Article

Exposure to Particulate Air Pollution and Cognitive Decline in Older Women

Rush Institute for Healthy Aging, Rush University Medical Center, Chicago, IL 60625, USA.
Archives of internal medicine (Impact Factor: 17.33). 02/2012; 172(3):219-27. DOI: 10.1001/archinternmed.2011.683
Source: PubMed

ABSTRACT

Chronic exposure to particulate air pollution may accelerate cognitive decline in older adults, although data on this association are limited. Our objective was to examine long-term exposure to particulate matter (PM) air pollution, both coarse ([PM 2.5-10 μm in diameter [PM(2.5-10)]) and fine (PM <2.5 μm in diameter [PM(2.5)]), in relation to cognitive decline.
The study population comprised the Nurses' Health Study Cognitive Cohort, which included 19,409 US women aged 70 to 81 years. We used geographic information system-based spatiotemporal smoothing models to estimate recent (1 month) and long-term (7-14 years) exposures to PM(2.5-10), and PM(2.5) preceding baseline cognitive testing (1995-2001) of participants residing in the contiguous United States. We used generalized estimating equation regression to estimate differences in the rate of cognitive decline across levels of PM(2.5-10) and PM(2.5) exposures. The main outcome measure was cognition, via validated telephone assessments, administered 3 times at approximately 2-year intervals, including tests of general cognition, verbal memory, category fluency, working memory, and attention.
Higher levels of long-term exposure to both PM(2.5-10) and PM(2.5) were associated with significantly faster cognitive decline. Two-year decline on a global score was 0.020 (95% CI, -0.032 to -0.008) standard units worse per 10 μg/m(3) increment in PM(2.5-10) exposure and 0.018 (95% CI, -0.035 to -0.002) units worse per 10 μg/m(3) increment in PM(2.5) exposure. These differences in cognitive trajectory were similar to those between women in our cohort who were approximately 2 years apart in age, indicating that the effect of a 10-μg/m(3) increment in long-term PM exposure is cognitively equivalent to aging by approximately 2 years.
Long-term exposure to PM(2.5-10) and PM(2.5) at levels typically experienced by many individuals in the United States is associated with significantly worse cognitive decline in older women.

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    • "Air pollution epidemiology has traditionally focused on cardiovascular and respiratory outcomes. These adverse associations have been extended to show the acceleration of cognitive decline of elderly communitybased populations12345and neurodevelopmental impairments of children[6,7]. The causes of cognitive impairment are being analyzed in rodent and cell models, which implicate neuroinflammatory responses to urban air pollutants891011. "
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    ABSTRACT: The basis for air pollution-associated neurodegenerative changes in humans is being studied in rodent models. We and others find that the ultrafine particulate matter (PM) derived from vehicular exhaust can induce synaptic dysfunction and inflammatory responses in vivo and in vitro. In particular, a nano-sized subfraction of particulate matter (nPM, PM0.2) from a local urban traffic corridor can induce glial TNFα production in mixed glia (astrocytes and microglia) derived from neonatal rat cerebral cortex. Here, we examine the role of TNFα in neurite dysfunctions induced by nPM in aqueous suspensions at 12 μg/ml. First, we show that the proximal brain gateway to nPM, the olfactory neuroepithelium (OE), rapidly responds to nPM ex vivo, with induction of TNFα, activation of macrophages, and dendritic shrinkage. Cell interactions were further analyzed with mixed glia and neurons from neonatal rat cerebral cortex. Microglia contributed more than astrocytes to TNFα induction by nPM. We then showed that the threefold higher TNFα in conditioned media (nPM-CM) from mixed glia was responsible for the inhibition of neurite outgrowth by small interfering RNA (siRNA) TNFα knockdown and by TNFα immunoneutralization. Despite lack of TNFR1 induction by nPM in the OE, experimental blocking of TNFR1 by TNFα receptor blockers restored total neurite length. These findings implicate microglia-derived TNFα as a mediator of nPM in air pollution-associated neurodegenerative changes which alter synaptic functions and neuronal growth.
    Full-text · Article · Dec 2016 · Journal of Neuroinflammation
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    • "PM exposure has been linked with CI in humans [21, 22, 23, 24]. While PM between 2.5 and 10 microns in size have been associated with a decrease in cognitive performance [22], PM smaller than 2.5 microns have also been linked to poor verbal learning, executive function and memory among elderly [23]. In a national study of 1,764 adults, every 10 microgram per cubic meter increase in PM levels resulted in a less than 1 unit decrease in DSST scores [24]. "
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    ABSTRACT: Recent studies report a link between common environmental exposures, such as particulate matter air pollution and tobacco smoke, and decline in cognitive function. The purpose of this study was to assess the association between exposure to polycyclic aromatic hydrocarbons (PAHs), a selected group of chemicals present in particulate matter and tobacco smoke, and measures of cognitive performance among elderly in the general population. This cross-sectional analysis involved data from 454 individuals aged 60 years and older from the 2001-2002 National Health and Nutrition Examination Survey. The association between PAH exposures (as measured by urinary biomarkers) and cognitive function (digit symbol substitution test (DSST)) was assessed using multiple linear regression analyses. After adjusting for age, socio-economic status and diabetes we observed a negative association between urinary 1-hydroxypyrene, the gold standard of PAH exposure biomarkers, and DSST score. A one percent increase in urinary 1-hydroxypyrene resulted in approximately a 1.8 percent poorer performance on the digit symbol substitution test. Our findings are consistent with previous publications and further suggest that PAHs, at least in part may be responsible for the adverse cognitive effects linked to tobacco smoke and particulate matter air pollution.
    Full-text · Article · Feb 2016 · PLoS ONE
    • "In one population cohort study comprising of 19,409 US women aged 70 to 81 years old, long-term exposure to coarse particulate matter (2.5 – 10 μm) as well as fine particulate matter (less than 2.5 μm) in air pollution was assessed in relation to cognitive decline. The results of study showed that long-term exposure to both coarse as well as fine particulate matter was associated with significantly faster cognitive decline in older women [50]. Similarly, a separate study analyzed the effects of exposure of black carbon, a marker of trafficrelated particles, on 671 older men and found that increased level of exposure during the previous 1 to 11 years was linked with worse cognitive function in older men [51]. "
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Questions & Answers about this publication

  • Luc LR Int Panis added an answer in Air Pollution:
    Air pollution epidemiology
    Several Epidemiological studies have consistently associated exposure to ambient air pollution with pulmonary and cardiovascular diseases and cancer.
    (Brunekreef et al. 2002; Pope et al. 2002; Loft et al.2008)
    Luc LR Int Panis
    Do not forget about the neurological effects of air pollution.
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      [Show abstract] [Hide abstract]
      ABSTRACT: Chronic exposure to particulate air pollution may accelerate cognitive decline in older adults, although data on this association are limited. Our objective was to examine long-term exposure to particulate matter (PM) air pollution, both coarse ([PM 2.5-10 μm in diameter [PM(2.5-10)]) and fine (PM <2.5 μm in diameter [PM(2.5)]), in relation to cognitive decline. The study population comprised the Nurses' Health Study Cognitive Cohort, which included 19,409 US women aged 70 to 81 years. We used geographic information system-based spatiotemporal smoothing models to estimate recent (1 month) and long-term (7-14 years) exposures to PM(2.5-10), and PM(2.5) preceding baseline cognitive testing (1995-2001) of participants residing in the contiguous United States. We used generalized estimating equation regression to estimate differences in the rate of cognitive decline across levels of PM(2.5-10) and PM(2.5) exposures. The main outcome measure was cognition, via validated telephone assessments, administered 3 times at approximately 2-year intervals, including tests of general cognition, verbal memory, category fluency, working memory, and attention. Higher levels of long-term exposure to both PM(2.5-10) and PM(2.5) were associated with significantly faster cognitive decline. Two-year decline on a global score was 0.020 (95% CI, -0.032 to -0.008) standard units worse per 10 μg/m(3) increment in PM(2.5-10) exposure and 0.018 (95% CI, -0.035 to -0.002) units worse per 10 μg/m(3) increment in PM(2.5) exposure. These differences in cognitive trajectory were similar to those between women in our cohort who were approximately 2 years apart in age, indicating that the effect of a 10-μg/m(3) increment in long-term PM exposure is cognitively equivalent to aging by approximately 2 years. Long-term exposure to PM(2.5-10) and PM(2.5) at levels typically experienced by many individuals in the United States is associated with significantly worse cognitive decline in older women.
      Full-text · Article · Feb 2012 · Archives of internal medicine