Long-term exposure to fine particulate matter and dementia incidence: A cohort study in Hong Kong

Ran, Jinjun; Schooling, CM; Han, Lefei; Sun, Shengzhi; Zhao, Shi; Zhang, Xiao­hong; Chan, King-Pan; Guo, Feifei; Lee, Ruby Siu-yin; Qiu, Yulan; Tian, Linwei

doi:10.1016/j.envpol.2020.116303

Cited by 38 publications

(27 citation statements)

References 47 publications

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“…In our prior review, approximately half of the studies used the following as surrogates for ambient pollutant concentrations at a person’s home: pollutant concentrations from a single monitoring station ( Chang et al. 2014 ; Ranft et al. 2009 ) or several ( Ailshire and Crimmins 2014 ; Ailshire and Clarke 2015 ; Chen and Schwartz 2009 ; Gatto et al.…”

Section: Resultsmentioning

confidence: 99%

“…2015 ) monitoring stations nearest to a participant’s residential location, city/county air pollution index values ( Zeng et al. 2010 ), or distance to road or traffic load measures ( Ranft et al. 2009 ; Schikowski et al.…”

Section: Resultsmentioning

confidence: 99%

“…For markers of traffic, excluding

and

, all older studies ( Power et al. 2011 ; Ranft et al. 2009 ; Schikowski et al.…”

Section: Resultsmentioning

confidence: 99%

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Exposure to Air Pollution in Relation to Risk of Dementia and Related Outcomes: An Updated Systematic Review of the Epidemiological Literature

Weuve

Bennett

Ranker

et al. 2021

Environ Health Perspect

114

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Background: Dementia is a devastating neurologic condition that is common in older adults. We previously reviewed the epidemiological evidence examining the hypothesis that long-term exposure to air pollution affects dementia risk. Since then, the evidence base has expanded rapidly. Objectives: With this update, we collectively review new and previously identified epidemiological studies on air pollution and late-life cognitive health, highlighting new developments and critically discussing the merits of the evidence. Methods: Using a registered protocol (PROSPERO 2020 CRD42020152943), we updated our literature review to capture studies published through 31 December 2020, extracted data, and conducted a bias assessment. Results: We identified 66 papers (49 new) for inclusion in this review. Cognitive level remained the most commonly considered outcome, and particulate matter (PM) remained the most commonly considered air pollutant. Since our prior review, exposure estimation methods in this research have improved, and more papers have looked at cognitive change, neuroimaging, and incident cognitive impairment/dementia, though methodological concerns remain common. Many studies continue to rely on administrative records to ascertain dementia, have high potential for selection bias, and adjust for putative mediating factors in primary models. A subset of 35 studies met strict quality criteria. Although high-quality studies of fine particulate matter with aerodynamic diameter ( ) and cognitive decline generally supported an adverse association, other findings related to and findings related to particulate matter with aerodynamic diameter ( , , and ) were inconclusive, and too few papers reported findings with ozone to comment on the likely direction of association. Notably, only a few findings on dementia were included for consideration on the basis of quality criteria. Discussion: Strong conclusions remain elusive, although the weight of the evidence suggests an adverse association between and cognitive decline. However, we note a continued need to confront methodological challenges in this line of research. https://doi.org/10.1289/EHP8716

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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Exposure to Air Pollution in Relation to Risk of Dementia and Related Outcomes: An Updated Systematic Review of the Epidemiological Literature

Weuve

Bennett

Ranker

et al. 2021

Environ Health Perspect

114

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“…The calculation of SI and its 95% CI were performed according to the approach raised by Hosmer and Andersson 19,20 . To further explore the association between the continuous scale of CBPAI or CBPAI′ and BPH risk in different alcohol consumption levels, we employed logistic regression models with natural cubic spline curve in never, light, and heavy drinking groups and fitted by a binomial‐distributed likelihood function using the maximal likelihood approach, with the degree of freedom (i.e., the knots) being determined by the fitting performance of Akaike information criterion (AIC) 21 . Statistical analysis was conducted in SPSS 22.0 except for the nonlinear regression analysis, which was performed by R statistical software version 3.6.1.…”

Section: Methodsmentioning

confidence: 99%

Joint effect between bisphenol A and alcohol consumption on benign prostatic hyperplasia: A case–control study in Hong Kong Chinese males

et al. 2021

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Background Whether bisphenol A (BPA) exposure is a contributing factor to benign prostatic hyperplasia (BPH) remains unclear. This study evaluated the association between chronic BPA exposure and BPH risk, and explored whether this association was modified by alcohol drinking. Methods This study included a total of 650 BPH cases and 650 controls recruited from the same hospital in Hong Kong during 2011–2016. Chronic BPA exposure level was estimated by a validated cumulative BPA exposure index (CBPAI). We performed unconditional logistic regression model to examine the association of BPH risk with potential sources of BPA exposure via oral intake and CBPAI. We further tested the interactions between CBPAI and alcohol consumption habits on BPH risk. Results A positive exposure–response relationship was observed between CBPAI and BPH risk. Frequent BPA exposure via oral intake of foods heated in a plastic box/bag (odds ratio [OR] = 3.52, 95% confidence interval [CI]: 1.51–8.22), cooling water in a plastic bottle (OR = 2.65, 95% CI: 1.33–5.27), or using a plastic cup to contain hot water (OR = 4.14, 95% CI: 1.02–16.89), was significantly associated with increased BPH risk. Compared with nonalcohol drinkers, alcohol drinkers was insignificantly associated with BPH risk (OR = 1.10, 95% CI: 0.77–1.57), but it demonstrated a more remarkable positive gradient between CBPAI exposure and BPH risk among alcohol drinkers, indicating an additive interaction between CBPAI and alcohol on BPH risk (synergy index = 4.24, 95% CI: 1.21–14.94). Conclusions Chronic oral BPA exposure increased BPH risk with a positive exposure–response relationship among Hong Kong Chinese, and alcohol drinking amplified the effect of BPA on BPH. Hence, minimizations of containing food or water/beverage in plastic containers and drinking alcohol are recommended in the community to mitigate BPH risk. Future larger and designated studies are warranted.

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“…An epidemiological investigation on a different population resident in Hon Kong also found that long term exposure (1998–2011) to PM 2.5 increased the incidence of both AD and vascular dementia [ 85 ]. All together these data indicate that air pollution affects AD and dementia risk in different racial populations.…”

Section: Herv Dysregulation Ad and Neurological Diseasesmentioning

confidence: 99%

Activation of Endogenous Retrovirus, Brain Infections and Environmental Insults in Neurodegeneration and Alzheimer’s Disease

Licastro

Porcellini

2021

IJMS

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Chronic neurodegenerative diseases are complex, and their pathogenesis is uncertain. Alzheimer’s disease (AD) is a neurodegenerative brain alteration that is responsible for most dementia cases in the elderly. AD etiology is still uncertain; however, chronic neuroinflammation is a constant component of brain pathology. Infections have been associated with several neurological diseases and viruses of the Herpes family appear to be a probable cause of AD neurodegenerative alterations. Several different factors may contribute to the AD clinical progression. Exogeneous viruses or other microbes and environmental pollutants may directly induce neurodegeneration by activating brain inflammation. In this paper, we suggest that exogeneous brain insults may also activate retrotransposons and silent human endogenous retroviruses (HERVs). The initial inflammation of small brain areas induced by virus infections or other brain insults may activate HERV dis-regulation that contributes to neurodegenerative mechanisms. Chronic HERV activation in turn may cause progressive neurodegeneration that thereafter merges in cognitive impairment and dementia in genetically susceptible people. Specific treatment for exogenous end endogenous pathogens and decreasing pollutant exposure may show beneficial effect in early intervention protocol to prevent the progression of cognitive deterioration in the elderly.

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Long-term exposure to fine particulate matter and dementia incidence: A cohort study in Hong Kong

Cited by 38 publications

References 47 publications

Exposure to Air Pollution in Relation to Risk of Dementia and Related Outcomes: An Updated Systematic Review of the Epidemiological Literature

Exposure to Air Pollution in Relation to Risk of Dementia and Related Outcomes: An Updated Systematic Review of the Epidemiological Literature

Joint effect between bisphenol A and alcohol consumption on benign prostatic hyperplasia: A case–control study in Hong Kong Chinese males

Activation of Endogenous Retrovirus, Brain Infections and Environmental Insults in Neurodegeneration and Alzheimer’s Disease

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