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.

Aerosols↗

PubMedDate not supplied

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.

Adolescent↗

PubMedDate not supplied

Controlled exposure to a mixture of SO2, NO2, and particulate air pollutants: effects on human pulmonary function and respiratory symptoms.

Exposure of 20 volunteers to sodium chloride (NaCl) aerosol or to a mixture containing NaCl plus irritant particles (zinc ammonium sulfate) and irritant gases (nitrogen dioxide and sulfur dioxide) produced no significant decrements in pulmonary function. There was a slight tendency for respiratory symptoms to be greater during the exposure to the mixture than during exposure to the NaCl aerosol alone; the differences were not statistically significant. The pollutant concentrations studied approximated worst-case ambient levels observed in the Los Angeles basin.

Adolescent↗

PubMedDate not supplied

Effects of short-term exposure to carbon monoxide in subjects with coronary artery disease.

Twenty-four male subjects with stable angina pectoris performed graded exercise tests after being exposed to either carbon monoxide (CO) or clean air in a randomized crossover double-blind experiment in which each subject acted as his own control. Subject's blood carboxyhemoglobin levels were increased from a baseline level of approximately 1.5% to 3% of saturation, post-CO exposure. Cardiographic and respiratory gas exchange data were obtained during the tests in which the subjects exercised to the point of onset of anginal pain. The goal of the study was to determine if low-level CO exposure compromised the ability of these individuals to perform work. Data were evaluated statistically using a two-factor analysis of variance with repeated measures; the factors were exposure ATMOSPHERE (clean air vs. CO) and ORDER of exposure (clean air first, CO second vs. CO first, clean air second). One-tailed tests were used, and differences were considered significant at the p less than .05 level. The time to onset of angina was reduced 6% (p = .046) after CO exposure relative to clean air. Oxygen uptake (VO2) at angina was reduced by approximately 3% (p = .04). A subgroup of individuals who exhibited depression in the ST segment of their electrocardiograph tracings showed a 12% reduction in time to onset of angina and a 20% reduction in the time to onset of 0.1 mV ST segment depression; both of these findings were also statistically significant.

Aged↗

PubMedDate not supplied

Urban ectopy in the mountains: carbon monoxide exposure at high altitude.

Environmental exposure to inhaled carbon monoxide (CO) increases coronary artery disease risk. Sudden cardiac death, a frequent manifestation of coronary artery disease, is usually a result of ventricular dysrhythmia. The effect of exposure to CO at sea level (CO/SL) and simulated high (2.1 km) altitudes (CO/HA) on the incidence of cardiac ectopy in subjects with coronary artery disease was investigated. A double-blind crossover study was conducted, with random-order assignment, and each subject served as his own control. Seventeen men with documented coronary artery disease and stable angina pectoris performed cardiopulmonary exercise stress tests after random exposure to either CO or clean air (CA) at sea level (CA/SL) or at a simulated 2.1-km high altitude (CA/HA). The individual CO and HA exposure conditions were each selected to reduce the percentage of oxygen saturation of the subjects' arterial blood by 4%. Subjects' blood carboxyhemoglobin levels were increased from an average of 0.62% after clean-air exposure to 3.91% of saturation after CO exposure. The percentage of oxygen saturation in arterial blood was reduced from a baseline level of 98% to approximately 94% after CO/SL or CA/HA and to approximately 90% after CO/HA. Compared with the CA/SL (i.e., 10 premature ventricular contractions [PVCs]), the average incidence of exercise-induced ventricular ectopy was approximately doubled after all exposures (CO/SL = 18 PVCs, CA/HA = 16 PVCs, and CO/HA = 19 PVCs), and a significant trend (p < .05) of increased ectopy with decreased oxygen saturation in arterial blood was observed. Yet, among subjects who were free from ectopy (n = 11) on CA/SL, only 2 subjects developed ectopy after CO/HA. No episodes of ventricular tachycardia or fibrillation occurred. The findings indicated that exposure to increased levels of hypoxemia, resulting from hypoxic and/or CO exposures, increased the susceptibility to ventricular ectopy during exercise in individuals with stable angina pectoris; however, this risk was nominal for those without ectopy.

Aged↗

PubMedDate not supplied

Urban angina in the mountains: effects of carbon monoxide and mild hypoxemia on subjects with chronic stable angina.

Seventeen men with stable angina pectoris who resided at or near sea level performed cardiopulmonary exercise stress tests after they were exposed to either carbon monoxide (3.9%), carboxyhemoglobin, or clean air. Investigators conducted the tests at sea level, and they simulated 2.1-km altitudes (i.e., reduced arterial oxygen saturation by approximately 4%) in a randomized double-blind experiment in which each subject acted as his or her own control. The duration of symptom-limited exercise, heart rate, indicators of cardiac ischemia and arrhythmia, blood pressure, and respiratory gas exchange were measured. Analyses of variance showed that both independent variables-altitude and carbon monoxide-significantly (p < or = .01) reduced total duration of exercise for the group as a whole (n=17) and reduced the time to onset of angina for a subset of 13 subjects who experienced angina during all four test conditions (p < .05). Time to onset of angina was reduced either after exposure to sea-level carbon monoxide (9%) or to simulated high-altitude clean-air exposures (11%), compared with clean air at sea level. Joint exposure to carbon monoxide at a simulated high altitude reduced the time to onset of angina, relative to clean air, by 18% (p < .05). Other cardiological, hemodynamic, and respiratory physiological parameters were also affected adversely by altitude and carbon monoxide exposures. None of the parameters measured were associated significantly with either altitude or carbon monoxide, indicating that the effects of carbon-monoxide-induced and high-altitude-induced hypoxia were additive. The results of this study suggest that high-altitude conditions exacerbate the effects of carbon monoxide exposures in unacclimatized individuals who have coronary artery disease.

Aged↗

PubMedDate not supplied

Effects of 0.2 ppm nitrogen dioxide on pulmonary function and response to bronchoprovocation in asthmatics.

To study the respiratory effects of nitrogen dioxide (NO2) at ambient concentrations, we exposed 31 asthmatic volunteers to purified air (control) and to 0.2 ppm NO2 for 2-h periods with light intermittent exercise. Bronchial reactivity (loss of forced expiratory performance in response to graded doses of methacholine chloride aerosol) was determined postexposure, using a newly developed apparatus that allowed accurate quantitation of methacholine dose. Forced expiratory performance, total respiratory resistance, and symptoms were also recorded immediately pre- and postexposure (prior to methacholine challenges). No significant direct effect of NO2 exposure on forced expiratory function or total respiratory resistance was observed. Symptoms showed a small significant (p less than 0.05) excess in purified air relative to NO2 exposures. Individual responses to methacholine varied greatly. About two-thirds of the subjects showed greater response after NO2 than after purified air, but the mean excess response was small. Mean changes attained significance in some but not all applicable statistical tests. Thus we cannot conclude unequivocally that NO2 exposure increased bronchial reactivity in this group, although there was some tendency in that direction.

Adolescent↗

PubMedDate not supplied

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Adult↗