TY - JOUR
T1 - Variation in echocardiographic and cardiac hemodynamic effects of PM and ozone inhalation exposure in strains related to Nppa and Npr1 gene knock-out mice
AU - Tankersley, Clarke G.
AU - Peng, Roger D.
AU - Bedga, Djahida
AU - Gabrielson, Kathleen
AU - Champion, Hunter C.
N1 - Funding Information:
This study was supported in part by National Institute of Health Grants (NIA AG-21057) and the NIEHS center grant (P30 ES003819) at Johns Hopkins University Bloomberg School of Public Health.
PY - 2010/7
Y1 - 2010/7
N2 - Elevated levels of ambient co-pollutants are associated with adverse cardiovascular outcomes shown by epidemiology studies. The role of particulate matter (PM) and ozone (O3) as co-pollutants in this association is unclear. We hypothesize that cardiac function following PM and O3 exposure is variably affected by genetic determinants (Nppa and Npr1 genes) and age. Heart function was measured before and after 2 days each of the following exposure sequence; (1) 2-h filtered air (FA) and 3-h carbon black (CB; 0.5 g/m3); (2) 2-h O3 (0.6ppm) and 3-h FA; (3) 5-h FA; and, (4) 2-h O3 and 3-h CB. Two age groups (5 and 18 months old (mo)) were tested in C57Bl/6J (B6) and 129S1/SvImJ (129) mice using echocardiographic (echo) and in vivo hemodynamic (IVH) measurements. With echo, posterior wall thickness was significantly (P<0.01) greater in 129 relative to B6 mice at baseline. With CB exposure, young B6 and older 129 mice show significant (P<0.01) reductions in fractional shortening (FS) compared to FA. With O3 exposure, FS was significantly (P<0.01) diminished in young 129, which was attributable to significant increases in end-systolic left ventricular diameter. With O3 and CB combined, notable (P<0.01) declines in heart rate and end-systolic posterior wall thickness occurred in young 129 mice. The IVH measurements showed striking (P<0.05) compromises in cardiac function after CB and O3 exposure; however, strain differences were undetectable. These results suggest that PM and O3 exposures, alone and combined, lead to different cardiac functional changes, and these unique changes are age-specific and dependent on Nppa and Npr1 genes.
AB - Elevated levels of ambient co-pollutants are associated with adverse cardiovascular outcomes shown by epidemiology studies. The role of particulate matter (PM) and ozone (O3) as co-pollutants in this association is unclear. We hypothesize that cardiac function following PM and O3 exposure is variably affected by genetic determinants (Nppa and Npr1 genes) and age. Heart function was measured before and after 2 days each of the following exposure sequence; (1) 2-h filtered air (FA) and 3-h carbon black (CB; 0.5 g/m3); (2) 2-h O3 (0.6ppm) and 3-h FA; (3) 5-h FA; and, (4) 2-h O3 and 3-h CB. Two age groups (5 and 18 months old (mo)) were tested in C57Bl/6J (B6) and 129S1/SvImJ (129) mice using echocardiographic (echo) and in vivo hemodynamic (IVH) measurements. With echo, posterior wall thickness was significantly (P<0.01) greater in 129 relative to B6 mice at baseline. With CB exposure, young B6 and older 129 mice show significant (P<0.01) reductions in fractional shortening (FS) compared to FA. With O3 exposure, FS was significantly (P<0.01) diminished in young 129, which was attributable to significant increases in end-systolic left ventricular diameter. With O3 and CB combined, notable (P<0.01) declines in heart rate and end-systolic posterior wall thickness occurred in young 129 mice. The IVH measurements showed striking (P<0.05) compromises in cardiac function after CB and O3 exposure; however, strain differences were undetectable. These results suggest that PM and O3 exposures, alone and combined, lead to different cardiac functional changes, and these unique changes are age-specific and dependent on Nppa and Npr1 genes.
KW - Air pollution
KW - Atrial natriuretic peptide
KW - Cardiac structure and function
KW - Cardiopulmonary regulation
KW - Myocardial contractility
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U2 - 10.3109/08958378.2010.487549
DO - 10.3109/08958378.2010.487549
M3 - Article
C2 - 20540624
AN - SCOPUS:77953567993
SN - 0895-8378
VL - 22
SP - 695
EP - 707
JO - Inhalation Toxicology
JF - Inhalation Toxicology
IS - 8
ER -