Violation of Allowable Work Intensity does not Augment Acute Kidney Injury Risk During Simulated Occupational Heat Stress
Authors: Hess Hayden , Heikkinen Molly , Hite M. Jo , Tourula Erica , Zoh Roger , Johnson Blair , Hostler David 
Published: May 2024

We recently demonstrated that violation of the National Institute of Occupational Safety and Health (NIOSH) heat stress recommendations by exceeding the allowable wet bulb globe temperature (WBGT) for a given moderate work intensity and work:rest ratio augmented acute kidney injury (AKI) risk. However, the role of work intensity (at a fixed work:rest ratio) on AKI risk during NIOSH compliant and non-compliant scenarios remains largely unknown. This study tested the hypothesis that violating the NIOSH recommendations by exceeding the allowable work intensity at a given WBGT and fixed work:rest ratio would augment AKI risk. Twelve healthy adults completed two NIOSH recommendation compliant trials and one noncompliant trial consisting of a 4 h exposure to a fixed WBGT and work intensity. Work-rest ratio was fixed at 30 min of walking and 30 min of rest each hour. Work intensity (i.e., Hprod) was prescribed as a function of WBGT— 412±51 W (27.3±0.3°C; high intensity compliant [Chigh]), 290±75 W (31.6±0.2°C; low intensity compliant [Clow]), and 410±61 W (31.7±0.2°C; high intensity noncompliant [NChigh]). All subjects were provided 237 mL of sport drink every 15 min and drank ad libitum. TC is presented as peak across the 4 h exposure. Urine samples were collected preexposure, and immediately and 1 h postexposure. Urinary inflammatory (monocyte chemotactic protein-1 [MCP-1]), oxidative stress (thioredoxin 1 [TRX-1]), and AKI risk (the product of insulin-like growth factor-binding protein 7 and tissue inhibitor of metalloproteinase 2 [IGFBP7·TIMP-2]) biomarkers were measured and normalized to urine flow rate. Urinary biomarkers were log transformed before statistical analysis and data are presented as mean ± SD. Peak Tc was higher during the NChigh trial (38.3±0.4°C) compared to the compliant trials (Chigh: 38.0±0.3°C; Clow: 37.8±0.4°C; p≤0.0095). Body weight change from pre- to postexposure did not differ between trials (p=0.7817). MCP-1 increased from pre- to immediately postexposure in all trials (p≤0.0031) but was not different between trials (p=0.1354). TRX-1 increased from pre- to immediately postexposure in all trials (p≤0.0085) but was not different between trials (p=0.6372). [IGFBP7·TIMP-2] increased from pre- to immediately postexposure in all trials (p=0.0454) but the increase was not different between trials (Chigh: -1.7±2.6 LOG [ng/mL2]/1000; Clow: -1.6±2.4 LOG [ng/mL2]/1000; NChigh:-1.2±2.3 LOG [ng/mL2]/1000; p=0.2076). Simulated occupational heat stress elevates AKI risk, likely due to both inflammation and oxidative stress. Violating the NIOSH recommendations by exceeding either the allowable WBGT (i.e., NChigh versus Chigh) or work intensity (i.e., NChigh versus Clow) resulted in a modest elevation in peak Tc but did not modify AKI risk and/or the urinary inflammatory and oxidative stress responses.

RCT: NCT04767347; Supported By: R01OH011528.

This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.