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. 2012 Jul;23(4):607-15.
doi: 10.1097/EDE.0b013e3182572563.

PM10-induced hospital admissions for asthma and chronic obstructive pulmonary disease: the modifying effect of individual characteristics

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PM10-induced hospital admissions for asthma and chronic obstructive pulmonary disease: the modifying effect of individual characteristics

Cristina Canova et al. Epidemiology. 2012 Jul.

Abstract

Background: Evidence suggests that oxidative stress is a unifying feature underlying the toxic actions of particulate matter (PM). We have investigated whether individual plasma antioxidant concentrations (uric acid and vitamins C, A, and E) and 10 antioxidant genes modify the response to PM with respect to hospital admissions for chronic obstructive pulmonary disease (COPD) or asthma.

Methods: Using a bidirectional, hospital-based, case-crossover study, 209 patients admitted for asthma or COPD to the Chelsea and Westminster Hospital (London), with 234 admissions, were recruited between May 2008 and July 2010. PM10 levels in the area of Kensington and Chelsea at the time of admission were compared with the levels 14 days before and 14 days after the event. Conditional logistic regression was used to estimate the effect of PM10 at several temporal lags, while controlling for confounders.

Results: An increase in asthma/COPD admission rate was related to a 10 μg/m increase in PM10, with the highest effect noted 0-3 days before the exacerbation (for lag 0-3, odds ratio = 1.35 [95% confidence interval = 1.04-1.76]). Serum vitamin C modified the effect of PM10 on asthma/COPD exacerbations. A similar (although weaker) influence was observed for low levels of uric acid and vitamin E, whereas vitamin A showed no effect modification. GSTP1 (rs1695), SOD2 (rs4880), and Nrf2 (rs1806649) were associated with a trend toward an increased risk of hospital admissions during periods of high PM10 levels.

Conclusions: Our study suggests that the concentration of antioxidants in patients' serum modifies the short-term effects of PM10 on asthma and COPD exacerbations.

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