November 7, 2005 

Health Effects Information Used In Cancer and Noncancer Risk Charac

For the 1999 National-Scale Assessment 

Introduction Hazard identification and dose-response assessment information for the 1999 national-scale assessment wa

sources and prioritized according to (1) conceptual consistency with EPA risk assessment guidelines and (2received. The prioritization process was aimed at incorporating into our assessment the best available scien

response information. The following sources were used. 

US Environmental Protection Agency (EPA) EPA has developed dose-response assessments for chronic exposure to many of the pollutants in this studytypically specify a reference concentration, or RfC (to protect against effects other than cancer) and/or a un

(to estimate the probability of contracting cancer). The RfC is an estimate, with uncertainty spanning perh

magnitude, of an inhalation exposure to the human population (including sensitive subgroups) that is likely appreciable risks of deleterious effects during a lifetime. The URE is the upper-bound excess cancer risk e

lifetime of continuous exposure to an agent at a concentration of 1 μg/m3 in air. In assessing a substance’s 

EPA evaluates various types of toxicological data and develops a weight-of-evidence (WOE) determinationassessments use an alphanumeric categorization (recommended by EPA’s 1986 guidelines for carcinogen r

assessments developed since 2002 characterize the WOE with a paragraph of descriptive text (recommende

revisions to the 1986 guidelines). EPA disseminates dose-response assessment information in several forms, depending on the level of intern

publishes dose-response assessments that have achieved full intra-agency consensus on its Integrated Risk 

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

undergone external scientific peer review. 
November 7, 2005 

Agency for Toxic Substances and Disease Registry (ATSDR) ATSDR, which is part of the US Department of Health and Human Services, develops and publishes Minim

for many toxic substances. The MRL is defined as an estimate of daily human exposure to a substance thaan appreciable risk of adverse effects (other than cancer) over a specified duration of exposure. MRLs can 

intermediate, and chronic duration exposures by the inhalation and oral routes. ATSDR describes MRLs aconcentrations to be used by health assessors to select environmental contaminants for further evaluation. with only 1 significant figure and are considered concentrations below which contaminants are unlikely to Concentrations above an MRL do not necessarily represent a threat, and MRLs are therefore not intended f

adverse health effects or for setting cleanup levels. Inhalation MRLs were used in the noncancer portion of this assessment when IRIS RfCs were not available definition, and derivation are philosophically consistent (though not identical) with the basis for EPA’s RfCreviewed by an expert panel of external peers and also by an interagency workgroup that includes EPA. M

pollutant-specific toxicological profile documents, and also in a table of “comparison values” that ATSDR 

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-response assessments for many substances, based both on carceffects other than cancer. The process for developing these assessments is similar to that used by the EPA tand incorporates significant external scientific peer review. The non-cancer information includes available 

guidance values expressed as chronic inhalation reference exposure levels (RELs). OEHHA defines the RElevel at (or below) which no health effects are anticipated, a concept that is substantially similar to EPA’s n

response assessment perspective. This assessment uses chronic RELs in the same way as RfCs when no IR

exist. OEHHA’s quantitative dose-response information on carcinogenicity by inhalation exposure is expressed i

defined similarly to EPA’s URE. This assessment uses specific OEHHA UREs in the same way as EPA’s exist. OEHHA’s dose response information for carcinogens and noncarcinogens is available on-line at 

http://www.oehha.ca.gov/air/hot_spots/index.html. 
November 7, 2005 

US EPA Health Effects Assessment Tables (HEAST) HEAST is a comprehensive listing consisting almost entirely of provisional UREs, RfCs, and other risk ass

chemicals of interest. Although the assessments summarized in HEAST have undergone review and have individual EPA program offices, and each is supported by an agency reference, they have not had enough r

as high-quality, EPA-wide consensus information. Because of these limitations, and the fact that HEAST h

since 1997 and exists only in hard copy (PB97-921199), this assessment uses HEAST information only whother sources described above are available. 

International Agency for Research on Cancer (IARC) The IARC, a branch of the World Health Organization, coordinates and conducts research on the causes of develops scientific strategies for cancer control. The IARC sponsors both epidemiological and laboratory r

disseminates scientific information through meetings, publications, courses and fellowships. As part of its mission, the IARC assembles evidence that substances cause cancer in humans and issues jud

of evidence. IARC’s “degrees of evidence” categories are Group 1 (carcinogenic in humans), Group 2A (pGroup 2B (possibly carcinogenic), Group 3 (not classifiable), and Group 4 (probably not carcinogenic). Th

may be applied to either single chemicals or mixtures. The IARC does not develop quantitative dose-respoUREs, however. IARC’s degrees of evidence for substances are included as supporting information for this assessment as a determinations, which do not cover all substances and in some cases may be out-of-date. The list of IARC available at http://monographs.iarc.fr/monoeval/grlist.html. 

Prioritization of Data Sources Some substances have been assessed for dose-response by more than one of the agencies used as sources fodifferent scientists developed these assessments at different times for purposes that were similar but not ide
November 7, 2005 

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

done many years apart. To resolve interagency discrepancies for this analysis, EPA applied a consistent pr

universe of dose-response information. Externally peer-reviewed assessments under development for the IRIS process were given first priority. Ththe most recent available toxicity information and data analysis, and were used in some cases to supersede 

Where externally peer reviewed IRIS draft assessments were not available, the next preferred source was EFor substances lacking IRIS assessments, ATSDR MRLs (available only for noncancer effects) received ne

by OEHHA RELs and UREs. 

Adjustments to Dose-Response Information Following the prioritization of dose-response information, EPA made the following adjustments based on p

• Oral carcinogens lacking inhalation assessments. For 13 carcinogenic substances, (benzotrichlorid

dichlorvos, 3,3'-dimethoxy benzidine, 3,3'-dimethylbenzidine, 1,4-dioxane, ethyl acrylate, isophoron

pentachloronitrobenzene, propylene dichloride, quinoline, and trifluralin) that currently lack inhalatisources described above, oral carcinogenic potency estimates were converted to inhalation UREs. T

risk (per mg/kg/d oral intake) to inhalation risk (per μg/m3 inhaled) was based on EPA’s standard as

body mass and 20 m3/d inhalation rate, as follows: 

Where: URE = Unit risk estimate for inhalation (risk per μg/m3) 

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

EPA understands that conversion of oral dose-response information to inhalation exposure is a prob

practice. However, the alternative to this would have been to omit these substances from quantitativ

estimates altogether, thereby making a de facto assumption of zero carcinogenic potency. For the pu

( )   ×  × ×   ⋅  =   − − g mg dm kg d kg mg CPS mg URE μ μ 1000 1 20 701 3 1 1 3
November 7, 2005 

scale assessment, EPA prefers to use the approach described above to screen these carcinogens for tcontributions to risk. If a substance is determined to be a potentially important contributor to risk, it 

further dose-response development through EPA’s IRIS process. 

• Hexavalent chromium compounds. The IRIS RfC for particulate hexavalent chromium was used in 

for chromic acid mists and dissolved aerosols. 

• Formaldehyde. EPA no longer considers the formaldehyde URE reported in IRIS, which is based o

represent the best available science in the peer-reviewed literature. Since that time, significant new d

become available. Accordingly, the 1999 risk estimates for formaldehyde are based on a dose-respo

the CIIT Centers for Health Research (formerly the Chemical Industry Institute of Toxicology) and 

assessment incorporates mechanistic and dosimetric information on formaldehyde that had been accdecade, and developed a URE using approaches that are consistent with EPA's guidelines for carcin

EPA had judged that this CIIT modeling effort currently represents the best application of available dosimetric science on the dose-response for portal of entry cancers due to formaldehyde exposures. reviewing the CIIT analysis and other recent information, including recently published epidemiolog

reassessment of our formaldehyde unit risk estimate (URE). 

• Glycol ethers. Most of the emission inventory information for the glycol ether category reports only 

entire group without distinguishing between individual glycol ether compounds. These individual cvary substantially in toxicity. In order to avoid underestimating the health hazard associated with gl

protectively applied the RfC for ethylene glycol methyl ether (the most toxic for which an assessme

group. 

• Diesel emissions. The 1999 national-scale assessment, as with the 1996 assessment, does not includ

risk estimates for diesel emissions because EPA has judged that toxicological data are not yet suffic

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

available for the 1996 assessment). 
November 7, 2005 

• Nickel. The IRIS URE for nickel inhalation shown in Table 1 below was derived from evidence of t

of insoluble nickel compounds in crystalline form. Soluble nickel species, and insoluble species in 

appear to produce genotoxic effects by the same toxic mode of action as insoluble crystalline nickel

information for some of the largest nickel-emitting sources (including oil combustion, coal combustsuggests that at least 35% of total nickel emissions may be soluble compounds. The remaining insoare not well-characterized, however. Consistent with this limited information, this analysis has cons65% of emitted nickel is insoluble, and that all insoluble nickel is crystalline. On this basis, the nick

subsulfide, and representative of pure insoluble crystalline nickel) was adjusted to reflect an assump

total mass of nickel may be carcinogenic. The ATSDR MRL in Table 2 was not adjusted, however, 

effects of nickel are not thought to be limited to the crystalline, insoluble form. 

• 2-Nitropropane. The assessment used a URE of 5.6 x 10-6 per ug/m3 for 2-nitropropane. This valu

by the Health Council of the Netherlands (available at: http://www.gr.nl/pdf.php?ID=423&p=1), ba

hepatocellular nodules in rats, and is consistent with weight-of-evidence determinations by the U.S. 

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

• Polycyclic organic matter (POM). The assessment divided POM emissions into eight categories. T

were assigned a URE equal to 5% of that for pure benzo[a]pyrene (the same assumption that the 199

all POM data). Categories 3-7 were composed of emissions that were reported as individual compo

were placed in the category with an appropriate URE. Category 8, composed of unspeciated carcino

aromatic hydrocarbons (a subset of POM called 7-PAH), was assigned a URE equal to 18% of that fDetails on the development of the 5% and 18% URE estimates are available here: http://www.epa.g

h.pdf. 

The process of URE estimation includes the following important sources of uncertainty: 

• Many of the substances in this assessment were classified as probable carcinogens, indicating tha

sufficient to prove these substances definitely cause cancer in humans. It is possible that some o

not human carcinogens at environmentally relevant doses, and that the true risk associated with t
November 7, 2005 

• All UREs used in this assessment were based on linear extrapolation from high to low doses. To 

dose-response relationships for some substances are nonlinear, this assumption may result in signunderestimates of risk. 

• UREs for most of these substances were developed from animal data using conservative method

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 sta

confidence limit (UCL) of the fitted dose-response curve. That means true risk would probably greater. A few (typically, those based on human data) were based on the statistical best fit (“max

estimate,” or MLE). UREs based on the MLE are identified in a footnote to Table 1. This differeMLE-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 information for both cancer and noncancer ef

national-scale assessment. The EPA and IARC weight-of-evidence (WOE) categories characterize the exte

data support the hypothesis that a pollutant causes cancer in humans. The EPA carcinogen categories are GGroup B1—probable, based on incomplete human data, Group B2—probable, based on adequate animal da

Group D—not classifiable, and Group E—evidence of non-carcinogenicity. The IARC categories are Grouhumans, Group 2A—probably carcinogenic, Group 2B—possibly carcinogenic, Group 3—not classifiable, 

not carcinogenic. The URE is the upper bound risk estimate of cancer risk from a lifetime exposure to a co

microgram per cubic meter. The “RfC” column lists reference concentrations and similar values (i.e., RELused in the initial 1996 national-scale assessment. The reference concentration (RfC) is an estimate, with u

perhaps an order of magnitude, of an inhalation exposure to the human population (including sensitive subgbe without appreciable risks of deleterious effects during a lifetime. The “target system” columns show up 

system adversely affected at the lowest dose in human or animal studies. Other information on individual s

footnotes. 
November 7, 2005 

Chemical Name CAS No.

EPA 

WOE

IARC 

WOE 

URE 

(  g/m3)-1

URE 

Source 

URE 

Date 

RfC1

(mg/m3)

RfC 

Source 

RfC 

Date 

Target 

System 1 

Acetaldehyde2 75070 B2 2B 0.000002 IRIS 1997 0.009 IRIS 1991 Respiratory Acetamide 60355 2B 0.00002 CAL 1999Acetonitrile 75058 D 0.06 IRIS 1999 Whole body Acrolein2 107028 3 0.00002 IRIS 2003 Respiratory Acrylamide2 79061 B2 2A 0.0013 IRIS 1997 0.0007 PCAL3 1997 Neurological Acrylic acid 79107 0.001 IRIS 1995 Respiratory Acrylonitrile2 107131 B1 2A 0.000068 IRIS 1991 0.002 IRIS 1997 Respiratory Allyl chloride 107051 C 3 0.000006 CAL 1999 0.001 IRIS 1991 Neurological Aniline 62533 B2 3 0.000001 CAL 1999 0.001 IRIS 1991 Spleen Antimony compounds 0.0002 IRIS 1995 Respiratory Arsenic2 7440382 A 1 0.0043 IRIS4 1997 0.00003 CAL 2000 DevelopmentalArsine 7784421 0.00005 IRIS 1994 HematologicalBenzene 71432 A 1 0.000007 IRIS4 2000 0.03 IRIS 2003 ImmunologicalBenzidine 92875 A 0.067 IRIS 1992 0.01 PCAL3 1997 Neurological Benzotrichloride 98077 B2 2B 0.0037 Conv. 

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Benzyl chloride 100447 B2 2B 0.000049 CAL 1999Beryllium compounds2 B1 1 0.0024 IRIS 1998 0.00002 IRIS 1998 Respiratory Bis(2-ethylhexyl) phthalate2 117817 B2 2B 0.000002 CAL 1999 0.01 CAL 1999 Respiratory Bis(chloromethyl) ether 542881 A 1 0.062 IRIS 1997Bromoform2 75252 B2 3 0.000001 IRIS 19971,3-Butadiene 106990 A 2A 0.00003 IRIS 2002 0.002 IRIS 2002 Reproductive Cadmium compounds2 B1 1 0.0018 IRIS 1992 0.00002 CAL 2000 Kidney Captan 133062 B2 3 0.000001 Conv. 

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Carbon disulfide 75150 0.7 IRIS 1995 Neurological Carbon tetrachloride2 56235 B2 2B 0.000015 IRIS 1991 0.04 CAL 2000 Liver Chlordane 57749 B2 2B 0.0001 IRIS 1998 0.0007 IRIS 1998 Liver 1 Includes EPA reference concentrations (RfCs) and similar values, i.e., California OEHHA reference exposure levels (RELs), and ATSDR 2 EPA is currently developing a new dose-response assessment for this chemical. This situation will change as these assessments are comp

assessments for other substances. A current status report for all EPA assessments is available at http://cfpub.epa.gov/iristrac/index.cfm. 

3 Proposed by California OEHHA; not yet adopted in final form. 4 Maximum likelihood URE. 5 Conversion of oral potency slope to inhalation unit risk estimate was based on the following assumptions: (1) whole-life, continuous expo

cubic meters of air per day, and (3) body mass of 70 kg. Further details are provided in the text, above. 
November 7, 2005 

Chemical Name CAS No.

EPA 

WOE

IARC 

WOE 

URE 

(  g/m3)-1

URE 

Source 

URE 

Date 

RfC1

(mg/m3)

RfC 

Source 

RfC 

Date 

Target 

System 1 

Chlorine 7782505 0.0002 CAL 2000 Respiratory 2-Chloroacetophenone 532274 0.00003 IRIS 1991 Respiratory Chlorobenzene 108907 1 CAL 2000 Reproductive Chlorobenzilate 510156 B2 0.000078 HEAST 1997Chloroform2 67663 B2 2B 0.098 ATSDR 1998 Liver Chloroprene2 126998 0.007 HEAST 1997 Respiratory Chromium VI compounds A 1 0.012 IRIS4 1998 0.0001 IRIS 1998 Respiratory Cobalt compounds2 7440484 0.0001 ATSDR 2001 Respiratory Coke Oven Emissions 8007452 A 0.00062 IRIS 1991Cresols (mixed) 1319773 C 0.6 CAL 2000 Neurological Cumene 98828 D 0.4 IRIS 1997 Kidney Cyanide compounds2 D 0.003 IRIS 1994 Neurological 1,2-Dibromo-3-chloropropane 96128 B2 0.002 CAL 1999 0.0002 IRIS 1991 Reproductive p-Dichlorobenzene2 106467 C 2B 0.000011 CAL 1999 0.8 IRIS 1994 Liver 3,3'-Dichlorobenzidine 91941 B2 2B 0.00034 CAL 1999Dichloroethyl ether 111444 B2 0.00033 IRIS 19971,3-Dichloropropene 542756 B2 2B 0.000004 IRIS 2000 0.02 IRIS 2000 Respiratory Dichlorvos 62737 B2 2B 0.000083 Conv. 

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2004 0.0005 IRIS 1994 Neurological 

Diesel emissions B1 0.005 IRIS 2003 Respiratory Diethanolamine 111422 0.003 CAL 2001 Respiratory 3,3'-Dimethoxy benzidine 119904 B2 2B 0.000004 Conv. 

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p-Dimethylamino azobenzene 60117 2B 0.0013 CAL 19993,3'-Dimethylbenzidine 119937 B2 0.0026 Conv. 

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Dimethyl formamide 68122 2B 0.03 IRIS 1999 Liver 2,4-Dinitrotoluene 121142 B2 2B 0.000089 CAL 1997 0.007 PCAL3 1997 Liver 1,4-Dioxane2 123911 B2 2B 0.000003 Conv. 

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2004 3 CAL 2000 Liver 

1,2-Diphenylhydrazine 122667 B2 0.00022 IRIS 1991Epichlorohydrin 106898 B2 2A 0.000001 IRIS 1997 0.001 IRIS 1992 Respiratory 1,2-Epoxybutane 106887 0.02 IRIS 1992 Respiratory Ethyl acrylate 140885 B2 2B 0.000014 Conv. 

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Chemical Name CAS No.

EPA 

WOE

IARC 

WOE 

URE 

(  g/m3)-1

URE 

Source 

URE 

Date 

RfC1

(mg/m3)

RfC 

Source 

RfC 

Date 

Target 

System 1 

Ethylbenzene2 100414 D 1 IRIS 1991 DevelopmentalEthyl carbamate 51796 2B 0.00029 CAL 1999Ethyl chloride 75003 10 IRIS 1991 DevelopmentalEthylene dibromide 106934 B2 2A 0.00022 IRIS 1997 0.0008 CAL 2001 Reproductive Ethylene dichloride2 107062 B2 2B 0.000026 IRIS 1997 2.4 ATSDR 2001 Liver Ethylene glycol 107211 0.4 CAL 2000 Respiratory Ethylene oxide2 75218 B1 1 0.000088 CAL 2004 0.03 CAL 2000 Neurological Ethylene thiourea 96457 B2 2B 0.000013 CAL 1999 0.003 PCAL3 1997 Endocrine Ethylidene dichloride 75343 C 0.000001 CAL 1999 0.5 HEAST 1992 Kidney Formaldehyde2 50000 B1 2A 5.5e-9 EPA 

OAQPS 

2004 0.0098 ATSDR 1999 Respiratory 

Glycol ether compounds2 0.02 EPA 

OAQPS 

2000 Reproductive 

Hexachlorobenzene 118741 B2 2B 0.00046 IRIS 1997 0.003 PCAL3 1997 Liver Hexachlorobutadiene2 87683 C 3 0.000022 IRIS 1997 0.09 PCAL3 1997 Reproductive Hexachlorocyclopentadiene2 77474 E 0.0002 IRIS 2001 Respiratory Hexachloroethane 67721 C 3 0.000004 IRIS 1997 0.08 PCAL3 1997 Kidney Hexamethylene-1,6-diisocyanate 

822060 0.00001 IRIS 1994 Respiratory 

n-Hexane2 110543 0.2 IRIS 1991 Neurological Hydrazine 302012 B2 2B 0.0049 IRIS 1997 0.0002 CAL 2000 Liver Hydrochloric acid 7647010 0.02 IRIS 1995 Respiratory Hydrofluoric acid 7664393 0.03 CAL 1999 Skeletal Isophorone 78591 C 2.7e-7 Conv. 

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2004 2 CAL 2001 Liver 

Lead2 7439921 B2 2B 0.0015 EPA 

OAQPS6

2003 Developmental

Lindane (all isomers) 2B 0.00053 IRIS 1988 0.0003 PCAL3 1997 Kidney Maleic anhydride 108316 0.0007 CAL 2001 Respiratory Manganese compounds D 0.00005 IRIS 1993 Neurological Mercury compounds C 0.00009 CAL 2000 Neurological Methanol2 67561 4 CAL 2000 Developmental6 EPA has not developed an RfC for lead. The value shown is the quarterly National Ambient Air Quality Standard for lead, which EPA b

adverse effects. 
November 7, 2005 

Chemical Name CAS No.

EPA 

WOE

IARC 

WOE 

URE 

(  g/m3)-1

URE 

Source 

URE 

Date 

RfC1

(mg/m3)

RfC 

Source 

RfC 

Date 

Target 

System 1 

Methyl bromide 74839 D 0.005 IRIS 1992 Respiratory Methyl chloride 74873 D 0.09 IRIS 2001 Neurological Methyl ethyl ketone 78933 5 IRIS 2003 DevelopmentalMethyl isobutyl ketone 108101 3 IRIS 2003 DevelopmentalMethyl isocyanate 624839 0.001 CAL 2001 Respiratory Methyl methacrylate 80626 E 0.7 IRIS 1998 Respiratory Methyl tert-butyl ether2 1634044 3 IRIS 1993 Liver 4,4'-Methylene bis(2-chloroaniline) 

101144 B2 2A 0.00043 CAL 1999

Methylene chloride2 75092 B2 2B 4.7e-7 IRIS 1997 1 ATSDR 2000 Liver Methylene diphenyl diisocyanate 

101688 D 0.0006 IRIS 1998 Respiratory 

4,4'-Methylenedianiline 101779 2B 0.00046 CAL 1999 0.02 CAL 2002 Ocular 

Naphthalene2 91203 C 2B 0.000034 CAL 2004 0.003 IRIS 1998 Respiratory Nickel compounds2 A 2B 0.00016 EPA 

OAQPS 

2004 0.000065 CAL 2000 Respiratory 

Nitrobenzene2 98953 D 2B 0.03 PCAL3 1997 Respiratory 

2-Nitropropane 79469 B2 2B 0.000005 EPA 

OAQPS 

2003 0.02 IRIS 1991 Liver 

Nitrosodimethylamine 62759 B2 2A 0.014 IRIS 1997

N-Nitrosomorpholine 59892 2B 0.0019 CAL 1999PCB Group 1336363 B2 2A 0.0001 IRIS 1999Pentachloronitrobenzene 82688 C 3 0.000074 Conv. 

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Pentachlorophenol2 87865 B2 2B 0.000005 CAL 1999 0.1 PCAL3 1997 Liver Phenol 108952 D 3 0.2 CAL 2000 Liver Phosgene2 75445 0.0003 PCAL3 1997 Respiratory Phosphine 7803512 D 0.0003 IRIS 1995 Whole body Phthalic anhydride 85449 0.02 CAL 2000 Respiratory Polycyclic organic matter7

group 12

8 0.000055 OAQPS 2004

Polycyclic organic matter group 22

8 0.000055 OAQPS 2004

7 A full discussion of the risk assessment for polycyclic organic matter is available at: http://www.epa.gov/ttn/atw/sab/appendix-h.pdf. 8 EPA WOE varies among individual compounds. 
November 7, 2005 

Chemical Name CAS No.

EPA 

WOE

IARC 

WOE 

URE 

(  g/m3)-1

URE 

Source 

URE 

Date 

RfC1

(mg/m3)

RfC 

Source 

RfC 

Date 

Target 

System 1 

Polycyclic organic matter group 32

8 0.1 OAQPS 2004

Polycyclic organic matter group 42

8 0.01 OAQPS 2004

Polycyclic organic matter group 52

8 0.001 OAQPS 2004

Polycyclic organic matter group 62

8 0.0001 OAQPS 2004

Polycyclic organic matter group 72

8 0.00001 OAQPS 2004

Polycyclic organic matter group 82

8 0.0002 OAQPS 2004

1,3-Propane sultone 1120714 2B 0.00069 CAL 1999Propylene dichloride 78875 B2 0.000019 Conv. 

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2004 0.004 IRIS 1991 Respiratory 

Propylene oxide 75569 B2 2B 0.000003 IRIS 1997 0.03 IRIS 1992 Respiratory Quinoline 91225 B2 0.0034 Conv. 

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Selenium compounds D 0.02 CAL 2001 Neurological Styrene2 100425 2B 1 IRIS 1992 Neurological Styrene oxide 96093 2A 0.006 PCAL3 1997 Respiratory 1,1,2,2-Tetrachloroethane 79345 C 3 0.000058 IRIS 1997Perchloroethylene2 127184 B2C 2A 0.000005 CAL 1999 0.27 ATSDR 1999 Neurological Titanium tetrachloride 7550450 2001 0.0001 ATSDR 1999 Respiratory Toluene2 108883 D 3 0.4 IRIS 1995 Respiratory 2,4-Toluene diamine 95807 B2 0.0011 CAL 19992,4-Toluene diisocyanate 26471625 2B 0.000011 CAL 1999 0.00007 IRIS 1995 Respiratory o-Toluidine 95534 B2 2B 0.000051 CAL 1999Toxaphene 8001352 B2 2B 0.00032 IRIS 19971,2,4-Trichlorobenzene 120821 D 0.2 HEAST 1993 Liver 1,1,2-Trichloroethane 79005 C 3 0.000016 IRIS 1997 0.4 PCAL3 1997 Liver 1,1,1-Trichloroethane2 71556 D 1 CAL 2000 Neurological Trichloroethylene2 79016 B2C 2A 0.000002 CAL 1999 0.6 CAL 2000 Ocular 2,4,6-Trichlorophenol 88062 B2 0.000003 IRIS 1997Triethylamine 121448 0.007 IRIS 1991 Respiratory 
November 7, 2005 

Chemical Name CAS No.

EPA 

WOE

IARC 

WOE 

URE 

(  g/m3)-1

URE 

Source 

URE 

Date 

RfC1

(mg/m3)

RfC 

Source 

RfC 

Date 

Target 

System 1 

Trifluralin 1582098 C 3 0.000002 Conv. 

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Vinyl acetate2 108054 2B 0.2 IRIS 1990 Respiratory Vinyl bromide 593602 B2 2A 0.000032 HEAST 1997 0.003 IRIS 1993 Liver Vinyl chloride 75014 A 1 0.000008 IRIS9 2000 0.1 IRIS 2000 Liver Vinylidene chloride2 75354 C 0.2 IRIS 2002 Liver Xylenes (mixed) 1330207 0.1 IRIS 2003 Neurological 9 URE based on whole life exposure was selected over a URE based on adult exposure only.