IARC MONOGRAPHS ON THE EVALUATION OF CARCINOGENIC ...

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Table 11 (contd) Reference Area Study base Type of analysis Exposure measures Outcome measures Sun et al. (2001) Yu et al. (1997a) Lu et al. (1998) Sun et al. (1999) Taiwan, China Same as Wang et al. (1996) Taiwan Male patients from Government Employee Central Clinics and a Taipei hospital, aged 30–65 during enrolment, 1988–92; n = 4841 HBsAgpositive, n = 2501 HBsAgnegative China Seven townships in Qidong. Men aged 20–60 years during enrolment; follow-up: 1987–97 China Men in 2 townships screened and found positive for chronic HBV infection, recruited in 1987–98; n = 145 Nested case–control analysis based on 79 cases and 149 controls, all HBsAgpositive Nested case–control on 43 cases and 2 matched controls per case, one HBsAg positive and one negative Nested case–control among HBsAg carriers; 30 cases and 5 controls per case (matched for age, place of residence) Aflatoxin–albumin adducts Baseline interviews and measurement of urinary aflatoxin and aflatoxin adducts AFB1–albumin adducts Cohort analysis AFM1 measured in 8 pooled urinary samples Same as Wang et al. (1996), 1991–97 Covariate Results Comments Same as Wang et al. (1996), anti-HCV, GSTM1, GSTT1 HCC Sociodemographic, alcohol, smoking Cases OR 95% CI Aflatoxin– 47 2.0 1.1–3.7 albumin adducts Cases OR 95% CI AFM1 23 6.0 1.2–29 AFP1 18 2.0 0.5–8.0 AFB1 17 2.0 0.7–5.8 AFB1–N7- 6 2.8 0.6–13 guanine adducts PLC Cases OR 95% CI HCC Anti-HCV, family history of HCC, smoking, alcohol AFB1- 23 3.5 [1.3–10] albumin adducts Cases RR 95% CI AFM1 17 4.5* 1.6–13 Statistically significant interaction with GSTT1 genotypes All analyses restricted to HBsAg-positive subjects Increased risks for HCC among anti-HCV (RR, 6.0) and those with family history of HCC (RR, 4.7) *Adjusted for anti-HCV and HCC family history AFB1, aflatoxin B1; AFM1, aflatoxin M1; AFP1, aflatoxin P1; CI, confidence interval; GST, glutathione S-transferase; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus; HCC, hepatocellular carcinoma; HCV, hepatitis C virus; NA, not applicable; OR, odds ratio; OV, Opisthorchis viverrini; PHC, primary hepatocellular carcinoma; p–yr, person–years; RR, relative risk; SMR, standardized mortality ratio; SPIR, standardized proportionate incidence ratio AFLATOXINS 201
202 IARC MONOGRAPHS VOLUME 82 history based on a frequency checklist of 45 food items usually consumed as an adult was combined with a set of independently measured aflatoxin levels in various local foods to derive a quantitative measure of dietary aflatoxin exposure. In a cohort-type analysis, using the lowest tertile of aflatoxin exposure as reference, the middle tertile had a relative risk (adjusted for age and smoking) of 1.6 (95% confidence interval [CI], 0.8–3.1; 25 cases) and the highest tertile had an odds ratio (OR) of 0.9 (95% CI, 0.4–1.9; 16 cases). To assess the risks in relation to biomarkers of aflatoxin exposure, a nested case– control study was conducted using 50 of the cases (Qian et al., 1994). Controls were selected from among subjects who had no history of liver cancer on the date of cancer diagnosis of the index cases and were matched to cases in ratios ranging from 10:1 to 3:1, yielding a total of 267 controls. For each case and control, urine samples were analysed for aflatoxins B 1, P 1 and M 1 and for aflatoxin B 1–N7-guanine adducts, and among a subgroup of 28 cases and their matched controls for aflatoxins G 1 and Q 1. HBsAg was measured by radioimmunoassay. Thirty-two out of 50 cases and 31 out of 267 controls were HBsAg-positive. Each of the six biomarkers of aflatoxin exposure was more frequently present among cases than controls. For 36 of the 50 liver cancer cases and 109 of 267 controls, results were positive in at least one of the four assays analysed for the full set of cases and controls (adjusted relative risk, 5.0; 95% CI, 2.1–12). The highest risks were found among subjects with aflatoxin B 1–N7-guanine adducts. Compared with subjects who had no aflatoxin biomarkers and were HBsAg-negative, the interaction of the two factors was supra-multiplicative, with relative risks as follows: aflatoxin biomarker only, 3.4 (95% CI, 1.1–10); HBsAg only, 7.3 (95% CI, 2.2–24); both factors, 59 (95% CI, 17–212). [The Working Group noted inconsistencies between analyses based on dietary questionnaires and biomarkers.] The Penghu Islets reportedly have the highest rates of HCC in Taiwan, China. Chen et al. (1996) enrolled 4691 men and 1796 women, aged 30–65 years, in a prospective cohort study. The subjects were selected from a housing register maintained by the local administration. Participants were interviewed on a variety of sociodemographic, dietary and medical history topics. Blood samples were collected and stored frozen. A two-stage screening process for HCC was undertaken which included serological markers and clinical assessments with ultrasonography. Subjects were further followed up with annual examinations. A total of 33 cases of HCC were diagnosed by December 1993, of whom two were negative for HBsAg. A total of 123 controls were selected from within the cohort among unaffected subjects, and matched with cases for age, sex, village and date of blood collection. Blood samples from cases and controls were analysed for HBsAg, for anti-hepatitis C virus (HCV) antibodies and aflatoxin B 1–albumin adducts, although samples for adduct analysis were usable for only 20 cases and 86 controls. Using logistic regression, with age and sex adjustment, and a detection limit for albumin adducts of 0.01 fmol/μg as the cut-off value, the OR for an association between presence of aflatoxin B 1–albumin adducts and HCC was 3.2 (13 cases; 95% CI, 1.1–8.9). When the statistical model also included several other covariates (HBsAg, anti-HCV, family history of liver cancer and cirrhosis), the odds ratio for aflatoxin B 1–albumin adducts
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WORLD HEALTH ORGANIZATION INTERNATI
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IARC MONOGRAPHS In 1969, the Intern
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iv IARC MONOGRAPHS VOLUME 82 3.2 Th
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vi IARC MONOGRAPHS VOLUME 82 SOME M
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IARC WORKING GROUP ON THE EVALUATIO
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PARTICIPANTS 5 Observer, representi
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PREAMBLE
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10 IARC MONOGRAPHS VOLUME 82 plasms
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12 IARC MONOGRAPHS VOLUME 82 collec
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14 agents present. For processes, i
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16 IARC MONOGRAPHS VOLUME 82 Finall
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18 IARC MONOGRAPHS VOLUME 82 and mi
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20 IARC MONOGRAPHS VOLUME 82 (c) St
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22 IARC MONOGRAPHS VOLUME 82 may le
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24 IARC MONOGRAPHS VOLUME 82 It is
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26 IARC MONOGRAPHS VOLUME 82 Data r
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28 when there is strong evidence th
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30 IARC MONOGRAPHS VOLUME 82 Vol. 7
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GENERAL REMARKS ON THE SUBSTANCES C
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SOME TRADITIONAL HERBAL MEDICINES
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44 which may include, for example,
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46 2. Use of Traditional Herbal Med
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48 IARC MONOGRAPHS VOLUME 82 decade
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50 IARC MONOGRAPHS VOLUME 82 Table
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52 3.2.1 Definition of herbal medic
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54 3.2.8 Individual supply Herbal m
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58 3.3.2 Germany (see Kraft, 1999;
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60 beyond placebo, and this informa
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62 3.3.5 Canada The Canadian Food a
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64 of adverse reactions to OTC drug
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66 IARC MONOGRAPHS VOLUME 82 3.3.12
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68 IARC MONOGRAPHS VOLUME 82 Jellin
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70 IARC MONOGRAPHS VOLUME 82 Simila
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72 IARC MONOGRAPHS VOLUME 82 Figure
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74 diameter of 4-6 cm or more, lobe
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76 1.2 Use 1.2.1 Aristolochia conto
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78 1.3.3 Aristolochia fangchi Compo
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80 1.6.2 Structural and molecular f
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82 chromatographic separation with
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84 may contain aristolochic acids.
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86 IARC MONOGRAPHS VOLUME 82 A bila
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88 received distilled water. The an
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90 IARC MONOGRAPHS VOLUME 82 Figure
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92 varied from undetectable (< 0.02
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94 lochic acids enhanced immune res
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96 4.4 Genetic and related effects
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Table 3 (contd) Details of study DN
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Table 4. DNA adduct formation with
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Table 4 (contd) Details of study Co
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Table 5 (contd) Species Treatment I
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Table 6. DNA adduct formation by ar
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Table 6 (contd) Test system Assay D
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Table 6 (contd) Test system Assay D
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Table 7. Polymerase action on arist
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Table 8 (contd) Test system Drosoph
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116 of the forestomach and lung of
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118 lochic acid II (three metabolit
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120 IARC MONOGRAPHS VOLUME 82 Che,
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122 IARC MONOGRAPHS VOLUME 82 Healt
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124 IARC MONOGRAPHS VOLUME 82 Nishi
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126 IARC MONOGRAPHS VOLUME 82 Schme
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128 IARC MONOGRAPHS VOLUME 82 Yang,
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130 Figure 1. Morinda officinalis H
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132 1.3.2 Morinda officinalis A num
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134 by Soxhlet extraction with ethy
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136 2.1 Case-control studies 2.1.1
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138 3. Studies of Cancer in Experim
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140 1,3-Dihydroxy-2-hydroxymethylan
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142 4.3 Reproductive and developmen
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Table 1 (contd) Test system Result
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146 5.1 Exposure data 5. Summary of
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148 IARC MONOGRAPHS VOLUME 82 Brigg
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Page 170 and 171: Riddelliine induced unscheduled DNA
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Page 213 and 214: Table 12. Summary of principal case
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Page 221 and 222: 214 3.4 Administration with known c
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Page 241 and 242: 234 In eight subjects (four from Ho
Page 243 and 244: Table 16 (contd) Test system Result
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Page 249 and 250: 242 difference between the two stud
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Page 253 and 254: 246 In a large cohort study in Shan
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252 IARC MONOGRAPHS VOLUME 82 Buetl
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254 IARC MONOGRAPHS VOLUME 82 Denis
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256 IARC MONOGRAPHS VOLUME 82 Galla
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258 IARC MONOGRAPHS VOLUME 82 Heino
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260 IARC MONOGRAPHS VOLUME 82 Jalon
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262 IARC MONOGRAPHS VOLUME 82 Kirk,
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264 IARC MONOGRAPHS VOLUME 82 Lunn,
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266 IARC MONOGRAPHS VOLUME 82 Olubu
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268 IARC MONOGRAPHS VOLUME 82 Roll,
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270 IARC MONOGRAPHS VOLUME 82 Stett
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272 IARC MONOGRAPHS VOLUME 82 Verge
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274 IARC MONOGRAPHS VOLUME 82 Yang,
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Table 1. IARC evaluations Previous
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278 kernels and in less than 0.1% o
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280 2.5.3 Cottonseed A. flavus is a
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282 IARC MONOGRAPHS VOLUME 82 aflat
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288 IARC MONOGRAPHS VOLUME 82 Figur
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294 IARC MONOGRAPHS VOLUME 82 8. Re
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296 IARC MONOGRAPHS VOLUME 82 Guo,
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298 IARC MONOGRAPHS VOLUME 82 Marti
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300 IARC MONOGRAPHS VOLUME 82 Sharm
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302 (d ) Solubility: Soluble in wat
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304 1.4 Occurrence Fumonisins have
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306 Table 1 (contd) IARC MONOGRAPHS
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308 (c) Formation in commodities ot
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312 IARC MONOGRAPHS VOLUME 82 3.1 O
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314 3.2.2 Rat IARC MONOGRAPHS VOLUM
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316 with NDEA and fumonisin B 1, wh
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318 IARC MONOGRAPHS VOLUME 82 In pi
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Figure 2. Allometric relationship b
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322 IARC MONOGRAPHS VOLUME 82 obser
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324 IARC MONOGRAPHS VOLUME 82 Hepat
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326 4.2.3 Related studies IARC MONO
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328 4.3.2 Experimental systems IARC
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330 and litters on postnatal day 21
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Table 4. Genetic and related effect
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334 IARC MONOGRAPHS VOLUME 82 The f
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336 IARC MONOGRAPHS VOLUME 82 (d )
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338 IARC MONOGRAPHS VOLUME 82 treat
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340 4.5.2 Interference with fatty a
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342 IARC MONOGRAPHS VOLUME 82 Figur
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344 5.2 Human carcinogenicity data
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346 IARC MONOGRAPHS VOLUME 82 Alber
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348 IARC MONOGRAPHS VOLUME 82 Chamb
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350 IARC MONOGRAPHS VOLUME 82 Floss
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352 IARC MONOGRAPHS VOLUME 82 Hiroo
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354 IARC MONOGRAPHS VOLUME 82 Lee,
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356 IARC MONOGRAPHS VOLUME 82 Mobio
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358 IARC MONOGRAPHS VOLUME 82 Prelu
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360 IARC MONOGRAPHS VOLUME 82 Savar
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362 IARC MONOGRAPHS VOLUME 82 Steve
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364 IARC MONOGRAPHS VOLUME 82 Flett
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366 IARC MONOGRAPHS VOLUME 82 Yu, C
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368 disulfide, carbon tetrachloride
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Table 1 (contd) Sample matrix Sampl
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Table 3. Naphthalene production (th
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374 1.4 Occurrence 1.4.1 Natural oc
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Table 5. Occupational exposure to n
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378 water assuming a water concentr
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380 (Scheepers & Bos, 1992). The av
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382 (d ) Biodegradation Studies on
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386 3.2 Inhalation exposure 3.2.1 M
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388 3.3.2 Rat Ten BD I and BD III r
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Figure 1. Main metabolic pathways o
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392 IARC MONOGRAPHS VOLUME 82 and t
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394 IARC MONOGRAPHS VOLUME 82 and 1
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396 IARC MONOGRAPHS VOLUME 82 1-240
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398 IARC MONOGRAPHS VOLUME 82 Perfu
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400 Siegel and Wason (1986) reviewe
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402 IARC MONOGRAPHS VOLUME 82 liver
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404 IARC MONOGRAPHS VOLUME 82 to id
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406 IARC MONOGRAPHS VOLUME 82 Alkal
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408 hyperplasia, atrophy, chronic i
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410 had deficient glucose-6-phospha
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Table 10. Genetic and related effec
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Table 10 (contd) Test system Micron
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416 assay with or without metabolic
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418 There is some evidence of devel
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420 IARC MONOGRAPHS VOLUME 82 Bjør
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422 IARC MONOGRAPHS VOLUME 82 Conkl
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424 IARC MONOGRAPHS VOLUME 82 Envir
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426 IARC MONOGRAPHS VOLUME 82 Ho, C
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428 IARC MONOGRAPHS VOLUME 82 Lynch
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430 IARC MONOGRAPHS VOLUME 82 O’B
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432 IARC MONOGRAPHS VOLUME 82 Schee
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434 IARC MONOGRAPHS VOLUME 82 Versc
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STYRENE This substance was consider
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EPA Method 8260B can be used to det
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Styrene is produced mainly by catal
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STYRENE 443 Table 3. Use patterns f
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STYRENE 445 most samples taken from
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STYRENE 447 successive layers of ch
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Table 4 (contd) Country and year of
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Table 5. Biological monitoring of o
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STYRENE 453 Since 1990, the long-te
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same products resulted in exposures
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STYRENE 457 Ambient air monitoring
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200 μg/kg, although 77% of the foo
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Table 8 (contd) Country or region Y
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2.1 Case reports 2. Studies of Canc
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Table 10 (contd) Reference (country
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Table 10 (contd) Reference (country
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STYRENE 469 (95% CI, 1.4-5.2; 10 de
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who had been employed in 1964-70 (t
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elationship for styrene became nega
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atio, 4.4; 95% CI, 1.1-17 in multip
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controls versus 32/32 treated). No
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3.4 Intraperitoneal administration
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Figure 1. Main metabolic pathways f
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STYRENE 483 a maximum and averaged
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(b) Distribution STYRENE 485 An ear
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STYRENE 487 rats with phenobarbital
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STYRENE 489 gavage (100-350 mg/kg b
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CYP2E1 and CYP2F2) inhibited nasal
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model indicated that absorbed styre
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female workers in the glass fibre-r
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STYRENE 497 continuously for seven
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STYRENE 499 exposure concentrations
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STYRENE 501 The frequency of sponta
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STYRENE 503 groups. Only minor gene
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concentrations of styrene in air we
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Table 12. Cytogenetic studies in ly
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Table 13. Genetic and related effec
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(b) Experimental systems (see Table
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Table 14 (contd) Test system Result
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STYRENE 515 styrene 7,8-oxide. Joha
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Styrene 7,8-oxide can bind to DNA w
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STYRENE 519 a small and non-signifi
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STYRENE 521 and immune systems, liv
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STYRENE 523 Artuso, M., Angotzi, G.
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STYRENE 525 Brugnone, F., Perbellin
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STYRENE 527 Coccini, T., Maestri, L
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STYRENE 529 Edling, C., Anundi, H.,
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STYRENE 531 Gobba, F., Galassi, C.,
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STYRENE 533 Horvath, E., Pongracz,
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STYRENE 535 logical Study and the I
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STYRENE 537 Linhart, I., Gut, I.,
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STYRENE 539 Miller, S.L., Branoff,
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STYRENE 541 Newhook, R. & Caldwell,
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STYRENE 543 Pryor, G.T., Rebert, C.
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STYRENE 545 Sielken, R.L. & Valdez-
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STYRENE 547 Tsuda, S., Matsusaka, N
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STYRENE 549 Boffetta, P. (1996b) Ex
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Agent SUMMARY OF FINAL EVALUATIONS
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554 IARC MONOGRAPHS VOLUME 82 DGAL:
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556 IARC MONOGRAPHS VOLUME 82 PMTDI
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558 IARC MONOGRAPHS VOLUME 82 Aldri
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560 IARC MONOGRAPHS VOLUME 82 Benz[
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562 β-Butyrolactone 11, 225 (1976)
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564 IARC MONOGRAPHS VOLUME 82 Chlor
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566 Cyproterone acetate 72, 49 (199
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568 IARC MONOGRAPHS VOLUME 82 Diepo
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570 Ethionamide 13, 83 (1977); Supp
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572 IARC MONOGRAPHS VOLUME 82 Haema
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574 L Lasiocarpine 10, 281 (1976);
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576 IARC MONOGRAPHS VOLUME 82 Methy
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578 IARC MONOGRAPHS VOLUME 82 Nicke
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580 O Ochratoxin A 10, 191 (1976);
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582 IARC MONOGRAPHS VOLUME 82 Polyb
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584 Rhodamine 6G 16, 233 (1978); Su
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586 Sulfafurazole 24, 275 (1980); S
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588 1,1,1-Trichloroethane 20, 515 (
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590 Y Yellow AB 8, 279 (1975); Supp
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Volume 31 Some Food Additives, Feed
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