Lupus · 2012
Atmospheric pollution: influence on hospital admissions in paediatric rheumatic diseases.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Vidotto J P, Pereira L A A, Braga A L F, Silva C A, Sallum A M, Campos L M, Martins L C, Farhat S C L
Аннотация
OBJECTIVE: To investigate the lag structure effects from exposure to atmospheric pollution in acute outbursts in hospital admissions of paediatric rheumatic diseases (PRDs).
METHODS: Morbidity data were obtained from the Brazilian Hospital Information System in seven consecutive years, including admissions due to seven PRDs (juvenile idiopathic arthritis, systemic lupus erythematosus, dermatomyositis, Henoch-Schönlein purpura, polyarteritis nodosa, systemic sclerosis and ankylosing spondylitis). Cases with secondary diagnosis of respiratory diseases were excluded. Daily concentrations of inhaled particulate matter (PM(10)), sulphur dioxide (SO(2)) nitrogen dioxide (NO(2)), ozone (O(3)) and carbon monoxide (CO) were evaluated. Generalized linear Poisson regression models controlling for short-term trend, seasonality, holidays, temperature and humidity were used. Lag structures and magnitude of air pollutants' effects were adopted to estimate restricted polynomial distributed lag models.
RESULTS: The total number of admissions due to acute outbursts PRD was 1,821. The SO(2) interquartile range (7.79 µg/m(3)) was associated with an increase of 1.98% (confidence interval 0.25-3.69) in the number of hospital admissions due to outcome studied after 14 days of exposure. This effect was maintained until day 17. Of note, the other pollutants, with the exception of O(3), showed an increase in the number of hospital admissions from the second week.
CONCLUSION: This study is the first to demonstrate a delayed association between SO(2) and PRD outburst, suggesting that oxidative stress reaction could trigger the inflammation of these diseases.
METHODS: Morbidity data were obtained from the Brazilian Hospital Information System in seven consecutive years, including admissions due to seven PRDs (juvenile idiopathic arthritis, systemic lupus erythematosus, dermatomyositis, Henoch-Schönlein purpura, polyarteritis nodosa, systemic sclerosis and ankylosing spondylitis). Cases with secondary diagnosis of respiratory diseases were excluded. Daily concentrations of inhaled particulate matter (PM(10)), sulphur dioxide (SO(2)) nitrogen dioxide (NO(2)), ozone (O(3)) and carbon monoxide (CO) were evaluated. Generalized linear Poisson regression models controlling for short-term trend, seasonality, holidays, temperature and humidity were used. Lag structures and magnitude of air pollutants' effects were adopted to estimate restricted polynomial distributed lag models.
RESULTS: The total number of admissions due to acute outbursts PRD was 1,821. The SO(2) interquartile range (7.79 µg/m(3)) was associated with an increase of 1.98% (confidence interval 0.25-3.69) in the number of hospital admissions due to outcome studied after 14 days of exposure. This effect was maintained until day 17. Of note, the other pollutants, with the exception of O(3), showed an increase in the number of hospital admissions from the second week.
CONCLUSION: This study is the first to demonstrate a delayed association between SO(2) and PRD outburst, suggesting that oxidative stress reaction could trigger the inflammation of these diseases.