Proinflammatory effects of cookstove emissions on human bronchial epithelial cells

Abstract

Approximately half the world’s population uses biomass fuel for indoor cooking and heating. This form of combustion typically occurs in open fires or primitive stoves. Human exposure to emissions from indoor biomass combustion is a global health concern, causing an estimated 1.5 million premature deaths each year. Many ‘improved’ stoves have been developed to address this concern; however, studies that examine exposure-response with cleaner-burning, more efficient stoves are few. The objective of this research was to evaluate the effects of traditional and cleaner burning stove emissions on an established model of the bronchial epithelium. We exposed well-differentiated, normal human bronchial epithelial (NHBE) cells to emissions from a single biomass combustion event using either a traditional three-stone fire or one of two energy-efficient stoves. Air-liquid interface cultures were exposed using a novel, aerosol-to-cell deposition system. Cellular expression of a panel of three pro-inflammatory markers was evaluated at 1 and 24 hours following exposure. Cells exposed to emissions from the cleaner burning stoves generated significantly fewer amounts of pro-inflammatory markers than cells exposed to emissions from a traditional, three stone fire. Particulate matter emissions from each cookstove were substantially different, with the three-stone fire producing the largest concentrations of particles (by both number and mass). This study supports emerging evidence that more efficient cookstoves have the potential to reduce respiratory inflammation in settings where solid fuel combustion is used to meet basic domestic needs.

A quantitative model of cookstove variability and field performance: Implications for sample size

“…The variability between users was estimated by comparing total carbon monoxide mass emissions from Water Boiling Test [23] results conducted at different facilities. Each laboratory independently operated a traditional three-stone fire [20,24,25]. Variability between users was estimated by the standard deviation of these independent studies.…”

In vitro exposure to isoprene-derived secondary organic aerosol by direct deposition and its effects on <i>COX-2</i> and <i>IL-8</i> gene expression

“…Other direct deposition studies have also used mRNA transcripts as a proxy for cytokine production (Hawley et al, 2014a, b;Hawley and Volckens, 2013;Volckens et al, 2009;Lichtveld et al, 2012). Changes in IL-8 and COX-2 mRNA levels were measured using a QuantiTect SYBR Green RT-PCR kit (Qiagen) and QuantiTect primer assays for Hs_ACTB_1_SG (catalog no.…”

“…Compared to exposure of cells in culture media to resuspended particles, direct particle deposition likely provides a more biologically relevant exposure model and enhances sensitivity of cells to air pollution particle exposures (Volckens et al, 2009;Lichtveld et al, 2012;Hawley et al, 2014a, b;Zavala et al, 2014;Hawley and Volckens, 2013). The Electrostatic Aerosol in Vitro Exposure System (EAVES) used in this study deposits particles, generated in our outdoor photochemical chamber, directly onto lung cells by electrostatic precipitation (de Bruijne et al, 2009).…”

Reducing Ultrafine Particle Emissions Using Air Injection in Wood-Burning Cookstoves

“…12 Although air injection can decrease total PM mass emitted, it is unclear if this technique reduces the number concentration of all PM emission sizes uniformly and may concurrently increase the number of ultrafine particles per mass of fuel burned, which may be more harmful to human health. 6,13 If total number of ultrafine particles per meal shifts to emit more particles smaller than 50 nm in diameter, then the total deposition of these ultrafine particles is expected to increase in all three primary lung regions: nasal pharyngeal, bronchial, and alveolar. Several researchers [14][15][16][17][18] show that particles smaller than 50 nm in diameter exhibit strong cytotoxicity in lung tissue including oxidative DNA damage and proinflamatory response.…”