Written by Angeline A. De Leon, Staff Writer. Blue LED light, when compared to red and green LED light, was more damaging to the retinal nerve cells of the participating mice. 

A growing number of studies continue to highlight the health risk of exposure to light-emitting diode (LED) lighting 1. Animal studies report that exposure to LEDs, especially blue light, is associated with retinal photochemical injury (RPI) 2,3. Blue light is known to induce the formation of reactive oxygen species (ROS) in the mitochondria of retinal cells 4,5, leading to impaired function of outer retinal cells and damage to essential biomolecules 6. Subsequently, light-induced damage is followed by retinal remodeling 7,8. Previous studies have suggested that RPI is a wavelength-dependent effect 2,9,10, with blue light showing the greatest potential to trigger retinal injury 3.  In a 2018 study 11 published in the International Journal of Ophthalmology, investigators sought to describe the risk of retinal photo toxicity associated with specific wavelengths of light (blue, green, red) under the same irradiance level in free-ranging animals.

A total of 202 adult Sprague-Dawley rats were used in the experiment, 40 serving as a control group, while the remaining 162 were divided into three groups and received programmed light exposure. Animals were exposed to single-wavelength blue LEDs (460 nm, irradiance at the level of cornea= 102.3 µW/cm2), green LEDs (530 nm, 102.8 µW/cm2), or red LEDs (620 nm, 102.7 µW/cm2) daily for a total exposure duration of up to 28 days under a 12h-dark/12h-light cycle. Before and after light treatment, rats were anesthetized and both eyes scanned for retinal electrical responses using electroretinography (ERG). At the end of exposure treatment, rats were sacrificed and their eyes removed and stained for histologic analysis (quantifying outer nuclear layer, ONL, and retina morphology alteration). In addition, transmission electron microscopy analysis (TEM) and terminal deoxynucleotidyl transferase duTP nick end labeling (TUNEL) were performed on retinal slices. Western blotting analysis was also conducted, along with immunohistochemical (IHC) staining.

ERG results showed that compared to controls, all three LED groups had a significant decrease in b-wave amplitude by the end of exposure treatment (p < 0.001), but that the blue LED group had the highest function loss after just three days of light exposure (p < 0.001). Histological analysis revealed exposure-induced retinal injuries in light-treated rats, including loss of photoreceptors and inner nuclear layer degeneration. ONL thickness of exposure groups were significantly reduced after 28 days of light exposure (p < 0.01 for green LED, p < 0.05 for red LED), with the blue LED group exhibiting greatest loss (p < 0.001). Apoptotic (cell death) analysis by TUNEL staining showed more apoptotic cells in the retina of exposure groups, as compared to controls, with highest fluorescence intensity (indicating cellular insult) for the blue LED group (p < 0.001). This was corroborated by IHC analysis, which showed that all exposure groups showed higher fluorescence intensity in the ONL, relative to controls, with the blue LED group exhibiting the highest response (p < 0.001 for each of the three antibodies used). Lastly, Western blot analysis revealed that the apoptotic marker PARP-1 showed greater densities after 3 days of blue and green light exposure (p < 0.001, p < 0.01, respectively), with PARP-1 activation showing a 3.8 times higher activation signal, relative to control, after blue light exposure.

Findings of the study confirm the health risk posed by excessive exposure to LED light, suggesting blue light to be the most harmful in terms of ROS production, apoptosis of retinal cells, and morphological alterations of the retina. Based on study evidence, exposure-induced RPE does appear to be wavelength dependent, a factor which should be considered in relation to commercial lighting choices. A notable strength of the present study is its use of a comprehensive methodological approach to studying the phototoxic effects of LED exposure on the retina. Investigators’ decision to allow animals to move freely in the cage during light exposure treatment also adds to the study’s ecological validity. The translation of current findings in a human model of retinal health would be an important next step.

Source: Shang YM, Wang GS, Sliney D, et al. Light-emitting-diode induced retinal damage and its wavelength dependency in vivo. Int J Opthalmol. 2018; 10(2). DOI: 10.18240/ijo.2017.02.03.

The Int. J. of Opthalmol. is an open access peer-reviewed journal.

Click here to read the full text study.

Posted July 29, 2019.

Angeline A. De Leon, MA, graduated from the University of Illinois at Urbana-Champaign in 2010, completing a bachelor’s degree in psychology, with a concentration in neuroscience. She received her master’s degree from The Ohio State University in 2013, where she studied clinical neuroscience within an integrative health program. Her specialized area of research involves the complementary use of neuroimaging and neuropsychology-based methodologies to examine how lifestyle factors, such as physical activity and meditation, can influence brain plasticity and enhance overall connectivity.

References:

  1. Behar-Cohen F, Martinsons C, Viénot F, et al. Light-emitting diodes (LED) for domestic lighting: any risks for the eye? Progress in retinal and eye research. 2011;30(4):239-257.
  2. Jaadane I, Boulenguez P, Chahory S, et al. Retinal damage induced by commercial light emitting diodes (LEDs). Free radical biology and medicine. 2015;84:373-384.
  3. Geiger P, Barben M, Grimm C, Samardzija M. Blue light-induced retinal lesions, intraretinal vascular leakage and edema formation in the all-cone mouse retina. Cell death & disease. 2015;6(11):e1985.
  4. Bravo-Nuevo A, Williams N, Geller S, Stone J. Mitochondrial deletions in normal and degenerating rat retina. Retinal Degenerations: Springer; 2003:241-248.
  5. Huang H, Li F, Alvarez RA, Ash JD, Anderson RE. Downregulation of ATP synthase subunit-6, cytochrome c oxidase-III, and NADH dehydrogenase-3 by bright cyclic light in the rat retina. Investigative ophthalmology & visual science. 2004;45(8):2489-2496.
  6. Donovan M, Cotter T. Caspase-independent photoreceptor apoptosis in vivo and differential expression of apoptotic protease activating factor-1 and caspase-3 during retinal development. Cell death and differentiation. 2002;9(11):1220.
  7. Marc RE, Jones B, Watt C, Vazquez-Chona F, Vaughan D, Organisciak D. Extreme retinal remodeling triggered by light damage: implications for age related macular degeneration. Molecular vision. 2008;14:782.
  8. Jones BW, Marc RE. Retinal remodeling during retinal degeneration. Experimental eye research. 2005;81(2):123-137.
  9. Bennet D, Kim M-G, Kim S. Light-induced anatomical alterations in retinal cells. Analytical biochemistry. 2013;436(2):84-92.
  10. Knels L, Valtink M, Roehlecke C, et al. Blue light stress in retinal neuronal (R28) cells is dependent on wavelength range and irradiance. European Journal of Neuroscience. 2011;34(4):548-558.
  11. Shang Y-M, Wang G-S, Sliney DH, Yang C-H, Lee L-L. Light-emitting-diode induced retinal damage and its wavelength dependency in vivo. International journal of ophthalmology. 2017;10(2):191.