Vision researchers have seen the damage intense blue light can do in the lab, but whether or not low levels of it can damage the eye over one's lifetime isn't clear cut. Against the backdrop of the development of intraocular lenses with a yellow tint designed to block blue light, this article looks at the research that's been done in search of a connection between blue light and retinal damage.

Acute Exposure
Using animals and tissue culture studies, researchers have made a strong connection between acute blue light exposure and ocular damage.1,2

In 1989, Swedish researchers exposed pigmented rabbits to light from a Xenon lamp for 3.5 hours straight. They passed the light through clear IOL material placed over one eye of each rabbit, and a material with a yellow filter over the other. Through electroretinography, they found that the retinal pigment epithelium and the neuroretina of the eye with the clear IOL sustained more damage. After about six days, the ERG readings returned to normal.3

When researchers postulate a connection between long-term blue light exposure and retinal damage, they often do so by extrapolating the data from these short-term studies and a couple of epidemiologic reports.

"I think chronic blue light is probably damaging," says Joshua Dunaief, MD, who has studied photic damage to the retina at the University of Pennsylvania. "The reason for that belief are the Chesapeake Bay Watermen Study and studies in a variety of animals, from mice to monkeys, that have shown blue light can cause photoreceptor and RPE toxicity. But exactly how they relate to long-term exposure in humans isn't clear, because some of the studies use intensities that are different from what people are exposed to routinely, and the duration is shorter." In his studies, he's exposed RPE cells in culture to a microscope light and then assessed their viability 24 hours later with stains. Blue light caused cell death more readily than green, but, he notes, the intensities are higher than what we're exposed to daily.

There's some evidence that blue light's damage may be related to the lipofuscin fluorophore A2E, a naturally occurring substance in the retina, and the release of free radicals in the RPE. In one study, researchers allowed RPE cells in culture to accumulate differing amounts of the fluorophore, then exposed the cells to 480 nm (blue) or 545 nm (green) light for 15 seconds to a minute.4

They found that nonviable cells were located in blue-light exposed zones of RPE cells that contained A2E, but cells outside those areas were viable. The number of nonviable cells increased with the duration of exposure and as a function of the concentration of the A2E in the cells. Illumination with the green light resulted in more viable cells.

 • The Watermen Study. This 1993 study attempted to bridge the gap between studies of acute and subacute exposure to intense levels of blue light and chronic, lifelong exposure to "normal" levels of blue light.5 The study followed the light exposure of 838 sailors in the oyster fleet of Maryland's Chesapeake Bay.

"In the Watermen Study, we used an occupational group with a very consistent work pattern," says the study's lead author, Hugh Taylor, MD, professor at the University of Melbourne in Australia, and director of the Center of Eye Research Australia. "When I say consistent, I mean consistent over 100 years. The only way you could dredge for oysters in Maryland was under sail.
"The Watermen were unique. First, they were regulated by law and by the seasonal nature of their work. Second, they had the potential for high sunlight exposure."

The study researchers took a series of measurements to work out the amount of light that reached the eyes of the watermen in a variety of different conditions, and they also took a detailed exposure history. Ultimately, they found no association between UV-A or UV-B and macular degeneration, but they did find an association with blue and visible light and ocular damage.

The University of Wisconsin's Beaver Dam Eye study also looked into a connection between sunlight and AMD. The researchers gathered information about sun exposure through a questionnaire at the baseline visit. Additional questions about earlier life patterns of exposure were asked at subsequent follow-up visits. The study doctors found that leisure time spent outdoors in the teenage years and the 30s was significantly associated with an early risk of age-related maculopathy, leading them to believe that there may be an association.6

"The eye seems to have developed a mechanism to protect itself," Dr. Dunaief says. "The reason the macula is yellow is because the compound lutein has deposited in front of the photoreceptors. It's very likely that it's deposited there because it's yellow and it helps protect the photoreceptors and RPE by absorbing blue light."

Lingering Doubts
It's been difficult for experts to definitely establish a connection between long-term exposure to ambient light and AMD, however, because many large-scale studies haven't been able to find one. In light of recent epidemiological studies, for example, Dr. Taylor isn't certain of a connection.

"Though intuitively I'd like to believe that maculopathy occurs over time due to sunlight," he says, "there's no data that I can say confirm it."

Dr. Taylor recently participated in a study in Australia designed to identify the risk factors for age-related maculopathy and AMD. Using 4,744 people from a mix of urban and rural areas, the researchers collected information on such factors as medical history, dietary intake and sun exposure.

The only risk factors uncovered for AMD were age, a history of smoking longer than 40 years and a history of ever taking angiotensin-converting enzyme inhibitors.7

"We used a simplified exposure history based on what had been used in the Watermen Study," says Dr. Taylor. "Because more than 80 percent of the ocular UV-B exposure is acquired during the summer months, we just concentrated on those months for the ocular history, between the hours of 9 and 5. This was a decision made to try to streamline the process because we were doing it on so many more people [than the Watermen Study]. That may have given a bit more noise in the measurement of UV or visible light exposure, but it still ranked the people in the right order."

Similarly, in a study that pooled epidemiologic findings from three major studies to look for trends, smoking emerged as the only preventable risk factor associated with AMD.8

One study even found sun sensitivity to be a confounding factor when its authors looked for a link between sun exposure and AMD. In the case-control study, the researchers compared 409 cases of AMD with 286 control subjects. The authors were surprised to find that, contrary to their original hypothesis, the control subjects had greater median annual ocular sun exposure than the patients with AMD.9

Should Something Be Done?
Despite conflicting reports of damage from everyday exposure to visible light, the damage to animal retinas and RPE cells in culture after acute exposure has generated discussion about blocking blue light in patients who have had their crystalline lenses removed through surgery. This culminated in the recent release of the AcrySof Natural lens (Alcon), which attenuates the transmission of light of wavelengths ranging from approximately 400 nm to around 500 nm.
Some surgeons, however, have reservations about a tinted lens.

"There's mounting evidence that the visual problems of older adults in dim environments increase with age, even when they don't have ocular media or retinal abnormalities," says Martin Mainster, PhD, MD, professor and vice chairman of ophthalmology at the University of Kansas Medical School, referring to a study of night vision and aging.10

"Scotopic (night vision) sensitivity declines more rapidly than photopic (day vision) sensitivity in older adults. Blue light is more important for scotopic than photopic vision because scotopic sensitivity peaks at 506 nm in the blue-green part of the optical spectrum, whereas photopic vision peaks at 555 nm in the green-yellow part." Dr. Mainster explains that this, theoretically, could cause a problem if a lens were designed to protect against long-term exposure damage from the lower intensity, blue-green part of the spectrum, since it might also reduce a patient's night vision. He's written an article for the British Journal of Ophthalmology, currently in press, on the topic of how much blue light an IOL should transmit.

"It's difficult at this time to design an ideal IOL because there's no definitive data on the action spectrum of the retinal phototoxicity potentially involved in AMD or how much blue light older patients need for scotopic activities," he says.

Jim Davison, MD, implanted 80 Natural lenses in 40 patients as part of the 297-patient Alcon U.S. Food and Drug Administration clinical trial. "In the study, there was no difference in color perception in this vs. the standard AcrySof lens," Dr. Davison says.

The trial also compared the contrast sensitivity of patients with the Natural lens to that of patients with the standard AcrySof in photopic and mesopic conditions. "There was no statistically significant difference between the lenses in mesopic or photopic conditions," says Dr. Davison.

"The vision that's attained through this implant is much like the vision the patients had with their natural crystalline lenses before their cataracts developed," says Robert Cionni, MD, another Natural lens investigator. "The light transmission is almost identical to that of a 50-year-old patient. It's not like wearing sunglasses at night."

At this early stage, Dr. Dunaief may speak for some surgeons who are intrigued by the possibility of decreasing a patient's risk of retinal damage with the lens, but are hesitant to be the first ones to implant them routinely.

"I think such a lens is a good idea," says Dr. Dunaief. "I don't think there's really any downside to it. Patients will probably not notice it much, if at all, and it may be protective. The only concerns I'd have is that it's a new device and, while I'm sure it's been tested carefully in preclinical trials, I'm not one to jump on new devices. I kind of like to wait a bit to see how they do for a while." 

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