Allergic Rhinitis and its Impact on Asthma (ARIA) 2008*
Authors: J. Bousquet, N. Khaltaev, A. A. Cruz, J. Denburg, W. J. Fokkens, A. Togias, T. Zuberbier, C. E. Baena‐Cagnani, G. W. Canonica, C. Van Weel, I. Agache, N. Aït‐Khaled, C. Bachert, M. S. Blaiss, S. Bonini, L.‐P. Boulet, P.‐J. Bousquet, P. Camargos, K.‐H. Carlsen, Y. Chen, A. Custovic, R. Dahl, P. Demoly, H. Douagui, S. R. Durham, R. Gerth Van Wijk, O. Kalayci, M. A. Kaliner, Y.‐Y. Kim, M. L. Kowalski, P. Kuna, L. T. T. Le, C. Lemiere, J. Li, R. F. Lockey, S. Mavale‐Manuel, E. O. Meltzer, Y. Mohammad, J. Mullol, R. Naclerio, R. E. O’Hehir, K. Ohta, S. Ouedraogo, S. Palkonen, N. Papadopoulos, G. Passalacqua, R. Pawankar, T. A. Popov, K. F. Rabe, J. Rosado‐Pinto, G. K. Scadding, F. E. R. Simons, E. Toskala, E. Valovirta, P. Van Cauwenberge, D.‐Y. Wang, M. Wickman, B. P. Yawn, A. Yorgancioglu, O. M. Yusuf, H. Zar, I. Annesi‐Maesano, E. D. Bateman, A. Ben Kheder, D. A. Boakye, J. Bouchard, P. Burney, W. W. Busse, M. Chan‐Yeung, N. H. Chavannes, A. Chuchalin, W. K. Dolen, R. Emuzyte, L. Grouse, M. Humbert, C. Jackson, S. L. Johnston, P. K. Keith, J. P. Kemp, J.‐M. Klossek, D. Larenas‐Linnemann, B. Lipworth, J.‐L. Malo, G. D. Marshall, C. Naspitz, K. Nekam, B. Niggemann, E. Nizankowska‐Mogilnicka, Y. Okamoto, M. P. Orru, P. Potter, D. Price, S. W. Stoloff, O. Vandenplas, G. Viegi, D. Williams
Journal: Allergy (2008)

Allergic rhinitis is a symptomatic disorder of the nose induced after allergen exposure by an immunoglobulin E (IgE)-mediated inflammation of the membranes lining the nose (1). It was defined in 1929 (2): ‘The three cardinal symptoms in nasal reactions occurring in allergy are sneezing, nasal obstruction and mucous discharge’. Allergic rhinitis is a global health problem that causes major illness and disability worldwide. Patients from all countries, all ethnic groups and of all ages suffer from allergic rhinitis. It affects social life, sleep, school and work. The economic impact of allergic rhinitis is often underestimated because the disease does not induce elevated direct costs. However, the indirect costs are substantial (1). Both allergic rhinitis and asthma are systemic inflammatory conditions and are often co-morbidities. Although asthma and other forms of allergic disease have been described in antiquity, ‘hay fever’ is surprisingly modern. Very rare descriptions can be traced back to Islamic texts of the 9th century and European texts of the 16th century. It was only in the early 19th century that the disease was carefully described, and at that time it was regarded as most unusual (3). In the 19th century, the disease followed the industrialization of westernized countries (4). By the end of the 19th century it had become commonplace in both Europe and North America. However, the prevalence of allergic rhinitis was still low and has considerably increased during the past 50 years. In some countries, over 50% of adolescents are reporting symptoms of allergic rhinitis (5). Using a conservative estimate, allergic rhinitis occurs in over 500 million people around the world. The prevalence of allergic rhinitis is increasing in most countries of the world, and particularly in areas with low or medium levels of prevalence. However, it may be plateauing or even decreasing in the highest prevalence areas. Rhinitis and allergic diseases are now taken seriously and the European Union (6) or countries such as Canada have specific programs to better understand, manage and prevent allergic diseases. Risk factors for allergic rhinitis are well identified. In the middle of the 19th century, the cause of hay fever was ascribed to pollens (7, 8). Indoor and outdoor allergens as well as occupational agents cause rhinitis and other allergic diseases. The role of indoor and outdoor pollution is probably very important, but has yet to be fully understood both for the occurrence of the disease and its manifestations. The diagnosis of allergic rhinitis is often easy, but in some cases it may cause problems and many patients are still underdiagnosed, often because they do not perceive the symptoms of rhinitis as a disease impairing their social life, school and work. The management of allergic rhinitis is well established and many guidelines have been issued although the first ones were not evidence based (9–11). In 1999, during the Allergic Rhinitis and its Impact on Asthma (ARIA) World Health Organization (WHO) workshop, the suggestions were made by a panel of experts and based on evidence using an extensive review of the literature available up to December 1999 (1). The statements of evidence for the development of these guidelines followed WHO rules and were based on those of Shekelle et al. (12). The second important achievement of ARIA was to propose a new classification for allergic rhinitis which was subdivided into ‘intermittent’ (IAR) or ‘persistent’ (PER) disease (1). Moreover, it is now recognized that allergic rhinitis comprises more than the classical symptoms of sneezing, rhinorrhoea and nasal obstruction. It is associated with impairments in how patients function in day-to-day life. The severity of allergic rhinitis was therefore classified as ‘mild’ or ‘moderate/severe’ depending on symptoms but also on quality of life (QOL; 1). Another important aspect of the ARIA guidelines was to consider co-morbidities of allergic rhinitis. Eye involvement in allergic rhinitis has been described for a long time (13). The nasal airways and their closely-associated paranasal sinuses are an integral part of the respiratory tract (1, 14–16). In the second century, Claudius Galenus, one of the fathers of modern respiratory physiology, defined the nose as a ‘respiratory instrument’ in his work De usu partium [on the usefulness of the (body) parts (17)]. The co-morbidities between the upper and lower airways were described with the clinical description of allergic rhinitis (3, 8). The nasal and bronchial mucosa present similarities, and one of the most important concepts regarding nose–lung interactions is the functional complementarity (14). Interactions between the lower and the upper airways are well known and have been extensively studied since 1990. Over 80% of asthmatics have rhinitis and 10–40% of patients with rhinitis have asthma (1). Most patients with asthma have rhinitis (18) suggesting the concept of ‘one airway one disease’ although there are differences between rhinitis and asthma (19, 20). The ARIA document was intended to be a state-of-the-art for the specialist as well as for the general practitioner and other healthcare professionals: to update their knowledge of allergic rhinitis; to highlight the impact of allergic rhinitis on asthma; to provide an evidence-based documented revision on diagnostic methods; to provide an evidence-based revision on treatments and to propose a stepwise approach to management. The ARIA document was not intended to be a standard-of-care document for individual countries. It was provided as a basis for doctors, healthcare professionals and organizations involved in the treatment of allergic rhinitis and asthma in various countries to facilitate the development of relevant local standard-of-care documents for patients. The ARIA workshop held at the WHO headquarters proposed the recommendations shown in Table 1. An update of the ARIA guidelines was needed because: a large number of papers have been published over the past 7 years extending our knowledge on the epidemiology, diagnosis, management and co-morbidities of allergic rhinitis. Other guidelines have been produced since 1999 (21), but these did not review the ongoing literature extensively using an evidence-based model; the ARIA recommendations were proposed by an expert group and needed to be validated in terms of classification and management; new evidence-based systems are currently available to guide recommendations and include safety and costs as well as efficacy of treatments (22, 23); there were gaps in our knowledge in the first ARIA document. In particular: some aspects of treatment like complementary and alternative medicine were not appropriately discussed; the links between the upper and lower airways in developing countries and deprived areas were not sufficiently developed even though, in the original ARIA document, a section was written on this subject in collaboration with the UNION (formerly IUATLD); sport and rhinitis in athletes and rhinitis and its links with asthma in preschool children. The ARIA update commenced in 2004. Several chapters of ARIA were extensively reviewed in an evidence-based model, and papers were published (or submitted) in peer-reviewed journals: tertiary prevention of allergy, complementary and alternative medicine, pharmacotherapy and anti-IgE treatment, allergen-specific immunotherapy, links between rhinitis and asthma and mechanisms of rhinitis (24–28). There was then a need for a global document based on the published papers to highlight the interactions between the upper and the lower airways and to: develop an evidence-based global document on a key problem of respiratory medicine including diagnosis, epidemiology, common risk factors, management and prevention; propose educational materials for healthcare professionals and patients; meet the objectives of the WHO Global Alliance against Chronic Respiratory Diseases (GARD; 29) in order to help coordinate the efforts of the different GARD organizations towards a better prevention and management of chronic respiratory diseases (CRD), to increase CRD awareness and also to fill some of the gaps in knowledge; focus on the prevention of chronic respiratory and allergic diseases; highlight gaps in knowledge, particularly in developing countries and deprived areas; prepare an executive summary and pocket guide for doctors, patients and healthcare professionals. Rhinitis is defined as an inflammation of the lining of the nose and is characterized by nasal symptoms including anterior or posterior rhinorrhoea, sneezing, nasal blockage and/or itching of the nose. These symptoms occur during two or more consecutive days for more than 1 h on most days (9). Allergic rhinitis is the most common form of noninfectious rhinitis and is associated with an IgE-mediated immune response against allergens. It is often associated with ocular symptoms. Several nonallergic conditions can cause similar symptoms: infections, hormonal imbalance, physical agents, anatomical anomalies and the use of certain drugs (30). Rhinitis is therefore classified as shown in Table 2 (1). The differential diagnosis of rhinitis is presented in Table 3 (1). Since the nasal mucosa is continuous with that of the paranasal sinuses, congestion of the ostia may result in sinusitis which does not exist without rhinitis. The term ‘rhinosinusitis’ should replace ‘sinusitis’ (31). Vasomotor rhinitis is a term which is not used in this document, as vasomotor symptoms can be caused by allergic and nonallergic rhinitis. Definition and classification of allergic rhinitis Allergic rhinitis is clinically defined as a symptomatic disorder of the nose induced after allergen exposure by an IgE-mediated inflammation. Allergic rhinitis is subdivided into IAR or PER disease. The severity of allergic rhinitis can be classified as ‘mild’ or ‘moderate/severe’. Allergic rhinitis impairs QOL, sleep, school and work. Many nonallergic triggers induce nasal symptoms which mimic allergic rhinitis. They include drugs (aspirin and other nonsteroidal anti-inflammatory agents), occupational agents, foods, physical, emotional and chemical factors and viral infections. 2.2.1.1. Clinical definition. Symptoms of allergic rhinitis include rhinorrhoea, nasal obstruction (32), nasal itching and sneezing which are reversible spontaneously or with treatment (2, 33–36). Postnasal drip mainly occurs either with profuse anterior rhinorrhoea in allergic rhinitis (37) or without significant anterior rhinorrhoea in chronic rhinosinusitis (CRS; 38, 39). Preschool children may just have nasal obstruction. However, when nasal obstruction is the only symptom, it is very rarely associated with allergy. Patients with nonallergic rhinitis may have similar symptoms (40). Allergic rhinitis is subdivided into ‘IAR’ or ‘PER’ disease. The severity of allergic rhinitis can be classified as ‘mild’ or ‘moderate/severe’ (1). 2.2.1.2. Definition for epidemiologic studies. The clinical definition of rhinitis is difficult to use in the epidemiologic settings of large populations where it is impossible to visit everybody individually or to obtain the laboratory evidence of each immune response. However, the standardization of the definition of rhinitis in epidemiologic studies is of crucial importance, especially when comparing the prevalence between studies. Initial epidemiologic studies have assessed allergic rhinitis on the basis of simple ‘working definitions’. Various standardized questionnaires have been used for this effect (41, 42). The first questionnaires assessing seasonal allergic rhinitis dealt with ‘nasal catarrh’ (British Medical Research Council, 1960; 43) and ‘runny nose during spring’ (British Medical Research Council, 1962; 44). Questions introducing the diagnostic term of ‘seasonal allergic rhinitis’ were successively used: ‘Have you ever had seasonal allergic rhinitis?’ or ‘Has a doctor ever told you that you suffer from seasonal allergic rhinitis?’ In the European Community Respiratory Health Survey (ECRHS) full-length questionnaire, the question asked on rhinitis was: ‘Do you have any nasal allergies including “seasonal allergic rhinitis”?’ (45). To identify the responsible allergen, the ECRHS study has included potential triggers of the symptoms. However, this question is not sensitive enough and some patients with nonallergic rhinitis answer ‘yes’. There are however problems with questionnaires. Many patients poorly perceive nasal symptoms of allergic rhinitis: some exaggerate symptoms, whereas many others tend to dismiss the disease (46). Moreover, a large proportion of rhinitis symptoms are not of allergic origin (47). In the Swiss Study on Air Pollution and Lung Diseases in Adults (SAPALDIA), the prevalence of current seasonal allergic rhinitis varied between 9.1% (questionnaire answer and a positive skin prick test to at least one pollen) and 14.2% (questionnaire answer only). Diagnostic criteria affect the reported prevalence rates of rhinitis (48–50). A score considering most of the features of allergic rhinitis (clinical symptoms, season of the year, triggers, parental history, individual medical history and perceived allergy) has recently been proposed (51). Using the doctor’s diagnosis (based on questionnaire, examination and skin tests to common aeroallergens) as a gold standard, these scores had good positive and negative predictive values (84% and 74%, respectively) in the identification of patients suffering from allergic rhinitis. Symptoms of perennial rhinitis have been defined as frequent, nonseasonal, nasal or ocular (‘rhinoconjunctivitis’). In one study, the length of the disease was also taken into consideration to differentiate perennial allergic rhinitis from the ‘common cold’ (viral upper respiratory infections; 52). Objective tests for the diagnosis of IgE-mediated allergy (skin prick test and serum-specific IgE) can also be used (53–55). The diagnostic efficiency of IgE, skin prick tests and Phadiatop® was estimated in 8 329 randomized adults from the SAPALDIA. The skin prick test had the best positive predictive value (48.7%) for the epidemiologic diagnosis of allergic rhinitis compared to the Phadiatop® (43.5%) or total serum IgE (31.6%) (56). Future working definitions may encompass not only clinical symptoms and immune response tests, but also nasal function and eventually specific nasal challenge (57). 2.2.2. Intermittent (IAR) and persistent allergic rhinitis (PER). Previously, allergic rhinitis was subdivided, based on the time of exposure, into seasonal, perennial and occupational (9, 10, 58, 59). Perennial allergic rhinitis is most frequently caused by indoor allergens such as dust mites, molds, insects (cockroaches) and animal danders. Seasonal allergic rhinitis is related to a wide variety of outdoor allergens such as pollens or molds. However, this classification is not entirely satisfactory as: in certain areas, pollens and molds are perennial allergens [e.g. grass pollen allergy in Southern California and Florida (60) or Parietaria pollen allergy in the Mediterranean area (61)]; symptoms of perennial allergy may not always be present all year round. This is particularly the case for a large number of patients allergic to house dust mites (HDM) suffering only from mild or moderate/severe IAR (62–65). This is also the case in the Mediterranean area where levels of HDM allergen are low in the summer (66); the majority of patients are sensitized to many different allergens and therefore exposed throughout the year (33, 62, 67–69). In many patients, perennial symptoms are often present and patients experience seasonal exacerbations when exposed to pollens or molds. It appears therefore that this classification is not adherent to real life; climatic changes modify the time and duration of the pollen season which may make predictions difficult; allergic patients travel and may be exposed to the sensitizing allergens in different times of the year; some patients allergic to pollen are also allergic to molds and it is difficult to clearly define the pollen season (70); some patients sensitized only to a single pollen species have perennial symptoms (71); due to the priming effect on the nasal mucosa induced by low levels of pollen allergens (72–77) and minimal PER inflammation of the nose in patients with symptom-free rhinitis (64, 78, 79), symptoms do not necessarily occur strictly in conjunction with the allergen season and nonspecific irritants such as air pollution may aggravate symptoms in symptomatic patients and induce symptoms in asymptomatic patients with nasal inflammation (80). Thus, a major change in the subdivision of allergic rhinitis was proposed in the ARIA document with the terms ‘IAR’ and ‘PER’ (1). It was shown that the classic types of seasonal and perennial rhinitis cannot be used interchangeably with the new classification of IAR/PER, as they do not represent the same stratum of disease. Thus, ‘IAR’ and ‘PER’ are not synonymous with ‘seasonal’ and ‘perennial’ (36, 62, 67, 81–83). In the original ARIA document, the number of consecutive days used to classify patients with PER was more than four per week (1). However, it appears that patients with PER usually suffer almost every day (84). Whereas the majority of patients have symptoms unrelated to seasons, it is possible to discriminate pollen seasons in some patients. In this case, patients experience symptoms during defined times of the year or have mild PER during most months of the year and more severe symptoms when exposed to high concentrations of allergens during pollen seasons. As most patients are polysensitized, it appears that the ARIA classification is closer to the patients’ needs than the previous one (85). Moreover, PER does not necessarily result from allergic origin (86). 2.2.3.1. Classical symptoms and signs. Allergic rhinitis is characterized by subjective symptoms which may be difficult to quantify due to the fact that they depend largely on the patient’s perception. 2.2.3.2. Symptoms associated with social life, work and school. It is now recognized that allergic rhinitis comprises more than the classical symptoms of sneezing, rhinorrhoea and nasal obstruction. It is associated with impairments in how patients function in day-to-day life. Impairment of QOL is seen in adults (10, 87, 88) and in children (89–92). Patients may also suffer from sleep disorders and emotional problems, as well as from impairment in activities and social functioning (93). Poorly-controlled symptoms of allergic rhinitis may contribute to sleep loss or disturbance (94–104). Moreover, H1-antihistamines with sedative properties can increase sedation in patients with allergic rhinitis (105, 106). Although sleep apnoea syndrome has been associated with nasal disturbances (107–109), it is unclear as to whether allergic rhinitis is associated with sleep apnoea (100, 107, 110). It has been shown that patients with moderate/severe symptoms of IAR or PER have an impaired sleep pattern by comparison to normal subjects and patients with mild rhinitis (111). It is also commonly accepted that allergic rhinitis impairs work (10, 84, 112, 113) and school performance (114–116). In several studies, the severity of allergic rhinitis, assessed using QOL measures, work productivity questionnaires or sleep questionnaires, was found to be somewhat independent of duration (67, 84, 111, 117). 2.2.3.3. Objective measures of severity. Objective measures of the severity of allergic rhinitis include: symptom scores; visual analogue scales (VAS ; 118, 119 ; Fig. 1) ; measurements of nasal obstruction, such as peak inspiratory flow measurements, acoustic rhinometry and rhinomanometry (120–122); measurements of inflammation such as nitric oxide (NO) measurements, cells and mediators in nasal lavages, cytology and nasal biopsy (121, 123); reactivity measurements such as provocation with histamine, methacholine, allergen, hypertonic saline, capsaicin or cold dry air (124) and measurements of the sense of smell (125). Mean mast cells, toludine blue staining, IgE+ and eosinophil cell counts/mm2 nasal biopsy tissues collected from patients with perennial allergic (PAR) and idiopathic (ID) rhinitis, and normal nonrhinitic subjects (N). (Horizontal bar + median counts; St1 = counts in epithelium; St2 = counts in superficial submucosa; St3 = counts in deep submucosa.) (Modified from Powe et al. 2001 (15) and reprinted with kind permission.) Measurements of VAS, nasal obstruction and smell are used in clinical practice. The other measurements are primarily used in research. 2.2.3.4. ARIA classification of allergic rhinitis. In the ARIA classification, allergic rhinitis can be classified as ‘mild’ or ‘moderate/severe’ depending on the severity of the symptoms and their impact on social life, school and work (Table 4). It has also been proposed to classify the severity as ‘mild’, ‘moderate’ or ‘severe’ (36, 126, 127). However, it seems that this proposal makes it more complex for the practicing doctor and does not provide any significant improvement to the patient, this more complex classification failing to translate to a difference in therapeutic options. The severity of allergic rhinitis is independent of its treatment. In asthma, the control level is also independent of asthma medications (128–132). Although such an independent relationship was suspected in a study on allergic rhinitis (67), this very important finding was confirmed in a recent study in which it was found that the severity of rhinitis is independent of its treatment (119). Thus, as for asthma, one of the problems to consider is to replace ‘severity’ by ‘control’, but sufficient data are not yet available. 2.3.1. Infectious rhinitis. For infectious rhinitis, the term rhinosinusitis is usually used. Rhinosinusitis is an inflammatory process involving the mucosa of the nose and one or more sinuses. The mucosa of the nose and sinuses form a continuum and thus, more often than not, the mucous membranes of the sinuses are involved in diseases which are primarily caused by an inflammation of the nasal mucosa. For this reason, infectious rhinitis is discussed under Rhinosinusitis. 2.3.2. Work-related rhinitis. Occupational rhinitis arises in response to an airborne agent present in the workplace and may be due to an allergic reaction or an irritant response (133). Causes include laboratory animals (rats, mice, guinea-pigs, etc.; 134), wood dust, particularly hard woods (Mahogany, Western Red Cedar, etc.; 135), mites (136), latex (137), enzymes (138), grains (bakers and agricultural workers; 139, 140) and chemicals such as acid anhydrides, platinum salts (141), glues and solvents (142). Occupational rhinitis is frequently underdiagnosed due to under-reporting and/or a lack of doctor awareness (133, 143). Diagnosis is suspected when symptoms occur in relation to work. Differentiating between immunologic sensitization and irritation may be difficult. Given the high prevalence of rhinitis in the general population, whatever the cause, then objective tests confirming the occupational origin are essential (144). Measures of inflammatory parameters via nasal lavage and the objective assessment of nasal congestion both offer practical means of monitoring responses (133). Growing experience with acoustic rhinometry and peak nasal inspiratory flow (PNIF) suggests that these methods may have a role in monitoring and diagnosing (145). The surveillance of sensitized workers may enable an early detection of occupational asthma. 2.3.3. Drug-induced rhinitis. Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) commonly induce rhinitis and asthma (Table 5). The disease has recently been defined as aspirin-exacerbated respiratory disease (146). In a population-based random sample, aspirin hypersensitivity was more frequent among subjects with allergic rhinitis than among those without (2.6%vs 0.3%; 147). In about 10% of adult patients with asthma, aspirin and other NSAIDs that inhibit cyclo-oxygenase (COX) enzymes (COX-1 and COX-2) precipitate asthma attacks and naso-ocular reactions (148). This distinct clinical syndrome, called aspirin-induced asthma, is characterized by a typical sequence of symptoms: an intense eosinophilic inflammation of the nasal and bronchial tissues combined with an overproduction of cysteinyl leukotrienes (CysLT; 149) and other prostanoids (150, 151). After the ingestion of aspirin or other NSAIDs, an acute asthma attack occurs within 3 hours, usually accompanied by profuse rhinorrhoea, conjunctival injection, periorbital edema and sometimes a scarlet flushing of the head and neck. Aggressive nasal polyposis and asthma run a protracted course, despite the avoidance of aspirin and cross-reacting drugs (152). Blood eosinophil counts are raised and eosinophils are present in nasal mucosa and bronchial airways. Specific anti-COX-2 enzymes are usually well tolerated in aspirin-sensitive patients (149) but many are no longer marketed. A range of other medications is known to cause nasal symptoms. These include: reserpine (154); guanethidine (155); phentolamine (156); methyldopa (155); ACE inhibitors (157); α-adrenoceptor antagonists; intraocular or oral ophthalmic preparations of β-blockers (158); chlorpromazine and oral contraceptives. The term rhinitis medicamentosa (159–161) applies to the rebound nasal obstruction which develops in patients who use intranasal vasoconstrictors chronically. The pathophysiology of the condition is unclear; however, vasodilatation and intravascular edema have both been implicated. The management of rhinitis medicamentosa requires the withdrawal of topical decongestants to allow the nasal mucosa to recover, followed by treatment of the underlying nasal disease (162). Cocaine sniffing is often associated with frequent sniffing, rhinorrhoea, diminished olfaction and septal perforation (163, 164). Amongst the multiuse aqueous nasal, ophthalmic and otic products, benzalkonium chloride is the most common preservative. Intranasal products containing this preservative appear to be safe and well tolerated for both long- and short-term clinical use (165). 2.3.4. Hormonal rhinitis. Changes in the nose are known to occur during the menstrual cycle (166), puberty, pregnancy (167, 168) and in specific endocrine disorders such as hypothyroidism (169) and acromegaly (170). Hormonal imbalance may also be responsible for the atrophic nasal change in postmenopausal women. A hormonal PER or rhinosinusitis may develop in the last trimester of pregnancy in otherwise healthy women. Its severity parallels the blood estrogen level (171). Symptoms disappear at delivery. In a woman with perennial rhinitis, symptoms may improve or deteriorate during pregnancy (172). 2.3.5. Nasal symptoms related to physical and chemical factors. Physical and chemical factors can induce nasal symptoms which may mimic rhinitis in subjects with sensitive mucous membranes and even in normal subjects if the concentration of chemical triggers is high enough (173, 174). Sudden changes in temperature can induce nasal symptoms in patients with allergic rhinitis (175). Chronic effects of cold dry air are important. Skier’s nose (cold, dry air; 176) has been described as a distinct entity. However, the distinction between a normal physiologic response and a disease is not clear and all rhinitis patients may exhibit an exaggerated response to unspecific physical or chemical stimuli. Little information is available on the acute or chronic effects of air pollutants on the nasal mucosa (177). The alterations of physiologic nasal respiration is of importance for any athlete. The impact of exercise on rhinitis and the effect of rhinitis on exercise received considerable attention before the 1984 Olympics, where evidence indicated that chronic rhinitis frequently occurs and deserves specific management in athletes (178). Athletes suffering from symptoms of rhinitis were shown to have impaired performances (179). Many active athletes suffer from allergic rhinitis during the pollen season (180, 181) and most of these receive treatment for their nasal symptoms. On the other hand, some conditions induce nasal symptoms. This is the case of the skier’s nose, a model of cold-induced rhinitis (176, 182–184), or rhinitis in competitive swimmers who inhale large quantities of chlorine gas or hypochlorite liquid (185–187). In runners, nasal resistance falls to about half of its resting values. Decongestion begins immediately after starting running and persists for around 30 min after (27). In multiple chemical sensitivities, nasal symptoms such as impaired odor perception may be present (188). 2.3.6. Rhinitis in smokers. In smokers, eye irritation and odor perception are more common than in nonsmokers (189). Tobacco smoke can alter the mucociliary clearance (190) and can cause an eosinophilic and ‘allergic’-like inflammation in the nasal mucosa of nonatopic children (191). Some smokers report a sensitivity to tobacco smoke including headache, nose irritation (rhinorrhoea, nasal congestion, postnasal drip and sneezing) and nasal obstruction (192). However, in normal subjects, smoking was not found to impair nasal QOL (193). Nonallergic rhinitis with eosinophilia syndrome (NARES) might be caused by passive smoking inducing an ‘allergy-like’ inflammatory response (194). 2.3.7. Food-induced rhinitis. Food allergy is a very rare cause of isolated rhinitis (195). However, nasal symptoms are common among the many symptoms of food-induced anaphylaxis (195). On the other hand, foods and alcoholic beverages in particular may induce symptoms by unknown nonallergic mechanisms. Gustatory rhinitis (hot, spicy food such as hot red pepper; 196) can induce rhinorrhoea, probably because it contains capsaicin. This is able to stimulate