Exposure to a firefighting overhaul environment without respiratory protection increases immune dysregulation and lung disease risk

Firefighting activities appear to increase the risk of acute and chronic lung disease, including malignancy. While self-contained breathing apparatuses (SCBA) mitigate exposures to inhalable asphyxiates and carcinogens, firefighters frequently remove SCBA during overhaul when the firegrounds appear clear of visible smoke. Using a mouse model of overhaul without airway protection, the impact of fireground environment exposure on lung gene expression was assessed to identify transcripts potentially critical to firefighter-related chronic pulmonary illnesses. Lung tissue was collected 2 hrs post-overhaul and evaluated via whole genome transcriptomics by RNA-seq. Although gas metering showed that the fireground overhaul levels of carbon monoxide (CO), carbon dioxide (CO2), hydrogen cyanine (HCN), hydrogen sulfide (H2S) and oxygen (O2) were within NIOSH ceiling recommendations, 3852 lung genes were differentially expressed when mice exposed to overhaul were compared to mice on the fireground but outside the overhaul environment. Importantly, overhaul exposure was associated with an up/down-regulation of 86 genes with a fold change of 1.5 or greater (p<0.5) including the immunomodulatory-linked genes S100a8 and Tnfsf9 (downregulation) and the cancer-linked genes, Capn11 and Rorc (upregulation). Taken together these findings indicate that, without respiratory protection, exposure to the fireground overhaul environment is associated with transcriptional changes impacting proteins potentially related to inflammation-associated lung disease and cancer.This work was supported by the Department of Homeland Security Fire Prevention and Safety Grant #EMW-2013-FP-00766 to G.H. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Ope

Switching from a high-fat cellulose diet to a high-fat pectin diet reverses certain obesity-related morbidities

Abstract Background Reducing caloric intake is a proven intervention for mitigating and modulating morbidities associated with overnutrition. Caloric restriction is difficult to affect clinically, therefore, dietary interventions that ameliorate the adverse consequences of overnutrition in the presence of a high-calorie diet would be of value. Methods Mice were fed an obesogenic diet containing 60% fat + 10% cellulose (HFC), or a control diet containing 10% fat + 10% cellulose (LFC) for 12 wks. Subgroups of mice were then switched from HFC to each of the following diets for an additional 5 wks: 1) 60% fat + 10% pectin (HFP), 2) LFC or 3) 10% fat + 10% pectin (LFP). To test for statistical differences, one-way or two-way ANOVAs were used with or without repeated measurements as needed. Results In comparison to HFC, HFP prevented additional weight gain while LFC and LFP triggered weight loss of 22.2 and 25.4%, respectively. Mice continued on HFC experienced a weight increase of 26% during the same 5 wk. interval. After 12 wks, HFC decreased mouse locomotion by 18% when compared to control diet, but a diet switch to LFC or LFP restored mouse movement. Importantly, HFP, LFC, and LFP reduced fasting blood glucose when compared to HFC. Likewise, HFP, LFC and LFP improved glucose tolerance and decreased fatty liver by 37.9, 49.8, 53.6 and 20.2%, 37.2, 43.7%, respectively. Conclusions Taken together, the results indicate that the dietary fiber pectin can mitigate some adverse consequences of overnutrition even in the presence of high-fat