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Bornehag, Carl-GustafORCID iD iconorcid.org/0000-0003-0417-1686
Alternative names
Publications (10 of 87) Show all publications
Vandenberg, L. N., Agerstrand, M., Beronius, A., Beausoleil, C., Bergman, A., Bero, L. A., . . . Ruden, C. (2016). A proposed framework for the systematic review and integrated assessment (SYRINA) of endocrine disrupting chemicals. Environmental health, 15, Article ID 74.
Open this publication in new window or tab >>A proposed framework for the systematic review and integrated assessment (SYRINA) of endocrine disrupting chemicals
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2016 (English)In: Environmental health, ISSN 1476-069X, E-ISSN 1476-069X, Vol. 15, article id 74Article in journal (Refereed) Published
Abstract [en]

Background: The issue of endocrine disrupting chemicals (EDCs) is receiving wide attention from both the scientific and regulatory communities. Recent analyses of the EDC literature have been criticized for failing to use transparent and objective approaches to draw conclusions about the strength of evidence linking EDC exposures to adverse health or environmental outcomes. Systematic review methodologies are ideal for addressing this issue as they provide transparent and consistent approaches to study selection and evaluation. Objective methods are needed for integrating the multiple streams of evidence (epidemiology, wildlife, laboratory animal, in vitro, and in silico data) that are relevant in assessing EDCs. Methods: We have developed a framework for the systematic review and integrated assessment (SYRINA) of EDC studies. The framework was designed for use with the International Program on Chemical Safety (IPCS) and World Health Organization (WHO) definition of an EDC, which requires appraisal of evidence regarding 1) association between exposure and an adverse effect, 2) association between exposure and endocrine disrupting activity, and 3) a plausible link between the adverse effect and the endocrine disrupting activity. Results: Building from existing methodologies for evaluating and synthesizing evidence, the SYRINA framework includes seven steps: 1) Formulate the problem; 2) Develop the review protocol; 3) Identify relevant evidence; 4) Evaluate evidence from individual studies; 5) Summarize and evaluate each stream of evidence; 6) Integrate evidence across all streams; 7) Draw conclusions, make recommendations, and evaluate uncertainties. The proposed method is tailored to the IPCS/WHO definition of an EDC but offers flexibility for use in the context of other definitions of EDCs. Conclusions: When using the SYRINA framework, the overall objective is to provide the evidence base needed to support decision making, including any action to avoid/minimise potential adverse effects of exposures. This framework allows for the evaluation and synthesis of evidence from multiple evidence streams. Finally, a decision regarding regulatory action is not only dependent on the strength of evidence, but also the consequences of action/inaction, e.g. limited or weak evidence may be sufficient to justify action if consequences are serious or irreversible.

Place, publisher, year, edition, pages
BioMed Central, 2016
Keyword
Endocrine disrupting chemicals, Systematic review, Study evaluation, Strength of evidence, Weight of evidence, Adverse effect, Endocrine disrupting activity, Evidence integration, Epidemiology, In vivo
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Research subject
Public Health Science
Identifiers
urn:nbn:se:kau:diva-44664 (URN)10.1186/s12940-016-0156-6 (DOI)000379994300001 ()27412149 (PubMedID)
Available from: 2016-08-12 Created: 2016-08-12 Last updated: 2017-12-06Bibliographically approved
Wang, I.-J., Chen, C.-Y. & Bornehag, C.-G. (2016). Bisphenol A exposure may increase the risk of development of atopic disorders in children. International journal of hygiene and environmental health (Print), 219(3), 311-316
Open this publication in new window or tab >>Bisphenol A exposure may increase the risk of development of atopic disorders in children
2016 (English)In: International journal of hygiene and environmental health (Print), ISSN 1438-4639, E-ISSN 1618-131X, Vol. 219, no 3, p. 311-316Article in journal (Refereed) Published
Abstract [en]

Background: Little is known about the effect of Bisphenol A (BPA) on atopic disorders. Objective: To investigated the associations (i) between postnatal BPA exposure and allergic diseases in children; (ii) between BPA and IgE levels for the possible disease pathogenesis; and (iii) gender-based differences. Methods: A total of 453 children from Childhood Environment and Allergic Diseases Study cohort with urine and blood samples were recruited in Taiwan. Urinary BPA glucoronide (BPAG) levels were measured by UPLC-MS/MS at ages 3 and 6 years. The associations between BPAG levels at different ages and IgE levels and the development of allergic diseases were evaluated by multivariate linear regression and logistic regression. A mediation analysis was also conducted to evaluate how much risk of allergic diseases in relation to BPA exposure is explained by IgE changes. Results: The BPAG levels at age 3 were positively associated with IgE levels at age 3 (beta = 64.85 kU/l per In-unit increase BPAG level; 95% Cl, 14.59-115.11 kU/l). Stratified by gender, BPAG levels at age 3 were positively associated with IgE levels at age 3, particularly in girls (beta = 139.23 kW; 95% Cl, 57.38-221.09 kU/l). Similar results were also found at age 6. Urinary BPAG levels at age 3 were significantly associated with asthma at ages 3 and 6, with OR (95%CI) of 1.29(1.08-1.55) and 1.27(1.04-1.55). We estimated that 70% of the total effect of BPA exposure on asthma is mediated by IgE levels. Conclusions: BPA exposures were associated with IgE levels and may increase the risk of development of allergic diseases in children particularly in girls.

Keyword
Allergic diseases, Bisphenol A, Children, Gender, IgE levels
National Category
Health Sciences
Research subject
Public Health Science
Identifiers
urn:nbn:se:kau:diva-42051 (URN)10.1016/j.ijheh.2015.12.001 (DOI)000374198800010 ()26765087 (PubMedID)
Available from: 2016-05-18 Created: 2016-05-18 Last updated: 2017-12-06Bibliographically approved
Choi, H., Schmidbauer, N. & Bornehag, C.-G. (2016). Non-microbial sources of microbial volatile organic compounds. Environmental Research, 148, 127-136
Open this publication in new window or tab >>Non-microbial sources of microbial volatile organic compounds
2016 (English)In: Environmental Research, ISSN 0013-9351, E-ISSN 1096-0953, Vol. 148, p. 127-136Article in journal (Refereed) Published
Abstract [en]

Background: The question regarding the true sources of the purported microbial volatile organic compounds (MVOCs) remains unanswered. Objective: To identify microbial, as well as non-microbial sources of 28 compounds, which are commonly accepted as microbial VOCs (i.e. primary outcome of interest is Sigma 28 VOCs). Methods: In a cross-sectional investigation of 390 homes, six building inspectors assessed water/mold damage, took air and dust samples, and measured environmental conditions (i.e., absolute humidity (AH, g/m(3)), temperature (degrees C), ventilation rate (ACH)). The air sample was analyzed for volatile organic compounds (mu g/m(3)) and; dust samples were analyzed for total viable fungal concentration (CFU/g) and six phthalates (mg/g dust). Four benchmark variables of the underlying sources were defined as highest quartile categories of: 1) the total concentration of 17 propylene glycol and propylene glycol ethers (Sigma 17 PGEs) in the air sample; 2) 2,2,4-trimethyl-1,3-pentanediol monoisobutyrate (TMPD-MIB) in the air sample; 3) semi-quantitative mold index; and 4) total fungal load (CFU/g). Results: Within severely damp homes, co-occurrence of the highest quartile concentration of either E17 PGEs or TMPD-MIB were respectively associated with a significantly higher median concentration of Sigma 28 VOCs (8.05 and 1338 mu g/m(3), respectively) compared to the reference homes (430 and 4.86 mu g/m(3), respectively, both Ps <= 0.002). Furthermore, the homes within the highest quartile range for Sigma fungal load as well as AH were associated with a significantly increased median Sigma 28 VOCs compared to the reference group (8.74 vs. 4.32 mu g/m(3), P=0.001). Within the final model of multiple indoor sources on E 28 VOCs, one natural log-unit increase in summed concentration of Sigma 17 PGEs, plus TMPD-MIB (Sigma 17 PGEs TMPD-MIB) was associated with 1.8-times (95% CI, 1.3-2.5), greater likelihood of having a highest quartile of Sigma 28 VOCs, after adjusting for absolute humidity, history of repainting at least one room, ventilation rate, and mold index (P-value =0.001). Homes deemed severely mold damaged (i.e., mold index =1) were associated with 1.7-times (95% CI, 0.8-3.6), greater likelihood of having a highest quartile of Sigma 28 VOCs, even though such likelihood was not significant (P-value =0.164). In addition, absolute humidity appeared to positively interact with mold index to significantly elevate the prevalence of the highest quartile category of Sigma 28 VOCs. Conclusion: The indoor concentration of Sigma 28 VOCs, which are widely accepted as MVOCs, are significantly associated with the markers of synthetic (i.e. E17 PGEs and TMPD-MIB), and to less extent, microbial (i.e., mold index) sources. (C) 2016 Elsevier Inc. All rights reserved.

Keyword
Indoor, Asthma, Allergies, Dampness, Mold, Paint
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Research subject
Public Health Science
Identifiers
urn:nbn:se:kau:diva-44548 (URN)10.1016/j.envres.2016.03.026 (DOI)000376712800016 ()27043176 (PubMedID)
Available from: 2016-08-04 Created: 2016-08-04 Last updated: 2017-12-06Bibliographically approved
Jernbro, C., Janson, S. & Bornehag, C.-G. (2015). Barns liv och hälsa i Värmland 2014.
Open this publication in new window or tab >>Barns liv och hälsa i Värmland 2014
2015 (Swedish)Report (Other (popular science, discussion, etc.))
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:kau:diva-35412 (URN)978-91-7063-628-8 (ISBN)
Available from: 2015-03-20 Created: 2015-03-20 Last updated: 2015-12-28
Ma, P., Liu, X., Wu, J., Yan, B., Zhang, Y., Lu, Y., . . . Yang, X. (2015). Cognitive deficits and anxiety induced by diisononyl phthalate in mice and the neuroprotective effects of melatonin. Scientific Reports, 5, Article ID 14676.
Open this publication in new window or tab >>Cognitive deficits and anxiety induced by diisononyl phthalate in mice and the neuroprotective effects of melatonin
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2015 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 5, article id 14676Article in journal (Refereed) Published
Abstract [en]

Diisononyl phthalate (DINP) is a plasticizer that is frequently used as a substitute for other plasticizers whose use is prohibited in certain products. In vivo studies on the neurotoxicity of DINP are however, limited. This work aims to investigate whether DINP causes neurobehavioral changes in mice and to provide useful advice on preventing the occurrence of these adverse effects. Behavioral analysis showed that oral administration of 20 or 200â mg/kg/day DINP led to mouse cognitive deficits and anxiety. Brain histopathological observations, immunohistochemistry assays (cysteine-aspartic acid protease 3 [caspase-3], glial fibrillary acidic protein [GFAP]), oxidative stress assessments (reactive oxygen species [ROS], glutathione [GSH], superoxide dismutase [SOD] activities, 8-hydroxy-2-deoxyguanosine [8-OH-dG] and DNA-protein crosslinks [DPC]), and assessment of inflammation (tumor necrosis factor alpha [TNF-Crossed D sign°[ and interleukin-1 beta [IL-1β]) of mouse brains showed that there were histopathological alterations in the brain and increased levels of oxidative stress, and inflammation for these same groups. However, some of these effects were blocked by administration of melatonin (50â mg/kg/day). Down-regulation of oxidative stress was proposed to explain the neuroprotective effects of melatonin. The data suggests that DINP could cause cognitive deficits and anxiety in mice, and that melatonin could be used to avoid these adverse effects.

Place, publisher, year, edition, pages
Nature Publishing Group, 2015
Keyword
Immunohistochemistry, Risk factors
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Research subject
Public Health Science
Identifiers
urn:nbn:se:kau:diva-42349 (URN)10.1038/srep14676 (DOI)000362087500001 ()2-s2.0-84942938338 (Scopus ID)
Available from: 2016-06-07 Created: 2016-05-23 Last updated: 2017-12-06Bibliographically approved
Deng, Q., Lu, C., Norback, D., Bornehag, C.-G., Zhang, Y., Liu, W., . . . Sundell, J. (2015). Early life exposure to ambient air pollution and childhood asthma in China. Environmental Research, 143, 83-92
Open this publication in new window or tab >>Early life exposure to ambient air pollution and childhood asthma in China
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2015 (English)In: Environmental Research, ISSN 0013-9351, E-ISSN 1096-0953, Vol. 143, p. 83-92Article in journal (Refereed) Published
Abstract [en]

Background: Early life is suggested to be a critical time in determining subsequent asthma development, but the extent to which the effect of early-life exposure to ambient air pollution on childhood asthma is unclear. Objectives: We investigated doctor-diagnosed asthma in preschool children due to exposure to ambient air pollution in utero and during the first year of life. Methods: In total 2490 children aged 3-6 years participated in a questionnaire study regarding doctor-diagnosed asthma between September 2011 and January 2012 in China. Children's exposure to critical air pollutants, sulfur dioxide (SO2) as proxy of industrial air pollution, nitrogen dioxide (NO2) as proxy of traffic pollution, and particulate matter <= 10 mu m in diameter (PM10) as a mixture, was estimated from the concentrations measured at the ambient air quality monitoring stations by using an inverse distance weighted (IDW) method. Logistic regression analysis was employed to determine the relationship between early-life exposure and childhood asthma in terms of odds ratio (OR) and 95% confidence interval (CI). Results: Association between early-life exposure to air pollutants and childhood asthma was observed. SO2 and NO2 had significant associations with adjusted OR (95% CI) of 1.45 (1.02-2.07) and 1.74 (1.15-2.62) in utero and 1.62 (1.01-2.60) and 1.90 (1.20-3.00) during the first year for per 50 mu g/m(3) and 15 mu g/m(3) increase respectively. Exposure to the combined high level of SO2 and NO2 in China significantly elevated the asthmatic risk with adjusted OR (95% CI) of 1.76 (1.18-2.64) in utero and 1.85 (1.22-2.79) during the first year compared to the low level exposure. The associations were higher for males and the younger children aged 3-4 than females and the older children aged 5-6. Conclusions: Early-life exposure to ambient air pollution is associated with childhood asthma during which the level and source of air pollution play important roles. The high level and nature of combined industrial and traffic air pollution in China may contribute to the recent rapid increase of childhood asthma. (C) 2015 Elsevier Inc. All rights reserved.

Keyword
Asthma, Children, In utero, Pregnancy, First year of life, Sulfur dioxide, Nitrogen dioxide, Particulate matter
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Research subject
Public Health Science
Identifiers
urn:nbn:se:kau:diva-40767 (URN)10.1016/j.envres.2015.09.032 (DOI)000365831400011 ()26453943 (PubMedID)
Available from: 2016-03-02 Created: 2016-03-02 Last updated: 2017-11-30Bibliographically approved
Tang, J., Yuan, Y., Wei, C., Liao, X., Yuan, J., Nånberg, E., . . . Yang, X. (2015). Neurobehavioral changes induced by di(2-ethylhexyl) phthalate and the protective effects of vitamin E in Kunming mice. Toxicology research, 4(4), 1006-1015
Open this publication in new window or tab >>Neurobehavioral changes induced by di(2-ethylhexyl) phthalate and the protective effects of vitamin E in Kunming mice
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2015 (English)In: Toxicology research, ISSN 2045-452X, Vol. 4, no 4, p. 1006-1015Article in journal (Refereed) Published
Abstract [en]

Di(2-ethylhexyl) phthalate (DEHP) is a plasticizer commonly used in PVC that may leach into the environment, and has been shown to adversely affect the health of humans and animals. We undertook a study to ascertain the neurotoxicity of DEHP in Kunming mice. This study included three rounds of testing. In the first round, Kunming mice were exposed to different concentrations of DEHP (0, 5, 50, 500 mg kg(-1) per day) after which their cognitive ability was assessed using the Morris water maze (MWM) test. The reactive oxygen species (ROS) content in tissue and the malondialdehyde (MDA) content of brains were also measured. In the second round, vitamin E (50 mg kg(-1) per day) was given daily as an anti-oxidant via the intragastric route. Cognitive deficits and locomotor activity, as well as ROS and MDA contents were tested employing the same methods. In the third round, the depressive mood of mice after DEHP exposure (500 mg kg(-1) per day) was measured using the open field test, the tail suspension test, and the forced swim test. The main findings of this study include: (1) a statistical association exists between DEHP oral exposure and spatial learning (DEHP 500 mg kg(-1) per day) and memory (DEHP 50 mg kg(-1) per day) dysfunction as ascertained by an MWM test of Kunming mice. (2) A statistical association was also found between DEHP oral exposure (50 and 500 mg kg(-1) per day) and oxidative stress (ROS and MDA) of mouse brain tissue. (3) Co-administration of vitamin E (50 mg kg(-1) per day) diminishes the elevation of ROS and MDA induced by DEHP (50 mg kg(-1) per day) from significant levels to non-significant levels. (4) Co-administration of vitamin E (50 mg kg(-1) per day) protects against mouse memory dysfunction induced by DEHP (50 mg kg(-1) per day) from being significant to being not significant. (5) In the 5 mg kg(-1) per day DEHP exposure groups, oxidative stress in brain tissue, and neurobehavioral changes were not found. (6) High dose DEHP exposure (500 mg kg(-1) per day) may induce behavioral despair in mice. Conclusions: These data suggest that DEHP is neurotoxic with regard to cognitive ability and locomotor activity.

Place, publisher, year, edition, pages
Royal Society of Chemistry, 2015
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Research subject
Public Health Science
Identifiers
urn:nbn:se:kau:diva-41647 (URN)10.1039/c4tx00250d (DOI)000356612300023 ()
Available from: 2016-04-11 Created: 2016-04-11 Last updated: 2016-05-12Bibliographically approved
Bornehag, C.-G. (2015). Phthalate exposure heralds birth defects. TrAC. Trends in analytical chemistry, 64, pp. VI-VI
Open this publication in new window or tab >>Phthalate exposure heralds birth defects
2015 (English)In: TrAC. Trends in analytical chemistry, ISSN 0165-9936, E-ISSN 1879-3142, Vol. 64, p. VI-VIArticle in journal, News item (Other academic) Published
Place, publisher, year, edition, pages
Amsterdam, Netherlands: Elsevier, 2015
National Category
Occupational Health and Environmental Health Public Health, Global Health, Social Medicine and Epidemiology
Research subject
Public Health Science
Identifiers
urn:nbn:se:kau:diva-41661 (URN)000349278500002 ()
Available from: 2016-04-11 Created: 2016-04-11 Last updated: 2018-01-10Bibliographically approved
Bornehag, C.-G., Carlstedt, F., Jonsson, B. A. G., Lindh, C. H., Jensen, T. K., Bodin, A., . . . Swan, S. H. (2015). Prenatal Phthalate Exposures and Anogenital Distance in Swedish Boys. Journal of Environmental Health Perspectives, 123(1), 101-107
Open this publication in new window or tab >>Prenatal Phthalate Exposures and Anogenital Distance in Swedish Boys
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2015 (English)In: Journal of Environmental Health Perspectives, ISSN 0091-6765, E-ISSN 1552-9924, Vol. 123, no 1, p. 101-107Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Phthalates are used as plasticizers in soft polyvinyl chloride (PVC) and in a large number of consumer products. Because of reported health risks, diisononyl phthalate (DiNP) has been introduced as a replacement for di(2-ethylhexyl) phthalate (DEHP) in soft PVC. This raises concerns because animal data suggest that DiNP may have antiandrogenic properties similar to those of DEHP. The anogenital distance (AGD)-the distance from the anus to the genitals-has been used to assess reproductive toxicity. OBJECTIVE: The objective of this study was to examine the associations between prenatal phthalate exposure and AGD in Swedish infants. METHODS: AGD was measured in 196 boys at 21 months of age, and first-trimester urine was analyzed for 10 phthalate metabolites of DEP (diethyl phthalate), DBP (dibutyl phthalate), DEHP, BBzP (benzylbutyl phthalate), as well as DiNP and creatinine. Data on covariates were collected by questionnaires. RESULTS: The most significant associations were found between the shorter of two AGD measures (anoscrotal distance; AGDas) and DiNP metabolites and strongest for oh-MMeOP [mono(4-methyl-7-hydroxyloctyl) phthalate] and oxo-MMeOP [mono-(2-ethyl-5-oxohexyl) phthalate]. However, the AGDas reduction was small (4%) in relation to more than an interquartile range increase in DiNP exposure. CONCLUSIONS: These findings call into question the safety of substituting DiNP for DEHP in soft PVC, particularly because a shorter male AGD has been shown to relate to male genital birth defects in children and impaired reproductive function in adult males and the fact that human levels of DiNP are increasing globally.

Keyword
Endocrine disrupting chemicals; in-utero exposure; male-rat; diisononyl phthalate; perinatal exposure; sexual development; gene-expression; dose-response; male infants; house-dust
National Category
Occupational Health and Environmental Health Public Health, Global Health, Social Medicine and Epidemiology
Research subject
Public Health Science
Identifiers
urn:nbn:se:kau:diva-41664 (URN)10.1289/ehp.1408163 (DOI)000347385000020 ()25353625 (PubMedID)
Available from: 2016-04-11 Created: 2016-04-11 Last updated: 2018-01-10Bibliographically approved
Choi, H., Thorne, P. & Bornehag, C.-G. (2015). Response to Miller [Letter to the editor]. Indoor Air, 25(1), 117-117
Open this publication in new window or tab >>Response to Miller
2015 (English)In: Indoor Air, ISSN 0905-6947, E-ISSN 1600-0668, Vol. 25, no 1, p. 117-117Article in journal, Letter (Other academic) Published
Place, publisher, year, edition, pages
Hoboken, USA: Wiley-Blackwell, 2015
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Research subject
Public Health Science
Identifiers
urn:nbn:se:kau:diva-41639 (URN)10.1111/ina.12131 (DOI)000348115500013 ()25594132 (PubMedID)
Available from: 2016-04-11 Created: 2016-04-11 Last updated: 2017-10-24Bibliographically approved
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ORCID iD: ORCID iD iconorcid.org/0000-0003-0417-1686

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