Chronic Household Air Pollution Exposure Is Associated with Impaired Alveolar Macrophage Function in Malawian Non-Smokers

Abstract

BackgroundHousehold 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.MethodsHealthy 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.ResultsVolunteers 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.ConclusionChronic 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.

Differential exposure and acute health impacts of inhaled solid-fuel emissions from rudimentary and advanced cookstoves in female CD-1 mice

“…PM exposure has also been shown to disrupt alveolar macrophage phagocytosis and intracellular killing (Lee, 2015), not unlike effects observed herein after exposure to the ND stove emissions. Studies of CS-using Malawian adults likewise showed that higher particle loading of macrophages was associated with impaired phagocytosis of pneumococci and mycobacteria (Rylance et al, 2015). Exposure may also disrupt lung barrier defenses and interfere with recruitment of neutrophils, effects similar to that observed in mice of the 3-S fire group.…”

ERS/ATS workshop report on respiratory health effects of household air pollution

“…The increased susceptibility to infection in subjects exposed to HAP is explained by recent ex vivo studies that show carbon loading of human alveolar macrophages results in impaired bacterial phagocytosis and decreased bacterial killing [56]. The degree of impairment is more severe with wood smoke exposure than with fine carbon black and while proteolysis is preserved, oxidative responses are impaired in proportion to smoke exposure [57]. The impairment of oxidative response of the alveolar macrophage allows an explanation of the apparent paradox of the often asymptomatic chronic human exposure to HAP.…”

Inflammatory periosteal reaction on ribs associated with lower respiratory tract disease: A method for recording prevalence from sites with differing preservation

“…This in turn may produce IPR on the ribs. Damage to the lungs caused by particulate matter also increases susceptibility to infectious pulmonary diseases (Rylance et al, ; van Eeden et al, ). Particulate pollution is of increasing concern today and is estimated to cause 4.2 million premature deaths around the world (World Health Organization, ).…”