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Departments of Environmental Health, Molecular and Cellular Physiology, Medicine, and Civil and Environmental Engineering, University of Cincinnati, Cincinnati, Ohio 45267
Recent studies suggest that genetic variability can influence
irritant-induced lung injury and inflammation. To begin identifying genes controlling susceptibility to inhaled irritants, seven inbred mouse strains were continuously exposed to nickel sulfate
(NiSO4), polytetrafluoroethylene, or ozone
(O3), and survival time was recorded. The A/J (A) mouse
strain was sensitive, the C3H/He (C3) strain was intermediate, and the
C57BL/6 (B6) strain was resistant to NiSO4-induced acute
lung injury. The B6AF1 offspring were also resistant. The
strain sensitivity pattern for NiSO4 exposure was similar
to that of polytetrafluoroethylene or ozone (O3). Pulmonary pathology was comparable for A and B6 mice. In the A strain, 15 µg/m3 of NiSO4 produced 20% mortality. The
strain sensitivity patterns for lavage fluid proteins (B6 > C3 > A) and neutrophils (A 
B6 > C3) differed from
those for acute lung injury. This phenotype discordance suggests that
these traits are not causally linked (i.e., controlled by independent
arrays of genes). As in acute lung injury, B6C3F1 offspring
exhibited phenotypes (lavage fluid proteins and neutrophils) resembling
those of the resistant parental strain. Agreement of acute lung injury
strain sensitivity patterns among irritants suggested a common
mechanism, possibly oxidative stress, and offspring resistance
suggested that sensitivity is inherited as a recessive trait.
acute respiratory distress syndrome; particulate matter; asthma; bronchitis; oxidant; ozone; air pollution; environmental genetics; nickel
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