Organic nitrogen in aerosols and precipitation at Barbados and Miami: Implications regarding sources, transport and deposition to the western subtropical North Atlantic

The deposition of anthropogenic nitrogen (N) species is believed to have a significant impact on the oligotrophic North Atlantic, but the magnitude of ecological effects remains uncertain because the deposition of water soluble organic N (WSON) is poorly quantified. Here we present measurements of water soluble inorganic N (WSIN) and WSON in aerosol and rain at two subtropical North Atlantic time series sites: Barbados and Miami. WSON total deposition rates ranged from 17.9 mmol m−2 yr−1 to 49.6 mmol m−2 yr−1, contributing on average only 6–14% of total N deposition, less than half the poorly constrained global average which is typically cited as 30%. On an event basis, biomass burning and dust events yielded the largest concentrations of WSON. However, biomass burning was relatively infrequent and highly variable in composition, and much of the organic N associated with dust appeared to be externally adsorbed from pollution sources. Conversely, in Miami pollution made relatively small contributions of WSON on an event basis, but impacts were relatively frequent, making pollution one of the largest sources of WSON during the year. The largest contributor to WSON was volatile basic organic N (VBON) species, which were present at concentrations 1–2 times higher than particulate WSON. Despite VBON inputs, samples associated with pollution-source trajectories yielded much more inorganic N than WSON. Consequently, we would expect that in the future as anthropogenic N emissions increase, inorganic nitrogen will remain the dominant form of N that is deposited to the western North Atlantic

Respiratory hospital admission risk near large composting facilities

AbstractBackgroundLarge-scale composting can release bioaerosols in elevated quantities, but there are few studies of health effects on nearby communities.MethodsA cross-sectional ecological small area design was used to examine risk of respiratory hospital admissions within 2500m of all 148 English large-scale composting facilities in 2008–10. Statistical analyses used a random intercept Poisson regression model at Census Output Area (COA) level (mean population 310). Models were adjusted for age, sex, deprivation and tobacco sales.ResultsAnalysing 34,963 respiratory hospital admissions in 4656 COAs within 250–2500m of a site, there were no significant trends using pre-defined distance bands of >250–750m, >750–1500m and >1500–2500m. Using a continuous measure of distance, there was a small non-statistically significant (p=0.054) association with total respiratory admissions corresponding to a 1.5% (95% CI: 0.0–2.9%) decrease in risk if moving from 251m to 501m. There were no significant associations for subgroups of respiratory infections, asthma or chronic obstructive pulmonary disease.ConclusionThis national study does not provide evidence for increased risks of respiratory hospital admissions in those living beyond 250m of an outdoor composting area perimeter. Further work using better measures of exposure and exploring associations with symptoms and disease prevalence, especially in vulnerable groups, is recommended to support regulatory approaches

Ambient air pollution exposure and chronic bronchitis in the Lifelines cohort

BACKGROUND: Few large studies have assessed the relationship of long-term ambient air pollution exposure with the prevalence and incidence of symptoms of chronic bronchitis and cough. METHODS: We leveraged Lifelines cohort data on 132 595 (baseline) and 65 009 (second assessment) participants linked to ambient air pollution estimates. Logistic regression models adjusted for sex, age, educational attainment, body mass index, smoking status, pack-years smoking and environmental tobacco smoke at home were used to assess associations of air pollution with prevalence and incidence of chronic bronchitis (winter cough and sputum almost daily for >/=3 months/year), chronic cough (winter cough almost daily for >/=3 months/year) and prevalence of cough and sputum symptoms, irrespective of duration. RESULTS: Associations were seen for all pollutants for prevalent cough or sputum symptoms. However, for prevalent and incident chronic bronchitis, statistically significant associations were seen for nitrogen dioxide (NO2) and black carbon (BC) but not for fine particulate matter (PM2.5). For prevalent chronic bronchitis, associations with NO2 showed OR: 1.05 (95% CI: 1.02 to 1.08) and with BC OR: 1.06 (95% CI: 1.03 to 1.09) expressed per IQR; corresponding results for incident chronic bronchitis were NO2 OR: 1.07 (95% CI: 1.02 to 1.13) and BC OR: 1.07 (95% CI: 1.02 to 1.13). In subgroup analyses, slightly stronger associations were observed among women, never smokers and younger individuals. CONCLUSION: This is the largest analysis to date to examine cross-sectional and longitudinal associations between ambient air pollution and chronic bronchitis. NO2 and BC air pollution was associated with increased odds of prevalent and incident chronic bronchitis

Atypical chemokine receptor ACKR2 controls branching morphogenesis in the developing mammary gland

Macrophages are important regulators of branching morphogenesis during development and postnatally in the mammary gland. Regulation of macrophage dynamics during these processes can therefore have a profound impact on development. We demonstrate here that the developing mammary gland expresses high levels of inflammatory CC-chemokines, which are essential in vivo regulators of macrophage migration. We further demonstrate that the atypical chemokine receptor ACKR2, which scavenges inflammatory CC-chemokines, is differentially expressed during mammary gland development. We have previously shown that ACKR2 regulates macrophage dynamics during lymphatic vessel development. Here, we extend these observations to reveal a novel role for ACKR2 in regulating the postnatal development of the mammary gland. Specifically, we show that Ackr2−/− mice display precocious mammary gland development. This is associated with increased macrophage recruitment to the developing gland and increased density of the ductal epithelial network. These data demonstrate that ACKR2 is an important regulator of branching morphogenesis in diverse biological contexts and provide the first evidence of a role for chemokines and their receptors in postnatal development processes

Small-area methods for investigation of environment and health

Small-area studies offer a powerful epidemiological approach to study disease patterns at the population level and assess health risks posed by environmental pollutants. They involve a public health investigation on a geographic scale (e.g. neighbourhood) with overlay of health, environmental, demographic and potential confounder data. Recent methodological advances, including Bayesian approaches, combined with fast growing computational capabilities permit more informative analyses than previously possible, including the incorporation of data at different scales, from satellites to individual-level survey information. Better data availability has widened the scope and utility of small-area studies, but also led to greater complexity, including choice of optimal study area size and extent, duration of study periods, range of covariates and confounders to be considered, and dealing with uncertainty. The availability of data from large, well-phenotyped cohorts such as UK Biobank enables the use of mixed-level study designs and the triangulation of evidence on environmental risks from small-area and individual-level studies, therefore improving causal inference, including use of linked biomarker and -omics data. As a result, there are now improved opportunities to investigate the impacts of environmental risk factors on human health, particularly for the surveillance and prevention of non-communicable diseases

Protective Effects of Smoke-free Legislation on Birth Outcomes in England: A Regression Discontinuity Design

Background: Environmental tobacco smoke has an adverse impact on preterm birth and birth weight. England introduced a new law to make virtually all enclosed public places and workplaces smoke free on July 1 2007. We investigated the effect of smoke-free legislation on birth outcomes in England using Hospital Episode Statistics (HES) maternity data. Methods: We used regression discontinuity, a quasi-experimental study design, which can facilitate valid causal inference, to analyse short-term effects of smoke-free legislation on birth weight, low birth weight, gestational age, preterm birth and small for gestational age. Results: We analysed 1,800,906 pregnancies resulting in singleton live-births in England between January 1 2005 and December 31 2009. In the one to five months following the introduction of the smoking-free legislation, for those entering their third trimester, the risk of low birth weight decreased by between 8% (95% CI: 4%-12%) and 14% (95% CI: 5%-23%), very low birth weight between 28% (95% CI: 19%-36%) and 32% (95% CI: 21%-41%), preterm birth between 4% (95% CI: 1%-8%) and 9% (95% CI: 2%-16%), and small for gestational age between 5% (95% CI: 2%-8%) and 9% (95% CI: 2%-15%). The impact of the smoke-free legislation varied by maternal age, deprivation, ethnicity and region. Conclusions: The introduction of smoke-free legislation in England had an immediate beneficial impact on birth outcomes overall, although this benefit was not observed across all age, ethnic, or deprivation groups

Common polygenic risk for autism spectrum disorder (ASD) is associated with cognitive ability in the general population

Acknowledgements Generation Scotland has received core funding from the Chief Scientist Office of the Scottish Government Health Directorates CZD/16/6 and the Scottish Funding Council HR03006. We are grateful to all the families who took part, the general practitioners and the Scottish School of Primary Care for their help in recruiting them and the whole Generation Scotland team, which includes interviewers, computer and laboratory technicians, clerical workers, research scientists, volunteers, managers, receptionists, health-care assistants and nurses. We acknowledge with gratitude the financial support received for this work from the Dr Mortimer and Theresa Sackler Foundation. For the Lothian Birth Cohorts (LBC1921 and LBC1936), we thank Paul Redmond for database management assistance; Alan Gow, Martha Whiteman, Alison Pattie, Michelle Taylor, Janie Corley, Caroline Brett and Caroline Cameron for data collection and data entry; nurses and staff at the Wellcome Trust Clinical Research Facility, where blood extraction and genotyping was performed; staff at the Lothian Health Board; and the staff at the SCRE Centre, University of Glasgow. The research was supported by a program grant from Age UK (Disconnected Mind) and by grants from the Biotechnology and Biological Sciences Research Council (BBSRC). The work was undertaken by The University of Edinburgh Centre for Cognitive Ageing and Cognitive Epidemiology, part of the cross council Lifelong Health and Wellbeing Initiative (MR/K026992/1). Funding from the Medical Research Council (MRC) and BBSRC is gratefully acknowledged. DJM is an NRS Career Research Fellow funded by the CSO. BATS were funded by the Australian Research Council (A79600334, A79906588, A79801419, DP0212016, DP0664638, and DP1093900) and the National Health and Medical Research Council (389875) Australia. MKL is supported by a Perpetual Foundation Wilson Fellowship. SEM is supported by a Future Fellowship (FT110100548) from the Australian Research Council. GWM is supported by a National Health and Medical Research Council (NHMRC), Australia, Fellowship (619667). We thank the twins and siblings for their participation, Marlene Grace, Ann Eldridge and Natalie Garden for cognitive assessments, Kerrie McAloney, Daniel Park, David Smyth and Harry Beeby for research support, Anjali Henders and staff in the Molecular Epidemiology Laboratory for DNA sample processing and preparation and Scott Gordon for quality control and management of the genotypes. This work is supported by a Stragetic Award from the Wellcome Trust, reference 104036/Z/14/Z.Peer reviewedPublisher PD

Air pollution, lung function and COPD: results from the population-based UK Biobank study

Ambient air pollution increases the risk of respiratory mortality, but evidence for impacts on lung function and chronic obstructive pulmonary disease (COPD) is less well established. The aim was to evaluate whether ambient air pollution is associated with lung function and COPD, and explore potential vulnerability factors.We used UK Biobank data on 303 887 individuals aged 40-69 years, with complete covariate data and valid lung function measures. Cross-sectional analyses examined associations of land use regression-based estimates of particulate matter (particles with a 50% cut-off aerodynamic diameter of 2.5 and 10 µm: PM2.5 and PM10, respectively; and coarse particles with diameter between 2.5 μm and 10 μm: PMcoarse) and nitrogen dioxide (NO2) concentrations with forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), the FEV1/FVC ratio and COPD (FEV1/FV