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Table 1: Lung cancer risks in four cohort studies (from US EPA, 1986) Study Number of subjects Lung cancer deaths Lung cancer SMR 90% confidence limits(CI) W. Virginia 1855 8 1.12 0.56, 2.02 8.5 Ontario 495 37 8.71 6.49, 11.45 1.4 Wales 967 145 5.28 4.58 – 6.03 1.2 Norway 2247 82 3.73 3.08, 4.48 1.3 * Note: the (SMR-1) is an estimate of excess relative risk Ratio of upper CI of (SMR-1) to (SMR-1) * The Ontario cohort study was determined to be the most appropriate for quantitative cancer risk assessment (CDHS, 1991). The main reason for choosing this cohort was that it was the only cohort with actual measurements of exposure associated with a relevant causal period with sufficient latency (available from 1948 on which is the most relevant period for the lung cancer deaths ascertained between 1963 and 1978). Animal Studies At the time that the CDHS (1991) report “Health Risk Assessment for Nickel” was written, inhalation exposure cancer bioassays had only examined insoluble forms of nickel for their carcinogenic potential. Likewise, only soluble forms of nickel had been evaluated by oral administration. Evidence of carcinogenic potential following inhalation exposure has been shown for nickel subsulfide (Ni 3 S 2 ) and suggested for nickel carbonyl. Inhalation exposure to metallic nickel resulted in very poor survival which was too short to properly evaluate carcinogenicity. Many rats exposed to metallic nickel by inhalation developed squamous metaplasia and peribronchial adenomatoses (Hueper and Payne, 1962). Exposure to metallic nickel by intratracheal instillation produced a significant increase in lung tumor incidence. Pott et al. (1987) administered nickel powder in a total intratracheal dose of 6 or 9 mg Ni/animal to female Wistar rats. Following treatment, animals were maintained for up to an additional 2.5 years. The lung tumor incidence in the saline control, 6 mg Ni (0.3 mg Ni × 20), and 9 mg Ni (0.9 mg × 10) treatment groups were 0%, 26% and 25%, respectively. The results from the nickel oxide (NiO) studies assessing the carcinogenicity of nickel oxide following inhalation exposure are negative in hamsters (Wehner et al., 1975, 1981) and inconclusive in rats (Takenaka et al., 1985; Glaser et al., 1986; Horie et al., 1985). These studies were also plagued by very poor survival rates. Intratracheal instillation of nickel oxide resulted in lung tumor induction. Female Wistar rats received a total dose of 0, 50, or 150 mg Ni/animal. Animals were maintained for an additional 2.5 years. The lung tumor incidence in the saline control, 50 (5 mg Ni × 10) and 150 mg Ni (15 mg Ni × 10) were 0%, 27% and 32%, respectively (Pott et al., 1987). Two studies produced positive results in evaluating the pulmonary tumorgenicity of nickel subsulfide, one utilizing inhalation exposure (Ottolenghi et al., 1974) and the other, intratracheal administration. In the Ottolenghi et al. study 122 male and 104 female Fischer-344 rats were exposed to 0.97 mg/m 3 nickel subsulfide via inhalation for 78-80 weeks (6 hours/day, 5 days/week). The control group, 120 379
male and 121 female rats, was exposed to clean air. The study design included two subtreatments in a 2 4 factorial arrangement. The two subtreatments were: 1) pre-exposure for one month to 0.97 mg/m 3 nickel subsulfide 6 hr/day, 5 day/week; and 2) injection of the pulmonary infarction agent, hexachlorotetrafluorobutane. Animals found moribund or succumbing during the study and those killed at the end of the observation period (i.e., 30 weeks) were necropsied. A small number of animals (18 in the exposed and 26 in the control groups) were not examined because of autolysis or cannibalism. The results demonstrated a significant increase in lung tumors (adenomas, adenocarcinomas, squamous cell carcinomas, and fibrosarcomas) in the exposed 110 male and 98 female rats examined as compared with the control 108 male and 107 female rats examined (Table 2). Table 2: Neoplastic Changes in Lungs of Rats Exposed to Nickel Subsulfide Tumors Controls Nickel Subsulfide Exposed Males Females Males Females Adenoma 0/108 (0%) 1/107 (1%) 8/110 (7%) b 7/98 (7%) a Adenocarcinoma 1/108 (1%) 0/107 (0%) 6/110 (5%) a 4/98 (4%) b Squamous cell 0/108 (0%) 0/107 (0%) 2/110 (2%) 1/98 (1%) carcinoma Fibrosarcoma 0/108 (0%) 0/107 (0%) 1/110 (1%) 0/98 (0%) a p < 0.01, Fisher’s Exact Test b p < 0.05, Fisher’s Exact Test The two subtreatments, described above, did not alter the effects produced by nickel subsulfide treatment (Ottolenghi et al., 1974). Sex of the exposed animal also did not appear to alter the effects produced by the nickel subsulfide treatment. The study results of Ottolenghi et al. (1974) for nickel subsulfide were selected for a quantitative risk assessment. At the time the CDHS (1991) risk assessment was conducted, injection administration (intramuscular) was the only route of exposure from which data were available for comparison of carcinogenic potency of a variety of nickel compounds. Injection studies by Sunderman (1984) and Skaug et al. (1984) demonstrate that based on the incidence of sarcomas produced at the injection site, nickel subsulfide and nickel oxide possess approximately equal potency following this route of exposure. None of the studies utilizing oral exposure has produced evidence of carcinogenic potential. However, it should be noted that only nickel sulfate (NiSO 4 ) has been adequately evaluated in rats by this route. IV. DERIVATION OF CANCER POTENCY Basis for Cancer Potency Nickel subsulfide has been observed to induce lung tumors in male and female rats (Ottolenghi et al., 1974). This study and the Ontario cohort study (Chovil et al., 1981; Roberts et al., 1984; Muir et al., 1985; ICNCM, 1990), which demonstrated an increased risk of lung cancer associated with 380
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Air Toxics Hot Spots Program Risk A
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Prepared by: John D. Budroe, Ph.D.
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This document is one of five docume
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TABLE OF CONTENTS PREFACE i INTRODU
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N-Nitrosodimethylamine 401 N-Nitros
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Hot Spots Unit Risk and Cancer Pote
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Additional ATES and PETS documents
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data. If several data sets (dose an
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US EPA Calculation of Carcinogenic
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exposure to a concentration of 1 µ
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incidences for each of the dose lev
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computes the surface area of a sphe
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Comparison of Hot Spots Cancer Unit
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Gold, L., de Veciana, M., Backman,
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Animal Studies Rats Woutersen et al
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ased on sufficient evidence of carc
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ACETAMIDE CAS No: 60-35-5 I. PHYSIC
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Methodology Expedited Proposition 6
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cancer mortality. However, US EPA (
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Table 2. Lung adenoma incidence in
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Table 3 (continued). Acrylamide-ind
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Robinson M, Bull RJ, Knutsen GL, Sh
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Also, a trend was observed correlat
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eported. Cause-specific expected de
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Bio/Dynamics Inc. conducted a study
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examination. Interim sacrifices wer
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Table 8. Tumor incidence in male an
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Gaffey WR and Strauss ME. 1981. A m
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(technical grade; 98% pure) by gava
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International Agency for Research o
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still alive in the low-dose control
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ANILINE CAS No: 62-53-3 I. PHYSICAL
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fibrosarcomas, stromal sarcomas, ca
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ARSENIC (INORGANIC) CAS No: 7440-38
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elationship between arsenic exposur
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al. (1988) did not induce lung tumo
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A risk assessment was also conducte
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Chen C, Chuang Y, You S, Lin T and
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Schrauzer G, White D, McGinness J,
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Table 1: Summary of epidemiologic s
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had at least one animal demonstrati
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mesothelioma, recommended lifetime
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National Institute for Occupational
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BENZENE CAS No: 71-43-2 I. PHYSICAL
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Animal Studies Available experiment
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Table 3: Summary of NTP bioassay re
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Table 4: Summary of benzene low-dos
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Maltoni C, Conti B and Cotti G. 198
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a benign tumor of the kidney. No ba
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al. (1968) found no tumors in lifet
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following relationship, where C(t 1
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Miakawa M. and Yoshida O. 1975. Pro
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human population and that BPDE-DNA
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demonstrated the tumor initiating a
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Table 4: Bronchoalveolar tumors fro
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Table 5: IARC groupings of PAHs, mi
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Table 6 (continued): IARC Group 3 P
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Potency Equivalency Factors (PEF) f
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This was rounded to a PEF of 0.1. 1
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experiment (Takayama et al., 1985)
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Deutsch-Wenzel RP, Brune H, Grimmer
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Krewski D, Thorslund T and Withey J
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U.S. Environmental Protection Agenc
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Sorahan et al. (1983) studied cance
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Lijinsky W. 1986. Chronic bioassay
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the drinking water (Schroeder and M
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Table II. Effective dose, upper-bou
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BIS(2-CHLOROETHYL)ETHER CAS No: 111
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IV. DERIVATION OF CANCER POTENCY Ba
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BIS(CHLOROMETHYL)ETHER CAS No: 542-
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Table 1. Bis(chloromethyl)ether-ind
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Drew RT, Laskin S, Kuschner M and N
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ates for the 1968 U.S. male populat
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Table 1: Incidence of primary tumor
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National Institute of Occupational
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was less than 0.05 when controlling
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up period. The final cohort include
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If the cadmium-exposed workers incl
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on personnel records (20%); (3) eva
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were exposed to a continuous (23.5
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procedure (NLIN), the parameters we
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International Agency for Research o
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Two reports were published on cance
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Mendel rats, respectively), and sub
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Eschenbrenner A and Miller E. 1946.
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III. CARCINOGENIC EFFECTS Human Stu
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cancers, were less than expected. T
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and no cases of cancer (although cl
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There was a statistically significa
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NTP (1982a) also conducted an carci
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Several pathologists have independe
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hepatocellular adenoma/carcinoma tu
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carcinogenic potency may decline in
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Cochrane W, Singh J and Miles W. 19
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North Atlantic Treaty Organization,
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CHLORINATED PARAFFINS (average chai
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ased on dose-response data for beni
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chloroform in drinking water with k
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Overall, the present epidemiologica
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female dogs received toothpaste bas
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Calculated q 1 * values from the ab
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Hogan MD, Chi Py, Hoel DG and Mitch
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Table 1. Study design summary for N
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V. REFERENCES California Environmen
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toluidine. Followup of this subcoho
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feeding studies on by NCI (1979) us
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CHROMIUM (HEXAVALENT) CAS No: 18540
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expected rate may be inflated becau
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Oral Borneff et al. (1968) exposed
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CREOSOTE (COAL TAR-DERIVED) CAS No:
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from an inhalation exposure study (
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Table 1. Study design summary for N
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Table 1. Experimental design for ca
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Hazardous Substance Data Bank (HSDB
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Table 1: Tumor induction in Fischer
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Hazardous Substance Data Bank (HSDB
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Table 1. Experimental design of 2,4
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Additional analysis of these data b
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Jackson RJ, Greene CJ, Thomas JT, M
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Table 1. Tumor incidence in rats ex
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Girard R, Tolot F, Martin P and Bou
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exposed more than 16 years before t
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interpretation of dose extrapolatio
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1, 1-DICHLOROETHANE CAS No: 75-34-3
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Table 1b. Study design for carcinog
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National Cancer Institute (NCI) 197
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mice, hepatocellular carcinoma inci
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V. REFERENCES California Department
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DAB/day by gavage for the life of t
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2,4-DINITROTOLUENE CAS No: 121-14-2
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Ellis et al.(1979) (also reported b
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Final Statement of Reasons for OAL,
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to the small sample size and short
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In an inhalation study, Torkelson e
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V. REFERENCES American Conference o
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EPICHLOROHYDRIN CAS No: 106-89-8 I.
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espiratory tumors were noted in the
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Table 4. Epichlorohydrin-induced fo
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Konishi Y, Kawabata A, Denda A, Ike
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exposed to arsenicals for 20 months
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espectively (all statistically sign
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ETHYLENE DICHLORIDE CAS No: 107-06-
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Several factors have been suggested
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myelogenous leukemias (4 and 8 year
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statistically significant. CDHS not
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combined with the incidence in the
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incidence of primary brain tumors.
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Table 6 (continued): Organ/Sex Mali
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An Upper 95% Confidence Limit (UCL)
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ETHYLENE THIOUREA (ETU) CAS No: 96-
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male and female rats. Tumor inciden
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FORMALDEHYDE CAS No: 50-00-0 I. PHY
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presented an extension of a previou
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Methodology In developing a spectru
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Casanova M, Morgan KT, Steinhagen W
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Tobe M, Kaneko T, Uchida Y, Kamata
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Table 1. Hexachlorobenzene-induced
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50 pups (F 1 ) of each sex were ran
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Ertürk E, Lambrecht RW, Peters HA,
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Table 1. Liver hepatoma incidence i
Page 337 and 338: 1988). An airborne unit risk factor
Page 339 and 340: HYDRAZINE CAS No: 302-01-2 I. PHYSI
Page 341 and 342: Methodology Inhalation A linearized
Page 343 and 344: LEAD AND LEAD COMPOUNDS (INORGANIC)
Page 345 and 346: and other occupational carcinogens
Page 347 and 348: y inhalation is similar for rats an
Page 349 and 350: Goyer RA. 1992. Nephrotoxicity and
Page 351 and 352: LINDANE (g-Hexachlorocyclohexane) C
Page 353 and 354: Using these relationships, a human
Page 355 and 356: METHYL TERT-BUTYL ETHER (MTBE) CAS
Page 357 and 358: Tumor incidences according to the r
Page 359 and 360: kidney changes indicative of chroni
Page 361 and 362: Interspecies scaling for oral doses
Page 363 and 364: Table 4 (continued): Dose Response
Page 365 and 366: Experimental Pathology Laboratories
Page 367 and 368: Animal Studies Male and female HaM/
Page 369 and 370: Gold L, Sawyer C, Magaw R, Backman
Page 371 and 372: Using the statistical tests (one-ta
Page 373 and 374: Table 1: Methylene chloride-induced
Page 375 and 376: Significant treatment-related incre
Page 377 and 378: National Toxicology Program (NTP) 1
Page 379 and 380: noted; however, the study duration
Page 381 and 382: Crump KS, Howe RB, Van Landingham C
Page 383 and 384: Table 1. Michler’s ketone-induced
Page 385 and 386: NICKEL AND NICKEL COMPOUNDS CAS No:
Page 387: the high exposure group was 14.0. A
Page 391 and 392: 2.1 - 2.6 × 10 -4 (µg/m 3 ) -1 .
Page 393 and 394: U.S. Environmental Protection Agenc
Page 395 and 396: The increased incidence of bladder
Page 397 and 398: A linearized multistage procedure w
Page 399 and 400: N-NITROSO-N-METHYLETHYLAMINE CAS No
Page 401 and 402: Hazardous Substance Data Bank (HSDB
Page 403 and 404: propylamine in drinking water at 0.
Page 405 and 406: N-NITROSODIETHYLAMINE CAS No: 55-18
Page 407 and 408: Table 2. Treatment groups, concentr
Page 409 and 410: California Department of Health Ser
Page 411 and 412: animals and the second generation t
Page 413 and 414: ationale for selection of the OEHHA
Page 415 and 416: A unit risk value based upon air co
Page 417 and 418: N-NITROSODIPHENYLAMINE CAS No: 86-3
Page 419 and 420: Methodology Dosage estimates of NDP
Page 421 and 422: Crump KS, Howe RB. 1984. The multis
Page 423 and 424: Table 1. P-Nitrosodiphenylamine-ind
Page 425 and 426: N-NITROSOMORPHOLINE CAS No: 59-89-2
Page 427 and 428: IV. DERIVATION OF CANCER POTENCY Ba
Page 429 and 430: N-NITROSOPIPERIDINE CAS No: 100-75-
Page 431 and 432: Table 3. N-Nitrosopiperidine-induce
Page 433 and 434: Crump KS, Howe RB, Van Landingham C
Page 435 and 436: testicular tumors were noted in the
Page 437 and 438: PARTICULATE MATTER FROM DIESEL-FUEL
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etired railroad workers who had had
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employment (χ 2 test for trend: p
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elevated smoking-adjusted risk esti
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Table 1 (continued): Reference Miln
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Table 1 (continued): Reference Damb
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Table 1 (continued): Reference Burn
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Table 1 (continued): Reference Raff
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Table 1 (continued): Epidemiologica
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Table 1 (continued): Epidemiologica
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Table 1 (continued): Reference Wegm
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Animal Studies Section 6.1 (Animal
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The variability, or heterogeneity,
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estimate for those studies for whic
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Figure 1: Estimates of Relative Ris
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q 1 * = Excess relative risk × CA
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Table 3: Number of Workers in the E
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u nexposed workers at zero concentr
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for each µg/m 3 of diesel exhaust
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Table 4: Values from Unit Risk for
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their findings that a reasonable es
Page 479 and 480:
Garshick E, Schenker M, Woskie S an
Page 481 and 482:
Lewis T, Green, FH MW, Burg J and L
Page 483 and 484:
Rothman K. 1986. Modern epidemiolog
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PENTACHLOROPHENOL CAS No: 87-86-5 I
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The default lifespan for mice is 10
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documented. An excess risk from ski
Page 491 and 492:
B6C3F 1 mice and F344/N rats were e
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This model, rather than a time depe
Page 495 and 496:
POLYCHLORINATED BIPHENYLS (PCBs) CA
Page 497 and 498:
several benign adenomatous lesions
Page 499 and 500:
Ito et al. (1973) exposed groups of
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could not be characterized by chlor
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exposure (all pathways and mixtures
Page 505 and 506:
National Toxicology Program 1993. T
Page 507 and 508:
Table 1. Potassium bromate-induced
Page 509 and 510:
1,3-PROPANE SULTONE CAS No: 1120-71
Page 511 and 512:
Page 513 and 514:
PROPYLENE OXIDE CAS No: 75-56-9 I.
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oxide. In the NTP carcinogenicity s
Page 517 and 518:
1,1,2,2-TETRACHLOROETHANE CAS No: 7
Page 519 and 520:
assumed a body weight of 70 kg and
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total); an untreated control group
Page 523 and 524:
TOLUENE DIISOCYANATE CAS No: 26471-
Page 525 and 526:
Animal Studies The National Toxicol
Page 527 and 528:
Mortillaro PT and Schiavon M. 1982.
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male or female rats. Increases in h
Page 531 and 532:
TRICHLOROETHYLENE CAS No: 79-01-6 I
Page 533 and 534:
A mortality analysis of a cohort of
Page 535 and 536:
elative to that of the controls whi
Page 537 and 538:
applied or metabolized. The range o
Page 539 and 540:
Katz RM and Jowett D. 1981. Female
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10,000 ppm 2,4,6-trichlorophenol in
Page 543 and 544:
Page 545 and 546:
Bionetics Research Laboratories. 19
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control; females: 6/10 exposed, 0/1
Page 549 and 550:
over controls (p < 0.04). Other tum
Page 551 and 552:
was increased (100/314 exposed vs.
Page 553 and 554:
Table 3. Cancer potency estimates f
Page 555 and 556:
Crouch E. 1983. Uncertainties in in
Page 557 and 558:
VINYL CHLORIDE CAS No: 75-01-4 I. P
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Table 1 (continued): A Summary of E
Page 561 and 562:
al., 1983). Histopathology of all o
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Table 3: Tumor incidences in 100 pp
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experiment, animals were exposed to
Page 567 and 568:
Experiment BT1 Most previous risk a
Page 569 and 570:
No statistical analyses of mortalit
Page 571 and 572:
Table 11 gives unit risk estimates
Page 573 and 574:
Bertazzi PA, Villa A, Foa V, Saia B
Page 575 and 576:
Nicholson WJ, Hammond EC, Seidman H
Page 577 and 578:
immunotoxicity, reproductive toxici
Page 579 and 580:
scheme. TEFs for two major noncance
Page 581 and 582:
NATO/CCMS (1988a) Pilot Study on In
Page 583 and 584:
Table 2 Toxicity Equivalency Factor
Page 585 and 586:
Table 4 A Comparison of CTEF- and I
Page 587 and 588:
Office of Environmental Health Haza
Page 589 and 590:
Group 4: The agent is probably not
Page 591 and 592:
TECHNICAL SUPPORT DOCUMENT FOR DESC
Page 593 and 594:
US EPA IRIS Inhalation Unit Risk an
Page 595 and 596:
TECHNICAL SUPPORT DOCUMENT FOR DESC
Page 597 and 598:
as appropriate, and revise IRIS fil
Page 599 and 600:
Chemical Exposure Route Study Type
Page 601 and 602:
Page 603 and 604:
Page 605 and 606:
Methyl tert-butyl ether p. 5: Added
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