Cold Stress and Strain

Abstract

The human body has the thermoregulatory capacity to maintain its body temperature within about 1°C of normal (i.e., 37°C) under a variety of external environmental temperatures. When the body's heat loss to the environment is greater than its ability to maintain its internal homeostatic temperature, the body undergoes cold strain in response to the external cold temperature stress. Prolonged exposure to any temperature less than normal body temperature to which the body's thermoregulatory capacity cannot accommodate may result in cold‐related injuries to tissues or cause other systemic changes, including hypothermia and death. Those injuries may involve local tissue damage that results when the tissue actually freezes (e.g., frostbite) or that can result from nonfreezing conditions in tissue sufficient to cause temporary or permanent vascular damage (e.g., chilblain, immersion foot). Heat loss sufficient to overcome the body's thermoregulatory mechanisms can produce a critical drop in the body's deep‐core temperature and eventually hypothermia and death. Exposure to cold stress may also produce physiological or metabolic changes or shifts in endocrine systems, affect judgment or behavior, or exacerbate existing medical conditions (e.g., cardiovascular disease). For acute exposures, the body's response to cold stress is a function of the rate of heat loss, the temperature to which the individual is exposed, and the duration of exposure. For chronic exposures which produce subtle endocrine and metabolic shifts, the diurnal or seasonal (e.g., circannual) periodicity of that exposure may be more important than the environmental temperature to which the person is exposed. In assessing the impacts of exposures to cold stress, one should differentiate between normal changes that result as the body accommodates to that stress (homeostatic response mechanisms) and actual damage or disruption that result when the body's homeostatic response mechanisms are exceeded.