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Statistical analysis of microbial genomic data within epidemiological cohort studies holds the promise to assess the influence of environmental exposures on both the host and the host-associated microbiome. However, the observational character of prospective cohort data and the intricate characteristics of microbiome data make it challenging to discover causal associations between environment and microbiome. Here, we introduce a causal inference framework based on the Rubin Causal Model that can help scientists to investigate such environment-host microbiome relationships, to capitalize on existing, possibly powerful, test statistics, and test plausible sharp null hypotheses. Using data from the German KORA cohort study, we illustrate our framework by designing two hypothetical randomized experiments with interventions of (i) air pollution reduction and (ii) smoking prevention. We study the effects of these interventions on the human gut microbiome by testing shifts in microbial diversity, changes in individual microbial abundances, and microbial network wiring between groups of matched subjects via randomization-based inference. In the smoking prevention scenario, we identify a small interconnected group of taxa worth further scrutiny, including Christensenellaceae and Ruminococcaceae genera, that have been previously associated with blood metabolite changes. These findings demonstrate that our framework may uncover potentially causal links between environmental exposure and the gut microbiome from observational data. We anticipate the present statistical framework to be a good starting point for further discoveries on the role of the gut microbiome in environmental health.

The link between elevated concentrations of ambient particulate matter (PM) and increased mortality has been investigated in numerous studies. Here we analyzed the role of different particle size fractions with respect to total and cardio-respiratory mortality in Erfurt, Germany, between 1995 and 2001. Number concentrations (NC) of PM were measured using an aerosol spectrometer consisting of a Differential Mobility Particle Sizer and a Laser Aerosol Spectrometer to characterize particles between 0.01 and 0.5 and between 0.1 and 2.5  μ m, respectively. We derived daily means of particle NC for ultrafine (0.01–0.1  μ m) and for fine particles (0.01–2.5  μ m). Assuming spherical particles of a constant density, we estimated the mass concentrations (MC) of particles in these size ranges. Concurrently, data on daily total and cardio-respiratory death counts were obtained from local health authorities. The data were analyzed using Poisson Generalized Additive Models adjusting for trend, seasonality, influenza epidemics, day of the week, and meteorology using smooth functions or indicator variables. We found statistically significant associations between elevated ultrafine particle (UFP; diameter: 0.01–0.1  μ m) NC and total as well as cardio-respiratory mortality, each with a 4 days lag. The relative mortality risk (RR) for a 9748 cm −3 increase in UFP NC was RR=1.029 and its 95% confidence interval (CI)=1.003–1.055 for total mortality. For cardio-respiratory mortality we found: RR=1.031, 95% CI: 1.003–1.060. No association between fine particle MC and mortality was found. This study shows that UFP, representing fresh combustion particles, may be an important component of urban air pollution associated with health effects.

Studies on the association between traffic noise and cardiovascular diseases have rarely considered air pollution as a covariate in the analyses. Isolated systolic hypertension has not yet been in the focus of epidemiological noise research. The association between traffic noise (road and rail) and the prevalence of hypertension was assessed in two study populations with a total of 4,166 participants 25-74 years of age. Traffic noise (weighted day-night average noise level; LDN) at the facade of the dwellings was derived from noise maps. Annual average PM2.5 mass concentrations at residential addresses were estimated by land-use regression. Hypertension was assessed by blood pressure readings, self-reported doctor-diagnosed hypertension, and antihypertensive drug intake. In the Greater Augsburg, Germany, study population, traffic noise and air pollution were not associated with hypertension. In the City of Augsburg population (n = 1,893), where the exposure assessment was more detailed, the adjusted odds ratio (OR) for a 10-dB(A) increase in noise was 1.16 (95% CI: 1.00, 1.35), and 1.11 (95% CI: 0.94, 1.30) after additional adjustment for PM2.5. The adjusted OR for a 1-μg/m3 increase in PM2.5 was 1.15 (95% CI: 1.02, 1.30), and 1.11 (95% CI: 0.98, 1.27) after additional adjustment for noise. For isolated systolic hypertension, the fully adjusted OR for noise was 1.43 (95% CI: 1.10, 1.86) and for PM2.5 was 1.08 (95% CI: 0.87, 1.34). Traffic noise and PM2.5 were both associated with a higher prevalence of hypertension. Mutually adjusted associations with hypertension were positive but no longer statistically significant.

There is evidence for adverse effects of outdoor air pollution on lung function of children. Quantitative summaries of the effects of air pollution on lung function, however, are lacking due to large differences among studies. We aimed to study the association between residential exposure to air pollution and lung function in five European birth cohorts with a standardized exposure assessment following a common protocol. As part of the European Study of Cohorts for Air Pollution Effects (ESCAPE) we analyzed data from birth cohort studies situated in Germany, Sweden, the Netherlands, and the United Kingdom that measured lung function at 6-8 years of age (n = 5,921). Annual average exposure to air pollution [nitrogen oxides (NO2, NOx), mass concentrations of particulate matter with diameters < 2.5, < 10, and 2.5-10 μm (PM2.5, PM10, and PMcoarse), and PM2.5 absorbance] at the birth address and current address was estimated by land-use regression models. Associations of lung function with estimated air pollution levels and traffic indicators were estimated for each cohort using linear regression analysis, and then combined by random effects meta-analysis. Estimated levels of NO2, NOx, PM2.5 absorbance, and PM2.5 at the current address, but not at the birth address, were associated with small decreases in lung function. For example, changes in forced expiratory volume in 1 sec (FEV1) ranged from -0.86% (95% CI: -1.48, -0.24%) for a 20-μg/m3 increase in NOx to -1.77% (95% CI: -3.34, -0.18%) for a 5-μg/m3 increase in PM2.5. Exposure to air pollution may result in reduced lung function in schoolchildren.

Epidemiological studies have reported associations between particulate matter (PM) concentrations and cancer and respiratory and cardiovascular diseases. DNA methylation has been identified as a possible link but so far it has only been analyzed in candidate sites. We studied the association between DNA methylation and short- and mid-term air pollution exposure using genome-wide data and identified potential biological pathways for additional investigation. We collected whole blood samples from three independent studies-KORA F3 (2004-2005) and F4 (2006-2008) in Germany, and the Normative Aging Study (1999-2007) in the United States-and measured genome-wide DNA methylation proportions with the Illumina 450k BeadChip. PM concentration was measured daily at fixed monitoring stations and three different trailing averages were considered and regressed against DNA methylation: 2-day, 7-day and 28-day. Meta-analysis was performed to pool the study-specific results. Random-effect meta-analysis revealed 12 CpG (cytosine-guanine dinucleotide) sites as associated with PM concentration (1 for 2-day average, 1 for 7-day, and 10 for 28-day) at a genome-wide Bonferroni significance level (p ≤ 7.5E-8); 9 out of these 12 sites expressed increased methylation. Through estimation of I2 for homogeneity assessment across the studies, 4 of these sites (annotated in NSMAF, C1orf212, MSGN1, NXN) showed p > 0.05 and I2 < 0.5: the site from the 7-day average results and 3 for the 28-day average. Applying false discovery rate, p-value < 0.05 was observed in 8 and 1,819 additional CpGs at 7- and 28-day average PM2.5 exposure respectively. The PM-related CpG sites found in our study suggest novel plausible systemic pathways linking ambient PM exposure to adverse health effect through variations in DNA methylation. Panni T, Mehta AJ, Schwartz JD, Baccarelli AA, Just AC, Wolf K, Wahl S, Cyrys J, Kunze S, Strauch K, Waldenberger M, Peters A. 2016. A genome-wide analysis of DNA methylation and fine particulate matter air pollution in three study populations: KORA F3, KORA F4, and the Normative Aging Study. Environ Health Perspect 124:983-990; http://dx.doi.org/10.1289/ehp.1509966.

Abstract Rationale Evidence of short-term effects of ultrafine particles (UFP) on health is still inconsistent and few multicenter studies have been conducted so far especially in Europe. Objectives Within the UFIREG project, we investigated the short-term effects of UFP and fine particulate matter (particulate matter with an aerodynamic diameter less than 2.5 μm [PM2.5]) on daily cause-specific hospital admissions in five Central and Eastern European cities using harmonized protocols for measurements and analyses. Methods Daily counts of cause-specific hospital admissions focusing on cardiovascular and respiratory diseases were obtained for Augsburg and Dresden (Germany), 2011–2012; Chernivtsi (Ukraine), 2013 to March 2014; and Ljubljana (Slovenia) and Prague (Czech Republic), 2012–2013. Air pollution and meteorologic data were measured at fixed monitoring sites in all cities. We analyzed city-specific associations using confounder-adjusted Poisson regression models and pooled the city-specific effect estimates using metaanalysis methods. Measurements and Main Results A 2,750 particles/cm3 increase (average interquartile range across all cities) in the 6-day average of UFP indicated a delayed and prolonged increase in the pooled relative risk of respiratory hospital admissions (3.4% [95% confidence interval, −1.7 to 8.8%]). We also found increases in the pooled relative risk of cardiovascular (exposure average of lag 2–5, 1.8% [0.1–3.4%]) and respiratory (6-d average exposure, 7.5% [4.9–10.2%]) admissions per 12.4 μg/m3 increase (average interquartile range) in PM2.5. Conclusions Our findings indicated delayed and prolonged effects of UFP exposure on respiratory hospital admissions in Central and Eastern Europe. Cardiovascular and respiratory hospital admissions increased in association with an increase in PM2.5. Further multicenter studies are needed using harmonized UFP measurements to draw definite conclusions on health effects of UFP.

Previous studies have reported increased risks of myocardial infarction in association with elevated ambient particulate matter (PM) in the previous hour(s). However, whether PM can trigger mechanisms that act on this time scale is still unclear. We hypothesized that increases in PM are associated with rapid changes in measures of heart rate variability and repolarization. We used data from panel studies in Augsburg, Germany, and Rochester, New York, USA, and two controlled human exposure studies in Rochester. Data included ECG recordings from all four studies, controlled exposures to (concentrated) ultrafine particles (UFP; particles with an aerodynamic diameter <100 nm) and ambient concentrations of UFP and fine PM (PM 2.5 , aerodynamic diameter <2.5 μm). Factor analysis identified three representative ECG parameters: standard deviation of NN-intervals (SDNN), root mean square of successive differences (RMSSD), and T-wave complexity. Associations between air pollutants and ECG parameters in the concurrent and previous six hours were estimated using additive mixed models adjusting for long- and short-term time trends, meteorology, and study visit number. We found decreases in SDNN in relation to increased exposures to UFP in the previous five hours in both of the panel studies (e.g. Augsburg study, lag 3 hours: −2.26%, 95% confidence interval [CI]: −3.98% to −0.53%; Rochester panel study, lag 1 hour: −2.69%; 95% CI: −5.13% to −0.26%) and one of the two controlled human exposure studies (1-hour lag: −13.22%; 95% CI: −24.11% to −2.33%). Similarly, we observed consistent decreases in SDNN and RMSSD in association with elevated PM 2.5 concentrations in the preceding six hours in both panel studies. We did not find consistent associations between particle metrics and T-wave complexity. This study provided consistent evidence that recent exposures to UFP and PM 2.5 can induce acute pathophysiological responses.

Here we compare PM(2.5) (particles with aerodynamic diameter less than 2.5 microm) mass and filter absorbance measurements with elemental carbon (EC) concentrations measured in parallel at the same site as well as collocated PM(2.5) and PM(10) (particles with aerodynamic diameter less than 10 microm) mass and absorbance measurements. The data were collected within the Traffic-Related Air Pollution on Childhood Asthma (TRAPCA) study in Germany, The Netherlands and Sweden. The study was designed to assess the health impact of spatial contrasts in long-term average concentrations. The measurement sites were distributed between background and traffic locations. Annual EC and PM(2.5) absorbance measurements were at traffic sites on average 43-84% and 26-76% higher, respectively, compared to urban background sites. The contrast for PM(2.5) mass measurements was lower (8-35%). The smaller contrast observed for PM(2.5) mass in comparison with PM(2.5) absorbance and EC documents that PM(2.5) mass underestimates exposure contrasts related to motorized traffic emissions. The correlation between PM(10) and PM(2.5) was high, documenting that most of the spatial variation of PM(10) was because of PM(2.5). The measurement of PM(2.5) absorbance was highly correlated with EC measurements and suggests that absorbance can be used as a simple, inexpensive and non-destructive method to estimate motorized traffic-related particulate air pollution. The EC/absorbance relation differed between countries and site type (background/traffic), supporting the need for site-specific calibrations of the simple absorbance method. While the ratio between PM(2.5) and PM(10) mass ranged from 0.54 to 0.68, the ratio of PM(2.5) absorbance and PM(10) absorbance was 0.96-0.97, indicating that PM(2.5) absorbance captures nearly all of the particle absorbance.

Background: Some studies have suggested that particulate matter (PM) levels during pregnancy may be associated with birth weight. Road traffic is a major source of fine PM (PM with aerodynamic diameter $< 2.5 \\mum$; PM2.5). Objective: We determined to characterize the influence of maternal exposure to atmospheric pollutants due to road traffic and urban activities on offspring term birth weight. Methods: Women from a birth cohort [the LISA (Influences of Lifestyle Related Factors on the Human Immune System and Development of Allergies in Children) cohort] who delivered a non-premature baby with a birth weight > 2,500 g in Munich metropolitan area were included. We assessed PM2.5, PM2.5absorbance (which depends on the blackness of PM2.5, a marker of traffic-related air pollution), and nitrogen dioxide levels using a land-use regression model, taking into account the type and length of roads, population density, land coverage around the home address, and temporal variations in pollution during pregnancy. Using Poisson regression, we estimated prevalence ratios (PR) of birth weight < 3,000 g, adjusted for gestational duration, sex, maternal smoking, height, weight, and education. Results: Exposure was defined for 1,016 births. Taking the lowest quartile of exposure during pregnancy as a reference, the PR of birth weight < 3,000 g associated with the highest quartile was 1.7 for PM2.5[95% confidence interval (CI), 1.2-2.7], 1.8 for PM2.5absorbance (95% CI, 1.1-2.7), and 1.2 for NO2(95% CI, 0.7-1.7). The PR associated with an increase of$1 \\mug/m^3$in PM2.5levels was 1.13 (95% CI, 1.00-1.29). Conclusion: Increases in PM2.5levels and PM2.5absorbance were associated with decreases in term birth weight. Traffic-related air pollutants may have adverse effects on birth weight.

Objectives: This paper presents the study design of the Berlin-Brandenburg Air study (BEAR-study). We measure air quality in Berlin and Brandenburg before and after the relocation of aircraft (AC) traffic from Tegel (TXL) airport to the new Berlin-Brandenburg airport (BER) and investigate the association of AC-related ultrafine particles (UFP) with health outcomes in schoolchildren. Methods: The BEAR-study is a natural experiment examining schoolchildren attending schools near TXL and BER airports, and in control areas (CA) away from both airports and associated air corridors. Each child undergoes repeated school-based health-examinations. Total particle number concentration (PNC) and meteorological parameters are continuously monitored. Submicrometer particle number size distribution, equivalent black carbon, and gas-phase pollutants are collected from long-term air quality monitoring stations. Daily source-specific UFP concentrations are modeled. We will analyze short-term effects of UFP on respiratory, cardiovascular, and neurocognitive outcomes, as well as medium and long-term effects on lung growth and cognitive development. Results: We examined 1,070 children (as of 30 November 2022) from 16 schools in Berlin and Brandenburg. Conclusion: The BEAR study increases the understanding of how AC-related UFP affect children’s health.