Air Pollution and Cognitive Decline
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
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 Thus, 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 morbidity.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
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. The creators recruited participants in 1992, 1999, and 2010. WHICAP administrators used these inclusion criteria: equal proportion of Hispanic, non-Hispanic Black, and non-Hispanic White participants; and equal proportion of participants age 65-74 years and > 75 years.
Subjects with substantial cognitive problems, history of dementia, or who could not 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, and no contraindications to MRI.
All individuals from this cohort attended 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. The analyses suggest 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. However, in NOMAS, there was no significant association between residential ambient air pollution and baseline cognitive decline or rate of decline in cognitive function.
COMMENTARY
The populations in WHICAP and NOMAS were similar in most aspects, except the NOMAS cohort was younger, with a median age of 70 years (±9.0) compared to WHICAP’s 75.2 years (±6.46), had a 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 there was less variability in pollutant levels in NOMAS. The authors cited these differences between WHICAP and NOMAS 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 higher 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 there were some limitations, and findings were not consistent between the two cohorts, the results of WHICAP add to the evidence base linking higher levels of ambient air pollution with accelerated cognitive decline. Further studies on this topic will help 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 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 these data to support ongoing public and political advocacy for clean air.
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- Peters A, Veronesi B, Calderón-Garcidueñas L, et al. Translocation and potential neurological effects of fine and ultrafine particles a critical update. Part Fibre Toxicol 2006;3:13.
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- Cullen B, Newby D, Lee D, et al. Cross-sectional and longitudinal analyses of outdoor air pollution exposure and cognitive function in U.K. Biobank. Sci Rep 2018;8:1-4.
- Peters R, Peters J, Booth A, Mudway I. Is air pollution associated with increased risk of cognitive decline? A systematic review. Age Ageing 2015;44:755-760.
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.
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