Birds or zebras?

In this issue of Allergy, Curtis et al. (1) report the results of indoor pigeon allergen sampling in dust and air in order to establish allergen contamination data of outdoor animals. They found high indoor levels of pigeon allergens in the vicinity of outdoor pigeon nests, but also in houses and hospitals that did not have pigeons in the immediate surroundings. Their study was undertaken following questions on indoor exposure by pigeon sensitive patients and an occupational physician. Because of the high allergenicity of pigeon allergens, they reasoned that even a low exposure to wild pigeon allergens may cause respiratory disease, especially ‘hypersensitivity pneumonitis’ (2–7). One could seriously wonder why such an effort should be undertaken. Should we really consider pigeon allergens as a cause of substantial morbidity? Are allergy or allergic alveolitis due to wild pigeons diseases that are underreported, misclassified, easy to miss, sometimes hard to prove, but nevertheless often seriously disabling and potentially fatal (8), or are they ‘zebras’ (9)? With respect to diagnostics, the current study has several implications, and raises new questions. Extrinsic allergic alveolitis, hypersensitivity pneumonitis, or allergic alveolitis (AA) which is the recently recommended term (10) owing to the fact that organic material was recognized as a separate disease almost 300 years ago (11). More than 40 specific etiologic agents, including animal proteins, bacteria, fungi, insect proteins, chemicals, and drugs, have been identified since the 1960s (8, 12). Owing to effective preventive measures in occupational medicine, AA nowadays mainly occurs as a result of domestic exposures, and bird allergens constitute the majority of the causative agents (8). The estimated prevalence of AA among pigeon breeders varies between 1 and 10%, depending on the definition used (13, 14). AA has also been described in pigeon breeder’s offspring (15–22), but the prevalence of AA or allergy owing to wild pigeons in the general population is unknown. City pigeons have been able to adapt and survive efficiently in the larger metropolitan areas in the West: it is estimated that pigeon populations equal roughly 2% of the size of the human population of large cities (Bundes Arbeitgruppe, Stadttauben, Germany, personal communication), and are mainly concentrated in the inner city areas. Pigeon allergens may cause more respiratory disease than is generally assumed for several reasons. The current study suggests that pigeon allergens can be present in sufficiently high concentrations in public buildings to cause AA or allergy to pigeon allergens. There is no doubt that the prevalence of allergy and asthma in the Western world is increasing (23). Hence, allergens may induce allergy and/or asthma more easily than a few decades ago. Typical inner city allergens from cockroach and mice have been implicated to play a role in the worldwide increase of prevalence of asthma and allergy (24–26), and pigeon allergens may act likewise in causing allergy, asthma, AA, or both (27). Traditionally, pigeon breeder’s lung has been described in adults keeping pigeons and, occasionally, in their offspring. It is never considered in patients who do not keep birds themselves. However, in the last 2 years four case reports appeared on AA owing to wild city pigeons (2–5), and the presence of AA in a teacher of the pigeoninfested high school reported by Curtis et al. (1) may be regarded as the fifth one. It seems highly unlikely that AA as a result of wild pigeons would be limited to these cases: we may be looking at the tip of an iceberg. As allergen avoidance does not really apply or cannot be realized for wild pigeons, it seems to be of most importance that general physicians and (pediatric) pulmonologists realize that AA owing to pigeons may Allergy 2002: 57: 566–569 Printed in UK. All rights reserved Copyright # 2002 Blackwell Munksgaard