SUMMARYTwctity-one symptomatic subjects with pigeon breeders' lung (PBL) and 10 asymptomatic pigeon breeders, with a similar exposure to pigeon antigens, underwent bronchoalveolar lavage. Total IgG, IgM and IgA in lavage fluid were determined as were specific antibody levels against antigens in pigeon serum and droppings. Results were converted to levels in epithelial lining fluid (ELF) using lavage and serum urea ratios. It was found that symptomatics represent a group that is hyperreactive to pigeon antigens compared with the asymptomatic group with significantly higher IgG, IgM, IgA levels as well as specific antibody levels against pigeon serum and droppings. Paired serum and ELF samples from 12 symptomatic subjects showed significantly elevated IgG, IgM and IgA levels in ELF compared with serum when values were expressed in terms of albumin. This strongly supports the concept of local production of immunoglobulins within the lung after inhaling immunogens as opposed to their diffusion from the vasculature. Results for IgA indicate that any putative protective role for this immunoglobulin is not valid in relation to the prevention of extrinsic allergic alveolitis. Analysis of smoking habits, lung immunoglobulins and response to inhalation challenge confirm the negative influence of smoking on total and functional lung immunoglobulins; however, levels in the ELF of ex-smokers suggest that the effect of smoking is not permanent. Smoking did not prevent responses to inhalation challenge.

Lavage fluids were investigated for 67 subjects in 6 groups: 12 with active sarcoidosis, 8 with inactive sarcoidosis, 17 with pigeon breeder's disease, 10 asymptomatic pigeon breeders, 12 with idiopathic pulmonary fibrosis (IPF) and 8 normal subjects. Albumin and urea per ml of bronchoalveolar lavage fluid (BALF) were determined for each subject together with percentage return of fluid (BAL%). Novel assay systems were employed to measure urea and albumin and these were compared with existing analytical techniques. When compared with the control group, we found that urea per ml of BALF was not statistically different for all other groups, except those with pigeon breeder's disease who had significantly raised levels. For albumin, however, three groups had significantly higher levels than the controls, namely those with active sarcoidosis, pigeon breeder's disease and IPF. BAL% return showed no significant differences for any group when compared with the controls. We conclude that since albumin is significantly raised in most patients with interstitial lung disease it does not represent a suitable marker for the quantitation of reactive proteins in BALF. Urea shows much less variability between groups than does albumin, and hence in the absence of a proven alternative represents the most reliable estimate available of epithelial lining fluid dilution during the lavage procedure, providing dwell time is kept to a minimum.

Extrinsic allergic alveolitides (EAA) are a group of hypersensitivity lung diseases caused by organic dusts of diverse origins. Despite the similar clinical, radiological, histological, serological and pulmonary function findings, the causative allergens in the dusts do not belong to a common molecular species. All EAA dusts have particles within the respirable range (i.e. up to 5 pm) some allergens are wholly soluble, some partly soluble and others associated with insoluble particles. EAA is not due to endotoxin in dusts, and the presence of specific antibodies and sensitized lymphocytes against the allergens provides a pointer to the hypersensitivity pathways that are activated to produce disease episodes. However, some EAA dusts can activate these pathways per se at high dust levels. Exposure to EAA dusts does not always lead to sensitization, yet some people respond to extremely low levels. Heredity has little influence on EAA, and although smoking reduces the immune response to EAA dusts, it does not prevent EAA. Prevention is dependent on reducing or abolishing exposure, and several techniques are outlined.

Giant lymph node hyperplasia (Castleman's Disease) is a rare cause of pleural effusion. We report the case of a 51 yr old West Indian male, who presented with a recurrent massive pleural effusion, due to a tumour arising from the pleura. He underwent parietal pleurectomy and subtotal excision of the tumour. Histological analysis of the specimen showed the features of multicentric Castleman's disease. Nine months following surgery he remains well, with no recurrence of the effusion.

Extrinsic allergic alveolitides (EAA) are a group of hypersensitivity lung diseases caused by organic dusts of diverse origins. Despite the similar clinical, radiological, histological, serological and pulmonary function findings, the causative allergens in the dusts do not belong to a common molecular species. All EAA dusts have particles within the respirable range (i.e. up to 5 μm) some