Objectives To investigate which air pollution characteristics are associated with biomarkers for acute nasal airway inflammation in healthy subjects. We hypothesised that associations would be ...strongest for oxidative potential (OP) of particles. Methods 31 volunteers were exposed to ambient air pollution at five sites in The Netherlands: two traffic sites, an underground train station, a farm and an urban background site. Each subject visited at least three sites between March and October 2009 and was exposed for 5 h per visit including exercise for 20 min every hour (h). Air pollution measurements during this 5-h-period included particulate matter (PM) mass concentration, elemental composition, elemental and organic carbon (OC), particle number concentration, OP, endotoxins, O3 and NO2. Pro-inflammatory biomarkers were measured before, 2 and 18 h postexposure, including cytokine IL-6 and IL-8, protein and lactoferrin in nasal lavage (NAL) as well as IL-6 in blood. One- and two-pollutant mixed models were used to analyse associations between exposure and changes in biomarkers. Results In two-pollutant models, cytokines in NAL were positively associated with OC, endotoxin and NO2; protein was associated with NO2; and lactoferrin was associated with all PM characteristics that were high at the underground site. In blood, associations with OC and endotoxin were negative. Conclusions We observed no consistent effects in two-pollutant models for PM mass concentration and OP. Instead, we found consistent associations with nasal inflammatory markers for other PM characteristics, specifically OC, endotoxin and NO2.
Several recent studies suggest an association between long-term exposure to traffic-related air pollution and health. Most studies use indicators of exposure such as outdoor air pollution or traffic ...density on the street of residence. Little information is available about the validity of these measurements as an estimate of long-term personal exposure to traffic-related air pollution. In this pilot study, we assessed outdoor and personal exposure to traffic-related air pollution in children living in homes on streets with different degree of traffic intensity.
The personal exposure of 14 children aged 9–12 years to ‘soot’, NO
x
(NO and NO
2) was assessed in Amsterdam between March and June 2003. Each child's personal exposure was monitored during four repeated 48-h periods. Concurrently, in- and outdoor NO
x
measurements were carried out at the school and at the home of each participating child. Measurements were supplemented by a questionnaire on time activity patterns and possible indoor sources. Flow-controlled battery operated pumps in a made-to-fit backpack were used to sample personal exposure to ‘soot’, determined from the reflectance of PM
2.5 filters. Exposure to NO
x
was assessed using Ogawa passive samplers. Children living near busy roads were found to have a 35% higher personal exposure to ‘soot’ than children living at an urban background location, despite that all children attended the same school that was located away from busy roads. Smaller contrasts in personal exposure were found for NO (14%), NO
2 (15%) and NO
x
(14%). This finding supports the use of ‘living near a busy road’ as a measure of exposure in epidemiological studies on the effects of traffic-related air pollution in children.
Evidence for the association between long-term exposure to ambient particulate matter components and mortality from natural causes is sparse and inconsistent. We evaluated this association in six ...large administrative cohorts in the framework of the Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE) project.
We analyzed data from country-wide administrative cohorts in Norway, Denmark, the Netherlands, Belgium, Switzerland and in Rome (Italy). Annual 2010 mean concentrations of copper (Cu), iron (Fe), potassium (K), nickel (Ni), sulfur (S), silicon (Si), vanadium (V) and zinc (Zn) in fine particulate matter (PM2.5) were estimated using 100 × 100 m Europe-wide hybrid land use regression models assigned to the participants' residential addresses. We applied cohort-specific Cox proportional hazard models controlling for area- and individual-level covariates to evaluate associations with natural mortality. Two pollutant models adjusting for PM2.5 total mass or nitrogen dioxide (NO2) were also applied. We pooled cohort-specific estimates using a random effects meta-analysis.
We included almost 27 million participants contributing more than 240 million person-years. All components except Zn were significantly associated with natural mortality pooled Hazard Ratios (HRs) (95% CI): 1.037 (1.014, 1.060) per 5 ng/m3 Cu; 1.069 (1.031, 1.108) per 100 ng/m3 Fe; 1.039 (1.018, 1.062) per 50 ng/m3 K; 1.024 (1.006, 1.043) per 1 ng/m3 Ni; 1.036 (1.016, 1.057) per 200 ng/m3 S; 1.152 (1.048, 1.266) per 100 ng/m3 Si; 1.020 (1.006, 1.034) per 2 ng/m3 V. Only K and Si were robust to PM2.5 or NO2 adjustment pooled HRs (95% CI) per 50 ng/m3 in K: 1.025 (1.008, 1.044), 1.020 (0.999, 1.042) and per 100 ng/m3 in Si: 1.121 (1.039, 1.209), 1.068 (1.022, 1.117) adjusted for PM2.5 and NO2 correspondingly.
Our findings indicate an association of natural mortality with most components, which was reduced after adjustment for PM2.5 and especially NO2.
Display omitted
•Assessed natural mortality following long-term exposure to eight particles components•Data from six European administrative cohorts with almost 27 million participants•Europe-wide hybrid land use regression models for concentrations estimation•Positive associations of natural mortality with all components•After PM2.5/NO2 adjustment only associations with potassium and silicon remained.
Background: Air pollution has consistently been associated with increased morbidity and mortality due to respiratory and cardiovascular disease. Underlying biological mechanisms are not entirely ...clear, and hemostasis and inflammation are suggested to be involved. Objectives: Our aim was to study the association of the variation in local concentrations of airborne particulate matter (PM) with aerodynamic diameter < 10 μm, carbon monoxide, nitrogen monoxide, nitrogen dioxide, and ozone with platelet aggregation, thrombin generation, fibrinogen, and C-reactive protein (CRP) levels in healthy individuals. Methods: From 40 healthy volunteers, we collected 13 consecutive blood samples within a 1-year period and measured light-transmittance platelet aggregometry, thrombin generation, fibrinogen, and CRP. We performed regression analysis using generalized additive models to study the association between the hemostatic and inflammatory variables, and local environmental concentrations of air pollutants for time lags within 24 hr before blood sampling or 24-96 hr before blood sampling. Results: In general, air pollutants were associated with platelet aggregation average, +8% per interquartile range (IQR), p < 0.01 and thrombin generation (average, +1% per IQR, p < 0.05). Platelet aggregation was not affected by in vitro incubation of plasma with PM. We observed no relationship between any of the air pollutants and fibrinogen or CRP levels. Conclusions: Air pollution increased platelet aggregation as well as coagulation activity but had no clear effect on systemic inflammation. These prothrombotic effects may partly explain the relationship between air pollution and the risk of ischemic cardiovascular disease.
Most studies investigating the health effects of long-term exposure to air pollution used traditional regression models, although causal inference approaches have been proposed as alternative. ...However, few studies have applied causal models and comparisons with traditional methods are sparse. We therefore compared the associations between natural-cause mortality and exposure to fine particulate matter (PM2.5) and nitrogen dioxide (NO2) using traditional Cox and causal models in a large multicenter cohort setting. We analysed data from eight well-characterized cohorts (pooled cohort) and seven administrative cohorts from eleven European countries. Annual mean PM2.5 and NO2 from Europe-wide models were assigned to baseline residential addresses and dichotomized at selected cut-off values (PM2.5: 10, 12, 15 μg/m³; NO2: 20, 40 μg/m³). For each pollutant, we estimated the propensity score as the conditional likelihood of exposure given available covariates, and derived corresponding inverse-probability weights (IPW). We applied Cox proportional hazards models i) adjusting for all covariates (“traditional Cox”) and ii) weighting by IPW (“causal model”). Of 325,367 and 28,063,809 participants in the pooled and administrative cohorts, 47,131 and 3,580,264 died from natural causes, respectively. For PM2.5 above vs. below 12 μg/m³, the hazard ratios (HRs) of natural-cause mortality were 1.17 (95% CI 1.13–1.21) and 1.15 (1.11–1.19) for the traditional and causal models in the pooled cohort, and 1.03 (1.01–1.06) and 1.02 (0.97–1.09) in the administrative cohorts. For NO2 above vs below 20 μg/m³, the HRs were 1.12 (1.09–1.14) and 1.07 (1.05–1.09) for the pooled and 1.06 (95% CI 1.03–1.08) and 1.05 (1.02–1.07) for the administrative cohorts. In conclusion, we observed mostly consistent associations between long-term air pollution exposure and natural-cause mortality with both approaches, though estimates partly differed in individual cohorts with no systematic pattern. The application of multiple modelling methods might help to improve causal inference.
299 of 300 words.
Display omitted
•We assessed associations between long-term PM2.5 and NO2 and natural-cause mortality.•We compared traditional Cox and causal inference models across large European cohorts.•We observed mostly consistent associations with both approaches.•Estimates partly differed in individual cohorts with no systematic pattern.•Application of multiple modelling methods is favorable to improve causal inference.
Oxidative potential (OP) of particulate matter (PM) has been proposed as a more health relevant metric than PM mass. However, little is known about the temporal and spatial variation of OP, which is ...crucial if OP were to be used as an exposure metric in epidemiological studies. We studied OP on routinely collected PM2.5 samples (every 6th day) from three regional, five urban background, and three street sites over a one-year period across the Netherlands. OP was measured as the ability to generate hydroxyl radicals in the presence of hydrogen peroxide using the electron spin resonance (OPESR).
OPESR correlated poorly with PM2.5 mass both spatially (Spearman's rs = 0.29) and temporally (median rs = 0.34). The temporal correlations across sites for OPESR were moderate (median rs = 0.50) compared to PM2.5 (median rs = 0.87), suggesting that exposure misclassification is higher when using OPESR as an exposure metric in time series studies. Street/urban background and street/regional background ratios for OPESR were 1.4 and 2.4 respectively; higher than for PM2.5 (ratio of 1.1 for both street/urban background and street/regional background).
This large scale, nationwide study found that PM2.5 correlated poorly with OPESR in space and time. Spatial contrasts were much larger for OPESR than for PM2.5, which offers the possibility to use OPESR to assess long-term exposure health effects.
•The spatial and temporal variations of oxidative potential (OPESR) were assessed.•OPESR was 2.4 higher at street sites than corresponding regional background sites.•Temporal correlations across and between different sites for OPESR were moderate.•Spatial contrasts were much larger for OPESR than for PM2.5.•PM2.5 correlated poorly with OPESR in space and time.
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.
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.
Of 3,081,244 individuals, we observed 803,373 death from natural causes during follow-up. We found significant positive associations between all-natural mortality with Si and K from both exposure modeling approaches (hazard ratios; 95% confidence intervals per interquartile range increase): SLR-Si (1.04; 1.03–1.05), RF-Si (1.01; 1.00–1.02), SLR-K (1.03; 1.02–1.04), and RF-K (1.06; 1.05–1.07). Strong associations of K and Si were detected with most causes of mortality except CKD and K, and diabetes and Si (the strongest associations for psychiatric disorders mortality). In addition, Fe was relevant for mortality from RD, lung cancer, CKD, and psychiatric disorders; Zn with mortality from CKD, RD, and lung cancer, and; Ni and V with lung cancer mortality.
We present novel results of the relevance of different PM2.5 components for different causes of death, with K and Si seeming to be most consistently associated with mortality in Denmark.
•Fine particulate matter (PM2.5) is linked to premature mortality.•Researches on which PM2.5 components are more responsible is limited.•With 3 million Danes, we studied how PM2.5 elemental components links with mortality.•Potassium and silicon were the most relevant PM2.5 components with mortality.•Different PM2.5 components were associated with different mortality outcomes.
A health impact assessment (HIA) of PM₁₀ and elemental carbon (EC) was performed for the period 1985–2008 in the city of Rotterdam. The spatial distribution of the concentrations was modeled by the ...URBIS model. The modeling results for 2008 were validated by PM₁₀ and EC measurements at various locations in Rotterdam. This paper describes the HIA related to improved air quality in the period 1985–2008: at urban background locations 18 μg m⁻³ PM₁₀ and 2 μg m⁻³ EC. The gain in life years saved due to long-term exposure to PM₁₀ and EC in this period was, respectively 13 and 12 month per person. The similar health impacts for PM₁₀ and EC suggests that reduction of combustion aerosol was important for the reduction in health impact of PM₁₀.
Oxidative potential (OP) has been suggested as a health-relevant measure of air pollution. Little information is available about OP spatial variation and the possibility to model its spatial ...variability. Our aim was to measure the spatial variation of OP within and between 10 European study areas. The second aim was to develop land use regression (LUR) models to explain the measured spatial variation.
OP was determined with the dithiothreitol (DTT) assay in ten European study areas. DTT of PM2.5 was measured at 16–40 sites per study area, divided over street, urban and regional background sites. Three two-week samples were taken per site in a one-year period in three different seasons. We developed study-area specific LUR models and a LUR model for all study areas combined to explain the spatial variation of OP.
Significant contrasts between study areas in OP were found. OP DTT levels were highest in southern Europe. DTT levels at street sites were on average 1.10 times higher than at urban background locations.
In 5 of the 10 study areas LUR models could be developed with a median R2 of 33%. A combined study area model explained 30% of the measured spatial variability. Overall, LUR models did not explain spatial variation well, possibly due to low levels of OP DTT and a lack of specific predictor variables.
•Oxidative potential (OP DTT) was measured in 10 European study areas.•OP DTT levels were the highest in southern and the lowest in northern Europe.•In 5 of the 10 study areas LUR models could be developed for OP DTT.
Epidemiologic studies have shown that ambient particulate matter (PM) has adverse effects on cardiovascular health. Effective mitigation of the health effects requires identification of the most ...harmful PM sources. The objective of our study was to evaluate relative effects of fine PM aerodynamic diameter $\leq 2.5 \mu m (PM_{2.5})$ from different sources on exercise-induced ischemia. We collected daily outdoor PM2.5 samples between autumn 1998 and spring 1999 in Helsinki, Finland. The mass of PM2.5 was apportioned between five sources. Forty-five elderly nonsmoking persons with stable coronary heart disease visited a clinic biweekly for submaximal exercise testing, during which the occurrence of ST segment depressions was recorded. Levels of PM2.5 originating from local traffic and long-range transport were associated with ST segment depressions > 0.1 mV, with odds ratios at 2-day lag of 1.53 95% confidence interval (CI), 1.19-1.97 and 1.11 (95% CI, 1.02-1.20) per $1 \mu g/m^3$, respectively. In multipollutant models, where we used indicator elements for sources instead of source-specific PM2.5, only absorbance (elemental carbon), an indicator of local traffic and other combustion, was associated with ST segment depressions. Our results suggest that the PM fraction originating from combustion processes, notably traffic, exacerbates ischemic heart diseases associated with PM mass.
PDF
