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  • 1.
    Andersson, John
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Air pollution and dementia in a low exposure setting: the role of noise, olfaction, and theapoe gene2023Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
    Abstract [en]

    Previous research indicates an association between air pollution exposure, and risk of dementia. Still, a number of factors that may play a role in this association remain to be explored. In addition, while most studies on air pollution and brain health have taken place in highly exposed large urban areas, the studies included in this thesis are conducted in an area with relatively low levels of air pollution and road traffic noise.

    The overall aim of this thesis is to investigate possible mechanisms - more specifically the role of noise, olfaction and the APOE-ε4 allele - in the association between air pollution and dementia, in a low exposure area. Because olfactory deficits have been linked to air pollution, and can be an early sign of dementia, an additional aim is to examine associations between exposure to air pollution and olfactory function.

    Methods: Participants were drawn from the Betula project – a prospective cohort study – in Umeå, Sweden. Modelled data on concentrations of nitrogenoxides (NOx), fine particle matter (PM2.5) and levels of road traffic noise, were matched with participants residential address at baseline. PM2.5 levels at the day of testing were obtained from a measuring station in the vicinity of the test location. Data on dementia diagnoses, APOE status, olfactory functions, and covariates, were drawn from the Betula project. Dementia assessment was primarily based on medical records, and conducted by a geropsychiatrist. Odor identification was assessed using the Scandinavian Odor Identification Test, and odor detection threshold by “sniffin’ sticks”. APOE genotype was determined by DNA analyses of blood samples.

    Study I. Where there is pollution, there is also often noise. In addition, exposure to noise can increase the risk of dementia. The aim of study I was to investigate the individual and combined effect of noise and air pollution on risk of dementia. The results showed an association between NOx and dementia. However, noise from road traffic did not contribute to this association.

    Study II. Olfactory deficits can be an early sign of dementia and might also becaused by air pollution. Olfactory receptor cells in the nasal cavity are exposed to inhaled air, and the olfactory bulb is one of the areas of the brain most affectedby air pollution. The APOE-ε4 allele is important to consider, as it is a risk factor for both dementia and declining olfactory functions. The aim of study II was to investigate the role of olfaction and the APOE-ε4 allele in the association between air pollution and dementia. Stratified analyses showed that associations between PM2.5 and dementia persisted only among APOE-ε4 carriers, and those with poor odor identification ability.

    Study III. The olfactory system may be vulnerable to air pollution, and olfactory dysfunction is an early sign of dementia. In addition, the moderating effect of odor identification ability found in study II, could be explained by air pollution increasing the risk of olfactory functions and dementia independent of each other. Thus, the aim of study III was to investigate the associations between PM2.5 (both long term exposure, and concentrations on the day of testing), and odor identification and detection. A positive association was observed between longterm air pollution exposure and odor identification ability. No association was found between long term air pollution exposure and odor detection, or between short term exposure and either olfactory outcome.

    Conclusion: Low levels of long-term exposure to air pollution increases the risk of dementia. APOE-ε4 carriers, and those with poor odor identification ability, seem particularly vulnerable. No residual confounding from road traffic noisewas found, suggesting that air pollution is the main component in the association between traffic related exposures and dementia in low-exposure areas. The positive association between air pollution and odor identification might be explained by socioeconomic status, and the links between olfaction and semantic memory.

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  • 2.
    Andersson, John
    et al.
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Oudin, Anna
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för hållbar hälsa.
    Nordin, Steven
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Forsberg, Bertil
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för hållbar hälsa.
    Nordin, Maria
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    PM2.5 exposure and olfactory functions2022Ingår i: International Journal of Environmental Health Research, ISSN 0960-3123, E-ISSN 1369-1619, Vol. 32, nr 11, s. 2484-2495Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Growing evidence indicates that air pollution can negatively impact cognitive functions. The olfactory system is interesting in this context as it is directly exposed to pollutants and also associated with cognitive functions. The aim of this study was to investigate long- and short-term PM2.5 exposure in association with olfactory functions. Scores from odor tests were obtained from the Betula project - a longitudinal cohort study. Estimates of annual mean PM2.5 concentrations at the participants' residential address were obtained from a dispersion-model. Daily mean PM2.5 concentrations were obtained from a measuring station close to the test location. We found a positive association between long-term PM2.5 exposure and odor identification, i.e. exposure was associated with a better ability to identify odors. We also found an interaction effect between PM2.5 and age on odor identification. We found no associations between any PM2.5 exposure and odor detection or between short-term PM2.5 exposure and olfactory functions.

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  • 3.
    Andersson, John
    et al.
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Oudin, Anna
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Yrkes- och miljömedicin.
    Sundström, Anna
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi. Umeå universitet, Samhällsvetenskapliga fakulteten, Enheten för demografi och åldrandeforskning (CEDAR).
    Forsberg, Bertil
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Yrkes- och miljömedicin.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Nordin, Maria
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Road traffic noise, air pollution, and risk of dementia: results from the Betula project2018Ingår i: Environmental Research, ISSN 0013-9351, E-ISSN 1096-0953, Vol. 166, s. 334-339Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: There is growing evidence for a negative impact of traffic-related air pollution on risk of dementia. However, the contribution of noise exposure to this association has been rarely examined.

    Objective: We aimed to investigate the individual and combined effect of noise and air pollution on risk of dementia.

    Methods: Data on dementia incidence over a 15 year period was obtained from the Betula project, a longitudinal study on health and ageing. Estimates of annual mean levels of nitrogen oxides (NOx) at the participants’ residential address were obtained using a land-use regression model. Modelled data provided road traffic noise levels (Leq. 24 h) at the participants’ residential address at baseline. Cox proportional hazard regression was used to calculate hazard ratios (HR).

    Results: Of 1721 participants at baseline, 302 developed dementia during the follow up period. Exposure to noise levels (Leq. 24 h) > 55 dB had no significant effect on dementia risk (HR 0.95; CI: 0.57, 1.57). Residing in the two highest quartiles of NOx exposure was associated with an increased risk of dementia. The risk associated with NOx was not modified by adjusting for noise. Moreover, we found no significant interaction effects between NOx and road traffic noise on dementia risk.

    Conclusion: We found no evidence that exposure to road traffic noise, either independently or in combination with traffic air pollution, was associated with risk of dementia in our study area. Our results suggest that pollution should be considered the main component in the association between traffic related exposures and dementia.

  • 4.
    Andersson, John
    et al.
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Sundström, Anna
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi. Umeå universitet, Samhällsvetenskapliga fakulteten, Enheten för demografi och åldrandeforskning (CEDAR). Department of Research and Development, Sundsvall Hospital, Sundsvall, Sweden.
    Nordin, Maria
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Segersson, David
    Swedish Meteorological and Hydrological Institute (SMHI), Norrköping, Sweden.
    Forsberg, Bertil
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Oudin, Anna
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin. Division of Occupational and Environmental Medicine, Lund University, Lund, Sweden.
    Pm2.5 and dementia in a low exposure setting: the influence of odor identification ability and APOE2023Ingår i: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 92, nr 2, s. 679-689Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Growing evidence show that long term exposure to air pollution increases the risk of dementia.

    Objective: The aim of this study was to investigate associations between PM2.5 exposure and dementia in a low exposure area, and to investigate the role of olfaction and the APOE ε4 allele in these associations.

    Methods: Data were drawn from the Betula project, a longitudinal study on aging, memory, and dementia in Sweden. Odor identification ability was assessed using the Scandinavian Odor Identification Test (SOIT). Annual mean PM2.5 concentrations were obtained from a dispersion-model and matched at the participants’ residential address. Proportional hazard regression was used to calculate hazard ratios.

    Results: Of 1,846 participants, 348 developed dementia during the 21-year follow-up period. The average annual mean PM2.5 exposure at baseline was 6.77 µg/m3, which is 1.77 µg/m3 above the WHO definition of clean air. In a fully adjusted model (adjusted for age, sex, APOE, SOIT, cardiovascular diseases and risk factors, and education) each 1 µg/m3 difference in annual mean PM2.5-concentration was associated with a hazard ratio of 1.23 for dementia (95% CI: 1.01–1.50). Analyses stratified by APOE status (ε4 carriers versus non-carriers), and odor identification ability (high versus low), showed associations only for ε4 carriers, and for low performance on odor identification ability.

    Conclusion: PM2.5 was associated with an increased risk of dementia in this low pollution setting. The associations between PM2.5 and dementia seemed stronger in APOE carriers and those with below average odor identification ability.

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  • 5.
    Li, Shenpan
    et al.
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Wu, LuYin
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Zeng, HuiXian
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Zhang, Jing
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Qin, ShuangJian
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Liang, Li-Xia
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Andersson, John
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Meng, Wen-Jie
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Chen, Xing-Yu
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Wu, Qi-Zhen
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Lin, Li-Zi
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Chou, Wei-Chun
    Center for Environmental and Human Toxicology, Department of Environmental and Global Health, College of Public Health and Health Professions, University of Florida, FL, Gainesville, United States.
    Dong, Guang-Hui
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Zeng, Xiao-Wen
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Hepatic injury and ileitis associated with gut microbiota dysbiosis in mice upon F–53B exposure2024Ingår i: Environmental Research, ISSN 0013-9351, E-ISSN 1096-0953, Vol. 248, artikel-id 118305Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Chlorinated polyfluorinated ether sulfonate (F–53B), a substitute of perfluorooctane sulfonic acid (PFOS), has attracted significant attention for its link to hepatotoxicity and enterotoxicity. Nevertheless, the underlying mechanisms of F–53B-induced enterohepatic toxicity remain incompletely understood. This study aimed to explore the role of F–53B exposure on enterohepatic injury based on the gut microbiota, pathological and molecular analysis in mice. Here, we exposed C57BL/6 mice to F–53B (0, 4, 40, and 400 μg/L) for 28 days. Our findings revealed a significant accumulation of F–53B in the liver, followed by small intestines, and feces. In addition, F–53B induced pathological collagen fiber deposition and lipoid degeneration, up-regulated the expression of fatty acid β-oxidation-related genes (PPARα and PPARγ, etc), while simultaneously down-regulating pro-inflammatory genes (Nlrp3, IL-1β, and Mcp1) in the liver. Meanwhile, F–53B induced ileal mucosal barrier damage, and an up-regulation of pro-inflammatory genes and mucosal barrier-related genes (Muc1, Muc2, Claudin1, Occludin, Mct1, and ZO-1) in the ileum. Importantly, F–53B distinctly altered gut microbiota compositions by increasing the abundance of Akkermansia and decreasing the abundance of Prevotellaceae_NK3B31_group in the feces. F–53B-altered microbiota compositions were significantly associated with genes related to fatty acid β-oxidation, inflammation, and mucosal barrier. In summary, our results demonstrate that F–53B is capable of inducing hepatic injury, ileitis, and gut microbiota dysbiosis in mice, and the gut microbiota dysbiosis may play an important role in the F–53B-induced enterohepatic toxicity.

  • 6.
    Oudin, Anna
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för hållbar hälsa. Department of Laboratory Medicine, Lund University, Lund, Sweden.
    Andersson, John
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Sundström, Anna
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Nordin Adolfsson, Annelie
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Oudin Åström, Daniel
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för hållbar hälsa.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Forsberg, Bertil
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för hållbar hälsa.
    Nordin, Maria
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Traffic-Related air pollution as a risk factor for dementia: no clear modifying effects of apoe ɛ4 in the betula cohort2021Ingår i: Alzheimer's disease and air pollution: the development and progression of a fatal disease from childhood and the opportunities for early prevention / [ed] Lilian Calderón-Garcidueñas, Amsterdam: IOS Press, 2021, s. 357-364Kapitel i bok, del av antologi (Refereegranskat)
    Abstract [en]

    It is widely known that the apolipoprotein E (APOE) ε4 allele imposes a higher risk for Alzheimer's disease (AD). Recent evidence suggests that exposure to air pollution is also a risk factor for AD, and results from a few studies indicate that the effect of air pollution on cognitive function and dementia is stronger in APOE ε4 carriers than in non-carriers. Air pollution and interaction with APOE ε4 on AD risk thus merits further attention. We studied dementia incidence over a 15-year period from the longitudinal Betula study in Northern Sweden. As a marker for long-term exposure to traffic-related air pollution, we used modelled annual mean nitrogen oxide levels at the residential address of the participants at start of follow-up. Nitrogen oxide correlate well with fine particulate air pollution levels in the study area. We had full data on air pollution, incidence of AD and vascular dementia (VaD), APOE ε4 carrier status, and relevant confounding factors for 1,567 participants. As expected, air pollution was rather clearly associated with dementia incidence. However, there was no evidence for a modifying effect by APOE ε4 on the association (p-value for interaction > 0.30 for both total dementia (AD+VaD) and AD). The results from this study do not imply that adverse effects of air pollution on dementia incidence is limited to, or stronger in, APOE ε4 carriers than in the total population.

  • 7.
    Oudin, Anna
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för hållbar hälsa. Department of Laboratory Medicine, Lund University, Lund, Sweden..
    Andersson, John
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Sundström, Anna
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Nordin Adolfsson, Annelie
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Oudin Åström, Daniel
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för hållbar hälsa.
    Adolfsson, Rolf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Psykiatri.
    Forsberg, Bertil
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för hållbar hälsa.
    Nordin, Maria
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Traffic-Related Air Pollution as a Risk Factor for Dementia: No Clear Modifying Effects of APOEɛ4 in the Betula Cohort2019Ingår i: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 71, nr 3, s. 733-740Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    It is widely known that the apolipoprotein E (APOE) ɛ4 allele imposes a higher risk for Alzheimer’s disease (AD). Recent evidence suggests that exposure to air pollution is also a risk factor for AD, and results from a few studies indicate that the effect of air pollution on cognitive function and dementia is stronger in APOE ɛ4 carriers than in non-carriers. Air pollution and interaction with APOE ɛ4 on AD risk thus merits further attention. We studied dementia incidence over a 15-year period from the longitudinal Betula study in Northern Sweden. As a marker for long-term exposure to traffic-related air pollution, we used modelled annual mean nitrogen oxide levels at the residential address of the participants at start of follow-up. Nitrogen oxide correlate well with fine particulate air pollution levels in the study area. We had full data on air pollution, incidence of AD and vascular dementia (VaD), APOE ɛ4 carrier status, and relevant confounding factors for 1,567 participants. As expected, air pollution was rather clearly associated with dementia incidence. However, there was no evidence for a modifying effect by APOE ɛ4 on the association (p-value for interaction > 0.30 for both total dementia (AD+VaD) and AD). The results from this study do not imply that adverse effects of air pollution on dementia incidence is limited to, or stronger in, APOE ɛ4 carriers than in the total population.

  • 8.
    Qin, Shuang-Jian
    et al.
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Zeng, Qing-Guo
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Zeng, Hui-Xian
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Li, Shen-Pan
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Andersson, John
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Zhao, Bin
    State Key Joint Laboratory of Environmental Simulation and Pollution Control, School of Environment, Tsinghua University, Beijing, China; State Environmental Protection Key Laboratory of Sources and Control of Air Pollution Complex, Beijing, China.
    Oudin, Anna
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin.
    Kanninen, Katja M.
    A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.
    Jalava, Pasi
    Department of Environmental and Biological Science, University of Eastern Finland, Kuopio, Finland.
    Jin, Nan-Xiang
    A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.
    Yang, Mo
    Department of Environmental and Biological Science, University of Eastern Finland, Kuopio, Finland.
    Lin, Li-Zi
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Liu, Ru-Qing
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Dong, Guang-Hui
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Zeng, Xiao-Wen
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Neurotoxicity of fine and ultrafine particulate matter: a comprehensive review using a toxicity pathway-oriented adverse outcome pathway framework2024Ingår i: Science of the Total Environment, ISSN 0048-9697, E-ISSN 1879-1026, Vol. 947, artikel-id 174450Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Fine particulate matter (PM2.5) can cause brain damage and diseases. Of note, ultrafine particles (UFPs) with an aerodynamic diameter less than or equal to 100 nm are a growing concern. Evidence has suggested toxic effects of PM2.5 and UFPs on the brain and links to neurological diseases. However, the underlying mechanism has not yet been fully illustrated due to the variety of the study models, different endpoints, etc. The adverse outcome pathway (AOP) framework is a pathway-based approach that could systematize mechanistic knowledge to assist health risk assessment of pollutants. Here, we constructed AOPs by collecting molecular mechanisms in PM-induced neurotoxicity assessments. We chose particulate matter (PM) as a stressor in the Comparative Toxicogenomics Database (CTD) and identified the critical toxicity pathways based on Ingenuity Pathway Analysis (IPA). We found 65 studies investigating the potential mechanisms linking PM2.5 and UFPs to neurotoxicity, which contained 2, 675 genes in all. IPA analysis showed that neuroinflammation signaling and glucocorticoid receptor signaling were the common toxicity pathways. The upstream regulator analysis (URA) of PM2.5 and UFPs demonstrated that the neuroinflammation signaling was the most initially triggered upstream event. Therefore, neuroinflammation was recognized as the MIE. Strikingly, there is a clear sequence of activation of downstream signaling pathways with UFPs, but not with PM2.5. Moreover, we found that inflammation response and homeostasis imbalance were key cellular events in PM2.5 and emphasized lipid metabolism and mitochondrial dysfunction, and blood-brain barrier (BBB) impairment in UFPs. Previous AOPs, which only focused on phenotypic changes in neurotoxicity upon PM exposure, we for the first time propose AOP framework in which PM2.5 and UFPs may activate pathway cascade reactions, resulting in adverse outcomes associated with neurotoxicity. Our toxicity pathway-based approach not only advances risk assessment for PM-induced neurotoxicity but shines a spotlight on constructing AOP frameworks for new chemicals.

  • 9.
    Wu, Qi-Zhen
    et al.
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Zeng, Hui-Xian
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Andersson, John
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Oudin, Anna
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin.
    Kanninen, Katja M.
    A.I.Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.
    Xu, Mu-Wu
    Department of Epidemiology and Environment Health, School of Public and Health Professions, University at Buffalo, Buffalo, United States.
    Qin, Shuang-Jian
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Zeng, Qing-Guo
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Zhao, Bin
    State Key Joint Laboratory of Environmental Simulation and Pollution Control, School of Environment, Tsinghua University, Beijing, China; State Environmental Protection Key Laboratory of Sources and Control of Air Pollution Complex, Beijing, China.
    Zheng, Mei
    SKL-ESPC, College of Environmental Sciences and Engineering, Center for Environment and Health, Peking University, Beijing, China.
    Jin, Nanxiang
    A.I.Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.
    Chou, Wei-Chun
    Center for Environmental and Human Toxicology, Department of Environmental and Global Health, College of Public Health and Health Professions, University of Florida, FL, Gainesville, United States.
    Jalava, Pasi
    Department of Environmental and Biological Science, University of Eastern Finland, Kuopio, Finland.
    Dong, Guang-Hui
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Zeng, Xiao-Wen
    Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou, China.
    Long-term exposure to major constituents of fine particulate matter and neurodegenerative diseases: a population-based survey in the Pearl River Delta Region, China2024Ingår i: Journal of Hazardous Materials, ISSN 0304-3894, E-ISSN 1873-3336, Vol. 470, artikel-id 134161Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Exposure to PM2.5 has been linked to neurodegenerative diseases, with limited understanding of constituent-specific contributions.

    Objectives: To explore the associations between long-term exposure to PM2.5 constituents and neurodegenerative diseases.

    Methods: We recruited 148,274 individuals aged ≥ 60 from four cities in the Pearl River Delta region, China (2020 to 2021). We calculated twenty-year average air pollutant concentrations (PM2.5 mass, black carbon (BC), organic matter (OM), ammonium (NH4+), nitrate (NO3-) and sulfate (SO42-)) at the individuals' home addresses. Neurodegenerative diseases were determined by self-reported doctor-diagnosed Alzheimer's disease (AD) and Parkinson's disease (PD). Generalized linear mixed models were employed to explore associations between pollutants and neurodegenerative disease prevalence.

    Results: PM2.5 and all five constituents were significantly associated with a higher prevalence of AD and PD. The observed associations generally exhibited a non-linear pattern. For example, compared with the lowest quartile, higher quartiles of BC were associated with greater odds for AD prevalence (i.e., the adjusted odds ratios were 1.81; 95% CI, 1.45–2.27; 1.78; 95% CI, 1.37–2.32; and 1.99; 95% CI, 1.54–2.57 for the second, third, and fourth quartiles, respectively).

    Conclusions: Long-term exposure to PM2.5 and its constituents, particularly combustion-related BC, OM, and SO42-, was significantly associated with higher prevalence of AD and PD in Chinese individuals.

    Environmental implication: PM2.5 is a routinely regulated mixture of multiple hazardous constituents that can lead to diverse adverse health outcomes. However, current evidence on the specific contributions of PM2.5 constituents to health effects is scarce. This study firstly investigated the association between PM2.5 constituents and neurodegenerative diseases in the moderately to highly polluted Pearl River Delta region in China, and identified hazardous constituents within PM2.5 that have significant impacts. This study provides important implications for the development of targeted PM2.5 prevention and control policies to reduce specific hazardous PM2.5 constituents.

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