Division of Sleep Medicine, Brigham and Womens Hospital, Boston, Massachusetts 02115; Division of Sleep Medicine, Harvard Medical School, Boston, Massachusetts 02115 (S.W.L., C.A.D.); and Department of Neurology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107 (G.C.B.)
Address correspondence to: Charles A. Czeisler, M.D., Harvard Medical School Brigham and Womens Hospital, Department of Medicine, 221 Longwood Avenue, Boston, Massachusetts 02115-5817. E-mail: caczeisler{at}gcrc.bwh.harvard.edu
Abstract
The endogenous circadian oscillator in mammals, situated in the
suprachiasmatic nuclei, receives environmental photic input from
specialized subsets of photoreceptive retinal ganglion cells. The human
circadian pacemaker is exquisitely sensitive to ocular light exposure,
even in some people who are otherwise totally blind. The magnitude of
the resetting response to white light depends on the timing, intensity,
duration, number and pattern of exposures. We report here that the
circadian resetting response in humans, as measured by the pineal
melatonin rhythm, is also wavelength dependent. Exposure to 6.5 h of
monochromatic light at 460 nm induces a two-fold greater circadian
phase delay than 6.5 h of 555 nm monochromatic light of equal photon
density. Similarly, 460 nm monochromatic light causes twice the amount
of melatonin suppression compared to 555 nm monochromatic light, and is
dependent on the duration of exposure in addition to wavelength. These
studies demonstrate that the peak of sensitivity of the human circadian
pacemaker to light is blue-shifted relative to the three-cone visual
photopic system, the sensitivity of which peaks at 555 nm. Thus
photopic lux, the standard unit of illuminance, is inappropriate when
quantifying the photic drive required to reset the human circadian
pacemaker.