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During this long campaign the Allied and Axis forces fought fiercely for every hill and every village.

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This is a digital copy of a book that was preserved for generations on library shelves before it was carefully scanned by Google as part of a project to make the world's books discoverable online. It has survived long enough for the copyright to expire and the book to enter the public domain. The overall approach, which is illustrated in Figures 2-1 and 2-2, consists of three components (relevant terms are defined in Box 2-1): Later chapters in this report provide details of the types of databases, assays, models, and tools that are available for evaluating acute toxicity, their integration, and next steps that are needed to begin implementing the committee’s framework and strategy. ACUTE TOXICITY OF CLASSICAL CHEMICAL-WARFARE AGENTS Historically, most chemical-warfare agents have belonged to the following chemical classes: nerve agents (such as sarin and soman), blister or vesicant agents (such as phosgene oxime and sulfur mustards), blood agents (such as cyanide), and pulmonary agents (such as chlorine and phosgene) (DHHS 2014). Knowledge of their mechanisms of toxicity can be useful in the development of therapeutic countermeasures (Sharma et al. For example, in vitro methods have been developed for the evaluation of cholinesterase inhibition by nerve-gas agents (Worek et al. Data on some early, sensitive responses to such agents can support development of acute exposure limits for the general public. For example, a number of studies indicate that pupil constriction (miosis) is the most sensitive acute response to human exposure to OP nerve agents (such as sarin), and such end points have been used as part of the basis of acute exposure limits (NRC 2005).

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