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This document presents answers to 24 questions relevant to reviewing European policies on air pollution and to addressing health aspects of these policies. The answers were developed by a large group of scientists engaged in the WHO project "Review of evidence on health aspects of air pollution -REVIHAAP". The experts reviewed and discussed the newly accumulated scientific evidence on the adverse effects on health of air pollution, formulating science-based answers to the 24 questions. Extensive rationales for the answers, including the list of key references, are provided. The review concludes that a considerable amount of new scientific information on the adverse effects on health of particulate matter, ozone and nitrogen dioxide, observed at levels commonly present in Europe, has been published in recent years. This new evidence supports the scientific conclusions of the WHO air quality guidelines, last updated in 2005, and indicates that the effects in some cases occur at air pollution concentrations lower than those serving to establish these guidelines. It also provides scientific arguments for taking decisive actions to improve air quality and reduce the burden of disease associated with air pollution in Europe.This publication arises from the project REVIHAAP and has been co-funded by the European Union. Keywords AIR POLLUTANTS AIR POLLUTION -ADVERSE EFFECTS ENVIRONMENT AND PUBLIC HEALTH EVIDENCE BASED PRACTICE GUIDELINES HEALTH POLICYAddress requests about publications of the WHO Regional Office for Europe to: Publications WHO Regional Office for Europe Scherfigsvej 8 DK-2100 Copenhagen Ø, Denmark Alternatively, complete an online request form for documentation, health information, or for permission to quote or translate, on the Regional Office web site (http://www.euro.who.int/pubrequest). © World Health Organization 2013All rights reserved. The Regional Office for Europe of the World Health Organization welcomes requests for permission to reproduce or translate its publications, in part or in full.The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate borderlines for which there may not yet be full agreement.The mention of specific companies or of certain manufacturers products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.All reasonable precautions have been taken by the World Health Organization to verify the information contained in this publication. However, the published material is being distributed without warranty of any kind, either express or implied. ...

Self-assembly of benzene-1,3,5-tricarboxylic acid (trimesic acid - TMA) monolayers at the alkanoic acid-graphite interface is revisited. Even though this archetypal model system for hydrogen bonded porous networks is particularly well studied, the analysis of routinely observed superperiodic contrast modulations known as moiré patterns lags significantly behind. Fundamental questions remain unanswered such as, are moiré periodicity and orientation always the same, i.e. is exclusively only one specific moiré pattern observed? What are the geometric relationships (superstructure matrices) between moiré, TMA, and graphite lattices? What affects the moiré pattern formation? Is there any influence from solvent, concentration, or thermal treatment? These basic questions are addressed via scanning tunneling microscopy experiments at the liquid-solid interface, revealing a variety of different moiré patterns. Interestingly, TMA and graphite lattices were always found to be ∼5° rotated with respect to each other. Consequently, the observed variation in the moiré patterns is attributed to minute deviations (<2°) from this preferred orientation. Quantitative analysis of moiré periods and orientations facilitates the determination of the TMA lattice parameter with picometer precision.

B ushfires and hazard reduction burns routinely expose Australians to fine particulate matter with an aerodynamic diameter of less than 2.5 mm (PM 2.5 ) with a range of health effects, including premature mortality. 1 Exposure to landscape fire smoke (LFS) will rise as the frequency of bushfires increases with climate change. 2 To estimate the health effects of PM 2.5 exposure attributable to LFS in Sydney, we assessed all-cause mortality and hospitalisations for cardiovascular and respiratory disease in the Sydney Greater Capital City Statistical Area 3 (GCCSA) during 2001e2013.Our methods are described in the online Appendix. In brief, we quantified the population-level health effects attributable to pollutant exposure on the basis of risk estimates from epidemiological studies and local estimates of exposure and disease incidence. Dates of verified LFS events affecting Sydney were retrieved from a previously validated database 4 that included events identified in media archives, agency records, and satellite images for all days on which 24-hour mean PM 2.5 levels exceeded the 95th percentile of the long term daily city-wide averages. For each day with a validated LFS event, the background PM 2.5 level was estimated from the mean of the values for the 30 nearest non-LFS calendar days in each year. Daily PM 2.5 concentrations were interpolated to Sydney GCCSA Statistical Area 3 (SA3) averages. The health burden was estimated for each SA3 from death and hospitalisation incidence rates, daily PM 2.5 exposure, and epidemiological risk estimates recommended by the World Health Organization. 5 Formal ethics approval was not required for this analysis of publicly available data.A total of 184 LFS days (3% of all days) were identified (Box); the mean increase in mean population-weighted PM 2.5 level attributable to LFS was 12.1 mg/m 3 (standard deviation, 12.1 mg/m 3 ). We estimated that 197 premature deaths (95% confidence interval [CI], 101e295 deaths), 436 cardiovascular hospitalisations (95% CI, 163e717 hospitalisations), and 787 respiratory hospitalisations (95% CI, 119e1494 hospitalisations) were attributable to fire smoke on these days.Exposure estimates were based on a small number of air pollution monitors (six). Our conservative methods were similar to those applied in a recent assessment of hazard reduction burning near Sydney during May 2016 which estimated that 14 premature deaths were caused by LFS exposure. 6 Our results indicate that the health impact of LFS exposure during 2001e2013 was similar to having a May 2016-like event every 12 months.Our analysis suggests that LFS is an important contributor to overall air pollution and the related population health burden. Our health risk estimates assumed short term, immediate impacts of increased PM 2.5 levels, but extended exposure is likely to have greater effects. Further, we included in our analysis only LFS events associated with PM 2.5 levels exceeding the 95th percentile of background values; our exposure estimates may therefore be conservative. The e...

Exposure to traffic related nitrogen dioxide (NO) air pollution is associated with adverse health outcomes. Average pollutant concentrations for fixed monitoring sites are often used to estimate exposures for health studies, however these can be imprecise due to difficulty and cost of spatial modeling at the resolution of neighborhoods (e.g., a scale of tens of meters) rather than at a coarse scale (around several kilometers). The objective of this study was to derive improved estimates of neighborhood NO concentrations by blending measurements with modeled predictions in Sydney, Australia (a low pollution environment). We implemented the Bayesian maximum entropy approach to blend data with uncertainty defined using informative priors. We compiled NO data from fixed-site monitors, chemical transport models, and satellite-based land use regression models to estimate neighborhood annual average NO. The spatial model produced a posterior probability density function of estimated annual average concentrations that spanned an order of magnitude from 3 to 35 ppb. Validation using independent data showed improvement, with root mean squared error improvement of 6% compared with the land use regression model and 16% over the chemical transport model. These estimates will be used in studies of health effects and should minimize misclassification bias.

Objectives To estimate the annual burden of mortality and the associated health costs attributable to air pollution from wood heaters in Armidale. Design Health impact assessment (excess annual mortality and financial costs) based upon atmospheric PM2.5 measurements. Setting Armidale, a regional Australian city (population, 24 504) with high levels of air pollution in winter caused by domestic wood heaters, 1 May 2018 – 30 April 2019. Main outcome measures Estimated population exposure to PM2.5 from wood heaters; estimated numbers of premature deaths and years of life lost. Results Fourteen premature deaths (95% CI, 12–17 deaths) per year, corresponding to 210 (95% CI, 172–249) years of life lost, are attributable to long term exposure to wood heater PM2.5 pollution in Armidale. The estimated financial cost is $32.8 million (95% CI, $27.0–38.5 million), or $10 930 (95% CI, $9004–12 822) per wood heater per year. Conclusions The substantial mortality and financial cost attributable to wood heating in Armidale indicates that effective policies are needed to reduce wood heater pollution, including public education about the effects of wood smoke on health, subsidies that encourage residents to switch to less polluting home heating (perhaps as part of an economic recovery package), assistance for those affected by wood smoke from other people, and regulations that reduce wood heater use (eg, by not permitting new wood heaters and requiring existing units to be removed when houses are sold).

Ambient fine particulate matter <2.5 µm (PM2.5) air pollution increases premature mortality globally. Some PM2.5 is natural, but anthropogenic PM2.5 is comparatively avoidable. We determined the impact of long-term exposures to the anthropogenic PM component on mortality in Australia. PM2.5-attributable deaths were calculated for all Australian Statistical Area 2 (SA2; n = 2310) regions. All-cause death rates from Australian mortality and population databases were combined with annual anthropogenic PM2.5 exposures for the years 2006–2016. Relative risk estimates were derived from the literature. Population-weighted average PM2.5 concentrations were estimated in each SA2 using a satellite and land use regression model for Australia. PM2.5-attributable mortality was calculated using a health-impact assessment methodology with life tables and all-cause death rates. The changes in life expectancy (LE) from birth, years of life lost (YLL), and economic cost of lost life years were calculated using the 2019 value of a statistical life. Nationally, long-term population-weighted average total and anthropogenic PM2.5 concentrations were 6.5 µg/m3 (min 1.2–max 14.2) and 3.2 µg/m3 (min 0–max 9.5), respectively. Annually, anthropogenic PM2.5-pollution is associated with 2616 (95% confidence intervals 1712, 3455) deaths, corresponding to a 0.2-year (95% CI 0.14, 0.28) reduction in LE for children aged 0–4 years, 38,962 (95%CI 25,391, 51,669) YLL and an average annual economic burden of $6.2 billion (95%CI $4.0 billion, $8.1 billion). We conclude that the anthropogenic PM2.5-related costs of mortality in Australia are higher than community standards should allow, and reductions in emissions are recommended to achieve avoidable mortality.

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