Doctors

Allergies > Doctors: Avoiding allergies

For the General information on Avoiding allergies

Avoiding Allergies

The progression and severity of allergic rhinitis are both correlated with environmental concentrations of the allergen causing the disease.

Studies involving movement of allergic patients to high altitude environments (where allergen exposure levels are low) and those following natural variations in allergen exposure have shown that lowering allergen concentrations can improve allergic disease symptoms. Most clinical trials of allergen avoidance strategies have been small, short-term, and poorly designed, but a few have shown successful allergen reduction with some clinical benefit in allergic patients.

The following sections recommend methods of avoiding particular allergens. Patients will vary in their willingness to employ these methods, and this will be influenced by the extent of action needed, their attitude to taking pharmacological treatments, and the severity of their disease. If necessary, allergen avoidance can be combined with therapeutic treatment.

Patients should also be advised to avoid general irritants such as cigarette smoke.

Please review the list below to find out more information on how to avoid exposure to:

- house dust mite allergens

- pet allergens

- pollen allergens

- indoor mould allergens

Product advertisements bombard us with the well-publicized allergy symptoms of sneezing and water eyes - but allergies are much more than a sneeze. Do you get headaches? what about stomachaches? Does your child seem overactive? Do their grades fluctuate? Is your sleep disturbed? Do you or your child experience cognitive fog, items when you can't think clearly? Do you eat a meal and then get indigestion because you ate too much? It could be WHAT you eat!

Food and inhaled allergies seriously impact our health. Recent studies (Brostoff, 1989; Darlington & Mansfield, 1983: Galland, 1989; Jaff, 1994; Marshall & Stroud, 1984; O'Banion & Armstrong, 1978; Rapp, 1978; Rapp, 1991; Ratner & Vigder, 1985; Schauss, 1981) implicate food allergies in profoundly affecting many behaviors, characteristics, and health concerns.

There are over seventy distinct food and environmental allergy symptoms.

The concept that the food we eat can provoke immunotoxic reactions deserves attention. Digestion is often assumed to be healthy: completely breaking foods into their elemental amino acids and peptides, glycerides and fatty acids, sugars, vitamins, minerals and cofactors. In healthy people, this is how digestion works. In people with chronic health problems, from myofacial and joint pain to irritability; from fatigue to chronic illness, disorder to digestion is the rule, occurring 82-100% of such cases (the more carefully digestive competence is studied, the more defects are documented). From dysbiosis to maldigestion, from abnormal mucous production to repair defects in the intestinal wall; from absorption uptake block to enteropathy disorders of digestion make immunoreactive digestive remnants available for attack on the internal immune defense and repair systems of the body. While maldigestion underlies these problems, the signs and symptoms of ill health are often systemic. Further, the translocation of intestinal antigens are known to be disruptive of host immune competence. Without overt intestinal symptomatology, many clinicians do not include immunologic provocation by digestive remnants in their differential diagnosis.

Cows milk, chicken egg, wheat, corn, soy and peanut sensitivity are common immunoreactors. This is partly due to their being complex, difficult-to-digest foods and partly to their common inclusion in processed, restructured foods. Previously, diagnosis has been difficult because accurate, patient-predictive specific information about reactive substances has been lacking.

Polls of nursing mothers show, for example, that over 75% drink approximately a quart of cow' milk a day, and eat eggs, wheat, soy, peanuts and corn on a regular basis. Moreover, women who do not breast feed their infants are likely to be giving them formulas that contain cow's milk or cow's milk proteins (whey, casein, lactoglobulin), and/or soy milk and corn syrup. In addition, when solid foods are started, most parents introduce cow's milk products (such as milk, ice-cream or cheese), wheat, corn, and eggs during the first year of life. Is this healthy? Probably not. These are complex, difficult-to-digest foods, especially for the still developing infant digestive tract which does not mature for 1-2 years. The immature intestine is highly permeable, designed for oligoantigenic breast milk. Given the digestive remnants commonly left in the child's intestine, the common association of food allergies/hypersensitivities to these foods are predictable.

The term food sensitivity/hypersensitivity (FS) can be defined as "a clinical manifestation of an immulogical response in which foods, their proteins, or their metabolic derivatives act as antigens and stimulate the production of antibodies (or cellular responses) against them". For example, in the case of cow's milk allergy (CMA), the proteins may be B-lactoglobulin, casein, or bovine immunoglobulin, casein or bovine immunoglobulin G (IgG), among others. There are two different types of immulogic response, depending on the clinical appearance: immediate or delayed. Some infants and/or children develop clinical manifestations in less than one hour, and indication of a Type 1, or immediate hypersensitivity reaction; this type of response is typically indicated by elevated total serum immunoglobulin E (IgE) and antigen-specific IgE Radio-allergosorbent (RAST) values. The short time between exposure and symptom provocation makes careful history useful in identifying offenders. However, more commonly infants/children exhibit a late or delay-in-onset response with clinical symptoms appearing later, from hours to days after exposure. In the past, most food allergies were believed to be IgE-mediated, but most infants were proven CMA/FA do not fall into the Type 1, immediate (IgE) category, but rather exhibit delay-in-onset responses of Type 11, 111 or 1V reactions. Unfortunately, these differences in timing and the fact that many of the symptoms are not always associated with an allergic ediology make diagnosis frustrating for the parent and difficult for the doctor. Thus, CMA and FS often escape recognition, especially when the symptomatic response is long delayed.

The symptoms and sign of CMA/FS are many, and children may suffer a variety of health consequences.

The most common clinical manifestations are:

cutaneous or skin-related, with eczema and urticaria;

gastrointestinal colic, vomiting (including projectile vomiting), diarrhea, and/or constipation;

respiratory wheezing/asthma, recurrent bronchitis, sinusitis, nasal congestion or rhinitis;

unexplained fatigue; and

myalgic, fibrositis or arthralgic pain.

However, recurrent middle ear disturbances, failure to thrive, anorexia, behavioral disorders, and/or musculoskeletal aches are also common. The frequency of CMA/FS in infants with no special family antecedents if reported range between 2.2 and 7%, and approached 25% when childhood eczema is present. Unfortunately, the diagnosis of CMA/FS is frequently not made until many months of unsuccessful therapies have been attempted to reduce symptoms. The possibility that CMA/FS may actually be the problem is too often considered only when other explanations for recurrent symptoms cannot be found. Many mothers report frustration about making numerous trips to their pediatrician without success. Only after proper laboratory diagnosis and substitution for the offending food(s) does the reactive child begin to thrive and behave in a normal, healthy fashion. One mom who experienced the maze of food allergies with her children said

"We bring these wonderful children into the world and in our hearts we want to do the best of everything for them. If we know that dairy, corn, and wheat are the most common allergens, why feed them to our kids? Why not avoid those foods for at least the first year? This may help to create a better balance in their overall growth and immune defenses in the future."

We think this is a sound and sensible approach.

Of all the substances, cow's milk seems to provoke the major health problems during the first year of life. Interestingly, the first indication that cow's milk may not be suitable for infants was noted long ago. Around the 1800s, if a mother was unable to nurse and a "wet-nurse" could not be employed, many infants were fed directly from the udder of cows, goats, or asses. Although infant mortality was extremely high in non-breast fed babies, the rates were lowest in infants fed ass-milk and highest among those fed cow's milk. More such evidence related to the health consequences of cow's milk emerged over the next decades.

As noted above, one clinical manifestation of CMA is middle ear disturbances or infections, and in the 1970's a physician stated that far too many children have tubes put in their ears before allergy is even considered. Today, as in the past, recurrent ear problems are often diagnosed as infections and treated unsuccessfully by prescribing antibiotics and then surgery, when in fact CMA was the problem. Most mothers would be willing to remove milk from their diet before submitting their infant to unnecessary surgery, if there were even a remote chance for success. In addition to its effects on ears, milk is regarded as the food most frequently associated with asthma, either as a causative or exacerbating agent. Some physicians believe that every patient in whom asthma is poorly controlled should be taken off milk products for at least a trial period of three weeks. Finally recent evidence suggests an association between cow's milk feeding in infancy and the subsequent development of juvenile onset diabetes. Clearly there is no harm in avoiding milk products during the first year, and there is a good chance that doing so will decrease the likelihood of having your infant, toddler, or child suffer needlessly, undergo useless therapies or invasive procedures, and/or develop other related diseases later on. It seems wise to attempt dietary approaches first.

COMMON CLINICAL SIGNS OF CMA/FS

Otis media, recurrent
Colic
Diarrhea with or without alternating diarrhea
Enteropathy (intestinal atrophy)
Headaches (chronic or migraine)
Hyperactivity
Attention Deficit Disorder
Flu, recurrent
Muscle aches, recurrent
Rhinitis
Sinusitis
Allergic 'shiners'

House Dust Mites Allergens

House dust mites infest warm, humid places such as mattresses, bedding, rugs, clothing, and upholstered furniture. The faecal particles of mites, found on house dust, contain most of the allergenic activity of dust mites.

As exposure is usually continuous throughout the year, house dust mites cause perennial allergic rhinitis. The heaviest exposure occurs when a person lies down to sleep.

- Many house dust mite allergens have been isolated; Der p I comprises up to 95% of the allergen content of mite faeces

To reduce exposure to house dust mite allergens, the following measures can be recommended (obviously only people with severe disease will be willing to carry out the more drastic of these). The bed is probably the most important site of allergen exposure, and the relative ease and success of interventions aimed at this site makes it a key target for allergen control.

- Wash bedding weekly at 60°C or higher*

- Encase bedding, box springs, and mattresses in fine weave, plastic, or vapour-permeable covering*

- Remove stuffed toys from beds

- Damp-clean furniture in bedrooms

- Vacuum clean weekly: ideally this should be done by a non-allergic person in the household; when this is not possible, suggest that the patient wears a mask whilst vacuuming and leaves room for 20 min afterwards

- Reduce indoor humidity* (most successful in climates with low humidity and well sealed houses)

- Use of acarides (eg benzyl benzoate, tannic acid) to reduce mite populations (reported outcomes vary, but clinical benefits unlikely)

- Replace carpets with wood flooring*

- Replace curtains with blinds

- Replace upholstered furniture with leather, vinyl, or wooden furniture

- Avoid living in basements

*has been proven to reduce allergen concentrations

Pet Allergens

The best way to avoid pet allergens is to find the pet a new home. Most pet owners are unlikely to consider this. The following actions should therefore be recommended:

- house the pet outside

- restrict the pet to certain areas, particularly those with hard floors rather than carpets (when cats are removed from rooms, aeroallergen levels drop by 70%)

- use high-efficiency air cleaners (was found to improve symptoms in asthmatic children sensitised to cat or dog allergens)

- if possible, wash the pet weekly (although a blinded, controlled study found that washing cats weekly did not reduce allergen exposure)

- replace carpets with wood flooring (carpets accumulate cat allergen much faster than wooden floors)

Pollen

Pollen is a very common allergen.

Grass, tree, and weed pollen can cause seasonal allergic rhinitis in areas in which these plants have seasonal pollen production. Familiarity with the pollinating season of local trees, grasses, and weeds will facilitate diagnosis.

- The length of seasonal exposure is dependent on geographic location and the plant species. The concentration of pollen in the environment also depends on weather variables (eg winds above 17 mph sweep pollen upwards and reduce ground exposure) and the aerodynamic characteristics of the allergens (eg smaller pollen grains tend to remain airborne for longer)

In some areas, pollen production may be continuous and can cause perennial disease. Patients can monitor pollen counts using weather forecasts.

Many pollen allergens have been isolated and characterised:

- Allergens from grass pollens are divided into 8 groups based on their physiochemical and immunochemical similarities. Major allergens have been found in groups I (eg rye grass, Lol p I) and V (eg timothy grass, Phl p I). Unlike ragweed and tree pollen allergens, grass pollen allergens show extensive cross-reactivity among different species. On skin testing with group I allergens, 90–95% of grass pollen-allergic individuals show reactivity

- Of the weed pollens, ragweed pollen is the most well studied. 90–95% of ragweed-sensitive individuals have skin test reactivity to Amb a I and Amb a II allergens. Cross-reactivity between ragweed and certain foods, eg melon, cucumber, and squash has been reported

- Allergenic fractions of trees are less well studied. Major allergens of birch, hazel, alder, and hornbeam are Bet v I, Cor a I, Aln g I, and Car b I respectively. The birch allergen has cross-reactivity to certain foods eg apple, pear, celery, carrot, and potato

Avoidance of pollen allergens is difficult, but the following actions can be recommended:

- keep house and car windows shut during the day in the pollen season

- use air conditioning

- restrict outdoor activities to later in the day, when pollen counts are lower

- avoid countryside when pollen counts are high

- take holidays by the sea during the pollen season as pollen counts are lower by the coast

Indoor Mould Allergens

Mould (fungi) spores

Mould spores (eg Alternaria and Cladosporium) may cause allergic rhinitis. These are not produced during distinct seasons, but as moulds tend to thrive in a moist environment, in temperate climates spore counts rise in spring with a peak in mid to late summer. In these situations they can cause seasonal allergic rhinitis. Perennial allergic rhinitis may be caused by continuous exposure to indoor mould spores.

- It is difficult to collect, identify, and prepare fungal extracts for diagnostic and therapeutic purposes. Determining the degree to which rhinitis symptoms are caused by fungal allergy is a problem due to the continuous production of spores

The following actions can be recommended to people affected by indoor mould spores:

- limit mould growth by maintaining relative humidity at 50% or less using an exhaust fan or dehumidifier

- remove mould with bleach

References

van Cauwenberge P, Bachert C, Passalacqua G, et al. Consensus statement on the treatment of allergic rhinitis. European Academy of Allergology and Clinical Immunology. Allergy 2000;55:116–134.

Boner AL, Niero E, Antolini I, Valleta EA, Gaburro D. Pulmonary function and bronchial hyperreactivity in asthmatic children with house dust mite allergy during a prolonged stay in the Italian Alps. Ann Allergy 1985;54:42–45.

Tovey E, Marks G. Methods and effectiveness of environmental control. J Allergy Clin Immunol 1999;103:179–191.

Cloostermann SG, Schermer TR, Bijl-Hofland ID, et al. Effects of house dust mite avoidance measures on Der p 1 concentrations and clinical condition of mild adult dust mite-allergic asthmatic patients, using no inhaled steroids. Clin Exp Allergy 1999;29:1336–1346.

Sheikh A, Hurwitz B. House dust mite avoidance measures for perennial allergic rhinitis (Cochrane Review). The Cochrane Library. Oxford: Update Software; 2001.

Eggleston PA, Bush RK. Environmental allergen avoidance: an overview. J Allergy Clin Immunol 2001;107:S403–S405.

Arlian LG, Platt-Mills TA. The biology of dust mites and the remediation of mite allergens in allergic disease. J Allergy Clin Immunol 2001;107:S406–S413.

van der Heide S, van Aalderen WM, Kauffmann HF, Dubois AE, de Monchy JG. Clinical effects of air cleaners in homes of asthmatic children sensitized to pet allergens. J Allergy Clin Immunol 1999;104:447–451.

Klucka CV, Ownby DR, Green J, Zoratti E. Cat shedding of Fel d I is not reduced by washings, Allerpet-C spray, or acepromazine. J Allergy Clin Immunol 1995;95:1164–1171.

Virant FS. Allergic rhinitis. Immunol Allergy Clin North Am 2000;20:265–282.