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| 2. |
- Claeson, Anna-Sara, 1974-, et al.
(författare)
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Symptoms from masked acrolein exposure suggest altered trigeminal reactivity in chemical intolerance
- 2017
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Ingår i: Neurotoxicology. - : Elsevier. - 0161-813X .- 1872-9711. ; 60, s. 92-98
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Tidskriftsartikel (refereegranskat)abstract
- Background: Chemical intolerance (CI) is a widespread occupational and public health problem characterized by symptoms that reportedly result from low-levels of chemical exposure. The mechanisms behind CI are unknown, however modifications of the chemical senses (rather than toxic processes) have been suggested as key components. The aim of this study was to investigate whether individuals with self-reported CI report more sensory irritation during masked acrolein exposure compared to controls without CI. Methods: Individuals with CI (n = 18) and controls without CI (n = 19) were exposed in an exposure chamber. Each participant took part in two exposure conditions – one with heptane (the masking compound), and one with heptane and acrolein at a dose below previously reported sensory irritation thresholds. The exposures lasted for 60 min. Symptoms and confidence ratings were measured continuously throughout the exposure as were measurements of electrodermal activity and self-reported tear-film break-up time. Participants were blind to exposure condition. Results: Individuals with CI, compared with controls reported greater sensory irritation in the eyes, nose and throat when exposed to acrolein masked with heptane. There was no difference during exposure to heptane. Conclusions: Masked exposure to acrolein at a concentration below the previously reported detection threshold is perceived as more irritating by individuals with CI compared with controls. The results indicate that there is altered trigeminal reactivity in those with CI compared to controls.
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| 3. |
- Feiler, Marina Oktapodas, et al.
(författare)
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The association between early-life relative telomere length and childhood neurodevelopment
- 2018
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Ingår i: NeuroToxicology. - : Elsevier BV. - 0161-813X .- 1872-9711. ; 65, s. 22-27
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: To examine the association between telomere length and neurodevelopment in children. Methods: We examined the relationship between relative telomere length (rTL) and neurodevelopmental outcomes at 9 and 30 months, and 5 years of age in children enrolled in the Seychelles Child Development Study Nutrition Cohort 1 (NC1). Relative telomere length was measured in cord blood and in child blood at age five. Multivariable linear regression examined associations between neurodevelopmental outcomes and rTL adjusting for relevant covariates. Results: Mean rTL was 1.18 at birth and 0.71 at age five. Increased cord blood rTL was associated with better scores on two neurodevelopmental tests, the psychomotor developmental index (β = 4.01; 95% confidence interval (CI) = 0.17, 7.85) at age 30 months, and the Woodcock Johnson test of achievement letter-word score (β = 2.88; CI = 1.21–4.56) at age five. The Woodcock Johnson test of achievement letter-word score remained statistically significant after two outliers were excluded (β = 2.83; CI = 0.69, 4.97); the psychomotor developmental index did not (β = 3.62; CI = −1.28, 8.52). None of the neurodevelopmental outcomes at age five were associated with five-year rTL. Conclusion: Although increased cord blood rTL was associated with better test scores for a few neurodevelopmental outcomes, this study found little consistent evidence of an association between rTL and neurodevelopment. Future studies with a larger sample size, longer follow-up, and other relevant biological markers (e.g. oxidative stress) are needed to clarify the role of rTL in neurodevelopment and its relevance as a potential surrogate measure for oxidative stress in the field of developmental neurotoxicity.
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| 5. |
- Legrand, M., et al.
(författare)
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Cell proliferation and cell death are disturbed during prenatal and postnatal brain development after uranium exposure
- 2016
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Ingår i: Neurotoxicology. - : Elsevier BV. - 0161-813X .- 1872-9711. ; 52, s. 34-45
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Tidskriftsartikel (refereegranskat)abstract
- The developing brain is more susceptible to neurotoxic compounds than adult brain. It is also well known that disturbances during brain development cause neurological disorders in adulthood. The brain is known to be a target organ of uranium (U) exposure and previous studies have noted that internal U contamination of adult rats induces behavioral disorders as well as affects neurochemistry and neurophysiological properties. In this study, we investigated whether depleted uranium (DU) exposure affects neurogenesis during prenatal and postnatal brain development. We examined the structural morphology of the brain, cell death and finally cell proliferation in animals exposed to DU during gestation and lactation compared to control animals. Our results showed that DU decreases cell death in the cortical neuroepithelium of gestational day (GD) 13 embryos exposed at 40 mg/L and 120 mg/L and of GD18 fetuses exposed at 120 mg/L without modification of the number of apoptotic cells. Cell proliferation analysis showed an increase of BrdU labeling in the dentate neuroepithelium of fetuses from GD18 at 120 mg/L. Postnatally, cell death is increased in the dentate gyrus of postnatal day (PND) 0 and PND5 exposed pups at 120 mg/L and is associated with an increase of apoptotic cell number only at PND5. Finally, a decrease in dividing cells is observed in the dentate gyrus of PND21 rats developmentally exposed to 120 mg/L DU, but not at PNDO and PND5. These results show that DU exposure during brain development causes opposite effects on cell proliferation and cell death processes between prenatal and postnatal development mainly at the highest dose. Although these modifications do not have a major impact in brain morphology, they could affect the next steps of neurogenesis and thus might disrupt the fine organization of the neuronal network.
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| 6. |
- Legrand, M., et al.
(författare)
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Exposure to depleted uranium during development affects neuronal differentiation in the hippocampal dentate gyrus and induces depressive-like behavior in offspring
- 2016
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Ingår i: Neurotoxicology. - : Elsevier BV. - 0161-813X .- 1872-9711. ; 57, s. 153-162
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Tidskriftsartikel (refereegranskat)abstract
- The developing brain is known to be sensitive to uranium (U) and exposure to this element during postnatal brain development results in behavioral disorders in adulthood. Moreover, we have previously shown that U exposure during gestation and lactation affects neurogenesis, in particular neural cell proliferation and cell death. In this study, we investigated whether exposure to depleted U (DU) affects neuronal differentiation during prenatal and postnatal brain development. We assessed in situ expression of specific genes involved in neuronal differentiation and expression of neuronal protein markers. The effects of DU on neurobehavioral function were investigated in parallel. Neuronal differentiation involves many signaling pathways that regulate the balance between cell proliferation and the transition to neuronal differentiation. In the present study pregnant rats were exposed from gestational day (GD) 1 throughout lactation to postnatal day (PND) 21. Using in situ hybridization, our results show decreased expression of Wnt3a in the hippocampal neuroepithelium in GD 13 embryos from DU exposed dams and decreased expression of Notch1 and increased expression of Mash1 in the hippocampal and dentate neuroepithelia of GD 18 fetuses from DU exposed dams. Expression of the NeuroD and NeuroD2 genes was not modified in the hippocampal neuroepithelium of GD18 fetuses from DU exposed dams. There was no change in the expression of any of these genes in the dentate gyrus of PND 5 pups from DU exposed dams. No change in nestin or doublecortin immunestaining was observed in the prenatal or early postnatal stages. However, the number of doublecortin-positive cells increased in the granular cell layer of PND 21 pups from DU exposed dams. Finally, depressive-like behavior was induced in PND21 rats, without modification of locomotor and exploratory activities or of spatial memory. In conclusion, these results showed that exposure of pregnant and lactating rats to DU affects brain development by causing disturbed cell proliferation and neuronal differentiation at the prenatal stage. Moreover, this exposure increased the pool of immature neurons in the dentate gyrus and induced depressive-like behavior in neonatal rats. Therefore, these data strongly suggest that exposure to DU during gestation and lactation affects brain development in embryos, fetuses and neonates with behavioral consequences in the offspring.
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| 9. |
- Wahlberg, Karin, et al.
(författare)
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Polymorphisms in manganese transporters show developmental stage and sex specific associations with manganese concentrations in primary teeth
- 2018
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Ingår i: NeuroToxicology. - : Elsevier BV. - 0161-813X .- 1872-9711. ; 64, s. 103-109
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Tidskriftsartikel (refereegranskat)abstract
- Background: Manganese (Mn) is an essential metal that can become neurotoxic at elevated levels with negative consequences on neurodevelopment. We have evaluated the influence of single nucleotide polymorphisms (SNPs) in Mn transporter genes SLC30A10 and SLC39A8 on Mn concentrations in dentine, a validated biomarker that reflects Mn tissue concentrations early in life. Methods: The study included 195 children with variable environmental Mn exposure. Mn concentrations in dentine representing fetal, early postnatal and early childhood developmental periods were measured using laser ablation-inductively coupled plasma mass spectrometry. SLC30A10 rs12064812 (T/C) and SLC39A8 rs13107325 (C/T) were genotyped by TaqMan real time PCR and SLC30A10 rs1776029 (G/A) by pyrosequencing; and SNPs were analyzed in association with Mn in dentine. Results: SLC39A8 rs13107325 rare allele (T) carriers had significantly higher Mn concentrations in postnatal dentine (110%, p = 0.008). For all SNPs we also observed non-significant associations with Mn concentrations in dentine in opposite directions for fetal and early postnatal periods. Furthermore, there were significant differences in the influence of SLC30A10 rs1776929 genotypes on Mn concentrations in dentine between sexes. Discussion: The findings from this study indicate that common SNPs in Mn transporters influence Mn homeostasis in early development and may therefore be important to consider in future studies of early life Mn exposure and health effects. Our results also suggest that the influence of these transporters on Mn regulation may differ by developmental stage, as well as between girls and boys.
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| 10. |
- Yi-Ting, Lin, et al.
(författare)
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Indole-3 acetic acid increased risk of impaired cognitive function in patients receiving hemodialysis
- 2019
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Ingår i: Neurotoxicology. - : Elsevier BV. - 0161-813X .- 1872-9711. ; 73, s. 85-91
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Tidskriftsartikel (refereegranskat)abstract
- Patients receiving hemodialysis (HD) have a higher risk of cognitive impairment and dementia than the general population. The accumulation of uremic toxins in the brain causes uremic encephalopathy, however, limited data exists to elucidate the effect of protein-bound uremic toxins on cognitive function. Here we investigate the effect of indole-3 acetic acid (IAA) and hippuric acid (HA), two different protein-bound uremic toxins from amino acid derivatives, on cognitive function by Silico and in a clinical study. Prevalent HD patients were enrolled in two independent hospitals. Serum IAA and HA were measured using mass spectrometry. Cognitive performance was measured using Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), and Cognitive Abilities Screening Instrument (CASI) by trained psychologists. Using silico data to predict the effect of blood-brain barrier penetration was performed. The silico data demonstrated that IAA and HA had positive blood-brain barrier penetration ability. Amongst the 230 HD patients, serum IAA was associated with poor MMSE score (beta = -0.90, 95% CI -1.61 to -0.19) and poor CASI score (beta = -3.29, 95% CI -5.69 to -0.88) in stepwise multiple linear regression analysis. In logistic regression model, Serum IAA was also associated with cognitive impairment based on MMSE definition (OR, 1.96, 95% CI 1.10, 3.5) and CASI definition (OR, 2.09, 95% CI 1.21, 3.61). There was no correlation between Serum HA levels and cognitive function status. In conclusion, IAA, not HA, was associated with cognitive impairment in HD patients. Further large scale and prospective studies are needed to confirm our findings.
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| 14. |
- Till, Christine, et al.
(författare)
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Caregiving and infants' neurodevelopment in rural Costa Rica : Results from the Infants’ Environmental Health Study (ISA)
- 2019
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Ingår i: NeuroToxicology. - : Elsevier BV. - 0161-813X. ; 74, s. 100-107
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Tidskriftsartikel (refereegranskat)abstract
- Early caregiving is one of the strongest influences on children's development, and among the most significant modifiable environmental factor. The aim of this study was to explore the association between quality of caregiver-infant interactions and neurodevelopment of infants living in banana-growing communities in rural Costa Rica characterized as having environmental toxic exposures. Home visits were conducted with 94 caregiver-infant dyads from the Infants’ Environmental Health Study (ISA), living within Matina county, Limón province. One-year infant neurodevelopmental outcomes were assessed using the Bayley Scales of Infant and Toddler Development®, Third Edition (Bayley-III). Quality of caregiver-infant interaction was assessed with a standardized observational task: Nursing Child Assessment Satellite Training Teaching scale (NCATS) at around two years of age. Multiple regression analyses examined associations between components of caregiver-infant interactions and neurodevelopmental outcomes, adjusting for mancozeb and manganese exposure and other potential confounders. Compared to NCATS normative data for U.S. Hispanic mothers, 35% of the sample had overall caregiving interaction scores ≤10th percentile cut-off, indicating less than optimal interactions. Higher quality of caregiver-infant interaction was associated with higher expressive communication ability in infants [ß = 0.03 (95% CI: 0.01, 0.06)], controlling for pesticide exposure and confounders. Aspects of caregiving such as stimulation and growth-fostering of infants were most strongly associated with language outcomes. Results suggest an association between positive caregiving on language development for infants living in a rural agricultural area in Costa Rica, and highlight aspects of caregiving that could be targeted to improve resilience of these children who live in vulnerable conditions.
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