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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.

It is unknown if ambient fine particulate matter (PM2.5) is associated with lower renal function, a cardiovascular risk factor. We investigated whether long-term PM2.5 exposure was associated with estimated glomerular filtration rate (eGFR) in a cohort of older men living in the Boston Metropolitan area. This longitudinal analysis included 669 participants from the Veterans Administration Normative Aging Study with up to four visits between 2000 and 2011 (n = 1,715 visits). Serum creatinine was measured at each visit, and eGFR was calculated according to the Chronic Kidney Disease Epidemiology Collaboration equation. One-year exposure to PM2.5 prior to each visit was assessed using a validated spatiotemporal model that utilized satellite remote-sensing aerosol optical depth data. eGFR was modeled in a time-varying linear mixed-effects regression model as a continuous function of 1-year PM2.5, adjusting for important covariates. One-year PM2.5 exposure was associated with lower eGFRs; a 2.1-μg/m3 interquartile range higher 1-year PM2.5 was associated with a 1.87 mL/min/1.73 m2 lower eGFR [95% confidence interval (CI): -2.99, -0.76]. A 2.1 μg/m3-higher 1-year PM2.5 was also associated with an additional annual decrease in eGFR of 0.60 mL/min/1.73 m2 per year (95% CI: -0.79, -0.40). In this longitudinal sample of older men, the findings supported the hypothesis that long-term PM2.5 exposure negatively affects renal function and increases renal function decline. Mehta AJ, Zanobetti A, Bind MC, Kloog I, Koutrakis P, Sparrow D, Vokonas PS, Schwartz JD. 2016. Long-term exposure to ambient fine particulate matter and renal function in older men: the VA Normative Aging Study. Environ Health Perspect 124:1353-1360; http://dx.doi.org/10.1289/ehp.1510269.

This study aimed to examine the association between work-unit level leadership quality and individual-level long-term sickness absence (LTSA) in the hospital sector and effect modification by chronic disorders. This longitudinal analysis included 33 025 Danish public hospital employees who were followed-up for one year after baseline in March 2014. Leadership quality was assessed by questionnaire with mean responses aggregated by work-unit and characterized in tertiles. LTSA during follow-up was determined from employer records. Chronic disorders at baseline was assessed from the Danish hospital and prescription registers. We performed multilevel logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI) adjusting for potential confounders. We evaluated interaction between chronic illness and low leadership quality on multiplicative and additive scales. We identified employees as healthy (60.8%) or with somatic (31.6%), mental (3.3%), or both somatic and mental (4.3%) disorders. During follow-up, 6% of employees registered a LTSA. Medium and high leadership quality were associated with lower risk of LTSA with OR of 0.84 (95% CI 0.76-0.94) and 0.73 (95% CI 0.65-0.82) respectively, compared to low leadership quality. Associations were similar for healthy employees and employees with only somatic disorders, whereas no association was observed for employees with mental disorders (in presence or absence of somatic disorders). No statistically significant (α=0.05) interactions between leadership quality and chronic disorders on LTSA were observed. The findings suggest that the quality of leadership in work units is associated with risk of long-term sick leave in the Danish public hospital sector and that strong leadership protects employees against LTSA.

BackgroundChildhood malnutrition is a major public health issue in Sub-Saharan Africa (SSA) and 61.4 million children under the age of five years in the region are stunted. Although insight from existing studies suggests plausible pathways between ambient air pollution exposure and stunting, there are limited studies on the effect of different ambient air pollutants on stunting among children.ObjectiveExplore the effect of early-life environmental exposures on stunting among children under the age of five years.MethodsIn this study, we used pooled health and population data from 33 countries in SSA between 2006 and 2019 and environmental data from the Atmospheric Composition Analysis Group and NASA’s GIOVANNI platform. We estimated the association between early-life environmental exposures and stunting in three exposure periods – in-utero (during pregnancy), post-utero (after pregnancy to current age) and cumulative (from pregnancy to current age), using Bayesian hierarchical modelling. We also visualise the likelihood of stunting among children based on their region of residence using Bayesian hierarchical modelling.ResultsThe findings show that 33.6% of sampled children were stunted. In-utero PM2.5 was associated with a higher likelihood of stunting (OR = 1.038, CrI = 1.002–1.075). Early-life exposures to nitrogen dioxide and sulphate were robustly associated with stunting among children. The findings also show spatial variation in a high and low likelihood of stunting based on a region of residence.Impact StatementThis study explores the effect of early-life environmental exposures on child growth or stunting among sub-Saharan African children. The study focuses on three exposure windows – pregnancy, after birth and cumulative exposure during pregnancy and after birth. The study also employs spatial analysis to assess the spatial burden of stunted growth in relation to environmental exposures and socioeconomic factors. The findings suggest major air pollutants are associated with stunted growth among children in sub-Saharan Africa.

ObjectivesTo explore the associations of long-term exposure to air pollution with onset of all human health conditions.DesignProspective phenome-wide association study.SettingDenmark.ParticipantsAll Danish residents aged ≥30 years on 1 January 2000 were included (N=3 323 612). After exclusion of individuals with missing geocoded residential addresses, 3 111 988 participants were available for the statistical analyses.Main outcome measureFirst registered diagnosis of every health condition according to the International Classification of Diseases, 10th revision, from 2000 to 2017.ResultsLong-term exposure to fine particulate matter (PM2.5) and nitrogen dioxide (NO2) were both positively associated with the onset of more than 700 health conditions (ie, >80% of the registered health conditions) after correction for multiple testing, while the remaining associations were inverse or insignificant. As regards the most common health conditions, PM2.5 and NO2 were strongest positively associated with chronic obstructive pulmonary disease (PM2.5: HR 1.06 (95% CI 1.05 to 1.07) per 1 IQR increase in exposure level; NO2: 1.14 (95% CI 1.12 to 1.15)), type 2 diabetes (PM2.5: 1.06 (95% CI 1.05 to 1.06); NO2: 1.12 (95% CI 1.10 to 1.13)) and ischaemic heart disease (PM2.5: 1.05 (95% CI 1.04 to 1.05); NO2: 1.11 (95% CI 1.09 to 1.12)). Furthermore, PM2.5 and NO2 were both positively associated with so far unexplored, but highly prevalent outcomes relevant to public health, including senile cataract, hearing loss and urinary tract infection.ConclusionsThe findings of this study suggest that air pollution has a more extensive impact on human health than previously known. However, as this study is the first of its kind to investigate the associations of long-term exposure to air pollution with onset of all human health conditions, further research is needed to replicate the study findings.

Abstract Background The association between psychosocial working environments and sickness absence is well-known. However, the potential for reducing sickness absences of different lengths through improvements in psychosocial work factors is not fully understood. We aim to quantify the potential for reducing short-, intermediate- and long-term sickness absence rates, respectively, through hypothetical improvements in several psychosocial work factors. Methods This longitudinal study includes 24 990 public hospital employees from the 2014 wave of the Well-being in Hospital Employees study. The 1-year sickness absence rate was divided into short- (1–3 days), intermediate- (4–28 days) and long-term (29 days or more) periods. We simulated hypothetical scenarios with improvements in 17 psychosocial work factors using the parametric g-formula and estimated resulting changes in sickness absence rate ratios (RRs) with 95% confidence intervals (95% CIs). Results Setting all 17 psychosocial work factors to their most desirable levels (vs. least desirable levels) was associated with an overall 54% lower rate of sickness absence (95% CI: 48–60%). Reducing bullying (no vs. yes RR: 0.86, 95% CI: 0.83–0.90) and perceived stress (low vs. high RR: 0.90, 95% CI: 0.87–0.92), and increasing skill discretion (high vs. low RR: 0.91, 95% CI: 0.89–0.94) held the largest potential for reducing the total sickness absence rate. Overall, associations were similar for short-, intermediate- and long-term sickness absence. Conclusions The psychosocial working environment was strongly associated with sickness absence. Improving the working environment may have a great impact on short-, intermediate- and long-term sickness absence rates.

Objectives. To examine whether subsidized housing, specifically public housing and rental assistance, is associated with asthma in the Boston, Massachusetts, adult population. Methods. We analyzed a pooled cross-sectional sample of 9554 adults taking part in 3 Boston Behavioral Risk Factor Surveillance System surveys from 2010 to 2015. We estimated odds ratios for current asthma in association with housing status (public housing development [PHD] resident, rental assistance [RA] renter, non-RA renter, nonrenter nonowner, homeowner as reference) in logistic regression analyses adjusting for year, age, sex, race/ethnicity, education, and income. Results. The odds of current asthma were 2.02 (95% confidence interval [CI] = 1.35, 3.03) and 2.34 (95% CI = 1.60, 3.44) times higher among PHD residents and RA renters, respectively, than among homeowners. We observed smoking-related effect modification (interaction P = .04); elevated associations for PHD residents and RA renters remained statistically significant (P < .05) only among ever smokers. Associations for PHD residents and RA renters remained consistent in magnitude in comparison with non-RA renters who were eligible for subsidized housing according to income. Conclusions. Public housing and rental assistance were strongly associated with asthma in this large cross-sectional sample of adult Boston residents.

Abstract Rationale There is limited evidence from population-based studies demonstrating incidence of spirometric-defined chronic obstructive pulmonary disease (COPD) in association with occupational exposures. Objectives We evaluated the association between occupational exposures and incidence of COPD in the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA). Measurements and Main Results Prebronchodilator ratio of forced expiratory volume in 1 second over forced vital capacity (FEV1/FVC) was measured in 4,267 nonasthmatic SAPALDIA participants ages 18–62 at baseline in 1991 and at follow-up in 2001–2003. COPD was defined by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criterion (FEV1/FVC < 0.70) and Quanjer reference equation (FEV1/FVC < lower limit of normal [LLN]), and categorized by severity (≥80% and <80% predicted FEV1 for stage I and stage II+, respectively). Using a job-exposure matrix, self-reported occupations at baseline were assigned exposures to biological dusts, mineral dusts, gases/fumes, and vapors, gases, dusts, or fumes (VGDF) (high, low, or unexposed as reference). Adjusted incident rate ratios (IRRs) of stage I and stage II+ COPD were estimated in mixed Poisson regression models. Statistically significant (P < 0.05) IRRs of stage II+ GOLD and LLN-COPD, indicating risks between two- and fivefold, were observed for all occupational exposures at high levels. Occupational exposure-associated risk of stage II+ COPD was observed mainly in males and ages ≥40 years, and remained elevated when restricted to nonsmokers. Conclusions In a Swiss working adult population, occupational exposures to biological dusts, mineral dusts, gases/fumes, and VGDF were associated with incidence of COPD of at least moderate severity.

BackgroundOccupational exposures have been associated with an increased risk of COPD. However, few studies have related objectively assessed occupational exposures to prospectively assessed incidence of COPD, using postbronchodilator lung function tests. Our objective was to examine the effect of occupational exposures on COPD incidence in the European Community Respiratory Health Survey.MethodsGeneral population samples aged 20–44 were randomly selected in 1991–1993 and followed up 20 years later (2010–2012). Spirometry was performed at baseline and at follow-up, with incident COPD defined using a lower limit of normal criterion for postbronchodilator FEV1/FVC. Only participants without COPD and without current asthma at baseline were included. Coded job histories during follow-up were linked to a Job-Exposure Matrix, generating occupational exposure estimates to 12 categories of agents. Their association with COPD incidence was examined in log-binomial models fitted in a Bayesian framework.Findings3343 participants fulfilled the inclusion criteria; 89 of them had COPD at follow-up (1.4 cases/1000 person-years). Participants exposed to biological dust had a higher incidence of COPD compared with those unexposed (relative risk (RR) 1.6, 95% CI 1.1 to 2.3), as did those exposed to gases and fumes (RR 1.5, 95% CI 1.0 to 2.2) and pesticides (RR 2.2, 95% CI 1.1 to 3.8). The combined population attributable fraction for these exposures was 21.0%.InterpretationThese results substantially strengthen the evidence base for occupational exposures as an important risk factor for COPD.

Background There is mixed evidence suggesting that air pollution may be associated with increased risk of developing psychiatric disorders. We aimed to investigate the association between air pollution and non-specific perceived stress, often a precursor to development of affective psychiatric disorders. Methods This longitudinal analysis consisted of 987 older men participating in at least one visit for the Veterans Administration Normative Aging Study between 1995 and 2007 (n = 2,244 visits). At each visit, participants were administered the 14-item Perceived Stress Scale (PSS), which quantifies stress experienced in the previous week. Scores ranged from 0–56 with higher scores indicating increased stress. Differences in PSS score per interquartile range increase in moving average (1, 2, and 4-weeks) of air pollution exposures were estimated using linear mixed-effects regression after adjustment for age, race, education, physical activity, anti-depressant medication use, seasonality, meteorology, and day of week. We also evaluated effect modification by season (April-September and March-October for warm and cold season, respectively). Results Fine particles (PM 2.5 ), black carbon (BC), nitrogen dioxide, and particle number counts (PNC) at moving averages of 1, 2, and 4-weeks were associated with higher perceived stress ratings. The strongest associations were observed for PNC; for example, a 15,997 counts/cm 3 interquartile range increase in 1-week average PNC was associated with a 3.2 point (95%CI: 2.1-4.3) increase in PSS score. Season modified the associations for specific pollutants; higher PSS scores in association with PM 2.5 , BC, and sulfate were observed mainly in colder months. Conclusions Air pollution was associated with higher levels of perceived stress in this sample of older men, particularly in colder months for specific pollutants.