Photobiomodulation of the Visual System and Human Health
Abstract
:1. Introduction
2. Spectral Band Terminology
3. Introduction to EM Biological Effects
4. Phototoxicity, Dosimetry, and Action Spectrum of the Visual System
4.1. The Eyelids
4.2. The Cornea
4.3. The Conjunctiva
4.4. The Iris and Crystalline Lens
4.5. The Aqueous Humor and Vitreous Humor
4.6. The Retina
4.7. Other Ophthalmic-Related Effects
5. Photobiomodulation Effects on Human Health
6. Conclusions
Author Contributions
Funding
Conflicts of Interest
Abbreviations
A2E | N-Retinylidene-N-retinylethanolamine |
AMD | Age-related macular degeneration |
ANSI | American National Standards Institute |
ATP | Adenosine triphosphate |
BCC | Basal cell carcinoma |
CIE | Commission Internationale de l’Eclairage |
COVID | Coronavirus disease |
DNA | Deoxyribonucleic acid |
EM | Electromagnetic |
EMR | Electromagnetic radiation |
HEV | High-energy visible (light) |
IR | Infrared |
ISO | International Organization for Standardization |
MERS | Middle East Respiratory Syndrome |
MPE | Maximum permissible exposure |
OSSN | Ocular surface squamous neoplasia |
PAR | Photosynthetically active radiation |
PBM | Photobiomodulation |
PDT | Photodynamic therapy |
POS | Reactive oxygen species |
PUFA | Polyunsaturated fatty acids |
RPE | Retinal pigment epithelium |
SARS | Severe acute respiratory syndrome |
SCC | Squamous cell carcinoma |
UV | Ultraviolet |
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Wavelength | EMR Phototoxicity and Dosimetry of the Lids | |
---|---|---|
Effect | Reference | |
UVB 280 < 315 nm | Average erythemal UV dose of Americans is about 25,000 J/m2/year. | [66] |
3X more carcinogenic than UVA (e.g., squamous cell carcinoma, SCC). | [66] | |
Squamous cell carcinomas account for about 8%, and melanomas about 2%, of all-cause cancer in Croatia. | [67] | |
Basal cell carcinomas (BCC) account for 80–90% of all malignant tumors of the eyelid. | [68] | |
Excess exposure increases risk of erythema, melanogeneisis, DNA damage, immune suppression, photo-aging. | [66] | |
UVB is major cause of sunburn, which is leading risk factor for melanoma and non-melanoma skin cancers. | [66] | |
BCC may be due to strong UVB exposure at a young age, whereas SCC appears due to chronic/cumulative exposure. | [10] | |
UVA 315 < 400 nm | Photoaging: main effect on the lids is sagging skin. | [66] |
Visible 380 < 760 nm | Intense visible (e.g., 532 nm laser pointer) has been shown to cause ecchymosis of upper and lower eyelids. | [69] |
Infrared | Photodynamic therapy (at 634 nm) is an effective treatment for basal cell carcinoma. | [70] |
Thermal radiation can cause burns ranging from mild to third degree and eventually skin death. | [71] | |
Exposure Limits (see text discussion) | UVR 3 mJ/cm2 for 8 h daily to avoid redness (erythemal), and this is one-third to one-quarter of the minimal erythemal dose. | [72] |
Wavelength | EMR Phototoxicity and Dosimetry of the Cornea | |
---|---|---|
Effect | Reference | |
UVC 100 < 280 nm | Momentary exposure to UVC can cause photokeratitis such as welders flash. | [73] |
Susceptibility to photokeratitis may peak at 270 nm with exposure thresholds as low as 3 mJ/cm2. | [74] | |
UVB 280 < 315 nm | 10 h of UVA or 23 min of UVB can cause photokeratitis. | [75] |
UVB absorption is 1.8 times higher in the anterior 100 nm of the human cornea than in the posterior layers. The absorption coefficients of the epithelium and Bowman’s membrane are higher than the stroma, but the stroma absorbs more due to thickness. Tryptophan and ascorbic acid absorb UVB. | [76] | |
300 nm causes apoptosis in all three layers of the cornea and induces keratitis. Apoptosis in all layers of the cornea occurs 5 h after exposure. | [77] | |
UVB light can accelerate the physiological loss of corneal epithelium be two mechanisms, shedding and apoptosis. | [10] | |
The biological damage potential at 295 nm is 375 times more than the biological damage potential at 320 nm. | [78] | |
UVA 315 < 400 nm | Climatic droplet keratopathy—chronic UVA and UVB. | [10] |
Corneal crosslinking: primary treatment for corneal ectatic disease, involves application of vitamin B2 (riboflavin) + 370 nm to stiffen the cornea. | [79] | |
Epithelium: pseudo-keratinization, polyhedral intermediate cells, necrosis, lymphatic infiltration. | [80] | |
Bowman’s membrane: detachment from epithelium, thickened, micro-bleedings. | [80] | |
Stroma: swelling and collagen disorganization, inflammatory cells, angiogenesis blood vessels. | [80] | |
Endothelial detachment. | [80] | |
Visible 380 < 760 nm | Punctate keratitis caused by 532 nm laser pointer. | [69] |
Climatic droplet keratopathy with higher blue (400–500 nm) light exposures, in addition to UVA and UVB. | [81] | |
NIR 760 < 1400 nm | The cornea transmits 96% of incident infrared in the 700–1400 nm range, limiting sensitivity to IR harm, especially in the 750–990 nm range. Significant exposure results in causing protein coagulation which can cause irreversible damage especially on endothelium layer. High-dose IR damage to the cornea causes immediate pain and vascularization, with potential of loss of transparency and opacification in response to burns that causes ulcers. | [71] |
Exposure Limits (see text discussion) | 315–400 nm: 1 J/cm2 for exposure time < 1000 s 1 mW/cm2 for time ≥ 1000 s 180–400 nm: 3 mJ/cm2 pulsed hazard 770–3000 nm 1.8t−0.75 W/cm2 for time < 20 s 0.1 W/cm2 for time > 20 s 1.8t0.25 J/cm2 for time < 45 s | [52] |
Wavelength | EMR Phototoxicity and Dosimetry of the Conjunctiva | |
---|---|---|
Effect | Reference | |
UVC 200–280 nm | Erythema: Although only 1% of 254 nm may penetrate the stratum corneum, mild erythema still results. | [74] |
UVB 280–315 nm | Ocular surface squamous neoplasia (OSSN) declines by 49% for each 10 degree increase in latitude. | [92] |
UVB, UVA and Visible | Pterygium: hyperplasia of the bulbar conjunctiva that grows over the cornea. | [10] |
Pterygium: Associated with long-term exposure to UVA and UVB. | [10] | |
Pterygium: High prevalence between latitudes ± 37 degrees. | [93] | |
Pterygium may initiate by UV-induced changes in corneal epithelial stem cells. | [94] | |
Pinguecula: fibro-fatty degenerative change in bulbar conjunctiva. | [10] | |
Pinguecula: Weak association with long-term UVA and UVB. | [10] | |
Pinguecula: May be a histological link with sun-induced skin changes. | [95] | |
448 nm at 0.8 mW/cm for 6 h resulted in lysosomal membrane permeabilization of the conjunctiva. | [96] | |
Conjunctival UV autofluorescence can be used to accurately determine the time spent outdoors. | [97] | |
Damage of conjunctiva caused by 532 nm laser pointer. | [69] | |
Exposure Limits (see text discussion) | 270 nm: 3 mJ/cm2 within minutes can cause conjunctival injection, chemosis, damaged epithelial cells, and the presence of inflammatory cells. | [98] |
Wavelength | EMR Phototoxicity and Dosimetry of the Crystalline Lens | |
---|---|---|
Phototoxic Effect | Reference | |
UVB 280 < 315 nm | 295–325 nm associated with crystalline lens damage and cataract formation. Cortical and posterior subcapsular cataracts associated with intense 295–325 nm exposure delivered over days. | [72,102] |
315 nm contributes significantly to cataract formation | [102] | |
Risk for cortical cataracts increased 1.6-fold when the cumulative UVB exposure doubled. No association of nuclear cataracts and UVB, or between cataracts and UVA—Chesapeake Bay Study. | [103] | |
Chronic UVB exposure linked to cortical cataract. | [72] | |
Variations in individual behavior can be a reason for up to a 18-fold difference in UVB exposure. | [104] | |
280–315 nm is the most biologically active EM radiation band. | [74] | |
Men with higher levels of average annual UVB were 1.36x more likely to have more severe cortical opacities than men with lower levels. | [105] | |
UVA 315 < 400 nm | If the radiant energy exposure was continuous and if no repair processes occurred, it would take 10 h of UVA to damage the cornea but 26 h to damage the lens. Lens damage due to UVB exposure would take 245 h, but the cornea would be damaged in 23 min. | [106] |
A generalization of the findings indicates that lens damage thresholds for UVA are in the J/cm2 range, and for UVB in the mJ/cm2 range. | [106] | |
315–400 nm accelerates crystalline lens aging. | [102] | |
325 nm at 260 J/cm2 created cataracts in rhesus monkeys. | [107] | |
Infrared | Cataracts induced in rats with 1090 nm, 197 W/cm2, multiple exposure times. | [108] |
Infrared causes lens changes in molecular weight and protein backbone structure, age-related types of cataract. | [109,110] | |
Exposure Limits (see text discussion) | 315–400 nm: 1 J/cm2 for exposure time < 1000 s 1 mW/cm2 for time ≥ 1000 s 180–400 nm: 3 mJ/cm2 pulsed hazard 770–3000 nm 1.8t−0.75 W/cm2 for time < 20 s 0.1 W/cm2 for time > 20 s 1.8t0.25 J/cm2 for time < 45 s | [52] |
Wavelength | EMR Phototoxicity and Dosimetry of the Retina | |
---|---|---|
Effect | Reference | |
UVC 200 < 280 nm | UVC causes time-dependent apoptosis of RPE cells. | [119] |
UVB 280 < 315 nm | UVB energy from 0.2 to 0.4 J/cm2 induces decreased phagocytic activity of RPE cells. | [120] |
UVA 315 < 400 nm | 338 nm: Lipofuscin, a conglomerate of modified lipids and bisretinoids, is susceptible to photochemical changes leading to irreparable cellular damage. | [121] |
A2E, a lipofuscin fluorophore, has two peak absorbance rates, including one in the UVA range at 338 nm. | [121] | |
325 nm can produce retinal lesions. | [122] | |
315–400 nm: AMD linked to strong UVA exposure, mitochondrial DNA and RPE cells are particularly susceptible to 390–400 nm radiation within UVA, 380 nm was noted to cause damage to rat photoreceptor cells—particularly rods. | [123] | |
Patients with macular degeneration have a higher rate of poor tanning ability and glare sensitivity. | [124] | |
The retina was exquisitely susceptible to damage by UVA light, requiring irradiances 50–80 times lower to cause permanent photoreceptor cell damage with this wave-band compared to green light. | [125] | |
Visible 380 < 760 nm | Re-analysis of the Chesapeake Bay watermen study demonstrated an association between blue light exposure and AMD. Individuals with more sunlight exposure are at a significantly increased risk of AMD. | [81,126] |
400–480 induces photoreceptor cell death via apoptosis, consequently killing RPE cells. | [123] | |
400–550 solar retinitis. Violet to blue light can cause temporary conditions such as ‘red vision’ (erythropsia) and reduction in night vision—especially in aphakic patients. | [72,102] | |
400–550 are toxic to the aging retina as it loses antioxidant protection contributing to AMD. | [127] | |
415–555 provided maximum loss of RPE. | [128] | |
390–550 can irradiate lipofuscin, compromising lysosomal integrity and impairing activities of catalase, superoxide dismutase, and cathepsin while inducing lipid peroxidation—ultimately damaging mitochondrial DNA and RPE cells. | [123] | |
Removal of the “blue” component of light significantly decreases retinal damage after high intensity exposure. | [129] | |
Toxicity of “blue” led light and A2E is associated to mitochondrial dynamics impairment in ARPE-19 cells: implications for age-related macular degeneration. | [130] | |
Short-wave light triggers cellular stress responses that may be involved in RPE disease development, which has implications for pathogenesis of AMD. | [131] | |
Short-wave light increases production of reactive oxygen species (ROS), inducing oxidative stress and triggering photoreceptor cell and RPE death, which are risk factors for AMD. | [132] | |
403 nm: regenerates rhodopsin. | [123] | |
404 nm: cytochrome oxidase and RPE inhibited. | [123] | |
430 nm: Maximum A2R excitation degrades RPE cells. | [123] | |
432 nm: Damage to RPE cells via absorbance of all-trans-retinal. | [121] | |
439 nm: Disrupt retina blood barrier in rats. | [123] | |
447 nm: Peak A2E excitation rate harms RPE cells. | [121] | |
448 nm: RPE disruption. | [96] | |
460 nm: greater retinal damage by blue (460 nm) compared to green (530 nm) and red (620 nm) LEDs. | [133] | |
470 nm: Damage to photoreceptor rods and RPE. | [123] | |
488 nm: RPE disruption above ANSI’s photochemical MPE. | [121] | |
Infrared | Thermal damage causing enzymes to denature which contributes to permanent damage to the photoreceptor and RPE. Deep retinal coagulation, may involve choroid. | [71] |
Exposure Limit (see text discussion) | 305–700 nm 2 mW/(cm2 sr) for time > 10,000 s (phakic eye) White light source 0.22 mW/cm2 for time > 10,000 s 380–1400 nm 0.7 W/cm2 for time > 10 s and retinal image diameter > 1.7 mm | [52] |
Wavelength | Ophthalmic-Related Effect | Reference |
---|---|---|
UVA 315–400 nm | Blurred vision: Secondary to photokeratitis. | [136] |
Myopia development: 360–400 nm might be important for both preventing myopia progression and the onset of myopia. | [63] | |
Visible 380 < 760 nm | Migraine sensitivity: 447, 590, and 627 nm aggravates migraines, while 530 nm lessens severity. | [137] |
Glare via fluorescence: Near UV or short visible wavelengths induces a blue green fluorescence, which can be a source of intraocular veiling glare. Exposure to near UV/blue wavelength sources can influence a glare intense enough to reduce visual performance. Exposure to wavelengths longer than 365 nm induce weaker but progresses more towards red color, with 365 nm a lens absorption peak rate. | [138] | |
Filtering 465–480 nm light may lead to a decrease in intraocular pressure by increasing melatonin levels in the anterior chamber. | [116] | |
Chromatic aberration: 2.50 D difference within the eye between violet (360 nm) and red wavelengths (760 nm): may impair high-frequency contrast. | [139] | |
Intrinsically photosensitive ganglion cells peak sensitivity at 480 nm. | [140] | |
Blue haze /visual range: veiling due to short-wave dominant atmospheric haze limits how far an individual can see. | [141] | |
High-intensity (blue or xenon) headlights: induce glare discomfort/disability particularly in older drivers. | [142] | |
Photophobia/glare discomfort: shorter wavelengths are monotonically related to higher photophobic (greater squint) and aversion responses. | [143] | |
Infrared | Infrared may decrease discomfort. | [102] |
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Buch, J.; Hammond, B. Photobiomodulation of the Visual System and Human Health. Int. J. Mol. Sci. 2020, 21, 8020. https://doi.org/10.3390/ijms21218020
Buch J, Hammond B. Photobiomodulation of the Visual System and Human Health. International Journal of Molecular Sciences. 2020; 21(21):8020. https://doi.org/10.3390/ijms21218020
Chicago/Turabian StyleBuch, John, and Billy Hammond. 2020. "Photobiomodulation of the Visual System and Human Health" International Journal of Molecular Sciences 21, no. 21: 8020. https://doi.org/10.3390/ijms21218020