RESUMO
The rapid growth of hydraulic fracturing for oil and gas extraction in the U.S. has led to 135 active "frac" sand mines, processing plants, and rail transfer stations in Wisconsin. Potential environmental health risks include increased truck traffic, noise, ecosystem loss, and groundwater, light, and air pollution. Emitted air contaminants include fine particulate matter (PM2.5) and respirable crystalline silica. Inhalation of fine dust particles causes increased mortality, cardiovascular disease, lung disease, and lung cancer. In the authors' pilot study, use of a filter-based ambient particulate monitor found PM2.5 levels of 5.82-50.8 µg/m3 in six 24-hour samples around frac sand mines and processing sites. Enforcement of the existing U.S. Environmental Protection Agency annual PM2.5 standard of 12 µg/m3 is likely to protect the public from silica exposure risks as well. PM2.5 monitoring around frac sand sites is needed to ensure regulatory compliance, inform nearby communities, and protect public health.
Assuntos
Poluentes Atmosféricos/análise , Exposição Ambiental , Monitoramento Ambiental , Fraturamento Hidráulico , Material Particulado/análise , Poluentes Atmosféricos/normas , Humanos , Tamanho da Partícula , Material Particulado/normas , Projetos Piloto , Saúde Pública , Dióxido de Silício/análise , Dióxido de Silício/normas , WisconsinRESUMO
Autophagy, the primary recycling pathway of cells, plays a critical role in mitochondrial quality control under normal growth conditions and in the response to cellular stress. The Hsp90-Cdc37 chaperone complex coordinately regulates the activity of select kinases to orchestrate many facets of the stress response. Although both maintain mitochondrial integrity, the relationship between Hsp90-Cdc37 and autophagy has not been well characterized. Ulk1, one of the mammalian homologs of yeast Atg1, is a serine-threonine kinase required for mitophagy. Here we show that the interaction between Ulk1 and Hsp90-Cdc37 stabilizes and activates Ulk1, which in turn is required for the phosphorylation and release of Atg13 from Ulk1, and for the recruitment of Atg13 to damaged mitochondria. Hsp90-Cdc37, Ulk1, and Atg13 phosphorylation are all required for efficient mitochondrial clearance. These findings establish a direct pathway that integrates Ulk1- and Atg13-directed mitophagy with the stress response coordinated by Hsp90 and Cdc37.