Increased Risk of Dementia in Patients Exposed to Nitrogen Dioxide and Carbon Monoxide: A Population-Based Retrospective Cohort Study

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Abstract

Background

The air pollution caused by vehicular emissions is associated with cognitive decline. However, the associations between the levels of nitrogen dioxide (NO ₂) and carbon monoxide (CO) exposure and dementia remain poorly defined and have been addressed in only a few previous studies.

Materials and Methods

In this study, we obtained data on 29547 people from the National Health Insurance Research Database (NHIRD) of Taiwan, including data on 1720 patients diagnosed with dementia between 2000 and 2010, and we evaluated the risk of dementia among four levels of air pollutant. Detailed data on daily air pollution were available from January 1, 1998 to December 31, 2010. Yearly average concentrations of pollutants were calculated from the baseline to the date of dementia occurrence, withdrawal of patients, or the end of the study, and these data were categorized into quartiles, with Q1 being the lowest level and Q4 being the highest.

Results

In the case of NO ₂, the adjusted hazard ratios (HRs) of dementia for all participants in Q2, Q3, and Q4 compared to Q1 were 1.10 (95% confidence interval (CI), 0.96–1.26), 1.01 (95% CI, 0.87–1.17), and 1.54 (95% CI, 1.34–1.77), and in the case of CO, the adjusted HRs were 1.07 (95% CI, 0.92–1.25), 1.37 (95% CI, 1.19–1.58), and 1.61 (95% CI, 1.39–1.85).

Conclusion

The results of this large retrospective, population-based study indicate that exposure to NO ₂ and CO is associated with an increased risk of dementia in the Taiwanese population.

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Most cited references 36

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Alcohol consumption as a risk factor for dementia and cognitive decline: meta-analysis of prospective studies.

Kaarin J. Anstey, Holly A Mack, Nicolas Cherbuin (2009)

The relationships between alcohol consumption and dementia and cognitive decline were investigated in a systematic review including meta-analyses of 15 prospective studies. Follow-ups ranged from 2 to 8 years. Meta-analyses were conducted on samples including 14,646 participants evaluated for Alzheimer disease (AD), 10,225 participants evaluated for vascular dementia (VaD), and 11,875 followed for any type of dementia (Any dementia). The pooled relative risks (RRs) of AD, VaD, and Any dementia for light to moderate drinkers compared with nondrinkers were 0.72 (95% CI = 0.61-0.86), 0.75 (95% CI = 0.57-0.98), and 0.74 (95% CI = 0.61-0.91), respectively. When the more generally classified "drinkers," were compared with "nondrinkers," they had a reduced risk of AD (RR = 0.66, 95% CI = 0.47-0.94) and Any dementia (RR = 0.53, 95% CI = 0.53-0.82) but not cognitive decline. There were not enough data to examine VaD risk among "drinkers." Those classified as heavy drinkers did not have an increased risk of Any dementia compared with nondrinkers, but this may reflect sampling bias. Our results suggest that alcohol drinkers in late life have reduced risk of dementia. It is unclear whether this reflects selection effects in cohort studies commencing in late life, a protective effect of alcohol consumption throughout adulthood, or a specific benefit of alcohol in late life.

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Long-term exposure to traffic-related particulate matter impairs cognitive function in the elderly.

Ulrich Ranft, Tamara Schikowski, Dorothee Sugiri … (2009)

Animal studies have suggested that fine particulate matter (PM) can translocate from the upper respiratory tract to the brain and cause brain inflammation. Brain inflammation is involved in the pathogenesis of neurodegenerative diseases. Hypothesizing therefore that long-term exposure to fine PM might contribute to the development of Alzheimer's disease (AD), the objective of this study was to investigate the association between exposure to fine PM and mild cognitive impairment (MCI) which is associated with a high risk of progression to AD. A study group of 399 women aged 68-79 years who lived for more than 20 years at the same residential address has been assessed for long-term exposure to PM and tested for MCI. The exposure assessment comprised background concentration of PM(10) and traffic-related PM indicated by the distance of the residential address to the next busy road. The women were assessed for MCI by a battery of several neuropsychological tests and their odor identification ability. Consistent effects of traffic-related air pollution exposure on test performances including a dose-response relation were found. The associations were adjusted for potential confounders using regression analysis. These results indicate that chronic exposure to traffic-related PM may be involved in the pathogenesis of AD.

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Air pollution combustion emissions: characterization of causative agents and mechanisms associated with cancer, reproductive, and cardiovascular effects.

Joellen Lewtas (2015)

Combustion emissions account for over half of the fine particle (PM(2.5)) air pollution and most of the primary particulate organic matter. Human exposure to combustion emissions including the associated airborne fine particles and mutagenic and carcinogenic constituents (e.g., polycyclic aromatic compounds (PAC), nitro-PAC) have been studied in populations in Europe, America, Asia, and increasingly in third-world counties. Bioassay-directed fractionation studies of particulate organic air pollution have identified mutagenic and carcinogenic polycyclic aromatic hydrocarbons (PAH), nitrated PAH, nitro-lactones, and lower molecular weight compounds from cooking. A number of these components are significant sources of human exposure to mutagenic and carcinogenic chemicals that may also cause oxidative and DNA damage that can lead to reproductive and cardiovascular effects. Chemical and physical tracers have been used to apportion outdoor and indoor and personal exposures to airborne particles between various combustion emissions and other sources. These sources include vehicles (e.g., diesel and gasoline vehicles), heating and power sources (e.g., including coal, oil, and biomass), indoor sources (e.g., cooking, heating, and tobacco smoke), as well as secondary organic aerosols and pollutants derived from long-range transport. Biomarkers of exposure, dose and susceptibility have been measured in populations exposed to air pollution combustion emissions. Biomarkers have included metabolic genotype, DNA adducts, PAH metabolites, and urinary mutagenic activity. A number of studies have shown a significant correlation of exposure to PM(2.5) with these biomarkers. In addition, stratification by genotype increased this correlation. New multivariate receptor models, recently used to determine the sources of ambient particles, are now being explored in the analysis of human exposure and biomarker data. Human studies of both short- and long-term exposures to combustion emissions and ambient fine particulate air pollution have been associated with measures of genetic damage. Long-term epidemiologic studies have reported an increased risk of all causes of mortality, cardiopulmonary mortality, and lung cancer mortality associated with increasing exposures to air pollution. Adverse reproductive effects (e.g., risk for low birth weight) have also recently been reported in Eastern Europe and North America. Although there is substantial evidence that PAH or substituted PAH may be causative agents in cancer and reproductive effects, an increasing number of studies investigating cardiopulmonary and cardiovascular effects are investigating these and other potential causative agents from air pollution combustion sources.

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Author and article information

Contributors

Gianluigi Forloni: Role: Editor

Journal

Journal ID (nlm-ta): PLoS One

Journal ID (iso-abbrev): PLoS ONE

Journal ID (publisher-id): plos

Journal ID (pmc): plosone

Title: PLoS ONE

Publisher: Public Library of Science (San Francisco, USA )

ISSN (Electronic): 1932-6203

Publication date Collection: 2014

Publication date (Electronic): 12 August 2014

Volume: 9

Issue: 8

Electronic Location Identifier: e103078

Affiliations

[1 ]Department of Public Health, China Medical University, Taichung, Taiwan

[2 ]Department of Medical Research, Taichung Veterans General Hospital, Taichung, Taiwan

[3 ]Department of Medical Laboratory Science and Biotechnology, School of Medical and Health Sciences, Fooyin University, Kaohsiung, Taiwan

[4 ]Management Office for Health Data, China Medical University Hospital, Taichung, Taiwan

[5 ]Graduate Institute of Clinical Medical Science, College of Medicine, China Medical University, Taiwan

[6 ]Department of Nuclear Medicine and PET Center, China Medical University Hospital, Taichung, Taiwan

“Mario Negri” Institute for Pharmacological Research, Italy

Author notes

* E-mail: d10040@ 123456mail.cmuh.org.tw

Competing Interests: The authors have declared that no competing interests exist.

Study concept and design: KHC CHK. Acquisition of data: KHC MYC CHM TNW CYC CHK. Analysis and interpretation of data: KHC CHM CHK. Drafting of the manuscript: KHC MYC CHM TNW CYC CHK. Critical revision of the manuscript for important intellectual content: KHC CHM CHK. Statistical analysis: CHM. Obtained funding: CHK. Administrative, technical, or material support: KHC MYC CHM TNW CYC CHK. Study supervision: CHK.

Article

Publisher ID: PONE-D-14-11777

DOI: 10.1371/journal.pone.0103078

PMC ID: 4130523

PubMed ID: 25115939

SO-VID: 1ae3862e-cfec-4bb4-85e3-ef1c7c594fb1

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

History

Date received : 15 March 2014

Date accepted : 25 June 2014

Page count

Pages: 8

Funding

The study was supported in part by China Medical University (CMU102-BC-2), Taiwan Ministry of Health and Welfare Clinical Trial and Research Center of Excellence (MOHW103-TDU-B-212-113002), Taiwan Ministry of Health and Welfare Cancer Research Center for Excellence (MOHW103-TD-B-111-03), and International Research-Intensive Centers of Excellence in Taiwan (I-RiCE) (NSC101-2911-I-002-303). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

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Data Availability The authors confirm that all data underlying the findings are fully available without restriction. All data and related metadata are deposited in an appropriate public repository: The study population's data were from Taiwan NHIRD ( http://w3.nhri.org.tw/nhird//date_01.html) are maintained by Taiwan National Health Research Institutes ( http://nhird.nhri.org.tw/) [27]. The National Health Research Institutes (NHRI) is a non-profit foundation established by the government. Air quality data were from Taiwan Air Quality Monitoring Network ( http://taqm.epa.gov.tw/taqm/en/PsiMap.aspx) in Taiwan Environmental Protection Administration ( http://www.epa.gov.tw/).

Increased Risk of Dementia in Patients Exposed to Nitrogen Dioxide and Carbon Monoxide: A Population-Based Retrospective Cohort Study

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Background

Materials and Methods

Results

Conclusion

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PLOS Climate

Most cited references 36

Alcohol consumption as a risk factor for dementia and cognitive decline: meta-analysis of prospective studies.

Long-term exposure to traffic-related particulate matter impairs cognitive function in the elderly.

Air pollution combustion emissions: characterization of causative agents and mechanisms associated with cancer, reproductive, and cardiovascular effects.

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