Estimating within-city variability in air pollution concentrations is important. Land use regression (LUR) models are able to explain such small-scale within-city variations. Transparency in LUR ...model development methods is important to facilitate comparison of methods between different studies. We therefore developed LUR models in a standardized way in 36 study areas in Europe for the ESCAPE (European Study of Cohorts for Air Pollution Effects) project.
Nitrogen dioxide (NO2) and nitrogen oxides (NOx) were measured with Ogawa passive samplers at 40 or 80 sites in each of the 36 study areas. The spatial variation in each area was explained by LUR modelling. Centrally and locally available Geographic Information System (GIS) variables were used as potential predictors. A leave-one out cross-validation procedure was used to evaluate the model performance.
There was substantial contrast in annual average NO2 and NOx concentrations within the study areas. The model explained variances (R2) of the LUR models ranged from 55% to 92% (median 82%) for NO2 and from 49% to 91% (median 78%) for NOx. For most areas the cross-validation R2 was less than 10% lower than the model R2. Small-scale traffic and population/household density were the most common predictors. The magnitude of the explained variance depended on the contrast in measured concentrations as well as availability of GIS predictors, especially traffic intensity data were important. In an additional evaluation, models in which local traffic intensity was not offered had 10% lower R2 compared to models in the same areas in which these variables were offered.
Within the ESCAPE project it was possible to develop LUR models that explained a large fraction of the spatial variance in measured annual average NO2 and NOx concentrations. These LUR models are being used to estimate outdoor concentrations at the home addresses of participants in over 30 cohort studies.
► LUR models were developed in 36 study areas in Europe using a standardized approach. ► NO2 models explained a large fraction of concentration variability (median R2 82%). ► Local traffic intensity data were important predictors for LUR model development.
The highly leukotoxic JP2 clone of Actinobacillus actinomycetemcomitans is strongly associated with aggressive periodontitis in adolescents of African descent. DNA fingerprinting using the frequently ...cutting restriction enzyme MspI and multilocus sequence typing (MLST) showed that five strains of this clone were genetically virtually identical, although ribotyping of the six rrn genes and EcoRI RFLP analysis of the seven IS150-like elements revealed differences. PCR analyses demonstrated that these multi-copy sequences are subject to intragenomic homologous recombination, resulting in translocations or large inversions. The genome rearrangements were reflected in differences among 25 strains representing the JP2 clone in DNA fingerprinting using the rare-cutting restriction enzyme XhoI and resolved by PFGE. XhoI DNA fingerprinting provides a tool for studying local epidemiology, including transmission of this particularly pathogenic clone of A. actinomycetemcomitans.
Few studies have investigated effects of air pollution on the incidence of cerebrovascular events.
We assessed the association between long-term exposure to multiple air pollutants and the incidence ...of stroke in European cohorts.
Data from 11 cohorts were collected, and occurrence of a first stroke was evaluated. Individual air pollution exposures were predicted from land-use regression models developed within the European Study of Cohorts for Air Pollution Effects (ESCAPE). The exposures were: PM2.5 particulate matter (PM) ≤ 2.5 μm in diameter, coarse PM (PM between 2.5 and 10 μm), PM10 (PM ≤ 10 μm), PM2.5 absorbance, nitrogen oxides, and two traffic indicators. Cohort-specific analyses were conducted using Cox proportional hazards models. Random-effects meta-analysis was used for pooled effect estimation.
A total of 99,446 study participants were included, 3,086 of whom developed stroke. A 5-μg/m3 increase in annual PM2.5 exposure was associated with 19% increased risk of incident stroke hazard ratio (HR) = 1.19, 95% CI: 0.88, 1.62. Similar findings were obtained for PM10. The results were robust to adjustment for an extensive list of cardiovascular risk factors and noise coexposure. The association with PM2.5 was apparent among those ≥ 60 years of age (HR = 1.40, 95% CI: 1.05, 1.87), among never-smokers (HR = 1.74, 95% CI: 1.06, 2.88), and among participants with PM2.5 exposure < 25 μg/m3 (HR = 1.33, 95% CI: 1.01, 1.77).
We found suggestive evidence of an association between fine particles and incidence of cerebrovascular events in Europe, even at lower concentrations than set by the current air quality limit value.
Epidemiological evidence on the association between ambient air pollution and breast cancer risk is inconsistent.
We examined the association between long-term exposure to ambient air pollution and ...incidence of postmenopausal breast cancer in European women.
In 15 cohorts from nine European countries, individual estimates of air pollution levels at the residence were estimated by standardized land-use regression models developed within the European Study of Cohorts for Air Pollution Effects (ESCAPE) and Transport related Air Pollution and Health impacts – Integrated Methodologies for Assessing Particulate Matter (TRANSPHORM) projects: particulate matter (PM) ≤2.5μm, ≤10μm, and 2.5–10μm in diameter (PM
, PM
, and PM
, respectively); PM
absorbance; nitrogen oxides (NO
and NO
); traffic intensity; and elemental composition of PM. We estimated cohort-specific associations between breast cancer and air pollutants using Cox regression models, adjusting for major lifestyle risk factors, and pooled cohort-specific estimates using random-effects meta-analyses.
Of 74,750 postmenopausal women included in the study, 3,612 developed breast cancer during 991,353 person-years of follow-up. We found positive and statistically insignificant associations between breast cancer and PM
{hazard ratio (HR)=1.08 95% confidence interval (CI): 0.77, 1.51 per 5 μg/m
}, PM
1.07 (95% CI: 0.89, 1.30) per 10 μg/m
, PM
1.20 (95% CI: 0.96, 1.49 per 5 μg/m
, and NO
1.02 (95% CI: 0.98, 1.07 per 10 μg/m
, and a statistically significant association with NO
1.04 (95% CI: 1.00, 1.08) per 20 μg/m
,
=0.04.
We found suggestive evidence of an association between ambient air pollution and incidence of postmenopausal breast cancer in European women. https://doi.org/10.1289/EHP1742.
Epidemiological evidence on the association between ambient air pollution and brain tumor risk is sparse and inconsistent.
In 12 cohorts from 6 European countries, individual estimates of annual mean ...air pollution levels at the baseline residence were estimated by standardized land-use regression models developed within the ESCAPE and TRANSPHORM projects: particulate matter (PM) ≤2.5, ≤10, and 2.5-10 μm in diameter (PM2.5, PM10, and PMcoarse), PM2.5 absorbance, nitrogen oxides (NO2 and NOx) and elemental composition of PM. We estimated cohort-specific associations of air pollutant concentrations and traffic intensity with total, malignant, and nonmalignant brain tumor, in separate Cox regression models, adjusting for risk factors, and pooled cohort-specific estimates using random-effects meta-analyses.
Of 282194 subjects from 12 cohorts, 466 developed malignant brain tumors during 12 years of follow-up. Six of the cohorts also had data on nonmalignant brain tumor, where among 106786 subjects, 366 developed brain tumor: 176 nonmalignant and 190 malignant. We found a positive, statistically nonsignificant association between malignant brain tumor and PM2.5 absorbance (hazard ratio and 95% CI: 1.67; 0.89-3.14 per 10-5/m3), and weak positive or null associations with the other pollutants. Hazard ratio for PM2.5 absorbance (1.01; 0.38-2.71 per 10-5/m3) and all other pollutants were lower for nonmalignant than for malignant brain tumors.
We found suggestive evidence of an association between long-term exposure to PM2.5 absorbance indicating traffic-related air pollution and malignant brain tumors, and no association with overall or nonmalignant brain tumors.
Several studies have indicated weakly increased risk for kidney cancer among occupational groups exposed to gasoline vapors, engine exhaust, polycyclic aromatic hydrocarbons and other air pollutants, ...although not consistently. It was the aim to investigate possible associations between outdoor air pollution at the residence and the incidence of kidney parenchyma cancer in the general population. We used data from 14 European cohorts from the ESCAPE study. We geocoded and assessed air pollution concentrations at baseline addresses by land‐use regression models for particulate matter (PM10, PM2.5, PMcoarse, PM2.5 absorbance (soot)) and nitrogen oxides (NO2, NOx), and collected data on traffic. We used Cox regression models with adjustment for potential confounders for cohort‐specific analyses and random effects models for meta‐analyses to calculate summary hazard ratios (HRs). The 289,002 cohort members contributed 4,111,908 person‐years at risk. During follow‐up (mean 14.2 years) 697 incident cancers of the kidney parenchyma were diagnosed. The meta‐analyses showed higher HRs in association with higher PM concentration, e.g. HR = 1.57 (95%CI: 0.81–3.01) per 5 μg/m3 PM2.5 and HR = 1.36 (95%CI: 0.84–2.19) per 10−5m−1 PM2.5 absorbance, albeit never statistically significant. The HRs in association with nitrogen oxides and traffic density on the nearest street were slightly above one. Sensitivity analyses among participants who did not change residence during follow‐up showed stronger associations, but none were statistically significant. Our study provides suggestive evidence that exposure to outdoor PM at the residence may be associated with higher risk for kidney parenchyma cancer; the results should be interpreted cautiously as associations may be due to chance.
What's new?
Ambient air pollution is an established cause of lung cancer. It is of considerable public health interest whether air pollution also causes other cancers. A few studies indicated that air pollution might cause kidney cancer. These authors investigated a possible link between kidney parenchyma cancer and air pollution at the residence of 289,002 participants of 14 European cohorts. They found an increased risk in association with particulate matter air pollution, although not statistically significant.
Abstract Background Ambient air pollution contains low concentrations of carcinogens implicated in the etiology of urinary bladder cancer (BC). Little is known about whether exposure to air pollution ...influences BC in the general population. Objective To evaluate the association between long-term exposure to ambient air pollution and BC incidence. Design, setting, and participants We obtained data from 15 population-based cohorts enrolled between 1985 and 2005 in eight European countries ( N = 303 431; mean follow-up 14.1 yr). We estimated exposure to nitrogen oxides (NO2 and NO x ), particulate matter (PM) with diameter <10 μm (PM10 ), <2.5 μm (PM2.5 ), between 2.5 and 10 μm (PM2.5–10 ), PM2.5absorbance (soot), elemental constituents of PM, organic carbon, and traffic density at baseline home addresses using standardized land-use regression models from the European Study of Cohorts for Air Pollution Effects project. Outcome measurements and statistical analysis We used Cox proportional-hazards models with adjustment for potential confounders for cohort-specific analyses and meta-analyses to estimate summary hazard ratios (HRs) for BC incidence. Results and limitations During follow-up, 943 incident BC cases were diagnosed. In the meta-analysis, none of the exposures were associated with BC risk. The summary HRs associated with a 10-μg/m3 increase in NO2 and 5-μg/m3 increase in PM2.5 were 0.98 (95% confidence interval CI 0.89–1.08) and 0.86 (95% CI 0.63–1.18), respectively. Limitations include the lack of information about lifetime exposure. Conclusions There was no evidence of an association between exposure to outdoor air pollution levels at place of residence and risk of BC. Patient summary We assessed the link between outdoor air pollution at place of residence and bladder cancer using the largest study population to date and extensive assessment of exposure and comprehensive data on personal risk factors such as smoking. We found no association between the levels of outdoor air pollution at place of residence and bladder cancer risk.
Background Cadmium is a known carcinogen that can disrupt endocrine signalling. Cigarette smoking and food are the most common routes of non-occupational exposure to cadmium. Cadmium accumulates in ...the kidney and can be measured in urine, making urine cadmium (U-Cd) a biomarker of long-term exposure. However dietary-cadmium (D-Cd) intake estimates are often used as surrogate indicator of cadmium exposure in non-smoking subjects. It is therefore important to investigate the concordance between D-Cd estimates obtained with Food Frequency Questionnaires and U-Cd. Methods U-Cd levels were compared with estimated dietary-cadmium (D-Cd) intake in 1764 post-menopausal women from the Danish Diet, Cancer and Health cohort. For each participant, a food frequency questionnaire, and measures of cadmium content in standard recipes were used to judge the daily intake of cadmium, normalized by daily caloric intake. Cadmium was measured by ICP-MS in spot urine sampled at baseline and normalized by urinary creatinine. Information on diet, socio-demographics and smoking were self-reported at baseline. Results Linear regressions between U-Cd and D-Cd alone revealed minimal but significant positive correlation in never smokers (R2 = 0.0076, Beta = 1.5% increase per 1 ng Cd kcal-1, p = 0.0085, n = 782), and negative correlation in current smokers (R2 = 0.0184, Beta = 7.1% decrease per 1 ng Cd kcal-1 change, p = 0.0006, n = 584). In the full study population, most of the variability in U-Cd was explained by smoking status (R2 = 0.2450, n = 1764). A forward selection model revealed that the strongest predictors of U-Cd were age in never smokers ( delta R2 = 0.04), smoking duration in former smokers ( delta R2 = 0.06) and pack-years in current smokers ( delta R2 = 0.07). Food items that contributed to U-Cd were leafy vegetables and soy-based products, but explained very little of the variance in U-Cd. Conclusions Dietary-Cd intake estimated from food frequency questionnaires correlates only minimally with U-Cd biomarker, and its use as a Cd exposure indicator may be of limited utility in epidemiologic studies.
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