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Lignite Fly Ash and the Interferon System

Lignite fly ash, the combustible product of lignite coal, is the largest constituent of the particulate emissions produced when coal is burned to generate electric power. An estimated million plus metric tons of fly ash were released into the atmosphere of the United States during 1974 (1). This atmospheric burden is predicted to increase with increased use of new technologies for coal combustion, such as fluidized bed combustion. Because coal fly ash contains mutagenic and carcinogenic agents (2,3), it may pose a potential hazard to human health.

Previous research has shown that certain chemicals and particulates can interfere with the production of interferon, a cellular defense mechanism.* The process of interferon induction is initiated in the cell by invading viruses. Among the agents known to interfere with the process are asbestos fibers (4), diesel engine emissions (5), mutagens (6), and carcinogens (7).

To determine if lignite fly ash has an inhibiting effect on the production of interferon, investigators at the National Institute for Occupational Safety and Health (NIOSH) have examined the effect of fly ash on the interferon system (8). The amount of interferon produced in the presence of various materials was assessed by measuring the degree to which Sendai virus activity was inhibited. Induction of interferon by influenza virus was evaluated in monolayers of Rhesus monkey kidney cells pretreated with lignite fly ash (9). Results indicated that about 50% less interferon was produced in these pretreated cells than in untreated cells. When interferon was added to the cells, however, the presence of fly ash did not impair the ability of the interferon to protect the cells against viral infection. In cells pretreated with fly ash, influenza virus multiplied to twice the levels noted in untreated cells. In contrast, unburned lignite coal had a minimal effect on viral growth and interferon induction; the degree of biologic activity was correlated with the "rank" of the coal (10).**

To study the nature of the inhibitor(s) present in lignite fly ash, the fly ash was extracted with both polar and nonpolar solvents and with horse serum. Interferon induction was inhibited by extracts of lignite fly ash when either polar (methanol) or nonpolar (dichloromethane) solvents were used; this finding suggests that there may be more than one inhibitor present. Fly ash was also extracted with horse serum, which forms complexes with some heavy metals and organic compounds and has a chemical constitution similar to alveolar fluids from the lung. These extracts, with and without the addition of disodium ethylenediamine tetraacetic acid (EDTA), a metal chelator, yielded additional compounds that suppressed the induction of interferon by viruses. Furthermore, the residual particulates of fly ash left after extraction with horse serum were able to inhibit the induction of interferon. These results indicate that several soluble components of lignite fly ash, and components in the particulate matrix as a whole, acting singly or together, may alter cellular defenses. Reported by Microbiology Section, Div of Respiratory Disease Studies, National Institute for Occupational Safety and Health, CDC.

Editorial Note

Editorial Note: The findings presented here demonstrate that lignite fly ash and several soluble components (both organic and inorganic) adsorbed to or inherent in these particulates adversely affected the induction of interferon. Because the growth of influenza virus was enhanced in vitro in the presence of lignite fly ash and correlated with suppression of interferon production, exposure to lignite fly ash may affect human host responses to viral infection.

Findings of this study indicate that studying the process of viral induction of interferon can be useful in detecting both soluble and particulate reactants potentially hazardous to human health. Future studies should attempt to detect the stage during coal combustion at which fly ash contains potentially harmful chemicals, to minimize these occurrences, and to determine the health risk, if any, to the workers in the plants and to persons in the communities nearby.


  1. Energy Research Development Administration. Coal extraction processing and combustion. Publication 116, Argonne National Laboratory, Argonne, Illinois, 1976; 3:3,16.

  2. Natusch DFS. Potentially carcinogenic species emitted to the atmosphere by fossil-fuel power plants. Environ Health Persp 1978;22:79-90.

  3. Chrisp CE, Fisher GL, Lammert JE. Mutagenicity of filtrates from respirable coal fly ash. Science 1978;199:73-5.

  4. Hahon N, Eckert HL. Depression of viral interferon induction in cell monolayers by asbestos fibers. Environ Res 1976;11:52-65.

  5. Hahon N, Booth JA, Wheeler R. Activity of diesel engine emission particulates on the interferon system. Environ Res 1982;28:443-55.

  6. Hahon N, Ong TM. Action of antischistosomal drugs, hycanthone and its analog IA-4 N-oxide, on viral interferon induction. J Toxicol Environ Health 1980;6:705-12.

  7. DeMaeyer E, DeMaeyer-Guignard J. Effect of different carcinogenic agents on the production of interferon in tissue culture and in the animal. In: GEW Wolstenholme, M O'Connor, eds. Interferon. Little, Brown: Boston, 1967, 218-39.

  8. Taylor-Papadimitriou J. Effects of interferon on cell growth and function. In: I Gresser, ed. Interferon Vol. 2, Academic Press: New York, 1980, 13-46.

  9. Hahon N, Booth JA, Eckert HL. Interferon assessment by the immunofluorescent, immunoperoxidase, and hemadsorption cell-counting techniques. Arch Virol 1975;48:239-43.

  10. Hahon N. Effect of coal rank on the interferon system. Environ Res 1983;30:72-9.

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