Dataset Information

Respiratory Inflammation and Short-Term Ambient Air Pollution Exposures in Adult Beijing Residents with and without Prediabetes: A Panel Study.

ABSTRACT:

Background

Accumulating evidence suggests that individuals with glucose metabolism disorders are susceptible to mortality associated with fine particles. However, the mechanisms remain largely unknown.

Objectives

We examined whether particle-associated respiratory inflammation differed between individuals with prediabetes and healthy control participants.

Methods

Based on a panel study [A prospective Study COmparing the cardiometabolic and respiratory effects of air Pollution Exposure on healthy and prediabetic individuals (SCOPE)] conducted in Beijing between August 2013 and February 2015, fractional exhaled nitric oxide (FeNO) was measured from 112 participants at two to seven visits to indicate respiratory inflammation. Particulate pollutants-including particulate matter with an aerodynamic diameter of ?2.5?m (PM2.5), black carbon (BC), ultrafine particles (UFPs), and accumulated-mode particles-were monitored continuously at a single central monitoring site. Linear mixed-effects models were used to estimate associations between ln-FeNO with pollutant concentrations at individual 1-h lags (up to 24 h) and with average concentrations at 8 and 24 h before the clinical visit. We evaluated glucose metabolism disorders as a potential modifier by comparing associations between participants with high vs. low average fasting blood glucose (FBG) and homeostasis model assessment insulin resistance (HOMA-IR) levels.

Results

FeNO was positively associated with all pollutants, with the strongest associations for an interquartile range increase in 1-h lagged exposures (ranging from 21.3% for PM2.5 to 74.7% for BC). Associations differed significantly according to average HOMA-IR values when lagged 6-18 h for PM2.5, 15-19 h for BC, and 6-15 h for UFPs, with positive associations among those with HOMA-IR?1.6 while associations were closer to the null or inverse among those with HOMA-IR<1.6. Associations between PM2.5 and FeNO were consistently higher among individuals with average FBG?6.1?mmol/L vs. low FBG, with significant differences for multiple hourly lags.

Discussion

Glucose metabolism disorders may aggravate respiratory inflammation following exposure to ambient particulate matter. https://doi.org/10.1289/EHP4906.

SUBMITTER: Chen X

PROVIDER: S-EPMC7263737 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Respiratory Inflammation and Short-Term Ambient Air Pollution Exposures in Adult Beijing Residents with and without Prediabetes: A Panel Study.

Chen Xi X Han Yiqun Y Chen Wu W Wang Yanwen Y Qiu Xinghua X Li Weiju W Hu Min M Wu Yusheng Y Wang Qi Q Zhang Hanxiyue H Zhu Tong T

Environmental health perspectives 20200601 6

<h4>Background</h4>Accumulating evidence suggests that individuals with glucose metabolism disorders are susceptible to mortality associated with fine particles. However, the mechanisms remain largely unknown.<h4>Objectives</h4>We examined whether particle-associated respiratory inflammation differed between individuals with prediabetes and healthy control participants.<h4>Methods</h4>Based on a panel study [A prospective Study COmparing the cardiometabolic and respiratory effects of air Polluti ...[more]

PMID: 32484751

Similar Datasets

Project description:Few epidemiologic studies have evaluated the effects of air pollution on the risk of Parkinson disease (PD).We investigated the associations of long-term residential concentrations of ambient particulate matter (PM) < 10 ?m in diameter (PM10) and < 2.5 ?m in diameter (PM2.5) and nitrogen dioxide (NO2) in relation to PD risk.Our nested case-control analysis included 1,556 self-reported physician-diagnosed PD cases identified between 1995 and 2006 and 3,313 controls frequency-matched on age, sex, and race. We geocoded home addresses reported in 1995-1996 and estimated the average ambient concentrations of PM10, PM2.5, and NO2 using a national fine-scale geostatistical model incorporating roadway information and other geographic covariates. Air pollutant exposures were analyzed as both quintiles and continuous variables, adjusting for matching variables and potential confounders.We observed no statistically significant overall association between PM or NO2 exposures and PD risk. However, in preplanned subgroup analyses, a higher risk of PD was associated with higher exposure to PM10 (ORQ5 vs. Q1 = 1.65; 95% CI: 1.11, 2.45; p-trend = 0.02) among women, and with higher exposure to PM2.5 (ORQ5 vs. Q1 = 1.29; 95% CI: 0.94, 1.76; p-trend = 0.04) among never smokers. In post hoc analyses among female never smokers, both PM2.5 (ORQ5 vs. Q1 = 1.79; 95% CI: 1.01, 3.17; p-trend = 0.05) and PM10 (ORQ5 vs. Q1 = 2.34; 95% CI: 1.29, 4.26; p-trend = 0.01) showed positive associations with PD risk. Analyses based on continuous exposure variables generally showed similar but nonsignificant associations.Overall, we found limited evidence for an association between exposures to ambient PM10, PM2.5, or NO2 and PD risk. The suggestive evidence that exposures to PM2.5 and PM10 may increase PD risk among female never smokers warrants further investigation. Citation: Liu R, Young MT, Chen JC, Kaufman JD, Chen H. 2016. Ambient air pollution exposures and risk of Parkinson disease. Environ Health Perspect 124:1759-1765;?http://dx.doi.org/10.1289/EHP135.

Project description:BACKGROUND:Residential proximity to major roadways, and prenatal exposures to particulate matter <2.5??m (PM2.5) and ozone (O3) are linked to poor fetal outcomes but their relationship with childhood development is unclear. OBJECTIVES:We investigated whether proximity to major roadways, or prenatal and early-life exposures to PM2.5 and O3 increase the risk of early developmental delays. STUDY DESIGN:Prospective cohort. SETTINGS:New York State excluding New York City. PARTICIPANTS:4089 singletons and 1016 twins born between 2008 and 2010. EXPOSURES:Proximity to major roadway was calculated using road network data from the NY Department of Transportation. Concentrations of PM2.5 and O3 estimated by the Environmental Protection Agency Downscaler models were spatiotemporally linked to each child's prenatal and early-life addresses incorporating residential history, and locations of maternal work and day-care. OUTCOMES:Parents reported their children's development at ages 8, 12, 18, 24, 30 and 36 months in five domains using the Ages and Stages Questionnaire. Generalized mixed models estimated the relative risk (RR) and 95% CI for failing any developmental domain per 10 units increase in PM2.5 and O3, and for those living <1000?m away from a major roadway compared to those living further. Models adjusted for potential confounders. RESULTS:Compared to those >1000?m away from a major roadway, those resided 50-100?m [RR: 2.12 (1.00-4.52)] and 100-500?m [RR: 2.07 (1.02-4.22)] away had twice the risk of failing the communication domain. Prenatal exposures to both PM2.5 and ozone during various pregnancy windows had weak but significant associations with failing any developmental domain with effects ranging from 1.6% to 2.7% for a 10??g/m3 increase in PM2.5 and 0.7%-1.7% for a 10?ppb increase in ozone. Average daily postnatal ozone exposure was positively associated with failing the overall screening by 8 months [3.3% (1.1%-5.5%)], 12 months [17.7% (10.4%-25.5%)], and 30 months [7.6%, (1.3%-14.3%)]. Findings were mixed for postnatal PM2.5 exposures. CONCLUSIONS:In this prospective cohort study, proximity to major roadway and prenatal/early-life exposures to PM2.5 and O3 were associated with developmental delays. While awaiting larger studies with personal air pollution assessment, efforts to minimize air pollution exposures during critical developmental windows may be warranted.

Project description:BACKGROUND:Mechanisms underlying the effects of traffic-related air pollution on people with asthma remain largely unknown, despite the abundance of observational and controlled studies reporting associations between traffic sources and asthma exacerbation and hospitalizations. OBJECTIVES:To identify molecular pathways perturbed following traffic pollution exposures, we analyzed data as part of the Atlanta Commuters Exposure (ACE-2) study, a crossover panel of commuters with and without asthma. METHODS:We measured 27 air pollutants and conducted high-resolution metabolomics profiling on blood samples from 45 commuters before and after each exposure session. We evaluated metabolite and metabolic pathway perturbations using an untargeted metabolome-wide association study framework with pathway analyses and chemical annotation. RESULTS:Most of the measured pollutants were elevated in highway commutes (p?<?0.05). From both negative and positive ionization modes, 17,586 and 9087 metabolic features were extracted from plasma, respectively. 494 and 220 unique features were associated with at least 3 of the 27 exposures, respectively (p?<?0.05), after controlling confounders and false discovery rates. Pathway analysis indicated alteration of several inflammatory and oxidative stress related metabolic pathways, including leukotriene, vitamin E, cytochrome P450, and tryptophan metabolism. We identified and annotated 45 unique metabolites enriched in these pathways, including arginine, histidine, and methionine. Most of these metabolites were not only associated with multiple pollutants, but also differentially expressed between participants with and without asthma. The analysis indicated that these metabolites collectively participated in an interrelated molecular network centering on arginine metabolism, underlying the impact of traffic-related pollutants on individuals with asthma. CONCLUSIONS:We detected numerous significant metabolic perturbations associated with in-vehicle exposures during commuting and validated metabolites that were closely linked to several inflammatory and redox pathways, elucidating the potential molecular mechanisms of traffic-related air pollution toxicity. These results support future studies of metabolic markers of traffic exposures and the corresponding molecular mechanisms.

Dataset Information

Respiratory Inflammation and Short-Term Ambient Air Pollution Exposures in Adult Beijing Residents with and without Prediabetes: A Panel Study.

Background

Objectives

Methods

Results

Discussion

Publications

Respiratory Inflammation and Short-Term Ambient Air Pollution Exposures in Adult Beijing Residents with and without Prediabetes: A Panel Study.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure