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In 2007, the International Agency for Research on Cancer (IARC) convened an expert working group who examined all relevant information and concluded that “Shiftwork that involves circadian disruption is probably carcinogenic to humans (Group 2A).”1 As a key element of their classification, IARC judged that there was “sufficient evidence in experimental animals for the carcinogenicity of light during the daily dark period (biological night) [emphasis added].”1 However, while IARC identified a key role for ‘biological night’ in animals, it is more difficult to define—and work with—a biological night in humans. This editorial suggests ‘how’ we can do this in practice to arrive at an epidemiological measure of circadian disruption.
Remarkably, the key link in the ‘probable’ chain of causation between shift work and cancer, that is, circadian disruption, is nowhere defined in the IARC monograph.1 However, we would expect it to occur in individuals who do work—usually associated with light—at times when their body anticipates—and is prepared for—sleep, that is, at their biological night. The possibly underlying cause of cancer may be conceptualised as consequences of chronodisruption, that is, a relevant disturbance of the circadian organisation of physiology, endocrinology, metabolism and behaviour.2 To understand the mechanisms by which disruptions of activity and rest and of wake and sleep states may contribute to disease will lie in the domain of laboratory studies. However, epidemiologists should also consider the concept of chronodisruption by comparing how much shift work-associated times overlap with workers’ biological nights.3
Biological night has been described as the time when the circadian clock promotes sleep.4 Importantly, humans vary as to when they tend to be awake and asleep in the course of 24 hours. This is evinced and captured by the chronotype …
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