RT Journal Article
SR Electronic
T1 Evaluation of cardiopulmonary effects and oxidative stress in sugarcane workers compared to a control population exposed to outdoor biomass air pollution
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP p4193
VO 38
IS Suppl 55
A1 Gustavo Prado
A1 Ubiratan Santos
A1 Mário Terra-Filho
A1 Dirce Zanetta
A1 Renato Paceli
YR 2011
UL http://erj.ersjournals.com/content/38/Suppl_55/p4193.abstract
AB Brazil is the world's largest producer of sugar and alcohol. The practice of burning the sugarcane field in the night before harvesting in order to facilitate cropping and thereby increase productivity is still very common. This biomass burning emits large amounts of particulate (PM) and gaseous pollutants to the atmosphere.With the aim of studying cardiopulmonary impacts and oxidative stress in a population of 113 sugarcane workers (SW) and 109 local healthy controls (C), we evaluated lung function tests (LFTs), blood pressure (BP), heart rate variability (HRV) – in submaximal treadmill protocol – and laboratory tests in pre-harvest and harvest periods. All subjects were male non-smokers. Data were submited to univariate and LMM multivariate analysis.Results: Median age was 28.4 (C) and 23 (SW); P=0.02.In the harvest period (median atmospheric PM2.5=75.3μg/m3 in sugarcane tillage area vs 27.7μg/m3 in city area) there was a significant higher increase in CPK levels in SW than in control subjects, as well as a higher reduction in LFTs. We also found a significant higher increase in diastolic BP and decrease in HRV among sugarcane workers in harvest period. Another important result, was the statistically significant reduction in antioxidants enzymes SOD, GST and GPX in the harvest period, much more expressive among sugarcane workers than in control subjects.We conclude, therefore, that even in healthy populations, exposure to biomass outdoor pollution can cause cardiopulmonary detrimental effects with potential clinical relevance and that such impacts can be probably explained by the physiopathologic pathway of oxidative stress.