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

Abstract

Background: There is an urgent need to provide access to cleaner end user energy technologies for the nearly 40% of the world's population who currently depend on rudimentary cooking and heating systems. Advanced cookstoves (CS) are designed to cut emissions and solid-fuel consumption, thus reducing adverse human health and environmental impacts.

Study premise: We hypothesized that, compared to a traditional (Tier 0) three-stone (3-S) fire, acute inhalation of solid-fuel emissions from advanced natural-draft (ND; Tier 2) or forced-draft (FD; Tier 3) stoves would reduce exposure biomarkers and lessen pulmonary and innate immune system health effects in exposed mice.

Results: Across two simulated cooking cycles (duration ~ 3h), emitted particulate mass concentrations were reduced 80% and 62% by FD and ND stoves, respectively, compared to the 3-S fire; with corresponding decreases in particles visible within murine alveolar macrophages. Emitted carbon monoxide was reduced ~ 90% and ~ 60%, respectively. Only 3-S-fire-exposed mice had increased carboxyhemoglobin levels. Emitted volatile organic compounds were FD ≪ 3-S-fire ≤ ND stove; increased expression of genes involved in xenobiotic metabolism (COX-2, NQO1, CYP1a1) was detected only in ND- and 3-S-fire-exposed mice. Diminished macrophage phagocytosis was observed in the ND group. Lung glutathione was significantly depleted across all CS groups, however the FD group had the most severe, ongoing oxidative stress.

Conclusions: These results are consistent with reports associating exposure to solid fuel stove emissions with modulation of the innate immune system and increased susceptibility to infection. Lower respiratory infections continue to be a leading cause of death in low-income economies. Notably, 3-S-fire-exposed mice were the only group to develop acute lung injury, possibly because they inhaled the highest concentrations of hazardous air toxicants (e.g., 1,3-butadiene, toluene, benzene, acrolein) in association with the greatest number of particles, and particles with the highest % organic carbon. However, no Tier 0-3 ranked CS group was without some untoward health effect indicating that access to still cleaner, ideally renewable, energy technologies for cooking and heating is warranted.

Keywords: Cookstoves; Incomplete combustion; Lung injury; Oxidative stress; Phagocytosis.

Figure 1.

Characterization of cookstove emissions within the NOEC. (A) Example of real-time particle counts generated by the ND stove across the cold start-up and two consecutive water boiling cycles, replicate 1 and 2; (B) mean of the particle volume diameter (nm) assessed by SMPS; (C) mean PM concentrations (μg/M³) for each CS system; (D) relative elemental carbon (EC) and organic carbon (OC) contained in emitted PM; and (E) mean carbon monoxide concentrations (ppm). Figures depict the mean (± SD) of the two replicates for each stove week.

Figure 2.

Volatile chemical speciation from representative canister collected samples of CS emissions. Mean concentrations (ppb) of two replicates for each stove week are depicted for (A) alkanes; (B) alkenes; (C) cyclic hydrocarbons or aromatics; and (D) carbonyl species based on emissions from the FD stove (white bars); ND stove (grey bars with hatching), or 3-S fire (solid black bars).

Figure 3.

Biomarkers of exposure to CS emissions. (A) Blood % carboxyhemoglobin concentrations at 0 h PE; (B) number of particles visible in macrophages obtained via lung lavage at 0, 4, and 24 h PE; and (C) dark field microscopy (40X magnification) images show particles (white dots) within cell boundaries of phagocytic cells at 24 h PE. Data represent the mean (±SE) of n = 8 mice/group for the FD (light bars), ND (grey bars with hatches), and 3-S fire (solid black bars) exposed groups. *Significantly different than the air control group at the corresponding time PE. ^#Significantly different than all other CS groups at the corresponding time PE.

Figure 4.

Cytokine concentrations of (A) IL-1_β and (B) TNF_α present in bronchoalveolar lavage fluid at 4 h PE. Data represent the mean (±SE) of n = 8 mice/group. *Significantly different than the air control group (p < 0.05). ^#Significantly different than all other CS groups (p < 0.05).

Figure 5.

Alterations in steady-state expression of eight genes related to lung inflammatory pathways (TNFα, MIP-2, IL-6), antioxidant status (GCLC, HO-1), or xenobiotic metabolism (COX-2, NQO1, CYP1A1) were evaluated in lung tissue homogenates at 0 h PE. Results are normalized to β-actin, and represent the mean (±SE) of n = 8 mice/group for the FD (light bars with horizontal hatching), ND (grey bars with hatching), and 3-S fire (solid black bars). *Significantly different than the air control group at the corresponding time PE (p < 0.05). ^£Significantly different than the FD stove group at the corresponding time PE (p < 0.05). ^#Significantly different than all other CS groups at the corresponding time PE (p < 0.05).