Data from: Chronic household air pollution exposure is associated with impaired alveolar macrophage function in Malawian non-smokers

Background: Household air pollution in low income countries is an
important cause of mortality from respiratory infection. We hypothesised
that chronic smoke exposure is detrimental to alveolar macrophage
function, causing failure of innate immunity. We report the relationship
between macrophage function and prior smoke exposure in healthy Malawians.
Methods: Healthy subjects exposed daily to cooking smoke at home
volunteered for bronchoalveolar lavage. Alveolar macrophage particulate
content was measured as a known correlate of smoke exposure. Phagocytosis
and intraphagosomal function (oxidative burst and proteolysis) were
measured by a flow cytometric assay. Cytokine responses in macrophages
were compared following re-exposure in vitro to wood smoke, before and
after glutathione depletion. Results: Volunteers had a range of alveolar
macrophage particulate loading. The macrophage capacity for phagosomal
oxidative burst was negatively associated with alveolar macrophage
particulate content (n = 29, r2 = 0.16, p = 0.033), but phagocytosis per
se and proteolytic function were unaffected. High particulate content was
associated with lower baseline CXCL8 release (ratio 0.51, CI 0.29–0.89)
and lower final concentrations on re-exposure to smoke in vitro (ratio
0.58, CI 0.34–0.97). Glutathione depletion augmented CXCL8 responses by
1.49x (CI 1.02–2.17) compared with wood smoke alone. This response was
specific to smoke as macrophages response to LPS were not modulated by
glutathione. Conclusion: Chronic smoke exposure is associated with reduced
human macrophage oxidative burst, and dampened inflammatory cytokine
responses. These are critical processes in lung defence against infection
and likely to underpin the relationship between air pollution and
pneumonia.