All active, adult kidney transplant centers listed on the UNOS website were eligible for inclusion (194). Centers were called up to 3 times for survey.RESULTS: 122 centers responded. 49 were willing to evaluate incarcerated individuals (34 public, 15 private), 43 willing to list (30 public, 13 private), and 42 willing to transplant (30 public, 12 private). 14 centers said yes, but on a case-by-case basis only. Reported considerations were type of crime, length of sentence, and likelihood of release. Frequently cited reasons for not treating inmates were: inadequate follow-up (28), insurance/funding (16), transportation (12), medication compliance (9), security (8), patient safety (8), and lack of social support (5). 24 centers refused to disclose their policy or did not have one. Two centers claimed incarceration was a contraindication to kidney transplantation.CONCLUSIONS: As prevalence of ESRD increases in the incarcerated population, barriers to transplant for inmates need to be addressed. A lack of understanding of the contraindications to transplant or a lack of knowledge about the prisoner system on behalf of transplant centers may contribute to these barriers. However, there is likely a component of implicit bias and ethical dilemma. We feel as transplant professionals it is our responsibility to assist vulnerable patients in overcoming barriers to transplantation and work to ensure equitable access to organs, regardless of incarceration status.

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Objective Airway exposure to nanoparticles is common in occupational settings. Inhaled nanoparticles have toxic effects on respiratory tissue. Vocal folds are also at direct risk from inhaled nanoparticles. This study investigated the effects of single-walled carbon nanotubes (SWCNT), a type of nanoparticle, on vocal fold epithelium and fibroblasts. These cell types were selected for study since the epithelium is the outer layer of the vocal folds and fibroblasts are the most common cell type in connective tissue underlying the epithelium. Methods Native porcine vocal fold epithelium and cultured human vocal fold fibroblasts were exposed to SWCNTs (100 ng/mL) and control (no SWCNT), in vitro. Epithelial and fibroblast viability were measured using MTT assay. Epithelial barrier integrity was assessed with transepithelial resistance and sodium fluorescein permeability. Epithelial tight junctional protein occludin expression was measured with the Western blot. Gene expressions of the fibroblast specific protein 1 (FSP-1), α-smooth muscle actin (α-SMA), and collagen III (Col-III) were assessed using quantitative polymerase chain reaction. Results Transcriptional expression of genes encoding FSP-1 and Col-III were increased significantly following SWCNT exposure. There were no significant differences between control and SWCNT groups on any of the other measures. Conclusions SWCNT exposure induces vocal fold fibroblasts to a fibrotic phenotype. These data help us understand vocal fold defense mechanisms and lay the groundwork for studying the physiological effects of nanoparticle exposure in vivo.

Objectives/Hypothesis Inhaled pollutants can contact vocal fold tissue and induce detrimental voice changes. Acrolein is a pollutant in cigarette smoke and can also be inhaled during the combustion of fossil fuels, animal fats, and plastics in the environment. However, the vocal fold pathological changes induced by acrolein and the underlying inflammatory pathways are not well understood. These biologic data are needed to understand why voice problems may result from pollutant exposure. Study Design In vivo prospective design with experimental and control groups. Methods Sprague‐Dawley male rats (N = 36) were exposed to acrolein (3 ppm) or filtered air (control) through a whole‐body exposure system for 5 hours/day, for 5 days/week, over 4 weeks. Histopathological changes, presence of edema, expression of proinflammatory cytokines and markers, and the phosphorylation of nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB) were investigated. Results Histological evaluation and quantification demonstrated that subacute acrolein exposure induced significant vocal fold edema. Acrolein exposure also induced epithelial sloughing and cell death. Quantitative polymerase chain reaction showed a significant upregulation of genes encoding interferon regulatory factor and chitinase‐3‐like protein 3. Western blot revealed a 76.8% increase in phosphorylation of NF‐κB P65 after subacute acrolein exposure. Conclusions These findings suggest that 4‐week exposures to 3 ppm acrolein induce vocal fold inflammation manifested as edema, related to the activation of NF‐κB signaling. The edema may underlie the voice changes reported in speakers exposed to pollutants. Level of Evidence NA Laryngoscope, 129:E313–E317, 2019