RESEARCH TRIANGLE PARK, NC—Temporary closure of a Utah Valley steel mill during a labor dispute yielded unprecedented epidemiological evidence for the health effects of particulate emissions. Researchers from the Environmental Protection Agency (EPA) now demonstrate that particles from the plant cause lung inflammation in healthy subjects.[1]

PLANT LINKED WITH ILLNESS

“This was the first study on air pollution particles that correlated effects from controlled human exposures with epidemiological data,” said Andrew Ghio, MD, a Research Medical Officer at the EPA’s National Health and Environmental Effects Laboratory in Research Triangle Park, NC. Dr. Ghio described the Utah Valley topography as “a bowl surrounded by the Rockies—there are frequent inversions in January, February, and March.” The inversions were associated with increases in human mortality, as well as in “a large number of indices of morbidity: for instance, hospitalization for bronchitis and for asthma in adults; and school absences, bronchitis, and asthma attacks in children,” Dr. Ghio noted. “In the fall of 1986, the steel mill closed as a result of a labor dispute … and reopened in the fall of 1987.” During the closure period, health indices affected by plant emissions were markedly reduced.

PLANT PARTICULATES CAUSE LUNG INFLAMMATION

In the new study, “we obtained filter samples collected by the Utah Department of Air Quality in January through March of the years before, during, and after the plant closure,” Dr. Ghio told PULMONARY REVIEWS. Particles collected during each period were then extracted, and equal-mass samples were instilled into the lungs of volunteers under bronchoscopy. “Twenty-four hours later, we did lavage,” said Dr. Ghio.

In subjects receiving particles from 1986, before the plant closure, “there was a neutrophilic inflammation in that part of the lung. There was also some injury, as indicated by an increase in protein, and a pro-coagulative tendency.” In contrast, Dr. Ghio emphasized, “When we instilled particulate extracts from the period of the plant closure, we had no such effects. We concluded that there was something in the [pre-closure] extracts associated with lung injury and inflammation.”

“We found the same in animals,” noted Dr. Ghio, citing recent work in rats demonstrating similarly elevated lung injury and neutrophilic inflammation with instillation of the steel mill particulates. Compared with animals whose lungs were instilled with particles collected during the mill closure or with saline, these rats also had an increased incidence of airway hyperresponsivity to acetylcholine. “These findings suggest that mass may not be the most appropriate metric … rather, specific components must be identified and addressed,” the authors said.

OXIDANTS LIKELY CAUSE OF DAMAGE

Dr. Ghio and colleagues already suspected probable culprits for the damage: “We analyzed filtrates for ability to generate oxidants. Filtrates from 1986 and 1987 [pre- and post-closure] were both associated with a lot of oxidant generation and lots of metals. Particulates were high in iron, copper, and zinc” but also contained elevated quantities of cationic (calcium, potassium, or magnesium) salts.

Previous studies had associated metal content with potential for oxidative damage to cells in vitro. Additionally, other, nonmetallic components of the particulate plant emissions appear to be responsible for impairing phagocytotic activity and for promoting apoptosis of alveolar macrophages in vitro.

—Mimi Zucker, PhD

Reference
1. Ghio AJ, Devlin RB. Inflammatory lung injury after bronchial instillation of air pollution particles. Am J Respir Crit Care Med. 2001;164:704-708.

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