Effects of concentrated ambient particles on heart rate, blood pressure, and cardiac contractility in spontaneously hypertensive rats during a dust storm event

Chuen-Chau Chang, Jing Shiang Hwang, Chang Chuan Chan, Peng Y. Wang, Tsun J. Cheng

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15 Citations (Scopus)


Epidemiological studies have suggested that cardiovascular mortality and morbidity increased during Asian dust events. The findings were still inconclusive though. We have shown an increased pulmonary toxicity in diseased animals during a dust storm event. However, the toxicity nature of dust storm particles remains unclear. It is our objective in this study to further investigate the cardiovascular effects of concentrated PM2.5 on spontaneously hypertensive rats during the same dust storm event. Four spontaneously hypertensive rats were implanted with radiotelemetry transmitters at the age of 10 wk. Baseline heart rate, mean blood pressure, and cardiac contractility (measured as QA interval, QAI) data were collected 4 wk before. Exposure group received concentrated ambient particles inhalation for 6 h during a dust storm event, while the control group received room air inhalation at the same time. Self-control data were collected 4 wk after the event during the same clock hours while there was no dust storm. Gravimetric analysis showed a particle mass concentration of 315.55 μg/m3 during the 6 h of exposure. A linear mixed-effects model revealed sigmoid increases in heart rate (to a maximum of 93.8 ± 18.8 bpm) and mean blood pressure (to a maximum of 14.8 ± 5.4 mm Hg), and a sigmoid decrease of QAI (to a maximum of - 3.5 ± 1.5 ms) during the exposure after an initial incubation period. We conclude that concentrated dust storm particles, which are different from products of automobile combustion process, may cause adverse cardiovascular effects on diseased animals.

Original languageEnglish
Pages (from-to)973-978
Number of pages6
JournalInhalation Toxicology
Issue number11
Publication statusPublished - Jan 2007


ASJC Scopus subject areas

  • Health, Toxicology and Mutagenesis
  • Toxicology

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