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Some comments on the dietary intake of butylated hydroxytoluene
Fd Chem. Toxic. Vol. 29, No. 1, pp. 73-75. 1991
PergamonPress pie. Printed in Great Britain
LETTERS TO THE EDITOR SOME COMMENTS ON THE DIETARY INTAKE OF BUTYLATED HYDROXYTOLUENE Sir,--Your recent article on the maximal daily dietary intake of butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) in The Netherlands (Verhagen et al., 1990) requires some comment in respect of the conclusions reached. In particular, the conclusion that " . . . it cannot be excluded that the acceptable daily intake for BHT (FAO/WHO: 0-0.125 mg/kg; EEC: 0-0.05 mg/kg) is exceeded in all age and sex groups, but particularly in children aged 1-6 years," is both misleading and not justified by the available data. The study is based on the consumption of fats in different foodstuffs in The Netherlands, and adopts a maximal approach, that is, all fats are assumed to contain a maximum permissible content of BHT (and BHA). This methodology has been used in a number of previous studies of this type, and is an acceptable approach in the absence of specific analytical data. However, after addressing the different practical factors that will actually reduce BHT levels very significantly, it makes the bland comment, "Consequently, actual BHA and/or BHT intakes may be lower than the estimated levels of intake." [my italics]. These factors deserve to be given much greater weight, and are considered in more detail below: (i) The need for use of an antioxidant or otherwise will depend upon a variety of factors, for example the type of oil or fat, its intended use etc. In many cases, none will be required and none will be used. (ii) The methodology assumes the use of only two antioxidants, BHA and/or BHT, and the maximal approach calculates levels on the basis of maximum permitted use of these products. In practice, there are a number of other antioxidants that are used, for example gallate esters, and it is common to use a combination of antioxidants in order to make use of the synergistic effects of many mixtures. Calculations based on the exclusive use of a single antioxidant to its maximum level will inevitably overestimate the overall consumption of BHT very considerably. (iii) The processing conditions used in the production of many foods such as cakes, biscuits and snacks lead to substantial losses of BHT at this stage (due to volatility/steam volatility), which may be as high as 90%, resulting in a reduced level of BHT in the final product. It should be noted that the major calculated BHT contribution in this study originates from the "pastry, cake and biscuits" category. Giving due weight to the above factors, a more realistic conclusion would seem to be that the likelihood of current ADIs being exceeded is very low. Such a conclusion is supported by a recent French study (Anonymous, 1990) that collected information on the actual use of BHT (and BHA) in foodstuffs, and also made analytical determinations on the occurrence of these antioxidants in a variety of food products. From this data, it estimated a maximum practical consumption of BHA/BHT for a young person of 50 kg body weight as 0.4 mg/person/day, which is equivalent to 0.008 mg/kg body weight/day for both antioxidants combined. A worst case calculation (a young person eating only cake and chewing gum) gave a total daily intake of 0.04 mg/kg body weight/day. The lower (EEC) ADI for BHT is 0.05 mg/kg body weight/day. This study supports the view that the consumption of BHT as part of the normal west European diet is unlikely to exceed the existing ADI. Even this study overlooks the fact that 80-99% of BHT in chewing gum is not extracted from the gum during chewing, and is therefore not actually ingested. Moreover, calculations of intake based on sales/usage of antioxidants to the food industry, modified by the 'loss in processing' factor, still give an overestimate of actual consumption. This is because significant portions of frying oils/fats are not consumed; they are discarded after one (or more) 'frying(s)', particularly in domestic use. When all these factors are considered it can be seen that the chances of exceeding even the lower ADI for BHT as set by the EEC, are remote. When balanced against the known risks (and waste) associated with rancid fats/oils it is clear that the benefit outweighs the risks. References
Anonymous (1990) Rapport sur rtvaluation de la consummation de certains additifs. Direction G~ntrale de la Concurrence de la Consummation et de la Rtpression des Fraudes, 13 Rue St Georges, Paris. 73
74
Letter to the Editor
Verhagen H., Deerenberg I., Marx A., ten Hoor F., Henderson P.Th. and Kleinjans J. C. S. (1990) Estimate of the maximal daily dietary intake of butylated hydroxyanisole and butylated hydroxytoluene in The Netherlands. Food and Chemical Toxicology 28, 215-220. C. J.
Nunn
European BHT Manufacturers Association, Avenue Louise 250 Bte. 72, B- 1050 Brussels, Belgium This letter was shown to Dr Verhagen et al. Their rejoinder follows:
S i r , - - D a t a on the amounts of food additives bought, sold or used by foodstuff-producing companies are generally confidential by nature and therefore not regularly available from literature sources, if at all. Therefore, in our study (Verhagen et al., 1990a) we used an alternative method to estimate the maximalpossible daily dietary intake of the food antioxidants B H A and B H T based on a maximal approach. The theoretical and practical limitations of this method as outlined by D r N u n n are in line with our own reservations about this method. Thus, in reality the daily dietary intake of B H T and B H A will actually be lower than the values derived from the applied maximal approach, as we have tried to indicate (Verhagen et al., 1990a). This is supported by data from the latest market basket study in The Netherlands, which included analyses of B H A and BHT; B H A was found in a few instances only while B H T could not be detected (van D o k k u m et al., 1982). We think that for a proper risk assessment more pertinent data should be made available on the actual dietary intake as well as on the mechanism underlying the tumorigenicity o f B H A and BHT. In order to address the first aspect, we have performed a limited experiment (too small to extrapolate the results to the general population) to assess the daily individual dietary intake o f BHA, but not of BHT, based on a biologicalmonitoring approach, utilizing the fact that 39% of a single oral dose of 0.5 mg B H A / k g body weight (the current A D I ) is recovered from the urine as phase-II conjugates of B H A with glucuronic acid and sulphate (Verhagen et al., 1989); we have published this small study as a conference abstract only. (Verhagen et al., 1990b). In part 1 of the experiment 22 volunteers (13 female, 9 male; 23 _ 1 years, mean _+ SD) collected their urine for a 24-hr period. In part 2 o f the experiment 6 volunteers consumed foodstuffs that might contain B H A or B H T (as indicated from the list of ingredients): salted biscuits, crunchy roasted nuts, chewing gum (which was entirely ingested; D r N u n n is right that hardly any B H T or B H A is extracted from chewing gum by chewing alone---H. Verhagen, unpublished data), frozen dinner, a tin of goulash or fish fingers (the last three food items were consumed after preparation). Volunteers subsequently collected their urine for 24 hr. Aliquots of urine were treated overnight with fl-glucuronidase/arylsulphatase in order to release B H A from its conjugates. Thereafter, B H A was extracted with diethylether and the organic phase washed with 1 N-NaOH and with 1 lq-HCl and evaporated to dryness at 0°C under N2. Levels of B H A in urine were quantitated by H P L C essentially as described previously (Verhagen et al., 1989). The limit o f detection was 25 ng B H A / m l urine. Taking the average body weight (68 _+ 10kg) and urinary volume (1107 _+466ml) into Table 1. Levels of BHA in 24-hr urine samples from humans* Body ng BHA/ pg BHA/kg % of Subject Sex Age weight ml urine body weight the ADI 1 f 21 65 <25 < 1 <0.2 2 f 22 85 <25 <1 <0.2 3 f 24 63 <25 <1 <0.2 4 f 22 69 <25 <1 <0.2 5 f 22 58 <25 <1 <0.2 6 f 21 53 <25 <1 <0.2 7 f 24 63 <25 <1 <0.2 8 f 24 54 <25 <1 <0.2 9 f 21 69 <25 <1 <0.2 10 f 23 59 <25 <1 <0.2 11 f 23 69 < 25 < 1 < 0.2 12t f 21 55 67 3.2 0.7 13 f 24 59 <25 <1 <0.2 14 m 24 83 <25 <1 <0.2 15 m 23 69 < 25 < 1 < 0.2 16 m 22 67 <25 <1 <0.2 17t m 26 82 99 5.1 1.0 1St m 22 75 51 1.5 0.3 19t m 25 78 84 4.0 O.S 20 m 24 70 < 25 <1 < 0.2 21 m 24 75 <25 <1 <0.2 22 m 22 69 <25 <1 <0.2 *Results from part 1 of the experiment detailed in the text. tPositive samples.
PergamonPress pie. Printed in Great Britain
LETTERS TO THE EDITOR SOME COMMENTS ON THE DIETARY INTAKE OF BUTYLATED HYDROXYTOLUENE Sir,--Your recent article on the maximal daily dietary intake of butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) in The Netherlands (Verhagen et al., 1990) requires some comment in respect of the conclusions reached. In particular, the conclusion that " . . . it cannot be excluded that the acceptable daily intake for BHT (FAO/WHO: 0-0.125 mg/kg; EEC: 0-0.05 mg/kg) is exceeded in all age and sex groups, but particularly in children aged 1-6 years," is both misleading and not justified by the available data. The study is based on the consumption of fats in different foodstuffs in The Netherlands, and adopts a maximal approach, that is, all fats are assumed to contain a maximum permissible content of BHT (and BHA). This methodology has been used in a number of previous studies of this type, and is an acceptable approach in the absence of specific analytical data. However, after addressing the different practical factors that will actually reduce BHT levels very significantly, it makes the bland comment, "Consequently, actual BHA and/or BHT intakes may be lower than the estimated levels of intake." [my italics]. These factors deserve to be given much greater weight, and are considered in more detail below: (i) The need for use of an antioxidant or otherwise will depend upon a variety of factors, for example the type of oil or fat, its intended use etc. In many cases, none will be required and none will be used. (ii) The methodology assumes the use of only two antioxidants, BHA and/or BHT, and the maximal approach calculates levels on the basis of maximum permitted use of these products. In practice, there are a number of other antioxidants that are used, for example gallate esters, and it is common to use a combination of antioxidants in order to make use of the synergistic effects of many mixtures. Calculations based on the exclusive use of a single antioxidant to its maximum level will inevitably overestimate the overall consumption of BHT very considerably. (iii) The processing conditions used in the production of many foods such as cakes, biscuits and snacks lead to substantial losses of BHT at this stage (due to volatility/steam volatility), which may be as high as 90%, resulting in a reduced level of BHT in the final product. It should be noted that the major calculated BHT contribution in this study originates from the "pastry, cake and biscuits" category. Giving due weight to the above factors, a more realistic conclusion would seem to be that the likelihood of current ADIs being exceeded is very low. Such a conclusion is supported by a recent French study (Anonymous, 1990) that collected information on the actual use of BHT (and BHA) in foodstuffs, and also made analytical determinations on the occurrence of these antioxidants in a variety of food products. From this data, it estimated a maximum practical consumption of BHA/BHT for a young person of 50 kg body weight as 0.4 mg/person/day, which is equivalent to 0.008 mg/kg body weight/day for both antioxidants combined. A worst case calculation (a young person eating only cake and chewing gum) gave a total daily intake of 0.04 mg/kg body weight/day. The lower (EEC) ADI for BHT is 0.05 mg/kg body weight/day. This study supports the view that the consumption of BHT as part of the normal west European diet is unlikely to exceed the existing ADI. Even this study overlooks the fact that 80-99% of BHT in chewing gum is not extracted from the gum during chewing, and is therefore not actually ingested. Moreover, calculations of intake based on sales/usage of antioxidants to the food industry, modified by the 'loss in processing' factor, still give an overestimate of actual consumption. This is because significant portions of frying oils/fats are not consumed; they are discarded after one (or more) 'frying(s)', particularly in domestic use. When all these factors are considered it can be seen that the chances of exceeding even the lower ADI for BHT as set by the EEC, are remote. When balanced against the known risks (and waste) associated with rancid fats/oils it is clear that the benefit outweighs the risks. References
Anonymous (1990) Rapport sur rtvaluation de la consummation de certains additifs. Direction G~ntrale de la Concurrence de la Consummation et de la Rtpression des Fraudes, 13 Rue St Georges, Paris. 73
74
Letter to the Editor
Verhagen H., Deerenberg I., Marx A., ten Hoor F., Henderson P.Th. and Kleinjans J. C. S. (1990) Estimate of the maximal daily dietary intake of butylated hydroxyanisole and butylated hydroxytoluene in The Netherlands. Food and Chemical Toxicology 28, 215-220. C. J.
Nunn
European BHT Manufacturers Association, Avenue Louise 250 Bte. 72, B- 1050 Brussels, Belgium This letter was shown to Dr Verhagen et al. Their rejoinder follows:
S i r , - - D a t a on the amounts of food additives bought, sold or used by foodstuff-producing companies are generally confidential by nature and therefore not regularly available from literature sources, if at all. Therefore, in our study (Verhagen et al., 1990a) we used an alternative method to estimate the maximalpossible daily dietary intake of the food antioxidants B H A and B H T based on a maximal approach. The theoretical and practical limitations of this method as outlined by D r N u n n are in line with our own reservations about this method. Thus, in reality the daily dietary intake of B H T and B H A will actually be lower than the values derived from the applied maximal approach, as we have tried to indicate (Verhagen et al., 1990a). This is supported by data from the latest market basket study in The Netherlands, which included analyses of B H A and BHT; B H A was found in a few instances only while B H T could not be detected (van D o k k u m et al., 1982). We think that for a proper risk assessment more pertinent data should be made available on the actual dietary intake as well as on the mechanism underlying the tumorigenicity o f B H A and BHT. In order to address the first aspect, we have performed a limited experiment (too small to extrapolate the results to the general population) to assess the daily individual dietary intake o f BHA, but not of BHT, based on a biologicalmonitoring approach, utilizing the fact that 39% of a single oral dose of 0.5 mg B H A / k g body weight (the current A D I ) is recovered from the urine as phase-II conjugates of B H A with glucuronic acid and sulphate (Verhagen et al., 1989); we have published this small study as a conference abstract only. (Verhagen et al., 1990b). In part 1 of the experiment 22 volunteers (13 female, 9 male; 23 _ 1 years, mean _+ SD) collected their urine for a 24-hr period. In part 2 o f the experiment 6 volunteers consumed foodstuffs that might contain B H A or B H T (as indicated from the list of ingredients): salted biscuits, crunchy roasted nuts, chewing gum (which was entirely ingested; D r N u n n is right that hardly any B H T or B H A is extracted from chewing gum by chewing alone---H. Verhagen, unpublished data), frozen dinner, a tin of goulash or fish fingers (the last three food items were consumed after preparation). Volunteers subsequently collected their urine for 24 hr. Aliquots of urine were treated overnight with fl-glucuronidase/arylsulphatase in order to release B H A from its conjugates. Thereafter, B H A was extracted with diethylether and the organic phase washed with 1 N-NaOH and with 1 lq-HCl and evaporated to dryness at 0°C under N2. Levels of B H A in urine were quantitated by H P L C essentially as described previously (Verhagen et al., 1989). The limit o f detection was 25 ng B H A / m l urine. Taking the average body weight (68 _+ 10kg) and urinary volume (1107 _+466ml) into Table 1. Levels of BHA in 24-hr urine samples from humans* Body ng BHA/ pg BHA/kg % of Subject Sex Age weight ml urine body weight the ADI 1 f 21 65 <25 < 1 <0.2 2 f 22 85 <25 <1 <0.2 3 f 24 63 <25 <1 <0.2 4 f 22 69 <25 <1 <0.2 5 f 22 58 <25 <1 <0.2 6 f 21 53 <25 <1 <0.2 7 f 24 63 <25 <1 <0.2 8 f 24 54 <25 <1 <0.2 9 f 21 69 <25 <1 <0.2 10 f 23 59 <25 <1 <0.2 11 f 23 69 < 25 < 1 < 0.2 12t f 21 55 67 3.2 0.7 13 f 24 59 <25 <1 <0.2 14 m 24 83 <25 <1 <0.2 15 m 23 69 < 25 < 1 < 0.2 16 m 22 67 <25 <1 <0.2 17t m 26 82 99 5.1 1.0 1St m 22 75 51 1.5 0.3 19t m 25 78 84 4.0 O.S 20 m 24 70 < 25 <1 < 0.2 21 m 24 75 <25 <1 <0.2 22 m 22 69 <25 <1 <0.2 *Results from part 1 of the experiment detailed in the text. tPositive samples.