Use of high-resolution metabolomics for the identification of metabolic signals associated with traffic-related air pollution

Liang, Donghai; Moutinho, Jennifer L.; Golan, Rachel; Yu, Tianwei; Ladva, Chandresh N; Niedzwiecki, Megan M.; Walker, Douglas I.; Sarnat, Stefanie Ebelt; Chang, Howard H.; Greenwald, Roby; Jones, Dean P.; Russell, Armistead G.; Sarnat, Jeremy A.

doi:10.1016/j.envint.2018.07.044

Cited by 127 publications

(111 citation statements)

References 76 publications

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“…In recent years, high-resolution metabolomics (HRM) has been used to relate internal exposure of participants to complex traffic-related air pollution mixtures (185). In one study, plasma and saliva samples collected from the participants and subjected to HRM revealed differences in endogenous signaling processes that were related to oxidative stress, inflammation, nucleic acid damage, and repair.…”

Section: Relevance Of Metabolomics In Chemical Exposure-induced Cvdmentioning

confidence: 99%

Use of an Exposome Approach to Understand the Effects of Exposures From the Natural, Built, and Social Environments on Cardio-Vascular Disease Onset, Progression, and Outcomes

Juárez

Hood

Song

et al. 2020

Front. Public Health

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Obesity, diabetes, and hypertension have increased by epidemic proportions in recent years among African Americans in comparison to Whites resulting in significant adverse cardiovascular disease (CVD) disparities. Today, African Americans are 30% more likely to die of heart disease than Whites and twice as likely to have a stroke. The causes of these disparities are not yet well-understood. Improved methods for identifying underlying risk factors is a critical first step toward reducing Black:White CVD disparities. This article will focus on environmental exposures in the external environment and how they can lead to changes at the cellular, molecular, and organ level to increase the personal risk for CVD and lead to population level CVD racial disparities. The external environment is defined in three broad domains: natural (air, water, land), built (places you live, work, and play) and social (social, demographic, economic, and political). We will describe how environmental exposures in the natural, built, and social environments "get under the skin" to affect gene expression though epigenetic, pan-omics, and related mechanisms that lead to increased risk for adverse CVD health outcomes and population level disparities. We also will examine the important role of metabolomics, proteomics, transcriptomics, genomics, and epigenomics in understanding how exposures in the natural, built, and social environments lead to CVD disparities with implications for clinical, public health, and policy interventions. In this review, we apply an exposome approach to Black:White CVD racial disparities. The exposome is a measure of all the exposures of an individual across the life course and the relationship of those exposures to health effects. The exposome represents the totality of exogenous (external) and endogenous (internal) exposures from conception onwards, simultaneously distinguishing, characterizing, and quantifying etiologic, mediating, moderating, and co-occurring risk and protective factors and their relationship to disease. Specifically, it assesses the biological mechanisms and underlying pathways through which chemical and non-chemical environmental Juarez et al. The Exposome and Cardiovascular Disease exposures are associated with CVD onset, progression and outcomes. The exposome is a promising approach for understanding the complex relationships among environment, behavior, biology, genetics, and disease phenotypes that underlie population level, Black: White CVD disparities.

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Section: Relevance Of Metabolomics In Chemical Exposure-induced Cvdmentioning

confidence: 99%

Use of an Exposome Approach to Understand the Effects of Exposures From the Natural, Built, and Social Environments on Cardio-Vascular Disease Onset, Progression, and Outcomes

Juárez

Hood

Song

et al. 2020

Front. Public Health

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“…In particular, major ubiquitous ambient air pollutants, including fine particulate matter (PM 2.5 ), nitrogen dioxide (NO 2 ), and ozone (O 3 ), may have both direct and indirect systemic impact on the human body by enhancing oxidative stress and inflammation, eventually leading to respiratory, cardiovascular, and immune system dysfunction and deterioration [9][10][11][12][13] .…”

Section: Introductionmentioning

confidence: 99%

Urban Air Pollution May Enhance COVID-19 Case-Fatality and Mortality Rates in the United States

Liang

Shi

Zhao

et al. 2020

Preprint

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Background:The novel human coronavirus disease 2019 pandemic has claimed more than 240,000 lives worldwide, causing tremendous public health, social, and economic damages. While the risk factors of COVID-19 are still under investigation, environmental factors, such as urban air pollution, may play an important role in increasing population susceptibility to COVID-19 pathogenesis. Methods:We conducted a cross-sectional nationwide study using zero-inflated negative binomial models to estimate the association between long-term (2010-2016) county-level exposures to NO 2 , PM 2.5 and O 3 and county-level COVID-19 case-fatality and mortality rates in the US. We used both single and multipollutant models and controlled for spatial trends and a comprehensive set of potential confounders, including state-level test positive rate, county-level healthcare capacity, phase-of-epidemic, population mobility, sociodemographic, socioeconomic status, behavior risk factors, and meteorological factors.Results: 1,027,799 COVID-19 cases and 58,489 deaths were reported in 3,122 US counties from January 22, 2020 to April 29, 2020, with an overall observed case-fatality rate of 5.8%. Spatial variations were observed for both COVID-19 death outcomes and long-term ambient air pollutant levels. County-level average NO 2 concentrations were positively associated with both COVID-19 case-fatality rate and mortality rate in single-, bi-, and tri-pollutant models (p-values<0.05). Per inter-quartile range (IQR) increase in NO 2 (4.6 ppb), COVID-19 case-fatality rate and mortality rate were associated with an increase of 7.1% (95% CI 1.2% to 13.4%) and 11.2% (95% CI 3.4% to 19.5%), respectively. We did not observe significant associations between long-term exposures to PM 2.5 or O 3 and COVID-19 death outcomes (p-values>0.05), although per IQR increase in PM 2.5 (3.4 ug/m 3 ) was marginally associated with 10.8% (95% CI: -1.1% to 24.1%) increase in COVID-19 mortality rate. Discussions and Conclusions:Long-term exposure to NO 2 , which largely arises from urban combustion sources such as traffic, may enhance susceptibility to severe COVID-19 outcomes, independent of longterm PM 2.5 and O 3 exposure. The results support targeted public health actions to protect residents from COVID-19 in heavily polluted regions with historically high NO 2 levels. Moreover, continuation of current efforts to lower traffic emissions and ambient air pollution levels may be an important component of reducing population-level risk of COVID-19 deaths.

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“…Notwithstanding such challenges, identifying metabolite perturbations caused by air pollution exposure is a particularly relevant and promising approach in characterizing the interactions of living organisms with their environment by identifying disregulated molecular pathways and predicting health endpoints [60]. It is not surprising, therefore, that to address issues such as differential toxicity, workers have adopted such an approach in both toxicological and epidemiological studies [61][62][63][64][65][66][67]. Experimental studies have investigated shifts in the metabolite profiles of bronchial wash (BW) and bronchoalveolar lavage (BAL) of healthy volunteers following exposure to biodiesel exhaust (BDE) compared with filtered air [61,62].…”

Section: Applications Of Omics Approaches To Explore Mechanisms Of Tomentioning

confidence: 99%

“…A key finding from these studies has been the identification of several oxidative stress and inflammationrelated pathways (including leukotriene, cytochrome P450, vitamin E, tyrosine, methionine and tryptophan metabolism) that were consistently associated with elevated pollution exposures. For example, in an analysis of healthy college students living close to a major urban highway, leukotriene, vitamin E, cytochrome P450 and methionine metabolic pathways were linked to longer-term (over 3 months) exposure to elevated traffic-related air pollution (TRAP), including black carbon (BC) and PM 2.5 [64]. As illustrated in figure 3, Liang et al [68] detected numerous significant metabolic perturbations associated with in-vehicle exposures during commuting, validated metabolites that were closely linked to several inflammatory and redox pathways and collectively implicated these mechanisms as part of the impact of TRAP toxicity in asthmatic individuals.…”

Section: Applications Of Omics Approaches To Explore Mechanisms Of Tomentioning

confidence: 99%

Toxicity of airborne particles—established evidence, knowledge gaps and emerging areas of importance

Kelly

Fussell

2020

Phil. Trans. R. Soc. A.

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Epidemiological research has taught us a great deal about the health effects of airborne particulate matter (PM), particularly cardiorespiratory effects of combustion-related particles. This has been matched by toxicological research to define underlying mechanistic pathways. To keep abreast of the substantial challenges that air pollution continues to throw at us requires yet more strides to be achieved. For example, being aware of the most toxic components/sources and having a definitive idea of the range of associated disease outcomes. This review discusses approaches designed to close some of these knowledge gaps. These include a focus on particles arising from non-exhaust PM at the roadside and microplastics—both of which are becoming more relevant in the light of a shift in PM composition in response to global pressure to reduce combustion emissions. The application of hypothesis-free approaches in both mechanistic studies and epidemiology in unveiling unexpected relationships and generating novel insights is also discussed. Previous work, strengthening the evidence for both the adverse effects and benefits of intervention tell us that the sooner we act to close knowledge gaps, increase awareness and develop creative solutions, the sooner we can reduce the public health burden attributable to these complex and insidious environmental pollutants. This article is part of a discussion meeting issue ‘Air quality, past present and future’.

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Use of high-resolution metabolomics for the identification of metabolic signals associated with traffic-related air pollution

Cited by 127 publications

References 76 publications

Use of an Exposome Approach to Understand the Effects of Exposures From the Natural, Built, and Social Environments on Cardio-Vascular Disease Onset, Progression, and Outcomes

Use of an Exposome Approach to Understand the Effects of Exposures From the Natural, Built, and Social Environments on Cardio-Vascular Disease Onset, Progression, and Outcomes

Urban Air Pollution May Enhance COVID-19 Case-Fatality and Mortality Rates in the United States

Toxicity of airborne particles—established evidence, knowledge gaps and emerging areas of importance

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