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.
References
Energy Research Development Administration. Coal extraction
processing and combustion. Publication 116, Argonne National
Laboratory, Argonne, Illinois, 1976; 3:3,16.
Natusch DFS. Potentially carcinogenic species emitted to the
atmosphere by fossil-fuel power plants. Environ Health Persp
1978;22:79-90.
Chrisp CE, Fisher GL, Lammert JE. Mutagenicity of filtrates
from
respirable coal fly ash. Science 1978;199:73-5.
Hahon N, Eckert HL. Depression of viral interferon induction
in
cell monolayers by asbestos fibers. Environ Res 1976;11:52-65.
Hahon N, Booth JA, Wheeler R. Activity of diesel engine
emission
particulates on the interferon system. Environ Res
1982;28:443-55.
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.
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.
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.
Hahon N, Booth JA, Eckert HL. Interferon assessment by the
immunofluorescent, immunoperoxidase, and hemadsorption
cell-counting techniques. Arch Virol 1975;48:239-43.
Hahon N. Effect of coal rank on the interferon system.
Environ
Res 1983;30:72-9.
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