Number 82 March 1996
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
- 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.
- International Programme on Chemical Safety (1992)
Diethylhexyl phthalate. Environmental Health Criteria 131,
publ. World Health Organisation, Geneva.
- International Programme on Chemical Safety (1992)
Diethylhexyl phthalate. Environmental Health Criteria 131,
publ. World Health Organisation, Geneva.
- Ministry of Agriculture, Fisheries and Food (1995)
Phthalates in paper and board packaging. Food Surveillance Information
Sheet 60.
- Castle, L., Gilbert, J. and Eklund, T. (1990) Migration
of plasticiser from poly(vinyl chloride) milk tubing. Food Addit. Contam.
7, 591-596.
- Cerbulis, J. and Byler, D.M. (1986) Isolation and
detection of dialkyl phthalates from pork. J. Agric. Food Chem. 34,
198-200.
- 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.
- Mayer, F.L., Jr. Stalling, D.L. and Johnson, J.L. (1972)
Phthalate esters as environmental contaminants. Nature (London) 238,
411-413.
- 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.
- Ministry of Agriculture, Fisheries and Food (1994) The
British diet: finding the facts. Food Surveillance Paper No. 40,
publ. HMSO, London.
- Gregory, J., Foster, K., Tyler, H. and Wiseman, M.
(1990) Dietary and nutritional survey of British adults, publ. HMSO, London.
- 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.
- 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.
- 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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