Associations between ambient air pollution and blood markers of inflammation and coagulation/fibrinolysis in susceptible populations

Rückerl, Regina; Hampel, Regina; Breitner, Susanne; Cyrys, Josef; Kraus, Ute; Carter, Jackie; Dailey, Lisa A.; Devlin, Robert B.; Díaz-Sánchez, David; Köenig, Wolfgang; Phipps, Richard P.; Silbajoris, Robert; Soentgen, Jens; Soukup, Joleen M.; Peters, Annette; Schneider, Alexandra

doi:10.1016/j.envint.2014.05.013

Cited by 135 publications

(88 citation statements)

References 72 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…[1][2][3][4] Although potential biological mechanisms for these adverse health effects are yet to be fully ascertained, inflammation and oxidative stress are likely to be involved. [5][6][7] In addition, several studies have reported an association between PM exposure and dysfunction of the automatic nervous system, which is known to increase cardiovascular risk. [8][9][10] Animal studies further implicated PM 2.5 as a stressor to the central nervous system that might induce a cascade of neuroendocrine responses.…”

mentioning

confidence: 99%

Particulate Matter Exposure and Stress Hormone Levels

et al. 2017

View full text Add to dashboard Cite

BACKGROUND:Exposure to ambient particulate matter (PM) is associated with a number of adverse health outcomes, but potential mechanisms are largely unknown. Metabolomics represents a powerful approach to study global metabolic changes in response to environmental exposures. We therefore conducted this study to investigate changes in serum metabolites in response to the reduction of PM exposure among healthy college students. METHODS:We conducted a randomized, double-blind crossover trial in 55 healthy college students in Shanghai, China. Real and sham air purifiers were placed in participants' dormitories in random order for 9 days with a 12-day washout period. Serum metabolites were quantified by using gas chromatography-mass spectrometry and ultrahigh performance liquid chromatography-mass spectrometry. Between-treatment differences in metabolites were examined using orthogonal partial least square-discriminant analysis and mixed-effect models. Secondary outcomes include blood pressure, corticotropin-releasing hormone, adrenocorticotropic hormone, insulin resistance, and biomarkers of oxidative stress and inflammation. RESULTS:The average personal exposure to PMs with aerodynamic diameters ≤2.5 μm was 24.3 μg/m 3 during the real purification and 53.1 μg/m 3 during the sham purification. Metabolomics analysis showed that higher exposure to PMs with aerodynamic diameters ≤2.5 μm led to significant increases in cortisol, cortisone, epinephrine, and norepinephrine. Between-treatment differences were also observed for glucose, amino acids, fatty acids, and lipids. We found significantly higher blood pressure, hormones, insulin resistance, and biomarkers of oxidative stress and inflammation among individuals exposed to higher PMs with aerodynamic diameters ≤2.5 μm. CONCLUSIONS:This study suggests that higher PM may induce metabolic alterations that are consistent with activations of the hypothalamuspituitary-adrenal and sympathetic-adrenal-medullary axes, adding potential mechanistic insights into the adverse health outcomes associated with PM. Furthermore, our study demonstrated short-term reductions in stress hormone following indoor air purification. ORIGINAL RESEARCH ARTICLE C onvincing epidemiological evidence suggests that exposure to higher levels of ambient particulate matters (PMs), especially fine PMs with aerodynamic diameters ≤2.5 μm (PM 2.5 ), may have adverse cardiovascular and metabolic consequences such as hypertension, coronary heart disease, stroke, and diabetes mellitus. CLINICAL TRIAL REGISTRATION:1-4 Although potential biological mechanisms for these adverse health effects are yet to be fully ascertained, inflammation and oxidative stress are likely to be involved. [5][6][7] In addition, several studies have reported an association between PM exposure and dysfunction of the automatic nervous system, which is known to increase cardiovascular risk. [8][9][10] Animal studies further implicated PM 2.5 as a stressor to the central nervous system that might induce a cascade of neuroendocrine responses...

show abstract

mentioning

confidence: 99%

Particulate Matter Exposure and Stress Hormone Levels

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Accumulation of lipid peroxidation products in vascular walls promotes disruption of vulnerable plaques,33, 34 which likely contributes to the risk of acute cardiovascular events. Some,14, 15, 16 but not all,17, 18 prior studies have found an association between short‐term air pollution and plasma myeloperoxidase. Ruckerl et al found higher myeloperoxidase levels were associated with the BC, NO, NO 2 , and PM 2.5 within 5 days in a group of potentially genetically susceptible participants who were free of type 2 diabetes or impaired glucose tolerance 14.…”

Section: Discussionmentioning

confidence: 95%

“…Some,14, 15, 16 but not all,17, 18 prior studies have found an association between short‐term air pollution and plasma myeloperoxidase. Ruckerl et al found higher myeloperoxidase levels were associated with the BC, NO, NO 2 , and PM 2.5 within 5 days in a group of potentially genetically susceptible participants who were free of type 2 diabetes or impaired glucose tolerance 14. However, Delfino et al reported no association between measured air pollutants and myeloperoxidase among 29 nonsmoking elderly participants with a history of coronary artery disease 17…”

Section: Discussionmentioning

confidence: 95%

See 1 more Smart Citation

Short‐Term Exposure to Air Pollution and Biomarkers of Oxidative Stress: The Framingham Heart Study

Wilker

Dorans

et al. 2016

JAHA

122

View full text Add to dashboard Cite

BackgroundShort‐term exposure to elevated air pollution has been associated with higher risk of acute cardiovascular diseases, with systemic oxidative stress induced by air pollution hypothesized as an important underlying mechanism. However, few community‐based studies have assessed this association.Methods and ResultsTwo thousand thirty‐five Framingham Offspring Cohort participants living within 50 km of the Harvard Boston Supersite who were not current smokers were included. We assessed circulating biomarkers of oxidative stress including blood myeloperoxidase at the seventh examination (1998–2001) and urinary creatinine‐indexed 8‐epi‐prostaglandin F2α (8‐epi‐PGF 2α) at the seventh and eighth (2005–2008) examinations. We measured fine particulate matter (PM 2.5), black carbon, sulfate, nitrogen oxides, and ozone at the Supersite and calculated 1‐, 2‐, 3‐, 5‐, and 7‐day moving averages of each pollutant. Measured myeloperoxidase and 8‐epi‐PGF 2α were loge transformed. We used linear regression models and linear mixed‐effects models with random intercepts for myeloperoxidase and indexed 8‐epi‐PGF 2α, respectively. Models were adjusted for demographic variables, individual‐ and area‐level measures of socioeconomic position, clinical and lifestyle factors, weather, and temporal trend. We found positive associations of PM 2.5 and black carbon with myeloperoxidase across multiple moving averages. Additionally, 2‐ to 7‐day moving averages of PM 2.5 and sulfate were consistently positively associated with 8‐epi‐PGF 2α. Stronger positive associations of black carbon and sulfate with myeloperoxidase were observed among participants with diabetes than in those without.ConclusionsOur community‐based investigation supports an association of select markers of ambient air pollution with circulating biomarkers of oxidative stress.

show abstract

“…30 The third (and most plausible hypothesis) is predicated on the premise that airborne particulates enter the bloodstream where they may then interact with tissue components to promote the observed pathologic effects 30,31 ; the latter is supported by emerging evidence suggesting that inhaled inert gold nanoparticles not only enter the bloodstream of healthy adult volunteers, but are detected in the urine within minutes after exposure, providing a proof of concept that inhaled nanoparticles get filtered and excreted by the kidney. 31 These three hypotheses provide contextual background to evaluate the experimental and clinical findings describing the extrapulmonary effect of particulate matter air pollution, where it has been reported that exposure to elevated levels of PM 2.5 is associated with increased inflammatory mediators (including TNF-a, IL-6, and plasminogen activator inhibitor-1), oxidative stress, [32][33][34] increased atherosclerotic plaque area, and exaggerated vasoconstrictor responses to phenylephrine and serotonin. 35 Evidence suggests that increased PM 2.5 concentrations are associated with significant decrease in flow-mediated dilatation, 36,37 increases in systolic BP and pulse pressure, [38][39][40] and disturbances in the hypothalamic-pituitary-adrenal axis.…”

Section: Discussionmentioning

confidence: 99%

Particulate Matter Air Pollution and the Risk of Incident CKD and Progression to ESRD

Bowe¹,

Xie²,

Li³

et al. 2017

JASN

266

236

View full text Add to dashboard Cite

Elevated levels of fine particulate matter ,2.5 mm in aerodynamic diameter (PM 2.5 ) are associated with increased risk of cardiovascular outcomes and death, but their association with risk of CKD and ESRD is unknown. We linked the Environmental Protection Agency and the Department of Veterans Affairs databases to build an observational cohort of 2,482,737 United States veterans, and used survival models to evaluate the association of PM 2.5 concentrations and risk of incident eGFR ,60 ml/min per 1.73 m 2 , incident CKD, eGFR decline $30%, and ESRD over a median follow-up of 8.52 years. In time-varying analyses, a 10-mg/m 3 increase in PM 2.5 concentration was associated with similarly increased risk of eGFR,60 ml/min per 1.73 m 2 , CKD, eGFR decline $30%, and ESRD. Spline analyses showed a linear relationship between PM 2.5 concentrations and risk of kidney outcomes. Exposure estimates derived from National Aeronautics and Space Administration satellite data yielded consistent results. Our findings demonstrate a significant association between exposure to PM 2.5 and risk of incident CKD, eGFR decline, and ESRD.

show abstract

Associations between ambient air pollution and blood markers of inflammation and coagulation/fibrinolysis in susceptible populations

Cited by 135 publications

References 72 publications

Particulate Matter Exposure and Stress Hormone Levels

Particulate Matter Exposure and Stress Hormone Levels

Short‐Term Exposure to Air Pollution and Biomarkers of Oxidative Stress: The Framingham Heart Study

Particulate Matter Air Pollution and the Risk of Incident CKD and Progression to ESRD

Contact Info

Product

Resources

About