Monitoring and assessment of dietary exposure to chemical contaminants Ramesh V. Baht a & Gerald G. Moyb
Introduction More than 10 million unique chemical entities are now known to scientists and several hundred thousand are in common use throughout the world. While the technologies associated with the use of these chemicals have resulted in a dramatic improvement in living conditions for most of the world's population, these technologies and related human activities have also resulted in the introduction of numerous chemicals, directly or indirectly, into the food supply. Only a few of these chemicals have been fully characterized in terms of their potential toxicities to animals and humans, particularly in relation to their long-term effects. Chemical contaminants present in food may result from their natural occurrence in soil (e.g. cadmium, lead, and mercury) or from mycotoxin contamination (e.g. aflatoxin), from pollution arising from industrial and other human activities (e.g. lead, mercury, cadmium, and polychlorinated biphenyls (PCBs)) from agricultural practices (e.g. pesticides, fertilizers, and drugs used in food animals) and from food processing and packaging (e.g. nitrosamines, certain polycyclic aromatic hydrocarbons and lead). These contaminants may present a potential hazard for human health if exposure exceeds tolerable levels. Food contamination monitoring is an essential component of ensuring the safety of food supplies and managing health and environment resources, since it provides information on the levels and sources of contaminants in foods, on the amounts of contaminants ingested by humans, and on trends in contamination levels. Prevention and control of food contamination are highly dependent on adequate and reliable food contamination monitoring programmes. Such programmes offer a number of important benefits to governments and are an integral part of the food safety programmes in most industrialized countries. At the international level, the need for a global assessment oflevels of chemicals in food and in the total diet led to the establishment of the Global Environment Monitoring System - Food Contamination Monitoring and Assessment Pro-
gramme (GEMS/Food) in 1976 which now includes participating institutions in more than 60 countries throughout the world. The main objective of the Programme is to inform governments, the Codex Alimentarius Commission, other relevant institutions and the public on levels and trends of contaminants in food, their contribution to total human exposure and significance with regard to public health and trade. The Programme is conducted globally, regionally, and nationally, as well as in local areas of special concern that serve as models - where appropriate -for remedial actions, food control and resource management. Supporting components of the Programme involve technical cooperation, training, analytical quality assurance studies and information exchange. GEMS/Food collects residue and intake data on the following 18 priority contaminations: • Industrial chemicals (4) -lead, cadmium, mercury, and polychlorinated biphenyls (PCBs); • Organochlorine pesticides (8) - aldrin/dieldrin, DDT-complex, heptachlor and heptachlor epoxide, hexachlorobenzene, total hexachlorocyclohexane (HCH) isomers, gammaHCH (lindane), endosulfan, and endrin; • Organophosphorus pesticides (5) - diazinon, fenitrothion, malathion, parathion, and parathion-methyl; • Mycotoxins ( 1) -Aflatoxin. The major source of information for this paper was data submitted to GEMS/Foodc as well as results of the most recent assessment of regional data on estimated total dietary intakes of contaminants in food (1). Additional data were obtained from national reports and from the literature.
Risk assessment of chemical contaminants in food If toxicological information and/ or exposure estimates suggest that adverse health effects might be expected as a result of a chemical contaminant in food, more detailed information should be obtained on its toxicity (hazard characterization) and on the actual human exposure (exposure assessment) in order to conduct a risk assessment of the
a
Deputy Director, National Institute of Nutrition, Hyderabad, India. Food Safety Scientist, Programme ofFood Safety and Food Aid, Division of Food and Nutrition, World Health Organization, Geneva, Switzerland
c Jelinek, C. Assessment of dietary intake of chemical contaminants,
b
joint UNEP/FAO/WHO Food Contamination Monitaring and Assessment Programme, WHO, Geneva, 1992 (Document WHO/ HPP /FOS/92.6).
132
Rapp. trimest. statist. sanit. mond., 50 (1997)
potential hazard.d As the risk becomes a matter of public health concern, various management options can be considered which can be addressed to the source of the contamination or to the affected food. Any risk management decision must also include consideration of relevant economic, social and political factors (2). Once an option is selected and, where appropriate, intervention programmes are designed and implemented, further monitoring will provide a basis for assessing the effectiveness of the programmes and for future management decisions. In the following sections, characterization of the risks posed by potential food borne hazards has been considered in the light of established safe levels, such as the Acceptable Daily Intake (ADI)
and the Provisional Tolerable Weekly Intake (PTWI) when these have been established by the Joint FAO/WHO Expert Committee on Food Additives (JECFA) or the Joint FAO/WHO Meeting on Pesticide Residues. In cases where these are not established, recommended national levels have been considered.
Dietary intake of lead Information from 23 countries, mostly industrialized, on the dietary intakes of lead by their adult populations was available for review. Average weekly lead intakes for adults in each of the various countries are given in Table 1. For a variety of factors, a strict comparison of the levels among the various countries cannot be made. The differences in years in which the studies were carried out and in the study approaches, and inadequacies in analytical quality control may account for much of the differences in intakes. This applies for all contaminants and countries discussed in this paper.
d
Application ofrisk analysis tofood standards issues. Report of a Joint FAO/WHO Consultation, 13-17 March 1995, WHO, Geneva, 1995 (Document WHO/FNU/FOS/95.3).
Table 1 Dietary intake of lead by adultsa Tableau 1 Doses de plomb ingerees avec les aliments par les adultesa Intake (~g/kg bw/wk) - Dose ingeree (~g/kg de poids corporeVsemaine) Country/areaPays/territoire Australia - Australie YearAn nee 1983 1984 1985 1987 1980 1982 1981 1988 1984 1980 1980 1980 1980 1985 1980 1981 1986 1984-88 1984-88 1983 1982 1987 1982 1984 1985 1988 MedianMediane 2.4 4.2 4.0 8.0 31.5 20.9 5.7 5.7 63.7 7.7 23.7 30.0 32.6 7.0 7.0 4.2 1.6 2.3 2.7 19.8 21.9 28.6 20.8 18.5 18.3 32.3 MeanMoyenne 90th percentile90• centile
Reference bfremarksReference bfremarques
10.6 17.1 95th percentile consumer- Consommateurs du 95e centile (3) Highest in Brussels- Valeurs les plus elevees a Bruxelles GEMS/Food; (4) (5) Beijingc- Pekinc
Belgium - Belgique
11.2 4.6 63.0
41.7 10.9 6.4 96.6 34.3
Canada China- Chine Cuba Denmark - Danemark
With 1/4 liter wine/day- Avec 1/4 I de vin par jour Near heavy traffic- A proximite d'une forte circulation automobile Near smelter- Pres de fonderies 10.5 (6) Mykkanen et al. (1984)
6.6
Finland- Finlande
(7) Market basket - Panier de Ia menagere (7) Duplicate diet- Rations en double
France Germany - Allemagne Guatemala
14.7 14.1 21.6 15.6 15.3 30.5
GEMS/Food; (8) 71.4 27.6 26.4 22.1 55.0 Urban Urban Urban Urban Zone Zone Zone Zone urbaine urbaine urbaine urbaine 133
Wid hlth statist.
quart., 5D (1997)
Table 1 (continued) Tableau 1 (suite) 1 (~g/kg (~g/kg
ntake
bw/wk) - Dose ingenle de poids corporel/semaine) MeanMoyenne 11.3 10.3 12.2 14.0 64.0 56.0 17.6 15.2 28.5 39.1 10.1 7.6 4.7d 9.9 5.6 5.6 9.8 15.4 3.4 4.0e 3.4 3.4 5.5 90th percentile90' centile
Country/areaPays/territoire Hungary- Hongrie
YearAn nee 1980 1982 1983 1984 1981 1981 1982 1985 1981 1982 1980 1981 1981 1983 1985 1987 1988 1980 1985 1984-85 1985 1984-86 1984-86 1988 1984-88 1982 1982 1982 1983 1983 1981-83 1987 1985 1985 1980 1980 1983 1984-88 1988 1984-88 1984-88 1980 1981 1981 1983 1985 1987 1988 1980 1982 1985 1986
MedianMediane 10.6 9.2 11.9 12.3
Reference bfremarksReterence bfremarques
17.0 18.7 17.4 20.2 (9) Duplicate diet- Rations en double (9) Market basket - Panier de Ia menagere
lndia-lnde Ireland -lrlande Italy - ltalie Japan - Japon
Rural families - Families rurales Rural families - Families rurales
6.2 5.9 11.3 4.6 4.4 4.8 6.4 3.3 3.3 15.4
10.9 13.4 (10) Rural females- Sexe feminin, milieu rural
Netherlands - Pays-Bas
16.8 9.8 8.1 15.2 47.6
Selected foods- Choix d'aliments Duplicate diet- Rations en double Duplicate diet- Rations en double (12) Duplicate diet- Rations en double Market basket - Panier de Ia menagere (13) Selected foods- Choix d'aliments (7) Market basket - Panier de Ia menagere
New Zealand Nouvelle-Zelande Poland - Pologne
7.0 5.6 7.9 1.9
24.9 20.2 16.5 22.4 14.0 10.5 11.5 4.6 d 12.3 d 2.7 3.0 3.8 1.75
55.0 44.8 60.5 39.9
Industrial area- Zone industrielle Non-industrial area- Zone non industrielle Industrial area- Zone industrielle Non-industrial area- Zone non industrielle (14) Wroclaw, Lublin (15) Lublin, Olzstyn, Poznan (11) Rural families- Families rurales (11) Seoul families- Families de Seoul (16) (17) (7) Average person; market basket- lndividu moyen; panier de Ia menagere (5, 18) Stockholmb (7) (7) Rural area- Zone rurale (19) High-lead water, Ayr- Eau aforte teneur en plomb, Ayr
Rep. of KoreaRepublique de Coree Sweden - Suede
3.0 9.2 7.7 30.8 6.9 6.6 6.7 6.9 7.9 5.5
Switzerland - Suisse Turkey- Turquie UK- Royaume-Uni
3.0 3.5 6.4 14.0 8.5 47.2 7.4 6.8 6.9 7.1 8.3 5.7 4.4 1.8
4.4 19.8 114.1 8.3 7.5 7.4 7.3 12.2 8.4
New study design - Nouveau plan experimental
134
Rapp. trimest. statist. sanit. mond., 50 (1997)
Table 1 (continued) Tableau 1 (suite) Intake (~g/kg bw/wk)- Dose ingenle (~g/kg de poids corporel/semaine) Country/areaPays/territoire YearAn nee MedianMediane MeanMoyenne 90th percentile90• centile Reference bfremarksReference bfremarques
1987 1986-88 1988
1.3 1.1 1.8
(5f ~g/kg
a FAO/WHO provisional tolerable weekly intake: 50 ~g/kg body weight.- Dose ingenle hebdomadaire tolerable proviso ire FAO/OMS : 50 b GEMS/Food unless otherwise referenced.- Reference GEMS/Food sauf indication contraire. c Non-smoking adult females, duplicate diet.- Femmes adultes non fumeuses, rations en double. d Geometric mean.- Moyenne geometrique. e Three-fold decrease from 1978.- Diminution d'un facteur 3 depuis 1978.
de poids corpore!.
Because the PTWI for lead refers to the maximum intake from all sources, not only the 90th percentile intakes, but even the median intakes should be well below 25 g/kg body weight. This is particularly true for intakes of infants and children because some of the young can ingest substantial amounts of lead from paint, dust and soil by handto-mouth activities in addition to exposure through air and water. Dietary intakes of lead by infants and children are given in Table 2. In view of the relative frequency that median and mean intakes oflead approached or exceeded the PTWI, more countries, both industrialized and developing, should carry out dietary intake studies for lead. Surveys should be conducted on a regular basis to determine the impact, if any, of prevention and control measures on levels of lead in food. More duplicate diet studies should be carried out in areas with heavy industrial activities, especially mining and metal processing, in areas with high lead levels in drinking water and in areas of high traffic density if leaded petrol is still in use. Since dietary intakes of lead relative to body weights are highest for infants and young children, who are also especially sensitive to the toxic effects of lead, and since lead passes the placental barrier readily, every effort should be made to reduce the levels of lead in foods for infants and children, in foods consumed by women of childbearing age and in drinking water. In addition, more' duplicate diet studies for lead should be conducted with pregnant and nursing women and with infants and young children.
kidneys, molluscs and crustacean had higher levels, these foods constitute much less of the average diet. The average weekly intakes of cadmium by infants and young children reported in surveys by the I 1 countries are given in Table 4. The average intakes reported from Cuba and Poland exceed the PTWI. The intakes reported from Finland, Germany, Canada, the United Kingdom and Niger were around 50% of the PTWI. In many of the reporting countries, the median or mean cadmium intakes constitute an appreciable percentage of the PTWI. Where the 90th percentiles were reported, they approached or exceeded the PTWI in some cases. Therefore, exposure to cadmium in the diet is of public health concern. Nationally representative dietary intake studies should be carried out by more countries and appropriate measures should be taken to minimize its occurrence in the diet. Well-designed duplicate diet studies should be conducted in locations of probable cadmium contamination, such as those near mining and metal extraction operations, phosphate fertilizer plants, high-cadmium bearing strata in the soil, municipal sludge-deposition areas, and shellfish areas affected by improperly treated industrial or municipal discharges. Caution should be observed in consuming meat organs, shellfish, vegetables, fruit and grains from areas of known cadmium contamination, and appropriate measures should be taken to minimize its occurrence in these areas.
Dietary intake of mercury Dietary intake of cadmium The average intakes from recent surveys in a number of countries are presented in Table 3. Because of their higher consumption, Canada, Denmark, Finland, the Netherlands and the United States of America identified cereals and their products, followed by potatoes and other vegetables, as the largest contributors to this intake. While animal Wid hlth statist.
Data reported from 15 countries on weekly adult dietary intake were available for assessment. The average total mercury intakes from each of the countries are presented in Table 5. The highest average intakes, from Poland and Denmark, are about 60% of the PTWI of 3.3 pg/kg body weight for methylmercury, or about 40% of the PTWI for total mercury. The average intakes from Germany, 135
quatt., 50 (1997)
Table 2 Dietary intake of lead by infants and childrena Tableau 2 Doses de plomb ingerees avec les aliments par les nourrissons et les enfantsa Country/areaPays/territoire Australia - Australie An nee 1983 1984 1985 1987 1981 1987 1987 1987 1987 1987 1987 1988 1984 1985 1985 1980 1980 1980 1980 1980 1983 1983 1983 1984 1984 1985 1984-85 1979 1983 1982 1981 1982 1982 1982 1982 1985 USA- Etats-Unis d'Amerique 1980 1982 1985 1986 1987 1986-88 1983 Year-
Age
MedianMediane 8.5 24.4 12.1 8.9
Mean90th Moyenne percentile90• centile
Reference bfrernarksReference bfremarques
9mo. 9 mo. 9mo. 9 mo. 0-6 mo. 0-12 mo. 0-12 mo. 0-12 mo. 0-12 mo.
32.9 12.1 118.0 8.3 38.4 11.5 13.7 16.5 16.5 3.4 6.6 7.6 7.2 22.4 18.2 106.2 18.2 95th percentile consumers - Consommateurs du 95e centile (20) (21) Ready-to-use formulae- Formule prate a l'emploic (21) Ready-to-use formulad- Formule prete a l'emploid (21) Concentrated formulae- Formule concentreec (21) Powdered formulae- Preparation en poudrec Selected foods- Choix d'aliments Market basket - Panier de Ia menagere (22) Breast-fed- Alimentation au sein Urban - Milieu urbain Urban- Milieu urbain Urban - Milieu urbain (B) Regular water- Eau normale High-lead- Eau aforte teneur en plomb Breast-fed - Alimentation au sein
Austria - Autriche Canada
Cuba Finland - Finlande Germany - Allemagne
Guatemala Hungary- Hongrie Niger Philippines Poland - Pologne
Sweden - Suede Switzerland - Suisse UK- Royaume-Uni
0-12 mo. 0-12 mo. 0-1 mo. 1-4 yr. 5.6 3-6 mo. 7.5 9-14 mo. 8.2 3 yr. 1 mo. 1 mo. 1 mo. 3 mo. 2.1 3 mo. 11.6 3 mo. 3.6 3 mo. 12.8 1-3 yr. 5.4 1-3 yr. 2.7 1-3 yr. 14.6 1-3 yr. 3 mo. 3 mo. 14.1 10 mo. <4 mo. 226.1 3.7 yr. 4 yr. 3.6 yr. 3.4 yr. 2 yr. 6mo. 6mo. 6-11 mo. 6-11 mo. 6-11 mo. 6-11 mo. 3 mo. 6.0 5.6 8.3 6.36 12.4
11.0 13.7 14.2
33.4 17.8 32.3 20.0 1.7
96.6 61.3 85.4
23.5 361.2 807.8 7.3 6.8 8.9 6.83 15.3 29.0 16.8 12.2 5.0 3.6 3.2 2.7 15.9 16.1 15.4 12.6 24.9
Industrial area- Zone industrielle Non-industrial area- Zone non industrielle Industrial area- Zone industrielle (14) Wroclaw (23) Breast-fed - Alimentation au sein (24) (25) (19) High-lead water, Ayr- Eau aforte teneur en plomb, Ayr Asian non-vegetarian- Sujets asiatiques non vegetariens caucasian non-vegetarian - Blancs non vegetariens (26, 27) Birmingham
New study design - Nouveau plan d'etude
Zaire - Za"ire
• FAO/WHO provisional tolerable weekly intake: 25 ~g/kg body weight.- Dose ingeree hebdomadaire tolerable provisoire FAO/OMS: 25 ~g/kg de poids corpore!. bGEMS/Food unless otherwise referenced.- Reference GEMS/Food saul indication contraire. c Non-lead-soldered cans.- Baltes de conserves non soudees au plomb. d Lead-soldered cans.- Baltes de conserves soudees au plomb. 136 Rapp.
trimest. statist. sanit. mond., 50 (1997)
Table 3 Dietary intake of cadmium by adults a Tableau 3 Doses de cadmium ingerees avec les aliments par les adultesa Country/areaPays/territoire Australia -Australia YearAn nee 1983 1984 1985 1987 1980 1982 MedianMediane 0.8 1.4 1.0 2.1 MeanMoyenne 90th percentile9{)0 centile
Reference bfremarksReference bfremarques
2.7 5.4 2.1
3.6 3.6
95th percentile consumer- Consommateurs du 95e centile (3) Brussels, Charleroi, Liege, 2 % > PTWI Bruxelles, Charleroi, Liege, 2 % > dose ingeree tolerable provisoire GEMS/Food; (4) (5) Beijingc- Pekin c GEMS/Food; (28). Havana - La Havane
Belgium - Belgique
1.8
Canada China- Chine Cuba Denmark - Danemark
1981 1988 1984 1980 1980 1985 1987 1980 1981 1986
1.3 1.0 1.9
1.5 1.0 1.4 3.2 4.1 2.5 2.0 1.5 1.4 0.8
3.5 1.0 3.7 7.5
Near lead smelter -A proximite de fonderies de plomb 3.6 (6) (29) High intakes with liver or wild mushrooms in meals - Fortes doses ingerees avec des repas a base de foie ou de cham pig nons
2.2
Finland - Finlande
France Germany- Allemagne Guatemala
Hungary- Hongrie
Italy- ltalie
Japan - Japon
1986 1984-88 1984-88 1983 1982 1987 1982 1984 1985 1988 1980 1982 1983 1984 1985 1981 1982 1986 1987 1980 1981 1981 1981 1982 1983 1984 1985 1986 1987 1985
1.1 1.2 1.2 3.5 3.5 2.7 4.6 1.8 2.2 2.8 0.8 0.4 0.6 0.5 5.6 4.8 1.8 3.2 3.7 0.9 0.4 0.6 0.6 0.9 7.8 6.4 4.7 3.4 4.9 4.3 5.6e 5.2e 4.5 4.1 4.9 3.7 4.1 3.4 2.4e 3.4e 2.9 1.1 1.1 2.0 1.2 2.1 13.4 7.4 2.4 4.3 7.4 1.5 0.7 1.0 1.0
(7) Market basket - Panier de Ia menagere (7) Duplicate diet- Rations en double
GEMS/Food; (8) Urban -Zone urbaine Urban -Zone urbaine Urban -Zone urbaine Urban - Zone urbaine
Rural families- Families rurales Rural families- Families rurales
4.7 4.8 4.2
8.0 5.7 (30) Rural families - Families rurales (31) Non-polluted areas- Zones non polluees 6.0 5.5 6.1 4.7 6.1 4.2 (11) Rural families- Families rurales (11) Seoul females- Sexe feminin, Seoul
3.8 3.9 4.3 3.9 2.9 2.8
Korea, Rep. of - Coree, Republique de
9.9
1985 1985 1984-86 Wid hlth statist.
Selected foods- Choix d'aliments Duplicate diet- Rations en double (12) Duplicate diet- Rations en double (15) Market basket- Panier de Ia menagere 137
quart., 50 (1997)
l
l
Table 3 (continued) Tableau 3 (suite) Country/areaPays/territoire YearAn nee 1988 1984-88 New Zealand Nouvelle-Zelande Poland - Pologne 1982 1982 1982 1983 1983 1981-83 1987 1980 1988 1988 1984-88 1984-88 1980 1981 1983 1985 1987 1988 1980 1982 1985 1986 1987 1986-88 1988 MedianMediane 2.3 2.3 5.9 5.3 4.4 5.1 2.4 2.2 3.8 1.0 1.2 1.0 1.8 0.8 2.8 1.9 1.9 1.9 2.2 2.2 2.8 2.8 1.9 1.6 1.5 1.1 1.0 Mean- 90th percentileMoyenne 90' centile Reference bfremarksReference bfremarques Selected foods - Choix d'aliments (1) Market basket - Panier de Ia menagere
8.8 0.6 2.9 0.6
94.5 87.5 23.1 8.1
Sweden - Suede
0.9
1.6
Switzerland - Suisse Turkey- Turquie UK- Royaume-Uni
Industrial area- Zone industrielle Non-industrial area - Zone non industrielle Industrial area- Zone industrielle Non-industrial area- Zone non industrielle (14) Lublin, Wroclaw (15) Lublin, Poznan, Olzstyn GEMS/FOOD; (16) (9) Average person; market basket- lndividu moyen; panier de Ia menagere (5, 18) Stockholmc (7) (7) Rural -Zone rurale
2.1 1.9 1.8 1.8 2.2 1.9 2.6 2.9
3.2 2.2 2.1 2.1 2.5 2.3 4.4 4.0 New study design- Nouveau plan d'etude
USA- Etats-Unis d'Amerique
Yugoslavia- Yougoslavie
1.0
(5) Zagrebc
• FAD/WHO provisional tolerable weekly intake: 7 ~g/kg body weight.- Doses ingerees hebdomadaires tolerables provisoires FAO/OMS: 7 ~g/kg de poids corpore!. bGEMS/Food unless otherwise referenced.- Reference GEMS/Food sauf indication contraire. c Non-smoking females.- Non-fumeurs de sexe fl!minin. d Geometric means.- Moyennes geometriques.
Table 4 Dietary intake of cadmium by infants and childrena Tableau 4 Doses de cadmium ingerees avec les aliments par les nourrissons et les enfantsa Intake (~g/kg bw/wk)- Dose ingeree (~g/kg de poids corporel/semaine) Country/areaPays/territoire Australia - Australia YearAn nee 1983 1984 1985 1987 1984-85 1986 1987 1987 Age MedianMediane 1.2 2.1 1.5 2.2 6.3 Mean90th Moyenne percentile90° centile Reference bfremarksReference bfremarques
9 mo. 9 mo. 9 mo. 9 mo. 3-6 mo. 0-1 mo. 0-12 mo. 0-12 mo.
5.25 3.0 9.8 1.1 2.4 4.4 19.9 95th percentile consumers - Consommateurs du 95e centile Urban - Milieu urbain (22) Breast-fed- Alimentation au sein (21) Ready-to-use formula, milk-based Formula prate aI' usage, a base de lait (21) Ready-to-use formula, soy-basedFormula prate aI' usage, a base de soja Rapp. trimest. statist. sanit. mond., 50 (1997)
Cuba Canada
138
Table 4 (continued) Tableau 4 (suite) Intake (~g/kg bw/wk) - Dose ingeree (~g/kg de poids corporel/semaine) Country/areaPayS/territoire YearAn nee 1987 1987 1980 1980 1980 1980 1983 1983 1984-85 1984 1984 1985 1983 1982 1982 1982 1982 1985 USA- Etats-Unis d'Amerique 1980 1982 1985 1986 1987 1986-88 Age MedianMediane 90th MeanMoyenne percentile9oe centile 2.8 2.9 3.9 3.2 7.6 3.2 2.8 2.0 2.7 1.3 2.7 4.4 6.5 2.7 7.5 0.1 2.0 1.9 2.4 2.5 2.9 9.8 9.4 3.5 2.9 2.2 2.3 14.5 9.7 15.6 (14) Wroclaw Industrial area- Zone industrielle Non-industrial area- Zone non industrielle Industrial and non-industrial areas- Zones industrielles et non industrielles (23) Breast-fed- Alimentation au sein
Reference bfremarksReference bfremarques Market basket - Panier de Ia mimagere Selected foods- Choix d'aliments (6)
Finland - Finlande Germany - Allemagne
0-12mo. 0-12 mo. 3 yr. 1 mo. 1 mo. 1 mo. 3 mo. 3 mo. 1-3 yr. 1-3 yr. 1-3 yr. 1-3 yr. 3 mo. 3.7 yr. 4 yr. 3-6 yr. 3-4 yr. 2 yr. 6 mo. 6 mo. 6-11 mo. 6-11 mo. 6-11 mo. 6-11 mo.
Regular water- Eau normale High-cadmium water- Eau aforte teneur en cadmium Breast-fed - Alimentation au sein
Niger Philippines Poland - Pologne
Sweden - Suede UK - Royaume-Uni
2.0 1.9 1.8 2.5 2.7
2.7 3.1 3.6 3.8 3.7
Asian non-vegetarian - Asiatiques non vegetariens Caucasian non-vegetarian - Blancs non vegetariens (26) Birmingham
New study design - Nouveau plan d'etude
a
FAO/WHO provisional tolerable weekly intake: 7 ~g/kg body weight.- Doses ingenles hebdomadaires tolerables proviso ires FAO/OMS: 7 ~g/kg de poids corpore!. bGEMS/Food unless otherwise referenced.- Reference GEMS/Food saul indication contraire.
Table 5 Dietary intake of mercury by adultsa Tableau 5 Doses de mercure ingerees avec les aliments par les adultesa Intake (~g/kg bw/wk) - Dose ingeree (~g/kg de poids corporel/semaine) Country/areaPays/territoire Australia - Australie Belgium- Belgique YearAn nee 1984 1982 MedianMediane 0.3 0.8 Mean- 90th percentileMoyenne 90• centile 1.6 Reference bfremarksReference bfremarques (3) Brussels, Charleroi, Liege, 2%>PTW1 Bruxelles, Charleroi, Liege, 2%> dose ingeree tolerable provisoire
Cuba Denmark - Danemark Finland - Finlande
1983 1985 1980 1984-88 1984-88
1.6
1.6 1.9 0.4 0.23 0.27
5.6C (6) (7) Market basket - Panier de Ia menagere (7) Duplicate diet - Rations en double 139
Wid hlth statist. quart., 50 (1997)
Table 5 (continued) Tableau 5 (suite) Intake (~g/kg bw/wk)- Dose ingeree (~g/kg de poids corporel/semaine) Country/areaPays/territoire YearAn nee MedianMediane MeanMoyenne 90th percentile9Qe centile Reference bfremarksReference bfremarques
France Germany- Allemagne Guatemala Italy - ltalie Netherlands- Pays-Bas
1980 1981 1982 1988 1982 1985 1985 1986 1986 1988 1982 1981-83
2.3 1.6 .68
1.2 2.6 1.5 1.3 0.2 0.2 0.07 0.07 1.1 0.6 1.0
3.9 (8)
(12)
0.06
(13)
New Zealand Nouvelle Zelande Poland - Pologne Sweden - Suede Thailand - Thailande UK- Royaume-Uni USA- Etats-Unis d'Amerique
1987 1988 1987 1985 1985 1986 1987 1986-88 0.7 0.23 0.8 0.3 0.3 0.2 0.2 0.3
2.0 1.3
(32) (14) Lublin, Wroclaw (15) Lublin, Olsztyn, Poznan
(33)
• FAD/WHO provisional tolerable weekly intake: total mercury- 5 ~g/kg body weight methylmercury- 3.3 ~g/kg body weight- Doses ingerees hebdomadaires tolerables provisoires FAD/OMS: mercure total 5 ~g/kg de poids corpore! methylmercure- 3,3 ~g/kg de poids corpore!. b GEMS/Food unless otherwise referenced.- Reference GEMS/Food saul indication contraire. c Maximum
Guatemala, Belgium, and Cuba, were around 50% of the PTWI for methylmercury. The lowest average intakes were reported from Finland, the United Kingdom, the United States and Sweden. The data available concerning weekly total mercury intakes by infants and children are given in Table 6 and are within the PTWI. In a study of breast milk in Sweden, mainly among fishermen's wives who consumed relatively large amounts of fish, intake levels for breast-feeding infants were about 50% of the PTWI. Because of concern for the toxic effects of methylmercury on the developing foetus, Sweden has advised pregnant women to avoid consuming too much fish containing high levels of mercury. In the data reviewed from 16 countries, the average adult intake did not exceed the PTWI in any instance. However, in several countries, it amounted to an appreciable portion of the PTWI. In view of these results, dietary intake studies should be continued in order to follow up on results obtained to date, and should be carried out in additional countries. Most of the studies reviewed have been carried out in industrialized countries. In the results to 140
date, there did not appear to be any correlation with the state of development of the country, but not enough data were available from developing countries to make a valid comparison. Not many results were available concerning dietary intakes of mercury by infants and young children, the age group most at risk. However, in all cases the intakes were equal to or higher than for adults. Representative studies on the dietary intakes of infants and children should be carried out in more countries. In addition, well-designed duplicate portion studies should be conducted in more countries with targeted groups, such as infants, children, pregnant and nursing women, those who consume greater amounts offish and those living near areas of metal pollution.
Dietary intake of polychlorinated biphenyls The available data from 9 countries on mean daily dietary intakes ofPCBs by adults are summarized in Table 7. Since fish generally contain higher levels of PCBs than any other food category, diets containing higher amounts of fish may be expected to lead to higher PCB intakes. Only Japan and the United Rapp. trimest. statist. sanit. mond., 50 (1997)
Table 6 Dietary intake of total mercury by infants and child rena Tableau 6 Doses de mercure totales ingerees par les nourrissons et les enfants a Weekly intake (~g/kg bw/Wk)Dose ingeree (~g/kg de poids corporeVsemaine) Country/areaPays/territoire Australia - Australie Finland - Finlande Poland - Pologne Sweden- Suede USA- Etats-Unis d'Amerique YearAn nee 1984 1984 1980 1985 1985 1988 1985 1986 1987 1986-88 1985 1986 1987 1986-88 1983 Age groupGroupe d'age 9mo. 2 yr. 3 yr. 3-7 yr. 1-3 yr. 3 mo. 6-11 6-11 6-11 6-11 mo. mo. mo. mo. MeanMoyenne 0.02C 0.5 c 1.5 2.5 3.1 2.6 0.3 0.2 0.3 0.4 0.6 0.4 0.5 0.5 1.7 c Reference bfremarksReference bfremarques
(6) (14)
(34) Among high fish consumers- Parmi les gros consommateurs de poisson
USA- Etats-Unis d'Amerique
Zaire - Zaire a
2 yr 2 yr. 2 yr. 2 yr. 3 mo.
FAO/WHO provisional tolerable weekly intake: 5.0 ~g/kg body weight.- Doses ingerees hebdomadaires tolerables provisoires FAO/OMS: 5.0 ~g/kg de poids corporel. bGEMS/Food unless otherwise referenced.- Reference GEMS/Food saul indication contraire. c Median - Mediane.
Table 7 Dietary intake of polychlorinated biphenyls by adultsa Tableau 7 Doses de biphenyls polychlores ingerees par les adultes a Country/areaPays/territoire Australia - Australie Finland - Finlande Guatemala Japan - Japan YearAnnee 1987 1984 1986 1988 1980 1982 1984 1986 1988 1984 1982 1983 1981 1985 1980 1982 1985 1986 1988 Mean daily intake (~g/kg bw/wk)Dose ingeree journaliere moyenne (~g/kg de poids corporel) 0.002 0.21 0.026 0.012 0.046 0.046 0.042 0.030 0.045 0.2 0.9 0.12 0.0005 Not detected - Non decele 0.0075 0.0029 0.0006 0.0025 0.001 Referenceb/RemarksReferenceb/remarques 95th percentile consumers- Consommateurs du 95e centile (35)
Netherlands - Pays-Bas New Zealand - Nouvelle-Zelande Switzerland - Suisse United Kingdom - Royaume-Uni USA- Etats-Unis d'Amerique
(36)
a
U.S. FDA suggested consumption maximum: 1 ~g/kg body weighVday.- Doses maxi males proposees par Ia FDA des Etats-Unis: 1 bGEMS/Food unless otherwise referenced.- Reference GEMS/Food saul indication contraire. Wid hlth statist. quart., 50 (1997)
~g/kg
de poids corpore I par jour.
141
States reported intakes over several years. Both countries reported mean intakes of less than 0.05llg/kg body weight/day over the 1980-1988 period. The United States intakes were an order of magnitude lower than those of Japan, probably because of the lower amount of fish in the United States diet. Substantially higher daily intakes in New Zealand were due primarily to the high PCB intake from dairy products. In this case, the mean intake of 0.9 11g/kg body weight/day approaches the FDA-suggested maximum of 1 g/kg body weight, while the daily mean intake of 1.5 11g/kg body weight for male teens exceeds it. Intakes reported from Australia and the United States for infants and young children were in the same range as those reported for adults. The average daily intakes of PCBs for infants, as estimated from levels in human milk reported from 8 countries, are presented in Table 8. The data from Denmark, Germany, Japan and the United Kingdom were submitted to GEMS/Food. The estimated intakes reported from all countries are above the U.S. Food and Drug Administration-suggested consumption maximum of 1 11g/kg body weight, except for India where the use of PCBs is greatly restricted. A mean intake of about 13 11g/kg body weight was calculated from data reported from PCB content in the breast milk of Inuit women from the Hudson Bay region of Northern Quebec. This high level in breast milk is ascribed to the markedly higher consumption of fish and marine mammals.
However, calculated mean intakes above 10 11g/kg body weight were also noted in Germany. In this connection, it should be noted that high PCB levels have been reported in fish and meat in certain areas of Germany, indicating localized high levels of environmental contamination. While the available information on dietary intakes of PCBs by adults is almost exclusively from industrialized countries, the intakes are usually well below the U.S. FDA guidance figure of 1 11g/kg body weight per day. Monitoring of PCBs in animal-derived foods, especially fish, should be carried out in all countries to determine possible sources of this contaminant in the diet, and dietary intake studies should be carried out, including areas of probable high intakes of PCB-contaminated food. The estimated intake of PCBs by the breast-fed infant was usually far in excess of this guidance value in virtually all reporting nations. In view of the high levels of PCBs found in human milk, surveys of this food should be conducted on a more regular basis in both industrialized and developing countries.
Dietary intake of pesticides Data on levels of residues of organochlorine and organophosphorous pesticides have been submitted to GEMS/Food for a wide variety of foods since 1980. Of the total of twenty countries submitting data, few submitted data on all the pesticides requested and fewer still on all the requested food
Table 8 Dietary intake of PCBs by infants from human milka Tableau 8 Doses de PCB d'origine alimentaire ingerees par des nourrissons avec le lait maternela Country/areaPays/territoire
YearAnnee
Mean daily intake (~g/kg bw/wk)Dose ingen§e journaliere moyenne (~g/kg de poids corpore!)
Referenceh/RemarksRefl§rencebfremarques
Canada Denmark - Danemark Finland - Finlande Germany- Allemagne Hong Kong lndia-lnde Japan - Japan
UK- Royaume-Uni
1988 1988 1982 1982 1982 1983 1985 1982 1980 1981 1982 1983 1984 1985 1980
13.32 3.12 3.32 1.92 10.5 11.9 2.19 Not detected - Non decele
(37) Inuit (37) Caucasians - Blancs (38) Helsinki
(39) Ethnic Chinese (40) Ahmedabab
2.28 2.40 2.52 2.52 2.16 1.80 1.86
a U.S. FDA suggested consumption maximum: 1 ~g/kg body weighVday.- Doses maximales proposees par Ia FDA des Etats-Unis: 1 ~g!kg de poids corpore! par jour.
b GEMS/Food unless otherwise referenced.- Reference GEMS/Food sauf indication contraire.
142
Rapp. trimest. statist. sanit. mond., 50 (1997)
groups. Certainly, one major reason for this is the non-usage or, in some cases, trivial usage of pesticides monitored by GEMS/Food in many countries. On the other hand, participation of developing countries is very low, even though in recent years they have been the main users of organochlorine pesticides, which have been banned in many of the industrialized countries. Data have been submitted to GEMS/Food by even fewer countries on dietary intakes of pesticides. For example, only 9 of the 20 countries providing food data to GEMS/ Food have also submitted dietary intake data. Nonetheless, the available information does offer some indication of the prevailing situation in certain parts of the world.
However, acute poisonings by organophosphorus pesticides are by far the leading cause of pesticide-associated deaths, especially in developing countries. For example, China reported 42 812 cases of pesticide poisoning, including 3 900 fatalities in 1994. About 80% of the cases were caused by organophosphorus pesticides, and in particular, parathion (52%) and methamidophos (14%) (42).
Dietary intake of aflatoxin Aflatoxin has been reported to occur in a wide variety of food commodities ( 43). Aflatoxin Bl' B2 , Gl' G 2 , and M 1 are the most common forms of aflatoxin, but aflatoxin B 1 is considered to be the most toxic. In plant products, aflatoxin contamination occurs directly as a result of fungal invasion mainly by Aspergillus jlavus and A. parasiticus. Aflatoxin, mainly in the form of its metabolites, can occur in animal products, such as milk, meat and eggs, as a result of feeding contaminated feed to animals (43). A global survey carried out in different parts of the world revealed that among the commodities, groundnut and maize are the most frequently contaminated foods (44). Aflatoxin exposure in human populations has been assessed using either analysis of foods and the total diet for aflatoxin or measurement of aflatoxin biomarkers in human biological fluids like urine, serum and breast milk. High levels of aflatoxin have been reported in these commodities particularly in regions of Mrica, South East Asia and Southern China (45).
Organochlorine pesticides In many countries, restrictions have been placed on the use of organochlorine pesticides for nonfood as well as food applications, because of persistence and potential for bioaccummulation in the food chain. In foods, they occur primarily in milk and dairy products, eggs, meat and animal fat, and fish. Even when they are used only in non-food applications, they can enter the food supply not only by direct drift onto crops, but they can ultimately contaminate animal-derived foods because of their chemical stability in the soil and waterways. GEMS/Food data on dietary intakes of aldrin and dieldrin, DDT-complex, total HCH isomers, gamma-HCH (lindane), hexachlorbenzene, heptachlor and heptachlor epoxide, endosulfah and endrin are largely limited to developed countries where exposure for the adult populations is generally very much below the respective AD Is. The limited data available from developing countries indicate a higher average exposure for adults, but, with a few exceptions, still within the ADis. However, based on the levels in breast milk, a significant portion of infants in both developed and developing countries are exposed to levels of organochlorine pesticides above the respective ADis. While the ADI was intended as a level which could be consumed safely over a lifetime, excessive exposure of infants and children to these substances is a concern. Consequently, additional research is required to better characterize the risks of these pesticides from both toxicological and exposure perspectives.
Health effects of dietary exposure to aflatoxin Dietary aflatoxin exposure has been examined in areas of sub-Saharan Mrica and South-East Asia where commodities like maize and groundnuts are consumed as dietary staples. Epidemiological investigations in these areas revealed that aflatoxin intake is associated with a number of acute and chronic liver diseases in the populations. Acute aflatoxin toxicity incidents in human populations have been rare and occurred only under stress conditions like unseasonal rains which damaged food crops and made them susceptible to heavy fungal contamination. The acute diseases mostly in the form of acute hepatitis and cirrhosis were associated with consumption of foods with very high levels of aflatoxin in the parts per million range (Table 9). Of the outbreaks with acute toxicities suggestive of aflatoxin, the most convincing evidence of aflatoxin involvement came from an acute hepatitis outbreak in western parts of India (50). More than 400' people were affected and more than 100 people died in the outbreak. The implicated food was a recently harvested, badly stored maize which had been affected by unseasonal rains. Analysis of the maize samples showed heavy Aspergillus jlavus infection and high 143
Organophosphorus pesticides Diazinon, fenitrothion, malathion, parathion and parathion-methyl are included in the GEMS/Food Programme, but have been reported by only a few countries. Almost all reports indicate that, with few exceptions, exposures are only a few percent of the corresponding ADis. Among the exceptions are reports oflevels offenitrothion reaching about 45% of the diet of adults and children in Australia (41 ). Wid hlth statist. quarl., 50 (1997)
Table 9 Reported exposure to aflatoxins in acute liver diseases in human populations in different countries Tableau 9 Exposition aux aflatoxines dans des cas d'affections hepatiques aigues chez des populations de differents pays Country/areaPays/territoire No. of casesNombre de cas Nature of toxicity (as reported)Nature de Ia toxicite (telle qu'indiquee dans le rapport) Food implicatedAliments incrimines Aflatoxin levels in foodConcentration d'aflatoxine dans !'aliment (mg/kg) Dietary aflatoxin ReferenceintakeReference Dose d'aflatoxine ingeree par Ia voie alimentaire (~g/day- jour)
Senegal - Senegal Uganda - Ouganda China (Prov. of Taiwan) -Chine (province de Taiwan) lndia-lnde lndia-lnde Kenya - Kenya Malaysia - Malaisie
2
Hepatitis - Hepatite Acute hepatitis Hepatite aigue Acute liver disease Affection hepatique aigue Indian childhood cirrhosisCirrhose indienne de l'enfant Acute hepatitis Hepatite aigue Acute hepatitis Hepatite aigue Acute hepatic and renal failure- Affection hepatique aigue et insuffisance renale
Groundnut meal Farine d'arachide Cassava - Manioc Rice- Riz
0.5-1.0 1.7 0.2 0.3 0.25- 15.6 1.6-12.0 Not reported Non indiquee
35- 140 100 Not reported Non indiquee
(46) (47) (48)
26 20 400
Groundnut meal Farine d'arachide Maize- Mais Maize- Mais Chinese noodles Nouilles chinoises
9- 18 2000-6000 Not reported Non indiquee Not reported Non indiquee
(49) (50) (51) (52)
13
aflatoxin levels ranging from 0.25-15.6 mg/kg. Individual aflatoxin intakes were calculated to be 2-6 mg/day (up to 120 pg/kgbodyweights) over a period of one month. Exposure to aflatoxin has been implicated in diseases like liver cirrhosis, kwashiorkor and Reye's syndrome. In individuals suffering from these diseases, aflatoxin, mostly aflatoxin Bl' B2 , M 1 and aflatoxicol, have been detected in liver biopsy, autopsied tissue samples and urine samples (53-55). Concern for effects of aflatoxin in humans is increasing in recent times owing to its hepatocarcinogenic properties. IARC concluded that there was sufficient evidence of carcinogenicity in humans for aflatoxin B 1 and classified it as a Group 1 carcinogen (45). Dietary aflatoxin exposure has been examined in areas of the world where primary liver cancer (PLC) is endemic and where aflatoxin contamination offoods is high (Table 10). It has been also assessed in normal populations exposed to high risk commodities in order to estimate the extent of risk. Epidemiological surveys in countries of sub-Saharan Mrica and South-East Asia showed a positive correlation between dietary aflatoxin intake and liver cancer incidence (58, 68). The major source of aflatoxin exposure in the diet was due to maize, groundnuts and sometimes rice. The frequency and level of aflatoxin contamination in these foods varied according to region, altitude and season. Regions with high rainfall showed higher levels of contamination. This was particularly observed in rice which showed high aflatoxin levels in rain-affected re144
gions of Thailand and India (64 ). Higher levels of contamination were observed during the rainy season when compared to the dry season. In The Gambia, the intakes were higher during the dry season when high aflatoxin levels occurred in groundnuts stored for consumption (63). The high prevalence of hepatitis B virus infection in these areas is also considered to be a risk factor for Primary Liver Cell Cancer (PLC) (69, 70). Correlation studies in PLC endemic areas addressing combined exposure to hepatitis B virus and aflatoxin concluded that aflatoxin exposure was a more important determinant of PLC incidence than hepatitis B virus infection (59, 66).
Presence of aflatoxin metabolites in human biological fluids Exposure to aflatoxin leads to their absorption, metabolic activation and subsequent covalent binding to cellular DNA and protein. The aflatoxins are primarily metabolized by the microsomal mixed function oxygenase system to a number of hydroxylated derivatives as well as an unstable highly reactive epoxide. This epoxide binds covalently to nucleic acids and proteins to exert the toxic and carcinogenic action of aflatoxin (71). A number of aflatoxin metabolites have been detected in urine, milk and serum of human populations exposed to dietary aflatoxin. Among these metabolites, aflatoxin-DNA and -protein adducts and aflatoxin M 1 are considered as biomarkers of aflatoxin exposure. Their measurement in urine Rapp. trimest. statist. sanit. mond., 50 (1997)
Table 10 Dietary aflatoxin exposure in human populations in different countries Tableau 10 Exposition des populations aux aflatoxines alimentaires dans differents pays Country/areaPays/territoire Period of samplingPeriode d'echantillonnage Type of foods sampledType d'aliments echantillonnes Aflatoxin levels in food•Concentrations d'aflatoxine dans les aliments• (~g/kg)
Estimated aflatoxin exposure (ng/kg bw/day)Exposition estimative aux aflatoxines (ng/kg de poids corpore! par jour)
ReferenceReference
Africa- Afrique Kenya Swaziland
1969 1972-1973
Prepared foods and beer Preparations alimentaires et biere Cooked diet - Aliments cuisines
0.1-0.4 (81 + 82)
Swaziland
1982-1983
Cooked foods and beer -Aliments cuisines et biere
Mozambique
1969-1974
Cooked diet - Aliments cuisines
11 - 700 (Total AF)(aflatoxines totales) 8 (Total AF)(aflatoxines totales)
4- 12 (81 + 82) 6-53 Not reported Non indiquee 3000- 18 000 IJg/day- jour (Total AF) 220 (Total AF) 17 (81) 15- 40 (81) 4- 120 (81) 5- 55 (81) 22 000 IJg/dayjour (8 1) 12- 2 000 (81) 4- 100 (81) 2.7 (81)
(56) (51)
(59)
(60)
Transkei Nigeria- Nigeria Gambia - Gambie Asia-Asie Thailand - Tha"ilande Philippines
1976-1977
Cooked diet - Aliments cuisines
(61) (62) (63) (64) (65)
1988 1969-1970
Cooked foods - Aliments cuisines Cooked diet- Aliments cuisines Market foods- Produits du marche
1 - >100 (81) Trace- >1000 (8 1 ) 0.6- 470 (81)
Southern ChinaChine du sud lndia-lnde USA- Etats-Unis d'Amerique
1978-1984 1990 1960-1979
Maize- Ma"is Cooked maize - Ma"is cuit Market foods- Produits du marche
1 - 9 (81)
(66) (68) (45)
a Type of aflatoxin is given in parentheses.- Type d'aflatoxine entre parentheses.
and serum using ELISA or HPLC techniques has been shown to reflect DNA damage by aflatoxin and to be directly related to the dietary intake (74, 77). These observations led to a better understanding and assessment of the relative roles of hepatitis B viral infection and aflatoxin in the etiologyofPLC. The level of urinary adducts reflects recent dietary exposure to aflatoxin (the previous 24-48 hours) whereas the level of aflatoxin-albumin adducts reflects aflatoxin exposure over the previous 2-3 months ( 45). Studies on levels of aflatoxinalbumin adducts in subjects from several countries in Mrica, South East Asia and Europe showed quantitative differences (Table 11). Exposure was significantly higher in regions of Mrica and Southern China than in the European region (76). The levels of aflatoxin-albumin adducts in sera of populations in different regions surveyed ranged from <5 pg to 720 pg aflatoxin Bclysine equivalents per mg of albumin. Wid hlth statist. quart., 50 (1997)
Aflatoxin has been shown to cross the placental barrier in humans. Their detection in cord sera has been reported from Thailand, Ghana, Nigeria and Gambia (Table 12). Several studies have demonstrated the presence of aflatoxin M 1 in human milk (Table 13). It was observed that only a small percentage (0.09-0.43%) of dietary aflatoxin intake was excreted in milk as aflatoxin M 1. Because of its importance for health and trade, aflatoxin contamination of maize, groundnuts and rice as well as other affected foods, such as tree nuts and figs, should continue to be a priority monitoring activity. When levels in staple foods are high, biomonitoring should be undertaken to provide an assessment .of the integrated exposure to aflatoxin in the diet. As currently recommended by JECFA, the levels of aflatoxins in food should be as low as feasible and interventions during production, harvest and storage of food should be considered to prevent or reduce contamination. 145
Table 11 Aflatoxin-albumin adducts in human seraa Tableau 11 Adduits aflatoxine-albumine presents dans les serums humainsa Adduct levels- Concentrations d'adduits (pg d'AFB 1 lysine eq/mg albumin/e) <5b 5-25 26-50 51-75 76-100 >100
Country/area (n)- Pays/territoires (n) Gambia- Gambie May- Mai (323) November- Novembre (67) Senegal - Senegal (29) Kenya (91) China- Chine Guangxi (93) Shandong (69) Thailand - Tha"ilande (84) France (44) Poland - Pologne (30) a Source: Ref.- Ref. (75)
Number of subjects- Nombre de suiets 7 0 0 48 28 69 73 44 30 53 39 20 26 35 0 10 0 0 76 13 6 5 13 0 1 0 0 49 7 2 1 6 0 0 0 0 40 3 1 5 2 0 0 0 0 98 5 0 6 9 0 0 0 0
b Limit of detection.- Concentration
mini male detectable.
Table 12 In utero exposure to aflatoxins Tableau 12 Exposition aux aflatoxines in utero Country/areaPays/territoires Thailand - Tha"ilande Ghana Nigeria - Nigeria Gambia- Gambie Type of sampleType d'echantillons Cord blood -Sang du cordon Maternal blood - Sang maternal Cord blood - Sang du cordon Cord blood - Sang du cordon Maternal blood - Sang maternal Cord blood - Sang du cordon Maternal blood - Sang maternal No. of samplesNombre d'echantillons 35 35 188 78 77 30 30 No. positive (%) Nombre d'echantillons positifs (%) 49 6 34 12 21 97 70 ReferenceReference
(77) (78) (62)
(79)
Table 13 Aflatoxin M1 detected in human milk in different countries Tableau 13 Aflatoxines M1 mises en evidence dans du lait humain de differents pays Country/area- Pays/territoires Zimbabwe Gambia- Gambie Ghana Sudan - Soudan Thailand - Tha"ilande Victoria, Australia - Australia 146
No. of samplesNombre d'echantillons 54 5 264 11 73
No. positive(%)- Nombre d'echantillons positifs (%) 11 100 22 45 15
Reference -Reference (45) (80)
(78) (81) (82) (82) Rapp. trimest statist. sanit. mond., 50 (1997)
Conclusions An assessment of the results of GEMS/Food and
other monitoring activities generally confirms the effectiveness of government efforts to prevent or reduce food contamination in industrialized countries. However, it is also recognized that better exposure estimates for infants and children and other vulnerable groups should be conducted. In developing countries, monitoring information is generally lacking and the health of hundreds of millions of people may be threatened. For these countries, and especially those that employ older agricultural and industrial technologies, basic food contamination monitoring and assessment programmes should be established for at least those contaminants of priority concern. In addition, these programmes can supply the essential information necessary for developing effective intervention strategies and for efficient management of health and environment resources. In all countries, accidental and sporadic contamination is an ever present danger and continual vigilance is necessary to safeguard public health. All countries should identify institutions with the analytical capability to support epidemiological investigations of outbreaks of disease that may be associated with consumption of chemical contaminants in food. All countries should participate in GEMS/Food to promote health-oriented, population-based monitoring of food contaminants in their countries.
established for at least those contaminants of priority concern. These programmes form an essential basis for developing effective intervention strategies and for efficient management of health and environment resources. In all countries, accidental and sporadic contamination is an ever present danger and continual vigilance is necessary to protect public health. All countries should identify institutions with the analytical capability to support epidemiological investigations of outbreaks of disease that may be associated with consumption of chemically contaminated food. All countries should participate in GEMS/Food to promote health-oriented, population-based monitoring at the national level.
Resume Suivi et evaluation de /'exposition d'origine alimentaire aux contaminants chimiques L'article expose les resultats obtenus par le systeme mondial de surveillance continue de l'environnement, par le programme de surveillance continue et d'evaluation de Ia contamination alimentaire (GEMS/Food) et autres programmes de surveillance, relatifs aux contaminants alimentaires prioritaires et, en particulier, au plomb, au cadmium, au mercure, aux biphenyles polychimes, aux residus de pesticides organochlores et organophosphores, ainsi qu'a l'aflatoxine. Ces resultats sont evalues compte tenu des doses acceptables ou tolerables fixees pour ces contaminants. Ces evaluations confirment generalement l'efficacite des efforts deployes par les pouvoirs publics des pays industrialises pour prevenir ou reduire Ia contamination alimentaire, mais il conviendrait de proceder a de meilleures estimations de !'exposition des nourrissons et des enfants ainsi que des autres groupes vulnerables. En ce qui concerne les pays en developpement, on ne possede guere de renseignements fiables, et des centaines de millions de personnes peuvent etre menacees sans qu'on le sac he. Dans ces pays, et notamment ceux qui ont recours a des techniques agricoles et industrielles anciennes, il faudrait mettre en place des programmes de surveillance et d'evaluation de Ia contamination des denrees alimentaires de base, au moins en ce qui concerne les contaminants prioritaires. Ces programmes sont essentiels pour Ia mise au point de strategies d'interventions efficaces et Ia bonne gestion des ressources sanitaires et environnementales. Dans tous les pays, Ia contamination accidentelle ou sporadique des aliments constitue un danger de chaque instant, et une vigilance sans faille est necessaire pour proteger Ia sante publique. Tous les pays devraient recenser les etablissements capables d'effectuer des analyses a l'appui des enquetes epidemiologiques portant sur des flambees de maladies susceptibles d'etre imputables a Ia consommation d'aliments contamines par des produits chimiques. lis devraient egalement tous participer au GEMS/Food afin d'encourager une surveillance a vocation sanitaire au sein de Ia population vivant sur leurs territoires. 147
Summary The results of the Global Environment Monitoring System I Food Contamination Monitoring and Assessment Programme (GEMS/Food) and other monitoring programmes for priority contaminants in the diet, including lead, cadmium, mercury, polychlorinated biphenyls, organochlorine and organophosphorus pesticide residues and aflatoxin, are presented. These results are assessed with respect to established acceptable or tolerable intakes for these contaminants. While the assessments generally confirm the effectiveness of government efforts to prevent or reduce food contamination in industrialized countries, better exposure estimates for infants and children and other vulnerable groups should be calculated. In developing countries, little reliable information is available on the occurrence of food contamination. Without such information, the health of hundreds of millions of people may be threatened. For these countries, and especially those that employ older agricultural and industrial technologies, basic food contamination monitoring and assessment programmes should be Wid hlth statist.
quatt., 50 (1997)
References/References 1. World Health Organization. Concern fur Europe's tomorrow. WHO European Centre for Environment and Health, WHO Regional Office for Europe, Wissenschaftliche Verlagsgesellshaft mbH, Stuttgart, Germany, 1995. 2. Food and Agriculture Organization of the United Nations. Risk management and food safety. Report of a Joint FAO /WHO Consultation, 27-31January 1997, Rome, Food and nutrition paper No. 65, FAO, Rome, 1997. 3. Buchet, J.P. et al. Oral daily intake of cadmium, lead, manganese, copper, chromium, mercury, calcium, zinc and arsenic in Belgium: a duplicate meal study. Food, chemistry and toxicology, 21: 19-24 ( 1983). 4. Dabeka, R. W. et al. Dietary in takes oflead, cadmium, arsenic and fluoride by Canadian adults: a 24-hour duplicate diet study. Food additives and contaminants, 89-102 (1987). 7 Vahter, M. & Slorach, S. Exposure monitaring of lead and cadmium: An international pilot study within the WHO/UNEP Human Exposure Assessment Location (HEAL) Programme. WHO and UNEP, Nairobi, 1990. 8. Weigert, P. et al. Arsenic, lead, cadmium and mercury in and on foods. Zentral Erfassungsund Bewertungstelle fiir Umweltchemikalien (ZEBS) - Hefte (Bundesgesundheitamt, Berlin) 1: 33-36 (1984). 9. Jathar, V.S. etal. Intake oflead through food in India. journal offood sciences and technology, 18: 240-242 (1981). 10. Ikeda, M. et al. Dietary intake of lead among Japanese farmers. Archives of environmental health, 44: 23-29 ( 1989). 11. Watanabe, T. et al. Pb and Cd levels among Korean populations. Bulletin of environmental contamination and toxicology, 38: 189-195 ( 1987). 12. Ellen, G. et al. Dietary intakes of some essential and nonessential trace elements, nitrate, nitrite and N-nitrosoamines by Dutch adults; estimated via a 24-hour duplicate portion study. Food additives and contaminants, 7: 207-221 (1990). 13. Van Dokkum, W. et al. Minerals and trace elements in total diets in the Netherlands. British journal of nutrition, 61: 7-15 (1989). 14. Szymczak,]. et al. Cadmium, lead and mercury in daily food rations of children aged 1-7 years. Roczniki Panstwowego Zakladu Higieny, 38: 230-236 ( 1987). 15. Marzec, Z. & Bulinski, R. Evaluation of cadmium, mercury and lead intake with reproduced diets. Roczniki Panstwowego ZakladuHigieny, 39:344-348 (1988). 16. Slorach, S. et al. Intakes oflead, cadmium and certain other metals via a typical Swedish weekly diet. Var Foda, Suppl. 1: 316 (1983). 17. Abdullah, M. et al. Essential and toxic inorganic elements in prepared meals- 24 hours sampling techniques. In: Braner, P. & Shramel, P. (eds). Trace element analytical chemistry in medicine and technology, Vol. 2. Berlin, Walter de Gruyter and Co., 1983. 18. Vahter, M. et al. Dietary intake of lead and cadmium in Sweden.VarFoda. 44: Suppl. 2:1-16 (1990). 19. Sherlock, J. et al. Assessment of lead intakes and doseresponse for a population in Ayr exposed to a plumbosolvent water supply. Human toxicology, 1: 115-122 (1982). 20. Haschke F. & Stefan, I. Lead intake with food and young infants in the years 1980 I 1981. Wiener Klinische Wochenschrift, 93: 613-616 (1981). 21. Dabeka, R.W. et al. Survey of lead, cadmium, cobalt and nickel in infant formulas and evaporated milks and estimation of dietary intakes of the elements by infants 0-12 months old. Science ofthe total environment, 89: 279-289 ( 1989). 22. Dabeka, R.W. &McKenzie, A.D. Lead and cadmium levels in commercial infant foods and dietary intake by infants 0-1 year old. Food additives and contaminants, 5: 333-342 (1988). 23. Larsson, B. et al. WHO collaborative breast feeding study II. Levels of lead and cadmium in Swedish human milk. Acta pediatrica scandinavia, 70: 281-284 (1981).
24. Yengar, G.V. & Parr, R.M. Trace element considerations in human milk from several global regions. International Workshop on composition and physiological properties of human milk, Kiel, Germany, 1985. 25. Erard, M. et al. Infants' exposure to lead cadmium and selenium by food. Transactions chimiques alimentaires hygiiniques, 73: 394-411 (1982). 26. Smart, G.A. et al. Dietary intakes oflead and other metals: a study of young children from an urban population in the UK. Food additives and contaminants, 5: 85-93 ( 1987). 27. Davies, D.J.A. et al. Lead intake and blood lead in two-year old U.K. urban children. Scienceofthetotalenvironment, 90: 1329 (1990). 28. Lierandi, G.B. et al. Estimation of the daily intake of cadmium which may be consumed by students 12-17 years old in secondary schools in the city of Havana. Die Nahrung, 33: 315-318 (1989). 29. Louekari, K. et al. Exposure to cadmium from foods, estimated by analysis and calculation, comparison of methods. Food additives and contaminants, 5: 111-117 (1987). 30. Watanabe, T. et al. Relationship of cadmium levels among blood, urine and diet in a general population. Bulletin of environmental contamination and toxicology, 38: 196-202 (1987). 31. Watanabe, T. et al. Dietary cadmium intakes of farmers in non polluted areas in japan, and the relation with blood lead levels. Environmental research, 37: 33-43 (1985). 32. Pickston, N.L. et al. The New Zealand diet: a survey of elements, pesticides, colours and preservatives. New Zealand joumaloftechnology, 1:81-89 (1985). 33. Ministry of Agriculture, Fisheries and Food. Survey ofmercury in food: second supplementary report. London, 1987. 34. Skerfving, S. Mercury in women exposed to methylmercury through fish consumption, and in their newborn babies and breast milk. Bulletin of environmental contamination and toxicology, 41:475-482 (1988). 35. Moilanen, R. et al. Average total dietary intakes of organochlorine compound from the Finnish diet. Zeitschrift filr Lebensmittel-Untersuchung und forschung, 182: 484-488 (1986). 36. Wuthrich, C. et al. Pesticides and other chemical residues in Swiss diet samples. Mitteilungenaus dem Gebieteder LebensmittelUntersuchung und hygiene, 76: 260-276 ( 1985). 37. Dewailly, E. et al. High levels ofPCBs in breast milk oflnuit women from Arctic Quebec. Bulletin of environmental contamination and toxicology, 43: 641-646 (1989). 38. Wickstrom, K. et al. Levels of chlordane, hexachlorobenzene and DDT compounds in Finnish human milk in 1982. Bulletin of environmental contamination and toxicology, 31: 251256 (1983). 39. Ip, H.M.H. & Phillips, D.J.H. Organochlorine residues in human breast milk in Hong Kong. Archives of environmental toxicology, 18: 490-494 ( 1989). 40. Jani, J.P. etal. Levels of organochlorine pesticides in human milk in Ahmedabad, India. International archives of environmental health, 60: 111-113 (1988). 41. National Health and Medical Research Council. The 1987 market basket survey. Canberra, Australian Government Publishing Service, 1-84 (1990). 42. World Health Organization. The Newsletter of the International Programme on Chemical Safety, Issue 8, WHO, Geneva, December 1995. 43. Bhat, R.V. Aflatoxins: Successes and failures of three decades of research. In: Fungi and mycotoxins in stured products: Proceedings of an international conference, Bangkok, Thailand, 23-25 April 1991. Champ B.R. et a!. (eds), Canberra, ACIAR Proceeding No. 36, pp 80-85, 1991. 44. Jelinek, C.F. et al. World-wide occurrence of mycotoxins in foods and feeds- an update. Journal ofthe Association ofOfficial Analytical Chemists, 72: 223-230 (1989).
148
Rapp. trimest. statist. sanit. mond., 50 (1997)
45. IARC. Monographs on the evaluation of carcinogenic risks to humans. Vol. 56. Some naturally occurring substances: rood items and constituents, heterocyclic aromatic amines and mycotoxins. Lyon, France, International Agency for Research on
Cancer, 1993. 46. Payet, M. et al. Two obseiVations of children who had consumed for a prolonged period flours contaminated with Aspergillus flavus. Presse medicate, 74: 649 (1966). 47. Serck-Hanssen, A. Aflatoxin-induced fatal hepatitis? A case report from Uganda. Archives of environmental health, 20: 729731 (1970). 48. Tung, T.C. & Ling, K.H. Study on aflatoxin offoodstuffs in Taiwan. journal of vitaminology, 14:48-52 (1968). 49. Arnla, I. et al. Cirrhosis in children from peanut meal contaminated by aflatoxin. American journal of clinical nutrition, 24: 609-614 (1971). 50. Krishnamachari, K.A. et al. Hepatitis due to aflatoxicosis An outbreak in Western India. Lancet, i: 1061-1063 (1975). 51. Ngindu, A. et al. Outbreak of acute hepatitis caused by aflatoxin poisoning in Kenya. Lancet, i: 1346-1348 (1982). 52. Chao, T.C. et al. An outbreak of aflatoxicosis and boric acid poisoning in Malaysia: a clinicopathological study. journal of pathology, 164: 225-33 (1991). 53. Dhatt, P .S. et al. Aflatoxins and Indian Childhood Cirrhosis. Indian journal of pediatrics, 19: 407-408 (1982). 54. Hendrickse, R.G. & Maxwell, S.M. Aflatoxin and child health in the tropics. Journal of toxicology. Toxin reviews, 8: 3141 (1989). 55. Shank, R.C. et al. Aflatoxin in autopsy specimens from Thai children with an acute disease of unknown aetiology. Food and cosmetics toxicology, 9: 501-507 (1971). 56. Peers, F.G. &Unsell, C.A. Dietaryaflatoxins and liver cancer -a population based study in Kenya. British journal of cancer, 27: 473-484 (1973). 57. Peers, F.G. et al. Dietary aflatoxin and human liver cancer. A study in Swaziland. International journal of cancer, 17: 167176 (1976). 58. Peers, F.G. & Unsell, C.A. Dietary aflatoxin and human liver cancer. Annates de la nutrition et de ['alimentation, 31: I 0051018 (1977). 59. Peers, F. et al. Aflatoxin exposure, hepatitis B virus infection and liver cancer in Swaziland. International journal of cancer, 39: 545-553 (1987). 60. van Rensburg, S.J. et al. Primary liver cancer rate and aflatoxin intake in a high cancer area. South African medical journa~ 48: 2508a-2508d (1974). 61. van Rensburg, S.J. et al. Primary liver cancer and aflatoxin in take in Transkei. Journal ofenvironmental pathology, toxicology and oncology, 10: 11-16 (1990). 62. Bean, T.A. & Yourtee, D.M. Aflatoxin metabolites in the urine of Nigerians. Comparison of chromatographic methods. journal of toxicology. Toxin reviews, 8: 43-52 (1989). 63. Wtl.d, C.P. et al. Dietary intake of aflatoxins and the level of albumin-bound aflatoxin in peripheral blood in The Gambia, West Mrica. Cancer, epidemiology, biomarkers and prevention, 1: 229-234 (1992). 64. Shank, R.C. et al. Dietary aflatoxins and human liver cancer, III Field suiVey of rural Thai families for ingested aflatoxins. Food and cosmetics toxicology, 10: 71-84 (1972).
65. Bulatao-Jayme, J. et al. A case-control dietary study of primary liver cancer risk from aflatoxin exposure. lnternationaljournalofepidemiology, 11:112-118 (1982). 66. Yeh, F.S. et al. Hepatitis B virus, aflatoxins and hepatocellular carcinoma in Southern Guanyxi, China. Cancer research, 49: 2506-2509 (1989). 67. Vasanthi, S. et al. Aflatoxin intake from Maize-based diets in a rural population in southern India. Journal of the science of food and agriculture, (in press) (1996). 68. Groopman, J.D. et al. Aflatoxin exposure in human populations: Measurements and relationships to cancer. CRC critical reviews of toxicology, 19: 113-144 (1988). 69. Campbell, T.C. et al. Non-association of aflatoxin with primary liver cancer in a cross-sectional ecological suiVey in the People's Republic of China. Cancer research, 50: 58826893 (1990). 70. Stoloff, L. Aflatoxin is not a probable human carcinogen. The published evidence is sufficient. Regulat1YYJ toxicology and pharmacology, 10: 272-283 (1989). 71. Eaton, D.L. & Callagher, E.P. Mechanisms of aflatoxin carcinogenesis. Annual review of pharmacology and toxicology, 34:135-172 (1994). 72. Groopman, J.D. et al. Molecular dosimetry of aflatoxin exposure. In: Groopman,J.D. & Skipper, P. (eds). Molecular dosimetry of human cancer: epidemiological, analytical and social considerations. Boca Raton, FL. CRC Press, pp 302-324, 1991. 73. Groopman, J.D. et al. A molecular dosimetry of urinary
74.
75.
76.
77.
78.
79. 80.
81. 82.
aflatoxin-DNA adducts in people living in Guangxi Autonomous Region, People's Republic of China. Cancer research, 52: 45-52 ( 1992). Groopm~, J.D. et al. Molecular dosimetry of aflatoxin-Nguanine in human urine obtained in The Gambia, West Mrica. Cancer, epidemiology, biomarners and prevention, 1: 221227 (1992). Wild, C.P. et al. Molecular dosimetry of aflatoxin exposure: contribution to understanding the multifactional etiopathogenesis of primary hepatocellular carcinoma with particular reference to hepatitis B virus. Environmental health perspectives, 99: 115-122 (1993). Zhu,J.Q. et al. Correlation of dietary aflatoxin Bllevels with excretion of aflatoxin Ml in human urine. Cancer research, 47: 1848-1852 (1987). Wilkinson, A.P. et al. Immunoassay of aflatoxin in food and human tissue. journal of toxicology. Toxin reviews, 8: 69-79 (1989). Lamp1ugh, S.M. et al. Aflatoxins in breast milk, neonatal cord blood and serum of pregnant women (short report). British medical journal, 296:968 ( 1988). Wild, C.P. et al. In utero exposure to aflatoxin in West Mrica [letter]. Lancet, 337:1602 (1991). Zarba, A. et al. Aflatoxin M 1 in human breast milk from The Gambia, West Mrica, quantified by combined monoclonal antibody immunoaffinity chromatography and HPLC. Carcinogenesis, 13: 891-894 ( 1992). Coulter,J.B.S. et al. Aflatoxins in human breast milk. Annals of tropical paediatrics, 4: 61-66 (1984). El Nezami, H.S. et al. Aflatoxin M1 in human breast milk samples from Victoria, Australia and Thailand. Food and chemical toxicology, 33: 173-179 (1995).
Wid hlth statist.
quart., 50 (1997)
149