Biomedical subjects

Peng-Yau Wang

Publications and source records attributed to Peng-Yau Wang.

8 recordsLinked to original sources

PubMed2005

Effects of concentrated ambient particles on heart rate variability in spontaneously hypertensive rats.

In the present study, the cardiovascular toxicity of PM(2.5) was determined in spontaneously hypertensive (SH) rats using the standard deviation of normal-to-normal intervals (SDNN) and root mean square of successive differences of adjacent normal-to-normal intervals (RMSSD) as outcome measurements. Four SH rats implanted with radiotelemetry transmitters were repeatedly exposed to concentrated PM(2.5) in nose-only exposure chambers. Gravimetric analysis revealed the mean post-concentrating mass concentration of particles during the 5 h of exposure was 202 mug/m(3). Using each animal as its own control and linear mixed-effects model, to adjust for circadian nature and individual differences, we found that SDNN decreased by 15% initially then gradually decreased to 60% of the initial value at the end of exposure. Our results indicate that concentrated PM(2.5) may decrease SDNN on SH rats during PM exposure. The study also showed that SDNN is more sensitive to PM induced effects than RMSSD.

Air Pollutants↗

PubMed2004

Effects of Asian dust event particles on inflammation markers in peripheral blood and bronchoalveolar lavage in pulmonary hypertensive rats.

The health impact of dust events from China has become a concern within China and in its neighboring countries. Previous epidemiological studies have demonstrated an association between particulate matter exposure and cardiopulmonary mortality. Here, we use pulmonary hypertensive rat models to examine inflammation markers in the lung and in peripheral blood after exposure to Asian dust storm particles. Using a nose-only inhalation system, eight pulmonary hypertensive rats were exposed to concentrated ambient particles (CAPs) from an actual Asian dust storm that took place between March 18 and 19, 2002; four control rats were also exposed to room air. Four rats exposed to CAPs of 315.6 g/m3 for 6 h were classified as the low-exposure group, and another four rats exposed to CAPs of 684.5 g/m3 for 4.5 h were classified as the high-exposure group. The animals were sacrificed 36 h after exposure. Inflammation markers in the peripheral blood and in the bronchoalveolar lavage (BAL) were analyzed, and IL-6 in BAL was also determined using ELISA. White blood cell counts in peripheral blood increased with increased CAP exposure levels (P<0.001, test for trend). In BAL analysis, total cell numbers and the proportion of neutrophil also increased with increased CAP levels (P<0.001, test for trend for both markers). Positive dose-response relationships between CAP exposure and total protein (P<0.05) and between CAPs and LDH activity (P<0.05) were also observed. Moreover, IL-6 protein in BAL increasing with CAP levels (P<0.05, test for trend) was demonstrated. Our results revealed that exposure to particulate matters during an Asian dust storm could increase lung inflammation and injury in pulmonary hypertensive rats. Further studies are needed to determine the components of dust storm particles that may contribute to the particle toxicity.

Air Pollutants↗

PubMed2004

Effects of concentrated ambient particles on heart rate, blood pressure, and cardiac contractility in spontaneously hypertensive rats.

Epidemiological studies have shown that particulate matter (PM) air pollution is associated with cardiovascular mortality and morbidity, especially for particles with aerodynamic diameters under 2.5 microm (PM(2.5)). Recent studies have revealed an association between PM pollution and autonomic functions including heart rate (HR), blood pressure (BP), and heart-rate variability. However, the association and linking mechanisms have not been clearly demonstrated in animal studies. Utilizing a novel approach that employs a mixed-effects model to overcome the problems of variations in diseased animals and circadian cycles, we have previously demonstrated an association between concentrated PM(2.5) and changes of HR and BP in pulmonary hypertensive rats. The objective of this study is to test the plausibility of this methodology and to demonstrate the particle effects under different pathophysiology. The feasibility of cardiac contractility (measured as QA interval, QAI) as an indicator for PM toxicology was also explored. Four spontaneously hypertensive (SH) rats were repeatedly exposed to concentrated PM(2.5) during spring and summer. The mass concentration of particles during the 5 h of exposure was 202.0 +/- 68.8 (mean +/- SE) and 141.0 +/- 54.9 microg/m(3) for spring and summer experiments, respectively. During spring exposures, the maximum increase of HR and mean BP noted at the end of exposure were 51.6 bpm (p <.001) and 8.7 mm Hg (p =.002), respectively. The maximum decrease of QAI noted at the same time was 1.6 ms (p =.001). Though a similar pattern was demonstrated during summer exposures, the responses were less prominent. We conclude that concentrated PM(2.5) may increase HR and mean BP and decrease QAI in SH rats. Our results also show that QAI may be used as an indicator in PM toxicology.

Air Pollutants↗

PubMed2003

Accumulation of urinary 2-thiothiazolidine-4-carboxylic acid (TTCA) among workers occupationally exposed to carbon disulfide for 1 week.

OBJECTIVES: To investigate if carbon disulfide (CS(2)) accumulates after a 1-week exposure period, and how the work-shift duration and exposure magnitude affects this accumulation for the workers in viscose rayon industry. METHODS: Six 8-h and seven 12-h workers in the spinning department historically known to be exposed to high air CS(2) were recruited as the exposed groups. Seven workers from other non-CS(2)-exposed departments were recruited as non-exposure controls. Exposure monitoring covered a full work shift with personal breathing zone monitoring. Urine was collected pre- and post-shift every day throughout the 5 consecutive days. 2-Thiothiazolidine-4-carboxylic acid levels in the urine (U-TTCA) were determined. RESULTS: No detectable values were found for airborne (<0.6 ppm) and urinary (<35 ng/ml) monitoring for the control groups. The exposure levels for a 12-h shift (11.3+/-1.47) (AM+/-S.D.) were significantly greater than for an 8-h shift (6.3+/-0.64). The linear accumulation trend for daily U-TTCA across the workdays was only significant for the 12-h shift at pre-shift. Statistical significance was found in the regression of the ratios for pre-shift U-TTCA to airborne CS(2) levels on the preceding day to the day of the exposure at pre-shift for a 12-h shift (r=0.98, P=0.02). CONCLUSIONS: The U-TTCA accumulation for occupational exposure to CS(2) was exposure-magnitude-dependent. The linear equations derived in this study indicated that the U-TTCA increment at pre-shift for each additional daily 12-h exposure, after an adjustment for the CS(2) exposure level, was 0.02 mg/g creatinine/ppm of CS(2). The long-term exposure response under such repeated and intermittent conditions should be noteworthy.

Adult↗

PubMed2003

Effects of concentrated ambient particles on heart rate and blood pressure in pulmonary hypertensive rats.

Epidemiologic studies have shown that increased concentrations of ambient particles are associated with cardiovascular morbidity and mortality. However, the exact mechanisms remain unclear. Recent studies have revealed that particulate air pollution exposure is associated with indicators of autonomic function including heart rate, blood pressure, and heart rate variability. However, this association has not been clearly demonstrated in animal studies. To overcome the problems of wide variations in diseased animals and circadian cycles, we adopted a novel approach using a mixed-effects model to investigate whether ambient particle exposure was associated with changes in heart rate and blood pressure in pulmonary hypertensive rats. Male Sprague-Dawley rats were implanted with radiotelemetry devices and exposed to concentrated ambient particles generated by an air particle concentrator. The rats were held in nose-only exposure chambers for 6 hr per day for 3 consecutive days and then rested for 4 days in each week during the experimental period of 5 weeks. These animals were exposed to concentrated particles during weeks 2, 3, and 4 and exposed to filtered air during weeks 1 and 5. The particle concentrations for tested animals ranged between 108 and 338 micro g/m(3). Statistical analysis using mixed-effects models revealed that entry and exit of exposure chamber and particle exposure were associated with changes in heart rate and mean blood pressure. Immediately after particle exposure, the hourly averaged heart rate decreased and reached the lowest at the first and second hour of exposure for a decrease of 14.9 (p < 0.01) and 11.7 (p = 0.01) beats per minute, respectively. The hourly mean blood pressure also decreased after the particle exposure, with a maximal decrease of 3.3 (p < 0.01) and 4.1 (p < 0.01) mm Hg at the first and second hour of exposure. Our results indicate that ambient particles might influence blood pressure and heart rate.

Air Pollutants↗

PubMed2002

Biological monitoring of carbon disulphide: kinetics of urinary 2-thiothiazolidine-4-carboxylic acid (TTCA) in exposed workers.

The objectives of this study was to establish the kinetics of urinary 2-thiothiazolidine-4-carboxylic acid (U-TTCA) for workers exposed to carbon disulphide (CS2) and to investigate the effects of volume and creatinine adjustment methods for urine measurement. Ten workers in the spinning department of a rayon factory were individually monitored for airborne CS2 concentrations, with consecutive urine samples collected for 24-38 hours after termination of exposure. The U-TTCA, urine volume and creatinine level were measured for each sample. First-order and biphasic kinetics were determined using the curve-fit method, for the measurement series. For the first-order kinetics linearity fit, statistically significant correlation coefficients of 0.74-0.98 and 0.86-0.99 were derived for the volume- and creatinine-adjusted methods, respectively. For the biphasic kinetics approach, the overall correlation coefficients were 0.544-0.999 and 0.171-0.999 for the first and second phases of the creatinine-adjusted method, respectively. A post-shift U-TTCA of 3.0 mg/g Cr. equivalent, 40% below the current BEI setting at nearly PEL exposed level, was found. In conclusion, first-order kinetic response was confirmed for U-ITCA. Both volume- and creatinine-based urine adjustment are satisfactory for TTCA assessment as a biomarker of individual CS2 exposure although the correlation for creatinine-based measurement was modestly superior to the volume-based analogue. Based on the results of this study,we recommend a re-evaluation of the current biological exposure index of 5 mg/g creatinine at a CS2 exposure level of 10 ppm.

Adult↗

PubMedDate not supplied

An automated exposure system for human inhalation study.

The authors developed a computer-based exposure system for human inhalation research to study the toxicokinetics of gases. The system uses a set of computer-controlled solenoid valves that regulates inhaled gases and collect exhaled breaths from the subject in accordance with a predetermined time schedule. The volunteer's breathing activity is monitored simultaneously with a real-time instrument, calibrated by both internal and external standards. The common air pollutant, 1,3-butadiene, was used for system validation. The results indicated that the errors were less than 3% relative to reference standards, and the error in the timing of the valve operation was negligible. The average difference between breath-monitoring methods was within 10%. The proposed system is an easy-to-use, reliable device for human studies; more than 130 subjects were tested in a companion study.

Administration, Inhalation↗

PubMedDate not supplied

Effects of concentrated ambient particles on airway responsiveness and pulmonary inflammation in pulmonary hypertensive rats.

Epidemiological studies have associated particulate air pollution with exacerbation of lung function in human populations. However, the relationship between ambient particles and lung function in animal studies has been inconsistent. In order to investigate the effects of concentrated ambient particles (CAPs) on airway responsiveness, we exposed pulmonary hypertensive rats to CAPs using particle concentrator at an EPA of Taiwan supersite, located at a traffic busy urban area nearing Taipei city. The exposure group (n = 5) was exposed to CAPs for 6 h each day for 3 consecutive days (mean mass concentration = 371.7 microg/m(3)), while a control group (n = 6) was exposed to HEPA-filtered air. Whole-body barometric plethysmography was used to measure respiratory frequency, tidal volume, and airway responsiveness before and after exposure. Enhanced pause (Penh) was used as an indicator of airway responsiveness. To improve the accuracy of airway responsiveness measurement, we controlled temperature and humidity. Further, airway responsiveness was determined 5 h after particle exposure to overcome the stress effect in nose-only exposure chambers. After CAPs exposure, we found decreased respiratory frequency and increased tidal volume (p < .05). Using the methacholine challenge test, a significant difference of Penh measured before and after experiment was observed in the CAPs group (p < .05), but not in the filtered air group. Further analysis showed that the Penh difference before and after exposure in the CAPs group was significantly greater than that in the filtered air group (p < .05). We conclude that CAPs could induce airway hyperresponsiveness in pulmonary hypertensive rats.

Air Pollutants↗