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Ultraviolet and blue light damage

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Dr Stuart Richer
OD PhD FAAO
Director, Ocular Preventative Medicine, James Lovell Federal Health Care Facility, Chicago IL, USA

 

Our sun, modern indoors LED lighting, and mobile phone, tablet and computer displays all emit damaging short wavelength high-energy visible blue radiation, defined as a wavelength band of approximately 445 nm +/- 30 nm. The amount of time spent under artificial blue dominant lighting, in particular, is increasing rapidly in all age groups.1

There is a need to assess the potential damage of not only UV but also this high-energy visible blue radiation band that impacts all ocular tissues. These include the anterior exposed cornea, through the internal tissues of the lens, vitreous and back to the retina.

Ocular exposure to sunlight, UVA and short blue light-emitting sources directed at the human eye results in an immediate inflammatory assault or, over a longer time-frame, combined inflammatory/photo-oxidative induced damage.2 The induction of cataracts and retinal degeneration typically results from long-term exposure.

Chronic exposure is particularly hazardous to infants, youngsters, teens and young adults with clear ocular lenses, but also after the age of 40 years as a result of lessened protective antioxidant systems combined with an increase in UV and visible light-absorbing endogenous chromophores. The latter efficiently produce singlet oxygen and other secondary reactive oxygen species. That is, during photo-oxidation reactions, phototoxic chromophores in the eye absorb light, are excited to a singlet state and then on to a triplet state. The triplet highly energetic state in turn produces free radicals and reactive oxygen species, which in turn damage the delicate DNA and macromolecular structures comprising ocular tissues.2

Cornea and conjunctiva impact

The vulnerable fully-exposed ocular surface tissues (cornea) and surrounding white semi-opaque tissue (conjunctiva) bear the major brunt of radiometric assault by both energetic UV and blue visible radiation.

The shorter the wavelength, the greater the energy, and the potential for biological damage is based on both intensity and duration of that exposure. Most of the UVC (220-280 nm) and some short wavelength UVB (280-320 nm) are filtered by an intact ozone layer. Ultraviolet A (320-420 nm) and visible light (400-700 nm) are typically the most damaging radiation reaching the conjunctiva, and contributing to the development of pinqueculas, a pathological overgrowth of conjunctival epithelium. Radiation not only impacts the cornea but also transverses this tissue itself.

Even on a cloudy day, 60 to 80 per cent of the sun’s rays can pass through the clouds and 50 per cent of the UVA received by the eye comes from reflected surfaces.3 In addition, radiometric data compiled by Wysecki and Stiles suggest that sunlight (6500 K colour temperature) contains as much as 25 per cent blue light. The atmospheric phenomenon of ‘blue haze’ comprises an even greater 40-50 per cent blue light.4

 

216-OL-Figure-1

Figure 1. Absorption and transmission of solar radiation of the eye. The cornea and crystalline lens filter out UVB and most UVA, so that the most energetic light reaching the retina is short wavelength blue-violet light. Image: Blue Light Hazard: report of a roundtable, March 16 2013. NY, NY, USA

 

Lens impact

The primary function of the lens is to transmit undistorted light to the retina. With the exception of aphakic patients and pseudophakic patients, all UV radiation below 295 nm is effectively filtered by the cornea. The human lens absorbs most UVA light, with the exact wavelength absorbed dependent on age. That is, very young lenses transmit UV to the vitreous/retina while ageing biologic lens ‘chromophores’ filter out most of the blue visible spectrum (400-500 nm). These yellow chromophores are 3-hydroxy kynurenine and its glucoside. However, as the lens ages, chromophores that were once protective are biochemically modified, producing phototoxic singlet oxygen.

The lens contains only two types of cells, an anterior lens epithelial layer and lens protein crystalline(s) making up the bulk of lens tissue. With age, there is a decrease in production of antioxidants and antioxidant enzymes combined with a defective ubiquitin lenticular protein repair system. As there is little lens cellular turnover, the process is insidious and cumulative, affecting not only retinal image quality but also the circadian rhythm or ‘biological clock’ serving sleep and endocrine competence. Regardless, the end result is a change in transparency of the lens, with clouding (cataract).

Cataract is the major cause of world-wide legal blindness. UVA and blue radiation induced oxidative stress on the human lens epithelial cells is the most important factor in cataract formation. LED lights having a colour temperature of 7378 K have been shown to cause overproduction of reactive oxygen species of human epithelial lens cells causing severe DNA damage, which triggers G2/M cell mitosis arrest and apoptotic cell arrest.5

Vitreous impact

The vitreous is an extracellular matrix comprising primarily water but also collagens and hyaluronan organised into a homogeneously transparent gel. The naturally ageing human lens limits short wavelength radiation to this tissue, by virtue of chromophores. However, blue light and stray UVA photons are able to reach back into the vitreous cavity. Scientists have not yet explored the role of light in the degeneration of the vitreous and formation of vitreal floaters, but the potential for UV and blue light damage is real.

Retinal impact

Visible light can cause retinal damage by photothermal but especially photochemical mechanisms. Blue light traversing the cornea and lens is able to reach the retina.

This ‘bad blue’ is particularly damaging to young children who do not have the natural build-up of crystalline lens pigment that comes with age to help protect them. As well, most post-operative pseudophakic patients are also vulnerable. Since children do not have the natural build-up of crystalline lens pigment, they need to be wearing blue light lenses and intake vegetables and fruits that are high in antioxidants and dietary carotenoids.

On the macro level, there are three levels of experimental cellular mechanistic evidence in murine (mice) retinal models that blue light is capable of damaging the retina. These include:

  • histological retinal thinning
  • visual electroretinogram degradation
  • immuno-histiochemical probes of increased double strand DNA breaks.6

There is now also putative biochemical and subcellular level evidence for the detrimental effect of blue light. Murine cells irradiated with blue light induce reactive oxygen species (ROS) production, ultimately resulting in apoptosis and photoreceptor cell death by both oxidative and endoplasmic reticulum stress using four distinct processes:7

  • subcellular mitochondrial damage and up-regulation of cytochrome C
  • photoreceptor S-opsin aggregation and endoplasmic reticulum stress
  • cell signalling MAPK activation and nuclear translocation of NF-kappa beta induces caspase activation
  • NF-kappa beta over-stimulation induced autophagy leading to cell death.

Ultimately, another chromophore called lipofuscin builds up in the retina with age and environmental assault. Lipofuscin is formed from incompletely digested photoreceptor outer segments and includes a molecule called A2e, which inhibits subcellular phago-lysosomal degradation of photoreceptor phospholipids. Blue light excites lipofuscin, producing damaging phototoxic singlet oxygen and secondary lipid peroxy radical chain reactions leading to photoreceptor death.

These lines of basic evidence are consistent with the epidemiologic results of The Beaver Dam Study, a longitudinal, population-based study of subjects age 43-86 years examined at baseline and five years later, for risk of age-related macular degeneration (AMD)  against sunlight exposure, using questionnaires.8

Leisure time spent outdoors during teenage and 30-39 years was significantly associated with the risk of early AMD (OR 2.09; 95% CI, 1.19-3.65). There was a protective effect for use of hats and sunglasses during teenage and 30-39 years (OR  0.72; 95% CI, 0.50-1.03). As well, lightly pigmented red-haired or blond-haired subjects were slightly more likely to develop early AMD than people with darker hair (OR 1.33; 95% CI, 0.97-1.83).

Uveal melanoma is the second-most common primary malignancy of the eye world-wide next to childhood retinoblastoma and is the principal fatal intraocular disease in adults. Cumulative epidemiological and experimental evidence now indicates that blue light is a credible risk factor for the development of this cancer.9

Conclusion

Ophthalmic lens manufacturers have embraced blue lens protection with a spectrum of new spectacle products. Those that block both UV and blue light are most desirable. The following population groups deserve protection:

  • infants and toddlers younger than three years with virtually transparent tissue
  • young children and teenagers exposed to blue light displays
  • older patients who have lost their natural ocular lens
  • persons with a family history of AMD or other retinal disease
  • persons on photo-sensitising medications
  • persons in occupations in manufacturing, lighting installation and outdoors work; surgeons, dentists, athletes
  • persons with prolonged exposure to blue light just before bed or ‘iPad insomnia’.

While the damage to the human eye from UV and blue light radiation is going to depend on intensity, chronicity and wavelength, as well as the health and age of the subject, there is an obvious need for ophthalmic radiation-blocking technology. Such protection should begin as early in life as possible. Beginning in middle age, antioxidant protection is depleted, leading to the formation of age-related cataracts and macular degeneration.

Another important consideration is the clinical measurement of macula pigment optical density. The spectrophotometric curve for the dietary (lutein and zeaxanthin)  carotenoids align precisely with the action spectra of damaging ‘bad blue’.  Denser macula pigment improves visual performance, and provides superior driving vision and emerging cognitive benefits while protecting against blue light.10,11 Thousands of practices in the United States and Europe are now offering macula pigment  measurement to their patients.12

The use of UV and blue light blocking lenses, as well as dietary carotenoid supplementation, can have a dramatic effect on the protection of vulnerable ocular human tissues, and make a positive contribution to public health and society.

 

1. The American Optometric Associations, American Eye-Q survey, 2014.

2.  Roberts JE, Dennison J. The photobiology of lutein and zeaxanthin in the eye. J Ophthalmol 2015. Article ID 687173, http://dx.doi.org/10.1155/2015/687173.

3.  Hammond BR Jr, Fletcher LM. Am J Clin Nutr 2012; 96: 1207S-1213S.

4.  Wyszecki G, Stiles WS. Color Science. Wiley 2000; 968 pages.

5.  Xie C1, Li X, Tong J, et al. Effects of white light-emitting diode (LED) light exposure with different correlated color temperatures (CCTs) on human lens epithelial cells in culture. Photochem Photobiol 2014; 90: 4: 853-859.

6.  Sasaki et al. Biological role of lutein induced retinal degeneration. J Nutr Biochem 2012; 23: 5: 423-429.

7.   Kuse Y et al. Damage of photoreceptor-derived cells in culture induced by light emitting diodes. Scientific Reports, 9 June 2014.

8.  Cruickshanks KJ, Klein R, Klein BE, Nondahl DM. Sunlight and the 5-year incidence of early age-related maculopathy: the Beaver Dam Eye Study. Arch Ophthalmol 2001; 119: 246-250.

9.  Logan P, Bernabreu M, Ferreira A, Burnier MN. Evidence for the role of blue light in the development of uveal melanoma. J Ophthalmol 2015. Article ID 386986, http://dx.doi.org/10.1155/2015/386986.

10. Richer S, Park DW, Epstein R, Wrobel JS, Thomas C. Macular re-pigmentation enhances driving vision in elderly adult males with macular degeneration. Clin Exp Ophthalmol 2012; 3: 217. doi:10.4172/2155-9570.1000217

11. Kemin Industries, Inc USA. Methods for Treating Ocular Disorders. US; 9,226,940, 2016.

12. [Internet]. 2016 [cited 3 November 2016]. Available from: http://www.eyepromise.com/doctors/ and www.elektron-healthcare.com/products/macular-pigment-screener.



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