Pulmonary exposure to peat smoke extracts in rats decreases expiratory time and increases left heart end systolic volume

References

• Abatzoglou JT, Williams AP. (2016). Impact of anthropogenic climate change on wildfire across western US forests. Proc Natl Acad Sci USA 113:11770–5.
   PubMed Web of Science ®Google Scholar
• Argacha JF, Bourdrel T, van de Borne P. (2017). Ecology of the cardiovascular system: A focus on air-related environmental factors. Trends Cardiovasc Med 28:112–26.
   PubMed Web of Science ®Google Scholar
• Baker KR, Woody MC, Valin L, et al. (2018). Photochemical model evaluation of 2013 California wild fire air quality impacts using surface, aircraft, and satellite data. Sci Total Environ 637–638:1137–49.
   PubMed Web of Science ®Google Scholar
• Brook RD, Rajagopalan S, Pope CA, 3rd, et al. (2010). Particulate matter air pollution and cardiovascular disease: an update to the scientific statement from the American Heart Association. Circulation 121:2331–78.
   PubMed Web of Science ®Google Scholar
• Carll AP, Haykal-Coates N, Winsett DW, et al. (2015). Cardiomyopathy confers susceptibility to particulate matter-induced oxidative stress, vagal dominance, arrhythmia and pulmonary inflammation in heart failure-prone rats. Inhal Toxicol 27:100–12.
   PubMed Web of Science ®Google Scholar
• Carll AP, Hazari MS, Perez CM, et al. (2013). An autonomic link between inhaled diesel exhaust and impaired cardiac performance: insight from treadmill and dobutamine challenges in heart failure-prone rats. Toxicol Sci 135:425–36.
   PubMed Web of Science ®Google Scholar
• Cascio WE. (2016). Proposed pathophysiologic framework to explain some excess cardiovascular death associated with ambient air particle pollution: insights for public health translation. Biochim Biophys Acta 1860:2869–79.
   PubMed Web of Science ®Google Scholar
• Chan EA, Buckley B, Farraj AK, Thompson LC. (2016). The heart as an extravascular target of endothelin-1 in particulate matter-induced cardiac dysfunction. Pharmacol Ther 165:63–78.
   PubMed Web of Science ®Google Scholar
• Cheng DC, Edelist G. (1988). Isoflurane and primary pulmonary hypertension. Anaesthesia 43:22–4.
   PubMed Web of Science ®Google Scholar
• Christou H, Reslan OM, Mam V, et al. (2012). Improved pulmonary vascular reactivity and decreased hypertrophic remodeling during nonhypercapnic acidosis in experimental pulmonary hypertension. Am J Physiol Lung Cell Mol Physiol 302:L875–90.
   PubMed Web of Science ®Google Scholar
• Cohen J. (1988). Statistical power analysis for the behavioral sciences. 2nd ed. Hillsdale, NJ: L. Erlbaum Associates.
   Google Scholar
• Deweirdt J, Quignard JF, Crobeddu B, et al. (2017). Involvement of oxidative stress and calcium signaling in airborne particulate matter - induced damages in human pulmonary artery endothelial cells. Toxicol In Vitro 45:340–50.
   PubMed Web of Science ®Google Scholar
• Emiroglu Y, Kargin R, Kargin F, et al. (2010). BNP levels in patients with long-term exposure to biomass fuel and its relation to right ventricular function. Pulm Pharmacol Ther 23:420–4.
   PubMed Web of Science ®Google Scholar
• Ewalenko P, Brimioulle S, Delcroix M, et al. (1997). Comparison of the effects of isoflurane with those of propofol on pulmonary vascular impedance in experimental embolic pulmonary hypertension. Br J Anaesth 79:625–30.
   PubMed Web of Science ®Google Scholar
• Farraj AK, Hazari MS, Winsett DW, et al. (2012). Overt and latent cardiac effects of ozone inhalation in rats: evidence for autonomic modulation and increased myocardial vulnerability. Environ Health Perspect 120:348–54.
   PubMed Web of Science ®Google Scholar
• Farraj AK, Walsh L, Haykal-Coates N, et al. (2015). Cardiac effects of seasonal ambient particulate matter and ozone co-exposure in rats. Part Fibre Toxicol 6:12.
   Google Scholar
• Gambone LM, Murray PA, Flavahan NA. (1997). Isoflurane anesthesia attenuates endothelium-dependent pulmonary vasorelaxation by inhibiting the synergistic interaction between nitric oxide and prostacyclin. Anesthesiology 86:936–44.
   PubMed Web of Science ®Google Scholar
• Gaveau DL, Salim MA, Hergoualc'h K, et al. (2014). Major atmospheric emissions from peat fires in Southeast Asia during non-drought years: evidence from the 2013 Sumatran fires. Scientific Reports 4:6112.
   PubMed Web of Science ®Google Scholar
• Gidding SS, Xie X, Liu K, et al. (1995). Cardiac function in smokers and nonsmokers: the CARDIA study. The Coronary Artery Risk Development in Young Adults Study. J Am Coll Cardiol 26:211–6.
   PubMed Web of Science ®Google Scholar
• Gorr MW, Youtz DJ, Eichenseer CM, et al. (2015). In vitro particulate matter exposure causes direct and lung-mediated indirect effects on cardiomyocyte function. Am J Physiol Heart Circ Physiol 309:H53–62.
   PubMed Web of Science ®Google Scholar
• Haikerwal A, Akram M, Del Monaco A, et al. (2015). Impact of fine particulate matter (PM2.5) exposure during wildfires on cardiovascular health outcomes. J Am Heart Assoc. doi: 10.1161/JAHA.114.001653.
   PubMed Web of Science ®Google Scholar
• Hayasaka H, Noguchi I, Putra EI, et al. (2014). Peat-fire-related air pollution in Central Kalimantan, Indonesia. Environ Pollut 195:257–66.
   PubMed Web of Science ®Google Scholar
• Hazari MS, Haykal-Coates N, Winsett DW, et al. (2011). TRPA1 and sympathetic activation contribute to increased risk of triggered cardiac arrhythmias in hypertensive rats exposed to diesel exhaust. Environ Health Perspect 119:951–7.
   PubMed Web of Science ®Google Scholar
• Horne BD, Joy EA, Hofmann MG, et al. (2018). Short-term elevation of fine particulate matter air pollution and acute lower respiratory infection. Am J Respir Critical Care Med 198:759–66.
   PubMed Web of Science ®Google Scholar
• Ilgenli TF, Akpinar O. (2007). Acute effects of smoking on right ventricular function. A tissue Doppler imaging study on healthy subjects. Swiss Med Wkly 137:91–6.
   PubMed Web of Science ®Google Scholar
• Kelly FJ, Fussell JC. (2017). Role of oxidative stress in cardiovascular disease outcomes following exposure to ambient air pollution. Free Radic Biol Med 110:345–67.
   PubMed Web of Science ®Google Scholar
• Kim YH, Tong H, Daniels M, et al. (2014). Cardiopulmonary toxicity of peat wildfire particulate matter and the predictive utility of precision cut lung slices. Part Fibre Toxicol 11:29.
   PubMed Web of Science ®Google Scholar
• Kim YH, Warren SH, Krantz QT, et al. (2018). Mutagenicity and lung toxicity of smoldering vs. flaming emissions from various biomass fuels: implications for health effects from wildland fires. Environ Health Perspect 126:017011.
   PubMed Web of Science ®Google Scholar
• Kou YR, Lai CJ. (1994). Reflex changes in breathing pattern evoked by inhalation of wood smoke in rats. J Appl Physiol 76:2333–41.
   PubMed Web of Science ®Google Scholar
• Kurhanewicz N, McIntosh-Kastrinsky R, Tong H, et al. (2017). TRPA1 mediates changes in heart rate variability and cardiac mechanical function in mice exposed to acrolein. Toxicol Appl Pharmacol 324:51–60.
   PubMed Web of Science ®Google Scholar
• Landis MS, Edgerton ES, White EM, et al. (2018). The impact of the 2016 fort McMurray Horse river wildfire on ambient air pollution levels in the Athabasca oil sands region, Alberta, Canada. Sci Total Environ 618:1665–76.
   PubMed Web of Science ®Google Scholar
• Laurance SG, Laurance WF. (2015). Peat fires: emissions likely to worsen. Nature 527:305.
   PubMed Web of Science ®Google Scholar
• Levy PT, Patel MD, Groh G, et al. (2016). Pulmonary artery acceleration time provides a reliable estimate of invasive pulmonary hemodynamics in children. J Am Soc Echocardiogr 29:1056–65.
   PubMed Web of Science ®Google Scholar
• Liu J, Ye X, Ji D, et al. (2018). Diesel exhaust inhalation exposure induces pulmonary arterial hypertension in mice. Environ Pollut 237:747–55.
   PubMed Web of Science ®Google Scholar
• Lumb AB, Slinger P. (2015). Hypoxic pulmonary vasoconstriction: physiology and anesthetic implications. Anesthesiology 122:932–46.
   PubMed Web of Science ®Google Scholar
• McGuinn LA, Ward-Caviness C, Neas LM, et al. (2017). Fine particulate matter and cardiovascular disease: comparison of assessment methods for long-term exposure. Environ Res 159:16–23.
   PubMed Web of Science ®Google Scholar
• Naeije R, Manes A. (2014). The right ventricle in pulmonary arterial hypertension. Eur Respir Rev 23:476–87.
   PubMedGoogle Scholar
• Newby DE, Mannucci PM, Tell GS, et al. (2015). Expert position paper on air pollution and cardiovascular disease. ESC Working Group on Thrombosis, European Association for Cardiovascular Prevention and Rehabilitation; ESC Heart Failure Association. Eur Heart J 36:83–93b.
   PubMed Web of Science ®Google Scholar
• Nielsen GD, Hougaard KS, Larsen ST, et al. (1999). Acute airway effects of formaldehyde and ozone in BALB/c mice. Hum Exp Toxicol 18:400–9.
   PubMed Web of Science ®Google Scholar
• Page SE, Hooijer A. (2016). In the line of fire: the peatlands of Southeast Asia. Philos Trans R Soc Lond B, Biol Sci. doi: 10.1098/rstb.2015.0176.
   Web of Science ®Google Scholar
• Perez CM, Hazari MS, Farraj AK. (2015a). Role of autonomic reflex arcs in cardiovascular responses to air pollution exposure. Cardiovasc Toxicol 15:69–78.
   PubMed Web of Science ®Google Scholar
• Perez CM, Hazari MS, Ledbetter AD, et al. (2015b). Acrolein inhalation alters arterial blood gases and triggers carotid body-mediated cardiovascular responses in hypertensive rats. Inhal Toxicol 27:54–63.
   PubMed Web of Science ®Google Scholar
• Rappold AG, Stone SL, Cascio WE, et al. (2011). Peat bog wildfire smoke exposure in rural North Carolina is associated with cardiopulmonary emergency department visits assessed through syndromic surveillance. Environ Health Perspect 119:1415–20.
   PubMed Web of Science ®Google Scholar
• Reid CE, Brauer M, Johnston FH, et al. (2016). Critical review of health impacts of wildfire smoke exposure. Environ Health Perspect 124:1334–43.
   PubMed Web of Science ®Google Scholar
• Robinson RK, Birrell MA, Adcock JJ, et al. (2018). Mechanistic link between diesel exhaust particles and respiratory reflexes. J Allergy Clin Immunol 141:1074–84.e1079.
   PubMed Web of Science ®Google Scholar
• Sequeira V, van der Velden J. (2017). The Frank–Starling Law: a jigsaw of titin proportions. Biophys Rev 9:259–67.
   PubMedGoogle Scholar
• Simkhovich BZ, Kleinman MT, Kloner RA. (2008). Air pollution and cardiovascular injury epidemiology, toxicology, and mechanisms. J Am Coll Cardiol 52:719–26.
   PubMed Web of Science ®Google Scholar
• Sommer N, Strielkov I, Pak O, Weissmann N. (2016). Oxygen sensing and signal transduction in hypoxic pulmonary vasoconstriction. Eur Respir J 47:288–303.
   PubMed Web of Science ®Google Scholar
• Tei C, Ling LH, Hodge DO, et al. (1995). New index of combined systolic and diastolic myocardial performance: a simple and reproducible measure of cardiac function-a study in normals and dilated cardiomyopathy. J Cardiol 26:357–66.
   PubMedGoogle Scholar
• Thibault HB, Kurtz B, Raher MJ, et al. (2010). Noninvasive assessment of murine pulmonary arterial pressure: validation and application to models of pulmonary hypertension. Circ Cardiovasc Imaging 3:157–63.
   PubMed Web of Science ®Google Scholar
• Thompson LC, Ledbetter AD, Haykal-Coates N, et al. (2017). Acrolein inhalation alters myocardial synchrony and performance at and below exposure concentrations that cause ventilatory responses. Cardiovasc Toxicol 17:97–108.
   PubMed Web of Science ®Google Scholar
• Tinling MA, West JJ, Cascio WE, et al. (2016). Repeating cardiopulmonary health effects in rural North Carolina population during a second large peat wildfire. Environ Health 15:12.
   PubMed Web of Science ®Google Scholar
• Urbancok D, Payne AJR, Webster RD. (2017). Regional transport, source apportionment and health impact of PM10 bound polycyclic aromatic hydrocarbons in Singapore's atmosphere. Environ Pollut 229:984–93.
   PubMed Web of Science ®Google Scholar
• Wang YC, Huang CH, Tu YK. (2018). Pulmonary hypertension and pulmonary artery acceleration time: a systematic review and meta-analysis. J Am Soc Echocardiogr 31:201–10.
   PubMed Web of Science ®Google Scholar
• Wauters A, Vicenzi M, De Becker B, et al. (2015). At high cardiac output, diesel exhaust exposure increases pulmonary vascular resistance and decreases distensibility of pulmonary resistive vessels. Am J Physiol Heart Circ Physiol 309:H2137–44.
   PubMed Web of Science ®Google Scholar
• Westerling AL, Hidalgo HG, Cayan DR, Swetnam TW. (2006). Warming and earlier spring increase western U.S. forest wildfire activity. Science (New York, NY) 313:940–3.
   Google Scholar