1 

### Health Effects Information Used In Cancer and Noncancer Risk

Characterization for the 2002 National-Scale Assessment

Introduction

Hazard identification and dose-response asse ssment information for the 2000 nationalscale assessment was obtained from various sources and pr ioritized according to (1)

conceptual consistency with EPA risk assessm ent guidelines and (2) the level of review

received. The prioritization process was aime d at incorporating into our assessment the

best available science with re spect to dose-response informa tion. The following sources

were used.



### US Environmental Protection Agency (EPA)

EPA has developed dose-respons e assessments for chronic exposure to many of the

pollutants in this study. Thes e assessments typically specify a reference concentration, or

RfC (to protect against effects other than canc er) and/or a unit risk estimate, or URE (to

estimate the probability of contracting cancer). The RfC is an estima te, with uncertainty

spanning perhaps an order of magnitude, of an inhalation exposure to the human

population (including sensitive subgr oups) that is likely to be without appreciable risks of

deleterious effects during a lifetime. The URE is the upper-bound excess cancer risk

estimated to result from a lifeti me of continuous exposure to an agent at a concentration

of 1 μg/m 3 

### in air. In assessing a substance’ s carcinogenic potential, EPA evaluates

various types of toxicological data a nd develops a weight-of-evidence (WOE)

determination. Older WOE assessment s use an alphanumeric categorization

(recommended by EPA’s 1986 guidelines for carcinogen risk assessment); assessments

developed since the 2005 revisions to the cancer guidelines (see:

http://cfpub.epa.gov/ncea/raf/ recordisplay.cfm?deid=116283 ) characterize the WOE with

a paragraph of descriptive text.

EPA disseminates dose-response assessment in formation in several forms, depending on

the level of internal review. EPA publis hes dose-response assessments that have

achieved full intra-agency consensus on its In tegrated Risk Information System (IRIS),

which is regularly updated and available on-line at http://www.epa.gov/iris . All IRIS

assessments since 1996 have also under gone external scientific peer review.



### Agency for Toxic Substances a nd Disease Registry (ATSDR)

ATSDR, which is part of the US Department of Health and Huma n Services, develops

and publishes Minimal Risk Levels (MRLs) for many toxic substances. The MRL is

defined as an estimate of daily human exposure to a substance that is lik ely to be without

an appreciable risk of adverse effects (oth er than cancer) over a specified duration of

exposure. MRLs can be deri ved for acute, intermediate, and chronic duration exposures

by the inhalation and oral routes. ATSDR describes MRLs as media-specific2 

### concentrations to be used by health assessors to select e nvironmental contaminants for

further evaluation. MRLs are presented with only 1 significant figure and are considered

concentrations below which contaminants are unlikely to pose a health threat.

Concentrations above an MR L do not necessarily represen t a threat, and MRLs are

therefore not intended fo r use as predictors of adverse he alth effects or for setting cleanup

levels.

Inhalation MRLs were used in the noncancer portion of this assessment when IRIS RfCs

were not available because their concept, definition, and deriva tion are philosophically

consistent (though not iden tical) with the basis for EPA’s RfCs. ATSDR MRLs are

reviewed by an expert panel of external peer s and also by an inte ragency workgroup that

includes EPA. MRLs are published in polluta nt-specific toxicological profile documents,

and also in a table of “comparison values” that ATSDR regularly updates and distributes

(available on-line at http://www.atsdr.cdc.gov/mrls.html ).



### California Office of Environmental Health Hazard Assessment (OEHHA)

The California OEHHA has developed dose-re sponse assessments for many substances,

based both on carcinogenicity and health e ffects other than cancer. The process for

developing these assessments is similar to that used by the EPA to develop IRIS values

and incorporates significant external scientific peer review. The non-cancer information

includes available inhalation health risk guid ance values expressed as chronic inhalation

reference exposure levels (RELs). OEHHA de fines the REL as a concentration level at

(or below) which no health effects are anticip ated, a concept that is substantially similar

to EPA’s non-cancer dose-response assessmen t perspective. This assessment uses

chronic RELs in the same way as RfCs when no IRIS or ATSDR values exist.

OEHHA’s quantitative dose-response informa tion on carcinogenicity by inhalation

exposure is expressed in terms of the URE, defined similarly to EPA’s URE. This

assessment uses specific OEH HA UREs in the same way as EPA’s when no IRIS or

values exist. OEHHA’s dose response info rmation for carcinogens and noncarcinogens

is available on-line at http://www.oehha.ca.gov/air/hot_spots/index.html

.



### US EPA Health Effects A ssessment Tables (HEAST)

HEAST is a comprehensive listi ng consisting almost entirely of provisional UREs, RfCs,

and other risk assessment information fo r chemicals of interest. Although the

assessments summarized in HEAS T have undergone review an d have the concurrence of

individual EPA progr am offices, and each is su pported by an agency reference, they have

not had enough review to be recognized as high-qu ality, EPA-wide consensus

information. Because of these limitations, a nd the fact that HEAST has not been updated

since 1997 and exists only in hard copy (PB9 7-921199), this assessment uses HEAST

information only when no values from the other sources described above are available.3 

### Prioritization of Data Sources

Some substances have been a ssessed for dose-response by more than one of the agencies

used as sources for this anal ysis. Because different scientis ts developed these assessments

at different times for purposes that were simi lar but not identical, it is inevitable that the

results are not totally consistent . In some cases interagency differences were substantial,

especially among assessments done many ye ars apart. To resolve interagency

discrepancies for this analysis, EPA applied a consistent priority scheme to the universe

of dose-response information.

Externally peer-reviewed assessments under development for the IRIS process were

given first priority. These assessments reflect the most recent available toxicity

information and data analysis, and were used in some cases to supersede existing values

on IRIS. Where externally peer reviewed IRIS draft assessmen ts were not available, the

next preferred source was EPA’s IRIS da tabase. For substances lacking IRIS

assessments, ATSDR MRLs (available only for noncancer effect s) received next

preference, followed by OE HHA RELs and UREs.



### Adjustments to Dose-Response Information

Following the prioritization of dose-response information, EPA made the following

adjustments based on professional judgment:

 Oral carcinogens lacking inhalation assessments. For 12 carcinogenic substances,

(benzotrichloride, captan, DDE, dich lorvos, 3,3'-dimethoxybenzidine, 3,3'-

dimethylbenzidine, 1,4-diox ane, isophorone, pentachlo ronitrobenzene, propylene

dichloride, quinoline, and trifluralin) that currently lack inhalation assessments

from the sources described above, oral carcinogenic potency estimates were

converted to inhalation UREs. The convers ion from oral risk (per mg/kg/d oral

intake) to inhalation risk (per μ g/m 3 

### inhaled) was based on EPA’s standard

assumptions of a 70-kg body mass and 20 m 3 

### /d inhalation rate, as follows:

Where: URE = Unit risk estimate for inhalation (risk per μ g/m 3 

### )

CPS = Carcinogenic potency slope for ingestion (risk per mg oral

intake per kg body mass per day)

OAQPS understands that method used for the conversion of oral dose-response

information to inhalation ex posure is a problematic ri sk assessment practice.

However, the alternative to this would ha ve been to omit these substances from

quantitative inhalation risk estima tes altogether, thereby making a de facto 

##    

 

 

 

  

 

 

 

   

 

 

 

        



g mg

d m

kg d kg

mg CPS

m

g URE

 

1000 1 20

70 1 3 1 1

34 

### assumption of zero carcinogenic potency. For the purposes of the national-scale

assessment, OAQPS prefers to use the appr oach described above to screen these

carcinogens for their potential contributions to risk. If a substance is determined

to be a potentially important contributor to risk, it will be prioritized for further

dose-response development th rough EPA’s IRIS process.

 Hexavalent chro mium compounds . The IRIS RfC for particulate hexavalent

chromium was used in preference to the RfC for chromic acid mists and dissolved

aerosols.

 Formaldehyde . EPA no longer considers the fo rmaldehyde URE reported in IRIS,

which is based on a 1987 study, to represent the best available science in the peerreviewed literature. Since that time, si gnificant new data and analyses have

become available. Accordingly, risk es timates for formaldehyde are based on a

dose-response value developed by the CIIT Centers for Health Research (formerly

the Chemical Industry Institute of Toxi cology) and published in 1999. This

assessment incorporates mechanistic and dosimetric information on formaldehyde

that had been accumulated over the past decade, and deve loped a URE using

approaches that are consistent with EPA's guidelines for carcinogenic risk

assessment. EPA had judged that this C IIT modeling effort currently represents

the best application of available mechan istic and dosimetric science on the doseresponse for portal of entry cancers due to formaldehyde exposures. EPA is

currently reviewing the CIIT analysis and other recent information, including

recently published epidemiological st udies, in our reassessment of our

formaldehyde unit risk estimate (URE).

 Glycol ethers . Most of the emission inventory information for the glycol ether

category reports only the total mass for the entire group without distinguishing

between individual glycol ether comp ounds. These individual compounds,

however, vary substantially in toxicity. In order to avoid underestimating the

health hazard associated w ith glycol ethers, EPA has protectively applied the RfC

for ethylene glycol methyl ether (the most toxic for which an a ssessment exists) to

the entire group.

 Diesel emissions . The national-scale assessme nts do not include quantitative

cancer risk estimates for diesel emis sions because EPA has judged that

toxicological data are not yet sufficien t to develop a URE. However, diesel

emissions have been assessed for effects other than cancer, using the 2003 IRIS

RfC.

 Nickel . The IRIS URE for nickel inhalati on shown in Table 1 below was derived

from evidence of the carcinogenic effect s of insoluble nickel compounds in

crystalline form. Soluble nickel species, and insoluble species in amorphous form,

do not appear to produce genotoxic effect s by the same toxic mode of action as5 

### insoluble crystalline nickel. Nickel specia tion information for so me of the largest

nickel-emitting sources (including oil co mbustion, coal combustion, and others)

suggests that at least 35% of total nick el emissions may be soluble compounds.

The remaining insoluble nickel emissions are not well-characterized, however.

Consistent with this limited information, this analysis has conservatively assumed

that 65% of emitted nickel is insoluble, an d that all insoluble nickel is crystalline.

On this basis, the nickel URE (based on nickel subsulfide, and representative of

pure insoluble crystalline nickel) was adju sted to reflect an assumption that 65%

of the total mass of nickel may be car cinogenic. The ATSDR MRL in Table 2

was not adjusted, however, because the non cancer effects of nickel are not thought

to be limited to the crys talline, insoluble form.

 2-Nitropropane. The assessment used a URE of 5.6 x 10-6 per ug/m 3 

### for 2-

nitropropane. This value was derived in 1999 by the Health Council of the

Netherlands (available at: http://www.gr.nl/pdf.php?ID=423&p=1 ), based on

induction of hepatocellular nodules in ra ts, and is consistent with weight-ofevidence determinations by the U.S. National Toxicology Program (“reasonably

anticipated to be a human carcinogen”) and the IARC (“possibly carcinogenic to

humans”).

 Polycyclic organic matter (POM) . The assessment divided POM emissions into

eight categories. The first two categories were assigned a URE equal to 5% of that

for pure benzo[a]pyrene (the same assump tion that the 1996 assessment used for

all POM data). Categories 3-7 were compos ed of emissions that were reported as

individual compounds. These compounds were placed in the category with an

appropriate URE. Category 8, composed of unspeciated carcinogenic polynuclear

aromatic hydrocarbons (a subset of POM called 7-PAH), was assigned a URE

equal to 18% of that for pure benzo[a]pyr ene. Details on the development of the

5% and 18% URE estimates are available here:

http://www.epa.gov/ttn/a tw/sab/appendix-h.pdf

.

The process of URE estimation includes the following important sources of

uncertainty:

 Many of the substances in this asse ssment were classified as probable

carcinogens, indicating that data were not sufficient to prove these substances

definitely cause cancer in humans. It is possible that some of these substances

are not human carcinogens at environmenta lly relevant doses, and that the true

risk associated w ith them is zero.

 All UREs used in this assessment were based on linear extrapolation from high

to low doses. To the ex tent that true dose-respon se relationships for some

substances are nonlinear, this assumpti on may result in significant over- or

underestimates of risk.6 

###  UREs for most of these substances we re developed from animal data using

conservative methods to extrapolate betw een species. Actual human responses

may differ from the predicted ones.

 Most UREs used in this assessment (typically, those based on animal data)

were based on the statistical upper confidence limit (UCL) of the fitted doseresponse curve. That means true risk would probably be less, but could be

greater. A few (typically, those base d on human data) were based on the

statistical best fit (“maximum likeliho od estimate,” or MLE). UREs based on

the MLE are identified in a footnote to Table 1. This difference between UCLand MLE-based assessments results in some UREs that are somewhat less

conservative than the rest.



### Table 1: Dose-Responses Values

This table lists includes dose-response values and supporting informa tion for both cancer

and noncancer effects used in the 2002 national-scale as sessment. The EPA weight-ofevidence (WOE) categories charact erize the extent to which available data support the

hypothesis that a pollutant causes cancer in humans. The EPA carcinogen categories are

Group A—known, Group B1—probable, base d on incomplete huma n data, Group B2—

probable, based on adequate animal data, Group C—possible, Group D—not classifiable,

and Group E—evidence of non-carcinogenic ity. The URE is the upper bound risk

estimate of cancer risk from a lifetime exposur e to a concentration of 1 microgram per

cubic meter. The “RfC” column lists referen ce concentrations and similar values (i.e.,

RELs, MRLs) that were used in this assessme nt. The reference concentration (RfC) is an

estimate, with uncertainty sp anning perhaps an order of magnitude, of an inhalation

exposure to the human population (including sensitive subgr oups) that is likely to be

without appreciable risks of deleterious e ffects during a lifetime. The “target system”

columns show up to three organs or organ system adversely a ffected at the lowest dose in

human or animal studies, but only the resp iratory and neurological endpoints were

assessed in the 2002 NATA b ecause these two endpoints were identified as the noncancer

drivers in previous NATA assessments. Ot her information on indivi dual substances is

shown in footnotes.7Chemical NameCAS No.EPAWOEURE(μg/m3)-1URESourceRfC1(mg/m3)RfCSourceTargetSystem 114TargetSystem 214TargetSystem 314Acetaldehyde 75070 B2 0.000002 IRIS 0.009 IRIS RespiratoryAcetamide 60355 0.00002 CALAcetonitrile 75058 D 0.06 IRIS Whole bodyAcrolein 107028 0.00002 IRIS RespiratoryAcrylamide 79061 B2 0.0013 IRIS 0.0007 PCAL2NeurologicalAcrylic acid 79107 0.001 IRIS RespiratoryAcrylonitrile 107131 B1 0.000068 IRIS 0.002 IRIS RespiratoryAllyl chloride 107051 C 0.000006 CAL 0.001 IRIS Neurological4-Aminobiphenyl 92671Aniline 62533 B2 0.0000016 CAL 0.001 IRIS Spleeno-Anisidine 90040Antimony compounds 7440360 0.00023IRIS RespiratoryArsenic compounds 7440382 A 0.0043 IRIS 0.00003 CAL DevelopmentalArsine 7784421 0.00005 IRIS HematologicalBenzene 71432 A 0.0000078 IRIS 0.03 IRIS ImmunologicalBenzidine 92875 A 0.10724IRIS 0.01 PCAL2Neurological LiverBenzotrichloride 98077 B2 0.0037 Conv. Oral5Benzyl chloride 100447 B2 0.000049 CALBiphenyl 92524 DBeryllium compounds 7440417 B1 0.0024 IRIS 0.00002 IRIS RespiratoryBis(2-ethylhexyl) phthalate 117817 B2 0.0000024 CAL 0.01 PCAL2Respiratory LiverBis(chloromethyl) ether 542881 A 0.062 IRISBromoform 75252 B2 0.0000011 IRIS1,3-Butadiene 106990 A 0.00003 IRIS 0.002 IRIS ReproductiveCalcium cyanamide 156627Cadmium compounds 7440439 B1 0.0018 IRIS 0.00002 CAL KidneyCaptan 133062 B2 0.000001 Conv. Oral5Carbaryl 63252Carbon disulfide 75150 0.7 IRIS NeurologicalCarbon tetrachloride 56235 B2 0.000015 IRIS 0.19 ATSDR LiverCarbonyl sulfide 4635811Includes EPA reference concentrations (RfCs) and similar values, i.e., California OEHHA reference exposure levels (RELs), andATSDR minimum risk levels (MRLs). Many ofthese chemicals are under review for the development of RfCs. Acurrent status report for all EPA assessments is available athttp://cfpub.epa.gov/iristrac/index.cfm.2Proposed by California OEHHA; not yet adopted in final form.3RfC used for antimony compounds is derived from RfC for antimony trioxide.4Includes age-related adjustment factor (1.6 x) to account for early childhood exposures to a known mutagenic agent. See document athttp://www.epa.gov/ttn/atw/childrens_supplement_final.pdffor further details.5Conversion of oral potency slope to inhalation unit risk estimate was based on the following assumptions: (1) whole-life, continuous exposure, (2) inhalation rate of 20 cubicmeters of air per day, and (3) body mass of 70 kg. Further details are provided in the text above.8Chemical NameCAS No.EPAWOEURE(μg/m3)-1URESourceRfC1(mg/m3)RfCSourceTargetSystem 114TargetSystem 214TargetSystem 314Catechol 120809Chlordane 57749 B2 0.0001 IRIS 0.0007 IRIS LiverChlorine 7782505 0.0002 CAL RespiratoryChloroacetic acid 791182-Chloroacetophenone 5322740.00003 IRIS RespiratoryChlorobenzene 108907 1 CAL Reproductive Kidney LiverChlorobenzilate 510156 B2 0.000078 HEASTChloroform 67663 B2 0.098 ATSDR LiverChloromethyl methyl ether 107302 AChloroprene 126998 0.007 HEAST RespiratoryChromium VI compounds 18540299 A 0.012 IRIS 0.0001 IRIS RespiratoryCobalt compounds 7440484 0.0001 ATSDR RespiratoryCoke Oven Emissions 8007452 A 0.00062IRISCresols (mixed) 1319773 C 0.6 CAL Neurological Whole body0-cresol695487 0.6 OAQPS Neurologicalm-cresol6108394 0.6 OAQPS Neurologicalp-cresol6106445 0.6 OAQPS NeurologicalCumene 98828 D 0.4 IRIS Kidney Endocrine2,4-d, salts and esters 94757DDE 72559 B2 0.000097 Conv. Oral5Diazomethane 334883Dibenzofurans 132649 DCyanide compounds 57125 D 0.0037IRIS Neurological Thyroid1,2-Dibromo-3-chloropropane 96128 B2 0.002 CAL 0.0002 IRIS ReproductiveDibutylphthalate 84742 Dp-Dichlorobenzene 106467 C 0.000011 CAL 0.8 IRIS Liver3,3'-Dichlorobenzidine 91941 B2 0.00034 CALDichloroethyl ether 111444 B2 0.00033 IRIS1,3-Dichloropropene 542756 B2 0.000004 IRIS 0.02 IRIS RespiratoryDichlorvos 62737 B2 0.000083 Conv. Oral50.0005 IRIS NeurologicalDiesel emissions 0.005 IRIS RespiratoryDiethanolamine 111422 0.003 CAL RespiratoryN,N-Dimethyl aniline 121697Diethyl sulfate 646753,3'-Dimethoxybenzidine 119904 B2 0.000004 Conv. Oral5p-Dimethylaminoazobenzene 60117 0.0013 CAL3,3'-Dimethylbenzidine 119937 B2 0.0026 Conv. Oral56The individual cresol and xylene isomers were modeled separately if their emissions were reported separately, and hazard quotients were generated for each isomer using the RfCfor their mixture. The final NATA results present their resultscombined under the HAP category of ‘cresol or xylene mixture’.7The RfC used is from the HAP, hydrogen cyanide.9Chemical NameCAS No.EPAWOEURE(μg/m3)-1URESourceRfC1(mg/m3)RfCSourceTargetSystem 114TargetSystem 214TargetSystem 314Dimethyl carbamoyl chloride 79447Dimethylformamide 68122 0.03 IRIS Liver1,1-Dimethylhydrazine 57147Dimethyl phthalate 131113 DDimethyl sulfate 77781 B24,6-Dinitro-o-cresol and salts 5345212,4-Dinitrophenol 512852,4-Dinitrotoluene 121142 B2 0.000089 CAL 0.007 PCAL2Liver Neurological1,4-Dioxane 123911 B2 0.0000077 CAL 3 CAL Liver Hematological Kidney1,2-Diphenylhydrazine 122667 B2 0.00022 IRISEpichlorohydrin 106898 B2 0.0000012 IRIS 0.001 IRIS Respiratory1,2-Epoxybutane 106887 0.02 IRIS RespiratoryEthyl acrylate 140885 B2Ethylbenzene 100414 D 1 IRIS DevelopmentalEthyl carbamate 51796 0.000464CALEthyl chloride 75003 10 IRIS DevelopmentalEthylene dibromide 106934 B2 0.0006 IRIS 0.009 IRIS RespiratoryEthylene dichloride 107062 B2 0.000026 IRIS 2.4 ATSDR LiverEthylene glycol 107211 0.4 CAL RespiratoryEthylene imine 151564Ethylene oxide 75218 B1 0.000088 CAL 0.03 CAL NeurologicalEthylene thiourea 96457 B2 0.000013 CAL 0.003 PCAL2EndocrineEthylidene dichloride 75343 C 0.0000016 CAL 0.5 HEAST KidneyFormaldehyde 50000 B1 5.5e-9 OAQPS 0.0098 ATSDR RespiratoryHeptachlor 76448 B2 0.0013 IRISGlycol ether compounds 0.028OAQPS ReproductiveHexachlorobenzene 118741 B2 0.00046 IRIS 0.003 PCAL2LiverHexachlorobutadiene 87683 C 0.000022 IRIS 0.09 PCAL2ReproductiveHexachlorocyclopentadiene 77474 E 0.0002 IRIS RespiratoryHexachloroethane 67721 C 0.000004 IRIS 0.08 PCAL2Kidney Liver NeurologicalHexamethylene-1,6-diisocyanate 822060 0.00001 IRIS Respiratoryn-Hexane 110543 0.7 IRIS Neurological RespiratoryHydrazine 302012 B2 0.0049 IRIS 0.0002 CAL Liver ThyroidHydrochloric acid 7647010 0.02 IRIS RespiratoryHydrofluoric acid 7664393 0.014 CAL SkeletalHydroquinone 1233198This RfC is for ethylene glycol methyl ether, the most toxicof this group for which an assessment exists. See note in textabove for a more complete explanation.10Chemical NameCAS No.EPAWOEURE(μg/m3)-1URESourceRfC1(mg/m3)RfCSourceTargetSystem 114TargetSystem 214TargetSystem 314Isophorone 78591 C 2.7e-7 Conv. Oral52 CAL Liver DevelopmentalLead compounds 7439921 B2 0.000159OAQPS NeurologicalLindane (all isomers) 0.00031 IRIS 0.0003 PCAL2Kidney Liver ReproductiveMaleic anhydride 108316 0.0007 CAL RespiratoryManganese compounds 7439965 D 0.00005 IRIS NeurologicalMercury compounds C 0.0003 IRIS NeurologicalMethanol 67561 4 CAL DevelopmentalMethoxychlor 72435 DMethyl bromide 74839 D 0.005 IRIS RespiratoryMethyl chloride 74873 D 0.09 IRIS NeurologicalMethyl isobutyl ketone 108101 3 IRIS DevelopmentalMethyl iodide 74884Methyl Hydrazine 60344Methyl isocyanate 624839 0.001 CAL Respiratory Whole bodyMethyl methacrylate 80626 E 0.7 IRIS RespiratoryMethyl tert-butyl ether 1634044 2.6e-7 CAL 3 IRIS Liver Kidney Ocular4,4'-Methylene bis(2-chloroaniline) 101144 B2 0.00043 CALMethylene chloride 75092 B2 4.7e-7 IRIS 1 ATSDR LiverMethylene diphenyl diisocyanate 101688 D 0.0006 IRIS Respiratory4,4'-Methylenedianiline 101779 0.00046 CAL 0.02 CAL OcularNaphthalene 91203 C 0.000034 CAL 0.003 IRIS RespiratoryNickel compounds A 0.00031210OAQPS 0.00009 D- ATSDR Respiratory ImmunologicalNitrobenzene 98953 C 0.00004 IRIS 0.009 IRIS Respiratory4-Nitrobiphenyl 929334-Nitrophenol 1000272-Nitropropane 79469 B2 0.0000056 OAQPS 0.02 IRIS LiverNitrosodimethylamine 62759 B2 0.014 IRISN-Nitrosomorpholine 59892 0.0019 CALParathion 56382 CPCB Group 1336363 B2 0.0001 IRISPentachloronitrobenzene 82688 C 0.000074 Conv. Oral5Pentachlorophenol 87865 B2 0.0000051 CAL 0.1 PCAL2Liver KidneyPhenol 108952 D 0.2 CAL Liverp-Phenylenediamine 106503Phosgene 75445 0.0003 IRIS RespiratoryPhosphine 7803512 D 0.0003 IRIS Whole bodyPhosphorus 77231409EPA has not developed an RfC for lead. The value shown is the quarterly National Ambient Air Quality Standard for lead, whichEPA believes to be without significant adverseeffects.10The URE used is derived by assuming 65% of the nickel subsulfide URE. See note in text above for a more complete explanation.11Chemical NameCAS No.EPAWOEURE(μg/m3)-1URESourceRfC1(mg/m3)RfCSourceTargetSystem 114TargetSystem 214TargetSystem 314Phthalic anhydride 85449 0.02 CAL Respiratory OcularPolycyclic organic matter11group 1120.0000884OAQPSPolycyclic organic matter group 2120.0000884,14OAQPSPolycyclic organic matter group 3120.164,14OAQPSPolycyclic organic matter group 4120.0164,14OAQPSPolycyclic organic matter group 5120.00164,14OAQPSPolycyclic organic matter group 6120.000164,14OAQPSPolycyclic organic matter group 7120.0000164,14OAQPSPolycyclic organic matter group 8120.000324,14OAQPS1,3-Propane sultone 1120714 0.00069 CALbeta-Propiolactone 57578Priopionaldehyde 123386 0.008 IRIS RespiratoryPropoxur 114261Propylene dichloride 78875 B2 0.000019 Conv. Oral50.004 IRIS RespiratoryPropylene oxide 75569 B2 0.0000037 IRIS 0.03 IRIS Respiratory1,2-Propylenimine 75558Quinoline 91225 B2Quinone 106514Selenium compounds 7782492 D 0.02 CAL Neurological Liver HematologicalStyrene 100425 1 IRIS NeurologicalStyrene oxide 96093 0.006 PCAL2Respiratory1,1,2,2-Tetrachloroethane 79345 C 0.000058 IRISPerchloroethylene 127184 B2C 0.0000059 CAL 0.27 ATSDR NeurologicalTitanium tetrachloride 7550450 0.0001 ATSDR RespiratoryToluene 108883 D 5.0 IRIS Respiratory Neurological2,4-Toluene diamine 95807 B2 0.0011 CAL2,4-Toluene diisocyanate 26471625 0.000011 CAL 0.00007 IRIS Respiratoryo-Toluidine 95534 B2 0.000051 CALToxaphene 8001352 B2 0.00032 IRIS1,2,4-Trichlorobenzene 120821 D 0.2 HEAST Liver1,1,2-Trichloroethane 79005 C 0.000016 IRIS 0.4 PCAL2Liver1,1,1-Trichloroethane 71556 D 1 CAL NeurologicalTrichloroethylene 79016 B2C 0.000002 CAL 0.6 CAL Neurological Ocular2,4,5-Trichlorophenol 959542,4,6-Trichlorophenol 88062 B2 0.0000031 IRISTriethylamine 121448 0.007 IRIS RespiratoryTrifluralin 1582098 C 0.0000022 Conv. Oral52,2,4-Trimethylpentane 54084111A full discussion of the risk assessment for polycyclic organic matter is available at: http://www.epa.gov/ttn/atw/sab/appendix-h.pdf.12EPA WOE varies among individual compounds.12Chemical NameCAS No.EPAWOEURE(μg/m3)-1URESourceRfC1(mg/m3)RfCSourceTargetSystem 114TargetSystem 214TargetSystem 314Vinyl acetate 1080540.2 IRIS RespiratoryVinyl bromide 593602 B2 0.000032 HEAST 0.003 IRIS LiverVinyl chloride 75014 A 0.0000088 IRIS130.1 IRIS LiverVinylidene chloride 75354 C 0.2 IRIS LiverXylenes (mixed) 1330207 0.1 IRIS Neurologicalo- Xylene695476 0.1 IRIS Neurologicalm-Xylene6108383 0.1 IRIS NeurologicalP-Xylene6106423 0.1 IRIS Neurological13URE based on whole life exposure was selected over a URE based on adult exposure only.14Multiple target organs listed if the concentration at the “critical effect” is the same at all targets.