Associations of preconception exposure to air pollution and greenness with offspring asthma and hay fever

We investigated if greenness and air pollution exposure in parents’ childhood affect offspring asthma and hay fever, and if effects were mediated through parental asthma, pregnancy greenness/pollution exposure, and offspring exposure. We analysed 1106 parents with 1949 offspring (mean age 35 and 6) from the Respiratory Health in Northern Europe, Spain and Australia (RHINESSA) generation study. Mean particulate matter (PM2.5 and PM10), nitrogen dioxide (NO2), black carbon (BC), ozone (O3) (µg/m3) and greenness (normalized difference vegetation index (NDVI)) were calculated for parents 0-18 years old and offspring 0-10 years old, and were categorised in tertiles. We performed logistic regression and mediation analyses for two-pollutant models (clustered by family and centre, stratified by parental lines, and adjusted for grandparental asthma and education). Maternal medium PM2.5 and PM10 exposure was associated with higher offspring asthma risk (odds ratio (OR) 2.23, 95%CI 1.32-3.78, OR 2.27, 95%CI 1.36-3.80), and paternal high BC exposure with lower asthma risk (OR 0.31, 95%CI 0.11-0.87). Hay fever risk increased for offspring of fathers with medium O3 exposure (OR 4.15, 95%CI 1.28-13.50) and mothers with high PM10 exposure (OR 2.66, 95%CI 1.19-5.91). The effect of maternal PM10 exposure on offspring asthma was direct, while for hay fever, it was mediated through exposures in pregnancy and offspring’s own exposures. Paternal O3 exposure had a direct effect on offspring hay fever. To conclude, parental exposure to air pollution appears to influence the risk of asthma and allergies in future offspring

Development of West-European PM2.5 and NO2 land use regression models incorporating satellite-derived and chemical transport modelling data

Satellite-derived (SAT) and chemical transport model (CTM) estimates of PM2.5 and NO2 are increasingly used in combination with Land Use Regression (LUR) models. We aimed to compare the contribution of SAT and CTM data to the performance of LUR PM2.5 and NO2 models for Europe. Four sets of models, all including local traffic and land use variables, were compared (LUR without SAT or CTM, with SAT only, with CTM only, and with both SAT and CTM). LUR models were developed using two monitoring data sets: PM2.5 and NO2 ground level measurements from the European Study of Cohorts for Air Pollution Effects (ESCAPE) and from the European AIRBASE network. LUR PM2.5 models including SAT and SAT+CTM explained ~60% of spatial variation in measured PM2.5 concentrations, substantially more than the LUR model without SAT and CTM (adjR(2): 0.33-0.38). For NO2 CTM improved prediction modestly (adjR(2): 0.58) compared to models without SAT and CTM (adjR(2): 0.47-0.51). Both monitoring networks are capable of producing models explaining the spatial variance over a large study area. SAT and CTM estimates of PM2.5 and NO2 significantly improved the performance of high spatial resolution LUR models at the European scale for use in large epidemiological studies

Air pollution and lung cancer incidence in 17 European cohorts: prospective analyses from the European Study of Cohorts for Air Pollution Effects (ESCAPE)

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Co-limitation towards lower latitudes shapes global forest diversity gradients

The latitudinal diversity gradient (LDG) is one of the most recognized global patterns of species richness exhibited across a wide range of taxa. Numerous hypotheses have been proposed in the past two centuries to explain LDG, but rigorous tests of the drivers of LDGs have been limited by a lack of high-quality global species richness data. Here we produce a high-resolution (0.025° × 0.025°) map of local tree species richness using a global forest inventory database with individual tree information and local biophysical characteristics from ~1.3 million sample plots. We then quantify drivers of local tree species richness patterns across latitudes. Generally, annual mean temperature was a dominant predictor of tree species richness, which is most consistent with the metabolic theory of biodiversity (MTB). However, MTB underestimated LDG in the tropics, where high species richness was also moderated by topographic, soil and anthropogenic factors operating at local scales. Given that local landscape variables operate synergistically with bioclimatic factors in shaping the global LDG pattern, we suggest that MTB be extended to account for co-limitation by subordinate drivers

Pollution and oral bioaccessibility of Pb in soils of villages and cities with a long habitation history. Special Issue of International Journal of Environmental Research and Public Health

The Dutch cities Utrecht and Wijk bij Duurstede were founded by the Romans around 50 B.C. and the village Fijnaart and Graft-De Rijp around 1600 A.D. The soils of these villages are polluted with Pb (up to ~5000 mg/kg). Lead isotope ratios were used to trace the sources of Pb pollution in the urban soils. In ~75% of the urban soils the source of the Pb pollution was a mixture of glazed potsherd, sherds of glazed roof tiles, building remnants (Pb sheets), metal slag, Pb-based paint flakes and coal ashes. These anthropogenic Pb sources most likely entered the urban soils due to historical smelting activities, renovation and demolition of houses, disposal of coal ashes and raising and fertilization of land with city waste. Since many houses still contain Pb-based building materials, careless renovation or demolition can cause new or more extensive Pb pollution in urban soils. In ~25% of the studied urban topsoils, Pb isotope compositions suggest Pb pollution was caused by incinerator ash and/or gasoline Pb suggesting atmospheric deposition as the major source. The bioaccessible Pb fraction of 14 selected urban soils was determined with an in vitro test and varied from 16% to 82% of total Pb. The bioaccessibility appears related to the chemical composition and grain size of the primary Pb phases and pollution age. Risk assessment based on the in vitro test results imply that risk to children may be underestimated in ~90% of the studied sample sites (13 out of 14)

Promoting respiratory public health through epigenetics research:an ERS Environment Health Committee workshop report

Epigenetics is a rapidly developing research field that is expected to unravel the complex interplay between genes and environmental exposures relevant for health and disease. Epigenetics is classically referred to as heritable phenotypic changes that cannot be explained by changes in DNA sequence. DNA methylation, which is the covalent binding of a methyl group to a cytosine followed by a guanine (CpG), is the most commonly used epigenetic marker in human studies to date. Epigenetics also refers to hydroxymethylation, chromatin remodelling, histone modifications and expression of noncoding RNAs. Recent epidemiological and experimental studies have shown that epigenetic changes are influenced by genetic factors, environmental exposures, ageing and disease processes. In particular, early-life events and exposures seem to strongly influence epigenetic processes such as DNA methylation [1, 2]. From the definition of epigenetics, heritable changes are implied and observations from pre-conceptual exposure studies raise the question whether epigenetic changes really can be inherited at the individual level from one generation to the next [3]. If so, this would have immense public health implications, since generations to come may have to face health consequences of the life their parents and grandparents lived, the diseases they had or the environmental factors they were exposed to. There are, however, many question marks around potential epigenetic effects across generations; from epidemiological and experimental evidence to mechanisms and potential health effects. Here, we report on an European Respiratory Society (ERS) Environment and Health Committee workshop held in March 2017 where epigenetics and transgenerational effects in the field of respiratory research were discussed. The aim of the meeting was to examine the role of ERS advocacy in promoting public health policy in relation to epigenetic mechanisms and to identify future research activities

Development of a sensitive real-time reverse transcriptase PCR assay with an internal control to detect and quantify chikungunya virus

International audienceBackground: The chikungunya virus (CHIKV; Alphavirus, Togaviridae) has emerged in the south Western Indian Ocean since early 2005. A major outbreak of CHIKV infection occurred in Reunion Island, where the virus is transmitted by Aedes albopictus mosquitoes. Facing an outbreak of unprecedented magnitude, we developed a rapid, sensitive, and reliable assay for the detection and quantification of CHIKV in plasma samples. Methods: A dual-color TaqMan 1-step reverse transcriptase PCR assay was developed in a LightCycler 2.0 system. A coextd. and coamplified chimerical RNA sequence was used as an internal control (IC) to eliminate false-neg. results. The CHIKV-specific and IC probes were labeled with 6-carboxyfluorescein (530 nm) and the wide span dye DYXL (705 nm), resp., eliminating the need for color compensation. A synthetic RNA was used as an external calibrator for CHIKV abs. quantification. Results: The detection limit was 350 copies/mL (3 copies/capillary). A further improvement to ∼40 copies/mL was obtained by use of a larger vol. of plasma. The assay specificity was confirmed in vitro and in silico. CHIKV in 343 patients was present at viral loads \textgreater108 copies/mL, mainly in newborns and seniors \textgreater60 years old. Long viremic phases of up to 12 days were seen in 6 patients. Conclusions: The assay is rapid, CHIKV-specific, and highly sensitive, and it includes an IC. It proved useful to detect and quantify CHIKV during the Reunion Island epidemic. The assay might be applicable to other CHIKV epidemics, esp. in the Indian subcontinent, where an extensive outbreak is ongoing. [on SciFinder(R)