Abstract:Acute exposure guideline levels (AEGLs) have been developed for the chemical warfare agents GB, GA, GD, GF, VX, and sulfur mustard. These AEGLs were approved by the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances after Federal Register publication and comment, and judged as scientifically valid by the National Research Council Committee on Toxicology Subcommittee on AEGLs. AEGLs represent general public exposure limits for durations ranging from 10 min to 8 h, and for t… Show more
“…scrotum, anal region) are highly sensitive to SM vapor (Kehe and Szinicz, 2005). The onset of symptoms depends on the absorbed agent dose and follows Haber's rule, where higher doses are known to shorten the symptom free latency period (Miller et al, 2000;Watson et al, 2006). However, in case of SM, the effect that increasing exposure shortens the latency period is not only governed by Haber's rule, but also influenced by the specific mechanism of SM toxicity: lower-dose exposures to SM predominantly result in DNA damage and effects become evident only after a latency period, when cells undergo cell cycle arrest and possibly apoptosis.…”
“…scrotum, anal region) are highly sensitive to SM vapor (Kehe and Szinicz, 2005). The onset of symptoms depends on the absorbed agent dose and follows Haber's rule, where higher doses are known to shorten the symptom free latency period (Miller et al, 2000;Watson et al, 2006). However, in case of SM, the effect that increasing exposure shortens the latency period is not only governed by Haber's rule, but also influenced by the specific mechanism of SM toxicity: lower-dose exposures to SM predominantly result in DNA damage and effects become evident only after a latency period, when cells undergo cell cycle arrest and possibly apoptosis.…”
“…Such is the case for the CWAs and TICs evaluated in the present assessment (NRC/COT 2002, 2003; Watson et al 2006a,b). …”
Section: Precedents and Sources Of Exposure Guidelinesmentioning
confidence: 65%
“…Army Corps of Engineers Baltimore District 2007; PARSONS 2007; DDESB 2008). These authorities consider the toxicity endpoints and uncertainty factors applied during development of arsine and sulfur mustard AEGL-2 concentrations to be protective (NRC/COT 2000, 2003; Watson et al 2006a). …”
Section: Precedents and Sources Of Exposure Guidelinesmentioning
In the event of a chemical terrorist attack on a transportation hub, post-event remediation and restoration activities necessary to attain unrestricted facility reuse and re-entry could require hours to multiple days. While restoration timeframes are dependent on numerous variables, a primary controlling factor is the level of pre-planning and decision-making completed prior to chemical terrorist release. What follows is the first of a two-part analysis identifying key considerations, critical information, and decision criteria to facilitate post-attack and post-decontamination consequence management activities. A conceptual site model and human health-based exposure guidelines are developed and reported as an aid to site-specific pre-planning in the current absence of U.S. state or Federal values designated as compound-specific remediation or re-entry concentrations, and to safely expedite facility recovery to full operational status. Chemicals of concern include chemical warfare nerve and vesicant agents and the toxic industrial compounds phosgene, hydrogen cyanide, and cyanogen chloride. This work has been performed as a national case study conducted in partnership with the Los Angeles International Airport and The Bradley International Terminal. All recommended guidelines have been selected for consistency with airport scenario release parameters of a one-time, short-duration, finite airborne release from a single source followed by compound-specific decontamination.
“…There is relatively little quantitative data on human inhalation exposures. Some early human exposures performed in 1918 and others performed in 1941–1942 and summarized by Watson (2006) suggest that exposure to SM at concentration × time doses of 1–100 mg × min/m 3 caused increasingly severe ocular effects and skin burns, with some evidence of mucosal exfoliation in the nasopharynx. Early exposures of rabbits summarized in the same review indicated that respiratory lesions occurred at exposures of approximately 600 mg × min/m 3 .…”
Context
sulfur mustard (SM) causes skin blistering and long-term pulmonary dysfunction. Its adverse effects have been studied in battlefield-exposed humans, but lack of knowledge regarding confounding factors makes interpretation challenging. Animal studies are critical to understanding mechanisms, but differences between animals and humans must be addressed. Studies of cultured human cells can bridge animal studies and humans.
Objective
Evaluate effects of SM vapor on airway cells.
Materials and methods
We examined responses of differentiated human tracheal/bronchial epithelial cells, cultured at an air-liquid interface, to SM vapors. SM effects on metabolic activity (Water Soluble Tetrazolium (WST) assay), cytokine and metalloproteinase secretion, and cellular heme oxygenase 1 (HO-1), an oxidative stress indicator, were measured after 24 h.
Results
At noncytotoxic levels of exposure, interleukin 8 and matrix metalloproteinase-13 were significantly increased in these cultures, but HO-1 was not significantly affected.
Discussion and conclusion
Exposure of differentiated airway epithelial cells to sub-cytotoxic levels of SM vapor induced inflammatory and degradative responses that could contribute to the adverse health effects of inhaled SM.
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