New clues to smog's effects on lungs.
There's little question that some of the constituents of photochemical smog-- most notably ozone and some sulfur oxides--are respiratory irritants. And that has concerned researchers and policymakers alike, because more than one-third of the U.S. population routinely breathes air that exceeds the federal smog standard (SN: 6/28/86, p. 405). What hasn't been understood is how serious these irritants are: whether they represent serious long-term hazards to human health, or even what kind of chronic respiratory hazards they might pose. But new animal studies at the University of California at Davis and the Massachusetts Institute of Technology are offering some clues. They suggest that smog may indeed be capable of causing potentially serious changes in the lungs.
In one study, monkeys exposed eight hours daily for one year to 0.61 parts per million ozone were found to have "abnormal' collagen (connective tissue) in their lungs. And once deposited, that abnormal collagen "doesn't go away,' says Jerold A. Last, who headed the project at Davis. Though the monkeys again synthesized normal collagen once the ozone exposures ended, Last notes that the normal tissue "didn't seem to replace the abnormal collagen.'
The altered collagen contains an unusually high number of chemical crosslinks that make the tissue stiffer and less elastic, report Last and his co-workers in the July TOXICOLOGY AND APPLIED PHARMACOLOGY. Such high numbers of crosslinks are characteristic of "changes we see in humans with fibrotic lung disease,' Last says. Fibrotic lung disease stiffens the lung and makes breathing difficult. In the most serious cases, it can compromise gas exchange and even cause death.
Since the levels of ozone used in the study are at least three to five times higher than what humans breathe in most smoggy regions, Last does not see death from fibrosis as an ozone health risk. But no one knows what the impacts of milder, unrecognized fibrosis might be, he says. It's possible it might make people more susceptible to other respiratory problems. For this reason, Last believes his data point toward the type of damage researchers might begin scouting for in people who have been chronically exposed to ozone.
At MIT, researchers are focusing on the respiratory effects of another component of smog: sulfur oxides, particularly those carried on the surface of submicron particles of metal oxides like zinc oxide (ZnO). Prevalent in emissions from coal burning, smelting and some steelmaking, ZnO is not a respiratory irritant by itself except at high concentrations. But it can catalyze sulfur dioxide (SO2)--also prevalent in industrial exhaust--to sulfuric acid (H2SO4), which is a potent respiratory irritant. New data from the group indicate that these metal oxides can increase the potency of sulfuric irritants --rendering them toxic at much lower levels than had been previously known.
Using guinea pigs, whose lungs provide a reasonable model for human asthmatics exposed to sulfur oxides, the researchers looked at factors such as the ability of these pollutants to limit the transfer of gases across membranes separating the lungs' small airways (alveoli) from capillaries. They found in this case that if 30 micrograms of sulfuric acid (a realistic figure) is layered on a tiny ZnO particle, it will produce the same effect-- roughly a 25 percent reduction in gas diffusion across the alveoli--as 10 times as much pure sulfuric acid in aerosol form. Mary O. Amdur, who directed the work, attributes this "order of magnitude difference' to the fact that the ultrafine size of the ZnO particles helps carry the H2SO4 that they create deep into the lung. Moreover, because this H2SO4 is concentrated on the particle's surface, all of it is readily available for reaction with the lung.
In the June 15 TOXICOLOGY AND APPLIED PHARMACOLOGY, Amdur's group also reports that sulfites, a little-studied class of respiratory toxicants in some smogs, similarly inhibit gas transfer deep within the lung. Moreover, sulfites, which can also ride small particles deep into the lung, proved six times more potent at constricting bronchial passages than SO2. Amdur suggests that an important way to limit these respiratory hazards might be to take away their transport by controlling industrial emissions of submicron aerosols.
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|Date:||Aug 8, 1987|
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