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The information in the archive was published by MAFF, Department of Health and the Scottish Executive before April 1st 2000 when the Food Standards Agency was established.

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Food Surveillance Information Sheet


Number 82   March 1996

MAFF UK - PHTHALATES IN FOOD


Index to MAFF UK Food Surveillance Information Sheets, 1996

see also:
60: MAFF UK - Phthalates in Paper and Board Packaging (May 1995)
83: MAFF UK - Phthalates in Infant Formulae (May 1996)
168: MAFF UK - Phthalates in Infant Formulae - Follow-Up Survey (December 1998)

Summary

MAFF's Food Safety Directorate has carried out a survey of the levels of total and individual phthalates in samples of composite fatty foods from the Total Diet Study (TDS). The survey was carried out using stored samples of food that had been collected in 1993.

Phthalates were detected in all TDS samples that were analysed There were considerable differences between the levels of phthalates found in retail samples in a pilot study and the levels found in the TDS samples. The reasons for this are unclear and MAFF will investigate further some of the issues raised by this study. Estimates of average dietary intakes of total phthalates range from 0.1 to 0.8 mg/person/day and high level (97.5th percentile) dietary intakes of total phthalates range from 0.4 to 1.6 mg/person/day. These are considerably below the Tolerable Daily Intakes set for some of these chemicals. The Department of Health has advised that there are unlikely to be any health risks to consumers from these dietary intakes of individual phthalates. This advice takes account of all available information on the possible effects of phthalates, including recent studies concerning oestrogenic activity.

Background

Phthalic acid diesters, commonly known as phthalates, are a group of organic chemicals that have a variety of industrial uses, including use as plasticisers in a wide range of household and consumer goods,2 uses in lubricating oils and uses as carriers for perfumes in cosmetics. The use of phthalates in plastic food packaging is limited, for example, to the manufacture of materials such as some adhesives and some printing inks. Phthalates are no longer used in the manufacture of cling film and most other food contact plastic materials.

The release of phthalates to the environment may occur during the production and distribution of phthalates, during the manufacture or use of products in which they are used, or after the dispersal of these products. Although some phthalates occur naturally in coal, crude oil and shale, the contribution of such sources to general environmental levels of phthalates is likely to be insignificant.3

As a result of their extensive use and their moderate resistance to degradation, phthalates are widely distributed in the environment and are often found at low levels in food. The toxicity of these substances has been considered by the EC Scientific Committee for Food (SCF), which has established Tolerable Daily Intakes (TDIs) for several of the chemicals in the group.

A recent survey by MAFF showed that two phthalates, dibutyl phthalate (DBP) and di-(2-ethylhexyl) phthalate (DEHP), were often present in paper and board packaging and were also present at generally low concentrations (typically less than 10 mg/kg) in foods packaged in paper and board.4 The concentrations of phthalates in samples of fat analysed in this recent survey would be expected to be lower in the core than at the surface if migration from packaging was the major source of contamination. In over half the samples, the concentrations of the phthalates at the core were about equal to or higher than the concentrations found at the surface. These results suggested that phthalates in food originate at least in part from general environmental contamination. Results from other surveys of milk and milk products,1,5 pork fat 6 and fish7,8 also indicate that phthalates are present in food from general environmental contamination rather than specific sources such as food packaging.

The current survey was conducted to estimate the intakes of total and individual phthalates from the average diet. TDS samples consist of retail food products, prepared as for consumption, then combined in amounts reflecting their relative importance in the average UK diet into twenty composite samples, each one representing a defined food group.9,10 Phthalates are fat soluble and therefore only those TDS food groups which make a major contribution to dietary fat intakes were selected for analysis. These were carcass meat, meat products, offals, poultry, eggs, fish, fats & oils, milk, and milk products.

A pilot study was undertaken to assess whether the normal preparation and storage of TDS samples may itself introduce phthalate contamination. Concentrations of total phthalates were compared in a selection of fatty food samples purchased from retail outlets in Norwich and split so that one portion of each sample was analysed directly and a second portion was analysed after having been processed in the manner used for regular TDS samples. The pilot study concluded that systematic contamination by phthalates in samples processed in the manner of TDS samples should not occur.

Method

All samples were analysed at CSL Food Science Laboratory, Norwich.

Identification and determination of individual phthalates

Food samples were extracted with diethyl ether/hexane (1:1) (liquid milk samples) or acetone/hexane (1:1) (all other food groups) and were fractionated by size exclusion chromatography then concentrated prior to analysis by gas chromatography/low resolution mass spectrometry (GC-MS) to identify individual phthalates. The limit of detection of the GC-MS instrument was typically 0.001 mg/kg for individual phthalates. The analytical methodology has only recently been developed and insufficient validation data are available for a robust quantitative measure of repeatability to be given. Further analyses were conducted using gas chromatography/high resolution mass spectrometry to confirm the identities of both major and minor peaks. These showed that some small peaks with relative retention times coincident with those of phthalate standards were, in fact, interfering compounds that had been co-extracted.

Concentrations of dipropyl phthalate (DPP), DBP, di-iso-butyl phthalate (DIBP), butylbenzyl phthalate (BBP) and DEHP were quantified after appropriate calibration. The presence of five other phthalates (di-iso-propyl phthalate, dihexyl phthalate, dicyclohexyl phthalate, diheptyl phthalate and dinonyl phthalate) could be confirmed by gas chromatography/high resolution mass spectrometry, but these compounds were not quantified. Dicyclohexyl phthalate and phthalates of higher molecular weight (dinonyl, didecyl, diundecyl and didodecyl isomers) were not detected in any of the samples analysed.

Some commercially-important phthalate esters, such as di-iso-octyl phthalate (DIOP) are complex mixtures of isomers that are dispersed over a wide range of retention times in capillary column gas chromatography. One sample of carcass meat, two of egg and two of milk were therefore analysed by high performance liquid chromatography/mass spectrometry (HPLC-MS) using an atmospheric pressure chemical ionisation interface, under which conditions the three mixtures of isomers represented by DIOP, di-iso-nonyl phthalate, and di-iso-decyl phthalate are each eluted as single peaks, thus allowing total dioctyl, dinonyl and didecyl phthalate concentrations to be established. The limit of detection of the HPLC-MS instrument was of the order of 0.01 mg/kg for each of the mixtures of phthalate isomers. Concentrations of total dioctyl phthalates are given in Table 1. Dinonyl and didecyl phthalates were not detected in any of the samples analysed.

Determination of total phthalates

Food samples were extracted with diethyl ether/hexane (1:1) (liquid milk samples) or acetone/hexane (1:1) (all other food groups) and phthalates were converted to dimethyl phthalate (DMP) by heating the extracts with methanolic potassium hydroxide solution and then with boron trifluoride/diethyl ether complex. These extracts were then fractionated by size exclusion chromatography and analysed by gas chromatography-mass spectrometry (GC-MS).

Preparation and analysis of all of the samples of a particular food type were completed in parallel, in a batch which included five process blank determinations. In all cases, the lower limit at which DMP extracted from samples could be measured securely was set by the presence of DMP in blanks rather than by instrumental sensitivity. The limit of quantification for each commodity was the mean plus three times the standard deviation of the corresponding blanks. Limits of quantification were below 0.2 mg/kg for most food types but were higher for fats and oils (0.24 mg/kg), milk (0.34 mg/kg) and carcass meat (0.41 mg/kg).

Quoted results are the mean of duplicate determinations. The average of the differences between duplicate determinations, expressed as a percentage of the corresponding mean ("mean duplicate difference") was below 10 percent for most commodities but was higher (around 35 percent) for milk and carcass meat.

Results

The mean concentrations of individual phthalates and of total phthalates (expressed as DMP) are shown in Table 1. Individual phthalates were measured in two samples of each of carcass meat, poultry, eggs and milk. Total phthalates were determined in ten samples of each of seven food groups (carcass meat, offals, poultry, fish, fats & oils, milk, and milk products) and in two samples of each of eggs and meat products.

The most abundant individual phthalate in each of the samples was DEHP. Earlier work had shown that DEHP accounted for 9 - 50 percent of total phthalate in a survey of retail cows' milk,1 and the results in this study are broadly comparable. The concentrations of DEHP measured by GC-MS and the total dioctyl phthalate measured by HPLC-MS for samples of carcass meat and eggs were similar, indicating that octyl phthalates other than DEHP were not present in these samples in appreciable quantities. In samples of milk, the total dioctyl phthalate concentration was considerably higher than that of DEHP, indicating contamination with other isomeric forms such as DIOP.

In the case of the two milk samples, the total quantity of individual phthalates found, expressed as the equivalent concentration of DMP, exceeded the measured total concentration. The precision and overall uncertainty inherent in the measurement of individual phthalate concentrations may be sufficient to account for this apparent discrepancy. For other commodities, a smaller proportion (2 percent - 23 percent) of the measured total was attributable to measured individual compounds.

The dietary intakes of phthalates have been estimated for average and high level UK consumers using food consumption data from the dietary and nutritional survey of British adults.11 Using this method to calculate intakes, dietary intakes of total phthalates, measured and expressed as DMP, were estimated to be 0.8 mg/person/day (mean intake) and 1.6 mg/person/day (high level intake).

Intake calculations using the results of analysis of the TDS samples suggested that the largest contributions to both mean and high level intakes are made by carcass meat (about 25 percent), eggs (about 15 percent), poultry (about 35 percent) and milk (about 10 percent). Individual phthalate esters were determined in two samples of each of these composite food groups. Using the concentrations found in the TDS samples gives estimates of intakes for each of the five individual phthalates quantified within the ranges 0.004 to 0.15 mg/person/day for mean intakes and 0.009 to 0.30 mg/person/day for high level intakes from these four foods (Table 2).

Interpretation

The levels of phthalates measured in TDS samples are at variance with those found in earlier surveillance1 and also with levels found in the pilot study, in which retail samples of a range of fatty foods and milk were analysed directly after purchase. Concentrations of phthalates found in the pilot study samples before and after preparation as for consumption are given in Table 3. Using the data on phthalates in retail samples of food (as purchased) for calculating dietary intakes gives an estimate of 0.1 mg/person/day for mean intakes and 0.4 mg/person/day for high level intakes. These are considerably below the estimates of 0.8 and 1.6 mg/person/day for average and high level dietary intakes of phthalates that were made on the basis of concentrations found in the TDS samples. This needs further investigation.

The toxicity of those phthalates permitted for use in food contact materials has been considered by the SCF. Sufficient toxicological data were available for the committee to set a TDI of 0.05 mg/kg bodyweight/day for DEHP and a temporary TDI for four of the other phthalates included in this survey: 0.1 mg/kg bodyweight/day for BBP; 0.05 mg/kg bodyweight for DBP; 0.1 mg/kg bodyweight/day for dicyclohexyl phthalate; and 0.2 mg/kg bodyweight/day for diethyl phthalate. Less toxicological data are available for the remaining phthalates used in food contact materials. The SCF has recommended a "group restriction" for the sum of these remaining compounds of 0.05 mg/kg bodyweight/day. Unlike the TDI, the group restriction is not a precise measure of potential risk to human health. Instead, it is a precautionary limit set to guide the food contact materials industry and enforcement authorities pending submission of further toxicological data.

The measurements of total phthalates found in the Total Diet Study give intake estimates of 0.013 and 0.027 mg/kg bodyweight/day for mean and high level adult consumers. Making a "worst case" assumption that all phthalates might have TDIs as low as DEHP or DBP, which is unlikely, then even high level consumers' total phthalate consumption is well within the lowest TDI of 0.05 mg/kg bodyweight/day. The total phthalate levels found in the pilot study (0.002 and 0.006 mg/kg bodyweight/day for mean and high level consumers, respectively) are even lower at around one-twenty-fifth to one-tenth of this TDI.

High level intakes of DEHP were estimated to be 0.30 mg/person/day, which is equivalent to 0.005 mg/kg bodyweight/day for a 60 kg adult. This level of intake is one-tenth of the TDI for this compound. Estimated intakes of BBP and DBP are considerably lower. Therefore consumption of foods containing the levels of phthalates found in the TDS samples would not result in mean or high level consumers exceeding the TDIs for DEHP, BBP and DBP.

The TDIs discussed above were set before the recent findings that some phthalates may have oestrogenic activity. Two phthalates, BBP and DBP, appear to have weak oestrogenic activity in vitro.12 That is, in "test tube" experiments they triggered some of the same effects as the natural hormone, oestradiol. However, they were about a million times less potent than oestradiol. The plasticisers, di-(2-ethylhexyl) adipate and DEHP, were not found to be active. Activity of BBP and DBP in vitro is not necessarily evidence that they will be active in the human body. To date only one of these phthalates, BBP, has been tested in laboratory rodents.13 Female rats were given BBP at a fixed concentration of 1 mg/l in their drinking water throughout pregnancy and lactation. Resulting intakes were estimated to range from 0.1 to 0.4 mg/kg bodyweight/day during the treatment period. This was reported to cause small reductions in testis weight and sperm production in the male offspring, who would have been exposed to BBP via the mother during the entirety of their most vulnerable period of testis development. These studies suggest that BBP and DBP may have weak oestrogenic activity but at this stage the data are very tentative and no firm conclusions can be drawn. Studies to confirm these effects and to establish a no-effect level would be needed.

Considering the individual phthalate measurements for BBP and DBP, and summing the high level consumer intakes, gives a combined estimated intake of 0.00085 mg/kg bodyweight/day. This is more than one-hundred fold below the dose range said to cause minimal effects in developing rodents. The Department of Health has advised that there are unlikely to be any health risks to consumers from the levels of individual or total phthalates found in the TDS samples.

References
  1. Sharman, M., Read, W.A., Castle, L. and Gilbert, J. (1994) Levels of di-(2-ethylhexyl)phthalate and total phthalate esters in milk, cream, butter and cheese. Food Addit. Contam. 11, 375-385.
  2. International Programme on Chemical Safety (1992) Diethylhexyl phthalate. Environmental Health Criteria 131, publ. World Health Organisation, Geneva.
  3. International Programme on Chemical Safety (1992) Diethylhexyl phthalate. Environmental Health Criteria 131, publ. World Health Organisation, Geneva.
  4. Ministry of Agriculture, Fisheries and Food (1995) Phthalates in paper and board packaging. Food Surveillance Information Sheet 60.
  5. Castle, L., Gilbert, J. and Eklund, T. (1990) Migration of plasticiser from poly(vinyl chloride) milk tubing. Food Addit. Contam. 7, 591-596.
  6. Cerbulis, J. and Byler, D.M. (1986) Isolation and detection of dialkyl phthalates from pork. J. Agric. Food Chem. 34, 198-200.
  7. Musial, C.J., Uthe, J.F., Sirota, G.R., Burns, B.G., Gilgan, M.W., Zitko, V. and Matheson, R.A. (1981) Di-n-hexyl phthalate (DHP), a newly identified contaminant in Atlantic herring (Clupea harengus harengus) and Atlantic mackerel (Scomber scombrus). Can. J. Fish. Aquat. Sci. 38, 856-859.
  8. Mayer, F.L., Jr. Stalling, D.L. and Johnson, J.L. (1972) Phthalate esters as environmental contaminants. Nature (London) 238, 411-413.
  9. Peattie, M.E., Buss, D.H., Lindsay, D.G. and Smart, G.A. (1983) Reorganisation of the British total diet study for monitoring food constituents from 1981. Food Chem. Toxic. 21, 503-507.
  10. Ministry of Agriculture, Fisheries and Food (1994) The British diet: finding the facts. Food Surveillance Paper No. 40, publ. HMSO, London.
  11. Gregory, J., Foster, K., Tyler, H. and Wiseman, M. (1990) Dietary and nutritional survey of British adults, publ. HMSO, London.
  12. Jobling, S., Reynolds, T., White, R., Parker, M.G. and Sumpter, J.P. (1995) A variety of environmentally persistent chemicals, including some phthalate plasticisers, are weakly oestrogenic. Environmental Health Perspectives 103, 582-587.
  13. Sharpe, R.M., Fisher, J.S., Millar, M.M., Jobling, S. and Sumpter, J.P. (1995) Gestational and lactational exposure of rats to xenoestrogens results in reduced testis size and sperm production. Environmental Health Perspectives 103, 1136-1143.
  14. Gilbert, J. (1994) The fate of environmental contaminants in the food chain. The Science of the Total Environment 143, 103-111.
Contact point

For further information, please contact:

Mr Steven Wearne
MAFF, Food Safety and Science Group
Food Contaminants Division
Ergon House, c/o Nobel House
17 Smith Square
London SW1P 3JR

Tel: +44 (0) 171 238 6227
Fax: +44 (0)171 238 5331


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These pages were last updated on 1 October 1996

 
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