Summary There was a reduced prevalence of symptoms of Extrinsic Allergic Alveolitis (EAA) among the cigarette smokers in a survey of 102 volunteer pigeon breeders. These smokers had a significantly lower antibody response against the inhaled antigens associated with the disease; only one of twenty‐three smokers (4.3%), but thirty‐nine of sixty‐five non‐smokers (55.4%) had elevated serum IgG antibody levels, despite similar degrees of avian exposure in each group. The appearance of antibody in six of fourteen ex‐smokers (42.9%) suggested that the apparent inhibitory effect of smoking on the antibody response was reversible. The smoking group had lower total serum IgG and IgA, higher serum IgD, and their total IgM and IgE levels were similar to the non‐smokers.

The purpose ofthis study was

SUMMARY Extrinsic allergic alveolitis (synonym: hypersensitivity pneumonitis) is caused by inhaling antigenic aerosols which induce hypersensitivity responses in susceptible individuals. It is an interstitial inflammatory disease affecting the distal, gas‐exchanging parts of the lung, in contrast to allergic asthma where the inflammation is more proximal, affecting the conducting airways. The aims of this review are to describe current concepts of the immunology of this model of lung inflammation, to describe some of the constitutional and environmental characteristics which affect disease susceptibility and development, and to describe topics for prospective study.

Extrinsic allergic alveolitis (also known as hypersensitivity pneumonitis) is caused by repeated inhalation of mainly organic antigens by sensitized subjects. This induces a hypersensitivity response in the distal bronchioles and alveoli and subjects may present clinically with a variety of symptoms. The aims of this review are to describe the current concepts of the immunological response, the diverse clinical presentation of this disease, the relevant investigations and management, and areas for future studies.

An association between pigeon breeders' disease and serum IgG antibodies to antigens derived from pigeon has been recognised since the first description of this type of hypersensitivity pneumonitis in 1965.'The relationship between exposure, circulating IgG antibody against pigeon protein antigens, and the development of pigeon breeders' disease remains uncertain,2 however, and this is reflected in the results of clinical studies. Patients reported in detail,3 usually with an acute, severe illness, typically have an intense antibody response and are rarely antibody negative4; whereas surveys conducted among the general population of pigeon fanciers regularly identify people who are apparently affected but who lack serum antibodies.5 6 Furthermore, these studies have found an appreciable proportion of healthy fanciers who do have circulating antibody against pigeon proteins, and it has been suggested that the humoral response largely reflects the intensity of exposure. used a radioimmunoassay technique to investigate the humoral antibody response and the factors which influence this and the development of pigeon breeders' disease in a large group of pigeon fanciers. MethodsPigeon fanciers in Central Scotland were approached through meetings organised at their local pigeon racing clubs and any person regularly exposed to pigeons, whether primarily engaged in the hobby or helping a relative with the pigeon husbandry, was asked to complete a questionnaire and provide a 20 ml venous blood sample. The questionnaire was divided into several sections, the questions generally requiring a simple "yes/no" reply. One section related to the circumstances and degree of exposure, another concerned the presence of any immediate or delayed symptoms after contact with the pigeons, and a further section recorded the details of any other illnesses. The completed questionnaires were coded and the data transferred to the disc storage of a PDPI 1/45 computer. Criteria for extrinsic allergic alveolitis were derived from Christensen et al,6 requiring a delayed (6-12 hours after exposure) respiratory symptom, 274 on 9 May 2018 by guest. Protected by copyright.