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Introduction
Adverse reaction to
foods
Adverse reaction to foods in humans is very
common; in milder cases it causes discomfort
and in the more severe cases it can cause
anaphylaxis and even death. Avoidance of the
offending food can in most cases alleviate this
problem; however, accidental exposure is very
common due to the unsuspected presence of
the offending food component in a wide range
of processed foods (e.g. peanut, soybean,
milk, egg and cereal proteins). Adverse
reaction to foods causes discomfort not only
when the offending food is consumed, but
also when an individual is exposed via
physical contact or inhalation of vapour or
particles of food.
Adverse reactions to foods may be classified
into two fundamental groups:
(1) food aversion; and
(2) food intolerance.
O. Fraser, S. Sumar and
N. Sumar
The authors
O. Fraser, S. Sumar and N. Sumar are all at the
Department of Surgery, St George's Hospotal Medical
School, University of London, UK.
Keywords
Food, Allergies
Abstract
Outlines the prevalence of adverse reactions to food and
what it means to the individual. Lists and describes the
known main food allergies.
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Nutrition & Food Science
Volume 30 . Number 5 . 2000 . pp. 236±242
# MCB University Press . ISSN 0034-6659
Food aversion is an unpleasant reaction to
food, which is caused by emotions associated
with the food rather than by the food itself.
Food intolerance, which includes food
allergy, is a general term referring to a nonpsychological, reproducible, unpleasant
reaction to a specific food or food ingredient.
Food intolerance is then further subdivided
into food allergy and non-immunologically
mediated food intolerance.
Food allergy is a specific adverse reaction
to food where there is evidence of an
abnormal immunological reaction to the
food.
Non-immunologically mediated food
intolerance can also occur in some
individuals. This may be due to a number of
mechanisms including:
.
the lack of a particular enzyme needed for
the digestion of food;
.
the presence of toxic substances;
.
irritant effects such as those caused by
highly spiced foods;
.
pharmacological effects of some food
components; and
.
indirect effects caused by fermentation
of unabsorbed food in the digestive
system.
In this review we will focus on foods which
elicit allergic (immunological) and nonallergic (non-immunological) response
in humans since these are of greater
importance when considering the safety of
the foods.
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O. Fraser, S. Sumar and N. Sumar
Prevalence
Allergic reactions to food
The true prevalence of adverse reaction to
food particularly food allergy is unknown.
Epidemiological data differ according to age
categories, country, public perception, and
study methods. Results of community surveys
have reported the perceived incidence of food
allergy to be 14 to 33 per cent. This wide
disparity in statistics is probably due to a
combination of improper terminology and
public misconceptions, and a lack of
challenge proven confirmation of symptoms
(Sloan and Powers, 1986). In 1982, a Finnish
study in which 866 children aged between one
and six years reported the prevalence of food
allergy as 19 per cent at one year of age, 27
per cent at three years, and 8 per cent at six
years (Kajosaari, 1982). Results were based
on history, effect of an elimination diet, and
non-blinded food challenges. A more rigorous
study looked prospectively at 1,749 Danish
infants for the development of cow's milk
allergy during their first year. About 7 per
cent of the children had suggestive clinical
symptoms, but only 2.2 per cent actually were
proven to have cow's milk allergy by food
challenges in the hospital (Host and Halken,
1990). These results were similar to an earlier
study from the Isle of Wight (2.5 per cent)
(Hidc and Guycr, 1983), and a more recent
study from The Netherlands (2.7 per cent)
(Schrander et al., 1993). In a prospective
study of children followed through the first
three years of life in a general paediatric
practice, Bock (1981), concluded that about
8 per cent of children have adverse reactions,
most of which are transient. It may be
concluded from these studies that 4 to 6 per
cent of children experience food
hypersensitivity in the first three years of life,
but only 1 to 2 per cent of the paediatric
population are still affected by their tenth
birthday. Figures were similar to those for the
adult population.
In the UK, studies carried out by the
Wycombe Health Authority in 1986 showed
that the occurrence of intolerance to food in
the general population was in the range of
0.01 to 0.23 per cent (between 1 in 500 and 1
in 10,000). A later study of the same
population showed that the number of
individuals actually showing a demonstrable
reaction was between 1.4 and 1.9 per cent
(between 1 in 50 and 1 in 70) (Young et al.,
1987; 1994).
The concept of foods generally consumed
within a population causing an allergic
reaction in some individuals has existed for
quite a long time and is expressed in the
vocabulary of the indigenous Amerindian in
South America as ``kinna''. If a person had a
``kinna'', this meant that when that person
consumed a particular food (the ``kinna''), he
would become ill. The first recorded
significant investigation into adverse reaction
to foods was in 1912 by two scientists,
Kustner and Prausnitz, who observed that an
intradermal injection of fish extracts into a
fish-sensitive individual, elicited an
immediate wheal and flare reaction. Of equal
importance was the observation that
immediate reactivity of the fish allergen could
be passively transferred to a non-atopic
subject by intradermal injection of sera from
fish sensitive individuals. Subsequently, the
passive transfer of hypersensitivity to other
allergens was also observed. The nature of
these reaginic antibodies remained unknown
for more than 40 years until lshizaka and
lshizaka (1967) identified IgE as the carrier of
reaginic activity in the serum of patients with
hayfever.
The discovery of IgE antibody has provided
the basis for immunochemical approaches to
the study of mechanisms underlying
immediate hypersensitivity reactions. It is
now well recognised that the major feature
distinguishing atopic individuals from nonatopic individuals is their capacity to develop
a sustained IgE response to an allergen. IgE
has the unique property of binding to highaffinity receptors on basophils and mast cells.
The cross-linking of specific membrane
bound IgE with an allergen triggers the
release of vasoactive mediators, leukocyte
chemotactic factors, and cytokines
responsible for the clinical manifestation of
immediate hypersensitivity reactions (Lebrer,
1986; Taylor et al., 1987).
The development of allergic reactions to
food most commonly occurs in two phases:
(1) sensitisation; and
(2) allergic response.
Sensitisation of an individual to an allergen
occurs when the initial or repeated exposure
to the food antigen results in the stimulation
of the immune system to produce food
antigen-specific IgE antibodies. This process
involves the antigen being presented to the
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O. Fraser, S. Sumar and N. Sumar
immune system by antigen presenting cells
(APC), which causes T-helper cell
stimulation (via cytokine IL4) of B cells to
produce antigen-specific IgE antibodies.
These IgE antibodies then bind to high
affinity receptors on the surface of mast cells
and basophils resulting in sensitisation. The
allergic reaction to the food antigen occurs on
subsequent exposure, which results in the
degranulation of mast cells or basophils
thereby releasing mediators responsible for
the manifestation of clinical symptoms
(Figure 1).
The major food allergens are water-soluble
glycoproteins, with molecular weights ranging
front 12.5kDa to 63kDa (Taylor et al., 1987).
Most of these allergens are heat and acid
stable and can survive protease digestion. The
antigens responsible for most of the morbidity
and mortality owing to food allergy will be
discussed individually. The importance of
these food antigens varies in different
countries, depending on dietary habit and
amount consumed.
Food antigens
Cow's milk
Cow's milk is one of the most common food
allergens in children, perhaps because it is
usually the first foreign protein encountered
by infants. Protein fractions from cow's milk
are subdivided into casein and whey proteins.
Although extensive heating may denature
some of these proteins, it does not
significantly decrease the allergenicity of most
protein fractions. Casein fractions are used
extensively in processed foods as well as
cheeses. The whey fraction consists of
-lactoglobulin, -lactalbumin, bovine
immunoglobulin, bovine serum albumin, and
small amounts of various other proteins. IgE
antibodies to these whey proteins have been
demonstrated in most milk-allergic patients.
Cross-reactivity among milk proteins
obtained from cows, goats and sheep has been
reported. Clinical reactivity to goat's milk has
been estimated to occur in 50 per cent of
children allergic to cow's milk (Clein, 1958).
Egg
Chicken's egg is probably the most common
cause of food allergic reactions in children.
The major protein allergens found in egg
white are ovomucoid, ovalbumin, and
ovotransferrin (Holen and Elsayed, 1990).
Egg yolk contains a variety of proteins namely
lipovitellin and lipovitellenin (lipo-proteins),
levitin (water-soluble protein), and phosvitin
(phospho-protein). Although the yolk is
considered to be less allergenic than egg
white, IgE antibodies to egg yolk proteins
have been demonstrated (Anet et al., 1985).
IgE antibodies from children allergic to
chicken's egg have been shown to cross-react
with eggs from other species (Langeland,
1983).
Soybean
Soybean, a legume, is another common cause
of food-allergic reactions, mainly in children.
It is used in many commercial foods since it is
an inexpensive source of high-quality protein.
Of the four major protein fractions identified,
no one fraction appears to be more allergenic
than the other in a study of eight children with
IgE-mediated hypersensitivity to soybean
(Butts et al., 1988). Soybean proteins have
been identified in some soybean oils, lecithin,
Figure 1 Shows a schematic representation of cellular events resulting in sensitisation and allergic reaction to food
allergens. Initial exposure to allergen in atopic individuals results in IgE production by B cells. This sensitises cells
such as mast cells and basophils so that on subsequent exposure to allergen, degranulation occurs, releasing preformed mediators and inducing the synthesis of newly-formed mediators to produce clinical symptoms
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and margarine, but the impact of this is yet to
be determined. Immunological crossreactivity among legumes has been
demonstrated. However, symptomatic
hypersensitivity to more than one legume is
rare (Bernhisel-Broadbent and Sampson,
1989).
Peanut
Allergic reactions to peanut occur quite
frequently in both children and adults. Peanut
allergy is probably the most common cause of
anaphylaxis. Peanut proteins are classified as
water-soluble albumins or non-water-soluble
globulins. Sixteen allergenic protein fractions
have been identified in unprocessed peanuts.
Two major allergens, Ara h 1 and Ara h 11
with molecular weight 63.5kDa and 17kDa
respectively, have been identified in peanuts
(Burks et al., 1992a). Thermal denaturation
does not alter the IgE specific binding
capacity of allergenic peanut proteins (Burks
et al., 1992b). Peanuts may be included as
flavouring in variety of foods including
confectioneries and condiments. Some
products may also contain deflavoured,
reflavoured and recoloured peanuts to
resemble walnuts, pecans, or almonds. This
poses a serious food safety hazard to
individuals allergic to peanut. Allergenic
protein fractions have also been isolated from
commercially refined peanut oil (Olszewski,
1998).
Tree nuts
Tree nuts are frequently implicated in allergic
reactions in both adults and children.
Walnuts, pecans, Brazil nuts, cashews,
hazelnuts, pine nuts and pistachios have all
been implicated as food allergens. Studies
have shown that allergy to individual tree nut
is mostly nut-specific, while multiple tree-nut
allergies, although rare, have been shown to
occur (Bock and Atkins, 1989). Crossreactivity with peanut and other legume
allergens is quite uncommon; however, crossreactivity with certain tree pollen and plant
``pan allergen'' profilin has been shown to
occur in some atopic individuals (Hirschwehr
et al., 1992).
Fish
Allergic reaction to fish is particularly
common in communities where fish is
handled and consumed on a large scale.
Several species are known to cause allergic
reactions, but only few of the offending
allergens have been studied in great depth.
The allergens present in codfish have been
studied quite extensively. Even though there
are several other allergenic proteins in codfish
protein extracts, Gad c 1 is considered to be
the major allergen (Dory et al., 1998;
Christina et al., 1992; Chopin et al., 1998).
The major allergen in codfish, Gad c 1 (also
known as allergen M), is a 12.5kDa
sarcoplasmic protein belonging to a group of
proteins known as parvalbumins. Crossreactivity of codfish allergens with those of
other fish, have been shown to occur in some
codfish allergic individuals (de Martino et al.,
1990; Hansen et al., 1997); however,
hypersensitivity to fish allergens are generally
species specific (Kelso et al., 1996; Nagpal,
1989).
Shellfish
Shellfish, which is made up of crustaceans
and molluscs, have been shown to be
allergenic. Crustaceans are by far the more
frequent offenders. Two major allergens
found in shrimp have been identified and
characterised. SA I and SA II of molecular
weight 20.5kDa and 38kDa respectively, are
myofibrilliar proteins (tropomyosin) (Nagpal,
1989). SA I is heat labile while SA II is heat
stable (Nagpal et al., 1989. The allergens
found in shrimp (including a 36kDa heat
stable protein) have been shown to be highly
cross-reactive with other allergens found in
snow crabs, fruit fly, lobster, squid and
cockroaches (Lebrer, 1986; Leung et al.,
1996).
Cereal grain
Cereal grains include wheat, rice, corn, rye,
barley and oats. The most common allergic
complaint with the cereal grains is
occupational asthma from respiratory
exposure to dusty work environment (Baldo
and Wrigley, 1984). Wheat is by far the most
frequent cereal grain involved in allergic
reactions in the USA and Europe where it is
consumed on a large scale. However, other
grains such as rice may be the more frequent
offenders in Asia. A total of 40 different
protein antigens have been identified in wheat
(Yunginger, 1991). Studies have shown that
the IgE in serum of atopic individuals with
high radioallergosorbent test (RAST) scores
for wheat flour tends to react to a greater
extent with albumins and globulins compared
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with the other major protein fractions, the
gliadins and glutenins (gluten complex)
(Hoffman, 1975). In rice, two major allergens
have been identified and characterised
(Shibasaki et al., 1975). These two major
allergens belong to the glutenin and globulin
protein fractions. Several antigenic wheat
proteins have been shown to cross-react with
rye antigens (Yunginger, 1991).
Non-immunological reactions to food
The incidence of non-immunological
reactions to food is much greater than that of
allergic reactions (Young et al., 1994). The
mechanisms by which foods and food
additives elicit non-immunological adverse
reactions are very diverse and beyond the
scope of this review. Several food components
and additives are known to elicit adverse
reactions. Most of these reactions are
normally not life threatening on their own;
however, when combined with other clinical
conditions such as asthma, they can then
result in death.
The most common offending food
components are wheat and milk. Wheat
protein gluten (gliadin and glutenin) is
responsible for causing Celiac disease
(Kagnoff, 1992). Celiac disease is a
permanent intolerance of the small bowel
mucosa to gluten. The avoidance of a glutencontaining diet normally results in the
disappearance of symptoms.
Intolerance to the milk sugar lactose is also
the source of discomfort in individuals. This
intolerance arises from the deficiency of the
enzyme -galactosidase in the small intestine
(Kocian, 1988). -galactosidase is necessary
for the hydrolysis of milk disaccharide,
lactose, into its constituent monosaccharides,
glucose and galactose. While glucose and
galactose can be absorbed and used for
metabolic energy, lactose cannot be absorbed
without prior hydrolysis. If -galactosidase
activity is insufficient, incomplete hydrolysis
of lactose from milk or dairy products occur.
Undigested lactose passes into the colon,
where the large numbers of bacteria will
convert it to CO2, H2, and H2O. Symptoms
associated with lactose intolerance include
abdominal cramps, flatulence, and frothy
diarrhoea.
Favism, which is caused by the ingestion of
fava beans, is an adverse reaction resulting
from a deficiency of a metabolic enzyme,
glucose-6-phosphate dehydrogenase (Mager
et al., 1980). Erythrocyte glucose-6phosphate dehydrogenase (G6PDH) is
essential for maintaining adequate levels of
the reduced form of glutathione (GSH) and
nicotinamide dinucleotide phosphate
(NADPH) in erythrocytes. GSH and
NADPH protect the erythrocyte membrane
from oxidation. Fava beans contain two
potent, naturally occurring oxidants, vicine
and convicine, which when consumed by
G6PDH-deficient individuals can result in
acute hemolytic anaemia (Mager et al., 1980).
The typical symptoms include fatigue,
abdominal and/or back pain, fever and chills,
and in more severe cases, renal failure.
Naturally occurring constituents in foods
are known to cause adverse reactions. Some
of these constituents exert pharmacological
effects on the sensitive individual.
Compounds such tyramine,
phenylethylamine, ethanol, caffeine and
phenolic flavanoids, which are present in
many foods such as cheese, chocolate and red
wine have been reported to cause migraines in
some individuals (Weber and Vaughan,
1991). Histamine poisoning can result from
the ingestion of foods with high histamine
content. Foods such as fish (tuna, mackerel,
herring and sardine), wine, vegetables
(spinach and eggplant), and some cheeses
(Parmesan, Roquefort and blue) have a high
histamine content. High histamine content in
scrombroid and non-scrombroid fish occurs
due to improper storage, resulting in bacterial
enzymic decarboxylation of histidine to
histamine. Histamine, when taken orally can
stimulate degranulation of mast cells and
basophils and is one of the mediators in the
production of symptoms in allergic reactions
(Baldwin, 1991).
Fungal, algal and bacterial toxins are quite
frequently the cause of adverse reaction to
food. Ciguatera poisoning (CP), diarrhetic
shellfish poisoning (DSP), amnesic shellfish
poisoning (ASP), and paralytic shellfish
poisoning (PSP) occur when contaminated
fish and shellfish (fish which have fed on toxic
dinoflagellate algae) are ingested. These
toxins (ciguatoxin in CP (Hokama and
Miyahara, 1986), saxotoxin in PSP (Shimizu,
1988), domoic acid in ASP (Wright et al.,
1989), and okadaic acid, dinophysistoxins
and pectenotoxins in DSP (Yasumoto and
Murata, 1990) are neurotoxins and ingestion
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O. Fraser, S. Sumar and N. Sumar
of these results in vomiting, diarrhoea,
abdominal cramps, and headaches and in the
most severe cases even death. Puffer fish
poisoning also results from the ingestion of
the puffer fish neurotoxin (tetrodotoxin)
(Taylor and Schantz, 1990).
Food additives used as preservatives,
thickeners, colourings, flavourings and antioxidants have all been implicated as causative
agents of adverse reaction to foods. The most
common additives known to cause a wide
range of clinical symptoms are sulphites,
salicylates, benzoates and parabens,
tartrazine, butylated hydroxyanisole (BHA),
butylated hydroxytoluene (BHT), nitrates,
nitrites, aspartame, and monosodium
glutamate (Weber et al., 1991).
Other contaminants commonly found in
food such as heavy metals, agricultural
chemicals and industrial waste pollutants
have also been known to cause adverse
reactions in human (Taylor, 1991).
Conclusion
Even though adverse reactions to food are
very common and have been shown to
increase two-fold over the last two decades,
very few of the offending food antigens have
been purified and characterised.
Furthermore, very little research has been
done to investigate the effects of post-harvest
handling and processing on the ability of these
food-components to elicit adverse reactions in
humans. With the increase in global trade in
foods and ever-changing eating habits, it is
conceivable that more people will come into
contact with an even wider diversity of food
antigens. In order to develop a more detailed
understanding of the chemistry of food
allergens and additives with respect to their
ability to cause adverse reactions in humans,
much further research is necessary.
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(1991), ``Part 3: adverse reaction to food additives'',
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a neuroexcitory amino acid, in toxic mussels from
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Yunginger, J.W. (1991), ``Food antigens'', in Metcalfe,
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242
Adverse reaction to
foods
Adverse reaction to foods in humans is very
common; in milder cases it causes discomfort
and in the more severe cases it can cause
anaphylaxis and even death. Avoidance of the
offending food can in most cases alleviate this
problem; however, accidental exposure is very
common due to the unsuspected presence of
the offending food component in a wide range
of processed foods (e.g. peanut, soybean,
milk, egg and cereal proteins). Adverse
reaction to foods causes discomfort not only
when the offending food is consumed, but
also when an individual is exposed via
physical contact or inhalation of vapour or
particles of food.
Adverse reactions to foods may be classified
into two fundamental groups:
(1) food aversion; and
(2) food intolerance.
O. Fraser, S. Sumar and
N. Sumar
The authors
O. Fraser, S. Sumar and N. Sumar are all at the
Department of Surgery, St George's Hospotal Medical
School, University of London, UK.
Keywords
Food, Allergies
Abstract
Outlines the prevalence of adverse reactions to food and
what it means to the individual. Lists and describes the
known main food allergies.
Electronic access
The current issue and full text archive of this journal is
available at
http://www.emerald-library.com
Nutrition & Food Science
Volume 30 . Number 5 . 2000 . pp. 236±242
# MCB University Press . ISSN 0034-6659
Food aversion is an unpleasant reaction to
food, which is caused by emotions associated
with the food rather than by the food itself.
Food intolerance, which includes food
allergy, is a general term referring to a nonpsychological, reproducible, unpleasant
reaction to a specific food or food ingredient.
Food intolerance is then further subdivided
into food allergy and non-immunologically
mediated food intolerance.
Food allergy is a specific adverse reaction
to food where there is evidence of an
abnormal immunological reaction to the
food.
Non-immunologically mediated food
intolerance can also occur in some
individuals. This may be due to a number of
mechanisms including:
.
the lack of a particular enzyme needed for
the digestion of food;
.
the presence of toxic substances;
.
irritant effects such as those caused by
highly spiced foods;
.
pharmacological effects of some food
components; and
.
indirect effects caused by fermentation
of unabsorbed food in the digestive
system.
In this review we will focus on foods which
elicit allergic (immunological) and nonallergic (non-immunological) response
in humans since these are of greater
importance when considering the safety of
the foods.
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O. Fraser, S. Sumar and N. Sumar
Prevalence
Allergic reactions to food
The true prevalence of adverse reaction to
food particularly food allergy is unknown.
Epidemiological data differ according to age
categories, country, public perception, and
study methods. Results of community surveys
have reported the perceived incidence of food
allergy to be 14 to 33 per cent. This wide
disparity in statistics is probably due to a
combination of improper terminology and
public misconceptions, and a lack of
challenge proven confirmation of symptoms
(Sloan and Powers, 1986). In 1982, a Finnish
study in which 866 children aged between one
and six years reported the prevalence of food
allergy as 19 per cent at one year of age, 27
per cent at three years, and 8 per cent at six
years (Kajosaari, 1982). Results were based
on history, effect of an elimination diet, and
non-blinded food challenges. A more rigorous
study looked prospectively at 1,749 Danish
infants for the development of cow's milk
allergy during their first year. About 7 per
cent of the children had suggestive clinical
symptoms, but only 2.2 per cent actually were
proven to have cow's milk allergy by food
challenges in the hospital (Host and Halken,
1990). These results were similar to an earlier
study from the Isle of Wight (2.5 per cent)
(Hidc and Guycr, 1983), and a more recent
study from The Netherlands (2.7 per cent)
(Schrander et al., 1993). In a prospective
study of children followed through the first
three years of life in a general paediatric
practice, Bock (1981), concluded that about
8 per cent of children have adverse reactions,
most of which are transient. It may be
concluded from these studies that 4 to 6 per
cent of children experience food
hypersensitivity in the first three years of life,
but only 1 to 2 per cent of the paediatric
population are still affected by their tenth
birthday. Figures were similar to those for the
adult population.
In the UK, studies carried out by the
Wycombe Health Authority in 1986 showed
that the occurrence of intolerance to food in
the general population was in the range of
0.01 to 0.23 per cent (between 1 in 500 and 1
in 10,000). A later study of the same
population showed that the number of
individuals actually showing a demonstrable
reaction was between 1.4 and 1.9 per cent
(between 1 in 50 and 1 in 70) (Young et al.,
1987; 1994).
The concept of foods generally consumed
within a population causing an allergic
reaction in some individuals has existed for
quite a long time and is expressed in the
vocabulary of the indigenous Amerindian in
South America as ``kinna''. If a person had a
``kinna'', this meant that when that person
consumed a particular food (the ``kinna''), he
would become ill. The first recorded
significant investigation into adverse reaction
to foods was in 1912 by two scientists,
Kustner and Prausnitz, who observed that an
intradermal injection of fish extracts into a
fish-sensitive individual, elicited an
immediate wheal and flare reaction. Of equal
importance was the observation that
immediate reactivity of the fish allergen could
be passively transferred to a non-atopic
subject by intradermal injection of sera from
fish sensitive individuals. Subsequently, the
passive transfer of hypersensitivity to other
allergens was also observed. The nature of
these reaginic antibodies remained unknown
for more than 40 years until lshizaka and
lshizaka (1967) identified IgE as the carrier of
reaginic activity in the serum of patients with
hayfever.
The discovery of IgE antibody has provided
the basis for immunochemical approaches to
the study of mechanisms underlying
immediate hypersensitivity reactions. It is
now well recognised that the major feature
distinguishing atopic individuals from nonatopic individuals is their capacity to develop
a sustained IgE response to an allergen. IgE
has the unique property of binding to highaffinity receptors on basophils and mast cells.
The cross-linking of specific membrane
bound IgE with an allergen triggers the
release of vasoactive mediators, leukocyte
chemotactic factors, and cytokines
responsible for the clinical manifestation of
immediate hypersensitivity reactions (Lebrer,
1986; Taylor et al., 1987).
The development of allergic reactions to
food most commonly occurs in two phases:
(1) sensitisation; and
(2) allergic response.
Sensitisation of an individual to an allergen
occurs when the initial or repeated exposure
to the food antigen results in the stimulation
of the immune system to produce food
antigen-specific IgE antibodies. This process
involves the antigen being presented to the
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O. Fraser, S. Sumar and N. Sumar
immune system by antigen presenting cells
(APC), which causes T-helper cell
stimulation (via cytokine IL4) of B cells to
produce antigen-specific IgE antibodies.
These IgE antibodies then bind to high
affinity receptors on the surface of mast cells
and basophils resulting in sensitisation. The
allergic reaction to the food antigen occurs on
subsequent exposure, which results in the
degranulation of mast cells or basophils
thereby releasing mediators responsible for
the manifestation of clinical symptoms
(Figure 1).
The major food allergens are water-soluble
glycoproteins, with molecular weights ranging
front 12.5kDa to 63kDa (Taylor et al., 1987).
Most of these allergens are heat and acid
stable and can survive protease digestion. The
antigens responsible for most of the morbidity
and mortality owing to food allergy will be
discussed individually. The importance of
these food antigens varies in different
countries, depending on dietary habit and
amount consumed.
Food antigens
Cow's milk
Cow's milk is one of the most common food
allergens in children, perhaps because it is
usually the first foreign protein encountered
by infants. Protein fractions from cow's milk
are subdivided into casein and whey proteins.
Although extensive heating may denature
some of these proteins, it does not
significantly decrease the allergenicity of most
protein fractions. Casein fractions are used
extensively in processed foods as well as
cheeses. The whey fraction consists of
-lactoglobulin, -lactalbumin, bovine
immunoglobulin, bovine serum albumin, and
small amounts of various other proteins. IgE
antibodies to these whey proteins have been
demonstrated in most milk-allergic patients.
Cross-reactivity among milk proteins
obtained from cows, goats and sheep has been
reported. Clinical reactivity to goat's milk has
been estimated to occur in 50 per cent of
children allergic to cow's milk (Clein, 1958).
Egg
Chicken's egg is probably the most common
cause of food allergic reactions in children.
The major protein allergens found in egg
white are ovomucoid, ovalbumin, and
ovotransferrin (Holen and Elsayed, 1990).
Egg yolk contains a variety of proteins namely
lipovitellin and lipovitellenin (lipo-proteins),
levitin (water-soluble protein), and phosvitin
(phospho-protein). Although the yolk is
considered to be less allergenic than egg
white, IgE antibodies to egg yolk proteins
have been demonstrated (Anet et al., 1985).
IgE antibodies from children allergic to
chicken's egg have been shown to cross-react
with eggs from other species (Langeland,
1983).
Soybean
Soybean, a legume, is another common cause
of food-allergic reactions, mainly in children.
It is used in many commercial foods since it is
an inexpensive source of high-quality protein.
Of the four major protein fractions identified,
no one fraction appears to be more allergenic
than the other in a study of eight children with
IgE-mediated hypersensitivity to soybean
(Butts et al., 1988). Soybean proteins have
been identified in some soybean oils, lecithin,
Figure 1 Shows a schematic representation of cellular events resulting in sensitisation and allergic reaction to food
allergens. Initial exposure to allergen in atopic individuals results in IgE production by B cells. This sensitises cells
such as mast cells and basophils so that on subsequent exposure to allergen, degranulation occurs, releasing preformed mediators and inducing the synthesis of newly-formed mediators to produce clinical symptoms
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and margarine, but the impact of this is yet to
be determined. Immunological crossreactivity among legumes has been
demonstrated. However, symptomatic
hypersensitivity to more than one legume is
rare (Bernhisel-Broadbent and Sampson,
1989).
Peanut
Allergic reactions to peanut occur quite
frequently in both children and adults. Peanut
allergy is probably the most common cause of
anaphylaxis. Peanut proteins are classified as
water-soluble albumins or non-water-soluble
globulins. Sixteen allergenic protein fractions
have been identified in unprocessed peanuts.
Two major allergens, Ara h 1 and Ara h 11
with molecular weight 63.5kDa and 17kDa
respectively, have been identified in peanuts
(Burks et al., 1992a). Thermal denaturation
does not alter the IgE specific binding
capacity of allergenic peanut proteins (Burks
et al., 1992b). Peanuts may be included as
flavouring in variety of foods including
confectioneries and condiments. Some
products may also contain deflavoured,
reflavoured and recoloured peanuts to
resemble walnuts, pecans, or almonds. This
poses a serious food safety hazard to
individuals allergic to peanut. Allergenic
protein fractions have also been isolated from
commercially refined peanut oil (Olszewski,
1998).
Tree nuts
Tree nuts are frequently implicated in allergic
reactions in both adults and children.
Walnuts, pecans, Brazil nuts, cashews,
hazelnuts, pine nuts and pistachios have all
been implicated as food allergens. Studies
have shown that allergy to individual tree nut
is mostly nut-specific, while multiple tree-nut
allergies, although rare, have been shown to
occur (Bock and Atkins, 1989). Crossreactivity with peanut and other legume
allergens is quite uncommon; however, crossreactivity with certain tree pollen and plant
``pan allergen'' profilin has been shown to
occur in some atopic individuals (Hirschwehr
et al., 1992).
Fish
Allergic reaction to fish is particularly
common in communities where fish is
handled and consumed on a large scale.
Several species are known to cause allergic
reactions, but only few of the offending
allergens have been studied in great depth.
The allergens present in codfish have been
studied quite extensively. Even though there
are several other allergenic proteins in codfish
protein extracts, Gad c 1 is considered to be
the major allergen (Dory et al., 1998;
Christina et al., 1992; Chopin et al., 1998).
The major allergen in codfish, Gad c 1 (also
known as allergen M), is a 12.5kDa
sarcoplasmic protein belonging to a group of
proteins known as parvalbumins. Crossreactivity of codfish allergens with those of
other fish, have been shown to occur in some
codfish allergic individuals (de Martino et al.,
1990; Hansen et al., 1997); however,
hypersensitivity to fish allergens are generally
species specific (Kelso et al., 1996; Nagpal,
1989).
Shellfish
Shellfish, which is made up of crustaceans
and molluscs, have been shown to be
allergenic. Crustaceans are by far the more
frequent offenders. Two major allergens
found in shrimp have been identified and
characterised. SA I and SA II of molecular
weight 20.5kDa and 38kDa respectively, are
myofibrilliar proteins (tropomyosin) (Nagpal,
1989). SA I is heat labile while SA II is heat
stable (Nagpal et al., 1989. The allergens
found in shrimp (including a 36kDa heat
stable protein) have been shown to be highly
cross-reactive with other allergens found in
snow crabs, fruit fly, lobster, squid and
cockroaches (Lebrer, 1986; Leung et al.,
1996).
Cereal grain
Cereal grains include wheat, rice, corn, rye,
barley and oats. The most common allergic
complaint with the cereal grains is
occupational asthma from respiratory
exposure to dusty work environment (Baldo
and Wrigley, 1984). Wheat is by far the most
frequent cereal grain involved in allergic
reactions in the USA and Europe where it is
consumed on a large scale. However, other
grains such as rice may be the more frequent
offenders in Asia. A total of 40 different
protein antigens have been identified in wheat
(Yunginger, 1991). Studies have shown that
the IgE in serum of atopic individuals with
high radioallergosorbent test (RAST) scores
for wheat flour tends to react to a greater
extent with albumins and globulins compared
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O. Fraser, S. Sumar and N. Sumar
with the other major protein fractions, the
gliadins and glutenins (gluten complex)
(Hoffman, 1975). In rice, two major allergens
have been identified and characterised
(Shibasaki et al., 1975). These two major
allergens belong to the glutenin and globulin
protein fractions. Several antigenic wheat
proteins have been shown to cross-react with
rye antigens (Yunginger, 1991).
Non-immunological reactions to food
The incidence of non-immunological
reactions to food is much greater than that of
allergic reactions (Young et al., 1994). The
mechanisms by which foods and food
additives elicit non-immunological adverse
reactions are very diverse and beyond the
scope of this review. Several food components
and additives are known to elicit adverse
reactions. Most of these reactions are
normally not life threatening on their own;
however, when combined with other clinical
conditions such as asthma, they can then
result in death.
The most common offending food
components are wheat and milk. Wheat
protein gluten (gliadin and glutenin) is
responsible for causing Celiac disease
(Kagnoff, 1992). Celiac disease is a
permanent intolerance of the small bowel
mucosa to gluten. The avoidance of a glutencontaining diet normally results in the
disappearance of symptoms.
Intolerance to the milk sugar lactose is also
the source of discomfort in individuals. This
intolerance arises from the deficiency of the
enzyme -galactosidase in the small intestine
(Kocian, 1988). -galactosidase is necessary
for the hydrolysis of milk disaccharide,
lactose, into its constituent monosaccharides,
glucose and galactose. While glucose and
galactose can be absorbed and used for
metabolic energy, lactose cannot be absorbed
without prior hydrolysis. If -galactosidase
activity is insufficient, incomplete hydrolysis
of lactose from milk or dairy products occur.
Undigested lactose passes into the colon,
where the large numbers of bacteria will
convert it to CO2, H2, and H2O. Symptoms
associated with lactose intolerance include
abdominal cramps, flatulence, and frothy
diarrhoea.
Favism, which is caused by the ingestion of
fava beans, is an adverse reaction resulting
from a deficiency of a metabolic enzyme,
glucose-6-phosphate dehydrogenase (Mager
et al., 1980). Erythrocyte glucose-6phosphate dehydrogenase (G6PDH) is
essential for maintaining adequate levels of
the reduced form of glutathione (GSH) and
nicotinamide dinucleotide phosphate
(NADPH) in erythrocytes. GSH and
NADPH protect the erythrocyte membrane
from oxidation. Fava beans contain two
potent, naturally occurring oxidants, vicine
and convicine, which when consumed by
G6PDH-deficient individuals can result in
acute hemolytic anaemia (Mager et al., 1980).
The typical symptoms include fatigue,
abdominal and/or back pain, fever and chills,
and in more severe cases, renal failure.
Naturally occurring constituents in foods
are known to cause adverse reactions. Some
of these constituents exert pharmacological
effects on the sensitive individual.
Compounds such tyramine,
phenylethylamine, ethanol, caffeine and
phenolic flavanoids, which are present in
many foods such as cheese, chocolate and red
wine have been reported to cause migraines in
some individuals (Weber and Vaughan,
1991). Histamine poisoning can result from
the ingestion of foods with high histamine
content. Foods such as fish (tuna, mackerel,
herring and sardine), wine, vegetables
(spinach and eggplant), and some cheeses
(Parmesan, Roquefort and blue) have a high
histamine content. High histamine content in
scrombroid and non-scrombroid fish occurs
due to improper storage, resulting in bacterial
enzymic decarboxylation of histidine to
histamine. Histamine, when taken orally can
stimulate degranulation of mast cells and
basophils and is one of the mediators in the
production of symptoms in allergic reactions
(Baldwin, 1991).
Fungal, algal and bacterial toxins are quite
frequently the cause of adverse reaction to
food. Ciguatera poisoning (CP), diarrhetic
shellfish poisoning (DSP), amnesic shellfish
poisoning (ASP), and paralytic shellfish
poisoning (PSP) occur when contaminated
fish and shellfish (fish which have fed on toxic
dinoflagellate algae) are ingested. These
toxins (ciguatoxin in CP (Hokama and
Miyahara, 1986), saxotoxin in PSP (Shimizu,
1988), domoic acid in ASP (Wright et al.,
1989), and okadaic acid, dinophysistoxins
and pectenotoxins in DSP (Yasumoto and
Murata, 1990) are neurotoxins and ingestion
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O. Fraser, S. Sumar and N. Sumar
of these results in vomiting, diarrhoea,
abdominal cramps, and headaches and in the
most severe cases even death. Puffer fish
poisoning also results from the ingestion of
the puffer fish neurotoxin (tetrodotoxin)
(Taylor and Schantz, 1990).
Food additives used as preservatives,
thickeners, colourings, flavourings and antioxidants have all been implicated as causative
agents of adverse reaction to foods. The most
common additives known to cause a wide
range of clinical symptoms are sulphites,
salicylates, benzoates and parabens,
tartrazine, butylated hydroxyanisole (BHA),
butylated hydroxytoluene (BHT), nitrates,
nitrites, aspartame, and monosodium
glutamate (Weber et al., 1991).
Other contaminants commonly found in
food such as heavy metals, agricultural
chemicals and industrial waste pollutants
have also been known to cause adverse
reactions in human (Taylor, 1991).
Conclusion
Even though adverse reactions to food are
very common and have been shown to
increase two-fold over the last two decades,
very few of the offending food antigens have
been purified and characterised.
Furthermore, very little research has been
done to investigate the effects of post-harvest
handling and processing on the ability of these
food-components to elicit adverse reactions in
humans. With the increase in global trade in
foods and ever-changing eating habits, it is
conceivable that more people will come into
contact with an even wider diversity of food
antigens. In order to develop a more detailed
understanding of the chemistry of food
allergens and additives with respect to their
ability to cause adverse reactions in humans,
much further research is necessary.
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