Principal Investigator: Judith T Zelikoff, Ph. D.
New York University Medical Center,
Institute of Environmental Medicine,
Over the past two decades, due to rising energy costs and the uncertain availability of petroleum and natural gas, homeowners in the United States have increasingly turned to the use of wood as an alternate home heating fuel. Human health risks associated with inhalation of woodsmoke, however, have been poorly studied and, thus, are not clearly defined. Epidemiological studies suggest that inhalation of woodsmoke increases the incidence, duration, and, possibly, severity of respiratory disease, particularly in children. The hypothesis of this toxological study is that inhalation exposure to woodsmoke compromises pulmonary host resistance to bacterial infections by altering immune defense mechanisms, particularly at the level of the macrophage.
Our studies have 3 major objectives. (a) to chemically characterize the woodsmoke emissions generated from the burning of Douglas Fir (commonly used for home heating in the Northwest United States) and Red Oak (a common firewood in the Northeastern U.S.), (b) to relate the epidemiological evidence to identifiable "health effects", host resistance to, and pulmonary clearance of, pathogenic bacteria, and (c) to determine the underlying mechanism(s) by which woodsmoke may alter pulmonary immunocompetence by examining effects on macrophage activities critical for maintaining host resistance to infectious diseases.
The system used for generation of the woodsmoke (see figure p. 2) was developed in our laboratory and consists of a feeder, a laboratory scale laminar flow drop-tube furnace, and a collection probe. Wood dusts, dry sieved to a diameter range between 53 and 63 um (to minimize variation in combustion kinetics during the combustion smoke/ash formation process), are suspended in the feeder using a vibrator, carried in a nitrogen gas stream, and injected axially downward into the furnace. The particles are then ignited and burned in a narrow zone along the furnace axis.
Whole effluents of smoke generated from the burning of Red Oak was characterized in terms of respirable suspended particulate (RSP) matter, carbon monoxide (CO) and NOX levels, as well as total polycyclic aromatic hydrocarbons [PAM; measured as benzo(a)pyrene]. Under the present burning conditions, RSP concentrations, determined gravimetrically, are maintained at a level of 750 ,ug/m3 for 1 hr; mass median diameter of the emitted particles is 0.15 ,um (sg = 1.8). Carbon monoxide levels recorded near the animal exposure port was 1ppm, and all (100%) of the gaseous material produced during burning was volatile. Levels of NOX (NO and NO2) were negligible, and the generated PAH concentration was 1.52 ppm. These measurements, generated under controlled conditions, are within the range of those produced indoors by the operation of airtight/nonairtight stoves.
Following a single 1 hr exposure, Sprague Dawley rats, exposed nose-only to Red Oak smoke effluents, were either anesthetized and intratracheally instilled with Staphylococcus aurevs to assess effects on pulmonary bacterial clearance, or sacrificed and their lungs ravaged to provide pulmonary macrophages (PM). Results from preliminary studies indicate that inhalation of smoke at the concentrations described above, reduces pulmonary bacterial clearance by 25% immediately after exposure. Phagocytic activity (as measured by the number of particles taken up per cell) by PM recovered from the lungs of exposed rats was depressed (compared to air-exposed controls) by 23% and 61% after 90 min and 2.5 hr, respectively.
Results from these early studies demonstrate that acute inhalation of woodsmoke effluents generated from a model system that produces emissions comparable to those produced in homes using wood burning devices, compromises important pulmonary immune defense mechanisms These findings may contribute to a better understanding of the epidemiological evidence that suggests an association between woodsmoke inhalation and increased incidence of respiratory infection. I am extremely grateful to the Center for Indoor Air Research for providing us with the support for these studies and to my co-investigators Drs. Lung Chi Chen and Mitchell Cohen for their intellectual input.
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