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  • 1.
    Ahmed, Sultan
    et al.
    International Centre for Diarrhoeal Disease Research, Dhaka, Bangladesh.
    Khoda, Sultana Mahabbat-E
    International Centre for Diarrhoeal Disease Research, Dhaka, Bangladesh.
    Rekha, Rokeya Sultana
    International Centre for Diarrhoeal Disease Research, Dhaka, Bangladesh.
    Gardner, Renee M.
    Institute of Environmental Medicine (IMM), Karolinska Institutet, Stockholm, Sweden.
    Ameer, Syeda Shegufta
    International Centre for Diarrhoeal Disease Research, Dhaka, Bangladesh.
    Moore, Sophie
    MRC International Nutrition Group, London School of Hygiene and Tropical Medicine, London, UK.
    Ekström, Eva-Charlotte
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health.
    Vahter, Marie
    Institute of Environmental Medicine (IMM), Karolinska Institutet, Stockholm, Sweden.
    Raqib, Rubhana
    International Centre for Diarrhoeal Disease Research, Dhaka, Bangladesh.
    Arsenic-Associated Oxidative stress, Inflammation, and Immune Disruption in Human Placenta and Cord Blood2011In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 119, no 2, p. 258-264Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Arsenic (As) exposure during pregnancy induces oxidative stress and increases the risk of fetal loss and low birth weight. OBJECTIVES: This study aimed to elucidate the effects of As exposure on immune markers in the placenta and cord blood, and the involvement of oxidative stress. METHODS: Pregnant women were enrolled around gestational week (GW) 8 in our longitudinal, population-based, mother-child cohort in Matlab, an area in rural Bangladesh with large variations in As concentrations in well water. Women (n=130) delivering at local clinics were included in the present study. We collected maternal urine twice during pregnancy (GW8 and 30) for measurements of As, and placenta and cord blood at delivery for assessment of immune and inflammatory markers. Placental markers were measured by immunohistochemistry and cord blood cytokines by multiplex cytokine assay. RESULTS: In multivariable adjusted models, maternal urinary As (U-As) exposure both at GW8 and 30 was significantly positively associated with placental markers of 8-oxoguanine (8-oxoG) and IL-1β, U-As at GW8 with TNF- α and IFN-γ, U-As at GW30 with leptin , and U-As at GW8 was inversely associated with CD3-T cells in the placenta. Cord blood cytokines (IL-1β, IL-8, IFN-γ, TNF-α) showed a U-shaped association with U-As at GW30. Placental 8-oxoG was significantly positively associated with placental pro-inflammatory cytokines. Multivariable adjusted analyses suggested that enhanced placental cytokine expression (TNF-α and IFN-γ) was primarily influenced by oxidative stress, while leptin expression appeared to be mostly mediated by As, and IL-1β appeared to be influenced by both oxidative stress and As. CONCLUSION: As exposure during pregnancy appeared to enhance placental inflammatory responses (in part by increasing oxidative stress), reduce placental T cells, and alter cord blood cytokines. These findings suggest that effects of As on immune function may contribute to impaired fetal and infant health.

  • 2. Akre, Olof
    et al.
    Boyd, Heather A.
    Ahlgren, Martin
    Wilbrand, Kerstin
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences.
    Westergaard, Tine
    Hjalgrim, Henrik
    Nordenskjoeld, Agneta
    Ekborn, Anders
    Melbye, Mads
    Maternal and gestational risk factors for hypospadias2008In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 116, no 8, p. 1071-1076Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: An increase in the prevalence of hypospadias has been reported, but the environmental causes remain virtually unknown. OBJECTIVES: Our goal was to assess the association between risk of hypospadias and indicators of placental function and endogenous hormone levels, exposure to exogenous hormones, maternal diet during pregnancy, and other environmental factors. METHODS: We conducted a case-control study in Sweden and Denmark from 2000 through 2005 using self-administered questionnaires completed by mothers of hypospadias cases and matched controls. The response rate was 88% and 81% among mothers of cases and controls, respectively. The analyses included 292 cases and 427 controls. RESULTS: A diet during pregnancy lacking both fish and meat was associated with a more than 4-fold increased risk of hypospadias [odds ratio (OR) 4.6, 95% confidence interval (CI), 1.6-13.3]. Boys born to obese [body mass index (BMI) > ;= 30] women had a more than 2-fold increased risk of hypospadias (OR = 2.6, 95% CI, 1.2-5.7) compared with boys born to mothers with a normal weight (BMI = 20-24). Maternal hypertension during pregnancy and absence of maternal nausea increased a boy's risk of hypospadias 2.0-fold (95% CI, 1.1-3.7) and 1.8-fold (95% CI, 1.2-2.8), respectively. Nausea in late pregnancy also appeared to be positively associated with hypospadias risk (OR = 7.6, 95% CI, 1.1-53). CONCLUSIONS: A pregnancy diet lacking meat and fish appears to increase the risk of hypospadias in the offspring. Other risk associations were compatible with a role for placental insufficiency in the etiology of hypospadias.

  • 3. Ali, Imran
    et al.
    Penttinen-Damdimopoulou, Pauliina E
    Mäkelä, Sari I
    Berglund, Marika
    Stenius, Ulla
    Akesson, Agneta
    Håkansson, Helen
    Halldin, Krister
    Institutet för miljömedicin, Karolinska Institutet.
    Estrogen-like effects of cadmium in vivo do not appear to be mediated via the classical estrogen receptor transcriptional pathway.2010In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 118, no 10, p. 1389-94Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Cadmium (Cd), a ubiquitous food contaminant, has been proposed to be an endocrine disruptor by inducing estrogenic responses in vivo. Several in vitro studies suggested that these effects are mediated via estrogen receptors (ERs).

    OBJECTIVE: We performed this study to clarify whether Cd-induced effects in vivo are mediated via classical ER signaling through estrogen responsive element (ERE)-regulated genes or if other signaling pathways are involved.

    METHODS: We investigated the estrogenic effects of cadmium chloride (CdCl2) exposure in vivo by applying the Organisation for Economic Co-operation and Development (OECD) rodent uterotrophic bioassay to transgenic ERE-luciferase reporter mice. Immature female mice were injected subcutaneously with CdCl2 (5, 50, or 500 µg/kg body weight) or with 17α-ethinylestradiol (EE2) on 3 consecutive days. We examined uterine weight and histology, vaginal opening, body and organ weights, Cd tissue retention, activation of mitogen-activated protein kinase (MAPK) pathways, and ERE-dependent luciferase expression.

    RESULTS: CdCl2 increased the height of the uterine luminal epithelium in a dose-dependent manner without increasing the uterine wet weight, altering the timing of vaginal opening, or affecting the luciferase activity in reproductive or nonreproductive organs. However, we observed changes in the phosphorylation of mouse double minute 2 oncoprotein (Mdm2) and extracellular signal-regulated kinase (Erk1/2) in the liver after CdCl2 exposure. As we expected, EE2 advanced vaginal opening and increased uterine epithelial height, uterine wet weight, and luciferase activity in various tissues.

    CONCLUSION: Our data suggest that Cd exposure induces a limited spectrum of estrogenic responses in vivo and that, in certain targets, effects of Cd might not be mediated via classical ER signaling through ERE-regulated genes.

  • 4.
    Alm, Henrik
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences, Toxicology.
    Scholz, Birger
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences, Toxicology.
    Fischer, Celia
    Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Physiology and Developmental Biology, Environmental Toxicology.
    Kultima, Kim
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences, Toxicology.
    Viberg, Henrik
    Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Physiology and Developmental Biology, Environmental Toxicology.
    Eriksson, Per
    Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Physiology and Developmental Biology, Environmental Toxicology.
    Dencker, Lennart
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences, Toxicology.
    Stigson, Michael
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences, Toxicology.
    Proteomic evaluation of neonatal exposure to 2,2,4,4,5-pentabromodiphenyl ether2006In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 114, no 2, p. 254-259Article in journal (Refereed)
    Abstract [en]

    Exposure to the brominated flame retardant 2,2 ,4,4 ,5-pentabromodiphenyl ether (PBDE-99) during the brain growth spurt disrupts normal brain development in mice and results in disturbed spontaneous behavior in adulthood. The neurodevelopmental toxicity of PBDE-99 has been reported to affect the cholinergic and catecholaminergic systems. In this study we use a proteomics approach to study the early effect of PBDE-99 in two distinct regions of the neonatal mouse brain, the striatum and the hippocampus. A single oral dose of PBDE-99 (12 mg/kg body weight) or vehicle was administered to male NMRI mice on neonatal day 10, and the striatum and the hippocampus were isolated. Using two-dimensional fluorescence difference gel electrophoresis (2D-DIGE), we found 40 and 56 protein spots with significantly (p < 0.01) altered levels in the striatum and the hippocampus, respectively. We used matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-ToF-MS) to determine the protein identity of 11 spots from the striatum and 10 from the hippocampus. We found that the levels of proteins involved in neurodegeneration and neuroplasticity (e.g., Gap-43/neuromodulin, stathmin) were typically altered in the striatum, and proteins involved in metabolism and energy production [e.g., alpha-enolase; gamma-enolase; ATP synthase, H+ transporting, mitochondrial F1 complex, beta subunit (Atp5b); and alpha-synuclein] were typically altered in the hippocampus. Interestingly, many of the identified proteins have been linked to protein kinase C signaling. In conclusion, we identify responses to early exposure to PBDE-99 that could contribute to persistent neurotoxic effects. This study also shows the usefulness of proteomics to identify potential biomarkers of developmental neurotoxicity of organohalogen compounds.

  • 5. Bergman, Ake
    et al.
    Heindel, Jerrold J.
    Kasten, Tim
    Kidd, Karen A.
    Jobling, Susan
    Neira, Maria
    Zoeller, R. Thomas
    Becher, Georg
    Bjerregaard, Poul
    Bornman, Riana
    Brandt, Ingvar
    Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Organismal Biology, Environmental toxicology.
    Kortenkamp, Andreas
    Muir, Derek
    Drisse, Marie-Noel Brune
    Ochieng, Roseline
    Skakkebaek, Niels E.
    Bylehn, Agneta Sunden
    Iguchi, Taisen
    Toppari, Jorma
    Woodruff, Tracey J.
    The Impact of Endocrine Disruption: A Consensus Statement on the State of the Science2013In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 121, no 4, p. A104-A106Article in journal (Other academic)
  • 6.
    Brantsaeter, Anne Lise
    et al.
    Norwegian Inst Publ Hlth, Dept Exposure & Risk Assessment, Div Environm Med, POB 4404, NO-0403 Oslo, Norway..
    Torjusen, Hanne
    Norwegian Inst Publ Hlth, Dept Exposure & Risk Assessment, Div Environm Med, POB 4404, NO-0403 Oslo, Norway.;Natl Inst Consumer Res SIFO, Oslo, Norway..
    Meltzer, Helle Margrete
    Norwegian Inst Publ Hlth, Dept Exposure & Risk Assessment, Div Environm Med, POB 4404, NO-0403 Oslo, Norway..
    Papadopoulou, Eleni
    Norwegian Inst Publ Hlth, Dept Exposure & Risk Assessment, Div Environm Med, POB 4404, NO-0403 Oslo, Norway..
    Hoppin, Jane A.
    N Carolina State Univ, Ctr Human Hlth & Environm, Dept Biol Sci, Raleigh, NC 27695 USA..
    Alexander, Jan
    Norwegian Inst Publ Hlth, Off Director Gen, POB 4404, NO-0403 Oslo, Norway..
    Lieblein, Geir
    Norwegian Univ Life Sci, Dept Plant Sci, As, Norway..
    Roos, Gun
    Natl Inst Consumer Res SIFO, Oslo, Norway..
    Holten, Jon Magne
    Oikos Organ Norway, Oslo, Norway..
    Swartz, Jackie
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience. Vidarkliniken, Jarna, Sweden..
    Haugen, Margaretha
    Norwegian Inst Publ Hlth, Dept Exposure & Risk Assessment, Div Environm Med, POB 4404, NO-0403 Oslo, Norway..
    Organic Food Consumption during Pregnancy and Hypospadias and Cryptorchidism at Birth: The Norwegian Mother and Child Cohort Study (MoBa)2016In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 124, no 3, p. 357-364Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The etiologies of the male urogenital anomalies hypospadias and cryptorchidism remain unclear. It has been suggested that maternal diet and environmental contaminants may affect the risk of these anomalies via placental or hormonal disturbances. OBJECTIVES: We examined associations between organic food consumption during pregnancy and prevalence of hypospadias and cryptorchidism at birth. METHODS: Our study includes 35,107 women participating in the Norwegian Mother and Child Cohort Study (MoBa) who delivered a singleton male infant. Information about use of six groups of organically produced food (vegetables, fruit, bread/cereal, milk/dairy products, eggs, and meat) during pregnancy was collected by a food frequency questionnaire. Women who indicated that they sometimes, often, or mostly consumed organic foods in at least one of the six food groups were classified as organic food consumers in analyses. Hypospadias and cryptorchidism diagnoses were retrieved from the Medical Birth Registry of Norway. We estimated odds ratios (ORs) and 95% confidence intervals (CIs) using multiple logistic regression. RESULTS: Seventy-four male newborns were diagnosed with hypospadias (0.2%), and 151 with cryptorchidism (0.4%). Women who consumed any organic food during pregnancy were less likely to give birth to a boy with hypospadias (OR = 0.42; 95% CI: 0.25, 0.70, based on 21 exposed cases) than women who reported they never or seldom consumed organic food. Associations with specific organic foods were strongest for vegetable (OR = 0.36; 95% CI: 0.15, 0.85; 10 exposed cases) and milk/dairy (OR = 0.43; 95% CI: 0.17, 1.07; 7 exposed cases) consumption. No substantial association was observed for consumption of organic food and cryptorchidism. CONCLUSIONS: Consumption of organically produced foods during pregnancy was associated with a lower prevalence of hypospadias in our study population. These findings were based on small numbers of cases and require replication in other study populations.

  • 7. Castro-Giner, Francesc
    et al.
    Künzli, Nino
    Jacquemin, Bénédicte
    Forsberg, Bertil
    de Cid, Rafael
    Sunyer, Jordi
    Jarvis, Deborah
    Briggs, David
    Vienneau, Danielle
    Norback, Dan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Occupational and Environmental Medicine.
    González, Juan R
    Guerra, Stefano
    Janson, Christer
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Respiratory Medicine and Allergology.
    Antó, Josep-Maria
    Wjst, Matthias
    Heinrich, Joachim
    Estivill, Xavier
    Kogevinas, Manolis
    Traffic-related air pollution, oxidative stress genes, and asthma (ECHRS)2009In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 117, no 12, p. 1919-1924Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Traffic-related air pollution is related with asthma, and this association may be modified by genetic factors. OBJECTIVES: We investigated the role of genetic polymorphisms potentially modifying the association between home outdoor levels of modeled nitrogen dioxide and asthma. METHODS: Adults from 13 cities of the second European Community Respiratory Health Survey (ECRHS II) were included (n = 2,920), for whom both DNA and outdoor NO(2) estimates were available. Home addresses were geocoded and linked to modeled outdoor NO(2) estimates, as a marker of local traffic-related pollution. We examined asthma prevalence and evaluated polymorphisms in genes involved in oxidative stress pathways [gluthatione S-transferases M1 (GSTM1), T1 (GSTT1), and P1 (GSTP1) and NAD(P)H:quinine oxidoreductase (NQO1)], inflammatory response [tumor necrosis factor alpha (TNFA)], immunologic response [Toll-like receptor 4 (TLR4)], and airway reactivity [adrenergic receptor beta2 (ADRB2)]. RESULTS: The association between modeled NO(2) and asthma prevalence was significant for carriers of the most common genotypes of NQO1 rs2917666 [odds ratio (OR) = 1.54; 95% confidence interval (CI), 1.10-2.24], TNFA rs2844484 (OR = 2.02; 95% CI, 1.30-3.27). For new-onset asthma, the effect of NO(2) was significant for the most common genotype of NQO1 rs2917666 (OR = 1.52; 95% CI, 1.09-2.16). A significant interaction was found between NQO1 rs2917666 and NO(2) for asthma prevalence (p = 0.02) and new-onset asthma (p = 0.04). CONCLUSIONS: Genetic polymorphisms in the NQO1 gene are related to asthma susceptibility among persons exposed to local traffic-related air pollution. This points to the importance of antioxidant pathways in the protection against the effects of air pollution on asthma.

  • 8. Gehring, Ulrike
    et al.
    Gruzieva, Olena
    Agius, Raymond M.
    Beelen, Rob
    Custovic, Adnan
    Cyrys, Josef
    Eeftens, Marloes
    Flexeder, Claudia
    Fuertes, Elaine
    Heinrich, Joachim
    Hoffmann, Barbara
    de Jongste, Johan C.
    Kerkhof, Marjan
    Kluemper, Claudia
    Korek, Michal
    Moelter, Anna
    Schultz, Erica S.
    Simpson, Angela
    Sugiri, Dorothea
    Svartengren, Magnus
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Occupational and Environmental Medicine.
    von Berg, Andrea
    Wijga, Alet H.
    Pershagen, Goeran
    Brunekreef, Bert
    Air Pollution Exposure and Lung Function in Children: The ESCAPE Project2013In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 121, no 11-12, p. 1357-1364Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: There is evidence for adverse effects of outdoor air pollution on lung function of children. Quantitative summaries of the effects of air pollution on lung function, however, are lacking due to large differences among studies. OBJECTIVES: We aimed to study the association between residential exposure to air pollution and lung function in five European birth cohorts with a standardized exposure assessment following a common protocol. METHODS: As part of the European Study of Cohorts for Air Pollution Effects (ESCAPE) we analyzed data from birth cohort studies situated in Germany, Sweden, the Netherlands, and the United Kingdom that measured lung function at 6-8 years of age (n = 5,921). Annual average exposure to air pollution [nitrogen oxides (NO2, NOx), mass concentrations of particulate matter with diameters < 2.5, < 10, and 2.5-10 mu m (PM2.5, PM10, and PMcoarse), and PM2.5 absorbance] at the birth address and current address was estimated by land-use regression models. Associations of lung function with estimated air pollution levels and traffic indicators were estimated for each cohort using linear regression analysis, and then combined by random effects meta-analysis. RESULTS: Estimated levels of NO2, NOx, PM2.5 absorbance, and PM2.5 at the current address, but not at the birth address, were associated with small decreases in lung function. For example, changes in forced expiratory volume in 1 sec (FEV1) ranged from -0.86% (95% CI: -1.48, -0.24%) for a 20-mu g/m(3) increase in NOx to -1.77% (95% CI: -3.34, -0.18%) for a 5-mu g/m(3) increase in PM2.5. CONCLUSIONS: Exposure to air pollution may result in reduced lung function in schoolchildren.

  • 9. Hodgson, Susan
    et al.
    Thomas, Laura
    Fattore, Elena
    Lind, Monica
    Institute of Environmental Medicine, Karolinska Institutet.
    Alfven, Tobias
    Hellström, Lennart
    Håkansson, Helen
    Carubelli, Grazia
    Fanelli, Roberto
    Jarup, Lars
    Bone mineral density changes in relation to environmental PCB exposure2008In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 116, no 9, p. 1162-1166Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Bone toxicity has been linked to organochlorine exposure following a few notable poisoning incidents, but epidemiologic studies in populations with environmental organochlorine exposure have yielded inconsistent results.

    OBJECTIVES: The aim of this study was to investigate whether organochlorine exposure was associated with bone mineral density (BMD) in a population 60-81 years of age (154 males, 167 females) living near the Baltic coast, close to a river contaminated by polychlorinated biphenyls (PCBs).

    METHODS: We measured forearm BMD in participants using dual energy X-ray absorptiometry; and we assessed low BMD using age- and sex-standardized Z-scores. We analyzed blood samples for five dioxin-like PCBs, the three most abundant non-dioxin-like PCBs, and p,p'-dichloro-phenyldichloroethylene (p,p'-DDE).

    RESULTS: In males, dioxin-like chlorobiphenyl (CB)-118 was negatively associated with BMD; the odds ratio for low BMD (Z-score less than -1) was 1.06 (95% confidence interval, 1.01-1.12) per 10 pg/mL CB-118. The sum of the three most abundant non-dioxin-like PCBs was positively associated with BMD, but not with a decreased risk of low BMD. In females, CB-118 was positively associated with BMD, but this congener did not influence the risk of low BMD in women.

    CONCLUSIONS: Environmental organochlorine exposures experienced by this population sample since the 1930s in Sweden may have been sufficient to result in sex-specific changes in BMD.

  • 10. 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
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Respiratory Medicine and Allergology.
    Jarvis, Deborah
    Al Kanaani, Zaina
    Keidel, Dirk
    Kuh, Diana
    Le Moual, Nicole
    Nieuwenhuijsen, Mark J.
    Marcon, Alessandro
    Modig, Lars
    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 Cohorts (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 mu g/m(3); p = 0.10] and nitrogen oxides (adjusted OR = 1.04; 95% CI: 0.99, 1.08 per 20 mu g/m(3); p = 0.08). Nonsignificant positive associations were estimated for PM10 (adjusted OR = 1.04; 95% CI: 0.88, 1.23 per 10 mu g/m(3)), PM2.5 (adjusted OR = 1.04; 95% CI: 0.88, 1.23 per 5 mu g/m(3)), 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 x 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 mu g/m(3)). 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.

  • 11.
    Johansson, Maria
    et al.
    Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Evolutionary Biology, Environmental Toxicology.
    Nilsson, S.
    Lund, B-O
    Interactions between methylsulfonyl PCBs and the glucocorticoid receptor1998In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 106, no 12, p. 769-772Article in journal (Refereed)
    Abstract [en]

    Persistent polychlorinated biphenyl (PCB) metabolites were studied with respect to their interaction with the human glucocorticoid receptor (GR). 3-Methylsulphonyl-2,5,6,2',4',5'-hexachlorobiphenyl (3-MeSO2-CB149) was shown to compete with 3H-dexamethasone for binding to the GR, with an IC50 (concentration that inhibits 50%) of approximately 1 microM. Using GRAF cells expressing human GR, glucocorticoid responsive element, and a reporter enzyme, we demonstrated that 3-MeSO2-CB149 functionally acts as an antagonist at the GR (IC50 = 2.7 microM). In accordance with the receptor binding, the antagonism mainly appeared to be of a competitive nature. When studying the competitive binding of 24 methylsulfonyl PCBs (relative to dexamethasone) to GR from mouse liver cytosol, seven compounds had a higher affinity to GR than 3-MeSO2-CB149. Structure-activity relationship studies indicated that the presence of three chlorine atoms in the ortho-position and chlorine and methyl sulfone groups on either end of the molecule (4 and 4'-position) increased the affinity to GR. The relevance of this finding for human health is not known, but PCB methyl sulfones are ubiquitous pollutants present in mother's milk. The results stress the need for studying endocrine disruptors that affect hormonal systems other than sex and thyroidogenic hormones.

  • 12.
    Kultima, Kim
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences, Toxicology.
    Nyström, Anna-Maja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences, Toxicology.
    Scholz, Birger
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences, Toxicology.
    Gustafson, Anne-Lee
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences, Toxicology.
    Dencker, Lennart
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences, Toxicology.
    Stigson, Michael
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences, Toxicology.
    Valproic acid teratogenicity: a toxicogenomics approach2004In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 112, no 12, p. 1225-1235Article in journal (Refereed)
    Abstract [en]

    Embryonic development is a highly coordinated set of processes that depend on hierarchies of signaling and gene regulatory networks, and the disruption of such networks may underlie many cases of chemically induced birth defects. The antiepileptic drug valproic acid (VPA) is a potent inducer of neural tube defects (NTDs) in human and mouse embryos. As with many other developmental toxicants however, the mechanism of VPA teratogenicity is unknown. Using microarray analysis, we compared the global gene expression responses to VPA in mouse embryos during the critical stages of teratogen action in vivo with those in cultured P19 embryocarcinoma cells in vitro. Among the identified VPA-responsive genes, some have been associated previously with NTDs or VPA effects [vinculin, metallothioneins 1 and 2 (Mt1, Mt2), keratin 1-18 (Krt1-18)], whereas others provide novel putative VPA targets, some of which are associated with processes relevant to neural tube formation and closure [transgelin 2 (Tagln2), thyroid hormone receptor interacting protein 6, galectin-1 (Lgals1), inhibitor of DNA binding 1 (Idb1), fatty acid synthase (Fasn), annexins A5 and A11 (Anxa5, Anxa11)], or with VPA effects or known molecular actions of VPA (Lgals1, Mt1, Mt2, Id1, Fasn, Anxa5, Anxa11, Krt1-18). A subset of genes with a transcriptional response to VPA that is similar in embryos and the cell model can be evaluated as potential biomarkers for VPA-induced teratogenicity that could be exploited directly in P19 cell-based in vitro assays. As several of the identified genes may be activated or repressed through a pathway of histone deacetylase (HDAC) inhibition and specificity protein 1 activation, our data support a role of HDAC as an important molecular target of VPA action in vivo.

  • 13.
    Kumar, Jitender
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Molecular epidemiology. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Lind, Monica
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Occupational and Environmental Medicine.
    Salihovic, Samira
    van Bavel, Bert
    Ingelsson, Erik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Molecular epidemiology. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiovascular epidemiology.
    Persistent Organic Pollutants and Inflammatory Markers in a Cross-Sectional Study of Elderly Swedish People: The PIVUS Cohort2014In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 122, no 9, p. 977-983Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Persistent organic pollutants (POPs) are compounds that are generated through various industrial activities and released in the surrounding environment. Different animal studies have shown effects of different POPs on various inflammatory markers. OBJECTIVE: Because very few studies have been conducted in humans, we assessed the associations between different POPs and inflammatory markers in a large population-based sample of elderly men and women (all 70 years of age) from Sweden. METHODS: This cross-sectional study investigated the concentrations of several polychlorinated biphenyls (PCBs), organochlorine pesticides, polychlorinated dibenzo-p-dioxin, and brominated diphenyl ether congeners and their association with a number of inflammatory markers [vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), E-selectin, C-reactive protein (CRP), total leucocyte count, tumor necrosis factor alpha (TNF-alpha), monocyte chemotactic protein 1 (MCP-1), and interleukin 6 (IL-6)] in 992 individuals. These individuals were recruited from the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) cohort. We used a total toxic equivalency (TEQ) value that measures toxicological effects with the relative potencies of various POPs. RESULTS: Following adjustment for potential confounders, the TEQ value (driven mainly by PCB-126) was significantly associated with levels of ICAM-1 (p < 10(-5)). A similar trend was also observed between sum of PCBs and VCAM-1 (p < 0.001). No significant associations were observed between levels of POPs and other inflammatory markers. CONCLUSIONS: TEQ values were associated with levels of ICAM-1, to a lesser degree also with VCAM-1, but not with CRP and several other inflammatory markers. These findings suggest an activation of vascular adhesion molecules by POPs, and particularly by PCB-126.

  • 14.
    Lejonklou, Margareta Halin
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Occupational and Environmental Medicine.
    Dunder, Linda
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Occupational and Environmental Medicine.
    Bladin, Emelie
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Occupational and Environmental Medicine.
    Pettersson, Vendela
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Occupational and Environmental Medicine.
    Rönn, Monika
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Occupational and Environmental Medicine.
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiovascular epidemiology.
    Waldén, Tomas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
    Lind, P. Monica
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Occupational and Environmental Medicine.
    Effects of Low-Dose Developmental Bisphenol A Exposure on Metabolic Parameters and Gene Expression in Male and Female Fischer 344 Rat Offspring.2017In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 125, no 6, article id 067018Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Bisphenol A (BPA) is an endocrine-disrupting chemical that may contribute to development of obesity and metabolic disorders. Humans are constantly exposed to low concentrations of BPA, and studies support that the developmental period is particularly sensitive.

    OBJECTIVES: The aim was to investigate the effects of low-dose developmental BPA exposure on metabolic parameters in male and female Fischer 344 (F344) rat offspring.

    METHODS: Pregnant F344 rats were exposed to BPA via their drinking water, corresponding to (BPA0.5; ) or (BPA50; ), from gestational day (GD) 3.5 until postnatal day (PND) 22, and controls were given vehicle (). Body weight (BW), adipose tissue, liver (weight, histology, and gene expression), heart weight, and lipid profile were investigated in the 5-wk-old offspring.

    RESULTS: Males and females exhibited differential susceptibility to the different doses of BPA. Developmental BPA exposure increased plasma triglyceride levels ( compared with , females BPA50 ; compared with , males BPA0.5 ) in F344 rat offspring compared with controls. BPA exposure also increased adipocyte cell density by 122% in inguinal white adipose tissue (iWAT) of female offspring exposed to BPA0.5 compared with controls ( number of adipocytes/HPF compared with number of adipocytes/HPF; ) and by 123% in BPA0.5 females compared with BPA50 animals ( number of adipocytes/high power field (HPF) compared with number of adipocytes/HPF; ). In iWAT of male offspring, adipocyte cell density was increased by 129% in BPA50-exposed animals compared with BPA0.5-exposed animals ( number of adipocytes/HPF compared with number of adipocytes/HPF; ). Furthermore, the expression of genes involved in lipid and adipocyte homeostasis was significantly different between exposed animals and controls depending on the tissue, dose, and sex.

    CONCLUSIONS: Developmental exposure to of BPA, which is 8-10 times lower than the current preliminary EFSA (European Food Safety Authority) tolerable daily intake (TDI) of and is within the range of environmentally relevant levels, was associated with sex-specific differences in the expression of genes in adipose tissue plasma triglyceride levels in males and adipocyte cell density in females when F344 rat offspring of dams exposed to BPA at were compared with the offspring of unexposed controls.

  • 15. Li, Li
    et al.
    Ekström, Eva-Charlotte
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health.
    Goessler, Walter
    Lönnerdal, Bo
    Nermell, Barbro
    Yunus, Mohammad
    Rahman, Anisur
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health.
    El Arifeen, Shams
    Persson, Lars Åke
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health.
    Vahter, Marie
    Nutritional status has marginal influence on the metabolism of inorganic arsenic in pregnant Bangladeshi women2008In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 116, no 3, p. 315-321Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The interindividual variation in metabolism of inorganic arsenic (iAs), involving methylation via one-carbon metabolism, has been well documented, but the reasons remain unclear. OBJECTIVES: In this population-based study we aimed to elucidate the effect of nutrition on As methylation among women in Matlab, Bangladesh, where people are chronically exposed to iAs via drinking water. METHODS: We studied effects of macronutrient status using body mass index (BMI) among 442 women in early pregnancy (gestational week 8), and effects of micronutrient status (plasma folate, vitamin B-12, zinc, ferritin, and selenium) among 753 women at gestational week 14. Arsenic metabolites in urine were measured by HPLC combined with hydride generation inductively coupled plasma mass spectrometry. RESULTS: The median concentration of As in urine was 97 mu g/L (range, 5-1,216 mu g/L, adjusted by specific gravity). The average proportions of iAs, monomethylarsonic acid, and dimethylarsinic acid in urine in gestational week 8 were 15%, 11%, and 74%, respectively. Thus, the women had efficient As methylation in spite of being poorly nourished (one-third had BMIs < 18.5 kg/m(2)) and having elevated As exposure, both of which are known to decrease As methylation. The metabolism of iAs was only marginally influenced by micronutrient status, probably because women, especially in pregnancy and with low folate intake, have an efficient betaine-mediated remethylation of homocysteine, which is essential for an efficient As methylation. CONCLUSIONS: In spite of the high As exposure and prevalent malnutrition, overall As methylation in women in early pregnancy was remarkably efficient. The As exposure level had the greatest impact on As methylation among the studied factors.

  • 16.
    Lind, Lars
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiovascular epidemiology.
    Lind, P. Monica
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Occupational and Environmental Medicine.
    Lejonklou, Margareta H
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Occupational and Environmental Medicine.
    Dunder, Linda
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Occupational and Environmental Medicine.
    Bergman, Åke
    Guerrero-Bosagna, Carlos
    Lampa, Erik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Lee, Hong Kyu
    Legler, Juliette
    Nadal, Angel
    Pak, Youngmi Kim
    Phipps, Richard P
    Vandenberg, Laura N
    Zalko, Daniel
    Ågerstrand, Marlene
    Öberg, Mattias
    Blumberg, Bruce
    Heindel, Jerrold J
    Birnbaum, Linda S
    Uppsala Consensus Statement on Environmental Contaminants and the Global Obesity Epidemic2016In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 124, no 5, p. A81-A83Article in journal (Refereed)
    Abstract [en]

    From the lectures presented at the 2nd International Workshop on Obesity and Environmental Contaminants, which was held in Uppsala, Sweden, on 8–9 October 2015, it became evident that the findings from numerous animal and epidemiological studies are consistent with the hypothesis that environmental contaminants could contribute to the global obesity epidemic. To increase awareness of this important issue among scientists, regulatory agencies, politicians, chemical industry management, and the general public, the authors summarize compelling scientific evidence that supports the hypothesis and discuss actions that could restrict the possible harmful effects of environmental contaminants on obesity.

  • 17.
    Lind, Monica
    et al.
    Institute of Environmental Medicine, Karolinska Institutet.
    Milnes, Matthew R
    Lundberg, Rebecca
    Bermudez, Dieldrich
    Orberg, Jan
    Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Physiology and Developmental Biology, Environmental Toxicology.
    Guillette, Louis J
    Abnormal bone composition in female juvenile American alligators from a pesticide-polluted lake (Lake Apopka, Florida)2004In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 112, no 3, p. 359-362Article in journal (Refereed)
    Abstract [en]

    Reproductive disorders have been found in pesticide-exposed alligators living in Lake Apopka, Florida (USA). These disorders have been hypothesized to be caused by exposure to endocrine- disruptive estrogen-like contaminants. The aim of this study was to expand our analysis beyond previous studies by investigating whether bone tissue, known to be affected by sex steroid hormones, is a potential target of endocrine disruptors. Long bones from 16 juvenile female alligators from Lake Apopka (pesticide-contaminated lake) and Lake Woodruff (control lake) were evaluated by peripheral quantitative computed tomography. We observed significant differences in bone composition, with female alligators from the contaminated lake having greater trabecular bone mineral density (BMD), total BMD, and trabecular mineral content compared with females from the control lake (p < 0.05). Increased trabecular and total BMD measurements suggest that juvenile female alligators from Lake Apopka were exposed to contaminants that created an internal environment more estrogenic than that normally observed. This estrogenic environment could be caused by both natural and anthropogenic compounds. Effects on BMD indicate interference with bone homeostasis. We hypothesize that contaminants present in the lake inhibit the natural and continuous resorption of bone tissue, resulting in increased bone mass. Although this is the only study performed to date examining effects of environmental estrogenic compounds on alligator bones, it supports previous laboratory-based studies in rodents. Further, this study is important in demonstrating that the alterations in morphology and physiology induced in free-ranging individuals living in environments contaminated with endocrine-active compounds are not limited to a few systems or tissues; rather, effects can be observed in many tissues affected by these hormones.

  • 18.
    Lind, Monica
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Occupational and Environmental Medicine.
    van Bavel, Bert
    Salihovic, Samira
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Circulating Levels of Persistent Organic Pollutants (POPs) and Carotid Atherosclerosis in the Elderly2012In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 120, no 1, p. 38-43Article in journal (Refereed)
    Abstract [en]

    Background and objective:

    Increased circulating levels of persistent organic pollutants (POPs) have been associated with myocardial infarction. Because myocardial infarction is an atherosclerotic disease, we investigated, in a cross-sectional study, whether POP levels are related to atherosclerosis.

    Methods:

    In the population-based Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) study (n = 1,016 participants 70 years of age), the prevalence of carotid artery plaques was determined by ultrasound. The number of carotid arteries with plaques (0, 1, or 2) was recorded. Also, the intima-media thickness (IMT) and gray scale median of the intima-media complex (IM-GSM) were measured. Twenty-three POPs, comprising 16 polychlorinated biphenyls (PCBs), 5 pesticides, 1 dioxin, and 1 brominated compound (brominated diphenyl ether congener BDE-47), were analyzed by high-resolution chromatography coupled to high-resolution mass spectrometry.

    Results:

    Seven of the POPs (PCB congeners 153, 156, 157, 170, 180, 206, and 209) were significantly associated with the number of carotid arteries with plaques even after adjusting for multiple risk factors (sex, waist circumference, body mass index, fasting blood glucose, systolic and diastolic blood pressure, high-density lipoprotein and low-density lipoprotein cholesterol, serum triglycerides, smoking, antihypertensive treatment, and statin use; p = 0.002-0.0001). Highly chlorinated PCBs (congeners 194, 206, and 209) were associated with an echolucent IM-GSM (p < 0.0001 after adjustment), whereas associations between POPs and IMT were modest.

    Conclusions:

    Circulating levels of PCBs were associated with atherosclerotic plaques and echogenicity of the intima-media complex independent of cardiovascular risk factors, including lipids. This suggests that POPs may be a risk factor for myocardial infarction, but associations need to be confirmed in prospective studies.

  • 19.
    Lindberg, Anna-Lena
    et al.
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Sohel, Nazmul
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health.
    Rahman, Mahfuzar
    Persson, Lars-Åke
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health.
    Vahter, Marie
    Impact of smoking and chewing tobacco on arsenic-induced skin lesions2010In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 118, no 4, p. 533-538Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: We recently reported that the main reason for the documented higher prevalence of arsenic-related skin lesions among men than among women is the result of less efficient arsenic metabolism. OBJECTIVE: Because smoking has been associated with less efficient arsenic methylation, we aimed to elucidate interactions between tobacco use and arsenic metabolism for the risk of developing skin lesions. METHODS: We used a population-based case-referent study that showed increased risk for skin lesions in relation to chronic arsenic exposure via drinking water in Bangladesh and randomly selected 526 of the referents (random sample of inhabitants > 4 years old; 47% male) and all 504 cases (54% male) with arsenic-related skin lesions to measure arsenic metabolites [methylarsonic acid (MA) and dimethylarsinic acid (DMA)] in urine using high-performance liquid chromatography (HPLC) and inductively coupled plasma mass spectrometry (ICPMS). RESULTS: The odds ratio for skin lesions was almost three times higher in the highest tertile of urinary %MA than in the lowest tertile. Men who smoked cigarettes and bidis (locally produced cigarettes; 33% of referents, 58% of cases) had a significantly higher risk for skin lesions than did nonsmoking men; this association decreased slightly after accounting for arsenic metabolism. Only two women smoked, but women who chewed tobacco (21% of referents, 43% of cases) had a considerably higher risk of skin lesions than did women who did not use tobacco. The odds ratio (OR) for women who chewed tobacco and who had < or = 7.9%MA was 3.8 [95% confidence interval (CI), 1.4-10] compared with women in the same MA tertile who did not use tobacco. In the highest tertile of %MA or %inorganic arsenic (iAs), women who chewed tobacco had ORs of 7.3 and 7.5, respectively, compared with women in the lowest tertiles who did not use tobacco. CONCLUSION: The increased risk of arsenic-related skin lesions in male smokers compared with nonsmokers appears to be partly explained by impaired arsenic methylation, while there seemed to be an excess risk due to interaction between chewing tobacco and arsenic metabolism in women.

  • 20.
    Lindhe, Örjan
    et al.
    Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Evolutionary Biology, Environmental Toxicology.
    Lund, Bert-Ove
    Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Evolutionary Biology, Environmental Toxicology.
    Bergman, Åke
    Brandt, Ingvar
    Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Evolutionary Biology, Environmental Toxicology.
    Irreversible binding and adrenocorticolytic activity of the DDT metabolite 3-methylsulfonyl-DDE examined in tissue-slice culture2001In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 109, no 2, p. 105-110Article in journal (Refereed)
    Abstract [en]

    The persistent adrenocorticolytic DDT metabolite 3-methylsulfonyl-DDE (MeSO(2)-DDE) was originally identified in Baltic grey seals, a population suffering from adrenocortical hyperplasia. In mice, MeSO(2)-DDE induces mitochondrial degeneration and cellular necrosis in the adrenal zona fasciculata. In this study, we used precision-cut tissue slice culture to examine local CYP11B1-catalyzed irreversible binding of MeSO(2)-DDE in the murine adrenal cortex. We also examined effects on steroid hormone secretion, histology, and ultrastructure. As determined by microautoradiography, selective binding occurred in zona fasciculata of slices exposed to MeSO(2)-[(14)C]-DDE. Quantification of binding by phosphorautoradiography revealed a 3-fold reduction of binding in slices co-exposed to the CYP11B1 inhibitor metyrapone. As measured by HPLC, corticosterone and 11-deoxycorticosterone secretion to the medium increased linearly for at least 24 hr. Addition of the ACTH analog tetracosactide caused an 8-fold increase in corticosterone secretion. Addition of metyrapone reduced corticosterone secretion 4-fold. Exposure of slices to MeSO(2)-DDE (50 microM) reduced the rate of corticosterone secretion by 90% after 24 hr of incubation. As determined by electron microscopy, vacuolated mitochondria were present in zona fasciculata of slices exposed to MeSO(2)-DDE (50 microM) for 24 hr. Our findings show that all effects of MeSO(2)-DDE previously reported in vivo could be reproduced in adrenal slice culture ex vivo. This test system allows analysis of zone-specific irreversible binding and effects on steroid hormone secretion and target cell ultrastructure. We propose adrenal slice culture as a simple ex vivo test system with which to examine the adrenocorticolytic activity of xenobiotics in human and wild animal tissue.

  • 21. Pond, Kathy
    et al.
    Kim, Rokho
    Carroquino, Maria-Jose
    Pirard, Philippe
    Gore, Fiona
    Cucu, Alexandra
    Nemer, Leda
    MacKay, Morag
    Smedje, Greta
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences. Arbets- och miljömedicin.
    Georgellis, Antonis
    Dalbokova, Dafina
    Krzyzanowski, Michal
    Workgroup report: developing environmental health indicators for European children: World Health Organization Working Group2007In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 115, no 9, p. 1376-1382Article in journal (Refereed)
    Abstract [en]

    A working group coordinated by the World Health Organization developed a set of indicators to protect children’s health from environmental risks and to support current and future European policy needs. On the basis of identified policy needs, the group developed a core set of 29 indicators for implementation plus an extended set of eight additional indicators for future development, focusing on exposure, health effects, and action. As far as possible, the indicators were designed to use existing information and are flexible enough to be developed further to meet the needs of policy makers and changing health priorities. These indicators cover most of the priority topic areas specified in the Children’s Environment and Health Action Plan for Europe (CEHAPE) as adopted in the Fourth Ministerial Conference on Health and Environment in 2004, and will be used to monitor the implementation of CEHAPE. This effort can be viewed as an integral part of the Global Initiative on Children’s Environmental Health Indicators, launched at the World Summit on Sustainable Development in 2002.

  • 22.
    Rahman, Anisur
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health.
    Vahter, Marie
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Ekström, Eva-Charlotte
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health.
    Persson, Lars-Åke
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health.
    Arsenic Exposure in Pregnancy Increases the Risk of Lower Respiratory Tract Infection and Diarrhea During Infancy in Bangladesh2011In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 119, no 5, p. 719-724Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Previous studies have reported associations between prenatal arsenic exposure and increased risk of infant mortality. An increase in infectious diseases has been proposed as the underlying cause of these associations, but there is no epidemiological research to support the hypothesis. We evaluated the association between arsenic exposure in pregnancy and morbidity during infancy. METHODS: This prospective population-based cohort study included 1,552 live-born infants of women enrolled during 2002 -2004 in Matlab, Bangladesh. Arsenic exposure was assessed by the concentrations of metabolites of inorganic arsenic in maternal urine samples collected at gestational week 8 and 30. Information on symptoms of lower respiratory tract infection (LRTI) and diarrhea in infants was collected by 7-days recalls at monthly home visits. RESULTS: In total 115,850 person-days of observation were contributed by the infants over a 12 months follow-up period. The estimated risk of LRTI and severe LRTI increased by 69% (adjusted relative risk (RR) 1.69, 95% confidence intervals (CI): 1.36 - 2.09) and 54% (RR 1.54, 95% CI: 1.21 - 1.97), respectively, for infants of mothers with urinary arsenic concentrations in the highest quintile (262 - 977 µg/L, average of arsenic concentrations measured in early and late gestation) relative to those with exposure in the lowest quintile (<39 µg/L). The corresponding figure for diarrhea was 20% (RR 1.20, 95% CI: 1.01 - 1.43). CONCLUSIONS: Arsenic exposure during pregnancy was associated with increased morbidity in infectious diseases during infancy. Taken together with the previous evidence of adverse effects on health, the findings strongly emphasize the need to reduce arsenic exposure via drinking water.

  • 23. Rahman, Mahfuzar
    et al.
    Vahter, Marie
    Sohel, Nazmul
    Yunus, Muhammad
    Wahed, Mohammad Abdul
    Streatfield, Peter Kim
    Ekström, Eva-Charlotte
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Maternal and Child Health (IMCH).
    Persson, Lars-Åke
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Maternal and Child Health (IMCH).
    Arsenic exposure and age- and sex-specific risk for skin lesions: A population-based case-referent study in Bangladesh2006In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 114, no 12, p. 1847-1852Article in journal (Refereed)
    Abstract [en]

    Background: The objective of this population-based case-referent study in Matlab, Bangladesh, was to assess the susceptibility to arsenic-induced skin lesions by age and sex, in a population drinking water from As-contaminated tube wells. Methods: Identification of As-related skin lesions was carried out in three steps: a) screening of the entire population > 4 years of age (n = 166,934) by trained field teams; b) diagnosis of suspected As-related cases by physicians; and c) confirmation by experts based on physicians' records and photographs, A total of 504 cases with skin lesions were confirmed. We randomly selected 2,201 referents from the Matlab health and demographic surveillance system; 1,955 were eligible, and 1,830 (94%) were available for participation in the study. Individual history of As exposure was based on information obtained during interviews and included all drinking-water sources used since 1970 and concentrations of As (assessed by atomic absorption spectrophotometry) in all the tube wells used. Results: Cases had been exposed to As more than referents (average exposure since 1970: male cases, 200 μg/L; female cases, 211 μg/L; male referents, 143 μg/L; female referents, 155 μg/L). We found a dose-response relationship for both sexes (p < 0.001) and increased risk with increasing socioeconomic status. Males had a higher risk of obtaining skin lesions than females (odds ratio 10.9 vs. 5.78) in the highest average exposure quintile (p = 0.005). Start of As exposure (cumulative exposure) before 1 year of age was not associated with higher risk of obtaining skin lesions compared to start of As exposure later in life. Conclusions: The results demonstrate that males are more susceptible than females to develop skin lesions when exposed to As in water from tube wells.

  • 24.
    Rentschler, Gerda
    et al.
    Department of Laboratory Medicine, Division of Occupational and Environmental Medicine, Lund University, Sweden.
    Kippler, Maria
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Axmon, Anna
    Department of Laboratory Medicine, Division of Occupational and Environmental Medicine, Lund University, Sweden.
    Raqib, Rubhana
    International Centre for Diarrhoeal Disease Research, Dhaka, Bangladesh (icddr,b).
    Ekström, Eva-Charlotte
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Maternal and Child Health (IMCH).
    Skerfving, Staffan
    Department of Laboratory Medicine, Division of Occupational and Environmental Medicine, Lund University, Sweden.
    Vahter, Marie
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Broberg, Karin
    Department of Laboratory Medicine, Division of Occupational and Environmental Medicine, Lund University, Sweden.
    Polymorphisms in Iron Homeostasis Genes and Urinary Cadmium Concentrations among Nonsmoking Women in Argentina and Bangladesh2013In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 121, no 4, p. 467-472Article in journal (Refereed)
    Abstract [en]

    Background:

    Cadmium (Cd) is a human toxicant and carcinogen. Genetic variation might affect long-term accumulation. Cd is absorbed via iron transporters.

    Objectives:

    We evaluated the impact of iron homeostasis genes [divalent metal transporter 1 (SLC11A2), transferrin (TF), transferrin receptors (TFR2 and TFRC), and ferroportin (SLC40A1)] on Cd accumulation.

    Methods:

    Subjects were nonsmoking women living in the Argentinean Andes [n = 172; median urinary Cd (U-Cd) = 0.24 µg/L] and Bangladesh (n = 359; U-Cd = 0.54 µg/L) with Cd exposure mainly from food. Concentrations of U-Cd and Cd in whole blood or in erythrocytes (Ery-Cd) were measured by inductively coupled plasma mass spectrometry. Fifty polymorphisms were genotyped by Sequenom. Gene expression was measured in whole blood (n = 72) with Illumina DirectHyb HumanHT-12 v4.0.

    Results:

    TFRC rs3804141 was consistently associated with U-Cd. In the Andean women, mean U-Cd concentrations were 22% (95% CI: –2, 51%), and they were 56% (95% CI: 10, 120%) higher in women with GA and AA genotypes, respectively, relative to women with the GG genotype. In the Bangladeshi women, mean U-Cd concentrations were 22% (95% CI: 1, 48%), and they were 58% (95% CI: –3, 157%) higher in women with GA and AA versus GG genotype, respectively [adjusted for age and plasma ferritin in both groups; ptrend = 0.006 (Andes) and 0.009 (Bangladesh)]. TFRC expression in blood was negatively correlated with plasma ferritin (rS = –0.33, p = 0.006), and positively correlated with Ery-Cd (significant at ferritin concentrations of < 30 µg/L only, rS = 0.40, p = 0.046). Rs3804141 did not modify these associations or predict TFRC expression. Cd was not consistently associated with any of the other polymorphisms evaluated.

    Conclusions:

    One TFRC polymorphism was associated with urine Cd concentration, a marker of Cd accumulation in the kidney, in two very different populations. The consistency of the findings supports the possibility of a causal association.

  • 25.
    Schlebusch, Carina M.
    et al.
    Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Ecology and Genetics, Evolutionary Biology. Uppsala University.
    Lewis Jr., C. M.
    Vahter, Marie
    Engström, Karin
    Tito, Raúl Y.
    Obregón-Tito, Alexandra J.
    Huerta, Doris
    Polo, Susan I.
    Medina, Ángel C.
    Brutsaert, Tom D.
    Concha, Gabriela
    Jakobsson, Mattias
    Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Ecology and Genetics, Evolutionary Biology. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Broberg, Karin
    Possible positive selection for an arsenic-protective haplotype in humans2013In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 121, no 1, p. 53-58Article in journal (Refereed)
    Abstract [en]

    Background: Arsenic in drinking water causes severe health effects. Indigenous people in the South American Andes have likely lived with arsenic-contaminated drinking water for thousands of years. Inhabitants of San Antonio de los Cobres (SAC) in the Argentinean highlands generally carry an AS3MT (the major arsenic-metabolizing gene) haplotype associated with reduced health risks due to rapid arsenic excretion and lower urinary fraction of the monomethylated metabolite.Objectives: We hypothesized an adaptation to high-arsenic living conditions via a possible positive selection for protective AS3MT variants and compared AS3MT haplotype frequencies among different indigenous groups. Methods: Indigenous groups we evaluated were a) inhabitants of SAC and villages near Salta in northern Argentina (n = 346), b) three Native American populations from the Human Genome Diversity Project (HGDP; n = 25), and c) five Peruvian populations (n = 97). The last two groups have presumably lower historical exposure to arsenic.Results: We found a significantly higher frequency of the protective AS3MT haplotype in the SAC population (68.7%) compared with the HGDP (14.3%, p &lt; 0.001, Fisher exact test) and Peruvian (50.5%, p &lt; 0.001) populations. Genome-wide microsatellite (n = 671) analysis showed no detectable level of population structure between SAC and Peruvian populations (measure of population differentiation FST = 0.006) and low levels of structure between SAC and HGDP populations (FST &lt; 0.055 for all pairs of populations compared). Conclusions: Because population stratification seems unlikely to explain the differences in AS3MT haplotype frequencies, our data raise the possibility that, during a few thousand years, natural selection for tolerance to the environmental stressor arsenic may have increased the frequency of protective variants of AS3MT. Further studies are needed to investigate this hypothesis.

  • 26. Schläwicke Engström, Karin
    et al.
    Strömberg, Ulf
    Lundh, Thomas
    Johansson, Ingegerd
    Vessby, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences.
    Hallmans, Göran
    Skerfving, Staffan
    Broberg, Karin
    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.

  • 27. Taylor, Kyla W.
    et al.
    Novak, Raymond F.
    Anderson, Henry A.
    Birnbaum, Linda S.
    Blystone, Chad
    DeVito, Michael
    Jacobs, David
    Koehrle, Josef
    Lee, Duk-Hee
    Rylander, Lars
    Rignell-Hydbom, Anna
    Tornero-Velez, Rogelio
    Turyk, Mary E.
    Boyles, Abee L.
    Thayer, Kristina A.
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiovascular epidemiology.
    Evaluation of the Association between Persistent Organic Pollutants (POPs) and Diabetes in Epidemiological Studies: A National Toxicology Program Workshop Review2013In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 121, no 7, p. 774-783Article, review/survey (Refereed)
    Abstract [en]

    BACKGROUND: Diabetes is a major threat to public health in the United States and worldwide. Understanding the role of environmental chemicals in the development or progression of diabetes is an emerging issue in environmental health. OBJECTIVE: We assessed the epidemiologic literature for evidence of associations between persistent organic pollutants (POPs) and type 2 diabetes. METHODS: Using a PubMed search and reference lists from relevant studies or review articles, we identified 72 epidemiological studies that investigated associations of persistent organic pollutants (POPs) with diabetes. We evaluated these studies for consistency, strengths and weaknesses of study design (including power and statistical methods), clinical diagnosis, exposure assessment, study population characteristics, and identification of data gaps and areas for future research. CONCLUSIONS: Heterogeneity of the studies precluded conducting a meta-analysis, but the overall evidence is sufficient for a positive association of some organochlorine POPs with type 2 diabetes. Collectively, these data are not sufficient to establish causality. Initial data mining revealed that the strongest positive correlation of diabetes with POPs occurred with organochlorine compounds, such as trans-nonachlor, dichlorodiphenyldichloroethylene (DDE), polychlorinated biphenyls (PCBs), and dioxins and dioxin-like chemicals. There is less indication of an association between other nonorganochlorine POPs, such as perfluoroalkyl acids and brominated compounds, and type 2 diabetes. Experimental data are needed to confirm the causality of these POPs, which will shed new light on the pathogenesis of diabetes. This new information should be considered by governmental bodies involved in the regulation of environmental contaminants.

  • 28. Verner, Marc-Andre
    et al.
    McDougall, Robin
    Glynn, Anders
    Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Organismal Biology, Environmental toxicology.
    Andersen, Melvin E.
    Clewell, Harvey J., III
    Longnecker, Matthew P.
    Is the Relationship between Prenatal Exposure to PCB-153 and Decreased Birth Weight Attributable to Pharmacokinetics?2013In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 121, no 10, p. 1219-1224Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: A recent meta-analysis based on data from > 7,000 pregnancies reported an -association between prenatal polychlorinated biphenyl (PCB)-153 exposure and reduced birth weight. Gestational weight gain, which is associated negatively with PCB levels in maternal and cord blood, and positively with birth weight, could substantially confound this association. OBJECTIVE: We sought to estimate the influence of gestational weight gain on the association between PCB-153 exposure and birth weight using a pharmacokinetic model. METHODS: We modified a recently published pharmacokinetic model and ran Monte Carlo simulations accounting for variability in physiologic parameters and their correlations. We evaluated the pharmacokinetic model by comparing simulated plasma PCB-153 levels during pregnancy to serial measurements in 10 pregnant women from another study population. We estimated the association between simulated plasma PCB-153 levels and birth weight using linear regression models. RESULTS: The plasma PCB-153 level profiles generated with the pharmacokinetic model were comparable to measured levels in 10 pregnant women. We estimated a 118-g decrease in birth weight (95% CI: -129, -106 g) for each 1-mu g/L increase in simulated cord plasma PCB-153, compared with the 150-g decrease estimated based on the previous meta-analysis. The estimated decrease in birth weight was reduced to -6 g (95% CI: -18, 6 g) when adjusted for simulated gestational weight gain. CONCLUSION: Our findings suggest that associations previously noted between PCB levels and birth weight may be attributable to confounding by maternal weight gain during pregnancy.

  • 29.
    Wålinder, Robert
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Ernstgård, Lena
    Johanson, Gunnar
    Norbäck, Dan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience.
    Venge, Per
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Wieslander, Gunilla
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Acute effects of a fungal volatile compound2005In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 113, no 12, p. 1775-1778Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: 3-Methylfuran (3-MF) is a common fungal volatile product with active biologic properties, and previous studies have indicated a contribution to airway disease. The aim of the present study was to assess the acute health effects of this compound in humans.

    DESIGN: Acute effects were assessed via chamber exposure to (1 mg/m3) 3-MF.

    PARTICIPANTS AND MEASUREMENTS: Twenty-nine volunteers provided symptom reports, ocular electromyograms, measurement of eye tear film break-up time,vital staining of the eye, nasal lavage, acoustic rhinometry, transfer tests, and dynamic spirometry.

    RESULTS: No subjective ratings were significantly increased during exposure. Blinking frequency and the lavage biomarkers myeloperoxidase and lysozyme were significantly increased, and forced vital capacity was significantly decreased during exposure to 3-MF compared with air control. CONCLUSIONS AND RELEVANCE TO CLINICAL PRACTICE: Acute effects in the eyes, nose, and airways were detected and might be the result of the biologically active properties of 3-MF. Thus, 3-MF may contribute to building-related illness.

  • 30.
    Zhao, Zhuohui
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Occupational and Environmental Medicine.
    Zhang, Zheng
    Wang, Zhuanhua
    Ferm, Martin
    Liang, Yanling
    Norbäck, Dan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Occupational and Environmental Medicine.
    Asthmatic Symptoms among Pupils in Relation to Winter Indoor and Outdoor Air Pollution in Schools in Taiyuan, China2008In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 116, no 1, p. 90-97Article in journal (Refereed)
    Abstract [en]

    Background: There are few studies on associations between children's respiratory heath and air pollution in schools in China. The industrial development and increased traffic may affect the indoor exposure to air pollutants in school environment. Moreover, there is a need to study respiratory effects of environmental tobacco smoke (ETS) and emissions from new building materials in homes in China.

    Objectives: We studied the associations between pupils' asthmatic symptoms and indoor and outdoor air pollution in schools, as well as selected home exposures, in a coal-burning city in north China.

    Methods: A questionnaire survey was administered to pupils (11–15 years of age) in 10 schools in urban Taiyuan, collecting data on respiratory health and selected home environmental factors. Indoor and outdoor school air pollutants and climate factors were measured in winter.

    Results: A total of 1,993 pupils (90.2%) participated ; 1.8% had cumulative asthma, 8.4% wheezing, 29.8% had daytime attacks of breathlessness. The indoor average concentrations of sulfur dioxide, nitrogen dioxide, ozone, and formaldehyde by class were 264.8, 39.4, 10.1, and 2.3 µg/m3, respectively. Outdoor levels were two to three times higher. Controlling for possible confounders, either wheeze or daytime or nocturnal attacks of breathlessness were positively associated with SO2, NO2, or formaldehyde. In addition, ETS and new furniture at home were risk factors for wheeze, daytime breathlessness, and respiratory infections.

    Conclusions: Indoor chemical air pollutants of mainly outdoor origin could be risk factors for pupils' respiratory symptoms at school, and home exposure to ETS and chemical emissions from new furniture could affect pupils' respiratory health.

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