Connecting Hay Fever To Bronchial Asthma – nasal and lung functions connected – includes related article on treatment

Jonathan Corren

Seasonal allergic rhinitis–more commonly known as “hay fever”–plagues some 35 million Americans. Once considered a trivial problem with minimal consequences. allergic rhinitis is now known to have a strong link to a variety of other important respiratory disorders, including chronic sinusitis, middle ear infections, nasal polyps, and bronchial asthma. It is the latter–the relationship between nasal allergies and asthma–which is of greatest concern to the medical community, given the recent increases in the prevalence of asthma as well as rising disability and medical costs attributable to the disease.

The first step in linking allergic rhinitis and asthma was taken centuries ago. Galen, a Greek physician and one of the fathers of Western medicine, postulated during the 2nd century A.D. that the nose serves a critical function in warming and filtering inspired air on its way to the lungs. He also believed that abnormal secretions originating from the interior of the skull–such as those seen during head colds–could drip into the chest and elicit lower respiratory symptoms such as cough.

In the 1500s however, human anatomists began to question the interconnectedness of the upper and lower airways. In fact, any discussion of a connection between the nose and lungs disappeared entirely from medical literature until early in the 20th century, when ear, nose and throat surgeons noticed that some cases of bronchitis and asthma showed striking improvements when chronic nasal and sinus conditions were successfully treated.

Still, it wasn’t until the mid-to late-20th century–when the prevalence of both allergic rhinitis and asthma began to rise–that physicians first took notice of how often the two disorders occurred together in the same patient. In fact, the most recent epidemiologic study of allergic diseases from the Johns Hopkins School of Medicine revealed that over 95 percent of patients who have allergic asthma also suffer from nasal allergies, in stark contrast to the general population, of which only 20 percent are allergy sufferers. Conversely, between 19 and 38 percent of allergic rhinitis patients are asthmatic as well, while only 3 to 5 percent of the general population suffer from asthma.


Results from research completed over the past two years suggest that patients who have both allergic rhinitis and asthma also suffer more debilitating chest symptoms than patients with asthma alone. A recent analysis of over 1200 asthmatics, half of whom had rhinitis and half of whom did not, showed that patients who had both rhinitis and asthma were much more likely to have nighttime awakening due to asthma (19.6 percent versus 11.8 percent), meet the criteria for “moderate to severe asthma” as defined by the National Asthma Education and Prevention Program (60.2 percent versus 51.2 percent), or miss work because of asthma attacks (24.1 percent versus 12.1 percent). In addition, these patients were more likely to require more potent medications, such as oral steroids, to treat their disease.

Once the connection between rhinitis and asthma had been made, the key question remaining was whether one condition predisposes a person to develop the other. In other words, which comes first, the asthma or the rhinitis? In a number of reports published during the past 30 years, up to 85 percent of patients with both asthma and rhinitis recalled having nasal symptoms that either preceded or started at the same time as their asthma. And in a long-term study of 690 students at Brown University, students who began their years at college with symptoms of allergic rhinitis–but without symptoms of asthma–were three times more likely to develop asthma during the ensuing 23 years of follow-up than were the students who did not have nasal allergies (a prevalence of 10.5 percent versus 3.6 percent).

On the strength of this evidence, some investigators are now attempting to determine which patients with allergic rhinitis are at highest risk for developing asthma. One way of discriminating between patients at risk for developing lower airway symptoms has been to perform measurements of bronchial reactivity. This tendency of the bronchial tubes to constrict–to go into bronchospasm–is thought to be an indicator of the degree of inflammation in the lower airways and is an important physiologic hallmark of asthma.

When tested, roughly one-quarter to one-half of all patients with either seasonal or perennial allergic rhinitis and no signs of asthma demonstrated a marked degree of bronchial hyperreactivity, and two small studies have suggested that it is these rhinitis patients who may go on to develop asthma. In fact, some investigators have postulated that asymptomatic bronchial hyperreactivity may represent an intermediate phase between uncomplicated nasal allergy and clinical asthma.

Researchers considering all of the above research now believe that nasal allergy may in fact be a significant but modifiable risk factor for the subsequent development of bronchial asthma, and is a condition that requires careful follow-up over time.


The co-existence of rhinitis and asthma may not seem all that surprising, considering the almost identical anatomy and histology of the tissues in the nose and lungs. In addition, both are exposed to the same airborne allergens and irritants and both respond similarly to such environmental insults. There are, however, other possible physiologic connections between the upper and lower airways which have only begun to be recognized and explored over the past two to three decades and which may shed even more light on the rhinitis-asthma link.

The NASAL-Bronchial Reflex

The first–and most widely accepted–of these theories is based on the idea that there are nerve fibers originating in the upper airway which connect to the lungs; this would allow irritants or allergic reactions in the nose to cause bronchial constriction as a sort of reflex. This idea is based on studies done in the late 1960s with five patients who had undergone surgical resection of the trigeminal nerve on just one side of their face as a last resort treatment for uncontrollable twitching of the facial muscles. These patients agreed to have a fine suspension of silica particles instilled into one or the other side of their nose on separate days, followed by measurement of their lung capacities. When the silica was sprayed into the nostril on the unoperated side of the face, the patients’ lung capacities dropped immediately, indicating an asthmatic reaction. However, when silica was administered into the nostril on the operated side of the face–the side on which the nerve was no longer in use–lung function did not change.

The same researchers later showed that bronchial constriction could be blocked by atropine, a medication that hinders the transmission of impulses through key parts of the nervous system. The results provided by these and similar experiments have provided powerful evidence that neural reflexes play a strong role in the connection between the nose and lungs (see “A Nervous Connection”).

Nasal Blockage Results in Increased Mouth Breathing

A second likely theory is based on the idea that the nasal blockage caused by allergic rhinitis may result in a shift from the normal pattern of nasal breathing to predominantly mouth breathing. What’s the connection between breathing patterns and asthma? One clinical investigation showed that when asthmatic patients exercised vigorously during periods of complete nasal obstruction, exercise-induced bronchospasm worsened significantly. When those same patients breathed entirely through the nose, however, bronchial constriction brought on by exercise was markedly improved.

In a similar experiment, patients were placed into a refrigerated chamber for several minutes and measurements were taken of both their lung capacity and the temperature within their trachea. On one of the experimental study days, the subjects were asked to breathe entirely through their nose; on the other, their nose was clipped tightly and they breathed through their mouth. The patients’ lung capacity dropped significantly on the mouth-breathing day of the experiment; this correlated highly with a significant cooling of the trachea. On the day they breathed only through their nose, however, their lower airway function changed only minimally and their intra-tracheal temperature remained close to normal. These studies demonstrate that nasal breathing has an important protective effect on the lower airways, most likely because the nose is more effective at warming and moisturizing inspired air before it passes into the lungs. In addition, a nose that is clear and free of inflammation is better able to filter and remove airborne allergens and pollutants than is the mouth.

Postnasal Drip of Inflammatoy Material

Patients with chronic nasal disease often complain that severe postnasal drip triggers episodes of coughing or wheezing. Since the 1920s, physicians have realized that substances placed in the nose and pharynx could later be recovered from the tracheobronchial tree. We now know that significant aspiration of upper airway secretions occurs during the night while people sleep. Since a large number of inflammatory chemicals (such as histamine and leukotrienes) and inflammatory cells (such as eosinophils) are present in the nose in patients with allergic rhinitis, it seems likely that as these factors drip into the lungs, they might increase lower airway inflammation and make asthma worse.


To date, the research into the asthma-rhinitis connection has told a compelling story: We now know that allergic rhinitis can be found in most patients with asthma, that it is associated with increased severity of asthma, and that it may contribute to the development of asthma. If so, the next logical step is to determine if physicians can reduce asthma severity or prevent asthma from occurring simply by treating rhinitis.

One of the earliest studies to address this question was performed in the early 1980s in children with chronic nasal blockage and asthma. After they were treated with a nasal steroid for four weeks, their nasal congestion decreased significantly and asthma brought on by exercise gradually improved. In a study in 1987, researchers at the Mayo Clinic investigating topical therapies for seasonal allergic rhinitis serendipitously found that wheezing and other asthma symptoms were greatly diminished in a group receiving steroid nasal sprays.

In 1992, my colleagues and I studied the effects of nasal steroids in patients with fall hay fever and mild asthma. Along with the usual assessments of upper and lower airway symptoms, we also performed tests to measure bronchial hyperreactivity at the beginning and end of the fall pollen season. In patients treated with placebo, there was a significant increase in lower airway hyperreactivity, consistent with the increase in lower airway inflammation during the pollen season. Study subjects treated with the active nasal steroid, however, showed no increase in bronchial hyperreactivity, suggesting the nasal therapy had a profound protective effect on the lungs.

More recently, clinical trials have been looking into the role of second-generation antihistamine medications in patients with both seasonal nasal allergies and asthma. The results have been very encouraging: This class of pharmaceuticals has not only significantly relieved patients’ hay fever, but has also reduced their asthma symptoms and improved the results of their lung function tests. In addition, these studies clearly demonstrate that antihistamines–particularly second-generation drugs such as loratadine and cetirizine–are extremely safe for use in patients with asthma.

The implications of these studies are quite striking. Put simply, they tell us that if hay fever is adequately treated, asthma will improve as well. Studies are now underway to see if we might go one step further and use aggressive intervention in allergic rhinitis to prevent or delay the eventual development of asthma. Thus, the rhinitis-asthma connection may ultimately lead us to ways to stop asthma in its tracks, at least in some patients.


By William W. Busse, M.D., FAAARI

Just as the frequency, triggers and symptoms of asthma are unique to each individual with the disease, so too are the treatment plans and medications prescribed. Nevertheless, there are two primary classes of pharmaceuticals available for the treatment of asthma: bronchodilators for short-term, fast-acting relief and anti-inflammatory medications for long-term symptom control.


During an asthma attack, the smooth muscles surrounding the airways constrict. Couple this with inflamed bronchial tubes, and an asthmatic can find it difficult to take in sufficient amounts of air. Some asthmatics describe the sensation as “trying to breathe through a straw.” At the start of an attack–or as soon as difficulty in breathing is experienced–patients with asthma are typically advised to take fast-acting bronchodilators to relax the constricted muscles. The most effective of these medications are inhaled beta-2 agonists such as albuterol, terbutaline and pirbuterol.

Anti-inflammatory Medications

The aforementioned inflamed bronchial tubes are chronic in asthma patients, and are part of what “defines” the disease. Chronic inflammation in the airways limits the amount of oxygen getting to the lungs and places the patient at risk for an asthma attack. Anti-inflammatory medications work to decrease airway swelling, and thus decrease the likelihood of an attack.

Physicians advocate that patients with persistent asthma use anti-inflammatories on a regular basis to ensure that they do not develop permanent changes called airway remodeling –alterations in the structure of the bronchial tubes that may result from untreated inflammation. Oral and inhaled corticosteriods are the most effective anti-inflammatory treatment available for asthma. Other anti-inflammatory medications for asthma include cromolyn, nedocromil and leukotriene modifiers.

Of course, the exact combination and method of administration of anti-inflammatory medications and bronchodilators depends on many factors. Still, asthma can be well controlled if patients remain involved in monitoring and managing their symptoms and medications.

Jonathan Corren. M.D. is Assistant Clinical Professor of Medicine and Pediatrics at the University of California, Los Angeles, School of Medicine and Co-Director of the UCLA Nasal and Sinus Disease Center. He has a full-time, private clinical and research practice in Los Angeles. Prior to his current position, he was attending physician and Instructor in Medicine at the National Jewish Center for Immunology and Respiratory Medicine in Denver, Colorado.

Corren’s research focuses on the interrelationship between the upper and lower airways, as well as the development of new treatments for allergic rhinitis and asthma. He has authored over 50 scientific articles, abstracts and book chapters in the areas of allergic disease and asthma.

Corren has been a member of the American Academy of Allergy, Asthma and Immunology (AAAAI) since 1990, and is currently Chair of the subcommittee on Clinical Use of Topical Corticosteroids for the Joint Task Force on Practice Parameters. He has previously served as Chair of the Antiinflammatory Committee for the AAAAI and as a member of the Practice Guidelines Committee for the American College of Allergy, Asthma and Immunology.

COPYRIGHT 1999 Discover

COPYRIGHT 2000 Gale Group

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