Comparative Cardiopulmonary Effects of Particulate Matter- And Ozone-Enhanced Smog Atmospheres in Mice

This study was conducted to compare the cardiac effects of particulate matter (PM)- (SA-PM) and ozone­(O3)-enhanced (SA-O3) smog atmospheres in mice. Based on our previous findings of filtered diesel exhaust we hypothesized that SA-O3 would cause greater cardiac dysfunction than SA-PM. Radiotelemete...

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Published inEnvironmental science & technology Vol. 52; no. 5; pp. 3071 - 3080
Main Authors Hazari, Mehdi S, Stratford, Kimberly M, Krantz, Q. Todd, King, Charly, Krug, Jonathan, Farraj, Aimen K, Gilmour, M. Ian
Format Journal Article
LanguageEnglish
Published United States American Chemical Society 06.03.2018
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Abstract This study was conducted to compare the cardiac effects of particulate matter (PM)- (SA-PM) and ozone­(O3)-enhanced (SA-O3) smog atmospheres in mice. Based on our previous findings of filtered diesel exhaust we hypothesized that SA-O3 would cause greater cardiac dysfunction than SA-PM. Radiotelemetered mice were exposed to either SA-PM, SA-O3, or filtered air (FA) for 4 h. Heart rate (HR) and electrocardiogram were recorded continuously before, during and after exposure. Both SA-PM and SA-O3 increased heart rate variability (HRV) but only SA-PM increased HR. Normalization of responses to total hydrocarbons, gas-only hydrocarbons and PM concentration were performed to assess the relative contribution of each phase given the compositional variability. Normalization to PM concentration revealed that SA-O3 was more potent in increasing HRV, arrhythmogenesis, and causing ventilatory changes. However, there were no differences when the responses were normalized to total or gas-phase only hydrocarbons. Thus, this study demonstrates that a single exposure to smog causes cardiac effects in mice. Although the responses of SA-PM and SA-O3 are similar, the latter is more potent in causing electrical disturbances and breathing changes potentially due to the effects of irritant gases, which should therefore be accounted for more rigorously in health assessments.
AbstractList This study was conducted to compare the cardiac effects of particulate matter (PM)- (SA-PM) and ozone(O )-enhanced (SA-O ) smog atmospheres in mice. Based on our previous findings of filtered diesel exhaust we hypothesized that SA-O would cause greater cardiac dysfunction than SA-PM. Radiotelemetered mice were exposed to either SA-PM, SA-O , or filtered air (FA) for 4 h. Heart rate (HR) and electrocardiogram were recorded continuously before, during and after exposure. Both SA-PM and SA-O increased heart rate variability (HRV) but only SA-PM increased HR. Normalization of responses to total hydrocarbons, gas-only hydrocarbons and PM concentration were performed to assess the relative contribution of each phase given the compositional variability. Normalization to PM concentration revealed that SA-O was more potent in increasing HRV, arrhythmogenesis, and causing ventilatory changes. However, there were no differences when the responses were normalized to total or gas-phase only hydrocarbons. Thus, this study demonstrates that a single exposure to smog causes cardiac effects in mice. Although the responses of SA-PM and SA-O are similar, the latter is more potent in causing electrical disturbances and breathing changes potentially due to the effects of irritant gases, which should therefore be accounted for more rigorously in health assessments.
This study was conducted to compare the cardiac effects of particulate matter (PM)- (SA-PM) and ozone­(O3)-enhanced (SA-O3) smog atmospheres in mice. Based on our previous findings of filtered diesel exhaust we hypothesized that SA-O3 would cause greater cardiac dysfunction than SA-PM. Radiotelemetered mice were exposed to either SA-PM, SA-O3, or filtered air (FA) for 4 h. Heart rate (HR) and electrocardiogram were recorded continuously before, during and after exposure. Both SA-PM and SA-O3 increased heart rate variability (HRV) but only SA-PM increased HR. Normalization of responses to total hydrocarbons, gas-only hydrocarbons and PM concentration were performed to assess the relative contribution of each phase given the compositional variability. Normalization to PM concentration revealed that SA-O3 was more potent in increasing HRV, arrhythmogenesis, and causing ventilatory changes. However, there were no differences when the responses were normalized to total or gas-phase only hydrocarbons. Thus, this study demonstrates that a single exposure to smog causes cardiac effects in mice. Although the responses of SA-PM and SA-O3 are similar, the latter is more potent in causing electrical disturbances and breathing changes potentially due to the effects of irritant gases, which should therefore be accounted for more rigorously in health assessments.
This study was conducted to compare the cardiac effects of particulate matter (PM)- (SA-PM) and ozone(O3)-enhanced (SA-O3) smog atmospheres in mice. Based on our previous findings of filtered diesel exhaust we hypothesized that SA-O3 would cause greater cardiac dysfunction than SA-PM. Radiotelemetered mice were exposed to either SA-PM, SA-O3, or filtered air (FA) for 4 h. Heart rate (HR) and electrocardiogram were recorded continuously before, during and after exposure. Both SA-PM and SA-O3 increased heart rate variability (HRV) but only SA-PM increased HR. Normalization of responses to total hydrocarbons, gas-only hydrocarbons and PM concentration were performed to assess the relative contribution of each phase given the compositional variability. Normalization to PM concentration revealed that SA-O3 was more potent in increasing HRV, arrhythmogenesis, and causing ventilatory changes. However, there were no differences when the responses were normalized to total or gas-phase only hydrocarbons. Thus, this study demonstrates that a single exposure to smog causes cardiac effects in mice. Although the responses of SA-PM and SA-O3 are similar, the latter is more potent in causing electrical disturbances and breathing changes potentially due to the effects of irritant gases, which should therefore be accounted for more rigorously in health assessments.
Author Krantz, Q. Todd
Stratford, Kimberly M
Farraj, Aimen K
Krug, Jonathan
King, Charly
Hazari, Mehdi S
Gilmour, M. Ian
AuthorAffiliation Curriculum in Toxicology
U.S. Environmental Protection Agency
Cardiopulmonary and Immunotoxicology Branch, Environmental Public Health Division, National Health and Environmental Effects Research Laboratory
University of North Carolina − Chapel Hill
Inhalation Toxicology Facilities Branch, Environmental Public Health Division, National Health and Environmental Effects Research Laboratory
Exposure Methods and Measurement Division, National Exposure Research Laboratory
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– name: Inhalation Toxicology Facilities Branch, Environmental Public Health Division, National Health and Environmental Effects Research Laboratory
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– name: 3 Inhalation Toxicology Facilities Branch, Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
– name: 1 Cardiopulmonary and Immunotoxicology Branch, Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
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Snippet This study was conducted to compare the cardiac effects of particulate matter (PM)- (SA-PM) and ozone­(O3)-enhanced (SA-O3) smog atmospheres in mice. Based on...
This study was conducted to compare the cardiac effects of particulate matter (PM)- (SA-PM) and ozone(O )-enhanced (SA-O ) smog atmospheres in mice. Based on...
This study was conducted to compare the cardiac effects of particulate matter (PM)- (SA-PM) and ozone(O3)-enhanced (SA-O3) smog atmospheres in mice. Based on...
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SubjectTerms Airborne particulates
Atmosphere
Atmospheres
Breathing
Comparative analysis
Diesel engines
EKG
Exposure
Gases
Heart diseases
Heart rate
Hydrocarbons
Mice
Ozone
Particulate emissions
Particulate matter
Particulates
Rodents
Smog
Variability
Title Comparative Cardiopulmonary Effects of Particulate Matter- And Ozone-Enhanced Smog Atmospheres in Mice
URI http://dx.doi.org/10.1021/acs.est.7b04880
https://www.ncbi.nlm.nih.gov/pubmed/29388764
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