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Subsections
Allergies can be a serious threat to life and can end as anaphylatic shock. The allergens in foods represent a hazard for those who suffer from allergies. According to the European Federation of Allergy and Airways Diseases Patients Association an estimated 4 per cent of adults and 8 percent of children in the European Union suffer from food Allergies.
First signs of an allergic reaction to food
- Running nose
- Itchy skin rash
- Tingling in the tongue, lips, or throat
- Swelling in the throat or other parts of the body
- Abdominal pain
- Eczema
- Dizziness
- Diarrhoea or vomiting
- Wheezing
Major serious food allergens
Cereals containing gluten (i.e. wheat, rye, barley, oats, spelt or their hybridised strains, and products thereof), fish, crustaceans, egg (globulin; albumin; Apovitellenin; livetin; ovalbumin; ovomucin; ovomucoid; ovovitellin; phosvitin), peanut, soybeans (soy protein, textured vegetable protein TPV, hydrolysed plant protein, hydrolysed soy protein, hydrolysed vegetable protein,), milk and dairy products including lactose (milk sugar), nuts i.g. almond (Amygdalus communis), hazelnut (Corylus avellana),walnut (Juglans regia), cashew (Anacardium occidentale),pecan nut(Carya illinoiesis), Brazil nut (Bertholletia excelsa), pistachio nut (Pistacia vera), macadamia nut, Queensland nut (Macadamia ternifolia), celery and other foods of the Umbelliferae family, mustard, sesame seed, sulphur dioxide and sulphites (at concentrations of more than 10 mg/kg or 10 mg/litre expressed as SO2) are the major serious food allergens.
The most common food allergens are found in a wide variety of processed foods and may cause allergies or intolerances in consumers endangering their health.
Food allergens are part of a wide group of adverse reactions to foods.
In order to provide all consumers with better information and to protect the health of certain consumers all ingredients must now be included in the list of ingredients.
| Foods |
Per cent |
|---|
| Milk (cow) |
42.0 |
| Egg (hen) |
|
| - Egg white |
14.6 |
| - Egg yolk |
9.0 |
| - Egg white and yolk |
9.7 |
| Fish |
11.0 |
| Citrus fruit |
4.5 |
| Legume |
2.5 |
| Horse meat |
1.3 |
| Meat |
1.0 |
| Vegetable |
1.0 |
| Onion |
1.0 |
| Nuts, chocolate and others |
2.0 |
Allergens
- Cereals containing gluten ( i.e. wheat, rye, barley, oats, spelt, kamut or their hybridised strains) and products thereof.) (Coeliac disease)
- Crustaceans and products thereof.
- Eggs and products thereof.
- Fish and products thereof.
- Peanuts and products thereof.
- Soybeans and products thereof.
- Milk and products thereof (including lactose).
- Nuts i. e. Almond (Amygdalus communis L.), Hazelnut (Corylus avellana), Walnut (Juglans regia), Cashew (Anacardium occidentale), Pecan nut (Carya illinoiesis (Wangenh.) K. Koch), Brazil nut (Bertholletia excelsa), Pistachio nut (Pistacia vera), Macadamia
nut and Queensland nut (Macadamia ternifolia) and products thereof.
- Celery and products thereof.
- Mustard and products thereof: Mustard protein allergic individuals may react to the protein content of the mustard oil. Individuals sensitised to and by the skin sensitising component allyl isothiocyanate may react to oil in the absence of mustard proteins.
- Sesame seeds and products thereof.
- Sulphur dioxide and sulphites at concentrations of more than 10 mg/kg or 10 mg/litre expressed as SO2.
Preservatives
A small part of
humans suffer fron allergy to preservatives. Labels like "Free of preservatives" must be true as some persons suffer heavy allergic responds to some preservatives. To avoid recourses due to cross over " No preservatives added" is being now labeled. This, however, does not solve the problem of allergic reactions.
Chafen and colleagues 2010 deplore the lacking of clear consensus regarding
the prevalence, most effective diagnostic, management and prevention of food
allergies. The term "food allergy" needs an universal definition. In this
review cow's milk, hen's eggs, peanuts, tree nuts, fish, and shellfish foods
were found responsible for 50% of all food allergies.
The authors also stress that more than 1% to 2% but less than 10% of the
population are affected by food allergies. Skin prick tests and serum
food-specific IgE presented no statistical advantage compared with food
challenge. No other valid testing methods exist.
Despite being the most important tool in the therapy of food allergies,
elimination diets are not sufficiently studied. The data on Immunotherapy are
insufficient and cannot be recommended. Standardized definitions of high risk and
hydrolysed formula do not exist to protect infants from cow's milk allergy. The
authors call for uniformity in the criteria for what constitutes a food allergy
and a set of evidence-based guidelines on which to make this diagnosis.
Accurate diagnosis of cow's milk allergy by determining the immunoglobulin E (IgE)-mediated response may be more useful than skin or blood tests performed with whole extracts. Fiocchi et al 2011 stresses that difficulties must be resoled to find and validate markers and correlate them to disease and patient profiles, meanwhile oral food challenge remains the reference standard for the diagnosis of this allergy.
Increasing amounts of foods that contain baked milk in the diets of children suffering with milk allergies may improve tolerance to milk and milk products.
Sampson et al 2011 report that approximately 75 percent of children, aged 2 to 17 years, with milk allergy, were found to tolerate foods containing baked milk, such as muffins, waffles and cookies. The high temperatures used in baking cause the proteins in milk to break down. This is believed to reduce the allergenicity.
After an initial muffin food challenge of six to twelve months, the children were given cheese pizza which is less heated than muffins and contains higher amount of unmodified milk protein. After three years of a diet containing cheese pizza At the end of the study period, 47 percent of the children could tolerate unheated milk products, such as skim milk, yoghurt and ice cream, compared to only 22 percent in a control group. The authors concluded that increased exposure to baked milk products helps to children outgrow milk allergies. Ovomucoid-specific IgE antibodies as predictors of whether children could tolerate heat-treated egg were assessed by Ando and colleagues 20008. They found that the quantitative measurements of specific IgE antibodies to both egg white and ovomucoid and the evaluation against the suggested positive and negative decision points for specific IgE may be useful in the diagnosis of egg allergy. The positive decision point was 7.4 kU(A)/L, and the negative decision point, was 0.6 kU(A)/L for raw egg white. For heated egg white the positive decision point was 10.8 kU(A)/L, and the negative decision point was 1.2 kU(A)/L.
Brand 2011 reports that the diagnosis of food allergy includes detailed history and reproducible symptoms and double-blind oral food challenges. Pattern must elicited from the history to confirm food allergy. Measuring specific immunoglobulin E in serum is not a help in the diagnosis of food allergy because asymptomatic sensitisation is common, says the author.
The 2011 revised version of the practice guideline on food hypersensitivity in infants of the Dutch College of General Practitioners also states that the examination of serum specific IgE levels should not be used in the diagnosis of food allergy, and a double-blind placebo-controlled food challenge is recommended. [6]
Nicolaou and Custovic 2011 write that the quantification of Ara h 2-specific IgE may accurately discriminate peanut allergy from tolerance may be more useful to predicting the presence and severity of clinical allergy than skin or blood tests based on whole extracts, however, until this is confirmed by further studies oral food challenge remains the gold standard for accurate diagnosis.
The authors report that different pollen and dietary exposures produce regional different results, for peanut-allergy sensitisation to Ara h 1-3 in the USA, to Ara h 9 in Spain and to Ara h 8 in Sweden. Soybean allergy sensitisation to Gly m 5 or Gly m 6 allergens may increase the risk to severe allergic reactions.
Ballmer-Weber and Hoffmann-Sommergruber 2011 report that celeriac, carrot and tomato are the most prevalent allergenic vegetables, whereas fruit allergy is mainly induced by apple, peach and kiwi. In kiwifruit allergy Act d 1 and Act d 3 were identified as potential marker allergens for severe symptoms. For celeriac allergy, however, such markers are still missing. The authors stress that the diagnosis of fruit and vegetable allergy in birch pollen-sensitized patients should not be excluded on a negative IgE testing to extracts, because Bet v 1-related allergens are often under-represented in extracts. [8] According to the PANACEA study the adherence to the Mediterranean type of diet is associated with lower prevalence of asthma symptoms, among 10 to 12 years old children: Greater adherence to the Mediterranean diet was inversely associated with ever had wheeze, exercise wheeze, ever had diagnosed asthma. No significant associations were found between asthma symptoms and consumption of fruits, vegetables, legumes, cereals, dairy, salty snacks, or margarine/butter consumption, while increased fish and meat intake was associated with less asthma symptoms. The authors suggest an inverse relationship between level of adherence to the Mediterranean diet and prevalence of asthma in school-aged children. Wang and Liu 2011 report that children with food allergies together with asthma are more likely to have near-fatal or fatal allergic reactions to food and more likely to have severe asthma. The authors stress that a causal link has not been determined, however, both condition together should increase the awareness of the severity of these ailments.
According to Järvinen 2011 peanut, tree nuts, and shellfish are the most commonly implicated foods in anaphylaxis, although milk is a common trigger in children, and asthma increases the risk of severe reactions. The authors stress that schools and restaurants have inadequate management plans and symptom and lack in staff education. Markers to predict risk of anaphylaxis and news therapies should be developed.
According to Patel et al. 2011, 4% to 6% of children and 1% to 2% of adults in the United States are suffering of food allergies. Direct medical costs and indirect costs of food-induced allergic reactions and anaphylaxis in the United States amount to half a billion dollars in 2007. Ambulatory visits accounted for more than half of the costs. Deaths caused by food-induced anaphylactic reactions are increasing, with most caused by food purchased outside the home. Bailey et al. 2011 report gaps in restaurant staff's knowledge of allergy. The authors stress the necessity to improve food allergy training practice for restaurant staff.
Goodman and Tetteh 2011 reviewing studies related to a possible allergenicity of genetic modified organisms found no documented proof of an adverse effect resulting from foods produced from GM plants. The authors suggest improvements for the allergenicity assessment of GMO plants.
Food allergens and Good Manufacturing Practice
According to the Institute of Food Science and Technology (IFST) the "greatest care must be taken by food manufacturers to formulate foods so as to avoid, whenever possible, inclusion of unnecessary major allergens as ingredients.
Food makers must organise raw material supplies, production schedules and cleaning procedures so as to prevent cross-contact of products by "foreign" allergens.
Training of all personnel should be focused on the understanding of necessary measures and the reasons for them.
Food manufacturers should comply with the relevant labelling legislation providing appropriate warning, to potential purchasers, of the presence of a major allergen in a product.
An appropriate system for recall of any product found to contain a major allergen not indicated on the label should be in place ". Many allergies and immune system diseases
have quadrupled in the last decade. Researchers suspect suspect modern
living, including the sterile homes, changes in diet, air pollution, obesity
and increasingly sedentary lifestyles to be responsible for the increase of
the ailments.
According to Minutolo and colleagues 2008, burning natural gas in home
appliances such as stove tops and water heaters ultrafine airborne particles
with diameters in the 1 nm to 10 nm size range are formed.
In home-heating burners these particles, formed in the flame region are oxidized
in the post-oxidation region, presenting no hazard. However, domestic stove
tops and water boilers do not have a post-oxidation region. The emit, therefore,
a high number of hazardous particles. Soot particles with size larger than 10 nm
are not formed.
Because of the size of the particle, they can penetrate the deepest part of
the lungs. Larger particles are generally filtered in the nose and throat and
do not cause problems, but particulate matter smaller than about 10
micrometers can settle in the bronchi and lungs and cause health problems.
Similarly, particles smaller than 2.5 micrometers tend to penetrate into the
gas-exchange regions of the lung, and very small particles (< 100
nanometers) may pass through the lungs to affect other organs. Particles
smaller than 100 nanometers can pass through cell membranes and migrate into
other organs, including the brain. It has been suggested that particulate
matter can cause similar brain damage as that found in Alzheimer patients.
Particles emitted from modern diesel engines are typically in the size range of
100 nanometers. In addition, these soot particles also carry carcinogenic
components like benzopyrenes adsorbed on their surface.
Pope and colleagues 2002 found that particles smaller than 2.5 micrometers
leads to high plaque deposits in arteries, causing vascular inflammation and
atherosclerosis.
Fine particulate and sulfur oxide-related pollution were associated with
all-cause, lung cancer, and cardiopulmonary mortality. The authors concluded that
long-term exposure to combustion-related fine particulate air pollution is an
important environmental risk factor for cardiopulmonary and lung cancer
mortality. The authors stress that the legislative limits for engines are
unsuitable to protect against particulate matter.
According to Valavanides and colleagues 2008 the inflammatory injury,
oxidative damage, and other biological effect are stronger for fine and
ultrafine particles, such those from exhaust particles from automobiles
because they can penetrate deeper into the airways of the respiratory tract.
These particles pollute urban areas.
The authors call for studies on the cytotoxic and carcinogenic mechanisms of
particulate matters in the lungs. They stress the importance to understand the
formation of particulate matter by internal combustion engines and other sources.
According to Fernando Martinez the hygiene hypothesis, as originally proposed,
postulated an inverse relation between the incidence of infectious diseases in
early life and the subsequent development of allergies and asthma. Researchers
say that microbial burden in general, and not any single acute infectious
illness, is the main source of "danger" signals which modulate the immune
response in early life. This may interact with genetic variations and result
in an inherited susceptibility to asthma and allergies.
Some are feeding high-risk children gradually larger amounts of
allergy-inducing foods, hoping to train the immune system not to overreact.
Others are testing benign bacteria or parts of bacteria. Still others have
patients with MS, colitis and related ailments swallow harmless parasitic
worms to try to calm their bodies' misdirected defences.
Robert Summers and colleagues 2004 postulated that helminth parasites mostly
have been eliminated in industrialized parts of the world, where the incidence
of inflammatory bowel disease became the highest. Therefore the authors
experimented with whipworms, proposing that helminths protect the bowel by
downregulating inflammatory responses. They call on the symbiotic effect of
helmnths and humans on developing and maintaining the immune system.
[21]
Although hay fever, eczema, asthma and food allergies seem quite different,
they are all "allergic diseases" because they are caused by the immune system
responding to substances that are ordinarily benign, such as pollen or
peanuts. Autoimmune diseases also result from the body's defence mechanisms
malfunctioning. But in these diseases, which include lupus, MS, Type 1
diabetes and inflammatory bowel disease, the immune system attacks parts of
the body such as nerves, the pancreas or digestive tract.
According to Jean-Francois Bach the immune systems are much less busy, resulting
in much more strong responses to much weaker stimuli, triggering allergies and
autoimmune diseases. The researcher stresses that children raised with pets or
older siblings are less likely to develop allergies, possibly because they are
exposed to more microbes and parasites. Children reared on farms were one-tenth
as likely to develop diseases such as asthma and hay fever. This was strongly
supported by Erika von Mutius of the Ludwig-Maximilians University in Munich.
[22]
The lack of exposure to potential threats early in life leaves the immune
system with fewer command-and-control cells known as regulatory T cells,
making the system more likely to overreact or run wild, says William Parker of the Duke University.
Ropbert Wood of the Johns Hopkins School of medicine is against the "hygiene
hypothesis" because it does not explain asthma which is common in poor
population which is exposed to cockroaches and rodents.
Other researchers blame processed foods or change in the balance of certain
vitamins, such as vitamins C and E and fish oil. This is being supported by
Thomas Platts-Mills
But many researchers believe the hygiene hypothesis is the strongest, and is
in connection with a genetic predisposition. William Cookson says to develop
allergies or autoimmune diseases both environmental factors and genetic
susceptibility are needed.
Some researches following the hypothesis that challenge is necessary to develop a
correct response, try to give increasing amounts of milk, egg and peanut to
children suffering from these allergies . At start tiny doses are given, trying to train the immune system, the studies are leaded by
Wesley Burks.
Other researches give patients microscopic parasitic worms to try to tamp down
the immune system. Multiple sclerosis patients who had intestinal parasites were
found to be in better conditions than those who did not. Professor John O.
Fleming and colleagues will therefore undertake experiments with pig worms on MS
patients. [23] [24]
Labelling
According to labelling Directive 2000/13, a full list of ingredient was considered not to be compulsory when the compound ingredient constitutes less than 25% of the finished product. Many of allergenic ingredients were so hidden.
The Directive 2003/89/EC amended Directive 2000/13. The mandatory inclusion on food labels of the most common food allergen ingredients and their derivate is contained in this directive which came into force in 2005.
A similar law goes into effect in the US on 1 January 20 due to the US Food Allergen and Consumer Protection Act (FALCPA). Food makers have to list in lain, common language, the presence of any of the eight major food allergens- milk, egg, peanut, tree nut, fish, shellfish, wheat and soy a product's label.
When cross-over of food allergens is not possible to be completely avoided, the warning " May contain traces of..." should be included in the label.
The EU directives regarding the indication of ingredients in food and Food
allergens are:
Directive 2003/89 Directive regarding the indication of ingredients in food.
[25]
Directive 2005/26 Ingredients provisionally excluded from Directive
2003/89/EC. [26]
Directive 2006/142 Directive listing ingredients which must appear on food
labels. [27]
Directive 2007/68 Listing ingredients exempt from labelling rules in
2003/89/EC. [28]
New labelling rules in European Directive (2003/89/EC) ensure that all consumers are given comprehensive ingredient listing information and make it easier for people with food allergies to identify ingredients they need to avoid.
The new rules came into force on 25 November 2004 establishing a list of 12 food allergens, which have to be indicated by reference to the source allergen whenever they, or ingredients made from them, are used at any level in pre-packed foods, including alcoholic drinks. The list consists of cereals containing gluten, crustaceans, eggs, fish, peanuts, nuts, soybeans, milk, celery, mustard, sesame, and sulphur dioxide at levels above 10mg/kg or 10 mg/litre expressed as SO2.
The new rules also removed the "25%" rule in the previous legislation, which meant that individual ingredients making up a compound ingredient did not have to be listed if the compound ingredient made up less than 25% of the finished products. So, apart from a few exceptions, all ingredients now have to be indicated on the label, even when they make up only a small proportion of the product.
Mustard and products thereof are included in the list of the Annex IIIa of the Directive 2003/89/EC [25].
Mustard seed from Brassica juncea are ground, tap water is added and the slurry is incubated at 50°C for 30 minutes. The allyl isothiocyanate is released
from its precursor by the enzyme myrosinase. The oil is obtained by steam distillation under reduced pressure. The mustard seed oil is separated from water by centrifugation and dried with sodium sulphate and filtered.
Mustard is known to trigger allergic reactions or intolerances in sensitive individuals and was therefore included in this list and must be labelled.. International Flavours & Fragrances (IFF) requested the European Commission exempt mustard seed oil from labelling European Food Safety Authority to evaluate the scientific data and came to the following conclusion:
IFF claims that mustard seed oil is not likely to trigger adverse reactions on the basis of two arguments: 1) the typical low levels of mustard seed oil in foods, and 2) the in vitro demonstration that proteins are not present in amounts higher than 1.5 microg/g in five samples of mustard seed oil analysed with an ELISA test developed by the applicant.
According to the Panel IFF did not take into account the known toxicity of allyl isothiocyanate and its role in causing allergic contact dermatitis, or the possibility that proteins not detectable with the ELISA test could cause an IgE-mediated reaction (Lerbaek et al., 2004; Kohl and Frosch, 1990).
The main volatile component of mustard seed oil is allyl isothiocyanate (97-100%). which has been classified as toxic by inhalation, in contact with the skin and if swallowed, and irritating to eyes, respiratory system and skin
Allergic reactions to mustard, including severe anaphylactic reactions, are well documented in clinical and laboratory studies. Mustard allergy may account for 1-7% of all food allergies with regional variations.
Mustard allergens are resistant to heat and to enzymatic degradation, and therefore are not markedly affected by food processing. The major mustard allergens identified are Sin a 1, belonging to the 2S albumin family, and Bra j 1, also from the 2S albumin family, with a MW.
A new major allergen in mustard seeds has been recently isolated and identified, an 11S globulin called Sin a 2 with a MW of 51 kDa (Palomares et al., 2005), but not all mustard allergens and their occurrence in different species are known. [30] [31]
In addition, allyl isothiocyanate is a major skin-sensitizing agent (non IgE-mediated mechanism). Mustard protein allergic individuals may react to the protein content of the oil. Individuals sensitised to the skin-sensitising component allyl isothiocyanate may react to oil even in the absence of mustard proteins (Lerbaek, 2004).
Taking account of the potential allergen content and well documented clinical allergic reactions in individuals sensitive to mustard (NDA, 2004a), it is appropriate for the Panel to assess the likelihood that mustard seed oil may cause an allergic reaction in mustard-allergic individuals.
Mustard seed oil (allyl isothiocyanate) will therefore not be exempted from labelling as allergen.
Some ingredients derived from the listed allergenic foods are so highly processed that they are no longer capable of triggering an adverse reaction. A list of products that are temporarily exempt (til 25 November 2007) from the labelling requirements of 2003/89/EC was published as Commission Directive 2005/26/EC
Manufacturers often use phrases such as "may contain nut traces" to show that
there could be traces of nut in a food product, either in the ingredients, or
because it has entered the product accidentally during the production process.
It is not a legal requirement to say on the label that a food might contain
traces of nut, but many manufacturers label their products in this way. Some
members of the public have expressed concern that "may contain" labelling is
used too much and could undermine valid warnings on products and restrict
people's choice unnecessarily.
Akiyama, Imai and Ebisawa 2011 describe the history of the food-labelling system for specific allergenic ingredients (i.e., egg, milk, wheat, buckwheat, and peanut) which became required by law in Japan on April 1, 2002. Foods containing walnut and soy bean must be labelled with subspecific allergenic ingredients, shrimp/prawn and crab has also become mandatory. Official guidelines of 2006 determine that any food containing allergen proteins at greater than 10mg/kg must be labelled under the Law.
EuroPrevall
EuroPrevall is an EU-funded multidisciplinary project aiming to improve quality of life for food allergenic people.
The partner organisations of the project will:
1- Characterise the pattern and prevalence of food allergies across Europe in infants, children and adults.
2- Develop methods to improve the quality of food allergic diagnosis, reducing the need for food challenge tests.
3- Determin the impact of food allergies on the quality of life and its economic cost for food allergic people and their families, workplace and employers, and healthcare.
EuroPrevall is a multi-disciplinary research project looking at the prevalence
cost and basis of food allergy in Europe to estimate the currently unknown
prevalence of food allergy and exposure to known or suspected risk factors for
food allergy across Europe. A protocol for the sampling strategy, the use of
questionnaires, and collection of blood samples for immunological analyses is
presented bei Kummeling and colleagues 2009.
Basic information on adverse reactions to foods in groups aged 7-10 years and 20-54 years were collected, together with a questionnaire on potential risks and
exposures. Blood sample were taken to allow serological analysis. Subjects
reporting adverse reactions to foods and sensitized to the same food(s) were
called in for a full clinical evaluation that included a double blind placebo
controlled food challenge. The authors hope that data of these studies will
improve disease prevention, diagnosis and management.
To assess global variations in the prevalence of food allergies the
EuroPrevall-INCO project has been developed to evaluate the prevalence of food
allergies in China, India and Russia using the methodology of the EuroPrevall
protocol applied in the EU, and compare the data with different European
countries. The authors hope that these Asian data added to Europe findings will
improve knowledge about the development of food allergy.
The Avon Longitudinal Study of Parents and Children was conceived to assess
the sensitization within a large birth cohort, the associations between
sensitization to different allergens and determine whether small groups of
allergen may be responsible for atopy, an allergic hypersensitivity affecting
parts of the body not in direct contact with the allergen.
Roberts and colleagues performed skin allergy tests at 7 years of age with
positive sensitization found with grass pollens (8.5%), house dust mite
(Dermatophagoides pteronyssinus 7.8%, Dermatophagoides farinae 3.6%), cat
(4.9%), dog (2.7%), horse (1.4%), rabbit (1.4%), peanut (1.4%) and mixed
tree nuts (1.0%). The authors concluded that aeroallergens are the most
important ones, and peanuts and tree nuts are most frequent food allergens.
Strong associations within and between different allergen classes such as
pollens, animals, foods, peanut and tree nuts were noted.
Shaker and Woodmansee 2009 stresses that 4 to 6% of US children have an
allergic reaction to at least one food, being influenced by a combination of
genetic influences, characteristics of food antigen processing, and timing of
food introduction. The authors point out that early introduction of allergenic
foods is being under trial because strict avoidance of allergenic foods
beyond 4-6 months may not be effective.
Current management of food allergy is summarized by the authors to depend on
accurate diagnosis, appropriate counseling regarding strict allergen
avoidance, emergency preparedness, instruction on the use of self-injectable
epinephrine, and ongoing surveillance for the possible development of tolerance.
Kim and Sicherer 2010 writes that strict allergen avoidance has been considered
to be the best strategy to prevent food allergy. It was found, however, that
children with milk and egg allergy tolerate extensively heated forms of these
foods, oral exposure can lead to desensitization, and delaying introduction of
highly allergenic foods to infants and young children does not prevent the
development of food allergy, and may even increase risks. Biomarkers are being
identified to select those patients who can profit from an early exposure to
allergens. The authors stress that, depending on the specific case, strict
avoidance is inevitable. [38]
Benhamou and colleagues 2009 write that egg allergy in children below the age of
three are the most frequent of allergies. Ovomucoid is the major allergen of
egg, and egg white proteins allergy may occur without clinical symptoms. The
diagnosis of egg allergy comprises IgE tests and standardized food challenges. Treatment of egg allergy includes strict avoidance of eggs and their products,
also tolerance induction protocols, in particular with egg proteins with reduced
allergenic properties in specific cases, are promising.
Patent Blue V, also called Food Blue 5 or Sulphan Blue, is a dark bluish
synthetic dye used as a food coloring. As a food additive, it has E number E131.
It is not widely used, but can be found in certain jelly sweets. Patent Blue V is
banned as a food colour in Australia, USA, and Norway.
In medicine, Patent Blue V is used in lymphangiography as a dye to colour
lymph vessels. It is also used in dental disclosing tablets as a stain to
show dental plaque on teeth.
It may cause allergic reactions, with symptoms ranging from itching and nettle
rash to nausea, hypotension, and in rare cases anaphylactic shock; it is not
recommended for children.
It was suggested that vitamin E and zinc intake during pregnancy might reduce the risk of wheeze and/or asthma in the offspring. Miyake and colleagues 2010
examining such associations found that higher maternal intake of green and
yellow vegetables, citrus fruit, and beta-carotene during pregnancy was
significantly associated with a reduced risk of eczema, but not wheeze, and
vitamin E consumption during pregnancy reduced the risk of infantile wheeze,
but not eczema.
The authors, however, found no protection against wheeze nor eczema generated
by higher maternal intake of total vegetables, vegetables other than green
and yellow vegetables, total fruit, apples, alpha-carotene, vitamin C, or zinc.
International Dairy Foods Association IDFA helped develop new guidelines for clear labeling of allergenic ingredients on food labels and supports the implementation of these guidelines, encourages disclousure of allergenic ingredients in clear and simple language, and is dedicated to assisting dairy processors in preventing cross contamination.
IDFA urges all members to review their policies and verify that they are operating within the new allergen guidelines. Further it ist being recommended that member companies follow these recommendations:
1- Review formulations to identify the presence, if any, of the 8 major allergens.
2- Contact ingredient suppliers to determine if ingredients they supply contain any allergen, including components of flavours, colors, incidental additives and processing aides, which may not be required to list specific ingredients.
3- Review their current labels to ensure that if any allergen are present they are included in the ingredient declaration in terms that are easily understood by consumers. The dairy industry is currently using the following labeling guidelines, which are among the options listed in the Allergy Labeling Guidelines issued by the Allergen Issues Alliance.
- Use of parenthetical statement following the ingredient name or class of names that identifies the presence of an allergic ingredient. For example, caseinate (derived from milk); and
- Use of a commonly understood name that identifies the presence of the allergen such as "natural walnut flavour."
4- Advisory statement should not be used as a substitute for Good Manufacturing Practices (GMP). Only use advisory label statements such as "may contain..." when all four of the criteria established in the Allergen Guidelines are met. These criteria are:
- The presence of a major food allergen is documented throughout visual examination or analytical testing of the processing line, equipment, ingredient or product, or other means.
- A major food allergen is present in some, but not all, of the product.
- The presence of a major food allergen is potentially hazardous.
- The risk of presence of a major food allergen is unavoidable even when current GMP's are followed.
Food allergy diagnosis
Food allergy is diagnosed by a process of elimination.
The first step is a detailed patient history to establish a pattern of reactions to foods in order to decide if the facts match with a food allergy. Other causes such as food intolerance or other health problems, should at this point be excluded.
The diagnosis is usually based on the symptom and dietary histories and subsequently confirmed via more specific investigations including skin prick tests, blood chemistry, and response to dietary restriction.
Test Diets
These are oral food
challenge tests.
Skin prick tests
These tests are performed if history, diet diary or elimination diet suggests a specific food allergy to be present.
A drop of allergen extract is placed on the skin of the lower arm, and the skin scratched with a needle. A positive reaction is shown by the rapid development of a localised reddening and swelling.
The only conclusive demonstration of food allergy (gold standard) is the result of a double-blind placebo-controlled food challenge, which must be performed in hospital with resuscitation facilities available because even extremely small doses can lead to a life-threatening reaction.
The sensitivity of in vitro immunoassays compared with prick/puncture skin tests has been reported to range from 50-90% with an average of about 70%. Skin testing, therefore, continues to be the preferred method for the diagnosis of IgE-mediated sensitivity.
Total serum IgE (Radio-Immuno-Sorbens-Test RIST
test)
RIST Test evaluates only the total amount
of IgE antibody. The RAST test is much more complicated but gives the answer to what allergen the patient is sensitive.
Allergen-specific IgE antibody testing (Radioallergosorbent RAST testing
The allergen-specific IgE antigen testing is done to screen for a type I hypersensitivity to a specific substance or substances in response to acute or chronic allergy-like symptoms in patients. The specific serum IgE Testing incorporates the use of microwell plastic strips, which have been coated with allergen proteins. Serum or plasma is exposed to the microwell and the bound IgE antibody is detected using an enzyme labelled anti-human IgE antibody. Peroxide substrate detects the levels of enzyme present, which is directly proportional to the level of specific IgE bound to the specific allergen.
Food Sensitivity Panel
The measure of high levels of IgG, IgA and IgM antibodies in serum for specific food antigens is a dependable diagnosis of specific forms of food sensitivity.
Testing about 96 different types of food indicates not only gastrointestinal diseases,but also neuromuscular and cardiovascular events, as well as cross reactivity of food antigens with tissue antigens as an initiating process in some autoimmune diseases.
Available are following test by ALLETESS Medical Laboratory of the serum of a patient [43]:
- IgG/IgA to Gliadin
- IgG/IgA to Gluten
- IgG/IgA to Casein
- IgG/IgA to lactalbumin
- IgG/IgA to Ovalbumin
- IgG/IgA to beta-lactalbumin
- Reticulin Antibodies
- Tissue Transglutaminase (tTG)(Specific to Endomysium) Antibody IgA Complete blood count (CBC), white blood cell differential count, eosinophil count, basophil count are blood tests for an indirect indication of an ongoing allergic process with special attention to the eosinophils and basophils. Elevation of their number suggest an allergy, but they may also be elevated for other reasons.[44]
| |
|
|
Skin reaction |
time of |
|---|
| Reaction |
Description |
Antibody |
and cellular infiltrate |
Onset |
|---|
| Type I |
Anaphylaxis |
IgE |
Allergy skin test |
1-20 min |
| |
|
|
eosinophils |
|
| Type II |
Cytotoxic |
IgG/IgM |
- |
- |
| Type III |
Immune |
IgG(IgM) |
Arthus reaction) |
7-10 hrs |
| |
complexes |
|
(PMNs) |
?-10 hrs |
| Type IV |
Delayed-type |
- |
TB skin test |
1-3 days |
| |
hypersensitivity (DTH) |
|
mononuclear cells |
|
At present there is no cure for food allergy, The only option is to avoid eating the problem food. Food allergic young people between 16 to 24 years are more likely to experience a severe allergic reaction leading to death.
The following measures can be taken:
- Avoidance of all allergens if possible
- Desensitisation (induce IgG)
- Drug:
Antihistamines and decongestants
Corticosteroids
Cromolyn sodium
Ephedrine and isoproterenol
Incidence of most common food allergies
A relative small group of foods or food products are responsible for most cases of food allergies.[45] Two out of a hundred babies under 12 month are allergic to cow's milk. It is the most common food allergen in childhood but nine out of ten milk allergic children are no longer allergic by the age of three.
It is unusual for adults to be milk allergic, but a small number of children have an anaphylactic reaction to milk and remain allergic into adulthood.
Because the proteins in milk are similar in sheep, goats and cows, people who are usually allergic to cow's milk are usually allergic to other milks and dietary calcium must be sourced from non-dairy foods.
Increasing amounts of foods that contain baked milk in the diets of children suffering with milk allergies may improve tolerance to milk and milk products.
Sampson et al 2011 report that approximately 75 percent of children, aged 2 to 17 years, with milk allergy, were found to tolerate foods containing baked milk, such as muffins, waffles and cookies. The high temperatures used in baking cause the proteins in milk to break down. This is believed to reduce the allergenicity.
After an initial muffin food challenge of six to twelve months, the children were given cheese pizza which is less heated than muffins and contains higher amount of unmodified milk protein. After three years of a diet containing cheese pizza At the end of the study period, 47 percent of the children could tolerate unheated milk products, such as skim milk, yoghurt and ice cream, compared to only 22 percent in a control group. The authors concluded that increased exposure to baked milk products helps to children outgrow milk allergies. Allergy to eggs also occurs in young children rather than adults. Most egg allergies disappear with time but whilst allergic to hen's eggs individuals are also allergic to other eggs.
Shellfish allergies
Shellfish allergies are unusual in children, but reactions to fish are found in both children and adults. Severe reactions are more frequently found with these foods, including anaphylaxis.
Cooking does not destroy the proteins responsible for the allergy, but some people may be allergic to the cooked food whilst they are able to eat raw fish.
Those who are allergic to cod are also allergic to hake, carp, pike and whiting. The protein that causes shellfish allergy are usually found in the flesh whilst the proteins responsible for allergy in foods such as shrimps are in the muscle and the shells.
Fruits and vegetable allergies
Generally they are mild. The proteins causing allergy in fruits and vegetables are similar to pollen proteins. Four out of ten individuals who are allergic to tree and weed pollens are also allergic to some fruits, and people who are allergic to birch pollen are likely to be allergic to apples.
Many of fruit and vegetable proteins are destroyed by cooking. The cooked food may be safe to eat. However, Kiwi fruit allergy , and peach and Rosaceae fruit allergies are severe and life-threatening. Their proteins are resistant to cooking and are found in fermented products such as wine and beer.
Peanuts allergies
Peanuts are not nuts
but legumes like soya, peas and beans. Peanuts are one of most allergenic foods and cause severe reactions. This allergy persists throughout life. Traces found in processed oils or on cooking or serving utensils can be sufficient to trigger anaphylaxis.
Cabanillas et al 2012 report a remarcable reduction of IgE-binding capacity of peanut allergens of roasted peanuts, submitted to autoclaving at 2.56 atm, for 30 min.
Antibodies against peanut allergens (Ara h 1, Ara h 2 and Ara h 3), digestion experiments, and circular dichroism spectroscopy analysis were performed by the authors. Obtained data suggest that the heat and pressure treatment increases the protein unfolding and digestibility. The authors concluded that the described treatment of peanuts may improve food safety.
Tree nuts allergies
They are also
called as true nuts and almond, Brazil nut, cashew nut, hazelnut, macadamia, pecan, pistachio, Queensland and walnut. Dr Shridhar Sathe and
colleagues 2008 studied the allergenic proteins of cashew nut (Anacardium
occidentale L.). They found that the three cashew nut allergens Ana o 1, Ana
o 2 and Ana o 3 were good marker proteins for the detection of cashew in foods
such as snacks, bakery products, deserts and sauces.
Searching for appropriate detection methodology of traces of cashew nuts in these
foods, the authors found that specific mouse monoclonal antibodies responded for
the three cashew nut allergens even after normal food processing, like
sterilisation, pasteurisation, microwaving and gamma irradiation. Ana o 2 was
found by the authors to be the most stable, and was also the major allergen of
cashew. Ana o 2 is therefore being suggested as best marker protein for cashew
detection. [49]
Our body has a host of defensive mechanisms to prevent food from making contact with our immune system. Even so some people have a tendency to react to particular foods and develop food allergies.
This tendency is present from birth and may be affected by environmental factors such as childhood infections.
Food tolerance is poorly developed in infancy and children become more susceptible to developing food allergies than adults. Children who are introduced to cow's under the age of 6 month are more likely to develop milk protein allergy. Some babies are sensitised to peanuts, milk and eggs at or around birth. It is possible that they were exposed to these allergens in the womb or during breath feeding.[45]
Peanut, vaccination and atopic allergic disease revision
The UK Department of Health advice issued by the Committee on Toxicity in Chemicals in Food, Consumer Products and the Environment (COT) issued in 1998 a precautionary advice that pregnant or breast-feeding women with a family history of atopy, may wish to avoid eating peanuts during pregnancy and lactation as this could increase the chances of peanut sensitisation in children.
Atopy or atopic syndrome is an allergic hypersensitivity affecting parts of the body not in direct contact with the allergen. There appears to be a strong hereditary component linked to genes such as 5q31-33 with a cluster of cytokine genes. The individual components, such as asthma, eczema or hay fever, are all caused at least in part by type I I hypersensitivity reactions.
[50] [51] Dr. Tara Dean and Dr.
Carina Venter assessed the compliance with this recommendation and its impact upon peanut sensitization.
In this study children sensitized to peanuts were found, but their mothers had not consumed peanuts during pregnacy. The scientists conclude therefore that maternal consumption of peanuts during pregnancy was not associated with peanut sensitization in the infant.
The majority of mothers avoided peanut consumption during pregnancy. The authors found that either the government advice is misunderstood by mothers, or that those who communicate the advice have not fully explained who it is targeted at, and stress the necessity of a review of the 1998 COT document. The authors call for clear, consistent factual advice and information about the real risks associated with peanut consumption during pregnancy/lactation and peanut allergy in the developing child, and specifically to whom these risks apply. [52] Despite highlighting that the increase in peanut allergy has been extraordinary,
with a 117.3 per cent increase in the prevalence of peanut allergy from 2001 to
2005 the report recommended to withdraw government guidance advising some
pregnant women and young children to avoid peanuts, alleging that abstinence from
peanuts during pregnancy and early life may actually increase the risk of
developing peanut allergy. The report refers to Israel, where peanuts are
commonly used in infants' weaning foods with a low incidence of peanut allergy.
The study of Saskia Willers and colleagues 2008 present new arguments against the
House of Lords report 2007 which speaks in favour of peanut consumption. Willers
found a strong association between daily versus rare nut product consumption
during pregnancy and symptoms of asthma in children.
The authors concluded that daily consumption of peanuts and their products
increased the asthma outcomes for about 50 per cent compared to rare consumption,
but no association was found for vegetable, fish, egg, milk or milk products
during pregnancy with asthma. The authors stress that the study deals with asthma
and not specifically with peanut allergy and call for caution on this respect.
Asthma, a complex heritable disease, affects notably developed countries.
Changes in DNA methylation resulting in aberrant gene transcription may
enhance their risk. Hollingsworth and colleagues 2008 report that a study
using mice found maternal diet supplemented with methyl donors (vitamine
folate) to enhance the
severity of allergic airway disease. Using a methyl-rich supplemented diet
the authors found that 82 gene-associated loci were differentially methylated
during gestation, increasing allergic reactions.
Important genes which were downregulated were Runt-related transcription factor
3 (Runx3), and Runx3 mRNA, which reduce the outcomes of allergic airway disease in progeny exposed in utero to a high-methylation diet. Treatment with a
demethylating agent caused the opposite effect.
The authors concluded that dietary factors can modify the heritable risk of
asthma through epigenetic mechanisms during fetal development in mice.
Rachel Miller, commenting the study of Hollingsworth and colleagues 2008
stresses that greater airway allergic inflammation and IgE production in F1 and,
to some extent, F2 progeny were noted using high-methylation diet during
gestation, but not during lactation or adulthood, suggesting that asthma-related
phenotypes across multiple generations via epigenetic mechanisms is acquired
during gestation. [57] Analysing prevalences of allergic sensitization and atopic disease in relation to vaccination coverage. Grüber and colleagues (2003) found that children with a higher vaccination coverage seemed to be transiently better protected against development of atopy in the first years of life. [58]
Grüber reassured in 2005 that common childhood vaccines are unlikely to promote atopic disease. He wrote that possible future development of atopic symptoms is most likely not causally related to vaccination but a coincidence. However, according to Grüber, vaccines specifically designed to down-regulate Th-2 type immunity have to be further elucidated if they are safe and effective in preventing the development of atopic disease. He concludes that effective protection against potentially life threatening or disabling infectious diseases should be offered to every child-atopic or not. [59]
According to Nakajima and colleagues in 2007 all few effects, which were seen in their study concerning vaccination and atopic disease, were small and age-dependent. The study supports numerous previous studies of no effect of vaccines on asthma. The authors conclude that the fear of their child developing atopic disease should not deter parents from immunising their children, especially when weighed against the benefits. [60] Contact with new drugs, cosmetics, exotic fruits and spices can be one cause of growing number of food allergies in the industrial countries. Results of studies suggest that a western lifestyle is associated with allergic diseases in childhood.[61]
For 1995-1996, the International Study of Asthma and Allergies in Childhood (ISAAC) found prevalence of self-reported asthma symptoms in children aged 13-14 years at 2.6 to 4.4 per cent in Albania, Roumania, Georgia, Greece and Russian Federation. In United Kingdom and Ireland these rates reached 32 percent, suggesting that western lifestyle is associated with allergic diseases in childhood.
| Land |
Prevalence |
|---|
| UK |
36% |
| Australia |
33% |
| New Zealand |
32% |
| Ireland |
28% |
| USA |
24% |
| South Africa |
16% |
| Japan |
13% |
| China |
<5% |
| Indonesia |
<5% |
| India |
<5% |
| |
|
|---|
(Source ISAAC Study)
Gut microflora and immune system
Changes in gut microflora caused by widespread use of antibiotics and today's high fat, lowfibre diet could be responsible for a major increase in allergies in recent years.
Gary Huffnagle is an associated professor of internal medicine and of microbiology and immunology at the University of Michigan. He says that researches indicates that microflora lining the walls of the gastrointestinal tract are a major underlying factor responsible for the immune system's ability to ignore inhaled allergens. Changes in the microflora in the gut upsets the immune system's balance between tolerance and sesitization.
To test this hypothesis, Balb/C laboratory mice were given a five-day course of antibiotics, killing their gut bacteria. A single oral introduction of Candida albicans stimulated an increase of growth of this yeast in the gut of the mice. This is a common side-effect of antibiotics.
An increased airway hypersensitivity to ovalbumin (egg whites) inserted via nasal cavities was noted.
Huffnagle says that differences in host genetics and the type of allergens does not matter as the response had been identical in all studies. It confirms that microflora are the key to maintain a balanced immune response. Changing the composition of microflora in the gut predisposes animals to allergic airway diseases. Allergic sensitization can also occur outside lungs [62].
However, an article by Sunia Foliaki, from the International Study of Asthma and Allergies in Childhood (ISAAC) published in the International Journal of Epidemiology in 2004 says that findings are generally not consistent with the hypothesis that antibiotic use increases the risk of asthma, rhinitis, or eczema. If there is a casual association of antibiotic use with asthma risk, it does not appear to explain the international differences in asthma prevalence.
It has been hypothesized that antibiotic use early in life may increase the subsequent risk of asthma. Foliaki conducted an ecological analysis of the relationship between antibiotics sales and the prevalence of symptoms of asthma, allergic rhinoconjunctivitis and atopic eczema in 99 centres from 28 countries[63].
The findings of Huffnagle gives a new dimension to the relationship between gut microflora and immunology trying to explain the different occurrence of East and West asthma.
Allergens
Allergens are macromolecules (usually proteins) which are involved in sensitising and eliciting allergic reactions.
The International Union of Immunological Societies (IUIS) published in 1986 the characterisation and nomenclature of allergen which was revised (Official list of allergens I.U.I.S. Allergen Nomenclature Sub-Committee 2003.03.02) http://www.allergen.org/Archive/Meetings/2003/List 20030302.pdf and List of allergens as of September 12, 2005 http://www.allergen.org/list.htm standardisation allergen preparations guidelines.
Food allergy is a very individual problem. Treatment of food allergy involves changes in the lifestyle. Food allergy is best treated by avoiding the
foods that cause it.
Special diets are the most often used treatment for food allergies. If the patient is allergic to only one or two foods, elimination of these foods may be the only treatment.
The best thing is to ban the foods which cause the problem from the kitchen. Ready to eat meals from the supermarket must be carefully screened to avoid the offending ingredients. New food labelling directives gives a better chance to avoid specific allergen.
Rotation diet
Rotation diets are necessary when a patient has multiple food allergies. The foods causing the allergy must be eliminated and all other foods should be eaten in intervals of four to five days. This reduces the exposure to many other foods to which the person has also unknown subclinical allergies. This will avoid future intolerance to these foods. The ideal rotation interval can vary from person to person and from food to food, but should never be less than four days.
No food should be eaten in extremely large quantities. Rice should not make up half of the food of the day. New and unusual foods should be included in the diet, to avoid eating one food in large quantities.
Medication
Mild allergies may be controlled by nonprescription antihistamines. More severe cases need epinephrine and antihistamine medication and a medical bracelet
Severe cases need an allergy kit that contains everything necessary for an epinephrine shot. All child caregivers should know how to recognise the signs of a severe allergic reaction and how to give an epinephrine shot.
Food intolerance
Food intolerance do not involve the immune system. It includes reactions to histamines and other amines found in the foods, and lactose intolerance, where individuals lack the enzyme necessary to break down lactose in the gut. Such adverse reactions to food do not involve the immune system and are also called non-allergic food hypersensitivity reactions. They are also called pseudoallergy.
Food, additives and drugs are the main responsibilities for pseudoallergies.
Substances which may trigger a pseudoallergy are: Food colours, preservatives such as benzoic acid and sulfite, acetysalicyl acid and other not steroidal antiphlogystica.
Salicilates contained in foods may cause pseudoallergies.
Foods high in salicilates are: Berry fruits, oranges, apricots (Prunus armeniaca), pineapple (Ananas comosus), cucumber (Cucumis sativa), olives (Olea europaea), grapes and wine. The treatment of pseudoallergies is similar to that of allergic diseases (antihistamine drugs, steroids, B2 agonists, epinephrine).
Biogenic amines such as histamine, cadaverine and putrescine can be present in foodstuffs or be formed during their storage by microbial decarboxylation of the corresponding amino acids, mainly during fermentation processes. Elevated concentrations of these compounds also indicate bad hygienic conditions during the fermentation process.
Foods produced with the help of bacteria have therefore often a high level of biogenic amines. These foods are yeast extract, some types of cheese, sauerkraut, red wine and spoiled foods containing meat or certain fishes.
Scombroid poisoning occur when the spiny-finned fish of the family of Scombridae undergoes improper storage resulting scombroid toxin. Susceptible fish include albacore, amberjack, anchovy, Australian salmon, bluefish, bonito, kahawai, herring, mackerel, mahi-mahi, needlefish, sauri, sardine, skipjack, wahoo and yellowfin tuna. Affected fish have a metallic or peppery taste.
Biogenic amines are responsible for a pseudoallergy reactions such as headache, skin irritation or changes in blood pressure.
Milk allergy is an immunologically mediated adverse reaction to one or more milk proteins. In some children the ingestion of milk can trigger the body into launching an inappropriate immune response to the proteins in milk resulting in an allergic reaction.
Currently the only treatment for milk allergies is total avoidance of milk proteins. Initially if the infants are breastfed, the lactating mothers are given an elimination diet. If symptoms are not relieved or if the infants are bottle-fed, milk substitute formulas are used to provide the infant with a complete source of nutrition. Milk substitutes include soy milk, rice milk, and hypoallergenic formulas based on hydrolysed protein or free amino acids.
Milk allergy is the most common food allergy. It affects somewhere between 2% and 3% of infants in developed countries, but approximately 85-90% of children lose clinical reactivity to milk once they surpass 3 years of age.
Lactose intolerance is marked by a relative or absolute absence of the enzyme lactase in the small intestine which prevents metabolism of lactose.
It is a clinical syndrome with symptoms including abdominal pain, diarrhoea, nausea, flatulence, and/or bloating after ingesting lactose-containing substances. Lactose is not absorbed in the gut, and can draw fluids into the intestine by osmosis, which produces diarrhoea, and the carbohydrate can be metabolised by certain intestinal bacteria that produce carbon dioxide, methane and hydrogen as waste products, thereby leading to flatulence.
Differences between primary, secondary, congenital, and developmental lactase deficiency are discussed in a review from the American Academy of Pediatrics (AAP).
Treatment consists of use of lactase-treated dairy products or oral lactase supplementation, limitation of lactose-containing foods, or dairy elimination. The American Academy of Pediatrics supports use of dairy foods as an important source of calcium for bone mineral health and of other nutrients such as protein, and riboflavin that facilitate growth in children and adolescents. If dairy products are eliminated, other dietary sources of calcium or calcium supplements need to be provided.
According to AAP pediatricians and other pediatric care providers should maintain awareness of the benefits and controversies related to the consumption of dietary milk products and milk-based infant formula. A lactose tolerance test, a hydrogen breath test, or a stool acidity test is required for a clinical diagnosis.
Most adults in the world are lactose-intolerant: the majority of humans stop producing significant amounts of lactase sometime between the ages of two and five. A relatively recent genetic change caused some populations, including many northern Europeans, to continue producing lactase into adulthood; these lactose-tolerant populations are in the minority. Lactose intolerance is an autosomal recessive trait, while lactase-persistence is the dominant allele.
Important lactose intolerant ethnic groups are gathered in the south of Africa, China and Hispanics ranging from 100 to 65% of cases. Meanwhile in UK, Germany and other states of northern Europe have only 2% of persons suffering from intolerance to lactose.
Yoghurts containing live cultures are well tolerated by people with lactose intolerance because the bacteria partially digest the lactose into glucose and galactose. Aged cheeses, such as Cheddar and Swiss, have lower lactose contents than other cheeses.
Kleber and her colleagues from the Germany's University of Hohenheim report that over70% of beta-lg antigenicity content in the sweet whey and 90% in skim milk were reduced using a wide range of lactic acid bacteria (Lactobacillus) independently or in mixture 1:1 with Streptococcus thermophilus subspecies salivarius incubated at 40°C for 24 hrs.
The research is important because 80 per cent of all cases of milk allergies is caused by the whey protein beta-lactoglobulin (beta-lg) which is not present in human milk.
Antigenicity refers to the capacity to induce an immune response. In this study only the antigenity of beta-lg was tested and not the allergenicity. The enzymes are reported to be more or less specific with some better at reducing the beta-lg content in milk and/ or whey.
The research has industrial relevance regarding new fermented milk products with reduced antigenic properties
Lactose intolerance is caused by a shortage of the enzyme lactase, which is produced by the cells that line the small intestine. Lactase breaks down milk sugar into two simpler forms of sugar called glucose and galactose, which are then absorbed into the bloodstream. Lactose intolerance occurs in about 25% of people in Europe; 50-80% of people of Hispanic origin, people from south India, black people, and Ashkenazi Jews; and almost 100% of people in Asia and American Indians.Lactose intolerance is a problem caused by the digestive system.
Symptoms are often the same of lactose intolerace. Cow's milk is an allergic reaction triggered by the immune system. Common symptoms, which range from mild to severe, include nausea, cramps, bloating, gas, and diarrhea. Symptoms begin about 30 minutes to 2 hours after eating or drinking foods containing lactose. The severity of symptoms depends on many factors, including the amount of lactose a person can tolerate and a person's age, ethnicity, and digestion rate.
There are sophisticated tests for the diagnosis of lactase malabsorption,like the Lactose Tolerance Test, the Hydrogen Breath Test and the Stool Acidity Test. However, the diagnosis can be made easily on the basis of clinical history. Improvement in symptoms after eliminating such foods and worsening when they are reintroduced confirms the diagnosis.
No treatment can improve the body's ability to produce lactase, but symptoms can be controlled through diet.
Lactase concentration after birth and declines after weaning. In primary lactase deficiency lactase concentrations declines at the age of weaning. It is associated with a recessive inherited trait, different between Europeans and Africans.
In primary lactase deficiency the development of
symptoms depends on how much lactose needs to be ingested before the available lactase is saturated. Thus, most people with primary lactase deficiency can ingest up to 240 ml of milk (12 g of lactose) without developing symptoms.
It may help to divide daily milk intake into several small portions and to take it with other foods. Yoghurt, curds, and cheeses are better tolerated, because lactose is partially hydrolysed by bacteria during their preparation and gastric emptying is slower as these products have a thicker consistency. People with lactose intolerance should be encouraged to gradually increase their intake of milk- this causes changes in the intestine that permit higher milk intake.
Milk-cereal mixtures delay the entry of lactose into the intestine, permitting better absorption. Since these are cheap and easily prepared at home, their use should be promoted.
It results from injury to the small bowel mucosal brush border secondary to viral or non-viral intestinal infection, common in developing countries. Treatment is directed at the underlying cause.
It is characterized by minimal or absent lactase immediately after birth. It is a rare disorder.
It occurs in premature infants, because lactase levels do not increase until the third trimester of a woman's pregnancy. The deficiecy, however, rapidly improves as the intestinal mucosa matures.
For those who react to very small amounts of lactose or have trouble limiting their intake of foods that contain it, the lactase enzyme is available without a prescription to help people digest foods that contain lactose. The tablets are taken with the first bite of dairy food. Lactase enzyme is also available as a liquid. Adding a few drops of the enzyme makes lactose more digestible for people with lactose intolerance.
Young children and infants with lactase deficiency should not consume lactose-containing formulas or foods until they are able to tolerate lactose digestion. Most older children and adults do not have to avoid lactose completely, but people differ in the amounts and types of foods they can handle.
Short periods of lactose intolerance are common after episodes of infective diarrhoea and may prolong the diarrhoeal illness. a meta-analysis has shown that most children with acute diarrhoea can safely continue to receive breast or undiluted animal milk Milk-cereal mixtures given at frequent intervals (nearly 2 g/kg/day of lactose or 40 ml/kg/day of milk) were well tolerated by most children with persistent diarrhoea.
Non-responders will benefit from reducing lactose intake below their current threshold of tolerance, followed by long term steps directed at improving adaptation of the intestine.
Recent research shows that yogurt with active cultures may be a good source of calcium for many people with lactose intolerance. Even though yogurt is fairly high in lactose, the bacterial cultures used to make it produce some of the lactase enzyme required for proper digestion. [68]
The Institute of Medicine released a report listing the requirements for daily calcium intake. How much calcium a person needs to maintain good health varies by age group. Recommendations from the report are shown in the following table.
| Age group |
Amount of calcium to consume |
|---|
| |
daily, in milligrams (mg) |
| |
|
| 0-6 months |
400 mg |
| 6-12 months |
600 mg |
| 1-5 years |
800 mg |
| 6-10 years |
1,200 mg |
| 11-24 years |
1,200-1,500 mg |
| 19-50 years |
1,000 mg |
| 51-70+ years |
1,500 mg |
In addition, pregnant and nursing women need between 1,200 and 1,500 mg of calcium daily Calcium sources.
Many non-dairy foods are high in calcium, including dark green vegetables such as broccoli, or fish with soft, edible bones, such as salmon and sardines.
[71]
| Vegetables |
Calcium |
Lactose |
|
Dairy products |
Calcium |
Lactose |
|---|
| |
mg |
g |
|
|
mg |
g |
| Soymilk, fotified, 1 cup |
200-300 |
0 |
|
Yoghurt,plain,low-fat |
415 |
5 |
| |
|
|
|
1 cup |
|
|
| Sardines,with edible bones, |
270 |
0 |
|
Milk,reduced fat |
295 |
11 |
| 3 oz. |
|
|
|
1 cup |
|
|
| |
|
|
|
|
|
|
| Salmon,canned, with edible |
205 |
0 |
|
Swiss cheese,1 oz. |
270 |
1 |
| bones, 3 oz. |
|
|
|
|
|
|
| |
|
|
|
|
|
|
| Broccoli, raw, 1 cup |
90 |
|
|
Ice cream,1/2 cup |
85 |
6 |
| |
|
|
|
|
|
|
| Orange, 1 medium |
50 |
0 |
|
Cottage cheese |
75 |
2-3 |
| |
|
|
|
1/2 cup |
|
|
| Pinto beans, 1/2 cup |
40 |
0 |
|
|
|
|
| Tuna,canned,3 oz. |
10 |
0 |
|
|
|
|
| Lettuce greens,1/2 cup |
10 |
0 |
|
|
|
|
Yoghurt with active cultures may be a good source of calcium for many people with lactose intolerance. Even though yoghurt is fairly high in lactose, the bacterial cultures used to make it produce some of the lactase enzyme required for proper digestion.
Clearly, many foods can provide the calcium and other nutrients the body needs, even when intake of milk and dairy products is limited. However, factors other than calcium and lactose content should be kept in mind when planning a diet. Some vegetables that are high in calcium (Swiss chard, spinach, and rhubarb, for example) are not listed in the chart because the body cannot use the calcium they contain because these foods also contain substances called oxalates, which stop calcium absorption.
Calcium is absorbed and used only when there is enough vitamin D in the body. A balanced diet should provide an adequate supply of vitamin D from sources such as eggs and liver. Sunlight also helps the body naturally absorb vitamin D, and with enough exposure to the sun, food sources may not be necessary. Although milk and foods made from milk are the only natural sources of lactose, it is often added to prepared foods. People with very low tolerance for lactose should know about the many food products that may contain even small amounts of lactose, such as:
Bread and other baked goods, processed breakfast cereals, instant potatoes, soups, and breakfast drinks, margarine, lunch meats (other than kosher), salad dressings, candies and other snacks, mixes for pancakes, biscuits, and cookies, powdered meal-replacement supplements.
Some products labeled non-dairy, such as powdered coffee creamer and whipped toppings, may actually include ingredients that are derived from milk and therefore contain lactose such as whey, curds, milk by-products, dry milk solids, and non-fat dry milk powder. They contain lactose.
About 5 per cent of the general population have some type of food allergy. Some bowl disorders seem to trigger food hypersensitivity. In case of Irritable Bowel Syndrome 65 percent of patients may be affected by food allergy.
IBS Irritable Bowel Syndrome
Irritable bowel syndrome is the most common functional disorder of the gastrointestinal tract, characterised by abdominal pain, bloating and irregular bowel function with constipation or diarrhoea. IBS is believed to affect more than 58 million people wordwide, and more women suffer from it than men. It is untreatable and intervention involves management of symptoms. It is not life threatening but it is a long-term condition that involves abdominal discomfort.
IBS patients had higher IgG4 titers to wheat (PiÜ< 0.001), beef (<0.001), pork (<0.001), and lamb(P=0.009), and soy beans (P=0.012) as compared with healthy controls.
The IgG4 titers to potatoes, rice, fish, chicken, yeast, tomato or shrimp were not significantly different to titers found in healthy people.
Probiotic bacteria has been widely researched for its impact on gut health but few strains have enough evidence to claim a benefit on IBS symptoms showing promise in normalising bowel movements. The probiotic bacteria Lp299v (Lactobacillus plantarum 299v) is the first probiotic targeting IBS symptoms. It helps to reduce intestinal discomfort and other symptoms.
International regulations mean that probiotic products cannot carry explicit disease prevention or treatment claims. Probiotics are, however, marketed with "friendly" or "good" bacteria that can redress the balance of flora in the gut and help the user to feel "better" , other address the improvement of the immune system.[72] Lactobacillus reuteri ATCC 55730 is a probiotic (health-promoting) lactic acid bacterium widely used as a dietary supplement to improve gastrointestinal, immune and oral health.
Dietary supplementation with the probiotic L. reuteri ATCC 55730 induces significant colonization of the stomach, duodenum, and ileum of healthy humans, and this is associated with significant alterations of the immune response in the gastrointestinal mucosa. [73] [74]
Probiotic bacteria taken by mothers may reduce the likelihood of eczema, also an allergic disease. Children who were exposed to probiotics around the time of birth were 40 per cent less likely to develop atopic eczema at four years of age than children in a placebo group.
However exposure to probiotics did not have any protective effect over asthma in this study.
Child care infants fed a formula supplemented with L reuteri or B lactis had fewer and shorter episodes of diarrhea, with no effect on respiratory illnesses. These effects were more prominent with L reuteri, which was also the only supplement to improve additional morbidity parameters. [75]
Dr Steve Allen is investigating the impact of probiotics on allergies giving Lactobcillus reuteri supplements to mothers for four weeks prior to birth of their babies and these babies are now being given probiotics for their first year.
Analysis of breast milk taken from the mothers a couple of days after giving birth showed increased levels of the anti-inflammatory cytokine (cell signal substance) IL-10 and reduced levels of TGF-beta-2. The cytokine IL-10 is central to regulation of the immune system and has anti-inflammatory properties. However the origine of TGF-B2 in breast milk is uncertain because it is produced by many cell types and there is the possibility of an association with a subclinical mastitis. [76]
Je-Ruei Liu and colleagues evaluated the effect of oral consumption of milk kefir and soymilk kefir on in vivo IgE and IgG1 production induced by ovalbumin (OVA) in mice. They found that both foods suppressed the IgE and IgG1 responses and altered the intestinal microflora. The intestinal populations of Bifidobacterium spp. and Lactobacillus spp. were increased and Clostridium spp., decreased. Disorder of the intestinal microflora is told to be closely related to food allergy development,
According to the authors, milk kefir and soymilk kefir may, therefore, help to prevente food allergy and enhancement of mucosal resistance to gastrointestinal pathogen infection.
Soybean lecithin and allergy
[77]
The protein fraction of soybeans are allergenic. The vast majority of this protein is removed in the soy lecithine manufacturing process. The remaining trace levels of soy proteins in lecithine are not suficient to produce allergic reactions in the majority of soy-allergic persons. Some of the more sensitive persons, however should avoid soy-lecithine when used as ingredient in food.Source labelling of soy-lecithine is provided in the Food Allergen Labeling and Consumer Protection Act of 2004.
Dr. Hefle and Dr. Taylor from the University of Nebraska advocate that no conceivable allergenic risk would occur from the use of shared equipment for products that contain soybean lecithin and products that do not. The transfered amount of soy protein will be verylow. An "allergen-cleanout" is according to these authors not necessary.
In a study performed in Switzerland, Denmark and Italy Barbara K.
Ballmer-Weber and colleagues 2007 reported that the no observed adverse
effect level (NOAEL) in Europe should be two milligrams for soy and 1
milligram for soy protein.
According to the authors 1% of patients with soy allergy would react
subjectively and objectively with 0.21 and 37.2 mg of soy protein, respectively.
this should be considered in food-labelling directives. Juana Frias and colleagues 2007 studied the reduction of the immunoreactivity
and improvement of amino acid content after fermentation of soybean flour.
The highest reduction in IgE immunoreactivity was obtained with Lactobacillus
plantarum fermenting milled soybean flour in liquid state, and most of the
total amino acids increased.
Cracked soybean in solid state fermentation with Bacillus subtilis presented
high reduction in immunoreactivity, alanine and threonine improved. Less
effective were fermentations with Aspergillus oryzae and Rhizopus oryzae.
The authors concluded that fermentation can decrease soy immunoreactivity, and
nutritious hypoallergenic soy products may be developed using this technology.
The biochemistry of allergies
The immune system produces immunoglobulins which act as defence against viral, microbial and fungal infections.
One particular for of immunoglobulins are immunoglobulin E (IgE) which respond to parasitic infections such as malaria agents. Some of this group of immunoglobulins are a response to contact with pollen, dust and food causing allergic reactions such as hay fever.
The normal function of the body produces IgG and IgA in response to food proteins. The immune reaction of certain predisposed individuals result in the so-called Th2 response which leads to the secretion of IgE immunoglobulins.
This response happens normally only in case of parasitic infectins such as malaria but also happens in case of hypersensitivity to food allergens. This is called Th2 response.
Allergies develop in two stages: Sensitisation occurs when an antigen
comes in contact with cells called progenitor B-lymphocytes. These cells break down the antigen in peptide fragments which are bound in special molecules called hystocompatibility complex class II complex. This complex is transported to the surface of the B-lymphocyte cell. The T-cell receptors of CD4 of another cell type, called T helper cell recognises the foreign peptide on the surface of the B-lymphocytes, triggering the secretion of specific antibodies, the IgE immunoglobulins. During the elicitation of an allergic
reaction, the IgE becomes associated with specific IgE receptors on the surface of basophile or mast cells. These cells are packed full of inflammatory mediators such as histamine.
The cell-bound IgE is crosslinked by the agent in case of a re-exposure. The mast cell is then caused to release the inflammatory mediators which trigger the allergic symptoms usually within minutes following exposure, resulting in asthma, vomiting, eczema and hives (nettle rash).
| Food |
Allergen |
|---|
| Milk |
Casein, beta-lactoglobulin, alfa-lactalbumin |
| Eggs |
Ovomucoid, ovalbumin |
| Fish |
Parvalbumin |
| Shell-fish and |
Tropomyosin |
| Seafood |
|
| Peanut |
7S seedstorage globulin, 11S seed storage globulins, 2S albumin |
| Soya |
7S seedstorage globulin, 11S seed storage globulins, |
| |
Bet v 1 homologue, inactive papain-related thiol protease |
| Tree nuts |
2S albumin, 7S storage globulins, 11S seed storage globulins |
| |
Non specific lipid transfer proteins, Bet v 1 homologue |
| Mustard, Sesame |
2S albumin |
| seeds |
|
| Cereals wheat |
Seed storage prolamins, alfa-amylase, trypsin inhibitors, |
| |
Glycosylated peroxidase |
| Fresh fruit and vegetables |
Homologues of the major birch pollen allergen Bet v1 |
| Kiwi, peach,celery |
Cysteineprotease, LTP |
| |
|
|---|
Food manufacturers must comply with directives calling for mandatory declaration of major allergens on labels. Special kits for the detection of some of these allergens are being developed to help food manufacturers to screen their raw ware and their production lines for unforeseen cross-over of traces of ingredients.
Many kits on the market only detect egg white and do not indicate the presence of egg yolk. Biotrace Tecra Egg Via Kit detects both. Other kits avilable using simple extraction methods and sensitive specific immunoassay techniques and " on-site" tests highly effective in the food industry as part of a HACCP programme: [80]
- Wheat gluten
- Milk proteins (caseins/caseinates; whey protein and albumin; lactoglobulin)
- Peanut and sesame tests are directed towards their major components. The antibodies are specific and can be used in a wide rage of food matrices, including chocolate-based foods, which can sometimes cause problems.
- Soya protein
- Sesame protein
- Tree nuts
ELISA Systems Kits to Detect Food Allergens
The following rapid Elisa (enzyme-linked immunosorbent assay) kits are available:[81]
- Almond (Prunus dulcis): It belongs to the tree nuts group. Almonds are a common cause to food allergy.
- Beta-lactalbumin and casein: Non-dairy products should be tested to ensure raw and finished products have not been contaminated with milk proteins. Either beta-lactalbumin or casein can be tested.
- Crustacean: Trompomyosin is a major protein in Crustaceans. It is the major shrimp allergen and presents evidences of cross-reactivity among crustaceans and molluscs.
- Egg: It tests only egg white.
- Hazelnut (Corylus avelana): Detects heat stable protein component of hazelnut.
- Peanut: The proteins Ara h1 and Ara h2 of peanuts are focused. Ara h2 is heat stable
- Sesame (Sesamum indicum): Allergy to sesame seeds is increasing. In Israel sesame is a major cause of food allergy. Anaphylaxis has been reported after ingestion of meat and sesame seed oil.
- Soy: The incidence of allergy to soybean proteins is quite low in comparison to other major food proteins. However, the increasing consumption of soybean products makes this test necessary.
Celery (Apium graveolens), together with peanuts, is a potent allergenic vegetable. Three celery allergens are known: Api g 1, Api g 4, and Api g 5. Gadermaier et al. 2010 identifed a new lipid transfer protein (nsLTP).from celery stalks consisting of a single isoallergen designated as Api g 2.0101 with a typical alfa-helical fold and high thermal stability and gastrointestinal digestion. Thermal denaturation did not affect the IgE binding of Api g 2. Therefore, patients with Api g 2 allergy may develop serious reactions responding to cooked celery stalks Api g 2-specific IgE antibodies cross-reacted with peach and mugwort pollen nsLTPs. The authors suggest to include the recombinant Api g 2 in the current panel of allergens for molecule-based diagnosis in celery allergy.
According to Harrer et al. 2010 the data on plant food allergies at the molecular level, the allergen structure,and stability, together with immunological methods at the level of IgE and T-cell reactivity can be integrated in computational algorithms to predict allergenicity of novel foods. Lipid-transfer proteins are important food allergens, being used in herbs and spice mixes. Over fifty allergenic non-specific lipid transfer protein (nsLTPs) are already know. All these data can be used in molecule-based diagnosis and future development of specific immunotherapy in plant food allergy. [83]
Faeste et al. 2010 developed a detection method for celery in food, using a sandwich celery ELISA using polyclonal anticelery antibodies, however, it may only be used for screening foods because of its cross-reactivity with potato and carrot proteins. It is based on the detection of nanoLC-ion-trap MS/MS proteins which are present in celery, potatoes and carrots. The authors also describe a novel patatin (Sola t 1)-like protein in celery and a flavin adenine dinucleotide binding domain-containing protein (Api g 5)-like protein in carrot. The authors suggest that further development of the MS-based screening method may be used to detect celery allergens in foods. Such a method is not yet available but it is needed to comply with the mandatory labelling of celery proteins in preprocessed foods.[84]
Ferrer et al. 2009 stresses the importance microarray technique to determine specific IgE against multiple allergens and allows the determination of IgG and IgM against the same allergens.. Microarray procedures are being developed not only for the determination of antibodies but also for cell activation tests and determination of cross-reactions. Microarray technique can help to improve the safety and efficacy of immunotherapy and increase knowledge on the physiopathology of allergic diseases.
Diagnosis of IgE-mediated allergies was improved with the development of flow-assisted analysis of allergen-specific activated basophils and component-resolved diagnosis (CRD). De Knop et al. 2010 reviewed the component-resolved allergy diagnosis by microarray, which allows an analysis of individual sensitization profiles with multiplexed purified and recombinant allergens which may facilitate the formulation of diagnostic algorithms. The authors, however, stresses that this method needs further assessment and it should be considered part of a complementary diagnostic and should not be used as final tool. [86]
Allergies and cross-reactivity
Milk allergy
There are at least 30 antigenic proteins in milk. Casein is the most commonly used milk protein in the food industry; lactalbumin, lactoglobulin, bovine albumin, and gama globulin are other protein groups within the milk.
Digested fractions of milk proteins may induce the production of IgE, IgA, and IgG antibodies and may trigger complex, variable immune responses. Skin tests with whole milk proteins are, therefore, misleading because secondary antigens of digested proteins are not detected.
Accurate diagnosis is important in case of an immediate symptomatic hypersensitivity to cow's milk protein because a milk-free diet with substitute formula should be established.
Many children who are allergic to cow's milk protein also show sensitivity to soy- based products. There are infant formulas in which the milk and soy proteins are degraded so the immune system does not recognise the allergen and the product can be consumed safely.
alfa-lactalbumin
alfa-lactalbumin and beta-lactalbumin are the major cow's milk allergens. The presence of cow's milk is widespread due also to its unlabelled inclusion as an ingredient, or to errors in cooking, processing and preparation, especially in restaurants. For this reason, individuals with milk allergies should avoid processed foods as much as they can and try to consume foods prepared at home; only food items with all the ingredients listed on the label should be consumed.
Hot dog, salad mayonnaise, dressings, and meat products are often produced using caseinates as emulsifier. Caseinates replaces egg yolk in these products which resist deep freezing. The same products produced with egg yolk are extremely sensitive to freezing.
A hot dog may contain caseinate.
Kiwi fruits allergies
Birch pollen and Kiwi allergy
Fruit allergy is frequently associated with birch pollen.
Kiwi allergy is a new manifestation of birch pollen-associated food allergy and is mediated by cross-reacting antigens in the kiwi fruit. Kiwi allergy can be expected in patients with birch pollen allergy exhibiting high levels of IgE to birch pollen. [87]
Fahlbusch and associated scientists at the Institute of Clinical Immunology, at the University of Jena, Germany found that the major allergen for kiwi allergy is the 30 kDa protein and additionally that the cross-rection between kiwi and birch pollen allergy is mainly due to carbohydrate moieties. [88] Basophil activation is
associated with the expression of CD63. In birch-pollen-associated food allergy to celery, carrot and apple, Bet v 1, Api g 1, Dau c 1 and Mal d 1 are major allergens. : Recombinant allergens have not yet been used in the CD63-based basophil activation test (BAT). However, the BAT using recombinant allergens provides a valuable new in vitro method for the detection of sensitization to foods.
In the presented study Erdmann determined specific IgE by the CAP method and basophil activation by flowcytometry upon double staining with anti-IgE/anti-CD63 monoclonal antibodies after incubating with purified recombinant Bet v 1, Bet v 2, Api g 1, Dau c 1 and Mal d.
According to Erdmann double-blind placebo-controlled food challenges remain the gold standard to confirm food allergy, however, the CD63-based BAT with recombinant allergens may supplement routine tests for allergy diagnosis.[89]
The basophil activation test (using either CD203c or CD63 as activation marker) has become a robust and reliable test for in vitro investigations of immediate allergy, complementary to other existing in vitro tests. Inter-laboratory standardization in clinical decision-making is necessary. Each allergen has to be assessed one by one to determine its optimal concentration as well as the definition of the threshold for positivity (using ROC analysis).[90] The green-fleshed
kiwi Actinidia deliciosa cv Hayward and the yellow-fleshed cultivar Actinidia chinensis cv Hort 16A are grown commercially. According to findings of Bublin and associated scientists of the Department of Pathophysiology, Medical University of Vienna, Austria. the IgE immunoblotting showed marked differences in the allergen compositions of green and gold kiwifruit extracts.
Phytocystatin which is a novel plant food allergen, and a thaumatin-like protein were allergens common for both cultivars. In the extract of gold kiwifruits two allergens with homologies to chitinases were found. Actinid was detected exclusively in green kiwifruits.
Green and gold kiwifruit extracts were shown to be highly cross-reactive as determined by the authors using IgE ELISA inhibition.
The authors conclude that the gold kiwifruit should be considered as new allergen source for patients allergic to green kiwifruits because of the presence of common allergens and the IgE cross-reactivity to green kiwifruit.[91] Fescue meadow pollen cross-sensitise
to kiwi fruits. This was found by Gavrovic-Jankulovic and associated scientists at the Department of Biochemistry from the University of Belgrade using the sera from polysensitized patients with specific IgE to grass pollen and kiwi fruit. According to their findings a 24 kDa kiwi glycoprotein represent potential major allergen, which share common epitopes with Fes p 4 and 36kDa meadow fescue allergen. [92]
Rye, timothy and mugwort pollen and kiwi allergy
The cross-reactivity to birch, rye, timothy, and mugwort pollen (Artemisia vulgaris) with kiwi was studied by Rudescko and associated scientists at the the Institute of Clinical Immunology, at the University of Jena, Germany.
They found that an extract of kiwi was able to bind immunoglobulin E from kiwi-allergic patients in the immunoblots and EIA. Immunoblots results revealed a broad spectrum of IgE specificities; 12 allergens were identified within a range of 15 to 94 kDa, 10 of which cross-reacted with birch, timothy, rye, and mugwort pollen, while two (25 and 30 kDa) were not inhibited homologously by pollen. EIA additionally revealed kiwi-specific allergens. Three proteins of the kiwi extract (25, 30, and 43 kDa) were considered to contain a carbohydrate miety.
Profilin seems to be relevant in cross-reactivity of kiwi allergens. [93]
People who are allergic to birch pollen react also to peanuts, hazelnuts, apples, strawberries, carrots, celery and pulses. Certain proteins in these foods are so similar in structure to the protein in birch pollen that triggers the allergy that the body manifests such cross allergy. According to Professor Dr. Dr. Andreas Hensel, President of the Federal Institute for Risk Assessment (BfR).BfR stresses that such cross allergy with soy products are possible.
The trigger of the cross allergy to soy is a protein (the PR-10 stress protein Gly m 4), which is found in soybeans and is similar in structure to the birch pollen allergen Bet v 1.
The activity of the soy protein Gly m 4 can be dampened through heating to high temperatures or the protein itself can be destroyed. Allergy sufferers can, therefore, eat most products with soy ingredients which were heated during processing without suffering any health disorders.
BfR does not believe that it makes sense for the packaging of soy products to carry additional warnings for allergy sufferers. Not all soy products contain the protein Gly m4 that triggers the allergy. At the present time, no official detection method is available. Furthermore, besides soy numerous other foods such as peanuts could trigger severe cross allergy in people with a birch pollen allergy. They include apples, hazelnuts, and celery. Warnings on soy products would not, therefore, protect people who are allergic to birch pollen from a cross allergy.
| Food |
Allergen |
IUIS |
Chemical Structure |
|---|
| |
|
Nomeclature |
|
| Milk |
beta-lactoglobulin |
|
|
| |
alfa-lactalbumin |
|
|
| |
Caseine |
|
|
| |
Serum albumin |
|
|
| |
Immunoglobulins |
|
|
| Chicken egg |
ovomucoid |
Gal d 1 |
Glycoprotein |
| |
Ovalbumin |
Gal d 2 |
Glycoprotein |
| |
Conalbumin |
Gal d 3 |
Glycoprotein |
| |
Lysozyme |
|
|
| |
Ovomucin |
|
Glycoprotein |
| |
Apovitellenin I |
|
|
| |
Apovitellenin IV |
|
|
| |
Livetin |
|
|
| |
Alfa-livetin |
|
Serum albumin |
| |
Beta-livetin |
|
|
| |
Gama-livetin |
|
|
| |
Phosvitin |
|
Glycophosphoprotein |
| Cod |
Allergen M |
Gad C 1 |
Glycoprotein |
| Common shrimp |
Antigen-I |
|
Glycoprotein |
| |
Antigen-II |
|
Glycoprotein |
| |
Sa-I |
|
|
| |
Sa-II |
Pen i-1 |
Trompomyosin |
| |
Sa-III |
|
tRNA |
| |
|
Pen a 1 |
Trompomyosin |
| |
|
Pen s 1 |
Trompomyosin |
| |
|
Met A 1 |
Trompomyosin |
| |
|
Par f 1 |
Trompomyosin |
| Peanuts |
Arachin |
|
Glycoprotein |
| |
Conarachin |
|
Glycoprotein |
| |
|
Ara h 1 |
Glycoprotein |
| |
|
Ara h 2 |
|
| |
Aglutinin |
|
|
| |
Peanut 1 |
|
Glycoprotein |
| |
Concanavalin-A-reactive |
|
Glycoprotein |
| |
glycoprotein |
|
|
| |
wheat germ-lectin-reactive |
|
Glycoprotein |
| |
material |
|
|
| Soybean |
Glycinin |
|
Protein |
| |
Beta-conglycinin |
|
Glycoprotein |
| |
2S-Globulin |
|
|
| |
Kunitz Soybean |
|
|
| |
Trypsin inhibitor |
|
|
| Wheat |
|
Tri v BD 47 |
Protein |
| |
|
Tri v BD 17 |
Protein |
| |
|
Tri v BD 15 |
Protein |
| |
0.28 alfa-amylase- inhibitor |
|
|
| |
Alfa-amylase-inhibitor |
|
Protein |
| |
WTAI-CM 16 |
|
|
| Barley |
Alfa-amylase (BMAI-1) |
|
|
| |
BTAI-CMb |
|
|
| Rice |
RP16KD |
|
|
| Tomato |
Profilin |
|
|
| |
Polygalacturonase 2A (PG2A) |
|
|
| |
Beta-fructofuranosidase |
|
|
| |
Superoxide dismutase (SOD) |
|
|
| |
pectinesterase (PE) |
|
|
| Avocado |
Prs a 1 |
|
Hevein-like domain |
| |
|
|
peptides |
| Mustard |
Sin a 1 |
|
2s-albumin |
| |
Bra j IE |
|
2s albumin |
| Kiwi |
24kDa kiwi glycoprotein |
|
Glycoprotein |
| |
43-kDa |
|
|
| |
Actinidin Act c 1 |
|
|
| Strawberry |
20/18-kDa |
|
homologues to Bet v 1 |
| Banana |
Class I chitinases |
|
|
| |
with hevein-like domain |
|
|
| |
33kDa |
|
|
| |
37 kDa |
|
|
| Appel |
Skin-allergen Mal d 1 |
|
Protein similar to |
| |
|
|
Bet v I (birch) |
| Food |
Allergen |
IUIS |
Chemical Structure |
|---|
| |
|
Nomeclature |
|
Starlink maize was developed inserting the Cry9C-gene
turning it resistant to plague insects. Starlink had been approved for use in feed and industrial uses, not for human consumption due to Cry9-protein potential's to cause allergic reactions. In September 2000 taco-shells in retail-stores contained meal from StarLink corn were found, triggering a recall. Aventis had to buy back all harvested Starlink maize as well as Starlink sowing seed.
In July 2001 EPA expert panel concluded that Starlink maize could result in allergy and decided that it should not be used for human consumption (www.epa.gov/scipoly/sap/). As contamination of maize for food purposes with fodder maize can not be avoided, cultivation of Starlink was no longer allowed. Although traces of Starlink can still be expected in the food chain, it has never been detected in products on EU-markets.
Carsten Bindslev-Jensen and colleagues studied the possible allergenicity of a wide variety of enzyme classes and origins, including enzymes produced by genetically modified organisms using prick test, histamine release and oral challenges.
Some positive skin prick test result or a positive histamine release were not supported by oral challenges using exaggerated dosages of the enzymes, and the findings were seen without clinical relevance.
No allergenic findings of clinical relevance were related and the authors concluded that ingestion of food enzymes in general is not considered to be a concern with regard to food allergy.
Current legislation allows manufacturers to use substances known as processing
aids during bread production without declaring so on the label. The "Real Bread
Campaign" says that these ingredients include enzymes such as xylanase,
transglutaminase, hemicellulase, phospholipase and fungal alpha-amylase some of
which are known allergens or may be produced using substances of animal or GM
origin.
Bakery enzymes are used to extend the shelf-life of baked goods, maintain bread
volume, crumb softness, crust crispiness and improves browning. Such enzymes
are:
- Amylases which convert starch to sugar and produce dextrins.
- Oxidases strengthen and bleach the dough.
- Proteases and hemicellulases reduce gluten elasticity.
- Hemicellulases improve gluten strength.
The Campaign stresses that the only essential ingredients of basic leavened
bread are flour, water and yeast, to which a small amount of salt may be
added, The campaign calls on bread producers to to stop the use of processing
aids during bread production or include a declaration of any and all added
enzymes and other processing aids used. The EU regulation 1331/2008 demands that enzymes used as
processing aids must be approved prior to their use. Approval was not required
before December 2008 [98].
Christophe Frossard and Philippe Eigenmann from the University Hospital of Geneva in a study published in March 2007 found that Lactococcus lactis, bioengineered to deliver murine IL-10, can decrease food-induced anaphylaxis. According to the authors, this may provide an option to prevent IgE-type sensitization to common food allergens. The anti-inflammatory interleukin-10 (IL-10) is a potential regulator for food tolerance.
The researchers administered the transfected Lactococcus lactis to mice and induced oral sensitization with beta-lactoglobulin in the presence of cholera toxin. Anaphylaxis and blood levels of antigen-specific immunoglobulin E (IgE) were found to be significantly reduced in mice which had received the L. lactis strain.
Liem and colleagues (2007) in a Canadian study, found that immaturity of the gastrointestinal tract or immune response of prematurity and low birth weight does not change the risk for development of IgE-mediated food allergies allergy in childhood.
The researchers disagree with previous studies indicating that at an age less than 3 years the immature gastrointestinal tracts result in an increased uptake of food antigens, increasing the risk for sensitization but in this study they found that food allergy was associated with a maternal history of asthma and food allergy.
The authors write that a development of immunologic tolerance of the immature immune system to orally ingested allergens may take place, preventing sensitivation.
They call for more studies to find out how early exposure to food antigens, such as pre- and probiotics traces of peanuts, may protect premature children by increasing immune tolerance to those antigens.
The PARSIFAL study - Prevention of Allergy Risk factors for Sensitisation in Children related to Farming and Anthroposophic Lifestyle
-looked at farm children from rural and suburban communities in Austria, Germany, the Netherlands, Sweden and Switzerland.
Waser and colleagues report that consumption of farm milk, whether boiled or not, was associated with a reduction in the occurrence of asthma by 26%, hay fever by 33%, and food allergy by 58%. No effect was observed for eczema. Other farm-produced products were not related to any allergy-related health outcome.
It is not know what components of the raw milk may be responsible for such effects, but it could be linked to the pathogenic and non-pathogenic microbe levels in the milk, a kind of action observed with probiotic bacteria which may reduce the risk of certain allergies.
The authors, however, warn that raw milk may contain pathogens such as salmonella or enterohaemorrhagic E coli and they do not recommend to drink unheated milk. The authors call for more studies on the omega-3 fatty acids profile in addition to the microbial content of the farm milk.
Soy is a common dietary constituent and allergic reactions to soy proteins are well described. Soy allergy prevalence studies are lacking, estimated prevalences are about 0.5% in the general population with about 3-6% of allergic children being allergic to soy proteins. Clinical reactions are similar to those observed with other major food allergens, such as milk, egg or peanut and include systemic anaphylaxis.
The ADM and Cargill asked for an exemption of allergy warning for natural mixed tocopherols (vitamin E, E306) and a range of D-alpha tocopherols acetate and succinate derived from vegetable oil (soybean oil). Natural mixed tocopherols are mainly used as antioxidants in fatty foods at a concentration of about 50 mg/kg (referring to the fat fraction of the specific food). Natural mixed tocopherols are also used as dietary supplements.
The application covers phytosterol esters produced from vegetable oil (soybean oil). Phytosterol esters are currently commercially available in selected foods in several EU countries. The EU regulations limit exposure to a maximum of 3 grams per day of phytosterols through labelling requirements and maximum concentrations in certain food categories in order to avoid intakes above the recommended limits from multiple sources of intake. Plant sterols under consideration are derived from soybean oil deodorised distillates.
Considering the information provided by the applicant regarding the starting material, the subsequent production process, and the demonstration of low residual protein content, the Panel of the European Food Safety Authority considers that it is unlikely that natural mixed tocopherol/D-alpha tocopherols from soybean sources and vegetable oils derived phytosterols and phytosterol esters from soybean sources will trigger a severe allergic reaction in susceptible individuals. The mixed tocopherols from soybean will therefore exempted from labelling of allergy warning.
Since wheat is relevant both as a source of epitopes known to induce coeliac disease and as a source of allergens triggering wheat allergy, it is appropriate to investigate wheat products, namely wheat starch hydrolysates, for their potential to induce coeliac disease or trigger wheat allergy.
The Association des Amidonneries de Cereales de l'Union Europeenne AAC provides information on wheat starch hydrolysates, particularly concerning the potential effects of wheat-based glucose syrups including dextrose in coeliac disease and wheat allergy. The history of safe use of wheat-based glucose syrups including dextrose is claimed based on the safe use of wheat starch-based gluten-free diet in coeliac disease.
Wheat-based glucose syrups including dextrose may contain low levels of proteins and peptides. It is not known at which levels of intake glucose syrups including dextrose would cause allergic reactions in wheat-allergic individuals. Nevertheless, taking into account all the scientific information provided and in particular the levels of wheat proteins reported in glucose syrups including dextrose, the Panel considers that it is not very likely that this product will trigger a severe allergic reaction in susceptible individuals.
For coeliac disease, assessment of the evidence provided including a new clinical study indicates that wheat-based glucose syrup is unlikely to cause an adverse reaction in individuals with coeliac disease provided that the (provisional) value of gluten considered by Codex Alimentarius for foods rendered gluten-free is not exceeded.
The Codex Standard for Gluten-Free Foods (Codex Stan 118-1983) specifies that the nitrogen content of food ingredients derived from gluten containing cereals may not exceed 0.05 g per 100 g on a dry basis (or 0.31 % protein/ds, Nx6.25), when they are used in a gluten-free food. [107]
Wheat (i.e. all Triticum species, such as durum wheat, spelt, and kamut), rye
and barley, have been identified as grains that are scientifically reported to
contain gluten. The gluten present in those grains can cause adverse health
effects to persons intolerant to gluten and therefore should be avoided by them.
Different people with intolerance to gluten may tolerate variable small amounts
of gluten within a restricted range. In order to enable individuals to find on
the market a variety of foodstuffs appropriate for their needs and for their
level of sensitivity, a choice of products should be possible with different low
levels of gluten within such a restricted range.
Under the new European Union regulation (EC) No 41/2009 of 20 January 2009 , two
claims are allowed: A maximum of 20 parts per million
of gluten are allowed. These products are intended for those who are extremely
sensitive to gluten. This declaration is allowed for
products which have up to 100 ppm of gluten. Foods with this label can be used
by persons which are less sensitive to gluten.
The claims of gluten specified in EC 41/2009 were also adopted in the Codex
Standard Codex Stan 118-1979, in the version of 2008.
The Association of European Coeliac Societies (AOECS) was founded in 1988. This
Association reviews problems of international importance, coordinates
international activities and matters of common interest of the members and
favours the exchange of information among the members for the benefit of
Europeans affected by the coeliac condition or dermatitis herpetiformis.
Early diagnosis and strict maintenance of a gluten-free diet will
significantly reduce the risk of problems associated with coeliac disease
stresses, says the Association of European Coeliac Societies (AOECS)
According to the Association population screening is the only way to identify
the majority of CD patients. A combination of serology and HLA-typing is the
only definitive way to screen for coeliac disease; a combined diagnosis
accounting for symptomatic, silent and latent CD patients aims for a 100%
specificity and sensitivity.
European Commission, therefore, designated 9.5M EUR towards research and
innovation for the diagnosis, monitoring and management of Coeliac Disease (CD).
The CD-MEDICS Integrated Project-Coeliac Disease Management Monitoring and
Diagnosis using Biosensors and an Integrated Chip System developes a
lab-on-a-chip device. In this system a drop of blood on a card is subjected the
a microstructured fluidic network of reagents. The special surface of the card
captures biological components being looked for and are detected by a sensor.
This enables a fast diagnosis of population screening, based on the combination
of serology and Human Leukocyte Antigen-typing (HLA-typing).
Biosensor devices also can precisely measure blood glucose using biosensor
for detecting blood glucose and other biological molecules using hollow
structures called single-wall carbon nanotubes anchored to gold-coated
"nanocubes." The device resembles a tiny cube-shaped tetherball anchored to
electronic circuitry by a nanotube. Timothy Fisher, from the Purdue
University develops such devices using nanotechnology, similar to the European
Project to monitore Coeliac Disease.
According to Fischer, the sensing portion of the system, the nanocubes,
extend out from the rest of the device and can more easily come into contact
with target molecules enhancing sensitivity.
Contrary to other sensors the nano-tetherball biosensor can detect wide range
of concentrations whereas other sensors work only in narrow rages of specific
concentrations.
The researchers grow nanotubes on a porous anodic alumina template. Paladium
nanocubes, coated with gold,are also formed. They are then connected with
biotin-streptavidin combination which is already being used to analyse
biological samples. Replacing the biotin with glucose oxidase the sensor became
sensitive to glucose concentrations. The enzyme causes an electrochemical
reaction in the presence of glucose and oxygen, generating an electrical signal,
explain the authors.
Accomando and colleagues 2010 reviewed the laboratory findings, histology
passing and genetics. The gluten is the main environmental factor targeting a
complex genetic background. HLA genes and also not HLA related genes are
supposed to increase the risk to the disease. Serological markers may monitor the
disease and a safe and effective gluten free diet. Special interest is given to
histology, where intra epithelial cell infiltration by several lymphocyte subsets
may increase further knowledge of the pathogenesis of the disease.
According to Hadjivassiliou and colleagues 20101 there are many manifestations of
the autoimmune disease to ingested gluten, among which the best known is coeliac
disease. The authors reviewed the neurological manifestations which leaded to
the concept of extraintestinal presentations of gluten sensitivity without
enteropathy. Rubio-Tapia and colleagues 2010 stressed that nearly 1% of the population
suffer from coeliac disease, and many remain undetected. The number of cases
increases. Mortality risk may be increased if not diagnosed. The genetic
pathway and the overlap with type 1 diabetes mellitus are explained. The
authors point out that diagnostic using novel deamidated gliadin peptides
antibodies produce better results than native gliadin-based tests.
In a review of 2008 Leeds, Hopper and Sanders report that in spite of the
development of more sensitive and specific serological markers diagnosis should
always be confirmed with a duodenal biopsy. Strict, lifelong gluten-free diet is
essential, however, alternatives to the gluten-free diet are about to go into
clinical studies. The authors also point to the controversy on complications of
coeliac disease, such as neurological effects,which are not widely accepted.
[116]
A life-long gluten-free diet is challenged in cases such as 'silent' and 'latent'
patients is under discussion, and tolerance to gluten may be acquired later in
life, but must be accompanied by a strict follow-up. The amount of gluten
permitted in gluten-free products is being discussed, however, the daily amount
of gluten that can be safely consumed is not defined. Oath are seen to be
tolerated by most patients with coeliac disease.
Rashtak and Murray 2009 stress that coeliac disease can affect people of any
age. The authors assessed the prevalence, clinical features, diagnosis, and
consequences of celiac disease in the elderly and adjusted particular
nutritional and nonnutritional to the needs of this group.
Mukherjee and colleagues 2010 compared coeliac disease effect in the elderly to
that of a population of young adults with coeliac disease. Diarrhoea was the
main presenting symptom in both groups. Autoimmune disease prevalence, the
degree of villous atrophy and prevalence of bone disease was similar in young
adults and in the elderly, but thyroid disease and neuropathy were more common in
the older group.
Neurological disorders occur with a frequency of up to 10% in patients
presenting symptoms of coeliac disease, and may also be the only symptom of
gluten sensitivity. Hadjivassiliou and colleagues 2008 identified a neuronal
transglutaminase isozyme which is the target of the immune response in
patients with such neurological dysfunction. The authors found that
anti-transglutaminase 2 IgA is linked with gastrointestinal disease, an
anti-transglutaminase 6 IgG and IgA response is prevalent in gluten ataxia,
independent of intestinal involvement.
The authors suggest that antibodies against transglutaminase 6 can serve as a
marker in addition to human leukocyte antigen type and anti-gliadin and
anti-transglutaminase 2 antibodies may identify patients with gluten
sensitivity who are at risk of neurological disease.
De Vivo and colleagues in a review 2009 discuss the role of transglutaminases
in neurodegenerative diseases. The authors point out that transglutaminase
TG2 is involved in the molecular mechanisms of celiac disease, and is also
engaged in human neurodegenerative diseases such as Alzheimer's disease,
Parkinson's disease, supranuclear palsy, Huntington's disease polyglutamine
diseases and others.
Armstrong, Robins and Howdle 2009 stress the high risk of siblings of coeliac
patients. Negative coeliac serology of these siblings can, however, are an
affirmation that they are very unlikely to develop the disease. Developments
in serological antibody testing turns screening programmes in the community
possible, however, early introduction of a gluten-free diet remains the best
action to reduce the risk of coeliac related complications. The authors point
out that altering the toxicity of cereal proteins opens promising alternatives
for the future.
Rawal and colleagues 2010 evaluated the plasma levels of zinc in deficient
patients with coeliac disease. The researchers found that plasma levels of zinc
were similar between patients which received gluten free diet without zinc
supplementation and a group of patient which received gluten free diet with zinc
supplementation. Plasma zinc levels rose in both groups and did not depend on
supplementation. The authors concluded that zinc levels rise with gluten free
diet and do not depend on supplementation.
Sealey-Voyksner and colleagues 2010 presented a new specific and sensitive
non-immunological liquid chromatography-mass spectrometry (LC-MS) based assay to
detect and quantify trace levels of six wheat gluten peptides in food and
consumer products. At present, immunochemistry is the leading analytical method
for gluten detection in food. Consequently, enzyme-linked immunosorbent assays
(ELISAs), such as the sandwich or competitive type assays, are the only
commercially available methods. The news LC-MS method detects and quantifies select target peptides in food over a range from 10pg/mg to 100ng/mg.
Vermeersch and colleagues 2010 report that the detection of IgG antibodies
against deamidated gliadin peptides (DGP) assays is more sensitive and more
specific for celiac disease than detection of IgG antibodies against native
gliadin. The authors compared these assays and found that the diagnostic accuracy
of the IgG anti-DGP assays was comparable to the diagnostic accuracy of the IgA
anti-tTG assays. The sensitivity of the IgG anti-DGP assays was significantly
better than sensitivity of the IgG anti-tTG assays and the specificity was better
than the IgA and IgG anti-gliadin assays.
Volta and colleagues 2010 compare the performance of DGP antibodies with that
of tTG antibodies. In coeliac disease, deamidation of gliadin peptides is induced by tissue transglutaminase (tTG). Serological tests based on the
detection of antibodies to deamidated gliadin peptides (DGP) have been
developed. although both tests represent a very good tool for identifying
coeliac patients, tTG antibodies display a higher predictive value than DGP
antibodies, and must still be considered the best serological test for CD
screening.
Volta and colleagues, in another recent study,recommend the combined search for
IgA tTGA and IgG DGP-AGA to provide the best diagnostic accuracy for coeliac
disease, reducing the number of tests and improving cost-efficacy. [127]
Duerksen and Leslie 2010 write that low bone density and osteoporosis is
associated with celiac disease. The authors stress that serological testing with
tissue transglutaminase (TTG) and immunoglobulin A endomysial (EMA) antibodies is
highly specific for celiac disease, while antigliadin antibody (AGA) testing is
less specific. Higher prevalence of osteosporosis and lower bone density in
TTG/EMA seropositive women compared with seronegative women were found by the
authors. Isolated AGA seropositivity showed no significant association with any
bone density measurements.
Arranz and Garrote point out that it is widely accepted that coeliac disease is based on adaptive immunity after T CD4(+)lymphocyte stimulation by tissue
transglutamine-modified gluten peptides and HLA-DQ2/DQ8 restriction, which
produce proinflammatory cytokines. Gluten also activates innate immunity and
epithelial cytotoxicity mediated by intraepithelial lymphocytes. The authors
stress that perception of serological and immunogenetic markers increased the
knowledge of coeliac disease and led to a reevaluation of diagnostic of the
disease in adults with minimal or atypical disease expression.
Hershcovici and colleagues 2010 state that coeliac disease is frequently
diagnosed after a long delay-period resulting in increased morbidity and
mortality. Mass screening for coeliac disease of the young-adult general
population to improved life quality and is a cost-effectiveness strategy is
being suggested. Rising awareness of health-care professionals is also being
mentioned as an alternative to mass screening, say the authors.
Kearby and colleagues report a case of pernio or chilblains a rare condition,
presenting blue toes exposed to cold or humid environments. Pernio is associated
with variety of systemic conditions such as cryoglobulinemia and celiac disease.
In the present case diagnosis of coeliac disease was confirmed. Medication and a
gluten free diet was successfu
BfR recommends strictly limiting levels in leather goods.
Studies by the regulatory authorities of the federal states reveal that many leather goods like gloves, shoes or watch straps which come into direct contact with the skin contain high levels of chromium (VI). Hexavalent chromium is a strong allergen and it can lead to allergic skin reactions like contact eczema in sensitised individuals. The typical clinical picture is allergic contact eczema on the areas of the skin which come into contact with chromium (VI). Clothing which has direct skin contact should not, therefore, contain any chromium (VI).
Even the lowest levels of chromium (VI) in leather are sufficient to trigger an allergic reaction in hypersensitive individuals. At a level of 5 mg per kg leather half of the sensitised individuals already manifested allergic skin reactions like for instance contact eczema. The only effective protection for them against skin disorders is to avoid any contact with products containing chromium (VI).
At the present time the chromium content of leather goods has not been regulated by law apart from industrial safety provisions. In 2006 a DIN standard stipulated that the chromium (VI) levels in work gloves must be below the detection limit of three milligrams chromium (VI) per kilogram leather.
In more than 50% of leather goods such as gloves and shoes and other ware which is worn close to the skin like watch straps, chromium IV was found up to 10 mg/kg.
Normally, chromium (III) sulphate is used as the tanning agent. Chromium (VI) either appears as an impurity in the tanning substance or it is formed through oxidation from chromium (III) in the ensuing processing stages. There are methods available which can considerably reduce the chromium levels in the leather or even completely remove the chromium (VI). Chromium-free tanning methods are another option.
Chromium free leather processing or mandatory declaration
The BfR believes that leather goods that come into contact with skin should not, if possible, contain any chromium (VI). At the very least, the levels should be reduced as far as possible. At the present time, the analytical detection limit is approximately 3 mg per kg leather. The studies by the regulatory authorities and the standard for work gloves prove that this limit can be complied with by using the corresponding technologies.
On the other hand, mandatory declaration could help allergy sufferers to consciously avoid purchasing products containing chromium (VI).
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