BLOG: Light exposure – wavelength, timing, moderation, diligence

A just-published study provides an interesting twist on our current thinking regarding UV light protection.

The results showed that violet light exposure (VL, identified as 360 nm to 400 nm, part of the UV-A spectrum) suppressed myopia progression.

The authors identified myopia as a worldwide growing problem, the incidence doubling in the U.S. and Europe and increasing by 60% in East Asia over the past 50 years.

The study contained two parts. In the first part, they used a chick model, which found that experimentally induced myopia was reduced with VL exposure, suppressing axial length elongation and causing significant upregulation of EGR1, a myopia suppressive gene. Repeating the experiments with blue light (peak wavelength 470 nm), the authors found minimal effect on myopia progression and upregulation of EGR1, while pointing out the danger blue light poses to the retina and circadian disruption.

In the second part, they performed a retrospective study of children wearing VL-protected spectacles and contact lenses versus unprotected children in regard to axial length elongation. Their results showed that children without VL protection had the least amount of axial length elongation, resulting in suppressed myopia progression.

The authors conclude that VL exposure is an important outdoor environmental factor for myopia control, yet many are excluded from exposure due to lack of outdoor activity and excessive UV protection provided in spectacles and contact lenses. In other words, those that are prone to myopia, which is exacerbated by an indoor, near point lifestyle, are made worse through the UV protection included in their refractive correction.

What this study illustrates is that good intentions can have unintended consequences. The ophthalmic lens industry has done an admirable job of developing UV-blocking lenses to protect the eye and ocular adnexa from skin cancers, pinguecula, pterygium, photokeratitis and cataract. Yet perhaps we need part of the UV spectrum for myopia control. The question becomes one of moderation: At what percent transmittance of 360 nm to 400 nm light through a lens and for what daily length of exposure is myopia progression controlled?

As we are in the infancy of understanding the consequences of blue light exposure, the same questions apply. While we know that short wavelength blue light (400 nm to 460 nm) contributes to photo-oxidative retinal damage and chromatic aberration (which contributes to digital eye strain), and that longer wavelength blue light (460 nm to 490 nm) contributes to circadian disruption, at what percent transmittance and at what times of day should 400 nm 500 nm light be regulated by ophthalmic lenses?

Consider that intrinsically photosensitive retinal ganglion cells (ipRGCs) were discovered a mere 15 years ago, and that the intricacies of their function are largely unknown. IpRGCs non-visually sense light through the photopigment melanopsin and have been shown to influence circadian rhythm and pupillary light reflexes, mediate pain avoidance (blinking, squinting) from bright light stimuli and regulate dopamine, influencing mesopic and scotopic vision. Studies also point to a link between circadian clock disruption and the development of psychiatric illnesses, including mood and substance abuse disorders. Yet lenses we are now prescribing for blue light protection may have some effect on ipRGC function.

As a profession, we have historically concentrated on bending light, that is, refraction. It seems we are now coming into a new era of prescribing for attenuation of light. Our good intentions may have unintended consequences.

To be clear, I am not advocating we abandon new blue light filtering technologies. However, it will be up to all of us to stay abreast of developments regarding light attenuation and insist on knowing the spectral transmittance characteristics of lenses we are prescribing and how they may affect our patients. After all, we prudently would not prescribe timolol to a severe asthmatic, would we?

References:

Matynia A. J Exp Neurosci. 2013;7:43-50. doi: 10.4137/JEN.S11267

Parekh PK, et al. Front Psychiatry. 2016;6:187. doi: 10.3389/fpsyt.2015.00187.

Torii H, et al. EBioMedicine. 2017;15:210-219. doi: http://dx.doi.org/10.1016/j.ebiom.2016.12.007.