The combustion of solid fuels, including coal and biomass, is a main anthropogenic source of atmospheric particulate matter (PM). The hidden costs have been underestimated due to lack of consideration of the toxicity of PM. Here we report the unequal toxicity of inhalable PM emitted from energy use in the residential sector and coal-fired power plants (CFPPs). The incomplete burning of solid fuels in household stoves generates much higher concentrations of carbonaceous matter, resulting in more than one order of magnitude greater toxicity than that from CFPPs. When compared with CFPPs, the residential sector consumed only a tenth of solid fuels in mainland China in 2017, but it contributed about 200-fold higher of the population-weighted toxic potency-adjusted PM2.5 exposure risk. We suggest that PM2.5-related toxicity should be considered when making air pollution emission control strategies, and incomplete combustion sources should receive more policy attention to reduce exposure risks.

Lipid droplets (LDs) are critical for lipid storage and energy metabolism. LDs form in the endoplasmic reticulum (ER). However, the molecular basis for LD biogenesis remains elusive. Here, we show that fat storage–inducing transmembrane protein 2 (FIT2) interacts with ER tubule-forming proteins Rtn4 and REEP5. The association is mainly transmembrane domain based and stimulated by oleic acid. Depletion of ER tubule-forming proteins decreases the number and size of LDs in cells and Caenorhabditis elegans, mimicking loss of FIT2. Through cytosolic loops, FIT2 binds to cytoskeletal protein septin 7, an interaction that is also required for normal LD biogenesis. Depletion of ER tubule-forming proteins or septins delays nascent LD formation. In addition, FIT2-interacting proteins are up-regulated during adipocyte differentiation, and ER tubule-forming proteins, septin 7, and FIT2 are transiently enriched at LD formation sites. Thus, FIT2-mediated nascent LD biogenesis is facilitated by ER tubule-forming proteins and septins.

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