Number 191      November 1999

MAFF UK - 1997 TOTAL DIET STUDY - ALUMINIUM, ARSENIC, CADMIUM, CHROMIUM, COPPER, LEAD, MERCURY, NICKEL, SELENIUM, TIN AND ZINC

Index to MAFF UK Food Surveillance Information Sheets, 1999

See also:
33: MAFF, UK: A survey of Cadmium, Arsenic, Mercury and Lead concentrations in Individual foods (July 1994)
34: MAFF UK - 1991 Total Diet Study (July 1994)
113: MAFF, UK: Survey of Lead and Cadmium in foods (June 1997)
119: MAFF UK - Survey of Mercury in foods (August 1997)
126: MAFF UK - Dietary Intake of Selenium
131: MAFF UK - 1994 Total Diet Study: Metals and Other Elements
137: MAFF UK - 1991 Total Diet Study - Nitrate and Nitrite (December 1997)
149: MAFF UK - 1994 Total Diet Study (Part 2) Dietary intakes of metals and other elements (May 1998)
152: MAFF UK - Summaries of Food Surveillance Papers - 'Lead, Arsenic and Other Metals in Food' and 'Cadmium, Mercury and Other Metals in Food' (June 1998)
166: MAFF UK - Metals and Other Elements in Vegetarian Foods (November 1998)
194: MAFF UK - Nutrient analysis of Bread and Morning Goods (January 2000)
199: MAFF UK - Multi-Element Survey of Wild Edible Fungi and Blackberries (March 2000)

• The Total Diet Study provides information on dietary exposures of the general UK population to chemicals such as nutrients and contaminants.
• Dietary exposures to aluminium, arsenic, cadmium, chromium, copper, lead, mercury, nickel, selenium, tin and zinc are regularly checked to see if there are any risks to health from the levels of these chemicals found in the UK diet.
• The results from the 1997 Total Diet Study show that dietary exposures to aluminium, arsenic, cadmium, chromium, copper, mercury, nickel, tin and zinc are similar to those from previous years and are not a concern to health.
• Dietary exposures to lead for UK consumers continue to fall and are well below the recommended safe level of exposure.
• The estimated selenium intake of the UK population is similar to those from 1994 and 1995 and is lower than those from 1991 and 1985. In considering the 1994 and 1995 estimates, the Committee on Medical Aspects of Food Policy (COMA) agreed that there was, at present, no evidence of adverse health consequences from current intakes.

Summary

Concentrations of eleven metals and other elements analysed in the 1997 Total Diet Study (TDS) are reported and have been used to estimate dietary exposures of the general UK population to these elements. Samples for the 20 TDS food groups were obtained from 20 towns in the UK in 1997 and analysed in 1998/99 for aluminium, arsenic, cadmium, chromium, copper, lead, mercury, nickel, selenium, tin and zinc.

Analyses for bromine, fluorine and iodine are also being carried out but are not reported here. When completed, the results of these analyses and the corresponding dietary exposure estimates will be reported in a separate Food Surveillance Information Sheet.

Dietary exposures to aluminium, arsenic, cadmium, chromium, copper, mercury, nickel, tin and zinc estimated from the results of the 1997 TDS are similar to those from previous TDSs and are below the appropriate recommended safe levels of exposure where these exist. Dietary exposure of the UK population to lead is falling as a result of successful measures taken to reduce lead contamination of the environment and food. There has been little change in estimates of selenium exposure since the 1994 TDS but current estimates are lower than those from the 1991 and 1985 TDSs.

Background

Metals and other elements in food
Environmental sources are the main contributors to contamination of food with most metals and other elements. Some elements (e.g. arsenic) are present naturally but the major sources of other elements (e.g. lead) in the environment are from pollution from industrial and other human activities. The presence of metals and other elements in food can also be the result of contamination by certain agricultural practices (e.g. cadmium from phosphate fertilisers) or manufacturing processes (e.g. tin in canned foods).

Metals and other elements in food are of interest because of their possible health effects. Some have no known beneficial biological function and long-term, high-level exposures may be harmful to health. For example, organic mercury compounds are neurotoxins, exposure to lead can be harmful to neuropsychological development, inorganic arsenic is a human carcinogen, and cadmium can affect renal function. Other elements can cause short-term health effects from one incidence of high-level exposure. For example, high concentrations of tin in food can cause stomach upsets. Some elements, such as copper, chromium, selenium and zinc are essential to health but may be toxic at high levels of exposure.^1,2

The risks to health from chemicals in food can be assessed by comparing estimates of dietary exposure with recommended safe levels of exposure. In the case of metals and other elements, these are the Provisional Tolerable Weekly Intakes (PTWIs) and Provisional Maximum Tolerable Daily Intakes (PMTDIs) recommended by the Joint Expert Committee on Food Additives of the Food and Agriculture Organization of the United Nations and the World Health Organization International Programme on Chemical Safety (JECFA). The PTWI or PMTDI is an estimate of the amount of a substance that can be ingested over a lifetime without appreciable risk.

The Joint Food Safety and Standards Group (JFSSG) carries out surveys to obtain information on the concentrations of metals and other elements in food. This information is used together with consumption data to estimate dietary exposures and assess the safety of foods consumed in the UK. The main source of information on dietary exposures of the general UK population to metals and other elements is the TDS which is described below.

Total Diet Study
The TDS is an important part of JFSSG surveillance programme for chemicals in food and has been carried out on a continuous annual basis since 1966. Results from the TDS are used to estimate dietary exposures of the general UK population to chemicals in food, such as nutrients and contaminants, to identify trends in exposure and make assessments on the safety and nutritional quality of the food supply.³

The design of the UK Total Diet Study has been described in detail elsewhere, but basically involves 119 categories of foods combined into 20 groups of similar foods for analysis.^3,4 The relative proportion of each food category within a group reflects its importance in the average UK household diet and is based on an average of three previous years of consumption data from the National Food Survey.⁵ Foods are grouped so that commodities known to be susceptible to contamination (e.g. offals, fish) are kept separate, as are foods which are consumed in large quantities (e.g. bread, potatoes, milk).^3,4

Analyses for metals and other elements in the TDS are carried out every three years. The foods making up the 20 groups analysed for metals and other elements are obtained from retail outlets in 20 locations throughout the UK. Samples are transported to one centre where they are prepared and cooked (where necessary) according to normal domestic practice. After preparation, the constituents of each food group are thoroughly homogenised and frozen until analysis.

Each food group obtained from each location (i.e. a total of 400 samples) in the 1997 TDS was analysed for aluminium, arsenic, cadmium, chromium, copper, lead, mercury, nickel, selenium, tin and zinc. The mean (average) concentrations from the 20 samples of each food group were used together with data on the consumption of these food groups to make estimates of dietary exposure for either the average UK household (i.e. population exposure estimates) or for individual adult consumers (i.e. consumer exposure estimates). Population exposure estimates are compared with those from previous years to identify trends in exposure. Consumer exposure estimates are compared with the appropriate PTWIs and PMTDIs to assess the safety of foods consumed by the general UK population.

Brand names
Brand names are not available as TDS samples are composites of a number of different foods.⁶

Methodology

Sample preparation
Individual components of the TDS food groups were purchased from retail outlets in 20 representative towns in the UK in 1997 and prepared as for consumption, including cooking where appropriate, before being combined into one of 20 food groups.^3,4 The 400 individual TDS samples analysed in this study were prepared and homogenised by the Institute of Food Research (Norwich).

Multi-Element Analysis
Samples were analysed for aluminium, arsenic, cadmium, chromium, copper, lead, mercury, nickel selenium, tin and zinc by the Central Science Laboratory, Norwich (CSL). Prior to analysis, the homogenised samples were digested in inert plastic vessels with nitric acid using microwave heating. All elements except mercury and selenium were analysed using Inductively Coupled Plasma-Mass Spectrometry (ICP-MS). Hydride Generation ICP-MS (HG-ICP-MS) was used for mercury and selenium analyses. All results were corrected for recovery. Details of the methods of analysis and quality control procedures have been reported previously.⁷

Quality control
CSL participated in and had consistently demonstrated a satisfactory performance in the appropriate rounds in FAPAS (Food Analysis Performance Assessment Scheme) and was accredited by UKAS (United Kingdom Accreditation Service) for multi-element analysis of food.

The quality control criteria used are as follows:

• Three National Institute of Standards and Technology (NIST) Certified Reference Materials (CRMs) were analysed with every batch of samples [i.e. NIST 1547 (Peach Leaves), NIST 1566a (Oyster tissue) and NIST 1577B (Bovine liver)]. Batches were rejected if results for 2 of the 3 CRMs were not within 40 per cent of the certified reference value.
• A calibration standard was analysed at the start and end of each run. Batches were rejected if the re-measured standard was outside of the original value by 20 per cent or more.
• 10 per cent of samples were run in duplicate in different batches. Results of duplicate analyses had to have Relative Standard Deviations (RSDs) of less than 25 per cent or differ by no more than 2 times the limit of detection (LOD) whichever was greater.
• LODs were defined as 3 times the standard deviation of measured values for reagent blanks after correction for typical sample weight and dilution. The LODs for aluminium, arsenic, cadmium, chromium, copper, lead, mercury, nickel, selenium, tin and zinc are given in Table 1.

Dietary exposure estimates
Two types of dietary exposures have been estimated from the results of the 1997 TDS for aluminium, arsenic, cadmium, chromium, copper, lead, mercury, nickel, selenium, tin and zinc:

1. Population exposure estimates. These are based on consumption data from the National Food Survey. These are compared with similarly derived estimates from previous TDSs to follow trends in dietary exposures of the general UK population.
2. Consumer exposure estimates. These are estimates of dietary exposures for individuals who eat average amounts of each food group (i.e. mean consumers) and those who eat significantly more than average [i.e. upper range (97.5th percentile) consumers] and are based on consumption data from the Dietary and Nutritional Survey of British Adults (Adults Survey).⁸ Exposure estimates (both mean and 97.5th percentile) of adult consumers are used for comparison with the PTWIs and PMTDIs to assess the risks to consumers.

The estimation of both these types of dietary exposures is discussed in more detail below.

Population exposure estimates
The quantities of foods that make up the TDS and the relative proportion of each food are largely based on an average of the available data from three previous years of the National Food Survey and are updated annually.⁵ For example, to determine the amounts of foods making up the 1997 TDS, an average consumption data of the 1993, 1994 and 1995 National Food Survey were used. Multiplying the amounts of foods consumed (based on consumption data from the appropriate years of the National Food Survey) by the corresponding mean concentrations of metals and other elements detected in each TDS food group gives an estimate of population average exposure (covering both adults and children) for that year. These estimates can be used to follow trends in exposure as they take into account changes in both consumption of the various foods making up the general UK diet and concentrations of metals and other elements in these foods.

Concentrations of metals and other elements in 1997 TDS samples are shown in Table 2. Population average exposures based on these concentrations and consumption data from the National Food Survey are shown in Table 3 and are compared with those from previous UK TDSs in Table 4.

Consumer exposure estimates
Mean and 97.5th percentile exposures for aluminium, arsenic, cadmium, chromium, copper, lead, mercury, nickel selenium, tin and zinc have also been estimated for adult consumers using the mean concentrations in each food group and consumption data from the Adults Survey (Table 3).⁸ Dietary exposures of adult consumers have been estimated for comparison with the appropriate PTWIs and PMTDIs (Table 5).

Consumer exposure estimates are less suitable for following trends in exposure than population estimates as they are based on consumption data from the Adults Survey which was carried only once in 1986 and 1987 and is not updated annually.⁸ They do not therefore take into account changes in consumption patterns and only reflect changes in concentrations of metals and other elements. However, consumer exposure estimates do take into account exposures by individuals rather than the population as a whole, and also consider those who consume above average amounts of food (i.e. 97.5th percentile consumers). These estimates therefore provide more accurate assessments of dietary exposures of individual consumers than population exposure estimates for comparison with PTWIs and PMTDIs.

Unless stated otherwise, the mean concentrations and dietary exposures reported in this Food Surveillance Information Sheet are all upper bound values. This means that for those results less than the LODs, it has been assumed that concentrations of the elements are equal to the LODs.

Mean concentrations calculated from these results are known as upper bound values. Dietary exposures estimated from these upper bound mean concentrations are likely to be slight over estimates of exposure.

Results

The mean concentrations of aluminium, arsenic, cadmium, chromium, copper, lead, mercury, nickel selenium, tin and zinc found in each food group from the 20 locations in the 1997 TDS for metals and other elements are shown in Table 2. Population average, and mean and 97.5th percentile consumer exposure estimates are given in Table 3. Population average exposures estimated from the results of the 1997 TDS are compared with those from TDSs carried out since 1976 in Table 4. Estimates for mean and 97.5th percentile adult consumers are compared with PTWIs and PMTDIs in Table 5.

The concentrations detected and dietary exposures for each element are discussed in detail in the ‘Interpretation’ section.

Interpretation

Aluminium
The highest mean concentrations of aluminium were found in the Bread (6.6 mg/kg) and Fish (6.1 mg/kg) groups (Table 2). These values are similar to the aluminium concentrations found in these food groups in previous TDSs (e.g. in the 1994 TDS, the Bread group had a mean aluminium concentration of 3.7 mg/kg and in the 1991 TDS, 4.6 mg/kg).^1,9 The mean aluminium concentration in the Miscellaneous cereals group in the 1997 TDS (i.e. 5.2 mg/kg) was similar to that of the 1988 TDS (i.e. 4.8 mg/kg) but was considerably lower than the 1994 TDS (i.e. 78 mg/kg) and 1991 TDS (i.e. 64 mg/kg).^1,9,10 The relatively high aluminium concentrations found in the Miscellaneous cereals group from the 1991 and 1994 TDSs were considered to be caused by the presence of aluminium-containing additives which are permitted for use in some of the bakery products included in the Miscellaneous cereals group.^1,9,11 The differences in concentrations between the 1988/1997 and 1991/1994 TDSs may be due to differences in the use of aluminium-containing additives in bakery products and/or in the individual products included in this food group in different years.

The average UK population dietary exposure to aluminium estimated from the results of the 1997 TDS (i.e. 3.4 mg/day) was similar to the 1988 TDS (i.e. 3.9 mg/day) but lower than those from the 1994 (i.e. 11 mg/day) and 1991 TDSs (i.e. 10 mg/day) (Table 4). These differences are due to the lower mean aluminium concentrations in the Miscellaneous cereals group in 1988 and 1997 (Table 2). The food groups which made the greatest contributions to dietary exposures of adult consumers in the 1997 TDS were Beverages (35 per cent), Bread (21 per cent) and Miscellaneous cereals (16 per cent). Beverages make a major contribution to exposure owing to the high rate of consumption of this food group rather than because of high concentrations of aluminium. The presence of higher concentrations in the Bread and Miscellaneous cereals groups combined with relatively high rates of consumption helps to explain the large contribution made by these groups to dietary exposure.

Exposure estimates of aluminium for mean (i.e. 3.2 mg/day) and 97.5th percentile (i.e. 5.7 mg/day) adult consumers from the 1997 TDS were lower than the JECFA PTWI of 7 mg/kg bodyweight which is equivalent of 60 mg/day for a 60 kg adult (Table 5).¹² Dietary exposure estimates from the UK TDS were similar to those from other countries. Dietary exposures to aluminium in the USA were reported to range from 0.7 mg/day in infants to 11.5 mg/day for 14 to 16 year old males.¹³ Dietary exposures from Italian TDSs were found to range between 2.3 mg/day and 6.3 mg/day.¹⁴

The Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment (COT) considered the health implications from aluminium in food on the basis of 1991 TDS exposure estimates (i.e. 10 mg/day as compared to the 1997 estimate of 3.4 mg/day) and concluded that ‘intakes, as estimated from average levels in food in the UK, are not a cause for toxicological concern’.¹ In an earlier statement, the COT noted that ‘the relationship between aluminium and Alzheimer’s disease remains unclear and is the subject of continuing research. There is no evidence that aluminium in food affects the occurrence of Alzheimer’s disease.’¹⁰

Arsenic
Arsenic is present in food in different forms (species) which vary in toxicity with inorganic forms being the most toxic. This is reflected in the JECFA PTWI (of 0.015 mg/kg bodyweight) which applies to inorganic arsenic only.¹² Most of the arsenic in the diet is present in the less toxic organic forms.^15,16 However, it is difficult to distinguish analytically between the different forms of arsenic in food, and for this reason most surveys including this one have measured total arsenic. A JFSSG-funded project is being carried out by CSL to develop a method suitable for the routine determination of the different forms of arsenic in food. If this project is successful, the method developed will be used to analyse samples from a future UK TDS to allow the estimation of dietary exposures to inorganic arsenic. This will allow direct comparisons to be made with the PMTDI for inorganic arsenic and more accurate assessment of the risks to health.

The population exposure of total arsenic estimated from the results of the 1997 TDS was 0.065 mg/day (Table 3). This is similar to population dietary exposures from previous TDSs (Table 4). The Fish group made the greatest contribution to population dietary exposure (i.e. 94 per cent) and also had the highest mean arsenic concentration (i.e. 4.4 mg/kg) (Tables 2 and 3).

Dietary exposure estimates to total arsenic for mean and 97.5th percentile adult consumers were 0.12 mg/day and 0.42 mg/day respectively. Although these values are similar to or greater than the PMTDI for inorganic arsenic, which is equivalent to 0.13 mg/day for a 60 kg adult (Table 5),¹² it should be noted that they refer to total arsenic and that most of the arsenic present in the diet is in the less toxic organic forms.^15,16 The COT considered 1991 TDS dietary exposure estimates, which are similar to 1997 TDS estimates, concluding that such levels are not a cause for toxicological concern.¹

Dietary exposures to total arsenic have also been estimated for other countries. Two TDSs carried out in the USA in 1990, and 1986 to 1991 found mean total arsenic exposures for adults of 0.051 mg/day and 0.038 mg/day respectively,^17,18 the average exposure of Canadian adults from a TDS carried out between 1985 and 1988 was 0.047 mg/day,¹⁹ exposure of male adults in New Zealand was estimated to be 0.15 mg/day,²⁰ a survey carried out in the Basque Country (Spain) in 1990 and 1991 found a mean total arsenic exposure of 0.286 mg/day,²¹ and a duplicate diet study of Japanese adults reported an exposure of 0.182 mg/day.²²

Cadmium
Cadmium is present at low concentrations in most foods, with those that are consumed in larger quantities making the greatest contributions to population dietary exposure (i.e. 0.012 mg/day in the 1997 TDS). For example, in the 1997 TDS, cadmium concentrations were highest in the Offals (i.e. 0.077 mg/kg) and Nuts (i.e. 0.059 mg/kg) groups, while the Bread and Potatoes groups made the greatest contributions (i.e. both 25 per cent) to dietary exposure of the general population (Tables 2 and 3). The dietary exposure of the general UK population estimated from the results of the 1997 TDS was slightly lower than those of previous years (e.g. 0.014 mg/day in the 1994 TDS and 0.018 mg/day in the 1991 TDS) (Table 4).^2,9

Dietary exposures of mean and 97.5th percentile adult consumers were estimated from the results of the 1997 TDS to be 0.014 mg/day and 0.024 mg/day respectively (Table 3). These values are below the JECFA PTWI of 0.007 mg/kg bodyweight which is equivalent to 0.06 mg/day for a 60 kg person (Table 5).²³ Smoking tobacco can also contribute to cadmium exposure. Smoking 20 cigarettes per day will result in inhalation of 2 micrograms to 4 micrograms of cadmium.²⁴ The COT commented in 1995 that ‘the intake of cadmium is below levels known to cause renal toxicity, although we note that the margin between average cadmium intakes and levels associated with toxicity is smaller than for most other metals. We are reassured that the average dietary intake of cadmium did not increase between 1982 and 1991, as we would view any increase with concern. We note that cadmium is recognised as a human carcinogen via inhalation of cadmium dusts and fumes in the workplace. There is inadequate evidence to assess the carcinogenicity of dietary cadmium.’ ²

Dietary exposures to cadmium of UK consumers estimated from the results of the 1997 TDS are within the range found in the European Union (EU). A study carried out by the European Commission in 1995 and 1996 found that dietary exposures to cadmium in the 15 Member States of the EU ranged from 0.007 mg/day to 0.057 mg/day.²⁵ Dietary exposure estimates have also been reported for the USA (i.e. 0.015 mg/day),¹⁷ Canada (i.e. 0.024 mg/day),²⁶ New Zealand (i.e. 0.028 mg/day for adult males),²⁰ and Egypt (i.e. 0.24 mg/day).²⁷

Chromium
Most of the chromium present in food is in the trivalent form (Cr³⁺) which is an essential nutrient.² To prevent deficiency, the Committee on Medical Aspects of Food Policy (COMA) has recommended that chromium intakes should be above 0.025 mg/day for adults and between 0.1 to 1.0 micrograms/kg bodyweight/day for children and adolescents.²⁸ The COMA also noted that no adverse effects had been observed from trivalent chromium. Although the hexavalent form of chromium (Cr⁶⁺) is more toxic, it is not normally found in food.²

The UK population exposure to chromium was estimated from the results of the 1997 TDS to be 0.1 mg/day. Dietary exposures of mean and 97.5th percentile adult consumers were estimated to be 0.1 mg/day and 0.17 mg/day respectively (Table 3). The JECFA have not set a PTWI for chromium. However, these dietary exposure estimates are similar to levels that the COT considered in 1995 did not warrant any major concern in terms of toxicity, or deficiency.²

This population exposure to chromium estimated from the 1997 TDS is lower than that from the 1994 TDS which was unexpectedly high (i.e. 0.34 mg/day) (Table 4).⁹ The high population exposure estimate from the 1994 TDS was caused by relatively high chromium concentrations in the Oils and fats, Milk, Dairy produce and Nuts groups.⁹ Chromium concentrations in these and other food groups in the 1997 TDS are similar to TDSs carried out before 1994.^2,9 The relatively high concentrations and exposure estimate from the 1994 TDS appear to be unique to that year and not part of a trend of increasing exposure to chromium of the UK population.

Copper
Copper is an essential element, but can be toxic at high levels of exposure. To reflect this, the COMA has recommended a Reference Nutrient Intake (RNI - enough, or more than enough for about 97 per cent of people in a population) for adults of 1.2 mg/day and JECFA has recommended a PMTDI of 0.5 mg/kg body weight (i.e. is equivalent to 30 mg/day for a 60 kg person).^28,29 Copper is present in most foods with offals and nuts containing the highest concentrations. For example in the 1997 TDS, mean copper concentrations in the Nuts and Offals groups were 8.5 mg/kg and 50 mg/kg respectively while mean concentrations in the other food groups ranged from 0.05 mg/kg to 2.1 mg/kg (Table 2).

Dietary exposures to copper for the general UK population have remained relatively constant. The UK population dietary exposure estimated from the 1997 TDS was 1.2 mg/day which is equal to the population dietary exposure estimated from the 1994 TDS (Table 4) and is similar to the copper intake (i.e. 1.01 mg/day) from the 1997 National Food Survey.^5,9 Dietary exposures for mean and 97.5th percentile adult consumers estimated from the 1997 TDS were 1.4 mg/day and 3.2 mg/day respectively. These values are below the PMTDI and approximately equal to the RNI and so are not a concern in terms of toxicity, or deficiency (Table 5).^28,29

Lead
Exposure to lead is of concern mainly because of possible detrimental effects on intelligence. Studies have indicated an adverse effect of low-level lead exposure neuropsychological development.³⁰ For example, it has been reported that a doubling of blood lead levels (from 10 to 20 micrograms/dl) is associated with a reduction in Intelligence Quotient (IQ) of around one to two IQ points.³¹

It is UK Government policy to reduce human exposure wherever practical and, more specifically, to reduce blood lead levels in children to below 10 micrograms/dl. Food is one of the major sources of lead exposure in the UK, the others are air (mainly lead dust originating from petrol) and drinking water. Exposure from these three sources has been reduced. This has been demonstrated by a marked reduction in blood lead levels over the past 15 years. Blood lead levels for the majority of the UK population are now below 10 micrograms/dl,³² and the mean blood lead level in children aged 31 months (this is the age when a child’s exposure to lead is considered to be highest) is 3.44 micrograms/dl.³³

Dietary exposures of the general UK population have declined from 0.12 mg/day estimated in the 1980 TDS to 0.026 mg/day in the 1997 TDS (Table 4). The cause of this decrease can be partly attributed to a lowering of the LOD from, for example, 0.05 mg/kg in the 1988 TDS to 0.0006 mg/kg - 0.005 mg/kg in the 1997 TDS (Table 1).¹ However, an actual decrease in exposure is also evident. Lower-bound population exposure estimates, in which results less than the LOD are assumed to be zero, fell from 0.036 mg/day in the 1982 TDS to 0.024 mg/day in 1997.³⁴ This decrease in dietary exposure reflects the success of measures taken to reduce lead exposure and contamination of food (e.g. lead-free petrol, greater use of welded cans, the banning of lead seals on wine bottles, etc.). Similar reductions in dietary exposure to lead have also been reported in other countries.^35,36

The mean lead concentration in the Green vegetables group in the 1997 was unexpectedly high at 0.061 mg/kg (Table 2). In comparison, the median concentration was 0.0065 mg/kg. An unusually high lead level in the Green vegetables group sample from one of the 20 locations was the cause of the disparity between the mean and median concentrations. This sample had a lead concentration of 1.0 mg/kg and also had the highest concentrations in the Green vegetables group of aluminium (i.e. 19 mg/kg), zinc (i.e. 8.3 mg/kg), arsenic (i.e. 0.02 mg/kg) and cadmium (i.e. 0.32 mg/kg). CSL carried out several repeat analyses of the homogenised sample provided to check these results. The presence of these elements at higher than average concentrations indicates contamination of the sample at some stage of the study. The relatively high mean lead concentration in the 1997 TDS has little influence on dietary exposure estimates as this food group makes little contribution (i.e. 8 per cent) to the dietary exposure estimate of the general population.

The Offals group contained the highest lead concentrations (i.e. 0.09 mg/kg) in the 1997 TDS (Table 2), but the Beverages group made the greatest contribution to dietary exposure of the general population (i.e. 54 per cent of total exposure). This is because of the high levels of consumption of the latter food group rather than the presence of high concentrations of lead. Dietary exposures of mean and 97.5th percentile adult consumers were 0.024 mg/day and 0.043 mg/day respectively and below the JECFA PTWI which is equivalent to 0.21 mg/day for a 60 kg person (Tables 3 and 5).²³ The PTWI for lead on 0.025 mg/kg bodyweight was maintained by JECFA at it 53rd meeting held in Rome in June 1999. Dietary exposures to lead in the UK are similar to those reported in the USA (i.e. 0.015 mg/day),¹⁷ Canada (i.e. 0.024 mg/day),²⁶ The Netherlands (i.e. 0.01 mg/day to 0.032 mg/day),³⁷ New Zealand (i.e. 0.033 mg/day for adult males),²⁰ and Spain (i.e. 0.039 mg/day).²¹

The COT reviewed the toxicity of lead in 1995 and stated that ‘we welcome the decline in lead levels compared with earlier surveys. It is encouraging that measures taken to reduce lead contamination of food and the environment appear to be reducing the average dietary intake of lead in the UK, although we recognise that changes in the preparation and analysis of the Total diet may be responsible for part of this apparent decline. Since it is not possible to identify, from epidemiological studies, a threshold for the association between exposure to lead and decrements in IQ, efforts should continue to reduce lead exposure from all sources.’ ¹

Mercury
The main sources of exposure to mercury (apart from occupational sources) are from the diet and dental amalgam.^40,41 Mercury is present in food naturally (e.g. in fish which take up mercury from marine sediments), or as a result of pollution (e.g. emissions from industrial processes, fossil fuel combustion).² The main dietary source of mercury is fish and this has lead to recent interest in the potential effects of exposure to mercury on the neurological development of children from populations (i.e. Faeroe Islands, Republic of the Seychelles) with high rates of fish consumption.^38,39

Exposure to mercury from dental amalgam is mainly to the metallic and inorganic forms of the element which are considered to be less toxic than the organic forms of mercury. Most of the mercury in food is present as methyl mercury or other organic forms.² This is reflected in the JECFA PTWI for mercury of 300 micrograms/person (equivalent to 0.043 mg/day for a 60 kg person), of which not more than 200 micrograms should be methyl mercury.⁴⁰ This methyl mercury PTWI of 0.0033 mg/kg bodyweight was maintained by JECFA at it 53rd meeting held in Rome in June 1999. To assess the risks to health from mercury in food it would be preferable to detect and thus estimate dietary exposures to both total mercury and methyl mercury. However, there is no suitable analytical method to routinely and accurately detect methyl mercury in food, and for this reason JFSSG surveys including the TDS, have measured total mercury concentrations. A JFSSG-funded research project is currently underway at the University of Plymouth to develop such an analytical method.

Dietary exposure of the general UK population to mercury, estimated from the results of the 1997 TDS, was 0.003 mg/day (Table 3). The Fish group contained the highest concentrations of mercury (i.e. 0.043 mg/kg) (Table 2) and made the greatest contribution (i.e. 33 per cent) to population dietary exposure. Mercury concentrations in the other food groups were very low. The population exposure to mercury estimated from the 1997 TDS was very similar to those from previous TDSs (Table 4). Dietary exposure estimates of mean and 97.5th percentile adult consumers were 0.0031 mg/day and 0.0064 mg/day respectively. These exposure estimates are both well within the PTWI for mercury and methyl mercury.⁴⁰ Therefore, the estimated mean and 97.5th percentile dietary exposures for adults to mercury do not give cause for toxicological concern (Table 5). Dietary exposures estimated from the UK TDS are similar to those from the USA (i.e. 0.008 mg/day),¹⁷ and The Netherlands (i.e. 0.002 mg/day),³⁷ but lower than those of the Basque Country of Spain (i.e. 0.018 mg/day),²¹ New Zealand (i.e. 0.013 mg/day for adult males),²⁰ and Egypt (i.e. 0.078 mg/day).²⁷

Nickel
The population dietary exposure estimated from the 1997 TDS (i.e. 0.13 mg/day) was the same as that from the 1994 TDS (Table 4). Dietary exposure estimates for mean and 97.5th percentile adult consumers were 0.12 mg/day and 0.21 mg/day respectively (Table 3). JECFA has not recommended a PTWI for nickel but the World Health Organization (WHO) has set a Tolerable Daily Intake (TDI) of 5 micrograms/kg bodyweight (equivalent to 0.3 mg/day for a 60 kg person).⁴²

Nickel has not been demonstrated to be an essential nutrient for humans but is considered to be a normal constituent of the diet. However, there are adverse health effects associated with nickel. Contact with nickel (e.g. from long-term contact with nickel containing jewellery) can cause dermatitis in sensitised individuals. The COT reviewed the toxicity of nickel in 1995 and concluded: ‘nickel is ubiquitous in the diet and we consider that the nickel content of food would be difficult to restrict. The levels of nickel in the diet are not a cause of concern other than for individuals sensitised to nickel, a few of whom may react adversely to nickel in food. There is limited evidence to suggest that, in these subjects, a diet low in nickel may reduce symptoms.’ ¹

Selenium
Selenium is an essential element for humans. The COMA has recommended RNIs of 0.06 mg/day in women and 0.075 mg/day in men.²⁸ The COMA has also recommended that the safe maximum exposure from all sources should be 0.45 mg/day for adult males.²⁸ Concerns have been raised that intakes of selenium in the UK are falling.^43,44 The JFSSG has previously estimated population dietary exposures of 0.063 mg/day and 0.06 mg/day in the 1985 and 1991 TDSs respectively, 0.043 mg/day in 1994, and 0.039 mg/day in the 1995 TDS (Table 4).^2,9,44 Dietary exposures for the UK population have also been estimated in other studies and reported to be 0.06 mg/day (1974) and 0.034 mg/day (1993/94).^45,46 The COMA considered the nutritional implications of selenium exposures estimated from the results of the 1994 and 1995 TDSs in 1997 and agreed that ‘(i) there is, at present, no evidence of adverse health consequences from current intakes; (ii) monitoring of selenium intakes and measurements of selenium status should continue; and (iii) further research should be encouraged to investigate whether the current levels of intake are adequate, and whether the body adapts to changing intakes.’ ^44,47

The general UK population dietary exposure estimated from the 1997 TDS was 0.039 mg/day (Table 3). This is the same as the population exposure estimated from the 1995 TDS and similar to that from the 1994 TDS (i.e. 0.043 mg/day) but is at the lower end of the reference range for adults recommended by the COMA (i.e. 0.04 mg/day). (It should be noted that dietary exposure estimates for selenium from the 1995 TDS are not directly comparable with those from other years as they are based on analyses of composite samples of each food from all the towns in the TDS rather than the upper bound mean concentrations of analyses of each food group from each town.) Population dietary exposures estimated from lower bound mean concentrations (in which concentrations below the LOD are assumed to be zero) were 0.053 mg/day, 0.041 mg/day and 0.039 mg/day in the 1991, 1994 and 1997 TDSs respectively. These results indicate that there has not been a decline in selenium intakes in recent years, but confirm that selenium intakes are now lower than those estimated from the 1991 and 1985 TDSs (Table 4).

Dietary exposures of mean and 97.5th percentile adult consumers estimated from the results of the 1997 TDS were 0.054 mg/day and 0.1 mg/day respectively (Table 3). These exposure estimates are below the safe maximum exposure recommended by the COMA.²⁸ The COT considered the toxicity of selenium in 1995 and concluded that dietary intakes of selenium, of which average intakes were then estimated at 0.06 mg/day, are not a concern in terms of toxicity, or deficiency.²

Tin
High concentrations of tin in food can irritate the gastrointestinal tract and may cause stomach upsets in some individuals. These short-term effects may occur in some individuals at tin concentrations above 200 mg/kg. Long-term effects are not expected from tin in the diet.² As there are health concerns regarding high concentrations of tin, the Tin in Food Regulations 1992 limit the maximum amount of tin in foods sold in the UK to 200 mg/kg.⁴⁸ The COT has supported this limit, which is intended to protect consumers against the potential short-term health effects caused by tin. The JECFA has recommended a PTWI for tin of 14 mg/kg body weight/week to protect against the risk of any long-term effects.⁴⁰

Most foods contain very low concentrations of tin, usually below 10 mg/kg, although canned foods may contain higher concentrations as a result of the slow dissolution of the tin coating used on the inside of some food cans to protect the steel body of the can from corrosion.⁴⁹ In the 1997 TDS, tin concentrations in all the food groups were below 0.1 mg/kg, except for Canned vegetables (41 mg/kg tin) and Fruit products (which include canned fruits; 7.2 mg/kg tin) (Table 2). Together, Canned vegetables and Fruit products accounted for 94 per cent of the UK population dietary exposure to tin of 1.8 mg/day (Table 3). Dietary exposure estimates for mean and 97.5th percentile adult consumers were 1.9 mg/day and 6.3 mg/day respectively and thus much lower than the PTWI which is equivalent to 120 mg/day for a 60 kg person (Table 5).⁴⁰ Therefore, dietary exposures to tin are not a cause for concern.

Zinc
Zinc is an essential element for human health and the COMA has recommended RNIs of 9.5 mg/day and 7.0 mg/day for adult males and females respectively.²⁸ However, high levels of exposure to zinc can be harmful and JECFA has recommended a PMTDI of 60 mg/day.⁵⁰ Dietary exposures of mean and 97.5th percentile adult consumers estimated from the results of the 1997 TDS were 11 mg/day and 20 mg/day respectively which are within the PMTDI (Tables 3 and 5).

Zinc exposure of the general UK population was estimated from the results of the 1997 TDS to be 8.4 mg/day. This is the same as the general population exposure estimate from the 1994 TDS (Table 4), and is comparable to the intake from the 1997 National Food Survey of 7.7 mg/day.^5,9 Zinc concentrations were highest in the Carcass meat and Offals groups (i.e. both 52 mg/kg) of the 1997 TDS and these food groups contributed 14 per cent to total dietary exposure (Table 2).

The COT considered the toxicity of zinc in 1995 and concluded that ‘the estimated average daily intake of zinc from food and beverages (10-12 mg) which is more than adequate for the nutritional needs of most people.²⁸ Excessive supplementation of the diet with zinc salts interferes with absorption of copper and iron from the diet, and may result in anaemia. One study indicated that the early stages of this process may be detectable even at total daily intakes as low as 18.5 mg, when zinc salts were added to a diet deficient in zinc.⁵¹ Some people exceed this daily intake from food and beverages alone, but there is no evidence that their health is at risk as a result. However, supplementation of the diet with zinc preparations in unnecessary and unwise, unless there is good evidence of deficiency.’ ²

Actions
Analyses of 1997 TDS samples for bromine, fluorine and iodine are being carried out. Dietary exposure estimates for these elements will be considered by the COT. These results and the COT’s conclusions will be released in a future Food Surveillance Information Sheet.

The JFSSG has issued a competitive tender for the analysis of inorganic and total arsenic concentrations in samples from the 1999 TDS.⁵² The results of these analyses will be used to estimate dietary exposures to inorganic arsenic for comparison with those for total arsenic and the PMTDI for inorganic arsenic. This information will allow more accurate assessment of the risks to consumers from arsenic in food than has previously been possible.

It is planned that analyses for metals and other elements will be carried out on samples from the 2000 TDS. Dietary exposures estimated from these results will be used to continue to monitor trends in exposure (e.g. for lead and selenium) and assess the risks to UK consumers from these elements in food.

Conclusions
Dietary exposures for the general UK population to aluminium, arsenic, cadmium, chromium, copper, lead, mercury, nickel, selenium, tin and zinc estimated from the results of the 1997 TDS are similar to or lower than those from previous years. Exposure estimates for individual adult consumers are lower than the relevant PMTDIs, PTWIs and TDIs. In 1995 the COT considered both the mean and 97.5th percentile estimated exposures of these 11 elements in the diet and advised that dietary exposures of these elements are not a cause for concern. However, the COT noted that the margin between mean cadmium exposures and levels associated with toxicity is smaller than for most other metals. Therefore, it is reassuring to note that dietary exposures to cadmium have not increased since 1982. Average daily exposures to zinc from food are more than adequate for the nutritional needs of most people and the COT regard that supplementation of the diet with zinc preparations as unnecessary or unwise, unless there is good evidence of deficiency.

Glossary of terms

Summary of units

References

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Further Information

Further information on this survey can be obtained from:
Dr Patrick Miller
MAFF, Joint Food Safety and Standards Group,
Food Contaminants Division
Room 238, Ergon House, c/o Nobel House
17 Smith Square
London SW1P 3JR, UK.

Tel: +44 (0) 20 7238 5751
Fax: +44 (0) 20 7238 5331
Email: p.miller@fsci.maff.gov.uk

Further copies of this and other Food Surveillance Information Sheets can be obtained from:

MAFF, Joint Food Safety and Standards Group, Publicity and Information Section
Room 303B, Ergon House, c/o Nobel House
17 Smith Square
London, SW1P 3JR, UK.

Tel: +44 (0) 20 7238 6223
Fax: +44 (0) 20 7238 6330
Email: s.h.fssginfo@fssg.maff.gov.uk

Copies of COT statements can be obtained from:

Mr Jonathan Lighthill
COT Secretariat
Room 652C, Skipton House
80 London Road
London SE1 6LW, UK

Tel: +44 (0) 20 7972 5007
Fax: +44 (0) 20 7972 5134
Email: jonathan.lighthill@doh.gsi.gov.uk

This material is Crown Copyright but may be reproduced without formal permission or charge for personal or in-house use © Crown Copyright 1999.

These pages were last updated on 29 October 1999.