Neurobehavioral effects of ambient air pollution on cognitive performance in US adults
Introduction
Ambient air pollution, especially the particulate matters (PM), has increasingly been appreciated as a threat to cardiopulmonary health (Kaiser, 2005, Nel, 2005). Following several reports in the early 1990s showing excessive mortality associated with unexpectedly low PM concentrations (Pope and Dockery, 2006), hundreds of epidemiologic studies have reported fairly consistent associations between elevated PM concentrations over short periods of 1 or several days and increased cardiovascular mortality and morbidity (e.g., hospitalizations, emergency visits). Recent meta-analyses also confirmed a consistent and positive association between short-term ambient ozone and cardiovascular mortality (Bell et al., 2005, Ito et al., 2005, Levy et al., 2005). Short-term elevations of PM and ozone can increase ischemic stroke mortality (Henrotin et al., 2007, Hong et al., 2002) and morbidity (Chan et al., 2006, Wellenius et al., 2005). In addition, large cohort studies have demonstrated that long-term exposures to ambient air pollutants are associated with increased cardiovascular mortality (Dockery et al., 1993, Pope et al., 2002) and PM exposure increases the risks for coronary heart diseases and stroke. (Miller et al., 2007) Paralleling this epidemiologic literature are intriguing findings from clinical experiments (Brook et al., 2002, Rundell et al., 2007) and in vivo animal models (Sun et al., 2005, Suwa et al., 2002), all pointing to the possibility that ambient air pollutants can perturb endothelial function, damage microvasculature, and eventually cause progression of atherosclerosis. Given the strong associations of cognitive aging with these clinical conditions and neuropathological processes (Knopman et al., 2001), it is plausible that long-term exposures to ambient air pollutants may affect neurocognitive function in humans. Various in vivo experiments with exposures to ozone, PM, or particles–ozone mixtures have found the neurotoxic effects in different animal models (Dorado-Martinez et al., 2001, Elder et al., 2006, Rivas-Arancibia et al., 1998, Sirivelu et al., 2006, Sorace et al., 2001), supporting the adverse neurocognitive effect of exposure to ambient air pollution. In the recent cross-sectional analysis of extant neurocognitive function data collected among 202 children enrolled in a birth cohort, high levels of black carbon (a marker for traffic particles) were associated with decreased cognitive function across assessments of verbal and nonverbal intelligence and memory constructs (Suglia et al., 2008). However, epidemiological data linking the cognitive function in adults with exposure to ambient air pollution are still lacking. The following study was carried out to address this significant data gap.
Section snippets
Study design
Our secondary analyses used the extant data on central nervous system (CNS) function from the Third National Health and Nutrition Examination Survey (NHANES III) conducted by the National Center for Health Statistics (NCHS) of the Centers for Disease Control and Prevention between 1988 and 1994. Details about this survey and related methods have been published (NCHS, 1995). In brief, the NHANES III followed a multi-stage stratified random sampling of the U.S. population, with oversampling of
Characteristics of study population
Table 1 shows the population characteristics of the source population of adult participants in NHANES-III, 1988–1991. Compared to participants with estimable air pollutant data (N = 3944), subjects with missing exposure data were slightly younger (p < 0.0001) and more likely to be non-Hispanic whites (p < 0.0001), had lower family income (p < 0.001), and more likely came from rural areas (p < 0.001) or communities with lower poverty-income ratio (p < 0.0001). These comparisons denoted that the missing data
Discussion
Our analyses demonstrated that, reduced performance in neurobehavioral tests in US adults (aged 20–59 years) was associated with estimated increasing levels of estimated annual exposure to ambient ozone prior to the examination in 1988–1991. Such a putatively ozone-associated CNS effect could not be completely attributable to the between-individual differences in demographics, socioeconomic factors, lifestyles, household characteristics, urban/rural locations, and conventional CVD risk factors.
Conclusions
Our study provided the first epidemiological data supporting the adverse effects of ambient air pollutants on CNS in adults. Longitudinal studies are needed to fully investigate whether long-term exposure to air pollution causes neurobehavioral changes and subsequent development of neurocognitive impairments, including cognitive decline (global and within specific domains) and dementia.
Conflict of interest
The authors declare that there are no conflicts of interest.
Acknowledgements
This work was supported in part by the National Institute of Environmental Health Sciences grant ES00002 and Environmental Protection Agency (EPA) grants EPA R827353 and R832416. The authors thank two anonymous reviewers for helpful comments.
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