S. Becker et al., EXPOSURE TO NITRIC-ACID STIMULATES HUMAN ALVEOLAR MACROPHAGE FUNCTIONBUT DOES NOT CAUSE INFLAMMATION OR CHANGES IN LUNG-FUNCTION, Inhalation toxicology, 8(2), 1996, pp. 185-200
Nitric acid (HNO3) is common component of air pollution possibly assoc
iated with increased risk for airway infection, airway injury, and inf
lammation. To experimentally address this question, we exposed 9 healt
hy nonsmoking volunteers once to HNO3 vapor (200 mu g/m(3), 0.08 ppm),
and once to filtered air, for 2 h with 100 min of moderate intermitte
nt exercise (ventilation rate 39 L/min). Pulmonary functions (spiromet
ry and airway resistance) were measured, as were subjective symptoms o
f response. Bronchoalveolar lavage (BAL) was performed 18 h after expo
sure, and cells and fluid were analyzed for indicators of airway injur
y and inflammation. As a measure of host defense capability against in
fectious disease, alveolar macrophages (AM) were tested for phagocytos
is of Candida albicans and for susceptibility to infection with respir
atory syncytial virus (RSV). Exposure to HNO3 did not change pulmonary
function nor measures of symptoms. Compared to air-exposed BAL, there
was no significant increase in protein, lactate dehydrogenase, fibron
ectin, prostaglandin E(2), leukotriene B-4, C3a, alpha-l-antitrypsin,
or interleukin 6 in the HNO3-exposed BAL, nor was there an increase in
polymorphonuclear neutrophils (PMN). This indicates that acute exposu
re to environmentally high levels of HNO3 vapor that can be encountere
d in ambient air does not cause permeability changes, cell damage, or
inflammation in the lung. On the other hand, there was a significant i
ncrease in the phagocytic activity of AM after HNO3 exposure. Phagocyt
osis of both unopsonized and serum-opsonized C. albicans was increased
by 85% and 24% respectively. Furthermore, HNO3-exposed AM showed incr
eased resistance to infection with RSV and released 72% less RSV than
AM from subjects exposed to filtered air. Superoxide anion production
in response to adherence was undetectable in the HNO3-exposed AM but w
as produced by the air-exposed cells. Thus, these results suggest that
HNO3 at 0.08 ppm does not cause acute injury in the lung. instead hos
t defense functions of AM such as phagocytic and antiviral activities
are stimulated after HNO3 inhalation.