Associations among plasma metabolite levels and short-term exposure to PM2.5 and ozone in a cardiac catheterization cohort

doi:10.1016/j.envint.2016.10.012

Environment International

Volume 97, December 2016, Pages 76-84

https://doi.org/10.1016/j.envint.2016.10.012 Get rights and content

Highlights

•
We explored associations between short-term exposures to PM_2.5 and ozone with plasma metabolite concentrations
•
PM_2.5 and ozone were associated with changes in plasma metabolite levels
•
Strongest association was seen for PM_2.5 with a lag of one day and decreased mean glycine concentrations
•
Our findings might help to understand the link between air pollution and cardiovascular disease

Abstract

Rationale

Exposure to ambient particulate matter (PM) and ozone has been associated with cardiovascular disease (CVD). However, the mechanisms linking PM and ozone exposure to CVD remain poorly understood.

Objective

This study explored associations between short-term exposures to PM with a diameter < 2.5 μm (PM_2.5) and ozone with plasma metabolite concentrations.

Methods and results

We used cross-sectional data from a cardiac catheterization cohort at Duke University, North Carolina (NC), USA, accumulated between 2001 and 2007. Amino acids, acylcarnitines, ketones and total non-esterified fatty acid plasma concentrations were determined in fasting samples. Daily concentrations of PM_2.5 and ozone were obtained from a Bayesian space-time hierarchical model, matched to each patient's residential address. Ten metabolites were selected for the analysis based on quality criteria and cluster analysis. Associations between metabolites and PM_2.5 or ozone were analyzed using linear regression models adjusting for long-term trend and seasonality, calendar effects, meteorological parameters, and participant characteristics.

We found delayed associations between PM_2.5 or ozone and changes in metabolite levels of the glycine-ornithine-arginine metabolic axis and incomplete fatty acid oxidation associated with mitochondrial dysfunction. The strongest association was seen for an increase of 8.1 μg/m³ in PM_2.5 with a lag of one day and decreased mean glycine concentrations (− 2.5% [95% confidence interval: − 3.8%; − 1.2%]).

Conclusions

Short-term exposures to ambient PM_2.5 and ozone is associated with changes in plasma concentrations of metabolites in a cohort of cardiac catheterization patients. Our findings might help to understand the link between air pollution and cardiovascular disease.

Introduction

Exposure to ambient air pollution affects a range of cardiovascular events (Brook et al., 2010, Rückerl et al., 2011). Acute (day-to-day) exposure to particulate matter (PM) with an aerodynamic diameter < 2.5 μm (PM_2.5) is associated with increased risk of cardiovascular mortality, myocardial infarction, heart failure exacerbation, stroke (Atkinson et al., 2014, Mustafic et al., 2012, Shah et al., 2013, Shah et al., 2015) and induction of a variety of adverse cardiovascular outcomes (Brook et al., 2010, McGuinn et al., 2015). Epidemiological and controlled-exposure studies also suggest that exposure to ambient ozone may increase cardiovascular morbidity (Arjomandi et al., 2015, Devlin et al., 2012, Green et al., 2016, Hampel et al., 2012, Lanzinger et al., 2014). The elderly and those with underlying diseases, for example, cardiovascular diseases or diabetes, are particularly susceptible to the health effects of PM_2.5 (Lanzinger et al., 2014, Rückerl et al., 2011, Shumake et al., 2013, Stafoggia et al., 2010); however, current evidence for the risks of ozone are inconclusive (Goodman et al., 2014).

The physiological mechanisms linking PM_2.5 exposure to cardiovascular disease have yet to be fully elucidated. Biological pathways thought to be important include: systemic inflammation; changes in the autonomic balance; local inflammatory response; and oxidative stress due to translocation of particles or particle constituents (Brook et al., 2010, Peters et al., 2011). Further, inhalation of ozone may cause systemic inflammation and autonomic dysfunction (Brook et al., 2010, Devlin et al., 2012, Hampel et al., 2012). However, exploring the possibility that PM_2.5- or ozone-induced changes in metabolic pathways may contribute to or mediate cardiometabolic outcomes is becoming increasing important for understanding potential mechanisms of these effects.

Metabolomics, or metabolomic profiling, refers to the comprehensive analysis of metabolites - low molecular weight chemicals including sugars, acylcarnitines, amino acids, and lipids - present in biological specimens (Rhee and Gerszten, 2012). Metabolomics has the potential for identifying novel biomarkers contributing to the onset or progression of cardiovascular disease (Shah et al., 2012a). Specific metabolomic profiles are associated with coronary artery disease (CAD) and atherosclerosis, and with major adverse cardiovascular events, including myocardial infarction, stroke, heart failure and death (Kordalewska and Markuszewski, 2015, Shah et al., 2012a, Würtz et al., 2015).

Current literature on short-term exposures to air pollution and blood chemistries has focused on traditional clinical parameters such as C-reactive protein or cytokines (e.g. Chuang et al., 2007, Rückerl et al., 2007, Tsai et al., 2012). However, evaluating associations between air pollution and metabolite levels could provide further evidence of air pollution-related physiologic changes and offer further insights into the pathophysiologic mechanisms by which short-term exposures to air pollution may increase the risk of acute cardiovascular events. So far, there has been only one epidemiological study exploring the association between air pollution and changes in metabolite levels (Menni et al., 2015). In this study using a subset of the TwinsUK cohort, long-term exposures to PM₁₀ and PM_2.5 were linked with metabolites related to reduced lung function. Only a small number of animal or toxicological studies have reported associations between inhaled toxicants and metabolite levels (Miller et al., 2015, Miller et al., 2016, Wang et al., 2012, Wang et al., 2015, Wei et al., 2013).

This study aimed to explore the influence of short-term exposures to PM_2.5 and ozone on selected metabolites in a cohort of individuals undergoing cardiac catheterization for suspected CAD. Moreover, we evaluated whether these associations were modified by participant or lifestyle characteristics. Since the study population was at high risk for cardiovascular disease, our findings may help to uncover and clarify air pollution-metabolomics associations in a population particularly susceptible to the health effects of air pollution.

Section snippets

Study population

This study was conducted using data from the CATHeterization GENetics (CATHGEN) cohort, a large cohort of patients undergoing cardiac catheterization for suspected cardiovascular disease between 2001 and 2010 at the Duke University Cardiac Catheterization Clinic (Durham, NC)(Kraus et al., 2015).

For each of these patients, home addresses were extracted from medical records. Addresses were geocoded within the Children's Environmental Health Initiative (http://cehi.snre.umich.edu/), adding

Participant characteristics

Table 1 describes the study population. On average, participants were 59 years old with a mean BMI of 30 kg/m². About 58% of the participants were men; approximately half were current smokers. The prevalence of CAD and hypertension was 50.4% and 67.9%, respectively; this reflects a population with increased risk for CAD.

Cluster analysis

Twenty-three of the 61 metabolites met all the inclusion criteria. Results of the cluster analysis are shown in Fig. 1. Most of the indices used to determine the relevant number

Summary

Prior day (1-day lag) increases in PM_2.5 were associated with decreases in the concentrations of the amino acids arginine and glycine; PM_2.5 was also associated with delayed increases in ornithine and C16:1. Increases in short-term exposures to ozone resulted in immediate and delayed increases of the amino acids aspartic acid/asparagine and ornithine; delayed increases were found for the acylcarnitines C10:1 and C16:1 as well as for total ketones. Results also suggested that there was effect

Disclaimer

Research described in this article was conducted under contract to the Health Effects Institute (HEI), and organization jointly funded by the United States Environmental Protection Agency (EPA) (Assistance Award No. R-82811201), and certain motor vehicle and engine manufacturers. The contents of this article do not necessarily reflect the views of HEI, or its sponsors, nor do they necessarily reflect the view and policies of the EPA or motor vehicle and engine manufacturers.

This work was

References (56)

S.C. Gray et al.
Race, socioeconomic status, and air pollution exposure in North Carolina
Environ. Res.
(2013)
M. Kordalewska et al.
Metabolomics in cardiovascular diseases
J. Pharm. Biomed. Anal.
(2015)
S. Lanzinger et al.
The impact of decreases in air temperature and increases in ozone on markers of endothelial function in individuals having type-2 diabetes
Environ. Res.
(2014)
D.B. Miller et al.
Inhaled ozone (O3)-induces changes in serum metabolomic and liver transcriptomic profiles in rats
Toxicol. Appl. Pharmacol.
(2015)
C.B. Newgard et al.
A branched-chain amino acid-related metabolic signature that differentiates obese and lean humans and contributes to insulin resistance
Cell Metab.
(2009)
S. Rizza et al.
Metabolomics signature improves the prediction of cardiovascular events in elderly subjects
Atherosclerosis
(2014)
L.D. Roberts et al.
Towards metabolic biomarkers of insulin resistance and type 2 diabetes: progress from the metabolome
Lancet Diab. Endocrinol.
(2014)
A.S.V. Shah et al.
Global association of air pollution and heart failure: a systematic review and meta-analysis
Lancet
(2013)
H. Sourij et al.
Arginine bioavailability ratios are associated with cardiovascular mortality in patients referred to coronary angiography
Atherosclerosis
(2011)
W.H. Tang et al.
Diminished global arginine bioavailability and increased arginine catabolism as metabolic profile of increased cardiovascular risk
J. Am. Coll. Cardiol.
(2009)

M. Arjomandi et al.

Exposure to medium and high ambient levels of ozone causes adverse systemic inflammatory and cardiac autonomic effects

Am. J. Physiol. Heart Circ. Physiol.

(2015)

R.W. Atkinson et al.

Epidemiological time series studies of PM2.5 and daily mortality and hospital admissions: a systematic review and meta-analysis

Thorax

(2014)

V.J. Berrocal et al.

A bivariate space-time downscaler under space and time misalignment

Ann. Appl. Stat.

(2010)

V.J. Berrocal et al.

A spatio-temporal downscaler for output from numerical models

J. Agric. Biol. Environ. Stat.

(2010)

V.J. Berrocal et al.

Space-time data fusion under error in computer model output: an application to modeling air quality

Biometrics

(2012)

R.D. Brook et al.

Particulate matter air pollution and cardiovascular disease: an update to the scientific statement from the American Heart Association

Circulation

(2010)

M. Charrad et al.

NbClust: an R package for determining the relevant number of clusters in a data set

J. Stat. Softw.

(2014)

K.J. Chuang et al.

The effect of urban air pollution on inflammation, oxidative stress, coagulation, and autonomic dysfunction in young adults

Am. J. Respir. Crit. Care Med.

(2007)

R.B. Devlin et al.

Controlled exposure of healthy young volunteers to ozone causes cardiovascular effects

Circulation

(2012)

Y. Ding et al.

Plasma glycine and risk of acute myocardial infarction in patients with suspected stable angina pectoris

J. Am. Heart Assoc.

(2016)

S.D. Dubowsky et al.

Diabetes, obesity, and hypertension may enhance associations between air pollution and markers of systemic inflammation

Environ. Health Perspect.

(2006)

P.H.C. Eilers et al.

Flexible smoothing with B-splines and penalties. With comments and a rejoinder by the authors

Stat. Sci.

(1996)

E. Ferrannini et al.

Early metabolic markers of the development of dysglycemia and type 2 diabetes and their physiological significance

Diabetes

(2013)

A. Floegel et al.

Identification of serum metabolites associated with risk of type 2 diabetes using a targeted metabolomic approach

Diabetes

(2013)

J.E. Goodman et al.

Weight-of-evidence evaluation of short-term ozone exposure and cardiovascular effects

Crit. Rev. Toxicol.

(2014)

R. Green et al.

Long- and short-term exposure to air pollution and inflammatory/hemostatic markers in midlife women

Epidemiology

(2016)

R. Hampel et al.

Immediate ozone effects on heart rate and repolarisation parameters in potentially susceptible individuals

Occup. Environ. Med.

(2012)

W.E. Kraus et al.

A guide for a cardiovascular genomics biorepository: the CATHGEN experience

J. Cardiovasc. Transl. Res.

(2015)

Cited by (51)

Association of short-term PM<inf>2.5</inf> exposure with airway innate immune response, microbiota and metabolism alterations in human airways
2024, Environmental Pollution
Exposure to fine particulate matter (PM_2.5) has been associated with impaired airway innate immunity, leading to diverse lung disorders. However, the mechanisms of the adverse effects of PM_2.5 on the airway innate immune system has not been adequately elucidated. This study aimed to investigate the association between short-term exposure to ambient PM_2.5 and airway innate immune responses. A panel study of 53 undergraduate students was conducted in November 2020 and April 2021. Levels of airway innate immune biomarkers including interleukin-1β (IL-1β), IL-4, IL-6, IL-8, IL-17, interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), myeloperoxidase (MPO), and matrix metalloproteinase-9 (MMP-9) in induced sputum were measured, and airway microbiota and metabolites examined. Linear mixed-effect model was used to evaluate the effects of short-term exposure to PM_2.5 on the above-listed airway immune biomarkers. The results indicated that for every 10 μg/m³ increase in PM_2.5 concentration (at lag3), was associated with an increase of 21.3 % (5.4 %–37.1 %), 26.2 % (0.30 %–52.1 %), 22.4 % (0.70 %–44.2 %), 27.4 % (6.6 %–48.3 %), 18.3 % (4.6 %–31.9 %), 3.9 % (0.20 %–7.6 %) or 2.4 % (0.10 %–4.7 %) in IL-6, TNF-α, IL-17, IL-4, IFN-γ, MPO, or MMP-9 levels, respectively. Meanwhile, exposure to higher levels of ambient PM_2.5 was found to significantly modulate airway microbiota and metabolite profile. Specifically, Prevotella and Fusobacterium, as well as 96 different metabolites were associated with PM_2.5 levels. The metabolic pathways associated with these metabolites mainly included amino acid biosynthesis and metabolism. Notably, PM_2.5 exposure-induced alterations of some airway microbiota were significantly correlated with specific airway metabolic change. Taken together, these results demonstrated that short-term exposure to PM_2.5 was associated with alterations of airway immune response, microbial dysbiosis and changes of metabolites. This study provided insights into the mechanisms underlying PM_2.5-induced airway innate immune responses.
Longitudinal associations between metabolites and immediate, short- and medium-term exposure to ambient air pollution: Results from the KORA cohort study
2023, Science of the Total Environment
Short-term exposure to air pollution has been reported to be associated with cardiopulmonary diseases, but the underlying mechanisms remain unclear. This study aimed to investigate changes in serum metabolites associated with immediate, short- and medium-term exposures to ambient air pollution.
We used data from the German population-based Cooperative Health Research in the Region of Augsburg (KORA) S4 survey (1999–2001) and two follow-up examinations (F4: 2006–08 and FF4: 2013–14). Mass-spectrometry-based targeted metabolomics was used to quantify metabolites among serum samples. Only participants with repeated metabolites measurements were included in this analysis. We collected daily averages of fine particles (PM_2.5), coarse particles (PM_coarse), nitrogen dioxide (NO₂), and ozone (O₃) at urban background monitors located in Augsburg, Germany. Covariate-adjusted generalized additive mixed-effects models were used to examine the associations between immediate (2-day average of same day and previous day as individual's blood withdrawal), short- (2-week moving average), and medium-term exposures (8-week moving average) to air pollution and metabolites. We further performed pathway analysis for the metabolites significantly associated with air pollutants in each exposure window.
Of 9,620 observations from 4,261 study participants, we included 5,772 (60.0%) observations from 2,583 (60.6%) participants in this analysis. Out of 108 metabolites that passed quality control, multiple significant associations between metabolites and air pollutants with several exposure windows were identified at a Bonferroni corrected p-value threshold (p < 3.9 × 10⁻⁵). We found the highest number of associations for NO₂, particularly at the medium-term exposure windows. Among the identified metabolic pathways based on the metabolites significantly associated with air pollutants, the glycerophospholipid metabolism was the most robust pathway in different air pollutants exposures.
Our study suggested that short- and medium-term exposure to air pollution might induce alterations of serum metabolites, particularly in metabolites involved in metabolic pathways related to inflammatory response and oxidative stress.
Metabolic pathways altered by air pollutant exposure in association with lipid profiles in young adults
2023, Environmental Pollution
Mounting evidence suggests that air pollution influences lipid metabolism and dyslipidemia. However, the metabolic mechanisms linking air pollutant exposure and altered lipid metabolism is not established. In year 2014–2018, we conducted a cross-sectional study on 136 young adults in southern California, and assessed lipid profiles (triglycerides, total cholesterol, high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol, very-low-density lipoprotein (VLDL)-cholesterol), and untargeted serum metabolomics using liquid chromatography-high-resolution mass spectrometry, and one-month and one-year averaged exposures to NO₂, O₃, PM_2.5 and PM₁₀ air pollutants at residential addresses. A metabolome-wide association analysis was conducted to identify metabolomic features associated with each air pollutant. Mummichog pathway enrichment analysis was used to assess altered metabolic pathways. Principal component analysis (PCA) was further conducted to summarize 35 metabolites with confirmed chemical identity. Lastly, linear regression models were used to analyze the associations of metabolomic PC scores with each air pollutant exposure and lipid profile outcome. In total, 9309 metabolomic features were extracted, with 3275 features significantly associated with exposure to one-month or one-year averaged NO₂, O₃, PM_2.5 and PM₁₀ (p < 0.05). Metabolic pathways associated with air pollutants included fatty acid, steroid hormone biosynthesis, tryptophan, and tyrosine metabolism. PCA of 35 metabolites identified three main PCs which together explained 44.4% of the variance, representing free fatty acids and oxidative byproducts, amino acids and organic acids. Linear regression indicated that the free fatty acids and oxidative byproducts-related PC score was associated with air pollutant exposure and outcomes of total cholesterol and LDL-cholesterol (p < 0.05). This study suggests that exposure to NO₂, O₃, PM_2.5 and PM₁₀ contributes to increased level of circulating free fatty acids, likely through increased adipose lipolysis, stress hormone and response to oxidative stress pathways. These alterations were associated with dysregulation of lipid profiles and potentially could contribute to dyslipidemia and other cardiometabolic disorders.
Overview of PM<inf>2.5</inf> and health outcomes: Focusing on components, sources, and pollutant mixture co-exposure
2023, Chemosphere
PM_2.5 varies in source and composition over time and space as a complicated mixture. Consequently, the health effects caused by PM_2.5 varies significantly over time and generally exhibit significant regional variations. According to numerous studies, a notable relationship exists between PM_2.5 and the occurrence of many diseases, such as respiratory, cardiovascular, and nervous system diseases, as well as cancer. Therefore, a comprehensive understanding of the effect of PM_2.5 on human health is critical. The toxic effects of various PM_2.5 components, as well as the overall toxicity of PM_2.5 are discussed in this review to provide a foundation for precise PM_2.5 emission control. Furthermore, this review summarizes the synergistic effect of PM_2.5 and other pollutants, which can be used to draft effective policies.
The pathophysiological and molecular mechanisms of atmospheric PM<inf>2.5</inf> affecting cardiovascular health: A review
2023, Ecotoxicology and Environmental Safety
Exposure to ambient fine particulate matter (PM_2.5, with aerodynamic diameter less than 2.5 µm) is a leading environmental risk factor for global cardiovascular health concern.
To provide a roadmap for those new to this field, we reviewed the new insights into the pathophysiological and cellular/molecular mechanisms of PM_2.5 responsible for cardiovascular health. Main findings: PM_2.5 is able to disrupt multiple physiological barriers integrity and translocate into the systemic circulation and get access to a range of secondary target organs. An ever-growing body of epidemiological and controlled exposure studies has evidenced a causal relationship between PM_2.5 exposure and cardiovascular morbidity and mortality. A variety of cellular and molecular biology mechanisms responsible for the detrimental cardiovascular outcomes attributable to PM_2.5 exposure have been described, including metabolic activation, oxidative stress, genotoxicity, inflammation, dysregulation of Ca²⁺ signaling, disturbance of autophagy, and induction of apoptosis, by which PM_2.5 exposure impacts the functions and fates of multiple target cells in cardiovascular system or related organs and further alters a series of pathophysiological processes, such as cardiac autonomic nervous system imbalance, increasing blood pressure, metabolic disorder, accelerated atherosclerosis and plaque vulnerability, platelet aggregation and thrombosis, and disruption in cardiac structure and function, ultimately leading to cardiovascular events and death. Therein, oxidative stress and inflammation were suggested to play pivotal roles in those pathophysiological processes.
Those biology mechanisms have deepen insights into the etiology, course, prevention and treatment of this public health concern, although the underlying mechanisms have not yet been entirely clarified.
Exposures to low-levels of fine particulate matter are associated with acute changes in heart rate variability, cardiac repolarization, and circulating blood lipids in coronary artery disease patients
2022, Environmental Research
Exposure to air pollution is a major risk factor for cardiovascular disease, disease risk factors, and mortality. Specifically, particulate matter (PM), and to some extent ozone, are contributors to these effects. In addition, exposures to these pollutants may be especially dangerous for susceptible populations. In this repeated-visit panel study, cardiovascular markers were collected from thirteen male participants with stable coronary artery disease. For 0–4 days prior to the health measurement collections, daily concentrations of fine PM (PM_2.5) and ozone were obtained from local central monitoring stations located near the participant's homes. Then, single (PM_2.5) and two-pollutant (PM_2.5 and ozone) models were used to assess whether there were short-term changes in cardiovascular health markers. Per interquartile range increase in PM_2.5, there were decrements in several heart rate variability metrics, including the standard deviation of the normal-to-normal intervals (lag 3, -5.8%, 95% confidence interval (CI) = −11.5, 0.3) and root-mean squared of successive differences (five day moving average, −8.1%, 95% CI = −15.0, −0.7). In addition, increases in PM_2.5 were also associated with changes in P complexity (lag 1, 4.4%, 95% CI = 0.5, 8.5), QRS complexity (lag 1, 4.9%, 95% CI = 1.4, 8.5), total cholesterol (five day moving average, −2.1%, 95% CI = −4.1, −0.1), and high-density lipoprotein cholesterol (lag 2, -1.6%, 95% CI = −3.1, −0.1). Comparisons to our previously published work on ozone were conducted. We found that ozone affected inflammation and endothelial function, whereas PM_2.5 influenced heart rate variability, repolarization, and lipids. All the health changes from these two studies were found at concentrations below the United States Environmental Protection Agency's National Ambient Air Quality Standards. Our results imply clear differences in the cardiovascular outcomes observed with exposure to the two ubiquitous air pollutants PM_2.5 and ozone; this observation suggests different mechanisms of toxicity for these exposures.

View all citing articles on Scopus

View full text

Full length articleAssociations among plasma metabolite levels and short-term exposure to PM2.5 and ozone in a cardiac catheterization cohort

Highlights

Abstract

Rationale

Objective

Methods and results

Conclusions

Introduction

Section snippets

Study population

Participant characteristics

Cluster analysis

Summary

Disclaimer

Environ. Res.

J. Pharm. Biomed. Anal.

Environ. Res.

Toxicol. Appl. Pharmacol.

Cell Metab.

Atherosclerosis

Lancet Diab. Endocrinol.

Lancet

Atherosclerosis

J. Am. Coll. Cardiol.

Exposure to medium and high ambient levels of ozone causes adverse systemic inflammatory and cardiac autonomic effects

Am. J. Physiol. Heart Circ. Physiol.

Epidemiological time series studies of PM2.5 and daily mortality and hospital admissions: a systematic review and meta-analysis

Thorax

A bivariate space-time downscaler under space and time misalignment

Ann. Appl. Stat.

A spatio-temporal downscaler for output from numerical models

J. Agric. Biol. Environ. Stat.

Space-time data fusion under error in computer model output: an application to modeling air quality

Biometrics

Particulate matter air pollution and cardiovascular disease: an update to the scientific statement from the American Heart Association

Circulation

NbClust: an R package for determining the relevant number of clusters in a data set

J. Stat. Softw.

The effect of urban air pollution on inflammation, oxidative stress, coagulation, and autonomic dysfunction in young adults

Am. J. Respir. Crit. Care Med.

Controlled exposure of healthy young volunteers to ozone causes cardiovascular effects

Circulation

Plasma glycine and risk of acute myocardial infarction in patients with suspected stable angina pectoris

J. Am. Heart Assoc.

Diabetes, obesity, and hypertension may enhance associations between air pollution and markers of systemic inflammation

Environ. Health Perspect.

Flexible smoothing with B-splines and penalties. With comments and a rejoinder by the authors

Stat. Sci.

Early metabolic markers of the development of dysglycemia and type 2 diabetes and their physiological significance

Diabetes

Identification of serum metabolites associated with risk of type 2 diabetes using a targeted metabolomic approach

Diabetes

Weight-of-evidence evaluation of short-term ozone exposure and cardiovascular effects

Crit. Rev. Toxicol.

Long- and short-term exposure to air pollution and inflammatory/hemostatic markers in midlife women

Epidemiology

Immediate ozone effects on heart rate and repolarisation parameters in potentially susceptible individuals

Occup. Environ. Med.

A guide for a cardiovascular genomics biorepository: the CATHGEN experience

J. Cardiovasc. Transl. Res.

Full length article
Associations among plasma metabolite levels and short-term exposure to PM_2.5 and ozone in a cardiac catheterization cohort