Cohorts based on administrative data have size advantages over individual cohorts in investigating air pollution risks, but often lack in-depth information on individual risk factors related to ...lifestyle. If there is a correlation between lifestyle and air pollution, omitted lifestyle variables may result in biased air pollution risk estimates. Correlations between lifestyle and air pollution can be induced by socio-economic status affecting both lifestyle and air pollution exposure.
Our overall aim was to assess potential confounding by missing lifestyle factors on air pollution mortality risk estimates. The first aim was to assess associations between long-term exposure to several air pollutants and lifestyle factors. The second aim was to assess whether these associations were sensitive to adjustment for individual and area-level socioeconomic status (SES), and whether they differed between subgroups of the population. Using the obtained air pollution–lifestyle associations and indirect adjustment methods, our third aim was to investigate the potential bias due to missing lifestyle information on air pollution mortality risk estimates in administrative cohorts.
We used a recent Dutch national health survey of 387,195 adults to investigate the associations of PM10, PM2.5, PM2.5-10, PM2.5 absorbance, OPDTT, OPESR and NO2 annual average concentrations at the residential address from land use regression models with individual smoking habits, alcohol consumption, physical activity and body mass index. We assessed the associations with and without adjustment for neighborhood and individual SES characteristics typically available in administrative data cohorts. We illustrated the effect of including lifestyle information on the air pollution mortality risk estimates in administrative cohort studies using a published indirect adjustment method.
Current smoking and alcohol consumption were generally positively associated with air pollution. Physical activity and overweight were negatively associated with air pollution. The effect estimates were small (mostly <5% of the air pollutant standard deviations). Direction and magnitude of the associations depended on the pollutant, use of continuous vs. categorical scale of the lifestyle variable, and level of adjustment for individual and area-level SES. Associations further differed between subgroups (age, sex) in the population. Despite the small associations between air pollution and smoking intensity, indirect adjustment resulted in considerable changes of air pollution risk estimates for cardiovascular and especially lung cancer mortality.
Individual lifestyle-related risk factors were weakly associated with long-term exposure to air pollution in the Netherlands. Indirect adjustment for missing lifestyle factors in administrative data cohort studies may substantially affect air pollution mortality risk estimates.
•Lifestyle factors were weakly associated with long-term air pollution exposure.•Lifestyle-air pollution associations diminished, but not fully explained by SES.•Mortality risk could be biased when lifestyle missing in administrative data cohorts.
Atmospheric pollutants and meteorological conditions are suspected to be causes of preterm birth. We aimed to characterize their possible association with the risk of preterm birth (defined as birth ...occurring before 37 completed gestational weeks). We pooled individual data from 13 birth cohorts in 11 European countries (71,493 births from the period 1994-2011, European Study of Cohorts for Air Pollution Effects (ESCAPE)). City-specific meteorological data from routine monitors were averaged over time windows spanning from 1 week to the whole pregnancy. Atmospheric pollution measurements (nitrogen oxides and particulate matter) were combined with data from permanent monitors and land-use data into seasonally adjusted land-use regression models. Preterm birth risks associated with air pollution and meteorological factors were estimated using adjusted discrete-time Cox models. The frequency of preterm birth was 5.0%. Preterm birth risk tended to increase with first-trimester average atmospheric pressure (odds ratio per 5-mbar increase = 1.06, 95% confidence interval: 1.01, 1.11), which could not be distinguished from altitude. There was also some evidence of an increase in preterm birth risk with first-trimester average temperature in the -5°C to 15°C range, with a plateau afterwards (spline coding, P = 0.08). No evidence of adverse association with atmospheric pollutants was observed. Our study lends support for an increase in preterm birth risk with atmospheric pressure.
Background: Long-term exposure to ambient air pollution has recently been linked to atherosclerosis and cardiovascular events. There are, however, very limited data in healthy young people. We ...examined the association between air pollutants and indicators of vascular damage in a cohort of young adults. Methods: We used data from the Atherosclerosis Risk in Young Adults study. We estimated exposure to nitrogen dioxide (NO2), particulate matter less than 2.5 μm in aerodynamic diameter (PM2.5), black smoke, sulfur dioxide (SO2), and various traffic indicators for participants' 2000 home addresses. Exposure for the year 2000 was estimated by land-use regression models incorporating regional background annual air pollution levels, land-use variables, population densities, and traffic intensities on nearby roads. Outcomes were common carotid artery intima-media thickness (n = 745), aortic pulse wave velocity (n = 524), and augmentation index (n = 729). Results: Exposure contrasts were substantial for NO2, SO2, and black smoke (5th—95th percentiles = 19.7 to 44.9, 2.5 to 5.2, and 8.6 to 19.4 μg/m³, respectively) and smaller for PM2.5 (16.5 to 19.9 μg/m³). The variability of carotid artery intima-media thickness was less than for pulse wave velocity and especially augmentation index (5–95th percentiles = 0.42 to 0.58 mm, 4.9 to 7.4 m/s and — 12.3% to 27.3%, respectively). No associations were found between any of the pollutants of traffic indicators and carotid artery intima-media thickness, although PM2.5 effect estimates were in line with previous studies. We observed a 4.1% (95% confidence interval = 0.1% to 8.0%) increase in pulse wave velocity and a 37.6% (2.2% to 72.9%) increase in augmentation index associated with a 25 μg/m³ increase in NO2, and a 5.3% (0.1% to 10.4%) increase in pulse wave velocity with a 5 μg/m³ increase in SO2. PM2.5 and black smoke were not associated with either of these 2 outcomes. Conclusions: Air pollution may accelerate arterial-wall stiffening in young adults. Small outcome variability and lack of residential mobility data may have limited the power to detect an effect on intima-media thickness.
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.
Preterm premature rupture of membranes (PROM) is the leading identifiable predisposing factor for preterm birth. Although maternal exposure to air pollution can potentially have an impact on preterm ...PROM, there is no available evidence on such an impact. In this study, based on 5,555 singleton births occurring in Barcelona, Spain (2002-2005), we investigated the associations of maternal exposure to nitrogen dioxide, nitrogen oxides, and particulate matter with aerodynamic diameters of ≤2.5 µm (PM2.5), 2.5 µm-10 µm, and ≤10 µm and PM2.5 light absorption with preterm PROM and gestational age at the rupture of membranes (ROM). We utilized temporally adjusted land-use regression models to predict pollutant levels at each subject's home address during each week of her pregnancy. We conducted matched (according to the length of exposure) case-control analyses to estimate the preterm PROM risk associated with 1 interquartile-range increase in exposure levels during the entire pregnancy and during the last 3 months prior to ROM. We found an increase in preterm PROM risk of up to 50% (95% confidence interval: 4, 116) and a 1.3-day (95% confidence interval: -1.9, -0.6) reduction in gestational age at ROM associated with PM2.5 absorbance, nitrogen dioxide exposure, and nitrogen oxide exposure during the entire pregnancy and the last 3 months prior to ROM.
Peritoneal dialysis (PD) is associated with functional and structural changes of the peritoneal membrane, also known as peritoneal remodeling. The peritoneal membrane is affected by many endogenous ...and exogenous factors such as cytokines, PD fluids, and therapeutic interventions. Here, we present an overview of various studies that have investigated pharmacologic interventions aimed at regression of peritoneal damage and prolongation of PD treatment.
The pathology of multiple sclerosis (MS) is characterized by breakdown of the blood-brain barrier (BBB), accompanied by infiltration of macrophages and T lymphocytes into the central nervous system ...(CNS). The migration of these cells into the CNS parenchyma may be partly regulated by chemokines. The aim of this study was therefore to investigate the cellular localization of the potent monocyte- and T-cell-attracting chemokine monocyte chemoattractant protein (MCP)-1 by immunohistochemistry on postmortem brain tissue from MS and normal control cases. Brain tissue samples of six MS patients and four patients without a history of brain disease were neuropathologically classified according to characteristic (immuno)histochemical staining patterns. Frozen tissue sections of active demyelinating MS lesions, chronic active demyelinating MS lesions, and normal control brain were immunohistochemically stained with a monoclonal antibody directed against MCP-1. In active demyelinating MS lesions as well as in chronic active MS lesions, reactive hypertrophic astrocytes were strongly immunoreactive for MCP-1, whereas perivascular and parenchymal foamy macrophages did not express MCP-1 protein. These results suggest a significant role for the β-chemokine MCP-1, synthesized
in vivo by reactive hypertrophic astrocytes, in the recruitment and activation of myelin-degrading macrophages and thereby contributing to the evolution of MS lesions.
Epidemiological studies have reported the association between hypertension and exposure to road traffic noise, but the association between noise frequency characteristics is not clear. This study ...investigated the association between exposure to different frequency components of road traffic noise and the prevalence of hypertension in central Taiwan.
We recruited 820 residents living near main roads for more than 3 years. Frequency components of traffic noise and traffic flow rates during 0900-1700 on weekdays were measured simultaneously in 2008. Multiple logistic regressions were conducted to estimate odds ratios (ORs) for diagnosed hypertension, adjusting for potential confounders and the total traffic flow rate.
The high-exposure group (≥ the median of noise levels decibels, dB) at 63 Hz, 125 Hz and 1000 Hz had ORs for hypertension of 2.77 (95% confidence interval CI: 1.17-6.52), 4.08 (95% CI: 1.57-10.63) and 1.98 (1.00-3.92) (95% CI: 1.00-3.92), respectively, compared to the low-exposure group (< the median of noise levels dB). There was an increasing trend in the prevalence of hypertension by exposure to road traffic noise at 63, 125 and 1000 Hz in all subjects and in men. Total subjects exposed to ≥ 51 dB at 125 Hz had an OR of 4.65 (95% CI = 1.46-14.83) compared to those exposed to < 47 dB.
With the possible bias of exposure misclassification and a bias from using diagnosed hypertension, these results suggest that exposure to road traffic noise at low and hearing-sensitive frequencies may be associated with hypertension and exposure to noise at 125 Hz may have the greatest risk for hypertension.
Several recent studies associated long-term exposure to air pollution with increased mortality. An ongoing cohort study, the Netherlands Cohort Study on Diet and Cancer (NLCS), was used to study the ...association between long-term exposure to traffic-related air pollution and mortality. Following on a previous exposure assessment study in the NLCS, we improved the exposure assessment methods.
Long-term exposure to nitrogen dioxide (NO
2), nitrogen oxide (NO), black smoke (BS), and sulphur dioxide (SO
2) was estimated. Exposure at each home address (
N=21
868) was considered as a function of a regional, an urban and a local component. The regional component was estimated using inverse distance weighed interpolation of measurement data from regional background sites in a national monitoring network. Regression models with urban concentrations as dependent variables, and number of inhabitants in different buffers and land use variables, derived with a Geographic Information System (GIS), as predictor variables were used to estimate the urban component. The local component was assessed using a GIS and a digital road network with linked traffic intensities. Traffic intensity on the nearest road and on the nearest major road, and the sum of traffic intensity in a buffer of 100
m around each home address were assessed. Further, a quantitative estimate of the local component was estimated.
The regression models to estimate the urban component explained 67%, 46%, 49% and 35% of the variances of NO
2, NO, BS, and SO
2 concentrations, respectively. Overall regression models which incorporated the regional, urban and local component explained 84%, 44%, 59% and 56% of the variability in concentrations for NO
2, NO, BS and SO
2, respectively.
We were able to develop an exposure assessment model using GIS methods and traffic intensities that explained a large part of the variations in outdoor air pollution concentrations.
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