These are exposure studies associated with the GO term and all of its children.
|Reference||Associated Study Title||Author's Summary||Study Factors||Stressor||Receptors||Country||Medium||Exposure Marker||Measurements||Outcome|
|1.||Clair HB, et al. (2018).||Anniston Community Health Survey (ACHS)||Toxicant-associated steatohepatitis was associated with increased exposures to specific PCB congeners, and the sum of PCBs had associations with insulin, leptin, adipocytokines, and hepatocyte apoptosis.||2,2',3,5,5',6-
||Subjects with disease:Fatty Liver | Subjects with disease:Liver Diseases | Study subjects||United States||serum||2,2',3,4',5',6-
||Details||Fatty Liver | positive regulation of cell death | regulation of apoptotic process|
|2.||Adad LM, et al. (2015).||In this study, we determined the mutagenic and cell death potential of pesticides through the increased frequency of micronuclei and other nuclear abnormalities in exposed individuals||abamectin | copper oxychloride | Dimethoate | glyphosate | Methyl Parathion | Triazines||Workers||Brazil||Details||cholinesterase activity | cytokinetic process | lipid metabolic process | micronucleus organization | nuclear fragmentation involved in apoptotic nuclear change|
|3.||Winckelmans E, et al. (2017).||Flemish Environment and Health Survey (FLEHS I) | Flemish Environment and Health Survey (FLEHS III)||In this exploratory study, we identified mitochondrial genes and pathways associated with particulate air pollution indicating upregulation of energy producing pathways as a potential mechanism to compensate for particulate matter-induced mitochondrial damage.||sex||Particulate Matter||Study subjects||Belgium||air | blood||ECHS1 | ECI2 | ETHE1 | GTPBP3 | MRPL16 | MRPL38 | OGG1 | Particulate Matter | POLG||Details||apoptotic process | electron transport chain | gene expression | mitochondrial genome maintenance | mitochondrial translation | tricarboxylic acid cycle|