A Panel Study on Lung Function and Bronchial Inflammation among Children Exposed to Ambient SO₂ from an Oil Refinery

To determine the acute effects on respiratory function of children exposed to sulphur dioxide (SO₂), we conducted two population-based longitudinal investigations near a major oil refinery. We enrolled 233 children, age 8⁻14, in Sarroch (Italy). The first study entailed five monthly spirometric visi...

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Veröffentlicht in:International journal of environmental research and public health 2019-03, Vol.16 (6), p.1057
Hauptverfasser: Barbone, Fabio, Catelan, Dolores, Pistelli, Riccardo, Accetta, Gabriele, Grechi, Daniele, Rusconi, Franca, Biggeri, Annibale
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Sprache:eng
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Zusammenfassung:To determine the acute effects on respiratory function of children exposed to sulphur dioxide (SO₂), we conducted two population-based longitudinal investigations near a major oil refinery. We enrolled 233 children, age 8⁻14, in Sarroch (Italy). The first study entailed five monthly spirometric visits (Panel 5). In a subgroup, children positive for history of respiratory symptoms were tested weekly (20 times) with spirometry and fractional exhaled nitric oxide (FeNO) measurement (Panel 20). Baseline questionnaires and daily diaries were recorded. SO₂, NO₂, PM and O₃ were measured by monitoring stations. Multiple regression models were fitted. Using a multipollutant model, we found that a 10 µg/m³ SO₂ increase at lag0⁻2 days determined a percent variation (PV) of -3.37 (90% confidence interval, CI: -5.39; -1.30) for forced expiratory volume after one second (FEV1) in Panel 5 and a PV = -3.51 (90% CI: -4.77; -2.23) in Panel 20. We found a strong dose-response relation: 1-h SO₂ peaks >200 µg/m³ at lag2 days = FEV1 PV -2.49. For FeNO, we found a PV = 38.12 (90% CI: 12.88; 69.01) for each 10 µg/m³ SO₂ increase at 8-h time lag and a strong dose-response relation. Exposure to SO₂ is strongly associated with reduction of lung function and an increase in airway inflammation. This new evidence of harmful effects of SO₂ peaks should induce regulatory intervention.
ISSN:1660-4601
1661-7827
1660-4601
DOI:10.3390/ijerph16061057