Allergic Rhinitis (Hay Fever and Rose Fever) and Chronic Nasal Congestion

Description

Alternative Names

Causes

The allergic process, called atopy, and its connection to asthma is not completely understood. It involves various airborne allergens or other triggers that set off a cascade of events in the immune system leading to inflammation and hyperreactivity in the airways. One description is as follows:

• The conductor in an orchestra of immune factors that contribute to allergies and asthma appears to be a category of white blood cells known as helper T-cells, in particular a subgroup called TH2-cells.
• TH2-cells overproduce interleukins (ILs), immune factors that are molecular members of a family called cytokines, powerful agents of the inflammatory process.

• Interleukins 4, 9, and 13, for example, may be responsible for a first-phase asthma attack. These interleukins stimulate the production and release of antibody groups known as immunoglobulin E (IgE). (People with both asthma and allergies appear to have a genetic predisposition for overproducing IgE.)
• During an allergic attack, these IgE antibodies can bind to special cells in the immune system called mast cells, which are generally concentrated in the lungs, skin, and mucous membranes. This bond triggers the release of a number of active chemicals, importantly potent molecules known as leukotrienes. These chemicals cause airway spasms, over-produce mucus, and activate nerve endings in the airway lining.
• Another cytokine, interleukin 5, appears to contribute to a late-phase inflammatory response. This interleukin attracts white blood cells known as eosinophils. These cells accumulate and remain in the airways after the first attack. They persist for weeks and mediate the release of other damaging particles that remain in the airways.

The Hygiene Theory: Early Infections as Protection Against Allergies and Asthma

An increasingly important theory blames the dramatic increase in asthma and allergies on the reductions in childhood infections that have occurred with modern hygiene and antibiotic use. The basic theory rests on the idea that infections stimulate production of specific immune factors called TH1 cells. As these cells build up, they replace other immune factors called TH2 cells, which react to allergens--a less serious threat to the body. Without infections to stimulate the production of the TH1 infection fighters, then the TH2 allergen fighters are not replaced and they persist at high levels, making the growing child more susceptible to allergies and asthma.

A number of different studies support this theory:

• Some studies suggest that being part of a large family or attending day care increases the risk for early respiratory infections but reduces the risk of childhood asthma. The occasional cold, then, may be protective.
• In a 2002 study, researchers measured levels of bacterial byproducts called endotoxins in the mattress dust of 812 children. Those with the highest levels had an 80% lower rate in allergies and asthma.
• A 2001 Swedish study further found a strong association between allergy development and the absence of certain beneficial bacteria (called probiotics) carried in the infants intestines. Infants who were born in more hygienic environments tended to lack these bacteria. Antibiotic over-use and modern hygiene may specifically be reducing these helpful organisms. (Probiotics can be obtained in active yogurt cultures and in supplements, which are being studied for protection.)

Of note: The standard vaccinations against serious childhood infections, according to important studies in 2002 and 2003, pose no risk for asthma. One of the studies even reported some lower risk for asthma and allergies in the second and third years after vaccinations. It should strongly be pointed out that infections killed thousands of children every year before immunization became widespread. Asthma, although serious, is rarely fatal in children. No one should stop giving their children vaccinations against childhood killers.

Overexposure to Indoor Allergens

Some evidence suggests that the increase in allergies and asthma may be due to over exposure to allergens. One study in Germany that tracked East German children after the country became unified reported that children in the areas previously under communism experienced a significant increase in allergies, particularly hay fever, when they were exposed to a Western lifestyle. Included in lifestyle changes were the following:

• Increases in wall-to-wall carpeting.
• Increases in cat ownership.
• Damper homes.
• Consumption of margarine (which has been associated with hay fever).

Some scientists believe that more children are developing allergies because they are spend hours indoors each day engaging in sedentary activities and so are overexposed to indoor allergens. This exposure is intensified by the recent trend of making homes more energy-efficient, which may result in more dust mites being trapped inside.

Triggers of Seasonal Allergic Rhinitis (Hay Fever or Rose Fever)

Seasonal allergic rhinitis occurs only during periods of intense airborne pollen or spores. It is commonly, although inaccurately, called hay fever or rose fever, depending on whether it occurs in the late summer or spring. No fever accompanies this condition, and the allergic response is not dependent on either hay or roses. In general, triggers of seasonal allergy in the US are the following:

• Ragweed. Ragweed is the most important cause of allergic rhinitis in the US, affecting about 75% of allergy sufferers. One plant can release one million pollen grains a day. Ragweed is everywhere in the US, although it is less prevalent along the West Coast, southern Florida, northern Maine, Alaska, and Hawaii. The effects of ragweed in the northern states are first felt in middle to late August and last until the first frost. Ragweed allergies tend to be most severe before midday.
• Grasses. Grasses affect people in mid-May to late June. Grass allergies are experienced more in the late afternoon.
• Tree Pollen. Small pollen grains from certain trees usually produce symptoms in late March and early April.
• Mold Spores. Mold spores that grow on dead leaves and release spores into the air are common allergens throughout the spring, summer and fall. Mold spores may peak on dry windy afternoons or on damp or rainy days in the early morning.

Major weather changes, such as El Nino, can affect the timing of allergy seasons. For example, in 1998, when the effects of El Nino were very strong, allergy attacks were markedly increased and maximum tree pollen counts occurred two to four weeks earlier and mold counts two to three months earlier than in 1997.

Triggers of Perennial (Year-Round) Allergic Rhinitis

Allergens in the House. Allergens in the house can trigger attacks in people with year-long allergic rhinitis, called perennial rhinitis. Household allergens may include the following:

• House dust and mites. Dust mites, specifically mite feces, are coated with enzymes that contain a powerful allergen.
• Cockroaches.
• Pet dander.
• Molds growing on wallpaper, house plants, carpeting, and upholstery.

It is important to note that studies are now suggesting that early exposure to some of these allergens, including dust mites and pets, may prevent allergies from developing in the first place in children.

Fossil Fuels. Although difficult to prove, a number of investigations, including European studies in 1999 and 2000, reported an association between traffic-related air pollution and allergic rhinitis. Of particular note, some experts believe that refined fossil fuels, such as diesel fuel and particularly kerosene, may be important triggers for allergic rhinitis. And, in people who already have allergies or asthma, exposure to such fossil fuels may worsen symptoms.