Allergic rhinitis (AR) has become the most common allergic/immunologic disorder among the U.S. population (Dykewicz et al., 1998). The rising prevalence of AR has been reported not only in children (Meltzer, 1997), but also in adults (Linneberg et al., 2000). Although the incidence of AR peaks during young adult years, it is also an important health concern in older adults.

Despite evidence supporting the contention that allergic potential declines with aging (al-Rayes et al., 1992), recent findings indicate that older adults commonly seek care from an allergy/immunology physician. A survey of members and fellows of the American College of Allergy, Asthma and Immunology (Lang et al., 2000) found that approximately one in every five patients cared for by allergy/immunology practitioners is 55 years of age or older (and 6% were 70 or older). The distribution of diagnoses indicated by survey respondents was remarkably similar across three patient age groups, suggesting that older adult allergy/immunology patients exhibit symptoms that reflect conditions similar to other adults who seek out and/or continue allergy/immunology care (Figure). These findings imply that older adults will continue to seek care for conditions within that specialty -- particularly AR. This observation is important, as AR in older adults may be trivialized and undertreated, leading to unnecessary impairment of quality of life, reduced work productivity, predisposing sufferers to secondary complications -- including sinusitis and sleep disturbances -- and a greater likelihood of poorly controlled symptoms in those with concomitant asthma (Corren, 2000; Dykewicz et al., 1998). Given this, and the realization that by the year 2020 one in six people in the United States is expected to be older than 65 years of age (Guralnik and FitzSimmons, 1986), the proper recognition and management of AR in older adults has become increasingly important.

Rhinitis may be defined as an inflammation of the nasal mucous membranes. The allergic response that underlies AR results from exposure to an allergen that cross-links at least two immunoglobulin E (IgE) antibodies bound to the high-affinity IgE receptor on presensitized effector cells such as mast cells or basophils (Bufe, 2001). The allergic response includes both an early and a late phase (Christodoulopoulos et al., 2000). The early phase occurs promptly and spans approximately one hour. The late phase generally begins in three to six hours, peaks at six to eight hours, and subsides in 12 to 24 hours. When studied in laboratory settings, almost half of subjects will exhibit this dual response. The symptoms of the early phase typically include sneezing, itching and clear rhinorrhea; symptoms characterizing the late phase may be indistinguishable, but tend to be characterized by more prominent congestion. The late phase is promoted by factors generated in the early phase that encourage release of inflammatory mediators and the activation and recruitment of cells to the nasal mucosa (Naclerio, 1997). Whereas histamine appears to be the major mediator of the early phase, the late phase is more a function of cytokines and chemokines that have both inflammatory and pro-inflammatory effects, which lead to recruitment of inflammatory cells such as eosinophils and basophils (Christodoulopoulos et al., 2000). Eosinophils play important roles in the late phase, including release of leukotrienes -- the release of which, as suggested by published data, is of greater importance than histamine for nasal congestion (Donnelly et al., 1995; Okuda et al., 1988). During a clinically relevant exposure (e.g., outdoors during the ragweed season or indoors in a home with several cats) in a sensitized individual, aeroallergens enter the nasal passages on a virtually continual basis; for this reason, it is frequently difficult to separate the early and late phases of the allergic response in the real-world setting. One can imagine that based on the incessant nature of aeroallergen exposure, affected individuals experience a perpetual late-phase response.

Recognition of individuals with AR requires a careful history and physical examination. The key components of the history that favor AR over other causes of rhinitis that must be considered in the differential diagnosis (Table 1) include: seasonality of symptoms, occurrence of symptoms with certain exposures or situations, improvement of symptoms during spring-fall seasons when in air-conditioned environments, and, most importantly, the experience of prominent pruritus of nose, eyes, ears, throat and/or palate. In older adults with chronic perennial rhinitis, AR is less frequently confirmed and alternative diagnoses for perennial rhinitis, such as cholinergic hyperactivity, pharmacologic causes (e.g.,

-adrenergic effects of antihypertensive drugs) and chronic sinusitis, are found more frequently (Dykewicz et al., 1998).

The diagnosis of AR requires 1) positive history; 2) demonstration of IgE-mediated response to inhalant allergens by skin or in vitro testing; and 3) correlation between history and skin or in vitro test findings. Skin testing is recommended as the preferred diagnostic study, as it is associated with reduced cost, is more sensitive and entails no delay in obtaining results (American College of Physicians, 1989). Individuals who have skin disorders or cannot suspend antihistamine medications, such that skin testing would be uninterpretable, are candidates for in vitro testing to detect elevated titers of specific IgE to inhalant allergens (Dykewicz et al., 1998).

The prevalence of comorbid conditions such as hypertension, congestive heart failure, diabetes mellitus, gastroesophageal reflux and orthopedic impairment is considerably higher among older adults (Gong, 1997; Montanaro, 1997). Changes in the immune system, pharmacokinetics and pharmacodynamics with aging (Fillit, 1994), and the greater potential for drug-drug interactions (Traver et al., 1993) commonly influence management outcomes. These coexisting conditions and confounding factors frequently complicate diagnosis and management of AR in older adults.

Confirming the diagnosis with skin (or in vitro) testing can also direct specific avoidance measures. Avoidance of clinically relevant allergens can lead to substantial reduction of symptoms and medication reliance (Dykewicz et al., 1998) and is arguably the most important element of AR management. Because of the greater potential for untoward reactions from medications (Montanaro, 1997), a program of aggressive aeroallergen avoidance assumes heightened importance in the successful management of AR in older adults.

The inhalant allergens that may account for AR include dust mites, cockroaches, pets, mold spores, trees, grasses and weeds. Individuals with AR are frequently sensitive to more than one allergen.

Air conditioning can be associated with dramatic reduction in exposures to outdoor pollens and mold spores while indoors (Solomon et al., 1980). Because we now spend the majority of our time indoors (Samet et al., 1987), the utility of air conditioning for reducing symptoms should not be underestimated.

Microscopic dust mites are a major source of allergen in house dust (Dykewicz et al., 1998). They rely on heat and humidity to survive and proliferate (Arlian and Platts-Mills, 2001). Allergy to dust mites is common in patients with AR. Recommended avoidance measures to reduce exposures to dust mites include encasement of mattress/box spring and pillows in impermeable covers, reducing indoor relative humidity, washing bedding weekly in hot cycle (>130° F) and, if possible, removal of carpets in favor of tiled or hardwood flooring (Arlian and Platts-Mills, 2001; Corren, 2000).

For individuals allergic to animal dander who are pet owners, no avoidance strategy can approach the benefit that will accrue with elimination of the pet from the home (Chapman and Wood, 2001). In view of the potential therapeutic value of pets (Fitzgerald, 1986), the decision to remove a pet from the home should be discussed openly and considered on a risk/benefit basis. If the pet is removed from the home, the allergen may persist for several months; understandably, clinical benefit may not occur promptly (Wood et al., 1989). When removal is not possible, second-best measures include restricting the pet from the allergic person's bedroom, use of high-efficiency particulate or electrostatic air cleaners, and removal of carpets that otherwise serve as a reservoir for allergens (Chapman and Wood, 2001). Bathing the pet cannot be recommended, as allergen reduction is transient and is unlikely to be associated with clinical benefit (Hodson et al., 1999; Klucka et al., 1995).

Because avoidance measures will likely be incomplete and patients with AR will continue to be exposed to clinically relevant allergens, virtually all patients with AR will benefit from the use of regular medication.

The most commonly prescribed medications for AR are H1-antihistamines (Day, 1999; Dykewicz et al., 1998). These drugs antagonize the action of histamine by blocking receptor sites on target cells. Although conventional or first-generation antihistamines are efficacious, they can be associated with drowsiness and performance impairment (Corren, 2000; Day, 1999). Impaired driving performance has been documented with use of conventional antihistamines, even in individuals with no subjective awareness of drowsiness (O'Hanlon and Ramaekers, 1995). Older adults may be more sensitive to the psychomotor impairment promoted by antihistamines and are at greater risk for complications such as fractures and subdural hematomas caused by falls (McCue, 1996). Prominent anticholinergic effects, including dryness of mouth and eyes, constipation, inhibition of micturition, and potential provocation of narrow angle glaucoma, may occur. Because of concomitant comorbid conditions (e.g., increased intraocular pressure, benign prostatic hypertrophy, pre-existing cognitive impairment and so on) that may increase the potential risk associated with regular or even intermittent use, first-generation antihistamines should be prescribed or recommended cautiously in older adults. Use of second-generation antihistamines, which lack the prominent central nervous system or anticholinergic properties of conventional antihistamines, are preferred (Corren, 2000; Day, 1999). The second-generation antihistamines are displayed in Table 2. In a minority of patients, cetirizine (Zyrtec) and intranasal azelastine (Astelin) may be associated with mild sedation, and patients should be so informed. While drowsiness is a possible side effect of fexofenadine (Allegra) and loratadine (Claritin), they have not been associated with an increased rate of sedation compared with placebo.

Oral decongestants primarily reduce nasal stuffiness and may attenuate drainage, but do not affect sneezing or itching; they are frequently helpful taken in combination with an antihistamine. These drugs may also be problematic for older adults (Day, 1999), because of possible CNS and cardiovascular adverse effects. In addition, they may raise intraocular pressure and provoke obstructive urinary symptoms. Although topical pseudoephedrine decongestants (Afrin and others) may be efficacious, use should be avoided for longer than four days due to the risk of rhinitis medicamentosa (Dykewicz et al., 1998).

Intranasal cromolyn is well-tolerated, but is more efficacious for preventing, rather than reversing, inflammation (Corren, 2000; Dykewicz et al., 1998). Although required qid dosing limits cromolyn's utility, it carries no risk for systemic adverse effects and so may be preferred for older adults.

Intranasal corticosteroids (IC) are the most efficacious agents for management of AR (Dykewicz et al., 1998). Because symptoms of AR reflect underlying inflammation promoted by aeroallergen exposure, use of an agent that can achieve a broad range of anti-inflammatory effects and act through multiple mechanisms would be expected to be associated with maximal relief of AR symptoms compared with other agents (Dykewicz et al., 1998; Naclerio, 1997). The therapeutic effects of IC include vasoconstriction and reduction of mucosal edema, inhibition of mediator release, suppression of cytokine production, and inhibition of inflammatory cell infiltration (Corren, 2000). Intranasal corticosteroids are effective for reducing nasal congestion, rhinorrhea and sneezing and may also relieve ocular symptoms (Dykewicz et al., 1998). Systemic effects are minimal at recommended doses (Szefler, 2001). The major adverse effect of IC is local irritation or epistaxis; patients should be instructed to suspend IC use at the first sign of bleeding or irritation and to direct the nasal spray laterally (away from the nasal septum).

Intranasal ipratropium (Atrovent) may be efficacious for rhinorrhea, but it has little benefit for other AR symptoms (Dykewicz et al., 1998). This medication may be helpful if rhinorrhea is refractory to the previously discussed medications or for people with vasomotor/irritant rhinitis (Grossman et al., 1995). Adverse effects include the potential for local irritation or epistaxis.

Allergen immunotherapy for AR entails the incremental administration of inhalant allergens for the purpose of inducing immune system changes in host response with natural exposure to these allergens (Dykewicz et al., 1998).

A trial of allergen immunotherapy can be considered for patients with AR complications such as sinusitis or otitis or when avoidance measures combined with use of regular pharmacotherapy lack sufficient efficacy. Allergen immunotherapy may also have utility for people with AR who do not tolerate or are disinclined to take regular medications.

The decision to begin allergen immunotherapy should be individualized and based on symptom severity, relative benefit with pharmacotherapy and whether comorbid conditions such as ß-blocker use are present (Lang, 1995). Comorbid conditions may increase the risk for serious anaphylaxis -- the major risk of allergen immunotherapy (Dykewicz et al., 1998).

Allergen immunotherapy is commonly administered for AR, and its efficacy is well-established (Durham et al., 1999; Ohman and Ohman, 1992). As with other studies of therapeutic interventions, the therapeutic utility of allergen immunotherapy has been documented in younger individuals. Due to changes in the immune system with aging (Fillit, 1994) and the greater frequency of comorbid conditions, there is a need for additional trials of allergen immunotherapy for AR in older adults.

The author thanks Mrs. Janel Leitner for expert secretarial assistance.

Dr. Lang is section chief of allergy/immunology in the department of medicine at Thomas Jefferson University in Philadelphia. He is board-certified in both internal medicine and allergy/immunology.

al-Rayes H, Pachas W, Mirza N et al. (1992), IgE regulation and lymphokine patterns in aging humans. J Allergy Clin Immunol 90(4 pt 1):630-636.

American College of Physicians (1989), Allergy testing. Ann Intern Med 110(4):317-320 [see comment].

Arlian LG, Platts-Mills TA (2001), The biology of dust mites and the remediation of mite allergens in allergic disease. J Allergy Clin Immunol 107(3 suppl):S406-S413.

Bufe A (2001), Significance of IgE-binding epitopes in allergic disease. J Allergy Clin Immunol 107(2):219-221.

Chapman MD, Wood RA (2001), The role and remediation of animal allergens in allergic diseases. J Allergy Clin Immunol 107(3 suppl):S414-S421.

Christodoulopoulos P, Cameron L, Durham S, Hamid Q (2000), Molecular pathology of allergic disease. II: Upper airway disease. J Allergy Clin Immunol 105(2 pt 1):211-223.

Corren J (2000), Allergic rhinitis: treating the adult. J Allergy Clin Immunol 105(6 pt 2):S610-S615.

Day J (1999), Pros and cons of the use of antihistamines in managing allergic rhinitis. J Allergy Clin Immunol 103(3 pt 2):S395-S399.

Donnelly AL, Glass M, Minkwitz MC, Casale TB (1995), The leukotriene D4-receptor antagonist, ICI 204,219, relieves symptoms of acute seasonal allergic rhinitis. Am J Respir Crit Care Med 151(6):1734-1739.

Durham SR, Walker SM, Varga EM et al. (1999), Long-term clinical efficacy of grass-pollen immunotherapy. N Engl J Med 341(7):468-475 [see comment pp522-524].

Dykewicz MS, Fineman S, Skoner DP et al. (1998), Diagnosis and management of rhinitis: complete guidelines of the Joint Task Force on Practice Parameters in Allergy, Asthma, and Immunology. American Academy of Allergy, Asthma, and Immunology. Ann Allergy Asthma Immunol 81(5 pt 2):478-518.

Fillit H (1994), Clinical immunology of aging. Reviews in Clinical Gerontology 4:187-197.

Gong H Jr (1997), Coexisting conditions that complicate asthma management in the elderly. In: Asthma in the Elderly, Barbee RA, Bloom JW, eds. New York: Marcel Dekker Inc., pp219-258.

Grossman J, Banov C, Boggs P et al. (1995), Use of ipratropium bromide nasal spray in chronic treatment of nonallergic perennial rhinitis, alone and in combination with other perennial rhinitis medications. J Allergy Clin Immunol 95(5 pt 2):1123-1127.

Guralnik JM, FitzSimmons SC (1986), Aging in America: a demographic perspective. Cardiol Clin 4(2):175-183.

Hodson T, Custovic A, Simpson A et al. (1999), Washing the dog reduces dog allergen levels, but the dog needs to be washed twice a week. J Allergy Clin Immunol 103(4):581-585.

Klucka CV, Ownby DR, Green J, Zoratti E (1995), Cat shedding of Fel d I is not reduced by washings, Allerpet-C spray, or acepromazine. J Allergy Clin Immunol 95(6):1164-1171.

Lang DM (1995), Anaphylactoid and anaphylactic reactions. Hazards of beta-blockers. Drug Saf 12(5):299-304.

Lang DM, Visintainer PF, Howland WC et al. (2000), Survey of the extent and nature of care for adults and older adults by allergy/immunology practitioners. Ann Allergy Asthma Immunol 85(2):106-110 [see comment pp85-86].

Linneberg A, Nielsen NH, Madsen F et al. (2000), Increasing prevalence of specific IgE to aeroallergens in an adult population: two cross-sectional surveys 8 years apart: the Copenhagen Allergy Study. J Allergy Clin Immunol 106(2):247-252.

McCue JD (1996), Safety of antihistamines in the treatment of allergic rhinitis in elderly patients. Arch Fam Med 5(8):464-468.

Meltzer EO (1997), The prevalence and medical and economic impact of allergic rhinitis in the United States. J Allergy Clin Immunol 99(6 pt 2):S805-S828.

Montanaro A (1997), Allergic disease in an aging population. Immunology and Allergy Clinics of North America 17(4):513-520.

Naclerio RM (1997), Pathophysiology of perennial allergic rhinitis. Allergy 52(36 suppl):7-13.

O'Hanlon JF, Ramaekers JG (1995), Antihistamine effects on actual driving performance in a standard test: a summary of Dutch experience, 1989-94. Allergy 50(3):234-242.

Ohman JL, Ohman JL Jr (1992), Allergen immunotherapy. Review of efficacy and current practice. Med Clin North Am 76(4):977-991.

Okuda M, Watase T, Mezawa A, Liu CM (1988), The role of leukotriene D4 in allergic rhinitis. Ann Allergy 60(6):537-540.

Samet JM, Marbury MC, Spengler JD (1987), Health effects and sources of indoor air pollution. Part I. Am Rev Respir Dis 136(6):1486-1508.

Solomon WR, Burge HA, Boise JR (1980), Exclusion of particulate allergens by window air conditioners. J Allergy Clin Immunol 65(4):305-308.

Szefler SJ (2001), Pharmacokinetics of intranasal corticosteroids. J Allergy Clin Immunol 108(1 suppl):S26-S31.

Traver GA, Cline MG, Burrows B (1993), Asthma in the elderly. J Asthma 30(2):81-91 [see comment pp77-79].

Wood RA, Chapman MD, Adkinson NF, Eggleston PA (1989), The effect of cat removal on allergen content in household-dust samples. J Allergy Clin Immunol 83(4):730-734.

Management of Allergic Rhinitis