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  • 1. Akesson, Agneta
    et al.
    Barregard, Lars
    Bergdahl, Ingvar A.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Nordberg, Gunnar F.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Nordberg, Monica
    Skerfving, Staffan
    Non-Renal Effects and the Risk Assessment of Environmental Cadmium Exposure2014In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 122, no 5, p. 431-438Article in journal (Refereed)
    Abstract [en]

    Background: Exposure to cadmium (Cd) has long been recognized as a health hazard, both in industry and in general populations with high exposure. Under the currently prevailing health risk assessment, the relationship between urinary Cd (U-Cd) concentrations and tubular proteinuria is used. However, doubts have recently been raised regarding the justification of basing the risk assessment on this relationship at very low exposure. Objectives: Our objective was to review available information on health effects of Cd exposure with respect to human health risk assessment. Discussion: The associations between U-Cd and urinary proteins at very low exposure may not be due to Cd toxicity, and the clinical significance of slight proteinuria may also be limited. More importantly, other effects have been reported at very low Cd exposure. There is reason to challenge the basis of the existing health risk assessment for Cd. Our review of the literature found that exposure to low concentrations of Cd is associated with effects on bone, including increased risk of osteoporosis and fractures, and that this observation has implications for the health risk assessment of Cd. Other effects associated with Cd should also be considered, in particular cancer, although the information is still too limited for appropriate use in quantitative risk assessment. Conclusion: Non-renal effects should be considered critical effects in the health risk assessment of Cd.

  • 2. Andersen, Zorana J.
    et al.
    Stafoggia, Massimo
    Weinmayr, Gudrun
    Pedersen, Marie
    Galassi, Claudia
    Jørgensen, Jeanette T.
    Oudin, Anna
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Olsson, David
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Oftedal, Bente
    Aasvang, Gunn Marit
    Aamodt, Geir
    Pyko, Andrei
    Pershagen, Göran
    Korek, Michal
    De Faire, Ulf
    Pedersen, Nancy L.
    Östenson, Claes-Göran
    Fratiglioni, Laura
    Eriksen, Kirsten T.
    Tjønneland, Anne
    Peeters, Petra H.
    Bueno-de-Mesquita, Bas
    Plusquin, Michelle
    Key, Timothy J.
    Jaensch, Andrea
    Nagel, Gabriele
    Lang, Alois
    Wang, Meng
    Tsai, Ming-Yi
    Fournier, Agnes
    Boutron-Ruault, Marie-Christine
    Baglietto, Laura
    Grioni, Sara
    Marcon, Alessandro
    Krogh, Vittorio
    Ricceri, Fulvio
    Sacerdote, Carlotta
    Migliore, Enrica
    Tamayo-Uria, Ibon
    Amiano, Pilar
    Dorronsoro, Miren
    Vermeulen, Roel
    Sokhi, Ranjeet
    Keuken, Menno
    de Hoogh, Kees
    Beelen, Rob
    Vineis, Paolo
    Cesaroni, Giulia
    Brunekreef, Bert
    Hoek, Gerard
    Raaschou-Nielsen, Ole
    Long-term exposure to ambient air pollution and incidence of postmenopausal breast cancer in 15 European cohorts within the ESCAPE project2017In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 125, no 10, article id 107005Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Epidemiological evidence on the association between ambient air pollution and breast cancer risk is inconsistent.

    OBJECTIVE: We examined the association between long-term exposure to ambient air pollution and incidence of postmenopausal breast cancer in European women.

    METHODS: In 15 cohorts from nine European countries, individual estimates of air pollution levels at the residence were estimated by standardized land-use regression models developed within the European Study of Cohorts for Air Pollution Effects (ESCAPE) and Transport related Air Pollution and Health impacts – Integrated Methodologies for Assessing Particulate Matter (TRANSPHORM) projects: particulate matter (PM) ≤2.5μm, ≤10μm, and 2.5–10μm in diameter (PM2.5, PM10, and PMcoarse, respectively); PM2.5 absorbance; nitrogen oxides (NO2 and NOx); traffic intensity; and elemental composition of PM. We estimated cohort-specific associations between breast cancer and air pollutants using Cox regression models, adjusting for major lifestyle risk factors, and pooled cohort-specific estimates using random-effects meta-analyses.

    RESULTS: Of 74,750 postmenopausal women included in the study, 3,612 developed breast cancer during 991,353 person-years of follow-up. We found positive and statistically insignificant associations between breast cancer and PM2.5 {hazard ratio (HR)=1.08 [95% confidence interval (CI): 0.77, 1.51] per 5 μg/m(3)}, PM10 [1.07 (95% CI: 0.89, 1.30) per 10 μg/m(3)], PMcoarse[1.20 (95% CI: 0.96, 1.49 per 5 μg/m(3)], and NO(2) [1.02 (95% CI: 0.98, 1.07 per 10 μg/m(3)], and a statistically significant association with NOx [1.04 (95% CI: 1.00, 1.08) per 20 μg/m(3), p=0.04].

    CONCLUSIONS: We found suggestive evidence of an association between ambient air pollution and incidence of postmenopausal breast cancer in European women.

  • 3. Armstrong, Ben
    et al.
    Sera, Francesco
    Vicedo-Cabrera, Ana Maria
    Abrutzky, Rosana
    Oudin Åström, Daniel
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Section of Sustainable Health.
    Bell, Michelle L
    Chen, Bing-Yu
    de Sousa Zanotti Stagliorio Coelho, Micheline
    Correa, Patricia Matus
    Dang, Tran Ngoc
    Diaz, Magali Hurtado
    Dung, Do Van
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Section of Sustainable Health.
    Goodman, Patrick
    Guo, Yue-Liang Leon
    Guo, Yuming
    Hashizume, Masahiro
    Honda, Yasushi
    Indermitte, Ene
    Íñiguez, Carmen
    Kan, Haidong
    Kim, Ho
    Kyselý, Jan
    Lavigne, Eric
    Michelozzi, Paola
    Orru, Hans
    Ortega, Nicolás Valdés
    Pascal, Mathilde
    Ragettli, Martina S
    Saldiva, Paulo Hilario Nascimento
    Schwartz, Joel
    Scortichini, Matteo
    Seposo, Xerxes
    Tobias, Aurelio
    Tong, Shilu
    Urban, Aleš
    De la Cruz Valencia, César
    Zanobetti, Antonella
    Zeka, Ariana
    Gasparrini, Antonio
    The Role of Humidity in Associations of High Temperature with Mortality: A Multicountry, Multicity Study2019In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 127, no 9, article id 097007Article in journal (Refereed)
    Abstract [en]

    Background: There is strong experimental evidence that physiologic stress from high temperatures is greater if humidity is higher. However, heat indices developed to allow for this have not consistently predicted mortality better than dry-bulb temperature.

    Objectives: We aimed to clarify the potential contribution of humidity an addition to temperature in predicting daily mortality in summer by using a large multicountry dataset.

    Methods: In 445 cities in 24 countries, we fit a time-series regression model for summer mortality with a distributed lag nonlinear model (DLNM) for temperature (up to lag 3) and supplemented this with a range of terms for relative humidity (RH) and its interaction with temperature. City-specific associations were summarized using meta-analytic techniques.

    Results: Adding a linear term for RH to the temperature term improved fit slightly, with an increase of 23% in RH (the 99th percentile anomaly) associated with a 1.1% [95% confidence interval (CI): 0.8, 1.3] decrease in mortality. Allowing curvature in the RH term or adding terms for interaction of RH with temperature did not improve the model fit. The humidity-related decreased risk was made up of a positive coefficient at lag 0 outweighed by negative coefficients at lags of 1–3 d. Key results were broadly robust to small model changes and replacing RH with absolute measures of humidity. Replacing temperature with apparent temperature, a metric combining humidity and temperature, reduced goodness of fit slightly.

    Discussion:The absence of a positive association of humidity with mortality in summer in this large multinational study is counter to expectations from physiologic studies, though consistent with previous epidemiologic studies finding little evidence for improved prediction by heat indices. The result that there was a small negative average association of humidity with mortality should be interpreted cautiously; the lag structure has unclear interpretation and suggests the need for future work to clarify.

  • 4. Fuks, Kateryna B.
    et al.
    Weinmayr, Gudrun
    Foraster, Maria
    Dratva, Julia
    Hampel, Regina
    Houthuijs, Danny
    Oftedal, Bente
    Oudin, Anna
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Panasevich, Sviatlana
    Penell, Johanna
    Nilsson Sommar, Johan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Sørensen, Mette
    Tiittanen, Pekka
    Wolf, Kathrin
    Xun, Wei W.
    Aguilera, Inmaculada
    Basagaña, Xavier
    Beelen, Rob
    Bots, Michiel L.
    Brunekreef, Bert
    Bueno-de-Mesquita, H. Bas
    Caracciolo, Barbara
    Cirach, Marta
    de Faire, Ulf
    de Nazelle, Audrey
    Eeftens, Marloes
    Elosua, Roberto
    Erbel, Raimund
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Fratiglioni, Laura
    Gaspoz, Jean-Michel
    Hilding, Agneta
    Jula, Antti
    Korek, Michal
    Krämer, Ursula
    Künzli, Nino
    Lanki, Timo
    Leander, Karin
    Magnusson, Patrik K.
    Marrugat, Jaume
    Nieuwenhuijsen, Mark J.
    Östenson, Claes-Göran
    Pedersen, Nancy L.
    Pershagen, Göran
    Phuleria, Harish C.
    Probst-Hensch, Nicole M.
    Raaschou-Nielsen, Ole
    Schaffner, Emmanuel
    Schikowski, Tamara
    Schindler, Christian
    Schwarze, Per E.
    Søgaard, Annee J.
    Sugiri, Dorothea
    Swart, Wim J.
    Tsai, Ming-Yi
    Turunen, Anu W.
    Vineis, Paolo
    Peters, Annette
    Hoffmann, Barbara
    Arterial blood pressure and long-term exposure to traffic-related air pollution: an analysis in the European Study of Cohorts for Air Pollution Effects (ESCAPE)2014In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 122, no 9, p. 896-905Article, review/survey (Refereed)
    Abstract [en]

    BACKGROUND: Long-term exposure to air pollution is hypothesized to elevate arterial blood pressure (BP). The existing evidence is scarce and country-specific. OBJECTIVES: We investigated the cross-sectional association of long-term traffic-related air pollution with BP and prevalent hypertension in European populations. METHODS: Fifteen population-based cohorts, participating in the European Study of Cohorts for Air Pollution Effects (ESCAPE), were analysed. Residential exposure to particulate matter and nitrogen oxides was modelled with land use regression using a uniform protocol. Traffic exposure was assessed with traffic indicator variables. We analysed systolic and diastolic BP in participants medicated and non-medicated with BP lowering medication (BPLM) separately, adjusting for personal and area-level risk factors and environmental noise. Prevalent hypertension was defined as ≥ 140 mmHg systolic, or ≥ 90 mmHg diastolic BP, or intake of BPLM. We combined cohort-specific results using random-effects meta-analysis. RESULTS: In the main meta-analysis of 113,926 participants, traffic load on major roads within 100 m of the residence was associated with increased systolic and diastolic BP in non-medicated participants (0.35 mmHg [95% CI: 0.02-0.68] and 0.22 mmHg [95% CI: 0.04-0.40] per 4,000,000 vehicles × m/day, respectively). The estimated odds ratio for prevalent hypertension was 1.05 [95% CI: 0.99-1.11] per 4,000,000 vehicles × m/day. Modelled air pollutants and BP were not clearly associated. CONCLUSIONS: In this first comprehensive meta-analysis of European population-based cohorts we observed a weak positive association of high residential traffic exposure with BP in non-medicated participants, and an elevated OR for prevalent hypertension. The relationship of modelled air pollutants with BP was inconsistent.

  • 5. Guastadisegni, Cecilia
    et al.
    Kelly, Frank J
    Cassee, Flemming R
    Gerlofs-Nijland, Miriam E
    Janssen, Nicole AH
    Pozzi, Roberta
    Brunekreef, Bert
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Mudway, Ian
    Determinants of the proinflammatory action of ambient particulate matter in immortalized murine macrophages2010In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 118, no 12, p. 1728-1734Article in journal (Refereed)
    Abstract [en]

    We found no evidence that PM collected from sites in close proximity to traffic sources displayed enhanced proinflammatory activity in RAW264.7 cells.

  • 6.
    Harlid, Sophia
    et al.
    Epigenetics and Stem Cell Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA.
    Adgent, Margaret
    Jefferson, Wendy N.
    Panduri, Vijayalakshmi
    Umbach, David M.
    Xu, Zongli
    Stallings, Virginia A.
    Williams, Carmen J.
    Rogan, Walter J.
    Taylor, Jack A.
    Soy formula and epigenetic modifications: analysis of vaginal epithelial cells from infant girls in the IFED study2017In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 125, no 3, p. 447-452Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Early-life exposure to estrogenic compounds affects the development of the reproductive system in rodent models and humans. Soy products, which contain phytoestrogens such as genistein, are one source of exposure in infants fed soy formula, and they result in high serum concentrations.

    OBJECTIVES: Our goal was to determine whether soy exposure is associated with differential DNA methylation in vaginal cells from soy-fed infant girls.

    METHODS: Using the Illumina HumanMethylation450 BeadChip, we evaluated epigenome-wide DNA methylation in vaginal cells from four soy formula-fed and six cow formula-fed girls from the Infant Feeding and Early Development (IFED) study. Using pyrosequencing we followed up the two most differentially methylated sites in 214 vaginal cell samples serially collected between birth and 9 months of age from 50 girls (28 soy formula-fed and 22 cow formula-fed). With a mouse model, we examined the effect of neonatal exposure to genistein on gene specific mRNA levels in vaginal tissue.

    RESULTS: The epigenome-wide scan suggested differences in methylation between soy formula-fed and cow formula-fed infants at three CpGs in the gene proline rich 5 like (PRR5L) (p < 10(4)). Pyrosequencing of the two feeding groups found that methylation levels progressively diverged with age, with pointwise differences becoming statistically significant after 126 days. Genistein-exposed mice showed a 50% decrease in vaginal Prr5l mRNA levels compared to controls.

    CONCLUSIONS: Girls fed soy formula have altered DNA methylation in vaginal cell DNA which may be associated with decreased expression of an estrogen-responsive gene.

  • 7.
    Harlid, Sophia
    et al.
    Epigenetics and Stem Cell Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA.
    Xu, Zongli
    Panduri, Vijayalakshmi
    Sandler, Dale P
    Taylor, Jack A
    CpG sites associated with cigarette smoking: analysis of epigenome-wide data from the Sister Study.2014In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 122, no 7, p. 673-8Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Smoking increases the risk of many diseases, and it is also linked to blood DNA methylation changes that may be important in disease etiology.

    OBJECTIVES: We sought to identify novel CpG sites associated with cigarette smoking.

    METHODS: We used two epigenome-wide data sets from the Sister Study to identify and confirm CpG sites associated with smoking. One included 908 women with methylation measurements at 27,578 CpG sites using the HumanMethylation27 BeadChip; the other included 200 women with methylation measurements for 473,844 CpG sites using the HumanMethylation450 BeadChip. Significant CpGs from the second data set that were not included in the 27K assay were validated by pyrosequencing in a subset of 476 samples from the first data set.

    RESULTS: Our study successfully confirmed smoking associations for 9 previously established CpGs and identified 2 potentially novel CpGs: cg26764244 in GNG12 (p = 9.0 × 10-10) and cg22335340 in PTPN6 (p = 2.9 × 10-05). We also found strong evidence of an association between smoking status and cg02657160 in CPOX (p = 7.3 × 10-7), which has not been previously reported. All 12 CpGs were undermethylated in current smokers and showed an increasing percentage of methylation in former and never-smokers.

    CONCLUSIONS: We identified 2 potentially novel smoking related CpG sites, and provided independent replication of 10 previously reported CpGs sites related to smoking, one of which is situated in the gene CPOX. The corresponding enzyme is involved in heme biosynthesis, and smoking is known to increase heme production. Our study extends the evidence base for smoking-related changes in DNA methylation.

  • 8. Hebels, Dennie G. A. J.
    et al.
    Georgiadis, Panagiotis
    Keun, Hector C.
    Athersuch, Toby J.
    Vineis, Paolo
    Vermeulen, Roel
    Portengen, Lützen
    Bergdahl, Ingvar A.
    Umeå University, Faculty of Medicine, Department of Biobank Research. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Biobank Research. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Palli, Domenico
    Bendinelli, Benedetta
    Krogh, Vittorio
    Tumino, Rosario
    Sacerdote, Carlotta
    Panico, Salvatore
    Kleinjans, Jos C. S.
    de Kok, Theo M. C. M.
    Smith, Martyn T.
    Kyrtopoulos, Soterios A.
    Performance in omics analyses of blood samples in long-term storage: opportunities for the exploitation of existing biobanks in environmental health research2013In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 121, no 4, p. 480-487Article in journal (Refereed)
    Abstract [en]

    Background: The suitability for omic analysis of biosamples collected in previous decades and currently stored in biobanks is unknown.

    Objectives: We evaluated the influence of handling and storage conditions of blood-derived biosamples on transcriptomic, epigenomic (CpG methylation), plasma metabolomic [UPLC-ToFMS (ultra performance liquid chromatography-time-of-flight mass spectrometry)], and wide-target proteomic profiles.

    Methods: We collected fresh blood samples without RNA preservative in heparin, EDTA, or citrate and held them at room temperature for ≤ 24 hr before fractionating them into buffy coat, erythrocytes, and plasma and freezing the fractions at -80oC or in liquid nitrogen. We developed methodology for isolating RNA from the buffy coats and conducted omic analyses. Finally, we analyzed analogous samples from the EPIC-Italy and Northern Sweden Health and Disease Study biobanks.

    Results: Microarray-quality RNA could be isolated from buffy coats (including most biobank samples) that had been frozen within 8 hr of blood collection by thawing the samples in RNA preservative. Different anticoagulants influenced the metabolomic, proteomic, and to a lesser extent transcriptomic profiles. Transcriptomic profiles were most affected by the delay (as little as 2 hr) before blood fractionation, whereas storage temperature had minimal impact. Effects on metabolomic and proteomic profiles were noted in samples processed ≥ 8 hr after collection, but no effects were due to storage temperature. None of the variables examined significantly influenced the epigenomic profiles. No systematic influence of time-in-storage was observed in samples stored over a period of 13-17 years.

    Conclusions: Most samples currently stored in biobanks are amenable to meaningful omics analysis, provided that they satisfy collection and storage criteria defined in this study.

  • 9. Jacquemin, Benedicte
    et al.
    Siroux, Valerie
    Sanchez, Margaux
    Carsin, Anne-Elie
    Schikowski, Tamara
    Adam, Martin
    Bellisario, Valeria
    Buschka, Anna
    Bono, Roberto
    Brunekreef, Bert
    Cai, Yutong
    Cirach, Marta
    Clavel-Chapelon, Francoise
    Declercq, Christophe
    de Marco, Roberto
    de Nazelle, Audrey
    Ducret-Stich, Regina E.
    Ferretti, Virginia Valeria
    Gerbase, Margaret W.
    Hardy, Rebecca
    Heinrich, Joachim
    Janson, Christer
    Jarvis, Deborah
    al Kanaani, Zaina
    Keidel, Dirk
    Kuh, Diana
    Le Moual, Nicole
    Nieuwenhuijsen, Mark J.
    Marcon, Alessandro
    Modig, Lars
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Pin, Isabelle
    Rochat, Thierry
    Schindler, Christian
    Sugiri, Dorothea
    Stempfelet, Morgane
    Temam, Sofia
    Tsai, Ming-Yi
    Varraso, Raphaelle
    Vienneau, Danielle
    Vierkoetter, Andrea
    Hansell, Anna L.
    Kraemer, Ursula
    Probst-Hensch, Nicole M.
    Sunyer, Jordi
    Kuenzli, Nino
    Kauffmann, Francine
    Ambient Air Pollution and Adult Asthma Incidence in Six European horts ESCAPE)2015In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 123, no 6, p. 613-621Article in journal (Refereed)
    Abstract [en]

    Background: Short-term exposure to air pollution has adverse effects among patients with asthma, but whether long-term exposure to air pollution is a cause of adult-onset asthma is unclear. Objective: We aimed to investigate the association between air pollution and adult onset asthma. Methods: Asthma incidence was prospectively assessed in six European cohorts. Exposures studied were annual average concentrations at home addresses for nitrogen oxides assessed for 23,704 participants (including 1,257 incident cases) and particulate matter (PM) assessed for 17,909 participants through ESCAPE land-use regression models and traffic exposure indicators. Meta-analyses of cohort-specific logistic regression on asthma incidence were performed. Models were adjusted for age, sex, overweight, education, and smoking and included city/area within each cohort as a random effect. Results: In this longitudinal analysis, asthma incidence was positively, but not significantly, associated with all exposure metrics, except for PMcoarse. Positive associations of borderline significance were observed for nitrogen dioxide [adjusted odds ratio (OR) = 1.10; 95% CI: 0.99, 1.21 per 10 μg/m3; p = 0.10] and nitrogen oxides (adjusted OR = 1.04; 95% CI: 0.99, 1.08 per 20 μg/m3; p = 0.08). Nonsignificant positive associations were estimated for PM10 (adjusted OR = 1.04; 95% CI: 0.88, 1.23 per 10 μg/m3), PM2.5 (adjusted OR = 1.04; 95% CI: 0.88, 1.23 per 5 μg/m3), PM2.5absorbance (adjusted OR = 1.06; 95% CI: 0.95, 1.19 per 10–5/m), traffic load (adjusted OR = 1.10; 95% CI: 0.93, 1.30 per 4 million vehicles × meters/day on major roads in a 100-m buffer), and traffic intensity (adjusted OR = 1.10; 95% CI: 0.93, 1.30 per 5,000 vehicles/day on the nearest road). A nonsignificant negative association was estimated for PMcoarse (adjusted OR = 0.98; 95% CI: 0.87, 1.14 per 5 μg/m3). Conclusions: Results suggest a deleterious effect of ambient air pollution on asthma incidence in adults. Further research with improved personal-level exposure assessment (vs. residential exposure assessment only) and phenotypic characterization is needed.

  • 10. Langrish, Jeremy P.
    et al.
    Bosson, Jenny A.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Newby, David E.
    Mills, Nicholas L.
    Atmospheric Interactions and Cardiac Arrhythmias: Langrish et al. espond2015In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 123, no 6, p. A144-A145Article in journal (Refereed)
  • 11.
    Langrish, Jeremy P.
    et al.
    University of Edinburgh, University/BHF Centre for Cardiovascular Science, Edinburgh, United Kingdom.
    Watts, Simon J.
    University of Edinburgh, University/BHF Centre for Cardiovascular Science, Edinburgh, United Kingdom.
    Hunter, Amanda J.
    University of Edinburgh, University/BHF Centre for Cardiovascular Science, Edinburgh, United Kingdom.
    Shah, Anoop S. V.
    University of Edinburgh, University/BHF Centre for Cardiovascular Science, Edinburgh, United Kingdom.
    Bosson, Jenny A
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Unosson, Jon
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Barath, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Lundbäck, Magnus
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Cassee, Flemming R.
    National Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands .
    Donaldson, Ken
    University of Edinburgh, University/BHF Centre for Cardiovascular Science, Edinburgh, United Kingdom.
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Newby, David E.
    University of Edinburgh, University/BHF Centre for Cardiovascular Science, Edinburgh, United Kingdom.
    Mills, Nicholas L.
    University of Edinburgh, University/BHF Centre for Cardiovascular Science, Edinburgh, United Kingdom.
    Controlled exposures to air pollutants and risk of cardiac arrhythmia2014In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 122, no 7, p. 747-753Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Epidemiological studies have reported associations between air pollution exposure and increases in cardiovascular morbidity and mortality. Exposure to air pollutants can influence cardiac autonomic tone and reduce heart rate variability, and may increase the risk of cardiac arrhythmias, particularly in susceptible patient groups. OBJECTIVES: We investigated the incidence of cardiac arrhythmias during and after controlled exposure to air pollutants in healthy volunteers and patients with coronary heart disease. METHODS: We analyzed data from 13 double-blind randomized crossover studies including 282 participants (140 healthy volunteers and 142 patients with stable coronary heart disease) from whom continuous electrocardiograms were available. The incidence of cardiac arrhythmias was recorded for each exposure and study population. RESULTS: There were no increases in any cardiac arrhythmia during or after exposure to dilute diesel exhaust, wood smoke, ozone, concentrated ambient particles, engineered carbon nanoparticles, or high ambient levels of air pollution in either healthy volunteers or patients with coronary heart disease. CONCLUSIONS: Acute controlled exposure to air pollutants did not increase the short-term risk of arrhythmia in participants. Research employing these techniques remains crucial in identifying the important pathophysiological pathways involved in the adverse effects of air pollution, and is vital to inform environmental and public health policy decisions.

  • 12.
    Liang, Yihuai
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Lei, Lijian
    Department of Occupational Health and Toxicology (Key Laboratory of Public Health Safety, Ministry of Education of China), School of Public Health, Fudan University, Shanghai, People’s Republic of China.
    Nilsson, Johan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Li, Huiqi
    Department of Occupational Health and Toxicology (Key Laboratory of Public Health Safety, Ministry of Education of China), School of Public Health, Fudan University, Shanghai, People’s Republic of China.
    Nordberg, Monica
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Bernard, Alfred
    Unit of Toxicology, Université catholique de Louvain, Brussels, Belgium.
    Nordberg, Gunnar F
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Bergdahl, Ingvar A
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Jin, Taiyi
    Department of Occupational Health and Toxicology (Key Laboratory of Public Health Safety, Ministry of Education of China), School of Public Health, Fudan University, Shanghai, People’s Republic of China.
    Renal function after reduction in cadmium exposure: an eight-year follow-up of residents in cadmium-polluted areas2012In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 120, no 2, p. 223-228Article in journal (Refereed)
    Abstract [en]

    Background and objective: Long-term exposure to cadmium (Cd) causes renal dysfunction, but its change with exposure is unknown. We aimed at assessing the evolution of Cd-induced renal effects after a reduction in dietary exposure to Cd in rice.

    Methods: 412 residents in previously Cd-polluted and non-polluted areas were examined twice: in 1998 and 2006. Changes in blood Cd, urinary Cd, and kidney function (N-acetyl-β-D-glucosaminidase = NAG, β2-microglobulin, and albumin in urine) were measured. Results: In the most polluted area, mean blood Cd was 8.9 μg/L in 1998 and 3.3 μg/L in 2006, and urinary Cd was 11.6 and 9.0 μg/g creatinine in 1998 and 2006, respectively. Urinary albumin in 1998 increased with urinary Cd but no such exposure-response appeared for 2006 albumin versus urinary Cd 1998, indicating recovery. Other biomarkers of kidney function were also elevated in 1998. Partial recovery was observed for NAG, among women, and suggested for β2-microglobulin, among young individuals. The probability of having a β2-microglobulin above the 95th percentile in 2006 was high in those with an elevated β2-microglobulin in 1998 (odds ratio: 24.8, 95% CI: 11.2-55.3), whereas corresponding estimates for albumin and NAG were 3.0 (1.2-7.5) and 2.6 (1.6-4.4), respectively.

    Conclusions: Results suggest that a Cd-mediated increase in urinary albumin excretion is reversible upon substantial reduction of exposure. For the markers of tubular effects, a tendency towards improvement, but not complete recovery, was observed. Data from repeated observations suggests that β2-microglobulin may be more informative than NAG as an indicator for the individual's future tubular function.

  • 13. Ljungman, Petter L S
    et al.
    Andersson, Niklas
    Stockfelt, Leo
    Andersson, Eva M
    Sommar, Johan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Section of Sustainable Health.
    Eneroth, Kristina
    Gidhagen, Lars
    Johansson, Christer
    Lager, Anton
    Leander, Karin
    Molnar, Peter
    Pedersen, Nancy L
    Rizzuto, Debora
    Rosengren, Annika
    Segersson, David
    Wennberg, Patrik
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Barregard, Lars
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Section of Sustainable Health.
    Sallsten, Gerd
    Bellander, Tom
    Pershagen, Göran
    Long-Term Exposure to Particulate Air Pollution, Black Carbon, and Their Source Components in Relation to Ischemic Heart Disease and Stroke2019In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 127, no 10, article id 107012Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Long-term exposure to particulate matter (PM) in ambient air has been associated with cardiovascular mortality, but few studies have considered incident disease in relation to PM from different sources.

    OBJECTIVES: We aimed to study associations between long-term exposure to different types of PM and sources, and incident ischemic heart disease (IHD) and stroke in three Swedish cities.

    METHODS: ), and black carbon (BC) from road wear, traffic exhaust, residential heating, and other sources in Gothenburg, Stockholm, and Umeå. Registry data for participants from four cohorts were used to obtain incidence of IHD and stroke for first hospitalization or death. We constructed time windows of exposure for same-year, 1- to 5-y, and 6- to 10-y averages preceding incidence from annual averages at residential addresses. Risk estimates were based on random effects meta-analyses of cohort-specific Cox proportional hazard models.

    RESULTS: exposure from residential heating.

    DISCUSSION: Few consistent associations were observed between different particulate components and IHD or stroke. However, long-term residential exposure to locally emitted BC from traffic exhaust was associated with stroke incidence. The comparatively low exposure levels may have contributed to the paucity of associations.

  • 14.
    Mansouri, Kamel
    et al.
    National Center for Computational Toxicology, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, USA.
    Abdelaziz, Ahmed
    Institute of Structural Biology, Helmholtz Zentrum Muenchen – German Research Center for Environmental Health (GmbH), Munich, Germany.
    Rybacka, Aleksandra
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Roncaglioni, Alessandra
    Environmental Chemistry and Toxicology Laboratory, IRCCS-Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy.
    Tropsha, Alexander
    Laboratory for Molecular Modeling, University of North Carolina, Chapel Hill, North Carolina, USA.
    Varnek, Alexandre
    Laboratoire de Chemoinformatique, University of Strasbourg, Strasbourg, France.
    Zakharov, Alexey
    National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
    Worth, Andrew
    Institute for Health and Consumer Protection (IHCP), Joint Research Centre of the European Commission in Ispra, Ispra, Italy.
    Richard, Ann M.
    National Center for Computational Toxicology, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, USA.
    Grulke, Christopher M.
    National Center for Computational Toxicology, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, USA.
    Trisciuzzi, Daniela
    Department of Pharmacy-Drug Sciences, University of Bari, Bari, Italy.
    Fourches, Denis
    Laboratory for Molecular Modeling, University of North Carolina, Chapel Hill, North Carolina, USA.
    Horvath, Dragos
    Laboratoire de Chemoinformatique, University of Strasbourg, Strasbourg, France.
    Benfenati, Emilio
    Environmental Chemistry and Toxicology Laboratory, IRCCS-Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy.
    Muratov, Eugene
    Laboratory for Molecular Modeling, University of North Carolina, Chapel Hill, North Carolina, USA.
    Wedebye, Eva Bay
    National Food Institute, Division of Toxicology and Risk Assessment, Technical University of Denmark, Copenhagen, Denmark.
    Grisoni, Francesca
    Milano Chemometrics and QSAR Research Group, University of Milano-Bicocca, Milan, Italy.
    Mangiatordi, Giuseppe F.
    Department of Pharmacy-Drug Sciences, University of Bari, Bari, Italy.
    Incisivo, Giuseppina M.
    Environmental Chemistry and Toxicology Laboratory, IRCCS-Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy.
    Hong, Huixiao
    National Center for Toxicological Research, Division of Bioinformatics and Biostatistics, U.S. Food and Drug Administration, Jefferson, Arizona, USA.
    Ng, Hui W.
    National Center for Toxicological Research, Division of Bioinformatics and Biostatistics, U.S. Food and Drug Administration, Jefferson, Arizona, USA.
    Tetko, Igor V.
    Institute of Structural Biology, Helmholtz Zentrum Muenchen – German Research Center for Environmental Health (GmbH), Munich, Germany.
    Balabin, Ilya
    High Performance Computing, Lockheed Martin, Research Triangle Park, North Carolina, USA.
    Kancherla, Jayaram
    National Center for Computational Toxicology, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, USA.
    Shen, Jie
    Research Institute for Fragrance Materials, Inc., Woodcliff Lake, New Jersey, USA.
    Burton, Julien
    Institute for Health and Consumer Protection (IHCP), Joint Research Centre of the European Commission in Ispra, Ispra, Italy.
    Nicklaus, Marc
    National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
    Cassotti, Matteo
    Milano Chemometrics and QSAR Research Group, University of Milano-Bicocca, Milan, Italy.
    Nikolov, Nikolai G.
    National Food Institute, Division of Toxicology and Risk Assessment, Technical University of Denmark, Copenhagen, Denmark.
    Nicolotti, Orazio
    Department of Pharmacy-Drug Sciences, University of Bari, Bari, Italy.
    Andersson, Patrik L.
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Zang, Qingda
    Integrated Laboratory Systems, Inc., Research Triangle Park, North Carolina, USA.
    Politi, Regina
    Laboratory for Molecular Modeling, University of North Carolina, Chapel Hill, North Carolina, USA.
    Beger, Richard D.
    National Center for Toxicological Research, Division of Systems Biology, U.S. Food and Drug Administration, Jefferson, Arizona, USA.
    Todeschini, Roberto
    Milano Chemometrics and QSAR Research Group, University of Milano-Bicocca, Milan, Italy.
    Huang, Ruili
    National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, Maryland, USA.
    Farag, Sherif
    Laboratory for Molecular Modeling, University of North Carolina, Chapel Hill, North Carolina, USA.
    Rosenberg, Sine A.
    National Food Institute, Division of Toxicology and Risk Assessment, Technical University of Denmark, Copenhagen, Denmark.
    Slavov, Svetoslav
    National Center for Toxicological Research, Division of Systems Biology, U.S. Food and Drug Administration, Jefferson, Arizona, USA.
    Hu, Xin
    National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, Maryland, USA.
    Judson, Richard S.
    National Center for Computational Toxicology, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, USA.
    CERAPP: Collaborative Estrogen Receptor Activity Prediction Project2016In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 124, no 7, p. 1023-1033Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Humans are exposed to thousands of man-made chemicals in the environment. Some chemicals mimic natural endocrine hormones and, thus, have the potential to be endocrine disruptors. Most of these chemicals have never been tested for their ability to interact with the estrogen receptor (ER). Risk assessors need tools to prioritize chemicals for evaluation in costly in vivo tests, for instance, within the U.S. EPA Endocrine Disruptor Screening Program. OBJECTIVES: We describe a large-scale modeling project called CERAPP (Collaborative Estrogen Receptor Activity Prediction Project) and demonstrate the efficacy of using predictive computational models trained on high-throughput screening data to evaluate thousands of chemicals for ER-related activity and prioritize them for further testing. METHODS: CERAPP combined multiple models developed in collaboration with 17 groups in the United States and Europe to predict ER activity of a common set of 32,464 chemical structures. Quantitative structure-activity relationship models and docking approaches were employed, mostly using a common training set of 1,677 chemical structures provided by the U.S. EPA, to build a total of 40 categorical and 8 continuous models for binding, agonist, and antagonist ER activity. All predictions were evaluated on a set of 7,522 chemicals curated from the literature. To overcome the limitations of single models, a consensus was built by weighting models on scores based on their evaluated accuracies. RESULTS: Individual model scores ranged from 0.69 to 0.85, showing high prediction reliabilities. Out of the 32,464 chemicals, the consensus model predicted 4,001 chemicals (12.3%) as high priority actives and 6,742 potential actives (20.8%) to be considered for further testing.CONCLUSION: This project demonstrated the possibility to screen large libraries of chemicals using a consensus of different in silico approaches. This concept will be applied in future projects related to other end points.

  • 15. Markunas, Christina A
    et al.
    Xu, Zongli
    Harlid, Sophia
    Epigenetics and Stem Cell Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA.
    Wade, Paul A
    Lie, Rolv T
    Taylor, Jack A
    Wilcox, Allen J
    Identification of DNA methylation changes in newborns related to maternal smoking during pregnancy.2014In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 122, no 10, p. 1147-53Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Maternal smoking during pregnancy is associated with significant infant morbidity and mortality, and may influence later disease risk. One mechanism by which smoking (and other environmental factors) might have long-lasting effects is through epigenetic modifications such as DNA methylation.

    OBJECTIVES: We conducted an epigenome-wide association study (EWAS) investigating alterations in DNA methylation in infants exposed in utero to maternal tobacco smoke, using the Norway Facial Clefts Study.

    METHODS: The Illumina HumanMethylation450 BeadChip was used to assess DNA methylation in whole blood from 889 infants shortly after delivery. Of 889 mothers, 287 reported smoking-twice as many smokers as in any previous EWAS of maternal smoking. CpG sites related to maternal smoking during the first trimester were identified using robust linear regression.

    RESULTS: We identified 185 CpGs with altered methylation in infants of smokers at genome-wide significance (q-value < 0.05; mean Δβ = ± 2%). These correspond to 110 gene regions, of which 7 have been previously reported and 10 are newly confirmed using publicly available results. Among these 10, the most noteworthy are FRMD4A, ATP9A, GALNT2, and MEG3, implicated in processes related to nicotine dependence, smoking cessation, and placental and embryonic development.

    CONCLUSIONS: Our study identified 10 genes with newly established links to maternal smoking. Further, we note differences between smoking-related methylation changes in newborns and adults, suggesting possible distinct effects of direct versus indirect tobacco smoke exposure as well as potential differences due to age. Further work would be needed to determine whether these small changes in DNA methylation are biologically or clinically relevant. The methylation changes identified in newborns may mediate the association between in utero maternal smoking exposure and later health outcomes.

  • 16. Martens, Dries S
    et al.
    Gouveia, Sandra
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Madhloum, Narjes
    Janssen, Bram G
    Plusquin, Michelle
    Vanpoucke, Charlotte
    Lefebvre, Wouter
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Nording, Malin
    Nawrot, Tim S
    Neonatal Cord Blood Oxylipins and Exposure to Particulate Matter in the Early-Life Environment: an ENVIRONAGE Birth Cohort Study2017In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 125, no 4, p. 691-698Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: As part of the lipidome, oxylipins are bioactive lipid compounds originating from oxidation of different fatty acids. Oxylipins could provide a new target in the developmental origins model or the ability of early life exposure to change biology.

    OBJECTIVES: We studied the association between in utero PM2.5 (particulate matter with aerodynamic diameter <2.5µm) exposure and oxylipin profiles in newborns.

    METHODS: Thirty-seven oxylipins reflecting the cyclooxygenase (COX), lipoxygenase (5-LOX and 12/15-LOX) and cytochrome P450 (CYP) pathways were assayed in 197 cord blood plasma samples from the ENVIRONAGE birth cohort. Principal component (PC) analysis and multiple regression models were used to estimate associations of in utero PM2.5 exposure with oxylipin pathways and individual metabolites.

    RESULTS: A principal component representing the 5-LOX pathway (6 metabolites) was significantly positively associated with PM2.5 exposure during the entire (multiple testing-adjusted q-value = 0.05) and second trimester of pregnancy (q = 0.05). A principal component representing the 12/15-LOX pathway (11 metabolites) was positively associated with PM2.5 exposure during the second trimester of pregnancy (q = 0.05). PM2.5 was not significantly associated with the COX pathway during any time period. There was a positive but non-significant association between second trimester PM2.5 and the CYP pathway (q = 0.16).

    CONCLUSION: In utero exposure to particulate matter, particularly during the second trimester, was associated with differences in the cord blood levels of metabolites derived from the lipoxygenase pathways. These differences may indicate an effect of air pollution during in utero life on the inflammatory state of the newborn at birth. Oxylipins may be important mediators between early life exposures and health outcomes later in life.

  • 17.
    Meister, Kadri
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Johansson, Christer
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Estimated short-term effects of coarse particles on daily mortality in Stockholm, Sweden2012In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 120, p. 431-436Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Whereas serious health effects associated with particles with an aerodynamic diameter ≤ 10 µm (PM10) and ≤ 2.5 µm (fine fraction; PM2.5) are documented in many studies, the effects of coarse particles with aerodynamic diameter between 2.5 and 10 µm (PM2.5-10) are still under debate. In this study we estimate the effects of short-term exposure of coarse particles on daily mortality in Stockholm.

    METHOD: We collected data on daily mortality for the years 2000-2008. Concentrations of PM10, PM2.5, O3 and CO were measured simultaneously in central Stockholm. We used additive Poisson regression models to examine the association between daily mortality and the coarse fraction at day of death and day before. Effect estimates were adjusted for other pollutants (two-pollutant models) during different seasons.

    RESULTS: We estimated a 1.68% increase [95% confidence interval (CI) 0.20, 3.15%] in daily mortality per 10 µg m-3 increase in PM2.5-10 (single-pollutant model). The association with PM2.5-10 was stronger for November - May when road dust is most important (1.69% increase, CI 0.21, 3.17%) compared to the rest of the year (1.31% increase, CI -2.08, 4.70%), although the difference was not statistically significant. When adjusted for other pollutants, particularly PM2.5, the effect estimates per 10 µg m-3 for coarse particles decreased slightly, but were still higher than corresponding effect estimates for PM2.5.

    CONCLUSIONS: Our analysis shows an increase in daily mortality associated with elevated urban background levels of coarse particles. Regulation of the coarse particle fraction should be considered, along with actions to specifically reduce coarse particle emissions, especially road dust suspension, in cities.

  • 18. Mills, Nicholas L
    et al.
    Robinson, Simon D
    Fokkens, Paul HB
    Leseman, Daan LAC
    Miller, Mark R
    Anderson, David
    Freney, Evelyn J
    Heal, Mathew R
    Donovan, Robert J
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    MacNee, William
    Boon, Nicholas A
    Donaldson, Ken
    Newby, David E
    Cassee, Flemming R
    Exposure to concentrated ambient particles does not affect vascular function in patients with coronary heart disease2008In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 116, no 6, p. 709-715Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Exposure to fine particulate air pollution is associated with increased cardiovascular morbidity and mortality. We previously demonstrated that exposure to dilute diesel exhaust causes vascular dysfunction in humans.

    OBJECTIVES: We conducted a study to determine whether exposure to ambient particulate matter causes vascular dysfunction. METHODS: Twelve male patients with stable coronary heart disease and 12 age-matched volunteers were exposed to concentrated ambient fine and ultrafine particles (CAPs) or filtered air for 2 hr using a randomized, double-blind cross-over study design. We measured peripheral vascular vasomotor and fibrinolytic function, and inflammatory variables-including circulating leukocytes, serum C-reactive protein, and exhaled breath 8-isoprostane and nitrotyrosine-6-8 hr after both exposures.

    RESULTS: Particulate concentrations (mean +/- SE) in the exposure chamber (190+/-37 microg/m(3)) were higher than ambient levels (31+/-8 microg/m(3)) and levels in filtered air (0.5+/-0.4 microg/m(3); p<0.001). Chemical analysis of CAPs identified low levels of elemental carbon. Exhaled breath 8-isoprostane concentrations increased after exposure to CAPs (16.9+/-8.5 vs. 4.9+/-1.2 pg/mL, p<0.05), but markers of systemic inflammation were largely unchanged. Although there was a dose-dependent increase in blood flow and plasma tissue plasminogen activator release (p<0.001 for all), CAPs exposure had no effect on vascular function in either group.

    CONCLUSIONS: Despite achieving marked increases in particulate matter, exposure to CAPs--low in combustion-derived particles--did not affect vasomotor or fibrinolytic function in either middle-aged healthy volunteers or patients with coronary heart disease. These findings contrast with previous exposures to dilute diesel exhaust and highlight the importance of particle composition in determining the vascular effects of particulate matter in humans.

  • 19.
    Odhiambo Sewe, Maquins
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Global Health. Graduate School in Population Dynamics and Public Policy, Umeå University.
    Bunker, Aditi
    Ingole, Vijendra
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Global Health. Graduate School in Population Dynamics and Public Policy, Umeå University; Vadu Rural Health Program, KEM Hospital Research Centre, Pune, India.
    Egondi, Thaddaeus
    Oudin Åström, Daniel
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine. Department of Clinical Science, Center for Primary Health Care Research, Lund University, Malmö.
    Hondula, David M.
    Rocklöv, Joacim
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Global Health.
    Schumann, Barbara
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Global Health. Umeå University, Faculty of Social Sciences, Centre for Demographic and Ageing Research (CEDAR).
    Estimated Effect of Temperature on Years of Life Lost: A Retrospective Time-Series Study of Low-, Middle-, and High-Income Regions2018In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 126, no 1, article id 017004Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Numerous studies have reported a strong association between temperature and mortality. Additional insights can be gained from investigating the effects of temperature on years of life lost (YLL), considering the life expectancy at the time of death.

    OBJECTIVES: The goal of this work was to assess the association between temperature and YLL at seven low-, middle-, and high-income sites.

    METHODS: We obtained meteorological and population data for at least nine years from four Health and Demographic Surveillance Sites in Kenya (western Kenya, Nairobi), Burkina Faso (Nouna), and India (Vadu), as well as data from cities in the United States (Philadelphia, Phoenix) and Sweden (Stockholm). A distributed lag nonlinear model was used to estimate the association of daily maximum temperature and daily YLL, lagged 0-14 d. The reference value was set for each site at the temperature with the lowest YLL.

    RESULTS: Generally, YLL increased with higher temperature, starting day 0. In Nouna, the hottest location, with a minimum YLL temperature at the first percentile, YLL increased consistently with higher temperatures. In Vadu, YLL increased in association with heat, whereas in Nairobi, YLL increased in association with both low and high temperatures. Associations with cold and heat were evident for Phoenix (stronger for heat), Stockholm, and Philadelphia (both stronger for cold). Patterns of associations with mortality were generally similar to those with YLL.

    CONCLUSIONS: Both high and low temperatures are associated with YLL in high-, middle-, and low-income countries. Policy guidance and health adaptation measures might be improved with more comprehensive indicators of the health burden of high and low temperatures such as YLL.

  • 20.
    Oudin, Anna
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Nordin Adolfsson, Annelie
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry.
    Lind, Nina
    Umeå University, Faculty of Social Sciences, Department of Psychology.
    Modig, Lars
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Nordin, Maria
    Umeå University, Faculty of Social Sciences, Department of Psychology.
    Nordin, Steven
    Umeå University, Faculty of Social Sciences, Department of Psychology.
    Adolfsson, Rolf
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry.
    Nilsson, Lars-Göran
    Umeå University, Faculty of Medicine, Umeå Centre for Functional Brain Imaging (UFBI). Aging research centre, Karolinska Institutet.
    Traffic-Related Air Pollution and Dementia Incidence in Northern Sweden: A Longitudinal Study2016In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 124, no 3, p. 306-312Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Exposure to ambient air pollution is suspected to cause cognitive effects, but a prospective cohort is needed to study exposure to air pollution at the home address and the incidence of dementia.

    OBJECTIVES: We aimed to assess the association between long-term exposure to traffic-related air pollution and dementia incidence in a major city in northern Sweden.

    METHODS: Data on dementia incidence over a 15-year period were obtained from the longitudinal Betula study. Traffic air pollution exposure was assessed with a Land Use Regression Model with a spatial resolution of 50 m x 50 m. Annual mean nitrogen oxide levels at the residential address of the participants at baseline (the start of follow-up) was used as a marker for long-term exposure to air pollution.

    RESULTS: Out of 1806 participants at baseline, 191 were diagnosed with Alzheimer's disease during follow-up, and 111 were diagnosed with vascular dementia. Participants in the highest exposure group were more likely to be diagnosed with dementia (Alzheimer's disease or vascular dementia), with a Hazard Ratio (HR) of 1.43 (95% Confidence Interval (CI): 0.998, 2.05 for the highest versus lowest quartile). The estimates were similar for Alzheimer's disease (HR 1.38) and vascular dementia (HR 1.47). The HR for dementia associated for the third quartile versus the lowest quartile was 1.48 (95% CI: 1.03, 2.11). A sub-analysis that excluded a younger sample that had been re-tested after only 5 years of follow-up suggested stronger associations with exposure than in the full cohort (HR = 1.71; 95% CI: 1.08, 2.73 for the highest versus lowest quartile).

    CONCLUSIONS: If the associations we observed are causal, then air pollution from traffic might be an important risk factor for vascular dementia and Alzheimer's disease.

  • 21.
    Oudin Åström, Daniel
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Tornevi, Andreas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Ebi, Kristie L
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Rocklöv, Joacim
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Global Health.
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Evolution of Minimum Mortality Temperature in Stockholm, Sweden, 1901-20092016In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 124, no 6, p. 740-744Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The mortality impacts of hot and cold temperatures have been thoroughly documented, with most locations reporting a U-shaped relationship with a minimum mortality temperature (MMT) at which mortality is lowest. How MMT may have evolved over past decades as global mean surface temperature increased has not been thoroughly explored.

    OBJECTIVE: We used observations of daily mean temperatures to investigate whether MMT changed in Stockholm, Sweden, from the beginning of the 20th century until 2009.

    METHODS: Daily mortality and temperature data for the period 1901-2009 in Stockholm, Sweden were used to model the temperature-mortality relationship. We estimated MMT using distributed lag non-linear Poisson regression models considering lags up to 21 days of daily mean temperature as the exposure variable. To avoid large influences on the MMT from intra and inter annual climatic variability, we estimated MMT based on 30-year periods. Further, we investigated whether there were trends in the absolute value of the MMT and the relative value of the MMT (the corresponding percentile of the same day temperature distribution) over the study period.

    RESULTS: Our findings suggest that both the absolute MMT and the relative MMT increased in Stockholm, Sweden over the course of the last century.

    CONCLUSIONS: The increase in MMT over the course of the last century suggests autonomous adaptation within the context of the large epidemiological, demographical and societal changes that occurred. Whether the rate of increase will be sustained with climate change is an open question.

  • 22. Pearce, Neil E
    et al.
    Blair, Aaron
    Vineis, Paolo
    Ahrens, Wolfgang
    Andersen, Aage
    Anto, Josep M
    Armstrong, Bruce K
    Baccarelli, Andrea A
    Beland, Frederick A
    Berrington, Amy
    Bertazzi, Pier A
    Birnbaum, Linda S
    Brownson, Ross C
    Bucher, John R
    Cantor, Kenneth P
    Cardis, Elisabeth
    Cherrie, John W
    Christiani, David C
    Cocco, Pierluigi
    Coggon, David
    Comba, Pietro
    Demers, Paul A
    Dement, John M
    Douwes, Jeroen
    Eisen, Ellen A
    Engel, Lawrence S
    Fenske, Richard A
    Fleming, Lora E
    Fletcher, Tony
    Fontham, Elizabeth
    Forastiere, Francesco
    Frentzel-Beyme, Rainer
    Fritschi, Lin
    Gerin, Michel
    Goldberg, Marcel
    Grandjean, Philippe
    Grimsrud, Tom K
    Gustavsson, Per
    Haines, Andy
    Hartge, Patricia
    Hansen, Johnni
    Hauptmann, Michael
    Heederik, Dick
    Hemminki, Kari
    Hemon, Denis
    Hertz-Picciotto, Irva
    Hoppin, Jane A
    Huff, James
    Järvholm, Bengt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Kang, Daehee
    Karagas, Margaret R
    Kjaerheim, Kristina
    Kjuus, Helge
    Kogevinas, Manolis
    Kriebel, David
    Kristensen, Petter
    Kromhout, Hans
    Laden, Francine
    Lebailly, Pierre
    LeMasters, Grace
    Lubin, Jay H
    Lynch, Charles F
    Lynge, Elsebeth
    't Mannetje, Andrea
    McMichael, Anthony J
    McLaughlin, John R
    Marrett, Loraine
    Martuzzi, Marco
    Merchant, James A
    Merler, Enzo
    Merletti, Franco
    Miller, Anthony
    Mirer, Franklin E
    Monson, Richard
    Nordby, Karl-Kristian
    Olshan, Andrew F
    Parent, Marie-Elise
    Perera, Frederica P
    Perry, Melissa J
    Pesatori, Angela C
    Pirastu, Roberta
    Porta, Miquel
    Pukkala, Eero
    Rice, Carol
    Richardson, David B
    Ritter, Leonard
    Ritz, Beate
    Ronckers, Cecile M
    Rushton, Lesley
    Rusiecki, Jennifer A
    Rusyn, Ivan
    Samet, Jonathan M
    Sandler, Dale P
    de Sanjose, Silvia
    Schernhammer, Eva
    Seniori Constantini, Adele
    Seixas, Noah
    Shy, Carl
    Siemiatycki, Jack
    Silvermann, Debra T
    Simonato, Lorenzo
    Smith, Allan H
    Smith, Martyn T
    Spinelli, John J
    Spitz, Margaret R
    Stallones, Lorann
    Stayner, Leslie T
    Steenland, Kyle
    Stenzel, Mark
    Stewart, Bernard W
    Stewart, Patricia A
    Symanski, Elaine
    Terracini, Benedetto
    Tolbert, Paige E
    Vainio, Harri
    Vena, John
    Vermeulen, Roel
    Victora, Cesar G
    Ward, Elizabeth M
    Weinberg, Clarice R
    Weisenburger, Dennis
    Wesseling, Catharina
    Weiderpass, Elisabete
    Zahm, Shelia H
    IARC Monographs: 40 Years of Evaluating Carcinogenic Hazards to Humans2015In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 123, no 6, p. 507-514Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Recently the International Agency for Research on Cancer (IARC) Programme for the Evaluation of Carcinogenic Risks to Humans has been criticized for several of its evaluations, and also the approach used to perform these evaluations. Some critics have claimed that IARC Working Groups' failures to recognize study weaknesses and biases of Working Group members have led to inappropriate classification of a number of agents as carcinogenic to humans.

    OBJECTIVES: The authors of this paper are scientists from various disciplines relevant to the identification and hazard evaluation of human carcinogens. We have examined here criticisms of the IARC classification process to determine the validity of these concerns. We review the history of IARC evaluations and describe how the IARC evaluations are performed.

    DISCUSSION: We conclude that these recent criticisms are unconvincing. The procedures employed by IARC to assemble Working Groups of scientists from the various discipline and the techniques followed to review the literature and perform hazard assessment of various agents provide a balanced evaluation and an appropriate indication of the weight of the evidence. Some disagreement by individual scientists to some evaluations is not evidence of process failure. The review process has been modified over time and will undoubtedly be altered in the future to improve the process. Any process can in theory be improved, and we would support continued review and improvement of the IARC processes. This does not mean, however, that the current procedures are flawed.

    CONCLUSIONS: The IARC Monographs have made, and continue to make, major contributions to the scientific underpinning for societal actions to improve the public's health.

  • 23. Samoli, Evangelia
    et al.
    Touloumi, Giota
    Schwartz, Joel
    Anderson, Hugh Ross
    Schindler, Christian
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Vigotti, Maria Angela
    Vonk, Judith
    Kosnik, Mitja
    Skorkovsky, Jiri
    Katsouyanni, Klea
    Short-term effects of carbon monoxide on mortality: an analysis within the APHEA project.2007In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 115, no 11, p. 1578-1583Article in journal (Refereed)
    Abstract [en]

    Objectives: We investigated the short-term effects of carbon monoxide on total and cardiovascular mortality in 19 European cities participating in the APHEA-2 (Air Pollution and Health: A European Approach) project.

    Methods: We examined the association using hierarchical models implemented in two stages. In the first stage, data from each city were analyzed separately, whereas in the second stage the city-specific air pollution estimates were regressed on city-specific covariates to obtain overall estimates and to explore sources of possible heterogeneity. We evaluated the sensitivity of our results by applying different degrees of smoothing for seasonality control in the city-specific analysis.

    Results: We found significant associations of CO with total and cardiovascular mortality. A 1-mg/m3 increase in the 2-day mean of CO levels was associated with a 1.20% [95% confidence interval (CI), 0.63–1.77%] increase in total deaths and a 1.25% (95% CI, 0.30–2.21%) increase in cardiovascular deaths. There was indication of confounding with black smoke and nitrogen dioxide, but the pollutant-adjusted effect of CO on mortality remained at least marginally statistically significant. The effect of CO on total and cardiovascular mortality was observed mainly in western and southern European cities and was larger when the standardized mortality rate was lower.

    Conclusions: The results of this large study are consistent with an independent effect of CO on mortality. The heterogeneity found in the effect estimates among cities may be explained partly by specific city characteristics.

  • 24.
    Schläwicke Engström, Karin
    et al.
    Department of Occupational and Environmental Medicine, Lund University Hospital, Lund, Sweden.
    Strömberg, Ulf
    Department of Occupational and Environmental Medicine, Lund University Hospital, Lund, Sweden.
    Lundh, Thomas
    Department of Occupational and Environmental Medicine, Lund University Hospital, Lund, Sweden.
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology.
    Vessby, Bengt
    Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Skerfving, Staffan
    Department of Occupational and Environmental Medicine, Lund University Hospital, Lund, Sweden.
    Broberg, Karin
    Department of Occupational and Environmental Medicine, Lund University Hospital, Lund, Sweden.
    Genetic variation in glutathione-related genes and body burden of methylmercury2008In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 116, no 6, p. 734-739Article in journal (Refereed)
    Abstract [en]

    Background: Exposure to toxic methylmercury (MeHg) through fish consumption is a large problem worldwide, and it has led to governmental recommendations of reduced fish consumption and blacklisting of mercury-contaminated fish. The elimination kinetics of MeHg varies greatly among individuals. Knowledge about the reasons for such variation is of importance for improving the risk assessment for MeHg. One possible explanation is hereditary differences in MeHg metabolism. MeHg is eliminated from the body as a glutathione (GSH) conjugate.

    Objectives: We conducted this study to assess the influence of polymorphisms in GSH-synthesizing [glutamyl-cysteine ligase modifier subunit (GCLM-588) and glutamyl-cysteine ligase catalytic subunit (GCLC-129)] or GSH-conjugating [glutathione S-transferase pi 1 (GSTP1–105 and GSTP1–114)] genes on MeHg retention.

    Methods: Based on information obtained from questionnaires, 292 subjects from northern Sweden had a high consumption of fish (lean/fat fish two to three times per week or more). We measured total Hg in erythrocytes (Ery-Hg) and long-chain n-3 polyunsaturated fatty acids in plasma (P-PUFA; an exposure marker for fish intake).

    Results: The GSTP1 genotype modified Ery-Hg; effects were seen for GSTP1–105 and −114 separately, and combining them resulted in stronger effects. We found evidence of effect modification: individuals with zero or one variant allele demonstrated a steeper regression slope for Ery-Hg (p = 0.038) compared with individuals with two or more variant alleles. The GCLM-588 genotype also influenced Ery-Hg (p = 0.035): Individuals with the GCLM-588 TT genotype demonstrated the highest Ery-Hg, but we saw no evidence of effect modification with increasing P-PUFA.

    Conclusions: These results suggest a role of GSH-related polymorphisms in MeHg metabolism.

  • 25. Semenza, Jan C.
    et al.
    Trinanes, Joaquin
    Lohr, Wolfgang
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Global Health.
    Sudre, Bertrand
    Löfdahl, Margareta
    Martinez-Urtaza, Jaime
    Nichols, Gordon L.
    Rocklöv, Joacim
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Global Health.
    Environmental Suitability of Vibrio Infections in a Warming Climate: An Early Warning System2017In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 125, no 10, article id UNSP 107004Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Some Vibrio spp. are pathogenic and ubiquitous in marine waters with low to moderate salinity and thrive with elevated sea surface temperature (SST). OBJECTIVES: Our objective was to monitor and project the suitability of marine conditions for Vibrio infections under climate change scenarios. METHODS: The European Centre for Disease Prevention and Control (ECDC) developed a platform (the ECDC Vibrio Map Viewer) to monitor the environmental suitability of coastal waters for Vibrio spp. using remotely sensed SST and salinity. A case-crossover study of Swedish cases was conducted to ascertain the relationship between SST and Vibrio infection through a conditional logistic regression. Climate change projections for Vibrio infections were developed for Representative Concentration Pathway (RCP) 4.5 and RCP 8.5. RESULTS: The ECDC Vibrio Map Viewer detected environmentally suitable areas for Vibrio spp. in the Baltic Sea in July 2014 that were accompanied by a spike in cases and one death in Sweden. The estimated exposure response relationship for Vibrio infections at a threshold of 16 degrees C revealed a relative risk (RR) = 1.14 (95% CI: 1.02, 1.27; p=0.024) for a lag of 2 wk; the estimated risk increased successively beyond this SST threshold. Climate change projections for SST under the RCP 4.5 and RCP 8.5 scenarios indicate a marked upward trend during the summer months and an increase in the relative risk of these infections in the coming decades. CONCLUSIONS: This platform can serve as an early warning system as the risk of further Vibrio infections increases in the 21st ritui due to climate change.

  • 26.
    van Ede, Karin I.
    et al.
    Institute for Risk Assessment Sciences, Utrecht University, Utrecht, the Netherlands.
    Andersson, Patrik L.
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Gaisch, Konrad P. J.
    Institute for Risk Assessment Sciences, Utrecht University, Utrecht, the Netherlands.
    van den Berg, Martin
    Institute for Risk Assessment Sciences, Utrecht University, Utrecht, the Netherlands.
    van Duursen, Majorie B. M.
    Institute for Risk Assessment Sciences, Utrecht University, Utrecht, the Netherlands.
    Comparison of Intake and Systemic Relative Effect Potencies of Dioxin-like Compounds in Female Mice after a Single Oral Dose2013In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 121, no 7, p. 847-853Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Risk assessment for mixtures of polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs) is performed using the toxic equivalency factor (TEF) approach. These TEF values are derived mainly from relative effect potencies (REPs) linking an administered dose to an in vivo toxic or biological effect, resulting in "intake" TEFs. At present, there is insufficient data available to conclude that intake TEFs are also applicable for systemic concentrations (e. g., blood and tissues). OBJECTIVE: We compared intake and systemic REPs of 1,2,3,7,8-pentachlorodibenzodioxin (PeCDD), 2,3,4,7,8-pentachlorodibenzofuran (4-PeCDF), 3,3', 4,4', 5-pentachlorobiphenyl (PCB-126), 2,3', 4,4', 5-pentachlorobiphenyl (PCB-118), and 2,3,3', 4,4', 5-hexachlorobiphenyl (PCB-156) in female C57BL/6 mice 3 days after a single oral dose. METHODS: We calculated intake REPs and systemic REPs based on administered dose and liver, adipose, or plasma concentrations relative to TCDD. Hepatic cytochrome P450 1Al-associated ethoxyresorufin-O-deethylase (EROD) activity and gene expression of Cyp1a1, 1a2 and 1b1 in the liver and peripheral blood lymphocytes (PBLs) were used as biological end points. RESULTS: We observed up to one order of magnitude difference between intake REPs and systemic REPs. Two different patterns were discerned. Compared with intake REPs, systemic REPs based on plasma or adipose levels were higher for PeCDD, 4-PeCDF, and PCB-126 but lower for the mono-ortho PCBs 118 and 156. CONCLUSIONS: Based on these mouse data, the comparison between intake REPs and systemic REPs reveals significant congener-specific differences that warrants the development of systemic TEFs to calculate toxic equivalents (TEQs) in blood and body tissues.

  • 27. Wang, Meng
    et al.
    Beelen, Rob
    Bellander, Tom
    Birk, Matthias
    Cesaroni, Giulia
    Cirach, Marta
    Cyrys, Josef
    de Hoogh, Kees
    Declercq, Christophe
    Dimakopoulou, Konstantina
    Eeftens, Marloes
    Eriksen, Kirsten T.
    Forastiere, Francesco
    Galassi, Claudia
    Grivas, Georgios
    Heinrich, Joachim
    Hoffmann, Barbara
    Ineichen, Alex
    Korek, Michal
    Lanki, Timo
    Lindley, Sarah
    Modig, Lars
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Mölter, Anna
    Nafstad, Per
    Nieuwenhuijsen, Mark J.
    Nystad, Wenche
    Olsson, David
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Raaschou-Nielsen, Ole
    Ragettli, Martina
    Ranzi, Andrea
    Stempfelet, Morgane
    Sugiri, Dorothea
    Tsai, Ming-Yi
    Udvardy, Orsolya
    Varró, Mihaly J.
    Vienneau, Danielle
    Weinmayr, Gudrun
    Wolf, Kathrin
    Yli-Tuomi, Tarja
    Hoek, Gerard
    Brunekreef, Bert
    Performance of multi-city land use regression models for nitrogen dioxide and fine particles2014In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 122, no 8, p. 843-849Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Land use regression (LUR) models have been developed mostly to explain intraurban variations in air pollution based on often small local monitoring campaigns. Transferability of LUR models from city to city has been investigated, but little is known about the performance of models based on large numbers of monitoring sites covering a large area.

    OBJECTIVES: We aimed to develop European and regional LUR models and to examine their transferability to areas not used for model development.

    METHODS: We evaluated LUR models for nitrogen dioxide (NO2) and particulate matter (PM; PM2.5, PM2.5 absorbance) by combining standardized measurement data from 17 (PM) and 23 (NO2) ESCAPE (European Study of Cohorts for Air Pollution Effects) study areas across 14 European countries for PM and NO2. Models were evaluated with cross-validation (CV) and hold-out validation (HV). We investigated the transferability of the models by successively excluding each study area from model building.

    RESULTS: The European model explained 56% of the concentration variability across all sites for NO2, 86% for PM2.5, and 70% for PM2.5 absorbance. The HV R2s were only slightly lower than the model R2 (NO2, 54%; PM2.5, 80%; PM2.5 absorbance, 70%). The European NO2, PM2.5, and PM2.5 absorbance models explained a median of 59%, 48%, and 70% of within-area variability in individual areas. The transferred models predicted a modest-to-large fraction of variability in areas that were excluded from model building (median R2: NO2, 59%; PM2.5, 42%; PM2.5 absorbance, 67%).

    CONCLUSIONS: Using a large data set from 23 European study areas, we were able to develop LUR models for NO2 and PM metrics that predicted measurements made at independent sites and areas reasonably well. This finding is useful for assessing exposure in health studies conducted in areas where no measurements were conducted.

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