Air pollution affects billions of people worldwide, yet ambient pollution measurements are limited for much of the world. Urban air pollution concentrations vary sharply over short distances (≪1 km) ...owing to unevenly distributed emission sources, dilution, and physicochemical transformations. Accordingly, even where present, conventional fixed-site pollution monitoring methods lack the spatial resolution needed to characterize heterogeneous human exposures and localized pollution hotspots. Here, we demonstrate a measurement approach to reveal urban air pollution patterns at 4-5 orders of magnitude greater spatial precision than possible with current central-site ambient monitoring. We equipped Google Street View vehicles with a fast-response pollution measurement platform and repeatedly sampled every street in a 30-km
area of Oakland, CA, developing the largest urban air quality data set of its type. Resulting maps of annual daytime NO, NO
, and black carbon at 30 m-scale reveal stable, persistent pollution patterns with surprisingly sharp small-scale variability attributable to local sources, up to 5-8× within individual city blocks. Since local variation in air quality profoundly impacts public health and environmental equity, our results have important implications for how air pollution is measured and managed. If validated elsewhere, this readily scalable measurement approach could address major air quality data gaps worldwide.
Several studies have recently identified strong epigenetic signals related to tobacco smoking. However, an aspect that did not receive much attention is the evolution of epigenetic changes with time ...since smoking cessation. We conducted a series of epigenome-wide association studies to capture the dynamics of smoking-induced epigenetic changes after smoking cessation, using genome-wide methylation profiles obtained from blood samples in 745 women from 2 European populations. Two distinct classes of CpG sites were identified: sites whose methylation reverts to levels typical of never smokers within decades after smoking cessation, and sites remaining differentially methylated, even more than 35 years after smoking cessation. Our results suggest that the dynamics of methylation changes following smoking cessation are driven by a differential and site-specific magnitude of the smoking-induced alterations (with persistent sites being most affected) irrespective of the intensity and duration of smoking. Analyses of the link between methylation and expression levels revealed that methylation predominantly and remotely down-regulates gene expression. Among genes whose expression was associated with our candidate CpG sites, LRRN3 appeared to be particularly interesting as it was one of the few genes whose methylation and expression were directly associated, and the only gene in which both methylation and gene expression were found associated with smoking. Our study highlights persistent epigenetic markers of smoking, which can potentially be detected decades after cessation. Such historical signatures are promising biomarkers to refine individual risk profiling of smoking-induced chronic disease such as lung cancer.
Type 2 diabetes is one of the major chronic diseases accounting for a substantial proportion of disease burden in Western countries. The majority of the burden of type 2 diabetes is attributed to ...environmental risks and modifiable risk factors such as lifestyle. The environment we live in, and changes to it, can thus contribute substantially to the prevention of type 2 diabetes at a population level. The ‘exposome’ represents the (measurable) totality of environmental, i.e. nongenetic, drivers of health and disease. The external exposome comprises aspects of the built environment, the social environment, the physico-chemical environment and the lifestyle/food environment. The internal exposome comprises measurements at the epigenetic, transcript, proteome, microbiome or metabolome level to study either the exposures directly, the imprints these exposures leave in the biological system, the potential of the body to combat environmental insults and/or the biology itself. In this review, we describe the evidence for environmental risk factors of type 2 diabetes, focusing on both the general external exposome and imprints of this on the internal exposome. Studies provided established associations of air pollution, residential noise and area-level socioeconomic deprivation with an increased risk of type 2 diabetes, while neighbourhood walkability and green space are consistently associated with a reduced risk of type 2 diabetes. There is little or inconsistent evidence on the contribution of the food environment, other aspects of the social environment and outdoor temperature. These environmental factors are thought to affect type 2 diabetes risk mainly through mechanisms incorporating lifestyle factors such as physical activity or diet, the microbiome, inflammation or chronic stress. To further assess causality of these associations, future studies should focus on investigating the longitudinal effects of our environment (and changes to it) in relation to type 2 diabetes risk and whether these associations are explained by these proposed mechanisms.
Graphical abstract
Investigating a single environmental exposure in isolation does not reflect the actual human exposure circumstance nor does it capture the multifactorial etiology of health and disease. The exposome, ...defined as the totality of environmental exposures from conception onward, may advance our understanding of environmental contributors to disease by more fully assessing the multitude of human exposures across the life course. Implementation into studies of human health has been limited, in part owing to theoretical and practical challenges including a lack of infrastructure to support
comprehensive exposure assessment, difficulty in differentiating physiologic variation from environmentally induced changes, and the need for study designs and analytic methods that accommodate specific aspects of the exposome, such as high-dimensional exposure data and multiple windows of susceptibility. Recommendations for greater data sharing and coordination, methods development, and acknowledgment and minimization of multiple types of measurement error are offered to encourage researchers to embark on exposome research to promote the environmental health and well-being of all populations.
Epidemiological evidence from prospective cohort studies on risk factors of Parkinson's disease (PD) is limited as case ascertainment is challenging due to a lack of registries and the disease course ...of PD. The objective of this study was to create a case ascertainment method for PD within two prospective Dutch cohorts based on multiple sources of PD information. This method was validated using clinical records from the general practitioners (GPs). Face validity of the case ascertainment was tested for three etiological factors (smoking, sex and family history of PD). In total 54825 participants were included from the cohorts AMIGO and EPIC-NL. Sources of PD information included self-reported PD, self-reported PD medication, a 9 item screening questionnaire (Tanner), electronical medical records, hospital discharge data and mortality records. Based on these sources we developed a likelihood score with 4 categories (no PD, unlikely PD, possible PD, likely PD). For the different sources of PD information and for the likelihood score we present the agreement with GP-validated cases. Risk of PD for established factors was studied by logistic regression as exact diagnose dates were not always available. Based on the algorithm, we assigned 346 participants to the likely PD category. GP validation confirmed 67% of these participants in EPIC-NL, but only 12% in AMIGO. PD was confirmed in only 3% of the participants with a possible PD classification. PD case ascertainment by mortality records (91%), EMR ICPC (82%) and self-reported information (62-69%) had the highest confirmation rates. The Tanner PD screening questionnaire had a lower agreement (18%). Risk estimates for smoking, family history and sex using all likely PD cases were comparable to the literature for EPIC-NL, but not for smoking in AMIGO. Using multiple sources of PD evidence in cohorts remains important but challenging as performance of sources varied in validity.
Despite extensive evidence showing that exposure to specific chemicals can lead to disease, current research approaches and regulatory policies fail to address the chemical complexity of our world. ...To safeguard current and future generations from the increasing number of chemicals polluting our environment, a systematic and agnostic approach is needed. The "exposome" concept strives to capture the diversity and range of exposures to synthetic chemicals, dietary constituents, psychosocial stressors, and physical factors, as well as their corresponding biological responses. Technological advances such as high-resolution mass spectrometry and network science have allowed us to take the first steps toward a comprehensive assessment of the exposome. Given the increased recognition of the dominant role that nongenetic factors play in disease, an effort to characterize the exposome at a scale comparable to that of the human genome is warranted.
Recently, there has been increasing evidence that exposure to air pollution is linked to neurodegenerative diseases, but little is known about the association with amyotrophic lateral sclerosis ...(ALS).
We investigated the association between long-term exposure to air pollution and risk of developing ALS.
A population-based case-control study was conducted in Netherlands from 1 January 2006 to 1 January 2013. Data from 917 ALS patients and 2,662 controls were analyzed. Annual mean air pollution concentrations were assessed by land use regression (LUR) models developed as part of the European Study of Cohorts for Air Pollution Effects (ESCAPE). Exposure estimates included nitrogen oxides (NO
, NO
), particulate matter (PM) with diameters of <2.5 μm (PM
), <10 μm (PM
), between 10 μm and 2.5 μm (PM
), and PM
absorbance. We performed conditional logistic regression analysis using two different multivariate models (model 1 adjusted for age, gender, education, smoking status, alcohol use, body mass index, and socioeconomic status; model 2 additionally adjusted for urbanization degree).
Risk of ALS was significantly increased for individuals in the upper exposure quartile of PM
absorbance OR=1.67; 95% confidence interval (CI): 1.27, 2.18, NO
(OR=1.74; 95% CI: 1.32, 2.30), and NO
concentrations (OR=1.38; 95% CI: 1.07, 1.77). These results, except for NO
, remained significant after adjusting additionally for urbanization degree.
Based on a large population-based case-control study, we report evidence for the association between long-term exposure to traffic-related air pollution and increased susceptibility to ALS. Our findings further support the necessity for regulatory public health interventions to combat air pollution levels and provide additional insight into the potential pathophysiology of ALS. https://doi.org/10.1289/EHP1115.
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•First LUR models for UFP on a national scale.•Combining targeted mobile monitoring with long-term regional background monitoring.•Different algorithms predicted external measurements ...well and correlated highly.•Deconvolution can improve large-area exposure assessment.•Models will be applied in Dutch nation-wide health studies.
Large nation- and region-wide epidemiological studies have provided important insights into the health effects of long-term exposure to outdoor air pollution. Evidence from these studies for the long-term effects of ultrafine particles (UFP), however is lacking. Reason for this is the shortage of empirical UFP land use regression models spanning large geographical areas including cities with varying topographies, peri-urban and rural areas. The aim of this paper is to combine targeted mobile monitoring and long-term regional background monitoring to develop national UFP models.
We used an electric car to monitor UFP concentrations in selected cities and towns across the Netherlands over a 14-month period in 2016–2017. Routes were monitored 3 times and concentrations were averaged per road segment. In addition, we used kriging maps based on regional background monitoring (20 sites; 3 × 2 weeks) over the same period to assess annual average regional background concentrations. All road segments were used to model spatial variation of UFP with three different land-use (regression) approaches: supervised stepwise regression, LASSO and random forest. For each approach, we also tested a deconvolution method, which segregates the average concentration at each road segment into a local and background signal. Model performance was evaluated with short-term (400 sites across the Netherlands; 3 × 30 minutes) and external longer-term measurements (42 sites in two major cities; 3 × 24 hours). We also compared predictions of all six models at 1000 random addresses spread over the country.
We found similar predictive performance for the six models, with validation R2 values from 0.25 to 0.35 for short-term measurements and 0.52 to 0.60 for longer-term external measurements. Models with and without deconvolution had similar predictive performance. All models based on the deconvolution method included a regional background kriging map as important predictor. Correlations between predictions at random addresses were high with Pearson correlations from 0.84 to 0.99. Models overestimated exposure at the short-term and long-term sites by about 20–30% in all cases, with small differences between regions and road types.
We developed robust nation-wide models for long-term UFP exposure combining mobile monitoring with long-term regional background monitoring. Minor differences in predictive performance between different algorithms were found, but the deconvolution approach is considered more physically realistic. The models will be applied in Dutch nation-wide health studies.
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