"Our study revealed significant deficits in lung function growth in children with long-term exposure to air pollutants," wrote Isabelle Romieu, M.D., M.P.H., lead author of the study.
"In addition to the important impact of lung health, early lung deficits may increase the risk of developing chronic obstructive lung disease later in life, as well as cardiovascular morbidity and general mortality.
These conclusions are the result of a three-year, multi-site prospective study that measured lung function growth in 3,170 eight-year-old children at 39 schools in Mexico City and analyzed it with respect to the children's exposure to common urban pollutants: ozone (O3), nitrogen dioxide (NO2), and particulate matter under 10 ėm (PM10).
Dr. Romieu, of the Instituto Nacional de Salud Publico in Mexico, and eight colleagues reported their findings in the second issue for August of the American Journal of Respiratory and Critical Care Medicine, published by the American Thoracic Society.
Previous studies have found that short-term exposure to pollutants is associated with acute but reversible deficits in lung function, but the effects of long-term exposure, like that experienced by residents of heavily polluted urban environments, had not been conclusively characterized.
The researchers analyzed forced vital capacity in one second (FVC1); forced expiratory flow, midexpiratory phase (FEF25-75); and forced expiratory volume in one second (FEV1) in the schoolchildren at six month increments over three years to determine the effects of pollutant exposure, which was measured by air monitoring stations within 2 km of the children's schools.
They conducted personal exposure assessments on 60 randomly selected children in the study to ensure that the air monitoring station data was an accurate representation of individual exposure.
Although all measurements of lung function increased over time, the researchers found that higher exposure to O3, NO2 and PM10 was significantly associated with growth deficits in FVC and FEV1.
"At the beginning of the study and at each phase of follow-up, children exposed to lower O3 and PM10 concentrations had better lung function values that children exposed to higher concentrations," wrote the researchers.
Strikingly, the effect of pollutant exposure on FEV1 among the children in their study was slighter greater than the effect of exposure to maternal smoking among children in the United States.
The study could not determine the mechanism by which pollutants change lung growth, but other studies have found differences in lung morphology related to O3 exposure, and suggested that chronic exposure to PM and O3 may be associated with small airway disease.
Recently, oxidative stress from oxidant compounds, including O3, NO2 and PM has been identified as a potential cause of an inflammatory response, which could then lead to chronic lung damage. The reversibility of the damage is unclear, but the authors note that previous studies have reported long-term deficits in lung function associated with air pollutants.
"Although we could not identify specific sources [of the pollutants], the effect is likely to be due to vehicular exhaust," wrote the researchers, concluding that "there is a clear need for stricter air pollution measures in Mexico City to protect lung growth in children living there."