Toxicity and risks with T-2 and HT-2 toxins in cereals

Abstract

The trichothecenes T-2 and HT-2 toxins have during recent years been found frequently in cereals grown in Europe. They are mainly produced by Fusarium langsethiae. High concentrations of the toxins are most commonly found in oats, but they are also detected frequently at lower concentrations in barley. Wheat is only rarely contaminated. Yearly surveys of T-2 and HT-2 toxins in oats from Northern Europe have shown that the occurrence and levels have increased from 2002, with very high levels in 2005-2007, followed by a decrease in 2008-2009.Raw oats delivered to mills for processing to food have also been highly contaminated with T-2 and HT-2 toxins during the period 2006-2009. The processing of oats in the mills by sorting-sieving and dehulling reduce the toxin concentrations in the final food products, flakes and meals, with more than 80% even at high levels in the raw oat. The concentrations of the toxins in the by-products from the process are instead increased. The by-products are mainly used as feed components.The toxic effects of T-2 and HT-2 toxins in animals and the toxicological information used in the risk evaluations are briefly described. Risk evaluations of the toxins in cereals for human consumption have been conducted by both EU-Scientific Committee on Food and by JECFA in 2001. Both evaluations resulted in the same temporary tolerable daily intake (t-TDI) for the sum of T-2 and HT-2 toxins. The group TDI for T-2 and HT-2 toxins, alone or in combination, became 60 ng/kg bw and day.The intake of T-2 and HT-2 toxins through oats is calculated from median concentrations in oat products and median consumption data from Norway. The intake was found to be 1.5-5.4% of the t-TDI.The toxic effects studied or expected in farm animals, horses and ruminants, consuming high amounts of oat in their feed are described and discussed.

Full text

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Proc. 11th European Fusarium Seminar, 20-23September 2010, Radzikow, Poland
TOXICITY AND RISKS WITH T-2 AND HT-2 TOXINS IN CEREALS
Pettersson, H.
Department of Animal Nutrition and Management, Swedish University of Agricultural
Sciences, P. O. Box 7024, SE-750 07 Uppsala, Sweden
The trichothecenes T-2 and HT-2 toxins have during recent years been found frequently
in cereals grown in Europe. They are mainly produced by Fusarium langsethiae. High
concentrations of the toxins are most commonly found in oats, but they are also detected
frequently at lower concentrations in barley. Wheat is only rarely contaminated with the
toxins and then at low levels. Yearly surveys of T-2 and HT-2 toxins in oats from
Northern Europe have shown that the occurrence and levels have increased from 2002,
with very high levels in 2005-2007, followed by a decrease in 2008-2009.
Raw oats delivered to mills for processing to food have also been highly contaminated
with T-2 and HT-2 toxins during the period 2006-2009. The decrease during the last
years can also be seen. The processing of oats in the mills by sorting-sieving and
dehulling reduce the toxin concentrations in the final food products, flakes and meals,
with more than 80 % even at high levels in the raw oat. The concentrations of the toxins
in the by-products from the process are instead increased. The by-products are mainly
used as feed components. The concentrations of T-2 and HT-2 in oats and oat products
will be summarized.
The toxic effects of T-2 and HT-2 toxins in animals and the toxicological information
used in the risk evaluations will be briefly described. Risk evaluations of the toxins in
cereals for human consumption have been conducted by both EU-Scientific Committee
on Food and by JECFA in 2001. Both evaluations resulted in the same tolerable daily
intake (TDI) for the sum of T-2 and HT-2 toxins. The group TDI for T-2 and HT-2
toxins, alone or in combination, became 60 ng/kg bw and day.
The intake of T-2 and HT-2 toxins through oats is calculated from median
concentrations in oat products and consumption by exposed population. Intake by
normal and high consumers of oat are compared with the TDI.
The toxic effects studied or expected in farm animals, horses and ruminants, consuming
high amounts of oat in their feed are described and discussed.
Key words: T-2 toxin, HT-2 toxin, Fusarium langsethiae, oats, toxin contamination,
toxicity, risk

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Proc. 11th European Fusarium Seminar, 20-23September 2010, Radzikow, Poland
Introduction
Cereal plants are worldwide infected with different Fusarium species and some of them
e.g. F. graminearum, F. culmorum are associated with plant diseases like Fusarium head
blight and grain contamination with toxins. Other Fusarium species e.g. F. poae, F.
langsethiae do not produced clear pathogenic symptoms but may still produce toxins.
The trichothecene deoxynivalenol mainly produced by F. graminearum is the most
frequently found fusarium toxin and present at the highest concentrations in especially
wheat. The more toxic trichothecenes T-2 and HT-2 toxins have during recent years
been found also frequently in cereals grown in Europe (Edwards et al. 2009, Pettersson
et al. 2008). They are mainly associated with F. langsethiae, but may be produced also
by F. sporotrichioides in cereals from East and South Europe. T-2 and HT-2 toxins have
most frequently been found at highest concentrations in oats followed by barley. Wheat
is much less contaminated.
Tricothecenes in cereals were risk evaluated by the EU Scientific Committee on Food
(SCF 2001) and JECFA (Joint FAO/WHO Expert Committee on Food Additives) in
2001. A combined provisional tolerable daily intake (p-TDI) of 0.06 µg/kg body weight
and day was established for T-2 and HT-2 toxins, since T-2 toxin is readably converted
into HT-2 toxin after consumption.
The European Union has introduced maximal tolerable levels of deoxynivalenol in
cereals intended for food and recommendation on guidance levels in feed (EC 2006a,b).
There are currently no legal limits for T-2 and HT-2 toxins in food or feed, although the
intention to introduce such is indicated in the legislation. The time table for introduction
has been prolonged, partly due to the high occurrence of the toxins in oats.
This paper will give a review of the occurrence of T-2 and HT-2 toxins in European
cereals, effect of processing, their toxicity and risks for human and animals.
Occurrence
Surveys of T-2 and HT-2 toxins in European cereals during the 1990-ties as reported by
SCOOP 2003 and JECFA 2001 showed that the toxins occurred most frequently in oats
followed by barley and maize. Wheat was much less contaminated. The mean levels for
the sum of T-2 and HT-2 toxins were generally relatively low (< 100 µg/kg) although
some max values in certain oat samples exceeded 1000 µg T-2+HT-2/kg. The surveys of
trichothecenes in cereals continued in Scandinavia and started in UK during the period
2000 to 2009. Results from the surveys of T-2 and HT-2 toxins in oats are presented in
table 1. High and increasing levels of T-2 and HT-2 toxins were found in oats from
Scandinavia and UK in 2002 to 2006. Thirty-three to 44 % of the samples from UK,
Finland, and Sweden exceeded 500 µg T-2+HT-2/kg during at least one year. Median
levels above 200 µg/kg were recorded and max concentrations up to 9990 µg/kg were
found. The levels decreased in oats from all survey countries during the period 2007-
2009.
The European Breakfast Cereal Association (CEEREAL) has analyzed T-2 and HT-2
toxins in 235 samples of raw oats delivered to their mills during 2006-2009 (Pettersson
2010). The overall median level was only 44 µg T-2+HT-2/kg with a max value of
841µg/kg in 20006. The decrease in the levels during 2008-2009 compared to 2006-
2007 was clear.

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Proc. 11th European Fusarium Seminar, 20-23September 2010, Radzikow, Poland
Barley and wheat have also been analyzed for T-2 and HT-2 toxins in Scandinavia, UK
and France during several years in the period 2000-2009. Concentrations above 50 µg T-
2+HT-2/kg have only rarely been detected in wheat. Barley samples above that level
occurred more frequently, but most positive samples had a concentration below. In the
French surveys of spring barley such low levels were frequently detected (Orlando et al.
2010). The adjusted mean concentrations for the years 2006-2008 were between 19 and
22 µg T-2+HT-2/kg. The toxins were much less frequently detected in winter barley
although fewer samples had been analyzed.
All oats for human consumption are processed in mills. Oats are cleaned by screening,
dehulled, sorted and flaked or milled. T-2 and HT-2 toxin concentration in the final
products used for food are reduced by an average of 80% during especially the dehulling
step. The effect of processing on the toxin levels in oats from UK mills are in detail
described by Scudamore et al. 2007. The toxin levels in the by-products (husks, debris,
small kernels) often used for feed will instead increase by on an average up to 3 times
compared to the raw oats.
The CEEREAL has also analyzed T-2 and HT-2 toxins in the oat-flakes and oat by-
products obtained in their mills during 2005-2009 (Pettersson 2010). The concentrations
in the raw oats, oat-flakes and oat by-products from the mills are given in table 2. The
mean and median concentrations in oat-flakes decrease by 81 and 73 % respectively
compared to raw oats and increased by 307 and 345 % in the oat-byproducts.
Toxicity
T-2 and HT-2 toxins exhibit their toxicity mainly by inhibiting DNA, RNA and protein
synthesis, the latter at the ribosomal level. The toxins are therefore highly cytotoxic and
more toxic compared to the other trichothecenes partly due to their more lipophilic
character and membrane permeability. T-2 toxin is rapidly converted into HT-2 toxin
after ingestion by animals. The toxicity of T-2 and HT-2 toxins in animals is thus
considered to be similar.
Several studies in mice and rats show that T-2 toxin causes cytotoxicity and proliferative
changes in the oesophagus- and forestomach epithelium. Several tests for genotoxicity in
vitro and in rodents in vivo, especially for clastogenic effects, were positive for T-2 and
HT-2. There is, however, limited evidence for carcinogenicity in experimental animals.
It induced hepatocellular- and pulmonary adenomas in male mouse (Schiefer et al.
1987).
The most important toxicity studies identified by the EU Scientific Committee on Food
(SCF, 2001) and the Joint FAO/WHO Expert Committee on Food Additives (JECFA,
2001) in their evaluation of T-2 and HT-2 toxicity are given in table 3. The LOAEL
(Lowest observed adverse effect levels) or NOAEL (No observed adverse effect levels)
are given for the critical effects. Both Committees, the JECFA and the SCF, used the
haematotoxicity and immunotoxicity of T-2 toxin in the subacute toxicity study by Rafai
et al. 1995a as the bases for their safety assessment. There are deficiencies in the toxicity
studies, e.g study duration, pair feeding of control animals, comparative studies on
metabolism and toxicokinetics. To account for this and the use of a LOAEL, the
Committes included an extra uncertainty factor of 5, giving an overall uncertainty factor
of 500. A temporary or provisional maximal Tolerable Daily Intake (t-TDI or PMTDI)

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Proc. 11th European Fusarium Seminar, 20-23September 2010, Radzikow, Poland
of 0.06 µg/ kg bodyweight and day was thus established for the sum of T-2 and HT-2
toxins.
The toxicity of T-2 and HT-2 toxins in farm animals was evaluated by Eriksen and
Pettersson 2004. The lowest effect level in feed for certain toxic effects in major feeding
studies with pigs and chickens are given in table 4. Guidance values for the highest T-2
and HT-2 concentrations in feed for pigs and chicken was suggested to 0.2 and 0.5
µg/kg respectively.
There are hardly any reports on toxic effects in ruminants fed T-2 and HT-2 toxins in
controlled studies. This may be due to that trichothecenes including T-2 and HT-2 toxins
are rapidly degraded and detoxified by microorganisms in the rumen. They are
deacetylated and de-epoxidated. The removal of the epoxide is the main detoxification
of trichothecenes. De-epoxidation activities have also been found in faeces from pigs
and horses (Eriksen et al. 2002; Pettersson et al. 2008), but it is unclear if this reaction
in the lower part of the gastro-intestinal tract may have an influence on the eventual
toxic effects.
Horses may be highly exposed to T-2 and HT-2 toxins but there are only few case
reports on their eventual toxic effects in horses. Most cases are from East Europe but T-
2 toxin has also been the cause of bean-hull poisoning of horses in Japan. Toxic effects
described are CNS toxicity, muscle contraction, tachycardia and colic. The exposure of
trotter horse to T-2 and HT-2 toxins through oats has been studied in Sweden (Pettersson
et al. 2007). Horses consuming an average of 2.6 mg T-2+HT-2 per day were compared
with a group consuming 0.7 mg toxins per day. No clear effects were seen on health and
performance of the horses.
Risks
Estimation of human intake of T-2 and HT-2 toxins through oats and comparison with
the established t-TDI can provide information on the risks with the toxins in food oats.
JECFA (2001) made intake calculations for the trichothecenes based on the toxin
database available for each cereal at that time and different cereal consumption
information. The calculated intakes were high for many population groups and the intake
for the sum of T-2 and HT-2 toxins exceeded the combined t-TDI in most high cereal
consumption groups. The toxin portion from oats was about 50% of the intake. The
mean concentration used for oats in the calculations was a weight mean (21 µg T-2/kg,
35 µg HT-2/kg) of all European analysis on unprocessed oats. This is not an appropriate
concentration value to use in the calculations since unprocessed oats are not consumed
and processing decrease the toxin concentrations with more than 80%.
The median concentration of T-2 and HT-2 toxins in oat-flakes for the year 2005-2009
from the study by CEEREAL are more correct to use. This concentration has been used
together with the detailed Norwegian oat consumption data for the calculation of intake
in table 5. Oat consumption in Norway is relatively high and a median consumption has
been used in the calculations. The intake of T-2 and HT-2 toxins from oats is then 1.5-5
% of the t-TDI depending on groups and much lower than in the JECFA calculations. If
the intake is calculated for high oat consumers (95th percentile consumption) and high
toxin concentration (90th percentile) in the oat-flakes, the toxin intake will become 48-77
% of the t-TDI.

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Proc. 11th European Fusarium Seminar, 20-23September 2010, Radzikow, Poland
About 75 % of the European oat crop is used in animal feed. Oats are mainly used in
feed for ruminants and horses. It is less popular in feeds for pigs and poultry due to the
relative high fiber content and low energy value. Oat by-products are only used in horse
and ruminant feed.
Oats with median T-2 and HT-2 toxin concentrations (Survey mean 90 µg/kg,
CEEREAL 42 µg/kg) can be used in feed to pigs and poultry without restrictions due to
toxin content and risk for exceeding feed guidance levels. The oat component in their
feeds rarely exceeds 50% of the diet. Oats containing high toxin levels equal to the 90th
percentile (208 µg/kg) in the CEEREAL study could also be used, but oats with
concentrations above 1000 µg T-2+HT-2/kg may cause adverse effects.
In adult ruminants even the highest T-2 and HT-2 toxin concentrations in oats are
expected to be degraded and detoxified by the rumen microbes. The highest toxin
concentrations may have a local contact effect causing erosions on the muzzle and in the
mouth. This has however not been described.
Athletic or working horses may be fed up to 6 kg oats per day in addition to the
roughage. If oats with a median toxin concentration (90 or 42 µg/kg) is used the daily
intake will be only 0.25-0.54 mg/day or calculated on a body weight of 500kg give 0.5-
1.1 µg/kg b.w. and day. The lowest adverse effect level of T-2 and HT-2 toxins in horses
is not known, but this daily amount will probably not cause adverse effects. Oats with T-
2 and HT-2 concentrations above 1000 µg/kg will give a daily consumption of more
than 6 mg/day or more than 12 µg/ kg b.w. and day. These amounts are expected to
cause toxic effects in the horses, although it was not noticed in the study on trotter
horses in Sweden. An explanation could be the degradation of trichothecenes in
intestinal and feces content of horses fed oats. A local cytotoxic contact effects caused
by high toxin concentrations could also be expected in the muzzel, mouth, stomach and
upper intestine of the horses. T-2 and HT-2 toxins are highly cytotoxic and cause cell
death at concentrations from 0.3-20 ng/ml in cell culture studies.
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Table 1. T-2 and HT-2 toxins in surveys of oats 2000-2009. (after Pettersson 2010)
Year Country Mean Median Max Reference
>50ppb >500ppb (µg/kg) (µg/kg) (µg/kg)
2000 Finland 25 36 8137 25 1369 Hietaniemi 2006
Norway 22 73 586 53 564 SCOOP 2003
2001 Finland 37 27 059 25 273 Hietaniemi 2006
Norway 24 0 0 10 10 10 SCOOP 2003
2002 Finland 30 37 078 38 427 Hietaniemi 2006
UK 92 70 16 311 106 4844 Edwards 2006
2003 Finland 30 63 13 305 116 1647 Hietaniemi 2006
UK 104 69 33 727 204 9990 Edwards 2006
2004 Finland 30 57 10 282 104 2850 Hietaniemi 2006
Norway 56 70 0106 86 334 Clasen 2006
UK 128 80 24 500 202 6997 Edwards 2006
2005 Finland 60 63 33 440 186 3500 Hietaniemi 2006
Sweden 41 61 17 255 90 1165 Pettersson 2006
Norway 126 87 13 283 180 2041 Clasen 2006
Denmark 18 94 6312 221 2560 Biselli 2006
UK 134 88 44 694 403 3188 Edwards 2006
2006 Finland 59 53 5163 47 1283 Hietaniemi 2007
Sweden 71 90 44 465 376 1416 Pettersson 2007
Norway 102 78 9218 145 1675 Clasen 2006
UK 100 96 43 795 404 6261 Edwards 2007
2007 Finland 80 53 5121 64 863 Hietaniemi 2007
Sweden 58 91 10 255 90 1165 Pettersson 2008
Norway 32 94 6217 177 980 Clasen 2008
UK 103 77 18 438 169 8399 Edwards 2008
2008 Finland 80 38 5100 32 1932 Hietaniemi 2009
Sweden 70 34 057 34 493 Pettersson 2009
Norway 33 64 062 55 145 Clasen 2009
UK 90 7120 47 1190 Edwards 2009
2009 Finland 80 39 485 25 1020 Hietaniemi 2010
Sweden 27 33 482 35 886 Pettersson 2010
Norway 30 67 6134 73 763 Clasen 2010
Number
of
Samples
Percentage of Samples

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Table 2. T-2 and HT-2 toxins in oats and oat products from European mills in the
CEEREAL study 2005-2009. (after Pettersson 2010).
Product Number Mean Median 90th % ile Max
of Samples (µg/kg) (µg/kg) (µg/kg) (µg/kg)
Oats raw 235 96 44 212 841
Oat flakes 435 18 12 41 197
Oat by-product 208 295 152 663 1711

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Table 3. Critical Toxicology studies on T-2 toxin identified by SCF in 2001. (after
Slatter 2004)
Study
Critical effect
NOAEL/LOAEL
Reference
(mg/kg b.w./day)
Mouse, 16 months
Pulmonary adenomas
0.23 (NOAEL)
Schiefer et al. 1987
Hepatocellular adenomas
0.23 (NOAEL)
Forestomach epithelial
hyperplasi
0.23 (NOAEL)
Rat, 4 week
Forestomach epithelial
hyperplasi
0.5 (NOAEL)
Ohtsubo and Saito 1977
Mouse, 5 days
Thymus athrophy,
decreased number of T- and
B-cells
0.75 (LOAEL)
Smith et al. 1994
Pig, 3 weeks (subacute)
Reduced number of
leukocytes, lymphocytes
and antibody production
against horse globulin.
Decrease in size of thymus
and spleen
0.03 (LOAEL)
Rafai et al. 1995
Monkey (15 days by gavage)
Leukopenia
0.1 (LOAEL)
Rukimini et al. 1980
Mouse, CD-1, two generations.
No dose showing effect
Embryo- or foetotoxicity
0.45 (NOAEL)
Rosseaux and Schiefer
1987
Rat, single dose
Neurotoxicity
0.4 (NOAEL)
Sirkka et al. 1992

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Table 4. Lowest effect level of T-2 toxin in feed for pigs and chicken.
Animal
Lowest
Effect level
Toxic Effect
Reference
(mg/kg feed)
Pig
0.5
Reduced immunedefence
Rafai et al. 1995b
1-2
Reduced growth and feed
intake
Rafai et al. 1995a, Friend
et al. 1992, Weaver et al.
1978
Chicken
0.4-1
Mucosa erosion
Wyatt et al. 1972, 1973
2
Reduced feed
consumption and growth
Wyatt et al. 1972, 1973

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Table 5. Intake of T-2 and HT-2 toxins from oats calculated on consumption data from
Norway. Median consumption and median toxin concentration from CEEREAL study.
Population
Body
Median
Toxin
conc.
Median Consumption
group
weight
Grain
Toxin intake
% of TDI
(kg)
(µg/kg)
(g/person
per day)
(ng/person
, day)
(ng/kg
b.w., day)
6 years
23
12
6.2
74.4
3.23
5.4
10 years
35
12
8.2
98.4
2.81
4.7
Males
16-29 years
75
12
7.5
90
1.20
2.0
30-59 years
83
12
7.6
91.2
1.10
1.8
60-79 years
79
12
6.5
78
0.99
1.6
Females
16-29 years
63
12
6.3
75.6
1.20
2.0
30-59 years
65
12
5.8
69.6
1.07
1.8
60-79 years
69
12
5.1
61.2
0.89
1.5