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Background: Studies have linked air pollution to lung cancer incidence and mortality, but few have compared these associations, which may differ due to cancer survival variations. We aimed to evaluate the association between long-term air pollution exposure and lung cancer incidence and compare findings with previous lung cancer mortality analyses within the same cohorts., Methods: We analyzed four population-based administrative cohorts in Denmark (2000-2015), England (2011-2017), Norway (2001-2016) and Rome (2001-2015). We assessed residential exposure to annual average fine particulate matter (PM 2.5 ), nitrogen dioxide (NO₂), black carbon (BC), and warm-season ozone (O 3 ) using Europe-wide land use regression models. We used Cox proportional hazard models to evaluate cohort-specific hazard ratios (HRs) and 95% confidence intervals (CIs) for lung cancer incidence identified using hospital admission records (English and Roman cohorts) or cancer registries (Danish and Norwegian cohorts). We evaluated the associations at low exposure levels using subset analyses and natural cubic splines. Cohort-specific HRs were pooled using random-effects meta-analyses, separately for incidence and mortality., Results: Over 93,733,929 person-years of follow-up, 111,949 incident lung cancer cases occurred. Incident lung cancer was positively associated with PM 2.5 , NO 2 and BC, and negatively associated with O 3 . The negative O 3 association became positive after adjustment for NO 2 . Associations were almost identical or slightly stronger for lung cancer incidence than mortality in the same cohorts, with respective meta-analytic HRs (95% CIs) of 1.14 (1.06, 1.22) and 1.12 (1.02, 1.22) per 5 μg/m 3 increase in PM 2.5 , and 1.10 (1.04, 1.16) and 1.09 (1.02, 1.16) per 10 μg/m 3 increase in NO 2 . Positive associations persisted for both incidence and mortality at low pollution levels with similar magnitude., Conclusions: We found similarly elevated risks of lung cancer incidence and mortality in association with residential exposure to PM 2.5 , NO 2 and BC in meta-analyses of four European administrative cohorts, which persisted at low pollution levels., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

End-stage kidney disease (ESKD) poses a high burden on patients and health systems. While numerous studies indicate an association between air pollution and chronic kidney disease, studies on ESKD are rare. We investigated the association of long-term exposure to nitrogen dioxide (NO₂), fine particulate matter (PM 2.5 ), black carbon (BC) and ozone (O 3 ) with ESKD incidence in two large population-based European cohorts. We followed individuals in the Austrian Vorarlberg Health Monitoring and Promotion Program (VHM&PP) and the Italian Rome Longitudinal Study (RoLS) using dialysis and kidney transplant registries. Long-term exposure to pollutants was estimated at the home address using Europe-wide land use regression models at 100x100m scale. Hazard ratios (HR) were determined from Cox-proportional hazard models adjusted for individual and neighbourhood level confounders. We observed 501 events among 136,823 individuals in VHM&PP (mean age 42.1 years; crude incidence rate (IR) 0.14 per 1000 person-years) and 3231 events among 1,939,461 individuals in RoLS (mean age 52.4 years; IR 0.22 per 1000 person-years). In VHM&PP, there was no evidence of an association between PM 2.5 or O 3 and ESKD. There were elevated HRs but with large confidence intervals for BC (HR 1.17 [95 % confidence interval (CI): 0.98, 1.39] for 0.5*10 -5 /m), and for NO₂ (HR 1.14 [95%CI: 0.96, 1.35] for 10 μg/m 3 ). In RoLS, ESKD was associated with PM 2.5 (HR 1.37 [95 % CI: 1.06, 1.76] for an increase of 5 μg/m 3 ), while there was no evidence of association with BC, NO 2 , or O 3 exposure. Our study suggests an association of air pollution with ESKD incidence, which differed between the two cohorts and may possibly be influenced by respective air pollution mixtures., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Introduction: Exposure to ambient air pollution from combustion-source emissions contributes to the prevalence of asthma, but the role of early-life exposure in asthma development is not well understood. The objective was to examine the effects of early-life exposure to multiple specific ambient air pollutants on incidence and prevalence of asthma and to determine the mechanistic basis for these effects., Methods: The study included all live-born singletons in Denmark during 1998-2016 (N = 1,060,154), participants in the Danish National Birth Cohort (DNBC 3 , N = 22,084), and participants in the Copenhagen Prospective Studies on Asthma in Childhood (COPSAC, N = 803). We modeled the concentrations of particulate matter ≤2.5 and ≤10 μm in aerodynamic diameter (PM 2.5 and PM 10 ), PM-related elemental carbon (EC), organic carbon (OC), sulfate (SO 4 2- ), nitrate (NO 3 - ), ammonium (NH 4 + ), secondary organic aerosols (SOA), and sea salt as well as nitrogen dioxide (NO 2 ), nitrogen oxides (NO x ), sulfur dioxide (SO 2 ), and ozone (O 3 ) - from all sources. Prenatal and postnatal time-weighted mean exposures were calculated for all residential addresses., We defined asthma incidence as the first registered asthma diagnosis for all and used parental recall at child aged 7 to determine the prevalence of doctor-diagnosed asthma ever and active asthma for the DNBC participants. For the COPSAC participants, we analyzed inflammatory markers in blood collected at 6 months of age; at 6 years of age, we analyzed nasal epithelial deoxyribonucleic acid (DNA) methylation, gene expression, immune mediators, and forced expiratory volume in 1 second (FEV 1 )., Cox proportional hazard models were fitted with fixed prenatal means and time-varying running annual means of a year before the event for the postnatal follow-up period for asthma incidence. Logistic regression models with cluster-robust standard errors and generalized estimating equations for dependence between women being included more than once were used for asthma prevalence. Mixed-effect linear regression models with random intercept for cohort were used to examine changes in lung function, and linear regression models were used to examine changes in biomarkers., Results: The prenatal mean and interquartile range (IQR) concentrations of PM 2.5 and NO 2 were 10.5 (2.4) and 17.5 (8.7) μg/m 3 . In the nationwide study the risk of asthma incidence increased with increasing prenatal exposure to all pollutants except for O 3 and sea salt. An IQR increase in prenatal exposure was associated with an adjusted hazard ratio (HR) and 95% confidence interval (CI) of 1.06 (95% CI: 1.04-1.08) for PM 2.5 and 1.04 (1.02-1.05) for NO 2 . The corresponding estimates for postnatal exposures were 1.08 (1.05-1.10) and 1.02 (1.01-1.04), respectively., In the DNBC participants, the asthma incidence results from models further adjusted with cohort-specific covariates were similar to models adjusted for register-based covariates only. Prenatal exposure to PM 2.5 , PM 10 , NO 2 , NO x , EC, SO 4 2- , and sea salt were weakly associated with elevated risk for asthma incidence. There was no evidence of associations with asthma prevalence., For the COPSAC children, an IQR of PM 2.5 and of NH 4 + was each associated with a 2%-3% (95% CI: 1%-5%) reduction in mean FEV 1 , consistently for prenatal and postnatal exposures. Prenatal exposure to PM and NO 2 was associated with immunological changes in blood and the airways but not with DNA methylation or gene expression changes., Conclusions: The results of these studies strengthen the evidence that long-term exposure to ambient air pollution contributes to the development of asthma in early life through an altered immune profile, even at these relatively low concentrations., (© 2024 Health Effects Institute. All rights reserved.)

Competing Interests: The authors declare that they have no conflicts of interest with regard to the content of this report.

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/m 3 , BC (1.26 (1.03-1.53) per 0.5 × 10 - 5 /m), NO 2 (1.13 (0.93-1.38) per 10 μg/m 3 ) and inverse for O 3 (0.71 (0.54-0.93) per 10 μg/m 3 ). 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., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Objective: There is limited study from low-and-middle income countries on the effect of perinatal exposure to air pollution and the risk of infection in infant. We assessed the association between perinatal exposure to traffic related air pollution and the risk of infection in infant during their first six months of life., Methods: A prospective cohort study was performed in Jakarta, March 2016-September 2020 among 298 mother-infant pairs. PM 2.5 , soot, NO x , and NO 2 concentrations were assessed using land use regression models (LUR) at individual level. Repeated interviewer-administered questionnaires were used to obtain data on infection at 1, 2, 4 and 6 months of age. The infections were categorized as upper respiratory tract (runny nose, cough, wheezing or shortness of breath), lower respiratory tract (pneumonia, bronchiolitis) or gastrointestinal tract infection. Logistic regression models adjusted for covariates were used to assess the association between perinatal exposure to air pollution and the risk of infection in the first six months of life., Results: The average concentrations of PM 2.5 and NO 2 were much higher than the WHO recommended levels. Upper respiratory tract infections (URTI) were much more common in the first six months of life than diagnosed lower respiratory tract or gastro-intestinal infections (35.6%, 3.5% and 5.8% respectively). Perinatal exposure to PM 2.5 and soot suggested increase cumulative risk of upper respiratory tract infection (URTI) in the first 6 months of life per IQR increase with adjusted OR of 1.50 (95% CI 0.91; 2.47) and 1.14 (95% CI 0.79; 1.64), respectively. Soot was significantly associated with the risk of URTI at 4-6 months age interval (aOR of 1.45, 95%CI 1.02; 2.09). All air pollutants were also positively associated with lower respiratory tract infection, but all CIs include unity because of relatively small samples. Adjusted odds ratios for gastrointestinal infections were close to unity., Conclusion: Our study adds to the evidence that perinatal exposure to fine particles is associated with respiratory tract infection in infants in a low-middle income country., (© 2024. The Author(s).)

Air pollution has been shown to significantly impact human health including cancer. Gastric and upper aerodigestive tract (UADT) cancers are common and increased risk has been associated with smoking and occupational exposures. However, the association with air pollution remains unclear. We pooled European subcohorts (N = 287,576 participants for gastric and N = 297,406 for UADT analyses) and investigated the association between residential exposure to fine particles (PM 2.5 ), nitrogen dioxide (NO 2 ), black carbon (BC) and ozone in the warm season (O 3w ) with gastric and UADT cancer. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. During 5,305,133 and 5,434,843 person-years, 872 gastric and 1139 UADT incident cancer cases were observed, respectively. For gastric cancer, we found no association with PM 2.5 , NO 2 and BC while for UADT the hazard ratios (95% confidence interval) were 1.15 (95% CI: 1.00-1.33) per 5 μg/m 3 increase in PM 2.5 , 1.19 (1.08-1.30) per 10 μg/m 3 increase in NO 2 , 1.14 (1.04-1.26) per 0.5 × 10 -5  m -1 increase in BC and 0.81 (0.72-0.92) per 10 μg/m 3 increase in O 3w . We found no association between long-term ambient air pollution exposure and incidence of gastric cancer, while for long-term exposure to PM 2.5 , NO 2 and BC increased incidence of UADT cancer was observed., (© 2024 The Authors. International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC.)

Objectives: To explore the associations of long-term exposure to air pollution with onset of all human health conditions., Design: Prospective phenome-wide association study., Setting: Denmark., Participants: All Danish residents aged ≥30 years on 1 January 2000 were included (N=3 323 612). After exclusion of individuals with missing geocoded residential addresses, 3 111 988 participants were available for the statistical analyses., Main Outcome Measure: First registered diagnosis of every health condition according to the International Classification of Diseases, 10th revision, from 2000 to 2017., Results: Long-term exposure to fine particulate matter (PM 2.5 ) and nitrogen dioxide (NO 2 ) were both positively associated with the onset of more than 700 health conditions (ie, >80% of the registered health conditions) after correction for multiple testing, while the remaining associations were inverse or insignificant. As regards the most common health conditions, PM 2.5 and NO 2 were strongest positively associated with chronic obstructive pulmonary disease (PM 2.5 : HR 1.06 (95% CI 1.05 to 1.07) per 1 IQR increase in exposure level; NO 2 : 1.14 (95% CI 1.12 to 1.15)), type 2 diabetes (PM 2.5 : 1.06 (95% CI 1.05 to 1.06); NO 2 : 1.12 (95% CI 1.10 to 1.13)) and ischaemic heart disease (PM 2.5 : 1.05 (95% CI 1.04 to 1.05); NO 2 : 1.11 (95% CI 1.09 to 1.12)). Furthermore, PM 2.5 and NO 2 were both positively associated with so far unexplored, but highly prevalent outcomes relevant to public health, including senile cataract, hearing loss and urinary tract infection., Conclusions: The findings of this study suggest that air pollution has a more extensive impact on human health than previously known. However, as this study is the first of its kind to investigate the associations of long-term exposure to air pollution with onset of all human health conditions, further research is needed to replicate the study findings., Competing Interests: Competing interests: All authors have completed the ICMJE uniform disclosure form at http://www.icmje.org/disclosure-of-interest/ and declare: no support from any organisation for the submitted work; ERH and LHM were partly supported by unrestricted grants from the Novo Nordisk Foundation, ZJA and Y-HL chaired the ERS Environment and Health Committee, BB has received a grant from the Health Effects Institute; no other relationships or activities that could appear to have influenced the submitted work., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

It is unclear whether cancers of the upper aerodigestive tract (UADT) and gastric cancer are related to air pollution, due to few studies with inconsistent results. The effects of particulate matter (PM) may vary across locations due to different source contributions and related PM compositions, and it is not clear which PM constituents/sources are most relevant from a consideration of overall mass concentration alone. We therefore investigated the association of UADT and gastric cancers with PM 2.5 elemental constituents and sources components indicative of different sources within a large multicentre population based epidemiological study. Cohorts with at least 10 cases per cohort led to ten and eight cohorts from five countries contributing to UADT- and gastric cancer analysis, respectively. Outcome ascertainment was based on cancer registry data or data of comparable quality. We assigned home address exposure to eight elemental constituents (Cu, Fe, K, Ni, S, Si, V and Zn) estimated from Europe-wide exposure models, and five source components identified by absolute principal component analysis (APCA). Cox regression models were run with age as time scale, stratified for sex and cohort and adjusted for relevant individual and neighbourhood level confounders. We observed 1139 UADT and 872 gastric cancer cases during a mean follow-up of 18.3 and 18.5 years, respectively. UADT cancer incidence was associated with all constituents except K in single element analyses. After adjustment for NO 2 , only Ni and V remained associated with UADT. Residual oil combustion and traffic source components were associated with UADT cancer persisting in the multiple source model. No associations were found for any of the elements or source components and gastric cancer incidence. Our results indicate an association of several PM constituents indicative of different sources with UADT but not gastric cancer incidence with the most robust evidence for traffic and residual oil combustion., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Leukemia and lymphoma are the two most common forms of hematologic malignancy, and their etiology is largely unknown. Pathophysiological mechanisms suggest a possible association with air pollution, but little empirical evidence is available. We aimed to investigate the association between long-term residential exposure to outdoor air pollution and risk of leukemia and lymphoma. We pooled data from four cohorts from three European countries as part of the "Effects of Low-level Air Pollution: a Study in Europe" (ELAPSE) collaboration. We used Europe-wide land use regression models to assess annual mean concentrations of fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ), black carbon (BC) and ozone (O 3 ) at residences. We also estimated concentrations of PM 2.5 elemental components: copper (Cu), iron (Fe), zinc (Zn); sulfur (S); nickel (Ni), vanadium (V), silicon (Si) and potassium (K). We applied Cox proportional hazards models to investigate the associations. Among the study population of 247,436 individuals, 760 leukemia and 1122 lymphoma cases were diagnosed during 4,656,140 person-years of follow-up. The results showed a leukemia hazard ratio (HR) of 1.13 (95% confidence intervals [CI]: 1.01-1.26) per 10 μg/m 3 NO 2 , which was robust in two-pollutant models and consistent across the four cohorts and according to smoking status. Sex-specific analyses suggested that this association was confined to the male population. Further, the results showed increased lymphoma HRs for PM 2.5 (HR = 1.16; 95% CI: 1.02-1.34) and potassium content of PM 2.5 , which were consistent in two-pollutant models and according to sex. Our results suggest that air pollution at the residence may be associated with adult leukemia and lymphoma., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)