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Why Is PM Hazardous to Your Health?
This page finalized May 18, 2004.
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Chairman's Air Pollution Seminar Series |
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Thursday, June 17, 2004 |
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Why Is PM Hazardous to Your Health? |
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Dr. Colin Solomon (UC San Francisco): 10:00 a.m. to 10:50 a.m. |
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- Webcast - |
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| Exposure to airborne particulate matter (PM) has been linked to thousands of deaths and to hundreds of thousands of cases of respiratory symptoms and asthma attacks in California each year. To investigate how exposure to PM might lead to these outcomes, the ARB funded a three-campus collaborative with researchers from UC San Francisco, UC Irvine, and UC Davis. The three groups used similar tissue sample collection methods, biological assays, and exposure conditions: a laboratory-generated PM mixture of ammonium nitrate and carbon black. Both human clinical studies on asthmatic volunteers and animal model studies were conducted. Investigators from each campus will present their findings and discuss how these findings help us understand the ways that particles affect human health. | ||
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Agenda |
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Dr. Colin Solomon |
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| This project investigated the effect of inhaled particles on airway inflammation in individuals with asthma. One experiment involved separate single exposures to each of filtered air (FA), carbon and ammonium nitrate particles (P), and P with ozone (PO). The second experiment involved separate single exposures to FA, P, and three serial-day exposures to P (P3). In PO, compared to FA and P, there were increases in airway inflammatory cells, proteins, and gene expression, and decreases in spirometric pulmonary function (SPF). Within the P3 condition there were decreases in SPF. The results indicate that exposure to the particles can lead to decreases in SPF function, but does not lead to any physiologically significant changes in airway cell distribution, protein, or gene expression. However, combined exposure to particles and ozone, in addition to decreases in SPF, does lead to increases in inflammatory cells, and protein and gene expression. These differential changes appear to be due primarily to the ozone component of the exposure environment. | ||
| Colin Solomon received his Ph.D. in physiology from the University of Queensland, Australia. He is an assistant professor in the Department of Medicine at the University of California at San Francisco. Dr. Solomon investigates the mechanisms of toxin-induced (gas and particle) airway inflammation in humans using controlled exposure experiments. | ||
Dr. Karron Power |
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| Alteration of heart function may underlie the increase in morbidity and mortality observed from exposure to ambient air particles and to ozone. Heart rate variability (HRV) measures the beat-to-beat changes in heart rate. Decreased HRV has been associated with increased cardiac mortality, and decreased HRV is seen with exposure to PM. The physiological mechanism underlying this effect is unknown, but may involve airway inflammation. An experiment was designed to test the hypothesis that controlled exposure to PM, and also to combined PM and ozone, would result in decreased HRV. Human subjects with allergic asthma were chosen for a controlled-exposure experiment because of the increased baseline airway inflammation inherent to asthma. Exposure to PM and ozone combined had a greater effect on HRV than exposure to PM alone. | ||
| Karron Power received her M.D. from the University of California at San Francisco and her M.P.H. in public health from the University of California at Berkeley. She is an assistant professor in the Department of Medicine at UCSF, in the Division of Occupational and Environmental Medicine. Dr. Power investigates the effects of air pollutants on cardiac autonomic function and airway inflammation using both controlled human exposures and epidemiologic studies. | ||
Dr. Michael T. Kleinman |
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| This project examined the effects of PM exposure in senescent (elderly) rats, using a laboratory-generated mixture of ammonium nitrate and elemental carbon (carbon black). Senescent rats exhibited changes in blood pressure and heart rate variability that were consistent with an adverse effect of PM on the heart. Humans and rats, exposed under similar conditions, both exhibited increased activation of macrophages. The results provided evidence of decreased heart rate variability after the exposures. This effect was also noted in the work conducted at UCSF by the previous speakers. | ||
| Michael T. Kleinman received his Ph.D. in environmental health sciences from New York University. He is a professor and Associate Director of the Air Pollution Health Effects Laboratory in the Department of Community and Environmental Medicine at University of California at Irvine. He currently serves as the Chair of the California Air Quality Advisory Committee and is a consultant to the U.S. EPA Science Advisory Board. Dr. Kleinman studies the health effects of exposures to environmental contaminants found in the ambient air. | ||
Dr. Kent Pinkerton |
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| This project examined rats that were sensitized to ovalbumin (egg whites) prior to PM exposure, in order to develop an animal model that physiologically mimics asthmatic conditions found in humans. The PM exposures in these rats led to effects such as altered airway epithelial cells and increased airway inflammation. This project also involved the assay of cellular endpoints in human lung tissue samples obtained from asthmatics exposed to PM at UCSF. Based on these assays, PM exposure led to detectable changes in levels of cytokine expression, which help generate immune responses. | ||
| Kent Pinkerton received his Ph.D. in pathology from Duke University Medical Center. He is a professor in the Department of Anatomy, Physiology, and Cell Biology in the School of Veterinary Medicine at the University of California at Davis, where he serves as director of the Center for Health and the Environment. He has been studying the effects of air pollutants on lung structure and function, the interaction of gases and airborne particles within specific sites and cell populations of the lungs, and the effects of environmental tobacco smoke and combustion emissions on lung growth and development. | ||
Dr. John Balmes |
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| Carbon and ammonium nitrate are two of the major constituents of airborne particulate matter (PM) in California. These two types of particles, however, have traditionally been considered non-toxic to humans at concentrations typically found in California ambient air. The results of previous CARB-funded work involving rats conducted at UC Davis and UC Irvine suggested that carbon and ammonium nitrate particles at a combined total concentration range of 250-300 µg/m3 can induce proliferative changes in airway tissue and changes in blood pressure and heart rate. CARB took the unique step of funding three University of California campuses (Davis, Irvine, and San Francisco) to conduct inter-related experiments designed to further investigate how these relatively biologically inert particles might induce airway and cardiovascular toxicity in susceptible humans as well as sensitive animal models. The animal model studied at UC Davis was the ovalbumin-sensitized Brown Norway rat exposed to aerosolized ovalbumin (a model of allergic airway inflammation that has some features of human asthma). The animal model studied at UC Irvine was the senescent Fischer 344N rat (a model relevant to elderly humans). The susceptible group studied at UCSF was allergic asthmatic individuals. The results of the UC Davis experiments confirmed that carbon and ammonium nitrate particles can induce proliferation of the airway lining cells as well as augment certain allergic inflammatory responses. The results of the UC Irvine experiments confirmed that inhalational exposure to these particles can also induce changes in blood pressure and heart rate. The results of the UCSF experiments showed little evidence of toxicity of carbon and ammonium nitrate particles alone but significant effects of combined exposure to the particles and ozone on lung function, airway inflammation, and heart rate variability. Taken together, the results of the experiments at the three UC campuses suggest that exposure to carbon and ammonium nitrate particles at concentrations approximately an order of magnitude higher than ambient air can induce adverse effects in animal models of allergic airway inflammation and the elderly as well as, in combination with a high-ambient exposure to ozone, in allergic asthmatic humans. | ||
| John R. Balmes received his M.D. from the Mount Sinai School of Medicine. He is a professor in the Department of Medicine at the University of California at San Francisco, Chief of the Division of Occupational and Environmental Medicine at San Francisco General Hospital, and Director of the Northern California Center for Occupational and Environmental Health. Dr. Balmes investigates the effects of various air pollutants on airway inflammation and respiratory health in humans using controlled human exposure and epidemiologic studies. | ||
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For more information on this Seminar, please contact
Ralph Propper |
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For a complete listing of the ARB Chairman's Seminar
Series and the related documentation |
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