Ambient Particulate Matter and Acrolein Co-Exposure Increases Myocardial Dyssynchrony in Mice via TRPA1
We have examined the potential for interactive cardiovascular effects of repeated, intermittent co-exposure to concentrated ambient particulate matter (CAPs) and acrolein, and the potential role of transient receptor potential cation channel A1 (TRPA1), which we previously linked to air pollution-induced cardiac arrhythmogenesis. Chemical and source characteristics of collected particles was evaluated, as well as wind and weather patterns during exposure. Female B6129 mice and Trpa1-/- mice (n=6) were exposed to filtered air (FA), CAPs (46 µg/m3 of PM2.5 approximately 160 nm diameter), Acrolein (0.42 ppm) or CAPs+Acrolein for 3hrs/day, 2days/week, for 4 weeks. Cardiac strain data, heart function and dimensions, and transmitral blood flow were investigated with echocardiography (40 MHz) before exposures, 1 day after the first exposure, and 1 day after the final exposure. Several other biological endpoints were evaluated but the key findings from ultrasound echocardiography assessments were: elapsed time between peak strain in adjacent wall segments (i.e. myocardial strain delay), a measure of myocardial dyssynchrony, increased by ~5-fold in B6129 mice after the final exposure to CAPs+Acrolein when compared to strain delay in B6129 mice exposed to FA, CAPs, or Acrolein alone, and when compared to strain delay in Trpa1-/- mice exposed to CAPs+Acrolein. There were no changes after the first exposure in any group.
This dataset is associated with the following publication:
Thompson, L., L. Walsh, B. Martin, J. Mcgee, C. Wood, K. Kovalcik, P. Pancras, N. Coates, A. Ledbetter, D. Davies, W. Cascio, M. Higuchi, M. Hazari, and A. Farraj. Ambient Particulate Matter and Acrolein Co-Exposure Increases Myocardial Dyssynchrony in Mice: Evidence for TRPA1 Involvement. TOXICOLOGICAL SCIENCES. Society of Toxicology, RESTON, VA, 167(2): 559-572, (2019).
Complete Metadata
| accessLevel | public |
|---|---|
| bureauCode |
[
"020:00"
]
|
| contactPoint |
{
"fn": "Leslie Thompson",
"hasEmail": "mailto:thompson.leslie@epa.gov"
}
|
| description | We have examined the potential for interactive cardiovascular effects of repeated, intermittent co-exposure to concentrated ambient particulate matter (CAPs) and acrolein, and the potential role of transient receptor potential cation channel A1 (TRPA1), which we previously linked to air pollution-induced cardiac arrhythmogenesis. Chemical and source characteristics of collected particles was evaluated, as well as wind and weather patterns during exposure. Female B6129 mice and Trpa1-/- mice (n=6) were exposed to filtered air (FA), CAPs (46 µg/m3 of PM2.5 approximately 160 nm diameter), Acrolein (0.42 ppm) or CAPs+Acrolein for 3hrs/day, 2days/week, for 4 weeks. Cardiac strain data, heart function and dimensions, and transmitral blood flow were investigated with echocardiography (40 MHz) before exposures, 1 day after the first exposure, and 1 day after the final exposure. Several other biological endpoints were evaluated but the key findings from ultrasound echocardiography assessments were: elapsed time between peak strain in adjacent wall segments (i.e. myocardial strain delay), a measure of myocardial dyssynchrony, increased by ~5-fold in B6129 mice after the final exposure to CAPs+Acrolein when compared to strain delay in B6129 mice exposed to FA, CAPs, or Acrolein alone, and when compared to strain delay in Trpa1-/- mice exposed to CAPs+Acrolein. There were no changes after the first exposure in any group. This dataset is associated with the following publication: Thompson, L., L. Walsh, B. Martin, J. Mcgee, C. Wood, K. Kovalcik, P. Pancras, N. Coates, A. Ledbetter, D. Davies, W. Cascio, M. Higuchi, M. Hazari, and A. Farraj. Ambient Particulate Matter and Acrolein Co-Exposure Increases Myocardial Dyssynchrony in Mice: Evidence for TRPA1 Involvement. TOXICOLOGICAL SCIENCES. Society of Toxicology, RESTON, VA, 167(2): 559-572, (2019). |
| distribution |
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{
"title": "CAPs Acrolein Biological Data.xlsx",
"mediaType": "application/vnd.openxmlformats-officedocument.spreadsheetml.sheet",
"downloadURL": "https://pasteur.epa.gov/uploads/10.23719/1411215/CAPs%20Acrolein%20Biological%20Data.xlsx"
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"title": "CAPs Acrolein Chamber and Weather Values.xlsx",
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"title": "CAPs Acrolein Elemental Analysis.xlsx",
"mediaType": "application/vnd.openxmlformats-officedocument.spreadsheetml.sheet",
"downloadURL": "https://pasteur.epa.gov/uploads/10.23719/1411215/CAPs%20Acrolein%20Elemental%20Analysis.xlsx"
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"mediaType": "application/vnd.openxmlformats-officedocument.spreadsheetml.sheet",
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|
| identifier | https://doi.org/10.23719/1411215 |
| keyword |
[
"Ambient air quality",
"Fine Particulate Matter",
"TRPA1",
"acrolein",
"air pollution exposure",
"co-exposure",
"echocardiography",
"heart function",
"multiple pollutants",
"myocardial dyssynchrony",
"myocardial synchrony"
]
|
| license | https://pasteur.epa.gov/license/sciencehub-license.html |
| modified | 2017-12-11 |
| programCode |
[
"020:094"
]
|
| publisher |
{
"name": "U.S. EPA Office of Research and Development (ORD)",
"subOrganizationOf": {
"name": "U.S. Environmental Protection Agency",
"subOrganizationOf": {
"name": "U.S. Government"
}
}
}
|
| references |
[
"https://doi.org/10.1093/toxsci/kfy262"
]
|
| rights |
null
|
| title | Ambient Particulate Matter and Acrolein Co-Exposure Increases Myocardial Dyssynchrony in Mice via TRPA1 |