Sources of particle number concentration and noise near London Gatwick Airport.

There is increasing evidence of potential health impacts from both aircraft noise and aircraft-associated ultrafine particles (UFP). Measurements of noise and UFP are however scarce near airports and so their variability and relationship are not well understood. Particle number size distributions and noise levels were measured at two locations near Gatwick airport (UK) in 2018-19 with the aim to characterize particle number concentrations (PNC) and link PNC sources, especially UFP, with noise. Positive Matrix Factorization was used on particle number size distribution to identify these sources. Mean PNC (7500-12,000 p cm-3) were similar to those measured close to a highly trafficked road in central London. Peak PNC (94,000 p cm-3) were highest at the site closer to the runway. The airport source factor contributed 17% to the PNC at both sites and the concentrations were greatest when the respective sites were downwind of the runway. However, the main source of PNC was associated with traffic emissions. At both sites noise levels were above the recommendations by the WHO (World Health Organisation). Regression models of identified UFP sources and noise suggested that the largest source of noise (LAeq-1hr) above background was associated with sources of fresh traffic and urban UFP depending on the site. Noise and UFP correlations were moderate to low suggesting that UFP are unlikely to be an important confounder in epidemiological studies of aircraft noise and health. Correlations between UFP and noise were affected by meteorological factors, which need to be considered in studies of short-term associations between aircraft noise and health.

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

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 PM10 collected in the vicinity of the steel plant. METHODS: The metal content of PM10 samples collected before during and after the closure was measured by ICP-MS in order to ascertain whether there was any significant alteration in PM10 composition during the steel plant closure. Biological activity was assessed by instillation of 24 hr PM10 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 PM10 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 PM10 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 PM10 collected during the reopened period, as well as significant increases in albumin (p < 0.05). Extracts of PM10 from the pre-closure and closure periods did not induce any significant alterations in inflammation or lung damage. The soluble and insoluble extractable PM10 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. PM10 from the re-opened period stimulated J774 macrophages to generate TNF-alpha protein and this was significantly prevented by chelating the metal content of the PM10 prior to addition to the cells. CONCLUSION: PM10-induced inflammation in the rat lung was related to the concentration of metals in the PM10 samples tested, and activity was found in both the soluble and insoluble fractions of the particulate pollutant.

Soluble transition metals cause the pro-inflammatory effects of welding fumes in vitro.

Epidemiological studies have consistently reported a higher incidence of respiratory illnesses such as bronchitis, metal fume fever (MFF), and chronic pneumonitis among welders exposed to high concentrations of metal-enriched welding fumes. Here, we studied the molecular toxicology of three different metal-rich welding fumes: NIMROD 182, NIMROD c276, and COBSTEL 6. Fume toxicity in vitro was determined by exposing human type II alveolar epithelial cell line (A549) to whole welding fume, a soluble extract of fume or the "washed" particulate. All whole fumes were significantly toxic to A549 cells at doses >63 microg ml(-1) (TD 50; 42, 25, and 12 microg ml(-1), respectively). NIMROD c276 and COBSTEL 6 fumes increased levels of IL-8 mRNA and protein at 6 h and protein at 24 h, as did the soluble fraction alone, whereas metal chelation of the soluble fraction using chelex beads attenuated the effect. The soluble fraction of all three fumes caused a rapid depletion in intracellular glutathione following 2-h exposure with a rebound increase by 24 h. In addition, both nickel based fumes, NIMROD 182 and NIMROD c276, induced significant reactive oxygen species (ROS) production in A549 cells after 2 h as determined by DCFH fluorescence. ICP analysis confirmed that transition metal concentrations were similar in the whole and soluble fractions of each fume (dominated by Cr), but significantly less in both the washed particles and chelated fractions. These results support the hypothesis that the enhanced pro-inflammatory responses of welding fume particulates are mediated by soluble transition metal components via an oxidative stress mechanism.