Long-Term Ambient Air Pollution Exposures and Brain Imaging Markers in Korean Adults: The Environmental Pollution-Induced Neurological EFfects (EPINEF) Study

Cho, Jaelim; Noh, Young; Kim, Sun Young; Sohn, Jungwoo; Noh, Juhwan; Kim, Woojin; Cho, Seong-Kyung; Seo, Hwasun; Seo, Gayoung; Lee, Seung Koo; Seo, Seongho; Koh, Shin Ok; Oh, Sung Soo; Kim, Hee Jin; Seo, Sang Won; Shin, Dae-Seock; Kim, Nakyoung; Kim, Ho; Lee, Jung Il; Kim, Chang-Soo

doi:10.1289/ehp7133

Cited by 41 publications

(31 citation statements)

References 51 publications

(71 reference statements)

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“…Healthy subjects were participants of the Environmental Pollution‐Induced Neurological EFfects (EPINEF) study, which is based on community. Through local advertisements, individuals without known neurological diseases (e.g., any kind of dementia, movement disorders, or stroke) were recruited and enrolled in this cohort (Cho et al, 2020). The 96 participants in the healthy group did not have subjective memory complaints and objective cognitive decline.…”

Section: Methodsmentioning

confidence: 99%

Early‐stage Parkinson's disease: Abnormal nigrosome 1 and 2 revealed by a voxelwise analysis of neuromelanin‐sensitive MRI

Sung

Noh

Kim

2021

Human Brain Mapping

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Previous pathologic studies evaluated the substantia nigra pars compacta (SNpc) of a limited number of idiopathic Parkinson's disease (IPD) patients with relatively longer disease durations. Therefore, it remains unknown which region of the SNpc is most significantly affected in early‐stage IPD. We hypothesized that a voxelwise analysis of thin‐section neuromelanin‐sensitive MRI (NM‐MRI) may help determine the significantly affected regions of the SNpc in early‐stage IPD and localize these areas in each nigrosome on high‐spatial‐resolution susceptibility map‐weighted imaging (SMwI). Ninety‐six healthy subjects and 50 early‐stage IPD patients underwent both a 0.8 × 0.8 × 0.8 mm3 NM‐MRI and a 0.5 × 0.5 × 1.0 mm3 multi‐echo gradient‐recalled echo imaging for SMwI. Both NM‐MRI and SMwI templates were created by using image data from the 96 healthy subjects. Permutation‐based nonparametric tests were conducted to investigate spatial differences between the two groups in NM‐MRI, and the results were displayed on both NM‐MRI and SMwI templates. The posterolateral and anteromedial regions of the SNpc in NM‐MRI were significantly different between the two groups, corresponding to the nigrosome 1 and nigrosome 2 regions, respectively, on the SMwI template. There were the areas of significant spatial difference in the hypointense SN on SMwI between early‐stage IPD patients and healthy subjects. These areas on SMwI were slightly greater than those on NM‐MRI, including the areas showing group difference on NM‐MRI. Our voxelwise analysis of NM‐MRI suggests that two regions (nigrosome 1 and nigrosome 2) of the SNpc are separately affected in early‐stage IPD.

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Section: Methodsmentioning

confidence: 99%

Early‐stage Parkinson's disease: Abnormal nigrosome 1 and 2 revealed by a voxelwise analysis of neuromelanin‐sensitive MRI

Sung

Noh

Kim

2021

Human Brain Mapping

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“…In addition, traffic-related pollution may contain elements characterized by neurotoxic effects, especially heavy metals such as lead, cadmium, mercury, and selenium already associated with ALS risk [61][62][63][64][65][66]. A neuroimaging study showed that long-term exposure to high ambient air pollution may lead to cortical thinning and reduced subcortical volume in adults [67].…”

Section: Discussionmentioning

confidence: 99%

Risk of Amyotrophic Lateral Sclerosis and Exposure to Particulate Matter from Vehicular Traffic: A Case-Control Study

Filippini

Mandrioli

Malagoli

et al. 2021

IJERPH

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(1) Background: Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease with still unknown etiology. Some occupational and environmental risk factors have been suggested, including long-term air pollutant exposure. We carried out a pilot case-control study in order to evaluate ALS risk due to particulate matter with a diameter of ≤10 µm (PM10) as a proxy of vehicular traffic exposure. (2) Methods: We recruited ALS patients and controls referred to the Modena Neurology ALS Care Center between 1994 and 2015. Using a geographical information system, we modeled PM10 concentrations due to traffic emissions at the geocoded residence address at the date of case diagnosis. We computed the odds ratio (OR) and 95% confidence interval (CI) of ALS according to increasing PM10 exposure, using an unconditional logistic regression model adjusted for age and sex. (3) Results: For the 132 study participants (52 cases and 80 controls), the average of annual median and maximum PM10 concentrations were 5.2 and 38.6 µg/m3, respectively. Using fixed cutpoints at 5, 10, and 20 of the annual median PM10 levels, and compared with exposure <5 µg/m3, we found no excess ALS risk at 5–10 µg/m3 (OR 0.87, 95% CI 0.39–1.96), 10–20 µg/m3 (0.94, 95% CI 0.24–3.70), and ≥20 µg/m3 (0.87, 95% CI 0.05–15.01). Based on maximum PM10 concentrations, we found a statistically unstable excess ALS risk for subjects exposed at 10–20 µg/m3 (OR 4.27, 95% CI 0.69–26.51) compared with those exposed <10 µg/m3. However, risk decreased at 20–50 µg/m3 (OR 1.49, 95% CI 0.39–5.75) and ≥50 µg/m3 (1.16, 95% CI 0.28–4.82). ALS risk in increasing tertiles of exposure showed a similar null association, while comparison between the highest and the three lowest quartiles lumped together showed little evidence for an excess risk at PM10 concentrations (OR 1.13, 95% CI 0.50–2.55). After restricting the analysis to subjects with stable residence, we found substantially similar results. (4) Conclusions: In this pilot study, we found limited evidence of an increased ALS risk due to long-term exposure at high PM10 concentration, though the high statistical imprecision of the risk estimates, due to the small sample size, particularly in some exposure categories, limited our capacity to detect small increases in risk, and further larger studies are needed to assess this relation.

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“…69 Imaging evidence of an association between PM2.5 exposure and neurodegenerative changes is provided by longitudinal studies of healthy patients with interval MRI scans, which have shown white matter loss in those exposed to greater concentrations of PM2.5. [70][71][72][73][74] PM(coarse) has been less well-studied and only a single report linking exposure in women to decreased mini-mental status examination (MMSE) score has been published. 75 Exposure to PM10, particularly in patients harboring the APOE4 allele, has been shown to associate both with dementia incidence and rate of cognitive decline, as well as front-temporal thinning on MRI.…”

Section: Dementiamentioning

confidence: 99%

“…75 Exposure to PM10, particularly in patients harboring the APOE4 allele, has been shown to associate both with dementia incidence and rate of cognitive decline, as well as front-temporal thinning on MRI. 66,74,[76][77][78] The effects of exposure to ground-level ozone (O3) remain less clear, as there have not been as strong associations with dementia incidence 76 , increased odds of amyloid PET positivity 68 , or MMSE score decline. 66 Nitrogenous gases have shown an association with vascular dementia 79 , global brain atrophy 74 , and a slightly faster rate of decline in those with the APOE4 allele, with differing results for MMSE-scored cognitive decline and all-cause dementia.…”

Section: Dementiamentioning

confidence: 99%

“…66,74,[76][77][78] The effects of exposure to ground-level ozone (O3) remain less clear, as there have not been as strong associations with dementia incidence 76 , increased odds of amyloid PET positivity 68 , or MMSE score decline. 66 Nitrogenous gases have shown an association with vascular dementia 79 , global brain atrophy 74 , and a slightly faster rate of decline in those with the APOE4 allele, with differing results for MMSE-scored cognitive decline and all-cause dementia. 63,64,66,75 Sulfur dioxide (SO2) exposure has also been associated with MMSE score decline.…”

Section: Dementiamentioning

confidence: 99%

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Neurology in a Changing Climate: A Scoping Review

Louis

Carlson

Suresh

et al. 2021

Preprint

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ImportanceAlthough the international community collectively seeks to reduce global temperature rise to less than 1.5ºC, there are already irreversible environmental changes that have occurred, and currently available evidence suggests these changes will continue to occur. As we begin to witness the effects of a warming planet on human health, it is imperative that as neurologists we anticipate the ways in which the epidemiology and incidence of neurologic disease may be affected.ObjectiveIn this review, we organize our analysis around three key themes related to climate change and neurologic health: extreme weather events and temperature fluctuations, emerging neuro-infectious diseases, and pollutant impacts. Across each of these key themes, we appraise and review recent literature relevant to neurological disease and the practice of neurology.Evidence ReviewStudies were identified using a set of relevant search terms relating to climate change and neurologic diseases in the PubMed repository for publications between 1990 and 2021. Studies were included if they pertained to human incidence or prevalence of disease, were in the English language, and were relevant to neurologic disease.FindingsWe identified a total of 136 articles, grouped into the three key themes of our study; extreme weather events and temperature fluctuations (23 studies), emerging neuro-infectious diseases (42 studies), and pollutant impacts (71 studies). Broadly, the studies included highlighted the relationships between neurologic symptom exacerbation and temperature variability, tick-borne infections and warming climates, and airborne pollutants and cerebrovascular disease incidence and severity.Conclusions and RelevanceOur work highlights three key priorities for further work; namely, neuro-infectious disease risk mitigation, an understanding of the pathophysiology of airborne pollutants on the nervous system, and research into how to improve delivery of neurologic care in the face of climate-related disruptions.Key PointsQuestionHow does climate change impact neurological disease?Findings136 articles were identified relating neurologic disease to climate change. Articles were grouped into three key themes, highlighting evidence linking neurologic disease exacerbation to temperature fluctuation, tick-borne infections with climate change, and airborne pollutants to cerebrovascular disease.MeaningA substantial body of literature suggests that neurologic disease incidence, morbidity, and mortality is directly impacted by climate change and its sequelae, but much remains to be uncovered.

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Long-Term Ambient Air Pollution Exposures and Brain Imaging Markers in Korean Adults: The Environmental Pollution-Induced Neurological EFfects (EPINEF) Study

Cited by 41 publications

References 51 publications

Early‐stage Parkinson's disease: Abnormal nigrosome 1 and 2 revealed by a voxelwise analysis of neuromelanin‐sensitive MRI

Early‐stage Parkinson's disease: Abnormal nigrosome 1 and 2 revealed by a voxelwise analysis of neuromelanin‐sensitive MRI

Risk of Amyotrophic Lateral Sclerosis and Exposure to Particulate Matter from Vehicular Traffic: A Case-Control Study

Neurology in a Changing Climate: A Scoping Review

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