Associations between daily mortality in London and combined oxidant capacity, ozone and nitrogen dioxide.

Both nitrogen dioxide (NO2) and ozone (O3) are powerful oxidants in ambient air that are intimately linked through atmospheric chemistry and which continuously interchange over very short timescales. Based upon atmospheric chemistry alone, there is a strong, a priori, reason for considering O3 and NO2 together in epidemiological studies, rather than either of the two pollutants separately in single-pollutant models. This paper compares two approaches to this, using Ox, defined as O3 + NO2, as a single metric and also using O3 and NO2 together in two-pollutant models. We hypothesised that the magnitude of the association between Ox and daily mortality would be greater than for NO2 and O3 individually. Using collocated hourly measurements for O3 and NO2 in London, from 2000 to 2005, we carried out a time series analysis of daily mortality. We investigated O3, NO2 and Ox individually in single-pollutant Poisson regression models and NO2 and O3 jointly in two-pollutant models in both all-year and season-specific analyses. We observed larger associations for mean 24-h concentrations of Ox (1.30 % increase in mortality per 10 ppb) than for O3 (0.87 %) and NO2 (0 %) individually. However, when analysed jointly in two-pollutant models, associations for O3 (1.54 %) and NO2 (1.07 %) were comparable to the Ox association. Season-specific analyses broadly followed this pattern irrespective of whether the Ox concentrations were driven by O3 production (summer) or depletion (winter). This novel approach in air pollution epidemiology captures the simultaneous impact of both oxidants whilst avoiding many of the statistical issues associated with two-pollutant models and potentially simplifies health impact calculations

Fine particle components and health--a systematic review and meta-analysis of epidemiological time series studies of daily mortality and hospital admissions.

Short-term exposure to fine particle mass (PM) has been associated with adverse health effects, but little is known about the relative toxicity of particle components. We conducted a systematic review to quantify the associations between particle components and daily mortality and hospital admissions. Medline, Embase and Web of Knowledge were searched for time series studies of sulphate (SO4(2-)), nitrate (NO3(-)), elemental and organic carbon (EC and OC), particle number concentrations (PNC) and metals indexed to October 2013. A multi-stage sifting process identified eligible studies and effect estimates for meta-analysis. SO4(2-), NO3(-), EC and OC were positively associated with increased all-cause, cardiovascular and respiratory mortality, with the strongest associations observed for carbon: 1.30% (95% CI: 0.17%, 2.43%) increase in all-cause mortality per 1 μg/m(3). For PNC, the majority of associations were positive with confidence intervals that overlapped 0%. For metals, there were insufficient estimates for meta-analysis. There are important gaps in our knowledge of the health effects associated with short-term exposure to particle components, and the literature also lacks sufficient geographical coverage and analyses of cause-specific outcomes. The available evidence suggests, however, that both EC and secondary inorganic aerosols are associated with adverse health effects

Epidemiological time series studies of PM2.5 and daily mortality and hospital admissions: a systematic review and meta-analysis

Background Short-term exposure to outdoor fine particulate matter (particles with a median aerodynamic diameter <2.5 μm (PM2.5)) air pollution has been associated with adverse health effects. Existing literature reviews have been limited in size and scope. Methods We conducted a comprehensive, systematic review and meta-analysis of 110 peer-reviewed time series studies indexed in medical databases to May 2011 to assess the evidence for associations between PM2.5 and daily mortality and hospital admissions for a range of diseases and ages. We stratified our analyses by geographical region to determine the consistency of the evidence worldwide and investigated small study bias. Results Based upon 23 estimates for all-cause mortality, a 10 µg/m3 increment in PM2.5 was associated with a 1.04% (95% CI 0.52% to 1.56%) increase in the risk of death. Worldwide, there was substantial regional variation (0.25% to 2.08%). Associations for respiratory causes of death were larger than for cardiovascular causes, 1.51% (1.01% to 2.01%) vs 0.84% (0.41% to 1.28%). Positive associations with mortality for most other causes of death and for cardiovascular and respiratory hospital admissions were also observed. We found evidence for small study bias in single-city mortality studies and in multicity studies of cardiovascular disease. Conclusions The consistency of the evidence for adverse health effects of short-term exposure to PM2.5 across a range of important health outcomes and diseases supports policy measures to control PM2.5 concentrations. However, reasons for heterogeneity in effect estimates in different regions of the world require further investigation. Small study bias should also be considered in assessing and quantifying health risks from PM2.

Long-term concentrations of nitrogen dioxide and mortality: a meta-analysis of cohort studies.

BACKGROUND: Concentrations of outdoor nitrogen dioxide (NO2) have been associated with increased mortality. Hazard ratios (HRs) from cohort studies are used to assess population health impact and burden. We undertook meta-analyses to derive concentration-response functions suitable for such evaluations and assessed their sensitivity to study selection based upon cohort characteristics. METHODS: We searched online databases and existing reviews for cohort studies published to October 2016 reporting HRs for NO2 and mortality. We calculated meta-analytic summary estimates using fixed/random effects models. RESULTS: We identified 48 articles analyzing 28 cohorts. Meta-analysis of HRs found positive associations between NO2 and all-cause (1.02 (95% CI: 1.01, 1.03); prediction interval (PI): (0.99, 1.06) per 10µg/m increment in NO2), cardiovascular (1.03 (95% CI: 1.02,1.05); PI: (0.98, 1.08)) , respiratory (1.03 (95% CI: 1.01,1.05); PI: (0.97, 1.10)) and lung cancer mortality (1.05 (95% CI: 1.02,1.08); PI: (0.94, 1.17)) with evidence of substantial heterogeneity between studies. In subgroup analysis, summary HRs varied by age at cohort entry, spatial resolution of pollution estimates, and adjustment for smoking and body mass index at the individual level; for some sub-groups the HR was close to unity, with lower confidence limits below 1. CONCLUSIONS: Given the many uncertainties inherent in the assessment of this evidence base and the sensitivity of health impact calculations to small changes in the magnitude of the HRs, calculation of the impact on health of policies to reduce long-term exposure to NO2 should use prediction intervals and report ranges of impact rather than focusing upon point estimates.This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal

'Dressage Is Full of Queens!' Masculinity, Sexuality and Equestrian Sport

Attitudes towards sexuality are changing and levels of cultural homophobia decreasing, yet there remain very few openly gay men within sport. As a proving ground for heteromasculinity, sport has traditionally been a hostile environment for gay men. This article is based on an ethnographic study within a sporting subworld in which gay men do appear to be accepted: equestrian sport. Drawing on inclusive masculinity theory, equestrian sport is shown to offer an unusually tolerant environment for gay men in which heterosexual men of all ages demonstrate low levels of homophobia. Inclusive masculinity theory is a useful framework for exploring the changing nature of masculinities and this study demonstrates that gay men are becoming increasingly visible and accepted within once unreceptive locales, such as sport and rural communities. However, this more tolerant attitude is purchased at the expense of a subordinated feminine Other, perpetuating the dominance of men within competitive sport. © The Author(s) 2012

Chemical characteristics of Pacific tropospheric air in the region of the Intertropical Convergence Zone and South Pacific Convergence Zone

The Pacific Exploratory Mission (PEM)-Tropics provided extensive aircraft data to study the atmospheric chemistry of tropospheric air in Pacific Ocean regions, extending from Hawaii to New Zealand and from Fiji to east of Easter Island. This region, especially the tropics, includes some of the cleanest tropospheric air of the world and, as such, is important for studying atmospheric chemical budgets and cycles. The region also provides a sensitive indicator of the global-scale impact of human activity on the chemistry of the troposphere, and includes such important features as the Pacific "warm pool," the Intertropical Convergence Zone (ITCZ), the South Pacific Convergence Zone (SPCZ), and Walker Cell circulations. PEM-Tropics was conducted from August to October 1996. The ITCZ and SPCZ are major upwelling regions within the South Pacific and, as such, create boundaries to exchange of tropospheric air between regions to the north and south. Chemical data obtained in the near vicinity of the ITCZ and the SPCZ are examined. Data measured within the convergent zones themselves are not considered. The analyses show that air north and south of the convergent zones have different chemical signatures, and the signatures are reflective of the source regions and transport histories of the air. Air north of the ITCZ shows a modest urban/industrialized signature compared to air south of the ITCZ. The chemical signature of air south of the SPCZ is dominated by combustion emissions from biomass burning, while air north of the SPCZ is relatively clean and of similar composition to ITCZ south air. Chemical signature differences of air north and south of the zones are most pronounced at altitudes below 5 km, and, as such, show that the ITCZ and SPCZ are effective low-altitude barriers to the transport of tropospheric air. At altitudes of 8 to 10 km, chemical signatures are less dissimilar, and air backward trajectories (to 10 days) show cross-convergent-zone flow. At altitudes below about 5 km, little cross-zonal flow is observed. Chemical signatures presented include over 30 trace chemical species including ultrafine, fine, and heated-fine (250°C) aerosol. Copyright 1999 by the American Geophysical Union

Role of dystrophin in airway smooth muscle phenotype, contraction and lung function

Dystrophin links the transmembrane dystrophin-glycoprotein complex to the actin cytoskeleton. We have shown that dystrophin-glycoprotein complex subunits are markers for airway smooth muscle phenotype maturation and together with caveolin-1, play an important role in calcium homeostasis. We tested if dystrophin affects phenotype maturation, tracheal contraction and lung physiology. We used dystrophin deficient Golden Retriever dogs (GRMD) and mdx mice vs healthy control animals in our approach. We found significant reduction of contractile protein markers: smooth muscle myosin heavy chain (smMHC) and calponin and reduced Ca2+ response to contractile agonist in dystrophin deficient cells. Immunocytochemistry revealed reduced stress fibers and number of smMHC positive cells in dystrophin-deficient cells, when compared to control. Immunoblot analysis of Akt1, GSK3β and mTOR phosphorylation further revealed that downstream PI3K signaling, which is essential for phenotype maturation, was suppressed in dystrophin deficient cell cultures. Tracheal rings from mdx mice showed significant reduction in the isometric contraction to methacholine (MCh) when compared to genetic control BL10ScSnJ mice (wild-type). In vivo lung function studies using a small animal ventilator revealed a significant reduction in peak airway resistance induced by maximum concentrations of inhaled MCh in mdx mice, while there was no change in other lung function parameters. These data show that the lack of dystrophin is associated with a concomitant suppression of ASM cell phenotype maturation in vitro, ASM contraction ex vivo and lung function in vivo, indicating that a linkage between the DGC and the actin cytoskeleton via dystrophin is a determinant of the phenotype and functional properties of ASM. © 2014 Sharma et al

Traffic pollution and the incidence of cardiorespiratory outcomes in an adult cohort in London.

OBJECTIVES: The epidemiological evidence for adverse health effects of long-term exposure to air and noise pollution from traffic is not coherent. Further, the relative roles of background versus near traffic pollution concentrations in this process are unclear. We investigated relationships between modelled concentrations of air and noise pollution from traffic and incident cardiorespiratory disease in London. METHODS: Among 211 016 adults aged 40-79 years registered in 75 Greater London practices between 2005 and 2011, the first diagnosis for a range of cardiovascular and respiratory outcomes were identified from primary care and hospital records. Annual baseline concentrations for nitrogen oxide (NOx), particulate matter with a median aerodynamic diameter <2.5 μm (PM2.5) attributable to exhaust and non-exhaust sources, traffic intensity and noise were estimated at 20 m(2) resolution from dispersion models, linked to clinical data via residential postcode. HRs were adjusted for confounders including smoking and area deprivation. RESULTS: The largest observed associations were between traffic-related air pollution and heart failure (HR=1.10 for 20 μg/m(3) change in NOx, 95% CI 1.01 to 1.21). However, no other outcomes were consistently associated with any of the pollution indicators, including noise. The greater variations in modelled air pollution from traffic between practices, versus within, hampered meaningful fine spatial scale analyses. CONCLUSIONS: The associations observed with heart failure may suggest exacerbatory effects rather than underlying chronic disease. However, the overall failure to observe wider associations with traffic pollution may reflect that exposure estimates based on residence inadequately represent the relevant pattern of personal exposure, and future studies must address this issue