PAH/29 ADD1 Final 4 December 2002
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EUROPEAN COMMISSION HEALTH and CONSUMER PROTECTION DIRECTORATE-GENERAL Directorate C - Scientific Opinions C2 - Management of scientific committees; scientific co-operation and networks Scientific Committee on Food SCF/CS/CNTM/PAH/29 ADD1 Final 4 December 2002 ANNEX Background document to the opinion of the Scientific Committee on Food on the risks to human health of Polycyclic Aromatic Hydrocarbons in food (expressed on 4 December 2002) Polycyclic Aromatic Hydrocarbons – Occurrence in foods, dietary exposure and health effects Summary of background information on polycyclic aromatic hydrocarbons with emphasis on occurrence in foods, dietary exposure and health effects. The summary is based on available background monographs prepared in other frameworks and contributions of members of the SCF Task Force on PAH. B-1049 Bruxelles / Brussels - Belgium. Telephone: exchange (32-2) 299 11 11. Fax: (32-2) 2994891. http://europa.eu.int/comm/food/fs/sc/scf/index_en.html Acknowledgements This background document was prepared by the SCF Task Force on PAH which was chaired by Dr. J.C. Larsen (Institute of Food Safety and Nutrition, Søborg). Other members of the task force were Dr. J. Alexander (Folkehelseinstituttet, Oslo), Professor H. Autrup (Aarhus University), Dr. S. Barlow (Independent consultant in toxicology), Dr. R. Crebelli (Istituto Superiore di Sanità, Rome), Dr. D. Gott (Food Standards Agency, London), Dr. A.G.A.C. Knaap (Rijksinstituut voor Volksgezondheid en Milieu, Bilthoven), Dr. C. Lambré (Agence française de sécurité sanitaire des aliments, Maisons-Alfort), Dr. F.X.R. van Leeuwen (Rijksinstituut voor Volksgezondheid en Milieu, Bilthoven), Dr. E. Menichini (Istituto Superiore di Sanità, Rome), Dr. J. Schlatter (Bundesamt für Gesundheit, Zürich), Professor R. Walker (Food Safety Group, School of Biological Sciences, University of Surrey, Guildford) and Dr. D. Yates (Food Standards Agency, London). A1 TABLE OF CONTENTS 1 EXPOSURE ASSESSMENT A5 1.1 Occurrence of PAH in foods A5 1.1.1 Sources of environmental PAH contamination A5 1.1.2 Physical and chemical properties of PAH influencing their occurrence in foods A6 1.1.3 Contamination of food with PAH during processing and smoking A8 1.1.4 Analytical methods A9 1.1.5 Examples of data for various contaminated foods A9 1.1.6 Measures to reduce PAH contamination of foods A15 1.2 Profile of PAH occurring in food A16 1.3 Intake estimates A31 1.3.1 Dietary intakes A31 1.3.2 Intake by children A39 1.3.3 Temporal trend of intake A39 1.3.4 The contribution from individual food groups to PAH intake A42 1.3.5 Comparison with the contribution to the PAH intake from other sources A49 1.3.6 Contribution from tobacco smoking to the benzo[a]pyrene intake A51 2 HAZARD IDENTIFICATION / CHARACTERISATION A52 2.1 Absorption, distribution, excretion and metabolism of PAH A52 2.1.1 Absorption A52 2.1.2 Distribution A53 2.1.3 Elimination and excretion A55 2.1.4 Enterohepatic cycling of PAH A56 2.1.5 Metabolism A56 2.1.6 Summary of absorption, distribution, metabolism and excretion of PAH A66 2.2 Significance of receptior mediated effects A67 2.2.1 Introduction A67 2.2.2 The Ah-receptor A67 2.2.3 Variation in AhR levels A70 2.2.4 PAH and AhR mediated effects A70 2.2.5 Other receptor mediated effects A72 A2 2.2.6 Other PAH-mediated effects A72 2.2.7 Structure-activity correlations A73 2.2.8 Potentiation A77 2.2.9 Summary A77 2.3 Variation in the susceptibility of humans A77 2.3.1 General aspects A77 2.3.2 Cytochrome P450 (CYP) A79 2.3.3 Glutathione S-Transferases (GST) A80 2.3.4 Others A82 2.3.5 DNA repair A83 2.3.6 Conclusion A84 2.4 Short- and long-term toxicity and carcinogenicity A86 2.4.1 Toxicity after a single exposure A86 2.4.2 Short-term toxicity A87 2.4.3 Special short-term assays for induction of preneoplastic lesions A89 2.4.4 Long-term toxicity A90 2.4.5 Oral carcinogenicity studies evaluated by IPCS (1998) A91 2.4.6 Carcinogenicity of PAH following other routes of administration A101 2.4.7 Carcinogenicity of complex mixtures containing PAH A103 2.4.8 Recent oral carcinogenicity studies on benzo[a]pyrene not evaluated by IPCS (1998) A104 2.5 Reproductive and developmental toxicity of PAH A106 2.5.1 Introduction A106 2.5.2 Placental transfer of PAH and formation of placental PAH-DNA adducts A106 2.5.3 Reproductive toxicity in experimental animals A107 2.5.4 Developmental toxicity in experimental animals A108 2.5.5 Reproductive and developmental toxicity in humans A111 2.5.6 Discussion and conclusions A114 2.6 Effects of PAH on the immune system A123 2.6.1 Immunosuppressive effects possibly leading to either increased susceptibility to cancer or infectious diseases A124 2.6.2 Mechanistic studies A125 2.6.3 Immunological effects observed in offsprings after treatment in utero A126 2.6.4 Observations in humans A127 2.6.5 Immunostimulation leading to allergy or contact hypersensitivity A128 A3 2.7 Genotoxicity of PAH A129 2.7.1 Introduction A129 2.7.2 Genotoxicity of selected polycyclic aromatic compounds A129 2.7.3 Mutagenicity of PAH mixtures A130 2.7.4 Relationship of genotoxicity with carcinogenicity A131 2.8 Special studies on cardiovascular effects of PAH A140 2.9 Observations in humans A141 2.9.1 Biomarkers of exposure to PAH A141 2.9.2 Effects of PAH exposures observed in humans A143 3 REFERENCES A148 Appendix 1 Further examples of PAH metabolism A186 Appendix 2 Toxic equivalency factors for PAH A190 A4 1EXPOSURE ASSESSMENT 1.1 Occurrence of PAH in foods Raw foods should usually not contain high levels of PAH. In areas remote from urban or industrial activities, the levels of PAH found in unprocessed foods reflect the background contamination, which originates from long distance airborne transportation of contaminated particles and natural emissions from volcanoes and forest fires. In the neighbourhood of industrial areas or along highways, the contamination of vegetation can be ten-fold higher than in rural areas (Hancock et al., 1970, personal communication from Lambré, C., 2002; Larsson and Sahlberg, 1982). Processing of food (such as drying and smoking) and cooking of foods at high temperatures (grilling, roasting, frying) are major sources generating PAH (Guillen et al., 1997; Phillips, 1999). Levels as high as 200 µg/kg food have been found for individual PAH in smoked fish and meat. In barbecued meat, 130 µg/kg has been reported whereas the average background values are usually in the range of 0.01-1 µg/kg in uncooked foods. Contamination of vegetable oils (including olive residue oils) with PAH usually occurs during technological processes like direct fire drying, where combustion products may come into contact with the oil seeds or oil (Speer et al., 1990; Standing Committee on Foodstuffs, 2001). Examples of PAH levels in a number of foods can be found in table 1.1.1. 1.1.1 Sources of environmental PAH contamination Foods can be contaminated by PAH that are present in air (by deposition), soil (by transfer) or water (deposition and transfer). The sources, natural and mostly anthropogenic, of PAH in the environment are numerous and include (IPCS, 1998): 4 Stubble burning (Ramdahl and Moller, 1983) and spreading of contaminated sewage sludge on agricultural fields (Hembrock-Heger and Konig, 1990; cited by IPCS, 1998). 4 Exhausts from mobile sources (motor vehicles and aircrafts). Close to an emission source such as a motorway, very high concentrations of PAH were detected in the surface layer, but soil at a depth of 4-8 cm was two times less contaminated (Butler et al., 1984; cited by IPCS, 1998). Close to highways, concentrations of PAH in the soil in the range of 2-5 mg/kg can be found whereas in unpolluted areas, the levels are in the range of 5-100 µg/kg. The distribution and concentration of PAH in soil, leaf litter, and soil fauna depend broadly on the distance from the roadside. A5 4 Industrial plants (e.g. aluminum foundries, incinerators). 4 Wood preservation, use of tar coated wood. Oysters and mussels grown in beds with tar or creosote coated wood posts may be contaminated with PAH. 4 Domestic heating with open fireplaces. Levels of PAH in the atmosphere appear to be higher in the winter than in the summer period. 4 Burning of coal for thermal and electric energy. The quantity emitted varies widely depending on the quality of coal and on the combustiton process. 4 Burning of automobile tires or of creosote treated wood releases considerable amounts of PAH. 4 PAH present in tobacco smoke contaminate both the atmosphere of the kitchen and the foods during preparation and cooking. 4 Oil pollution of surface waters and soils. 4 Forest fires and volcanic eruptions (Hites et al., 1980; cited in IPCS, 1998). 1.1.2 Physical and chemical properties of PAH influencing their occurrence in foods The occurrence of PAH in foods is influenced by the same physicochemical characteristics that determine their absorption and distribution in man. These are their relative solubility in water and organic solvents, which determine their capacity for transport and distribution between different environmental compartments and their uptake and accumulation by living organisms. The transportation of PAH in the atmosphere is influenced by their volatility. The chemical reactivity of PAH influences adsorption to organic material or degradation in the environment. All these factors determine the persistence and capacity of PAH to bioaccumulate in the food chain. PAH are lipophilic and generally have a very poor aqueous solubility.