Evaluation of a real-time passive personal particle monitor in fixed site residential indoor and ambient measurements.

Recent experimental findings in animals and humans indicate adverse respiratory effects from short-term exposures to particulate air pollutants, especially in sensitive subpopulations such as asthmatics. The relationship between air pollution and asthma has mainly been determined using particulate matter (PM) measurements from central sites. Validated tools are needed to assess exposures most relevant to health effects. Recently, a personal passive particulate sampler (personal Data-RAM, pDR, MIE Inc., Bedford, MA) has become available for studying personal exposures to PM with time resolution at 1 min. The pDR measures light scatter from PM in the 0.1-10 microM range, the significant range for health effects. In order to assess the ability of the pDR in predicting gravimetric mass, pDRs were collocated with PM2.5 and PM10 Harvard Impactors (HI) inside and outside nine homes of asthmatic children and at an outdoor central Air Pollution Control District site. Results are presented of comparisons between the HI samplers and the pDR in various modes of operation: passive, active, and active with a heated inlet. When used outdoors at fixed sites the pDR readings exhibit interference from high relative humidity (RH) unless operated with a method for drying inlet air such as a heater, or if readings at times of high RH are adjusted. The pDR correlates more highly with the HI PM2.5 than with the HI PM10 (r2 = 0.66 vs. 0.13 for outdoors, r2 = 0.42 vs. 0.20 for indoors). The pDR appears to be a useful tool for an epidemiologic study that aims to examine the relationship between health outcomes and personal exposure to peaks in PM.

Toxicity of chemical components of ambient fine particulate matter (PM 2.5) inhaled by aged rats.

The toxicity of two important chemical components of fine ambient particulate matter (PM 2.5)-ammonium bisulfate (ABS) and elemental carbon (C)-was studied using aged (senescent) rats. The study tested the hypotheses that fine particle exposure can damage lungs and impair host defenses in aged rats and that ozone would potentiate the toxicity of these particles. Ammonium bisulfate aerosols were generated by nebulization of dilute aqueous solutions. Elemental carbon was generated from an aqueous suspension of carbon black. Carbon and ABS mixtures were generated by nebulization of a suspension of carbon black in a dilute aqueous solution of ABS. Rats were exposed, nose-only, for 4 h a day, three consecutive days a week, for 4 weeks. The rats were exposed to one of six atmospheres: (1) purified air; (2) C, 50 microg m(-3), 0.3 microm mass median aerodynamic diameter (MMAD); (3) ABS, 70 microg m(-3), 0.3 microm MMAD; (4) O3, 0.2 ppm; (5) ABS + C, 0.46 microm MMAD; and (6) ABS + C + O3, 0.45 microm MMAD. Data were analyzed using ANOVA and Tukey multiple comparison tests; a two-tailed significance level of 0.05 was used. The nuclei of lung epithelial and interstitial cells were examined to determine the labeling of the DNA of dividing cells by 5-bromo-2-deoxyuridine and to identify the location of injury-repair-related cell replication. Increased labeling of both epithelial and interstitial lung cells occurred following all pollutant exposures. Although epithelial cells are most likely impacted by inhaled particles first, the adjacent interstitial cells were the cells that showed the greatest degree of response. Exposure to the ABS + C + O3 mixture resulted in losses of lung collagen and increases in macrophage respiratory burst and phagocytic activities that were statistically significant. Our results demonstrate that ozone can increase the toxicity of inhaled particles (or vice versa), and suggest that detailed study of mixtures could provide a more comprehensive understanding of the mechanisms by which inhaled pollutants adversely affect human health.

Breathing pattern and metabolic rate responses of rats exposed to ozone.

Breathing pattern (frequency and tidal volume), minute ventilation (VE), oxygen consumption (MO2), and rectal temperature (TR) were measured from rats exposed to 0.8, 0.6, 0.4, and 0.2 ppm O3 to determine the relation between breathing pattern responses to O3 and metabolic rate. In 0.8 ppm O3, rapid-shallow breathing began at 60 min exposure while VE and MO2 declined beginning at 40 min. In comparison to clean air exposed animals, rats (n = 8) during the third hour of 0.8 ppm O3 exposure had a 27% increase in frequency, 35% decline in tidal volume, 20% decrease in VE, 24% decrease in MO2, and 1.3 degrees C decrease in TR. At lower O3 concentrations, responses were diminished in magnitude, and in rats exposed to 0.2 ppm O3, only MO2 was significantly decreased, irritant-induced depression of VE did not imply a state of hypoventilation or hypoxia because ventilation equivalent for O2 (VE/MO2) did not decline during O3 exposures. Body temperature and metabolic rate depression have not been observed during the development of rapid-shallow breathing in dogs or humans exposed to these low levels of O3, and the present observations in rats may reflect a more labile thermoregulatory physiology among rodents. Ventilatory and metabolic rate depression in response to irritant inhalation can be an effective pulmonary defense in rodents and other heterothermic mammals.

A rodent treadmill for inhalation toxicological studies and respirometry.

A 10-runway treadmill was enclosed for inhalation toxicological studies of rodents under exercise exposure to environmental pollutants. The exposure system was lined with sheet stainless steel to minimize scrubbing of charged particles and reactive gases. Average metabolic gas exchange of exercising animals was derived from measurements of inlet or outlet airflow and data from an O2 analyzer in conjunction with either a CO2 or N2 analyzer. An airflow rate of 400 l X min-1 ensured a response time of 1 min to reach 95% of a step change in metabolic rate and held scrubbing losses of an O3 test atmosphere to less than 2% of treadmill inlet concentration. Gas exchange averaged for 10 rats during incremental exercise up to their highest collective performance was similar to published data for rats tested individually.