- Email: [email protected]
IARC Monographs on the evaluation of carcinogenic risks to humans: Volume 51. Coffee, tea, mate, methylxanthines and methylglyoxal
Fd Chem. Toxic. Vol. 29, No. 9, pp. 647~48, 1991
Pergamon Press plc. Printed in Great Britain
Review Section REVIEWS OF RECENT PUBLICATIONS
IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Volume 51. Coffee, Tea, Mate, Methylxanthines and Methylglyoxal. Lyon, 1991. pp. 513. Sw. fr. 80.00. ISBN 92 832 1251 7. Volume 50. Pharmaceutical Drugs. Lyon, pp. 415. Sw. ft. 65.00. ISBN 92 832 1250 9.
1990.
Volume 49. Chromium, Nickel and Welding. Lyon, 1990. pp. 677. Sw. ft. 95.00. ISBN 92 832 1249 5. Volume 48. Some Flame Retardants and Textile Chemicals, and Exposures in the Textile Manufacturing Industry. Lyon, 1990. pp. 345. Sw. fr. 65.00. ISBN 92 832 1248 7. Headlines linking coffee-drinking and cancer are by no means infrequent, indeed they often seem to be weekly events. The epidemiologists are certainly warranted in giving coffee-drinking a good deal of attention; any habit indulged in by so many must be scrutinized carefully for possible impact on health. The communication difficulties arise from the inability of journalists to view individual epidemiological study reports as only one brick in what might be a very large wall of previous relevant work. The headlines are invariably based on the latest findings in isolation, and no attention is given to whether the previous work points to the same conclusion. As a consequence, the public are continually and vigorously told of all the iconoclastic results, but never hear of the ones that conform to the status quo. An IARC Working Group that met in the spring of 1990 has done all thinking commentators a great service, therefore, in reviewing all the available cancer studies on coffee; for a few years at least there will be less excuse for the media not to view things in a wider perspective. Case-control studies have looked pretty carefully for a link between coffee-drinking and increased risk of developing cancers of the upper digestive tract, large bowel, stomach and breast, and have found none; indeed, in the case of the large bowel, the collective evidence is that coffee may be slightly protective. On the less reassuring side, there is some indication that coffee drinkers may be at a slightly higher risk of developing pancreatic or ovarian cancer, or cancer of the bladder and urinary tract. The Working Group was slightly more confident about the bladder carcinogenicity than the activity at the other 'positive' sites, and the bladder findings were the basis of the overall assignment of coffee to Group 2B (possibly carcinogenic to humans). Tea did not escape the experts' attention. Epidemiological studies were fewer in number--probFCT 29/~-E
ably reflecting US dominance in epidemiology and American cultural preference for coffee over t e a - and in general gave no convincing indication of carcinogenic activity. The oesophagus seemed to be the most likely susceptible site, if any. A number of studies have reported the ingestion of hot tea to be associated with an increased risk of oesophageal cancer, but the Working Group thought the high temperature of the beverage was the more likely stimulus of the cancer process. The overall verdict was that tea was not classifiable as to its carcinogenicity to humans (Group 3). The methylxanthine-containing beverage from South America, mate, was also found to have a temperature problem. Hot mate-drinking was considered probably carcinogenic to humans (Group 2A), again the oesophagus takes the carcinogenic pounding, whereas no data were available to evaluate the risks of drinking cooler mate. The Working Group's attempts to review the cancer status of theophyUine, theobromine, caffeine and methylglyoxal proved unsuccessful and each finished up in Group 3. Of the pharmaceutical compounds on the agenda of the Working Group that deliberated in the Autumn of 1989, two were considered to be proven human carcinogens (Group 1). Cyclosporin, an immunosuppressive agent, is associated with cancer of the lymphatic system, and the cytostatic agent thiotepa induces leukaemia. Azacitidine and chlorozotocin were judged to be probably carcinogenic to humans (Group 2A) on the basis of the laboratory animal cancer profile, and chloramphenicol was similarly ranked mainly because of limited human evidence. Sufficient evidence of carcinogenicity in laboratory animals for dantron and trichlormethine meant a Group 2B classification. Among the Group 3 materials were ampicillin, cimetidine and paracetamol. The Working Group invited to Lyon in the summer of 1989 updated previous evaluations of chromium and nickel, and considered, for the first time, occupational exposure to welding fumes. The last item was assigned to Group 2B because of limited epidemiological evidence, in particular an increased lung cancer rate. Chromium VI and nickel are both Group 1 materials, based on increased cancers of the lung and sinonasal cavity in workers involved in chromate or chromate pigment production, or chromium plating, and lung and nasal cancers in workers exposed to nickel sulphate, or combinations of nickel sulphides and oxides in the nickel refining industry. For the individual metal salts, sufficient evidence of carcinogenicity in laboratory animals was found for calcium, lead, strontium and zinc chromates, and nickel monoxides, crystalline sulphides, hydroxides and metallic nickel. 647
648
Reviews of recent publications--Fd Chem. Toxic. Vol. 29, No. 9
The Working Group meeting in February 1989, under the chairmanship of Dr Martin Gardner, considered textile chemicals. The experts concluded that there was limited evidence that working in the textile manufacturing industry entails a carcinogenic risk (Group 2B), a suspicion based on findings of bladder cancer among dyers and weavers, and of cancers of the nasal cavity among weavers and other textile workers. Of the individual compounds used in the industry that were evaluated by Dr Gardner and his group, p-chloro-o-toluidine and its strong acid salts were concluded to be possibly carcinogenic to man (Group 2A), the limited evidence of activity in man adding to the burden of sufficient evidence seen in laboratory animals. Data from laboratory animals alone ensured that chlorendic acid, Disperse Blue 1, nitrilotriacetic acid and its salts, and some chlorinated paraffins (average carbon chain length C~2 and degree of chlorination approximately 60%) finished up in Group 2B. Decabromodiphenyl oxide, dimethyl hydrogen phosphite, tetrakis-(hydroxymethyl) phosphonium salts, tris(2-chloroethyl)phosphate, Disperse Yellow 3, Vat Yellow 4 and 4-nitro-o-toluidine were each assigned to Group 3. [James Hopkins--BIBRA]
Haiogenated Biphenyls, Terphenyls, Naphthalenes, Dibenzodioxins and Related Products. Edited by R. D. Kimbrough and A. A. Jensen. 2nd Edition. Topics in Environmental Health 4. Elsevier, Amsterdam, 1989. pp. xv + 518. £197.50, Dfl. 375.00. ISBN 0-44481029-3. (ISBN Series 0.444-41597-1). The return of a favourite book in a new edition always raises questions. Does it match up to its predecessor? Has it advanced in line with current knowledge? For this multi-author volume the answers must be, with some reservations, yes. Chapters have been removed or added, contracted or expanded, to accommodate a slightly different emphasis from the first edition. Some additional structure has also been incorporated by division of the book into sections. In the first section, the co-ordination of the contributions from different authors has slipped. Formerly, the first chapter described the production of each of the title compounds in industrial use; now it is limited to the polychlorinated biphenyls. Cross-references in later chapters to some of the title compounds go unfulfilled. Otherwise, this section provides detailed,
up-to-date descriptions of the commercial use, properties and analysis of the title compounds and their transformation products in the environment. The last chapter explains how so few of the episodes of wildlife loss can be linked unambiguously with specific compounds, as a result of analytical sensitivity, environmental persistence and the ubiquity of many of the compounds. The toxicology section commences with a thorough consideration of the absorption, distribution and metabolism of the halogenated aromatics. It also addresses the problems of their bioavailability when they are adsorbed on particulate materials such as soils and fly-ash. The chapter on general toxicity and carcinogenesis is disappointing; it is almost a word-for-word repeat of the corresponding entry in the earlier edition, with only the addition of a few scattered references. Reproductive and developmental toxicity, and also genetic toxicity, have each been assigned their own chapter, and recent research in these areas is well covered. The chapter on mechanism of action is extremely useful; although only concerned with the polychlorodibenzo-p-dioxins and analogues, it presents evidence that supports the concept of 'toxic equivalents' for this series of compounds. If this chapter has defects, they can be attributed to the multiplicity of toxic effects caused by the dioxins and the limitations on the space available for a discussion of each. Two chapters on environmental exposure and background levels in various populations introduce the discussion of human health effects. These, with a chapter on transformer accidents, illustrate how difficult it is to establish examples of toxicity of the polychlorinated biphenyls in the general population. This indicates the importance of the poisoning episodes in Japan and Taiwan, which are summarized next. Accounts of the two episodes of toxicity attributable to localized environmental dispersal of 2,3,7,8-tetrachlorodibenzo-p-dioxin, in Seveso and Missouri, are updated and lead into a discussion of occupational exposure. This book is a valuable reference source. However, in this capacity the index fails. Entries for individual compounds are inconsistent and, in many cases, missing. Also, the overall plan lacks a coherent discussion of the carcinogenic hazards of these compounds. This is particularly noticeable in the chapter on animal toxicity (less than a page devoted to the topic), and human epidemiology is only briefly discussed. [John G r e i g - - M R C Toxicology Unit, Carshalton]
Pergamon Press plc. Printed in Great Britain
Review Section REVIEWS OF RECENT PUBLICATIONS
IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Volume 51. Coffee, Tea, Mate, Methylxanthines and Methylglyoxal. Lyon, 1991. pp. 513. Sw. fr. 80.00. ISBN 92 832 1251 7. Volume 50. Pharmaceutical Drugs. Lyon, pp. 415. Sw. ft. 65.00. ISBN 92 832 1250 9.
1990.
Volume 49. Chromium, Nickel and Welding. Lyon, 1990. pp. 677. Sw. ft. 95.00. ISBN 92 832 1249 5. Volume 48. Some Flame Retardants and Textile Chemicals, and Exposures in the Textile Manufacturing Industry. Lyon, 1990. pp. 345. Sw. fr. 65.00. ISBN 92 832 1248 7. Headlines linking coffee-drinking and cancer are by no means infrequent, indeed they often seem to be weekly events. The epidemiologists are certainly warranted in giving coffee-drinking a good deal of attention; any habit indulged in by so many must be scrutinized carefully for possible impact on health. The communication difficulties arise from the inability of journalists to view individual epidemiological study reports as only one brick in what might be a very large wall of previous relevant work. The headlines are invariably based on the latest findings in isolation, and no attention is given to whether the previous work points to the same conclusion. As a consequence, the public are continually and vigorously told of all the iconoclastic results, but never hear of the ones that conform to the status quo. An IARC Working Group that met in the spring of 1990 has done all thinking commentators a great service, therefore, in reviewing all the available cancer studies on coffee; for a few years at least there will be less excuse for the media not to view things in a wider perspective. Case-control studies have looked pretty carefully for a link between coffee-drinking and increased risk of developing cancers of the upper digestive tract, large bowel, stomach and breast, and have found none; indeed, in the case of the large bowel, the collective evidence is that coffee may be slightly protective. On the less reassuring side, there is some indication that coffee drinkers may be at a slightly higher risk of developing pancreatic or ovarian cancer, or cancer of the bladder and urinary tract. The Working Group was slightly more confident about the bladder carcinogenicity than the activity at the other 'positive' sites, and the bladder findings were the basis of the overall assignment of coffee to Group 2B (possibly carcinogenic to humans). Tea did not escape the experts' attention. Epidemiological studies were fewer in number--probFCT 29/~-E
ably reflecting US dominance in epidemiology and American cultural preference for coffee over t e a - and in general gave no convincing indication of carcinogenic activity. The oesophagus seemed to be the most likely susceptible site, if any. A number of studies have reported the ingestion of hot tea to be associated with an increased risk of oesophageal cancer, but the Working Group thought the high temperature of the beverage was the more likely stimulus of the cancer process. The overall verdict was that tea was not classifiable as to its carcinogenicity to humans (Group 3). The methylxanthine-containing beverage from South America, mate, was also found to have a temperature problem. Hot mate-drinking was considered probably carcinogenic to humans (Group 2A), again the oesophagus takes the carcinogenic pounding, whereas no data were available to evaluate the risks of drinking cooler mate. The Working Group's attempts to review the cancer status of theophyUine, theobromine, caffeine and methylglyoxal proved unsuccessful and each finished up in Group 3. Of the pharmaceutical compounds on the agenda of the Working Group that deliberated in the Autumn of 1989, two were considered to be proven human carcinogens (Group 1). Cyclosporin, an immunosuppressive agent, is associated with cancer of the lymphatic system, and the cytostatic agent thiotepa induces leukaemia. Azacitidine and chlorozotocin were judged to be probably carcinogenic to humans (Group 2A) on the basis of the laboratory animal cancer profile, and chloramphenicol was similarly ranked mainly because of limited human evidence. Sufficient evidence of carcinogenicity in laboratory animals for dantron and trichlormethine meant a Group 2B classification. Among the Group 3 materials were ampicillin, cimetidine and paracetamol. The Working Group invited to Lyon in the summer of 1989 updated previous evaluations of chromium and nickel, and considered, for the first time, occupational exposure to welding fumes. The last item was assigned to Group 2B because of limited epidemiological evidence, in particular an increased lung cancer rate. Chromium VI and nickel are both Group 1 materials, based on increased cancers of the lung and sinonasal cavity in workers involved in chromate or chromate pigment production, or chromium plating, and lung and nasal cancers in workers exposed to nickel sulphate, or combinations of nickel sulphides and oxides in the nickel refining industry. For the individual metal salts, sufficient evidence of carcinogenicity in laboratory animals was found for calcium, lead, strontium and zinc chromates, and nickel monoxides, crystalline sulphides, hydroxides and metallic nickel. 647
648
Reviews of recent publications--Fd Chem. Toxic. Vol. 29, No. 9
The Working Group meeting in February 1989, under the chairmanship of Dr Martin Gardner, considered textile chemicals. The experts concluded that there was limited evidence that working in the textile manufacturing industry entails a carcinogenic risk (Group 2B), a suspicion based on findings of bladder cancer among dyers and weavers, and of cancers of the nasal cavity among weavers and other textile workers. Of the individual compounds used in the industry that were evaluated by Dr Gardner and his group, p-chloro-o-toluidine and its strong acid salts were concluded to be possibly carcinogenic to man (Group 2A), the limited evidence of activity in man adding to the burden of sufficient evidence seen in laboratory animals. Data from laboratory animals alone ensured that chlorendic acid, Disperse Blue 1, nitrilotriacetic acid and its salts, and some chlorinated paraffins (average carbon chain length C~2 and degree of chlorination approximately 60%) finished up in Group 2B. Decabromodiphenyl oxide, dimethyl hydrogen phosphite, tetrakis-(hydroxymethyl) phosphonium salts, tris(2-chloroethyl)phosphate, Disperse Yellow 3, Vat Yellow 4 and 4-nitro-o-toluidine were each assigned to Group 3. [James Hopkins--BIBRA]
Haiogenated Biphenyls, Terphenyls, Naphthalenes, Dibenzodioxins and Related Products. Edited by R. D. Kimbrough and A. A. Jensen. 2nd Edition. Topics in Environmental Health 4. Elsevier, Amsterdam, 1989. pp. xv + 518. £197.50, Dfl. 375.00. ISBN 0-44481029-3. (ISBN Series 0.444-41597-1). The return of a favourite book in a new edition always raises questions. Does it match up to its predecessor? Has it advanced in line with current knowledge? For this multi-author volume the answers must be, with some reservations, yes. Chapters have been removed or added, contracted or expanded, to accommodate a slightly different emphasis from the first edition. Some additional structure has also been incorporated by division of the book into sections. In the first section, the co-ordination of the contributions from different authors has slipped. Formerly, the first chapter described the production of each of the title compounds in industrial use; now it is limited to the polychlorinated biphenyls. Cross-references in later chapters to some of the title compounds go unfulfilled. Otherwise, this section provides detailed,
up-to-date descriptions of the commercial use, properties and analysis of the title compounds and their transformation products in the environment. The last chapter explains how so few of the episodes of wildlife loss can be linked unambiguously with specific compounds, as a result of analytical sensitivity, environmental persistence and the ubiquity of many of the compounds. The toxicology section commences with a thorough consideration of the absorption, distribution and metabolism of the halogenated aromatics. It also addresses the problems of their bioavailability when they are adsorbed on particulate materials such as soils and fly-ash. The chapter on general toxicity and carcinogenesis is disappointing; it is almost a word-for-word repeat of the corresponding entry in the earlier edition, with only the addition of a few scattered references. Reproductive and developmental toxicity, and also genetic toxicity, have each been assigned their own chapter, and recent research in these areas is well covered. The chapter on mechanism of action is extremely useful; although only concerned with the polychlorodibenzo-p-dioxins and analogues, it presents evidence that supports the concept of 'toxic equivalents' for this series of compounds. If this chapter has defects, they can be attributed to the multiplicity of toxic effects caused by the dioxins and the limitations on the space available for a discussion of each. Two chapters on environmental exposure and background levels in various populations introduce the discussion of human health effects. These, with a chapter on transformer accidents, illustrate how difficult it is to establish examples of toxicity of the polychlorinated biphenyls in the general population. This indicates the importance of the poisoning episodes in Japan and Taiwan, which are summarized next. Accounts of the two episodes of toxicity attributable to localized environmental dispersal of 2,3,7,8-tetrachlorodibenzo-p-dioxin, in Seveso and Missouri, are updated and lead into a discussion of occupational exposure. This book is a valuable reference source. However, in this capacity the index fails. Entries for individual compounds are inconsistent and, in many cases, missing. Also, the overall plan lacks a coherent discussion of the carcinogenic hazards of these compounds. This is particularly noticeable in the chapter on animal toxicity (less than a page devoted to the topic), and human epidemiology is only briefly discussed. [John G r e i g - - M R C Toxicology Unit, Carshalton]