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SERUM CONCENTRATION OF ACE, NEOPTERIN, TNF-α AND SIL-2R IN HEALTHY WORKERS EXPOSED TO DIFFERENT METAL DUSTS

Harald C Ott, Christian Prior, Manfred Herold, Markus Riha, Guenter OttDepartment of Cardiac Surgery, Department of Medicine, University Hospital Innsbruck

PATIENTS:

155 healthy employees of a glass manufacturer company, a hard-metal plant, a tool manufacturer company and a biochemical plant were examined:

• 57 workers exposed to lead dust and fumes

• 38 workers exposed to hard-metal dust

• 14 workers exposed to molybdenum dust and fumes

• 17 workers exposed to hard-metal grinding-coolant aerosol

• 29 workers exposed to organic dust

METHODS:

Blood samples were collected during a routine medical check up, the serum was separated and the serum probes were kept frozen auntil further analysis.

Serum concentrations were determined using commercially available enzyme assays

RESULTS:

CONCLUSION:

Each of the studied inhalative exposures seemes to induce a characteristic cytokine pattern and therefore a specific inflammatory answer. This can be considered as an early adverse effect.

Increased levels of the serum markers measured in this study are a common finding in patients suffering from active interstitial lung disease. Wether our observations highlight an ongoing disease or indicate only a physiological reaction remains unclear.

INTRODUCTION:

Chronic lead and hard-metal exposure can cause severe occupational lung disease.

The aim of the study was to detect early adverse effects of chronic inhalative metal dust and fume exposure by measurement of different serum markers.

Corresponding author:

Harald C Ott MD, Department of Cardiac Surgery, University Hospital Innsbruck, Anichstraße , 6020

Innsbruck, AUSTRIA, Fax: 00435125042528, Phone: 00435125043806, e-mail: [email protected]

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Fig.1 to 4: Serum levels of Neopterin, sIL-2R, ACE and TNF-alpha in different groups of workers

p<0,001

p<0,01

p<0,05

Lead exposure triggers sIL-2R and TNF-α release. Hard-metal exposure induces TNF-α release. Grinding-coolant exposure induces TNF-α and neopterin release. Molybdenum exposure causes Neopterin release.

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