By Soroush Nomigolzar, MD, and Nancy Selfridge, MD
Dr. Nomigolzar is Clinical Skills Facilitator, Department of Clinical Foundations at Ross University School of Medicine, Barbados, West Indies
Dr. Selfridge is Professor, Department of Clinical Foundations at Ross University School of Medicine, Barbados, West Indies
Dr. Nomigolzar and Dr. Selfridge report no financial relationships relevant to this field of study.
• Despite evidence of a pathological central nervous system vascular inflammatory effect of air pollution from animal experiments and human autopsy studies, cohort study results relating longitudinal exposure to air pollution and cognitive decline have been mixed.
• In this analysis of data from two large prospective study cohorts living in the same limited geographical area in northern Manhattan, researchers investigated the relationship between exposure to air pollution and evidence of cognitive decline. They based their findings on global cognition scores measured by periodic administration of validated neuropsychological testing.
• Evidence of cognitive decline was associated with higher levels of ambient air pollution in both cross-sectional and longitudinal analyses for one large cohort, but not the other.
SYNOPSIS: In this large prospective cohort study of subjects in Manhattan, researchers demonstrated an association between exposure to air pollution and decline in cognitive function over time in one cohort, but not the other.
SOURCE: Kulick ER, Wellenius GA, Boehme AK, et al. Long-term exposure to air pollution and trajectories of cognitive decline among older adults. Neurology 2020;94:e1782-1792.
Air pollutants are potent oxidants that can lead to oxidative stress and inflammation.1 As a result, ambient air pollution has been associated with various cardiovascular and respiratory diseases.2-3 Recently, there has been a growing interest in a potential link between air pollution and neurological damage, especially in the elderly, for whom cognitive decline is a major mobidity.4 Despite evidence of a pathological central nervous system vascular inflammatory effect of air pollution from animal experiments and human autopsy studies, cohort study results relating longitudinal exposure to air pollution and cognitive decline have been mixed.5-9
In the study reviewed, Kulick et al used data from two prospective cohorts of individuals residing in the northern Manhattan area of New York City to investigate the association between long-term exposure to ambient air pollution and cognitive decline, both cross-sectionally and longitudinally. The data collection was obtained from two ongoing prospective cohort studies of residents in northern Manhattan: the Washington Heights-Inwood Community Aging Project (WHICAP) and the Northern Manhattan Study (NOMAS). WHICAP is a study of aging and dementia and recruited its participants in three different waves in 1992, 1999, and 2010. WHICAP used the following inclusion criteria:
- equal proportion of Hispanic, non-Hispanic Black, and non-Hispanic White participants;
- equal proportion of participants age 65-74 years and > 75 years.
Subjects with substantial cognitive problems, history of dementia, or who were unable to speak English or Spanish were excluded. Additional participants were selected from the NOMAS project, established to study stroke risk factors prospectively in multiethnic individuals living in the same community. Participants were recruited between 1993 and 2001 and 2003 and 2008. A subcohort of NOMAS recruits received neuropsychological assessment as a baseline between 2003 and 2008. Inclusion criteria for this group were:
- age > 50 years;
- no clinical stroke or clinically identified dementia;
- no contraindications to magnetic resonance imaging.
All individuals from this cohort had at least one follow-up neuropsychological assessment after five years. The final sample selected by Kulick et al for data analysis (n = 5,330 from WHICAP; n = 1,093 from NOMAS) included those subjects with no baseline dementia, at least one neuropsychological exam during the study, whose primary address was in New York City, and no missing data for the confounding variables.
Satellite and Environmental Protection Agency data for nitrogen dioxide (NO2), fine particulate matter (PM2.5), and respirable particulate matter (PM10) were used in validated, regionalized, universal geostatistical kriging models to estimate the residential air pollution exposure in the calendar year prior to enrollment. Cognitive function, represented by a global cognitive score, was calculated using validated neuropsychological tests assessing three domains of cognitive function (memory, executive function, language) and standardized as Z-scores with cohort-specific means and standard deviations. Sociodemographic data for analysis included age at time of cognitive testing, race-ethnicity, and educational level. A summary Z-score for socioeconomic status was calculated for each subject based on census information of neighborhood measures of wealth, education and occupation. Data from the WHICAP and NOMAS cohorts were analyzed separately. Linear mixed models were used for repeated measures assessing the relationship between exposure to air pollutants and both baseline cognitive function and cognitive decline. Data analysis suggests that in the WHICAP cohort, higher levels of ambient air pollution were associated with cognitive decline at baseline as well as a higher rate of cognitive decline over time. (See Table 1.) However, in NOMAS, there was no significant association between residential ambient air pollution and baseline cognitive decline or rate of decline in cognitive function.
The populations in WHICAP and NOMAS were similar in most aspects except that NOMAS had a younger cohort, with a median age of 70 years (±9.0) compared to WHICAP’s 75.2 years (±6.46), lower prevalence of cardiovascular disease, and included a higher percentage of Hispanic individuals (43% in WHICAP, 66% in NOMAS). The mean levels of air pollutants also were similar between the two groups, but NOMAS had less variability in pollutant levels. These differences between WHICAP and NOMAS were cited by the authors as possible explanations for the differences in observed outcomes between the two cohorts. The younger NOMAS cohort could explain the better baseline cognition as well as less decline in cognition upon follow-up for this group. Moreover, individuals in the WHICAP cohort had more cardiovascular diseases, which may have contributed to greater decline in cognition.
Interestingly, the greater percentage of Hispanic individuals in the NOMAS cohort suggests a potential underlying protective factor in Hispanic populations, possibly as the result of genetics or lifestyle factors, such as nutrition, exercise, and alcohol use. Another factor that might have influenced outcomes is that WHICAP was a significantly larger cohort, which increases the power of the data analysis compared to NOMAS. Finally, the NOMAS data excluded individuals with pre-existing dementia and history of stroke or cardiac events, creating a potential selection bias.
Even though this study had some limitations, and findings were not consistent between the two cohorts, the results of WHICAP adds to the evidence base linking higher levels of ambient air pollution with accelerated cognitive decline. Further studies on this topic will help to solidify the association between ambient air pollution and cognitive decline. In the meantime, the findings can help physicians become more sensitive to the possibility of accelerated cognitive decline in their patients and maintain increased vigilance for early symptoms and signs. Although many patients may not be able to move away from high pollution, awareness of this modifiable risk factor can help physicians focus on preventive measures, such as increasing indoor air quality with air purifiers and patient education concerning home cleaning and regular air filter changes. Finally, physicians who are so inclined may use this data to support ongoing public and political advocacy for clean air.
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