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Background
This is a broad and diverse group of diseases which lead to a variety of histologic patterns of interstitial lung disease.
OUTLINE
EPIDEMIOLOGY CHARACTERIZATION SYNONYMS INCIDENCE AGE RANGE-MEDIAN GEOGRAPHY
DISEASE ASSOCIATIONS CHARACTERIZATION ALUMINUM
Aluminum welding fume-induced pneumoconiosis.Hull MJ, Abraham JL.
School of Medicine, SUNY Upstate Medical University, Syracuse, NY.
Hum Pathol 2002 Aug;33(8):819-25 Abstract quote Chronic exposure to high concentrations of fumes during aluminum arc welding causes a severe pneumoconiosis characterized by diffuse pulmonary accumulation of aluminum metal and a corresponding reduction in lung function. Aluminum fume-induced pneumoconiosis is a rarely reported entity, of which the true incidence is unknown.
We report the clinical, radiographic, microscopic, and microanalytic results of 2 coworkers, employed by the same aluminum shipbuilding facility, who died of complications from this disease. Scanning electron microscopy and energy dispersive x-ray analysis of the exogenous particle content in the lung tissue of these cases revealed the highest concentrations of aluminum particles (average of 9.26 billion aluminum particles per cm(3) of lung tissue) among the 812 similar analyses in our pneumoconiosis database.
One patient had an original clinical diagnosis of sarcoidosis but no evidence of granulomatous inflammation.
BERYLLIOSIS FLOUR MILL LUNG
Flour mill lung: a pneumoconiosis of mixed aetiology.Sundaram P, Kamat R, Joshi JM.
Department of Respiratory Medicine, TN. Medical College and B.YL. Nair Hospital, Mumbai.
Indian J Chest Dis Allied Sci 2002 Jul-Sep;44(3):199-201 Abstract quote We report two cases of mixed dust fibrosis which occurred in the setting of poorly ventilated flour mills where various kinds of grain, chiefly wheat, were ground using stones whose silica content was analysed to be greater than 80 percent. While one patient was a non-smoker and the other was an ex-smoker, both cooked on kerosene stoves in the same room.
We propose the term 'Flour mill lung' for this form of pneumoconiosis. A larger study would be required to establish the entity and its incidence among flour mill workers.
SILICOSIS
PATHOGENESIS CHARACTERIZATION CYTOKINES
Tumor necrosis factor-alpha gene promoter polymorphism in coal workers' pneumoconiosis.Kim KA, Cho YY, Cho JS, Yang KH, Lee WK, Lee KH, Kim YS, Lim Y.
Department of Occupational and Environmental Medicine, St Mary's Hospital, The Catholic University of Korea, Youngdunpo-gu, Seoul.
Mol Cell Biochem 2002 May-Jun;234-235(1-2):205-9 Abstract quote Tumor necrosis factor-alpha (TNF-alpha) is believed to play a central role in the pathogenesis of pneumoconiosis. TNF2, a polymorphism in the TNF-a gene promoter, has been associated with an increase in TNF-alpha production and airway inflammation.
To investigate the frequency of TNF2 in patients who have coal workers' pneumoconiosis (CWP) and to determine whether it is associated with development of a large opacity in CWP, we investigated the expression ofthe TNF2 allele in 80 patients who had CWP and in 54 healthy controls using restriction fragment length polymorphism (RFLP). Compared to controls (10.2%), the frequency of the TNF2 allele was greater in the CWP patients (20.6%).
Furthermore, the TNF2 allele was very common in patients who had a large opacity (28.2%) in comparison with 13.4% in those with simpleCWP. From these data, we suggest that the TNF2 allele is associated with the development of a large opacity in CWP.
Cytokine polymorphisms in silicosis and other pneumoconioses.Yucesoy B, Vallyathan V, Landsittel DP, Simeonova P, Luster MI.
Ankara University, Faculty of Pharmacy, Department of Toxicology, Turkey.
Mol Cell Biochem 2002 May-Jun;234-235(1-2):219-24 Abstract quote Silicosis and coal workers' pneumoconiosis are complex multifactorial lung diseases whose etiopathogenesis are not well defined.
It is generally accepted that fibrotic lung disorders are mediated by macrophage-derived cytokines and growth factors. There is evidence showing a crucial role for tumor necrosis factor-a (TNF-alpha) and interleukin-1 (IL-1) in inflammation caused by silica dust and in the transition from simple to progressive massive fibrosis.
In this review we discuss genetic polymorphisms responsible for regulating the production of these proinflammatory cytokines and their role in modifying silicosis severity.
LABORATORY/RADIOLOGIC/
OTHER TESTSCHARACTERIZATION RADIOLOGIC LABORATORY MARKERS
GROSS APPEARANCE/
CLINICAL VARIANTSCHARACTERIZATION GENERAL VARIANTS
HISTOLOGICAL TYPES CHARACTERIZATION GENERAL VARIANTS
SPECIAL STAINS/IMMUNOPEROXIDASE/
OTHERCHARACTERIZATION SPECIAL STAINS IMMUNOPEROXIDASE
DIFFERENTIAL DIAGNOSIS KEY DIFFERENTIATING FEATURES
PROGNOSIS AND TREATMENT CHARACTERIZATION PROGNOSTIC FACTORS MALIGNANCY SILICOSIS
Silica, silicosis, and lung cancer: a risk assessment.Finkelstein MM.
Occupational Health Program, McMaster University, Hamilton, Ontario, Canada
Am J Ind Med 2000 Jul;38(1):8-18 Abstract quote BACKGROUND: To investigate exposure-response relationships for silica, silicosis, and lung cancer.
METHODS: Quantitative review of the literature identified in a computerized literature search.
RESULTS: The risk of silicosis (ILO category 1/1 or more) following a lifetime of exposure at the current OSHA standard of 0.1 mg/m(3) is likely to be at least 5-10% and lung cancer risk is likely to be increased by 30% or more. The exposure-response relation for silicosis is nonlinear and reduction of dust exposures would have a greater than linear benefit in terms of risk reduction. Available data suggests that 30 years exposure at 0.1 mg/m(3) might lead to a lifetime silicosis risk of about 25%, whereas reduction of the exposure to 0.05 mg/m(3) might reduce the risk to under 5%.
CONCLUSIONS: The lifetime risk of silicosis and lung cancer at an exposure level of 0.1 mg/m(3) is high. Lowering exposures to the NIOSH recommended limit if 0.05 mg/m(3) may have substantial benefit.
TREATMENT Henry JB. Clinical Diagnosis and Management by Laboratory Methods. Twentieth Edition. WB Saunders. 2001.
Rosai J. Ackerman's Surgical Pathology. Eight Edition. Mosby 1996.
Sternberg S. Diagnostic Surgical Pathology. Third Edition. Lipincott Williams and Wilkins 1999.
Robbins Pathologic Basis of Disease. Sixth Edition. WB Saunders 1999.
DeMay RM. The Art and Science of Cytopathology. Volume 1 and 2. ASCP Press. 1996.
Last Updated 9/19/2002
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