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Inflammatory responses to the occupational inhalation of metal fume

¹ Medical Research Council (MRC) Environmental Epidemiology Unit, ³ Infection, Inflammation and Repair Division, University of Southampton, Southampton, and ⁴ School of Pharmacy and Biomedical Sciences, Institute of Biomedical and Biomolecular Sciences, University of Portsmouth, Portsmouth, UK, ² The Royal Naval Hospital, Gibraltar.

CORRESPONDENCE: K. Palmer, MRC Environmental Epidemiology Unit, Southampton General Hospital, Southampton SO16 6YD, UK. Fax: 44 2380704021. E-mail: ktp{at}mrc.soton.ac.uk

Keywords: Inflammation, metal fume, occupational, pneumonia, welding

Received: May 4, 2005
Accepted October 19, 2005

Occupational exposure to metal fume promotes a reversible increase in the risk of pneumonia, but by mechanisms which are unclear. To investigate, the current authors measured various markers of host defence function in welders and nonwelders.

Induced sputum and venous blood samples were collected from 27 welders with regular long-term exposure to ferrous metal fume and 31 unexposed matched controls. In sputum, the present authors measured cell counts, the soluble and cellular iron concentration, and levels of interleukin-8, tumour necrosis factor-, myeloperoxidase, matrix metalloproteinase-9, immunoglobulin (Ig)A, ₂-macroglobulin and unsaturated iron-binding capacity. Blood samples were assayed for evidence of neutrophil activation and pneumococcal IgG antibodies.

Welders had significantly higher iron levels and a substantially lower unsaturated iron-binding capacity in their sputum, but, despite a high iron challenge, there was a noteworthy absence of an inflammatory response. Only blood counts of eosinophils and basophils were significantly related to the extent of welding. Weak nonsignificant trends were observed for several other measures, consistent with low-grade priming of neutrophils.

In conclusion, these data suggest that chronic exposure to metal fume blunts responsiveness to inhaled particulate matter. However, the mechanism behind the lack of detectable local inflammatory response requires further investigation.

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