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Oudin, Anna
Publications (10 of 91) Show all publications
Wu, Q.-Z., Zeng, H.-X., Andersson, J., Oudin, A., Kanninen, K. M., Xu, M.-W., . . . Zeng, X.-W. (2024). Long-term exposure to major constituents of fine particulate matter and neurodegenerative diseases: a population-based survey in the Pearl River Delta Region, China. Journal of Hazardous Materials, 470, Article ID 134161.
Open this publication in new window or tab >>Long-term exposure to major constituents of fine particulate matter and neurodegenerative diseases: a population-based survey in the Pearl River Delta Region, China
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2024 (English)In: Journal of Hazardous Materials, ISSN 0304-3894, E-ISSN 1873-3336, Vol. 470, article id 134161Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
Elsevier, 2024
Keywords
Alzheimer's disease, China, Health risk, Parkinson's disease, PM2.5 constituent
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-223230 (URN)10.1016/j.jhazmat.2024.134161 (DOI)2-s2.0-85189547708 (Scopus ID)
Available from: 2024-04-19 Created: 2024-04-19 Last updated: 2024-04-19Bibliographically approved
de Crom, T. O., Ginos, B. N., Oudin, A., Ikram, M. K., Voortman, T. & Ikram, M. A. (2023). Air pollution and the risk of dementia: the Rotterdam study. Journal of Alzheimer's Disease, 91(2), 603-613
Open this publication in new window or tab >>Air pollution and the risk of dementia: the Rotterdam study
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2023 (English)In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 91, no 2, p. 603-613Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Exposure to air pollution has been suggested to increase the risk of dementia, but studies on this link often lack a detailed screening for dementia and data on important confounders.

OBJECTIVE: To determine the association of exposure to air pollution with the risk of dementia and cognitive decline in the population-based Rotterdam Study.

METHODS: Between 2009 and 2010, we determined air pollutant concentrations at participants residential addresses using land use regression models. Determined air pollutants include particulate matter <10μm (PM10) and <2.5μm (PM2.5), a proxy of elemental carbon (PM2.5 absorbance), nitrogen oxide (NOx), and nitrogen dioxide (NO2). As the individual air pollutant levels were highly correlated (r = 0.71-0.98), we computed a general marker covering all air pollutants based on a principal component analysis. We followed participants up for dementia until 2018 and determined cognitive performance during two subsequent examination rounds. Using Cox and linear mixed models, we related air pollution to dementia and cognitive decline.

RESULTS: Of the 7,511 non-demented participants at baseline, 545 developed dementia during a median follow-up of 7 years. The general marker of all air pollutants was not associated with the risk of dementia (hazard ratio [95% confidence interval]: 1.04 [0.95-1.15]), neither were the individual air pollutants. Also, the general marker of all air pollutants or the individual air pollutant levels were not associated with cognitive decline.

CONCLUSION: In this study, we found no clear evidence for an association between exposure to air pollution and the risk of dementia or cognitive decline.

Place, publisher, year, edition, pages
IOS Press, 2023
Keywords
Air pollution, Alzheimer’s disease, cognition, dementia, nitrogen oxide, particulate matter
National Category
Occupational Health and Environmental Health Neurology
Identifiers
urn:nbn:se:umu:diva-204471 (URN)10.3233/JAD-220804 (DOI)000912515600009 ()36463450 (PubMedID)2-s2.0-85147045381 (Scopus ID)
Funder
Swedish Research Council
Available from: 2023-02-17 Created: 2023-02-17 Last updated: 2023-04-04Bibliographically approved
Richter, J. C., Flanagan, E., Taj, T. M., Al-Nahar, L., Jakobsson, K. & Oudin, A. (2023). An investigation of child health in relation to housing renovations for a disadvantaged immigrant population in Malmö, Sweden. Scandinavian Journal of Public Health, 51(3), 472-482
Open this publication in new window or tab >>An investigation of child health in relation to housing renovations for a disadvantaged immigrant population in Malmö, Sweden
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2023 (English)In: Scandinavian Journal of Public Health, ISSN 1403-4948, E-ISSN 1651-1905, Vol. 51, no 3, p. 472-482Article in journal (Refereed) Published
Abstract [en]

AIMS: The aim of the study was to describe child health in relation to housing renovations in more than 800 rental units, consisting of repairs of dilapidated kitchens and bathrooms, in the disadvantaged neighbourhood of Herrgården in Rosengård, Malmö, Sweden.

METHODS: Data on housing conditions and self-reported health were collected during home visits to families living in Herrgården (building renovations area) and a comparison area (neighbouring Törnrosen, with generally better housing conditions). At baseline, 130 families with 359 children participated, while 51 families with 127 children participated at follow-up. All data were collected between 2010 and 2012. Additionally, regional register data on health-care usage/in- and outpatient contacts within the public health-care system between 2008 and 2013 were also collected for all 8715 children registered as living in the two areas.

RESULTS: Self-reported health seemed to somewhat improve in both areas, with 74% versus 86% and 78% versus 88% reporting good or very good health in Herrgården and in the comparison area at baseline and follow-up, respectively. In Herrgården, crowdedness increased, while it decreased in the comparison area. The number of health-care contacts remained stable over time in Herrgården, while it decreased in the comparison area.

CONCLUSIONS: Partial housing renovations did not seem to result in clear health improvements as measured with the indicators used in the present study. This could possibly be due to persisting health effects due to increased crowdedness or persisting poor housing conditions, as only kitchens and bathrooms were renovated.

Place, publisher, year, edition, pages
Sage Publications, 2023
Keywords
Immigrant health, child health, child health inequality, housing renovations, indoor environment
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:umu:diva-201856 (URN)10.1177/14034948221138998 (DOI)000893128400001 ()36457214 (PubMedID)2-s2.0-85143643314 (Scopus ID)
Funder
Swedish Research Council Formas, 2011:1233000Swedish Research Council Formas, 2012:1185000
Available from: 2022-12-21 Created: 2022-12-21 Last updated: 2023-06-19Bibliographically approved
Thacher, J. D., Oudin, A., Flanagan, E., Mattisson, K., Albin, M., Roswall, N., . . . Sørensen, M. (2023). Exposure to long-term source-specific transportation noise and incident breast cancer: A pooled study of eight Nordic cohorts. Environment International, 178, Article ID 108108.
Open this publication in new window or tab >>Exposure to long-term source-specific transportation noise and incident breast cancer: A pooled study of eight Nordic cohorts
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2023 (English)In: Environment International, ISSN 0160-4120, E-ISSN 1873-6750, Vol. 178, article id 108108Article in journal (Refereed) Published
Abstract [en]

Background: Environmental noise is an important environmental exposure that can affect health. An association between transportation noise and breast cancer incidence has been suggested, although current evidence is limited. We investigated the pooled association between long-term exposure to transportation noise and breast cancer incidence.

Methods: Pooled data from eight Nordic cohorts provided a study population of 111,492 women. Road, railway, and aircraft noise were modelled at residential addresses. Breast cancer incidence (all, estrogen receptor (ER) positive, and ER negative) was derived from cancer registries. Hazard ratios (HR) were estimated using Cox Proportional Hazards Models, adjusting main models for sociodemographic and lifestyle variables together with long-term exposure to air pollution.

Results: A total of 93,859 women were included in the analyses, of whom 5,875 developed breast cancer. The median (5th–95th percentile) 5-year residential road traffic noise was 54.8 (40.0–67.8) dB Lden, and among those exposed, the median railway noise was 51.0 (41.2–65.8) dB Lden. We observed a pooled HR for breast cancer (95 % confidence interval (CI)) of 1.03 (0.99–1.06) per 10 dB increase in 5-year mean exposure to road traffic noise, and 1.03 (95 % CI: 0.96–1.11) for railway noise, after adjustment for lifestyle and sociodemographic covariates. HRs remained unchanged in analyses with further adjustment for PM2.5 and attenuated when adjusted for NO2 (HRs from 1.02 to 1.01), in analyses using the same sample. For aircraft noise, no association was observed. The associations did not vary by ER status for any noise source. In analyses using <60 dB as a cutoff, we found HRs of 1.08 (0.99–1.18) for road traffic and 1.19 (0.95–1.49) for railway noise.

Conclusions: We found weak associations between road and railway noise and breast cancer risk. More high-quality prospective studies are needed, particularly among those exposed to railway and aircraft noise before conclusions regarding noise as a risk factor for breast cancer can be made.

Place, publisher, year, edition, pages
Elsevier, 2023
Keywords
Air pollution, Aircraft noise, Breast cancer, Estrogen receptor, Noise, Railway noise, Traffic, Traffic noise
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-212484 (URN)10.1016/j.envint.2023.108108 (DOI)37490787 (PubMedID)2-s2.0-85165505340 (Scopus ID)
Funder
NordForsk, 83597Forte, Swedish Research Council for Health, Working Life and Welfare
Available from: 2023-08-01 Created: 2023-08-01 Last updated: 2023-08-01Bibliographically approved
Kitaba, N. T., Knudsen, G. T., Johannessen, A., Rezwan, F. I., Malinovschi, A., Oudin, A., . . . Holloway, J. W. (2023). Fathers’ preconception smoking and offspring DNA methylation. Clinical Epigenetics, 15(1), Article ID 131.
Open this publication in new window or tab >>Fathers’ preconception smoking and offspring DNA methylation
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2023 (English)In: Clinical Epigenetics, E-ISSN 1868-7083, Vol. 15, no 1, article id 131Article in journal (Refereed) Published
Abstract [en]

Background: Experimental studies suggest that exposures may impact respiratory health across generations via epigenetic changes transmitted specifically through male germ cells. Studies in humans are, however, limited. We aim to identify epigenetic marks in offspring associated with father’s preconception smoking.

Methods: We conducted epigenome-wide association studies (EWAS) in the RHINESSA cohort (7–50 years) on father’s any preconception smoking (n = 875 offspring) and father’s pubertal onset smoking < 15 years (n = 304), using Infinium MethylationEPIC Beadchip arrays, adjusting for offspring age, own smoking and maternal smoking. EWAS of maternal and offspring personal smoking were performed for comparison. Father’s smoking-associated dmCpGs were checked in subpopulations of offspring who reported no personal smoking and no maternal smoking exposure.

Results: Father’s smoking commencing preconception was associated with methylation of blood DNA in offspring at two cytosine-phosphate-guanine sites (CpGs) (false discovery rate (FDR) < 0.05) in PRR5 and CENPP. Father’s pubertal onset smoking was associated with 19 CpGs (FDR < 0.05) mapped to 14 genes (TLR9, DNTT, FAM53B, NCAPG2, PSTPIP2, MBIP, C2orf39, NTRK2, DNAJC14, CDO1, PRAP1, TPCN1, IRS1 and CSF1R). These differentially methylated sites were hypermethylated and associated with promoter regions capable of gene silencing. Some of these sites were associated with offspring outcomes in this cohort including ever-asthma (NTRK2), ever-wheezing (DNAJC14, TPCN1), weight (FAM53B, NTRK2) and BMI (FAM53B, NTRK2) (p < 0.05). Pathway analysis showed enrichment for gene ontology pathways including regulation of gene expression, inflammation and innate immune responses. Father’s smoking-associated sites did not overlap with dmCpGs identified in EWAS of personal and maternal smoking (FDR < 0.05), and all sites remained significant (p < 0.05) in analyses of offspring with no personal smoking and no maternal smoking exposure. Conclusion: Father’s preconception smoking, particularly in puberty, is associated with offspring DNA methylation, providing evidence that epigenetic mechanisms may underlie epidemiological observations that pubertal paternal smoking increases risk of offspring asthma, low lung function and obesity.

Place, publisher, year, edition, pages
BioMed Central (BMC), 2023
Keywords
DNA methylation, Epigenetic, Epigenome-wide association study, Paternal effects, Preconception, RHINESSA, Tobacco smoke
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:umu:diva-214269 (URN)10.1186/s13148-023-01540-7 (DOI)001058561300001 ()37649101 (PubMedID)2-s2.0-85169230897 (Scopus ID)
Funder
The Research Council of Norway, 274767The Research Council of Norway, 214123The Research Council of Norway, 228174The Research Council of Norway, 230827The Research Council of Norway, 273838EU, Horizon 2020, 633212Swedish Heart Lung FoundationSwedish Asthma and Allergy Association
Available from: 2023-09-12 Created: 2023-09-12 Last updated: 2023-09-12Bibliographically approved
Azzouz, M., Xu, Y., Barregard, L., Zöller, B., Molnar, P., Oudin, A., . . . Stockfelt, L. (2023). Long-term ambient air pollution and venous thromboembolism in a population-based Swedish cohort. Environmental Pollution, 331, Article ID 121841.
Open this publication in new window or tab >>Long-term ambient air pollution and venous thromboembolism in a population-based Swedish cohort
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2023 (English)In: Environmental Pollution, ISSN 0269-7491, E-ISSN 1873-6424, Vol. 331, article id 121841Article in journal (Refereed) Published
Abstract [en]

Air pollution is a major contributor to the global burden of disease and has been linked to several diseases and conditions, including cardiovascular disease. The biological mechanisms are related to inflammation and increased coagulability, factors that play an important role in the pathogenesis of venous thromboembolism (VTE, i.e., deep vein thrombosis or pulmonary embolism). This study investigates if long-term exposure to air pollution is associated with increased VTE incidence. The study followed 29 408 participants from the Malmö Diet and Cancer (MDC) cohort, which consists of adults aged 44–74 recruited in Malmö, Sweden between 1991 and 1996. For each participant, annual mean residential exposures to particulate matter <2.5 μg (PM2.5) and <10 μg (PM10), nitrogen oxides (NOx) and black carbon (BC) from 1990 up to 2016 were calculated. Associations with VTE were analysed using Cox proportional hazard models for air pollution in the year of the VTE event (lag0) and the mean of the prior 1–10 years (lag1-10). Annual air pollution exposures for the full follow-up period had the following means: 10.8 μg/m3 for PM2.5, 15.8 μg/m3 for PM10, 27.7 μg/m3 for NOx, and 0.96 μg/m3 for BC. The mean follow-up period was 19.5 years, with 1418 incident VTE events recorded during this period. Exposure to lag1-10 PM2.5 was associated with an increased risk of VTE (HR 1.17 (95%CI 1.01–1.37)) per interquartile range (IQR) of 1.2 μg/m3 increase in PM2.5 exposure. No significant associations were found between other pollutants or lag0 PM2.5 and incident VTE. When VTE was divided into specific diagnoses, associations with lag1-10 PM2.5 exposure were similarly positive for deep vein thrombosis but not for pulmonary embolism. Results persisted in sensitivity analyses and in multi-pollutant models. Long-term exposure to moderate concentrations of ambient PM2.5 was associated with increased risks of VTE in the general population in Sweden.

Place, publisher, year, edition, pages
Elsevier, 2023
Keywords
Air pollution, Deep vein thromboembolism, Particulate matter, Survival analysis, Venous thromboembolism
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-209186 (URN)10.1016/j.envpol.2023.121841 (DOI)001013282600001 ()37209899 (PubMedID)2-s2.0-85160406991 (Scopus ID)
Available from: 2023-06-20 Created: 2023-06-20 Last updated: 2023-09-05Bibliographically approved
Roswall, N., Thacher, J. D., Ögren, M., Pyko, A., Åkesson, A., Oudin, A., . . . Sørensen, M. (2023). Long-term exposure to traffic noise and risk of incident colon cancer: A pooled study of eleven Nordic cohorts. Environmental Research, 224, Article ID 115454.
Open this publication in new window or tab >>Long-term exposure to traffic noise and risk of incident colon cancer: A pooled study of eleven Nordic cohorts
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2023 (English)In: Environmental Research, ISSN 0013-9351, E-ISSN 1096-0953, Vol. 224, article id 115454Article in journal (Refereed) Published
Abstract [en]

Background: Colon cancer incidence is rising globally, and factors pertaining to urbanization have been proposed involved in this development. Traffic noise may increase colon cancer risk by causing sleep disturbance and stress, thereby inducing known colon cancer risk-factors, e.g. obesity, diabetes, physical inactivity, and alcohol consumption, but few studies have examined this.

Objectives: The objective of this study was to investigate the association between traffic noise and colon cancer (all, proximal, distal) in a pooled population of 11 Nordic cohorts, totaling 155,203 persons.

Methods: We identified residential address history and estimated road, railway, and aircraft noise, as well as air pollution, for all addresses, using similar exposure models across cohorts. Colon cancer cases were identified through national registries. We analyzed data using Cox Proportional Hazards Models, adjusting main models for harmonized sociodemographic and lifestyle data.

Results: During follow-up (median 18.8 years), 2757 colon cancer cases developed. We found a hazard ratio (HR) of 1.05 (95% confidence interval (CI): 0.99–1.10) per 10-dB higher 5-year mean time-weighted road traffic noise. In sub-type analyses, the association seemed confined to distal colon cancer: HR 1.06 (95% CI: 0.98–1.14). Railway and aircraft noise was not associated with colon cancer, albeit there was some indication in sub-type analyses that railway noise may also be associated with distal colon cancer. In interaction-analyses, the association between road traffic noise and colon cancer was strongest among obese persons and those with high NO2-exposure.

Discussion: A prominent study strength is the large population with harmonized data across eleven cohorts, and the complete address-history during follow-up. However, each cohort estimated noise independently, and only at the most exposed façade, which may introduce exposure misclassification. Despite this, the results of this pooled study suggest that traffic noise may be a risk factor for colon cancer, especially of distal origin.

Place, publisher, year, edition, pages
Elsevier, 2023
Keywords
Colon cancer, Distal, Pooled cohort study, Proximal, Railway noise, Road traffic noise
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-205486 (URN)10.1016/j.envres.2023.115454 (DOI)000951077000001 ()36764429 (PubMedID)2-s2.0-85148731232 (Scopus ID)
Funder
NordForsk, 83597
Available from: 2023-03-15 Created: 2023-03-15 Last updated: 2023-09-05Bibliographically approved
Pyko, A., Roswall, N., Ögren, M., Oudin, A., Rosengren, A., Eriksson, C., . . . Pershagen, G. (2023). Long-term exposure to transportation noise and ischemic heart disease: a pooled analysis of nine Scandinavian cohorts. Journal of Environmental Health Perspectives, 131(1), Article ID 17003.
Open this publication in new window or tab >>Long-term exposure to transportation noise and ischemic heart disease: a pooled analysis of nine Scandinavian cohorts
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2023 (English)In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 131, no 1, article id 17003Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Transportation noise may induce cardiovascular disease, but the public health implications are unclear. OBJECTIVES: The study aimed to assess exposure-response relationships for different transportation noise sources and ischemic heart disease (IHD), including subtypes. METHODS: Pooled analyses were performed of nine cohorts from Denmark and Sweden, together including 132,801 subjects. Time-weighted long-term exposure to road, railway, and aircraft noise, as well as air pollution, was estimated based on residential histories. Hazard ratios (HRs) were calculated using Cox proportional hazards models following adjustment for lifestyle and socioeconomic risk factors. RESULTS: A total of 22,459 incident cases of IHD were identified during follow-up from national patient and mortality registers, including 7,682 cases of myocardial infarction. The adjusted HR for IHD was 1.03 [95% confidence interval (CI) 1.00, 1.05] per 10 dB formula presented for both road and railway noise exposure during 5 y prior to the event. Higher risks were indicated for IHD excluding angina pectoris cases, with HRs of 1.06 (95% CI: 1.03, 1.08) and 1.05 (95% CI: 1.01, 1.08) per 10 dB formula presented for road and railway noise, respectively. Corresponding HRs for myocardial infarction were 1.02 (95% CI: 0.99, 1.05) and 1.04 (95% CI: 0.99, 1.08). Increased risks were observed for aircraft noise but without clear exposure-response relations. A threshold at around 55 dB formula presented was suggested in the exposure-response relation for road traffic noise and IHD. DISCUSSION: Exposure to road, railway, and aircraft noise in the prior 5 y was associated with an increased risk of IHD, particularly after exclusion of angina pectoris cases, which are less well identified in the registries. 

Place, publisher, year, edition, pages
Environmental Health Perspectives, 2023
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-203555 (URN)10.1289/EHP10745 (DOI)36607286 (PubMedID)2-s2.0-85145955612 (Scopus ID)
Funder
NordForsk, 83597
Available from: 2023-01-19 Created: 2023-01-19 Last updated: 2023-03-15Bibliographically approved
Nilsson Sommar, J., Segersson, D., Flanagan, E. & Oudin, A. (2023). Long-term residential exposure to source-specific particulate matter and incidence of diabetes mellitus: A cohort study in northern Sweden. Environmental Research, 217, Article ID 114833.
Open this publication in new window or tab >>Long-term residential exposure to source-specific particulate matter and incidence of diabetes mellitus: A cohort study in northern Sweden
2023 (English)In: Environmental Research, ISSN 0013-9351, E-ISSN 1096-0953, Vol. 217, article id 114833Article in journal (Refereed) Published
Abstract [en]

Diabetes mellitus (DM) incidence have been assessed in connection with air pollution exposure in several studies; however, few have investigated associations with source-specific local emissions. This study aims to estimate the risk of DM incidence associated with source-specific air pollution in a Swedish cohort with relatively low exposure. Individuals in the Västerbotten intervention programme cohort were followed until either a DM diagnosis or initiation of treatment with glucose-lowering medication occurred. Dispersion models with high spatial resolution were used to estimate annual mean concentrations of particulate matter (PM) with aerodynamic diameter ≤10 μm (PM10) and ≤2.5 μm (PM2.5) at individual addresses. Hazard ratios were estimated using Cox regression models in relation to moving averages 1-5 years preceding the outcome. During the study period, 1479 incident cases of DM were observed during 261,703 person-years of follow-up. Increased incidence of DM was observed in association with PM10 (4% [95% CI: -54-137%] per 10 μg/m3), PM10-traffic (2% [95% CI: -6-11%] per 1 μg/m3) and PM2.5-exhaust (11% [95% CI: -39-103%] per 1 μg/m3). A negative association was found for both PM2.5 (-18% [95% CI: -99-66%] per 5 μg/m3), but only in the 2nd exposure tertile (-10% [95% CI: -25-9%] compared to the first tertile), and PM2.5-woodburning (-30% [95% CI: -49-4%] per 1 μg/m3). In two-pollutant models including PM2.5-woodburning, there was an 11% [95% CI: -11-38%], 6% [95% CI: -16-34%], 13% [95% CI: -7-36%] and 17% [95% CI: 4-41%] higher risk in the 3rd tertile of PM10, PM2.5, PM10-traffic and PM2.5-exhaust, respectively, compared to the 1st. Although the results lacked in precision they are generally in line with the current evidence detailing particulate matter air pollution from traffic as an environmental risk factor for DM.

Place, publisher, year, edition, pages
Elsevier, 2023
Keywords
Air pollution, Cohort, Diabetes mellitus, Exhaust, Particulate matter, Traffic emissions
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-201854 (URN)10.1016/j.envres.2022.114833 (DOI)000895272700010 ()36402182 (PubMedID)2-s2.0-85145580527 (Scopus ID)
Funder
Swedish Research Council Formas, 2017–00898
Available from: 2022-12-21 Created: 2022-12-21 Last updated: 2023-01-12Bibliographically approved
Lepistö, T., Lintusaari, H., Oudin, A., Barreira, L. M. .., Niemi, J. V., Karjalainen, P., . . . Rönkkö, T. (2023). Particle lung deposited surface area (LDSAal) size distributions in different urban environments and geographical regions: Towards understanding of the PM2.5 dose–response. Environment International, 180, Article ID 108224.
Open this publication in new window or tab >>Particle lung deposited surface area (LDSAal) size distributions in different urban environments and geographical regions: Towards understanding of the PM2.5 dose–response
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2023 (English)In: Environment International, ISSN 0160-4120, E-ISSN 1873-6750, Vol. 180, article id 108224Article in journal (Refereed) Published
Abstract [en]

Recent studies indicate that monitoring only fine particulate matter (PM2.5) may not be enough to understand and tackle the health risk caused by particulate pollution. Health effects per unit PM2.5 seem to increase in countries with low PM2.5, but also near local pollution sources (e.g., traffic) within cities. The aim of this study is to understand the differences in the characteristics of lung-depositing particles in different geographical regions and urban environments. Particle lung deposited surface area (LDSAal) concentrations and size distributions, along with PM2.5, were compared with ambient measurement data from Finland, Germany, Czechia, Chile, and India, covering traffic sites, residential areas, airports, shipping, and industrial sites. In Finland (low PM2.5), LDSAal size distributions depended significantly on the urban environment and were mainly attributable to ultrafine particles (<100 nm). In Central Europe (moderate PM2.5), LDSAal was also dependent on the urban environment, but furthermore heavily influenced by the regional aerosol. In Chile and India (high PM2.5), LDSAal was mostly contributed by the regional aerosol despite that the measurements were done at busy traffic sites. The results indicate that the characteristics of lung-depositing particles vary significantly both within cities and between geographical regions. In addition, ratio between LDSAal and PM2.5 depended notably on the environment and the country, suggesting that LDSAal exposure per unit PM2.5 may be multiple times higher in areas having low PM2.5 compared to areas with continuously high PM2.5. These findings may partly explain why PM2.5 seems more toxic near local pollution sources and in areas with low PM2.5. Furthermore, performance of a typical sensor based LDSAal measurement is discussed and a new LDSAal2.5 notation indicating deposition region and particle size range is introduced. Overall, the study emphasizes the need for country-specific emission mitigation strategies, and the potential of LDSAal concentration as a health-relevant pollution metric.

Place, publisher, year, edition, pages
Elsevier, 2023
Keywords
Exposure, Human respiratory tract, Particulate matter, Regional aerosol, Ultrafine particles, Urban air quality
National Category
Meteorology and Atmospheric Sciences Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-214972 (URN)10.1016/j.envint.2023.108224 (DOI)2-s2.0-85172305525 (Scopus ID)
Funder
EU, Horizon 2020, 814978
Available from: 2023-10-16 Created: 2023-10-16 Last updated: 2023-10-16Bibliographically approved
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