A national cohort study (2000–2018) of long-term air pollution exposure and incident dementia in older adults in the United States
Air pollution may increase risk of Alzheimer’s disease and related dementias (ADRD) in the U.S., but the extent of this relationship is unclear. Here, we constructed two national U.S. population-based cohorts of those aged ≥65 from the Medicare Chronic Conditions Warehouse (2000–2018), combined with...
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Published in | Nature communications Vol. 12; no. 1; pp. 6754 - 9 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
19.11.2021
Nature Publishing Group Nature Portfolio |
Subjects | |
Online Access | Get full text |
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Abstract | Air pollution may increase risk of Alzheimer’s disease and related dementias (ADRD) in the U.S., but the extent of this relationship is unclear. Here, we constructed two national U.S. population-based cohorts of those aged ≥65 from the Medicare Chronic Conditions Warehouse (2000–2018), combined with high-resolution air pollution datasets, to investigate the association of long-term exposure to ambient fine particulate matter (PM
2.5
), nitrogen dioxide (NO
2
), and ozone (O
3
) with dementia and AD incidence, respectively. We identified ~2.0 million incident dementia cases (
N
= 12,233,371; dementia cohort) and ~0.8 million incident AD cases (
N
= 12,456,447; AD cohort). Per interquartile range (IQR) increase in the 5-year average PM
2.5
(3.2 µg/m
3
), NO
2
(11.6 ppb), and warm-season O
3
(5.3 ppb) over the past 5 years prior to diagnosis, the hazard ratios (HRs) were 1.060 (95% confidence interval [CI]: 1.054, 1.066), 1.019 (95% CI: 1.012, 1.026), and 0.990 (95% CI: 0.987, 0.993) for incident dementias, and 1.078 (95% CI: 1.070, 1.086), 1.031 (95% CI: 1.023, 1.039), and 0.982 (95%CI: 0.977, 0.986) for incident AD, respectively, for the three pollutants. For both outcomes, concentration-response relationships for PM
2.5
and NO
2
were approximately linear. Our study suggests that exposures to PM
2.5
and NO
2
are associated with incidence of dementia and AD.
Air pollution has been linked to neurodegenerative disease. Here the authors carried out a population-based cohort study to investigate the association between long-term exposure to PM
2.5
, NO
2
, and warm-season O
3
on dementia and Alzheimer’s disease incidence in the United States. |
---|---|
AbstractList | Air pollution may increase risk of Alzheimer's disease and related dementias (ADRD) in the U.S., but the extent of this relationship is unclear. Here, we constructed two national U.S. population-based cohorts of those aged ≥65 from the Medicare Chronic Conditions Warehouse (2000-2018), combined with high-resolution air pollution datasets, to investigate the association of long-term exposure to ambient fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3) with dementia and AD incidence, respectively. We identified ~2.0 million incident dementia cases (N = 12,233,371; dementia cohort) and ~0.8 million incident AD cases (N = 12,456,447; AD cohort). Per interquartile range (IQR) increase in the 5-year average PM2.5 (3.2 µg/m3), NO2 (11.6 ppb), and warm-season O3 (5.3 ppb) over the past 5 years prior to diagnosis, the hazard ratios (HRs) were 1.060 (95% confidence interval [CI]: 1.054, 1.066), 1.019 (95% CI: 1.012, 1.026), and 0.990 (95% CI: 0.987, 0.993) for incident dementias, and 1.078 (95% CI: 1.070, 1.086), 1.031 (95% CI: 1.023, 1.039), and 0.982 (95%CI: 0.977, 0.986) for incident AD, respectively, for the three pollutants. For both outcomes, concentration-response relationships for PM2.5 and NO2 were approximately linear. Our study suggests that exposures to PM2.5 and NO2 are associated with incidence of dementia and AD.Air pollution may increase risk of Alzheimer's disease and related dementias (ADRD) in the U.S., but the extent of this relationship is unclear. Here, we constructed two national U.S. population-based cohorts of those aged ≥65 from the Medicare Chronic Conditions Warehouse (2000-2018), combined with high-resolution air pollution datasets, to investigate the association of long-term exposure to ambient fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3) with dementia and AD incidence, respectively. We identified ~2.0 million incident dementia cases (N = 12,233,371; dementia cohort) and ~0.8 million incident AD cases (N = 12,456,447; AD cohort). Per interquartile range (IQR) increase in the 5-year average PM2.5 (3.2 µg/m3), NO2 (11.6 ppb), and warm-season O3 (5.3 ppb) over the past 5 years prior to diagnosis, the hazard ratios (HRs) were 1.060 (95% confidence interval [CI]: 1.054, 1.066), 1.019 (95% CI: 1.012, 1.026), and 0.990 (95% CI: 0.987, 0.993) for incident dementias, and 1.078 (95% CI: 1.070, 1.086), 1.031 (95% CI: 1.023, 1.039), and 0.982 (95%CI: 0.977, 0.986) for incident AD, respectively, for the three pollutants. For both outcomes, concentration-response relationships for PM2.5 and NO2 were approximately linear. Our study suggests that exposures to PM2.5 and NO2 are associated with incidence of dementia and AD. Air pollution may increase risk of Alzheimer’s disease and related dementias (ADRD) in the U.S., but the extent of this relationship is unclear. Here, we constructed two national U.S. population-based cohorts of those aged ≥65 from the Medicare Chronic Conditions Warehouse (2000–2018), combined with high-resolution air pollution datasets, to investigate the association of long-term exposure to ambient fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ), and ozone (O 3 ) with dementia and AD incidence, respectively. We identified ~2.0 million incident dementia cases ( N = 12,233,371; dementia cohort) and ~0.8 million incident AD cases ( N = 12,456,447; AD cohort). Per interquartile range (IQR) increase in the 5-year average PM 2.5 (3.2 µg/m 3 ), NO 2 (11.6 ppb), and warm-season O 3 (5.3 ppb) over the past 5 years prior to diagnosis, the hazard ratios (HRs) were 1.060 (95% confidence interval [CI]: 1.054, 1.066), 1.019 (95% CI: 1.012, 1.026), and 0.990 (95% CI: 0.987, 0.993) for incident dementias, and 1.078 (95% CI: 1.070, 1.086), 1.031 (95% CI: 1.023, 1.039), and 0.982 (95%CI: 0.977, 0.986) for incident AD, respectively, for the three pollutants. For both outcomes, concentration-response relationships for PM 2.5 and NO 2 were approximately linear. Our study suggests that exposures to PM 2.5 and NO 2 are associated with incidence of dementia and AD. Air pollution may increase risk of Alzheimer’s disease and related dementias (ADRD) in the U.S., but the extent of this relationship is unclear. Here, we constructed two national U.S. population-based cohorts of those aged ≥65 from the Medicare Chronic Conditions Warehouse (2000–2018), combined with high-resolution air pollution datasets, to investigate the association of long-term exposure to ambient fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3) with dementia and AD incidence, respectively. We identified ~2.0 million incident dementia cases (N = 12,233,371; dementia cohort) and ~0.8 million incident AD cases (N = 12,456,447; AD cohort). Per interquartile range (IQR) increase in the 5-year average PM2.5 (3.2 µg/m3), NO2 (11.6 ppb), and warm-season O3 (5.3 ppb) over the past 5 years prior to diagnosis, the hazard ratios (HRs) were 1.060 (95% confidence interval [CI]: 1.054, 1.066), 1.019 (95% CI: 1.012, 1.026), and 0.990 (95% CI: 0.987, 0.993) for incident dementias, and 1.078 (95% CI: 1.070, 1.086), 1.031 (95% CI: 1.023, 1.039), and 0.982 (95%CI: 0.977, 0.986) for incident AD, respectively, for the three pollutants. For both outcomes, concentration-response relationships for PM2.5 and NO2 were approximately linear. Our study suggests that exposures to PM2.5 and NO2 are associated with incidence of dementia and AD.Air pollution has been linked to neurodegenerative disease. Here the authors carried out a population-based cohort study to investigate the association between long-term exposure to PM2.5, NO2, and warm-season O3 on dementia and Alzheimer’s disease incidence in the United States. Air pollution may increase risk of Alzheimer's disease and related dementias (ADRD) in the U.S., but the extent of this relationship is unclear. Here, we constructed two national U.S. population-based cohorts of those aged ≥65 from the Medicare Chronic Conditions Warehouse (2000-2018), combined with high-resolution air pollution datasets, to investigate the association of long-term exposure to ambient fine particulate matter (PM ), nitrogen dioxide (NO ), and ozone (O ) with dementia and AD incidence, respectively. We identified ~2.0 million incident dementia cases (N = 12,233,371; dementia cohort) and ~0.8 million incident AD cases (N = 12,456,447; AD cohort). Per interquartile range (IQR) increase in the 5-year average PM (3.2 µg/m ), NO (11.6 ppb), and warm-season O (5.3 ppb) over the past 5 years prior to diagnosis, the hazard ratios (HRs) were 1.060 (95% confidence interval [CI]: 1.054, 1.066), 1.019 (95% CI: 1.012, 1.026), and 0.990 (95% CI: 0.987, 0.993) for incident dementias, and 1.078 (95% CI: 1.070, 1.086), 1.031 (95% CI: 1.023, 1.039), and 0.982 (95%CI: 0.977, 0.986) for incident AD, respectively, for the three pollutants. For both outcomes, concentration-response relationships for PM and NO were approximately linear. Our study suggests that exposures to PM and NO are associated with incidence of dementia and AD. Air pollution has been linked to neurodegenerative disease. Here the authors carried out a population-based cohort study to investigate the association between long-term exposure to PM2.5, NO2, and warm-season O3 on dementia and Alzheimer’s disease incidence in the United States. Air pollution may increase risk of Alzheimer’s disease and related dementias (ADRD) in the U.S., but the extent of this relationship is unclear. Here, we constructed two national U.S. population-based cohorts of those aged ≥65 from the Medicare Chronic Conditions Warehouse (2000–2018), combined with high-resolution air pollution datasets, to investigate the association of long-term exposure to ambient fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ), and ozone (O 3 ) with dementia and AD incidence, respectively. We identified ~2.0 million incident dementia cases ( N = 12,233,371; dementia cohort) and ~0.8 million incident AD cases ( N = 12,456,447; AD cohort). Per interquartile range (IQR) increase in the 5-year average PM 2.5 (3.2 µg/m 3 ), NO 2 (11.6 ppb), and warm-season O 3 (5.3 ppb) over the past 5 years prior to diagnosis, the hazard ratios (HRs) were 1.060 (95% confidence interval [CI]: 1.054, 1.066), 1.019 (95% CI: 1.012, 1.026), and 0.990 (95% CI: 0.987, 0.993) for incident dementias, and 1.078 (95% CI: 1.070, 1.086), 1.031 (95% CI: 1.023, 1.039), and 0.982 (95%CI: 0.977, 0.986) for incident AD, respectively, for the three pollutants. For both outcomes, concentration-response relationships for PM 2.5 and NO 2 were approximately linear. Our study suggests that exposures to PM 2.5 and NO 2 are associated with incidence of dementia and AD. Air pollution has been linked to neurodegenerative disease. Here the authors carried out a population-based cohort study to investigate the association between long-term exposure to PM 2.5 , NO 2 , and warm-season O 3 on dementia and Alzheimer’s disease incidence in the United States. |
ArticleNumber | 6754 |
Author | Schwartz, Joel Zhang, Yuhan Ilango, Sindana D. Shi, Liuhua Chang, Howard H. Steenland, Kyle Lyles, Robert H. Weber, Rodney J. Requia, Weeberb J. Wingo, Thomas Liu, Pengfei Li, Haomin |
Author_xml | – sequence: 1 givenname: Liuhua orcidid: 0000-0001-8165-4644 surname: Shi fullname: Shi, Liuhua email: liuhua.shi@emory.edu organization: Gangarosa Department of Environmental Health, Rollins School of Public Health, Emory University – sequence: 2 givenname: Kyle surname: Steenland fullname: Steenland, Kyle organization: Gangarosa Department of Environmental Health, Rollins School of Public Health, Emory University – sequence: 3 givenname: Haomin surname: Li fullname: Li, Haomin organization: Department of Epidemiology, Rollins School of Public Health, Emory University – sequence: 4 givenname: Pengfei surname: Liu fullname: Liu, Pengfei organization: School of Earth and Atmospheric Sciences, Georgia Institute of Technology – sequence: 5 givenname: Yuhan surname: Zhang fullname: Zhang, Yuhan organization: Department of Epidemiology, Rollins School of Public Health, Emory University – sequence: 6 givenname: Robert H. surname: Lyles fullname: Lyles, Robert H. organization: Department of Biostatistics and Bioinformatics, Rollins School of Public Health, Emory University – sequence: 7 givenname: Weeberb J. orcidid: 0000-0002-7564-3364 surname: Requia fullname: Requia, Weeberb J. organization: School of Public Policy and Government, Fundação Getúlio Vargas – sequence: 8 givenname: Sindana D. surname: Ilango fullname: Ilango, Sindana D. organization: Department of Epidemiology, School of Public Health, University of Washington – sequence: 9 givenname: Howard H. surname: Chang fullname: Chang, Howard H. organization: Gangarosa Department of Environmental Health, Rollins School of Public Health, Emory University, Department of Biostatistics and Bioinformatics, Rollins School of Public Health, Emory University – sequence: 10 givenname: Thomas orcidid: 0000-0002-7679-6282 surname: Wingo fullname: Wingo, Thomas organization: Department of Neurology and Human Genetics, School of Medicine, Emory University – sequence: 11 givenname: Rodney J. surname: Weber fullname: Weber, Rodney J. organization: School of Earth and Atmospheric Sciences, Georgia Institute of Technology – sequence: 12 givenname: Joel orcidid: 0000-0001-6168-378X surname: Schwartz fullname: Schwartz, Joel organization: Department of Environmental Health, Harvard T.H. Chan School of Public Health |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34799599$$D View this record in MEDLINE/PubMed |
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ContentType | Journal Article |
Copyright | The Author(s) 2021 2021. The Author(s). The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
Copyright_xml | – notice: The Author(s) 2021 – notice: 2021. The Author(s). – notice: The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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Snippet | Air pollution may increase risk of Alzheimer’s disease and related dementias (ADRD) in the U.S., but the extent of this relationship is unclear. Here, we... Air pollution may increase risk of Alzheimer's disease and related dementias (ADRD) in the U.S., but the extent of this relationship is unclear. Here, we... Air pollution has been linked to neurodegenerative disease. Here the authors carried out a population-based cohort study to investigate the association between... |
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SubjectTerms | 692/617/375/132/1283 704/844/4081 Aged Aged, 80 and over Air Pollutants - adverse effects Air pollution Air Pollution - adverse effects Air Pollution - statistics & numerical data Alzheimer's disease Chronic conditions Cohort analysis Confidence intervals Dementia Dementia - epidemiology Dementia - etiology Dementia disorders Environmental Exposure - adverse effects Environmental Exposure - statistics & numerical data Environmental Monitoring - statistics & numerical data Exposure Female Follow-Up Studies Humanities and Social Sciences Humans Incidence Male multidisciplinary Neurodegenerative diseases Nitrogen dioxide Older people Particulate matter Particulate Matter - adverse effects Pollutants Population studies Risk Factors Science Science (multidisciplinary) United States - epidemiology |
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Title | A national cohort study (2000–2018) of long-term air pollution exposure and incident dementia in older adults in the United States |
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