS 66101 FTS: 276-7619 Com: (913)
From page 581...
... 581 ' : ~ ,, I ~ r' o o PI ~ Z V ~Lit


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