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Air pollution poses a threat to human health, with pregnant women and their developing fetuses being particularly vulnerable. A high dual burden of ambient and indoor air pollution exposure has been identified in Ethiopia, but studies investigating their effects on adverse birth outcomes are currently lacking. This study explores the association between ambient air pollution (NO

Luftföroreningar står för ett av åtta förtida dödsfall i världen, och utgör därmed ett stort hot mot människors hälsa. HIA (hälsokonsekvensbedömningar) av hypotetiska förändringar i luftföroreningshalter kan användas som ett sätt att bedöma hälsoeffekter, planer och projekt som beslutsfattare behöver för att förhindra sjukdom. Syftet med denna studie var att beräkna hälsoeffekter som kan tillskrivas hypotetisk nedgång i luftföroreningshalter i Malmö i södra Sverige om en policy med avgasfri innerstad skulle genomföras. Air pollution is responsible for one in eight premature deaths worldwide, and thereby a major threat to human health. Health impact assessments of hypothetic changes in air pollution concentrations can be used as a mean of assessing the health impacts of policy, plans and projects, and support decision-makers in choices to prevent disease. The aim of this study was to estimate health impacts attributable to a hypothetical decrease in air pollution concentrations in the city of Malmö in Southern Sweden corresponding to a policy on-road transportations without tail-pipe emissions in the municipality. We used air pollution data modelled for each of the 326,092 inhabitants in Malmö by a Gaussian dispersion model combined with an emission database with >40,000 sources. The dispersion model calculates Nitrogen Oxides (NO) (later transformed into Nitrogen Dioxide (NO)) and particulate matter with an aerodynamic diameter

Individual differences in cognitive performance increase with advancing age, reflecting marked cognitive changes in some individuals along with little or no change in others. Genetic and lifestyle factors are assumed to influence cognitive performance in ageing by affecting the magnitude and extent of age-related brain changes (i.e., brain maintenance or atrophy), as well as the ability to recruit compensatory processes. The purpose of this review is to present findings from the Betula study and other longitudinal studies, with a focus on clarifying the role of key biological and environmental factors assumed to underlie individual differences in brain and cognitive ageing. We discuss the vital importance of sampling, analytic methods, consideration of non-ignorable dropout, and related issues for valid conclusions on factors that influence healthy neurocognitive ageing.

SummaryPsychological factors such as anxiety and depression are prevalent in patients with asthma. The purpose of this study was to investigate the relationship between respiratory symptoms and psychological status and to estimate the importance of psychological status in comparison with other factors that are known to be associated with respiratory symptoms.This study included 2270 subjects aged 20–44 (52% female) from Sweden, Iceland, and Norway. Each participant underwent a clinical interview including questions on respiratory symptoms. Spirometry and methacholine challenge were performed. Symptoms of depression and anxiety were measured using the Hospital Anxiety and Depression Scale (HADS).Eighty-two percent of the subjects reported no anxiety or depression whatsoever, 11% reported anxiety, 2.5% depression and 4% reported both anxiety and depression. All respiratory symptoms, such as wheezing, breathlessness and nightly symptoms, were more common, at a statistically significant level, in participants who had depression and anxiety, even after adjusting for confounders (ORs 1.33–1.94). The HADS score was the most important determinant for nightly symptoms and attacks of breathlessness when at rest whereas bronchial responsiveness was the most important determinant for wheezing, and breathlessness when wheezing. The probability of respiratory symptoms related to HADS score increased with increasing HADS score for all respiratory symptoms.In conclusion, there is a strong association between respiratory symptoms and psychological status. There is therefore a need for interventional studies designed to improve depression and anxiety in patients with respiratory symptoms.

BACKGROUND: Few studies on long-term exposure to air pollution and mortality have been reported from Europe. Within the multicentre European Study of Cohorts for Air Pollution Effects (ESCAPE), we aimed to investigate the association between natural-cause mortality and long-term exposure to several air pollutants. METHODS: We used data from 22 European cohort studies, which created a total study population of 367,251 participants. All cohorts were general population samples, although some were restricted to one sex only. With a strictly standardised protocol, we assessed residential exposure to air pollutants as annual average concentrations of particulate matter (PM) with diameters of less than 2.5 μm (PM2.5), less than 10 μm (PM10), and between 10 μm and 2.5 μm (PMcoarse), PM2.5 absorbance, and annual average concentrations of nitrogen oxides (NO2 and NOx), with land use regression models. We also investigated two traffic intensity variables-traffic intensity on the nearest road (vehicles per day) and total traffic load on all major roads within a 100 m buffer. We did cohort-specific statistical analyses using confounder models with increasing adjustment for confounder variables, and Cox proportional hazards models with a common protocol. We obtained pooled effect estimates through a random-effects meta-analysis. FINDINGS: The total study population consisted of 367,251 participants who contributed 5,118,039 person-years at risk (average follow-up 13.9 years), of whom 29,076 died from a natural cause during follow-up. A significantly increased hazard ratio (HR) for PM2.5 of 1.07 (95% CI 1.02-1.13) per 5 μg/m(3) was recorded. No heterogeneity was noted between individual cohort effect estimates (I(2) p value=0.95). HRs for PM2.5 remained significantly raised even when we included only participants exposed to pollutant concentrations lower than the European annual mean limit value of 25 μg/m(3) (HR 1.06, 95% CI 1.00-1.12) or below 20 μg/m(3) (1.07, 1.01-1.13). INTERPRETATION: Long-term exposure to fine particulate air pollution was associated with natural-cause mortality, even within concentration ranges well below the present European annual mean limit value. FUNDING: European Community's Seventh Framework Program (FP7/2007-2011).

e439 www.thelancet.com/oncology Vol 14 October 2013 on day 15. We acknowledged the lower proportion of responses in the placebo group, but we cannot agree with Zheng and colleagues’ simplistic projection of longer overall survival by assumption of an arbitrary response rate. Proof of statistical signifi cance is a vigorous exercise using actual and accurate data. Zheng and colleagues’ simple correlative interpretation is not in accordance with basic statistical principles. The pharmacodynamic separation model is an interesting preclinical theory. We attempted to validate this theory with FASTACT and FASTACT-2, and only found benefi t in patients with EGFR mutations. As explained in our discussion, we no longer believe that the avoidance of G1 arrest is the only mechanism contributing to positive outcomes; early exposure of patients with heterogeneous tumours to chemotherapy is the other major reason for better survival. Zheng and colleagues might also have misunderstood table 3 on poststudy treatment. Low percentage of exposure to second-line taxane (1%) or pemetrexed (2%) in the placebo group is explained by the high percentage (85%) of patients who received second-line EGFR tyrosinekinase inhibitors. In other words, 88% of patients from the placebo group received second-line therapy whereas only 39% from the treatment group did. Furthermore, overall survival benefi t is confi ned to only patients with EGFR mutations. The mutation-positive control group contained 48 patients, thus only seven (not 34) patients did not receive a second-line EGFR tyrosinekinase inhibitors. This cannot be the sole reason for the 10 month diff erence in median overall survival. We agree with Zheng and colleagues’ fi nal comment on not acting too fast—we have never intended to do so anyway.