Redefining idiopathic interstitial lung disease into occupational lung diseases by analysis of chemical composition of inhaled dust particles in induced sputum and/or lung biopsy specimens.

There has been increased public awareness of the potential danger from exposure to hazardous dust in various occupations. This study aims to validate the qualitative analysis of scanning electron microscopy (SEM) of lung samples by 1) correlation of induced sputum (IS) findings to clinical findings, 2) comparing hazardous particles in IS to those in biopsied lung specimens, and 3) assessing whether the particles present in the lungs of transplanted patients correlate with occupational history of dust exposure. Forty patients with occupational history were included; of whom 35 filled in questionnaires. Twenty-four of them had SEM analysis of their IS, and 11 of these 24 also had SEM analysis of their lung tissue. Another 11 lung biopsies from patients with occupational history were scanned by SEM and compared with 10 lung biopsies from patients with no occupational history. SEM analysis of IS was as efficient for detecting hazardous particles as was SEM analysis of lung tissue; silica was detected better in sputum. Exposure to silica was the main chemical element associated with a high likelihood to show abnormalities in IS (Odds ratio 19.41 CI = 0.270-1398.33). The average number of detected hazardous chemical elements in patients with an occupational history of exposure was 4 +/- 1.61 in IS and 3.55 +/- 2.02 in lung tissue (P = 0.57); it was 1.5 +/- 0.85 from transplanted occupationally exposed patients compared with 0.36 +/- 0.67 in transplanted non-exposed patients (P = 0.003). SEM analysis of particles in IS and lung tissue can elucidate the causative agent(s) of otherwise idiopathic interstitial lung disease among occupationally exposed workers.

Sarcoidosis: an organized pattern of reaction from immunology to therapy.

Advances in our understanding of sarcoidosis and other granulomatous disorders were discussed at a recent meeting. In particular, the role of cytokines and cell interactions, and the expression of specific T-cell receptor molecules, were considered in relation to the regulation of the pathogenesis of these diseases in humans.

IgE values in the allergic and healthy Israeli population.

This study was designed to establish IgE values in different allergic diseases in an Israeli population and healthy controls. The geometric mean IgE in the control group was 41 IU/mL (range = 15 to 111 IU/mL) and in the atopic group 142 IU/mL (range = 36 to 556 IU/mL). The highest values were found in patients with asthma plus allergic rhinitis plus atopic dermatitis and asthma plus atopic dermatitis. The lowest values were from patients with urticaria. There was a gradual increase in IgE levels from 4 to 10 years and then a gradual decrease. IgE was significantly higher in males, particularly in the 21 to 40-year age group and above 60 years. There was no difference in IgE levels in the various ethnic groups. There was a correlation between IgE levels and the number of positive skin tests. Peripheral eosinophilia was found in one-third of the patients with low IgE and in 2/3 of the patients with IgE above 500 IU/mL. An IgE of 120 IU/mL or more was found in 56% of patients with asthma in addition to other atopic diseases. Only 10% of normal controls had an IgE value of 120 IU/mL or more. These results are similar to those reported from European and North American countries.

Suppressor cell activity of human alveolar macrophages in interstitial lung diseases.

It has been shown that alveolar macrophages (AM) are able to modulate lymphocyte proliferation in vitro. The purpose of this study was to evaluate the effect of AM on the proliferation of autologous peripheral lymphocytes (APL) in patients with interstitial lung disease (ILD) compared to controls. Thirty patients were investigated: eight with idiopathic pulmonary fibrosis (IPF), nine with sarcoidosis(SA), seven with rheumatoid arthritis (RA) and six controls (CO). AM and APL were co-cultured at an increasing macrophage/lymphocyte ratio: 1%, 10%, 20% and 50%. A dose-dependent effect was observed and related to the number of AM added to APL, enhancing at low ratios and suppressing at high ratios. Suppression of proliferation by 50% AM differed in the four groups tested: 94.6% (92-98) in IPF, 73.0% (49-100) in SA, 43% (25-57) in RA, 32.4% (22-41) in the CO (P less than 0.01, P less than 0.05, and P0.05 respectively, compared to CO). Suppressive cell activity of AM from patients with ILD was higher than suppressive cell activity of the CO group. Suppression with 10% of AM in ILD group was 18% (2.2-62) compared with 2.58% (-13-17) in the CO group (P less than 0.05). 20% AM in ILD group showed 35% (3-76) suppression in comparison with 9.76% (-11-27) in the control group (P less than 0.01), 50% AM in ILD have a suppressive activity of 71% (25-100) in contrast to 32.4% (22-41) in control (P less than 0.01). In conclusion, AM from patients with interstitial lung diseases have a significantly stronger suppressive effect on the proliferation of autologous peripheral lymphocytes than controls. This is a new aspect of the study of activation of AM in these kinds of disorders.