1,721,805 research outputs found
Hallmarks of Environmental Insults
No full textEnvironmental insults impair human health around the world. Contaminated air, water, soil and food, occupational and household settings expose humans of all ages to a plethora of chemicals and environmental stressors. We propose eight hallmarks of environmental insults which jointly underpin the damaging impact of environmental exposures during the life-span. Specifically, they include oxidative stress and inflammation, genomic alterations and mutations, epigenetic alterations, mitochondrial dysfunction, endocrine disruption, altered intercellular communication, altered microbiome communities, and impaired nervous system function. They provide a framework to understand why complex mixtures of environmental exposures induce severe health effects even at relatively modest concentrations
Levels of the hemoglobin adduct N-(2,3-Dihydroxypropyl)-valine in cord and maternal blood: Prenatal transfer of glycidol in the ENVIRONAGE birth cohort
No full textBACKGROUND: Glycidol, a probable human carcinogen, is a reactive chemical released in the gastrointestinal tract from glycidyl fatty acid esters, which are heat-induced dietary contaminants. OBJECTIVES: To investigate the prenatal transfer of glycidol, a specific hemoglobin adduct was measured as a biomarker for internal glycidol exposure in paired cord and maternal blood samples. METHODS: In 100 mother-newborn pairs from the Belgian ENVIRONAGE (ENVIRonmental influence ON AGEing in early life) birth cohort, we studied the correlation between levels of the glycidol-derived hemoglobin adduct N-(2,3-dihydroxypropyl)-valine (2,3-diHOPr-Val) in paired cord and maternal blood samples. The adduct levels were determined after cleavage with a modified Edman degradation by using ultra-high performance liquid chromatography-tandem mass spectrometry and an isotope-labeled reference standard. RESULTS: 2,3-DiHOPr-Val was detectable in all 100 maternal blood samples and in 96 cord blood samples (LOD =0.5 pmol 2,3-diHOPr-Val/g hemoglobin), with medians of 5.4 (range: 2.3-29.2) and 1.6 (range: LOD - 8.9) pmol/g hemoglobin), respectively. In blood samples of mothers who smoked during pregnancy and in the cord blood samples of their newborns (n = 6), the median 2,3-diHOPr-Val levels were 16.7 (range: 6.4-29.2) and 6.2 (range: LOD - 8.6) pmol/g hemoglobin, respectively. The median ratio of 2,3-diHOPr-Val levels of cord to maternal blood was 0.35 (range: 0.19-1.14) (n = 49). The Spearman correlation coefficient between 2,3-diHOPr-Val levels in cord and maternal blood samples was 0.63 (p < 0.001) among all mother-newborn pairs and 0.59 (p < 0.001) among mother-newborn pairs of non-smoking mothers. DISCUSSION: Maternal data confirm widespread exposure to glycidol, also in non-smokers. Neonatal levels indicate prenatal exposure to glycidol, due to an obviously relatively unhindered passive transfer through the placental barrier. Possible health effects of fetal (and postnatal) glycidol exposure in children may be addressed in epidemiological studies.sponsorship: The ENVIRONAGE birth cohort is supported by grants from the European Research Council (ERC-2012-StG310898) and the Research Foundation - Flanders (FWO, 1516112N/G.0873.11.N.10). Janneke Hogervorst was partly funded by a postdoctoral research fellow grant from the Research Foundation - Flanders (FWO) (no. 12J9516N). (European Research Council|ERC-2012-StG310898, Research Foundation - Flanders (FWO)|1516112N/G.0873.11.N.10, Research Foundation - Flanders (FWO)|12J9516N)status: Publishe
Dynamics of skin microvascular blood flow in 4-6-years-old children in association with prenatal and childhood air pollution exposure
No full textDynamics of skin microvascular blood flow in 4-6-years-old children in association with prenatal and childhood air pollution exposure
No full textGestational acrylamide exposure and biomarkers of fetal growth: Probing the mechanism underlying the association between acrylamide and reduced fetal growth
No full textIntroduction: Four epidemiological studies have shown a negative association between prenatal acrylamide exposure and birth size. In order to shed light on the possible underlying mechanism(s), we analysed associations between acrylamide biomarkers and biomarkers related to fetal growth. Methods: In newborns of the ENVIRONAGE birth cohort (n ranges from 215 to 434), we investigated the association between prenatal acrylamide exposure (acrylamide and glycidamide hemoglobin adduct levels in cord blood) and thyroid hormones (TSH, T3, T4 and the ratio of T4 to T3 in cord plasma), insulin-related factors (cord plasma insulin and IGF1, and placental IGF2), neurotrophins (cord plasma BDNF, and placental NGF, NT3 and NT4), and cord plasma homocysteine and progesterone, using multiple linear regression analysis. In addition, we investigated whether the biomarkers mediated the associations between prenatal acrylamide exposure and birth outcomes. Results: We observed lower cord plasma TSH (−10.2% [95% CI: −15.0, −4.3]) and higher placental NGF levels (10.0% [95% CI 3.7, 17.4]) for a twofold increase of acrylamide adducts, a decrease in the ratio of cord plasma free T4 and free T3 with higher acrylamide and glycidamide adducts of −2.9% (95% CI: −5.7, −0.1) and −3.9% (95% CI: −6.2, −1.6) for a twofold increase in acrylamide and glycidamide adduct levels, respectively, and higher cord plasma free T3 with increases in both acrylamide and glycidamide adducts of 2.8% (95% CI: 0.2, 5.6) and 3.6% (95% CI: 0.8, 6.6) for a twofold increase in acrylamide and glycidamide adduct levels, respectively. Additionally, a twofold increase in glycidamide adducts was associated with lower cord plasma insulin levels, particularly among newborns of non-smoking mothers (−11.2% [95% CI: −19.5, −0.1]).Cord plasma insulin seemed to mediate the association between glycidamide adducts and birth weight. Conclusions: A decrease in cord plasma insulin levels may be (a marker of) a mechanism by which gestational acrylamide exposure is associated with decreased fetal growth. The possible health consequences of the associations between gestational acrylamide exposure and thyroid hormones and neurotrophins warrant future study
Omgeving en leefstijfactoren: al vroeg in het leven van invloed op telomeerlengte
No full textTelomeren zij n de beschermende uiteinden van chromosomen en nemen in lengte af naarmate we verouderen. Telomeren zij n een indicator voor de gevoeligheid om ouderdomsgerelateerde ziekten te ontwikkelen. Verschillen in telomeerlengtes worden voornamelij k verklaard door een complex samen-spel van genetische, leefstij l-en omgevingsfactoren. Eerdere studies toonden aan dat een gezonde leefstij l belangrij k is in termen van ziektepreventie. Recent onderzoek toont aan dat leefstij l ook in verband wordt gebracht met essentiële biologische processen die betrokken zij n bij veroudering, zoals telomeerverkorting. Dit kan gedeeltelij k verklaren waarom er een verband is tussen leefstij l en ontwik-keling van ziekten. Dit benadrukt dat een gezonde leefstij l niet alleen direct bij draagt aan het voorkomen van ziekten, maar ook indirect via biologische processen die de veroudering reguleren en daarbij de gevoeligheid voor het ontstaan van ziekte verminderen. Deze omgevings-en leefstij lfactoren kunnen al voor de geboorte aanzienlij k invloed uitoefenen op de variatie in telomeerlengte bij pasgeborenen. Hoewel bij de geboorte ieder kind even oud is, is dat niet zo als we kij ken naar de biologische leeftij d op basis van de lengte van de telomeren. Met andere woorden, de lengte van de telomeren bij de geboorte vormt één van de mechanismen die verschillen in veroudering en ziektegevoeligheid gedurende het le-ven mee bepalen. Dit benadrukt het belang van een gezonde leefstij l en omgeving voor het bevorderen van een lang en gezond leven vanaf de preconceptie, niet alleen voor onszelf, maar ook voor toekomstige generaties. (NED TIJ DSCHR LEEFSTIJ LGENEESKD 2025;3(2):69-75) 1 PhD-student, 2 hoogleraar faculteit Wetenschappen, 3 gast FWO postdoctoraal onderzoeker, 4 Centrum voor Milieukunde, Universiteit Hasselt, Hasselt, België, 5 departement Maatschappelij ke Gezondheidszorg en Eerstelij nszorg, KU Leuven, Leuven, België. Correspondentie graag richten aan: dhr. prof. dr. T.S. Nawrot, Universiteit Hasselt, Centrum voor Milieukunde, Agoralaan gebouw D, 3590 Diepenbeek, België, tel: +32 490 57 70 13, e-mailadres: [email protected] Belangenconflict: geen gemeld. Financiële ondersteuning: D.S. Martens is houder van een postdoctoraatbeurs bij het Fonds Wetenschap-pelij k Onderzoek-Vlaanderen (FWO 12X9623N). Trefwoorden: gezondheid, leefstij lfactoren, preventie, telomeerlengte, veroudering
Blood pressure and hypertension in relation to lead exposure updated according to present-day blood lead levels
No full textLead is an environmental hazard that should be addressed worldwide. Over time, human exposure to lead in the Western world has fallen drastically to the levels comparable to those in humans living in the pre-industrial era, who were mainly exposed to natural sources of lead. To re-evaluate the health risks possibly associated with present-day lead exposure, a three-pronged approach was applied. First, we critically assessed the recently published population metrics describing the adverse health effects associated with lead exposure at the population level. Next, we summarized the key results of the Study for Promotion of Health in Recycling Lead (SPHERL; NCT02243904) and analyzed these results in the context of the published population metrics. Last but not least, we performed a brief literature review on the present-day lead exposure level in Poland. To our best knowledge, SPHERL is the first prospective study that accounted for interindividual variation in vulnerability to the toxic effects of lead exposure by assessing the participants' health status before and after occupational lead exposure, with blood pressure and hypertension as the primary outcomes. The overall conclusion of this comprehensive review on blood pressure and hypertension is that mainstream ideas about the public and occupational health risks related to lead exposure need to be urgently updated because a large part of the available literature has become obsolete given present-day exposure levels that sharply declined over the past 40 years.Funding:
The International Lead Association (www.ila-lead.org) provided an unrestricted grant to the Research Unit Hypertension and Cardiovascular Epidemiology, KU Leuven Department of Cardiovascular Sciences, partially supporting data collection and management and statistical analysis of the SPHERL project. The Non-Profit Research Association Alliance for the Promotion of Preventive Medicine, Mechelen, Belgium (URL, www.appremed.org) received a nonbinding grant from OMRON Healthcare Co Ltd, Kyoto, Japan. These funders played no role in the decision to submit this review article
Omgeving en leefstijfactoren: al vroeg in het leven van invloed op telomeerlengte
No full textTelomeren zij n de beschermende uiteinden van chromosomen en nemen in lengte af naarmate we verouderen. Telomeren zij n een indicator voor de gevoeligheid om ouderdomsgerelateerde ziekten te ontwikkelen. Verschillen in telomeerlengtes worden voornamelij k verklaard door een complex samen-spel van genetische, leefstij l-en omgevingsfactoren. Eerdere studies toonden aan dat een gezonde leefstij l belangrij k is in termen van ziektepreventie. Recent onderzoek toont aan dat leefstij l ook in verband wordt gebracht met essentiële biologische processen die betrokken zij n bij veroudering, zoals telomeerverkorting. Dit kan gedeeltelij k verklaren waarom er een verband is tussen leefstij l en ontwik-keling van ziekten. Dit benadrukt dat een gezonde leefstij l niet alleen direct bij draagt aan het voorkomen van ziekten, maar ook indirect via biologische processen die de veroudering reguleren en daarbij de gevoeligheid voor het ontstaan van ziekte verminderen. Deze omgevings-en leefstij lfactoren kunnen al voor de geboorte aanzienlij k invloed uitoefenen op de variatie in telomeerlengte bij pasgeborenen. Hoewel bij de geboorte ieder kind even oud is, is dat niet zo als we kij ken naar de biologische leeftij d op basis van de lengte van de telomeren. Met andere woorden, de lengte van de telomeren bij de geboorte vormt één van de mechanismen die verschillen in veroudering en ziektegevoeligheid gedurende het le-ven mee bepalen. Dit benadrukt het belang van een gezonde leefstij l en omgeving voor het bevorderen van een lang en gezond leven vanaf de preconceptie, niet alleen voor onszelf, maar ook voor toekomstige generaties. (NED TIJ DSCHR LEEFSTIJ LGENEESKD 2025;3(2):69-75) 1 PhD-student, 2 hoogleraar faculteit Wetenschappen, 3 gast FWO postdoctoraal onderzoeker, 4 Centrum voor Milieukunde, Universiteit Hasselt, Hasselt, België, 5 departement Maatschappelij ke Gezondheidszorg en Eerstelij nszorg, KU Leuven, Leuven, België. Correspondentie graag richten aan: dhr. prof. dr. T.S. Nawrot, Universiteit Hasselt, Centrum voor Milieukunde, Agoralaan gebouw D, 3590 Diepenbeek, België, tel: +32 490 57 70 13, e-mailadres: [email protected] Belangenconflict: geen gemeld. Financiële ondersteuning: D.S. Martens is houder van een postdoctoraatbeurs bij het Fonds Wetenschap-pelij k Onderzoek-Vlaanderen (FWO 12X9623N). Trefwoorden: gezondheid, leefstij lfactoren, preventie, telomeerlengte, veroudering
Urinary lead in relation to combustion-derived air pollution in urban environments. A longitudinal study of an international panel.
No full textBACKGROUND: Urinary lead (Pb) is generally considered to have limited use in biomonitoring environmental exposure to lead. Carbon load in airway macrophages (AM BC) is an internal marker to assess long-term exposure to combustion-derived aerosol particles. In urban environments, atmospheric Pb and black carbon may have common sources. We aimed to study the temporal change of urinary Pb (U-Pb) when exposure to outdoor air pollution changes, and the relationship between U-Pb and AM BC. METHODS: A panel of 50 young healthy adults [mean (SD) 26.7 (5.2) years], including 17 long-term (>1 year) residents in Leuven, Belgium (BE), 15 and 18 newcomers (arrived <3 weeks) from low- and middle-income countries (LMIC) and high-income countries (HIC), respectively, underwent 8 repeated measurements at 6 weeks intervals. In urine spot samples obtained at 5 time points (T1, T2, T4, T6, T8), 24 trace elements were quantified by inductively coupled plasma-mass spectrometry. At each time point, AM BC was quantified as the median surface of black inclusions (in μm2) by means of image analysis of 25 macrophages obtained by induced sputum. Changes in urinary metal concentrations (with and without creatinine correction) and the relationship between U-Pb and AM BC were estimated using linear mixed models adjusted for covariates and potential confounders. RESULTS: Only U-Pb differed between groups and exhibited significant time trends. Participants from the LMIC group had significantly higher initial U-Pb (1.18 μg/g creat) than the HIC group (0.44 μg/g creat) and BE group (0.45 μg/g creat). In the LMIC group, U-Pb decreased significantly with time by 0.061 μg/g creatinine per 30 days [95% confidence interval (CI): 0.034, 0.088]. U-Pb remained unchanged in the other two groups. An increase in AM BC of 1 μm2 was associated with an increase in U-Pb of 0.369 μg/g creat (95% CI: 0.145, 0.593). CONCLUSION: This panel study demonstrates that U-Pb may be a valid alternative to blood Pb for biomonitoring changes in exposure to lead, at least at group level. In addition, we identified a positive association between U-Pb and AM BC, a biomarker of exposure to traffic-related air pollution, suggesting the existence of common sources of Pb and black carbon in urban environments
Mitochondrial DNA methylation in placental tissue: a proof of concept study by means of prenatal environmental stressors
No full textWhile previous studies have demonstrated that prenatal exposure to environmental stressors is associated with mitochondrial DNA (mtDNA) methylation, more recent investigations are questioning the accuracy of the methylation assessment and its biological relevance. In this study, we investigated placental mtDNA methylation while accounting for methodological issues such as nuclear contamination, bisulphite conversion, and PCR bias. From the ENVIRONAGE birth cohort, we selected three groups of participants (n = 20/group). One group with mothers who smoked during pregnancy (average 13.2 cig/day), one group with high air pollutant exposure (PM2.5: 16.0 +/- 1.4 mu g/m(3), black carbon: 1.8 +/- 0.3 mu g/m(3)) and one control group (non-smokers, PM2.5: 10.6 +/- 1.7 mu g/m(3), black carbon: 0.9 +/- 0.1 mu g/m(3)) with low air pollutant exposure. DNA methylation levels were quantified in two regions of the displacement loop control region (D-loopandLDLR2) by bisulphite pyrosequencing. Additionally, we measured DNA methylation on nuclear genes involved in mitochondrial maintenance (PINK1, DNA2, andPOLG1) and assessed mtDNA content using qPCR. AbsoluteD-loopmethylation levels were higher for mothers that smoked extensively (+0.36%, 95% CI: 0.06% to 0.66%), and for mothers that were highly exposed to air pollutants (+0.47%, 95% CI: 0.20% to 0.73%). The relevance of our findings is further supported, asD-loopmethylation levels were correlated with placental mtDNA content (r = -0.40, p = 0.002) and associated with birth weight (-106.98 g, 95% CI: -209.60 g to -4.36 g for an IQR increase inD-loopmethylation). Most notably, our data demonstrates relevant levels of mtDNA methylation in placenta tissue, with significant associations between prenatal exposure to environmental stressors andD-loopmethylation.This work was supported by the Research Foundation Flanders [G082317N]; Research Foundation Flanders [N1518119].Janssen, BG (corresponding author), Hasselt Univ, Ctr Environm Sci, B-3590 Diepenbeek, Belgium.
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