Modelling of ambient particle number concentrations (PNC) has been implemented in the Danish air quality modelling system DEHM/UBM/AirGIS and evaluated with long-term measurements. We implemented ...particle dynamical processes in the regional scale model DEHM using the M7 aerosol dynamics module (presented in the accompanying article by Frohn et al., 2021), and we developed models for PNC at the local scale (UBM) and street scale (OSPM), in a first approximation without including the particle dynamics as presented in this article.
Outdoor concentration estimates are provided at the front door of all residential address locations in Denmark for the past 40 years (1979–2018) with a spatial resolution of 1 km × 1 km taking all emission sectors in Denmark into account and additionally at the street location, with significant traffic (>500 vehicles/day).
We evaluated our model with up to 18-year long measurement time series of particle number size distributions (PNSD) at Danish street, urban and rural background stations. Two particle size ranges were used for evaluation: PNC>10 (count of particles with diameter larger than 10 nm) and PNC30_250 (diameter range 30–250 nm), in order to exclude nucleation events from the measurements and to obtain a consistent long-term measured time series.
When comparing our model estimates with PNC30_250 measurements, we obtain Pearson correlation coefficients (Rp) in the range 0.39–0.95 depending on station location (street, urban background, rural) and averaging time (hour, day, month, year). The highest correlations were found for yearly averages at a monitoring station located at a street with dense traffic (Rp = 0.95) whereas shorter time averages and comparisons with monitoring stations at urban and rural background locations provided lower correlations. The model performance for PNC in terms of correlation coefficients with respect to measurements is comparable to the performance for other pollutants such as NOX, PM2.5 and better than the performance for PM10.
The model generally overestimated the observed concentrations, Normalized Mean Bias (NMB) was in the range 6%–190% compared to PNC>10 and 90%–290% compared to PNC30_250. These relatively high NMBs are probably caused by uncertainties in the modelling process, especially the estimation of particle number emissions, which largely determine the ambient concentrations of PNC. Furthermore, uncertainties might as well originate from the complexity of modelling particle dynamical processes accurately and the great challenges in performing long-term PNC measurements.
The presented model can estimate PNC at all Danish addresses over the last 40 years with a 1-h time resolution. The data seem to provide a good indication of the relative differences in PNC at Danish addresses.
•Particle number concentrations (PNC) implemented in the Danish air quality modelling system DEHM/UBM/AirGIS.•Outdoor concentrations are provided at the front door of all residential addresses in Denmark for 40 years (1979–2018)•Spatial resolution of 1 km × 1 km taking all emission sectors in Denmark into account.•Additionally at the street locations consider the local traffic contribution, all done in 1 hour time resolution.•Comparing model with PNC30_250 measurementsgives Pearson correlation coefficients in the range 0.39–0.95.•Model overestimated the observed concentrations, Normalized Mean Bias in the range 6%–190% compared to PNC>10.
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.
Physical activity enhances the uptake of air pollutants, possibly reducing its beneficial effects. We examined the effects of leisure-time and transport-related physical activities on the risk of ...myocardial infarction (MI), and whether potential benefits on MI are reduced by exposure to traffic-related air pollution.
A group of 57 053 participants (50-65 years of age) from the Danish Diet, Cancer, and Health cohort reported physical activity at baseline (1993-1997) and were linked to registry data on hospital contacts and out-of-hospital deaths caused by MI, until December 2015. Nitrogen dioxide levels were estimated at participants' baseline residences. We used Cox regressions to associate participation in sports, cycling, walking, and gardening with incident and recurrent MI, and tested for interaction by nitrogen dioxide. Of 50 635 participants without MI at baseline, 2936 developed incident MI, and of 1233 participants with MI before baseline, 324 had recurring MI during follow-up. Mean nitrogen dioxide concentration was 18.7 μg/m
at baseline (1993-1997). We found inverse statistically significant associations between participation in sports (hazard ratio; 95% confidence interval: 0.85; 0.79-0.92), cycling (0.91; 0.84-0.98), gardening (0.87; 0.80-0.95), and incident MI, while the association with walking was statistically nonsignificant (0.95; 0.83-1.08). Recurrent MI was statistically nonsignificantly inversely associated with cycling (0.80; 0.63-1.02), walking (0.82, 0.57-1.16), and gardening (0.91; 0.71-1.18), and positively with sports (1.06; 0.83-1.35). There was no effect modification of the associations between physical activity and MI by nitrogen dioxide.
Benefits of physical activity on both the incidence and the recurrence of MI are not reduced by exposure to high levels of air pollution.
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.
What's new?
Exposure to long‐term ambient air pollution increases mortality and cancer incidence. However, most evidence exists for high exposure levels and lung cancer. In this large European study focusing on air pollution levels even below current EU standards, long‐term exposure to fine particles, nitrogen dioxide and black carbon increased the incidence of upper aerodigestive tract cancers, while no association was found with gastric cancer. These results indicate that ambient air pollution may increase the risk of upper aerodigestive tract cancers, and support the need for aligning current EU air pollution levels with the new WHO Air Quality Guidelines.
Exposure to traffic noise has been associated with adverse effects on neuropsychological outcomes in children, but findings with regard to behavioral problems are inconsistent.
We investigated ...whether residential road traffic noise exposure is associated with behavioral problems in 7-year-old children.
We identified 46,940 children from the Danish National Birth Cohort with complete information on behavioral problems at 7 years of age and complete address history from conception to 7 years of age. Road traffic noise (Lden) was modeled at all present and historical addresses. Behavioral problems were assessed by the parent-reported Strengths and Difficulties Questionnaire (SDQ). Associations between pregnancy and childhood exposure to noise and behavioral problems were analyzed by multinomial or logistic regression and adjusted for potential confounders.
A 10-dB increase in average time-weighted road traffic noise exposure from birth to 7 years of age was associated with a 7% increase (95% CI: 1.00, 1.14) in abnormal versus normal total difficulties scores; 5% (95% CI: 1.00, 1.10) and 9% (95% CI: 1.03, 1.18) increases in borderline and abnormal hyperactivity/inattention subscale scores, respectively; and 5% (95% CI: 0.98, 1.14) and 6% (95% CI: 0.99, 1.12) increases in abnormal conduct problem and peer relationship problem subscale scores, respectively. Exposure to road traffic noise during pregnancy was not associated with child behavioral problems at 7 years of age.
Residential road traffic noise in early childhood may be associated with behavioral problems, particularly hyperactivity/inattention symptoms.
Road traffic noise at normal urban levels can lead to stress and sleep disturbances. Both excess of stress hormones and reduction in sleep quality and duration may lead to higher risk for type 2 ...diabetes.
We investigated whether long-term exposure to residential road traffic noise is associated with an increased risk of diabetes.
In the population-based Danish Diet, Cancer and Health cohort of 57,053 people 50-64 years of age at enrollment in 1993-1997, we identified 3,869 cases of incident diabetes in a national diabetes registry between enrollment and 2006. The mean follow-up time was 9.6 years. Present and historical residential addresses from 1988 through 2006 were identified using a national register, and exposure to road traffic noise was estimated for all addresses. Associations between exposure to road traffic noise and incident diabetes were analyzed in a Cox regression model.
A 10-dB higher level of average road traffic noise at diagnosis and during the 5 years preceding diagnosis was associated with an increased risk of incident diabetes, with incidence rate ratios (IRR) of 1.08 (95% CI: 1.02, 1.14) and 1.11 (95% CI: 1.05, 1.18), respectively, after adjusting for potential confounders including age, body mass index, waist circumference, education, air pollution (nitrogen oxides), and lifestyle characteristics. After applying a stricter definition of diabetes (2,752 cases), we found IRRs of 1.11 (95% CI: 1.03, 1.19) and 1.14 (95% CI: 1.06, 1.22) per 10-dB increase in road traffic noise at diagnosis and during the 5 years preceding diagnosis, respectively.
Exposure to residential road traffic noise was associated with a higher risk of diabetes. This study provides further evidence that urban noise may adversely influence population health.
Air pollution causes lung cancer, but associations with other cancers have not been established. We investigated whether long‐term exposure to traffic‐related air pollution is associated with the ...risk of the general population for leukaemia. We identified 1,967 people in whom leukaemia was diagnosed in 1992–2010 from a nation‐wide cancer registry and selected 3,381 control people at random, matched on sex and year of birth, from the entire Danish population. Residential addresses since 1971 were traced in a population registry, and outdoor concentrations of NOx and NO2, as indicators of traffic‐related air pollution, were calculated at each address in a dispersion model. We used conditional logistic regression to estimate the risk for leukaemia after adjustment for income, educational level, cohabitation status and co‐morbidity. In linear analyses, we found odds ratios for acute myeloid leukaemia of 1.20 (95% confidence interval: 1.04–1.38) per 20 µg/m3 increase in NOx and 1.31 (1.02–1.68) per 10 µg/m3 increase in NO2, calculated as time‐weighted average exposure at all addresses since 1971. We found no association with chronic myeloid or lymphocytic leukaemia. This study indicates an association between long‐term exposure to traffic‐related air pollution and acute myeloid leukaemia in the general population, but not for other subtypes of leukaemia.
What's new?
Outdoor air pollution is classified by the International Agency for Research on Cancer (IARC) as a human lung carcinogen. Further, several known and suspected leukaemogens are present in outdoor air at low concentrations. It is, however, uncertain whether outdoor air pollution detectably increases the risk of general populations for leukaemia. In this large population‐wide case–control study, we found an association between long‐term exposure to traffic‐related air pollution outside the residence and risk for acute myeloid leukaemia but not for other subtypes of leukaemia.
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.
Cancer initiation is presumed to occur in utero for many childhood cancers and it has been hypothesized that advanced paternal age may have an impact due to the increasing number of mutations in the ...sperm DNA with increasing paternal age. We examined the association between paternal age and specific types of childhood cancer in offspring in a large nationwide cohort of 1,904,363 children born in Denmark from 1978 through 2010. The children were identified in the Danish Medical Birth Registry and were linked to information from other national registers, including the Danish Cancer Registry. In total, 3,492 children were diagnosed with cancer before the age of 15 years. The adjusted hazard ratio of childhood cancer according to paternal age was estimated using Cox proportional hazards regressions. We found a 13% (95% confidence interval: 4–23%) higher hazard rate for every 5 years advantage in paternal age for acute lymphoblastic leukemia, while no clear association was found for acute myeloid leukemia (hazard ratio pr. 5 years = 1.02, 95% confidence interval: 0.80–1.30). The estimates for neoplasms in the central nervous system suggested a lower hazard rate with higher paternal age (hazard ratio pr. 5 years = 0.92, 95% confidence interval: 0.84–1.01). No clear associations were found for the remaining childhood cancer types. The findings suggest that paternal age is moderately associated with a higher rate of childhood acute lymphoblastic leukemia, but not acute myeloid leukemia, in offspring, while no firm conclusions could be made for other specific cancer types.
What's new?
Do older fathers impart more mutations to their children, leading to more frequent childhood cancer? To investigate, these authors looked at data from a cohort of children born in Denmark during the years 1978–2010. They found a higher rate of acute lymphoblastic leukemia, but not acute myeloid leukemia, among children born to fathers over age 45 years. Conversely, children with older fathers seemed to experience fewer central nervous system neoplasms. Other childhood cancers showed no clear link to the father's age.
Physical activity enhances uptake of air pollutants in the lung, possibly augmenting their harmful effects on chronic lung disease during exercise.
To examine whether benefits of physical activity ...with respect to the risk of asthma and chronic obstructive pulmonary disease (COPD) are moderated by exposure to high air pollution levels in an urban setting.
A total of 53,113 subjects (50-65 yr) from the Danish Diet, Cancer, and Health cohort reported physical activity at recruitment (1993-1997) and were followed until 2013 in the National Patient Register for incident hospitalizations for asthma and COPD. Levels of nitrogen dioxide (NO
) were estimated at subject residences at the time of recruitment. We used Cox regression to associate physical activities and NO
(high/medium/low) with asthma and COPD, and then introduced an interaction term between each physical activity and NO
.
A total of 1,151 subjects were hospitalized for asthma and 3,225 for COPD during 16 years. We found inverse associations of participation in sports (hazard ratio 95% confidence interval: 0.85 0.75-0.96) and cycling (0.85 0.75-0.96) with incident asthma, and of participation in sports (0.82 0.77-0.89), cycling (0.81 0.76-0.87), gardening (0.88 0.81-0.94), and walking (0.85 0.75-0.95) with incident COPD admissions. We found positive associations between NO
and incident asthma (1.23 1.04-1.47) and COPD (1.15 1.03-1.27) hospitalizations (comparing ≥21.0 μg/m
to <14.3 μg/m
). We found no interaction between associations of any physical activity and NO
on incident asthma or COPD hospitalizations.
Increased exposure to air pollution during exercise does not outweigh beneficial effects of physical activity on the risk of asthma and COPD.
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