Air pollutants such as NO2 and PM2.5 have consistently been linked to mortality, but only few previous studies have addressed associations with long-term exposure to black carbon (BC) and ozone (O3).
...We investigated the association between PM2.5, PM10, BC, NO2, and O3 and mortality in a Danish cohort of 49,564 individuals who were followed up from enrollment in 1993–1997 through 2015. Residential address history from 1979 onwards was combined with air pollution exposure obtained by the state-of-the-art, validated, THOR/AirGIS air pollution modelling system, and information on residential traffic noise exposure, lifestyle and socio-demography.
We observed higher risks of all-cause as well as cardiovascular disease (CVD) mortality with higher long-term exposure to PM2.5, PM10, BC, and NO2. For PM2.5 and CVD mortality, a hazard ratio (HR) of 1.29 (95% CI: 1.13–1.47) per 5 μg/m3 was observed, and correspondingly HRs of 1.16 (95% CI: 1.05–1.27) and 1.11 (95% CI: 1.04–1.17) were observed for BC (per 1 μg/m3) and NO2 (per 10 μg/m3), respectively. Adjustment for noise gave slightly lower estimates for the air pollutants and CVD mortality. Inverse relationships were observed for O3. None of the investigated air pollutants were related to risk of respiratory mortality. Stratified analyses suggested that the elevated risks of CVD and all-cause mortality in relation to long-term PM, NO2 and BC exposure were restricted to males.
This study supports a role of PM, BC, and NO2 in all-cause and CVD mortality independent of road traffic noise exposure.
•Higher exposure to PM2.5, PM10, NO2 and black carbon was associated with mortality.•Associations of air pollutants and CVD mortality were independent of noise exposure.•O3 exposure was not associated with increased mortality risk.
The search for the genetic factors underlying complex neuropsychiatric disorders has proceeded apace in the past decade. Despite some advances in identifying genetic variants associated with ...psychiatric disorders, most variants have small individual contributions to risk. By contrast, disease risk increase appears to be less subtle for disease-predisposing environmental insults. In this study, we sought to identify associations between environmental pollution and risk of neuropsychiatric disorders. We present exploratory analyses of 2 independent, very large datasets: 151 million unique individuals, represented in a United States insurance claims dataset, and 1.4 million unique individuals documented in Danish national treatment registers. Environmental Protection Agency (EPA) county-level environmental quality indices (EQIs) in the US and individual-level exposure to air pollution in Denmark were used to assess the association between pollution exposure and the risk of neuropsychiatric disorders. These results show that air pollution is significantly associated with increased risk of psychiatric disorders. We hypothesize that pollutants affect the human brain via neuroinflammatory pathways that have also been shown to cause depression-like phenotypes in animal studies.
•Premature mortality associated to fine particles (PM2.5) over Europe is estimated.•Excess mortality rate from PM2.5 in Europe is 904,000 premature deaths/year.•This mortality rate will increase by ...73% in the year 2050 under RCP8.5 scenario.•Increase in premature mortality is associated fundamentally to the aging of population.
The World Health Organization estimates that around 7 million people die every year from exposure to fine particles (PM2.5) inpolluted air. Here, the number of premature deaths in Europe from different diseases associated to the ambient exposure to PM2.5 have here been studied both for present (1991–2010) and future periods (2031–2050, RCP8.5 scenario). This contribution combines different state-of-the-art approaches (use of high-resolution climate/chemistry simulations over Europe for providing air quality data; use of different baseline mortality data for specific European regions; inclusion of future population projections and dynamical changes for 2050 obtained from the United Nations (UN) Population Projections or use of non-linear exposure–response functions) to estimate the premature mortality due to PM2.5. The mortality endpoints included in this study are Lung Cancer (LC), Chronic Obstructive Pulmonary Disease (COPD), Cerebrovascular Disease (CEV), Ischemic Heart Disease (IHD), Lower Respiratory Infection (LRI) and other Non-Communicable Diseases (other NCDs). Different risk ratio and baseline mortalities for each disease end each age range have been estimated individually. The results indicate that the annual excess mortality rate from fine particulate matter in Europe is 904,000 95% confidence interval (95% CI) 733,100–1,067,800, increasing by 73% in 2050s (1,560,000; 95% CI 1,260,000–1,840,000); meanwhile population decreases from 808 to 806 million according to the UN estimations. The results show that IHD is the main cause of premature mortality in Europe associated to PM2.5 (around 48%) both for the present and future periods. Despite several marked regional differences, premature deaths associated to all the endpoints included in this study will increase in the future period due to the climate penalty but especially because of changes in the population projected and its aging.
•Primary carbonaceous particle and SOA exposure was associated with mortality.•Primary carbonaceous particle and SIA exposure was associated with CVD mortality.•Sea salt exposure was not associated ...with increased mortality risk.
Studies on health effects of long-term exposure to specific PM2.5 constituents are few. Previous studies have reported an association between black carbon (BC) exposure and cardiovascular diseases (CVD) and a few studies have found an association between sulfate exposure and mortality. These studies, however, relied mainly on exposure data from centrally located air-monitoring stations, which is a crude approximation of personal exposure.
We focused on specific chemical constituents of PM2.5, i.e. elemental and primary organic carbonaceous particles (BC/OC), sea salt, secondary inorganic aerosols (SIA, i.e. NO3–, NH4+, and SO42-), and secondary organic aerosols (SOA), in relation to all-cause, CVD and respiratory disease mortality.
We followed a Danish cohort of 49,564 individuals from enrollment in 1993–1997 through 2015. We combined residential address history from 1979 onwards with mean annual air pollution concentrations obtained by the AirGIS air pollution modelling system, lifestyle information from baseline questionnaires and socio-demography obtained by register linkage.
During 895,897 person-years of follow-up, 10,193 deaths from all causes occurred – of which 2319 were CVD-related and 870 were related to respiratory disease. The 15-year time-weighted average concentrations of PM2.5, BC/OC, sea salt, SIA and SOA were 13.8, 2.8, 3.4, 4.9, and 0.3 µg/m3, respectively. For all-cause mortality, a higher risk was observed with higher exposure to PM2.5, BC/OC and SOA with adjusted hazard ratios of 1.03 (95% confidence intervals: 1.01, 1.05), 1.06 (1.03, 1.09), and 1.08 (1.03, 1.13) per interquartile range, respectively. The associations for BC/OC and SOA remained after adjustment for PM2.5 in two-pollutant models. For CVD mortality, we observed elevated risks with higher exposure to PM2.5, BC/OC and SIA. The results showed no clear relationship between sea salt and mortality.
In this study, we observed a relationship between long-term exposure to PM2.5, BC/OC, and SOA and all-cause mortality and between PM2.5, BC/OC, and SIA and CVD mortality.
•We included spatially-varying relationships in our Europe-wide models.•We built spatially- and temporally-varying models to estimate annual air pollution.•Spatially-varying linear regression was ...more robust than a machine learning method.
Previous European land-use regression (LUR) models assumed fixed linear relationships between air pollution concentrations and predictors such as traffic and land use. We evaluated whether including spatially-varying relationships could improve European LUR models by using geographically weighted regression (GWR) and random forest (RF). We built separate LUR models for each year from 2000 to 2019 for NO2, O3, PM2.5 and PM10 using annual average monitoring observations across Europe. Potential predictors included satellite retrievals, chemical transport model estimates and land-use variables. Supervised linear regression (SLR) was used to select predictors, and then GWR estimated the potentially spatially-varying coefficients. We developed multi-year models using geographically and temporally weighted regression (GTWR). Five-fold cross-validation per year showed that GWR and GTWR explained similar spatial variations in annual average concentrations (average R2 = NO2: 0.66; O3: 0.58; PM10: 0.62; PM2.5: 0.77), which are better than SLR (average R2 = NO2: 0.61; O3: 0.46; PM10: 0.51; PM2.5: 0.75) and RF (average R2 = NO2: 0.64; O3: 0.53; PM10: 0.56; PM2.5: 0.67). The GTWR predictions and a previously-used method of back-extrapolating 2010 model predictions using CTM were overall highly correlated (R2 > 0.8) for all pollutants. Including spatially-varying relationships using GWR modestly improved European air pollution annual LUR models, allowing time-varying exposure-health risk models.
•Early-life exposure to air pollution may increase asthma risk in young children.•Children living in low socio-economy areas may be more susceptible.•Air pollution have adverse health effects even at ...low concentrations.
Asthma is a complex, heterogeneous disease and one of the most common chronic diseases among children. Exposure to ambient air pollution in early life and childhood may influence asthma aetiology, but it is uncertain which specific components of air pollution and exposure windows are of importance. The role of socio-economic status (SES) is also unclear. The aims of the present study are, therefore, to investigate how various exposure windows of different pollutants affect risk-induced asthma in early life and to explore the possible effect SES has on that relationship.
The study population was constructed using register data on all singleton births in the greater Stockholm area between 2006 and 2013. Exposure to ambient black carbon (BC), fine particulate matter (PM2.5), primary organic carbon (pOC) secondary organic aerosols (SOA), secondary inorganic aerosols, and oxidative potential at the residential address was modelled as mean values for the entire pregnancy period, the first year of life and the first three years of life. Swedish national registers were used to define the outcome: asthma diagnosis assessed at hospital during the first six years of life. Hazard ratios (HRs) and their 95% confidence intervals (CIs) were modelled with Cox proportional hazards model with age as the underlying time-scale, adjusting for relevant potential confounding variables.
An increased risk for developing childhood asthma was observed in association with exposure to PM2.5, pOC and SOA during the first three years of life. With an interquartile range increase in exposure, the HRs were 1.06 (95% CI: 1.01–1.10), 1.05 (95% CI: 1.02–1.09) and 1.02 (95% CI: 1.00–1.04), for PM2.5, pOC and SOA, respectively, in the fully adjusted models. Exposure during foetal life or the first year of life was not associated with asthma risk, and the other pollutants were not statistically significantly associated with increased risk. Furthermore, the increase in risk associated with PM2.5 and the components BC, pOC and SOA were stronger in areas with lower SES.
Our results suggest that exposure to air pollution during the first three years of life may increase the risk for asthma in early childhood. The findings further imply a possible increased vulnerability to air pollution-attributed asthma among low SES children.
Ambient air pollution has been linked to stroke, but few studies have examined in detail stroke subtypes and confounding by road traffic noise, which was recently associated with stroke. Here we ...examined the association between long-term exposure to air pollution and incidence of stroke (overall, ischemic, hemorrhagic), adjusting for road traffic noise. In a nationwide Danish Nurse Cohort consisting of 23,423 nurses, recruited in 1993 or 1999, we identified 1,078 incident cases of stroke (944 ischemic and 134 hemorrhagic) up to December 31, 2014, defined as first-ever hospital contact. The full residential address histories since 1970 were obtained for each participant and the annual means of air pollutants (particulate matter with diameter < 2.5 µm and < 10 µm (PM2.5 and PM10), nitrogen dioxide (NO2), nitrogen oxides (NOx)) and road traffic noise were determined using validated models. Time-varying Cox regression models were used to estimate hazard ratios (HR) (95% confidence intervals (CI)) for the associations of one-, three, and 23-year running mean of air pollutants with stroke adjusting for potential confounders and noise. In fully adjusted models, the HRs (95% CI) per interquartile range increase in one-year running mean of PM2.5 and overall, ischemic, and hemorrhagic stroke were 1.12 (1.01–1.25), 1.13 (1.01–1.26), and 1.07 (0.80–1.44), respectively, and remained unchanged after adjustment for noise. Long-term exposure to ambient PM2.5 was associated with the risk of stroke independent of road traffic noise.
•A nationwide, register-based, case-control study with 12 928 brain tumor cases.•State of the art air pollution modeling for all addresses 10 years before diagnosis.•Primary emitted carbonaceous ...particles was associated with malignant brain tumors.•Results need replication.
Air pollution is an established carcinogen. Evidence for an association with brain tumors is, however, inconclusive. We investigated if individual particulate matter constituents were associated with brain tumor risk.
From comprehensive national registers, we identified all (n = 12 928) brain tumor cases, diagnosed in Denmark in the period 1989–2014, and selected 22 961 controls, matched on age, sex and year of birth. We established address histories and estimated 10-year mean residential outdoor concentrations of particulate matter < 2.5 µm, primarily emitted black carbon (BC) and organic carbon (OC), and combined carbon (OC/BC), as well as secondary inorganic and organic PM air pollutants from a detailed dispersion model. We used conditional logistic regression to calculate odds ratios (OR) per inter quartile range (IQR) exposure. We adjusted for income, marital and employment status as well as area-level socio-demographic characteristics.
Total tumors of the brain were associated with OC/BC (OR: 1.053, 95%CI: 1.005–1.103, per IQR). The data suggested strongest associations for malignant tumors with ORs per IQR for OC/BC, BC and OC of 1.063 (95% CI: 1.007–1.123), 1.036 (95% CI: 1.006–1.067) and 1.030 (95%CI: 0.979–1.085), respectively. The results did not indicate adverse effects of other PM components.
This large, population based study showed associations between primary emitted carbonaceous particles and risk for malignant brain tumors. As the first of its kind, this study needs replication.
Purpose
The etiology of Hodgkin lymphoma (HL) is obscure. Research on air pollution and risk of HL provides inconsistent results. We aimed to investigate the association between long-term residential ...exposure to air pollution and risk of adult Hodgkin lymphoma in Denmark.
Methods
We performed a nationwide register-based case–control study, including all (
n
= 2,681) Hodgkin lymphoma cases registered in the nationwide Danish Cancer Registry between 1989 and 2014. We randomly selected 8,853 age- and sex-matched controls from the entire Danish population using the Civil Registration System, and identified 20-year residential address history for all cases and controls. We modeled outdoor air pollution concentrations at all these addresses using the high-resolution multiscale air pollution model system DEHM/UBM/AirGIS. We used conditional logistic regression to estimate odds ratios adjusted for individual and neighborhood level sociodemographic variables.
Results
There was no association between 1, 5, 10, and 20 years’ time-weighted average exposure to fine particles (PM
2.5
), O
3
, SO
2,
NO
2,
or the PM
2.5
constituents OC, NH
4
, NO
3
, and SO
4
and risk of Hodgkin lymphoma.
Conclusion
Residential exposure to ambient air pollution does not seem to increase the risk of developing Hodgkin lymphoma.
BACKGROUNDAir pollution has been linked to mortality, but there are few studies examining the association with different exposure time windows spanning across several decades. The evidence for the ...effects of green space and mortality is contradictory.OBJECTIVEWe investigated all-cause mortality in relation to exposure to particulate matter (PM2.5 and PM10), black carbon (BC), nitrogen dioxide (NO2), ozone (O3) and greenness (normalized difference vegetation index - NDVI) across different exposure time windows.METHODSThe exposure assessment was based on a combination of the Danish Eulerian Hemispheric Model and the Urban Background Model for the years 1990, 2000 and 2010. The analysis included a complete case dataset with 9,135 participants from the third Respiratory Health in Northern Europe study (RHINE III), aged 40-65 years in 2010, with mortality follow-up to 2021. We performed Cox proportional hazard models, adjusting for potential confounders.RESULTSAltogether, 327 (3.6 %) persons died in the period 2010-2021. Increased exposures in 1990 of PM2.5, PM10, BC and NO2 were associated with increased all-cause mortality hazard ratios of 1.40 (95 % CI1.04-1.87 per 5 μg/m3), 1.33 (95 % CI: 1.02-1.74 per 10 μg/m3), 1.16 (95 % CI: 0.98-1.38 per 0.4 μg/m3) and 1.17 (95 % CI: 0.92-1.50 per 10 μg/m3), respectively. No statistically significant associations were observed between air pollution and mortality in other time windows. O3 showed an inverse association with mortality, while no association was observed between greenness and mortality. Adjusting for NDVI increased the hazard ratios for PM2.5, PM10, BC and NO2 exposures in 1990. We did not find significant interactions between greenness and air pollution metrics.CONCLUSIONLong term exposure to even low levels of air pollution is associated with mortality. Opening up for a long latency period, our findings indicate that air pollution exposures over time may be even more harmful than anticipated.
PDF
