Chronic Inhalation Exposure to Coal Dust and/or Diesel Exhaust:
Effects on the Alveolar Macrophages of Rats
The use of diesel-powered equipment in underground mines has
raised questions regarding possible toxic interactions between coal
dust and diesel emissions. The National Institute for Occupational
Safety and Health (NIOSH) has studied in rats the effects of coal
dust, alone and in combination with diesel engine exhausts, on
physiologic properties of the alveolar macrophages (the pulmonary
cell
that provides the first line of defense against inhaled
particulates)
(1). These pneumocytes were obtained after the animals were
subjected
to chronic exposure to aerosols containing coal dust and/or diesel
exhausts.
The rats were exposed by inhalation for 7 hours a day, 5 days a
week, for 2 years. In addition to a control group (exposed only to
filtered air), groups of rats were exposed to atmospheres
containing 2
mg/m((3)) coal dust, 2 mg/m((3)) diesel particulates, or 1
mg/m((3))
coal dust plus 1 mg/m((3)) diesel particulates. At the end of
exposure, alveolar macrophages were obtained at necropsy by lavage
of
the rat lungs with phosphate-buffered saline, pH = 7.4 (2).
The following physiologic parameters of these cells were
measured: (1) membrane integrity, as indicated by maintenance of a
constant cell volume and absence of protein and lysosomal enzymes
in
acellular fluid from the pulmonary lavage; (2) viability, as
indicated
by lack of affect on cellular protein content, cellular lysosomal
enzyme activity, or oxygen consumption; (3) metabolic activity,
i.e.,
enhanced secretion of reactive forms of oxygen (e.g., superoxide,
hydrogen peroxide, and hydroxyl radical); and (4) morphologic
changes
indicating phagocytic activity, such as "spreading" of the cell and
"ruffling" of its surface, as observed by scanning electron
microscopy.
The results of these tests suggested that chronic exposure to
coal
dust and/or diesel exhaust did not alter the membrane integrity of
the
alveolar macrophages. However, exposure to coal dust activates
alveolar macrophages, while diesel exhaust depresses them. In
other
words, exposure to coal dust in situ increased the number of
macrophages obtained by lavage, enhanced the secretion of reactive
forms of oxygen, and increased cellular spreading. In contrast,
exposure to diesel-engine exhausts resulted in decreased secretion
of
reactive forms of oxygen and less formation of surface ruffling.
The
combination of coal dust and diesel-engine exhausts resulted in
degrees of secretory activity and surface morphology intermediate
between the effects of separate exposures.
Reported by Div of Respiratory Disease Studies, NIOSH, CDC.
Editorial Note
Editorial Note: The data reported here may have implications for
understanding the development of emphysema in coal miners, i.e.,
hypersecretion of reactive forms of oxygen may act to destroy
pulmonary tissue. Furthermore, exposure to diesel-engine exhaust
may
adversely affect the lungs by decreasing the phagocytic capacity of
alveolar macrophages. These laboratory investigations point up the
complexity of predicting the pulmonary response to combined
exposures,
thus emphasizing the need for careful epidemiologic investigations
of
workers exposed to combined coal-diesel emissions.
References
Green GM. The J. Burns Amberson Lecture--In defense of the
lung.
Am Rev Respir Dis 1970;102:691-703.
Myrvik QN, Leake ES, Fariss B. Lysozyme content of alveolar
and
peritoneal macrophages from the rabbit. J Immunol
1961;86:133-6.
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