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Urban climate policy offers a significant opportunity to promote improved public health. The evidence around climate and health cobenefits is growing but has yet to translate into widespread integrated policies. This article presents two systematic reviews: first, looking at quantified cobenefits of urban climate policies, where transportation, land use, and buildings emerge as the most studied sectors; and second, looking at review papers exploring the barriers and enablers for integrating these health cobenefits into urban policies. The latter reveals wide agreement concerning the need to improve the evidence base for cobenefits and consensus about the need for greater political will and leadership on this issue. Systems thinking may offer a way forward to help embrace complexity and integrate health cobenefits into decision making. Knowledge coproduction to bring stakeholders together and advance policy-relevant research for urban health will also be required. Action is needed to bring these two important policy agendas together.

Epidemiological cohort studies have consistently found associations between long-term exposure to outdoor air pollution and a range of morbidity and mortality endpoints. Recent evaluations by the World Health Organization and the Global Burden of Disease study have suggested that these associations may be nonlinear and may persist at very low concentrations. Studies conducted in North America in particular have suggested that associations with mortality persisted at concentrations of particulate matter with an aerodynamic diameter of less than 2.5 μm (PM2.5) well below current air quality standards and guidelines. The uncertainty about the shape of the concentration-response function at the low end of the concentration distribution, related to the scarcity of observations in the lowest range, was the basis of the current project. Previous studies have focused on PM2.5, but increasingly associations with nitrogen dioxide (NO2) are being reported, particularly in studies that accounted for the fine spatial scale variation of NO2. Very few studies have evaluated the effects of long-term exposure to low concentrations of ozone (O3). Health effects of black carbon (BC), representing primary combustion particles, have not been studied in most large cohort studies of PM2.5. Cohort studies assessing health effects of particle composition, including elements from nontailpipe traffic emissions (iron, copper, and zinc) and secondary aerosol (sulfur) have been few in number and reported inconsistent results.

Rationale: Ambient air pollution exposure has been linked to mortality from chronic cardiorespiratory diseases, while evidence on respiratory infections remains more limited. Objectives: We examined the association between long-term exposure to air pollution and pneumonia-related mortality in adults in a pool of eight European cohorts. Methods: Within the multicenter project ELAPSE (Effects of Low-Level Air Pollution: A Study in Europe), we pooled data from eight cohorts among six European countries. Annual mean residential concentrations in 2010 for fine particulate matter, nitrogen dioxide (NO2), black carbon (BC), and ozone were estimated using Europe-wide hybrid land-use regression models. We applied stratified Cox proportional hazard models to investigate the associations between air pollution and pneumonia, influenza, and acute lower respiratory infections (ALRI) mortality. Measurements and Main Results: Of 325,367 participants, 712 died from pneumonia and influenza combined, 682 from pneumonia, and 695 from ALRI during a mean follow-up of 19.5 years. NO2 and BC were associated with 10–12% increases in pneumonia and influenza combined mortality, but 95% confidence intervals included unity (hazard ratios, 1.12 [0.99–1.26] per 10 μg/m3 for NO2; 1.10 [0.97–1.24] per 0.5 1025m21 for BC). Associations with pneumonia and ALRI mortality were almost identical. We detected effect modification suggesting stronger associations with NO2 or BC in overweight, employed, or currently smoking participants compared with normal weight, unemployed, or nonsmoking participants. Conclusions: Long-term exposure to combustion-related air pollutants NO2 and BC may be associated with mortality from lower respiratory infections, but larger studies are needed to estimate these associations more precisely.

Background: The evidence linking ambient air pollution to bladder cancer is limited and mixed. Methods: We assessed the associations of bladder cancer incidence with residential exposure to fine particles (PM2.5), nitrogen dioxide (NO2), black carbon (BC), warm season ozone (O3) and eight PM2.5 elemental components (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) in a pooled cohort (N = 302,493). Exposures were primarily assessed based on 2010 measurements and back-extrapolated to the baseline years. We applied Cox proportional hazard models adjusting for individual- and area-level potential confounders. Results: During an average of 18.2 years follow-up, 967 bladder cancer cases occurred. We observed a positive though statistically non-significant association between PM2.5 and bladder cancer incidence. Hazard Ratios (HR) were 1.09 (95% confidence interval (CI): 0.93–1.27) per 5 µg/m3 for 2010 exposure and 1.06 (95% CI: 0.99–1.14) for baseline exposure. Effect estimates for NO2, BC and O3 were close to unity. A positive association was observed with PM2.5 zinc (HR 1.08; 95% CI: 1.00–1.16 per 10 ng/m3). Conclusions: We found suggestive evidence of an association between long-term PM2.5 mass exposure and bladder cancer, strengthening the evidence from the few previous studies. The association with zinc in PM2.5 suggests the importance of industrial emissions.

Background Nickel allergy is the most prevalent contact allergy. It belongs to a different hypersensitivity type to asthma and rhinoconjunctivitis. The aim of this analysis was to assess whether self-reported nickel allergy is associated with incident wheezing, asthma and rhinoconjunctivitis in young German adults, taking into account potential effect modification by sex. Methods In total, 2051 (70.6%) participants aged 19–24 years took part in the second phase of SOLAR (Study on Occupational Allergy Risks), a follow-up study of ISAAC II (the second phase of the International Study of Asthma and Allergies in Childhood) in Germany. Self-reported nickel allergy, as well as having pierced ears, and the three outcomes incident wheezing, asthma and rhinoconjunctivitis, were analysed stratified for sex. Logistic regression adjusted for potential confounders was performed. Results An association between self-reported nickel allergy and incident wheezing was observed for men and women, while only in males did pierced ears show a significant association with the outcome (adjusted OR 2.26, 95% CI 1.10–4.62). Also only in males, self-reported nickel allergy was associated with elevated odds for incident asthma (adjusted OR 4.34, 95% CI 1.22–15.41). Neither in men nor in women was a significant association observed for incident rhinoconjunctivitis. Conclusion Our results suggest that self-reported nickel allergy is associated with incident wheezing. Whether this association is due to environmental or genetic predisposition, or due to an overlap of the mechanisms of type I and type IV hypersensitivity, needs to be elucidated., Self-reported nickel allergy is associated with incident wheezing in young German males and females, and with incident asthma in males, whereas no significant association was observed for self-reported nickel allergy and incident rhinoconjunctivitis http://bit.ly/2YHmwBA

Ambient air pollution is an established risk factor for premature mortality from chronic cardiovascular, respiratory and metabolic diseases, while evidence on neurodegenerative diseases and psychiatric disorders remains limited. We examined the association between long-term exposure to air pollution and mortality from dementia, psychiatric disorders, and suicide in seven European cohorts. Within the multicenter project ‘Effects of Low-Level Air Pollution: A Study in Europe’ (ELAPSE), we pooled data from seven European cohorts from six countries. Based on the residential addresses, annual mean levels of fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC), ozone (O3), and 8 PM2.5 components were estimated using Europe-wide hybrid land-use regression models. We applied stratified Cox proportional hazard models to investigate the associations between air pollution and mortality from dementia, psychiatric disorders, and suicide. Of 271,720 participants, 900 died from dementia, 241 from psychiatric disorders, and 164 from suicide, during a mean follow-up of 19.7 years. In fully adjusted models, we observed positive associations of NO2 (hazard ratio [HR] = 1.38; 95 % confidence interval [CI]: 1.13, 1.70 per 10 µg/m3), PM2.5 (HR = 1.29; 95 % CI: 0.98, 1.71 per 5 µg/m3), and BC (HR = 1.37; 95 % CI: 1.11, 1.69 per 0.5 × 10−5/m) with psychiatric disorders mortality, as well as with suicide (NO2: HR = 1.13 [95 % CI: 0.92, 1.38]; PM2.5: HR = 1.19 [95 % CI: 0.76, 1.87]; BC: HR = 1.08 [95 % CI: 0.87, 1.35]), and no association with dementia mortality. We did not detect any positive associations of O3 and 8 PM2.5 components with any of the three mortality outcomes. Long-term exposure to NO2, PM2.5, and BC may lead to premature mortality from psychiatric disorders and suicide.

Particulate matter air pollution and diesel engine exhaust have been classified as carcinogenic for lung cancer, yet few studies have explored associations with liver cancer. We used six European adult cohorts which were recruited between 1985 and 2005, pooled within the “Effects of low-level air pollution: A study in Europe” (ELAPSE) project, and followed for the incidence of liver cancer until 2011 to 2015. The annual average exposure to nitrogen dioxide (NO 2), particulate matter with diameter 2.5), black carbon (BC), warm-season ozone (O 3), and eight elemental components of PM 2.5 (copper, iron, zinc, sulfur, nickel, vanadium, silicon, and potassium) were estimated by European-wide hybrid land-use regression models at participants' residential addresses. We analyzed the association between air pollution and liver cancer incidence by Cox proportional hazards models adjusting for potential confounders. Of 330 064 cancer-free adults at baseline, 512 developed liver cancer during a mean follow-up of 18.1 years. We observed positive linear associations between NO 2 (hazard ratio, 95% confidence interval: 1.17, 1.02-1.35 per 10 μg/m 3), PM 2.5 (1.12, 0.92-1.36 per 5 μg/m 3), and BC (1.15, 1.00-1.33 per 0.5 10 −5/m) and liver cancer incidence. Associations with NO 2 and BC persisted in two-pollutant models with PM 2.5. Most components of PM 2.5 were associated with the risk of liver cancer, with the strongest associations for sulfur and vanadium, which were robust to adjustment for PM 2.5 or NO 2. Our study suggests that ambient air pollution may increase the risk of liver cancer, even at concentrations below current EU standards.

BACKGROUND AND AIM: The epidemiological evidence on associations between ambient air pollution and bladder cancer is limited. We aimed to evaluate the associations between long-term exposure to amb...

BackgroundLong-term exposure to ambient air pollution has been linked to childhood-onset asthma, although evidence is still insufficient. Within the multicentre project Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), we examined the associations of long-term exposures to particulate matter with a diameter 2.5), nitrogen dioxide (NO2) and black carbon (BC) with asthma incidence in adults.MethodsWe pooled data from three cohorts in Denmark and Sweden with information on asthma hospital diagnoses. The average concentrations of air pollutants in 2010 were modelled by hybrid land-use regression models at participants’ baseline residential addresses. Associations of air pollution exposures with asthma incidence were explored with Cox proportional hazard models, adjusting for potential confounders.ResultsOf 98 326 participants, 1965 developed asthma during a mean follow-up of 16.6 years. We observed associations in fully adjusted models with hazard ratios of 1.22 (95% CI 1.04–1.43) per 5 μg·m−3 for PM2.5, 1.17 (95% CI 1.10–1.25) per 10 µg·m−3 for NO2 and 1.15 (95% CI 1.08–1.23) per 0.5×10−5 m−1 for BC. Hazard ratios were larger in cohort subsets with exposure levels below the European Union and US limit values and possibly World Health Organization guidelines for PM2.5 and NO2. NO2 and BC estimates remained unchanged in two-pollutant models with PM2.5, whereas PM2.5 estimates were attenuated to unity. The concentration–response curves showed no evidence of a threshold.ConclusionsLong-term exposure to air pollution, especially from fossil fuel combustion sources such as motorised traffic, was associated with adult-onset asthma, even at levels below the current limit values.

Background: The SITLESS programme comprises exercise referral schemes and self-management strategies and has been evaluated in a trial in Denmark, Spain, Germany and Northern Ireland. The aim of this qualitative study was to understand the implementation and contextual aspects of the intervention in relation to the mechanisms of impact and to explore the perceived effects. Methods: Qualitative methodologies were nested in the SITLESS trial including 71 individual interviews and 12 focus groups targeting intervention and control group participants from postintervention to 18-month follow-up in all intervention sites based on a semi-structured topic guide. Results: Overarching themes were identified under the framework categories of context, implementation, mechanisms of impact and perceived effects. The findings highlight the perceived barriers and facilitators to older adults’ engagement in exercise referral schemes. Social interaction and enjoyment through the group-based programmes are key components to promote adherence and encourage the maintenance of targeted behaviours through peer support and connectedness. Exit strategies and signposting to relevant classes and facilities enabled the maintenance of positive lifestyle behaviours. Conclusions: When designing and implementing interventions, key components enhancing social interaction, enjoyment and continuity should be in place in order to successfully promote sustained behaviour change., publishedVersion

This study analyzes the association of work-related stress with incident asthma and rhinitis in young adults with a special focus on gender-specific differences. Incident asthma, wheezing and rhinitis were measured in a cohort of 2051 young German adults (aged 16–18 years at baseline) recruited by the prospective population-based SOLAR study (Study of Occupational Allergy Risks). Work-related stress was measured by the Trier Inventory for the Assessment of Chronic Stress (TICS). Two TICS scales, work overload and work discontent, were analysed. Logistic regression was conducted to calculate odds ratios (OR) and 95% confidence intervals (CI). In females, the odds for incident asthma were found to be 17% higher for each increase of the work discontent score by one point (OR 1.17, 95% CI 1.04–1.31). In males, no association was statistically significant. Incident rhinitis showed no association with any exposure variable. This study shows a link between work-related stress and incident asthma which seems to be confined to women. This study adds evidence about the association of work-related stress and asthma in young adults and can contribute to prevention for that particular age group.

BACKGROUND: Inconsistent associations between long-term exposure to particles with an aerodynamic diameter ≤ 2.5 μ m [fine particulate matter ( PM 2.5 )] components and mortality have been reported, partly related to challenges in exposure assessment. OBJECTIVES: We investigated the associations between long-term exposure to PM 2.5 elemental components and mortality in a large pooled European cohort; to compare health effects of PM 2.5 components estimated with two exposure modeling approaches, namely, supervised linear regression (SLR) and random forest (RF) algorithms. METHODS: We pooled data from eight European cohorts with 323,782 participants, average age 49 y at baseline (1985-2005). Residential exposure to 2010 annual average concentration of eight PM 2.5 components [copper (Cu), iron (Fe), potassium (K), nickel (Ni), sulfur (S), silicon (Si), vanadium (V), and zinc (Zn)] was estimated with Europe-wide SLR and RF models at a 100 × 100 m scale. We applied Cox proportional hazards models to investigate the associations between components and natural and cause-specific mortality. In addition, two-pollutant analyses were conducted by adjusting each component for PM 2.5 mass and nitrogen dioxide ( NO 2 ) separately. RESULTS: We observed 46,640 natural-cause deaths with 6,317,235 person-years and an average follow-up of 19.5 y. All SLR-modeled components were statistically significantly associated with natural-cause mortality in single-pollutant models with hazard ratios (HRs) from 1.05 to 1.27. Similar HRs were observed for RF-modeled Cu, Fe, K, S, V, and Zn with wider confidence intervals (CIs). HRs for SLR-modeled Ni, S, Si, V, and Zn remained above unity and (almost) significant after adjustment for both PM 2.5 and NO 2 . HRs only remained (almost) significant for RF-modeled K and V in two-pollutant models. The HRs for V were 1.03 (95% CI: 1.02, 1.05) and 1.06 (95% CI: 1.02, 1.10) for SLR- and RF-modeled exposures, respectively, per 2 ng / m 3 , adjusting for PM 2.5 mass. Associations with cause-specific mortality were less consistent in two-pollutant models. CONCLUSION: Long-term exposure to V in PM 2.5 was most consistently associated with increased mortality. Associations for the other components were weaker for exposure modeled with RF than SLR in two-pollutant models. https://doi.org/10.1289/EHP8368.

Objective To investigate the associations between air pollution and mortality, focusing on associations below current European Union, United States, and World Health Organization standards and guidelines. Design Pooled analysis of eight cohorts. Setting Multicentre project Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE) in six European countries. Participants 325 367 adults from the general population recruited mostly in the 1990s or 2000s with detailed lifestyle data. Stratified Cox proportional hazard models were used to analyse the associations between air pollution and mortality. Western Europe-wide land use regression models were used to characterise residential air pollution concentrations of ambient fine particulate matter (PM 2.5 ), nitrogen dioxide, ozone, and black carbon. Main outcome measures Deaths due to natural causes and cause specific mortality. Results Of 325 367 adults followed-up for an average of 19.5 years, 47 131 deaths were observed. Higher exposure to PM 2.5 , nitrogen dioxide, and black carbon was associated with significantly increased risk of almost all outcomes. An increase of 5 µg/m 3 in PM 2.5 was associated with 13% (95% confidence interval 10.6% to 15.5%) increase in natural deaths; the corresponding figure for a 10 µg/m 3 increase in nitrogen dioxide was 8.6% (7% to 10.2%). Associations with PM 2.5 , nitrogen dioxide, and black carbon remained significant at low concentrations. For participants with exposures below the US standard of 12 µg/m 3 an increase of 5 µg/m 3 in PM 2.5 was associated with 29.6% (14% to 47.4%) increase in natural deaths. Conclusions Our study contributes to the evidence that outdoor air pollution is associated with mortality even at low pollution levels below the current European and North American standards and WHO guideline values. These findings are therefore an important contribution to the debate about revision of air quality limits, guidelines, and standards, and future assessments by the Global Burden of Disease.

Background/aim: Ambient air pollution has been associated with lung cancer, but the shape of the exposure-response function - especially at low exposure levels - is not well described. The aim of this study was to address the relationship between long-term low-level air pollution exposure and lung cancer incidence. Methods: The “Effects of Low-level Air Pollution: a Study in Europe” (ELAPSE) collaboration pools seven cohorts from across Europe. We developed hybrid models combining air pollution monitoring, land use data, satellite observations, and dispersion model estimates for nitrogen dioxide (NO2), fine particulate matter (PM2.5), black carbon (BC), and ozone (O3) to assign exposure to cohort participants’ residential addresses in 100 m by 100 m grids. We applied stratified Cox proportional hazards models, adjusting for potential confounders (age, sex, calendar year, marital status, smoking, body mass index, employment status, and neighborhood-level socio-economic status). We fitted linear models, linear models in subsets, Shape-Constrained Health Impact Functions (SCHIF), and natural cubic spline models to assess the shape of the association between air pollution and lung cancer at concentrations below existing standards and guidelines. Results: The analyses included 307,550 cohort participants. During a mean follow-up of 18.1 years, 3956 incident lung cancer cases occurred. Median (Q1, Q3) annual (2010) exposure levels of NO2, PM2.5, BC and O3 (warm season) were 24.2 µg/m3 (19.5, 29.7), 15.4 µg/m3 (12.8, 17.3), 1.6 10−5m−1 (1.3, 1.8), and 86.6 µg/m3 (78.5, 92.9), respectively. We observed a higher risk for lung cancer with higher exposure to PM2.5 (HR: 1.13, 95% CI: 1.05, 1.23 per 5 µg/m3). This association was robust to adjustment for other pollutants. The SCHIF, spline and subset analyses suggested a linear or supra-linear association with no evidence of a threshold. In subset analyses, risk estimates were clearly elevated for the subset of subjects with exposure below the EU limit value of 25 µg/m3. We did not observe associations between NO2, BC or O3 and lung cancer incidence. Conclusions: Long-term ambient PM2.5 exposure is associated with lung cancer incidence even at concentrations below current EU limit values and possibly WHO Air Quality Guidelines.

Improving the capacity for physical activity interventions to maintain behavior change is a key public health concern and an important strategy for the health and independence of older adults. Ways of ensuring effective maintenance of physical activity levels in older adults are unclear. This study includes the objective measure of moderate-to-vigorous physical activity (MVPA); self-reported self-efficacy; and self-regulation at four timepoints (baseline, intervention completion at 4 months, 12-, and 18-month follow-up) from the SITLESS study, a clinical trial conducted with a cohort of community-dwelling older adults (≥65 years) from Denmark, Germany, Spain, and the United Kingdom. A cross-lagged analysis found that self-regulation and self-efficacy may be key determinants of MVPA behavior in community-dwelling older adults. More specifically, the use of behavioral support strategies represents an important correlate of MVPA behavior, and its association with MVPA may be mediated by self-regulation and self-efficacy in older adults in the short and long term.

We developed Europe-wide models of long-term exposure to eight elements (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) in particulate matter with diameter

Reduced lung function is associated with overall and cardiovascular mortality. Chronic low grade systemic inflammation is linked to impaired lung function and cardiovascular outcomes. We assessed the association of lung function with overall 8-year mortality in 867 individuals of the Activity and Function in the Elderly study using confounder-adjusted Cox proportional hazards models (including gait speed and daily walking time as measures of physical function) without and with adjustment for inflammatory and cardiac markers. Forced expiratory volume in 1 s/forced vital capacity ( FEV1/FVC) but not FVC was related to mortality after adjustment for physical function and other confounders. Additional adjustment for inflammatory and cardiac markers did not change the hazard ratios (HR) markedly, e.g. for a FEV1/ FVC below 0.7 from 1.55 [95% confidence-interval (CI) 1.14���2.11] to 1.49 (95% CI 1.09���2.03). These independent associations were also observed in the apparently lung healthy subpopulation with even higher HRs up to 2.76 (95% CI 1.52���4.93). A measure of airflow limitation but not vital capacity was associated with overall mortality in this community-dwelling older population and in the subgroup classified as lung healthy. These associations were independent of adjustment for inflammatory and cardiac markers and support the role of airflow limitation as independent predictor of mortality in older adults., publishedVersion

Motivated by a growing recognition of the climate emergency, reflected in the 26th Conference of the Parties (COP26), we outline untapped opportunities to improve health through ambitious climate actions in cities. Health is a primary reason for climate action yet is rarely integrated in urban climate plans as a policy goal. This is a missed opportunity to create sustainable alliances across sectors and groups, to engage a broad set of stakeholders, and to develop structural health promotion. In this statement, we first briefly review the literature on health co-benefits of urban climate change strategies and make the case for health-promoting climate action; we then describe barriers to integrating health in climate action. We found that the evidence-base is often insufficiently policy-relevant to be impactful. Research rarely integrates the complexity of real-world systems, including multiple and dynamic impacts of strategies, and consideration of how decision-making processes contend with competing interests and short-term electoral cycles. Due to siloed-thinking and restrictive funding opportunities, research often falls short of the type of evidence that would be most useful for decision-making, and research outputs can be cryptic to decision makers. As a way forward, we urge researchers and stakeholders to engage in co-production and systems thinking approaches. Partnering across sectors and disciplines is urgently needed so pathways to climate change mitigation and adaptation fully embrace their health-promoting potential and engage society towards the huge transformations needed. This commentary is endorsed by the International Society for Environmental Epidemiology (ISEE) and the International Society for Urban Health (ISUH) and accompanies a sister statement oriented towards stakeholders (published on the societies’ websites).

BACKGROUND: Previous studies showed controversial results for the influence of pregnancy-related and perinatal factors on subsequent respiratory and atopic diseases in children. The aim of this study was to assess the association between perinatal variables and the prevalence of asthma, bronchial hyperreactivity (BHR), flexural eczema (FE), allergic rhinitis, and sensitization in childhood and early adulthood. METHODS: The studied population was first examined in Munich and Dresden in 1995/1996 at age 9-11 years. Participants were followed until age 19-24 years using questionnaires and clinical examinations. Associations between perinatal data and subsequent atopic diseases were examined using logistic regression analyses adjusting for potential confounders. RESULTS: Cesarean section was statistically significantly associated with BHR in early adulthood (odds ratio 4.8 [95% confidence interval 1.5-15.2]), while assisted birth was associated with presence of asthma symptoms in childhood (2.2 [1.2-3.9]), FE symptoms (2.2 [1.2-4.3]) and doctor's diagnosis of atopic dermatitis (1.9 [1.0-3.4]) in childhood, and sensitization in early adulthood (2.2 [1.1-4.3]). Lower birth length (1.9 [1.1-3.2]), lower birthweight (0.5 [0.3-0.9]), and higher birthweight (0.6 [0.4-1.0]) were predictive of sensitization in early adulthood compared to average birth length and birthweight, respectively. None of the other perinatal factors showed statistically significant associations with the outcomes. CONCLUSIONS: Our results indicate that children who are born by cesarean section and especially by assisted birth, might be at greater risk for developing asthma, FE, and sensitization and should hence be monitored. Prenatal maternal stress might partly explain these associations, which should be further investigated.

Several studies have indicated weakly increased risk for kidney cancer among occupational groups exposed to gasoline vapors, engine exhaust, polycyclic aromatic hydrocarbons and other air pollutant ...

Background: An association between long-term exposure to fine particulate matter (PM2.5) and lung cancer has been established in previous studies. PM2.5 is a complex mixture of chemical components from various sources and little is known about whether certain components contribute specifically to the associated lung cancer risk. The present study builds on recent findings from the “Effects of Low-level Air Pollution: A Study in Europe” (ELAPSE) collaboration and addresses the potential association between specific elemental components of PM2.5 and lung cancer incidence. Methods: We pooled seven cohorts from across Europe and assigned exposure estimates for eight components of PM2.5 representing non-tail pipe emissions (copper (Cu), iron (Fe), and zinc (Zn)), long-range transport (sulfur (S)), oil burning/industry emissions (nickel (Ni), vanadium (V)), crustal material (silicon (Si)), and biomass burning (potassium (K)) to cohort participants’ baseline residential address based on 100 m by 100 m grids from newly developed hybrid models combining air pollution monitoring, land use data, satellite observations, and dispersion model estimates. We applied stratified Cox proportional hazards models, adjusting for potential confounders (age, sex, calendar year, marital status, smoking, body mass index, employment status, and neighborhood-level socio-economic status). Results: The pooled study population comprised 306,550 individuals with 3916 incident lung cancer events during 5,541,672 person-years of follow-up. We observed a positive association between exposure to all eight components and lung cancer incidence, with adjusted HRs of 1.10 (95% CI 1.05, 1.16) per 50 ng/m3 PM2.5 K, 1.09 (95% CI 1.02, 1.15) per 1 ng/m3 PM2.5 Ni, 1.22 (95% CI 1.11, 1.35) per 200 ng/m3 PM2.5 S, and 1.07 (95% CI 1.02, 1.12) per 200 ng/m3 PM2.5 V. Effect estimates were largely unaffected by adjustment for nitrogen dioxide (NO2). After adjustment for PM2.5 mass, effect estimates of K, Ni, S, and V were slightly attenuated, whereas effect estimates of Cu, Si, Fe, and Zn became null or negative. Conclusions: Our results point towards an increased risk of lung cancer in connection with sources of combustion particles from oil and biomass burning and secondary inorganic aerosols rather than non-exhaust traffic emissions. Specific limit values or guidelines targeting these specific PM2.5 components may prove helpful in future lung cancer prevention strategies.

Exposure to ambient fine particulate matter (PM 2.5 ) is a major global health concern. Quantitative estimates of attributable mortality are based on disease-specific hazard ratio models that incorporate risk information from multiple PM 2.5 sources (outdoor and indoor air pollution from use of solid fuels and secondhand and active smoking), requiring assumptions about equivalent exposure and toxicity. We relax these contentious assumptions by constructing a PM 2.5 -mortality hazard ratio function based only on cohort studies of outdoor air pollution that covers the global exposure range. We modeled the shape of the association between PM 2.5 and nonaccidental mortality using data from 41 cohorts from 16 countries—the Global Exposure Mortality Model (GEMM). We then constructed GEMMs for five specific causes of death examined by the global burden of disease (GBD). The GEMM predicts 8.9 million [95% confidence interval (CI): 7.5–10.3] deaths in 2015, a figure 30% larger than that predicted by the sum of deaths among the five specific causes (6.9; 95% CI: 4.9–8.5) and 120% larger than the risk function used in the GBD (4.0; 95% CI: 3.3–4.8). Differences between the GEMM and GBD risk functions are larger for a 20% reduction in concentrations, with the GEMM predicting 220% higher excess deaths. These results suggest that PM 2.5 exposure may be related to additional causes of death than the five considered by the GBD and that incorporation of risk information from other, nonoutdoor, particle sources leads to underestimation of disease burden, especially at higher concentrations.

Background/aim Epidemiological cohort studies have consistently found associations between long-term exposure to outdoor air pollution and a range of morbidity and mortality endpoints. Recent evaluations by World Health Organisation and Global Burden of Disease study suggested that these associations may be non-linear and persist at very low concentrations. Methods We focus on analyses contributing to knowledge about health effects of air pollution concentrations at low concentrations, defined as less than current EU, EPA and WHO Limit Values or guidelines for PM2.5, NO2 and O3. Studies have focused especially on PM2.5, but increasingly associations with NO2 are reported. Very few studies have evaluated long-term morbidity and mortality effects of O3. We perform analyses of all-cause and cause-specific mortality and morbidity endpoints in a pooled dataset of 10 ESCAPE study cohorts and the Danish Nurse Cohort with detailed individual data (~3 80 000 subjects) and in seven very large European administrative cohorts (~35 million subjects). We focus on PM2.5, NO2, O3, and exploit rich monitoring data of black carbon (BC) available from the ESCAPE study. Results The first results are expected mid 2018. So far, we completed exposure assessment – using hybrid LUR models we made European maps of 2010 concentrations for PM2.5, NO2, O3 and BC. As individual cohort data are pooled, we developed common codebook harmonising variables between cohorts. We also obtained additional residential addresses histories. Further, we developed data transfer and management procedures. Data from all cohorts has been transferred and checked. Follow up is extended until 2013. We established secure remote access environment so that analysts involved can perform analyses without physically travelling to Utrecht. Finally, common statistical analysis scripts have been developed and afterwards demonstrated and discussed during the Stat Workshop (Utrecht, 25–27 Oct 2017). Conclusion There are no conclusions yet from this study.

Background/Aim: Previous analysis from the large European multicentre ESCAPE study showed an association of particulate matter

Background. Epidemiological evidence on the association between ambient air pollution and brain tumor risk is sparse and inconsistent. Methods. In 12 cohorts from 6 European countries, individual estimates of annual mean air pollution levels at the baseline residence were estimated by standardized land-use regression models developed within the ESCAPE and TRANSPHORM projects: Particulate matter (PM) ≥2.5,≥10, and 2.5-10 FÊm in diameter (PM2.5, PM10, and PMcoarse), PM2.5 absorbance, nitrogen oxides (NO2 and NOx) and elemental composition of PM. We estimated cohort-specific associations of air pollutant concentrations and traffic intensity with total, malignant, and nonmalignant brain tumor, in separate Cox regression models, adjusting for risk factors, and pooled cohort-specific estimates using random-effects meta-analyses. Results. Of 282 194 subjects from 12 cohorts, 466 developed malignant brain tumors during 12 years of follow-up. Six of the cohorts also had data on nonmalignant brain tumor, where among 106 786 subjects, 366 developed brain tumor: 176 nonmalignant and 190 malignant. We found a positive, statistically nonsignificant association between malignant brain tumor and PM2.5 absorbance (hazard ratio and 95% CI: 1.67; 0.89.3.14 per 10.5/m3), and weak positive or null associations with the other pollutants. Hazard ratio for PM2.5 absorbance (1.01; 0.38.2.71 per 10-5/m3) and all other pollutants were lower for nonmalignant than for malignant brain tumors. Conclusion. We found suggestive evidence of an association between long-term exposure to PM2.5 absorbance indicating traffic-related air pollution and malignant brain tumors, and no association with overall or nonmalignant brain tumors. © 2018 The Author(s). Chemicals/CAS: nitric oxide, 10102-43-9; nitrogen dioxide, 10102-44-0

We aimed to prospectively assess changes in chronic stress among young adults transitioning from high school to university or working life. A population-based cohort in Munich and Dresden (Germany) was followed from age 16–18 (2002–2003) to age 20–23 (2007–2009) (n = 1688). Using the Trier Inventory for the Assessment of Chronic Stress, two dimensions of stress at university or work were assessed: work overload and work discontent. In the multiple ordinal generalized estimating equations, socio-demographics, stress outside the workplace, and job history were additionally considered. At follow-up, 52% of the population were university students. Work overload increased statistically significantly from first to second follow-up, while work discontent remained constant at the population level. Students, compared to employees, reported a larger increase in work overload (adjusted odds ratio (OR): 1.33; 95% confidence interval (95% CI): 1.07, 1.67), while work discontent did not differ between the groups. In conclusion, work overload increases when young adults transition from school to university/job life, with university students experiencing the largest increase.

BACKGROUND: Epidemiological evidence on the association between ambient air pollution and breast cancer risk is inconsistent. OBJECTIVE: We examined the association between long-term exposure to ambient air pollution and incidence of postmenopausal breast cancer in European women. METHODS: In 15 cohorts from nine European countries, individual estimates of air pollution levels at the residence were estimated by standardized land-use regression models developed within the European Study of Cohorts for Air Pollution Effects (ESCAPE) and Transport related Air Pollution and Health impacts - Integrated Methodologies for Assessing Particulate Matter (TRANSPHORM) projects: particulate matter (PM) ≤2:5 μm, ≤10 μm, and 2:5–10 μm in diameter (PM2:5, PM10, and PMcoarse, respectively); PM2:5 absorbance; nitrogen oxides (NO2 and NOx); traffic intensity; and elemental composition of PM. We estimated cohort-specific associations between breast cancer and air pollutants using Cox regression models, adjusting for major lifestyle risk factors, and pooled cohort-specific estimates using random-effects meta-analyses. RESULTS: Of 74,750 postmenopausal women included in the study, 3,612 developed breast cancer during 991,353 person-years of follow-up. We found positive and statistically insignificant associations between breast cancer and PM2:5 {hazard ratio (HR) =1:08 [95% confidence interval (CI): 0.77, 1.51] per 5 μg/m3 }, PM10 [1.07 (95% CI: 0.89, 1.30) per 10 μg/m3 ], PMcoarse [1.20 (95% CI: 0.96, 1.49 per 5 μg/m3 ], and NO2 [1.02 (95% CI: 0.98, 1.07 per 10 μg/m3 ], and a statistically significant association with NOx [1.04 (95% CI: 1.00, 1.08) per 20 μg/m3, p =0:04]. CONCLUSIONS: We found suggestive evidence of an association between ambient air pollution and incidence of postmenopausal breast cancer in European women. © 2017, Public Health Services, US Dept of Health and Human Services. All rights reserved. Chemicals/CAS: copper, 15158-11-9, 7440-50-8; iron, 14093-02-8, 53858-86-9, 7439-89-6; nickel, 7440-02-0; nitrogen oxide, 11104-93-1; potassium, 7440-09-7; silicon, 7440-21-3; sulfur, 13981-57-2, 7704-34-9; vanadium, 7440-62-2; zinc, 7440-66-6, 14378-32-6

Background Tobacco smoke exposure increases the risk of cancer in the liver, but little is known about the possible risk associated with exposure to ambient air pollution. Objectives We evaluated the association between residential exposure to air pollution and primary liver cancer incidence. Methods We obtained data from four cohorts with enrolment during 1985–2005 in Denmark, Austria and Italy. Exposure to nitrogen oxides (NO 2 and NO X ), particulate matter (PM) with diameter of less than 10 µm (PM 10 ), less than 2.5 µm (PM 2.5 ), between 2.5 and 10 µm (PM 2.5–10 ) and PM 2.5 absorbance (soot) at baseline home addresses were estimated using land-use regression models from the ESCAPE project. We also investigated traffic density on the nearest road. We used Cox proportional-hazards models with adjustment for potential confounders for cohort-specific analyses and random-effects meta-analyses to estimate summary hazard ratios (HRs) and 95% confidence intervals (CIs). Results Out of 174,770 included participants, 279 liver cancer cases were diagnosed during a mean follow-up of 17 years. In each cohort, HRs above one were observed for all exposures with exception of PM 2.5 absorbance and traffic density. In the meta-analysis, all exposures were associated with elevated HRs, but none of the associations reached statistical significance. The summary HR associated with a 10-μg/m 3 increase in NO 2 was 1.10 (95% confidence interval (CI): 0.93, 1.30) and 1.34 (95% CI: 0.76, 2.35) for a 5-μg/m 3 increase in PM 2.5 . Conclusions The results provide suggestive evidence that ambient air pollution may increase the risk of liver cancer. Confidence intervals for associations with NO 2 and NO X were narrower than for the other exposures.

The authors wish to make the following amendments to their paper published in International Journal of Environmental Research and Public Health [1][...]

Background: Long-term exposures to particulate matter air pollution (PM2.5 and PM10) and high traffic load have been associated with markers of systemic inflammation. Epidemiological investigations have focused primarily on total PM, which represents a mixture of pollutants originating from different sources. Objective: We investigated associations between source-specific PM and high-sensitive C-reactive protein (hs-CRP), an independent predictor of cardiovascular disease. Methods: We used data from the first (2000–2003) and second examination (2006–2008) of the Heinz Nixdorf Recall study, a prospective population-based German cohort of initially 4,814 participants (45–75 years of age). We estimated residential long-term exposure to local traffic- and industry-specific fine particulate matter (PM2.5) at participants’ residences using a chemistry transport model. We used a linear mixed model with a random participant intercept to estimate associations of source-specific PM and natural log-transformed hs-CRP, controlling for age, sex, education, body mass index, low- and high-density lipoprotein cholesterol, smoking variables, physical activity, season, humidity, and city (8,204 total observations). Results: A 1-μg/m3 increase in total PM2.5 was associated with a 4.53% increase in hs-CRP concentration (95% CI: 2.76, 6.33%). hs-CRP was 17.89% (95% CI: 7.66, 29.09%) and 7.96% (95% CI: 3.45, 12.67%) higher in association with 1-μg/m3 increases in traffic- and industry-specific PM2.5, respectively. Results for PM10 were similar. Conclusions: Long-term exposure to local traffic-specific PM (PM2.5, PM10) was more strongly associated with systemic inflammation than total PM. Associations of local industry-specific PM were slightly stronger but not significantly different from associations with total PM. Citation: Hennig F, Fuks K, Moebus S, Weinmayr G, Memmesheimer M, Jakobs H, Bröcker-Preuss M, Führer-Sakel D, Möhlenkamp S, Erbel R, Jöckel KH, Hoffmann B, Heinz Nixdorf Recall Study Investigative Group. 2014. Association between source-specific particulate matter air pollution and hs-CRP: local traffic and industrial emissions. Environ Health Perspect 122:703–710; http://dx.doi.org/10.1289/ehp.1307081