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Part B Results

Part B Results

Introduction

The purpose of the ATDS is to estimate the dietary exposure of Australian consumers to a range of pesticide residues and contaminants that can be found in the food supply. These exposures are estimated by determining the mean level of residue in each food and multiplying this by the respective amount of food consumed. Total dietary exposures for each pesticide or contaminant are estimated by adding together all contributions from the various foods in the Australian diet.

The results section of this report has been split into two sections: the first section covers contaminants and the second section covers pesticides. Within each of these sections there are subsections on each individual contaminant or pesticide. All the dietary exposure assessments are in the appendixes while the analytical results and background data can be found in the supplementary information on ANZFA' s website.

All analytical results are expressed in milligrams per kilogram (mg/kg) of the edible portion of food prepared for consumption. Dietary exposure estimates for metal contaminants are presented as micrograms per kilogram body weight (µg/kg bw) per day. Dietary exposure estimates for pesticide residues are presented as nanograms per kilogram body weight (ng/kg bw) per day.

Contaminants

The metals examined in this survey for all foods were antimony, total arsenic, cadmium, copper, lead, mercury, selenium, tin and zinc. In addition, seafood was analysed for inorganic arsenic. The LORs for each metal are given overleaf.

Table 1: Limits of reporting for metal contaminants

Metal

Limit of reporting mg/kg

Antimony

0.01

Arsenic, total

0.01

Arsenic, inorganic

0.05

Cadmium

0.005

Copper

0.01

Lead

0.01

Mercury

0.01

Selenium

0.02

Tin

0.02

Zinc

0.01

Dibutyl tin/tributyl tin

0.001

Information on the methods of analysis for the metal contaminants is included in Part 5 of the supplementary information available on ANZFA' s website.

Consistent with previous surveys, total dietary exposures were estimated for the following age - gender categories:

  • adult males aged 25 - 34 years;
  • adult females aged 25 - 34 years;
  • boys aged 12 years;
  • girls aged 12 years;
  • toddlers aged two years; and
  • infants aged nine months.

The food consumption and body weights data for each of the age - gender diets are included in Tables 3 and 5, respectively, of the supplementary information.

Dietary exposure estimates for toddlers were expected to be higher than the other population groups because of their high food consumption relative to body weight. This was apparent in the resulting dietary exposure estimates for metal contaminants.

The estimated dietary exposures to contaminants for these age gender categories are given in Appendix 1. Comparisons between dietary exposures from the 19th ATDS and the revised 1996 AMBS could only be made for arsenic, cadmium, lead and mercury as these were the only metals included in the 1996 AMBS.

The following figures represent the dietary exposure to metal contaminants as a percentage of the tolerable limit. Information on the tolerable limit of each contaminant is available in Table 8 of the supplementary information on ANZFA' s website.

Figure 1: Range of estimated dietary exposure to metal contaminants for adult males (25 - 34 years) as a percentage of the tolerable limit

Figure 2: Range of estimated dietary exposure to metal contaminants for adult females (25 - 34 years) as a percentage of the tolerable limit

Figure 3: Range of estimated dietary exposure to metal contaminants for boys (12 years) as a percentage of the tolerable limit

Figure 4: Range of estimated dietary exposure to metal contaminants for girls (12 years) as a percentage of the tolerable limit

Figure 5: Range of estimated dietary exposure to metal contaminants for toddlers (2 years) as a percentage of the tolerable limit

Figure 6: Range of estimated dietary exposure to metal contaminants for infants (9 months) as a percentage of the tolerable limit

Antimony

Antimony is found in low-level concentrations in water, soil and air. However, it is widely used as an industrial chemical in the manufacture of alloys and in the production of fireproofing chemicals and textiles.

The WHO/FAO Joint Expert Committee on Food Additives and Contaminants has not made any evaluation of antimony and therefore no tolerable limit has been set. However, an oral reference dose for antimony of 0.4 µg/kg bw/day was assigned by the United States Environmental Protection Agency (USEPA 1991). This level has been adopted by ANZFA as a tolerable limit for the purposes of dietary modelling.

The mean, median, maximum and minimum levels of antimony found in foods analysed in the 19th survey are given in Table 9 in the supplementary information on ANZFA' s website. The estimated dietary exposures to antimony for each age - gender category are given in Appendix 1.

The highest calculated mean exposure to antimony was for toddlers because of their high food consumption relative to body weight. This calculated exposure for toddlers gave a wide range (4% to 240% of the tolerable limit). The lower limit was calculated by assuming that foods contained no antimony if they were reported as containing less than the LOR (0.01 mg/kg) and the upper limit was calculated by assuming that foods contained 0.01 mg/kg of antimony if they were reported as containing less than the LOR. The wide range results from limitations of the current analytical method, which can measure antimony levels down to 0.01 mg/kg but no lower, and the high proportion of results that were reported as less than the LOR. The actual exposure for antimony lies within this calculated range and it is not possible with the current method to be more precise.

In the recent ANZFA review of the Food Standards Code, more comprehensive data on antimony levels in food were available than in the 19th ATDS. Estimated dietary exposure to antimony was lower than reference health standards. The review concluded that there was no cause for concern for public health and safety. The review recommended, however, that the ATDS continue to monitor dietary exposures to antimony. For future surveys, ANZFA will request antimony analyses with a lower LOR to enable more specific exposures to be calculated.

Recommendation

It is recommended that analyses with a lower LOR for antimony be undertaken in future surveys so that more accurate dietary exposure assessments can be calculated. ANZFA has been informed that methods are now available that can detect antimony to a LOR of 0.002 mg/kg and ANZFA will be seeking to use these methods in future surveys.

Arsenic

Arsenic occurs naturally in both organic and inorganic forms. In the past, arsenic compounds were commonly used in drugs, but the main uses today are in pesticides, veterinary drugs and industrial applications. Inorganic arsenic is registered for use in timber preservatives and for control of termites in timber. There are no registered uses in food crops or for animal production. DSMA (disodium methyl arsonate) is registered as a herbicide for turfs and lawns. MSMA (monosodium methyl arsonate) is registered as a herbicide for use in cotton and sugarcane production, on rights-of-way and for non-crop uses.

Most foods contain low levels of arsenic due to its wide distribution in the environment and, to some extent, to its use in agriculture. Dietary arsenic represents the major source of arsenic exposure for most of the population. Some types of seafood contain up to 10 times the arsenic of other foods. People who consume large amounts of seafood may therefore ingest significant amounts of arsenic (primarily in organic form). However, inorganic arsenic is more toxic than organic arsenic (WHO 1981).

This survey examined total arsenic in all foods and inorganic arsenic in crocodile, fish fillets, mussels, canned red salmon and canned crab. Inorganic arsenic was only measured in seafood and crocodile because of the generally higher levels of arsenic that these foods contain.

A level of approximately 0.0029 mg/kg bw/day is the lowest observable effects level (LOEL) based on a review of available epidemiological data conducted by ANZFA. This level was rounded off to 0.003 mg/kg bw/day to be the tolerable limit for inorganic arsenic for the purposes of dietary modelling.

The mean, median, maximum and minimum levels of total arsenic and inorganic arsenic found in the foods analysed are given in Tables 10 and 11 in the supplementary information on ANZFA' s website. The estimated dietary exposure to total arsenic and inorganic arsenic for each age - gender category are given in Appendix 1.

Inorganic arsenic analyses are more expensive than total arsenic analyses. To make the best use of the available funds for analytical testing, total arsenic, rather than inorganic arsenic, is determined in most cases. There is no accepted ratio that can be used for all foods to convert the total arsenic content to inorganic arsenic. For this reason and to enable comparison of the results with the tolerable limit for inorganic arsenic, it was assumed that all arsenic detected in each food was in the form of the more toxic inorganic arsenic. This is an overestimate because not all arsenic is present as inorganic arsenic.

Even with the overestimation for inorganic arsenic content, all estimated dietary exposures were below the tolerable limit for inorganic arsenic. The highest mean exposure to arsenic was for two-year-olds because of their high food consumption relative to body weight. This exposure ranged from 36% of the tolerable limit up to 57%. The wide range results from limitations of the analytical method, which can measure arsenic down to 0.01 mg/kg but no lower, and the high proportion of results reported as ' less than the LOR ' . Dietary exposures to arsenic are within acceptable health standards.

Seafood makes the greatest contribution to the dietary intake of arsenic. Although total arsenic levels were higher in seafood than in other foods, the more toxic inorganic arsenic levels were found to be low in mussels and were less than the LOR in crocodile, fish fillets, canned red salmon and canned crab.

Recommendation

It is recommended that analyses with a lower LOR for arsenic be undertaken in future surveys so that more accurate dietary exposure assessments can be calculated.

Cadmium

Cadmium is a metallic element that occurs naturally at low levels in the environment. Food, rather than air or water, represents the major source of cadmium exposure, although tobacco smoking adds significantly to the body' s burden.

Long-term exposure to high levels of cadmium may lead to considerable accumulation in the liver and kidneys, particularly the renal cortex, resulting in kidney damage.

Additional cadmium has been added to the environment through industrial processes such as cadmium metal production. Further cadmium has been added to agricultural soils through the use of phosphate fertilisers and certain organic fertilisers based on manures.

The tolerable limit for cadmium, set at the 33rd meeting of the WHO/FAO Joint Expert Committee on Food Additives, is 7 µg/kg bw/week (WHO 1989).

The mean, median, maximum and minimum levels of cadmium found in the foods analysed are given in Table 12 in the supplementary information on ANZFA' s website. The estimated dietary exposures to cadmium for each age - gender category are given in Appendix 1.

The highest mean exposure to cadmium was for two-year-olds because of their high food consumption relative to body weight. This exposure ranged from 17% to 58% of the tolerable limit. This range results from limitations of the analytical method, which can measure cadmium levels down to 0.01 mg/kg but no lower, and the high proportion of results reported as ' less than the LOR ' . All estimated dietary exposures were below the tolerable limit of 7 µg/kg bw/week. Dietary exposures to cadmium are within acceptable safety standards.

Recommendation

It is recommended that analyses with a lower LOR for cadmium be undertaken in future surveys so that more accurate dietary exposure assessments can be calculated.

Copper

Copper is widely distributed in nature. Copper and its compounds have many industrial, urban and agricultural uses. Copper salts, in the form of Bordeaux mixture, have been used since the 19th century as a fungicide for grapes and other crops. Organic growers' associations consider Bordeaux acceptable for use in organic food production.

Copper is an essential element. Enzymes containing copper are important for the body to transport and use iron. Anaemia is therefore one of the first symptoms of copper deficiency. Copper deficiency, however, is not common, as copper is widely distributed in food, particularly in meat, liver, kidney, heart and other forms of offal, fish and green vegetables.

Copper is stored in the liver, heart, brain, kidneys and muscles. Copper toxicity is rare, except in those suffering Wilson s disease (a hereditary disease resulting in excessive uptake and accumulation of copper by the body, especially in the liver and brain).

The mean, median, maximum and minimum levels of copper in foods are given in Table 13 in the supplementary information on ANZFA' s website. The estimated dietary exposures to copper for each age - gender category are given in Appendix 1.

In 1996 a joint FAO/International Atomic Energy Agency/WHO expert consultation set an upper limit for the safe range of population mean exposures for adults of 0.2 mg/kg bw/day. This value has been used as the tolerable limit for the purposes of dietary modelling (WHO 1996).

All estimated mean intakes are below the tolerable limit. Because of their high food consumption relative to body weight, the highest mean exposure to copper was for two-year-olds, calculated at 21% of the tolerable limit. No range has been presented for copper because a specific amount of copper was reported for all samples and no allowance had to be made for results reported as containing ' less than the LOR ' . Dietary exposures to copper are within acceptable health standards.

Lead

Lead is found almost everywhere, although lead concentrations are low in environments where there has been little human activity. Lead has been used for centuries because it is easily extracted from its ores. Lead is used for a number of industrial, domestic and rural purposes - the largest use is in lead batteries.

A significant source of exposure to lead is via food. This is due to lead-contaminated soil and dust finding its way into the food and water supply. Lead can also be unintentionally added to food during processing. Canned foods can be a source of lead, if lead solder has been used in the can seam; however, most cans now in use in Australia have welded seams. In addition, the level of lead in food has been falling due to technological improvements in food manufacturing.

Lead is a cumulative toxin that can primarily affect the blood, nervous system and kidneys. In the blood at high concentrations, lead inhibits red blood cell formation and eventually results in anaemia. The effects of high concentrations of lead on the nervous system can vary from hyperactive behaviour and mental retardation to seizures and cerebral palsy. As the kidneys are the primary route for lead excretion, lead tends to accumulate in these organs, causing irreversible damage.

Infants and children are considered particularly vulnerable to lead exposure. This is due to their higher energy requirements, their higher fluid, air and food intake per unit of body weight, and the immaturity of their kidneys, liver, nervous and immune systems. In addition, their rapid body growth, their different body composition and the development of their organs and tissues, in particular the brain, may increase their lead absorption. Behavioural characteristics of infants and children, such as the sucking of hands and other objects and the ingestion of non-food items (pica) may also result in a higher exposure to lead compared with adults. Dietary lead is not the only source of lead exposure. In particular, other important sources of exposure for infants and children to lead are from lead paint, soil and dust (Friberg et al. 1979).

The tolerable limit for lead, set at the 30th meeting of the WHO/FAO Joint Expert Committee on Food Additives, is 25 µg/kg bw/week (WHO 1987b).

The mean, median, maximum and minimum levels of lead in foods are given in Table 14 in the supplementary information on ANZFA' s website. Estimated dietary exposures to lead for each age - gender category are given in Appendix 1.

The highest mean exposure to lead was for two-year-olds because of their high food consumption relative to body weight. This exposure ranged from 33% to 53% of the tolerable limit. This range results from limitations of the analytical method, which can measure lead down to 0.01 mg/kg but no lower, and the high proportion of results reported as ' less than the LOR ' . All estimated intakes of lead were below the tolerable limit of 25 µg/kg bw/week. Dietary exposures to lead are within acceptable safety standards.

Recommendation

It is recommended that analyses with a lower LOR for lead be undertaken in future surveys so that more accurate dietary exposure assessments can be calculated.

Mercury

Mercury is found naturally in the environment. It is usually found concentrated only in certain areas, geographically known as mercuriferous belts. Apart from industrial activities, mercury is also released into the environment during earthquakes and volcanic activity.

Mercury is found in various forms (elemental, inorganic and organic), all of which have different toxicological properties. The most toxic to humans is the organic form, the most common organic form being methyl mercury. Methyl mercury is largely produced from the methylation of inorganic mercury by microbial activity. This is most likely to occur in marine and freshwater sediments. Methyl mercury is rapidly taken up and concentrated by filter-feeding organisms upon which fish feed.

In general, the diet is the major source of exposure to mercury. Seafoods specifically contain much higher levels of mercury, largely in the toxic methyl mercury form, whereas most other foods contain very low levels of mercury, almost entirely in the inorganic form. In this survey, total mercury, which included both organic and inorganic mercury, was measured.

Methyl mercury accumulates in the brain. The developing nervous system in the foetus is at particular risk. Effects include retarded psychomotor development, mental retardation and seizures.

The tolerable limit for mercury, set at the 16th meeting of the Joint FAO/WHO Expert Committee on Food Additives and maintained after reconsideration at the 22nd meeting of the same committee, is 0.3 mg per person per week, equivalent to 5 µg/kg bw/week (WHO 1978).

The mean, median, maximum, and minimum levels of mercury in foods are given in Table 15 in the supplementary information on ANZFA' s website. Seafood was shown to be the greatest source of mercury in all the diets for all age- gender categories. Of the foods analysed, fish fillets had the highest level of mercury. Estimated dietary exposures to mercury for all age - gender categories are given in Appendix 1.

Because of their high food consumption relative to body weight, the highest mean exposure to mercury was for two-year-olds and infants, where this exposure ranged from 5% up to 140% of the tolerable limit for two-year-olds, and from 2% up to 150% of the tolerable limit for infants. This range results from limitations of the analytical method, which can measure mercury down to 0.01 mg/kg but no lower, and the high proportion of samples reported as containing ' less than the LOR ' .

The upper limits of these ranges indicate that the exposure to mercury could be above the acceptable health standard. However, the upper limit of the range is an overestimate because it assumes that foods contain 0.01 mg/kg of mercury if these foods are reported as containing less than the LOR (0.01 mg/kg). Similarly, the lower limit of the range is an underestimate because it assumes that foods contain no mercury if these foods are reported as containing less than the LOR.

In the recent ANZFA review of the Food Standards Code, more comprehensive data on mercury levels in food were available than in the 19th ATDS. Estimated dietary exposures to mercury were lower than reference health standards for the general population. There was, however, cause for concern about the potential exposure to mercury for pregnant women consuming large amounts of fish with high mercury levels, because of the sensitivity of the foetus to mercury. As a result of the review ANZFA has developed an advisory statement for pregnant women on mercury in fish, in consultation with health professionals and the fishing industry.

Recommendation

It is recommended that analyses with a lower LOR for mercury be undertaken in future surveys so that more accurate dietary exposure assessments can be calculated. ANZFA has been informed that methods are now available that can detect mercury to a LOR of 0.002 mg/kg and ANZFA will be seeking to use these methods in future surveys.

Selenium

Selenium is a metalloid, both essential and toxic to humans. Selenium is widely distributed in rocks and soils; however, its distribution is uneven.

Selenium was known as a toxicant before being recognised as a nutrient. It may produce symptoms associated with changes in nail pathology, hair loss and dental decay. Selenium is also essential to humans, in that it helps maintain cell membrane integrity and has an antioxidant role in the body. Selenium deficiency can lead to diseases such as Keshan disease and Kaschin-Beck disease. Both diseases have been reported in selenium-deficient areas such as parts of China.

The Australian Recommended Dietary Intake (RDI) of selenium was set by the NHMRC in 1987. The RDIs are 85 µg/day (1.13 µg/kg bw) for adult males; 70 µg/day (1.18 µg/kg bw) for adult females; 85 µg/day (2.14 µg/kg bw) for boys; 70 µg/day (1.68 µg/kg bw) for girls; 25 µg/day (2.03 µg/kg bw) for toddlers; and 15 µg/day (1.65 µg/kg bw) for infants (NHMRC 1991).

As yet, the WHO has made no recommendation regarding tolerable limits of selenium (WHO 1987a). However, the US National Research Council has suggested that toxicity will occur after prolonged ingestion of upwards of 3 000 µg/day (Reilly 1980) which is equivalent to 50µg/kg bw/day (based on the WHO reference weight of 60 kg for an adult).

Based on limited human data, the biochemical changes (reduction in the ratio of plasma selenium levels to erythrocyte selenium) linked with exposure of humans to selenium at 750 µg/day is interpreted to represent the first indicator of chronic selenium toxicity and therefore is a LOEL. Chronic selenium intake of 750 µg/day is proposed as the tolerable limit for selenium. This corresponds to an intake of 12.5 µg/kg bw/day for adults, assuming a 60 kg adult body weight.

The mean, median, maximum and minimum levels of selenium in foods are given in Table 16 in the supplementary information on ANZFA' s website. Estimated dietary exposure to selenium for all age - gender categories are given in Appendix 1.

Because of their high food consumption relative to body weight, the highest mean exposure to selenium was for two-year-olds, where this exposure ranged from 20% to 29% of the tolerable limit of 750 µg/day (12.5 µg/kg bw/day). This range results from limitations of the analytical method, which can measure selenium down to 0.01 mg/kg but no lower, and the proportion of samples reported as containing ' less than the LOR ' .

All estimated mean intakes of selenium for all age - gender categories are below the suggested tolerable limit of 3 000 µg/day (50 µg/kg bw/day). Dietary exposures to selenium are within acceptable health standards.

Estimated dietary exposures to selenium were in the same range as the RDI for each age - gender group (see table below). The lower dietary exposure estimates (based on zero values for non-detect results) were lower than the RDI for female adults, boys, girls and infants but exceeded the RDI for male adults and toddlers. The higher dietary exposure estimate (based on numerical values for non-detect results) exceeded the RDI in all cases, except for boys and girls aged 12 years. However, since RDIs are established so that the nutrient requirements of virtually all the population are met, it is likely that actual requirements for selenium will be met for most people in these age groups.

Table 2: Estimated dietary exposures to selenium

Adult males

Adult females

Boys

Girls

Toddlers

Infants

25 - 34 years

25 - 34 years

12 years

12 years

2 years

9 months

µg/kg bw/day

µg/kg bw/day

µg/kg bw/day

µg/kg bw/day

µg/kg bw/day

µg/kg bw/day

RDI*

1.13

1.18

2.14

1.68

2.03

1.65

Dietary exposure

1.2 - 1.7

0.97 - 1.4

1.5 - 2

1.1 - 1.5

2.5 - 3.6

1.0 - 2.9

Recommendation

It is recommended that analyses with a lower LOR for selenium be undertaken in future surveys so that more accurate dietary exposure assessments can be calculated.

Tin

Tin is a metal that has been used since ancient times as an alloy in combination with copper to produce bronze. Today tin is used in plating, solders and alloys. Tin is also used extensively for food containers and food-processing equipment as it is generally resistant to corrosion and easy to solder.

The main route of exposure to tin is through food, although levels are generally low. Higher levels are found in canned foods as a result of the coating or plate breaking down. Exposure to tin contamination is greatly reduced when the cans are lacquered.

Toxicity from tin exposure is low. However, high levels of tin may produce acute gastrointestinal disturbances such as nausea, vomiting and diarrhoea. Small children and infants are also more likely to consume high levels of tin from a single source, on a body weight basis.

The WHO/FAO Joint Expert Committee on Food Additives, at its 33rd meeting, set a tolerable limit of 14 mg/kg bw/week for inorganic tin (WHO 1989), and recommended that efforts be made to keep tin levels in canned foods as low as practical, consistent with the application of good manufacturing practice.

The mean, median, maximum and minimum levels of tin in canned foods are given in Table 17 in the supplementary information on ANZFA' s website. Estimated dietary exposures to tin for all age - gender categories are given in Appendix 1.

Because of their high food consumption relative to body weight, the highest mean exposure to tin was for two-year-olds, where this exposure ranged from 1.5% to 1.6% of the tolerable limit. All estimated exposures to tin for all age - gender categories are well below the tolerable limit for tin of 14 mg/kg bw/week.

All results were below the current maximum permitted concentrations (MPCs) listed in Standard A12 of the Food Standards Code for tin in canned foods. Canned peas and canned pineapple contained the highest concentrations of tin.

Dibutyl and tributyl tin

Tributyl tin compounds are used as antifouling agents on boats as well as for fungal control on timber. Occupational exposure represents the most significant hazard to humans with respect to exposure to organotin compounds.

Mussels were analysed for dibutyl tin (DBT) and tributyl tin (TBT) which were detected in approximately half the samples. The concentrations ranged from less thantheLOR (<0.001 mg/kg) to 0.021 mg/kg for dibutyl tin and from less than theLOR(<0.001 mg/kg) to 0.033 mg/kg for tributyl tin. From this data, the median level for both DBT and TBT was 0.005 mg/kg.

The margin of safety for this amount of TBT/DBT can be determined by comparing the intake level of TBT in humans with the intake level known to cause toxic effects in experimental animals. The lowest level shown to have marginal toxic effects in animals is 0.25 mg/kg bw/day (WHO 1990b).

The median concentration for TBT in mussels is 0.005 mg TBT /kg and the median concentration for DBT in mussels was 0.005 mg DBT/kg. If it were assumed that DBT was as toxic as TBT then the total median TBT equivalent concentration would be 0.010 mg/kg.

A high consumer of molluscs (95th percentile for males aged 25 34) is estimated to consume 402 grams per day (1995 National Nutrition Surv

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