Abstract
Biomass smoke is one of the major air pollutants and contributors of household air pollution worldwide. More than 3 billion people use biomass fuels for cooking and heating, while other sources of exposure are from the occurrence of bushfires and occupational conditions. Persistent biomass smoke exposure has been associated with acute lower respiratory infection (ALRI) as a major environmental risk factor. Children under the age of five years are the most susceptible in developing severe ALRI, which accounts for 940,000 deaths globally. Around 90% of cases are attributed to viral infections, such as influenza, adenovirus, and rhinovirus. Although several epidemiological studies have generated substantial evidence of the association of biomass smoke and respiratory infections, the underlying mechanism is still unknown. Using an in vitro model, primary human lung fibroblasts were stimulated with biomass smoke extract (BME), specifically investigating hardwood and softwood types, and human rhinovirus-16 for 24 h. Production of pro-inflammatory mediators, such as IL-6 and IL-8, were measured via ELISA. Firstly, we found that hardwood and softwood smoke extract (1%) up-regulate IL-6 and IL-8 release (p ≤ 0.05). In addition, human rhinovirus-16 further increased biomass smoke-induced IL-8 in fibroblasts, in comparison to the two stimulatory agents alone. We also investigated the effect of biomass smoke on viral susceptibility by measuring viral load, and found no significant changes between BME exposed and non-exposed infected fibroblasts. Activated signaling pathways for IL-6 and IL-8 production by BME stimulation were examined using signaling pathway inhibitors. p38 MAPK inhibitor SB239063 significantly attenuated IL-6 and IL-8 release the most (p ≤ 0.05). This study demonstrated that biomass smoke can modulate rhinovirus-induced inflammation during infection, which can alter the severity of the disease. The mechanism by which biomass smoke exposure increases inflammation in the lungs can be targeted and inhibited via p38 MAP kinase pathway.
Highlights
Biomass smoke is the result of the combustion of different types of biomass fuels, such as wood, animal dung, crop residues, and coal generated by more than 3 billion people for cooking and heating
We investigated lower concentrations (0.01%, 0.1%, and 1%) of hardwood and softwood smoke extract and found no toxic effects of biomass smoke extract by trypan blue exclusion assays (Figure 2A,B) and LDH assays (Figure 2C,D)
We found a significant increase of both IL-6 and IL-8 release from 1% hardwood and softwood smoke extract stimulation (Figure 3)
Summary
Biomass smoke is the result of the combustion of different types of biomass fuels, such as wood, animal dung, crop residues, and coal generated by more than 3 billion people for cooking and heating. As much as 97% of the population, living in rural areas in the least developed countries, rely solely on biomass fuels for household energy purposes [2]. Several studies have shown that women and children have the highest biomass smoke exposure due to cultural practices, such as indoor cooking in housing with very poor air ventilation [3]. During the burning of these fuels, people indoors can be exposed with up to 30,000 μg/m3 of particulate matter (PM) sized 10 μm or smaller (PM10), while an average concentration throughout the day is approximately 300–5000 μg/m3. Since most women and children stay indoors, they are exposed to these high concentrations of particulate matter and other toxic air pollutants for about 3–7 h a day [6]. The Global Burden of Disease 2010 study found that household air pollution is the second highest risk factor of ill health for women and girls globally [7]
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