Outdoor Ultrafine Particulate Matter and Risk of Lung Cancer in Southern California.

Rationale: Particulate matter ⩽2.5 µm in aerodynamic diameter (PM2.5) is an established cause of lung cancer, but the association with ultrafine particulate matter (UFP; aerodynamic diameter < 0.1 µm) is unclear. Objectives: To investigate the association between UFP and lung cancer overall and by histologic subtype. Methods: The Los Angeles Ultrafines Study includes 45,012 participants aged ⩾50 years in southern California at enrollment (1995-1996) followed through 2017 for incident lung cancer (n = 1,770). We estimated historical residential ambient UFP number concentrations via land use regression and back extrapolation using PM2.5. In Cox proportional hazards models adjusted for smoking and other confounders, we estimated associations between 10-year lagged UFP (per 10,000 particles/cm3 and quartiles) and lung cancer overall and by major histologic subtype (adenocarcinoma, squamous cell carcinoma, and small cell carcinoma). We also evaluated relationships by smoking status, birth cohort, and historical duration at the residence. Measurements and Main Results: UFP was modestly associated with lung cancer risk overall (hazard ratio [HR], 1.03 [95% confidence interval (CI), 0.99-1.08]). For adenocarcinoma, we observed a positive trend among men; risk was increased in the highest exposure quartile versus the lowest (HR, 1.39 [95% CI, 1.05-1.85]; P for trend = 0.01) and was also increased in continuous models (HR per 10,000 particles/cm3, 1.09 [95% CI, 1.00-1.18]), but no increased risk was apparent among women (P for interaction = 0.03). Adenocarcinoma risk was elevated among men born between 1925 and 1930 (HR, 1.13 [95% CI, 1.02-1.26] per 10,000) but not for other birth cohorts, and was suggestive for men with ⩾10 years of residential duration (HR, 1.11 [95% CI, 0.98-1.26]). We found no consistent associations for women or other histologic subtypes. Conclusions: UFP exposure was modestly associated with lung cancer overall, with stronger associations observed for adenocarcinoma of the lung.

Long-term exposure to air pollution and incidence of gastric and the upper aerodigestive tract cancers in a pooled European cohort: The ELAPSE project.

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 (PM2.5), nitrogen dioxide (NO2), black carbon (BC) and ozone in the warm season (O3w) 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 PM2.5, NO2 and BC while for UADT the hazard ratios (95% confidence interval) were 1.15 (95% CI: 1.00-1.33) per 5 µg/m3 increase in PM2.5, 1.19 (1.08-1.30) per 10 µg/m3 increase in NO2, 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/m3 increase in O3w. We found no association between long-term ambient air pollution exposure and incidence of gastric cancer, while for long-term exposure to PM2.5, NO2 and BC increased incidence of UADT cancer was observed.

Hyperlocal Air Pollution Mapping: A Scalable Transfer Learning LUR Approach for Mobile Monitoring.

Addressing the challenge of mapping hyperlocal air pollution in areas without local monitoring, we evaluated unsupervised transfer learning-based land-use regression (LUR) models developed using mobile monitoring data from other cities: CORrelation ALignment (Coral) and its inverse distance-weighted modification (IDW_Coral). These models mitigated domain shifts and transferred patterns learned from mobile air quality monitoring campaigns in Copenhagen and Rotterdam to estimate annual average air pollution levels in Amsterdam (50m road segments) without involving any Amsterdam measurements in model development. For nitrogen dioxide (NO2), IDW_Coral outperformed Copenhagen and Rotterdam LUR models directly applied to Amsterdam, achieving MAE (4.47 µg/m3) and RMSE (5.36 µg/m3) comparable to a locally fitted LUR model (AMS_SLR) developed using Amsterdam mobile measurements collected for 160 days. IDW_Coral yielded an R2 of 0.35, similar to that of the AMS_SLR based on 20 collection days, suggesting a minimum requirement of 20-day mobile monitoring to capture city-specific insights. For ultrafine particles (UFP), IDW_Coral's citywide predictions strongly correlated with previously published mixed-effect models fitted with 160-day Amsterdam measurements (Pearson correlation of 0.71 for UFP and 0.72 for NO2). IDW_Coral demands no direct measurements in the target area, showcasing its potential for large-scale applications and offering significant economic efficiencies in executing mobile monitoring campaigns.

Validity of Mobility-Based Exposure Assessment of Air Pollution: A Comparative Analysis with Home-Based Exposure Assessment.

Air pollution exposure is typically assessed at the front door where people live in large-scale epidemiological studies, overlooking individuals' daily mobility out-of-home. However, there is limited evidence that incorporating mobility data into personal air pollution assessment improves exposure assessment compared to home-based assessments. This study aimed to compare the agreement between mobility-based and home-based assessments with personal exposure measurements. We measured repeatedly particulate matter (PM2.5) and black carbon (BC) using a sample of 41 older adults in the Netherlands. In total, 104 valid 24 h average personal measurements were collected. Home-based exposures were estimated by combining participants' home locations and temporal-adjusted air pollution maps. Mobility-based estimates of air pollution were computed based on smartphone-based tracking data, temporal-adjusted air pollution maps, indoor-outdoor penetration, and travel mode adjustment. Intraclass correlation coefficients (ICC) revealed that mobility-based estimates significantly improved agreement with personal measurements compared to home-based assessments. For PM2.5, agreement increased by 64% (ICC: 0.39-0.64), and for BC, it increased by 21% (ICC: 0.43-0.52). Our findings suggest that adjusting for indoor-outdoor pollutant ratios in mobility-based assessments can provide more valid estimates of air pollution than the commonly used home-based assessments, with no added value observed from travel mode adjustments.

Air pollution exposure and mortality from neurodegenerative diseases in the Netherlands: A population-based cohort study.

BACKGROUND: Long-term exposure to ambient air pollution has been linked with all-cause mortality and cardiovascular and respiratory diseases. Suggestive associations between ambient air pollutants and neurodegeneration have also been reported, but due to the small effect and relatively rare outcomes evidence is yet inconclusive. Our aim was to investigate the associations between long-term air pollution exposure and mortality from neurodegenerative diseases. METHODS: A Dutch national cohort of 10.8 million adults aged ≥30 years was followed from 2013 until 2019. Annual average concentrations of air pollutants (ultra-fine particles (UFP), nitrogen dioxide (NO2), fine particles (PM2.5 and PM10) and elemental carbon (EC)) were estimated at the home address at baseline, using land-use regression models. The outcome variables were mortality due to amyotrophic lateral sclerosis (ALS), Parkinson's disease, non-vascular dementia, Alzheimer's disease, and multiple sclerosis (MS). Hazard ratios (HR) were estimated using Cox models, adjusting for individual and area-level socio-economic status covariates. RESULTS: We had a follow-up of 71 million person-years. The adjusted HRs for non-vascular dementia were significantly increased for NO2 (1.03; 95% confidence interval (CI) 1.02-1.05) and PM2.5 (1.02; 95%CI 1.01-1.03) per interquartile range (IQR; 6.52 and 1.47 µg/m3, respectively). The association with PM2.5 was also positive for ALS (1.02; 95%CI 0.97-1.07). These associations remained positive in sensitivity analyses and two-pollutant models. UFP was not associated with any outcome. No association with air pollution was found for Parkinson's disease and MS. Inverse associations were found for Alzheimer's disease. CONCLUSION: Our findings, using a cohort of more than 10 million people, provide further support for associations between long-term exposure to air pollutants (PM2.5 and particularly NO2) and mortality of non-vascular dementia. No associations were found for Parkinson and MS and an inverse association was observed for Alzheimer's disease.

Hourly land-use regression modeling for NO2 and PM2.5 in the Netherlands.

Annual average land-use regression (LUR) models have been widely used to assess spatial patterns of air pollution exposures. However, they fail to capture diurnal variability in air pollution and consequently might result in biased dynamic exposure assessments. In this study we aimed to model average hourly concentrations for two major pollutants, NO2 and PM2.5, for the Netherlands using the LUR algorithm. We modelled the spatial variation of average hourly concentrations for the years 2016-2019 combined, for two seasons, and for two weekday types. Two modelling approaches were used, supervised linear regression (SLR) and random forest (RF). The potential predictors included population, road, land use, satellite retrievals, and chemical transport model pollution estimates variables with different buffer sizes. We also temporally adjusted hourly concentrations from a 2019 annual model using the hourly monitoring data, to compare its performance with the hourly modelling approach. The results showed that hourly NO2 models performed overall well (5-fold cross validation R2 = 0.50-0.78), while the PM2.5 performed moderately (5-fold cross validation R2 = 0.24-0.62). Both for NO2 and PM2.5 the warm season models performed worse than the cold season ones, and the weekends' worse than weekdays'. The performance of the RF and SLR models was similar for both pollutants. For both SLR and RF, variables with larger buffer sizes representing variation in background concentrations, were selected more often in the weekend models compared to the weekdays, and in the warm season compared to the cold one. Temporal adjustment of annual average models performed overall worse than both modelling approaches (NO2 hourly R2 = 0.35-0.70; PM2.5 hourly R2 = 0.01-0.15). The difference in model performance and selection of variables across hours, seasons, and weekday types documents the benefit to develop independent hourly models when matching it to hourly time activity data.

Short-term residential exposure to endotoxin emitted from livestock farms in relation to lung function in non-farming residents.

BACKGROUND: Evidence on the public health relevance of exposure to livestock farm emissions is increasing. Research mostly focused on chemical air pollution, less on microbial exposure, while endotoxins are suggested relevant bacterial components in farm emissions. Acute respiratory health effects of short-term exposure to livestock-related air pollution has been shown for NH3 and PM10, but has not yet been studied for endotoxin. We aimed to assess associations between lung function and short-term exposure to livestock farming emitted endotoxin in co-pollutant models with NH3 and PM10. METHODS: In 2014/2015, spirometry was conducted in 2308 non-farming residents living in a rural area in the Netherlands. Residential exposure to livestock farming emitted endotoxin during the week prior to spirometry was estimated by dispersion modelling. The model was applied to geo-located individual barns within 10 km of each home address using provincial farm data and local hourly meteorological conditions. Regional week-average measured concentrations of NH3 and PM10 were obtained through monitoring stations. Lung function parameters (FEV1, FVC, FEV1/FVC, MMEF) were expressed in %-predicted value based on GLI-2012. Exposure-response analyses were performed by linear regression modelling. RESULTS: Week-average endotoxin exposure was negatively associated with FVC, independently from regional NH3 and PM10 exposure. A 1.1% decline in FVC was estimated for an increase of endotoxin exposure from 10th to 90th percentile. Stratified analyses showed a larger decline (3.2%) for participants with current asthma and/or COPD. FEV1 was negatively associated with week-average endotoxin exposure, but less consistent after co-pollutant adjustment. FEV1/FVC and MMEF were not associated with week-average endotoxin exposure. CONCLUSIONS: Lower lung function in non-farming residents was observed in relation to short-term residential exposure to livestock farming emitted endotoxin. This study indicates the probable relevance of exposure to microbial emissions from livestock farms considering public health besides chemical air pollution, necessitating future research incorporating both.

Single- and two-pollutant Concentration-Response Functions for PM2.5 and NO2 for Quantifying Mortality Burden in Health Impact Assessments.

OBJECTIVE: Health Impact Assessments (HIAs) for air pollutant mixtures are challenging because risk estimates are primarily derived from single-pollutant models. Combining risk estimates from multiple pollutants requires new approaches, as a simple addition of single pollutant risk estimates from correlated air pollutants may result in double counting. We investigated approaches applying concentration-response functions (CRFs) from single- and two-pollutant models in HIAs, focusing on long-term exposure to particulate matter with a diameter less than 2.5 micrometers (PM2.5) and nitrogen dioxide (NO2) and their associations with all-cause mortality. METHODS: A systematic literature search of MEDLINE and EMBASE identified cohort studies employing single- and two-pollutant models of long-term exposure to PM2.5 and NO2 with all-cause mortality. Pooled CRFs were calculated through random-effects meta-analyses of risk estimates from single- and two-pollutant models. Coefficient differences were calculated by comparing single- and two-pollutant model estimates. Four approaches to estimating population-attributable fractions (PAFs) were compared: PM2.5 or NO2 single-pollutant models to represent the mixture, the sum of single-pollutant models, the sum of two-pollutant models and the sum of single-pollutant models from a larger body of evidence adjusted by coefficient difference. RESULTS: Seventeen papers reported both single and two-pollutant estimates. Pooled hazard ratios (HRs) for mortality from single- and two-pollutant models were 1.053 (95% confidence interval: 1.034-1.071) and 1.035 (1.014-1.057), respectively, for a 5 µg/m3 increase in PM2.5. HRs for a 10 µg/m3 increase in NO2 were 1.032 (1.014-1.049) and 1.024 (1.000-1.049) for single- and two-pollutant models, respectively. The average coefficient difference between single- and two-pollutant models was 0.017 for PM2.5 and 0.007 for NO2. Combined PAFs for the PM2.5-NO2 mixture using joint HRs from single- and two-pollutant model CRFs were 0.09 and 0.06, respectively. CONCLUSION: Utilizing CRFs from two-pollutant models or applying the coefficient difference to a more extensive evidence base seems to mitigate the potential overestimation of mixture health impacts from adding single-pollutant CRFs.

Implementing co-created citizen science in five environmental epidemiological studies in the CitieS-Health project.

BACKGROUND AND AIM: Scientists and scientific institutions are adopting more extensive participatory models, hoping to revisit the existing relationship between science and society. Though citizen science has become more common in environmental monitoring, it is seldom utilized in environmental epidemiology. In the CitieS-Health project, we co-created epidemiological studies with citizens in five European countries. The aim of this paper is to share our experiences and impart methodological insight into the application of co-created citizen science strategies in environmental epidemiology. METHODS: We applied the CitieS-Health framework, involving citizens in all the phases of the studies: identifying research questions, designing research protocols, collecting data, analysing data, interpreting data, formulating conclusions, authoring scientific articles and communicating the results to diverse audiences. These epidemiological studies, conducted in specific areas in Italy, Lithuania, the Netherlands, Slovenia and Spain, covered diverse local environmental issues and health effects ranging from air pollution and mental health to industrial pollution and kidney disease. RESULTS: Together with citizens, we successfully conducted environmental epidemiological studies that generated new scientific knowledge reflecting the concerns and knowledge of citizens. Citizens contributed in all the research activities, including activities beyond formulating the research questions, though the researchers initiated several design discussions and conducted time-consuming and complex tasks (e.g. data analysis, measurement of specific exposures and health outcomes). The challenges we encountered were engaging effectively with citizens throughout the study, harmonizing citizens' knowledge and values with the academics' expertise, managing civic expectations, making complex concepts understandable to citizens and representativeness of participating citizens. The co-created studies were able to empower citizens to address local health concerns by sharing and using scientific knowledge generated from studies. CONCLUSIONS: Integration of co-created citizen science in environmental epidemiology is feasible and has the potential to improve the quality of research whilst promoting civic trust in research and results.

Long-term exposure to ambient air pollution and risk of lung cancer - A comparative analysis of incidence and mortality in four administrative cohorts in the ELAPSE study.

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 (PM2.5), nitrogen dioxide (NO2), black carbon (BC), and warm-season ozone (O3) 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 PM2.5, NO2 and BC, and negatively associated with O3. The negative O3 association became positive after adjustment for NO2. 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/m3 increase in PM2.5, and 1.10 (1.04, 1.16) and 1.09 (1.02, 1.16) per 10 µg/m3 increase in NO2. 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 PM2.5, NO2 and BC in meta-analyses of four European administrative cohorts, which persisted at low pollution levels.

Long-term exposure to air pollution and chronic kidney disease-associated mortality-Results from the pooled cohort of the European multicentre ELAPSE-study.

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 (NO2), black carbon (BC), ozone (O3), particulate matter ≤2.5 µm (PM2.5) and several elemental constituents of PM2.5. 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 PM2.5 (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), NO2 (1.13 (0.93-1.38) per 10 µg/m3) and inverse for O3 (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.

Does residential address-based exposure assessment for outdoor air pollution lead to bias in epidemiological studies?

BACKGROUND: Epidemiological studies of long-term exposure to outdoor air pollution have consistently documented associations with morbidity and mortality. Air pollution exposure in these epidemiological studies is generally assessed at the residential address, because individual time-activity patterns are seldom known in large epidemiological studies. Ignoring time-activity patterns may result in bias in epidemiological studies. The aims of this paper are to assess the agreement between exposure assessed at the residential address and exposures estimated with time-activity integrated and the potential bias in epidemiological studies when exposure is estimated at the residential address. MAIN BODY: We reviewed exposure studies that have compared residential and time-activity integrated exposures, with a focus on the correlation. We further discuss epidemiological studies that have compared health effect estimates between the residential and time-activity integrated exposure and studies that have indirectly estimated the potential bias in health effect estimates in epidemiological studies related to ignoring time-activity patterns. A large number of studies compared residential and time-activity integrated exposure, especially in Europe and North America, mostly focusing on differences in level. Eleven of these studies reported correlations, showing that the correlation between residential address-based and time-activity integrated long-term air pollution exposure was generally high to very high (R > 0.8). For individual subjects large differences were found between residential and time-activity integrated exposures. Consistent with the high correlation, five of six identified epidemiological studies found nearly identical health effects using residential and time-activity integrated exposure. Six additional studies in Europe and North America showed only small to moderate potential bias (9 to 30% potential underestimation) in estimated exposure response functions using residence-based exposures. Differences of average exposure level were generally small and in both directions. Exposure contrasts were smaller for time-activity integrated exposures in nearly all studies. The difference in exposure was not equally distributed across the population including between different socio-economic groups. CONCLUSIONS: Overall, the bias in epidemiological studies related to assessing long-term exposure at the residential address only is likely small in populations comparable to those evaluated in the comparison studies. Further improvements in exposure assessment especially for large populations remain useful.

A co-created citizen science project on the short term effects of outdoor residential woodsmoke on the respiratory health of adults in the Netherlands.

BACKGROUND AND AIM: Woodsmoke from household fireplaces contributes significantly to outdoor air pollution in the Netherlands. The current understanding of the respiratory health effects of exposure to smoke from residential wood burning is limited. This study investigated the association between short-term changes in outdoor woodsmoke exposure and lung function, respiratory symptoms, and medication use in adults in the Netherlands. METHODS: This study was co-created with citizen scientists and other relevant stakeholders. A panel study was conducted with repeated observations in 46 adults between February and May 2021 in four Dutch towns. Participants recorded their symptoms and medication use in daily diaries, and conducted morning and evening home spirometry measurements. Woodsmoke exposure was characterized by measuring levoglucosan (most specific marker for woodsmoke exposure), black/brown carbon, fine and ultrafine particulate matter at central monitoring sites. Individual woodsmoke perception (smell) was recorded in daily diaries. Linear and logistic regression models were used to investigate the association between respiratory health and woodsmoke exposure. Models were adjusted for time-varying confounders and accounted for repeated observations within participants. RESULTS: Consistent positive associations were found between levoglucosan and shortness of breath (SOB) during rest and extra respiratory medication use. Odds ratios for current day exposure to levoglucosan were 1.12 (95% CI: 0.97, 1.30) for SOB during rest and 1.19 (95% CI: 1.07, 1.33) for extra medication use, expressed per interquartile range of levoglucosan concentrations (69.16 ng/m3). Positive non-significant associations were found between levoglucosan and nasal symptoms, cough and waking up with SOB. No consistent association was found between levoglucosan and lung function. Associations found between woodsmoke markers, SOB during rest and extra medication use remained after the inclusion of PM2.5 and UFP in two-pollutant models. CONCLUSIONS: Adults experienced more SOB during rest, nasal symptoms and used more medication to treat respiratory symptoms on days with higher levels of outdoor woodsmoke concentrations.

Perinatal exposure to traffic related air pollutants and the risk of infection in the first six months of life: a cohort study from a low-middle income country.

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. PM2.5, soot, NOx, and NO2 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 PM2.5 and NO2 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 PM2.5 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.

Long-term air pollution exposure and malignant intracranial tumours of the central nervous system: a pooled analysis of six European cohorts.

BACKGROUND: Risk factors for malignant tumours of the central nervous system (CNS) are largely unknown. METHODS: We pooled six European cohorts (N = 302,493) and assessed the association between residential exposure to nitrogen dioxide (NO2), fine particles (PM2.5), black carbon (BC), ozone (O3) and eight elemental components of PM2.5 (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) and malignant intracranial CNS tumours defined according to the International Classification of Diseases ICD-9/ICD-10 codes 192.1/C70.0, 191.0-191.9/C71.0-C71.9, 192.0/C72.2-C72.5. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. RESULTS: During 5,497,514 person-years of follow-up (average 18.2 years), we observed 623 malignant CNS tumours. The results of the fully adjusted linear analyses showed a hazard ratio (95% confidence interval) of 1.07 (0.95, 1.21) per 10 µg/m³ NO2, 1.17 (0.96, 1.41) per 5 µg/m³ PM2.5, 1.10 (0.97, 1.25) per 0.5 10-5m-1 BC, and 0.99 (0.84, 1.17) per 10 µg/m³ O3. CONCLUSIONS: We observed indications of an association between exposure to NO2, PM2.5, and BC and tumours of the CNS. The PM elements were not consistently associated with CNS tumour incidence.

Long-term exposure to air pollution and risk of SARS-CoV-2 infection and COVID-19 hospitalisation or death: Danish nationwide cohort study.

BACKGROUND: Early ecological studies have suggested links between air pollution and risk of coronavirus disease 2019 (COVID-19), but evidence from individual-level cohort studies is still sparse. We examined whether long-term exposure to air pollution is associated with risk of COVID-19 and who is most susceptible. METHODS: We followed 3 721 810 Danish residents aged ≥30 years on 1 March 2020 in the National COVID-19 Surveillance System until the date of first positive test (incidence), COVID-19 hospitalisation or death until 26 April 2021. We estimated residential annual mean particulate matter with diameter ≤2.5 µm (PM2.5), nitrogen dioxide (NO2), black carbon (BC) and ozone (O3) in 2019 by the Danish DEHM/UBM model, and used Cox proportional hazards regression models to estimate the associations of air pollutants with COVID-19 outcomes, adjusting for age, sex, individual- and area-level socioeconomic status, and population density. RESULTS: 138 742 individuals were infected, 11 270 were hospitalised and 2557 died from COVID-19 during 14 months. We detected associations of PM2.5 (per 0.53 µg·m-3) and NO2 (per 3.59 µg·m-3) with COVID-19 incidence (hazard ratio (HR) 1.10 (95% CI 1.05-1.14) and HR 1.18 (95% CI 1.14-1.23), respectively), hospitalisations (HR 1.09 (95% CI 1.01-1.17) and HR 1.19 (95% CI 1.12-1.27), respectively) and death (HR 1.23 (95% CI 1.04-1.44) and HR 1.18 (95% CI 1.03-1.34), respectively), which were strongest in the lowest socioeconomic groups and among patients with chronic respiratory, cardiometabolic and neurodegenerative diseases. We found positive associations with BC and negative associations with O3. CONCLUSION: Long-term exposure to air pollution may contribute to increased risk of contracting severe acute respiratory syndrome coronavirus 2 infection as well as developing severe COVID-19 disease requiring hospitalisation or resulting in death.

Integrating large-scale stationary and local mobile measurements to estimate hyperlocal long-term air pollution using transfer learning methods.

Mobile air quality measurements are collected typically for several seconds per road segment and in specific timeslots (e.g., working hours). These short-term and on-road characteristics of mobile measurements become the ubiquitous shortcomings of applying land use regression (LUR) models to estimate long-term concentrations at residential addresses. This issue was previously found to be mitigated by transferring LUR models to the long-term residential domain using routine long-term measurements in the studied region as the transfer target (local scale). However, long-term measurements are generally sparse in individual cities. For this scenario, we propose an alternative by taking long-term measurements collected over a larger geographical area (global scale) as the transfer target and local mobile measurements as the source (Global2Local model). We empirically tested national, airshed countries (i.e., national plus neighboring countries) and Europe as the global scale in developing Global2Local models to map nitrogen dioxide (NO2) concentrations in Amsterdam. The airshed countries scale provided the lowest absolute errors, and the Europe-wide scale had the highest R2. Compared to a "global" LUR model (trained exclusively with European-wide long-term measurements), and a local mobile LUR model (using mobile data from Amsterdam only), the Global2Local model significantly reduced the absolute error of the local mobile LUR model (root-mean-square error, 6.9 vs 12.6 µg/m3) and improved the percentage explained variances compared to the global model (R2, 0.43 vs 0.28, assessed by independent long-term NO2 measurements in Amsterdam, n = 90). The Global2Local method improves the generalizability of mobile measurements in mapping long-term residential concentrations with a fine spatial resolution, which is preferred in environmental epidemiological studies.

Exposure to ambient ultrafine particles and allergic sensitization in children up to 16 years.

BACKGROUND: Few epidemiological studies so far have investigated the role of long-term exposure to ultrafine particles (UFP) in inhalant and food allergy development. OBJECTIVES: The purpose of this study was to assess the association between UFP exposure and allergic sensitization to inhalant and food allergens in children up to 16 years old in the Netherlands. METHODS: 2295 participants of a prospective birth cohort with IgE measurements to common inhalant and food allergens at ages 4, 8, 12 and/or 16 were included in the study. Annual average UFP concentrations were estimated for the home addresses at birth and at the time of the IgE measurements using land-use regression models. Generalized estimating equations were used for the assessment of overall and age-specific associations between UFP exposure and allergic sensitization. Additionally, single- and two-pollutant models with NO2, PM2.5, PM2.5 absorbance and PM10 were assessed. RESULTS: We found no significant associations between UFP exposure and allergic sensitization to inhalant and food allergens (OR (95% CI) ranging from 1.02 (0.95-1.10) to 1.05 (0.98-1.12), per IQR increment). NO2, PM2.5, PM2.5 absorbance and PM10 showed significant associations with sensitization to food allergens (OR (95% CI) ranging from 1.09 (1.00-1.20) to 1.23 (1.06-1.43) per IQR increment). NO2, PM2.5, PM2.5 absorbance and PM10 were not associated with sensitization to inhalant allergens. For NO2, PM2.5 and PM2.5 absorbance, the associations with sensitization to food allergens persisted in two-pollutant models with UFP. CONCLUSION: This study found no association between annual average exposure to UFP and allergic sensitization in children up to 16 years of age. NO2, PM2.5, PM2.5 absorbance and PM10 were associated with sensitization to food allergens.

Multiple myeloma risk in relation to long-term air pollution exposure - A pooled analysis of four European cohorts.

BACKGROUND: 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. METHODS: We pooled four European cohorts (N = 234,803) and assessed the association between residential exposure to nitrogen dioxide (NO2), fine particles (PM2.5), black carbon (BC), and ozone (O3) and multiple myeloma. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. RESULTS: 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 NO2, 1.04 (0.82, 1.33) per 5 µg/m³ PM2.5, 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 O3. CONCLUSIONS: We did not observe an association between long-term ambient air pollution exposure and incidence of multiple myeloma.

Long-term exposure to elemental components of fine particulate matter and all-natural and cause-specific mortality in a Danish nationwide administrative cohort study.

BACKGROUND: Fine particulate matter (PM2.5) is a well-recognized risk factor for premature death. However, evidence on which PM2.5 components are most relevant is unclear. METHODS: We evaluated the associations between mortality and long-term exposure to eight PM2.5 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 PM2.5 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 PM2.5 mass. RESULTS: 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. CONCLUSIONS: We present novel results of the relevance of different PM2.5 components for different causes of death, with K and Si seeming to be most consistently associated with mortality in Denmark.