This study shows an association between secular improvements in air quality in southern California and measurable improvements in lung-function development in children. Improved lung function was most strongly associated with lower levels of particulate pollution (PM 2.5 and PM 10 ) and nitrogen dioxide. These associations were observed in boys and girls, Hispanic white and non-Hispanic white children, and children with asthma and children without asthma, which suggests that all children have the potential to benefit from improvements in air quality.

In addition to improvements in lung-function development from 11 to 15 years of age, we also found a strong association between a reduction in air pollution and a reduction in the proportion of children with clinically low FEV 1 and FVC at 15 years of age. In general, the age range of 11 to 15 years captures a period during which lungs are developing rapidly in both boys and girls. Lung-function development continues in girls until their late teens and in boys until their early 20s, but at a much-reduced rate as compared with the rate during the earlier adolescent period.15,16 It is therefore likely that the improved function we observed in the children who were less exposed to the pollutants will persist into their adulthood. A higher level of lung function in early adulthood may decrease the risk of respiratory conditions.17 However, the greatest benefit of improvements in lung-function development may occur later in life, because it has been shown that greater lung function in adulthood can contribute to lower risks of premature death and other adverse health outcomes.18-24 Consistent with the growth effects we have observed in children, there is evidence that reduced exposure to pollution in adulthood can slow the decline in lung function25 and increase life expectancy.26,27

In southern California, motor vehicles are a primary source of PM 2.5 , PM 10 , and nitrogen dioxide, through direct tailpipe emissions as well as downwind physical and photochemical reactions of vehicular emissions.28,29 Gasoline-powered and diesel-powered engines contribute to high levels of these pollutants, and improved emission standards for both types of vehicles have contributed to the observed declines in air pollutants. Control strategies implemented in the 1970s and 1980s focused primarily on reducing the levels of ozone, a pollutant with a long history of demonstrated acute health effects.30 Although levels of ozone continued to decline in the 1990s and 2000s, the changes were smaller than for nitrogen dioxide and particulate matter, and we did not observe ozone-related effects on lung-function growth. This finding is consistent with our previous report that decreased lung-function growth was related to increased exposure to nitrogen dioxide and particulate matter but not to ozone.6 Only a few other studies have addressed the long-term effects of ozone on lung function in children, and the results have been inconsistent.31 Because of high correlations among reductions of PM 2.5 , PM 10 , and nitrogen dioxide (Table S6 in the Supplementary Appendix), we could not assess the independent associations between lung function and each of these pollutants. Many other studies have also been unable to identify the health effects of specific pollutants that are constituents of a multipollutant mixture.3,32 However, the results of our investigation make it clear that broad-based efforts to improve general air quality are associated with substantial and measurable public health benefits.

A main directive of the 1970 U.S. Clean Air Act was to establish “…ambient air quality standards…allowing an adequate margin of safety…requisite to protect the public health….” A basic tenet of the act is that changes in airborne pollutant levels can lead to improved public health and that the scientific evidence needed to determine the appropriate levels for those standards can be identified. Our observation of improvements in air quality and subsequent improvements in longitudinal respiratory health outcomes may provide objective evidence in support of that basic tenet.

The data necessary to conduct this study were collected over a period of nearly two decades. Strengths of the study include the use of consistent protocols for collecting health, covariate, and air-quality data over the entire study period. Although the extended follow-up period can be viewed as a strength, it also presented several challenges. A change in spirometers during the course of the study was necessary to replace aging equipment and raises the issue of instrumental comparability. To address this, we conducted an additional analysis to show that our findings are robust to the use of different spirometers (Table S7 in the Supplementary Appendix).

The change from annual testing in cohorts C and D to testing every other year in cohort E, as a result of budgetary constraints, may raise concern about dropout of participants in cohort E. In general, bias can occur in a cohort study if dropout depends simultaneously on both outcome and exposure. In our study, however, participant attrition during the follow-up period was not jointly associated with baseline lung function and several measures of exposure, including cohort membership and cohort-specific mean levels of nitrogen dioxide and particulate matter, the pollutants that showed significant associations with lung-function growth. In addition, the magnitude and significance of our observed growth effects were similar among participants with complete follow-up (Table S4 in the Supplementary Appendix), making it unlikely that selective dropout is responsible for our observed associations.

The shift in ethnic background across cohorts to a more Hispanic population, synchronous with general trends occurring more broadly in southern California,33,34 raises potential concerns about confounding by factors specific to ethnic background. Also, because this is an observational study, it is possible that one or more additional factors associated with both lung-function growth and change in air quality over time could confound our pollution analyses. However, we conducted many sensitivity analyses and found that none of these factors appreciably affected our estimates or inferences. Furthermore, because the mean growth in height from 11 to 15 years of age did not vary over the study period, one might conclude that the change in growth is specific to the lung, with improvement in air quality serving as an important contributing factor.

Another limitation of our study is the lack of a pure “control” community — that is, a community in which there was no change in pollution during the study period. However, we studied five different communities with differing magnitudes of improvement in air quality, which collectively serve as five replicate experiments of our within-community temporal-trend experiment. We conducted an additional analysis that showed that the expected gain in lung function over time within any one community was aligned with the magnitude of improvement in air quality within that community (Fig. S5 in the Supplementary Appendix). The trends in these effects suggest that if we had had a pure control community, we would have seen little change in lung-function growth. This analysis also suggests that even modest improvements in air quality can lead to improved health, although with only five communities included in the study, we caution that we do not have adequate data to make definitive conclusions about the exposure–response relationship.