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Ambient air pollution, including black carbon, entails a serious public health risk because of its carcinogenic potential and as climate pollutant. To date, an internal exposure marker for black carbon particles that have cleared from the systemic circulation into the urine does not exist. To develop and validate a novel method to measure black carbon particles in a label-free way in urine. We detected urinary carbon load in 289 children (aged 9-12 yr) using white-light generation under femtosecond pulsed laser illumination. Children's residential black carbon concentrations were estimated based on a high-resolution spatial temporal interpolation method. We were able to detect urinary black carbon in all children, with an overall average (SD) of 98.2 × 10 (29.8 × 10 ) particles/ml. The urinary black carbon load was positively associated with medium-term to chronic (1 mo or more) residential black carbon exposure: +5.33 × 10 particles/ml higher carbon load (95% confidence interval, 1.56 × 10 to 9.10 × 10 particles/ml) for an interquartile range increment in annual residential black carbon exposure. Consistently, children who lived closer to a major road (≤160 m) had higher urinary black carbon load (6.93 × 10 particles/ml; 95% confidence interval, 0.77 × 10 to 13.1 × 10 ). Urinary black carbon mirrors the accumulation of medium-term to chronic exposure to combustion-related air pollution. This specific biomarker reflects internal systemic black carbon particles cleared from the circulation into the urine, allowing investigators to unravel the complexity of particulate-related health effects.

Studies on the association between atherosclerosis and long-term exposure to ambient air pollution suggest that carotid intima-media thickness (CIMT), a marker of subclinical atherosclerosis, is positively associated with particulate matter (PM) exposure. However, there is heterogeneity between the different studies concerning the magnitude of this association. We performed a meta-analysis to determine the strength of the association between CIMT and particulate air pollution. We queried PubMed citation database and Web of Knowledge up to March 2015 in order to identify studies on CIMT and particulate air pollution. Two investigators selected and computerized all relevant information, independently. Eight of the reviewed epidemiological publications provided sufficient details and met our inclusion criteria. Descriptive and quantitative information was extracted from each selected study. The meta-analysis included 18,349 participants from eight cohorts for the cross-sectional association between CIMT and PM and 7,268 participants from three cohorts for the longitudinal analysis on CIMT progression and PM exposure. The average exposure to PM2.5 in the different study populations ranged from 4.1 to 20.8 µg/m3 and CIMT averaged (SD) 0.73 (0.14) mm. We computed a pooled estimate from a random-effects model. In the combined cross-sectional studies, an increase of 5 µg/m3 PM2.5 was associated with a 1.66% (95% CI: 0.86 to 2.46; P<0.0001) thicker CIMT, which corresponds to an average increase of 12.1 µm. None of the studies moved the combined estimate outside the confidence interval of the overall estimate. A funnel plot suggested absence of publication bias. The combined longitudinal estimate showed for each 5 µg/m3 higher PM2.5 exposure, a 1.04 µm per year (95% CI: 0.01 to 2.07; P=0.048) greater CIMT progression. Our meta-analysis supports the evidence of a positive association between CIMT, a marker of subclinical atherosclerosis, and long-term exposure to particulate air pollution.

Background Daily changes in ambient concentrations of particulate matter, nitrogen oxides and ozone are associated with increased cardiopulmonary morbidity and mortality, with the lungs and their function being a vulnerable target. Methods To evaluate the association between daily changes in air pollution and lung function in healthy adults we obtained annual lung function measurements from a routine worker health surveillance program not designed for research purposes. Forced Vital Capacity (FVC), Forced Expiratory Volume in the first second (FEV1), FEV1/FVC and Peak Expiratory flow (PEF) from a cohort of 2449 employees were associated with daily measurements of PM 10 , NO 2 and ozone at a nearby monitoring station in the North of Belgium. Repeated measures were available for the period 2011–2015. Results The mean (SD) PM 10 concentration on the day of the lung function test was 24.9 (15.5) μg/m 3 . A 10 μg PM 10 /m 3 increase on the day of the clinical examination was associated with a 18.9 ml lower FVC (95% CI: -27.5 to −10.3, p  < 0.0001), 12.8 ml lower FEV1 (−19.1 to −6.5; p  < 0.0001), and a 51.4 ml/s lower PEF (−75.0 to −27.0; p  < 0.0001). The FEV1/FVC-ratio showed no associations. An increase of 10 μgNO 2 /m 3 was associated with a reduction in PEF (−66.1 ml/s (−106.6 to −25.6; p  < 0.001)) on the day of the examination. Conclusions We found negative associations between daily variations in ambient air pollution and FVC, FEV1 and PEF in healthy adults.

Background Particulate matter exposure during in utero life may entail adverse health outcomes later in life. The microvasculature undergoes extensive, organ-specific prenatal maturation. A growing body of evidence shows that cardiovascular disease in adulthood is rooted in a dysfunctional fetal and perinatal development, in particular that of the microcirculation. We investigate whether prenatal or postnatal exposure to PM 2.5 (particulate matter with a diameter ≤ 2.5 μm) or NO 2 is related to microvascular traits in children between the age of four and six. Methods We measured the retinal microvascular diameters, the central retinal arteriolar equivalent (CRAE) and central retinal venular equivalent (CRVE), and the vessel curvature by means of the tortuosity index (TI) in young children (mean [SD] age 4.6 [0.4] years), followed longitudinally within the ENVIR ON AGE birth cohort. We modeled daily prenatal and postnatal PM 2.5 and NO 2 exposure levels for each participant’s home address using a high-resolution spatiotemporal model. Results An interquartile range (IQR) increase in PM 2.5 exposure during the entire pregnancy was associated with a 3.85-μm (95% CI, 0.10 to 7.60; p  = 0.04) widening of the CRVE and a 2.87-μm (95% CI, 0.12 to 5.62; p  = 0.04) widening of the CRAE. For prenatal NO 2 exposure, an IQR increase was found to widen the CRVE with 4.03 μm (95% CI, 0.44 to 7.63; p  = 0.03) and the CRAE with 2.92 μm (95% CI, 0.29 to 5.56; p  = 0.03). Furthermore, a higher TI score was associated with higher prenatal NO 2 exposure. We observed a postnatal effect of short-term PM 2.5 exposure on the CRAE and a childhood NO 2 exposure effect on both the CRVE and CRAE. Conclusions Our results link prenatal and postnatal air pollution exposure with changes in a child’s microvascular traits as a fundamental novel mechanism to explain the developmental origin of cardiovascular disease.

An imbalance between energy uptake and energy expenditure is the most important reason for increasing trends in obesity starting from early in life. Extracellular miRNAs are expressed in all bodily fluids and their expression is influenced by a broad range of stimuli. We examined whether screen time, physical activity and BMI are associated with children’s salivary extracellular miR-222 and miR-146a expression. In 80 children the extracellular fraction of saliva was obtained by means of differential centrifugation and ultracentrifugation. Expression levels of miR-222 and miR-146a were profiled by qPCR. We studied the association between children’s salivary extracellular miRNA expression and screen time, physical activity and BMI using mixed models, while accounting for potential confounders. We found that higher screen time was positively associated with salivary extracellular miR-222 and miR-146a levels. On average, one hour more screen time use per week was associated with a 3.44% higher miR-222 (95% CI: 1.34 to 5.58; p = 0.002) and 1.84% higher miR-146a (95% CI: −0.04 to 3.75; p = 0.055) level in saliva. BMI and physical activity of the child were not significantly associated with either miR-222 or miR-146a. A sedentary behaviour, represented by screen time use in children, is associated with discernible changes in salivary expression of miR-146a and or miR-222. These miRNA targets may emerge attractive candidates to explore the role of these exposures in developmental processes of children’s health.

Cardiovascular risk factors are usually better tolerated, and can therefore be perceived as less harmful, at a young age. However, over time the effects of these adverse factors may persist or accumulate and lead to excess morbidity and mortality from cardiovascular diseases later in life. Until now, reference values for the basic cardiovascular health characteristics of 4-to-6 year-old children are lacking. Within a follow-up study of the ENVIR ON AGE (ENVIRonmental influence ON early AGE) birth cohort we assessed various cardiovascular measurements in 288 children aged 4–5 years. For the macrovasculature, we measured their blood pressure and examined the intima-media thickness of the carotid artery (CIMT), the arterial elasticity (including the pulse-wave velocity (PWV), carotid distensibility (DC) and compliance (CC) coefficients), the carotid β stiffness index (SIβ) and Young’s Elastic Modulus (YEM). Retinal microvascular traits included the Central Retinal Arteriolar Equivalent (CRAE) and Central Retinal Venular Equivalent (CRVE). Age of the study population averaged (±SD) 4.2 (±0.4 years. Mean systolic and diastolic blood pressure were 97.9 (±8.1) mmHg and 54.7(±7.6) mmHg, respectively. CIMT for the total population averaged 487.1 (±68.1) µm. The average stiffness values for DC, CC, SIβ, and PWV were 78.7 (±34.2) 10 − ³/kPa, 1.61 (±0.59) mm 2 /kPa and 4.4 (±2.4), and 3.7 m/s (±0.9) respectively. The mean determined for YEM was 163.2 kPa (±79.9). Concerning the microvasculature, the average CRAE was 180.9 (±14.2) µm and the corresponding value for CRVE was 251.0 (±19.7) µm. In contrast to the macrovasculature, a significant gender-related difference existed for the microvasculature: in boys, both the CRAE (178.8 µm vs 182.6 µm; p = 0.03) and CRVE (247.9 µm vs 254.0 µm; p = 0.01) were narrower than in girls. We have provided reference values for young children to understand changes in the early cardiovascular health trajectory. Establishing these reference values of cardiovascular phenotypes at this young age is necessary to develop targeted health promotion strategies as well as for better understanding of the life course changes of both small and large blood vessels.

Background Ultrafine particles (<100 nm) are ubiquitous present in the air and may contribute to adverse cardiovascular effects. Exposure to air pollutants can alter miRNA expression, which can affect downstream signaling pathways. miRNAs are present both in the intracellular and extracellular environment. In adults, miR-222 and miR-146a were identified as associated with particulate matter exposure. However, there is little evidence of molecular effects of ambient air pollution in children. This study examined whether exposure to fine and ultrafine particulate matter (PM) is associated with changes in the extracellular content of miR-222 and miR-146a of children. Methods Saliva was collected from 80 children at two different time points, circa 11 weeks apart and stabilized for RNA preservation. The extracellular fraction of saliva was obtained by means of differential centrifugation and ultracentrifugation. Expression levels of miR-222 and miR-146a were profiled by qPCR. We regressed the extracellular miRNA expression against recent exposure to ultrafine and fine particles measured at the school site using mixed models, while accounting for sex, age, BMI, passive smoking, maternal education, hours of television use, time of the day and day of the week. Results Exposure to ultrafine particles (UFP) at the school site was positively associated with miR-222 expression in the extracellular fraction in saliva. For each IQR increase in particles in the class room (+8504 particles/cm 3 ) or playground (+28776 particles/cm 3 ), miR-222 was, respectively 23.5 % (95 % CI: 3.5 %–41.1 %; p =  0.021) or 29.9 % (95 % CI:10.6 %–49.1 %; p =  0.0027) higher. No associations were found between miR-146a and recent exposure to fine and ultrafine particles. Conclusions Our results suggest a possible epigenetic mechanism via which cells respond rapidly to small particles, as exemplified by miR-222 changes in the extracellular fraction of saliva.

Neurocognitive functions develop rapidly in early childhood and depend on the intrinsic cooperation between cerebral structures and the circulatory system. The retinal microvasculature can be regarded as a mirror image of the cerebrovascular circulation. To investigate the association between retinal vessel characteristics and neurological functioning in children aged 4 to 5 years. In this cohort study, mother-child pairs were recruited at birth from February 10, 2010, to June 24, 2014, and renewed consent at their follow-up visit from December 10, 2014, to July 13, 2018. Participants were followed up longitudinally within the prospective Environmental Influence on Aging in Early Life birth cohort. A total of 251 children underwent assessment for this study. Data were analyzed from July 17 to October 30, 2019. Retinal vascular diameters, the central retinal arteriolar equivalent (CRAE), central retinal venular equivalent (CRVE), vessel tortuosity, and fractal dimensions were determined. Attention and psychomotor speed, visuospatial working memory, and short-term visual recognition memory were assessed by the Cambridge Neuropsychological Test Automated Battery, including the following tasks: Motor Screening (MOT), Big/Little Circle (BLC), Spatial Span (SSP), and Delayed Matching to Sample (DMS). Among the 251 children included in the assessment (135 girls [53.8%]; mean [SD] age, 4.5 [0.4] years), for every 1-SD widening in CRVE, the children performed relatively 2.74% (95% CI, -0.12 to 5.49; P = .06) slower on the MOT test, had 1.76% (95% CI, -3.53% to -0.04%; P = .04) fewer correct DMS assessments in total, and made 2.94% (95% CI, 0.39 to 5.29; P = .02) more errors given a previous correct answer in the DMS task on multiple linear regression modeling. For every 1-SD widening in CRAE, the total percentage of errors and errors given previous correct answers in the DMS task increased 1.44% (95% CI, -3.25% to 0.29%; P = .09) and 2.30% (95% CI, -0.14% to 4.61%; P = .07), respectively. A 1-SD higher vessel tortuosity showed a 4.32% relative increase in latency in DMS task performance (95% CI, -0.48% to 9.12%; P = .07). Retinal vessel characteristics were not associated with BLC and SSP test outcomes. These findings suggest that children's microvascular phenotypes are associated with short-term memory and that changes in the retinal microvasculature may reflect neurological development during early childhood.

Introduction Studies on the association between atherosclerosis and long-term exposure to ambient air pollution suggest that carotid intima-media thickness (CIMT), a marker of subclinical atherosclerosis, is positively associated with particulate matter (PM) exposure. However, there is heterogeneity between the different studies concerning the magnitude of this association. We performed a meta-analysis to determine the strength of the association between CIMT and particulate air pollution. Methods We queried PubMed citation database and Web of Knowledge up to March 2015 in order to identify studies on CIMT and particulate air pollution. Two investigators selected and computerized all relevant information, independently. Eight of the reviewed epidemiological publications provided sufficient details and met our inclusion criteria. Descriptive and quantitative information was extracted from each selected study. The meta-analysis included 18,349 participants from eight cohorts for the cross-sectional association between CIMT and PM and 7,268 participants from three cohorts for the longitudinal analysis on CIMT progression and PM exposure. Results The average exposure to PM2.5 in the different study populations ranged from 4.1 to 20.8 mu g/m3 and CIMT averaged (SD) 0.73 (0.14) mm. We computed a pooled estimate from a random-effects model. In the combined cross-sectional studies, an increase of 5 mu g/m3 PM2.5 was associated with a 1.66% (95% CI: 0.86 to 2.46; P<0.0001) thicker CIMT, which corresponds to an average increase of 12.1 mu m. None of the studies moved the combined estimate outside the confidence interval of the overall estimate. A funnel plot suggested absence of publication bias. The combined longitudinal estimate showed for each 5 mu g/m3 higher PM2.5 exposure, a 1.04 mu m per year (95% CI: 0.01 to 2.07; P=0.048) greater CIMT progression. Conclusion Our meta-analysis supports the evidence of a positive association between CIMT, a marker of subclinical atherosclerosis, and long-term exposure to particulate air pollution.