TY - JOUR
T1 - Light at night, chronodisruption, melatonin suppression, and cancer risk
T2 - A review
AU - Reiter, Russel J.
AU - Tan, Dun Xian
AU - Korkmaz, Ahmet
AU - Erren, Thomas C.
AU - Piekarski, Claus
AU - Tamura, Hiroshi
AU - Manchester, Lucien C.
PY - 2007
Y1 - 2007
N2 - Light exposure during the night is becoming progressively more common throughout the world, particularly in areas where electricity is commonly used. Also, the availability of artificial light has allowed humans to work or recreate throughout the 24-hour day. Based on photographs taken of the Earth from outer space, it is also apparent that true darkness is disappearing. For years it was assumed that polluting the daily dark period with light was inconsequential in terms of animal/human physiology. That assumption, however, has proven incorrect. Light at night has two major physiological actions, i.e., it disrupts circadian rhythms and suppresses the production of melatonin by the pineal gland. Moreover, both these changes are light intensity and wavelength dependent. Both human epidemiological and experimental studies on animals have documented that a potential negative consequence of chronodisruption and nocturnal melatonin inhibition is cancer initiation and growth. In epidemiological studies, the frequency of each of the following cancers has been reportedly increased in individuals who routinely work at night or whose circadian rhythms are disrupted for other reasons (e.g., due to jet lag): breast, prostate, endometrial, and colorectal. Likewise, in experimental animals, cancer growth is exaggerated when the animals are repeatedly phase advanced (as occurs during easterly flights) or exposed to light at night. A variety of mechanisms have been examined to explain how the suppression of melatonin exaggerates cancer risk. Mechanistically, how chronodisruption (without a consideration of melatonin suppression) would enhance cancer frequency is less clear. In addition to cancer, there may be other diseases that result from the chronic suppression of melatonin by light at night.
AB - Light exposure during the night is becoming progressively more common throughout the world, particularly in areas where electricity is commonly used. Also, the availability of artificial light has allowed humans to work or recreate throughout the 24-hour day. Based on photographs taken of the Earth from outer space, it is also apparent that true darkness is disappearing. For years it was assumed that polluting the daily dark period with light was inconsequential in terms of animal/human physiology. That assumption, however, has proven incorrect. Light at night has two major physiological actions, i.e., it disrupts circadian rhythms and suppresses the production of melatonin by the pineal gland. Moreover, both these changes are light intensity and wavelength dependent. Both human epidemiological and experimental studies on animals have documented that a potential negative consequence of chronodisruption and nocturnal melatonin inhibition is cancer initiation and growth. In epidemiological studies, the frequency of each of the following cancers has been reportedly increased in individuals who routinely work at night or whose circadian rhythms are disrupted for other reasons (e.g., due to jet lag): breast, prostate, endometrial, and colorectal. Likewise, in experimental animals, cancer growth is exaggerated when the animals are repeatedly phase advanced (as occurs during easterly flights) or exposed to light at night. A variety of mechanisms have been examined to explain how the suppression of melatonin exaggerates cancer risk. Mechanistically, how chronodisruption (without a consideration of melatonin suppression) would enhance cancer frequency is less clear. In addition to cancer, there may be other diseases that result from the chronic suppression of melatonin by light at night.
KW - Cancer
KW - Chronodisruption
KW - Circadian rhythms
KW - Light pollution
KW - Melatonin
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U2 - 10.1615/CritRevOncog.v13.i4.30
DO - 10.1615/CritRevOncog.v13.i4.30
M3 - Review article
C2 - 18540832
AN - SCOPUS:43249103529
SN - 0893-9675
VL - 13
SP - 303
EP - 328
JO - Critical Reviews in Oncogenesis
JF - Critical Reviews in Oncogenesis
IS - 4
ER -