Effects of ozone and fine particulate matter (PM2.5) on rat system inflammation and cardiac function

Wang, Guanghe; Jiang, Rongfang; Zhao, Zhuohui; Song, Weimin

doi:10.1016/j.toxlet.2012.11.009

Cited by 119 publications

(71 citation statements)

References 46 publications

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“…While these results corroborate both our previous findings and those of others (Barath et al, 2013; Farraj et al, 2012; Farraj et al, 2015; Wang et al, 2013; Wu et al, 2010) they also highlight the fact that the cardiovascular response to low level or near-ambient ozone is quite variable and requires further investigation. We assumed a role for TRPA1 given the findings of Taylor-Clark and Undem (Taylor-Clark and Undem, 2006) who showed activation of TRPA1 on airway C-fibers by high concentrations of ozone (approximately 7.2 ppm) in an ex-vivo system.…”

Section: Discussionsupporting

confidence: 92%

“…Acrolein produced abnormal modulation of autonomic balance and an increased incidence of arrhythmia through TRPA1, which also mediated an increase in LVDP. In contrast, exposure to ozone did not appear to cause any significant effects despite the fact that mild cardiovascular effects of ozone at similar levels have been documented by our lab in the past and by others (Barath et al, 2013; Farraj et al, 2012; Farraj et al, 2015; Kurhanewicz et al, 2014; Wang et al, 2013; Wu et al, 2010). …”

Section: Discussionsupporting

confidence: 61%

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TRPA1 mediates changes in heart rate variability and cardiac mechanical function in mice exposed to acrolein

Kurhanewicz

McIntosh-Kastrinsky

Tong

et al. 2017

Toxicology and Applied Pharmacology

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Short-term exposure to ambient air pollution is linked with adverse cardiovascular effects. While previous research focused primarily on particulate matter-induced responses, gaseous air pollutants also contribute to cause short-term cardiovascular effects. Mechanisms underlying such effects have not been adequately described, however the immediate nature of the response suggests involvement of irritant neural activation and downstream autonomic dysfunction. Thus, this study examines the role of TRPA1, an irritant sensory receptor found in the airways, in the cardiac response of mice to acrolein and ozone. Conscious unrestrained wild-type C57BL/6 (WT) and TRPA1 knockout (KO) mice implanted with radiotelemeters were exposed once to 3 ppm acrolein, 0.3 ppm ozone, or filtered air. Heart rate (HR) and electrocardiogram (ECG) were recorded continuously before, during and after exposure. Analysis of ECG morphology, incidence of arrhythmia and heart rate variability (HRV) were performed. Cardiac mechanical function was assessed using a Langendorff perfusion preparation 24 h post-exposure. Acrolein exposure increased HRV independent of HR, as well as incidence of arrhythmia. Acrolein also increased left ventricular developed pressure in WT mice at 24 h post-exposure. Ozone did not produce any changes in cardiac function. Neither gas produced ECG effects, changes in HRV, arrhythmogenesis, or mechanical function in KO mice. These data demonstrate that a single exposure to acrolein causes cardiac dysfunction through TRPA1 activation and autonomic imbalance characterized by a shift toward parasympathetic modulation. Furthermore, it is clear from the lack of ozone effects that although gaseous irritants are capable of eliciting immediate cardiac changes, gas concentration and properties play important roles.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 61%

TRPA1 mediates changes in heart rate variability and cardiac mechanical function in mice exposed to acrolein

Kurhanewicz

McIntosh-Kastrinsky

Tong

et al. 2017

Toxicology and Applied Pharmacology

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“…To investigate whether the heart injury induced by PM 2.5 was in relation with the increased inflammatory activity, we measured expression of the pro-inflammatory cytokines, such as TNF-α, IL-6 and IL-1β, which are known to be elevated in the serum of heart disease patients [38]. reported that PM 2.5 deposition and myocardial inflammation were 15 observed in high-dose PM 2.5 rats (3.2 mg PM 2.5 /rat) in cardiac histopathology results, along with significant increases of TNF-α and IL-6 levels in rat serum [39]. Kvietys and Granger (2012) reviewed the reactive oxygen and nitrogen species contributed significantly to the diverse vascular responses in inflammation [40].…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial damage: An important mechanism of ambient PM2.5 exposure-induced acute heart injury in rats

Kou

Geng

et al. 2015

Journal of Hazardous Materials

139

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“…PM 2.5 and PM 10 are a major threat to children because of their higher exposure to ambient PM, mostly when involved in outdoor activities as compared to adults and because of their immature state of the lung and immune system function [72,76]. In addition to ENX and TMET, other particle pollutants such as PAH, NO 2 , SO 2 , and O 3 have also been associated with the pathogenesis of asthma and the increase of ER visits and hospitalizations of children; inflammation and oxidative stress are considered the major factors responsible for such adverse conditions [48,53,77-78]. A recent report has suggested an epigenetic and genetic variant in ADCYAP1R1 associated with asthma in Puerto Rican children [79].…”

Section: Discussionmentioning

confidence: 99%

African Dust Storms Reaching Puerto Rican Coast Stimulate the Secretion of IL-6 and IL-8 and Cause Cytotoxicity to Human Bronchial Epithelial Cells (BEAS-2B)

Rodríguez-Cotto¹,

Ortiz-Martínez²,

Rivera-Ramírez³

et al. 2013

Health

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African dust storm events (ADE) travel across the Atlantic Ocean (ADEAO) and reach the Puerto Rican coast (ADEPRC), potentially impacting air quality and human health. To what extent seasonal variations in atmospheric particulate matter (PM) size fractions, composition and sources trigger respiratory-adverse effects to Puerto Ricans is still unclear. In the present study, we investigated the pro-inflammatory and cytotoxic effects of PM samples harvested during ADEAO (PM10), ADEPRC (PM2.5 and PM10) and Non-ADE (Preand Post-ADEAO and Non-ADEPRC), using BEAS-2B cells. Endotoxins (ENX) in PM2.5 and PM10 extracts and traces of metals (TMET) in PM2.5 extracts were also examined. IL-6 and IL-8 secretion and cytotoxicity were used as endpoints. ADEAO and ADEPRC extracts were found to be more cytotoxic than Non-ADE and ADEAO were more toxic than ADEPRC extracts. PM10 extracts from ADEAO and Post-ADEAO caused significant secretion of IL-8. IL-6 and IL-8 secretion was higher following treatment with PM10 and PM2.5 ADEPRC than with Non-ADEPRC extracts. ENX levels were found to be higher in PM10 ADEAO than in the rest of the samples tested. TMET levels were higher in PM2.5 ADEPRC than in Non-ADEPRC extracts. Deferoxamine significantly reduced cytotoxicity and IL-6 and IL-8 secretion whereas Polymyxin B did not. TMET in PM2.5 fractions is a major determinant in ADEPRC-induced toxicity and work in conjunction with ENX to cause toxicity to lung cells in vitro. ENX and TMET may be responsible, in part, for triggering PM-respiratory adverse responses in susceptible and predisposed individuals.

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Effects of ozone and fine particulate matter (PM2.5) on rat system inflammation and cardiac function

Cited by 119 publications

References 46 publications

TRPA1 mediates changes in heart rate variability and cardiac mechanical function in mice exposed to acrolein

TRPA1 mediates changes in heart rate variability and cardiac mechanical function in mice exposed to acrolein

Mitochondrial damage: An important mechanism of ambient PM2.5 exposure-induced acute heart injury in rats

African Dust Storms Reaching Puerto Rican Coast Stimulate the Secretion of IL-6 and IL-8 and Cause Cytotoxicity to Human Bronchial Epithelial Cells (BEAS-2B)

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