Abstract
RationaleBiomass is the energy source for cooking and heating for billions of people worldwide. Despite their prevalent use and their potential impact on global health, the effects of these fuels on lung biology and function remain poorly understood.MethodsWe exposed human small airway epithelial cells and C57BL/6 mice to dung biomass smoke or cigarette smoke to compare how these exposures impacted lung signaling and inflammatory and proteolytic responses that have been linked with disease pathogenesis.ResultsThe in vitro exposure and siRNA studies demonstrated that biomass and cigarette smoke activated ERK to up regulate IL-8 and MMP-1 expression in human airway epithelial cells. In contrast to cigarette smoke, biomass also activated p38 and JNK within these lung cells and lowered the expression of tissue inhibitor of matrix metalloproteinase-1 (TIMP-1). Similarly, in the lungs of mice, both biomass and cigarette smoke exposure increased macrophages, activated ERK and p38 and up regulated MMP-9 and MMP-12 expression. The main differences seen in the exposure studies was that mice exposed to biomass exhibited more perivascular inflammation and had higher G-CSF and GM-CSF lavage fluid levels than mice exposed identically to cigarette smoke.ConclusionBiomass activates similar pathogenic processes seen in cigarette smoke exposure that are known to result in the disruption of lung structure. These findings provide biological evidence that public health interventions are needed to address the harm associated with the use of this fuel source.
Highlights
In the developing world, it is estimated that air pollution from biomass smoke accounts for 2.2 to 2.5 million deaths annually [1]
A small but significant increase in endotoxin levels was measured in biomass smoke extract (BSE) at a concentration of 5% (Fig. 2B)
To determine whether the effects of biomass were endotoxin mediated, MMP-1 and IL-8 levels were measured in the BSE and cigarette smoke extract (CSE) before and after endotoxin removal (Fig. 2C)
Summary
It is estimated that air pollution from biomass smoke accounts for 2.2 to 2.5 million deaths annually [1]. Epidemiologic studies have implicated biomass use in the development of chronic obstructive pulmonary disease (COPD) in adults and acute lower respiratory infection in children [2,3]. Women are affected given their daily usage of these fuel sources for cooking. Several studies have found increased markers of inflammation and oxidative stress in premenopausal women exposed to biomass smoke [5,6,7]. It is estimated that three billion people utilize biomass as their primary source of domestic energy [8]. Understanding how biomass smoke affects lung biology and function is an important question that has significant public health implications
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