Based on our results, exposure to traffic in general (distance to roadways) appears to have adverse effects on lung function in adults with asthma and rhinitis. To our knowledge, ours is the first study to report associations between traffic exposure and lung function among adults with known airway disease. Somewhat surprisingly, our findings suggest that it is not just exposure to traffic from major roadways with high traffic density which affects lung function in persons with asthma because distance to nearest roadway of any type was as strong of a predictor of lung function as distance to major roadway. This result was not likely due solely to the effect of major roadways because very few of our subjects lived near such roadways and the magnitude of the effect was similar for distance to nearest roadway of any type (usually a local road).
While multiple previous studies have assessed the effect of traffic exposures on asthma prevalence or risk of wheezing (e.g., risk of disease), there has been relatively little study of disease severity, with the few such studies limited to children. Thus, the effects of such exposures on health outcomes among adults with asthma are not well characterized. A 10-year retrospective study of health care utilization by adult asthmatic patients living in areas of Buffalo, NY, near the heavily trafficked U.S.-Canadian border crossing showed an association with traffic volume and asthma hospitalizations 29
. A somewhat similar ecological study showed that there were more hospitalizations for asthma in urbanized compared to rural areas of six Pennsylvania counties 30
. Daily vehicular traffic count and miles of roads/highways were two of the parameters of urbanization used in the Pennsylvania study. As noted in the introduction, poor asthma control was reported more frequently in adult survey respondents with the disease living within 500 ft of intersections with the highest quintile of traffic density in Southern California communities 13
A strength of the current analysis is its nesting within a larger population of adults with airway disease who have been well characterized and longitudinally followed. The health outcomes used here have been validated in other analyses of the study population 17, 18, 21, 31
. Another strength is the relatively robust traffic data available in California that is not always the case in other jurisdictions. Finally, unlike the Buffalo and Pennsylvania ecological studies, we were able to adjust for potential confounding of the relationships between traffic exposure metrics and asthma outcomes by SES using individual household income, smoking, and BMI data. This adjustment did not affect the associations with lung function, and did not substantively improve the associations with health status and asthma QoL
A major limitation to our study is potential exposure misclassification due to lack of measurements of concentrations of traffic-generated pollutants at participants’ homes as well as the fact that few of our participants lived close to major roadways, for example, in inner city areas or within 75 m of a freeway or highway. In addition, exposures to traffic emissions also occur away from home and our traffic exposure assignments were based solely on residential address. The measurement error inherent in our approach to traffic exposure assessment has likely led to an underestimate of traffic-related effects on lung function. Another limitation is the relatively small sample size, which may have limited our power to find statistically significant associations between traffic exposures and general health status or asthma quality of life. Although there are more subjects in the larger cohort, we limited this analysis to those with complete data for both spirometry and traffic exposures. Our study may not be generalizable beyond northern California, an area with generally low exposures to certain ambient pollutants, in particular, sulfur dioxide and acid sulfates. Because adult asthma is largely a disease of women, our cohort was predominantly female, reducing potential generalizablility to males.
Our results showing a positive association with distance to roadways and lung function in asthmatic adults are consistent with findings in non-asthmatic children and adults reported in several studies 27, 32, 33
. What is less clear, however, is why we did not find an association with either general health status or asthma-specific QoL, especially given that we have reported previously that neighborhood characteristics, including perceived exposure to traffic, were associated with the latter outcome in the larger cohort 19
. We used GIS-modeed traffic exposures for this analysis and self-report of traffic exposure has been shown to be only modestly correlated with modeled exposures 34
The mechanisms by which traffic emissions might cause reduced lung function are only partially understood, but it is known that such emissions induce a lower airway inflammatory response 35, 36
. Traffic emissions include both gases and particles that are capable of inducing oxidant injury. In particular, diesel exhaust particles emitted by heavy-duty vehicles have been shown to be cytotoxic as well as to enhance allergic inflammatory responses in sensitized individuals 37
. Airway remodeling has been hypothesized to be a consequence of recurrent or chronic oxidant injury 38
. A recent study of the effects of a 2-hour exposure to traffic in asthmatic subjects that documented both acute lung function decrements and increased sputum myeloperoxidase provides biological plausibility for airway remodeling from repeated exposures over long time periods.36
In summary, we have shown that distance to nearest roadway and nearest major roadway are associated with reduced lung function in a cohort of asthmatic adults. These results confirm similar findings reported in studies of children and suggest the need to control traffic emissions as a whole rather than the specific pollutant-by-pollutant approach that is currently used in both Europe and North America.