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Background  In the year 2000 Corus closed its steel plant operations in Redcar, NE of England temporarily for refurbishment of its blast furnace. This study investigates the impact of the closure on the chemical composition and biological activity of PM 10  collected in the vicinity of the steel plant.    Methods  The metal content of PM 10  samples collected before during and after the closure was measured by ICP-MS in order to ascertain whether there was any significant alteration in PM 10  composition during the steel plant closure. Biological activity was assessed by instillation of 24 hr PM 10  samples into male Wistar rats for 18 hr (n = 6). Inflammation was identified by the cellular and biochemical profile of the bronchoalveolar lavage fluid. Metal chelation of PM 10  samples was conducted using Chelex beads prior to treatment of macrophage cell line, J774,  in vitro  and assessment of pro-inflammatory cytokine expression.    Results  The total metal content of PM 10  collected before and during the closure period were similar, but on reopening of the steel plant there was a significant 3-fold increase (p < 0.05) compared with the closure and pre-closure samples. Wind direction prior to the closure was predominantly from the north, compared to south westerly during the closure and re-opened periods. Of metals analysed, iron was most abundant in the total and acid extract, while zinc was the most prevalent metal in the water-soluble fraction. Elevated markers of inflammation included a significant increase (p < 0.01) in neutrophil cell numbers in the bronchoalveolar lavage of rats instilled with PM 10  collected during the reopened period, as well as significant increases in albumin (p < 0.05). Extracts of PM 10  from the pre-closure and closure periods did not induce any significant alterations in inflammation or lung damage. The soluble and insoluble extractable PM 10  components washed from the reopened period both induced a significant increase in neutrophil cell number (p < 0.05) when compared to the control, and these increases when added together approximately equalled the inflammation induced by the whole sample. PM 10  from the re-opened period stimulated J774 macrophages to generate TNF-α protein and this was significantly prevented by chelating the metal content of the PM 10  prior to addition to the cells.    Conclusion  PM 10 -induced inflammation in the rat lung was related to the concentration of metals in the PM 10  samples tested, and activity was found in both the soluble and insoluble fractions of the particulate pollutant.

The effect of refurbishing a UK steel plant on PM10 metal composition and ability to induce inflammation