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Background Assessment of the cumulative effect of correlated exposures is an open methodological issue in environmental epidemiology. Most previous studies have applied regression models with interaction terms or dimension reduction methods. The combined effect of pollutants has been also evaluated through the use of exposure scores that incorporate weights based on the strength of the component-specific associations with health outcomes. Methods We compared three approaches addressing multi-pollutant exposures in epidemiological models: main effects models, the adaptive least absolute shrinkage and selection operator (LASSO) and a weighted exposure score. We assessed the performance of the methods by simulations under various scenarios for the pollutants’ correlations. We further applied these methods to time series data from Athens, Greece in 2007–12 to investigate the combined effect of short-term exposure to six regulated pollutants on all-cause and respiratory mortality. Results The exposure score provided the least biased estimate under all correlation scenarios for both mortality outcomes. The adaptive LASSO performed well in the case of low and medium correlation between exposures while the main effect model resulted in severe bias. In the real data application, the cumulative effect estimate was similar between approaches for all-cause mortality ranging from 0.7% increase per interquartile range (IQR) (score) to 1.1% (main effects), while for respiratory mortality conclusions were contradictive and ranged from − 0.6% (adaptive LASSO) to 2.8% (score). Conclusions Τhe use of a weighted exposure score to address cumulative effects of correlated metrics may perform well under different exposure correlation and variability in the health outcomes. [ABSTRACT FROM AUTHOR]

Abstract: Introduction: Doña Ana County in New Mexico regularly experiences severe air pollution episodes associated with windblown dust and fires. Residents of Hispanic/Latino origin constitute the largest population group in the region. We investigated the associations of ambient particulate matter and ozone with hospital emergency room and admissions for respiratory and cardiovascular visits in adults. Methods: We used trajectories regression analysis to determine the local and regional components of particle mass and ozone. We applied Poisson generalized models to analyze hospital emergency room visits and admissions adjusted for pollutant levels, humidity, temperature and temporal and seasonal effects. Results: We found that the sources within 500km of the study area accounted for most of particle mass and ozone concentrations. Sources in Southeast Texas, Baja California and Southwest US were the most important regional contributors. Increases of cardiovascular emergency room visits were estimated for PM10 (3.1% (95% CI: −0.5 to 6.8)) and PM10−2.5 (2.8% (95% CI: −0.2 to 5.9)) for all adults during the warm period (April–September). When high PM10 (>150μg/m3) mass concentrations were excluded, strong effects for respiratory emergency room visits for both PM10 (3.2% (95% CI: 0.5–6.0)) and PM2.5 (5.2% (95% CI: −0.5 to 11.3)) were computed. Conclusions: Our analysis indicated effects of PM10, PM2.5 and O3 on emergency room visits during the April–September period in a region impacted by windblown dust and wildfires. [Copyright &y& Elsevier]

Air pollution is a growing concern worldwide, with significant impacts on human health. Multiple myeloma is a type of blood cancer with increasing incidence. Studies have linked air pollution exposure to various types of cancer, including leukemia and lymphoma, however, the relationship with multiple myeloma incidence has not been extensively investigated. We pooled four European cohorts (N = 234,803) and assessed the association between residential exposure to nitrogen dioxide (NO 2), fine particles (PM 2.5), black carbon (BC), and ozone (O 3) and multiple myeloma. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. During 4,415,817 person-years of follow-up (average 18.8 years), we observed 404 cases of multiple myeloma. The results of the fully adjusted linear analyses showed hazard ratios (95% confidence interval) of 0.99 (0.84, 1.16) per 10 μg/m³ NO 2 , 1.04 (0.82, 1.33) per 5 μg/m³ PM 2.5 , 0.99 (0.84, 1.18) per 0.5 10−5 m−1 BCE, and 1.11 (0.87, 1.41) per 10 μg/m³ O 3. We did not observe an association between long-term ambient air pollution exposure and incidence of multiple myeloma. • Studies focusing on air pollution effects on multiple myeloma incidence are few • We obtained a large sample size by pooling four cohorts with harmonized covariates • Air pollution exposure was modelled for participants' baseline residential address • Results did not suggest air pollution as a risk factor for multiple myeloma [ABSTRACT FROM AUTHOR]

Despite the known link between air pollution and cause-specific mortality, its relation to chronic kidney disease (CKD)-associated mortality is understudied. Therefore, we investigated the association between long-term exposure to air pollution and CKD-related mortality in a large multicentre population-based European cohort. Cohort data were linked to local mortality registry data. CKD-death was defined as ICD10 codes N18–N19 or corresponding ICD9 codes. Mean annual exposure at participant's home address was determined with fine spatial resolution exposure models for nitrogen dioxide (NO 2), black carbon (BC), ozone (O 3), particulate matter ≤2.5 μm (PM 2.5) and several elemental constituents of PM 2.5. Cox regression models were adjusted for age, sex, cohort, calendar year of recruitment, smoking status, marital status, employment status and neighbourhood mean income. Over a mean follow-up time of 20.4 years, 313 of 289,564 persons died from CKD. Associations were positive for PM 2.5 (hazard ratio (HR) with 95% confidence interval (CI) of 1.31 (1.03–1.66) per 5 μg/m3, BC (1.26 (1.03–1.53) per 0.5 × 10− 5/m), NO 2 (1.13 (0.93–1.38) per 10 μg/m3) and inverse for O 3 (0.71 (0.54–0.93) per 10 μg/m3). Results were robust to further covariate adjustment. Exclusion of the largest sub-cohort contributing 226 cases, led to null associations. Among the elemental constituents, Cu, Fe, K, Ni, S and Zn, representing different sources including traffic, biomass and oil burning and secondary pollutants, were associated with CKD-related mortality. In conclusion, our results suggest an association between air pollution from different sources and CKD-related mortality. • Large population-based European cohort and fine-scale exposure resolution. • PM2.5 is positively associated with chronic kidney disease (CKD) mortality. • PM2.5 elemental constituents from different sources are related to CKD mortality. • The observed associations manifest below current European PM2.5 limit values. [ABSTRACT FROM AUTHOR]

Fine particulate matter (PM 2.5) is a well-recognized risk factor for premature death. However, evidence on which PM 2.5 components are most relevant is unclear. We evaluated the associations between mortality and long-term exposure to eight PM 2.5 elemental components [copper (Cu), iron (Fe), zinc (Zn), sulfur (S), nickel (Ni), vanadium (V), silicon (Si), and potassium (K)]. Studied outcomes included death from diabetes, chronic kidney disease (CKD), dementia, and psychiatric disorders as well as all-natural causes, cardiovascular disease (CVD), respiratory diseases (RD), and lung cancer. We followed all residents in Denmark (aged ≥30 years) from January 1, 2000 to December 31, 2017. We used European-wide land-use regression models at a 100 × 100 m scale to estimate the residential annual mean levels of exposure to PM 2.5 components. The models were developed with supervised linear regression (SLR) and random forest (RF). The associations were evaluated by Cox proportional hazard models adjusting for individual- and area-level socioeconomic factors and total PM 2.5 mass. Of 3,081,244 individuals, we observed 803,373 death from natural causes during follow-up. We found significant positive associations between all-natural mortality with Si and K from both exposure modeling approaches (hazard ratios; 95% confidence intervals per interquartile range increase): SLR-Si (1.04; 1.03–1.05), RF-Si (1.01; 1.00–1.02), SLR-K (1.03; 1.02–1.04), and RF-K (1.06; 1.05–1.07). Strong associations of K and Si were detected with most causes of mortality except CKD and K, and diabetes and Si (the strongest associations for psychiatric disorders mortality). In addition, Fe was relevant for mortality from RD, lung cancer, CKD, and psychiatric disorders; Zn with mortality from CKD, RD, and lung cancer, and; Ni and V with lung cancer mortality. We present novel results of the relevance of different PM 2.5 components for different causes of death, with K and Si seeming to be most consistently associated with mortality in Denmark. • Fine particulate matter (PM 2.5) is linked to premature mortality. • Researches on which PM 2.5 components are more responsible is limited. • With 3 million Danes, we studied how PM 2.5 elemental components links with mortality. • Potassium and silicon were the most relevant PM 2.5 components with mortality. • Different PM 2.5 components were associated with different mortality outcomes. [ABSTRACT FROM AUTHOR]

Background In the wider framework of the RESPOZE (ReSPiratory effects of OZone Exposure in Greek children) panel study, we investigated possible determinants of O 3 exposure of school children, measured with personal passive samplers, in Athens and Thessaloniki, Greece. Methods Personal exposure to O 3 was measured for five weeks spread along the academic year 2013-14, in 186 school children in Athens and Thessaloniki, Greece. At the same time, at-school outdoor measurements were performed and ambient levels of 8-h daily maximum O 3 from fixed sites were collected. We also collected information on lifestyle and housing characteristics through an extended general questionnaire (GQ) and each participant completed daily time activity diaries (TADs) during the study period. Results Mean outdoor concentrations were higher during the warmer months, in the suburbs of the cities and in Athens. Personal exposure concentrations were significantly lower compared to outdoor. Daily levels of at-school outdoor and ambient levels of O 3 from fixed sites were significant determinants of personal exposure to O 3 . For a 10 μg/m 3 increase in at-school outdoor O 3 concentrations and PM 10 measurements a 20.9% (95% CI: 13%, 28%) increase in personal exposure to O 3 was found. For a half an hour more spent in transportation an average increase of 7% (95% CI: 0.3%, 14.6%) in personal exposure to O 3 was observed. Among other possible determinants, time spent in transportation (TAD variable) and duration of open windows were the ones associated with personal O 3 exposure levels. Conclusions Our results support the use of outdoor and ambient measurements from fixed sites in epidemiological studies as a proxy of personal exposure to O 3 , but this has to be calibrated taking into account personal measurements and time-activity patterns. [ABSTRACT FROM AUTHOR]

Background : Particulate matter (PM) is classified as a group 1 human carcinogen. Previous experimental studies suggest that particles in diesel exhaust induce oxidative stress, inflammation and DNA damage in kidney cells, but the evidence from population studies linking air pollution to kidney cancer is limited. Methods : We pooled six European cohorts (N = 302,493) to assess the association of residential exposure to fine particles (PM 2.5), nitrogen dioxide (NO 2), black carbon (BC), warm season ozone (O 3) and eight elemental components of PM 2.5 (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) with cancer of the kidney parenchyma. The main exposure model was developed for year 2010. We defined kidney parenchyma cancer according to the International Classification of Diseases 9th and 10th Revision codes 189.0 and C64. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. Results : The participants were followed from baseline (1985–2005) to 2011–2015. A total of 847 cases occurred during 5,497,514 person-years of follow-up (average 18.2 years). Median (5–95%) exposure levels of NO 2 , PM 2.5 , BC and O 3 were 24.1 μg/m3 (12.8–39.2), 15.3 μg/m3 (8.6–19.2), 1.6 10−5 m−1 (0.7–2.1), and 87.0 μg/m3 (70.3–97.4), respectively. The results of the fully adjusted linear analyses showed a hazard ratio (HR) of 1.03 (95% confidence interval [CI]: 0.92, 1.15) per 10 μg/m³ NO 2 , 1.04 (95% CI: 0.88, 1.21) per 5 μg/m³ PM 2.5 , 0.99 (95% CI: 0.89, 1.11) per 0.5 10−5 m−1 BCE, and 0.88 (95% CI: 0.76, 1.02) per 10 μg/m³ O 3. We did not find associations between any of the elemental components of PM 2.5 and cancer of the kidney parenchyma. Conclusion : We did not observe an association between long-term ambient air pollution exposure and incidence of kidney parenchyma cancer. •A large sample size was obtained by pooling six cohorts with harmonized covariates. •A newly developed Europe-wide spatial land-use regression model was applied. •Results did not indicate a role of air pollutants in development of kidney cancer. [ABSTRACT FROM AUTHOR]

Although there is evidence on the effects of short-term ozone (O 3) exposures on children's respiratory health, few studies have reported results on the effects of long-term exposures. We report the effects of long-term exposure to O 3 on respiratory health outcomes in 10–11-year old children. We conducted a panel study in a sample of the general population of school children in two cities with high average O 3 concentrations, Athens and Thessaloniki, Greece. All 186 participating students were followed up intensively for 5 weeks spreading across a school year. Data was collected through questionnaires, weekly personal O 3 measurements, spirometry, FeNO and time-activity diaries. Long-term O 3 exposure was assessed using fixed site measurements and modeling, calibrated for personal exposures. The associations between measured lung function parameters and lung function growth over the study period, as well as FeNO and the occurrence of symptoms with long-term O 3 exposure were assessed through the application of multiple mixed effects 2-level regression models, adjusting for confounders and for short-term exposures. A 10 μg/m3 increase in calibrated long-term O 3 exposure, using measurements from fixed site monitors was associated with lower FVC and FEV 1 by 17 mL (95% Confidence Interval: 5–28) and 13 mL (3–21) respectively and small decreases in lung growth: 0.008% (0.002–0.014%) for FVC and 0.006% (0.000–0.012%) in FEV 1 over the study period. No association was observed with PEF, FeNO or the occurrence of symptoms. A similar pattern was observed when the exposure estimates from the dispersion models were employed. Our study provides evidence that long-term O 3 exposure is associated with reduced lung volumes and growth. • We investigated the effects of long-term exposure to ambient ozone on respiratory health outcomes in children. • This study shows adverse associations between long-term O 3 exposure and children's lung development, which may be of clinical relevance for a subset of the general population. • These early life impacts of long-term O 3 exposure may provide an explanation for premature mortality and increased morbidity in later life. [ABSTRACT FROM AUTHOR]