History Of Dust Exposure Research Articles

Cell markers, cytokines, and immune parameters in cement mason apprentices

Cement masons are known to have significant silica exposure, and silica exposure and silicosis are thought to increase risk of autoimmune disease. Because the mechanisms remain obscure, with inconclusive reports of systemic immune effects following silica exposure, our goal was to identify potential early markers of silica-related immunologic and respiratory effects. We conducted a cross-sectional study of cement mason apprentices and electrician (control) apprentices. Demographics, dust exposure history, symptoms, spirometry, exhaled nitric oxide, and blood (for immunoglobulins, cytokines, cell counts, and surface markers) were obtained from 11 cement mason apprentices and a comparison group of 21 electrician apprentices. Masons had significantly higher (P < 0.05) masonry dust exposure (42 versus 9 dust-hour-years), serum interleukin-1beta (IL-1beta; 12 versus 9 pg/ml), IL-2 (20 versus 8 pg/ml), IL-4 (193 versus 67 pg/ml), IL-10 (44 versus 21 pg/ml), and interferon-gamma (139 versus 65 pg/ml) compared with electricians. In contrast, masons had significantly lower percentages of CD25+ (12% versus 20%) and CD69+ (4% versus 9%) lymphocytes. Mason apprentices had higher levels of serum proinflammatory cytokines and lower percentages of CD25+ and CD69+ lymphocytes than did electrician apprentices. These preliminary findings suggest that mason apprentices may be at greater risk of a systemic proinflammatory state that is potentially linked to immune dysregulation. Although distinct limitations of this preliminary data are recognized, this is consistent with early biologic effects leading to increased incidence of autoimmune disease among silica-exposed workers. Prospective studies are needed to validate these initial findings and clarify the temporal sequence of observed relationships.

Recurrent pneumonia in a 38-year-old female

A 38-year-old Japanese female was referred to Kurume University Hospital (Kurume, Japan) because of recurrent pneumonia. She had no particular medical history, had never undergone a blood transfusion and was taking no regular medication or treatment. She had a negative smoking history, did not own any pets and denied a history of dust exposure. Her family history was unremarkable. She had successfully completed three vaginal deliveries and had been well until the age of 35 years, which is when she experienced her first episode of pneumonia. The pneumonia was cured by the administration of β-lactam antibiotics. She then suffered three more episodes of pneumonia within 3 years. She denied any history of accidental aspiration, weight loss or haemoptysis, and did not have pyrexia, night sweats or sputum production between the episodes of pneumonia.

Antithetical effect of tumor necrosis factor-αgene polymorphism on coal workers' pneumoconiosis (CWP)

Inter-individual variation in the severity of pneumoconiosis has been described, even with the same environmental exposure. We hypothesized that TNF-alpha promoter polymorphisms associate with lung responses to environmental exposure in coal worker's pneumoconiosis (CWP) patients. We examined polymorphisms at -238, -308, and -376 in 124 patients with CWP who had similar dust exposure history and in 122 non-exposed controls. CWP patients were divided into two groups: (1) nodular CWP (n = 84); (2) progressive massive fibrosis (PMF) (n = 44). The -308 A allele frequency was higher in patients with CWP compared to controls (6.35% and 2.05%, P < 0.01). It was also higher in patients with nodular CWP compared to PMF (P < 0.05). Logistic regression analysis revealed that patients with the -308 A allele were 3.8 times (P = 0.036) and those with smoking habit were 2.3 times (P < 0.002) more likely to have nodular CWP than PMF. TNF-alpha-308 A allele might interact with smoking to enhance susceptibility to nodular CWP.

British Thoracic Society study of cryptogenic fibrosing alveolitis: current presentation and initial management. Fibrosing Alveolitis Subcommittee of the Research Committee of the British Thoracic Society.

Mortality due to cryptogenic fibrosing alveolitis (CFA) is increasing, particularly in the elderly. Optimum management remains uncertain and previous studies of the disease have largely been from specialist centres. A national study was carried out of the presentation and initial management of CFA in the UK. All respiratory physicians in England, Scotland and Wales were invited to enter patients with newly diagnosed CFA over a two year period. CFA was diagnosed on histological grounds or according to clinical criteria which included the absence of a defined connective tissue disorder or pneumoconiosis. Participating physicians (n = 150) completed a questionnaire at patient entry and at all subsequent follow up visits and death. A total of 588 patients (373 men, 63%) were studied of whom 441 (75%) were referrals from primary care. Their mean (SD) age was 67.4 (10.0) years and median duration of symptoms at presentation was 9.0 months. Clubbing was more common in men (203/373; 54%) than in women (86/ 215; 40%); 209 patients (36%) were graded as severely breathless at presentation. A history of dust exposure (organic or inorganic) was present in 274 patients (47%) of whom 87 had had some exposure to asbestos. Subjects exposed to dust were more likely to have smoked and had slightly higher mean lung volumes, but were otherwise indistinguishable from those not exposed in terms of clinical presentation, management, and outcome. Transbronchial biopsy specimens were taken in 164 patients (28%) and open lung biopsy specimens in 73 (12%), but 60% had no histological diagnostic procedure. Biopsy procedures were more likely to be performed in younger patients, those with better lung function, and those with a history of asbestos exposure. At presentation a decision not to initiate specific treatment was made in 284 cases (48%). The decision to initiate treatment was made predominantly on symptomatic grounds. Two years after the close of entry to the study 266 patients (45%) had died. CFA is predominantly a disease of elderly patients and has a poor prognosis. Physicians generally considered CFA to be a clinical diagnosis and did not initiate treatment in up to half of patients at presentation.

Identification of inorganic dust particles in bronchoalveolar lavage macrophages by energy dispersive x-ray microanalysis.

This study shows that energy dispersive x-ray microprobe analysis to identify and quantify intracellular particles in macrophages obtained by the minimally invasive method of bronchoalveolar lavage (BAL) can detect inorganic dust exposures of many different kinds. Bronchoalveolar lavage macrophages from 22 patients have been examined. Twelve patients had occupational exposure to asbestos, talc, silica, hard metal or printing ink, while 10 had no known history of dust exposure. X-ray microprobe analysis identified particles which related to the known exposures, superimposed on a background of other particles related to smoking (kaolinite and mica) or to the general environment (silicon, titanium, and iron). The particle identification provided useful objective confirmation of the known exposures, except for silica, which could not be distinguished from the general background levels. X-ray microanalysis using BAL macrophages can be helpful for clarification of mixed dust exposures, to identify particles when light microscopy indicates retained dust in patients with no known history of exposure, and to monitor retained particles after removal from exposure.

Honeycomb Lung (Interstitial Fibrosis)

<h3>Common</h3> [Cystic bronchiectasis] Histiocytosis X (especially eosinophilic granuloma) Idiopathic interstitial fibrosis (Hamman-Rich ) Pneumoconiosis Sarcoidosis <h3>Uncommon</h3> Amyloidosis Chemical inhalation (late stage) Desquamative interstitial pneumonitis (DIP) Drug sensitivity, chronic or recurrent (eg, nitrofurantoin, hexamethonium, busulfan) Gaucher disease Lipoid pneumonia (eg, mineral oil aspiration) [Lymphangiomyomatosis] Oxygen toxicity [Mucoviscidosis] Neurofibromatosis Rheumatoid lung Scleroderma; dermatomyositis Sensitivity pneumonitis, recurrent (eg, farmer's lung, bagassosis) Tuberous sclerosis (Entities in brackets can be confused roentgenographically with true honeycomb lung. ) <h3>Diagnosis</h3> Eosinophilic granuloma. <h3>COMMENTS</h3> In analyzing this Gamut, a number of the possibilities offered, such as chemical inhalation, rheumatoid lung, and scleroderma are excluded by the lack of specific clinical information. Of the common causes, cystic bronchiectasis tends to show fluid in the cysts and to expand on inspiration; pneumoconiotics have a history of dust exposure. Therefore, idiopathic interstitial fibrosis (the

Eosinophilic granuloma of the lung.

Eosinophilic granuloma limited to the lung has not to our knowledge been previously reported. Two histologically proved cases recently observed, and carefully followed, are recorded in the following pages. Eosinophilic granuloma involving both lung and bone, diagnosed by biopsy of the osseous lesions, has been reported on three occasions (6, 8, 9). To these three cases another is added. The cases presented here have all been confirmed by surgical biopsy and histologic study. This, we believe, is the first report of histologic confirmation of the lung lesion. Finzi (1), in 1929, recorded the first case of eosinophilic granuloma of the bone. His diagnosis was“a myeloma with preponderance of eosinophilic cells.” Otani and Ehrlich (5) and Lichtenstein and Jaffe (3) established the condition as an entity in 1940. Since these early descriptions there has been a tendency to expand the entity to include cases in which there are multiple bone lesions and even extra-osseous lesions, such as those involving lymph nodes, skin, lungs, and other organs (2). We feel that with the present report a further step is taken in this direction. Eosinophilic Granuloma Limited to the Lung Case I: A 32-year-old white male had a chronic cough developing during the winter of 1948–49, with the production of 50 to 120 c.c. of sputum daily. He complained of fatigue and night sweats but denied having fever or chills. A provisional diagnosis of pulmonary tuberculosis was made and he was admitted to Fitzsimons Army Hospital. He had lost 40 pounds in weight. He gave a history of dust exposure from September 1947 to January 1948. Physical examination was negative except for the presence of râles in both lungs. X-ray examination revealed a diffuse and patchy granulomatous type of pulmonary infiltrate (Fig. 1) widely disseminated throughout both lung fields, showing a peculiar nodular quality. The nodules ranged in size from almost miliary dimensions to 1.5 cm. in diameter. Their margins were hazy. They were made more apparent, or striking, by scattered areas of lucency interpreted as emphysema. In the background, throughout, the films showed a mild degree of fibrosis. The total white blood count was 18,500, with 83 per cent polymorphonuclear neutrophils but no eosinophils. A tuberculin (PPD, 1st strength) skin reaction was 1 plus; histoplasmin skin reaction 2 plus; coccidioidin skin test negative. Repeated examinations of sputum were negative for acid-fast bacilli and fungi. On Aug. 24, 1949, a left thoracotomy was performed. Lung tissue from the left lower lobe was submitted for examination.