Environmental research · 2007
Short-term exposure to air pollution and inflammation-sensitive biomarkers.
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Steinvil Arie, Kordova-Biezuner Levana, Shapira Itzhak, Berliner Shlomo, Rogowski Ori
Аннотация
OBJECTIVES: To evaluate the effect of short-term exposure to air pollutants on inflammation-sensitive biomarkers in apparently healthy individuals.
METHODS: We enrolled all participants from The Tel-Aviv Sourasky Medical Center inflammation survey held between 2003 and 2006, excluding participants with an acute or chronic inflammatory disease, pregnancy, steroidal or nonsteroidal treatment, or a recent invasive procedure. Additional subjects were excluded for living more than 11km from the nearest air pollution monitoring station. Analysis was performed separately for men and women. Linear regression models were fitted for each inflammatory variable against air pollutant variables (particulate matter under 10microm, sulfur dioxide, nitrogen dioxide, carbon monoxide, and ozone) for increasing lag times of up to 7 days, and adjusted for all possible and known confounding parameters.
RESULTS: The study population comprised 3659 individuals (2203 males and 1456 females). We found a statistically significant negative correlation in the male population between air pollutants, mainly NO2, SO2, and CO, and fibrinogen in several lag days. A positive correlation was found for PM10 at day 7. No such correlation was found for CRP and WBC, or for the female population.
CONCLUSION: Our findings do not support the potential link between short-term exposure to air pollution and enhanced inflammation as a possible explanation for increased cardiovascular morbidity. Additional large-scale population-based studies with good methodological design are needed in order to clarify this issue.
METHODS: We enrolled all participants from The Tel-Aviv Sourasky Medical Center inflammation survey held between 2003 and 2006, excluding participants with an acute or chronic inflammatory disease, pregnancy, steroidal or nonsteroidal treatment, or a recent invasive procedure. Additional subjects were excluded for living more than 11km from the nearest air pollution monitoring station. Analysis was performed separately for men and women. Linear regression models were fitted for each inflammatory variable against air pollutant variables (particulate matter under 10microm, sulfur dioxide, nitrogen dioxide, carbon monoxide, and ozone) for increasing lag times of up to 7 days, and adjusted for all possible and known confounding parameters.
RESULTS: The study population comprised 3659 individuals (2203 males and 1456 females). We found a statistically significant negative correlation in the male population between air pollutants, mainly NO2, SO2, and CO, and fibrinogen in several lag days. A positive correlation was found for PM10 at day 7. No such correlation was found for CRP and WBC, or for the female population.
CONCLUSION: Our findings do not support the potential link between short-term exposure to air pollution and enhanced inflammation as a possible explanation for increased cardiovascular morbidity. Additional large-scale population-based studies with good methodological design are needed in order to clarify this issue.