BLBS102-c42 BLBS102-Simpson March 21, 2012 14:27 Trim: 276mm X 219mm Printer Name: Yet to Come
42 Food Allergens 807and tropomyosin are muscle cell proteins. To date, eight major
IgE-binding epiopes have been identified in shrimp tropomyosin
(Lehrer et al. 2003).
Exposure, including handling, consumption and inhalation of
air-borne particles from fish and fish ingredients, can induce
allergic reaction in sensitised individuals. Seafood-induced al-
lergic reactions are generally similar to responses induced by
many of the other allergenic foods. A study conducted using
30 shrimp-sensitive and 37 fish-allergic individuals reported al-
lergic symptoms ranging from generalised itching, urticaria to
swelling of the lips and tongue (Lehrer et al. 2003). Other re-
ported symptoms include difficulty breathing, gastrointestinal
distress and anaphylactic shock (O’Neil et al. 1993, Daul et al.
1993a, 1993b).
Additionally, occupational reactions among a variety of
seafood workers (e.g. fish and prawn workers, seafood pro-
cessing workers, fishermen, canners, restaurant cooks and other
workers in the seafood industry) have been reported. Cartier
et al. (1984) showed that workers in the seafood industry were
exposed to occupational allergens through direct contact with
seafood products as well as inhalation of bits of seafood or wa-
ter droplets generated during processing. Out of the 303 crab
workers investigated, 18% reported rhinitis or conjunctivitis,
about 24% some sort of skin rash and over a third reported of
asthma.
Very little work has been done on the effect of process-
ing on the allergenicity of seafood. As with other allergens,
highly refined products from seafoods that do not contain resid-
ual proteins (e.g. refined fish oils, gelatine and isinglass) do
not pose a risk to allergic consumers. However, processing
techniques that leave seafood protein fragments in the finished
product may pose serious allergenic risk to sensitised individ-
uals. As consumers and the food industry become increasingly
aware of the health benefits of fish, consumption and utili-
sation of fish and fish products is likely to increase, which
could increase the allergen risk for fish- and shellfish-sensitised
individuals.ALLERGENS IN CEREALS
Certain cereal grains contain proteins that induce immune-
mediated responses in individuals who are predisposed to CD or
who have specific cereal allergy. As the mechanisms involved
in celiac disease are distinctly different from those involved in
IgE-mediated cereal allergy, they will be discussed separately.Celiac DiseaseCD also sometimes known as gluten-sensitive enteropathy or
gluten intolerance is an abnormal immunological response to
gluten/gliadin, which frequently results in a diseased state char-
acterised by damage of the lining of the gut (villous atrophy). In
these individuals, the T lymphocytes in the small intestines re-
spond abnormally to gluten, causing inflammation and damage
to the absorptive epithelium of the small intestine, resulting in
malabsorption and disorders such as diarrhoea, bloating, weightloss, anaemia, weakness and muscle cramps. In children, CD
leads to growth retardation and underweight. Symptoms linger
for some days even after the offending food is avoided due to
the fact that the damaged intestine requires time to heal. Mortal-
ity rate has not been reported but patients are likely to develop
malignant lymphomas (Ferguson 1997).
CD occurs more commonly in Caucasians than in Blacks,
Asians and Hispanics according to present knowledge. Whether
this is due to under-diagnosis or true biosocial/genetic differ-
ence is not clear. Reported prevalence rates are 1:200–400
in Europe, 1:133 in America, 1:100–300 in a UK study and
1:120 in a Belfast study (Rostami et al. 1999, Gomez et al.
2001, Fasano and Catassi 2001, Fasano et al. 2003, Garc ́ıa
Novo et al. 2007). CD appears to be genetic with 10% preva-
lence rates reported among first-degree relatives of CD patients
and 70–100% concordance rates amongst twins. Higher preva-
lence rates are reported in women likely due to higher rates of
diagnoses.
The primary offending foods for celiacs are wheat, barley and
rye. The major proteins present in these cereals are albumins,
globulins, gliadin (prolamin) and glutenin (glutelin) and the of-
fending protein for celiacs is the gluten fraction in these cereals,
which are the prolamins and glutelins, particularly the prolamins
(i.e. hordein (barley), secalin (rye) and gliadin (wheat)). Several
repeating peptide sequences (e.g. QQPFP, QQQP, QQPY, QPYP,
PSQQ) in the primary structure of these proteins have been
blamed (Osman et al. 2001, Kahlenberg et al. 2006, Darewicz
et al. 2008). Although the mechanism involved in the pathogen-
esis of the disease is unclear, tissue transglutaminase is believed
to play a key role in the deamidation of glutamine converting it
to glutamic acid, which allows the immune cells to bind, provok-
ing continued immune response (Anderson et al. 2000, Mazzeo
et al. 2003). The principal organ targeted is the gut (i.e. small
intestine); however, damage to other parts of the body such as
the skin (dermatitis herpetiformis), the teeth and the liver has
been reported (Lohi 2010). Severity of the disease increases sig-
nificantly with delays in diagnosis (i.e. age of diagnosis) and the
degree of susceptibility increase with the rate of gluten consump-
tion (quantity). Tolerance thresholds for the general population
of CD patients are not known but some workers have reported
values ranging between 10 and 100 mg gluten (Collin et al. 2004,
Hischenhuber et al. 2006, Catassi et al. 2007).IgE-Mediated Cereal AllergyIgE-mediated cereal allergy is distinctly different from CD. This
type of allergy is an immediate-type hypersensitivity occurring
minutes to hours after consumption of the offending food. Symp-
toms are similar to those described for the other allergens and
include oral allergy syndrome (e.g. swelling of lips), respira-
tory difficulties (e.g. asthma), skin reaction (e.g. eczema, atopic
dermatitis) and gastrointestinal distress (e.g. nausea, diarrhoea,
vomiting and cramps). There is no accurate data available on the
prevalence, but as is the case for the other allergens, genetic sus-
ceptibility has been suggested (Becker et al. 2004). Severity of
IgE-mediated cereal allergy depends on the immune state of the
patient (degree of sensitisation/tolerance) and the concentration